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Cardiovascular assessment and monitoring 

Cardiovascular assessment and monitoring
Chapter:
Cardiovascular assessment and monitoring
Author(s):

Heather Baid

, Fiona Creed

, and Jessica Hargreaves

DOI:
10.1093/med/9780198701071.003.0006
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date: 25 September 2020

Cardiovascular assessment

If an actual or potential cardiovascular abnormality has been identified during a general ABCDE assessment (see Cardiovascular assessment and monitoring p. [link]) or while monitoring the patient, a more detailed and focused cardiovascular assessment can provide further information to guide clinical management.

Focused health history

Subjective information about the cardiovascular history can be taken from the patient if they are awake, or from other sources (e.g. family, caregivers, or patient notes). For an overview of history taking, see Cardiovascular assessment and monitoring p. [link].

Cardiovascular symptom enquiry

  • Chest pain, indigestion, and arm or jaw numbness.

  • Palpitations.

  • Shortness of breath—in the daytime and/or at night.

  • Syncope.

  • Fatigue.

  • Oedema.

  • Leg cramps.

  • Cough—if productive, note the type, amount, and colour of sputum.

  • Previous hypertension, angina, or myocardial infarction.

Focused physical assessment

  • Supporting therapies—oxygen, inotropes, intra-aortic balloon pump, pacing, oxygen, non-invasive or invasive mechanical ventilation.

  • Obvious signs of discomfort or distress.

  • Fluid assessment (see Cardiovascular assessment and monitoring p. [link]).

  • Cardiovascular-focused assessment of the face, neck, thorax, and peripheries (see Table 6.1).

Table 6.1 Cardiovascular-focused assessment

Normal

Abnormal

Inspection

  • Pink, moist mucous membranes

  • Symmetrical precordium

  • Pink peripheries

  • Central cyanosis

  • Dry mucous membranes

  • Raised JVP

  • Precordial wounds, drains, scarring, or bruising

  • Oedema

  • Signs of VTE

  • Peripheries pale, cyanotic, or mottled

Palpation

  • Point of maximal impulse fifth intercostal space, mid-clavicular line

  • Bilateral, strong, regular pulses

  • Capillary refill < 2 s

  • Warm peripheries

  • Thrills, heaves, and thrusts

  • Displaced point of maximal impulse

  • Pulses—weak, absent, bounding, or irregular

  • Capillary refill > 2 s

  • Peripheries cool, cold, hot, or diaphoretic

Auscultation

  • Clear S1 and S2 heart sounds

  • No bruits

  • Clear breath sounds

  • Heart sounds—murmur, S3, S4, split, rub, or muffled

  • Bruits—carotid, aortic, renal, or iliac

  • Breath sounds—crackles, wheeze, or diminished

Precordial landmarking

The following landmarking areas (see Figure 6.1) are used for precordial palpation to rule out thrills, heaves, and thrusts and for auscultation of heart sounds:

  • aortic area—second intercostal space, right sternal border

  • pulmonary area—second intercostal space, left sternal border

  • Erb’s point—third intercostal space, left sternal border

  • tricuspid area—fourth intercostal space, left sternal border

  • mitral area—fifth intercostal space, left mid-clavicular line.


Figure 6.1 Precordial landmarking.

Figure 6.1 Precordial landmarking.

(Adapted with permission from Spiers C (2011) Cardiac auscultation. British Journal of Cardiac Nursing 6(10), 482–6. © MA Healthcare.)

Causes of key abnormalities

  • Chest pain—angina, acute coronary syndromes, non-cardiac cause.

  • Irregular pulse—arrhythmia, ectopics.

  • Bounding pulse—sepsis.

  • Weak pulse—hypovolaemia, hypotension, left ventricular failure.

  • Peripheral oedema—right ventricular failure, sepsis.

  • Cool, diaphoretic skin.

  • Peripheral cyanosis—hypoxia, poor tissue perfusion.

  • Absent or weak pedal pulses—left ventricular failure, oedema, vascular insufficiency.

  • Prolonged capillary refill—poor tissue perfusion.

Laboratory investigations

See Cardiovascular assessment and monitoring p. [link] for normal values and further explanation of the following blood tests which are relevant to check for a cardiovascular review:

  • FBC

  • U&E

  • LFTs

  • clotting

  • troponin T

  • arterial blood gas analysis, including lactate

  • glucose.

Cardiovascular monitoring: a brief introduction

There is clearly a need for effective and accurate cardiovascular monitoring of all critically ill patients. There are a number of monitoring tools available for this, and these will be described in more detail in Chapter 7.

Standardized cardiovascular monitoring tools include:

  • continuous electrocardiogram (either a 3- or 5-lead system)

  • arterial blood pressure recording

  • central venous pressure measurement

  • cardiac output measurement (several tools are available)

  • fluid balance assessment

  • central temperature recording.

Hypotension

Definition

Hypotension is normally defined as a low blood pressure. The National Institute for Health and Care Excellence (NICE)1 defines normal blood pressure as being within a range of values. Normal systolic blood pressure is in the range 100–139 mmHg, and normal diastolic blood pressure is in the range 60–89 mmHg.

In critical care it may be more useful to define hypotension as a systolic blood pressure below 90 mmHg or a mean arterial pressure below 60 mmHg. Hypotension needs to be recognized and treated quickly, as all of the body’s organs require sufficient arterial pressure to maintain perfusion. Inadequate blood pressure will lead to reduced organ perfusion, organ dysfunction, and organ failure.

Assessment findings

When assessing for signs of hypotension in the critically ill patient it is essential to review other vital signs, as other changes may indicate cardiovascular deterioration. This includes changes in:

  • heart rate

  • respiratory rate (if self-ventilating)

  • peripheral perfusion

  • vascular resistance

  • urine output

  • level of consciousness (if not sedated)

  • blood pH.

It is suggested that it may be more beneficial for the critically ill patient if parameters of effective cardiac output are managed, rather than basing assessment and management on one parameter alone. To that end, Soni and Watson2 have highlighted a number of criteria that might suggest cardiac output is effective. These include:

  • warm, well-perfused peripheries (normal skin colour, cap refill < 3 seconds, palpable peripheral pulses)

  • blood pressure within acceptable limits

  • heart rate within acceptable range

  • evidence of functioning organs (e.g. urine output > 0.5 ml/kg/hr)

  • absence or improvement of acidosis.

Ineffective cardiac output can occur in the critically ill patient for a number of reasons. However, hypotension is commonly linked to various forms of shocks, including:

  • hypovolaemic shock

  • cardiogenic shock

  • septic shock or systemic inflammatory response syndrome (SIRS)

  • anaphylactic shock

  • neurogenic shock

  • obstructive shock

  • trauma shock.

