ANAESTHESIA FOR PATIENTS WITH CARDIAC DISEASE UNDERGOING NON-CARDIAC SURGERY

Dr Sock Huang Koh, Queen Elizabeth Hospital, Birmingham,
Dr James Rogers, Frenchay Hospital, Bristol

Introduction		Aortic Stenosis
Assessment of Perioperative Risk		Aortic Regurgitation
Ischaemic Heart Disease (IHD)		Mitral Stenosis
Heart Failure		Mitral Regurgitation
Valvular Heart Disease

INTRODUCTION

Major surgery stresses the cardiovascular system in the perioperative period. This stress leads to an increase in cardiac output which can be achieved easily by normal patients, but which results in substantial morbidity and mortality in those with cardiac disease. Postoperative events which cause death include myocardial infarction (MI), arrhythmias, and multiple organ failure secondary to low cardiac output. If the different mechanisms involved in different cardiac disease states are understood, then the most suitable anaesthetic can be given. The skill with which the anaesthetic is selected and delivered is more important than the drugs used. Previous articles on cardiovascular physiology and pharmacology (Updates 10 & 11) provide background information and should be read in conjunction with this article.

ASSESSMENT OF PERIOPERATIVE RISK

The Goldman Cardiac Risk Index attempts to quantify the risk of adverse perioperative cardiac events (Table 1). The index scores each of a range of various conditions including cardiac disease, age and the nature and urgency of the proposed surgery. The total score predicts the likelihood of complications and death. For certain operations this risk can be minimised by avoiding general anaesthesia and using local anaesthetic techniques. Examples include peribulbar eye blocks for cataract surgery and brachial plexus blocks for upper limb surgery.

There have been more recent indices of risk, including one study of patients undergoing major elective non-cardiac surgery¹. This identified six independent predictors of complications: high-risk type of surgery, history of ischaemic heart disease, history of congestive cardiac failure, history of cerebrovascular disease, preoperative treatment with insulin, and a raised serum creatinine.

The American Heart Association and College of Cardiology have issued guidelines for perioperative cardiovascular evaluation for non-cardiac surgery², giving levels of risk to certain clinical markers, functional capacity, and types of surgery (Table 2). In addition to identifying the presence of cardiac disease, it is essential to determine severity, stability, and prior treatment of the disease.

It is important to remember that the above schemes to identify populations of high risk patients will not predict accurately the perioperative problems facing any particular individual. However, they do allow planning of perioperative care. Depending on available resources, this includes: (a) optimisation of medical treatment and specific perioperative drug therapy, (b) preoperative surgical treatment of ischaemic and valvular disease, and (c) use of postoperative intensive care facilities.

ISCHAEMIC HEART DISEASE (IHD)

In developed countries 5-10% of patients presenting for surgery have some degree of ischaemic heart disease. Patients with IHD are at increased risk of perioperative myocardial infarction (MI), which is associated with an in-hospital mortality of some 30%. This is usually the consequence of “silent” myocardial ischaemia, that is ischaemia without the characteristic symptoms of angina. The strong association between postoperative silent ischaemia and other adverse cardiac events makes it important to use anaesthetic techniques which minimise the chance of such ischaemia developing.

Pathophysiology

Ischaemic heart disease is the result of the build-up in larger coronary arteries of plaques of atheroma - consisting of cholesterol and other lipids. This causes narrowing of the vessels, restricting coronary blood flow. There may be insufficient myocardial blood supply during times of high demand eg exercise, leading to the effort related chest pain of stable angina. The more serious conditions of unstable angina (pain at rest), silent ischaemia and myocardial infarction are thought to be due to rupture of the atheromatous plaques causing thrombus formation, as well as vasoconstriction of the coronary vessels. There are several factors in the perioperative period which make these more likely:

• high levels of adrenaline and other catecholamines as a consequence of surgery, causing tachycardia, coronary vasoconstriction, and increasing platelet “stickiness”.
• an increased tendency for blood to coagulate, making thrombosis in coronary vessels more likely.

Anaesthesia

• All anaesthetic techniques must aim to keep myocardial oxygen supply greater than demand, and therefore avoid ischaemia. The relevant factors are summarized in Table 3. The essential requirements of general anaesthesia for IHD are avoiding tachycardia and extremes of blood pressure, both of which adversely affect the balance between oxygen supply and demand. These are discussed in detail below during each phase of an operation.
• Pre-medication. A nervous patient may be tachycardic and require an anxiolytic premedication. Beta-blockers also reduce tachycardia, and prevent perioperative myocardial ischaemia. A regime of intravenous atenolol followed by postoperative oral treatment resulted in a reduction in both morbidity and mortality for two years after surgery in IHD patients3. In a similar fashion, alpha2-agonist drugs such as clonidine reduce noradrenaline release from synapses, causing both sedation and analgesia, also a reduction in intraoperative myocardial ischaemia.
  
  
• Induction. All intravenous anaesthetic agents have a direct depressant action on the myocardium, and may also reduce vascular tone. This causes hypotension (especially in the hypovolaemic patient), often with a compensatory tachycardia,, which may cause myocardial ischaemia. In general all agents can be used safely if given slowly in small increments. However, ketamine is unique in causing indirect stimulation of the sympathetic nervous system, leading to both hypertension (increased afterload) and tachycardia. This will be dangerous for a patient with IHD and should be avoided.
  
  
• Intubation. Laryngoscopy is a powerful stressor, causing hypertension and tachycardia. This can be avoided with a supplemental dose of intravenous induction agent or opioid eg alfentanil, just prior to laryngoscopy.
  
  
• Maintenance. Volatile agents have minimal effects on cardiac output, although they do reduce myocardial contractility, especially halothane. They cause vasodilation, and isoflurane has been implicated in the ‘coronary steal’ syndrome. The theory is that pre-stenotic vasodilation diverts blood away from already ischaemic areas of the myocardium. However, there is doubt as to the clinical significance of this phenomenon. Vagal stimulation due to halothane can cause bradycardias and nodal rhythms. Bradycardias can be beneficial by allowing greater coronary diastolic filling, providing blood pressure is maintained. Ether, despite being a direct myocardial depressant, causes indirect sympathetic stimulation with tachycardia, and therefore can aggravate ischaemia.

• Analgesia. High doses of opioids reduce the stressor response to surgery. Theoretically, non-steroidal anti-inflammtory drugs (NSAIDs) may have both a useful postoperative analgesic action and an anti-platelet effect which may reduce coronary thrombosis.
  
  
• Reversal and recovery. Reversal of muscle relaxation with a combined anti-cholinesterase/anti-muscarinic causes tachycardias, and extubation in itself is a stressor. Problems in the recovery phase which can cause ischaemia include; tachycardia, pain, hypothermia, shivering, hypoxia, and anaemia. These should be treated not just in the immediate postoperative period, but throughout the hospital admission. The use of supplemental oxygen in the postoperative period is one of the simplest, yet most effective measures in preventing myocardial ischaemia.
  
  
• Monitoring. As discussed above, the prime anaesthetic goals are to avoid tachycardias and extremes of blood pressure. It follows that it is most useful to monitor heart rate and blood pressure, also pulse oximetry to detect hypoxia. An ECG, if available, will give indications of arrhythmias, and ST segment depression may indicate ischaemia, although an observer will usually only detect the minority of such events. Rarely used techniques to detect ischaemia involve intraoperative transoesophageal echocardiography to assess ventricular wall motion abnormalities, and measuring serum troponin levels in the postoperative period.

The use of regional anaesthetic techniques has theoretical advantages: epidural anaesthesia reduces preload and afterload, coagulation responses, and in the case of thoracic epidurals, causes coronary vasodilation. These effects should reduce perioperative myocardial ischaemia, but this is not supported by research. However, good epidural analgesia may reduce the incidence of tachycardias arising due to postoperative pain. In a patient with IHD, local anaesthetic techniques such as brachial plexus block should be encouraged in order that the haemodynamic responses to general anaesthesia are avoided. However, even under local anaesthesia, the patient will be subject to the stresses of the surgical procedure itself, which can have marked haemodynamic effects.

HEART FAILURE

Heart failure is the inability of the heart to pump enough blood to match tissue requirements. It occurs in 1-2 % of the population, rising to 10% in the over 75 year old age group, and is associated with increased mortality following anaesthesia. The commonest cause is ischaemic heart disease. Other causes include hypertension, valvular heart disease and cardiomyopathies. One third of untreated patients with an ejection fraction of less than 40% will die within a year.

Pathophysiology

Cardiac output is lower in heart failure because stroke volume is reduced for the same left ventricular end-diastolic volume as compared to a normal heart. Starling’s law of the heart demonstrates the relationship between ventricular end-diastolic volume and stroke volume (Figure 1). Since the failing heart has a limited ability to increase stroke volume, the only response to a greater preload is an increase in heart rate, which in turn can cause ischaemia. In addition, high end-diastolic ventricular pressures tend to oppose blood flow to the endocardium.

Curves A and B illustrate the rise in cardiac output with increases in ventricular end-diastolic volume (pre-load) in the normal heart. Note that with an increase in contractility there is a greater cardiac output for the same ventricular end- diastolic volume.

In the diseased heart (C and D), cardiac output is less, and falls if ventricular end-diastolic volume rises to high levels, as in heart failure or overload.

Preoperative assessment

The aim is to assess disease severity and myocardial contractility. Limited exercise tolerance, orthopnoea, and paroyxsmal nocturnal dyspnoea are indicators of disease severity. Drug treatments may include ACE (angiotensin converting enzyme) inhibitors, diuretics and nitrates. In some patients with mild to moderate heart failure, cardioselective beta blockers may be used in an attempt to control the heart rate, but the risk is that they may block the low level sympathetic nervous activity which maintains contractility in the failing heart. Useful investigations are an ECG (looking for evidence of ischaemia), CXR, and, if available, an echocardiogram to assess ejection fraction. This is the proportion of end-diastolic blood volume ejected by the left ventricle during systole, and values of less than 30% equate to severe heart failure.

Anaesthesia

Safe anaesthesia for a patient in heart failure involves:

• Optimisation of ventricular filling - preload can be reduced with diuretics and nitrates, and both central venous and pulmonary artery pressures can be monitored.Trans-oesophageal echocardiography, if available, is a useful tool to visualize overall cardiac performance.
  
  
• Maintenance of myocardial contractility - in particular inotropes may be needed to oppose the cardiodepressant action of anaesthetic agents.
  
  
• Reduction of afterload by vasodilation, for example as a secondary effect of spinal or epidural anaesthesia. This not only reduces myocardial work, but helps maintain cardiac output. However, the benefit of such actions may be limited by falls in blood pressure which can compromise blood flow to vital organs such as the brain and kidneys.

VALVULAR HEART DISEASE

Pathology affecting valves on the left side of the heart is more common than on the right side. The same general principles of providing a haemodynamically stable anaesthetic apply as outlined in the section on ischaemic heart disease. In general, patients with valvular disease require antibiotic prophylaxis against infective endocarditis when undergoing certain operations (Table 4). Symptomatic regurgitant disease is usually better tolerated in the perioperative period than stenotic lesions, which sometimes need treatment such as valvotomy prior to non-cardiac surgery.

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