Intensive care after cardiac surgery

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Chapter 22 Intensive care after cardiac surgery

Raymond F. Raper

Coronary artery bypass surgery is one of the most frequently undertaken surgical procedures. Because of the prevalence of cardiac disease, cardiac surgery has significant health and economic implications. Intensive care may account for up to 40% of the total hospital costs for these patients and much of the short-term morbidity and mortality is based on perioperative events.

The overall mortality of cardiac surgery is low (approximately 3%). However, this ranges from less than 1% for elective coronary artery bypass grafting to in excess of 30% for more complicated surgery in patients with significant myocardial dysfunction and associated disorders. Usually, intensive care post-cardiac surgery involves a short period of recovery before discharge to the ward but, for a small percentage of patients, at least potentially remediable complications may require the complete intensive care armamentarium, with a highly significant impact on the intensive care unit (ICU) and hospital budgets and resources.

ORGANISATION

The convergence of large numbers of patients with very similar problems in the cardiac ICU provides an ideal environment for the standardisation of care based on protocols and clinical pathways. One of the traps of postoperative cardiac care is that the sameness of the patients tends to obscure their particularity. Individual patient assessment must carefully address the multisystemic manifestations of cardiovascular and degenerative diseases.

Cardiac surgery involves a continuum of care from presentation to postdischarge management and rehabilitation. The intensive care specialist must be involved in this continuum, not functioning in isolation from surgeons, anaesthetists, cardiologists and family practitioners.

The postoperative stage is largely set by the preoperative and operative phases of management. A component of postoperative management is active participation both in principle and in particular in patient selection and preparation as well as in the conduct of anaesthesia and surgery. Relevant aspects include suitability and preparation for surgery, advanced care planning and more technical issues such as temperature management, invasive monitoring, haemodynamic management and transport. Movement from the operating theatre to the ICU and later to the ward will only appear seamless if the management systems have been well coordinated in advance.

CARDIOVASCULAR MANAGEMENT

The first step in the intensive care management of the newly arrived patient who has undergone cardiac surgery involves a simple transfer of ventilation, monitoring and drug administration from transport to ICU systems. This should be structured to minimise disruption.

• Confirm integrity and position of endotracheal and gastric tubes and intravascular catheters.
• Re-establish mechanical ventilation of both lungs.
• Undertake chest radiography; to assess lung expansion, pleural integrity and catheter placement.
• Perform early 12-lead electrocardiography to exclude or identify acute ischaemia.

Management is conveniently dictated by standardised protocols, which should cover investigations, fluid and electrolyte management, vasoactive and other drug administration and mechanical ventilation. Standardisation is probably more important than the particulars of the protocol, which might vary considerably among institutions. Optimal cardiovascular management requires a sound knowledge of normal and abnormal cardiovascular physiology. It also requires an understanding of the haemodynamic changes usually seen in the postoperative patient (Figure 22.1).1

image

Figure 22.1 Haemodynamic changes following cardiac surgery. Systemic vascular resistance index (SVRI).

MONITORING

Electrocardiography and continuous invasive blood pressure and central venous pressure monitoring are standard. Flotation pulmonary artery (PA) catheterisation has become somewhat controversial. It is now reasonably well established that PA catheterisation is safe but may not alter outcomes.2

• Surgery can be safely undertaken at least in low-risk patients without PA catheterisation.3
• Collateral evidence supports PA catheter use in more complicated cases.
• It is essential that the known limitations and complications of PA catheters are considered in usage and interpretation.4

Cardiac output measurement by pulse contour analysis and a variety of ultrasound techniques is becoming more commonplace. A precise role for these techniques is not established, especially in the postsurgical patient, where Doppler-enabling windows may be difficult to obtain. Pulse contour analysis is invalidated by intra-aortic counterpulsation. Nevertheless, these techniques and continuous mixed venous saturation monitoring are attractive and very useful in individual patients.

Transoesophageal echocardiography is now almost routine in the operating theatre, at least for more complicated patients. The technique is less suitable for monitoring in the ICU but is helpful in the diagnosis and management of cardiovascular instability in postoperative patients.

FLUID AND ELECTROLYTE MANAGEMENT

Despite generous intraoperative fluid administration, effective hypovolaemia is common in the early postoperative period, especially as warming with associated vasodilatation occurs.

RESUSCITATION FLUID

• Use of isotonic fluid is essential.
• No benefit for any particular resuscitation fluid has been established. The suggestion that albumin may not be safe has been essentially dispelled.5
• Larger volumes of crystalloid than colloid solutions are required.

Polyuria is frequently observed in the early postoperative period, possibly related to hypothermia, haemodilution and the after-effects of non-pulsatile cardiopulmonary bypass on stretch and baroreceptors. This usually settles within the first 6 hours but often necessitates considerable volume replacement in the meantime.

POTASSIUM AND MAGNESIUM HOMEOSTASIS

Hypomagnesaemia and hypokalaemia are frequent in the early postoperative stage. These are exacerbated by polyuria. Late hyperkalaemia is also quite common, especially in patients with renal impairment or prior angiotensin-converting enzyme (ACE) inhibitor administration. Treatment for hyperkalaemia is rarely required in the absence of significant renal impairment. Especially in patients with atrial or ventricular ectopy or tachydysrhythmias, potassium and magnesium levels must be maintained in the high normal range.

Calcium homeostasis is generally not threatened by cardiopulmonary bypass. Massive transfusion, however, frequently causes hypocalcaemia. Ionised calcium levels are now easily monitored by ward-based blood gas machines.

HYPOTENSION

Hypotension is both a consequence and a cause of myocardial dysfunction. The major causes include:

• hypovolaemia
• vasodilation
• pericardial tamponade
• heart failure

Other causes of low cardiac output state (Table 22.1) should be considered and excluded. Whatever the cause, hypotension frequently causes myocardial ischaemia and consequent heart failure, especially if it occurs in the first 12–24 hours postoperatively. Angiography during this time almost always shows a significant reduction in the calibre of native coronary arteries, indicating increased coronary resistance and, presumably, altered coronary vasodilator reserve. Treatment of hypotension is urgent if a spiral of ischaemia and heart failure is to be averted.

Table 22.1 Low cardiac output

Preload
• Hypovolaemia, including haemorrhage
• Tamponade, pericardial constriction
• Left ventricular diastolic dysfunction
• Hypertrophy
• Ischaemia
• Oedema
• Cardiomyopathy
• Pulmonary hypertension
• Right ventricular failure

Afterload
• Excessive vasoconstriction
• Aortic stenosis
• Functional left ventricular obstruction
• Obstructive cardiomyopathy
• Systolic anterior motion of the mitral valve

Myocardial function
• Mechanical (ventricular septal defect, valve pathology)
• Cardiomyopathy
• Ischaemia, postischaemic stunning
• Metabolic, electrolyte abnormalities, pharmacolgical depression

MANAGEMENT

Successful management of hypotension depends on:

• rapid diagnostic assessment
• diagnosis-specific intervention

Context is very helpful. Early hypotension in patients with well-preserved ventricular function and no obvious ischaemia usually responds well to fluid administration. Patients with poor ventricular function and increasing inotrope requirement are likely to have a more sinister pathophysiology.

Vasoconstrictors may be useful in breaking the cycle of hypotension–ischaemia–hypotension but must be used cautiously in patients with impaired ventricular function, and especially in patients with major vascular or aortic pathology, for whom a hypertensive overshoot may be catastrophic.

HYPERTENSION

Complications associated with hypertension include:

• bleeding
• heart failure
• vascular (especially aortic) injury
• myocardial ischaemia

Significant postoperative hypertension is more common in patients having a history of hypertension and with cessation of β-blockade, but is reasonably common in the early postoperative period. Both absolute pressure and dp/dt are important factors in vascular injury. Vascular resistance declines over the first few hours (see Figure 22.1), so that therapy during this period is best undertaken with agents with a short duration of action. Nitroglycerine is theoretically more appropriate than nitroprusside because of the possibility of coronary steal with the latter agent.6 In practice, this is almost never apparent and nitroprusside appears to be more effective. Simple measures such as the provision of adequate analgesia and sedation should also be considered.

The target blood pressure varies with the indication. Excessive reduction of blood pressure risks reducing myocardial oxygen supply more than demand. Under most circumstances, a mean arterial pressure between 90 and 100 mmHg (12.0 and 13.5 kPa) seems optimal.7 Much lower target pressures may be applicable for the management of heart failure or in the presence of a vulnerable aorta, such as occurs with aortic trauma, dissection or aneurysm. Reduction of dp/dt with beta-blockade is more important than absolute blood pressure control in the management of aortic dissection.

LOW CARDIAC OUTPUT

The aetiology of a low cardiac output following heart surgery is diverse (see Table 22.1). The most common causes include:

• intravascular volume depletion
• systolic heart failure
• pericardial tamponade

Transient, reversible myocardial depression may follow an episode of acute ischaemia (preoperative or intraoperative) and is especially problematic where intraoperative myocardial protection has been difficult or suboptimal. Recognition of a low-output state in the absence of invasive monitoring may be difficult. Many of the usual signs of low output are also consequences of anaesthesia and surgery. Tachycardia may be obscured by drugs, hypothermia and heart disease, and even lactic acidosis may be an unreliable marker in this patient group.1

In the early postoperative period, a relatively low cardiac output may not warrant intervention, providing tissue oxygen delivery is adequate. Since beta-blockade is beneficial in the postoperative cardiac patient, beta-agonists should not be used unquestioningly. Nevertheless, optimisation of cardiac function does confer some benefit8 and intervention is clearly required when tissue oxygen delivery is inadequate.

Low cardiac output is associated with increased gastrointestinal, renal and neurological complications.

MANAGEMENT OPTIONS

1 Establish the diagnosis, including aetiology. Distinguishing tamponade from heart failure may require cardiac imaging with transthoracic or transoesophageal echocardiography. This should be the first recourse when uncertainty remains following conventional haemodynamic assessment. Tamponade may not be detectable using transthoracic echocardiography in the early phase after surgery.9 The principal role of echocardiography is thus the investigation of possible alternate diagnoses.
2 Correct all easily reversible factors, including hypovolaemia, tamponade, acute myocardial ischaemia, electrolyte abnormalities and dysrhythmias.
3 Vasodilators are helpful in the presence of hypertension and ventricular dilatation. Postsurgical vasodilation after the first 4–8 hours often obviates any ongoing role for these agents.
4 Use of inotropic agents. Because of the associated vasodilatation, ino-constricting agents are frequently required, alone or in combination. Useful agents include:

• dobutamine, an essentially pure β1-agonist with inotropic, lusotropic and some chronotropic effects
• noradrenaline (norepinephrine), metaraminol, vasopressin and high-dose dopamine which, being predominantly vasoconstrictors, are hazardous in the presence of hypovolaemia and should probably not be used alone in the presence of a low cardiac output
• adrenaline (epinephrine), the metabolic effects of which (especially lactic acidosis) make usage in cardiac surgical patients problematic.10 Adrenaline is, nevertheless, a potent ino-constrictor and recent studies suggest that it is as effective and as safe as noradrenaline, in the general patient population at least
• milrinone, which has a long duration of action and potent vasodilating properties. These make milrinone relatively difficult to introduce and to wean. It is, however, a very effective inotropic agent, especially in patients with beta-receptor downregulation
• levosimendan, a novel calcium-sensitising agent, has a promising role both perioeratively and as rescue therapy for postsurgery heart failure11

5 Intra-aortic balloon counterpulsation (IABC; see below).
6 Ventricular assist devices (VAD) are expensive and technically far more demanding than IABC. They are effective in resting the heart while supporting organ and tissue oxygen delivery. Indications for implantation have not been well established but include intractable heart failure, and failure to wean from cardiopulmonary bypass in spite of full cardiovascular support. A combination of haemodynamic and cardiac support-level criteria seems most useful and early utilisation offers improved outcomes.12,13 Usage is relatively infrequent so that management expertise is difficult to acquire. Some centres thus prefer to re-establish or continue cardiopulmonary bypass as short-term, biventricular support. Most published VAD data relate to non-surgical patients in whom the role of heart assist devices is increasingly established as both ‘bridge to transplant’ and as ‘destination therapy’.
7 Delayed sternal closure has an established role in improving outcome after cardiac surgery.14 Cardiac output is increased and inotropic requirement reduced. Subsequent sternal closure has an acceptably low complication rate. The sternum may be left open following an initial attempt at closure or reopened with later deterioration. Sternal retraction may be required.
8 Mechanical ventilation is generally continued throughout the period of low output. This reduces cardiac workload by removing the work of breathing. Positive intrathoracic pressure reduces left ventricular afterload, which is beneficial to the dilated left ventricle. Positive pressure may be detrimental, however, in the presence of diastolic ventricular dysfunction or hypovolaemia, where the reduction in venous return may further reduce ventricular preload.

INTRA-AORTIC BALLOON COUNTERPULSATION

IABC has an established role in support of cardiac surgery. Its two actions are: (1) augmentation of diastolic coronary perfusion pressure; and (2) left ventricular afterload reduction. This is achieved by balloon inflation (30–50 ml capacity) within the aorta during diastole and rapid deflation of the balloon immediately before aortic valve opening. The catheter is usually inserted using a Seldinger technique, but can be placed by femoral artery cutdown or directly into the descending thoracic aorta. Timing of inflation and deflation is critical to optimal function. This is best achieved using the pressure waveform and a 1:2 ratio (Figure 22.2).

image

Figure 22.2 Intra-aortic balloon counterpulsation pressure waveform.

Inflation is timed to coincide with the dicrotic notch. Deflation is timed to occur as late as possible in diastole,ensuring that the IABC end-diastolic pressure is lower than the patient’s end-diastolic pressure. IABC increases cardiac index and coronary perfusion and reduces left ventricular filling pressure, myocardial lactate production and oxygen extraction percentage.

Indications for IABC are summarised in Table 22.2.

Table 22.2 Indications for intra-aortic balloon counterpulsation

Prophylactic
• Cardiac surgery

• Two of: left main > 70%, left ventricular ejection fraction < 0.4, unstable angina, reoperation

• Non-cardiac procedures

• Severe left ventricular impairment, unstable angina

• Failure to wean from cardiopulmonary bypass
• Cardiogenic shock

• Reversible myocardial depression
• Support for reperfusion, revascularisation
• Bridge to transport

IABC improves:

• mortality in high-risk cardiac surgery15,16
• clinical outcomes when used in support of infarct-related, non-surgical coronary reperfusion17

IABC is not helpful in the management of cardiogenic shock from irremediable causes except as a bridge to transplant. Complications are:

• limb ischaemia (6–16%)
• vascular trauma, dissection
• infection (cutdown > percutaneous)
• balloon rupture
• bleeding
• thrombocytopenia
• malposition, vascular obstruction
• malfunction, failure to unwrap

Limb ischaemia is the most frequent complication and optimal management requires early recognition based on routine, systematic observation.

ISCHAEMIA

Postoperative myocardial ischaemia predicts a more complicated course.18 Recognition is enhanced by automated multilead ST analysis with confirmatory electrocardiography, although diagnosis may be difficult in the presence of preoperative electrocardiographic abnormalities.

Ischaemia may be due to graft failure. Remedial options include coronary angiography and/or reoperation. Angiography offers the potential for tailored reoperation or non-operative intervention. Management decisions may be influenced by surgical factors such as the availability of further conduit and the state of the native arteries. Thus close liaison among ICU personnel, cardiologists and surgeons is essential.

DIASTOLIC DYSFUNCTION

Ventricular hypertrophy is the commonest cause of diastolic dysfunction, and is exacerbated by poor myocardial protection during surgical procedures. Myocardial ischaemia, right ventricular (RV) dilatation and pericardial abnormalities (including tamponade) can also reduce left ventricular volume in spite of elevated filling pressures.19 Recognition and management can be very difficult.

Diagnosis generally requires:

• demonstration of small ventricular volumes (using echocardiography or other techniques)
• the presence of increased pressures

MANAGEMENT

• Treatable causes should be addressed.
• Blood volume must be maintained, with blood transfusion where necessary.
• Maintenance of sinus rhythm is helpful, if not essential.
• Atrial pacing at an enhanced heart rate is often beneficial since the stroke volume is fixed and the diastolic filling time is foreshortened.
• β-agonists and milrinone improve diastolic relaxation and hence ventricular compliance.

DYSRHYTHMIAS

Ventricular and supraventricular dysrhythmias are common. Prevention and treatment of electrolyte abnormalities may be prophylactic. New occurrence of complex ventricular dysrhythmias should stimulate a search for causal ischaemia and graft malfunction.

• Ventricular fibrillation and pulseless ventricular tachycardia require rapid defibrillation, preferably before external cardiac massage, which may cause mechanical injury poststernotomy. If haemodynamic stability cannot be rapidly restored, open cardiac massage should be instituted.
• Facilities for atrioventricular pacing are essential as transient heart block is common.

ATRIAL FIBRILLATION (AF)

AF is the most common complication of cardiac surgery.20,21 Its incidence varies from 10 to 40% in patients undergoing coronary artery surgery and up to 50% with some valvular procedures. Predisposing factors include a history of AF, valvular heart disease (especially mitral valve pathology), increasing age and prolonged P-wave duration. AF can be effectively treated and its recurrence prevented with intraoperative radiofrequency ablation and left atrial reduction during cardiac surgery.22 AF is probably less frequently observed following ‘off-pump’ surgery, and is most frequently encountered around the second and third postoperative days, but may occur weeks after surgery and hospital discharge.

AF is a potentially serious complication. Apart from discomfort, it may provoke or complicate haemodynamic instability. The major complication of AF, however, is stroke, with an increased risk of approximately threefold. Based on echocardiography, there is the potential for embolic stroke within 3 days of onset of AF.

AF is also associated with:

• increase in inotrope usage
• increased use of IABC
• increased reoperation for bleeding
• prolonged ICU and hospital stay
• increased costs

Several strategies are beneficial in preventing AF:23

• β-blockade
• amiodarone
• sotolol
• diltiazem
• atrial pacing
• dexamethasone

Treatment should be tempered with an understanding that spontaneous reversion to sinus rhythm is frequent. A treatment strategy is summarised in Table 22.3.

• Beta-blockade is best established.
• Digitalis is not more effective than placebo at reverting AF and may not be helpful in ventricular rate control in the presence of catecholamine stimulation.
• Anticoagulation should be considered where AF persists for longer than 48 hours and in all cases where elective cardioversion is undertaken.
• Early cardioversion tends to be ineffective and potentially harmful and should only be undertaken to correct severe haemodynamic compromise.

Table 22.3 Management of atrial fibrillation (AF)

Rate control
• β-blockade
• Calcium channel blockers
• Amiodarone
• Sotolol
• Digitalis

Cardioversion
• Ibuletide
• Amiodarone
• Magnesium
• Electrical cardioversion
Anticoagulation
• Always for elective cardioversion
• Consider if atrial fibrillation persists beyond 48 hours

RIGHT VENTRICULAR DYSFUNCTION

RV failure following cardiac surgery is reasonably common. Aetiological factors include:

• direct RV ischaemia or infarction
• poor myocardial protection
• anteriorly placed RV
• bypass-related pulmonary hypertension

Management involves:

• volume resuscitation
• maintenance of RV perfusion pressure with vasoconstrictors
• IABC as required
• inotrope administration
• RV afterload reduction

Useful afterload-reducing agents include nitric oxide,24 prostaglandins and sildenafil.25 Conventional vasodilators tend to produce excessive systemic vasodilatation. Occasionally, RV balloon counterpulsation or an RV assist device may be required. Delayed sternal closure has an established role.

EMERGENCY REOPERATION

Emergency re-sternotomy is indicated as part of resuscitation when haemodynamic stability cannot be rapidly re-established with conventional means.26,27 Advantages compared to closed-chest resuscitation include:

• establishment of the cause of instability
• correction of the cause (e.g. tamponade, kinked graft)
• more effective cardiac massage
• direct establishment of atrial and ventricular pacing

Re-sternotomy also enables the re-establishment of cardiopulmonary bypass and regrafting or correction of mechanical abnormalities as required. Infectious complications of emergency re-sternotomy are probably increased but the incidence is not prohibitive.

RESPIRATORY MANAGEMENT

Postoperative mechanical ventilation remains routine in cardiac surgical patients. Immediate extubation appears to offer little patient benefit28 but may be expedient. Neither is routine ventilation beyond 12 hours essential.29 Extubation can be safely undertaken with simple protocols. Reintubation is rarely required, but is more likely in older patients with pre-existing lung and vascular disease and impaired ventricular function. Reoperative surgery and bleeding requiring massive transfusion also increase the likelihood of early extubation failure.30

Hypoxia is very common in the early postoperative period. It is mostly attributable to atelectasis and responds well to simple measures such as positive end-expiratory pressure (PEEP), prolonged inspiration and simple recruitment manoeuvres. Atelectasis is a consequence of cardiopulmonary bypass and intraoperative ventilation with high inspired oxygen and without PEEP. Long-term sequelae are rare. Incentive spirometry and chest physiotherapy are commonly utilised in the postoperative period, without good supportive evidence. Early mobilisation appears most beneficial. Adequate analgesia facilitates physiotherapy and mobilisation. Local analgesic initiatives may be helpful31 whereas some non-steroidal agents may increase the risk of complications.32

More sinister causes of hypoxia include severe heart failure and hypoxaemic respiratory failure (acute respiratory distress syndrome: ARDS). The aetiology of ARDS is diverse, but includes shock, massive blood product administration and cardiopulmonary bypass itself. Management is not particular to this group of patients. Occasionally, profound hypoxia accompanies minor atelectasis with moderate pulmonary hypertension. Patent foramen ovale (which is seen in 10–15% of the normal population) with right-to-left intracardiac shunt is the likely mechanism.

Pulmonary embolism is an uncommon complication of cardiac surgery, probably due to bypass-induced platelet dysfunction, routine postoperative antiplatelet therapy and thromboprophylaxis.33 ‘Off-pump’ surgery may be associated with an increase in this complication and so may warrant a more aggressive prophylactic regimen.34

POSTOPERATIVE COMPLICATIONS

HAEMORRHAGE

Excessive postoperative bleeding is a major cause of increased morbidity and mortality. Mechanisms are complex and include preoperative anticoagulation, thrombolysis and antiplatelet therapy as well as activation of haemostatic mechanisms, including fibrinolysis. ‘Off-pump’ surgery may be associated with excessive bleeding because of administration of anticoagulant and antiplatelet therapy out of fear of early graft closure.

Most studies of pharmacological strategies to minimise postoperative blood loss have involved preoperative or intraoperative intervention. Extrapolation to the postoperative phase is intuitive rather than established. Aprotinin and the lysine analogues aminocaproic acid and tranexamic acid reduce bleeding and exposure to blood and blood products. Aprotinin has been associated with an increased risk of serious end-organ damage.35 Desmopressin is probably less effective and has been associated with an increased risk of myocardial infarction.36

Effective postoperative measures include reversal of residual heparin (including ‘heparin rebound’) and correction of coagulopathy with blood products. Application of PEEP has been shown to be effective in some studies, but not others. Retransfusion of shed blood reduces autologous transfusion requirements without apparent side-effects. Controlled tamponade with discontinuation of drain suction and even clamping of drains has also been reported.37 Finally, at least in reasonably stable patients, reduction of the transfusion threshold to at least 80 g/l reduces exposure to autologous blood transfusion38 without adverse consequences.

RENAL FAILURE

Depending on definition and patient groups, acute renal failure is observed in 1–5% of patients undergoing cardiac surgery. Risk factors include increasing age, heart failure, prolonged bypass, diabetes, pre-existing renal impairment and postoperative shock.39 Surgery without cardiopulmonary bypass may be relatively protective.40 Morbidity, mortality and costs are significantly increased. Effective preventive strategies beyond careful haemodynamic management and minimisation of associated nephrotoxic insults have not been established. Nevertheless, attention to urine output in the presence of known risk factors appears warranted.

SHIVERING

Shivering is frequent following cardiac surgery. Mechanisms are complex and not entirely related to core temperature. Shivering causes a significant increase in metabolic rate and hence cardiac workload. This is especially important in the patient with impaired cardiac function and limited reserve. Effective preventive agents include dexamethasone, clonidine, high-dose morphine and external warming. Pethidine effectively reduces the duration of shivering. Short-term neuromuscular blockade is occasionally required.

STERNAL INFECTION

Deep sternal wound infection is uncommon (0.5–2.5%). Associated morbidity and mortality are significant. Risk factors have been variously reported but consistently include diabetes, obesity and use of internal mammary arteries, especially if bilateral. Other contributing factors include prolonged surgery, chronic lung disease, male sex, low postoperative cardiac output, blood transfusion, sternal reopening and dialysis. Rigid control of blood sugar levels in diabetics41 and preoperative nasal and oropharyngeal decontamination42 may help prevent infection.

NEUROLOGICAL COMPLICATIONS

Neurological complications of cardiac surgery include neuropsychiatric deterioration as a consequence of cardiopulmonary bypass, delirium and a range of peripheral neuropathies, the most frequent of which is a unilateral phrenic nerve palsy. Paraplegia is a recognised complication of thoracic aortic surgery.

The most devastating neurological complication is cerebral infarction. The incidence varies with patient selection, but ranges from 1 to 5%. The pathophysiology is mostly embolic. Risk factors include carotid artery stenosis, hypertension, AF, aortic atheroma, impaired ventricular function and peripheral vascular disease.43 ‘Off-pump’ surgery is almost certainly protective and other operative techniques may also reduce the incidence.

GASTROINTESTINAL COMPLICATIONS

Peptic ulcer disease, pancreatitis, cholecystitis, gut ischaemia, ileus and hepatic dysfunction are uncommon (< 1%) after cardiac surgery. Morbidity, however, is quite high. Risk factors include increased age, more complicated surgery and postoperative shock. The incidence of gastrointestinal complications may be reduced with ‘off-pump’ surgery.44

LONG-TERM CONSIDERATIONS

Patients surviving cardiac surgery have a continuing risk of disease progression. It is important that effective secondary prevention strategies be considered or recommenced in the postoperative period. Initiatives with proven long term benefit in patients with ischaemic heart disease include anti-platelet therapy, beta blockade, ACE inhibitors, lipid-lowering statins and exercise. Treatment for hypertension, diabetes and other intercurrent disorders should also be reinstituted.

A small percentage of patients require long-term ICU management for a variety of complications. Excellent long-term survival and quality of life are possible in this group of patients, especially if the prolonged ICU stay results from pulmonary complications rather than severe heart failure or neurological dysfunction.45

NON-CARDIAC SURGERY

Non-cardiac surgery poses a significant risk to the patient with cardiac disease.46,47 Postoperative cardiac complications result in significantly increased immediate and late mortality. Simple preoperative assessment enables risk stratification which might lead to deferment or cancellation of non-essential surgery. Indications for specific investigations and treatments are probably not different in the preoperative patient. However, this might be the first time that a cardiac assessment has been undertaken and hence significant cardiac pathology identified. Risk factors are summarised in Table 22.4. Cumulative factors are more than additive. Patients undergoing vascular procedures have a high risk of associated coronary artery disease and should be carefully assessed preoperatively. Perioperative risk can be modified by anaesthetic technique and by optimal medical (or surgical) management of heart disease, which might include myocardial revascularisation.46

Table 22.4 Risk factors for cardiac patients undergoing non-cardiac surgery

• High-risk surgery (abdominal, thoracic, major vascular)
• History of ischaemic heart disease
• History of congestive heart failure
• History of cerebrovascular disease
• Treatment with insulin
• Renal impairment

High risk: three or more factors.

The principles of postoperative management are the same as those outlined for the cardiac surgical patient. The period of risk for cardiac complications extends for some days after surgery and close monitoring to identify and manage events during this time is desirable in high-risk patients. The immediate perioperative period poses risks associated with anaesthesia, bleeding, fluid and electrolyte imbalance, haemodynamic instability and temperature abnormalities. These can be effectively managed. Early reinstitution of protective treatment (aspirin, beta-blockers, ACE inhibition, statins, antihypertensive therapy) may protect against later complications.

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