Shock is a syndrome of cardiovascular system failure resulting in inadequate tissue perfusion. Hypotension is a common but not universal feature. Shock is often a feature of patients suffering sepsis, pneumonia, multiple trauma or multiple organ failure. Consequently, it is commonly seen in general intensive care units.

The clinical features vary depending on the cause and the physiological response. Two patterns are typically recognized, although there is a continuum from one to the other:

Hyperdynamic shock: Warm, pink, vasodilated, a tachycardia, with high cardiac output and hypotension. (typical of septic shock, see p. 33)

Hypodynamic shock: Cold, grey, sweaty, vasoconstricted, peripherally shut down with low cardiac output, blood pressure may be relatively well maintained (typical of cardiac shock, see p. 108).

Other features of shock may include an increased or decreased core temperature, hypoventilation or hyperventilation, renal and hepatic dysfunction, disseminated intravascular coagulation, and altered mental status. (See Systemic inflammatory response syndrome, p. 326 and Multiorgan dysfunction syndrome, p. 327.) The young fit patient with an adequate cardiac reserve may well be able to initially compensate for the pathophysiological disturbances leading to shock. Consequently, shock occurring in an otherwise fit young person often represents a greater physiological disturbance or a later stage of illness as compared with the situation in an elderly patient, in whom conditions such as fixed cardiac output, peripheral and coronary artery disease and reduced organ function reduce the ‘physiological reserve’.

The aetiology of shock is frequently multifactorial. Typical causes are listed in Table 4.1. Although all causes of shock are seen on the ICU, the commonest in practice is septic shock (see Septic shock, p. 331).

TABLE 4.1 Typical causes of shock^*

* Note, more than one cause may be present in an individual patient.

Apart from the mechanical causes of shock, in which relief of the mechanical obstruction may take priority, the principles of managing shock states are similar in all patients regardless of aetiology. They include:

treatment of the underlying pathology

optimization of circulating blood volume

optimization of cardiac output

optimization of blood pressure

optimization of oxygen delivery

support for any organ failure.

You should understand the factors that influence tissue perfusion and oxygen delivery, oxygen consumption and cardiac output.

Oxygen delivery is defined as the total amount of oxygen delivered to the tissues (body) per minute. It depends on the cardiac output (CO) and the oxygen content of arterial blood, as shown:

Therefore, ignoring dissolved oxygen, which is insignificant at atmospheric pressure, typical figures are:

Oxygen consumption is the total amount of oxygen consumed by the tissues (body) per minute. It can be calculated from the difference in oxygen content of arterial and mixed venous blood (SO₂).

If cardiac index is used in the above calculations (see below), then oxygen delivery and oxygen consumption can also be expressed as an index relative to body surface area. Typical normal values are shown in Table 4.2.

TABLE 4.2 Typical adult values for oxygen delivery and oxygen consumption

Under normal circumstances, oxygen consumption by the tissues is only about 25% of the oxygen delivered. This provides a large margin for safety, so that if oxygen requirements increase, for example in exercise, more oxygen can be extracted and utilized. In disease states however, while oxygen requirements may be raised, the ability of the tissues to extract and utilize oxygen may be impaired. Under these circumstances, utilization of oxygen by the tissues may be limited by the available supply. Oxygen delivery may be increased by manipulation of cardiac output, improvement in oxygen saturation and transfusion (see below). Oxygen extraction cannot be significantly influenced except by general improvement in the patient’s condition.

From the formula for oxygen delivery above, it follows that oxygen delivery can be improved by:

Ensuring adequate arterial oxygen saturation.

Optimizing haemoglobin (see below).

Optimizing cardiac output (see Optimizing haemodynamic status, p. 78).

If oxygen delivery remains critical, then tracheal intubation and assisted ventilation with paralysis (muscle relaxants) may help to reduce the muscle utilization of oxygen and reduce oxygen requirements.

Since haemoglobin (Hb) carries oxygen to the tissues, one might assume that raising a patient’s Hb to 15 g / dL might provide optimal oxygen delivery. However, clinical studies have not confirmed that raising the haemoglobin concentration improves outcome and indeed, the opposite is likely to be true. Evidence from the Canadian Multicentre Clinical Trials Group suggests that restrictive transfusion strategies produce the best outcome in critically ill patients and that the optimal level in most cases is a Hb of 8–10 g / dL. (See Indications for blood transfusion, p. 246.) This study excluded patients, however, with significant coronary artery and vascular disease, who may benefit from a higher Hb. If in doubt about optimal haemoglobin for an individual patient, seek senior advice.