Key cardiovascular assessment findings for each type of shock are summarized in Table 6.2.

Table 6.2 Key cardiovascular changes for each type of shock

Type of shock

Heart rate

Cardiac output

Systemic vascular resistance

Central venous pressure

Hypovolaemic

Cardiogenic

Septic or SIRS

*

Anaphylactic

Neurogenic

Obstructive

Trauma

* Cardiac output may be low with late sepsis.

Hypovolaemic shock

Definition

Hypovolaemia is an ineffective cardiac output status related to low volume within the vascular compartment. There are many causes of hypovolaemia, including:

  • excessive blood loss

  • haemorrhage

  • excessive vomiting and/or diarrhoea

  • excessive diuresis

  • plasma loss (e.g. severe burns)

  • third spacing

  • excessive dialysis.

Assessment findings

The hypovolaemic patient may present with some or all of the following findings on assessment:

  • tachycardia

  • decreased blood pressure (narrowing of pulse pressure)

  • pallor and diaphoresis

  • increased systemic vascular resistance (SVR)

  • extended capillary refill time

  • low central venous pressure

  • decreased urine output.

Management

This should relate to establishing and treating the cause of hypovolaemia (e.g. a patient who is haemorrhaging may require surgical intervention). Common aspects of management include:

  • appropriate fluid replacement (see Cardiovascular assessment and monitoring p. [link])

  • electrolyte replacement

  • continuous monitoring (blood pressure, heart rate, CVP, and JVP)

  • careful assessment of renal function (see Cardiovascular assessment and monitoring p. [link])

  • prevention of organ damage related to low perfusion.

Cardiogenic shock

Definition

Cardiogenic shock is a low cardiac output status related to reduced cardiac function. The heart does not pump effectively because of damage to the muscle. Poor cardiac output is then worsened by increased peripheral resistance resulting from normal compensatory mechanisms. The main causes of cardiogenic shock are:

  • myocardial infarction

  • cardiac tamponade

  • cardiac valve disease (particularly mitral valve disease)

  • cardiac arrhythmias.

Assessment findings

The patient with cardiogenic shock will present with all or some of the following symptoms:

  • hypotension

  • tachycardia

  • arrhythmias

  • increased SVR

  • signs of heart failure (increased CVP, pulmonary oedema, shortness of breath, hypoxia increased JVP).

Management

Treatment will focus on supporting the failing cardiovascular system to ensure adequate but not excessive fluid balance, and includes:

  • ensuring accurate fluid assessment to prevent both fluid overload and dehydration

  • careful and appropriate use of inotropic support

  • reduction in peripheral resistance

  • cautious use of glyceryl trinitrate (GTN)

  • intra-aortic balloon pump

  • left ventricular assist devices.

Septic shock and systemic inflammatory response syndrome (SIRS)

Definition

An acute inflammatory response as a result of either severe infection or another inflammatory injury. This is a distributive form of shock, resulting in profound vasodilatation and increased microvascular permeability.

Assessment findings

The patient with septic shock or SIRS will present with some or all of the following symptoms:

  • tachycardia

  • initial widening of pulse pressure, followed by hypotension in the later stages

  • initially increased and then decreased cardiac output

  • increased or decreased temperature

  • decreased SVR

  • relative hypovolaemia.

Management

For details of the management of sepsis and SIRS, see Cardiovascular assessment and monitoring p. [link].

Anaphylactic shock

Definition

This is a distributive form of shock related to severe allergic reaction following exposure to an antigen. Anaphylaxis triggers profound vasodilatation, misdistribution of fluid, and capillary leakage. It is treated as a medical emergency, as deterioration may be rapid, and prompt effective treatment is required (see Cardiovascular assessment and monitoring p. [link]). It may be caused by exposure to a number of antigens that may be infused, inhaled, or ingested. Examples include:

  • infusion or drug reactions

  • blood transfusion

  • latex

  • immunoglobulins

  • ingested food substances.

Assessment findings

The patient with anaphylactic shock will present with all or some of the following symptoms:

  • hypotension

  • tachycardia

  • increased respiration

  • decreased SVR

  • bronchospasm, laryngeal oedema, and/or stridor

  • pulmonary oedema

  • nausea and vomiting

  • urticaria

  • angio-oedema.

Management

Treatment should follow the Resuscitation Council guidelines3 (see Cardiovascular assessment and monitoring pp. [link] and p. [link] for further details).

Neurogenic shock

Definition

This is another distributive form of shock, in which severe vasodilatation is caused by disruption of sympathetic nerve activity that normally regulates and maintains vasomotor tone. It may occur within hours, and can persist for 1–3 weeks after spinal cord injury above T1 level, or more rarely after severe head injury affecting the medulla.

Assessment findings

The patient with neurogenic shock will present with all or some of the following symptoms:

  • hypotension

  • bradycardia

  • decreased SVR

  • loss of reflexes

  • warm dry skin

  • poikilothermia.

Management

This relates to protection of the spine, management of hypotension, and supportive measures until the period of neurogenic shock has passed. It includes:

  • stabilization of the spinal cord

  • assessment and management of other injuries

  • protection of the airway and supportive ventilation if needed

  • fluid replacement

  • inotropic support (increased SVR is the goal of support)

  • atropine or pacing for bradycardia

  • careful temperature regulation.

Obstructive shock

Definition

This is a form of shock caused by an inherent problem within the thoracic cavity that prevents effective cardiac contraction and the forward flow of blood through the cardiovascular system. It may be caused by:

  • pulmonary embolism

  • pericardial tamponade

  • tension pneumothorax.

Assessment findings

The patient with obstructive shock will present with all or some of the following symptoms:

  • tachycardia

  • cardiac arrhythmias

  • paradoxical pulse

  • hypotension

  • increased CVP

  • increased JVP

  • cardiac or respiratory arrest.

Treatment

Treatment focuses on removal of the obstructive mechanism. Therefore treat the cause as follows:

  • pneumothorax—chest drain insertion

  • pulmonary embolism—thrombolysis if appropriate

  • pericardial tamponade—drain tamponade.

Traumatic shock

Definition

Although trauma patients may present with any of the other forms of shock discussed previously, trauma practitioners have observed a specific form of shock following blunt trauma. Traumatic shock represents a unique pathological condition that appears to follow severe trauma and may lead to multi-organ dysfunction syndrome. This form of shock is characterized by an overwhelming inflammatory response, and supportive care is required for multi-organ dysfunction syndrome. See Cardiovascular assessment and monitoring p. [link] for more details of trauma assessment and management.

