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Cardiac emergencies 

Cardiac emergencies
Chapter:
Cardiac emergencies
Author(s):

Punit S. Ramrakha

, Kevin P. Moore

, and Amir H. Sam

DOI:
10.1093/med/9780198797425.003.0001
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date: 04 August 2020

Adult basic life support

Basic life support is the backbone of effective resuscitation following a cardiorespiratory arrest. The aim is to maintain adequate ventilation and circulation until the underlying cause for the arrest can be reversed. A duration of 3–4min without adequate perfusion (less if the patient is hypoxic) will lead to irreversible cerebral damage. The usual scenario is an unresponsive patient found by staff who alert the cardiac arrest team. The initial assessment described next should have already been performed by the person finding the patient. The same person should have also started cardiopulmonary resuscitation (CPR). Occasionally, you will be the first to discover the patient and it is important to rapidly assess the patient and begin CPR. The various stages in basic life support are described here and summarized in Fig. 1.1.

Fig. 1.1 Adult basic life support. Send or go for help as soon as possible, according to guidelines. For further information, see the Resuscitation Council (UK) website  http://www.resus.org.uk

Fig. 1.1 Adult basic life support. Send or go for help as soon as possible, according to guidelines. For further information, see the Resuscitation Council (UK) website http://www.resus.org.uk

1. Assessment of the patient

  • Ensure safety of the rescuer and victim.

  • Check whether the patient is responsive. Gently shake the victim and ask loudly, ‘Are you all right?’

    • If the victim responds, place them in the recovery position and get help.

    • If the victim is unresponsive, shout for help and move on to assess airway.

2. Airway assessment

  • Open the airway. With two fingertips under the point of the chin, tilt the head up. If this fails, place your fingers behind the angles of the lower jaw, and apply steady pressure upwards and forwards. Remove ill-fitting dentures and any obvious obstruction. If the patient starts breathing, roll the patient over into the recovery position and try to keep the airway open until an oropharyngeal airway can be inserted (see Fig. 1.2).

  • Keep airway open; look, listen, and feel for breathing. Look for chest movements; listen at the victim’s mouth for breathing sounds, and feel for air on your cheek (for no more than 10s).

    • If the patient is breathing, turn them into the recovery position, check for continued breathing, and get help.

    • If the patient is not breathing or making occasional gasps or weak attempts at breathing, send someone for help. Start rescue breaths by giving two slow, effective breaths, each resulting in a visible rise and fall in the chest wall.

Fig. 1.2 Insertion of an oropharyngeal and nasopharyngeal airway.

Fig. 1.2 Insertion of an oropharyngeal and nasopharyngeal airway.

3. Assessment of circulation

  • Assess signs of circulation by feeling the carotid pulse for no more than 10s.

    • If there are signs of circulation, but no breathing, continue rescue breaths and check for a circulation every 10 breaths (approximately every minute).

    • If there are no signs of circulation, start chest compression at a rate of 100 times per minute. Combine rescue breaths and compression at a rate of 30 compressions to two effective breaths.

  • The ratio of compressions to lung inflation remains the same for resuscitation with two persons.

Adult advanced life support

  • It is unlikely that an effective spontaneous cardiac activity will be restored by basic life support without more advanced techniques (intubation for effective ventilation, drugs, defibrillation, etc.). Do not waste time. As soon as help arrives, delegate CPR to someone less experienced in advanced life support (ALS), so that you are able to continue.

  • Attach the patient to a cardiac monitor as soon as possible to determine the cardiac rhythm, and treat appropriately (Cardiac emergencies Universal treatment algorithm, pp. [link][link]).

  • Oropharyngeal (Guedel) or nasopharyngeal airways help maintain the patency of the airway by keeping the tongue out of the way (see Fig. 1.2). They can cause vomiting if the patient is not comatose. Endotracheal (ET) intubation is the best method of securing the airway. Do not attempt this if you are inexperienced.

  • Establish venous access. Central vein cannulation (internal jugular or subclavian) is ideal but requires more training and practice and is not for the inexperienced. If venous access fails, drugs may be given via an ET tube (ETT) into the lungs (except for bicarbonate and calcium salts). Double the doses of drugs if using this route, as absorption is less efficient than intravenously (IV).

Post-resuscitation care

  • Try to establish the events that precipitated the arrest from the history, staff, witnesses, and hospital notes of the patient. Is there an obvious cause [myocardial infarction (MI), hypoxia, hypoglycaemia, stroke, drug overdose or interaction, electrolyte abnormality, etc.]? Record the duration of the arrest in the notes, with the interventions and drugs (and doses) in chronological order.

  • Examine the patient to check both lung fields are being ventilated. Check for ribs that may have broken during CPR. Listen for any cardiac murmurs. Check the neck veins. Examine the abdomen for an aneurysm or signs of peritonism. Insert a urinary catheter. Consider a nasogastric (NG) tube if the patient remains unconscious. Record the Glasgow Coma Scale (GCS) score (Cardiac emergencies Glasgow Coma Scale, p. [link]), and perform a brief neurological assessment (Cardiac emergencies Coma: assessment, pp. [link][link]).

  • Investigations: electrocardiogram (ECG)—looking for MI, ischaemia, tall T-waves (Cardiac emergencies K+); arterial blood gas (ABG)—mixed metabolic and respiratory acidosis is common and usually responds to adequate oxygenation and ventilation once the circulation is restored. If severe, consider bicarbonate; chest X-ray (CXR)—check position of ETT, look for pneumothorax; urea and electrolytes (U&Es); and glucose.

  • After early and successful resuscitation from a primary cardiac arrest, the patient may rapidly recover completely. The patient must be transferred to the high dependency unit (HDU) or coronary care unit (CCU) for monitoring for 12–24h. Commonly, the patient is unconscious post-arrest and should be transferred to the intensive therapy unit (ITU) for ventilation and haemodynamic monitoring and support for ≥24h.

  • Change any venous lines that were inserted at the time of arrest for central lines inserted with a sterile technique. Insert an arterial line, and consider a pulmonary artery (PA) catheter (Swan–Ganz) if requiring inotropes.

  • Remember to talk to the relatives. Keep them informed of events, and give a realistic (if bleak) picture of the arrest and possible outcomes.

  • When appropriate, consider the possibility of organ donation and do not be frightened to discuss this with the relatives. Even if discussion with the relatives is delayed, remember corneas and heart valves may be used up to 24h after death (Cardiac emergencies Brain death, p. [link]).

Universal treatment algorithm

  • Cardiac rhythms of cardiac arrest can be divided into two groups (see Fig. 1.3):

    • Ventricular fibrillation (VF)/ventricular tachycardia (VT).

    • Non-VF/VT [asystole and pulseless electrical activity (PEA)].

  • The principal difference in treatment of the two groups of arrhythmias is the need for attempted defibrillation in the VF/VT group of patients.

  • Fig. 1.3 summarizes the algorithm for management of both groups of patients.

Fig. 1.3 Adult Advanced Life Support algorithm.

Fig. 1.3 Adult Advanced Life Support algorithm.

Reproduced with the kind permission of the Resuscitation Council (UK), © 2014–19.

VF/VT

VF/VT are the most common rhythms at the time of cardiac arrest. Success in treatment of VF/VT is dependent on prompt defibrillation. With each passing minute in VF, the chance of successful defibrillation declines by 7–10%.

  • Defibrillation in the current guidelines involves a single shock of 150–200J biphasic (or 360J monophasic). Chest compressions should be continued while the defibrillator is charged.

  • Each shock should be immediately followed by CPR, without reassessing the rhythm or feeling for a pulse. This is because if a perfusing rhythm has not been restored, delay in trying to palpate the pulse will further compromise the myocardium. If a perfusing rhythm has been restored, the pulse is rarely palpable immediately after defibrillation, and giving compressions does not enhance the chance of VF recurring. In the event of post-shock asystole, compressions may induce VF.

  • Current guidelines suggest a ratio of 30 chest compressions to 2 breaths. When the airway is secured, chest compressions can be continued without pausing during ventilation.

  • Continue CPR for 2min, and then pause briefly to check the monitor.

  • If VF/VT persists, give a further (2nd shock) of 150–360J biphasic (or 360J monophasic).

  • Resume CPR immediately and continue for 2min, then pause briefly to check the monitor.

  • If VF/VT persists, give a 3rd shock of 150–360J biphasic (360J monophasic) and resume CPR. Give adrenaline 1mg and amiodarone 300mg once chest compressions have restarted.

  • Continue CPR for 2min, then pause briefly to check the monitor.

  • Give adrenaline before alternate shocks (approximately every 3–5min): 1mg IV or via intra-osseous route.

  • In between cycles of defibrillation, reversible factors must be identified and corrected, the patient intubated (if possible), and venous access obtained. If organized electrical activity is seen (when the monitor is checked at points suggested earlier in this algorithm), check for a pulse.

    • If present: start post-resuscitation care.

    • If pulse absent: switch to the non-VF/VT side of the algorithm.

  • Precordial thump. This has a low success rate for cardioversion of a shockable rhythm and is only effective if given within the first few seconds of the onset of a shockable rhythm. It must not delay defibrillation. It is therefore only really appropriate in a witnessed, monitored arrest, e.g. on the CCU or in the cardiac catheter laboratory.

Non-VF/VT (asystole and PEA)

  • The outcome from these rhythms is generally worse than for VF/VT, unless a reversible cause can be identified and treated promptly.

  • Chest compressions and ventilation (30:2) should be undertaken for 2min with each loop of the algorithm. When airway is secured, chest compressions can be continued without pausing during ventilation.

  • Recheck the rhythm after 2min. If organized electrical activity is seen, check for a pulse.

    • If present: start post-resuscitation care.

    • If absent: continue CPR.

    • If VF/VT: change to the VF/VT side of the algorithm.

  • Give adrenaline 1mg IV as soon as intravascular access is achieved and with alternate loops (every 3–5min).

  • In asystole, if P waves are present on the strip/monitor, pacing (external or transvenous) must be considered.

  • Identification of the underlying cause (see Fig. 1.3) and its correction are both vital for successful resuscitation. Resuscitation must be continued while reversible causes are being sought.

Acute coronary syndrome

Acute coronary syndrome (ACS) is an operational term used to describe a constellation of symptoms resulting from acute myocardial ischaemia. An ACS resulting in myocardial injury is termed an MI. ACS includes the diagnosis of unstable angina (UA), non-ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI). The term ACS is generally assigned by ancillary/triage personnel on initial contact with the patient. Guidelines for identification of ACS are summarized on Cardiac emergencies Non-ST-elevation myocardial infarction/unstable angina, pp. [link][link].

Definition

The current nomenclature divides ACS into two major groups, on the basis of delivered treatment modalities (see Fig. 1.4).

  • STEMI: ACS where patients present with ischaemic chest discomfort and ST-segment elevation on ECG. This group of patients must undergo reperfusion therapy on presentation.

  • NSTEMI and UA: ACS where patients present with ischaemic chest discomfort associated with transient or permanent non-ST-elevation ischaemic ECG changes. If there is biochemical evidence of myocardial injury, the condition is termed NSTEMI, and in the absence of biochemical myocardial injury, the condition is termed UA (see Fig. 1.4). This group of patients is not treated with thrombolysis.

Fig. 1.4 Nomenclature of ACS. Patients with ACS may present with or without ST-elevation on the ECG. The majority of patients with ST-elevation (large arrows) ultimately develop Q-wave MI (QwMI), whereas a minority (small arrow) develop a non-Q-wave MI (NQ-MI). Patients without ST-elevation experience either UA or an NSTEMI, depending on the absence or presence of cardiac enzymes (e.g. troponin) detected in the blood.

Fig. 1.4 Nomenclature of ACS. Patients with ACS may present with or without ST-elevation on the ECG. The majority of patients with ST-elevation (large arrows) ultimately develop Q-wave MI (QwMI), whereas a minority (small arrow) develop a non-Q-wave MI (NQ-MI). Patients without ST-elevation experience either UA or an NSTEMI, depending on the absence or presence of cardiac enzymes (e.g. troponin) detected in the blood.

Reprinted from Progress in Cardiovascular Diseases, 46(5), Kamineni R, et al. ‘Acute coronary syndromes: initial evaluation and risk stratification’, 379–92, Copyright 2004, with permission from Elsevier.

Initial management of ACS

  • All patients with suspected ACS should be placed in an environment with continuous ECG monitoring and defibrillation capacity.

  • Give aspirin and clopidogrel (300mg PO of each if no contraindications), and do not give any intramuscular (IM) injections (causes a rise in total creatine kinase (CK) and risk of bleeding with thrombolysis/anticoagulation). There is some evidence that a loading dose of 600mg of clopidogrel achieves quicker platelet inhibition and should be considered for patients going to the cardiac cathlab for immediate percutaneous coronary intervention (PCI).

Immediate assessment should include:

  • Rapid examination to exclude hypotension and note the presence of murmurs, and to identify and treat acute pulmonary oedema.

  • Secure IV access.

  • 12-lead ECG should be obtained and reported within 10min.

  • Give high-flow oxygen (O2) [initially only 28% if history of chronic obstructive pulmonary disease (COPD)].

  • Diamorphine 2.5–10mg IV as required (PRN) for pain relief.

  • Metoclopramide 10mg IV for nausea.

  • Glyceryl trinitrate (GTN) spray two puffs (unless hypotensive).

  • Take blood for:

    • Full blood count (FBC)/U&Es: supplement K+ to keep it at 4–5mmol/L.

    • Glucose: may be acutely elevated post-MI, even in non-diabetics, and reflects a stress–catecholamine response, which may resolve without treatment.

    • Biochemical markers of cardiac injury (see Box 1.4).

    • Lipid profile: total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglycerides.

    • Serum cholesterol and HDL remain close to baseline for 24–48h but fall thereafter and take ≥8 weeks to return to baseline.

  • Portable CXR to assess cardiac size and for pulmonary oedema, and to exclude mediastinal enlargement.

  • General examination should include peripheral pulses, fundoscopy, abdominal examination for organomegaly, and aortic aneurysm.

  • Consider alternative diagnoses (see Box 1.1).

ST-elevation myocardial infarction (STEMI)

Patients with an ACS who have ST-segment elevation/left bundle branch block (LBBB) on their presenting ECG benefit significantly from immediate reperfusion and are treated as one group under the term STEMI.

Presentation

  • Chest pain usually similar in nature to angina, but of greater severity and longer duration, and not relieved by sublingual (SL) GTN. Associated features include nausea and vomiting, sweating, breathlessness, and extreme distress.

  • The pain may be atypical, such as epigastric, or radiate through to the back.

  • Diabetics, the elderly, and hypertensives may suffer painless (‘silent’) infarcts and/or atypical infarction. Women and certain ethnic groups are more likely to have an atypical presentation. Features include breathlessness from acute pulmonary oedema, syncope or coma from arrhythmias, acute confusional states (mania/psychosis), diabetic hyperglycaemic crises, hypotension/cardiogenic shock, central nervous system (CNS) manifestations resembling stroke secondary to sudden reduction in cardiac output, and peripheral embolization.

Management

Diagnosis is normally made on presentation, followed by rapid stabilization to ensure prompt reperfusion therapy. This is in contrast to non-ST-elevation (NSTE)-ACS where the diagnosis may evolve over a period of 24–72h (Cardiac emergencies Non-ST-elevation myocardial infarction/unstable angina, pp. [link][link]). The management principles of the various stages are outlined here and expanded on subsequently (also see Box 1.2).

  • Stabilizing measures are generally similar for all ACS patients (Cardiac emergencies Acute coronary syndrome, pp. [link][link]).

    • All patients with suspected STEMI should have continuous ECG monitoring in an area with full resuscitation facilities.

    • Patients should receive immediate aspirin 300mg PO and clopidogrel 300mg PO (if no contraindications), analgesia, and O2.

    • Rapid examination to exclude hypotension and note the presence of murmurs, and to identify and treat acute pulmonary oedema. Examine for signs of aortic dissection [e.g. aortic regurgitation (AR) murmur, unequal blood pressure (BP) in the arms]. Right ventricular failure (RVF) out of proportion to left ventricular failure (LVF) suggests right ventricular (RV) infarction (Cardiac emergencies Right ventricular infarction, p. [link]).

    • Blood for FBC, biochemical profile, markers of cardiac injury, lipid profile, and glucose, and portable CXR.

  • Diagnosis must be made on the basis of history, ECG (ST-elevation/new LBBB), and biochemical markers of myocardial injury (NB If ECG changes diagnostic, reperfusion must not be delayed to wait for biochemical markers) (Cardiac emergencies STEMI: diagnosis 2, p. [link]). Echocardiography (Echo) can be helpful to look for regional hypokinesia.

  • Treatment:

    • General medical measures (Cardiac emergencies STEMI: general measures, pp. [link][link])

    • Reperfusion (Cardiac emergencies STEMI: reperfusion therapy (thrombolysis) 1, pp. [link][link]).

  • All patients with STEMI should be admitted to the CCU.

  • Discharge and risk prevention (Cardiac emergencies STEMI: predischarge risk stratifi cation, pp. [link][link]).

STEMI: diagnosis 1

This is based on a combination of history, ECG, and biochemical markers of cardiac injury. In practice, history and ECG changes are normally diagnostic, resulting in immediate reperfusion/medical treatment. Biochemical markers of cardiac injury usually become available later and help reconfirm the diagnosis, as well as provide prognostic information (magnitude of rise).

ECG changes

(Also see Box 1.3.)

  • ST-segment elevation occurs within minutes and may last for up to 2 weeks. ST-elevation of ≥2mm in adjacent chest leads and ≥1mm in adjacent limb leads is necessary to fulfil thrombolysis criteria. Persisting ST-elevation after 1 month suggests formation of LV aneurysm. Infarction site can be localized from ECG changes, as indicated in Table 1.1.

  • Pathological Q waves indicate significant abnormal electrical conduction but are not synonymous with irreversible myocardial damage. In the context of a ‘transmural infarction’, they may take hours or days to develop and usually remain indefinitely. In the standard leads, the Q wave should be ≥25% of the R wave and 0.04s in duration, with negative T waves. In the precordial leads, Q waves in V4 should be >0.4mV (four small squares) and in V6 >0.2mV (two small squares), in the absence of LBBB (QRS width <0.1s or three small squares).

  • ST-segment depression (ischaemia at distance) in a 2nd territory (in patients with ST-segment elevation) is secondary to ischaemia in a territory other than the area of infarction (often indicative of multi-vessel disease) or reciprocal electrical phenomena. Overall it implies a poorer prognosis.

  • PR-segment elevation/depression and alterations in the contour of the P wave are generally indicative of atrial infarction. Most patients will also have abnormal atrial rhythms such as atrial fibrillation (AF)/flutter and wandering atrial pacemaker and atrioventricular (AV) nodal rhythms.

  • T-wave inversion may be immediate or delayed and generally persists after the ST-elevation has resolved.

  • Non-diagnostic changes, but the ones that may be ischaemic, include new LBBB or right bundle branch block (RBBB), tachyarrhythmias, transient tall peaked T waves or T-wave inversion, axis shift (extreme left or right), or AV block.

Table 1.1 Localization of infarcts from ECG changes

Anterior

ST elevation and/or Q waves in V1–V4/V5

Anteroseptal

ST elevation and/or Q waves in V1–V3

Anterolateral

ST elevation and/or Q waves in V1–V6, I, and aVL

Lateral

ST elevation and/or Q waves in V5–V6 and T-wave inversion/ST elevation/Q waves in I and aVL

Inferolateral

ST elevation and/or Q waves in II, III, aVF, and V5–V6 (sometimes I and aVL)

Inferior

ST elevation and/or Q waves in II, III, and aVF

Inferoseptal

ST elevation and/or Q waves in II, III, aVF, and V1–V3

True posterior

Tall R waves in V1–V2 with ST depression in V1–V3

T waves remain upright in V1–V2

This can be confirmed with electrodes on the back for a posterior ECG. Usually occurs in conjunction with an inferior or lateral infarct

RV infarction

ST-segment elevation in the right precordial leads (V3R–V4R)

Usually found in conjunction with inferior infarction. This may only be present in the early hours of infarction

STEMI: diagnosis 2

Biochemical markers of cardiac injury

Serial measurements evaluating a temporal rise and fall should be obtained to allow a more accurate diagnosis. CK and creatine kinase-muscle/brain (CK-MB) from a skeletal muscle source tend to remain elevated for a greater time period, in comparison to a cardiac source.

CK

  • Levels twice the upper limit of normal are taken as being abnormal.

  • Serum levels rise within 4–8h post-STEMI and fall to normal within 3–4 days. The peak level occurs at about 24h but may be earlier (12h) and higher in patients who have had reperfusion (thrombolysis or PCI); enzymes from the damaged muscle are ‘washed out’ of the infarcted area with restored circulation.

  • False positive rates of ~15% occur in patients with alcohol intoxication, muscle disease or trauma, vigorous exercise, convulsions, IM injections, hypothyroidism, pulmonary embolism (PE), and thoracic outlet syndrome.

CK-MB isoenzyme is more specific for myocardial disease. Levels may be elevated despite a normal total CK. However, CK-MB is also present in small quantities in other tissues (skeletal muscle, tongue, diaphragm, uterus, and prostate), and trauma or surgery may lead to false positive results. If there is doubt about myocardial injury with CK-MB levels obtained, a cardiac troponin must be measured.

Cardiac troponins (TnT, TnI)

  • Both TnI and TnT are highly sensitive and specific markers of cardiac injury.

  • Serum levels start to rise by 3h post-MI, and elevation may persist up to 7–14 days. This is advantageous for diagnosis of late MI.

  • In most STEMI cases, the diagnosis can be made using a combination of the clinical picture and serial CK/CK-MB levels. In the event of normal CK-MB levels and suspected non-cardiac sources of CK, troponins can be used.

  • Troponins can also be elevated in non-ischaemic myocyte damage such as myocarditis, cardiomyopathy, and pericarditis.

Other markers

There are multiple other markers, but with increasing clinical availability of troponins, measurements are not recommended. These include aspartate transaminase (AST) (rise 18–36h post-MI) and lactate dehydrogenase (LDH) (rise 24–36h post-MI).

The time course of the various markers is seen in Fig. 1.5.

Fig. 1.5 Timing of biomarkers after myocardial infarction.

Fig. 1.5 Timing of biomarkers after myocardial infarction.

Reprinted from Journal of the American College of Cardiology, 48(1), Jaffe AS et al., ‘Biomarkers in acute cardiac disease: the present and the future’, 1–11, Copyright 2006, with permission from the American College of Cardiology Foundation. © 2006 by the American College of Cardiology Foundation.

For key points on non-ACS causes of raised troponin, see Box 1.4.

STEMI: general measures

(See Box 1.6.)

Immediate stabilizing measures

These are as outlined in Cardiac emergencies Acute coronary syndrome, pp. [link][link].

Control of cardiac pain

  • Diamorphine 2.5–10mg IV is the drug of choice and may be repeated to ensure adequate pain relief, unless evidence of emerging toxicity (hypotension, respiratory depression). Nausea and vomiting should be treated with metoclopramide (10mg IV) or a phenothiazine.

  • O2 to be administered at 2–5L/min if O2 saturation <90%. Hypoxaemia is frequently seen post-MI due to ventilation–perfusion abnormalities secondary to LVF. In patients with refractory pulmonary oedema, continuous positive airways pressure (CPAP) or via formal ET intubation may be necessary. Beware of carbon dioxide (CO2) retention in patients with COPD.

  • Nitrates may lessen pain and can be given, providing that the patient is not hypotensive (SL or IV). They need to be used cautiously in inferior STEMI, especially with RV infarction, as venodilation may impair RV filling and precipitate hypotension. Nitrate therapy has no effect on mortality (ISIS-4).

Correction of electrolytes

Both low potassium and magnesium may be arrhythmogenic and must be supplemented, especially in the context of arrhythmias.

Strategies to limit infarct size

β‎-blockade, angiotensin-converting enzyme inhibitor (ACEI), and reperfusion.

Beta-blockade

  • Early β‎-blockade in limiting infarct size, reducing mortality, and early malignant arrhythmias. All patients (including primary PCI and thrombolysis patients) should have early β‎-blockade, but those with the following features will benefit most:

    • Hyperdynamic state (sinus tachycardia, Cardiac emergenciesBP)

    • Ongoing or recurrent pain/reinfarction

    • Tachyarrhythmias such as AF.

  • Absolute contraindications: HR <60bpm, systolic BP (SBP) <100mmHg, moderate to severe heart failure, AV conduction defect, severe airways disease.

  • Relative contraindications: asthma, current use of calcium channel blocker and/or β‎-blocker, severe peripheral vascular disease with critical limb ischaemia, large inferior MI involving the RV.

  • Use a short-acting agent IV initially (metoprolol 1–2mg at a time, repeated at 1- to 2-min intervals to a maximum dose of 15–20mg) under continuous ECG and BP monitoring. Aim for a pulse rate of 60bpm and SBP of 100–110mmHg. If haemodynamic stability continues 15–30min after last IV dose, start metoprolol 50mg three times daily (tds). Esmolol is an ultra-short-acting IV β‎-blocker, which may be tried if there is concern whether the patient will tolerate β‎-blockers.

ACEIs

After receiving aspirin, β‎-blockade (if appropriate), and reperfusion, all patients with STEMI/LBBB infarction should receive an ACEI within the first 24h of presentation.

  • Patients with high-risk/large infarcts, particularly with an anterior STEMI, a previous MI, heart failure, or impaired LV function on imaging (Echo) or those who are elderly will benefit most.

  • The effect of ACEIs appears to be a class effect—use the drug with which you are familiar [e.g. ramipril 1.25mg once daily (od)].

STEMI: reperfusion by primary percutaneous coronary intervention

Time is of the essence for reperfusion, and each institution should have its recommended protocol. It is imperative that there are no delays in both the decision-making and implementation processes for reperfusion. If primary PCI is chosen, one telephone call should ensure a rapid response.

Primary PCI

  • Primary PCI is the current gold standard reperfusion strategy for treatment of STEMI.

  • Primary PCI requires significant coordination between the emergency services, community hospitals, and invasive centres. It must only be performed if:

    • A primary PCI programme is available and

    • The patient presents to an invasive centre and can undergo catheterization without delay.

