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Acute cardiology 

Acute cardiology
Chapter:
Acute cardiology
Author(s):

Kenneth McKinlay

and Naomi Johnston

DOI:
10.1093/med/9780199692958.003.0023
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Out-of-hospital cardiac arrest

Introduction

Cardiovascular disease is the leading cause of death in the developed world. There is a wide variation in the reported incidence and outcome of patients who have out-of-hospital cardiac arrest (OOHCA). It is unfortunately a common event with a high mortality, and survival rate to discharge home is typically <10%. The most common cause for adult cardiac arrest is acute coronary syndrome (ACS), however it is important to eliminate other potential causes and treat them appropriately.

Principles of management

  • Effective cardiopulmonary resuscitation (CPR) with minimal interruption

  • Optimize oxygenation

  • Early defibrillation

  • Appropriate drug treatment.

During circulatory arrest, organ injury can result from hypoxia, which is further exacerbated by reperfusion injury once return of spontaneous circulation (ROSC) is established. This insult can result in systemic inflammatory response syndrome (SIRS) and subsequent multiorgan failure (MOF). Early, aggressive management of these patients has potential to significantly influence their outcome and neurological status.

Post-cardiac care bundle (AHA guidelines)

1. Early coronary reperfusion

Early PCI is superior to thrombolysis with lower stroke, death, and reinfarction rates.

2. Hemodynamic optimization

Following cardiac arrest there is often a period of transient myocardial dysfunction; hypotension, reduced CO, frequent arrhythmias, and impaired contractility. Treatment includes:

  • IABP may augment the failing myocardium by both offloading the heart and increasing coronary perfusion

  • Inotropic/vasopressor support

  • Invasive cardiac monitoring.

3. Control of ventilation

Management should aim to avoid ALI:

  • Aim for normocarbia and oxygen saturation 94–98%

  • Lung protective ventilation strategies:

    • Tidal volumes 6mL/kg

    • Use of PEEP

    • FiO2 <60%

    • Permissive hypercapnia with plateau pressures <30cmH2O.

4. Blood glucose control

Blood glucose should be kept within 6–10mmol/L.

5. Treatment of seizures

Seizures are common following hypoxic neurological insult:

  • Insufficient evidence for prophylactic treatment.

  • Tonic clonic seizures treated with phenytoin/sodium valproate/benzodiazepines.

  • Myoclonus can be treated with clonazepam.

  • The use of EEG monitoring allows for identification of subclinical seizures, or seizure activity in paralysed patients.

6. Temperature control

Pyrexia is common in the 48 hours following cardiac arrest; poor neurological outcome has been associated with temperatures of 38°C and above.

Therapeutic hypothermia

There is increasing interest in the use of therapeutic hypothermia following OOHCA. Two landmark randomized control trials (RCTs) looked at the effect of cooling patients following VF arrest. Both trials demonstrated improvement in anoxic neurological injury, relating to improved functional outcomes and reduced mortality.

The International Liaison Committee on Resuscitation (ILCOR) recommends the use of therapeutic hypothermia in patients who have ROSC though remain comatose following OOHCA regardless of initial presenting rhythm.

Indications for therapeutic hypothermia

Patients accepted for ICU treatment directly or via the catheter lab with following features:

  • OOHCA with ROSC regardless of presenting rhythm

  • Comatose at the initial point of treatment with GCS score <9

  • Cerebral irritation following ROSC requiring intubation

  • No other known cause of coma (e.g. metabolic, trauma)

  • No coma state prior to arrest

  • No terminal illness

  • Not pregnant (request HCG test if <50 years)

  • Not haemodynamically unstable, e.g. high dose of inotropic support

  • No severe respiratory compromise.

Due to the adverse physiological effects of cooling, it is important to assess the risk of benefit versus harm on an individual basis.

Temperature monitoring (in order of preference)

  • PAFC

  • Bladder

  • Rectal

  • Oesophageal

  • Do not use tympanic probe for temperature monitoring—this is inaccurate.

Protocol for therapeutic hypothermia

See Fig. 23.1.

Figure 23.1 (a) and (b) An example of a protocol for therapeutic hypothermia. Reproduced with kind permission from Jorg Prinzlin and Kenneth McKinlay, Copyright Golden Jubilee National Hospital.

Figure 23.1 (a) and (b) An example of a protocol for therapeutic hypothermia. Reproduced with kind permission from Jorg Prinzlin and Kenneth McKinlay, Copyright Golden Jubilee National Hospital.

Further reading

Intensive Care Society (ICS), UK. Standards for the Management of Patients After Cardiac Arrest. Acute cardiology<http://www.ics.ac.uk/ics-homepage/guidelines-standards/>.