A guide to the balance between oxygen delivery and oxygen consumption can be obtained by the measurement of mixed venous oxygen saturation. Traditionally mixed venous oxygen was measured in blood from the pulmonary artery via a pulmonary artery catheter, either intermittently (by blood gas measurement) or continuously (using an oximetric catheter.) More recently, measurement of oxygen saturation of blood from a central catheter in the superior vena cava (S_cO₂) has been shown to correlate with the true SO₂ sufficiently closely to be used almost interchangeably in clinical practice.

Resuscitation guided by SO₂ or S_cO₂ has been shown to improve outcome by reducing the severity of organ failure and the duration of intensive care. Normal SO₂ is 55–75%. Values below this imply inadequate oxygen delivery. Values above this imply either supranormal oxygen delivery or reduced oxygen consumption. Conditions that may result in impaired oxygen consumption include sepsis, metabolic poisoning and widespread cellular death.

In a healthy heart there is little change in stroke volume with fluctuations in heart rate occurring within the physiological range (70–160 beats/min). Therefore, as heart rate increases, CO increases. The elderly, those with pre-existing heart disease, and critically ill patients, however tolerate a much narrower range of heart rates, and values outside 100–120 beats/min may significantly compromise CO.

At low heart rates, SV may be maintained but CO falls as a function of heart rate. At high rates, inadequate filling leads to a fall in SV and a subsequent reduction in CO. Tachycardias associated with abnormalities of cardiac rhythm (e.g. atrial fibrillation) further reduce ventricular filling and CO. Tachycardias also lead to increased myocardial oxygen consumption, while simultaneously reducing the time for diastolic perfusion of the ventricles. In patients with ischaemic heart disease, this may produce significant myocardial ischaemia, which may further compromise CO.

The stroke volume is the volume of blood ejected with each heartbeat, and is the difference between the volume of the full ventricle (end diastolic volume) and the volume of the ventricle after ejection of blood is completed (end systolic volume). Traditionally, SV has been thought of as being determined by preload, contractility and afterload.

Preload

This is defined as the ventricular wall tension at the end of diastole. In simple terms preload refers to the degree of ventricular filling. According to the Frank–Starling law of the heart, the greater the degree of ventricular filling, the greater the force of myocardial contraction and thus SV. Above a certain point, however, the ventricle becomes over-stretched and further filling may result in a fall in SV. Heart failure and pulmonary oedema may then develop (see Fig. 4.1).

Fig. 4.1 Diagrammatic representation of Frank–Starling Curves. (a) Increasing LVEDV leads to increased SV. (b) Effect of increased contractility, e.g. as a result of inotropes.

Preload is therefore a function of the volume status of the patient. It also depends upon adequate ventricular relaxation in order to allow ventricular filling to take place. Ventricular relaxation is an active process. In critically ill patients, failure of ventricular relaxation (diastolic failure) may result in the ventricle becoming stiff and non-compliant. When this occurs, the ventricle cannot fill normally, regardless of the patient’s volume status and cardiac output is reduced.

A more recent approach to understanding the interdependency of preload contractility and afterload and the effects thereof, on cardiac output and stroke volume, is to consider pressure–volume–flow loops of the left ventricle (see Fig. 4.2).

Fig. 4.2 (A) Pressure–volume loops of the left ventricle. (B) Effect of increased end diastolic volume (preload) (C) Effect of reduced contractility (S) and diastolic dysfunction (D).

End diastolic volume, which represents ventricular filling, is a function of venous return (pressure) and the diastolic compliance. Increased venous pressure leads to increased ventricular filling and this additional filling is greatest where diastolic compliance is optimal. Where diastolic dysfunction or failure occurs, the diastolic compliance is reduced (with a steeper diastolic compliance curve) and higher venous pressures are required to achieve adequate ventricular filling. Diastolic dysfunction may be seen in hypoxia, myocardial ischaemia, metabolic derangement or as a consequence of mechanical compromise such as pericardial effusion or tamponade.

The end systolic point describes the relationship between the end systolic volume (the volume of blood remaining in the ventricle at the end of systole) and the ejection systolic pressure. This point is determined by a combination of contractility and outflow resistance (afterload). The end systolic point moves upwards and to the right if the ejection systolic pressure is increased (e.g. increased afterload), and downwards to the left if the ejection systolic pressure is reduced (e.g. decreased afterload). Thus under conditions of vasodilation, (e.g. sepsis) there is reduced afterload, lower ejection systolic pressure and reduced end systolic volume. Conversely, vasoconstriction (increased afterload) leads to increased ejection systolic pressure, and increased end systolic volume.