Assessment findings

Rapid deterioration may be seen in this form of shock, and the patient may appear to be presenting with other forms of shock, including hypovolaemic shock and distributive shock (e.g. hypovolaemic shock without any other clinical signs of haemorrhage, or marked vasodilatation without other clinical signs of sepsis). See Chapter 18 (Cardiovascular assessment and monitoring p. [link]) for further details about trauma assessment and management.

The patient with trauma shock may present with very sudden deterioration and some or all of the following symptoms:

  • severe hypotension

  • vasodilatation

  • tachycardia

  • tachypnoea

  • symptoms of SIRS (see Cardiovascular assessment and monitoring p. [link]).

Treatment

Treatment focuses on:

  • surgery or other interventions addressing the specific cause of the trauma

  • effective management of blood pressure

  • effective fluid resuscitation (see Cardiovascular assessment and monitoring p. [link])

  • treatment of the symptoms of SIRS (see Cardiovascular assessment and monitoring p. [link])

  • possible use of corticosteroids.

Other causes of hypotension

Hypotension in the critically ill patient may be unrelated to shock status, and other mechanisms may be responsible for a fall in blood pressure and the associated effects on effective cardiac output status.

In these cases it is important to isolate and treat the causative factor. This may include:

  • side effects of medications such as sedatives or muscle relaxants

  • hypoadrenalism

  • hypopituitarism

  • poisoning.

References

1 National Institute for Health and Care Excellence (NICE). Hypertension: clinical management of primary hypertension in adults. CG127. NICE: London, 2011. Cardiovascular assessment and monitoring www.nice.org.uk/guidance/cg127Find this resource:

2 Soni N and Watson D. Cardiovascular support. In: GR Nimmo and M Singer (eds) ABC of Intensive Care, 2nd edn. Wiley-Blackwell: Chichester, 2011.Find this resource:

3 Resuscitation Council (UK). Emergency Treatment of Anaphylactic Reaction: guidelines for health care workers. Resuscitation Council (UK): London, 2008.Find this resource:

Hypertension

Definition

Hypertension is currently classified by NICE according to the level of the blood pressure above recognized normal limits.4 NICE defines normal blood pressure as being within a range of values. Normal systolic blood pressure is in the range 100–139 mmHg, and normal diastolic blood pressure is in the range 60–89 mmHg.

NICE4 classifies hypertension as follows:

  • Stage 1 hypertension—systolic pressure above 140 mmHg and diastolic pressure above 90 mmHg.

  • Stage 2 hypertension—systolic pressure above 160 mmHg and diastolic pressure above 100 mmHg.

  • Stage 3 hypertension—systolic pressure above 180 mmHg and diastolic pressure above 110 mmHg.

A combination of medication in the form of angiotensin-converting enzyme (ACE) inhibitors, calcium-channel blockers, and thiazide diuretics is recommended to reduce elevated blood pressure. The combination depends on the level of elevation and the type of hypertension. There are many causes of chronic elevation of blood pressure, and these are treated in accordance with the NICE guidelines.

The critically ill patient may also present with a hypertensive crisis. This is clinically defined as an acute elevation of blood pressure (greater than 180/120 mmHg).

Causes

There are many causes of a hypertensive crisis, including:

  • exacerbation of chronic hypertension

  • sudden withdrawal of antihypertensive medication

  • phenochromocytoma

  • pre-eclampsia and eclampsia

  • raised intracranial pressure

  • idiopathic causes

  • autonomic dysreflexia.

Assessment findings

In an acute hypertensive crisis the patient may present with various signs and symptoms, including:

  • cardiovascular changes—elevated blood pressure, chest pain, palpitations

  • neurological changes—headaches, visual disturbances, acute confusion, papilloedema, nausea and vomiting, seizures

  • renal changes—acute kidney injury, proteinurea.

Treatment

Patients who present with a hypertensive crisis require immediate medical intervention, but care should be taken to ensure that the blood pressure is not reduced dramatically. Recommendations are as follows:

  • Reduce the mean arterial pressure by no more than 25% in the initial hour.

  • Gradually reduce the blood pressure once that goal has been achieved using appropriate antihypertensive therapy.

  • Ensure that the patient receives adequate haemodynamic monitoring to facilitate continuous arterial pressure recordings to prevent sudden falls in blood pressure.

  • Monitor for side effects of hypertensive crisis, such as neurological and/or other organ damage.

Reference

4 National Institute for Health and Care Excellence (NICE). Hypertension: clinical management of primary hypertension in adults. CG127. NICE London, 2011. Cardiovascular assessment and monitoringwww.nice.org.uk/guidance/cg127Find this resource:

Acute coronary syndrome

Definition

Acute coronary syndrome (ACS) refers to a number of clinical conditions, including:

  • ST-segment elevation myocardial infarction (STEMI)

  • non-ST-segment elevation myocardial infarction (NSTEMI)

  • unstable angina (no changes to biological markers of ischaemia).

It is important that patients with ACS receive timely care to prevent further deterioration, potential irreversible damage to the myocardial wall, and potential heart failure. ACS has a high mortality rate, and approximately one-third of patients will die within 24 h of onset of symptoms. Risk factors for ACS include:

  • smoking

  • hypertension

  • diabetes

  • hyperlipidaemia.

Assessment findings

Chest pain is the main symptom associated with ACS, and a careful assessment of the pain is essential. It may be helpful to use the SOCRATES mnemonic (see Table 6.3).

Table 6.3 SOCRATES mnemonic

Site

Where is the pain?

Onset

When did it start?

Characteristics

What is the pain like? (stabbing, aching, tight, crushing)

Radiation

Does it spread or radiate anywhere?

Associated symptoms

Are there any other symptoms associated with the pain?

Timing

What is the timing of the pain, and how long does it last?

Exacerbating factors

Does anything relieve the pain symptoms?

Severity

How severe is the pain (perhaps using a numerical scale of 1 to 5)?

In addition to pain, patients may also present with:

  • anxiety

  • increased parasympathetic activation (nausea and vomiting)

  • increased sympathetic activity (sweating, tachycardia, increased respiratory rate, pallor, and a slight increase in blood pressure).5

It is important to remember that atypical presentation may occur, and that some groups of patients may present with no symptoms or atypically. This is common in:

  • elderly patients

  • female patients

  • patients with diabetes.

NICE6 emphasizes the importance of careful history taking, which should include:

  • the type of pain

  • associated symptoms, including nausea, vomiting, sweating, and shortness of breath

  • family history of cardiovascular disease

  • risk factors for the development of cardiovascular disease

  • previous investigations and treatments.

Clinical diagnosis of STEMI is made on the basis of:

  • presentation and patient history

  • 12-lead ECG changes

  • cardiac markers.