Endocarditis

Introduction

Endocarditis is inflammation of the endocardium, which may or may not include the heart valves. Despite advances in medicine over the last 30 years neither the incidence nor mortality of the condition has changed. However, both the predisposing factors and causative agents have altered. Previously considered a disease of the young with rheumatic heart disease, now this condition is associated with older patients following invasive procedures with or without prosthetic heart valves.

Predisposing factors

  • Male > female

  • Increasing age

  • IV drug abuse

  • Valve prostheses

  • Degenerative valve sclerosis

  • Multiple invasive procedures

  • Chronic haemodialysis

  • Diabetes

  • Intravascular devices.

Microbiology

85% of cases are blood culture positive for the following typical bacteria:

  • Staphylococcus aureus: commonest causative bacteria, coagulase negative Staphylococcus is frequently associated with prosthetic valve endocarditis (PVE)

  • Streptococcus; S. sangius,S. mitis,S. salivarius,S. mutans, and Gemella morbillorum. Infection with S. milleri and S. anginosus is associated with abscess formation and disseminated disease

  • Enterococcus; E. faecalis,E. faecium,E. durans.

Blood cultures are frequently negative with the following organisms:

  • Variant Streptococcus

  • Gram-negative bacilli

  • HACEK group (Haemophilus,Actinobacillus,Cardiobacterium,Eikenella,Kingella)

  • Brucella, and fungi.

Up to 5% of cases are the result of Coxiella burnetii (Q fever), Bartonella,Legionella,Mycoplasma, and Chlamydia. These organisms will always have negative blood cultures and can only be identified with serology and cell culture.

Common presenting features

  • New regurgitant murmur

  • Embolic event—30% patients present with brain, lung, or spleen infarction

  • Fever, signs of sepsis, pyrexia of unknown origin (PUO).

Additional features

  • Splinter haemorrhages (particularly on nail beds)

  • Janeway lesions (painless macular erythematous lesions)

  • Roth spots (retinal haemorrhages)

  • Osler’s nodes (painful nodules on digits)

  • Rigors, fatigue, anaemia, night sweats, microscopic haematuria.

Diagnosis

The Duke criteria for diagnosis of infective endocarditis require 2 major or 1 major and 3 minor or 5 minors:

Major criteria

  • Positive blood cultures: either typical organism in 2 sets, or persistently positive blood cultures (3+ sets >12 hours apart), or single positive blood culture for Q fever/phase 1 IgG antibody titre > 1:800.

  • Endocardium involvement: echocardiogram evidence of vegetation/abscesses or new valvular incompetence.

Minor criteria

  • Predisposing factors

  • Pyrexia > 38°C

  • Positive blood cultures

  • Echocardiogram that do not meet major criteria

  • Vascular or immunological signs.

Investigations

  • Blood cultures: at least 3 sets taken 30 minutes apart from separate sites.

  • Echocardiogram: TTE is first line in all patients; TOE has a higher sensitivity and specificity and is indicated in patients with a high suspicion of infective endocarditis (IE) despite a negative TTE and in all patients who have a positive TTE (abscess/vegetations visualized). In patients in whom a high suspicion remains despite previously negative findings should be rescanned 7–10 days later.

  • Urinalysis: microscopic haematuria.

  • CXR: cardiomegaly.

  • ECG: conduction abnormalities, typically 1st-degree heart block.

  • Blood tests: normochromic, normocytic anaemia, leukopenia, raised ESR and CRP.

Management

Early antibiotic therapy has been shown to reduce mortality.

Empirical therapy for native valves with acute presentation:

  • Flucloxacillin 8–12g/day in 4–6 doses with gentamycin 1mg/kg/day three times a day.

  • In penicillin allergic patients: vancomycin 1g/12 hours, and gentamycin 1mg/kg/day three times a day.

Subacute presentation:

  • Penicillin 7.2g in 6 divided doses with gentamycin 1mg/kg/day three times a day, or

  • Amoxicillin 12g/day in 6 divided doses (more activity against HACEK organisms).

Prosthetic valves

  • Vancomycin and gentamycin doses as previously with the addition of rifampicin 600–1200mg/day in two oral doses.

Once organism is isolated therapy should be directed in accordance with microbiological advice.

Early surgery prevents progressive heart failure and valvular destruction; however it also carries a higher mortality risk. The indications for surgery are:

  • Uncontrolled infection despite treatment

  • Prevention of emboli

  • Heart failure.

Prophylaxis

Certain patients are considered at a higher risk of developing endocarditis:

  • Patients with prosthetic valves/material for cardiac valve repair

  • Patients with previous infective endocarditis

  • Structural congenital heart disease—not including isolated atrial septal defect, repaired ventricular septal defect, or patent ductus arteriosus

  • Hypertrophic cardiomyopathy

  • Acquired valve heart disease (stenosis/incompetence).