Assuming contractility is unchanged, the ejection systolic point at the end of any heart beat will fall along a curve. Changes in contractility will shift the position of this curve (Fig. 4.2). Increased contractility for example as a result of inotropic drugs, shifts the curve upwards and to the left, so that the same ejection systolic pressure is associated with an increased ejection fraction, greater stroke volume and reduced end systolic volume. Reduced contractility, for example resulting from intrinsic heart disease, or from the myocardial depressant effects of acidosis, hypoxia or sepsis shifts the curve to the right and flattens it. The same systolic blood pressure is associated with a reduced ejection fraction and stroke volume and a much greater end systolic volume.

Arterial cannulation allows beat-to-beat measurement of arterial blood pressure and easy serial blood gas sampling. Significant respiratory variation in the amplitude of the arterial pressure wave (‘respiratory swing’) is characteristic of hypovolaemia. This pulse pressure variability (which relates to stroke volume variability caused by changes in venous return) can be formally measured by modern monitoring systems and is described as a percentage. Pulse variability less than 10% implies adequate filling and has been used as an end point for volume resuscitation. (See Arterial cannulation, p. 372.)

Central venous catheterization provides a route of delivery for drugs and fluids and enables measurement of right heart filling pressures (CVP). Central venous access can be achieved via the jugular, subclavian, brachial or femoral routes. (See Central venous cannulation, p. 376, and Optimizing filling status, p. 376.)

Pulmonary artery (PA) catheterization has for a number of years been the gold standard cardiovascular monitoring tool in ICU. This technique enables the measurement of pulmonary artery pressure, pulmonary artery occlusion pressure (PAOP) and CO, and also allows many other haemodynamic variables to be calculated or derived. Typical values are given in Table 4.4.

TABLE 4.4 Normal values of common haemodynamic variables derived from PA catheterization

These ‘normal values’ provide a guide only. They may not be achievable or appropriate for all critically ill patients (See Goal directed therapy, p. 78).

The value of pulmonary artery catheters has recently been questioned and the technique has been the subject of a number of major multicentre trials leading to a critical re-evaluation of the role of PA catheterization. Recent trials failed to show benefit or harm in a mixed adult ICU population with the suggestion that it should be reserved for the more complicated case where specific questions about the dynamic variables are required to be answered. The use of PA catheterization has fallen significantly with the introduction of alternative forms of monitoring. Relatively non-invasive systems for continuous cardiac output monitoring are available based on transthoracic bioimpedance, oesophageal Doppler, pulse contour and pulse power analysis.

Currently, systems based on pulse contour analysis are perhaps the most likely to enter widespread use. In general terms these require venous access (peripheral or central) and an arterial line with a sensor either built in or attached. To calibrate the system an indicator is injected into the venous catheter and is detected by the arterial line producing a standard dilutional CO measurement. From this the systems are able to provide continuous CO, SV and systemic vascular resistance by analysis of the pulse waveform. To maintain accuracy they must be calibrated every 8–12 h or whenever there is a significant change in cardiovascular status. A popular device using this technique is the Picco system, which combines pulse contour analysis with intermittent calibration by thermodilution. The thermodilution calibration curves can also be used to estimate thermal volumes of distribution in the chest, providing a reasonably well validated measure of global end diastolic volume (a surrogate for filling) and extra vascular lung water, useful in resuscitation and the management of acute lung injury.

A related approach is an analysis of the area under the curve of the arterial waveform. This is known as ‘pulse power analysis’ and has some theoretical advantages over pulse contour analysis. In particular, it does not require proximal arterial cannulation and should in theory be slightly more robust under conditions of damping. It is used commercially in the LiDCO system. This device combines pulse power analysis with calibration using lithium dilution every 12–24 h. An injection of a very low dose of lithium into a vein (not necessarily a central vein) is accompanied by measurement of a dilation curve in an artery. Blood is pumped from the arterial line across an electrode calibrated to measure monovalent cations. In theory, the only such ion whose concentration varies in the time course of the measurement is lithium. Injection of other charged substances at the same time invalidate the measurement. In practice, the only common confounding factor is recent injection of atracurium (a positively charged quaternary nitrogen compound).

A Doppler ultrasound probe is placed in the oesophagus and directed to obtain a signal from the descending aorta. The signal obtained is displayed on the screen and indicates peak velocity and flow time. By making a number of assumptions about the nature of flow in the aorta, the cross-sectional area of the aorta (estimated from body surface area and age) and the percentage of CO passing down the thoracic aorta, SV and CO can be estimated. Trends in values and response to changes in therapy are more useful than absolute values. It is particularly useful for assessing response to fluid challenges but is rather operator-dependent.

Transthoracic echocardiography is minimally invasive and can be repeated at short intervals to assess cardiac function and response to therapy. The key information available from echocardiography is shown in Table 4.5.