Indications for primary PCI

  • All patients with chest pain and ST-segment elevation or new LBBB fulfil primary PCI criteria (compare with indications for thrombolysis).

  • This will include a group of patients where ST-segment elevation may not fulfil the thrombolysis criteria.

  • In general, patients in whom thrombolysis is contraindicated should be managed by primary PCI. Cases where there is a significant risk of bleeding must be managed individually.

Outcome in primary PCI

  • Data from >10 large randomized trials demonstrate a superior outcome in patients with STEMI who are treated with primary PCI, in comparison to thrombolysis.

  • There is a significant short-term, as well as long-term, reduction in mortality and major adverse cardiac events (MACE) (death, non-fatal reinfarction, and non-fatal stroke) in STEMI patients treated with primary PCI. Furthermore, primary PCI patients have overall better LV function, a higher vessel patency rate, and less recurrent myocardial ischaemia.

  • Multiple studies (including PRAGUE-2 and DANAMI-2) have also demonstrated that interhospital transportation for primary PCI (community hospital to invasive centre) is safe and primary PCI continues to remain superior to thrombolysis despite the time delays involved.

Complications

  • These include bleeding from arterial puncture site, stroke, recurrent infarction, need for emergency coronary artery bypass graft (CABG), and death, which are similar to high-risk PCI cases (1%).

  • The best results are obtained from high-volume centres with experience of primary PCI.

  • Each primary PCI centre will have its own policy for management of cases, including the use of low-molecular weight heparin (LMWH)/unfractionated heparin (UFH) and antiplatelet agents (e.g. IIb/IIIa). It is generally accepted that, in the acute phase, only the ‘culprit’ lesion(s)/vessel(s) will be treated. The pattern of disease in the remainder of the vessels will determine whether total revascularization should be performed as an inpatient or elective case at some stage in the future.

  • STEMI patients treated with primary PCI can be discharged safely within 72h of admission without the need for further risk stratification.

  • Primary PCI is more cost-effective in the long term, with significant savings from fewer days in hospital, a lower need for readmission, and less heart failure.

  • Post-discharge care, secondary prevention, and rehabilitation remain identical to other MI cases.

Rescue PCI

As an adjunct to thrombolysis, PCI should be reserved for patients who remain symptomatic post-thrombolysis (failure to reperfuse) or develop cardiogenic shock (Cardiac emergencies Cardiogenic shock, pp. [link][link]). We recommend all patients who do not settle post-thrombolysis [ongoing symptoms and ongoing ST elevation with/without symptoms (<50% resolution of ST elevation at 90min post-lysis)] should be discussed with the local cardiac centre for urgent catheterization and revascularization.

For key points on STEMI, see Boxes 1.5 and 1.6.

STEMI: reperfusion therapy (thrombolysis) 1

Reperfusion occurs in 50–70% of patients who receive thrombolysis within 4h of onset of pain (compared with ~20% of controls). As with primary PCI, thrombolysis also results in reduction in mortality, LV dysfunction, heart failure, cardiogenic shock, and arrhythmias. However, the magnitude of the benefits obtained is smaller. Furthermore, patients must undergo cardiac catheterization to delineate their coronary anatomy before revascularization (achieved at the same time with primary PCI). Time is, once again, of paramount importance and thrombolysis should be administered as soon as possible (see Box 1.5).

Indications for thrombolysis

  • Typical cardiac pain within previous 12h and ST elevation in two contiguous ECG leads (>1mm in limb leads or >2mm in V1–V6).

  • Cardiac pain with new/presumed new LBBB on ECG.

  • If ECG is equivocal on arrival, repeat at 15- to 30-min intervals to monitor progression.

  • Thrombolysis should not be given if the ECG is normal or if there is isolated ST depression (must exclude true posterior infarct).

  • Remember patients with diabetes may present with dyspnoea or collapse without chest pain. Look for new ST elevation on the ECG.

  • True posterior infarction presents with ST depression in anterior chest leads (V1–V3), often with ST changes in inferior leads as well. If suspected, administer thrombolysis.

Timing of thrombolysis

  • Greatest benefit is achieved with early thrombolysis (especially if given within 4h of onset of first pain).

  • Patients presenting between 12 and 24h from onset of pain should be thrombolysed if there are any persisting symptoms and/or ST-segment elevation on the ECGs.

  • Patients presenting within 12–24h from the onset of pain whose clinical picture and ECGs appear to have settled should be managed initially as an NSTEMI, followed by early catheterization.

Choice of thrombolytic agent

  • This is partly determined by the local thrombolysis strategy.

  • Allergic reactions and episodes of hypotension are greater with streptokinase (SK).

  • Bolus agents are easier and quicker to administer, with a decrease in drug errors, in comparison to first-generation infusions.

  • Recombinant tissue plasminogen activator (rtPA) has a greater reperfusion capacity and a marginally higher 30-day survival benefit than SK, but an Cardiac emergencies risk of haemorrhage.

  • More recent recombinant plasminogen activator (rPA) derivatives have a higher 90-min TIMI-III flow rate, but similar 30-day mortality benefit to rtPA.

  • An rtPA derivative should be considered for any patient with:

    • Large anterior MI, especially if within 4h of onset

    • Previous SK therapy or recent streptococcal infection

    • Hypotension (SBP <100mmHg)

    • Low risk of stroke (age <55 years, SBP <144mmHg)

    • Reinfarction where immediate PCI facilities are not available.

The characteristics of the major thrombolytic agents are given in Box 1.7.

Patients who gain greatest benefit from thrombolysis

  • Anterior infarct.

  • Marked ST elevation.

  • Age >75 years.

  • Impaired LV function or LBBB, hypotensive.

  • SBP <100mmHg.

  • Patients presenting within 1h of onset of pain.

STEMI: thrombolysis 2

Complications of thrombolysis

  • Bleeding is seen in up to 10% of patients. Most are minor at sites of vascular puncture. Local pressure is sufficient, but occasionally transfusion may be required. In extreme cases, SK may be reversed by tranexamic acid (10mg/kg slow IV infusion).

  • Hypotension during the infusion is common with SK. Lay the patient supine, and slow/stop the infusion until the BP rises. Treatment with cautious (100–500mL) fluid challenges may be required, especially in inferior/RV infarction. Hypotension is not an allergic reaction and does not warrant treatment as such.

  • Allergic reactions are common with SK and include low-grade fever, rash, nausea, headaches, and flushing. Give hydrocortisone 100mg IV, with chlorphenamine 10mg IV.

  • Intracranial haemorrhage is seen in ~0.3% of patients treated with SK and ~0.6% of those with rtPA.

  • Reperfusion arrhythmias (most commonly a short, self-limiting run of idioventricular rhythm) may occur as the metabolites are washed out of the ischaemia tissue (Cardiac emergencies Ventricular tachyarrhythmia post-MI, p. [link]; Cardiac emergencies Bradyarrhythmias and indications for pacing, p. [link]; Cardiac emergencies Bradyarrhythmias post-MI, p. [link]).

  • Systemic embolization may occur from lysis of thrombus within the left atrium (LA), left ventricle (LV), or aortic aneurysm.

Absolute contraindications to thrombolysis

  • Active internal bleeding.

  • Suspected aortic dissection.

  • Recent head trauma and/or intracranial neoplasm.

  • Previous haemorrhagic stroke at any time.

  • Previous ischaemic stroke within the past 1 year.

  • Previous allergic reaction to a fibrinolytic agent.

  • Trauma and/or surgery within the past 2 weeks at risk of bleeding.

Relative contraindications to thrombolysis

  • Trauma and/or surgery >2 weeks previously.

  • Severe uncontrolled hypertension (BP >180/110) with/without treatment.

  • Non-haemorrhagic stroke over 1 year ago.

  • Known bleeding diathesis or current use of anticoagulation within therapeutic range [international normalized ratio (INR) 2 or over].

  • Significant liver or renal dysfunction.

  • Prolonged (>10min) of CPR.

  • Prior exposure to SK (especially previous 6–9 months).

  • Pregnancy or postpartum.

  • LP (lumbar puncture) within previous 1 month.

  • Menstrual bleeding or lactation.

  • History of chronic severe hypertension.

  • Non-compressible vascular punctures (e.g. subclavian central venous lines).

  • Proliferative diabetic retinopathy (risk of intraocular bleed).

Surgery for acute STEMI

Emergency surgical revascularization (CABG) cannot be widely applied to patients who suffer an MI outside of the hospital. CABG in uncomplicated STEMI patients after 6h from presentation is contraindicated secondary to significant haemorrhage into areas of infarction. Unstable patients have a very high perioperative mortality.

CABG in the context of an acute STEMI is of value in the following situations:

  • Persistent or recurrent chest pain despite thrombolysis/primary PCI.

  • High-risk coronary anatomy on catheterization [left main stem (LMS), left anterior descending artery (LAD) ostial disease].

  • Complicated STEMI [acute mitral regurgitation (MR), ventricular septal defect (VSD)].

  • Patients who have undergone successful thrombolysis, but with surgical coronary anatomy on catheterization.

  • Patients known to have surgical coronary anatomy on catheterization performed prior to admission with STEMI.

STEMI: additional measures

Low-molecular weight and unfractionated heparin

LMWH

  • There are trial data for the use of LMWH and thrombolysis [e.g. enoxaparin 30mg IV bolus, then 1mg/kg subcutaneously (SC) every 12h].

  • LMWH can be used at a prophylactic dose to prevent thromboembolic events in patients slow to mobilize, as an alternative to UFH.

UFH

  • There is no indication for ‘routine’ IV heparin following SK.

  • IV heparin [4000U/max. IV bolus, followed by 1000U/h max. adjusted for an activated partial thromboplastin time (APTT) ratio of 1.5–2.0 times control] should be used routinely, following rtPA and its derivatives, for 24–48h.

Clopidogrel (and other antiplatelets, e.g. prasugrel, ticagrelor)

  • The addition of clopidogrel to aspirin and fibrinolytics has been shown to reduce the incidence of death or MACE by 20% at 30 days.

  • If coronary stents are deployed, the patient should remain on dual anti- platelet therapy (DAPT) ideally for 12 months, as for patients with NSTEMI.

Glycoprotein IIb/IIIa inhibitors

  • There does not appear to be any benefit of glycoprotein (GP) IIb/IIIa in combination with full- or reduced-dose thrombolytics in STEMI.

  • GP IIb/IIIa inhibitors are recommended routinely in the context of STEMI patients treated with primary PCI. Best data are with abciximab.

  • They can also be used in the context of rescue PCI, subsequent to failed thrombolysis, although there is a greater risk of bleeding. Each case must be judged on its merits.

Magnesium

  • Earlier trials giving Mg2+ before or with thrombolytics showed some benefit in mortality. ISIS-4 showed no benefit from the routine use of IV Mg2+ post-MI. However, Mg2+ was given late (6h) after thrombolysis, by which time its protective effect on reperfusion injury may have been lost. Trials are ongoing.

  • Current accepted role for Mg2+ is confined to Mg2+-deplete patients and patients with reperfusion, supraventricular, and ventricular arrhythmias.

  • Dose: 8mmol in 20mL of 5% glucose over 20min, followed by 65mmol in 100mL of 5% glucose over 24h (contraindications: serum creatinine >300 micromol/L, third-degree AV block).

Calcium antagonists

  • Best avoided, especially in the presence of LV impairment.

  • Diltiazem and verapamil started after day 4–5 in post-MI patients with normal LV function have a small beneficial effect.

  • Amlodipine is safe to be used in patients with poor LV post-MI.

  • Nifedipine has been shown to increase mortality and should be avoided.

Digoxin

  • Has little role in the management of an acute STEMI and heart failure complicating an acute MI.

  • Can be used safely in the management of arrhythmias and heart rate (HR).

Right ventricular infarction

  • RV infarction results in elevated right-sided pressures [(right atrial (RA), right ventricular end-diastolic pressure (RVEDP)] and low left-sided pressures [BP, cardiac output (CO)].

  • It is common in inferior STEMI.

Diagnosis

  • Clinical: signs of right heart failure (Cardiac emergenciesJVP, Kussmaul’s sign, pulsus paradoxus), with absence of pulmonary oedema, in the context of a low output state (Cardiac emergenciesBP, cold peripheries).

  • ECG: in patients with inferior STEMI, a 0.1mV (>1mm) ST-segment elevation in any one of leads V4R–V6R is highly sensitive and specific for RV infarction. See Fig. 1.6 for different ECG patterns identified in right-sided precordial leads. Changes may be transient and present in the early stages only.

  • Echo: looking for RV dilatation and wall motion abnormalities.

Fig. 1.6 ST elevation and T-wave configuration in lead V4R in inferoposterior acute MI. Proximal occlusion of the RCA produces ST elevation of ≥1mm and a positive T wave. Distal occlusion is characterized by a positive T wave, but no ST elevation. Occlusion of the circumflex artery produces a negative T wave and ST depression of at least 1mm.

Fig. 1.6 ST elevation and T-wave configuration in lead V4R in inferoposterior acute MI. Proximal occlusion of the RCA produces ST elevation of ≥1mm and a positive T wave. Distal occlusion is characterized by a positive T wave, but no ST elevation. Occlusion of the circumflex artery produces a negative T wave and ST depression of at least 1mm.

From N Engl J Med, Wellens HJ, ‘The value of the right precordial leads of the electrocardiogram’, 340, 381–3. Copyright © 1999 Massachusetts Medical Society. Reprinted with permission from Massachusetts Medical Society.

Management

  • Aim to maintain a high RV preload:

    • Initially give 1–2L of colloid rapidly.

    • Avoid use of nitrates and diuretics, as they reduce preload and can worsen hypotension.

    • In patients requiring pacing, AV synchrony must be maintained to ensure maximal CO (atrial and ventricular wires).

    • Cardiovert any arrhythmias [supraventricular tachycardia (SVT), AF/flutter, or ventricular rhythms].

  • Reduce afterload:

    • This is particularly important if there is concomitant LV dysfunction.

    • Insert intra-aortic balloon pump (IABP).

    • Arterial vasodilators (sodium nitroprusside, hydralazine) or ACEIs can be used with caution.

  • Inotropic support should ideally be avoided and used only if all other measures fail to restore the haemodynamic status.

  • Reperfusion of the right coronary artery (RCA) (PCI or thrombolysis) has been demonstrated to improve RV function and reduce mortality.

STEMI: predischarge risk stratification

It is important to identify the subgroup of patients who have a high risk of reinfarction or sudden death. They should undergo coronary angiography, with a view to revascularization prior to discharge (if not treated with primary PCI), and/or electrophysiological investigations as necessary (see Fig. 1.7).

Fig. 1.7 Suggested strategy post-STEMI in patients who have undergone thrombolysis to determine the need for inpatient angiography/electrophysiological studies.

Fig. 1.7 Suggested strategy post-STEMI in patients who have undergone thrombolysis to determine the need for inpatient angiography/electrophysiological studies.

Source: data from Antman EM (2000). Cardiovascular Therapeutics, 2nd edn. Saunders, Philadelphia, PA.

Primary PCI group

  • STEMI patients treated with primary PCI are at a much lower risk of developing post-MI complications.

  • There is ongoing debate about whether patients treated with primary PCI should have total revascularization as an inpatient or whether this can be achieved after functional testing on an outpatient basis. Follow your local policy.

  • Patients who should have electrophysiological assessment prior to discharge are listed under Cardiac emergencies Electrophysiological study, p. [link].

Thrombolysis group

Patients treated with thrombolysis should be risk-stratified prior to discharge, and high-risk patients should have inpatient (or early outpatient) angiography. High-risk patients include those with:

  • Significant post-infarct angina or UA.

  • Positive exercise test (modified Bruce protocol) with angina, >1mm ST depression, or fall in BP.

  • Cardiomegaly on CXR, poor LV function on Echo [ejection fraction (EF) <40%].

  • Documented episodes of regular ventricular extrasystoles (VEs) and VT 24h post-infarction.

  • Frequent episodes of silent ischaemia on Holter monitoring.

Electrophysiological study

All STEMI patients with (1) non-sustained VT and documented EF <40% or (2) sustained/pulseless VT/VF (regardless of EF) should undergo electrophysiological testing prior to discharge (MADIT and MUSTT trials), with a view to defibrillator implantation.

Discharge and secondary prevention

  • Length of hospital stays in uncomplicated patients. The thrombolysis group needs to undergo risk stratification prior to discharge and tends to have a mean hospital stay of 5–7 days. The primary PCI group has a shorter hospital stay of between 3 and 4 days.

  • Prior to discharge, an agreed plan between patient (and patient’s family) and physician is necessary to address modifiable risk factors, beneficial medication, and rehabilitation programme.

  • Modifiable risk factors include:

    • Management of lipids and use of statins

    • Detection and treatment of diabetes

    • Ensuring BP is adequately controlled

    • Counselling to discontinue smoking

    • Advice on a healthy diet and weight loss.

  • It is vital patients understand the medical regimen and, in particular, the importance of long-term ‘prognostic medication’. Unless there are contraindications, all patients should be on a minimum of:

    • Aspirin 75mg od (if true allergy, use clopidogrel 75mg od alone)

    • Clopidogrel 75mg od (for 12 months)

    • ACEI at the recommended dosage

    • Statin at the recommended dosage

    • The role of long-term formal anticoagulation is controversial.

  • All patients must be offered a cardiac rehabilitation programme.

STEMI: complications

Complications

  • Continuing chest pain.

  • Fever.

  • New systolic murmur: VSD, acute MR, or pericarditis.

  • Arrhythmia: VT, AV block ectopics, and bradycardia.

  • Pump failure: hypotension, cardiac failure, and cardiogenic shock.

Complications are encountered more commonly in patients post-STEMI but can also be found in NSTEMI patients (Cardiac emergencies Non-ST-elevation myocardial infarction/unstable angina, pp. [link][link]). In NSTEMI patients, complications are more common where multiple cardiac events have occurred.

Further chest pain

  • Chest pain post-MI is not necessarily angina. A careful history is needed to characterize the pain. If there is doubt about the aetiology of the pain in the absence of ECG changes, stress/thallium imaging may aid diagnosis.

  • A bruised sensation and musculoskeletal pain are common in the first 24–48h, especially in patients who have received CPR or repeated direct current (DC) shock. Use topical agents for skin burns.

  • Recurrent infarction is an umbrella term including both extension of infarction in the original territory and repeated infarct in a 2nd territory.

    • Usually associated with recurrent ST elevation.

    • If cardiac enzymes are not yet back to normal, a significant change is a 2-fold rise above the previous nadir.

    • Patients should ideally undergo immediate PCI. Thrombolysis is an alternative, but a less attractive, approach. Standard thrombolysis criteria must be met (Cardiac emergencies STEMI: reperfusion therapy (thrombolysis) 1, pp. [link][link]). Bleeding is a risk (NB SK should not be used on a 2nd occasion).

  • Post-infarction angina (angina developing within 10 days of MI) should be treated with standard medical therapy. All patients with angina prior to discharge should undergo cardiac catheterization and revascularization as an inpatient.

  • Pericarditis presents as sharp, pleuritic, and positional chest pain, usually 1–3 days post-infarct. It is more common with STEMI. A pericardial friction rub may be audible. ECG changes are rarely seen. Treat with high-dose aspirin [600mg four times daily (qds) PO], covering with a proton pump inhibitor (PPI) (e.g. lansoprazole 30mg od PO). Other NSAIDs have been associated with a higher incidence of LV rupture and Cardiac emergencies coronary vascular resistance and are probably best avoided.

  • Pericardial effusion is more common with anterior MI, especially if complicated by cardiac failure. Tamponade is rare and the result of ventricular rupture and/or haemorrhagic effusions. Detection is with a combination of clinical features and Echo. Most small effusions resolve gradually over a few months, with no active intervention.

  • Pulmonary thromboembolism can occur in patients with heart failure and prolonged bed rest. Routine use of prophylactic LMWH and UFH, combined with early mobilization, has a reduced incidence of PE. Sources include lower limb veins and/or the RV (Cardiac emergencies Pulmonary embolism (PE): assessment, p. [link]).

  • Fever may be seen and peaks 3–4 days post-MI. It is associated with an elevated white cell count (WCC) and raised C-reactive protein (CRP). Other causes of fever should be considered—infection, thrombophlebitis, venous thrombosis, drug reaction, and pericarditis.

Ventricular septal defect post-myocardial infarction (MI)

  • Classically seen 24h (highest risk) to 10 days post-MI and affects 2–4% of cases.

  • Clinical features include rapid deterioration, with a harsh pan-systolic murmur (maximal at the lower left sternal edge), poor perfusion, and pulmonary oedema. The absence of a murmur in the context of a low output state does not rule out a VSD.

Diagnosis

  • Echocardiography: the defect may be visualized on two-dimensional (2D)-Echo, and colour flow Doppler shows the presence of left-to-right shunt. Anterior infarction is associated with apical VSD, and inferior MI with basal VSD. Failure to demonstrate a shunt on Echo does not exclude a VSD.

  • PA catheter (especially in the absence of Echo or inconclusive Echo results): a step-up in O2 saturation from RA to RV confirms the presence of a shunt, which may be calculated by:

    Qp:Qs=(Art sat RA sat)(ArtsatPAsat)

    where Qp = pulmonary blood flow; Qs = systemic blood flow.

  • Cardiovascular magnetic resonance imaging (MRI) can visualize the VSD but also allow for accurate calculation of the Qp:Qs.

Management

Stabilization measures are all temporizing until definitive repair can take place. Hypotension (Cardiac emergencies Hypotension and shock post-MI, p. [link]) and pulmonary oedema (Cardiac emergencies Hypotension and shock post-MI, p. [link]) should be managed as described elsewhere. Important principles are given here:

  • Invasive monitoring (PA catheter and arterial line) to dictate haemodynamic management. RA and pulmonary capillary wedge pressure (PCWP) dictate fluid administration or diuretic use. CO, mean arterial pressure (MAP), and arterial resistance determine the need for vasodilator therapy.

  • If SBP >100mmHg, cautious use of vasodilator therapy, generally with nitroprusside, will lower the systemic vascular resistance (SVR) and reduce the magnitude of the shunt. Nitrates will cause venodilatation and increase the shunt and should be avoided. Not to be used with renal impairment.

  • Inotropes if severely hypotensive (initially dobutamine, but adrenaline may be required, depending on haemodynamic response). Increasing systemic pressure will worsen shunt.

  • Consider IABP in most cases.

  • Liaise with surgeons early for possible repair. Operative mortality is high (20–70%), especially in the context of perioperative shock, inferoposterior MI, and RV infarction. Current recommendations are for high-risk early surgical repair, combined with CABG ± mitral valve (MV) repair/replacement.

  • If the patient has been weaned off pharmacological and/or mechanical support, it may be possible to postpone surgery for 2–4 weeks to allow for some level of infarct healing. Patients should ideally undergo catheterization prior to surgical repair to ensure culprit vessel(s) are grafted.

  • Closure of the VSD with catheter placement of an umbrella-shaped device (Amplatzer) has been reported to stabilize critically ill patients until definitive repair is possible.

Acute mitral regurgitation post-MI

  • MR due to ischaemic papillary muscle dysfunction or partial rupture is seen 2–10 days post-MI. Complete rupture causes torrential MR and is usually fatal.

  • Presentation is acute-onset, severe breathlessness, with hypoxia, acute pulmonary oedema, diaphoresis, and rapid deterioration.

  • More commonly associated with inferior MI (posteromedial papillary muscle) than anterior MI (anterolateral papillary muscle).

  • ‘Silent MR’ is quite frequent and must be suspected in any post-MI patient with unexplained haemodynamic deterioration.

  • Diagnosis is by Echo. In severe MR, PA catheterization will show a raised pressure, with a large v wave on the PCWP.

Management

(Cardiac emergencies Acute mitral regurgitation, pp. [link][link].)

  • Treatment with vasodilators, generally nitroprusside, should be started as early as possible once haemodynamic monitoring is available. IABP could also be considered.

  • Mechanical ventilation may be necessary.

  • Liaise with surgeons early for possible repair or replacement.

Pseudoaneurysm and free wall rupture

  • Demonstrated in up to 6% of STEMI patients and leads to sudden death in two-thirds.

  • A proportion present subacutely with cardiogenic shock, allowing time for intervention.

  • Diagnosis of subacute cases can be made on a combination of clinical features of pericardial effusion, tamponade, and Echo.

  • Patients who have undergone early thrombolysis have a lower chance of wall rupture.

  • Stabilization of the patient follows similar lines to cardiogenic shock (Cardiac emergencies Cardiogenic shock, pp. [link][link]). Case must be discussed with surgeons immediately, with a view to repair.

Cocaine-induced MI

  • The incidence of cocaine-induced MI, LV dysfunction, and arrhythmias are on the increase (see Box 1.8).

  • It has been estimated that 14–25% of young patients presenting to urban emergency departments with non-traumatic chest pain may have detectable levels of cocaine and its metabolites in their circulation. Of this group, 6% have enzymatic evidence of MI (figures are from the United States).

  • Most patients are young, non-white, ♂ cigarette smokers, without other risk factors for IHD.

Diagnosis

  • Can be difficult and must be suspected in any young individual with chest discomfort at low risk of developing OHD.

  • Chest pain occurs most commonly within 12h of cocaine use. Effects can return up to 24–36h later, secondary to long-lasting active metabolites.

  • ECG is abnormal, with multiple non-specific repolarization changes in up to 80% of cases, and ~40% may have diagnostic changes of STEMI qualifying for reperfusion therapy (Cardiac emergencies STEMI: diagnosis 1, p. [link]).

  • Biochemical markers of cardiac injury can be misleading, as most patients will have elevated CK levels secondary to rhabdomyolysis. TnT and TnI are vital to confirm myocardial injury.

Management

General measures

  • These are the same as for anyone presenting with MI. High-flow O2 5–10L, unless there is a contraindication; analgesia; aspirin 75mg od.

  • GTN: to be given at high doses as IV infusion (>10mg/h final levels) and dose titrated to symptoms and haemodynamic response (Cardiac emergencies STEMI: general measures, pp. [link][link]).

  • Benzodiazepines: are critical to reduce anxiety and tachycardia.