Prophylactic antibiotics:

  • No longer indicated for all dental or non-dental procedures as the risk of anaphylaxis outweighs the benefit of use.

  • Advice is given regarding recognizing symptoms, good oral hygiene, and avoidance of potential causative procedures.

  • However, if a high risk patient has an infection which requires antibiotics, and is undergoing GU/GI surgery at the site of the infection then antibiotics given should cover organisms causative for IE.

Prognosis is dependent on four features:

  • Patient factors: elderly, PVE, coexisting disease – respiratory, renal, cardiac, or IDDM.

  • Infective organism: fungi, Staphylococcus aureus, and Gram-negative bacilli all have poorer outcomes.

  • Complications of IE are heart or renal failure, CVA, and septic shock.

  • Echocardiogram evidence of pulmonary hypertension, severe valvular incompetence, raised diastolic pressure and reduced LV ejection fraction.

Further reading

Habib G, Hoen B, Tornos P, Thuny F, Prendergast B, Vilacosta I, et al. Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (new version 2009): the Task Force on the Prevention, Diagnosis, and Treatment of Infective Endocarditis of the European Society of Cardiology (ESC). Eur Heart J 2009;30:2369–413.Find this resource:

Aortic dissection

Introduction

Separation of the intima and media layers of the aortic wall results in the formation of both false and true lumens. Blood within the false lumen can then sequestrate and result in the dissection extending and potentially rupturing.

Risk factors

  • Male > female

  • 50–70 years

  • Hypertension, smoking, and hyperlipidaemia.

Causes

  • Congenital: Marfan’s syndrome, Ehler–Danlos syndrome, Turner’s syndrome

  • Degenerative: age >60

  • Atherosclerotic: hypertension, smoking, and hyperlipidaemia are all risk factors

  • Inflammatory: Takayasu’s disease, Behçet’s disease, giant cell arteritis, rheumatoid arthritis, and Ormond’s disease

  • Traumatic: deceleration injury—road traffic collision, fall from height

  • Surgical/iatrogenic: cross-clamp or aortic cannula placement, angiography, or angioplasty

  • Toxic: bacterial and fungal aortitis

  • Drugs: cocaine and amphetamine use

  • Pregnancy.

Classification

See Fig. 23.2.

Figure 23.2 Classification of aortic dissection. Adapted from The Annals of Thoracic Surgery, 10, 3, Daily PO, Trueblood HW, Stinson EB, Wuerflein RD, Shumway NE, Management of acute aortic dissections, pp. 237–247. Copyright 1970, with permission from The Society of Thoracic Surgeons, and from Journal of Thoracic Cardiovascular Surgery, 49, DeBakey ME et al., Surgical management of dissecting aneurysms of the aorta, pp. 130–149. Copyright Elsevier 1965.

Figure 23.2 Classification of aortic dissection. Adapted from The Annals of Thoracic Surgery, 10, 3, Daily PO, Trueblood HW, Stinson EB, Wuerflein RD, Shumway NE, Management of acute aortic dissections, pp. 237–247. Copyright 1970, with permission from The Society of Thoracic Surgeons, and from Journal of Thoracic Cardiovascular Surgery, 49, DeBakey ME et al., Surgical management of dissecting aneurysms of the aorta, pp. 130–149. Copyright Elsevier 1965.

Stanford1

  • Type A: the ascending aorta is involved in the dissection.

  • Type B: no involvement of the ascending aorta.

DeBakey (further subdivides the dissection)2

  • Type I the whole aorta is involved.

  • Type II only the ascending aorta is involved.

  • Type III only the descending aorta is involved in the dissection.

A new classification includes the aetiology of the dissection (Table 23.1).

Table 23.1 European Society of Cardiology classification of aortic dissection

Class 1

Classical aortic dissection

Class 2

Intramural haematoma/haemorrhage

Class 3

Subtle, discrete aortic dissection

Class 4

Plaque rupture/ulceration

Class 5

Traumatic/iatrogenic aortic dissection

Reproduced from Erbel R. et al., 'Diagnosis and management of aortic dissection: Task Force on Aortic Dissection, European Society of Cardiology', European Heart Journal, 2001, 22, 18, pp. 1642–1681, by permission of the European Society of Cardiology.

Presentation

  • Abrupt onset of severe chest pain, typically radiating through to back.

  • Pain often described as sharp, tearing, ripping, or stabbing.

  • Associated syncope, cardiac failure, cardiac tamponade, aortic regurgitation, hypo/hypertension.

  • Depending on the anatomy of the extension, aortic root occlusion can occur, affecting arms/legs (20%), renal (15%), brain (5%), cardiac (10%), and bowel (3%).