TABLE 4.5 Key information available from echocardiography

There is increasing availability of bedside, transthoracic and to a lesser extent transoesophageal, echocardiography in intensive care, for use by suitably trained intensive care staff, as opposed to cardiologists or sonographers. Abbreviated training packages have been developed for this purpose, which enable individuals to undertake focused examinations (e.g. FATE). All these packages accept the limitations of examinations by non-specialists and emphasize the need for formal referral to echocardiography where there is doubt about the findings. Nevertheless it seems likely that echocardiography will increasingly become an extension of the traditional clinical examination of patients in ICU. All patients will be likely to receive a focused echocardiography examination on admission and at intervals and the findings used to guide haemodynamic therapy.

The availability of so many measured haemodynamic variables (above) led to attempts to improve the outcome of critically ill patients by manipulation of the variables to achieve ‘standard goals’. Shoemaker, for example, compared measured variables in trauma survivors and non-survivors and suggested that outcome could be improved by manipulating haemodynamics to achieve supranormal values of cardiac index (4.5 L / min / m²), oxygen delivery index (650 mL / min / m²) and oxygen consumption index (165 mL/min/m²). There is little evidence, however, that this approach improves outcome in the general population of critically ill patients.

The difficulty with population-based targets of this sort is that they risk over- or under-treating individual patients. The more modern approach therefore is to optimize cardiovascular performance of each individual patient by titration of fluids and vasoactive drugs to achieve the ‘optimal response’ for that individual.

Avoid aiming to achieve absolute numbers for CO and other variables. Use ‘normal values’ only as a guide and think in terms of achieving adequate haemodynamic performance for the individual patient. A rational approach is to optimize fluid (filling) status first and then to add an inotrope or vasoconstrictor as required. Figure 4.3 provides a simple algorithm for optimizing haemodynamic status and the management of shock regardless of the underlying cause.

Fig. 4.3 Optimization of the haemodynamic system.

There is a tendency to refer to all vasoactive drugs as inotropes. This is not only incorrect but can lead to confusion when deciding which agent to choose in any given circumstance. By classifying the available agents according to their receptor pharmacology and actions, a rational approach to their use can be achieved. Table 4.6 shows the effects of agonists at various receptors.

TABLE 4.6 Effects of agonists on cardiovascular receptors

On the basis of activity at these receptors, drugs can be classified as inotropes (directly increase cardiac contractility), vasodilators, vasopressors, or a combination of these, e.g. inodilator or inopressor. Classifying agents in this way enables rational choices to be made in selecting agents for use. (See Optimizing cardiac output and Optimizing perfusion pressure below.)

The use of right atrial pressure (CVP) and to a lesser extent, left atrial pressure (PAOP) to guide fluid therapy is commonplace. Fluids are often given to achieve a predetermined CVP or PAOP. This approach should be avoided.

The relationship between filling pressure and volume status (ventricular end-diastolic volume) is complex and depends on the compliance of the ventricle. This compliance varies both between individuals and in different disease states. It may also change acutely in a single individual in response to pathophysiological changes such as myocardial ischaemia or acidosis.

Any predetermined figure for CVP / PAOP is bound, therefore, to be somewhat arbitrary and may not be optimal for an individual patient. Rather than aiming for a specific CVP or PAOP, try and determine the filling pressure which produces the best haemodynamic response from an individual patient.

Put bed head down or lift legs as a quick way to increase venous return and assess effect.

Give fluid to increase the CVP or PAOP in small increments and observe the increase in CO or SV

Continue until there is no further improvement or until there is deterioration in arterial blood gases or evidence of pulmonary oedema. (Note: stroke volume index of 50 mL / m² represents a full ventricle.)

Remember also that optimal filling may actually mean use of fluid restriction, diuretics and vasodilators to reduce preload in patients with heart failure.

Care should also be taken in the presence of renal failure when excessive fluid is not excreted.

Increased recognition that the concept of using ‘filling pressure’ (CVP or PAOP) as a measure of ventricular filling status is flawed has led to the development of monitoring systems capable of directly measuring (estimating) volume status. Detailed description is beyond the scope of this book. A guide to normal values for volume indices is given in Table 4.7.

TABLE 4.7 Typical values of volumetric haemodynamic variables

There is currently no consensus as to which of these variables is the most useful in assessing volume status. As with other haemodynamic variables, it is the trend and response to therapy which is more important than the absolute values obtained. If volumetric monitoring is available in your unit seek senior advice on interpretation of the information provided. If volumetric monitoring is not available, echocardiography can also be used to provide useful information about filling status.

If despite optimal filling CO remains inadequate, inotropes may be added to improve cardiac performance (Fig. 4.2). The rational use of inotropes requires an understanding of the receptor pharmacology of the commonly used agents. These are summarized in Table 4.8.