Acute coronary syndrome: ECG findings

12-lead ECG changes

Diagnosis of STEMI is based on the following criteria:7

  • new ST-segment elevation at the J point in two contiguous leads with the cut-points: ≥0.1 mV in all leads other than leads V2–V3 where the following cut points apply: ≥0.2 mV in men ≥40 years; ≥0.25 mV in men <40 years, or ≥0.15 mV in women7

  • new left bundle branch block.

A 12-lead ECG showing STEMI is illustrated in Figure 6.2.


Figure 6.2 12-lead ECG showing STEMI.

Figure 6.2 12-lead ECG showing STEMI.

(Reproduced from Creed F and Spiers C, Care of the Acutely Ill Adult: an essential guide for nurses, 2010, with permission from Oxford University Press.)

Diagnosis of NSTEMI is more complicated and requires further investigations, but in summary the patient may experience acute chest pain without the presence of persistent ST-segment elevation. Subtle ECG changes may be seen, including7:

  • new horizontal or down-sloping ST-segment depression ≥ 0.05 mV in 2 continguous leads and/or

  • T-wave inversion ≥ 0.1 mV in two contiguous leads with prominent R wave or R/S ratio >1.

However, the ECG may be normal. Cardiac markers (troponins) will be elevated. If cardiac markers are unchanged the patient may be diagnosed with unstable angina.

Acute coronary syndrome: treatment for STEMI

The goals of treatment of STEMI include:

  • alleviating the patient’s pain

  • monitoring their CVS status

  • restoring patency to the occluded artery or arteries

  • reducing the patient’s anxiety

  • monitoring for complications of STEMI.

Pain alleviation strategies

  • Assessment using an appropriate tool.

  • Opiate-based analgesia (usually morphine or diamorphine). Caution should be exercised if the patient is hypotensive or if they have underlying respiratory pathophysiology. Care should be taken to observe for signs of respiratory depression. Anti-emetics should be administered alongside analgesia to prevent further nausea and vomiting.

  • Nitrates may be given either sublingually or intravenously, taking care to monitor the effect on blood pressure. Nitrates will reduce preload and afterload as well as dilating the coronary arteries, so they act to reduce myocardial oxygen demand and enhance myocardial perfusion.

  • Intravenous beta blockers may also be given to reduce oxygen demand and thus help to alleviate pain.

  • Oxygen may be administered to keep oxygen saturation ≥ 94%, but there is no clinical evidence that routine use of oxygen reduces pain or improves myocardial oxygenation.8,9

Monitoring of CVS status

  • Careful monitoring is required to enable observation both of the effects of STEMI on the cardiovascular system, and of the side effects of treatment.

  • Careful assessment should include monitoring of blood pressure, heart rate, heart rhythm, and fluid balance.

  • The patient should be monitored using a continuous ECG and automated blood pressure recordings.

Restoring patency to the occluded artery or arteries

  • The most important aspect of treatment is the reperfusion of the myocardium.

  • Low-dose aspirin should be administered as soon as possible.

  • The gold-standard treatment for STEMI is considered to be primary percutaneous coronary intervention (P-PCI). This should be undertaken as quickly as possible, and within 1 h of the initial presenting symptoms.

  • If P-PCI is not available or is not suitable for the patient, thrombolysis medication (second or third generation) may be given to break down the fibrin thrombus. This should only be administered if it is not contraindicated (see Box 6.1 for contraindications to thrombolysis).

  • The patient should be closely monitored for reperfusion arrhythmias and potential haemorrhage.

Reduction of anxiety

  • Anxiety may exacerbate the sympathetic response, and the patient will require reassurance.

  • Opiate-based analgesia will help to reduce anxiety, as will reassurance, effective communication, and a confident professional approach to care delivery.

Monitoring for complications of STEMI

  • Some STEMI patients may be at higher risk of developing complications.

  • Patients in whom STEMI affects the anterior left ventricle and patients with left bundle branch block (LBBB) are at increased risk.

  • Complications to monitor for include:

    • left ventricular failure (LVF)

    • right ventricular failure (RVF)

    • cardiogenic shock

    • arrhythmias and cardiac arrest.

Acute coronary syndrome: treatment for NSTEMI

Treatment focuses on assessment and management of pain, and managing the patient’s NSTEMI with medication. It is currently recommended that the following groups of medication are administered10:

  • antiplatelet therapy

  • antithrombin therapy

  • nitrates

  • beta blockers.

References

5 Spiers C. Cardiovascular assessment and care. In: F Creed and C Spiers (eds) Care of the Acutely Ill Adult: an essential guide for nurses. Oxford University Press: Oxford, 2010. pp. 59–104.Find this resource:

6 National Institute for Health and Care Excellence (NICE). Myocardial Infarction with ST-Segment Elevation: the acute management of myocardial infarction with ST-segment elevation. CG167. NICE: London, 2013. Cardiovascular assessment and monitoringwww.nice.org.uk/guidance/cg167Find this resource:

7 Thygesen K et al. Universal definition of myocardial infarction. Circulation 2007; 116: 2634–53.Find this resource:

8 British Thoracic Society. BTS guideline for emergency oxygen use in adult patients. Thorax 2008; 63 (Suppl. 6 ): vi1–68.Find this resource:

9 Cabello JB et al. Oxygen therapy for acute myocardial infarction. Cochrane Database of Systematic Reviews 2013; Issue 8. Art. No.: CD007160.Find this resource:

10 National Institute for Health and Care Excellence (NICE). Unstable angina and NSTEMI: the early management of unstable angina and non-ST-segment-elevation myocardial infarction. CG94. NICE: London, 2013. https://www.nice.org.uk/guidance/cg94.

Acute heart failure

Definition

Heart failure is defined by NICE as ‘a complex clinical syndrome that suggests impairment of the heart as a pump supporting physiological circulation. It is caused by structural or functional abnormalities of the heart.’11

Acute heart failure represents a potential life-threatening emergency that requires immediate assessment and treatment, and is usually characterized by rapid onset of symptoms. The heart may fail in several ways:

  • left-sided heart failure (left ventricular failure)

  • right-sided heart failure (cor pulmonale or right ventricular failure)

  • both sides (biventricular failure).

A number of factors may cause heart failure. These include:

  • acute coronary syndrome

  • arrhythmias

  • cardiac valve disorders

  • cardiomyopathy

  • pulmonary embolism

  • cardiac tamponade

  • sepsis.

Assessment findings

The patient may present with:

  • acute breathlessness, dyspnoea, hypoxaemia, and reduced oxygen saturations

  • hypotension and tachycardia

  • pallor, sweating, capillary refill > 3 seconds and cyanosis

  • cool peripheries

  • metabolic acidosis (raised lactate levels)

  • altered level of consciousness

  • increased anxiety.