Diagnosis

Early diagnosis requires good history taking and a high index of suspicion in patients with risk factors.

  • ECG: eliminate acute MI as the diagnosis. Extension of the dissection involving the coronary ostia may present as ischaemia on the ECG.

  • CXR: mediastinal widening, cardiomegaly, aortic knuckles, pleural capping, deviation of trachea to right, and blunted costophrenic angles secondary to haemothorax.

  • CT: high sensitivity and specificity of dissection, rapid test, and able to establish the extent of the lesion.

  • MRI: highest sensitivity and specificity for diagnosis, also allows for functional assessment of aortic valve and left ventricle. May be impractical in critically ill patient.

  • TOE: allows for real time assessment of dissection, involvement of the aortic valve, degree of regurgitation, and left ventricular cardiac function can be assessed.

  • Aortography: previously considered the gold standard, though inappropriate in unstable patient.

Differential diagnosis

  • ACS

  • Aortic regurgitation

  • Aortic aneurysm without dissection

  • Pericarditis

  • PE

  • Pleurisy.

Management

Type A aortic dissection

  • Requires surgical intervention and has a higher mortality compared to type B (60% vs 10%).

  • Mortality increases 1–2% per hour in the untreated acute ascending aorta dissections in the first 48 hours.

Type B aortic dissection

  • Medical therapy is aimed at reducing hypertension.

  • No evidence to suggest an improved survival in patients who have a surgical repair of type B aortic dissections.

  • Surgery or interventional radiology may be considered in this group if the dissection is causing organ ischaemia.

Initial management

Strategy should be to prevent further extension of the dissection and vessel rupture:

  • A, B, C.

  • Tight BP control: IV labetalol to maintain systolic BP 80–100mmHg. Sodium nitroprusside (SNP), GTN and hydralazine are alternatives.

  • Reduce LV contractility without comprising coronary perfusion.

  • Adequate analgesia.

  • IV access, cross-match, full blood count, coagulation, U&Es, lactate.

  • Establish invasive monitoring—arterial line ideally placed in left radial artery as innominate artery may be involved in dissection, affecting right radial readings.

Conduct of anaesthesia

  • Maintain haemodynamic stability.

  • Type B dissections—thoracotomy incisions require double-lumen tube placement, usually left.

  • Depending on position of aortic clamp patients are at risk of bowel or renal ischaemia and anterior spinal artery syndrome/paralysis.

  • Meticulous review of urine output, metabolic status, and coagulation is important to anticipate any complications.

  • TOE can help guide surgical decision-making.

  • CPB—it may be necessary to establish CPB rapidly in a patient in extremis and femoral bypass can be established prior to sternotomy.

Deep hypothermic circulatory arrest (DHCA)

CPB allows for the maintenance of organ perfusion following cardioplegia induced cardiac arrest. Complete circulatory arrest can be advantageous in aortic surgery, providing improved operating conditions and reducing basal metabolic rate (BMR) and organ ischaemia. By reducing the body temperature to 18–20°C prolongation of the CPB and aortic cross-clamp times are possible. Periods of up to 30 minutes of DHCA are tolerated without significant neurological dysfunction; longer durations are linked to a sharp increase in neurological injury and poorer outcome.

It is possible to selectively perfuse the cerebral circulation, using retrograde cerebral perfusion or selective antegrade cerebral perfusion. By using these methods DHCA can be prolonged safely.

Postoperative care

  • Establish normothermia.

  • Correct any coagulopathy and acidosis.

  • Maintain MAP ∼65mmHg for at least the first 4 hours following the operation and if no significant bleeding noted increase the MAP ∼75mmHg.

  • Careful fluid balance, risk of cerebral oedema formation, may require mannitol or frusemide therapy.

  • Keep the patient ventilated and sedated initially, once haemodynamically stable for >12 hours and no signs of bleeding, wean patients and assess neurological status.

Further reading

Erbel R, Alfonso F, Boileau C, Dirsch O, Eber B, Haverich A, et al. Diagnosis and management of aortic dissection. Eur Heart J 2001;22:1642–81.Find this resource:

Hebballi R, Swanevelder J. Diagnosis and management of aortic dissection. CEACCP 2009;9:14–18.Find this resource:

    Notes:

    1 Reprinted from The Annals of Thoracic Surgery, 10, 3, Daily PO, Trueblood HW, Stinson EB, Wuerflein RD, Shumway NE, Management of acute aortic dissections,pp. 237–247. Copyright 1970, with permission from The Society of Thoracic Surgeons.

    2 This classification was published in Journal of Thoracic Cardiovascular Surgery, 49, DeBakey ME et al., Surgical management of dissecting aneurysms of the aorta, pp. 130–149. Copyright Elsevier 1965.