From the table and notes above, select the most appropriate inotrope for the patient’s clinical condition. Generally:

If despite low CO mean arterial blood pressure is well maintained, use dobutamine or dopexamine to increase CO, reduce afterload and improve perfusion.

If low CO is associated with low blood pressure use adrenaline (epinephrine).

If you are uncertain, the mixed actions of dopamine make it a reasonable choice in most settings. It is commonly used as a first-line agent in Europe; however, in the UK it has tended to be used less.

Start infusions at the lowest infusion rate possible to achieve the desired effect and continually reassess the response. Potential adverse effects include tachycardia, arrhythmias and increased myocardial oxygen consumption. Hyperglycaemia and lactic acidosis may also occur. Where the response is poor, alternative / additional agents may be used. Agents which effectively ‘bypass’ the β receptors may be particularly useful in heart failure, where down regulation of β receptors may occur. Two classes of drug are available (see Cardiogenic shock, p. 106).

There is increasing evidence that in profound shock states vasopressin or antidiuretic hormone (ADH), which is normally secreted by the posterior pituitary, becomes depleted. Replacement at physiological rather than pharmacological doses, by infusion of vasopressin at 0.1–0.4 μg / kg / min, may help to restore vascular reactivity and tone. It is usually used as a second line agent in combination with other vasopressor agents. Bolus doses of terlipressin, which is a longer acting agent in this class, can also be used.

As the patient’s condition improves, inotropes and vasoconstrictor agents can be gradually reduced. Ensure optimal filling at all times and reduce drugs according to the results of haemodynamic monitoring.

In intensive care short periods of hypertension, for example during weaning from ventilation, are not uncommon and do not generally result in any harm unless there is associated myocardial, cerebral or vascular disease. Therefore:

Do not over-treat hypertension.

If using an arterial line check the blood pressure reading using a blood pressure cuff. The readings sometimes disagree, in which case the non-invasive measurement may be the more accurate (see Arterial cannulation, p. 372).

Ensure adequate analgesia and sedation.

Check blood gases are acceptable.

Ensure normal fluid status. Consider diuretics or haemodialysis / filtration if fluid overloaded.

Correct hypothermia.

Reduce or stop inotropes and vasoconstrictors as appropriate.

Treatment will depend upon the absolute blood pressure, age and condition of the patient. The typical hypertensive patient is the elderly postoperative arteriopath with ischaemic heart disease. Treatment is generally only required if there is sustained diastolic blood pressure >110 mmHg, systolic >200 mmHg or associated myocardial ischaemia. If treatment is required consider:

Nifedepine 10–20 mg oral or sublingual. (Caution; sublingual nifedipine can cause a rapid fall in blood pressure.)

Hydralazine 10 mg i.v. repeated as necessary.

GTN infusion. Particularly if hypertensive episodes are associated with myocardial ischaemia or failure.

Labetalol is used in small incremental boluses (5–10 mg) and by infusion.

The young patient with unexplained sustained hypertension, particularly if associated with end organ damage, for example left ventricular hypertrophy, warrants further investigation. Consider other causes such as renal artery stenosis and phaeochromocytoma. Seek advice on appropriate treatment. (See Phaeochromocytoma, p. 221.)

This is common and generally represents an appropriate response to a clinical stress. Management is, therefore, correction of the underlying cause(s).

Bradycardia is arbitrarily described as a heart rate < 60 bpm. As heart rate falls cardiac output becomes compromised. While younger fitter patients may tolerate heart rates below this, many older patients will not and even rates above this may be insufficient to maintain an adequate cardiac output. The key concept therefore is maintenance of an adequate heart rate for the individual.

Bradycardia frequently reflects intrinsic disease of pacemaker tissue or the conducting system. It may be precipitated by increased vagal tone, hypoxia (particularly in children) and the myocardial depressant effect of drugs. Potentially important / reversible causes are shown in Box 4.3.

Initially, as heart rate falls, CO is maintained by increases in SV. Thereafter, as heart rate falls further, CO and blood pressure will fall. Junctional or ventricular escape rhythms may appear.

The algorithm for the management of bradycardia is shown in Fig. 4.4.

Fig. 4.4 Management of bradycardia.

(from Resuscitation Council UK 2005, with permission)

In the intensive care unit, if bradycardia occurs in association with significant hypotension, then consider adrenaline (epinephrine). Give 50–100 μg (0.5–1 mL of 1:10000 adrenaline) boluses and titrate to effect.

SVT encompasses all forms of tachydysrhythmia originating above the ventricles. In practice it is useful to distinguish atrial fibrillation and atrial flutter from other forms of SVT. In SVT the QRS complexes are always narrow (narrow complex tachycardia) unless there is an associated conduction defect (Fig. 4.5).

Fig. 4.5 Narrow complex tachycardia (SVT).