In right-sided failure the patient may present with:

  • peripheral oedema

  • raised CVP

  • raised JVP

  • clear breath sounds.

In left-sided heart failure the patient may present with:

  • evidence of pulmonary oedema (pink frothy sputum, and fine crackles on auscultation)

  • pleural effusion

  • cardiomegaly

  • cardiogenic shock (see Cardiovascular assessment and monitoring p. [link]).

Investigations may include:

  • chest X-ray

  • echocardiogram

  • biochemical markers of heart failure

  • assessment of fluid status and fluid balance

  • 12-lead ECG

  • cardiac output studies.

Treatment

If possible the cause of the heart failure should be identified, as this will facilitate treatment.

Left-sided heart failure treatment

  • Position the patient upright and support them with pillows (this reduces venous return and facilitates gas exchange).

  • Give oxygen therapy to maintain oxygen saturations ≥ 94%.

  • CPAP may be useful for the treatment of pulmonary oedema (this improves oxygenation and prevents further formation of pulmonary oedema).

  • Mechanical ventilation may be required in cases of severe respiratory failure.

  • Careful monitoring of cardiovascular status, fluid balance, and urine output is required.

  • Give diamorphine or morphine (this has anxiolytic properties and facilitates venous dilation) and anti-emetic cover.

  • Give a loop diuretic if there is evidence of hypervolaemia (this reduces blood volume and preload).

  • Administer IV nitrates with caution to prevent severe hypotension.

  • Give inotropic support with caution. See Cardiovascular assessment and monitoring p. [link].

  • Use an intra-aortic balloon pump if there is no improvement in response to medication. See Cardiovascular assessment and monitoring p. [link].

  • Use a left ventricular assist device if there is no improvement in response to medication.

Right-sided heart failure treatment

  • Position the patient upright and support them with pillows.

  • Give oxygen therapy to maintain oxygen saturations ≥ 94%.

  • Careful monitoring of cardiovascular status, fluid balance, and urine output is required.

  • Give anti-arrhythmic therapy if arrhythmias are present.

  • Volume loading should be undertaken with caution (100–200 mL) to try to improve ventricular contractility.

  • Provide inotropic support with an appropriate inotropic agent. See Cardiovascular assessment and monitoring p. [link].

  • Use an intra-aortic balloon pump (see Cardiovascular assessment and monitoring p. [link]).

Treatment for cardiogenic shock is described on Cardiovascular assessment and monitoring p. [link].

Reference

11 National Institute for Health and Care Excellence (NICE). Chronic Heart Failure: management of chronic heart failure in adults in primary and secondary care. CG108. NICE: London, 2010. Cardiovascular assessment and monitoringwww.nice.org.uk/guidance/cg108Find this resource:

Pericarditis

Definition

The pericardium is a double-walled fibrous inelastic sac that surrounds the heart. Its purpose is to:

  • fix the heart to the mediastinum

  • prevent dilatation of the heart

  • function as a barrier to infection.

Pericarditis is inflammation of the layers of the pericardium, which may be caused by:

  • viral infection

  • malignancy

  • tuberculosis

  • connective tissue disorders

  • hypothyroidism

  • idiopathic causes

  • cardiac surgery

  • myocardial infarction (late-onset pericarditis after MI is referred to as Dressler’s syndrome, and is thought to be an autoimmune response).

Assessment findings

The patient with pericarditis may present with all or some of the following symptoms:

  • chest pain (usually localized to the retrosternal area and left precordium); the pain may lessen if the patient sits forward, and it may worsen if the patient lies flat

  • pericardial rub on cardiac auscultation

  • 12-lead ECG changes (ECGs are abnormal in 90% of patients with acute pericarditis, and generally show diffuse ST-segment elevation in almost all of the 12-lead ECG).

Treatment

  • Treat the cause where possible.

  • Give non-steroidal anti-inflammatory medication.

  • Observe for complications of pericarditis, which may include:

    • pericardial effusion

    • pericardial tamponade.

Pericardial effusion

Definition

A pericardial effusion is the abnormal accumulation of fluid (usually more than 50 mL) in the pericardial sac. Effusions may be non-compressive or compressive. Non-compressive effusions do not interfere with normal cardiac functioning, and may present with fewer symptoms. Compressive effusions may cause sudden increases in pericardial pressure which may lead to cardiac tamponade. The factors that affect the impact of the effusion include:

  • the volume of fluid

  • the rate of fluid accumulation

  • the compliance of the pericardium.

Assessment findings

The patient may be asymptomatic (if non-compressive), or may have any of the following:

  • dull chest pain

  • signs of cardiac compression

  • 12-lead ECG changes, especially a dampening effect (reduced voltage) because of the insulation effect of the accumulated fluid; the QRS height may also fluctuate between beats because of the fluid accumulation

  • pericardial rub may be reduced because of the insulating effect of the fluid

  • reduced percussion (dull) over the left lung (Ewart’s sign), due to compression atelectasis.

The ECG should be considered to aid diagnosis.

Treatment

This involves pericardial drainage using pericardiocentesis.

Pericardial tamponade

Definition

Pericardial tamponade is a life-threatening condition that requires emergency medical intervention. It is caused by the accumulation of fluid that results in compression of the heart muscle and prevents normal cardiac contraction. The high pressure changes within the pericardium prevent ventricular filling, which leads to significantly reduced cardiac output, haemodynamic compromise, and potential circulatory collapse. Pericardial tamponade may be caused by:

  • infection

  • cardiac surgery

  • aortic dissection

  • trauma

  • malignancy

  • myocardial infarction

  • central line insertion

  • biopsy.

Assessment findings

Pericardial tamponade should be suspected if a patient with pericarditis or pericardial effusion shows signs of significant haemodynamic instability or compromise. Key findings may include:

  • systemic hypotension

  • tachycardia

  • dyspnoea

  • tachypnoea

  • cool peripheries, pallor and capillary refill > 3 seconds

  • raised JVP

  • increased CVP

  • quiet heart sounds on auscultation

  • paradoxical pulse.

The patient may suffer cardiac arrest if the tamponade is not quickly identified and treated.

Treatment

  • Pericardial drainage using pericardiocentesis. This may be performed either by open surgery, or percutaneously using echocardiography.

  • Cardiac resuscitation may be required if the patient has suffered cardiac arrest (see Cardiovascular assessment and monitoring p. [link]).

Infective endocarditis

Definition

The endocardium is the innermost lining of the heart, and its cells are biologically similar to the endothelial cells that line blood vessels. It has an important role in ensuring smooth blood flow through the heart.