Second-line agents

  • Verapamil is given in high doses and has the dual function of reducing cardiac workload, hence restoring O2 supply and demand, as well as reversing coronary vasoconstriction. Should be given cautiously as 1- to 2-mg IV bolus at a time (up to 10mg total), with continuous haemodynamic monitoring. This should be followed by a high-dose oral preparation to cover the 24-h period for at least 72h after the last dose of cocaine (80–120mg PO tds).

  • Phentolamine is an α‎-adrenergic antagonist and readily reverses cocaine-induced vasoconstriction (2–5mg IV and repeated if necessary). It can be used in conjunction with verapamil.

  • Labetalol has both α‎- and β‎-adrenergic activity and can be used after verapamil and phentolamine if the patient remains hypertensive. It is effective in lowering cocaine-induced hypertension but has no effect on coronary vasoconstriction.

  • Reperfusion therapy: evidence for use of thrombolysis is limited and generally associated with poor outcome secondary to hypertension-induced haemorrhagic complications. If the patient fails to settle after implementing first-line measures, verapamil, and phentolamine, they should undergo immediate coronary angiography, followed by PCI if appropriate (evidence of thrombus/vessel occlusion). In the event that angiography is not available, thrombolytic therapy can be considered.

Caution

β‎-blockers must be avoided. They exacerbate coronary vasoconstriction by allowing unopposed action of the adrenergic receptors.

Ventricular tachyarrhythmia post-MI

Accelerated idioventricular rhythm

  • Common (up to 20%) in patients with early reperfusion in first 48h.

  • Usually self-limiting and short-lasting, with no haemodynamic effects.

  • If symptomatic, accelerating sinus rate with atrial pacing or atropine may be of value. Suppressive antiarrhythmic therapy (lidocaine, amiodarone) is only recommended with degeneration into malignant ventricular tachyarrhythmias.

Ventricular premature beats (VPB)

  • Common and not related to incidence of sustained VT/VF.

  • Generally treated conservatively. Aim to correct acid–base balance and electrolyte abnormalities (aim K+ >4.0mmol/L and Mg2+ >1.0mmol/L).

  • Peri-infarction β‎-blockade reduces VPB.

Non-sustained and monomorphic VT

  • Associated with a worse clinical outcome.

  • Correct reversible features such as electrolyte abnormalities and acid–base balance (aim K+ >4.5mmol/L and Mg2+ >1.0mmol/L).

  • DC cardioversion for haemodynamic instability.

  • Non-sustained VT and haemodynamically stable VT (slow HR <100bpm) can be treated with amiodarone (300mg bolus IV over 30min, followed by 1.2g infusion over 24h). Lidocaine is no longer recommended as first line. Procainamide is an effective alternative but is arrhythmogenic.

  • For VT despite amiodarone, consider overdrive pacing.

Ventricular fibrillation and polymorphic VT

  • A medical emergency and requires immediate defibrillation.

  • In refractory VF, consider vasopressin 40U IV bolus.

  • Amiodarone 300mg IV bolus to be continued as an infusion (see previous section) if output restored.

  • Manage as cardiac arrest with usual ALS protocol (Cardiac emergencies Adult advanced life support, pp. [link][link]).

Atrial tachyarrhythmia post-MI

  • Includes SVT, AF, and atrial flutter.

  • If the patient is haemodynamically unstable, they must undergo immediate synchronized DC cardioversion (press the ‘synch’ button on the defibrillator).

  • Haemodynamically stable patients can be treated with digoxin, β‎-blockers, and/or calcium channel blockers (see Table 1.8).

  • Amiodarone can be used to restore sinus rhythm. However, it is not very effective in controlling rate. Class I agents should generally be avoided, as they increase mortality.

  • In AF and atrial flutter, patients should undergo anticoagulation to reduce embolic complications if there are no contraindications.

Table 1.8 Dosages of selected antiarrhythmics for treatment of SVT

Drug

Loading dose

Maintenance dose

Digoxin

IV 0.5–1mg in 50mL of saline over 1–2h

PO 0.5mg every 12h for two doses, then 0.25mg every 12h for 2 days

0.0625–0.25mg od (IV or PO)

Amiodarone

IV 300mg over 60min via central line, followed by 900mg IV over 23h

or

PO 200mg tds × 1 week, then 200mg PO bd × 1 week

or

PO 400mg tds for 3 days

200–400mg od (IV or PO)

Drug

Dosage

Propranolol

IV 1mg over 1min, repeated every 2min up to max. 10mg

PO 10–40mg 3–4 times a day

Atenolol

IV 2–10mg by slow injection

PO 25–100mg daily

Sotalol

IV 20–60mg by slow injection

PO 80–160mg bd

Verapamil

IV 5mg over 2min; repeated every 5min up to max. 20mg

PO 40–120mg tds

Procainamide

IV 100mg over 2min; repeated every 5min up to max. 1g

PO 250mg every 6h

Disopyramide

IV 50mg over 5min; repeated every 5min up to max. 150mg

PO 100–200mg every 6h

Flecainide

IV 2mg/kg over 10min (max. 150mg)

or

PO 100–200mg bd

Metoprolol

IV 5mg

PO 25–100mg

Bradyarrhythmias and indications for pacing

Alternating or isolated RBBB/LBBB do not need pacing, unless haemodynamically unstable or progression to higher levels of block. New bifascicular block [RBBB with either left axis deviation (LAD) or right axis deviation (RAD)] or bundle branch block with first-degree AV block may require prophylactic pacing, depending on the clinical picture. Indications for pacing should not delay reperfusion therapy. Venous access (femoral or internal jugular vein) should be obtained first, and pacing wire inserted later. External temporary cardiac pacing, atropine (300 micrograms to 3mg IV bolus), and isoprenaline can be used to buy time.

Bradyarrhythmias post-MI

First-degree AV block

  • Common and no treatment required.

  • Significant PR prolongation (>0.20s) is a contraindication to β‎-blockade.

Second-degree AV block

  • This indicates a large infarction affecting the conducting systems, and mortality is generally Cardiac emergencies in this group of patients.

    • Mobitz type I is self-limiting, with no symptoms. Generally, requires no specific treatment. If symptomatic or progression to complete heart block (CHB), will need temporary pacing.

    • Mobitz type II, 2:1, 3:1 should be treated with temporary pacing, regardless of whether it progresses to CHB.

Third-degree AV block

  • In the context of an inferior MI, can be transient and does not require temporary pacing, unless there is haemodynamic instability or an escape rhythm of <40bpm.

  • Temporary pacing is required with anterior MI and unstable inferior MI.

Hypotension and shock post-MI

(See Cardiac emergencies Cardiogenic shock, pp. [link][link].)

The important principles in managing hypotensive patients with MI are:

  • If the patient is well perfused peripherally, no pharmacological intervention is required. Consider lying the patient flat, with the legs elevated if necessary, provided there is no pulmonary oedema.

  • Try to correct any arrhythmia, hypoxia, or acidosis.

  • Arrange for an urgent Echo to exclude a mechanical cause for hypotension (e.g. MR, VSD, ventricular aneurysm) that may require urgent surgery.

Patients may be divided into two subgroups

Hypotension with pulmonary oedema

(Also see Cardiac emergencies Pulmonary oedema: assessment, pp. [link][link].)

  • Secure central venous access: internal jugular lines are preferable if the patient may have received thrombolytic therapy.

  • Commence inotropes (Cardiac emergencies Cardiogenic shock, pp. [link][link]).

  • Further invasive haemodynamic monitoring, as available (PA pressures and wedge pressure monitoring, arterial line).

  • Ensure optimal filling pressures, guided by physical signs and PA diastolic or wedge pressure. Significant MR will produce large v waves on the wedge trace and give spuriously high estimates of left ventricular end-diastolic pressure (LVEDP).

  • Ensure rapid coronary reperfusion (if not already done), either with primary PCI or thrombolysis, depending on availability.

  • Intra-aortic balloon counterpulsation (Cardiac emergencies Intra-aortic balloon counterpulsation 1, p. [link]) may allow stabilization until PCI can be performed.

Hypotension without pulmonary oedema

This may be due to either RV infarction or hypovolaemia.

Diagnosis

  • Check the JVP and RA pressure. This will be low in hypovolaemia and high in RV infarction.

  • RV infarction on ECG is seen in the setting of inferior MI and ST elevation in right-sided chest leads (V3R–V4R).

Management

  • In either case, cardiac output will be improved by cautious plasma expansion. Give 100–200mL of colloid over 10min and reassess.

  • Repeat once if there is some improvement in BP and the patient has not developed pulmonary oedema.

  • Invasive haemodynamic monitoring with a PA catheter (Swan–Ganz) is helpful to ensure hypotension is not due to low left-sided filling pressures. Aim to keep PCWP of 12–15mmHg.

  • Start inotropes if BP remains low despite adequate filling pressures.

  • Use IV nitrates and diuretics with caution, as venodilatation will compromise RV and LV filling and exacerbate hypotension.

See Cardiac emergencies Right ventricular infarction, p. [link] for management of RV infarction.

Cardiogenic shock

  • Affects between 5 and 20% of patients, and up to 15% of MI patients can present with cardiogenic shock.

  • Management involves a complex interaction between many medical, surgical, and intensive care teams. with multiple invasive and non-invasive measures. Despite significant advances, prognosis remains poor. Therefore, the absolute wishes of the patient with regard to such an invasive strategy should be respected from the outset.

Diagnosis

A combination of clinical and physiological measures:

  • Clinical: marked, persistent (>30min) hypotension with SBP <80–90mmHg.

  • Physiological: low cardiac index (<1.8L/mm/m2), with elevated LV filling pressure (PCWP >18mmHg).

Management

  • Complex and must be quick.

  • Correct reversible factors, including:

    • Arrhythmias and aim to restore sinus rhythm.

    • Acid–base balance, electrolyte abnormalities.

    • Ventilation abnormalities: intubate if necessary.

  • Rapid haemodynamic, echocardiographic, and angiographic evaluation:

    • Haemodynamic: to ensure adequate monitoring and access, including central venous lines, Swan–Ganz, arterial line insertion, urinary catheter.

    • Echocardiographic: to assess ventricular systolic function and exclude mechanical lesions, which may need to be dealt with by emergency cardiac surgery, including MR (NB Tall v waves on PCWP trace), VSD, and ventricular aneurysm/pseudoaneurysm.

    • Angiographic: with a view to PCI or CABG if appropriate.

  • Aim to improve haemodynamic status, achieving SBP ≥90mmHg, guided by physical signs and LV filling pressures. As a general guide:

    • PCWP <15mmHg: cautious IV fluids (colloids) in 100–200mL aliquots.

    • PCWP >15mmHg: inotropic support with diuretics (if pulmonary oedema).

  • Inotropes should be avoided, if at all possible, in acutely ischaemic patients. The aim should be to rapidly restore/maximize coronary flow and offload the LV. Early revascularization is vital and has been shown to decrease mortality. IABP will partially help achieve improved coronary perfusion, reduce LVEDP, and improve BP, although has not been shown to improve survival in randomized trials.

  • If haemodynamic status does not improve post-revascularization and IABP insertion, inotropes should be used. Choice of agent can be difficult and should partly be guided by local protocols and expertise. Generally accepted choices depend on the clinical picture and include:

    • If patient is hypotensive (with pulmonary oedema): start with dopamine (up to 5 micrograms/kg/min), and if ineffective, substitute with adrenaline and/or noradrenaline (NA).

    • If patient has adequate BP (with pulmonary oedema): dobutamine to increase CO (starting at 2.5–5 micrograms/kg/min and increasing to 10 micrograms/kg/min), titrating to HR and haemodynamics. Phosphodiesterase inhibitors (PDIs) can be used as an alternative. If hypotension and tachycardia complicate dobutamine/PDI inhibitor treatment, (nor)adrenaline can be added as a 2nd agent to achieve desired haemodynamic effect.

  • Use of diuretics, thrombolysis, GP IIb/IIIa antagonists, and LMWH/UFH should follow normal principles and be based on the clinical picture.

Non-ST-elevation acute coronary syndromes (NSTE-ACS)

NSTE-ACS are closely related conditions with similar clinical presentation, treatment, and pathogenesis, but of varying severity. If there is biochemical evidence of myocardial damage, the condition is termed NSTEMI, and in the absence of damage UA.

The diagnosis of NSTE-ACS may not be definitive on presentation and evolves over subsequent hours to days. Therefore, management of patients with NSTE-ACS is a progression through a number of risk stratification processes, dependent on history, clinical features, and investigative results, which, in turn, determine the choice and timing of a number of medical and/or invasive treatment strategies (see Fig. 1.8).

Fig. 1.8 NSTE-ACS—integrated care pathway.

Fig. 1.8 NSTE-ACS—integrated care pathway.

Clinical presentation

There are three distinct presentations:

  • Rest angina—angina when the patient is at rest.

  • New-onset severe angina.

  • Increasing angina—previously diagnosed angina which has become more frequent, longer in duration, or lower in threshold.

General examination (as indicated for all ACS; Cardiac emergencies Acute coronary syndrome, pp. [link][link]) must be undertaken, in particular to rule out pulmonary oedema and assess haemodynamic stability, cardiac valve abnormalities, and diaphoresis.

Integrated management plan

We recommend that all patients follow a local integrated care pathway on presentation. The various stages are broadly outlined here. See relevant pages for further information.

  • Initial stabilization (see also Cardiac emergencies Acute coronary syndrome, pp. [link][link]):

    • Transfer the patient to an area with continuous ECG monitoring and defibrillator facility.

    • Strict bed rest.

    • Give O2, aspirin 300mg PO, SL nitrate, and mild sedation if required.

    • If pain persists, give diamorphine 2.5–5mg IV PRN, with metoclopramide 10mg IV.

  • General investigations: similar to STEMI patients (Cardiac emergencies ST-elevation myocardial infarction (STEMI), pp. [link][link]; Cardiac emergencies STEMI: diagnosis 1, p. [link]; Cardiac emergencies STEMI: diagnosis 2, p. [link]), including blood for FBC, biochemical profile and markers of myocardial injury, and lipid profile, as well as CRP and thyroid function test (TFT) (if persistent tachycardia). Arrange portable CXR (rule out LVF and mediastinal abnormalities).

  • Confirm diagnosis (Cardiac emergencies NSTEMI/UA: diagnosis, p. [link]).

  • Risk stratification (Cardiac emergencies NSTEMI/UA: risk stratification, p. [link]) in order to determine appropriate medical and invasive treatment strategies. High-risk patients should be admitted to the CCU, and low/intermediate-risk patients to monitored beds in step-down unit.

  • Treatment is based on the patient’s risk and includes:

    • Medical strategies:

      • Anti-ischaemic (Cardiac emergencies NSTEMI/UA: medical management 1, p. [link]).

      • Antiplatelet (Cardiac emergencies NSTEMI/UA: medical management 2, pp. [link][link]).

      • Antithrombic (Cardiac emergencies NSTEMI/UA: medical management 2, pp. [link][link]).

    • Invasive strategies (Cardiac emergencies NSTEMI/UA: invasive versus non-invasive strategies, p. [link]).

  • Secondary prevention and discharge.

NSTE-ACS: diagnosis

Diagnosis in NSTE-ACS is an evolving process and may not be clear on presentation. A combination of history, serial changes in ECG, and serial changes in biochemical markers of myocardial injury determines the diagnosis. Once a patient has been designated a diagnosis of ACS with probable/possible NSTE-ACS ,they will require the following.

Serial ECGs

Changes can be transient and/or fixed, especially if a diagnosis of NSTEMI is made. See Table 1.1 for localization of infarcts from ECG changes.

  • ST-segment depression of ≥0.05mV is highly specific of myocardial ischaemia (unless isolated in V1–V3 suggesting a posterior STEMI).

  • T-wave inversion is sensitive, but non-specific, for acute ischaemia, unless very deep (≥0.3mV).

  • Rarely Q waves may evolve or there may be transient/new LBBB.

Serial biochemical markers of cardiac injury

These are used to differentiate between NSTEMI and UA, as well as to determine prognosis. We recommend levels at 6, 12, 24, and 48h after the last episode of pain. A positive biochemical marker (CK, CK-MB, or troponin) in the context of one or more of the aforementioned ECG changes is diagnostic of NSTEMI. If serial markers over a 24- to 72-h period from the last episode of chest pain remain negative, UA is diagnosed.

  • Cardiac TnT and TnI: are both highly cardiac-specific and sensitive, can detect ‘microinfarction’ in the presence of normal CK-MB, are not affected by skeletal muscle injury, and convey prognostic information (worse prognosis if positive). Troponins can be raised in non-atherosclerotic myocardial damage (cardiomyopathy, myocarditis, pericarditis) and should therefore be interpreted in the context of the clinical picture. Both TnT and TnI rise within 3h of infarction. TnT may persist up to 10–14 days, and TnI up to 7–10 days. Results must be interpreted with caution in patients with chronic renal failure (CRF). See Fig. 1.5.

  • CK levels do not always reach the diagnostic twice the upper limit of normal and generally have little value in diagnosis of NSTEMI.

  • CK-MB has low sensitivity and specificity; CK-MB isoforms improve sensitivity (CK-MB2 >1U/L or CK-MB2:CK-MB1 ratio >1.5), but isoform assays are not widely available clinically.

  • Myoglobin is non-cardiac-specific, but levels can be detected as early as 2h after onset of symptoms. A negative test is useful in ruling out myocardial necrosis.

Continuous ECG monitoring

Can detect episodes of silent ischaemia and arrhythmia. Both have been shown to be more prolonged in NSTEMI than in UA.

NSTE-ACS: risk stratification

NSTE-ACS are a heterogeneous group of conditions with variable outcomes. An assessment of risk for adverse outcome is vital to ensure formation of an adequate management plan.

Risk stratification should begin on initial evaluation and continue throughout the hospital stay. At each stage, patients with a high chance of a poor outcome should be identified and managed appropriately.

We recommend at least two formal risk stratification processes.

Early risk stratification

(See Table 1.2.) This should take place on presentation and forms part of the initial assessment used to make a diagnosis. It involves a combination of clinical features, ECG changes, and biochemical markers of cardiac injury, as demonstrated in Table 1.2. Patients are divided into high risk and intermediate/low risk.

  • High-risk patients should be admitted to the CCU, follow an early invasive strategy, and be managed with a combination of:

    • Acetyl salicylic acid (ASA), clopidogrel/ticagrelor, LMWH, IIb/IIIa inhibitor.

    • Anti-ischaemic therapy (first-line β‎-blocker, GTN).

    • Early invasive strategy (inpatient catheterization and PCI within 48h of admission).

  • Intermediate/low-risk patients should be admitted to a monitored bed on a step-down unit and undergo a 2nd inpatient risk stratification once their symptoms have settled, to determine the timing of invasive investigations. Initial management should include:

    • ASA, clopidogrel/ticagrelor, LMWH.

    • Anti-ischaemic therapy (first-line β‎-blocker, GTN).

    • Undergoing late risk stratification in 48–72h from admission.

Table 1.2 Short-term risk of death from non-fatal MI in patients with UA*

Feature

High risk (at least one of the following features must be present)

Intermediate risk (no high-risk feature but must have one of the following features)

Low risk (no high- or intermediate-risk feature but may have any of the following features)

History

Accelerating tempo of ischaemic symptoms in preceding 48h

Prior MI, peripheral or cerebrovascular disease, or CABG, prior aspirin use

Character of pain

Prolonged ongoing (>20min) rest pain

Prolonged (>20min) rest angina, now resolved, with moderate or high likelihood of CAD

Rest angina (<20min) or relieved with rest or SL GTN

New-onset or progressive CCS Class III or IV angina the past 2 weeks without prolonged (>20min) rest pain but with moderate or high likelihood of CAD

Clinical findings

Pulmonary oedema, most likely due to ischaemia

New or worsening MR murmur

S3 or new/worsening rales

Hypotension, bradycardia, tachycardia

Age >75 years

Age >70 years

ECG

Angina at rest with transient ST-segment changes >0.05mV

Bundle branch block, new or presumed new

Sustained ventricular tachycardia

T-wave inversion >0.2mV

Pathological Q waves

Normal or unchanged ECG during an episode of chest discomfort

Cardiac markers

Elevated (e.g. TnT or TnI >0.1ng/mL)

Slightly elevated (e.g. TnT >0.01 but <0.1ng/mL)

Normal

* Reproduced from Anderson JL, et al. ‘ACC/AHA 2007 Guidelines for the management of patients with unstable angina/non–ST-elevation myocardial infarction’, J Am Coll Cardiol, 50:1–157, copyright 2007 with permission from Wolters Kluwer Health, Inc. Cardiac emergencies http://circ.ahajournals.org/content/116/7/e148.

Late risk stratification

(See Cardiac emergencies STEMI: reperfusion therapy (thrombolysis) 1, pp. [link][link].) This involves a number of non-invasive tests to determine the optimal timing for invasive investigations in intermediate/low-risk patients. Suggested guidelines are summarized under Cardiac emergencies NSTE-ACS: late risk stratification, p. [link]. It is generally performed if there have been no further episodes of pain/ischaemia at 24–48h after admission.

  • Intermediate/low-risk patients who develop recurrent pain and/or ischaemic ECG changes at any point during their admission, heart failure, or haemodynamic instability in the absence of a non-cardiac cause should be managed as high-risk patients (early invasive strategy ± IIb/IIIa inhibitor).

  • Fig. 1.8 is a summary of a recommended integrated care pathway combining diagnosis, risk stratification, and treatment.

  • There are other risk stratification assessment scores, including Braunwald and TIMI. As recommended earlier, high-risk patients from these assessments should also follow an early invasive strategy, and intermediate/low-risk patients a more conservative strategy.

NSTE-ACS: late risk stratification

The highest risk of adverse outcome in patients who are designated as intermediate/low risk on presentation is during the early phase of admission. Therefore, it is important that the 2nd risk stratification process occurs within 24–48h of admission if the patient is stable.

Late risk stratification is based on non-invasive investigations. Computed tomography (CT) coronary angiography provides anatomic information and is a useful rule-out in lower-risk patients. Stress testing with dobutamine echocardiography or radionuclide imaging provides functional information. Exercise testing is still used, although the sensitivity and specificity are lower, compared to other non-invasive stress tests.

A patient is regarded as being at high risk of adverse outcome if they fulfil one of the features listed here. These patients should have inpatient cardiac catheterization.

CT coronary angiography

  • Requires a HR of ~60 or below and sinus rhythm for diagnostic imaging.

  • Directly images coronary arteries; however, no functional information.

  • Soft plaques may be underestimated.

  • Excellent test in low-risk patients to rule out CAD.

Stress radionuclide myocardial perfusion imaging

  • Abnormal tracer distribution in >1 territory.

  • Cardiac enlargement.

LV imaging

  • Stress echocardiography:

    • Rest EF <35%.

    • Wall motion score index >1.

  • Stress radionuclide ventriculography:

    • Rest EF <35%.

    • Fall in EF >10%.

Exercise ECG test

  • Horizontal/downsloping ST depression with:

    • Onset at HR <120bpm or <6.5 metabolic equivalents (METS).

    • Magnitude of >2.0mm.

    • Post-exercise duration of changes >6min.

    • Depression in multiple leads, reflecting multi-vessel disease.

  • Abnormal SBP response:

    • Sustained decrease of >10mmHg or flat BP response with abnormal ECG.

  • Other:

    • Exercise-induced ST-segment elevation.

    • VT.

    • Prolonged elevation of HR.

NSTE-ACS: medical management 1

Anti-ischaemic therapy

All patients should be treated with a combination of the listed agents to ensure adequate symptom control and a favourable haemodynamic status (SBP Cardiac emergencies 100–110mmHg, PR 860). All patients should be treated with adequate analgesia, IV nitrates, β‎-blockers, and statins (if no contraindications). Other agents can also be added, depending on the clinical picture.

  • Analgesia: diamorphine 2.5–5mg IV (with metoclopramide 10mg IV). Acts as anxiolytic. Reduces pain and SBP through venodilatation and reduction in sympathetic arteriolar constriction. Can result in hypotension (responsive to volume therapy) and respiratory depression (reversal with naloxone 400 micrograms–2mg IV).

  • Nitrates: GTN infusion (50mg in 50mL of normal saline at 1–10mL/h), titrated to pain and keeping SBP >100mmHg. Tolerance to continuous infusion develops within 24h, and the lowest efficacious dose should be used. Common side effects are headache and hypotension, both of which are reversible on withdrawal of medication. Absolute contraindication is use of sildenafil in the previous 24h. This can result in exaggerated and prolonged hypotension.

  • β‎-blockers: should be started on presentation, unless contraindicated. Initially use a short-acting agent (e.g. metoprolol 12.5–100mg PO tds), which, if tolerated, may be converted to a longer-acting agent (e.g. atenolol 25–1000mg od). Rapid β‎-blockade may be achieved using short-acting IV agents such as metoprolol (Cardiac emergencies Beta-blockers, p. [link]). Aim for HR of ~50–60bpm. Mild LVF is not an absolute contraindication to β‎-blocker therapy. Pulmonary congestion may be due to ischaemic LV systolic dysfunction and/or reduced compliance. If there is overt heart failure, β‎-blockade is contraindicated and a calcium antagonist (amlodipine 5–10mg od) can be used. By reducing HR and BP, β‎-blockers reduce myocardial O2 demand, and thus angina. When either used alone or in combination with nitrates and/or calcium antagonists, β‎-blockers are effective in reducing the frequency and duration of both symptomatic and silent ischaemic episodes.

  • Calcium antagonists: diltiazem 60–360mg PO, verapamil 40–120mg PO tds. Their use aims to reduce HR and BP and is a useful adjunct to treatment with analgesia/nitrates/β‎-blockers. Amlodipine/felodipine 5–10mg PO od can be used with pulmonary oedema and in poor LV function. Calcium antagonists alone do not appear to reduce mortality or risk of MI in patients with UA. However, when combined with nitrates and/or β‎-blockers, they are effective in reducing symptomatic and silent ischaemic episodes, non-fatal MI, and the need for revascularization.

  • Statins (HMG-CoA reductase inhibitors): high-dose statins (atorvastatin 80mg od) have been shown to reduce mortality and recurrent MI in the acute setting. The role of statins in primary and secondary prevention of future cardiovascular events is well documented.

  • ACEIs: unlike patients with STEMI in whom early introduction of an ACEI has significant prognostic benefits, specific trials in the NSTE-ACS setting are lacking. However, there is good evidence that both patients with low and high risk of cardiovascular disease will benefit from long-term ACE inhibition (HOPE and EUROPA trials).

NSTE-ACS: medical management 2

Antiplatelet therapy

All patients should be given aspirin and clopidogrel/ticagrelor (unless contraindicated). IIb/IIIa antagonists for high-risk patients only.

  • Aspirin (300mg PO): should be administered immediately in the emergency department and continued indefinitely (unless contraindicated). It has been shown to consistently reduce mortality and recurrent ischaemic events in many trials. In patients with aspirin hypersensitivity or major gastrointestinal (GI) intolerance, clopidogrel 75mg od should be used.

  • Thienopyridines: clopidogrel (300mg) or ticagrelor (180mg) should be given on admission to all patients with proven NSTE-ACS, regardless of risk, and be continued [75mg od clopidogrel, 90mg twice daily (bd) ticagrelor] for at least 12 months. The PLATO trial showed a decrease in recurrent MI and stroke with ticagrelor, compared to clopidogrel; however, there was a greater incidence of fatal intracranial bleeding. Clopidogrel/ticagrelor should be withheld in patients requiring CABG for 5–7 days to reduce haemorrhagic complications.

  • GP IIb/IIIa antagonists: there are multiple short- and long-acting commercially available molecules. These agents may be used in conjunction with aspirin, clopidogrel/ticagrelor, and LMWH (or UFH). Eptifibatide and tirofiban should be used in high-risk patients with ongoing ischaemia and elevated troponin, in whom an early invasive management strategy is not planned/available (<24h). In patients with an early invasive strategy, all IIb/IIIa antagonists can be used. Infusion is generally continued for 12h post-PCI. Taken as a group, these agents protect NSTE-ACS patients from death and non-fatal MI during the acute phase of their presentation and 24h post-intervention. See Box 1.9 for doses and administration regimen.

Antithrombotic therapy

All patients should be given an LMWH.

  • LMWHs: have been shown to be as good as, or superior to, UFH in short-term reduction of death, MI, and revascularization in patients with NSTE-ACS. They should be used in conjunction with aspirin and clopidogrel in all patients on presentation and be continued for 2–5 days after the last episode of pain and ischaemic ECG changes. Other advantages over UFH include SC administration, lack of monitoring, and reduced resistance and thrombocytopenia. Box 1.9 lists the doses of various agents in use for treating NSTE-ACS.

  • UFH: multiple trials have demonstrated a reduction in the risk of death and MI in patients with UA/NSTEMI. UFH should be started on presentation, as an alternative to LMWH, in conjunction with aspirin and clopidogrel. Infusion should be continued for 2–5 days subsequent to the last episode of pain and/or ischaemic ECG changes. An initial bolus of 60–70U/kg (maximum 5000U) should be followed by an infusion of 12–15U/kg/h (Cardiac emergencies 1000U/h). The infusion rate should be altered to achieve an APTT value of 1.5–2.0 times control. Coagulation should be checked initially every 6h, followed by once every 24h after two consistent values have been obtained.

Thrombolysis

There is no evidence to suggest that combining thrombolytic agents with aspirin, LMWH, and conventional anti-ischaemic therapy is of benefit. In the TIMI IIIB trial, the rtPA group had a worse outcome at 6 weeks and the risk of bleeding was also greater in the thrombolysis group.

For management key points for NSTEMI, see Box 1.10.

NSTE-ACS: invasive versus non-invasive strategies

Current evidence supports early angiography and revascularization in patients who present with either high-risk features or intermediate/low-risk features with ongoing symptoms. Furthermore, low- and intermediate-risk patients who settle on medical therapy should undergo symptom-limited, non-invasive stress testing to identify the cohort of patients with an Cardiac emergencies risk of adverse outcome. This 2nd group will also benefit from early invasive management.

Patients managed with an early conservative strategy tend to have an Cardiac emergencies need for antianginal therapy and rehospitalization for angina, and many undergo coronary angiography within the year.

The following groups are recommended to benefit from an early invasive strategy (inpatient cardiac catheterization and PCI):

  • Patients with high-risk features of NSTE-ACS:

    • Recurrent angina/ischaemic ECG changes despite optimal medical therapy.

    • Elevated troponin.

    • New/presumed new ST-segment depression.

    • Chest pain with clinical features of heart failure (pulmonary oedema, new/worsening MR, S3 gallop).

    • Haemodynamic instability.

    • Sustained VT.

  • Poor LV systolic function (EF <40%).

  • Patients allocated to low/medium risk, in whom subsequent non-invasive testing demonstrates high-risk features.

  • PCI in previous 6 months.

  • Previous CABG.

  • Patients with other comorbidities (e.g. malignancy, liver failure, renal disease), in whom risks of revascularization are not likely to outweigh benefits.

NSTE-ACS: discharge and secondary prevention

  • Length of hospital stay: will be determined by symptoms and the rate of progression through the NSTE-ACS pathway. Generally patients are hospitalized for 3–7 days.

  • Secondary prevention: remains of paramount importance and is similar in principle to STEMI patients (Cardiac emergencies STEMI: predischarge risk stratification, pp. [link][link]).

Arrhythmias: general approach

Both tachyarrhythmias and bradyarrhythmias may present with significant symptoms and haemodynamic compromise. The approach to patients with arrhythmias depends upon:

  • The effects of the rhythm on the patient.

  • The diagnosis from the ECG and the rhythm.

  • Any underlying cardiac abnormality or identifiable precipitant (see Box 1.11).

Effects of the rhythm on the patient

Patients with signs of severe haemodynamic compromise

  • Impending cardiac arrest.

  • Severe pulmonary oedema.

  • Shock: SBP <90mmHg.

  • Depressed consciousness.

If the patient is in cardiac arrest, then follow the ALS protocol. If the patient is conscious, but severely compromised, then seek urgent anaesthetic support and urgent synchronized DC cardioversion to manage tachyarrhythmias. For bradyarrhythmias, inotropic support (e.g. isoprenaline), external pacing, or temporary transvenous pacing should be considered (Cardiac emergencies Bradyarrhythmias: general approach, pp. [link][link]).

Patients with mild to moderate compromise

  • Mild pulmonary oedema.

  • Low cardiac output, with cool peripheries and oliguria.

  • Angina at rest.

Try to record a 12-lead ECG, if possible, and a long rhythm strip before giving any pharmacological agents and/or defibrillation. This will be invaluable for long-term management. If they deteriorate, treat as for severe haemodynamic compromise.

Diagnosing the arrhythmia

The main distinctions to make are:

  • Tachy- (>120/min) versus brady- (<60/min) arrhythmia.

  • Narrow (≤120ms or three small squares) versus broad QRS complex.

  • Regular versus irregular rhythm.

Tachyarrhythmias heart rate >120bpm

(See Box 1.12.)

History

Previous cardiac disease, palpitations, dizziness, chest pain, symptoms of heart failure, recent medication, and family history, particularly of cardiac conditions or sudden cardiac death. Ask specifically about conditions known to be associated with certain cardiac arrhythmias (e.g. AF: alcohol, thyrotoxicosis, MV disease, IHD, pericarditis; VT: previous MI, LV aneurysm).

Examination

BP, heart sounds and murmurs, signs of heart failure, carotid bruits.

Investigations

If the patient is haemodynamically stable:

  • 12-lead ECG and rhythm strip:

    • Regular versus irregular rhythm.

    • Narrow versus broad QRS complex.

  • Blood tests:

    • FBC, biochemistry, glucose (urgently).

    • Ca2+, Mg2+ (especially if on diuretics).

    • Biochemical markers of myocardial injury.

  • Where appropriate:

    • Blood cultures, CRP, erythrocyte sedimentation rate (ESR).

    • TFTs.

    • Drug levels.

    • ABGs.

  • CXR:

    • Heart size.

    • Evidence of pulmonary oedema.

    • Other pathology (e.g. Ca bronchus Cardiac emergencies AF, pericardial effusion Cardiac emergencies sinus tachycardia, hypotension ± AF).

In haemodynamically unstable patients, some of these investigations might need to be completed after restoration of stable rhythm.

Management

Haemodynamically unstable patients

  • Arrhythmias causing severe haemodynamic compromise (cardiac arrest, SBP <90mmHg, severe pulmonary oedema, evidence of cerebral hypoperfusion) require urgent correction, usually with external defibrillation. Drug therapy requires time and haemodynamic stability.

  • The only exception is a patient in chronic AF with an uncontrolled ventricular rate—defibrillation is unlikely to cardiovert to sinus rhythm. Rate control and treatment of the precipitant are first line. At the same time, factors that could increase the HR in a previously stable AF patient should be considered, such as infection.

  • Sedate awake patients with midazolam (2.5–10mg IV) ± diamorphine (2.5–5mg IV + metoclopramide 10mg IV) for analgesia. Beware respiratory depression and have an anaesthetist, flumazenil, and naloxone to hand, and always ask for anaesthetic assistance if not experienced in this.

  • Formal anaesthesia with propofol is preferred, but remember the patient may not have an empty stomach and precautions should be taken to prevent aspiration (e.g. cricoid pressure, ET intubation).

  • Start at 150J biphasic synchronized shock, and increase as required.

  • If tachyarrhythmia recurs or is unresponsive, try to correct Cardiac emergenciesPaO2, Cardiac emergenciesPaCO2, acidosis, or Cardiac emergenciesK+. Give Mg2+ (8mmol IV stat) and shock again. Amiodarone 150–300mg bolus IV may also be used.

  • Give specific antiarrhythmic therapy (see Table 1.3).

Table 1.3 Treatment options in tachyarrhythmias

Sinus tachycardia

Look for cause; β‎-blockade if anxious

Atrial fibrillation

Atrial flutter

SVT

(Cardiac emergencies Narrow complex tachyarrhythmias (SVT), pp. [link][link])

Rate control (AV node)

  • Digoxin

  • β‎-blockade

  • Calcium blocker (e.g. verapamil)

Cardioversion to sinus rhythm

  • Flecainide

  • Amiodarone

  • Sotalol

  • Disopyramide

  • Synchronized DC shock

Prevention

  • Amiodarone

  • Sotalol

  • Quinidine

  • Procainamide

Junctional tachycardias (AVNRT)

(Cardiac emergencies Atrioventricular nodal re-entry tachycardia, p. [link])

  • Adenosine

  • β‎-blockade

  • Verapamil

  • (Vagal stimulation)

  • Digoxin

  • Flecainide

  • Synchronized DC shock

Accessory pathway tachycardias (i.e. AVRT)

(Cardiac emergencies Accessory pathway tachycardia (AV re-entrant tachycardia), p. [link])

At AV node

  • Adenosine

  • β‎-blockade

At accessory pathway

  • Sotalol

  • Flecainide

  • Disopyramide

  • Quinidine

  • Amiodarone

Termination only

  • Synchronized DC shock

VT

(Cardiac emergencies Ventricular tachycardia: drugs, p. [link])

Termination and prevention

  • Lidocaine

  • Procainamide

  • Amiodarone

  • Magnesium

  • DC shock

  • Flecainide

  • Disopyramide

  • Propafenone

  • β‎-blockade

Haemodynamically stable patients

  • Admit and arrange for continuous ECG monitoring and 12-lead ECG.

  • Try vagotonic manoeuvres [e.g. Valsalva or carotid sinus massage (CSM); Cardiac emergencies Narrow complex tachyarrhythmias (SVT), pp. [link][link]].

  • If diagnosis is clear, introduce appropriate treatment.

  • If there is doubt regarding the diagnosis, give adenosine 6mg as a fast IV bolus, ideally in a big antecubital vein, followed promptly by 5–10mL of saline flush. (Consider starting with a lower dose in patients taking dipyridamole.) If no response, try 9, 12, and 18mg in succession, with continuous ECG rhythm strip.

  • Definitive treatment should start as soon as the diagnosis is known (Cardiac emergencies Treatment options in tachyarrhythmias, p. [link]; Cardiac emergencies Broad complex tachycardia: diagnosis, p. [link]; Cardiac emergencies Monomorphic ventricular tachycardia (MVT), pp. [link][link]; Cardiac emergencies Polymorphic ventricular tachycardia, pp. [link][link]; Cardiac emergencies Ventricular tachycardia: drugs, p. [link]; Cardiac emergencies Narrow complex tachyarrhythmias (SVT), pp. [link][link]; Cardiac emergencies Dosages of selected antiarrhythmics for SVT, p. [link]; Cardiac emergencies Atrial fibrillation: assessment, pp. [link][link]; Cardiac emergencies Atrial fibrillation: management, pp. [link][link]; Cardiac emergencies Atrial fibrillation: rate control, p. [link]; Cardiac emergencies Atrial flutter, p. [link]; Cardiac emergencies Multifocal atrial tachycardia, p. [link]; Cardiac emergencies Accessory pathway tachycardia (AV re-entrant tachycardia), p. [link]; Cardiac emergencies Atrioventricular nodal re-entry tachycardia, p. [link]).

Treatment options in tachyarrhythmias

(See Table 1.3.)

Broad complex tachycardia: diagnosis

(QRS width >120ms or >3 small squares)

Diagnostic approach

The following principles can be used to distinguish between different forms of broad complex tachyarrhythmia.

1. Examine the rhythm strip. Is it regular or irregular?

Regular

  • VT (mono-/polymorphic).

  • SVT or atrial flutter with bundle branch block.

  • Atrial flutter or SVT with pre-excitation (e.g. WPW).

Irregular

  • AF, atrial flutter, or multifocal atrial tachycardia with bundle branch block.

  • Pre-excited AF (e.g. WPW).

  • Torsades de pointes (polymorphic VT).

2. Are there any features on the 12-lead ECG that help distinguish VT from SVT with aberrancy?

Factors favouring SVT

  • A grossly irregular broad complex tachycardia with rates ≥200/min suggests AF with conduction over an accessory pathway.

  • Slowing or termination by vagotonic manoeuvres.

  • Evidence of atrial and ventricular coupling (e.g. with 1:2 AV block).

Factors favouring or diagnostic of VT

  • Cycle length stability (<40ms R–R variation).

  • QRS >140ms (3.5 small squares), especially with normal duration when compared with previous ECG in sinus rhythm.

  • Marked LAD (negative in lead II).

  • QRS concordance in chest leads. If the predominant deflection of the QRS is positive, this is highly suggestive of VT.

  • In patients with previous LBBB or RBBB, it is difficult to distinguish VT from SVT with aberrancy. A different QRS morphology in tachycardia suggests VT (other clues are given in Table 1.4).

  • Fusion or capture beats.

  • Independent atrial activity.

  • Documented CAD or reduced EF.

Table 1.4 Differentiating broad complex tachyarrhythmias*

RBBB

LBBB

Lead V1

rSR’ with R’ > r

RS with R > S

rS or QS with time to S wave nadir <70ms

Lead V6

If a Q wave is present, it must be 40ms and <0.2mV

R wave with no Q wave

Sensitivity 90%; specificity 67–85%.*

* Source: data from Griffith MJ, et al. (1994). ‘Ventricular tachycardia as default diagnosis in broad complex tachycardia.’ Lancet 343: 386–8.

3. What are the effects of adenosine?

The transient AV block produces one of three results:

  • The s adenosine (and experienced chest tightness with the injection). Higher doses are required in patients on theophyllines. The diagnosis is most likely to be VT.

If there is any doubt about the diagnosis in the acute setting, the patient must be treated as VT, until proven otherwise.

Morphologic rules

For any broad complex tachycardia with ‘bundle branch block’ morphology, assume it is VT unless features are present, as shown in Table 1.4, which could support the diagnosis of an SVT.

Monomorphic ventricular tachycardia (MVT)

Management

(See Box 1.13.)

1. Assess airway, breathing, and circulation immediately.

2. If patient is haemodynamically unstable

  • If develops VT while monitored, consider precordial thump—this can induce a mechanical premature ventricular complex, interrupting the VT circuit and terminating the arrhythmia. It must not delay external defibrillation.

  • Immediate unsynchronized external defibrillation (200J, 200J, 360J). Patient is often unconscious and if so, no sedation is required.

3. If patient is haemodynamically stable

  • Patient should initially be treated with IV pharmacological agents. If this is unsuccessful, they can be electrically cardioverted under sedation/anaesthesia.

  • Chemical cardioversion is empiric, and the choice of agent depends on local policy and expertise. We recommend IV amiodarone, sotalol, or procainamide as first-line agents. Amiodarone is the agent of choice in the context of poor LV function. Second-line agents include lidocaine and β‎-blockers (the latter is particularly valuable in the setting of MI/acute ischaemia).

  • Give IV magnesium (8mmol bolus over 2–5min, followed by 60mmol in 50mL of glucose over 24h) for all patients, especially if there is a risk of hypomagnesaemia (e.g. diuretics, excessive ethanol intake). With recurrent VT, a bolus dose can be repeated safely. Save a serum sample for analysis later.

4. Correct reversible factors

  • Ischaemia must be treated, especially in the context of post-infarction VT. This can initially be achieved with β‎-blockers. Patients should undergo revascularization at the earliest opportunity (Cardiac emergencies STEMI: reperfusion by primary percutaneous coronary intervention, pp. [link][link]).

  • Electrolyte abnormalities must be corrected (aim K+ ≥4.0–4.5, Mg2+ ≥1.0).

  • Acidosis: if severe (pH ≤7.1), give bicarbonate (8.4% sodium bicarbonate 50mL via a central line over 20min).

5. If there is recurrent or persistent VT

  • Synchronized DC shock under sedation or anaesthesia, with an anaesthetist present in case of sudden deterioration.

  • Overdrive pacing using a temporary transvenous wire may be used to terminate VT. The combination of prolonged temporary pacing and antiarrhythmics for recurrent VT is particularly effective in situations where the VT is provoked by bradycardia. If possible, rhythm strips of onset of runs of VT must be analysed, looking for bradycardia, heart block, or sick sinus syndrome. Dual-chamber temporary pacing may improve cardiac output by restoring AV synchrony.

6. Maintenance therapy

  • Usually oral and depends on the aetiology of VT. Patient must be discussed with the cardiac electrophysiologist early and options for EPS, radiofrequency ablation of VT focus, and/or implantable cardioverter–defibrillator (ICD) implantation explored. Patient will need ambulatory ECG monitor, exercise testing, or more invasive stimulation tests to monitor effectiveness of therapy.

Investigations

  • ECG: acute MI, prolonged QT interval.

  • CXR: cardiomegaly, pulmonary oedema.

  • U&Es: hypokalaemia, renal impairment.

  • Mg2+, Ca2+: ? deficiency.

  • Cardiac enzymes: small rises common after DC shock.

  • ABG: ? hypoxia, acidosis.

  • Echo: for LV function and to exclude structural abnormality (e.g. aneurysm).

Once the acute episode is over, consider referral to a cardiologist for:

  • Holter monitoring.

  • Exercise testing.

  • Coronary angiography.

  • VT stimulation (provocation) testing.

Polymorphic ventricular tachycardia

General management principles are identical to those for MVT. Most patients will be haemodynamically unstable and must undergo external defibrillation. Polymorphic ventricular tachycardia (PVT) occurring in the following circumstances requires specific therapy:

  • Ischaemic PVT in the context of MI.

  • Non-ischaemic PVT with QT prolongation (torsades de pointes).

  • PVT associated with Brugada syndrome.

Ischaemic PVT

  • Occurs in conjunction with acute MI and chronic myocardial ischaemia.

  • MVT in the context of MI can convert to PVT.

  • Primary treatment is complete revascularization. This must be followed by Holter monitoring, exercise ECG, and electrophysiological evaluation to determine the arrhythmia threshold.

  • A subset of patients, especially with poor LV function or where MVT degenerates into PVT, may require ICD implantation.

Non-ischaemic PVT with prolonged QT interval (torsades de pointes)

This is an irregular polymorphic VT (often self-limiting), which appears to ‘twist’ about the isoelectric line. It occurs in the setting of prolongation of the QT interval (QTc >500ms) (see Box 1.14), but the relationship between the degree of prolongation and the risk of serious arrhythmias is unpredictable. It may present as recurrent syncope or dizziness. Quite often, patients are mistaken as having seizures.

Brugada syndrome

  • Brugada syndrome1 is characterized by the triad of:

    • ST elevation in V1–V3 (may only be present on provocation test)

    • RBBB.

    • Sudden death (or family history of sudden death) from VF.

  • It is common in Japan and in South East Asia. Men are affected more than women.

  • The inheritance pattern is autosomal dominant, and some families have a mutation in the cardiac sodium channel SCN5A.

  • Must obtain specialist advice from a cardiac electrophysiologist. Patients will require electrophysiological studies, with a view to ICD implantation.

  • Diagnosis is made by serial ECGs after administration of flecainide 2mg/kg body weight IV in 10min or procainamide 10mg/kg IV in 10min. The test is positive if an additional 1mm ST elevation appears in leads V1, V2, and V3. All positive individuals should undergo EPS and further specialist evaluation.

Management

Congenital long QT

  • PVT in congenital QT prolongation is adrenergically driven, and treatment must include long-term β‎-blockade (e.g. propranolol).

  • Other adjunctive treatment includes pacemaker implantation and left stellate ganglionectomy.

  • Patients should be considered for ICD therapy. On occasions, decisions may be difficult because of the young age of patients.

Acquired long QT

  • The primary principle is to correct QT prolongation.

  • Offending agent(s) must be identified and discontinued immediately.

  • PVT in acquired QT prolongation is often secondary to prolonged pauses, which must be avoided.

  • All patients should receive IV Mg2+ (8mmol as a bolus over 2–5min, followed by a 60mmol infusion over 24h).

  • Overdrive temporary pacing (either ventricular or atrial) terminates the arrhythmia. Continued pacing prevents recurrence of PVT.

  • Isoprenaline may be used, while preparations are being made for pacing. This accelerates the atrial rate and captures the ventricles. Aim for a rate of 110–120bpm.

References

1. Cardiac emergencies http://www.brugada.org

Ventricular tachycardia: drugs

(See Table 1.5.)

Table 1.5 Dosages of selected antiarrhythmics for acute treatment of VT

Drug

Loading dose

Maintenance dose

Magnesium sulfate

8mmol (2g) IV over 2–15min (repeat once if necessary)

60mmol/48mL of saline at 2–3mL/h

Lidocaine

100mg IV over 2min (repeat once if necessary)

4mg/min for 30min

2mg/min for 2h

1–2mg/min for 12–24h

Procainamide

100mg IV over 2min. Repeat every 5min to max. of 1g

2–4mg/min IV infusion

250mg every 6h PO

Amiodarone

300mg IV over 60min via central line, followed by 900mg IV over 23h, 200mg PO tds × 1 week, then 200mg PO bd × 1 week

200–400mg od IV or PO

Disopyramide

50mg IV over 5min, repeated up to max. of 150mg IV, 200mg PO

2–5mg/min IV infusion

100–200mg every 6h PO

Flecainide

2mg/kg IV over 10min (max. 150mg)

1.5mg/kg IV over 1h, then 100–250 micrograms/kg/h IV for 24h or 100–200mg PO bd

Bretylium

5–10mg/kg (7500mg) IV over 10–15min

1–2mg/min IV infusion

Narrow complex tachyarrhythmias (SVT)

These originate within the atrium or the conduction system above the bundle of His (see Fig. 1.9). The important distinction to make is between regular and irregular tachyarrhythmias (see Table 1.6). Features of the different arrhythmias are shown in Table 1.7. The diagnosis not to miss is atrioventricular re-entrant tachycardia (AVRT) (tachycardias involving an accessory pathway), as digoxin and verapamil are contraindicated.

Fig. 1.9 Types of supraventricular tachycardia.

Fig. 1.9 Types of supraventricular tachycardia.

Table 1.6 Features of regular versus irregular tachycardia

Regular tachycardia

Irregular tachycardia

  • Sinus tachycardia

  • Atrial flutter (with 2:1 or greater block)

  • AVRT (i.e. with accessory pathway, e.g. WPW)

  • AVNRT

  • Intra-atrial re-entry tachycardia

  • AF

  • Atrial flutter with variable block

  • MAT

Table 1.7 Differential diagnosis of SVT

Arrhythmia

P wave configuration

Effect of adenosine

Comment

Sinus tachycardia (100–200/min)

Normal P waves

Transient AV block

Atrial fibrillation (<200/min)

f waves. Chaotic

Transient AV block

Irregular rhythm. Adenosine causes rate to slow briefly.

Fast AF with broad QRS seen in AVRT (e.g. WPW)

Atrial flutter (75–175/min)

Flutter waves (saw-tooth) (II, III, aVF, and VI)

Transient AV block

Adenosine may convert to AF

AVNRT (140–200/min)

Inverted buried in QRS (usually not seen)

Terminates

Most common recurrent SVT in adults

AVRT (e.g. WPW or accessory pathway) (150–250/min)

Inverted after QRS (inferior leads, RP > PR interval)

Terminates

Normal QRS if antegrade down AV node; broad QRS if antegrade down pathway

Atrial tachycardia (Intra-atrial re-entry) (100–200/min)

Abnormal P wave (PR < RP), 2:1 AV block may be seen

Transient AV block

Digoxin toxicity, lung disease, organic heart disease

MAT (100–130/min)

Multiple P wave morphologies

Transient AV block

Associated with lung disease and hypoxaemia

NB Any of these may be associated with broad QRS complexes from either a pre-existing bundle branch block or a rate-related intraventricular conduction abnormality.

Making the diagnosis

This can be done by careful examination of the 12-lead tachycardia ECG rhythm strip and the effect of inducing AV block.

Examination of ECG Important features to demonstrate are whether the rhythm is regular or irregular, and to examine for the presence/absence and morphology of P waves.

Irregular rhythm

  • No P waves visible:

    • Irregular rhythm with no discernible P wave (chaotic baseline with f waves): treat as AF (Cardiac emergencies Atrial fibrillation: assessment, pp. [link][link]).

    • Irregular rhythm with no discernible P wave and ‘saw-tooth’ flutter waves (especially in inferior leads and V1): treat as atrial flutter with variable block (Cardiac emergencies Atrial flutter, p. [link]).

  • P waves visible:

    • Irregular rhythm with multiple P wave morphologies (>3) and varying PR intervals: treat as multifocal atrial tachycardia (MAT) (Cardiac emergencies Multifocal atrial tachycardia, p. [link]).

Regular rhythm

  • No P waves visible:

    • No discernible P wave and ‘saw-tooth’ flutter waves (especially in inferior leads and V1): treat as atrial flutter with block (Cardiac emergencies Atrial flutter, p. [link]).

  • P waves visible:

    • P waves with normal morphology: treat as sinus tachycardia or sinus node re-entry tachycardia.

    • P waves within, or distorting the start or end of, QRS complex: treat as atrioventricular nodal re-entry tachycardia (AVNRT) (Cardiac emergencies Atrioventricular nodal re-entry tachycardia, p. [link]).

    • QRS complex may/may not be followed by P waves with different morphology to sinus P waves: treat as AVRT (Cardiac emergencies Accessory pathway tachycardia (AV re-entrant tachycardia), p. [link]).

Induce AV block

By vagotonic manoeuvres (e.g. Valsalva, CSM) and, if unsuccessful, with adenosine. [Adenosine 6mg fast IV bolus (3mg if via central line), followed promptly by 5–10mL of saline flush. If no response, try 9mg, 12mg, and then 18mg.] Check that the patient has received a therapeutic dose of adenosine (and experienced chest tightness with the injection). Higher doses are required in patients on theophyllines, lower in patients on dipyridamole.

  • AVNRT and AVRT may terminate with adenosine.

  • Transient AV block will unmask AF, flutter, and atrial tachycardia, but will not terminate.

  • The exact diagnosis may be left to an experienced cardiologist.

  • If there is degeneration of the rhythm into broad complex tachyarrhythmia and/or haemodynamic compromise, the patient must be electrically cardioverted immediately.

It is important to remember that SVT with previous bundle branch block/aberrancy or AVRT with pre-excitation can present with broad complex tachycardia. Differentiation from VT may be difficult, and if in doubt, the patient must be treated as VT until proven otherwise. ECG features to distinguish between the two are outlined under Cardiac emergencies Broad complex tachycardia: diagnosis, p. [link].

Dosages of selected antiarrhythmics for SVT

(See Table 1.8.)

Atrial fibrillation: assessment

Presentation

  • AF may present with palpitations, chest pain, breathlessness, collapse, or hypotension. Less commonly, it may present with an embolic event (stroke, peripheral embolus) or be asymptomatic. It occurs in 10–15% of patients post-MI.

  • Look for signs of an underlying cause (see Box 1.15).

  • Try to establish the duration of the AF—this will determine subsequent management (see later sections).

Investigations

These should be directed at looking for a precipitant and underlying heart disease. All patients should have:

  • ECG:

    • Broad QRS if aberrant conduction.

    • ST-T-wave changes may be due to rapid rate, digoxin, or underlying cardiac disease.

  • CXR: cardiomegaly, pulmonary oedema, intrathoracic precipitant, valve calcification (mitral stenosis).

  • U&Es: hypokalaemia, renal impairment.

  • Cardiac enzymes: ? MI. Small rise after DC shock.

  • Thyroid function: thyrotoxicosis may present as AF only.

  • Drug levels: especially if taking digoxin.

  • Mg2+, Ca2+.

  • ABG: if hypoxic, shocked, or ? acidotic.

  • Transthoracic (TTE)/transoesophageal echocardiography (TOE): for LV function and valve lesions and to exclude intracardiac thrombus or particularly thrombus in the LA appendage prior to cardioversion to sinus rhythm.

  • Other investigations depend on suspected precipitant.

Immediate management

Stabilize the patient

  • General measures (Cardiac emergencies Tachyarrhythmias heart rate >120bpm, pp. [link][link]) are as for any patient with an arrhythmia. Obtain venous access. Send bloods (Cardiac emergencies Tachyarrhythmias heart rate >120bpm, pp. [link][link]) and, if possible, check K+ immediately on an ITU machine.

  • Correct any electrolyte abnormality.

  • If severe acidosis (pH ≤7.1), give 8.4% sodium bicarbonate 50mL slowly IV over 20min.

  • CSM or IV adenosine may help confirm the diagnosis, revealing chaotic atrial activity. This is particularly helpful in patients with a rate of 150 bpm where atrial flutter should always be considered. CSM or adenosine will slow the ventricular rate and reveal flutter waves.

  • Does the ECG in AF show intermittent or constant delta waves? This suggests WPW, and digoxin and verapamil are contraindicated.

Further management

  • Cardiovert to sinus rhythm, if appropriate.

  • Control the ventricular response rate.

  • Try to prevent further episodes of AF.

Atrial fibrillation: management

(See Box 1.16.)

Rate control versus cardioversion

  • Important principles required to make a decision are:

    • Are there advantages in immediate cardioversion (e.g. ongoing ischaemia with fast ventricular rhythm, pulmonary oedema, Cardiac emergencies consciousness, haemodynamic instability)?

    • If the patient is cardioverted, will they remain in sinus rhythm (e.g. underlying sepsis/thyroid disease, large LA, poor LV, MV disease)?

    • What are the risks of thromboembolic complications and is anticoagulation required (helpful to calculate the CHADS2 and CHA2D2-Vasc scores)?

  • Cardioversion can be achieved chemically or with external defibrillation.

Haemodynamically unstable patients

  • All hypotensive patients should undergo external defibrillation using a synchronized shock of initially150J biphasic DC (Cardiac emergencies DC cardioversion 1, pp. [link][link]).

  • Do not attempt to defibrillate hypotensive patients with known chronic AF or a known underlying cause driving a fast ventricular response. Chances of success are very low (e.g. mitral stenosis, severe LV dysfunction, hyperthyroidism, sepsis).

  • Relative contraindications to defibrillation need to be weighed against the patient’s clinical condition. If possible, aim to optimize the clinical picture before cardioversion:

    • Hypokalaemia may be quickly corrected by giving 20mmol over 1h in 100mL of normal saline via a central line.

    • If digoxin toxicity is a possibility, ensure K+ is 4.5–5mmol/L and give magnesium sulfate 8mmol in 50mL of normal saline over 15min, before attempting defibrillation at low energies initially (e.g. 20–50J).

    • AF of >48h duration carries a significant risk of thromboembolic complications, unless the patient is on long-term anticoagulation and INR has been therapeutic. Consider performing TOE first.

  • The procedure is detailed under Cardiac emergencies DC cardioversion 1, pp. [link][link].

  • If DC shock fails initially:

    • Give IV amiodarone 300mg over 60min via a central line (followed by IV infusion of 900–1200mg over 24h).

    • Correct hypokalaemia (aim for K+ 4.5–5.0mmol/L).

    • Attempt further DC shock.

Haemodynamically stable patients

  • The initial aim should be rapid pharmacological rate control, followed by a decision regarding restoration of sinus rhythm if appropriate.

  • When making a decision regarding restoration of sinus rhythm, current evidence must be taken into account:

    • Management of AF with a rhythm control strategy alone has no survival benefit over a rate control strategy, as long as moderate- and high-risk patients are anticoagulated.

    • Rate control is not inferior to rhythm control for prevention of death and cardiovascular morbidity in patients with persistent AF after electrical cardioversion.

    • Patients in sinus rhythm are more likely to report a better ‘quality of life’ than those in AF.

AF >2 days’ duration

  • Control the ventricular rate using one of, or a combination of, digoxin and class II and IV agents (including: β‎-blocker, verapamil, diltiazem). Can be given as IV preparation to achieve rapid rate control, followed by oral preparations (see Table 1.8 for doses).

  • If patient not anticoagulated, start LMWH/UFH (UFH: give bolus of 5000U, followed by infusion, aiming for an APTT ratio of 2–3) until warfarinization is adequate (aim for an INR of 2–3).

  • Sinus rhythm may be restored by class Ia, Ic, and III agents (we recommend amiodarone, sotalol, quinidine, disopyramide, and flecainide).

  • If the patient needs to be electrically cardioverted, TOE must be performed to look for intracardiac thrombus or spontaneous contrast (a marker of very sluggish flow). If negative, DC cardioversion may be performed safely. Give a bolus of LMWH/UFH before cardioversion, if not already on LMWH/UFH.

  • Discharge when stable. Consider readmission following 4–6 weeks of warfarin for DC cardioversion.

AF <2 days’ duration

  • Although the risk of embolism in new-onset AF is low, we recommend anticoagulation at presentation with LMWH/UFH and subsequently warfarin (see previous section).

  • Attempt chemical cardioversion if there are no contraindications to potential agents. Chances of success are much higher with shorter duration of AF. Possible agents include:

    • Flecainide 2mg/kg IV over 10min (max. dose 150mg). Must be avoided in patients with known IHD and/or poor LV function.

    • Disopyramide 50–100mg IV. Ventricular rate may increase and fibrillatory waves coarsen before reverting to sinus rhythm, so load with digoxin/β‎-blocker/verapamil before giving this.

    • Amiodarone may be used IV/PO. Dosing requires a central line, and it may take 24–48h for sinus rhythm to be achieved. Amiodarone has relatively poor rate control properties and may need to be combined with a β‎-blocker or verapamil initially.

  • If cardioversion inappropriate or unsuccessful, achieve rate control as indicated in the previous section.

  • DC cardioversion can be attempted if rate control is difficult.

    • Discharge when stable. Anticoagulation may be achieved on an outpatient basis, if appropriate.

Atrial fibrillation: rate control

Controlling the ventricular response rate

  • Check that there is no history of WPW and that no delta waves are visible on the ECG.

  • We recommend β‎-blockers and calcium channel blockers (verapamil and diltiazem) as first-line agents for rate control. They both have the advantage of maintaining the ventricular rate during exertion. If a single agent is not adequate: either (1) combine β‎-blockers and calcium channel blockers (if BP adequate) or (2) add digoxin or amiodarone.

  • Digoxin is an alternative drug and can equally be used as a first-line agent. Patients should initially be given a full loading dose. The maintenance dose varies (0.0625–0.25mg od), depending on body mass, renal function, age, etc. Digoxin is poor at controlling the ventricular rate during exertion.

  • In patients with poor LV function, calcium channel blockers may not be appropriate, inducing heart failure, reflex tachycardia, and hypotension. β‎-blockers might be appropriate to help both with the heart failure (when not acute) and HR. Digoxin, with or without amiodarone, is a good combination (amiodarone will increase the plasma digoxin level, so halve the maintenance digoxin dose).

  • Other drugs that may be tried to control the ventricular rate are listed in Table 1.8.

  • If controlling the ventricular rate is difficult, consider alternative diagnosis, in particular MAT. Digoxin may make the arrhythmia worse (Cardiac emergencies Multifocal atrial tachycardia, p. [link]).

Long-term management

  • Look for causes (see Box 1.15), and arrange an Echo.

  • Patients successfully cardioverted acutely should be commenced on a prophylaxis regimen using class Ia, Ic, or III agents (e.g. sotalol, amiodarone, flecainide, propafenone). The choice of agent must be individualized:

    • Lone AF: use class Ic agents first, followed by class III or Ia if it fails.

    • Poor LV function: amiodarone and some β‎-blockers are the agents of choice.

    • IHD: class III agents and β‎-blockers (prevent ischaemia and, as a result, ischaemia-driven AF) are agents of choice.

  • If subsequently considered to be at low risk, treatment may be stopped at 1 month. Seek cardiac opinion if in doubt.

  • Patients cardioverted electively should remain on warfarin and rhythm prophylaxis for 1 month, pending outpatient review. The current trend is to keep patients at moderate or high risk of thromboembolism on anticoagulation life-long, unless there are concerns.

  • Patients with paroxysmal AF require long-term therapy to try to maintain sinus rhythm (classes III, Ic, and Ia). Digoxin only controls the ventricular rate and does not prevent AF. These patients may need long-term anticoagulation, depending on:

    • Frequency and length of AF paroxysms

    • Presence of underlying structural or cardiac abnormalities, and

    • Other systemic risk factors of thromboembolic complications.

Atrial flutter

  • This is rarely seen in the absence of underlying CAD, valve disease, myocardial disease, pericarditis, PE, or thyrotoxicosis.

  • The atrial rate is 280–320/min, and atrial activity is seen as flutter waves in inferior leads and V1 on the ECG.

  • The AV node conduction is slower (most commonly 2:1 block, sometimes 3:1 or 4:1), and this determines the ventricular rate.

  • Vagotonic manoeuvres and adenosine increase the AV block and reveal the flutter waves but only very rarely terminate the arrhythmia.

Management

  • Atrial flutter should be treated in exactly the same way as AF.

  • DC cardioversion is the therapy of choice, as flutter can be resistant to pharmacological therapy.

    • Lower energies are needed (50–100J).

    • If flutter has been present >48h, perform TOE and then cardiovert, with LMWH/UFH cover (as for AF).

  • Medical management:

    • Pharmacological agents recommended are similar to AF. Rate control and reversion rates can be low.

    • Digoxin, verapamil, and β‎-blockers can all be used to slow ventricular response. IV preparations can be used for more rapid action. The overall response can be poor. IV verapamil (2.5–5mg over 1–2min, repeated every 5min to a maximum dose of 20mg) will slow the response rate and occasionally restore sinus rhythm in 15–20% of patients.

    • Ibutilide and dofetilide have been reported to have reversion rates of 50% and 70%, respectively. Alternative agents are amiodarone, flecainide, quinidine, and procainamide.

    • NB Class Ia drugs can enhance AV conduction and must always be used after rate control has been achieved.

  • Flutter ablation can be performed, particularly in resistant and/or recurrent atrial flutter. Discuss with a cardiac electrophysiologist, as with increasing success of the procedure and reduced risk, this should be considered for all patients with resistant or recurrent flutter.

Multifocal atrial tachycardia

  • Commonly occurs in critically ill patients, especially with obstructive airways disease, who may be hypoxaemic and hypercapnic. Theophylline toxicity should be excluded.

  • Characterized by at least three different P wave morphologies with varying PP and PR intervals. Atrial nodal rate is 120–180 with 1:1 conduction.

  • Rapid regular rhythm may be difficult to differentiate from AF. However, differentiation is very important, as MAT is not responsive to DC cardioversion and is exacerbated by digoxin.

Management

  • The only true effective treatment is to treat the underlying illness. If associated with lung disease, aim to improve PaO2 and PaCO2.

  • Electrolyte abnormalities must be corrected. High-dose Mg2+ IV may restore sinus rhythm (15g over 5h).

  • There is increasing evidence from small trials that metoprolol is the most effective therapy. Use cautiously IV. However, most patients with MAT and COPD may not tolerate even a cardioselective β‎-blocker.

  • Verapamil is an alternative agent (5mg IV over 2min and repeated every 5min up to a maximum of 20mg; then 40–120mg PO tds) if the ventricular rate is consistently over >100/min and the patient is symptomatic.

  • DC shock and digoxin are ineffective.

Accessory pathway tachycardia (AV re-entrant tachycardia)

  • The three most common accessory pathways that produce paroxysmal tachycardias are described in Cardiac emergencies Types of accessory pathways, p. [link].

  • During re-entry tachycardia, the delta wave is lost, as the accessory pathway is only conducting retrogradely.

  • AF may produce very rapid ventricular rates, as the accessory pathway has rapid antegrade conduction (unlike the AV node). The ECG will show the delta wave in some or all of the QRS complexes.

Management

  • DC cardioversion should be used early if the tachycardia is poorly tolerated.

  • Class Ia, Ic, and II agents are suitable for chemical cardioversion. We recommend IV flecainide or disopyramide. β‎-blocker may also be given, especially if other agents are contraindicated (see Table 1.8).

  • Digoxin and verapamil should be avoided, as they may accelerate conduction down the accessory pathway. Amiodarone is dangerous, unless given very slowly (e.g. 300mg IV over 2–4h).

  • If recurrent symptoms, the patient should be referred for electrophysiological assessment and radiofrequency ablation. Seek specialist advice for long-term medical management.

Types of accessory pathways

Kent bundle (Wolff–Parkinson–White syndrome)

  • ECG: short PR interval and delta wave:

  • Associated with Ebstein’s, hypertrophic obstructive cardiomyopathy (HOCM), and mitral valve prolapse.

• Type A

Positive δ‎ wave in V1–V6

Negative in lead I

(Posterior left atrial pathway)

• Type B

Biphasic or negative δ‎ wave in V1–V3

Positive in lead I

(Lateral right atrial pathway)

• Concealed

No δ‎ wave visible, as pathway only conducts retrogradely.

Mahaim pathway (rare)

Pathway connects the AV node to the right bundle, resulting in a tachycardia with LBBB morphology.

James pathway (Lown–Ganong–Levine syndrome) (rare)

  • Short PR interval, but no delta wave.

  • Pathway connects the atria to the AV node, the bundle of His, or the fascicles.

Atrioventricular nodal re-entry tachycardia

  • AVNRT occurs secondary to a micro re-entrant circuit in the AV node.

  • General principles are as outlined under Cardiac emergencies Tachyarrhythmias heart rate >120bpm, pp. [link][link] (HR >120bpm apply).

  • Rate control can be achieved with (IV and PO) digoxin, β‎-blockers, and calcium channel blockers. β‎-blockers and calcium channel blockers can also promote reversion into sinus rhythm.

  • Class Ic and Ia agents (we recommend flecainide) can also be used for chemical cardioversion and maintenance of sinus rhythm long term.

  • If arrhythmia is resistant to treatment, consider electrical cardioversion.

  • Patients with recurrent symptoms should be referred for electrophysiological assessment and possible radiofrequency ablation.

Bradyarrhythmias: general approach

  • Ask specifically about previous cardiac disease, palpitations, blackouts, dizziness, chest pain, symptoms of heart failure, and recent drugs.

  • Examine carefully, noting the BP, JVP waveform (? cannon waves), heart sounds and murmurs, and signs of heart failure.

Investigations

  • 12-lead ECG and rhythm strip:

    • Look specifically for the relationship between P waves and QRS complex.

    • A long rhythm strip is sometimes necessary to detect CHB if atrial and ventricular rates are similar.

  • Blood tests:

    • FBC, biochemistry, glucose (urgently).

    • Ca2+, Mg2+ (especially if on diuretics).

    • Biochemical markers of cardiac injury.

  • Where appropriate:

    • Blood cultures, CRP, ESR.

    • TFTs.

    • Drug levels.

    • ABGs.

  • CXR:

    • Heart size.

    • ? signs of pulmonary oedema.

Management

Haemodynamically unstable patients

  • Give O2 via face mask if the patient is hypoxic on air.

  • Keep nil by mouth (NBM) until definitive therapy has been started to reduce the risk of aspiration in case of cardiac arrest or when the patient lies supine for temporary wire insertion.

  • Secure peripheral venous access.

  • Bradyarrhythmias causing severe haemodynamic compromise (cardiac arrest, asystole, SBP <90mmHg, severe pulmonary oedema, evidence of cerebral hypoperfusion) require immediate treatment and temporary pacing (the technique is described under Cardiac emergencies Indications for temporary pacing, pp. [link][link]).

    • Give atropine 1mg IV (Min-I-Jet®) bolus; repeat, if necessary, up to a maximum of 3mg.

    • Give isoprenaline 0.2mg IV (Min-I-Jet®) if there is a delay in pacing and the patient remains unstable. Set up an infusion (1mg in 100mL bag of normal saline, starting at 1mL/min, titrating to HR).

    • Set up an external pacing system (see Box 1.17), if available, and arrange for transfer to a screening room for transvenous pacing. If fluoroscopy is not available, ‘blind’ transvenous pacing using a balloon-tipped pacing wire may be attempted.

  • Bradycardia in shock is a poor prognostic sign. Look for a source of blood loss, and begin aggressive resuscitation with fluids and inotropes.

Haemodynamically stable patients

  • Admit to CCU with continuous ECG monitoring.

  • Keep atropine drawn up and ready in case of acute deterioration.

  • Does the patient require a temporary wire immediately? It may be of value to have appropriate central venous access (femoral or internal jugular vein) in place in case of need for emergency temporary wire insertion.

  • Refer the patient to a cardiologist.

Sinus bradycardia or junctional rhythm

(HR <50 bpm)

Causes

  • Young, athletic individual (physiological bradycardia).

  • Drugs (β‎-blockers, morphine).

  • Hypothyroidism.

  • Hypothermia.

  • Cardiac emergencies vagal tone:

    • Vasovagal attack.

    • Nausea or vomiting.

    • Carotid sinus hypersensitivity.

    • Acute MI (especially inferior).

  • Ischaemia or infarction of the sinus node.

  • Chronic degeneration of sinus or AV nodes or atria.

  • Cholestatic jaundice.

  • Raised intracranial pressure (ICP).

Management

  • If hypotensive or pre-syncopal, treat as described under Cardiac emergencies Bradyarrhythmias: general approach, pp. [link][link]:

    • Atropine 600 micrograms–3mg IV bolus, repeating as necessary.

    • Isoprenaline 0.5–10 micrograms/min IV infusion.

    • Temporary pacing.

    • Avoid and take steps to correct precipitants (see Cardiac emergencies Causes, p. [link]).

    • Stop any drugs that may suppress the sinus or AV nodes.

  • Long-term treatment:

    • If all possible underlying causes removed and if symptomatic bradycardia remains, refer for permanent pacing.

    • Consider Holter monitoring in patients with possible episodic bradycardia. R–R intervals >2.5s may require permanent pacing, especially if associated with symptoms.

Intraventricular conduction disturbances

Common causes of bundle branch block

  • IHD.

  • Hypertensive heart disease.

  • Valve disease (especially aortic stenosis).

  • Conduction system fibrosis (Lev and Len’gre syndromes).

  • Myocarditis or endocarditis.

  • Cardiomyopathies.

  • Cor pulmonale (RBBB) (acute or chronic).

  • Trauma or post-cardiac surgery.

  • Neuromuscular disorders (myotonic dystrophy).

  • Polymyositis.

Management

  • General principles (Cardiac emergencies Bradyarrhythmias: general approach, pp. [link][link]) apply.

  • Interventricular conduction disturbances on their own do not require temporary pacing. However, when associated with haemodynamic disturbance or progression to higher levels of block (even if intermittent), insertion of a transvenous pacing wire must be considered. The need for longer-term pacing is dependent on the persistence of symptoms and underlying cause. Consult a cardiologist. See Cardiac emergencies Indications for temporary pacing, pp. [link][link] for situations where temporary pacing is indicated.

Types of atrioventricular conduction block

First-degree heart block

  • Prolongation of the PR interval (>0.22s, >5 small squares).

Second-degree heart block

  • Mobitz type 1 (Wenckebach): progressive increase in PR interval, with intermittent complete AV block (P wave not conducted).

  • Mobitz type 2: the PR interval is constant, but there is intermittent failure to conduct the P wave. Often occurs in the presence of broad QRS complex.

  • 2:1, 3:1, etc.: as in Mobitz type 2, the PR interval is constant, but every second (in 2:1) or third (in 3:1) P wave is not conducted on a regular basis.

Third-degree (complete) heart block

Complete AV dissociation. If the P and QRS rates are similar, a long rhythm strip or exercise (to speed up the atrial rate) will help demonstrate dissociation.

Causes

  • Associated with acute infarction or ischaemia.

  • Drugs (β‎-blockers, digitalis, calcium channel blockers).

  • Conduction system fibrosis (Lev and Len’gre syndromes).

  • Cardiac emergencies vagal tone.

  • Trauma or following cardiac surgery.

  • Hypothyroidism (rarely thyrotoxicosis).

  • Hypothermia.

  • Hyperkalaemia.

  • Hypoxia.

  • Valvular disease (aortic stenosis, incompetence, endocarditis).

  • Myocarditis (diphtheria, rheumatic fever, viral, Chagas’ disease).

  • Associated with neuromuscular disease, i.e. myotonic dystrophy.

  • Collagen vascular disease [systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), scleroderma].

  • Cardiomyopathies (haemochromatosis, amyloidosis).

  • Granulomatous disease (sarcoid).

  • Congenital heart block.

  • Congenital heart disease [atrial septal defect (ASD), Ebstein’s, patent ductus arteriosus (PDA)].

Management

  • Principles are listed under Cardiac emergencies Bradyarrhythmias: general approach, pp. [link][link].

  • In summary, all symptomatic patients must have pacing (temporary or permanent). The higher the level of block (irrespective of symptoms), the greater the progression to CHB and/or chances of asystole.

  • See Cardiac emergencies Indications for temporary pacing, pp. [link][link] for situations when temporary pacing is indicated. Some cardiologists may prefer to implant a permanent system straightaway.

Pulmonary oedema: assessment

Presentation

  • Acute breathlessness, cough, frothy bloodstained (pink) sputum.

  • Collapse, cardiac arrest, or shock.

  • Associated features may reflect underlying cause:

    • Chest pain or palpitations: ? IHD/MI, arrhythmia.

    • Preceding history of dyspnoea on exertion: ? IHD, poor LV.

    • Oliguria, haematuria: ? acute renal failure (ARF) (Cardiac emergencies Acute kidney injury 1, pp. [link][link]).

    • Seizures, signs of intracranial bleed.

Causes

A diagnosis of pulmonary oedema or ‘heart failure’ is not adequate. An underlying cause must be sought in order to direct treatment appropriately. These may be divided into:

  • Cardiac emergencies pulmonary capillary pressure (hydrostatic).

  • Cardiac emergencies pulmonary capillary permeability.

  • Cardiac emergencies intravascular oncotic pressure.

Often a combination of factors are involved (e.g. pneumonia, hypoxia, cardiac ischaemia) (see Box 1.19).

The main differential diagnosis is acute (infective) exacerbation of COPD (previous history, quiet breath sounds, wheeze, fewer crackles). It may be difficult to differentiate the two clinically, and indeed sometimes they could coexist.

Principles of management

  1. 1. Stabilize the patient—relieve distress and begin definitive treatment.

  2. 2. Look for an underlying cause.

  3. 3. Address haemodynamic and respiratory issues.

  4. 4. Optimize and introduce long-term therapy.

Initial rapid assessment

  • If the patient is very unwell (e.g. unable to speak, hypoxic, SBP <100mmHg), introduce stabilizing measures and begin treatment immediately before detailed examination and investigations (see Box 1.18).

  • If the patient is stable and/or if there is doubt as to the diagnosis, give O2 and diuretic, but await the outcome of clinical examination and CXR before deciding on definitive treatment.

Urgent investigations for all patients

  • ECG: sinus tachycardia most common. ? any cardiac arrhythmia (AF, SVT, VT). ? evidence of acute ST change (STEMI, NSTEMI, UA). ? evidence of underlying heart disease [left ventricular hypertrophy (LVH), p mitrale].

  • CXR: to confirm the diagnosis, look for interstitial shadowing, enlarged hila, prominent upper lobe vessels, pleural effusion, and Kerley B lines. Cardiomegaly may or may not be present. Also exclude pneumothorax, PE (oligaemic lung fields), and consolidation.

  • ABG: typically Cardiac emergenciesPaO2. PaCO2 levels may be Cardiac emergencies (hyperventilation) or Cardiac emergencies, depending on the severity of pulmonary oedema. Pulse oximetry may be inaccurate if peripherally shut down.

  • U&Es: ? pre-existing renal impairment. Regular K+ measurements (once on IV diuretics).

  • FBC: ? anaemia or leucocytosis indicating the precipitant.

  • Echo: as soon as practical to assess LV function, valve abnormalities, VSD, or pericardial effusion.

Pulmonary oedema: causes

Look for an underlying cause for pulmonary oedema (see Box 1.19).

Pulmonary oedema: management 1

Stabilize the patient

  • Patients with acute pulmonary oedema should initially be continuously monitored and managed where full resuscitation facilities are available.

  • Sit the patient up in bed.

  • Give 60–100% O2 by face mask (unless contraindicated—COPD).

  • If the patient is severely distressed, summon the ‘on-call’ anaesthetist and inform ITU. If dyspnoea cannot be significantly improved by acute measures (see following text), the patient may require CPAP or mechanical ventilation.

  • Treat any haemodynamically unstable arrhythmia—urgent synchronized DC shock may be required.

  • Give:

    • Diamorphine 2.5–5mg IV (caution abnormal ABGs).

    • Metoclopramide 10mg IV.

    • Furosemide 40–120mg slow IV injection.

  • Secure venous access, and send blood for urgent U&Es, FBC, and cardiac enzymes (including troponin).

  • Unless thrombolysis is indicated, take ABG.

  • If SBP is ≥90mmHg and the patient does not have aortic stenosis:

    • Give SL GTN spray (two puffs).

    • Start IV GTN infusion 1–10mg/h; increase the infusion rate every 15–20min, titrating against BP (aiming to keep SBP ~100mmHg).

  • If SBP is <90mmHg, treat the patient as cardiogenic shock (Cardiac emergencies Cardiogenic shock, pp. [link][link]).

  • Insert a urinary catheter to monitor urine output, if appropriate.

  • Repeat ABG and K+ if the clinical condition deteriorates/fails to improve, or after 2h if there is improvement and the original sample was abnormal (serial K+ monitoring could also be performed from venous blood).

  • Monitor pulse, BP, RR, O2 saturation with a pulse oximeter (if an accurate reading can be obtained), and urine output.

Further management

Subsequent management of the patient is aimed at ensuring adequate ventilation/gas exchange, ensuring haemodynamic stability, and correcting any reversible precipitants of acute pulmonary oedema.

  • Assess the patient’s respiratory function:

    • Does the patient require respiratory support?(Cardiac emergencies Respiratory failure: assessment, pp. [link][link])

  • Assess the patient’s haemodynamic status:

    • Is the patient in shock? (Cardiac emergencies Non-VF/VT (asystole and PEA), pp. [link][link])

  • Look for an underlying cause (Cardiac emergencies Pulmonary oedema: causes, p. [link])

  • Conditions that require specific treatment:

    • Acute AR and MR (Cardiac emergencies Acute mitral regurgitation, pp. [link][link]).

    • Diastolic LV dysfunction (Cardiac emergencies Hypotension and shock post-MI, p. [link]).

    • Fluid overload (Cardiac emergencies Pulmonary oedema: specific conditions, p. [link]).

    • Renal failure (Cardiac emergencies Acute kidney injury 2, pp. [link][link]).

    • Severe anaemia.

    • Hypoproteinaemia (Cardiac emergencies Pulmonary oedema: specific conditions, p. [link]).

    • Sepsis (Cardiac emergencies Sepsis syndrome and septic shock, pp. [link][link]).

Pulmonary oedema: management 2

If the patient remains unstable and/or deteriorates, take the following steps.

Assess the patient’s respiratory function

  • Wheeze may be caused by interstitial pulmonary oedema. If there is a history of asthma, give nebulized salbutamol (2.5–5mg), nebulized ipratropium bromide (500 micrograms), and hydrocortisone (200mg) IV. Consider commencing an aminophylline infusion. This will relieve bronchospasm, as well as ‘offload’ by systemic vasodilatation (Cardiac emergencies Acute severe asthma: immediate therapy, p. [link]). However, it may worsen tachycardia, and it can be arrhythmogenic and lower potassium levels (K+) (supplement to ensure K+ levels are 4–5mmol/L).

  • Indications for further respiratory support include:

    • Patient exhaustion or continuing severe breathlessness.

    • Persistent PaO2 <8kPa.

    • Rising PaCO2.

    • Persistent or worsening acidosis (pH <7.2).

  • CPAP: this may be tried for cooperative patients, who can protect their airway, have adequate respiratory muscle strength, and are not hypotensive. The positive pressure reduces venous return to the heart and may compromise BP.

  • ET intubation and mechanical ventilation may be required, and some positive end-expiratory pressure (PEEP) should be used (Cardiac emergencies Positive end-expiratory pressure, p. [link]).

  • Discuss the patient with the on-call anaesthetist or ITU team EARLY.

Assess the patient’s haemodynamic status

It is important to distinguish between cardiogenic and non-cardiogenic pulmonary oedema, as further treatment is different between the two groups. This may be difficult clinically. A PA (Swan–Ganz) catheter can be considered in experienced centres if the patient’s condition will allow.

  • Non-cardiogenic pulmonary oedema occurs when the hydrostatic pressure within the capillary system overcomes the plasma oncotic pressure. In patients with hypoalbuminaemia, this will occur at PCWP <15mmHg. The critical PCWP may be estimated by serum albumin (g/L) × 0.57. Thus, a patient with a serum albumin of 15g/L will develop hydrostatic pulmonary oedema at an LA pressure of 8mmHg; a serum albumin of 30g/L will require an LA pressure of >17mmHg, etc.

  • Cardiogenic pulmonary oedema is often associated with significant systemic hypotension or low output states. Contributing factors include conditions where there is ‘mechanical’ impairment to forward flow [e.g. valvular heart disease (especially if acute), VSD] or severe myocardial disease (large MI, myocarditis, cardiomyopathy).

  • The gradient between PA diastolic pressure and PCWP (PAD–PCWP) is generally <5mmHg in cardiogenic, and >5mmHg in non-cardiogenic, pulmonary oedema (e.g. ARDS).

  • The pulse and BP are most commonly elevated due to circulating catecholamines and overactivity of the renin–angiotensin system. Examination reveals sweating, cool and ‘shut-down’ peripheries, and high pulse volume (assess the carotid or femoral pulses).

Management

(See Box 1.20.)

The general approach involves combination of diuretics, vasodilators, and inotropes. Patients may be divided into two groups:

  • Patients in shock (with SBP <100mmHg) (Cardiac emergencies Pulmonary oedema: management 3, pp. [link][link]).

  • Haemodynamically stable patients with SBP >100mmHg (Cardiac emergencies Pulmonary oedema: management 3, pp. [link][link]).

Pulmonary oedema: management 3

Patients with SBP <100mmHg

  • The patient is in incipient (or overt) shock. The most common aetiology is cardiogenic shock, but remember non-cardiogenic causes (e.g. ARDS, septic shock; Cardiac emergencies Shock, pp. [link][link]).

  • Optimal monitoring and access: central line ± PA catheter (Swan–Ganz), urinary catheter, arterial line (monitoring BP and ABGs). Internal jugular lines are preferable, as the risk of pneumothorax is lower.

  • Ensure the patient is not underfilled, using PCWP as a guide (<10mmHg) (mistaken diagnosis, e.g. septic shock from bilateral pneumonia).

  • Is there a mechanical cause that may require emergency surgery?

    • Arrange an urgent Echo to rule out:

    • VSD and acute MR in all patients with recent MI with/without new murmur (Cardiac emergencies STEMI: complications, pp. [link][link]).

    • Prosthetic heart valve dysfunction (e.g. dehiscence, infection) or pre-existing native aortic or mitral disease that may require surgery.

    • Discuss the patient early on with a cardiologist/cardiac surgeon.

The choice of inotropic agent depends on the clinical condition of the patient and, to some extent, the underlying diagnosis.

  • Treatment of septic shock is discussed elsewhere (Cardiac emergencies Sepsis syndrome and septic shock, pp. [link][link]).

  • SBP 80–100mmHg and cool peripheries: start dobutamine infusion at 5 micrograms/kg/min, increasing by 2.5 micrograms/kg/min every 10–15min to a maximum of 20 micrograms/kg/min until BP >100mmHg. This may be combined with dopamine (2.5–5 micrograms/kg/min). However, tachycardia and/or hypotension secondary to peripheral vasodilatation may limit its effectiveness. PDIs (enoximone or milrinone) should be considered where dobutamine fails.

  • SBP <80mmHg: give a slow IV bolus of adrenaline (2–5mL of 1 in 1000 solution Min-I-Jet®), and repeat if necessary.

    • Dopamine at doses of >2.5 micrograms/kg/min has a pressor action, in addition to direct and indirect inotropic effects, and may be used at higher doses (10–20 micrograms/kg/min) if the BP remains low. However, it tends to raise the pulmonary capillary filling pressure further and should be combined with vasodilators (e.g. nitroprusside or hydralazine) once the BP is restored (Cardiac emergencies Hypertensive emergencies: drug treatment, pp. [link][link]). Beware of arrhythmias at these doses.

    • Adrenaline infusion may be preferred to high-dose dopamine as an alternative inotrope. Once the BP is restored (>100mmHg), vasodilators, such as nitroprusside/hydralazine or GTN infusion, should be added to counteract the pressor effects. Adrenaline can be combined with dobutamine and/or a PDI, especially in the context of a poor ventricle.

  • Intra-aortic balloon counterpulsation should also be used with/without inotropes in the context of a potentially reversible cause for pulmonary oedema and shock (e.g. ongoing myocardial ischaemia, VSD, acute MR) (Cardiac emergencies Ventricular septal defect post-myocardial infarction (MI), pp. [link][link]).

  • Further doses of diuretic may be given.

Patients with SBP ≥100mmHg

  • Further doses of diuretic may be given—furosemide 40–80mg IV every 3–4h or as an infusion (e.g. 160–240mg over 24h).

  • Continue the GTN infusion, increasing the infusion rate every 15–20min up to 10mg/h, titrating against the BP (aiming to keep SBP ~100mmHg).

  • ACEIs can be used if BP is adequate and there are no other known contraindications (e.g. renal artery stenosis, renal failure), although most clinicians will wait after the acute heart failure has settled, as ACEIs might decrease diuresis in this context. Arteriolar vasodilators (nitroprusside or hydralazine) may also be added to, or used instead of, GTN in patients with adequate BP. Arterial pressure should be monitored continuously via an arterial line to prevent inadvertent hypotension.

Long-term management

  • Unless a contraindication exists, start an ACEI, increasing the dose to as near the recommended maximal dose as possible. In the context of LV impairment, ACEIs have significant prognostic benefit.

  • If ACEIs are contraindicated or not tolerated, consider the use of hydralazine and a long-acting oral nitrate in combination.

  • For all patients with impaired EF and New York Heart Association (NYHA) classes III/IV, consider the addition of spironolactone (25–50mg). (NB Monitor renal function and serum potassium.)

  • In the context of stable patients (no clinical features of failure) and poor LV function, β‎-blockers have significant mortality and some symptomatic benefit (NB Start at a very small dose, and increase gradually every 2 weeks, with regular monitoring). Bisoprolol, carvedilol, and metoprolol slow-release (not available in the UK) can all be used.

  • Ensure all arrhythmias are treated (Cardiac emergencies Tachyarrhythmias heart rate >120bpm, pp. [link][link]).

  • Digoxin can be used for symptomatic improvement.

  • Consider multi-site pacing (biventricular) in the context of severe LV dysfunction, broad QRS complex, or Echo evidence of dyssynchrony.

  • Patients with AF or poor LV function should be considered for long-term anticoagulation.

  • Patients <60 years with severe irreversible LV dysfunction and debilitating symptoms must be considered for cardiac transplantation and other LV support devices such as left ventricular assist devices (LVADs) as bridge to destination therapy.

Pulmonary oedema: specific conditions

Diastolic LV dysfunction

  • This typically occurs in elderly hypertensive patients with LVH where there is impaired relaxation of the ventricle in diastole. There is marked hypertension, pulmonary oedema, and normal or only mild systolic LV impairment.

  • With tachycardia, diastolic filling time shortens. As the ventricle is ‘stiff’ in diastole, LA pressure is Cardiac emergencies and pulmonary oedema occurs (exacerbated by AF, as filling by atrial systole is lost).

  • Treatment involves control of hypertension with IV nitrates (and/or nitroprusside), calcium blockers (verapamil or nifedipine), and even selective β‎-blockers (e.g. carvedilol).

Fluid overload

  • Standard measures are usually effective.

  • In extreme circumstances, venesection may be necessary.

  • Check the patient is not anaemic [haemoglobin (Hb) ≥10g/dL]. Remove 500mL of blood via a cannula in a large vein, and repeat if necessary.

  • If anaemic (e.g. renal failure) and acutely unwell, consider dialysis (Cardiac emergencies Acute kidney injury 1, pp. [link][link]).

Known (or unknown) renal failure

  • Unless the patient is permanently anuric, large doses of IV furosemide may be required (up to 1g, given at 4mg/min), in addition to standard treatment.

  • If such treatment fails, or the patient is known to be anuric, dialysis will be required.

  • In patients not known to have renal failure, an underlying cause should be sought (see Box 4.2).

Anaemia

  • Cardiac failure may be worsened or precipitated by the presence of significant anaemia. Symptoms may be improved in the long term by correcting this anaemia.

  • Generally, transfusion is unnecessary with Hb >9g/dL, unless there is a risk of an acute bleed. Treatment of pulmonary oedema will result in haemoconcentration and a ‘rise’ in Hb.

  • If anaemia is thought to be exacerbating pulmonary oedema, ensure that adequate diuresis is obtained prior to transfusion. Give slow transfusion (3–4h per unit) of packed cells, with IV furosemide 20–40mg before each unit.

Hypoproteinaemia

  • The critical LA pressure at which hydrostatic pulmonary oedema occurs is influenced by the serum albumin and approximates to [serum albumin concentration (g/L) × 0.57].

  • Treatment involves diuretics, cautious albumin replacement, spironolactone (if there is secondary hyperaldosteronism), and importantly treatment of the underlying cause for hypoproteinaemia.

Infective endocarditis (IE)

Clinical presentation of IE is highly variable and dependent on a combination of intracardiac pathology, evolution of the infection, and possible extracardiac involvement. Presentation can be insidious, as in streptococcal infections, with striking constitutional symptoms, such as with Staphylococcus aureus.

Presenting features can include the following:

  • Symptoms and signs of the infection: these include malaise, anorexia, weight loss, fever, rigors, and night sweats. Long-standing infection produces anaemia, clubbing, and splenomegaly.

  • Cardiac manifestations of the infection: congestive cardiac failure (CCF), palpitations, tachycardia, new murmur, pericarditis, or AV block.

  • Symptoms and signs due to immune complex deposition:

    • Skin: petechiae (most common), splinter haemorrhages, Osler’s nodes [small tender nodules (pulp infarcts) on hands and feet, which persist for hours to days], Janeway lesions (non-tender, erythematous, and/or haemorrhagic areas on the palms and soles).

    • Eye: Roth spots (oval retinal haemorrhages with a pale centre, located near the optic disc), conjunctival splinter haemorrhages, retinal flame haemorrhages.

    • Renal: microscopic haematuria, glomerulonephritis, and renal impairment.

    • Cerebral: toxic encephalopathy.

    • Musculoskeletal: arthralgia or arthritis.

Complications of the infection

  • Local effects:

    • Valve destruction results in a new or changing murmur. This may result in progressive heart failure and pulmonary oedema.

    • A new harsh pan-systolic murmur and acute deterioration may be due to perforation of the interventricular septum or rupture of the sinus of Valsalva aneurysm into the RV.

    • High-degree AV block (2–4% of IE) occurs with intracardiac extension of the infection into the interventricular septum (e.g. from aortic valve endocarditis).

    • Intracardiac abscess may be seen with any valve infection (25–50% of aortic endocarditis, 1–5% of mitral, but rarely with tricuspid) and is most common in prosthetic valve endocarditis (PVE).

  • Embolic events:

    • Septic emboli are seen in 20–45% of patients and may involve any circulation (brain, limbs, coronary, kidney, or spleen); PEs with tricuspid endocarditis.

    • Forty to 45% of patients who have had an embolic event will have another.

    • The risk depends on the organism (most common with Gram negative infections, S. aureus, or Candida) (see Box 1.22) and the presence and size of vegetations (emboli in 30% of patients with no vegetation on Echo, 40% with vegetations of <5mm, and 65% with vegetations of >5mm).

Ask specifically for a history of dental work, infections, surgery, IV drug use, or instrumentation, which may have led to bacteraemia. Examine for any potential sources of infection, especially teeth or skin lesions. Risk factors for endocarditis are shown in Box 1.21.

IE: diagnosis

Clinical features can be non-specific, and diagnosis difficult. A high index of suspicion must be maintained if patients present with unexplained fever, a predisposing cardiac lesion, bacteraemia, and an embolic phenomenon.

The Duke classification has been devised to help with the diagnosis:

  • Definite endocarditis: two major criteria, or one major and three minor criteria, or five minor criteria.

  • Possible endocarditis: findings which fall short of definite endocarditis but are not rejected.

  • Rejected diagnosis: firm alternative diagnosis, or sustained resolution of clinical features with <4 days of antibiotic therapy.

Major criteria

Positive blood culture

  • Typical microorganism for IE from two separate blood cultures.

  • Persistently positive blood culture.

Evidence of endocardial involvement

  • Positive echocardiogram:

    • Oscillating intracardiac mass (vegetation).

    • Abscess.

    • New partial dehiscence of prosthetic valve.

    • New valve regurgitation.

Minor criteria

  • Predisposing condition or drug use.

  • Fever >38°C.

  • Vascular phenomena: arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial and conjunctival haemorrhage, Janeway lesions.

  • Immunologic phenomena: glomerulonephritis, Osler’s nodes, Roth spots, rheumatoid factor.

  • Microbiological evidence: positive blood cultures, but not meeting major criteria, or serological evidence of organism consistent with IE.

  • Echo: positive for IE, but not meeting major criteria.

For common organisms in IE, see Box 1.22.

IE: investigations

  • Blood cultures

Take 3–4 sets of cultures from different sites at least an hour apart, and inoculate a minimum of 10mL/bottle for the optimal pick-up rate. Both aerobic and anaerobic bottles must be used. Lab should be advised that IE is a possibility, especially if unusual organisms are suspected. In stable patients on antibiotic therapy, doses must be delayed to allow culture on successive days. Ask for prolonged (fungal) cultures in IV drug users.

  • FBC

May show normochromic, normocytic anaemia (exclude haematinic deficiency), fragmented red blood cells (RBCs), and low haptoglobins, with mechanical valves, neutrophil leucocytosis, and perhaps thrombocytopenia.

  • U&Es

May be deranged (this should be monitored throughout treatment).

  • LFTs

May be deranged, especially with an increase in alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT). Raised LDH if there is RBC fragmentation.

  • ESR/CRP

Acute phase reaction.

  • Urinalysis

Microscopic haematuria ± proteinuria.

  • Immunology

Polyclonal elevation in serum immunoglobulins (Igs), complement levels.

  • ECG

May have changes associated with any underlying cause. There may be AV block or conduction defects (especially aortic root abscess) and rarely (embolic) acute MI.

  • CXR

May be normal. Look for pulmonary oedema or multiple infected or infarcted areas from septic emboli (tricuspid endocarditis) and to exclude chest cause for sepsis.

  • Echo

TTE may confirm the presence of valve lesions and/or demonstrate vegetations if >2mm in size. TOE is more sensitive for aortic root and mitral leaflet involvement. A normal Echo does not exclude the diagnosis.

  • MRI

Useful in investigation of paravalvular extension, aortic root aneurysm, and fistulae.

  • Dentition

All patients should have an orthopentamograph (OPG)—a panoramic dental X-ray, and a dental opinion.

  • Swabs

Any potential sites of infection (skin lesions).

  • V/Q scan

In cases where right-sided endocarditis is suspected, this may show multiple mismatched defects.

  • Save serum for

Aspergillus precipitins, Candida antibodies (rise in titre), Q fever (Coxiella burnetti), complement fixation test, Chlamydia complement fixation test, Brucella agglutinins, Legionella antibodies, Bartonella spp.

IE: antibiotics

‘Blind’ treatment for endocarditis

IE is usually a clinical diagnosis and must be considered in any patient with a typical history, fever, and a murmur with no other explanation. Often antibiotics need to be started before the culture results are available. Be guided by the clinical setting (see Table 1.9); see Box 1.23 for suggested doses.

Table 1.9 Antibiotic treatment of IE*

Presentation

Choice of antibiotic

Gradual onset (weeks)

Benzylpenicillin + gentamicin

Acute onset (days) or history of skin trauma

Flucloxacillin + gentamicin

Recent valve prosthesis [possible meticillin-resistant S. aureus (MRSA), diphtheroid, Klebsiella, Corynebacterium, or nosocomial staphylococci)

Vancomycin (or teicoplanin) + gentamicin + rifampicin

IV drug user

Vancomycin

* Oakley CM; The medical treatment of culture-negative infective endocarditis, European Heart Journal 1995; 16 (suppl_B): 90–93, doi:10.1093/eurheartj/16.suppl_B.90. (Translated and) Reprinted by permission of Oxford University Press on behalf of the European Society of Cardiology.

Duration of treatment

  • This is controversial, with a trend towards shorter courses. Microbiology and infectious disease (ID) opinion is important, especially in resistant and/or uncommon organisms. Box 1.24 shows one suggested protocol.

  • The duration of treatment varies, depending on the severity of infection and the infecting organism. IV therapy is usually for at least 2 weeks, and total antibiotic therapy is for 4–6 weeks.

  • If the patient is well following this period, antibiotic treatment may be stopped. Provided no surgery is indicated (Cardiac emergencies Surgery for IE, pp. [link][link]), the patient may be discharged and followed up in outpatient clinic.

  • Patients should be advised of the need for endocarditis prophylaxis in the future (see Table 1.10).

  • Patients with valvular damage following infection should be followed long term, and patients with VSDs should be considered for closure.

Table 1.10 Antibiotic prophylaxis

1 hour before

6 hours after

Minimal regimen

No penicillin allergy

Amoxicillin 3g PO

No 2nd dose

Allergy to penicillin

Clindamycin 300–600mg PO

No 2nd dose

Maximal regimen

No penicillin allergy

Amoxicillin 2g IV

+

Gentamicin 1.5mg/kg IM/IV

Vancomycin 1g IV over 1h

1–1.5g PO

No 2nd dose

1g IV at 12h

Allergy to penicillin

+

Gentamicin 1.5mg/kg IM/IV

No 2nd dose

Flexible modifications, depending on ‘degree of risk’

  • Additional doses after procedure.

  • Additional aminoglycosides.

  • Parenteral administration.

IE: monitoring treatment

Patients need careful clinical monitoring both during and for several months after the infection. Reappearance of features suggestive of IE must be investigated thoroughly to rule out recurrent infection or resistance to the treatment regimen.

Clinical features

  • Signs of continued infection, persistent pyrexia, and persistence of systemic symptoms.

  • Persistent fever may be due to drug resistance, concomitant infection (central line, urine, chest, septic emboli to lungs or abdomen), or allergy (? eosinophilia, ? leucopenia, ? proteinuria: common with penicillin but may be due to any antibiotic; consider changing or stopping antibiotics for 2–3 days).

  • Changes in any cardiac murmurs or signs of cardiac failure.

  • Development of any new embolic phenomena.

  • Inspect venous access sites daily. Change peripheral cannulae every 3–4 days.

Echo

  • Regular (weekly) TTEs may identify clinically silent, but progressive, valve destruction and development of intracardiac abscesses or vegetations.

  • The tips of long-standing central lines may develop sterile fibrinous ‘fronds’, which may be visible on TOE—change the line and send the tip for culture.

  • ‘Vegetations’ need not be due to infection (see Box 1.25).

ECG

Looking specifically for AV block or conduction abnormalities suggesting intracardiac extension of the infection. A daily ECG must be performed.

Microbiology

  • Repeated blood cultures (especially if there is continued fever).

  • Regular aminoglycoside and vancomycin levels (ensuring the absence of toxic levels and the presence of therapeutic levels). Gentamicin ototoxicity may develop with prolonged use, even in the absence of toxic levels.

  • Back titration to ensure that minimum inhibitory and bactericidal concentrations are being achieved.

Laboratory indices

  • Regular (daily) urinalysis.

  • Regular U&Es and LFTs.

  • Regular CRP (ESR every 2 weeks).

  • FBC: rising Hb and falling WCC suggests successful treatment; watch for β‎-lactam-associated neutropenia.

  • Serum magnesium (if on gentamicin).

References

2. Michel PL, Acar J (1995). Native cardiac disease predisposing to infective endocarditis. Eur Heart J 16(suppl B):2–6.Find this resource:

Culture-negative endocarditis

  • The most common reason for persistently negative blood cultures is prior antibiotic therapy, and this affects up to 15% of patients with a diagnosis of IE (see Box 1.26).

  • If the clinical response to the antibiotics is good, these should be continued.

  • For persisting fever:

    • Withhold antibiotics if not already started.

    • Consider other investigations for a ‘pyrexia of unknown origin’ (PUO) (Cardiac emergencies Pyrexia of unknown origin, p. [link]).

    • If clinical suspicion of IE is high, it warrants further investigation.

    • Repeated physical examination for any new signs.

    • Regular Echo and TOE. ‘Vegetations’ need not be due to infection (see Box 1.25).

    • Repeated blood cultures, especially when the temperature is raised. Discuss with microbiology about prolonged culturing times (4+ weeks) and special culturing and subculturing techniques. Most HACEK-group organisms can be detected (see Box 1.26).

  • Consider unusual causes of endocarditis.

  • Q-fever (Coxiella burnetii): complement fixation tests identify antibodies to phase 1 and 2 antigens. Phase 2 antigens are raised in acute illness, and phase 1 antigens in chronic illnesses such as endocarditis. Polymerase chain reaction (PCR) can be performed on operative specimens. Treat with indefinite (life-long) oral doxycycline ± co-trimoxazole, rifampicin, or quinolone.

  • Chlamydia psittaci: commonly, there is a history of exposure to birds and there may be an associated atypical pneumonia. Diagnosis is confirmed using complement fixation tests to detect raised antibody titres.

  • Brucellosis: blood cultures may be positive, although organisms may take up to 8 weeks to grow. Serology usually confirms the diagnosis.

  • Fungi: Candida is the most common species and may be cultured. Detection of antibodies may be helpful, although levels may be raised in normals. Detection of a rising titre is of more use. Other fungal infections (e.g. histoplasmosis, aspergillosis) are rare but may be diagnosed with culture or serology, although these are commonly negative. Antigen assays may be positive, or the organism may be isolated from biopsy material. Fungal IE is more common in patients with prosthetic valves and IV drug users. Bulky vegetations are common. Treatment is with amphotericin ± flucytosine. Prosthetic valves must be removed. Mortality is >50%.

* HACEK: Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella spp.

Right-sided endocarditis

  • May present as multiple infected PEs (abscesses).

  • Always consider this diagnosis in IV drug users (or patients with venous access).

  • Endocarditis on endocardial permanent pacemaker leads is a rare, but recognized, cause.

  • Patients most commonly have staphylococcal infection and are unwell, requiring immediate treatment and often early surgery.

  • Lesions may be sterilized with IV antibiotics.

  • Surgery may be required for:

    • Resistant organisms (S. aureus, Pseudomonas, Candida, and infection with multiple organisms).

    • Increasing vegetation size in spite of therapy.

    • Infections on pacemaker leads (surgical removal of lead and repair or excision of tricuspid valve).

    • Recurrent mycotic emboli.

Prosthetic valve endocarditis

Conventionally divided into early (<2 months post-operatively) and late (>2 months post-operatively).

Early prosthetic valve endocarditis

  • Most commonly due to staphylococci, Gram-negative bacilli, diphtheroids, or fungi.

  • Generally, infection has begun either perioperatively or in the immediate post-operative period.

  • Often a highly destructive, fulminant infection, with valve dehiscence, abscess formation, and rapid haemodynamic deterioration.

  • Discuss with surgeons early. They commonly require re-operation. Mortality is high (45–75%).

Late prosthetic valve endocarditis

  • The pathogenesis is different. Abnormal flow around the prosthetic valve ring produces microthrombi and non-bacterial thrombotic vegetations (NBTVs), which may be infected during transient bacteraemia. The source is commonly dental or urological sepsis or indwelling venous lines.

  • Common organisms are coagulase-negative staphylococci, S. aureus, S. viridans, or enterococci.

  • Frequently needs surgical intervention, and this carries a high mortality, but less than for early PVE.

  • It may be possible to sterilize infections on bioprostheses with IV antibiotics only. Surgery (Cardiac emergencies Surgery for IE, pp. [link][link]) may then be deferred.

Surgery for IE

Discuss early with the regional cardiothoracic centre—immediate intervention may be appropriate.

  • Surgical intervention may be necessary either during active infection or later because of the degree of valve destruction. Optimal timing depends on a number of factors:

    • Haemodynamic tolerance of lesion.

    • Outcome of the infection.

    • Presence of complications.

  • Choice of antimicrobial therapy should be modified, depending on microbiological results from intraoperative specimens. Samples should be sent for culture, staining, immunological testing, and PCR, depending on the suspected organism.

  • Duration of antimicrobial treatment is dependent on the clinical picture:

    • Culture-negative operative specimens: 2–3 weeks for valve infection and 3–4 weeks for abscess.

    • Culture-positive operative specimens: 3–4 weeks for valve infection and 4–6 weeks for abscess.

  • Timing is dictated by the clinical picture. Indications for urgent surgery are listed in Box 1.27. In patients with neurological injury, surgery should be delayed to avoid intracranial haemorrhage if cardiac function permits (embolic infarct: delay 10–14 days; haemorrhage: 21–28 days and when ruptured mycotic aneurysms have been repaired).

  • Box 1.27 summarizes the absolute and relative indications for surgery.

Haemodynamic tolerance of lesion

  • If the patient is haemodynamically stable, surgery may be delayed until after the antibiotic course is completed. Final management depends on the valve affected, the degree of destruction, and its effect on ventricular function. Severe AR and MR usually require surgery; tricuspid regurgitation, if well tolerated, is managed medically.

  • Decompensation (severe CCF or low cardiac output syndrome with functional renal failure) may respond to surgery, but mortality is high.

  • ‘Metastable’ patients who have been successfully treated after an episode of acute decompensation should be considered for early operation after 2–3 weeks of antibiotic therapy.

Outcome of infection

  • Persistence or relapse of infection (clinical and laboratory indices), despite appropriate antibiotics at an adequate dose, may be due to either a resistant organism or an abscess (paravalvular, extracardiac). Consider valve replacement if no extracardiac focus is found.

  • The organism may influence the decision—consider early surgery for fungal endocarditis or PVE with Escherichia coli or S. aureus.

Presence of complications

Urgent surgery indications comprise:

  • High-degree AV block.

  • Perforation of interventricular septum.

  • Rupture of the sinus of Valsalva aneurysm into the RV.

  • Intracardiac abscess.

  • Recurrent septic emboli.

  • PVE, especially associated with an unstable prosthesis.

Endocarditis prophylaxis

NB This is one regimen (after Leport et al.).3 Refer to your local policy.

See Boxes 1.28 and 1.29.

Box 1.21 shows cardiac conditions at risk of IE. High and moderate risk requires prophylaxis; ‘low’ risk does not.

The regimen may be modified, depending on the ‘degree of risk’ (both patient- and procedure-related), as shown in Table 1.10.

References

3. Leport C, Horstkotte D, Burckhardt D (1995). Antibiotic prophylaxis from an international group of experts towards a European consensus. Group of Experts of the International Society for Chemotherapy. Eur Heart J 16(Suppl B):126–31.Find this resource:

Acute aortic regurgitation

Presentation

  • Sudden, severe AR presents as cardiogenic shock and acute pulmonary oedema.

  • The haemodynamic changes are markedly different from those seen in chronic AR. The previous normal-sized LV results in a smaller effective forward flow and higher LVEDP for the same degree of AR.

  • Patients are often extremely unwell, tachycardic, and peripherally shut down, and often have pulmonary oedema. Unlike chronic AR, pulse pressure may be near normal.

  • If available, ask for a history of previous valvular heart disease, hypertension, features of Marfan’s syndrome, and risk factors for IE (see Box 1.21).

  • Physical signs of severe AR include a quiet aortic closure sound (S2), an ejection systolic murmur over the aortic valve (turbulent flow), a high-pitched and short early diastolic murmur (AR), and a quiet S1 (premature closure of the MV).

  • Examine specifically for signs of an underlying cause (see Box 1.30).

  • Where there is no obvious underlying cause (e.g. acute MI), assume IE until proven otherwise.

Diagnosis

Based on a combination of clinical features and TTE and/or TOE.

Management

Acute AR is a surgical emergency, and all other management measures are only aimed at stabilizing the patient until urgent aortic valve replacement (AVR) can take place. The patient’s clinical condition will determine the urgency of surgery (and mortality). Liaise immediately with local cardiologists.

General measures

  • Admit the patient to intensive care or medical HDU.

  • Give O2; begin treating any pulmonary oedema with diuretics.

  • Monitor blood gases; mechanical ventilation may be necessary.

  • Blood cultures × 3 are essential (Cardiac emergencies IE: investigations, p. [link]).

  • Serial ECG: watch for developing AV block or conduction defects.

Specific measures

  • Every patient must be discussed with the regional cardiothoracic centre.

  • In the context of good systemic BP, vasodilators, such as sodium nitroprusside or hydralazine, may temporarily improve forward flow and relieve pulmonary oedema.

  • Inotropic support may be necessary if hypotensive. However, inotropes are best avoided, as any increase in systemic pressures may worsen AR.

  • All patients with haemodynamic compromise should have immediate or urgent AVR.

  • IE: indications for surgery are given in Box 1.27.

  • IABP must be avoided, as it will worsen AR.

Acute mitral regurgitation

Presentation

  • Patients most commonly present with acute breathlessness and severe pulmonary oedema. Symptoms may be less severe or spontaneously improve, as LA compliance increases. There may be a history of previous murmur, angina, or MI.

  • The signs are different to those seen in chronic MR, because of the presence of a non-dilated and relatively non-compliant LA. Acute MR results in a large LA systolic pressure wave (v-wave), and hence pulmonary oedema.

  • Patients may be acutely unwell, with tachycardia, hypotension, peripheral vasoconstriction, and pulmonary oedema and a pan-systolic murmur of MR.

  • Later in the illness, probably because of sustained high LA and pulmonary venous pressures, right heart failure develops.

  • Examine for signs of any underlying conditions (see Box 1.31).

  • The important differential diagnosis is a VSD. TTE and Doppler studies can readily differentiate between the two conditions. Alternatively, if Echo is not available, PA catheterization in acute MR will exclude the presence of a left-to-right shunt and the PCWP trace will demonstrate a large v-wave.

  • Where there is no obvious underlying cause (e.g. acute MI), assume the patient has IE until proven otherwise.

Diagnosis

Based on a combination of clinical features and Echo. TTE can readily diagnose and quantify MR. It also provides information on LV status (in particular, regional wall motion abnormalities which can give rise to MR). TOE can provide specific information about the aetiology of valve dysfunction, including papillary muscle rupture and MV leaflet (anterior and posterior) structural abnormalities. This information will be vital for a decision regarding definitive management.

General measures

  • Admit the patient to intensive care or medical HDU.

  • Give O2; begin treating any pulmonary oedema with diuretics.

  • Monitor blood gases; mechanical ventilation may be necessary.

  • Blood cultures × 3 are essential (Cardiac emergencies IE: investigations, p. [link]).

  • If present, MI should be treated in the standard manner.

Specific measures

  • Pulmonary oedema may be very resistant to treatment.

  • In the presence of good BP, reduction in preload (GTN infusion) and afterload, especially with ACEIs, is important. Systemic vasodilators, such as hydralazine (12.5–100mg tds), can also be added in.

  • An IABP will help decrease the LVEDP and also increase coronary blood flow.

  • Patients may require inotropic support. There are multiple combinations, and the aetiology of MR, haemodynamic status, and local policy/expertise should dictate the choice of agent.

  • CPAP and intubation and positive pressure ventilation are extremely useful and must be considered in all severe and/or resistant cases.

  • Haemodynamic disturbance and severe pulmonary oedema in the context of acute MR is a surgical emergency.

  • IE: indications for surgery are given under Cardiac emergencies Surgery for IE, pp. [link][link].

  • Post-infarct MR: management depends upon the patient’s condition following resuscitation. Patients who are stabilized may have mitral valve replacement (MVR) deferred because of the risks of surgery in the post-infarct patient. Their preoperative management should consist of diuretics and vasodilators, including ACEIs if tolerated. Advise patients regarding endocarditis prophylaxis.

Deep vein thrombosis (DVT): assessment

Presentation

  • Most commonly asymptomatic. Minor leg discomfort or isolated swelling (>65%) in the affected limb are the most common clinical features. Breathlessness or chest pain may be secondary to PE.

  • Signs include erythema and swelling of the leg, dilated superficial veins, and calf discomfort on dorsiflexion of the foot (Homan’s sign—this is nowadays rarely used, in view of the risk of dislodging and embolization of a clot). The thrombus may be palpable as a fibrous cord in the popliteal fossa. Confirm the presence of swelling (>2cm) by measuring the limb circumference 15cm above and 10cm below the tibial tuberosity.

  • In all cases of leg swelling, abdominal and rectal (and pelvic in women) examination must be carried out to exclude an abdominal cause.

Risk factors for DVT

Procoagulant states

Congenital

  • Factor V Leiden.

  • Antithrombin III deficiency.

  • Protein C deficiency.

  • Protein S deficiency.

Acquired

  • Malignant disease (~5%).

  • Antiphospholipid syndrome.

  • Myeloproliferative disorders.

  • Oral contraceptive pill (especially with factor V Leiden mutation).

  • Nephrotic syndrome (via renal AT III losses).

  • Homocystinuria.

  • Paroxysmal nocturnal haemoglobinuria.

Venous stasis

  • Immobility (e.g. long journeys).

  • Recent surgery.

  • Pelvic mass.

  • Pregnancy or recent childbirth.

  • Severe obesity.

Miscellaneous

  • Hyperviscosity syndromes (see Cardiac emergencies Hyperviscosity syndrome, p. [link]).

  • Previous DVT or PE.

  • Family history of DVT/PE.

Investigations

  • Venous compression ultrasonography of leg veins is largely replacing venography as the initial investigation of choice. It is quick and non-invasive, with a sensitivity and specificity of >90%, and does not carry a risk of contrast allergy or phlebitis. It can simultaneously assess the extent of proximal progression of the thrombus, in particular extension into pelvic vessels.

  • D-dimers have a high negative predictive value for DVT. A low clinical probability of DVT and a negative D-dimer might not require further investigation; however, chronic DVT might have normal D-dimer results. A positive D-dimer result should be followed by ultrasonography.

  • Venography: use if results uncertain and clinical suspicion is high.

  • Consider baseline investigations—FBC, U&Es, ECG, CXR, urinalysis, and pulse oximetry (± ABG)—on all patients.

  • If appropriate, look for an underlying cause.

    • Coagulation screen.

    • Procoagulant screen: refer to the local screening policy and get haematology advice (e.g. CRP, ESR, protein C and S, antithrombin III levels, factor V Leiden mutation, autoantibody screen, Igs and immunoelectrophoretic strip, anticardiolipin antibody, Ham’s test, etc.).

    • Screen for malignancy: ultrasound (US) ± CT (abdomen and pelvis), CXR, LFTs, prostate-specific antigen (PSA), carcinoembryonic antigen (CEA), CA-125, CA-19.9, β‎-human chorionic gonadotrophin (HCG), etc.

For the Wells rule to estimate the probability of DVT, see Table 1.11.

Table 1.11 Wells rule to estimate the probability of DVT*

Clinical feature

Score

Active cancer (including treatment up to 6 months previously)

1

Paralysis, paresis, or recent plaster immobilization of the lower extremity

1

Recently bedridden for >3 days or major surgery within 4 weeks

1

Localized tenderness along the distribution of the deep venous system

1

Entire limb swollen

1

Calf swelling by >3cm when compared with the asymptomatic leg

1

Pitting oedema (greater in the symptomatic leg)

1

Dilated collateral superficial veins (non-varicose)

1

Previously documented DVT

1

Alternative diagnosis as likely or more possible than that of DVT

–2

Clinical probability of DVT with score**

Score >3 High

Score 1–2 Moderate

Score <1 Low

* Reprinted from The Lancet, 350, Wells PS, et al. ‘Value of assessment of pretest probability of deep-vein thrombosis in clinical management’, 1795–8, Copyright (1997), with permission from Elsevier.

** Source: data from Oudega R, et al. (2005). Ann Intern Med 143: 101.

DVT: management

  • If there is a high clinical suspicion of DVT, start empiric anticoagulation with LMWH. (Stop this if subsequent investigations are negative.)

  • Below-knee DVT: treat with compression stockings and SC prophylactic doses of LMWH until mobile, to deter proximal propagation of the thrombus.

  • Above-knee DVT: thrombi within the thigh veins warrant full anticoagulation with LMWH/UFH and subsequently oral anticoagulant.

  • See management algorithm in Fig. 1.10.

Anticoagulation

Heparin

  • LMWHs have now superseded UFH for both DVT and PE.

  • Treat with LMWH before starting oral anticoagulation.

  • LMWH are administered primarily as a once-daily SC injection, and the dosage is determined by patient weight.

Warfarin

  • Always start LMWH before starting warfarin and continue until the INR is within therapeutic range. Protein C (a vitamin K-dependent anticoagulant) has a shorter half-life than the other coagulation factors and levels fall sooner, resulting in a transient procoagulant tendency.

  • Continue warfarin (INR 2–2.5) for 3 months (this varies, depending on the cause of DVT, from 6 weeks to life).

  • If recurrent DVT, or patient is at high risk of recurrence, consider life-long anticoagulation.

Novel anticoagulants

Direct acting oral anticoagulants (dabigatran, apixaban, rivaroxaban and edoxaban) are licensed for treatment of DVT or PE and do not require routine testing.

  • Dabigatran and edoxaban should be started after 5 days of treatment with LMWH. The oral anticoagulant and LMWH should not be given together (see BNF for details).

  • Apixaban and rivaroxaban do not require LMWH treatment before use, but require an initial period of treatment with a higher dose of the oral anticoagulant followed by a lower maintenance dose (see BNF for details).

Thrombolysis

  • This should be considered for recurrent, extensive proximal venous thrombosis (e.g. femoral or iliac veins), as it is more effective than anticoagulation alone in promoting clot dissolution and produces a better clinical outcome. Given the lack of evidence base for this approach, an experienced clinician should be involved in this decision.

  • Catheter-directed thrombolytic therapy (rtPA or SK) is superior to systemic thrombolysis.

  • One approach is SK 250 000U over 30min, then 100 000U every hour for 24–72h (see data sheet). For contraindications to thrombolysis, see Cardiac emergencies STEMI: thrombolysis 2, pp. [link].

Further management

  • Women taking the combined oral contraceptive pill (OCP) should be advised to stop this.

  • If there are contraindications to anticoagulation, consider the insertion of a caval filter to prevent PE; however, such filters are best removed after 2 weeks to prevent long-term peripheral oedema from venous stasis.

  • All patients should be treated with thigh-high compression stockings to try to reduce symptomatic venous distension when mobilizing.

Pulmonary embolism (PE): assessment

Symptoms

  • Classically presents with sudden-onset, pleuritic chest pain, associated with breathlessness and haemoptysis. Additional symptoms include postural dizziness or syncope.

  • Massive PE may present as cardiac arrest [particularly with electromechanical dissociation (EMD)] or shock.

  • Presentation may be atypical, i.e. unexplained breathlessness or unexplained hypotension or syncope only.

  • PEs should be suspected in all breathless patients with risk factors for DVT or with clinically proven DVT (Cardiac emergencies DVT: management, pp. [link][link]).

  • Recurrent PEs may present with chronic pulmonary hypertension and progressive right heart failure.

Signs

  • Examination may reveal tachycardia and tachypnoea only. Look for postural hypotension (in the presence of raised JVP).

  • Look for signs of raised right heart pressures and cor pulmonale (raised JVP with prominent ‘a’ wave, tricuspid regurgitation, parasternal heave, RV S3, loud pulmonary closure sound with wide splitting of S2, pulmonary regurgitation).

  • Cyanosis suggests a large PE.

  • Examine for a pleural rub (may be transient) or effusion.

  • Examine lower limbs for obvious thrombophlebitis.

  • Mild fever (>37.5°C) may be present. There may be signs of coexisting COPD.

Causes

  • Frequently secondary to DVT (leg >> arm; Cardiac emergencies DVT: management, pp. [link][link]).

  • Other causes:

    • Rarely secondary to RV thrombus (post-MI).

    • Septic emboli (e.g. tricuspid endocarditis).

    • Fat embolism (post-fracture).

    • Air embolism (venous lines, diving).

    • Amniotic fluid.

    • Parasites.

    • Neoplastic cells.

    • Foreign materials (e.g. venous catheters).

Prognostic features

The prognosis in patients with PEs varies greatly, associated in part with any underlying condition. Generally worse prognosis is associated with larger PEs; poor prognostic indicators include:

  • Hypotension.

  • Hypoxia.

  • ECG changes (other than non-specific T-wave changes).

PE: investigations 1

General investigations

  • ABG: a normal ABG does not exclude a PE. Cardiac emergenciesPaO2 is invariable with larger PEs. Other changes include mild respiratory alkalosis and Cardiac emergenciesPaCO2 (due to tachypnoea) and metabolic acidosis (secondary to shock).

  • ECG: commonly shows sinus tachycardia and non-specific ST- and T-wave changes in the anterior chest leads. The classical changes of acute cor pulmonale, such as S1Q3T3, right axis deviation, or RBBB, are only seen with massive PE. Less common findings include atrial flutter or AF.

  • CXR: may be normal, and a near-normal chest film in the context of severe respiratory compromise is highly suggestive of a PE. Less commonly may show focal pulmonary oligaemia (Westermark’s sign), a raised hemidiaphragm, a small pleural effusion, wedge-shaped shadows based on the pleura, sub-segmental atelectasis, or dilated proximal PAs.

  • Blood tests: there is no specific test. FBC may show neutrophil leucocytosis; mildly elevated CK, troponin, and bilirubin may be seen.

  • Echo/TOE: insensitive for diagnosis but can exclude other causes of hypotension and raised right-sided pressures (e.g. tamponade, RV infarction; Cardiac emergencies Right ventricular infarction, p. [link]). In PE, it might show RV dilatation and global hypokinesia, with sparing of the apex (McConnell’s sign), and PA dilatation. Doppler may show tricuspid/pulmonary regurgitation, allowing estimation of RV systolic pressure.Sometimes, in bigger PE, the thrombus in the PA may be visible.

For underlying causes, see Box 1.32.

Specific investigations

D-dimer

  • A highly sensitive, but non-specific, test in acute PE.

  • Useful in ruling out PE in patients with low or intermediate probability.

  • Results can be affected by advancing age, pregnancy, trauma, surgery, malignancy, and inflammatory states.

Ventilation/perfusion lung scanning

A perfusion lung scan (with IV technetium-99-labelled albumin) should be performed in all suspected cases of PE. A ventilation scan (inhaled xenon-133) in conjunction increases the specificity by assessing whether the defects in the ventilation and perfusion scans ‘match’ or ‘mismatch’. Pre-existing lung disease makes interpretation difficult.

  • A normal perfusion scan rules out significant-sized PE and is reported as low probability for PE.

  • Abnormal scans are reported as medium or high probability:

    • A high probability scan is strongly associated with PE, but there is a significant minority of false positives.

    • A low probability scan with low clinical suspicion of PE should prompt a search for another cause for the patient’s symptoms.

    • If the clinical suspicion of PE is high and the scan is of low or medium probability, alternative investigations are required [usually computed tomography pulmonary angiogram (CTPA) or bilateral leg ultrasound scan (USS)].

PE: investigations 2

CTPA

  • This is the recommended initial lung imaging modality in patients with non-massive PE.

  • Allows direct visualization of emboli, as well as other potential parenchymal disease, which may provide an alternative explanation for symptoms.

  • Sensitivity and specificity are high (>90%) for lobar PAs, but not so high for segmental and sub-segmental PAs.

  • A patient with a positive CTPA does not require further investigation for PE.

  • A patient with a negative CTPA in the context of a high/intermediate probability of a PE should undergo further investigation.

Evaluation of leg veins with USS

  • Not very reliable. Almost half of patients with PE do not have evidence of a DVT and therefore, a negative result cannot rule out a PE.

  • Useful second-line investigation as an adjunct to CTPA and V/Q scan.

  • Outcome studies have demonstrated that it would be safe not to anticoagulate patients with a negative CTPA and lower limb USS who have an intermediate/low probability of a PE.

Pulmonary angiography

  • Is the ‘gold standard’ investigation.

  • It is indicated in patients in whom a diagnosis of embolism cannot be established by non-invasive means. Look for sharp cut-off of vessels or obvious filling defects.

  • An invasive investigation, and can be associated with 0.5% mortality.

  • If there is an obvious filling defect, the catheter, or a guidewire passed through the catheter, may be used to disobliterate the thrombus.

  • After angiography, the catheter may be used to give thrombolysis directly into the affected PA (Cardiac emergencies PE: management 1, p. [link]).

  • The contrast can cause systemic vasodilatation and haemodynamic collapse in hypotensive patients.

Magnetic resonance pulmonary angiography

  • Results are comparable to pulmonary angiography in preliminary studies.

  • It can simultaneously assess ventricular function.

Fig. 1.11 summarizes one proposed pathway for investigation of potential PE patients.

Fig. 1.11 Proposed pathway for investigation of patients with suspected PE.

Fig. 1.11 Proposed pathway for investigation of patients with suspected PE.

PE: management 1

1. Stabilize the patient

  • Unless an alternative diagnosis is made, the patient should be treated as for a PE until this can be excluded.

  • Monitor cardiac rhythm, pulse, BP, and respiratory rate (RR) every 15min with continuous pulse oximetry and a cardiac monitor. Ensure full resuscitation facilities are available.

  • Obtain venous access and start IV fluids (crystalloid or colloid).

  • Give maximal inspired O2 via face mask to correct hypoxia. Mechanical ventilation may be necessary if the patient is tiring (beware of cardiovascular collapse when sedation is given for ET intubation).

  • Give LMWH or UFH to all patients with high or intermediate risk of PE until diagnosis is confirmed. A meta-analysis of multiple trials has shown LMWH to be superior to UFH, with a reduction in mortality and bleeding complications. For doses, consult the local formulary.

  • If there is evidence of haemodynamic instability (systemic hypotension, features of right heart failure) or cardiac arrest, patients may benefit from thrombolysis with rtPA or SK—beware as doses used are different from treatment of STEMI (see Box 1.33).

2. Analgesia

  • Patients may respond to oral NSAIDs (remember gastric protection, as these patients are also anticoagulated).

  • Opiate analgesia to be used with caution. The vasodilatation caused by these drugs may precipitate or worsen hypotension. Give small doses (1–2mg diamorphine IV) slowly. Hypotension should respond to IV colloid.

  • Avoid IM injections (anticoagulation and possible thrombolysis).

3. Investigations with a view to a definite diagnosis

See Cardiac emergencies PE: investigations 1, p. [link] and Cardiac emergencies PE: investigations 2, p. [link].