The management of SVT depends on the degree of haemodynamic disturbance and likely origin. As shown in Fig. 4.6, DC cardioversion is indicated if there is associated shock. Adenosine may terminate a re-entry tachycardia. Amiodarone may be the drug of choice for the treatment of persistent SVT not associated with haemodynamic compromise. Atrial fibrillation is considered separately (see below).

Fig. 4.6 Management of narrow complex tachycardia.

(from Resuscitation Council UK 2005, with permission)

This is the commonest dysrhythmia seen in the ICU (Fig. 4.7), particularly in the elderly patient with ischaemic heart disease, intercurrent sepsis, electrolyte disturbance or inotrope dependency. AF may not settle until the patient’s general condition improves. Consider the underlying causes of dysrhythmia above.

Fig. 4.7 Atrial fibrillation.

Treatment depends on the ventricular rate and the degree of associated haemodynamic disturbance as shown in Fig. 4.6. When sudden in onset, restoration of sinus rhythm (where possible) should be attempted. Synchronized DC cardioversion is indicated for sudden onset atrial fibrillation associated with rapid ventricular rate and significant haemodynamic compromise. Amiodarone is the agent of choice for most patients with lower ventricular rates and without haemodynamic compromise.

Chronic AF may be associated with ischaemic heart disease or mitral valve disease. Restoration of sinus rhythm is unlikely and control of the ventricular rate is the main aim. Digoxin remains the usual therapy, but seek cardiology advice.

Digoxin 0.5 mg i.v. over 30 min, followed by 0.25–0.5 mg after 2 h if necessary. Once-daily dose thereafter, depending on response and levels.

In atrial flutter, the atrial rate is about 300 beats per minute and the P waves have a saw tooth appearance The AV node cannot conduct all the P waves to the ventricle and there is often associated 2:1 AV block (Fig. 4.8). Suspect if the ventricular rate is 150. Use a 12-lead ECG to identify flutter waves: Treatment is synchronized DC cardioversion or control of rate with β-blockers. Seek advice.

Fig. 4.8 Atrial flutter (with 2:1 block).

VPBs occur normally in the general population and their significance is uncertain. They are more common in the presence of heart disease and may be increased by the effects of digoxin toxicity, catecholamines and hypokalaemia. Asymptomatic unifocal VPBs occurring fewer than five times per minute are considered to be benign. Treatment may be indicated if associated with poor haemodynamic state, if multifocal, or if occurring in runs of two or more.

Correct hypoxia, hypercarbia, acidosis and hypokalaemia.

Consider lidocaine (lignocaine) 1 mg / kg followed by infusion 2 mg / min.

Consider magnesium.

Broad complex tachycardia (Fig. 4.9) is usually ventricular in origin, but may occasionally be supraventricular if there is an associated conduction defect, e.g. bundle branch block. Haemodynamic status is a poor guide to the underlying rhythm. An ECG may help to distinguish between the two. ECG features of ventricular tachycardia are shown in Box 4.4.

Fig. 4.9 Broad complex tachycardia.

If in doubt, broad complex tachycardia should be assumed to be ventricular in origin until proved otherwise. Management of broad complex tachycardia is shown in Fig. 4.10.

Fig. 4.10 Management of broad complex tachycardia.

(from Resuscitation Council UK 2005, with permission)

Torsade de pointes (Fig. 4.11) is a form of VT in which the complexes have a pointed shape, vary from beat to beat and the axis of the rhythm constantly changes. It is usually self-limiting, but may give rise to VF. Hypokalaemia, prolonged QT interval, bradycardia and antidysrhythmic drugs may be causes. Seek expert help.

Give magnesium 10 mmol i.v. stat followed by 50 mmol infusion over 12 h.

Consider β blockers.

Consider overdrive pacing and DC cardioversion.

Fig. 4.11 Polymorphic ventricular tachycardia (‘torsades de pointe’).

(See Defibrillation and DC cardioversion, p. 396.)

PR interval >0.2 s (1 large square on standard ECG trace). This does not require treatment but is indicative of underlying heart disease, electrolyte disturbance or drug toxicity, e.g. digoxin.

This may be of two types:

Mobitz type 1 (Wenckebach phenomenon). There is progressive lengthening of the PR interval followed by a P wave, which is not conducted to the ventricle, and then repetition of the cycle. This is usually self-limiting.

Mobitz type 2. The PR interval is constant but occasional P waves are not conducted to the ventricle. If high levels of block are present, e.g. 2:1 or 3:1 block, there is a significant risk that this will progress to complete heart block.

No atrial electrical activity is conducted to the ventricle. This may result in ventricular standstill (no CO!) or there may be an idioventricular escape rhythm. In this case, there is no discernible relationship between visible P waves and QRS complexes on the ECG.