Infective endocarditis is an infection that affects the endocardium, usually caused by a bacterial translocation from another area of the body. During the infection organisms are able to adhere to the surface of the valve and destroy the valvular leaflets. Vegetations may develop and these may break off, causing emboli distal to the heart (e.g. in the brain, gut, or limbs). Infective endocarditis may lead to heart failure. It may be divided into:

  • acute endocarditis, in which symptoms progress rapidly

  • subacute endocarditis, in which symptoms may develop over several months.

Endocarditis may be caused by:

  • invasive procedures that may allow bacterial infiltration (e.g. pacing wires, CVP lines)

  • cancer

  • dental manipulation

  • poor dental care

  • IV drug abuse.

Assessment findings

Patients with infective endocarditis may present with:

  • fever

  • breathlessness

  • signs of cardiac failure

  • effects of thromboemboli (e.g. stroke)

  • vascular changes (haemorrhagic lesions on the palms and soles, and splinter haemorrhages underneath the nail beds)

  • cardiac murmurs

  • arrhythmias

  • signs of chronic illness.

Treatment

  • High-dose intravenous antibiotics (often for several weeks).

  • Treatment of specific disorders (e.g. heart failure, arrhythmias).

  • Surgery to replace the affected valve.

Cardiac arrhythmias

Introduction

A common cardiac problem for critically ill patients is the development of cardiac arrhythmias. In health, normal cardiac electrical activity is stimulated by the sinoatrial node, and the normal cardiac rhythm is one that originates from the sinoatrial node and causes a normal sinus rhythm (see Figure 6.3).


Figure 6.3 ECG showing sinus rhythm.

Figure 6.3 ECG showing sinus rhythm.

(Reproduced from Creed F and Spiers C, Care of the Acutely Ill Adult: an essential guide for nurses, 2010, with permission from Oxford University Press.)

However, critically ill patients may develop:

  • disorders of impulse formation—this may lead to the cardiac rhythm being stimulated by another pacemaker cell within the heart

  • disorders of impulse conduction—this may lead to electrical impulses being slowed , blocked, or using an alternative pathway.

There are many factors that may contribute to arrhythmia and conduction disturbances in the critically ill, including:

  • cardiac disease

  • acute coronary syndrome

  • factors that affect autonomic control (e.g. neurological damage)

  • electrolyte disturbances

  • acid–base imbalances

  • endocrine influences

  • side effects of medication

  • invasive monitoring.

Brief diagnosis and management of common arrhythmias seen in critical care is discussed in the remainder of this chapter.

Analysing the ECG rhythm strip

It is important to adopt a systematic approach to ECG rhythm interpretation, as advocated by Spiers.12 Each part of the ECG requires attention. The normal ECG complex is shown in Figure 6.4.

  • Rate—the rate may be calculated by counting the number of small squares between two R waves and dividing into 1500.

  • Rhythm—the rhythm should be inspected to see if it is regular or irregular. Even a normal sinus rhythm may be irregular in some individuals (sinus arrhythmia).

  • P:QRS ratio—there should be one P wave for each QRS complex.

  • PR interval—this should be counted from the beginning of the P wave to the beginning of the R wave, and should be between 120–200 ms (milliseconds). A long PR interval may indicate first-degree heart block. A short PR interval may indicate ventricular pre-excitation syndromes.

  • QRS complex—this should be narrow and less than 120 ms in width. A widened QRS complex may indicate conduction problems or ventricular hypertrophy.

  • ST segment—this should be flat and on the isoelectric line at the J point which is the end of the QRS complex. Any deviation may indicate ischaemia or infarction, but a 12-lead ECG is required to determine this.

  • T waves—the T wave should always be in the same direction as the QRS complex.

Sinus bradycardia

Definition

In sinus bradycardia the rhythm originates from the sinoatrial node, and so presents with a normal P wave and normal QRS complex. However, the rate is slower than normal (usually < 60 beats/min) (see Figure 6.5).


Figure 6.5 Sinus bradycardia.

Figure 6.5 Sinus bradycardia.

(Reproduced from Creed F and Spiers C, Care of the Acutely Ill Adult: an essential guide for nurses, 2010, with permission from Oxford University Press.)

Causes

Sinus bradycardia may be normal for patients who are physically fit or in patients who are monitored while they are asleep. Pathophysiological causes of sinus bradycardia include:

  • hypothermia

  • inferior myocardial infarction

  • raised intracranial pressure

  • hypothyroidism

  • medication—for example :

    • beta blockers

    • calcium-channel blockers

    • digoxin.

Assessment findings

The patient will present with a slow heart rate (< 60 beats/min). Sinus bradycardia may be asymptomatic, or there may be symptoms such as hypotension or syncope.

Treatment

This is rarely needed, but if required because of haemodynamic consequences it is best to treat the underlying cause. For example:

  • Review medication if the condition is related to cardiac drugs.

  • Slowly increase the body temperature if the patient is hypothermic.

  • Correct hypothyroidism.

In some instances where the patient is adversely affected by bradycardia they may receive IV atropine and if this is ineffective, adrenaline may be given as an IV infusion. Pacing may also be considered if bradycardia is related to cardiac problems.

Sinus tachycardia

Definition

In sinus tachycardia the rhythm originates from the sinoatrial node and so presents with a normal P wave and normal QRS complex. However, the rate is faster than normal (usually > 100 beats/min) (see Figure 6.6).


Figure 6.6 Sinus tachycardia.

Figure 6.6 Sinus tachycardia.

(Reproduced from Creed F and Spiers C, Care of the Acutely Ill Adult: an essential guide for nurses, 2010, with permission from Oxford University Press.)

Causes

Sinus tachycardia is a normal physiological response to stress and exercise. Pathophysiological causes of sinus tachycardia include:

  • high temperature

  • most forms of shock (except neurogenic shock)

  • low cardiac output states

  • heart disease

  • respiratory disease

  • hyperthyroidism

  • pain

  • stimulants

  • some medications (e.g. salbutamol).

Assessment findings

The patient will present with a heart rate of > 100 beats/min. They may be asymptomatic or there may be haemodynamic consequences. Diastolic filling will be reduced, so blood pressure may be affected and the patient may present with hypotension. Coronary artery filling is also reduced, so the patient may present with chest pain if they have cardiac disease.

Treatment

Treatment necessitates establishing the cause. For example:

  • If the patient is hypovolaemic, fluid should be administered to correct hypovolaemia.

  • If the patient is pyrexial, the cause of the high temperature should be addressed.

  • Pain should be managed with appropriate assessment and treatment.

  • On some occasions, medications may be required to slow the heart rate (e.g. beta blockers or digoxin).

