Intercurrent disease and anaesthesia

Preoperative assessment

The preoperative assessment of patients with ischaemic heart disease (IHD) should follow a stepwise approach.

Clinical features

A detailed history and examination should identify recent or previous MI, unstable angina, significant arrhythmias or valvular heart disease. Diabetes, stroke, renal insufficiency and pulmonary disease are significant related comorbidities. The presence of one or more of the following active conditions is considered to make a patient at high risk for MACE:

• acute coronary syndrome (ACS), unstable angina or recent MI;

• decompensated heart failure;

• significant arrhythmias; and/or

• severe valvular disease (aortic stenosis with a gradient >40 mmHg/valve area <1.0 cm ² or symptomatic mitral stenosis)

The presence of these active conditions requires urgent management and may result in delay to non-urgent surgery.

Functional capacity

A simple assessment of physiological reserve can be made by quantifying a patient's metabolic equivalents (METs) (see Chapter 19 ). If a patient has no major cardiac risk factors and can achieve more than 4 METs of activity without significant cardiorespiratory symptoms, then the perioperative risk of an adverse cardiac event is low. A more detailed assessment of reserve can be made through the use of cardiopulmonary exercise (CPEX) testing. It may be possible to improve cardiorespiratory reserve before surgery in some patients (see Chapter 30 ).

Extent of surgery

The extent of surgery determines the level of physiological stress which the patient will experience. Examples of high-risk (cardiac morbidity >5%), intermediate-risk (cardiac morbidity 1%–5%) and low-risk (cardiac morbidity <1%) procedures are shown in Table 20.1 .

Cardiac risk stratification

The revised cardiac risk index (RCRI) can be used to identify several risk factors in patients undergoing non-cardiac surgery. It includes six predictors of risk:

• 1.

  High-risk surgery

• 2.

  History of IHD

• 3.

  Biventricular cardiac failure

• 4.

  Cerebrovascular disease

• 5.

  Preoperative treatment with insulin

• 6.

  Renal impairment (serum creatinine >177 µmol L ^–1 )

The presence of two risk factors has been equated to a risk of MACE approaching 7% and three risk factors, 11%.

The American College of Surgeons National Surgical Quality Improvement Program (ACS NSQIP) surgical risk calculator (available as an Internet-based calculator) has been developed to provide surgery-specific risk calculation. Up to 21 patient variables are used to calculate the risk of 10 outcomes, including MACE and death.

Management

Having made the assessment, subsequent management may be outlined as shown in Fig. 20.1 .

• If the patient requires emergency non-cardiac surgery, they should proceed to surgery without any further cardiac testing.

• If the surgery is elective, but the patient has evidence of ACS , surgery should be deferred. The patient should undergo further cardiac assessment. Once optimised, the patient's perioperative risk should be reassessed.

• In patients scheduled for elective surgery without any evidence of ACS , a risk assessment of MACE should be made based on surgery type, RCRI or NSQIP tools.

• Those patients with a risk of MACE estimated to be < 1% should proceed to surgery. No further testing is required in this group of patients.

• The management of patients with a risk of MACE ≥ 1% depends on their functional capacity. In the group of patients with an unknown or poor functional capacity (<4 METs), consideration should be given to non-invasive cardiac testing. Cardiac testing, however, should only be undertaken if results are going to change anaesthetic or surgical management; those patients with a good functional capacity (≥ 4 METs) should proceed to surgery.

Investigations

Recent guidelines from the UK National Institute for Health and Care Excellence (NICE) have reviewed the tests recommended before elective surgery, and these are discussed in detail in Chapter 19 .

Management of pre-existing cardiovascular disease

Previous percutaneous coronary intervention.

Percutaneous coronary intervention (PCI) has become a standard and increasingly common intervention in patients suffering from ACS. Fewer than 10% of patients undergo angioplasty alone; the remaining patients have an intracoronary stent inserted to maintain coronary artery patency. The major risk with coronary stents is restenosis by thrombus formation or re-endothelialisation resulting in an MI, which may be associated with a mortality of up to 50%. Bare metal stents (BMS) are only used in up to 15% of cases. The remainder are drug-eluting stents (DES), which have a lower restenosis rate. A cytotoxic agent is released by the DES to limit the risk of endothelialisation. In both types of stents, dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 inhibitor (e.g. clopidogrel; see Chapter 14 ) is recommended to reduce stent thrombosis. Current guidelines recommend DAPT after PCI for a minimum of 1 month in patients with BMS and 6 months with DES. If DAPT is tolerated without risk of bleeding, it may be reasonable for it to be continued beyond 12 months. This is an important clinical problem as it is estimated that as many as 5%–10% of patients with coronary stents may present for surgery within 1 year of stent implantation.

Guidelines now recommend elective non-cardiac surgery should be delayed 14 days after balloon angioplasty and 30 days after BMS implantation. In patients with DES the highest risk of stent thrombosis persists for the 3 months postimplantation, and surgery should initially be deferred if possible. With newer second-generation–type DES, the risk of stent thrombus falls at 6 months. At that point DAPT can be discontinued to allow surgery. Between 3 and 6 months it is a balance of risk, considering urgency of surgery, risk of bleeding if DAPT is continued perioperatively and risk of thrombus if it is discontinued. Low-dose aspirin should be continued perioperatively provided surgical bleeding risk allows and P2Y12 inhibitors should be restarted postoperatively. More recently an alternative type of polymer-free stent has been introduced (e.g. BioFreedom). This type of stent is claimed to have a restenosis risk similar to that of DES, with the advantage of requiring DAPT for only 1 month. This may represent a significant advantage in those patients who are at high risk of bleeding if prescribed long-term DAPT. Appropriate management will require discussion with the patient, surgeon and cardiologists ( Fig. 20.2 ).

Hypertension

Raised arterial pressure is one of the major preventable causes of morbidity and mortality in the general population. It is a major risk factor for ischaemic and haemorrhagic stroke, MI, heart failure, chronic kidney disease (CKD) and premature death. British Hypertension Society guidelines recommend starting antihypertensive therapy for sustained pressures greater than 140/90 mmHg. However, in the perioperative setting there is little evidence that patients with stage 2 hypertension (<180/110 mmHg) and no evidence of end-organ damage have an increased risk of cardiovascular complications. Isolated hypertension below this level is classified as a low risk factor. If hypertension is identified preoperatively the risks of anaesthesia and surgery are dependent on the presence and severity of end-organ damage.

Current UK recommendations are that a patient with a recorded blood pressure measurement less than 160/100 mmHg in the preceding 12 months should proceed to surgery. In those patients without a recording in the preceding 12 months, a blood pressure of less than 180/110 mmHg at the time of preassessment is acceptable to proceed with surgery. For non-urgent surgery, patients with severe hypertension (i.e. >180/110 mmHg) should be referred back to primary care for blood pressure control. Patients with hypertension, both controlled and uncontrolled, have a more labile haemodynamic profile intraoperatively. The perioperative management of antihypertensive medication is discussed in Chapter 19 .

Heart failure

Decompensated heart failure is a significant risk factor for perioperative MACE. Patients may have systolic or diastolic dysfunction, with or without preserved ejection fraction. Treatment should be optimised as far as possible preoperatively and investigation of underlying coronary artery disease undertaken as appropriate.

Pulmonary hypertension

A mean pulmonary artery pressure >25 mmHg is diagnostic of pulmonary hypertension. This may be idiopathic in nature or secondary to left-sided heart disease, lung disease or chronic thromboembolic disease. Diagnosis is confirmed by echocardiography and right-sided heart catheterisation. Perioperative mortality in non-cardiac surgery may be as high as 18% and morbidity of up to 42%, associated with respiratory failure, heart failure, dysrhythmias and MI. Intraoperative management can be complex, requiring a balance of maintaining right ventricular output and avoiding excessive afterload. Senior experienced management is essential.

Cerebrovascular disease

A history of previous ischaemic stroke is a recognised risk factor for MACE as measured by the RCRI. There may be up to a fivefold increase in risk of 30-day mortality and MACE regardless of timing between stroke and surgery. This risk is highest in those patients suffering a stroke less than 3 months before surgery and appears to stabilise after 9 months. The type of surgery does not seem to affect the risk of cerebrovascular event.

Treatment and additional interventions

General anaesthetic principles in patients with cardiovascular disease

Having ensured that management of the patient's cardiovascular disease is optimised (see Chapters 19 & 30 ), anaesthesia should comprise a balanced technique aimed at maintaining cardiovascular stability. A variety of options may be suitable, including general or regional anaesthesia or a combination of both. Tachycardia should be avoided and an adequate arterial pressure maintained; there should not be a sustained reduction in arterial pressure of >20% of the patient's normal blood pressure. Coronary perfusion and myocardial oxygen delivery are thus maintained without increasing myocardial work and oxygen requirements.

The level of intraoperative monitoring should be dictated by risk assessment. The following should be considered in addition to standard monitoring:

• Five-lead ECG. The usual ECG configuration for anaesthetic monitoring is standard limb lead II. Whilst this is useful for identifying arrhythmias, myocardial ischaemia occurs most commonly in the left ventricle and is detected more sensitively with a CM5 configuration.

• Direct arterial pressure recording.

• CVP monitorin g (with or without central venous oxygen saturations).

• Oesophageal Doppler or transoesophageal echocardiography (TOE). These provide a measurement of cardiac function, output and intravascular filling.

• Minimally invasive cardiac output monitors . These are devices that derive cardiac output and other variables from the arterial pressure waveform using internal algorithms. Some (FloTrac or LiDCO (Lithium Dilution Cardiac Output) devices) use a standard arterial catheter, whereas others (PiCCO (Pulse Index Continuous Cardiac Output)) require a dedicated thermistor-tipped catheter in a proximal (femoral or axillary) artery.

For patients identified as high-risk, specific consideration should be given to reducing the surgical stress response (see Chapter 13 ). Measures to achieve this are dictated by the patient and operative factors. These include:

• Use of neuraxial blockade. This has been associated with reduced risk of perioperative myocardial ischaemia and infarction. However, this must be balanced against the accompanying sympathetic block and associated hypotension, which may be pronounced, particularly with a high spinal block. Early judicious use of vasopressors, coupled with maintenance of intravascular volume, should limit this problem. However, neuraxial blockade, particularly spinal block, is relatively contraindicated if there is severely limited cardiovascular reserve and if maintenance of adequate arterial pressure is critical, such as in severe aortic stenosis.

• Effective perioperative analgesia. This is essential because pain is a potent stimulator of the stress response, and uncontrolled sympathetic activation increases myocardial work and oxygen demand, predisposing to myocardial ischaemia or infarction.

• Maintaining oxygenation, normocapnia and electrolyte balance at all times.

• Close attention to fluid balance. This begins preoperatively when fluid depletion secondary to factors such as excessive fasting times and bowel preparation should be corrected. As far as possible, euvolaemia should be maintained. Intravascular volume depletion is known to compromise organ perfusion and oxygen delivery, but there is increasing evidence that postoperative recovery is also compromised by excessive volume and sodium loading in the immediate perioperative period.

• Monitoring haemoglobin concentrations. Patients at high risk from cardiovascular disease do not tolerate anaemia. The optimal concentration of haemoglobin is the subject of much discussion but is probably around 100 g L ⁻¹ .

• Active patient warming to avoid hypothermia. Hypothermia activates the stress response, predisposes to arrhythmias and increases oxygen consumption postoperatively as a result of shivering.

Before embarking on anaesthesia and surgery, the patient's management and destination postoperatively should be planned; for example, would benefit be derived from a period of mechanical ventilation or continued close monitoring in HDU/ICU? Good communication between all the relevant clinicians, including anaesthesia, critical care, surgical and cardiology teams, is important.

General principles

• The patient's functional reserve is a good indicator of the severity of a valve lesion.

• Routine antibiotic prophylaxis is no longer recommended for all patients with valvular heart disease.

• Patients with valvular heart disease may be receiving anticoagulants; adhering to local bridging protocols is necessary.

• No specific anaesthetic technique is preferred for valvular heart disease. The aim is to maintain cardiovascular stability. In severe disease this is often best achieved using a general anaesthetic technique with opioids and controlled ventilation.

• Invasive monitoring is often required in these patients.

Aortic stenosis

Isolated aortic stenosis is associated most commonly with calcification, often on a congenitally bicuspid valve. In rheumatic heart disease, aortic stenosis occurs rarely in the absence of mitral disease and is combined usually with regurgitation. The diagnosis is suggested by the findings of an ejection systolic murmur, low pulse pressure and clinical and ECG evidence of left ventricular hypertrophy. It is important to distinguish between aortic stenosis and the murmur of aortic sclerosis found in some older patients. Clinical signs provide a guide: a slow-rising, low-volume pulse with reduced pulse pressure; reduced intensity of the second heart sound; and the presence of a click are suggestive of stenosis, as is evidence of left ventricular hypertrophy on ECG. However, echocardiography with Doppler flow monitoring is essential for confirmation and assessment of severity. The American Heart Association classification of aortic stenosis is shown in Table 20.3 . The heart size on chest radiograph is normal until late in the disease, whereas symptoms of angina, exertional syncope and left ventricular failure indicate advanced disease. Untreated severe symptomatic stenosis has a 50% 1-year survival rate.

Perioperative mortality is increased in patients with aortic stenosis. Left ventricular systolic function is usually good, but the hypertrophied ventricle has reduced compliance. Tachycardia and arrhythmias that compromise ventricular filling are poorly tolerated and should be avoided. In aortic stenosis, up to 40% of ventricular filling results from atrial systole; therefore, maintenance of sinus rhythm is important. Tachycardia also reduces the duration of coronary perfusion, compromising blood supply to the hypertrophied ventricle, particularly if there is concomitant coronary artery disease. The resulting myocardial ischaemia causes further cardiovascular deterioration, which may be catastrophic. Excessive bradycardia also compromises cardiac output. Adequate venous return must be maintained to ensure ventricular filling, and hypotension, which compromises coronary flow, must be avoided.

Mitral stenosis

Mitral stenosis is usually a manifestation of rheumatic heart disease. Characteristic features include AF, arterial embolism, pulmonary oedema (may be acute and precipitated by AF), pulmonary hypertension and right-sided heart failure. Patients with mitral stenosis who present for surgery are often receiving digoxin, diuretics and anticoagulants. Preoperative control of ventricular rate, treatment of pulmonary oedema and management of anticoagulant therapy (see Chapter 19 ) are necessary. During anaesthesia, control of heart rate is important. Tachycardia reduces diastolic ventricular filling and thus cardiac output, whereas bradycardia also results in decreased cardiac output because stroke output is limited. As with aortic stenosis, drugs which produce vasodilatation and neuroaxial block may cause severe hypotension. As a result of pre-existing pulmonary hypertension, patients are particularly vulnerable to hypoxaemia. Both hypoxaemia and acidaemia are potent pulmonary vasoconstrictors and may produce acute right ventricular failure. Thus opioid analgesics should be prescribed cautiously and airway obstruction avoided.

Aortic regurgitation

Acute aortic regurgitation (e.g. resulting from infective endocarditis) causes rapid left ventricular failure and may require emergency valve replacement, even in the presence of unresolved infection. Chronic aortic regurgitation is asymptomatic for many years. Left ventricular dilatation occurs, with eventual left ventricular failure. Patients with mild or moderate aortic regurgitation without left ventricular failure or major ventricular dilatation tolerate anaesthesia well. A slightly increased heart rate of approximately 100 beats min ⁻¹ is desirable because this reduces left ventricular dilatation. Bradycardia causes ventricular distension and should be avoided. Vasodilator therapy increases net forward flow by decreasing afterload and is useful in severe aortic regurgitation; isoflurane anaesthesia may be beneficial. Vasopressors should be avoided.

Mitral regurgitation

Leaflet mitral regurgitation usually results from infective endocarditis, rheumatic fever or mitral valve prolapse. Chordal or papillary muscle mitral regurgitation is more commonly secondary to ischaemia or MI. If occurring acutely, pulmonary oedema results and urgent valve replacement is required. Left ventricular failure with ventricular dilatation may cause functional mitral regurgitation. Chronic mitral regurgitation is commonly associated with mitral stenosis. In pure mitral regurgitation, left atrial dilatation occurs with a minimal increase in atrial pressure. The degree of regurgitation may be limited by reducing the volume of the left ventricle and the impedance to left ventricular ejection. Thus inotropic agents and vasodilators may be useful, whereas vasopressors should be avoided. A slight increase in heart rate is desirable unless there is concomitant stenosis.

Mitral valve prolapse

Mitral valve prolapse is most common in young women and may be an incidental finding in up to 5% of patients. It is associated with atypical chest pains, palpitations and embolic phenomena. Patients may be taking antiarrhythmic agents which need to be continued perioperatively.

Infective endocarditis

This is caused predominantly by the viridans group of streptococci, occasionally by gram-negative organisms or enterococci, and also by staphylococci, especially after cardiac surgery or in i.v. drug abusers. Coxiella burnetii also accounts for some cases. Patients with rheumatic or congenital heart disease, including asymptomatic lesions (e.g. bicuspid aortic valve), are at higher risk.

Hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy (HOCM) is a genetic cardiac disorder affecting 1 in 500 adults. There is a variable degree of ventricular muscle hypertrophy affecting mainly the interventricular septum. Patients may remain asymptomatic, or they may suffer dyspnoea, angina and syncope as a result of muscle hypertrophy and subsequent left ventricular outflow obstruction. Hypertrophic cardiomyopathy is also a cause of sudden cardiac death caused by arrhythmias. Diagnosis is confirmed by echocardiography. Anaesthetic issues include the following:

• Acute changes in volume status cause severe haemodynamic consequences, and hypovolaemia should be avoided.

• Outflow obstruction is exacerbated by catecholamines so inotropic agents should be avoided.

• Patients are usually receiving a β-blocker, which should be continued perioperatively.

• Patients with previous malignant ventricular arrhythmias are likely to have an ICD in situ.

History

Of the six cardinal symptoms of respiratory disease (cough, sputum, haemoptysis, dyspnoea, wheeze and chest pain), dyspnoea provides the best indication of functional impairment. Specific questioning is required to elicit the extent to which activity is limited by dyspnoea. Dyspnoea at rest or on minor exertion clearly indicates severe disease. A cough productive of purulent sputum indicates active infection. Chronic copious sputum production may indicate bronchiectasis. A history of heavy smoking or occupational exposure to dust may suggest pulmonary pathology.

A detailed drug history is important. Long-term steroid therapy (≥ prednisolone 5 mg day ^–1 or equivalent ( Table 20.4 )) within 3 months of the date of surgery necessitates augmented cover for the perioperative period (see later; Table 20.9 ); adverse effects include hypokalaemia and hyperglycaemia. Bronchodilators should be continued during the perioperative period. Patients with cor pulmonale may be receiving digoxin and diuretics.

Examination

A full physical examination is required, with emphasis on detecting signs of airway obstruction, increased work of breathing, active infection which may be treated preoperatively, and evidence of right-sided heart failure. The presence of obesity, cyanosis or dyspnoea should be noted. In addition, a simple forced expiratory manoeuvre may reveal prolonged expiration, and a simple test of exercise tolerance may be useful, such as a supervised walk test (see Chapter 19 ). Measurement of oxygen saturation provides a quick and useful indication of oxygenation; Sp o ₂ greater than 95% on air excludes significant hypoxaemia and, by inference, hypercapnia.

Investigations

These are discussed in Chapter 19 .

Effects of anaesthesia and surgery

The effects of anaesthesia alone on respiratory function are generally minor and short lived but may tip the balance towards respiratory failure in patients with severe disease. These effects include:

• mucosal irritation by anaesthetic agents;

• ciliary paralysis;

• introduction of infection by aspiration or tracheal intubation; and

• respiratory depression by neuromuscular blocking agents (NMBAs), opioid analgesics or volatile anaesthetic agents.

In addition, anaesthesia is associated with a decrease in functional residual capacity (FRC), especially in older and obese patients. This leads to closure of basal airways and shunting of blood through inadequately ventilated areas of lung, an effect which is magnified by inhibition of the hypoxic pulmonary vasoconstrictor reflex. After recovery from anaesthesia, residual concentrations of anaesthetic agents and the presence of opioids inhibit the hyperventilatory responses to both hypercapnia and hypoxaemia so that, without close monitoring with pulse oximetry and appropriate blood gas analysis, serious hypoxaemia and hypercapnia may occur. After thoracic and upper abdominal surgery, the decrease in FRC is more profound and persists for 5–10 days, with a parallel increase in alveolar–arterial oxygen tension difference. Complications, including atelectasis and pneumonia, occur in approximately 20% of these patients. The effects of surgery are dependent on its type and magnitude. Clearly, patients with pre-existing respiratory disease are at much greater risk after upper abdominal and thoracic surgery than after limb, head and neck or lower abdominal surgery.

The use of appropriate regional anaesthetic techniques, where possible, confers several advantages in patients with respiratory disease both intra- and postoperatively, including:

• avoidance of tracheal intubation and controlled ventilation;

• reduced or absent requirement for respiratory depressant agents such as volatile anaesthetic agents and opioids;

• effective analgesia, allowing the patient to undergo chest physiotherapy and take deep breaths thereby maintaining FRC. This may potentially reduce hypoxaemia.

Chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease is characterised by the presence of productive cough for at least 3 months in two successive years. Airways obstruction is caused by broncho­constriction which has minimal or no reversibility, bronchial oedema and hypersecretion of mucus. In the postoperative period, pulmonary atelectasis and pneumonia result if sputum is not cleared. Severe disease may be accompanied by the signs and symptoms of right-sided heart failure.

Preoperative management

The current state of the patient's disease is assessed by:

• history – frequency and severity of attacks, factors provoking attacks, recent episodes of infection, drug history;

• examination – presence or absence of wheeze, prolonged expiratory phase, overdistension, evidence of infection (cough, sputum, temperature, raised white cell count);

• pulmonary function tests – peak expiratory flow rate (PEFR) or forced expiratory volume in 1 s (FEV ₁ )/forced vital capacity (FVC) before and after inhalation of bronchodilator; and

• blood gas analysis, including changes in P a co ₂ to varying inspired oxygen concentrations.

Anaesthesia

The anaesthetic technique in obstructive airways disease should be guided by the nature of the surgery and also the severity of the disease.