Asymptomatic 1st or 2nd degree heart block generally does not require treatment. All symptomatic episodes of heart block do require treatment:

See bradycardia algorithm above.

Consider pacing: external or temporary pacing wire.

Indications for temporary cardiac pacing are given in Box 4.5.

The following ECG changes are typical of acute myocardial infarction:

ST segment elevation > 1 mm in precordial leads or > 2 mm in limb leads which persists for more than 24 h. Usually returns to normal within 2 weeks. (Persistent ST elevation at 1 month suggests development of left ventricular aneurysm.)

Reciprocal ST segment depression in the opposite leads.

Development of new Q waves greater than 25% of the ‘R’ wave and 0.04 s duration.

T wave inversion. (This is not diagnostic by itself.)

The location of these changes on the ECG identifies the region of the infarction (Table 4.11).

TABLE 4.11 Myocardial infarction and ECG patterns

Biomarkers are used to indicate the extent, if any, of muscle damage sustained during an acute myocardial ischaemic event. Previously enzymes released from damaged cardiac muscles were used for this purpose but these have now been largely superseded by the use of troponin assays. Cardiac troponin (troponin I) is a protein released by damaged myocardial cells and is a sensitive indicator of the extent of cellular damage. The measured level in fit and healthy people is normally less than 0.1 μg / L. Values above this usually indicate an acute myocardial ischaemic event or infarction.

In critically ill patients, however, myocardial damage may arise from causes other than ischaemia and minor rises in cardiac troponin may occur. The diagnostic threshold for an acute ischaemic event or myocardial infarction in intensive care patients is therefore a little higher. Levels above 0.5 μg / L are strongly suggestive of myocardial infarction.

If troponin assay is not available, creatine phosphokinase (CK) and creatinine phosphokinase isoenzyme (CK–MB) can be used. CK is released from all damaged muscle cells, whereas CK–MB is ‘specific’ to heart muscle. If the total CK is raised and the ratio of CK–MB to CK is greater than 6–8%, myocardial infarction is highly likely.

Based on the interpretation of ECG findings and biomarkers, three principle patterns of acute coronary syndrome can be described as shown in Table 4.12.

TABLE 4.12 Patterns of acute coronary syndrome

The importance of understanding acute coronary syndromes in this way is the ability to stratify the risk of myocardial infarction and therefore target appropriate treatment. In reality, biomarkers such as troponin do not rise until a number of hours after muscle damage has occurred, and therefore the initial management decisions are made on the basis of ECG changes. Patients with ST segment elevation are at high risk of developing a Q-wave infarction (significant muscle damage) and should be referred to cardiology for urgent percutaneous angioplasty / stenting where available or thrombolysis where not (see below). Patients without ST elevation are at low risk of developing a Q-wave infarction and can be managed conservatively in the first instance with subsequent management guided by progress and troponin levels.

Patients with acute coronary syndrome without ST elevation are at low risk of developing infarction and are usually managed conservatively in the first instance:

Give aspirin 300 mg oral followed by 75 mg daily unless contraindicated.

Consider clopidogrel 300 mg oral followed by 75 mg daily.

Start low molecular weight heparin according to local protocol, e.g. enoxaparin 1 mg / kg s.c. twice a day.

Consider β blocker (e.g. atenolol 25–100 mg daily, bisoprolol 12.5–5 mg twice daily) if there are no contraindications (bradycardia, hypotension, heart failure, asthma).

Consider GTN infusion to reduce preload and reduce myocardial work. 1–2 mg / h and titrate to response.

Patients who continue to have chest pain, or who have persistent ECG changes or in whom troponin levels are raised will require coronary angiography. Seek urgent cardiology advice.

Patients may be admitted to intensive care following a myocardial infarct or may suffer an infarction during their stay on intensive care. The diagnosis of myocardial infarction is made on the basis of a characteristic history of chest pain, ECG changes, and (subsequent) elevation of cardiac biomarkers (indicating heart muscle damage) Patients in the ICU may not be able to give a history of classic chest pain and great reliance has to be placed on the clinical picture, which may include .the sudden development of hypotension, cardiac failure (3rd or 4th heart sound), pericardial rub and pyrexia.

Give oxygen.

Give analgesia. e.g. morphine.

Give aspirin 300 mg oral, followed by 75 mg daily unless contraindicated.

Consider β-blocker unless contraindicated (bradycardia, hypotension, heart failure, asthma).

Consider GTN infusion to reduce preload and reduce myocardial work; 1–2 mg / h. Titrate to response.

Patients with acute ST elevation are assumed to have a high risk of developing a Q wave infarction and the main goal of therapy is to restore coronary blood flow to reduce the damage to the heart muscle. Seek urgent cardiology advice regarding angiography / angioplasty or thrombolysis (see below).

Thrombolysis

The gold standard management of all ST elevation myocardial infarction is urgent restoration of the coronary blood flow to the affected area. This is best achieved by ‘percutaneous coronary intervention’ (PCI) comprising coronary angiography, angioplasty and stenting of the affected coronary arteries. If this is not achievable (e.g. small hospital or remote locations) or the patient is unstable thrombolysis is an alternative. Consider

Either streptokinase 1.5 × 10⁶ units in 100–200 mL 0.9% saline i.v. over 1 h.

Or tissue plasminogen activator (TPA) 100 mg over 90 min (follow local protocol).

Thrombolysis is only indicated if there is irrefutable ECG evidence of acute infarction and should be started as soon as possible, preferably within 6 h of the onset of chest pain. Many patients in intensive care will, however, have a contraindication to thrombolysis (Box 4.6). Always seek advice from a cardiologist.

Box 4.6 Contraindications to thrombolysis

Recent major surgery

Intracranial pathology, e.g. previous CVA

Previous Gl haemorrhage

Bleeding from any site

Allergy to streptokinase

Prolonged external cardiac massage

Both mitral valve disease and chronic pulmonary disease may result in pulmonary hypertension and subsequent right heart failure. This is a very difficult condition to manage. When pulmonary artery and right ventricular pressures are high, any fall in systemic pressure will impair perfusion of the right ventricle. This results in worsening right ventricular performance and rapid deterioration.

Maintain systemic arterial blood pressure. Avoid drugs that lower systemic arterial pressure. Vasoconstrictors may be necessary to maintain systemic blood pressure and right ventricular perfusion. Consider intra-aortic balloon counter pulsation pumps to maintain systemic diastolic pressure. (See Cardiogenic shock below.)

Optimal filling of the right ventricle is vital. Use volumetric haemodynamic monitoring or right heart ejection fraction pulmonary artery catheters if available to directly estimate right ventricular end-diastolic volume.

Consider inotropes to improve right ventricular contractility.

Consider measures to reduce pulmonary vascular pressures and right ventricular afterload. Epoprostenol (prostacyclin) is effective but is not selective and may also reduce systemic blood pressure. Nitric oxide is more selective and may be useful although the evidence for improved outcome is limited. Seek senior advice.

The chances of a successful outcome from VF are thought to be best if defibrillation is achieved within 90 s of onset and decrease with time thereafter. In a witnessed arrest a single precordial thump may terminate fibrillation, after which the application of defibrillating DC shock should not be delayed.

The chances of recovery from asystolic arrest are poor. Check that the ECG leads are correctly attached and that the gain on the monitor is maximal. If VF cannot be excluded, then management commences as for VF. Severe hypoxaemia is one cause for a terminal bradycardia progressing to asystole.

Previously referred to as electromechanical dissociation. This term is used to describe the situation where electrical activity is present on the ECG but there is no discernable cardiac output. Hypovolaemia and mechanical obstruction of the cardiac output (e.g. tension pneumothorax and cardiac tamponade) should be excluded.

Patients who are resuscitated from cardiac arrest outside the ICU frequently require admission to intensive care. This may be because of failure to regain adequate conscious level, or inadequate cardiac, respiratory or renal function. The management of these patients depends upon the underlying clinical condition, the type of arrest and the timing and adequacy of the initial resuscitation measures [see the Intensive Care Society’s Standards for the management of patients after cardiac arrest 2008 (www.ics.ac.uk) and Resuscitation council UK’s guidelines 2005 (www.resus.org.uk)].

The commonest problem posed by these patients is difficulty determining the extent and nature of neurological injury resulting from the period of hypoxia. It is very difficult to make any assessment of this in the first 24–48 h and most patients, therefore, will require a period of stabilization and assessment:

Institute positive pressure ventilation according to arterial blood gases.

Optimize haemodynamic status.

Correct acidosis and electrolyte abnormalities.

Correct hyperglycaemia.

Treat any underlying conditions appropriately.

If required, use short-acting drugs for sedation.

If the patient’s neurological condition fails to improve over 48 h, then the outcome is likely to be poor. Seek advice. (See Hypoxic brain injury, p. 294.)

There is some evidence that cooling patients after (VF) cardiac arrest for 24 h post-resuscitation improves neurological outcome and this is now practised in many centres. The techniques used to achieve cooling, the optimum target temperature, the optimum duration of cooling, and the benefit in other forms of cardiac arrest have not yet been fully defined. Typically patients are cooled using exposure, cold air blankets and infusion of cold fluids, to a temperature of 33–34°C for a period of 24 h and then passively rewarmed. Seek local advice and protocols.