Extrasystoles

Definition

Extrasystoles are premature beats that arise from an ectopic focus in the atria, the junctional area, or the ventricles. The beat is earlier than anticipated, and is followed by a compensatory pause. The normal heart rhythm may follow the compensatory pause, or further arrhythmias may be precipitated. The shape of the waveform of the ectopic beat will be determined by the focus. Therefore atrial and junctional extrasystoles are usually narrow complexes with an abnormal or absent preceding P wave. Ventricular extrasystoles have wide, often bizarre waveforms, and the T wave is normally in the opposite direction to the QRS complex (see Figure 6.7).


Figure 6.7 Ventricular extrasystole.

Figure 6.7 Ventricular extrasystole.

(Reproduced from Creed F and Spiers C, Care of the Acutely Ill Adult: an essential guide for nurses, 2010, with permission from Oxford University Press.)

Causes

Occasional extrasystoles are common, even in healthy individuals. However, they may be caused by:

  • stimulants

  • cardiac disease

  • hypoxaemia

  • electrolyte disturbances

  • acid–base disturbances.

Assessment findings

ECG changes will be noted by the nurse, but occasional extrasystoles that do not precipitate arrhythmias will be unlikely to have any haemodynamic consequences for the patient. If the patient is having frequent extrasystoles and they are awake, they may be aware of ‘palpitations.’ Care should be taken if the extrasystoles are frequent or if they are multifocal (different shaped), as this may precipitate the development of arrhythmias.

Treatment

There is usually no need to treat atrial or junctional extrasystoles. However, treatment may be required for frequent or multifocal ventricular extrasystoles. This may include:

  • checking serum electrolyte levels (especially potassium ) and correcting any deficiencies

  • increasing supplemental oxygen if the patient is hypoxic

  • correcting the acid–base balance

  • checking digoxin levels if the patient is receiving digoxin, as frequent extrasystoles may be a sign of digoxin toxicity.

Atrial fibrillation

Definition

Atrial fibrillation is the commonest arrhythmia seen in critically ill patients. It is generally a fast arrhythmia and usually caused by a re-entry circuit within the atria. In atrial fibrillation there is no coordinated conduction, and atrial contraction is ineffective. Ventricular conduction is normally faster than 100 beats/min. Atrial fibrillation may be classified as paroxysmal, persistent, or permanent, and is illustrated in Figure 6.8.


Figure 6.8 Atrial fibrillation.

Figure 6.8 Atrial fibrillation.

(Reproduced from Creed F and Spiers C, Care of the Acutely Ill Adult: an essential guide for nurses, 2010, with permission from Oxford University Press.)

Causes

There are many causes of atrial fibrillation, including:

  • underlying cardiac disease

  • cardiac ischaemia

  • congenital defects

  • trauma

  • hypoxia

  • age over 50 years.

Assessment findings

The impact of atrial fibrillation is rate dependent. Atrial fibrillation will cause loss of atrial kick, which accounts for about 20% of stroke volume, so blood pressure may quickly become affected. There is an associated risk of blood clot development. Patients may present with:

  • hypotension

  • palpitations

  • chest pain

  • breathlessness

  • syncope.

Treatment

Treatment options are complex, and depend on the cause, nature, and duration of the arrhythmia.12 Sudden onset should be reported immediately to the doctors, and NICE has provided guidelines on treatment.13

Supraventricular tachycardia

Definition

Supraventricular tachycardia (SVT) is a narrow complex tachycardia with a very fast rate, normally in the range 140–250 beats/min. In this arrhythmia, P waves are normally absent or obscured by the QRS complex, and the QRS remains narrow. SVT is illustrated in Figure 6.9.


Figure 6.9 Supraventricular tachycardia.

Figure 6.9 Supraventricular tachycardia.

(Reproduced from Creed F and Spiers C, Care of the Acutely Ill Adult: an essential guide for nurses, 2010, with permission from Oxford University Press.)

Causes

SVT may be seen in healthy patients, and in this group may be caused by alcohol or stimulants.

In patients who are ill it may be caused by ischaemic heart disease or Wolff–Parkinson–White syndrome.

Assessment findings

Symptoms are likely to be rate related, but patients may experience:

  • hypotension

  • palpitations

  • breathlessness

  • syncope.

It may be necessary to slow the rate to facilitate diagnosis, and this can be done using:

  • carotid sinus massage

  • adenosine administration.

Treatment

Persistent SVT may require:

  • administration of anti-arrhythmic medications such as amiodarone

  • cardioversion.

Heart blocks

Definition

Heart blocks are caused by a conduction delay between the atria and ventricles, and may be referred to as atrioventricular (AV) block. Different types of block occur, including:

  • first-degree heart block (see Figure 6.10)

  • second-degree heart block:

    • Wenckebach (see Figure 6.11)

    • Mobitz type 2 (see Figure 6.12)

  • third-degree or complete heart block (see Figure 6.13).


Figure 6.10 First-degree block.

Figure 6.10 First-degree block.

(Reproduced from Creed F and Spiers C, Care of the Acutely Ill Adult: an essential guide for nurses, 2010, with permission from Oxford University Press.)


Figure 6.11 Wenckebach block.

Figure 6.11 Wenckebach block.

(Reproduced from Creed F and Spiers C, Care of the Acutely Ill Adult: an essential guide for nurses, 2010, with permission from Oxford University Press.)


Figure 6.12 Mobitz type 2 block.

Figure 6.12 Mobitz type 2 block.

(Reproduced from Creed F and Spiers C, Care of the Acutely Ill Adult: an essential guide for nurses, 2010, with permission from Oxford University Press.)


Figure 6.13 Complete heart block.

Figure 6.13 Complete heart block.

(Reproduced from Creed F and Spiers C, Care of the Acutely Ill Adult: an essential guide for nurses, 2010, with permission from Oxford University Press.)

Third-degree heart block usually requires clinical intervention. The other forms may or may not be asymptomatic. First- and second-degree blocks can precipitate third-degree block.

Assessment findings

Patients may or may not be symptomatic. If symptomatic, they may present with:

  • hypotension

  • breathlessness

  • syncope.

The ECG changes are summarized in Table 6.4.

Table 6.4 ECG changes associated with heart block

Heart block

Changes seen

First degree

  • Prolonged PR interval

  • Regular rhythm

Wenckebach (second degree)

  • Progressive lengthening of PR interval until a beat is dropped

  • Regularly irregular rhythm

Mobitz type 2 (second degree)

Varying conduction to ventricle leading to 2:1 or 3:1 block. The PR interval and QRS complex are constant

Complete (third degree)

There is no conduction between the atria and ventricles, so no distinguishable relationship between P waves and QRS complexes

Treatment

Treatment depends on the haemodynamic consequences of the block. Third-degree block may require temporary or permanent pacing.