4. Anticoagulate

  • Patients with a positive diagnosis must undergo anticoagulation with warfarin (or one of the newer licensed novel oral anticoagulants—this will depend on local protocols). There should be a period of overlap with LMWH/UFH until INR values are therapeutic. Target INR is 2–3 for most cases (see Box 1.34).

  • Standard duration of anticoagulation is:

    • 4–6 weeks for temporary risk factor.

    • 3 months for first idiopathic cases.

    • At least 6 months for other cases.

    • With recurrent events and underlying predisposition to thromboembolic events (e.g. antiphospholipid antibody syndrome), life-long anticoagulation may be needed (as well as higher target INR >3).

PE: management 2

Cardiac arrest

(Also see Cardiac emergencies Universal treatment algorithm, pp. [link][link].)

  • Massive PE may present as cardiac arrest with EMD. Exclude the other causes of EMD (Cardiac emergencies Universal treatment algorithm, pp. [link][link]).

  • Chest compressions may help break up the thrombus and allow it to progress more distally, thereby restoring some cardiac output.

  • If clinical suspicion of PE is high and there is no absolute contraindication to thrombolysis, give rtPA [similar in dose to STEMI, with a maximum of 50mg (see Box 1.33), followed by heparin].

  • If cardiac output returns, consider pulmonary angiography or inserting a PA catheter to try to mechanically disrupt the embolus.

Hypotension

The acute increase in pulmonary vascular resistance (PVR) results in RV dilatation and pressure overload, which mechanically impairs LV filling and function. Patients require a higher than normal right-sided filling pressure but may be worsened by fluid overload.

  • Insert an internal jugular sheath prior to anticoagulation. This can be used for access later, if necessary.

  • If hypotensive, give colloid (e.g. 500mL of Haemaccel® stat).

  • If hypotension persists, invasive monitoring and/or inotropic support is required. The JVP is a poor indicator of left-sided filling pressures in such cases. Adrenaline is the inotrope of choice.

  • Femoro-femoral cardiopulmonary bypass or extracorporeal membrane oxygenation in a specialized centre may be used to support the circulation until thrombolysis or surgical embolectomy can be performed.

  • Pulmonary angiography in a hypotensive patient is hazardous, as the contrast may cause systemic vasodilatation and cardiovascular collapse.

Pulmonary embolectomy

  • In patients who have contraindications to thrombolysis and are in shock requiring inotropic support, there may be a role for embolectomy if appropriate skills are on site.

  • This can be performed percutaneously in the catheterization laboratory using a number of devices or surgically on cardiopulmonary bypass.

  • Percutaneous procedures may be combined with peripheral or central thrombolysis.

  • Seek specialist advice early. Best results are obtained before onset of cardiogenic shock.

  • Radiological confirmation of extent and site of embolism is preferable before thoracotomy.

  • Mortality is ~25–30%.

Inferior vena cava filter

  • Infrequently used, as little to suggest improved short- or long-term mortality.

  • Filters are positioned percutaneously and, if possible, patients must remain anticoagulated to prevent further thrombus formation.

  • Most are positioned infrarenally (bird’s nest filter) but can also be suprarenal (Greenfield filter).

  • Indications for inferior vena cava (IVC) filter use include:

    • Anticoagulation contraindicated, e.g. active bleeding, heparin-induced thrombocytopenia, planned intensive chemotherapy

    • Anticoagulation failure despite adequate therapy

    • Prophylaxis in high-risk patients, e.g. progressive venous thrombosis, severe pulmonary hypertension.

Fat embolism

Commonly seen in patients with major trauma. There is embolization of fat and microaggregates of platelets, RBCs, and fibrin in systemic and pulmonary circulation. Pulmonary damage may result directly from the emboli (infarction) or by chemical pneumonitis and ARDS (Cardiac emergencies Adult respiratory distress syndrome 1, p. [link]).

Clinical features

  • There may be a history of fractures, followed (24–48h later) by chest pain, breathlessness, cough, haemoptysis, confusion, and rash.

  • Examination reveals fever (38–39°C), widespread petechial rash (25–50%), cyanosis, and tachypnoea. There may be scattered crepitations in the chest, although examination may be normal. Changes in mental state may be the first sign with confusion, drowsiness, seizures, and coma. Examine the eyes for conjunctival and retinal haemorrhages; occasionally, fat globules may be seen in the retinal vessels. Severe fat embolism may present as shock.

Investigations

  • ABG: hypoxia and respiratory alkalosis (with low PaCO2), as for thromboembolic PE.

  • FBC: thrombocytopenia, acute intravascular haemolysis.

  • Coagulation: disseminated intravascular coagulation (DIC).

  • U&Es and glucose: renal failure, hypoglycaemia.

  • Ca2+: may be low.

  • Urine: microscopy for fat and dipstick for Hb.

  • ECG: usually non-specific (sinus tachycardia; occasionally signs of right heart strain).

  • CXR: usually lags behind the clinical course. There may be patchy bilateral air space opacification. Effusions are rare.

  • CT head: consider if there is a possibility of head injury with expanding subdural or epidural bleed.

Differential diagnosis

Pulmonary thromboembolism, other causes of ARDS (Cardiac emergencies Adult respiratory distress syndrome 1, p. [link]), septic shock, hypovolaemia, cardiac or pulmonary contusion, head injury, aspiration pneumonia, transfusion reaction.

Management

  • Treat respiratory failure (Cardiac emergencies Respiratory failure: management, pp. [link][link]). Give O2 (maximal via face mask; CPAP and mechanical ventilation if necessary).

  • Ensure adequate circulating volume and cardiac output. Central venous pressure (CVP) is not a good guide to left-sided filling pressures, and a PA catheter (Swan–Ganz) should be used to guide fluid replacement. Try to keep PCWP 12–15mmHg, and give diuretics if necessary. Use inotropes to support circulation, as required (Cardiac emergencies Adult respiratory distress syndrome 3, pp. [link][link]).

  • Aspirin, heparin, and dextran 40 (500mL over 4–6h) are of some benefit in the acute stages but may exacerbate bleeding from sites of trauma.

  • High-dose steroids (methylprednisolone 30mg/kg q8h for three doses) have been shown to improve hypoxaemia,4 but steroids are probably most effective if given prophylactically.

References

4. Lindeque BG, Schoeman HS, Dommisse GF, Boeyens MC, Vlok AL (1987). Fat embolism syndrome and the fat embolism syndrome. A double-blind therapeutic study. Bone Joint Surg Br 69:128–31.Find this resource:

Hypertensive emergencies

Hypertensive crisis

Hypertensive crisis is defined as a severe elevation in BP [SBP >200mmHg, diastolic BP (DBP) >120mmHg]. Rate of change in BP is important. A rapid rise is poorly tolerated and leads to end-organ damage, whereas a gradual rise in a patient with existing poor BP control is tolerated better. Hypertensive crisis is classified as:

  • Hypertensive emergency where a high BP is complicated by acute target organ dysfunction (see Box 1.35) and includes:

    • Hypertensive emergency with retinopathy where there is marked elevation in BP (classically DBP >140mmHg), with retinal haemorrhages and exudates (previously called accelerated hypertension), and

    • Hypertensive emergency with papilloedema, with a similarly high BP and papilloedema (previously called malignant hypertension).

  • Hypertensive urgency where there is a similar rise in BP, but without target organ damage.

Conditions which may present with hypertensive emergency

  • Essential hypertension.

  • Renovascular hypertension: atheroma, fibromuscular dysplasia, acute renal occlusion.

  • Renal parenchymal disease: acute glomerulonephritis, vasculitis, scleroderma.

  • Endocrine disorders: phaeochromocytoma, Cushing’s syndrome, primary hyperaldosteronism, thyrotoxicosis, hyperparathyroidism, acromegaly, adrenal carcinoma.

  • Eclampsia and pre-eclampsia.

  • Vasculitis.

  • Drugs: cocaine, amphetamines, monoamine oxidase inhibitor (MAOI) interactions, ciclosporin, β‎-blocker, and clonidine withdrawal.

  • Autonomic hyperactivity in the presence of spinal cord injury.

  • Coarctation of the aorta.

Presentation

  • Occasionally, minimal non-specific symptoms such as mild headache and nosebleed.

  • A small group of patients present with symptoms resulting from BP-induced microvascular damage:

    • Neurological symptoms: severe headache, nausea, vomiting, visual loss, focal neurological deficits, fits, confusion, intracerebral haemorrhage, coma.

    • Chest pain (hypertensive heart disease, MI, or aortic dissection) and CCF.

    • Symptoms of renal failure: renal impairment may be chronic (secondary to long-standing hypertension) or acute (from necrotizing vasculitis of malignant hypertension).

  • Patients may present with hypertension as one manifestation of an underlying ‘disease’ (renovascular hypertension, CRF, CREST syndrome, phaeochromocytoma, pregnancy).

  • Examination should be directed at looking for evidence of end-organ damage, even if the patient is asymptomatic (heart failure, retinopathy, papilloedema, focal neurology).

Hypertensive emergencies: management

Priorities in management

  • Confirm the diagnosis and assess the severity.

  • Identify those patients needing specific emergency treatment.

  • Plan long-term treatment.

Diagnosis and severity

  • Ask about previous BP recordings, previous and current treatment, sympathomimetics, antidepressants, non-prescription drugs, and recreational drugs.

  • Check the BP yourself, in both arms, after a period of rest and, if possible, on standing. Monitor the patient’s BP regularly while they are in accident and emergency (A&E).

  • Examine carefully for clinical evidence of cardiac enlargement or heart failure, peripheral pulses, renal masses, or focal neurological deficit. Always examine the fundi—dilate if necessary.

Investigations

All patients should have:

  • FBC: MAHA with malignant hypertension.

  • U&Es: renal impairment and/or Cardiac emergenciesK+ (diffuse intrarenal ischaemia and secondary hyperaldosteronism).

  • Coagulation screen: DIC with malignant hypertension.

  • CXR: cardiac enlargement:

    • Aortic contour (? dissection).

    • Pulmonary oedema.

  • Urinalysis: protein and red cells ± casts.

  • ECG: voltage criteria for LVH (see Box 1.36).

Other investigations, depending on the clinical picture and possible aetiology, include:

  • 24-h urine collection:

    • Creatinine clearance.

    • Free catecholamines, metanephrines, or vanillyl mandelic acid (VMA).

  • Echo: LVH, aortic dissection.

  • Renal USS and Doppler: size of kidneys and renal artery stenosis.

  • Magnetic resonance (MR) renal angiogram: renal artery stenosis.

  • CT/MR brain: intracranial bleed.

  • Drug screen: cocaine, amphetamine, others.

Indications for admission

  • DBP persistently ≥120mmHg.

  • Retinal haemorrhages, exudates, or papilloedema.

  • Renal impairment.

Treatment principles

  • Rapid reduction in BP must be avoided and can be very dangerous. This can result in cerebral and cardiac hypoperfusion (an abrupt change of >25% in BP will exceed cerebral BP autoregulation).

  • Initial BP reduction of 25% to be achieved over 1–4h, with a less rapid reduction over 24h to a DBP of 100mmHg.

  • The only two situations where BP must be lowered rapidly are in the context of aortic dissection and MI.

Treatment

(Also see Cardiac emergencies Hypertensive emergencies: drug treatment, p. [link].)

  • The majority of patients who are alert and otherwise well may be treated with oral therapy to lower BP gradually.

  • For stable patients, first-line treatment should be with a low-dose calcium antagonist (e.g. amlodipine 5mg). Alternatively, a β‎-blocker, ACEI, or diuretic may be used.

  • Urgent invasive monitoring (arterial line) prior to drug therapy is indicated for patients with:

    • Evidence of hypertensive encephalopathy.

    • Complications of hypertension (e.g. aortic dissection, acute pulmonary oedema, or renal failure).

    • Treatment of an underlying condition (e.g. glomerulonephritis, phaeochromocytoma, CREST crisis).

    • Patients with persistent DBP ≥140mmHg.

    • Eclampsia.

  • Sublingual nifedipine must be avoided.

Conditions requiring specific treatment are listed in Box 1.37.

Long-term management

  • Investigate, as appropriate, for an underlying cause.

  • Select a treatment regimen that is tolerated and effective. Tell the patient why long-term therapy is important.

  • Try to reduce all cardiovascular risk factors by advising the patient to stop smoking, giving appropriate dietary advice (cholesterol), and aiming for optimal diabetic control.

  • Monitor long-term control and look for end-organ damage (regular fundoscopy, ECG, U&Es). Even poor control is better than no control.

Hypertensive emergencies: drug treatment

(See Tables 1.12 and 1.13.)

Table 1.12 Drugs for the treatment of hypertensive emergencies: IV therapy

Drug

Dosage

Onset of action

Comments

Labetalol

20–80mg IV bolus q10min

20–200mg/min by IV infusion, increasing every 15min

2–5min

Drug of choice in suspected phaeochromocytoma (Cardiac emergencies Thrombotic thrombocytopenic purpura and haemolytic uraemic syndrome, p. [link]) or aortic dissection (Cardiac emergencies Aortic dissection: management 2, pp. [link][link]). Avoid if there is LVF. May be continued PO (see below)

Nitroprusside

0.25–8 micrograms/kg/min IV infusion

Seconds

Drug of choice in LVF and/or encephalopathy

GTN

1–10mg/h IV infusion

2–5min

Mainly venodilatation. Useful in patients with LVF of angina

Hydralazine

5–10mg IV over 20min 50–300 micrograms/min IV infusion

10–15min

May provoke angina

Esmolol hydrochloride

500m/kg/min IV loading dose 50–200 micrograms/kg/min IV infusion

Seconds

Short-acting β‎-blocker also used for SVTs

Phentolamine

2–5mg IV over 2–5min PRN

Seconds

Drug of choice in phaeochromocytoma (Cardiac emergencies Thrombotic thrombocytopenic purpura and haemolytic uraemic syndrome, p. [link]), followed by labetalol (PO) when BP controlled

NB It is dangerous to reduce the BP quickly. Aim to reduce the DBP to 100–110mmHg within 2–4h. Unless there are good reasons to commence IV therapy, always use oral medicines.

Fig. 1.13 Right atrial pressure (RAP) tracing in tamponade. There is a paradoxical rise in RAP during inspiration.

Fig. 1.13 Right atrial pressure (RAP) tracing in tamponade. There is a paradoxical rise in RAP during inspiration.

Table 1.13 Drugs for the treatment of hypertensive emergencies: oral therapy

Drug

Dosage

Comment

Amlodipine

5–10mg od

Minimal drug interactions

Atendol

50–100mg PO od

There are numerous alternative β‎-blockers—see BNF

Nifedipine

10–20mg PO q8h (q12h if slow release)

Avoid sublingual as the fall in BP is very rapid

Labetalol

100–400mg PO q12h

Use if phaeochromocytoma suspected. Safe in pregnancy

Hydralazine

25–50mg PO q8h

Safe in pregnancy

Minoxidil

5–10mg PO od

May cause marked salt and water retention. Combine with a loop diuretic (e.g. furosemide 40–240mg daily)

Clonidine

0.2mg PO, followed by 0.1mg hourly max. 0.8mg total for urgent therapy, or 0.05–0.1mg PO q8h, increasing every 2 days

Sedation common. Do not stop abruptly as there is a high incidence of rebound hypertensive crisis

NB Aim to reduce DBP to 100–110mmHg in 2–4h and normalize BP in 2–3 days.

Hypertensive emergency with retinopathy (accelerated and malignant hypertension)

This is part of a continuum of disorders characterized by hypertension (DBP often >120mmHg) and acute microvascular damage (seen best in the retina, but present in all organs). It may be difficult to decide whether the damage in some vascular beds is the cause or effect of hypertension. An example is in the context of acute glomerulonephritis.

  • Accelerated hypertension (grade 3 retinopathy; see Box 1.38) may progress to malignant hypertension, with widespread necrotizing vasculitis of the arterioles (and papilloedema).

  • Presentation is commonly with headache or visual loss and varying degrees of confusion. More severe cases present with renal failure, heart failure, microangiopathic haemolytic anaemia (MAHA), and DIC.

Management

  • Transfer the patient to medical HDU/ITU.

  • Insert an arterial line, and consider a central venous line if there is evidence of necrotizing vasculitis and DIC. Catheterize the bladder.

  • Monitor the neurological state, ECG, and fluid balance.

  • Aim to lower the DBP to 100mmHg or by 15–20mmHg, whichever is higher, over the first 24h.

  • Those with early features may be treated successfully with oral therapy (β‎-blockers, calcium channel blockers).

  • Patients with late symptoms or who deteriorate should be given parenteral therapy, aiming for more rapid lowering of BP.

  • If there is evidence of pulmonary oedema or encephalopathy, give furosemide 40–80mg IV.

  • If there is no LVF, give a bolus of labetalol, followed by an infusion. For patients with LVF, nitroprusside or hydralazine is preferable.

  • Consult the renal team for patients with ARF or evidence of acute glomerulonephritis (>2+ proteinuria, red cell casts). ARF is managed as described under Cardiac emergencies Acute kidney injury: management, pp. [link][link]. Dopamine should be avoided, as it may worsen hypertension.

  • Consider giving an ACEI. High circulating renin levels may not allow control of hypertension, which, in turn, causes progressive renal failure. ACEIs will block this vicious circle. There may be marked first-dose hypotension, so start cautiously.

  • Haemolysis and DIC should recover with control of BP.

Hypertension in the context of acute stroke/intracranial bleed

  • Stroke/bleed may be the result of hypertension, or vice versa.

  • In the acute setting, there is impaired autoregulation of cerebral blood flow and autonomic function. Small changes in systemic BP may result in catastrophic falls in cerebral blood flow.

  • Systemic BP should not be treated, unless DBP >130mmHg and/or presence of severe cerebral oedema (with clinical manifestations).

  • In most cases, BP tends to settle over 24–36h. If treatment is indicated, BP reduction principles, as listed earlier, must be adhered to and a combination of nitroprusside, labetalol, and calcium channel blockers can be used.

  • Centrally acting agents must be avoided, as they cause sedation.

  • In patients with subarachnoid haemorrhage (SAH), a cerebroselective calcium channel blocker, such as nimodipine, is used to decrease cerebral vasospasm.

  • Systemic BP must also be treated if it qualifies with the principles listed earlier and/or if it remains elevated after 24h. There is no evidence that this reduces further events in the acute phase.

Hypertensive encephalopathy

  • Caused by cerebral oedema secondary to loss of cerebral autoregulatory function.

  • Usually gradual onset and may occur in previously normotensive patients at BPs as low as 150/100mmHg. It is rare in patients with chronic hypertension and pressures are also much higher.

Symptoms

  • Headache, nausea and vomiting, confusion, grade III and IV hypertensive retinopathy.

  • Late features consist of focal neurological signs, fits, and coma.

Diagnosis

  • A diagnosis of exclusion and other differential diagnoses must be ruled out (e.g. stroke, encephalitis, tumours, bleeding, vasculitis).

  • History is helpful, particularly of previous seizures, SAH usually being sudden in onset, and strokes being associated with focal neurological deficit.

  • Always exclude hypoglycaemia.

  • Starting BP-lowering treatment for hypertension associated with a stroke can cause extension of the stroke.

  • An urgent MRI or CT brain must be obtained to rule out some of the differential diagnoses.

Management

  • The primary principle of BP control is to reduce DBP by 25% or reduce DBP to 100mmHg, whichever is higher, over a period of 1–2h.

  • Transfer the patient to ITU for invasive monitoring (Cardiac emergencies Hypertensive emergency with retinopathy (accelerated and malignant hypertension), pp. [link][link]).

  • Monitor the neurological state, ECG, and fluid balance.

  • Correct electrolyte abnormalities (K+, Mg2+, Ca2+).

  • Give furosemide 40–80mg IV.

  • Nitroprusside is the first-line agent, as it allows easy control of BP changes, despite its tendency to increase cerebral blood flow.

  • Labetalol and calcium channel blockers are second-line agents and should be added in, if necessary.

  • It is vital to avoid agents with potential sedative action such as β‎-blockers, clonidine, and methyldopa.

  • In selected patients who are stable and present at the very early stages, oral therapy with a combination of β‎-blockers and calcium blockers may be sufficient.

Aortic dissection: assessment

Aortic dissection is a surgical/medical emergency and, untreated, has a 1-year mortality of >90%. Dissection begins with formation of a tear in the intima, and the force of the blood cleaves the media longitudinally to various lengths. Predisposing factors are summarized in Box 1.39.

* Marfan’s syndrome: arm span > height, pubis to sole > pubis to vertex, depressed sternum, scoliosis, high-arched palate, upward lens dislocation, thoracic aortic dilatation/aortic regurgitation, Cardiac emergenciesurinary hydroxyprolene (some).

Classification

There are three classifications, as illustrated in Fig. 1.12 (DeBakey, Stanford, and descriptive). Dissections involving the ascending and/or aortic arch are surgical emergencies, and those exclusive to the descending aorta are treated medically.

Fig. 1.12 Classification of aortic dissection.

Fig. 1.12 Classification of aortic dissection.

Presentation

  • Chest pain: classically abrupt onset of very severe, most commonly anterior, chest pain radiating to the interscapular region. Usually tearing in nature and, unlike the pain of MI, most severe at its onset. Pain felt maximally in the anterior chest is associated with ascending aortic dissection, whereas interscapular pain suggests dissection of the descending aorta. Patients often use adjectives such as ‘tearing’, ‘ripping’, ‘sharp’, and ‘stabbing’ to describe the pain.

  • Sudden death or shock: usually due to aortic rupture or cardiac tamponade.

  • CCF: due to acute aortic incompetence and/or MI from dissection extending into the coronary arteries (usually RCA).

  • Patients may also present with symptoms and signs of occlusion of one of the branches of the aorta. Examples include:

    • Stroke or acute limb ischaemia: due to compression or dissection.

    • Paraplegia with deficits: spinal artery occlusion.

    • MI infarction: usually the RCA.

    • Renal failure and renovascular hypertension.

    • Abdominal pain: coeliac axis or mesenteric artery occlusion.

  • Aortic dissection may be painless.

  • Ask specifically about history of hypertension, previous heart murmurs or aortic valve disease, and previous CXRs that may be useful for comparison.

Examination

  • This may be normal.

  • Most patients are hypertensive on presentation. Hypotension is more common in dissections of the ascending aorta (20–25%) and may be due to blood loss, acute aortic incompetence (which may be accompanied by heart failure), or tamponade (distended neck veins, tachycardia, pulsus paradoxus).

  • Pseudohypotension may be seen if flow to either or both subclavian arteries is compromised. Look for unequal BP in the arms, and document the presence of peripheral pulses carefully. Absent or changing pulses suggest extension of the dissection.

  • Auscultation may reveal aortic valve regurgitation and occasionally a pericardial friction rub. Descending aortic dissections may rupture or leak into the left pleural space, and the effusion results in dullness in the left base.

  • Neurologic deficits may be due to carotid artery dissection or compression (hemiplegia) or spinal artery occlusion (paraplegia with sensory loss).

Differential diagnosis

  • The chest pain may be mistaken for acute MI, and acute MI may complicate aortic dissection. Always look for other signs of dissection (see Box 1.37), as thrombolysis will be fatal.

  • Severe chest pain and collapse may also be due to PE, spontaneous pneumothorax, acute pancreatitis, and penetrating duodenal ulcer.

  • Pulse deficits without backache should suggest other diagnoses: atherosclerotic peripheral vascular disease, arterial embolism, Takayasu’s arteritis, etc.

  • Acute cardiac tamponade with chest pain is also seen in acute viral or idiopathic pericarditis and acute MI with external rupture.

Aortic dissection: investigations

General

  • ECG: may be normal or non-specific (LVH, ST/T abnormalities). Look specifically for evidence of acute MI (inferior MI is seen if the dissection compromises the RCA ostium).

  • CXR: may appear normal but, with hindsight, is almost always abnormal. Look for widened upper mediastinum, haziness or enlargement of the aortic knuckle, irregular aortic contour, separation (>5mm) of intimal calcium from outer aortic contour, displacement of trachea to the right, enlarged cardiac silhouette (pericardial effusion), and pleural effusion (usually on the left). Compare with previous films, if available.

  • Bloods: baseline FBC, U&Es, cardiac enzymes, as well as cross-match. A novel monoclonal antibody assay to smooth muscle myosin heavy chains can accurately differentiate an acute dissection from an MI.

Diagnostic

  • Echocardiography: TTE may be useful in diagnosing aortic root dilatation, AR, and pericardial effusion/tamponade. TOE is the investigation of choice, as it allows better evaluation of both the ascending aorta and descending aorta, may identify the origin of the intimal tear, allows evaluation of the origins of the coronary arteries in relation to the dissection flap, and provides information on aortic insufficiency. It is not good at imaging the distal ascending aorta and proximal arch.

  • MR angiography: is the gold standard for diagnosing aortic dissection. It has all the positive features of TOE and, in particular, also provides accurate information on all segments of the ascending/arch/descending aorta, entry/exit sites, and branch vessels. Images can be displayed in multiple views, as well as reconstructed in three dimensions. However, there are a number of disadvantages, including: (1) availability of service out of hours and cost; (2) presence of metallic valves or pacemakers may preclude the patient from having an MRI; and (3) monitoring of unstable patients in the scanner can be difficult and unsafe.

  • Spiral (helical) CT with contrast: allows three-dimensional display of all segments of the aorta and adjacent structures. True and false lumens are identified by differential contrast flow and enter and exit sites of the intimal flap, as well as pleural and pericardial fluids. However, it cannot demonstrate disruption of the aortic valve, which may be associated with ascending aortic dissection.

  • Angiography: using the femoral or axillary approach, may demonstrate altered flow in the two lumens, aortic valve incompetence, involvement of the branches, and the site of the intimal tear. It is invasive and associated with a higher risk of complications in an already high-risk patient. It has largely been superseded by CT/MRI and TOE.

Selecting a diagnostic modality

(See Box 1.40.)

  • Confirm or refute a diagnosis of dissection.

  • Is the dissection confined to the descending aorta or does it involve the ascending aorta/aortic arch?

  • Identify the extent, sites of enter and exit, and presence and absence of thrombus.

  • To see whether there is AR, coronary involvement or pericardial effusions.