References

12 Spiers C. Cardiovascular assessment and care. In: F Creed and C Spiers (eds) Care of the Acutely Ill Adult: an essential guide for nurses. Oxford University Press: Oxford, 2010. pp. 59–104.Find this resource:

13 National Institute for Health and Care Excellence (NICE). Atrial Fibrillation: the management of atrial fibrillation. CG180. NICE: London, 2014. Cardiovascular assessment and monitoringwww.nice.org.uk/guidance/cg180Find this resource:

Life-threatening cardiac arrhythmias

Ventricular tachycardia and ventricular fibrillation

Definition

All ventricular arrhythmias are potentially life-threatening and require urgent medical intervention. Ventricular tachycardia (VT) is a ventricular arrhythmia that most commonly occurs in patients with serious cardiac disease and in other critically ill patients. Ventricular fibrillation (VF) is a cardiac arrest scenario. In cases of VT and VF, immediate medical attention and resuscitation are required.

Assessment findings

In VT, the ECG (see Figure 6.14) shows no discernible P waves, and the QRS complexes are wide and bizarre. The patient may have lost consciousness and have no cardiac output (cardiac arrest), or they may demonstrate signs of severe haemodynamic compromise.


Figure 6.14 Ventricular tachycardia.

Figure 6.14 Ventricular tachycardia.

(Reproduced from Creed F and Spiers C, Care of the Acutely Ill Adult: an essential guide for nurses, 2010, with permission from Oxford University Press.)

In VF, the ECG shows irregular chaotic waveforms with no discernible P waves or QRS complexes (see Figure 6.15). The patient will be unconscious and present with no cardiac output.


Figure 6.15 Ventricular fibrillation.

Figure 6.15 Ventricular fibrillation.

(Reproduced from Creed F and Spiers C, Care of the Acutely Ill Adult: an essential guide for nurses, 2010, with permission from Oxford University Press.)

Treatment

For details of treatment for cardiac arrest, see Cardiovascular assessment and monitoring p. [link].

Asystole

Definition

Asystole is a cardiac arrest situation in which there is no electrical activity in the heart.

Assessment findings

The ECG will show an apparently flat line that may be undulating in nature (see Figure 6.16). A completely ‘flat line’ normally indicates detachment of the ECG leads. The patient will be unconscious, with no cardiac output.


Figure 6.16 Asystole.

Figure 6.16 Asystole.

(Reproduced from Creed F and Spiers CCreed F and Spiers C, Care of the Acutely Ill Adult: an essential guide for nurses, 2010, with permission from Oxford University Press.)

Treatment

For details of treatment for cardiac arrest, see Cardiovascular assessment and monitoring p. [link].

Pulseless electrical activity

Definition

Pulseless electrical activity (PEA) is a cardiac arrest situation in which there is electrical activity in the heart but no mechanical contraction associated with the electrical activity.

Assessment findings

The ECG will show a normal ECG complex with a defined P wave, QRS complex, and T wave. The ECG rate may be slower than normal. The patient will be unconscious, with no cardiac output.

Treatment

For details of treatment for cardiac arrest, see Cardiovascular assessment and monitoring p. [link].

Cardiovascular medication

Anti-arrhythmic medications

Several anti-arrhythmic medications are available, and the medical team will determine which of these is required. Medication is administered to restore the heart to a regular rhythm. Anti-arrhythmic medications are classified according to their effect on the cardiac action potential and whether they block sodium, potassium, or calcium channels or β‎-adrenoreceptor sites.

  • Class 1 anti-arrhythmic medication (sodium-channel blockers)—this is further subdivided into types i, ii, and iii. All types block the sodium channel and thus affect action potential duration. Class 1 drugs are not generally used, as they may cause life-threatening arrhythmias.14 Examples include quinidine, disopyramide, and flecainide.

  • Class 2 anti-arrhythmic medication (β‎-adrenoreceptor blockers)—this class has an effect on β‎-adrenoreceptor sites and is considered the best type of anti-arrhythmic drug for general use. Examples include propranolol and esmolol.

  • Class 3 anti-arrhythmic medication (potassium-channel blockers)—drugs in this class lengthen the action potential and thus increase the refractory period. Examples include amiodarone and ibutilide.

  • Class 4 anti-arrhythmic medication (calcium-channel blockers)—drugs in this class inhibit the inward movement of calcium ions and lengthen repolarization. Examples include verapamil and diltiazem.

  • Unclassified anti-arrhythmic medication—this category includes medications with other mechanisms of action. Examples include adenosine, atropine, digoxin, and magnesium sulfate.

Antihypertensive medication

It may be necessary to treat potentially life-threatening hypertension, or hypertension that may be detrimental to the patient’s health. Several antihypertensive agents are available, and the medical team will determine which antihypertensive is required. There is no evidence to suggest optimal drug therapy, so different medications may be used. Medications that may be utilized include the following.

Sodium nitroprusside

  • This is a vasodilator that has an immediate effect on blood pressure.

  • It is given intravenously, and care must be taken to avoid a profound drop in blood pressure.

  • It may cause cerebral vasodilatation and hence may raise ICP.

  • Ideally it should not be administered for more than 24 h, as it may cause metabolic acidosis.

  • Side effects include headache, palpitations, dizziness, and nausea.

Glyceryl trinitrate (GTN)

  • This is a vasodilator that, when given intravenously, takes effect within 1–2 min.

  • Nitrates cause arterial and venous vasodilatation, and may also lead to cerebral vasodilatation and a risk of increased ICP.

  • Side effects include headache, tachycardia, and nausea.

Hydralazine

  • This is a peripheral vasodilator that, when given intravenously, will take effect within 15–30 min.

  • Side effects include nausea, headaches, palpitations, and flushing.

Labetalol

  • This acts by blocking α‎- and β‎-adrenergic receptors.

  • It is given intravenously and will take effect within less than 5 min.

  • Side effects include headache, rashes, and nausea.

Esmolol

  • This is a short-acting selective β‎-adrenergic blocker.

  • It is given by continuous infusion as it has a short half-life.

  • When given intravenously it takes effect immediately.

  • Side effects include bronchospasm, bradycardia, nausea, and vomiting.

Enalapril

  • This is an angiotensin-converting enzyme (ACE) inhibitor.

  • It takes effect within 10–15 min.

  • Its mechanism of action includes:

    • inhibition of the conversion of angiotensin I to angiotensin II

    • reduction in secretion of aldosterone

    • increased peripheral vasodilatation.

  • Side effects include hyperkalaemia, angioedema, cough, and sometimes profound hypotension.

Reference

14 Morton PG and Fontaine DK. Critical Care Nursing: a holistic approach, 10th edn. Lippincott Williams & Wilkins: Philadelphia, PA, 2012.Find this resource: