define the fitness of the patient for the proposed anaesthetic and surgery

 delineate the level of risk of the procedure

 decide on the most appropriate anaesthetic technique

 assess the requirement for preoperative therapy to be initiated, for example β-blockade or blood transfusion

 assess the level of perioperative monitoring required

 decide on the patient’s postoperative management, including where this should take place.

 high-risk surgery (defined as intraperitoneal, intrathoracic or suprainguinal vascular surgery)

 ischaemic heart disease diagnosed either from the history or investigation

 congestive heart failure

 cerebrovascular disease

 insulin-dependent diabetes mellitus

 renal impairment (creatinine >177 μmol L^− 1).

History: Symptoms of cardiovascular disease include chest pain, dyspnoea, palpitations, ankle swelling and intermittent claudication. Past medical history and medical records usually reveal the nature and severity of disease, as many patients with cardiovascular symptoms will already have undergone relevant investigations.

Examination: Preoperative cardiovascular examination should include measurement of heart rate, arterial pressure and assessment of peripheral pulses and perfusion. Signs of heart failure should be sought, including a third heart sound, elevated jugular venous pressure and fine basal crepitations on auscultation of the lung fields. The heart should be auscultated for murmurs indicative of valvular disease. In particular, it is vital to make the diagnosis of aortic stenosis pre-operatively.

Testing the patient’s exercise capacity in the ward or on a flight of stairs is a simple, but useful, assessment of functional reserve. The inability to climb two flights of stairs indicates a very high risk of cardiopulmonary complications after major high-risk surgery.

Risk Stratification: Assessment of the patient’s risk of a perioperative cardiac event provides prognostic information. These issues may be discussed with the patient and appropriate written information provided. Adequate provision of information and the opportunity to ask questions has been shown to allay preoperative anxiety. Assessment also guides perioperative investigation and management.

In patients with an active cardiac condition defined as unstable coronary syndrome, decompensated heart failure, significant arrhythmias or severe valvular disease (Table 18.3), only emergency procedures should be considered. Elective procedures should be postponed for evaluation, testing and optimization of the patient’s active cardiac condition to minimize perioperative risk. The need for evaluation and further testing depends on the risks associated with a particular surgical procedure, the patient’s physiological reserve or functional capacity, and whether testing would change management. Patients undergoing low-risk surgery, or those with proven good functional capacity undergoing intermediate or higher risk surgery, can usually proceed to surgery. They will only require further invasive cardiac investigations if it would change management (i.e. they would require medical optimization or be a candidate for coronary revascularization) (Fig. 18.1).

For example, patients who have sustained a myocardial infarction (MI) within the 30 days before proposed surgery are a high-risk group. As a result of increased sympathetic stimulation and the coagulation activation secondary to surgery, such patients have a very high risk (up to 28%) of perioperative MI, which carries a high (10–15%) mortality. A history of uncomplicated MI more than 30 days before surgery is no longer considered an absolute contraindication to elective surgery, provided that the patient is symptom-free and has a good exercise capacity (see Table 18.1).

If there is no urgency for surgery however, it is best to wait until 3 months after MI when, if patients are asymptomatic with a good exercise capacity, they rejoin the low-risk group.

Asymptomatic patients who have undergone successful coronary artery bypass grafting more than 6 weeks before surgery constitute a low-risk group. Indeed, the mortality in this group is less than in a matched group with well-controlled angina on medical therapy. However, the risk of coronary artery surgery itself negates this benefit. It is therefore recognized that major cardiac interventions such as bypass grafting are indicated before non-cardiac surgery only if the patient’s underlying cardiac condition merits intervention for its own sake. This is the case for patients with severe triple vessel disease or significant left main stem stenosis.

Increasing numbers of patients now present for non-cardiac surgery having undergone percutaneous coronary interventions (PCI), particularly intracoronary stenting (ICS). Guidelines for the optimal perioperative management of these patients have been produced (Fig. 18.2). There are a number of important points. Firstly, it is beneficial to discuss the patient’s management with an experienced cardiologist. The risk of non-cardiac surgery in patients with intracoronary stents depends on the timing of surgery related to insertion of the stent and the type of stent used. Bare metal stents have been largely superseded by drug-eluting stents, which contain a cytotoxic agent. This is slowly released from the ICS to limit endothelialization, which reduces the incidence of thrombosis and stenosis within the stent itself. However, more prolonged and intensive antiplatelet therapy is required for drug-eluting stents because they are at increased risk of thrombosis until re-endothelialization has occurred. Following insertion of any ICS, there is an initial requirement for dual antiplatelet therapy (e.g. aspirin and clopidogrel). Non-cardiac surgery should be avoided during this time if possible. If antiplatelet therapy is stopped, the risk of stent thrombosis (which carries a 7% mortality) is high, while continuing therapy increases the risk of perioperative bleeding. The duration of dual antiplatelet therapy should be a minimum of one month after bare metal stents and up to 12 months for drug-eluting stents. It is recommended that even urgent surgery should be postponed for at least 4–6 weeks after ICS insertion, and elective surgery deferred for 3 months after bare metal stent, and for 12 months after drug-eluting stent insertion. If possible, even beyond these times, aspirin should be continued throughout the perioperative period, particularly because abrupt cessation of aspirin increases thrombogenicity. In the future, the possibility of bridging therapy with short-acting glycoprotein IIb/IIa inhibitors such as tirofiban may be considered.

As with coronary revascularization procedures, and due to the risks outlined, there is no place for prophylactic coronary stenting before surgery unless this is independently indicated for the cardiac condition.

Investigations: Standard investigations including haematology, biochemistry, an ECG and chest X-ray are necessary in all patients with proven or suspected cardiovascular disease. A coagulation screen may be indicated.

Subsequent investigations depend on the assessed risk for the patient and the clinical findings.

All patients found to have a murmur should have preoperative echocardiography. Significant aortic stenosis, for example, is associated with an increased risk of perioperative cardiovascular events and may be difficult to confirm and grade on clinical grounds alone. Echocardiography also provides useful information on left ventricular function.

Additional cardiovascular investigations are indicated only if they influence management. The incidence of asymptomatic coronary artery disease in the population is approximately 4%, and screening tests are unlikely to be helpful in patients with no cardiac symptoms. Patients with active cardiac conditions, in whom specific management of cardiovascular disease is indicated independent of the need for non-cardiac surgery, should undergo non-invasive cardiac testing, with or without coronary angiography and further treatment as indicated.

Between these two extremes lies a group of patients at increased risk of perioperative cardiovascular events in whom further assessment is indicated because perioperative care is influenced by the results. Moreover, accurate determination of risk to the patient may help decision-making with regard to the need for surgery and/or the type of operation and anaesthetic (Fig. 18.1).

Patients who should be considered for further pre-operative testing include:

The choice of preoperative test is dictated by local and patient factors, but commonly it includes exercise stress testing, dobutamine stress echocardiography and dipyridamole thallium scanning. Cardiological advice should be sought for both the test required and interpretation of the results with regard to predicting the perioperative risk of a serious cardiovascular event.

Pre-Existing Cardiovascular Disease: Ischaemic heart disease. Medical therapy should be reviewed and optimized if symptoms are poorly controlled.

Hypertension. Raised arterial pressure is a major cause of morbidity and mortality in the general population because of the detrimental effects on the myocardial, cerebrovascular and renal circulations. It is now recognized that both hypertension and isolated systolic hypertension should be treated because effective control of arterial pressure reduces the incidence of complications from target organ damage. The British Hypertension Society guidelines recommend starting antihypertensive therapy for sustained pressures above 140/90 mmHg. However, in the perioperative setting, there is little evidence that patients with isolated hypertension of less than 180/110 mmHg have a significantly increased risk of cardiovascular complications and isolated hypertension below this level is classified as a low-risk factor. If hypertension is identified preoperatively, evidence of target organ damage should be sought. If target organ damage is found, then the risks of anaesthesia and surgery are dependent on this. Subsequent investigation and management should be based on target organ function rather than on the hypertension per se. Postoperative follow-up and treatment are indicated.

For non-urgent surgery, patients with severe hypertension, i.e. > 180/110 mmHg, should be treated to lower the arterial pressure in a controlled manner before embarking on surgery. In the case of urgent surgery, more rapid control may be achieved. In light of their beneficial effects in high-risk cardiovascular patients, β-blockers are probably the agents of choice. Care must be taken, however, because rapid decreases in arterial pressure may be detrimental.

Antihypertensive therapy should be continued as far as possible throughout the perioperative period.

Many patients seen at preadmission clinic or admitted to hospital have hypertension which subsequently settles or which is not in keeping with the recordings made by their general practitioner. There is no evidence that so called ‘white coat hypertension’ carries an increased perioperative risk. Often, these patients benefit from a benzodiazepine premedication.

Heart failure. A history of treated heart failure and low left ventricular ejection fraction are intermediate clinical risk factors. Treatment should be optimized as far as possible pre-operatively and investigation of underlying coronary artery disease undertaken as appropriate, as outlined above.

Treatment and Additional Interventions: β-Blockers. Established β-blocker therapy should be maintained throughout the perioperative period either orally or intravenously if necessary. Sudden preoperative cessation may be associated with rebound effects such as angina, myocardial infarction, arrhythmias and hypertension. The dose of β-blocker may be reduced if there is undue bradycardia preoperatively (< 50 beat min⁻¹). Intraoperative bradycardia usually responds to intravenous atropine or glycopyrrolate. Some studies have shown that institution of perioperative β-blockade reduces short and long term cardiovascular morbidity and mortality in patients with definite evidence of ischaemic heart disease undergoing high-risk surgery.

These advantages are not seen in patients receiving chronic therapy and do not appear to be restricted to any particular β-blocker. Beta blockade should therefore be considered for these patients but the optimal time to begin therapy and the optimal duration of β-blockade are uncertain. In a non-urgent situation, it may be preferable to introduce β-blockade cautiously over several weeks, particularly if there is evidence of left ventricular dysfunction. It should be noted that several studies in lower risk patients (e.g. those with risk factors for ischaemic heart disease but no symptoms) have shown no overall benefit from perioperative β-blockade. In the POISE study, perioperative β-blockade actually increased the overall mortality and the incidences of stroke, bradycardia and hypotension.

Angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers. These agents have disease-modifying effects in patients with vascular disease, cardiac failure and diabetes, with a reduction in cardiac morbidity and mortality. They may predispose to renal failure and hyperkalaemia and may be associated with intractable intraoperative hypotension. There is currently no consensus as to whether or not these agents should be continued intraoperatively.

Antiplatelet agents. Aspirin and clopidogrel are used increasingly in combination to maintain vessel patency following percutaneous coronary intervention (PCI) and to reduce thrombosis in patients with unstable angina or recent MI. Both agents have irreversible effects on platelet action and their effect therefore continues for the life of the platelet. Aspirin inhibits cyclo-oxygenase-mediated production of thromboxane. Clopidogrel is a non-competitive antagonist of platelet ADP receptors. They have a synergistic effect in inhibiting platelet aggregation. Both agents need to be stopped for at least 7 days to see these effects reversed by new platelet production. Whether or not these agents are continued perioperatively depends on the perceived risk of bleeding against the increased risk of cardiovascular events. If the drugs are continued, both the surgeon and anaesthetist must be aware of the increased risk of haemorrhage and take appropriate anticipatory measures. Platelet transfusion is the only effective therapy for uncontrolled haemorrhage secondary to these agents.

In general, if a patient is anticoagulated (see below) or receiving clopidogrel, neuraxial blockade is contraindicated because of the increased risk of haematoma and neurological damage. Aspirin alone is not considered a significant risk factor.

Anticoagulants. Where long-term therapy is indicated, perioperative control must be monitored closely. Warfarin should be stopped at least 48 h preoperatively and the prothrombin time monitored daily. The prothrombin time should be less than 1.5 times control at the time of surgery. If prolonged, the use of vitamin K may be considered; however, this takes 6–12 h to act and may compromise subsequent anticoagulation, so its use depends on the reasons for anticoagulation. In an emergency or where excessive haemorrhage occurs, fresh frozen plasma should be given to supply coagulation factors. For patients at high risk from thrombosis, e.g. with a prosthetic heart valve, an intravenous heparin infusion should be started when the prothrombin time decreases and continued until 2 h preoperatively. After minor surgery with low risk of haemorrhage, warfarin may be restarted postoperatively. After major surgery, an infusion of unfractionated heparin should be used to maintain anticoagulation until warfarin therapy is reinstituted safely. The heparin infusion may be titrated to activated partial thromboplastin time (aPTT) to maintain good control and if necessary may be reversed rapidly with intravenous protamine. Protamine should be given slowly to avoid hypotension and if given in excessive dose is itself an anticoagulant.

Statins. Statins reduce morbidity and mortality in patients with vascular disease even in the presence of a normal cholesterol concentration. This is thought to result from stabilization of atheromatous plaques. There is also increasing evidence in patients undergoing high-risk vascular surgery that initiating statin therapy may reduce cardiovascular complications. The introduction of a statin preoperatively should therefore be considered in this group. Again, the optimal timing of this intervention is unknown but it has been suggested that therapy should be started 1 month before surgery.

α₂-Agonists. Drugs such as clonidine reduce sympathetic activity, reduce arterial pressure and heart rate and have analgesic properties. There is some evidence to suggest they may be of benefit in patients at high risk of perioperative cardiovascular events, but this is insufficient to recommend their routine use.

Continued administration mandates a greater degree of cardiovascular monitoring, particularly with regard to maintenance of intravascular volume. Vasoactive agents may be required to maintain an adequate arterial pressure.

Preoptimization. Measures to improve cardiac output and oxygen delivery have been shown to improve outcome in some high-risk patients with limited physiological reserve undergoing major surgery. These measures include monitored fluid therapy, vasoactive support, blood transfusion and mechanical ventilation, and are aimed at improving tissue oxygen delivery and hence oxygen delivery/consumption balance. The level of monitoring required, patient selection and the risk/benefit balance of increasing myocardial oxygen demand in the face of ischaemic heart disease, versus improving cardiac output and hence oxygen delivery, need to be considered on an individual basis.

This management strategy may be undertaken in a critical care area or in the anaesthetic room and requires close cooperation between relevant medical staff.

It is not known yet if combining preoptimization with preoperative therapy with agents such as β-blockers is helpful. However, the two approaches are not necessarily mutually exclusive.

Premedication: Anxiety is a cause of sympathetic nervous system activation which may be detrimental in patients with cardiovascular disease. While not all patients require anxiolytic premedication, there should be a low threshold for use in these patients. A benzodiazepine such as temazepam is usually satisfactory. In patients with low or fixed cardiac output states, e.g. mitral or aortic stenosis, constrictive pericarditis or congestive cardiac failure, and other high-risk patients, it is important to avoid hypotension or excessive sedation, respiratory depression and hypoxaemia which could result from premedication, and in these situations it may be preferable to omit sedative premedication.

The patient’s usual cardiac medications and any additional therapy started preoperatively should be continued and included in the premedication.

High-risk patients benefit from oxygen therapy before transfer to the anaesthetic room, especially if sedative premedication has been given.

 Anaesthesia should comprise a balanced technique aimed at maintaining cardiovascular stability. A variety of options may be suitable, including both general and regional anaesthesia or a combination.

 Tachycardia should be avoided and an adequate arterial pressure maintained (there should not be a sustained reduction in arterial pressure of more than 20% of the patient’s normal pressure). Coronary perfusion and myocardial oxygen delivery are thus maintained without increasing myocardial work and oxygen requirements.

 For patients identified as high risk, consideration should be given to stress reduction. Measures to achieve this are dictated by the patient and operative factors. These include the following:

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

 Patients should be well oxygenated and normocapnic.

 Close attention to fluid balance is mandatory. This begins preoperatively when fluid depletion secondary to factors such as excessive fasting times and bowel preparation should be corrected. As far as possible, normovolaemia 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.

 Patients at high risk from cardiovascular disease do not tolerate anaemia. The optimal level of haemoglobin is the subject of much discussion but is probably around 10 g L⁻¹.

 Patients should be actively warmed to avoid hypothermia, which activates the stress response, predisposes to arrhythmias and increases oxygen consumption postoperatively as a result of shivering.

 Effective perioperative analgesia is essential. 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.

 Before embarking on anaesthesia and surgery, consideration needs to be given to the patient’s management and destination postoperatively, e.g. would benefit be derived from a period of artificial ventilation or continued close monitoring in a high dependency or intensive care area postoperatively?

 Good communication between all of the relevant carers, including cardiology, critical care and the surgical team, is important.

Anaesthetic Agents: Most intravenous anaesthetic induction agents are cardiovascular depressants, causing both vasodilatation and myocardial depression. This is exaggerated in patients with low fixed cardiac output states and by concurrent hypovolaemia. Of the agents in regular use, etomidate is the least cardiac depressant. Care with dosing and rate of administration limits the hypotension caused by drugs such as propofol or thiopental. Co-induction with more than one agent may be beneficial in reducing the dose requirements of each and limiting hypotension. Concurrent administration of midazolam and a short-acting opioid (alfentanil or fentanyl) is often used. Remifentanil may be useful in these patients, in a low-dose infusion of 0.1–0.2 μg kg⁻¹ min⁻¹. It limits the dose of induction agent required and blunts the cardiovascular response to laryngoscopy and tracheal intubation. However, used in high doses, it may induce respiratory muscle stiffness and make bag and mask ventilation difficult before the onset of neuromuscular blockade.

For patients naive to β-blockers, esmolol (a short- acting i.v. β-blocker) may be used to obtund the cardiovascular response to airway manoeuvres.

Of the neuromuscular blocking agents, rocuronium and vecuronium are the most cardiostable.

Brief periods of cardiac ischaemia provide protection against the damaging effects of subsequent more prolonged episodes; this is known as ischaemic preconditioning. Much is now known about the physiology of this in experimental situations, including the fact that volatile anaesthetic agents and opioids help to induce ischaemic preconditioning, while other agents, e.g. the sulphonylureas, inhibit it.

There is clinical evidence of its relevance, e.g. patients with pre-infarct angina generally have a better prognosis than those who are asymptomatic, and this may be a result of preconditioning. The clinical application of these findings is as yet unknown, but may favour the use of volatile agents in this high-risk group.

 bradyarrhythmia unresponsive to atropine if associated with syncope, hypotension or ventricular arrhythmias

 risk of asystole

 complete heart block

 second-degree heart block (Mobitz 2)

 first-degree heart block associated with bifascicular block

 sick sinus syndrome.

Intraoperative Arrhythmias: Arrhythmias are common in the perioperative period and are often self-limiting and require no specific treatment. However, precipitants of these arrhythmias should be sought and corrected if possible as they are more likely to occur and cause cardiovascular compromise in patients with underlying heart disease.

Factors predisposing to intraoperative arrhythmias include the following.

Patient factors:

Autonomic effects:

Direct stimulation:

Drugs:

Management: This depends on the nature of the arrhythmia, likely causes and the degree of haemodynamic compromise.

Intraoperative Bradyarrhythmias: Bradyarrhythmias may often be prevented and may be treated using an intravenous anticholinergic, e.g. atropine or glycopyrrolate.

External pacing defibrillators are now widely available and can be used for temporary cardiac pacing for patients unresponsive to anticholinergics pending insertion of a transvenous pacemaker.

Intraoperative Tachyarrhythmias: These are either supraventricular or ventricular in origin. Generally, but not exclusively, supraventricular arrhythmias are narrow-complex, in distinction to broad-complex ventricular arrhythmias.

Supraventricular tachycardia. If there is haemodynamic compromise, the treatment of choice is synchronized DC cardioversion, particularly as the patient is already anaesthetized. This applies to all supraventricular tachyarrhythmias. If cardioversion fails, amiodarone 300 mg be given i.v. over 10–20 min and electrical cardioversion re-attempted.

If the patient is not severely compromised, management depends on the individual arrhythmia:

Permanent Pacemakers: Many patients with these devices have underlying heart disease which should be managed accordingly.

Permanent pacemakers are inserted in an increasing number of patients and are becoming increasingly complex. Pacemakers are classified by a series of 5 letters relating to the functions they possess (Table 18.4).

Specific Issues in Anaesthetic Management:

Implantable Cardioverter Defibrillators (ICDs): Increasingly, these devices are used for the management of patients with recurrent life-threatening episodes of VF and VT. ICDs may also have a pacemaker function. As with permanent pacemakers, they may be subject to electromagnetic interference and the same precautions apply.

The antitachycardia and defibrillator actions should be switched off before surgery involving diathermy. Diathermy could be interpreted as VF and a shock delivered unnecessarily. An external defibrillator must be available and the patient should be in a high-dependency area postoperatively until the ICD is checked and reactivated.

 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; perioperative heparinization 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.

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

 Outflow obstruction is exacerbated by catecholamines so that 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.

Chest X-ray: The preoperative chest X-ray is a poor indicator of functional impairment but may be indicated in certain situations:

ECG: This may indicate right atrial enlargement or right ventricular hypertrophy (P pulmonale in II; dominant R wave in III, V_1–3). Associated ischaemic heart disease is common, and ECG abnormalities may confirm this (Fig. 18.1).

Haematology: Polycythaemia occurs secondary to chronic hypoxaemia, while anaemia aggravates tissue hypoxia. Leucocytosis may indicate active infection.

Sputum Culture: Sputum culture is essential in patients with chronic lung disease or suspected acute infection.

Pulmonary Function Tests: Peak expiratory flow rate, forced expiratory volume in 1 s (FEV₁) and forced vital capacity (FVC) can be measured easily at the bedside. The FEV₁:FVC ratio is decreased in obstructive lung disease and normal in restrictive disease. In the presence of obstructive disease, the test should be repeated 5–10 min after administration of a bronchodilator aerosol to provide an indication of reversibility. An FVC < 1–1.5 L is indicative of limited ability to take large sigh breaths, expand lung bases and clear secretions by coughing.

Fuller investigation involves measurement of functional residual capacity (FRC), residual volume and total lung capacity, but these are rarely of value in determining clinical management.

Blood Gas Measurement: Arterial blood gas measurement is indicated in patients with chronic respiratory disease scheduled to undergo significant surgery and also if there is suspected acute hypoxaemia. It is also advisable when pulmonary function tests are markedly abnormal, e.g. in obstructive disease where the FEV₁ is less than 1.5 L. A raised PaCO₂ with normal pH indicates chronic hypercapnia with renal compensation; a combined raised PaCO₂ and acidosis indicates an acute event. Hypercapnia, particularly if acute, associated with acidosis, is likely to be associated with postoperative pulmonary complications. With a PaCO₂ of 6.7 kPa (50 mmHg) or greater, elective controlled ventilation may be required after major surgery. The combination of a low preoperative arterial oxygen tension (PaO₂) and dyspnoea at rest is also associated with a high likelihood of the need for planned ventilation after abdominal surgery.

 mucosal irritation by anaesthetic agents

 ciliary paralysis

 introduction of infection by aspiration or tracheal intubation

 respiratory depression by muscle relaxants, opioid analgesics or volatile anaesthetic agents.

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

The effects of surgery are dependent on its type and magnitude. Clearly, patients with pre-existing respiratory disease are at much greater risk following upper abdominal and thoracic surgery than after limb, head and neck or lower abdominal surgery.

Laparoscopic Surgery: The use of laparoscopic techniques for cholecystectomy, fundoplication and other abdominal procedures has markedly reduced postoperative pulmonary morbidity with the result that patients with severe pulmonary disease can usually undergo these procedures without the need for postoperative ventilatory support. The reasons for reduced morbidity include the relative lack of postoperative pain and the preservation of lung volumes postoperatively. These techniques should be encouraged in patients with chronic pulmonary disease. Nevertheless, cardiopulmonary function may be considerably compromised intraoperatively by raised intra-abdominal pressure, and judicious use of invasive haemodynamic monitoring has been recommended in patients with severe cardiorespiratory disease.

 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, WBC).

 Pulmonary function tests – peak expiratory flow rate or FEV₁/FVC before and after inhalation of bronchodilator.

 Blood gas analysis including changes in PaCO₂ to varying inspired oxygen concentrations.

An Approach with Minimal Intervention: Spontaneous ventilation with the option of local or regional anaesthesia is indicated for minor body surface operations. The use of a laryngeal mask airway (LMA) avoids tracheal intubation with its attendant risk of provoking bronchoconstriction, and if undue respiratory depression occurs, manifested by an increased PaCO₂, ventilation may be readily assisted via the LMA. Volatile anaesthetic agents, being bronchodilators, are well tolerated in asthmatics. Plexus blocks and low subarachnoid or epidural anaesthesia enable limb, lower abdominal or pelvic surgery in patients with severe respiratory impairment. Sedation should be administered carefully to avoid respiratory compromise.

Elective Mechanical Ventilation: A decision may be made to undertake intermittent positive-pressure ventilation (IPPV) during anaesthesia and for a variable period after operation, at least until elimination of neuromuscular blockers and anaesthetic agents has occurred. This also permits optimal provision of analgesia without fear of opioid-induced depression of ventilation. This technique is usually preferred if the preoperative PaCO₂ is greater than 6.7 kPa (50 mmHg) or if major thoracic or abdominal surgery is planned. Care should be taken with ventilator settings. A sufficiently long expiratory phase should be allowed to enable lung deflation and prevent gas trapping, while the inspiratory time should be adequate to avoid unduly high inflation pressures, with the attendant risk of pneumothorax.

Regional Anaesthesia: A combined general/epidural anaesthetic technique is often useful for major abdominal or thoracic surgery, as there is good evidence of a reduction in postoperative pulmonary complications with effective epidural analgesia. This approach may avoid a need for postoperative IPPV in some patients or may be usefully combined with noninvasive ventilation.

Anaesthetic Agents: Drugs which are associated with histamine release, e.g. atracurium and morphine, are perhaps best avoided, whilst rocuronium and fentanyl are preferred. β-Blocking drugs should also be avoided. If bronchospasm occurs during anaesthesia, it may result from easily remedied causes such as light anaesthesia or tracheal tube irritation and these should be corrected. If bronchospasm persists, nebulized salbutamol 2.5–5 mg should be administered into the anaesthetic breathing system and if this is not immediately beneficial, salbutamol 125–250 μg or aminophylline 250 mg should be administered by slow i.v. injection over at least 20 minutes, under ECG monitoring. The aminophylline dose should be modified if the patient is receiving oral theophylline. Thereafter, an infusion of aminophylline, up to 0.5–0.8 mg kg⁻¹ h⁻¹, or salbutamol, possibly in combination with nebulized salbutamol by positive-pressure ventilation (solution of 50–100 μg mL⁻¹ of water, run at 3–20 μg min⁻¹), should be maintained until improvement occurs. Hydrocortisone 200 mg i.v. should be given simultaneously, although it has no immediate effect. Inhaled volatile anaesthetic agents, e.g. sevoflurane, and intravenous ketamine have also been used with success when other agents have failed to relieve acute bronchospasm. Intravenous magnesium should also be considered in refractory cases.

Oxygen and Respiratory Care: Asthmatic patients rarely lose carbon dioxide responsiveness, and therefore high inspired oxygen concentrations are well tolerated and should be given. In patients with COPD, a controlled concentration of oxygen is generally required during spontaneous ventilation, using a 24% or 28% Venturi mask. Arterial blood gases should be checked frequently to ensure an adequate PaO₂ (> 8 kPa) without excessive carbon dioxide retention (PaCO₂ < 7.5–8 kPa). Using a pulse oximeter, the FiO₂ may be titrated to achieve an SpO₂ of around 90%. Hypoxaemia may seriously aggravate existing pulmonary hypertension and precipitate right ventricular failure.

Percutaneous cricothyroid puncture and insertion of a minitracheostomy permits aspiration of secretions while preserving the ability of the patient to cough and speak. This may be indicated postoperatively if sputum retention is a major problem.

The use of non-invasive respiratory support via a face-mask may be beneficial in the postoperative period. Non-invasive ventilation with a bilevel ventilator may aid carbon dioxide clearance and avoid postoperative invasive ventilation, or bridge the gap from invasive ventilation to spontaneous breathing. Face mask CPAP increases lung volumes and may prevent or treat lung atelectasis, with consequent improvement in oxygenation but without any significant effect on CO₂ clearance.

Techniques such as intermittent positive-pressure breathing (IPPB) supervised by a physiotherapist after surgery, can be used to expand the lungs and aid clearance of secretions. These techniques may also be effective if used and taught preoperatively in patients with large volumes of pulmonary secretions.

Analgesia: Simple, non-opioid analgesics and/or local and regional techniques should be used where possible. Non-steroidal anti-inflammatory drugs (NSAIDs) such as diclofenac or ibuprofen are useful in reducing the opioid requirements following major surgery and may be adequate on their own after minor surgery. However, NSAIDs may aggravate bronchospasm in some asthmatics as a result of increased leukotriene production. These agents should not be given to patients with a history of aspirin hypersensitivity or to asthmatics who have never taken NSAIDs previously. Opioid analgesics are best administered, where necessary, in small i.v. doses, under direct supervision, or using patient-controlled analgesia. Physiotherapy, bronchodilators and antibiotics should be continued postoperatively.

Sodium: Sodium retention occurs in renal failure, and through increased secretion of ADH, is associated with water retention, oedema and hypertension.

Hyponatraemia is also common in renal disease. It is the result either of sodium losses through the kidney or gastrointestinal tract, or of water overload causing dilutional hyponatraemia. The renal tubules may have a reduced ability to conserve sodium, e.g. in pyelonephritis, analgesic nephropathy or recovering acute renal failure, or sodium may be lost through diuretic therapy, vomiting or diarrhoea. Dilutional hyponatraemia is caused by either inappropriate fluid administration (glucose 5%), inappropriate ADH secretion, or both. Following transurethral prostatectomy, hyponatraemia may result from absorption of glycine irrigation fluid. Diagnosis of the cause of hyponatraemia involves measurement of urinary and plasma osmolality and urinary sodium concentration.

Potassium: Hyperkalaemia occurs typically in renal failure, frequently in association with metabolic acidosis. It causes delayed myocardial conduction and, if untreated, leads to cardiac arrest in asystole or ventricular fibrillation.

Hyperkalaemia should be treated promptly when the serum potassium concentration exceeds 6 mmol L⁻¹ or when ECG changes are evident:

Hypokalaemia occurs commonly in patients receiving diuretic therapy. These patients require preoperative measurement of serum potassium concentration and replacement if necessary. Hypokalaemia is associated with ventricular irritability, notably in patients taking digoxin.

Calcium: Retention of phosphate and vitamin D depletion (1,25-dihydroxycholecalciferol) in chronic renal failure lead to hyperparathyroidism. The development of a parathyroid adenoma leads to hypercalcaemia (tertiary hyperparathyroidism).

 a raised plasma renin concentration secondary to decreased perfusion of the juxtaglomerular apparatus results in hypertension through increased secretion of angiotensin and aldosterone

 fluid retention also causes hypertension by increasing the circulating blood volume.

 patients are frequently receiving concurrent medication for attendant problems, e.g. antihypertensive therapy

 many drugs are renally excreted; dosages require modification and plasma concentrations may require monitoring, e.g. aminoglycosides, digoxin

 some drugs have active metabolites which are renally excreted, e.g. morphine, midazolam. Dosage requires careful titration, or use of alternative agents should be considered, e.g. fentanyl, oxycodone

 some drugs adversely affect renal function, even in normal dosage. NSAIDs and the newer specific cyclo-oxygenase 2 inhibitors inhibit vasodilator prostaglandin production in the kidney and thus reduce glomerular blood flow and sodium excretion. This may be critical in septic or shocked patients, those with pre-existing renal dysfunction or those undergoing surgery associated with major blood loss. Their use should be avoided in such high-risk patients.

Treatment Regimens: Oral hypoglycaemic agents:

Insulins:

Insulin therapy is required by all type 1 diabetics and some type 2 patients. Most insulins in clinical use are now human insulins produced via recombinant DNA technology. The durations of action of insulin preparations vary:

Insulin is given by subcutaneous injection and the patient’s specific regimen is tailored to provide optimal glycaemic control. Often this is a twice-daily biphasic insulin injection. However, with the increasing requirement to achieve near normoglycaemia, more complex regimens are increasingly seen, e.g. a single ‘background’ injection of long-acting insulin with soluble insulin given before meals.

In well-controlled diabetic patients it is not usually necessary to change the insulin regimen on the day before surgery. Often, a change of regimen results in poorer control.

Acromegaly: Acromegaly is caused by increased secretion of growth hormone from eosinophil cell tumours of the anterior pituitary gland. If this occurs before fusion of the epiphyses, gigantism results. Problems for the anaesthetist include the following:

Treatment involves hypophysectomy which requires steroid cover preoperatively and steroid, thyroxine and possibly ADH replacement thereafter.

Cushing’s Disease: Cushing’s disease results from basophil adenomas, which secrete ACTH (see below).

Hypopituitarism (Simmonds’ Disease): Causes include chromophobe adenoma, tumours of surrounding tissues, e.g. craniopharyngioma, skull fractures, infarction following postpartum haemorrhage and infection. Clinical features include loss of axillary and pubic hair, amenorrhoea, features of hypothyroidism and adrenal insufficiency, including hypotension, but with a striking pallor, in contrast to the pigmentation of Addison’s disease (see p. 408).

The fluid and electrolyte disturbances are not as marked as in primary adrenal failure as a result of intact aldosterone production, but may be unmasked by surgery, trauma or infection. Anaesthesia in these patients requires steroid cover (pp. 408–409), cautious administration of induction agent and volatile anaesthetic agents, and careful cardiovascular monitoring.

Diabetes Insipidus: This is caused by disease or damage affecting the hypothalamic posterior pituitary axis. Common causes are pituitary tumour, craniopharyngioma, basal skull fracture and infection, or it may occur as a sequel to pituitary surgery. In 10% of cases, diabetes insipidus is renal in origin.

Dehydration with hypernatraemia follows excretion of large volumes of dilute urine. Patients require fluid replacement and treatment with parenteral vasopressin, or desmopressin, which can be also be given orally or intranasally.

Goitre: Thyroid swelling may result from iodine deficiency (simple goitre), autoimmune (Hashimoto’s) thyroiditis, adenoma, carcinoma or thyrotoxicosis. Nodules of the thyroid gland may be ‘hot’ (secreting thyroxine) or ‘cold’.

The goitre may occasionally cause respiratory obstruction. Retrosternal goitre may also cause superior vena caval obstruction. The presence of a goitre should alert the anaesthetist to the possibility of tracheal compression or displacement. A preoperative X-ray of neck and thoracic inlet may be useful, and a selection of small-diameter, armoured tracheal tubes should be available. Preoperative assessment of thyroid function is essential.

Thyrotoxicosis: This is characterized by excitability, tremor, tachycardia and arrhythmias (commonly atrial fibrillation), weight loss, heat intolerance and exophthalmos. Diagnosis is confirmed by measurement of total serum thyroxine, tri-iodothyronine (T₃) and TSH concentrations.

Elective surgery should not be carried out in hyperthyroid patients; they should first be rendered euthyroid with carbimazole or radioactive iodine. However, urgent surgery and elective subtotal thyroidectomy may be carried out safely in hyperthyroid patients using β-adrenergic blockade alone or in combination with potassium iodide to control thyrotoxic symptoms and signs. Emergency surgery carries a significant risk of thyrotoxic crisis. Control is best achieved in these circumstances by i.v. potassium iodide and a nonselective β-blocker (e.g. propranolol). If patients are unable to absorb oral medication, i.v. infusion is indicated (for propranolol, the daily i.v. dose is approximately one-tenth of the oral dose).

The doses of sedative drugs for premedication, and of anaesthetic agents, should be increased to compensate for faster distribution and elimination. Larger doses of sedative drugs than normal are required to avoid anxiety when procedures are carried out under regional anaesthesia.

Hypothyroidism: This may result from primary thyroid failure, Hashimoto’s thyroiditis, as a consequence of thyroid surgery, or secondary to pituitary failure. The diagnosis is suggested by tiredness, cold intolerance, loss of appetite, dry skin and hair loss. It may be confirmed by the finding of a low serum thyroxine concentration associated, in primary thyroid failure, with a raised serum TSH concentration.

Basal metabolic rate is decreased. Cardiac output is decreased, with little myocardial reserve, and hypothermia may be present. Treatment is with thyroxine, which should be started in a small dose of 25–50 μg daily. Rapid correction of hypothyroidism may be achieved using i.v. T₃, but this is inadvisable in elderly patients and those with ischaemic heart disease, which is common in hypothyroidism, as the sudden increase in myocardial oxygen demand may provoke ischaemia or infarction. ECG monitoring is advisable during treatment. Elective surgery should be avoided in myxoedematous patients, but if emergency surgery is necessary, close cardiovascular, ECG and blood gas monitoring is essential. Drug distribution and metabolism are slowed, and thus all anaesthetic agents must be administered in reduced doses.

Hypersecretion of Cortisol (Cushing’s Syndrome): Most instances are caused by pituitary adenomas which secrete ACTH and thus cause bilateral adrenocortical hyperplasia (Cushing’s disease). In 20–30% of patients, an adrenocortical adenoma or carcinoma is present. Rarely, an oat-cell carcinoma of bronchus, secreting ACTH, is the cause. ACTH and corticosteroid therapy present similar pictures. Clinical features include obesity, hypertension, proximal myopathy and diabetes mellitus. Biochemically, there is a metabolic alkalosis with hypokalaemia. Depending on the cause, treatment may involve hypophysectomy or adrenalectomy.

Anaesthetic management of these patients involves preoperative treatment of hypertension and congestive cardiac failure, and correction of hypokalaemia. Intraoperative management is directed towards careful monitoring of arterial pressure and maintenance of cardiovascular stability, with careful choice and administration of anaesthetic agents and muscle relaxants. Etomidate and atracurium or rocuronium would be an appropriate choice of induction agent and neuromuscular blocker, respectively. Postoperative steroid therapy is required for hypophysectomy and adrenalectomy (see below). Fludrocortisone 0.1–0.3 mg daily is required after bilateral adrenalectomy.

Primary Hypersecretion of Aldosterone (Conn’s Syndrome): Conn’s syndrome is caused by an adenoma of the zona glomerulosa of the adrenal cortex and presents with hypertension, hypernatraemia, hypokalaemia and oliguria. Anaesthetic management involves preoperative treatment of hypertension, administration of spironolactone and potassium replacement; meticulous intra- and postoperative monitoring of arterial pressure is essential.

Adrenocortical Hypofunction: Primary adrenocortical insufficiency (Addison’s disease) may be caused by an autoimmune process, tuberculosis, HIV infection, amyloid, metastatic carcinoma, or bilateral adrenalectomy. Haemorrhage into the glands during meningococcal septicaemia may cause acute adrenal failure in association with septic shock. Secondary failure results from hypopituitarism or prolonged corticosteroid therapy. In secondary failure resulting from pituitary insufficiency, aldosterone secretion is maintained, and fluid and electrolyte disturbances are less marked.

Clinical features include weakness, weight loss, hyperpigmentation, hypotension, vomiting, diarrhoea and volume depletion. Hypoglycaemia, hyponatraemia, hyperkalaemia and metabolic acidosis are characteristic but late biochemical findings. The stress of infection, trauma or surgery provokes profound hypotension. Diagnosis is made by measurement of plasma cortisol concentration and the response to ACTH stimulation.

All surgical procedures in these patients must be covered by increased steroid administration (see below). Patients with acute adrenal insufficiency require urgent fluid and sodium replacement with arterial pressure and CVP monitoring, glucose infusion to combat hypoglycaemia and hydrocortisone 100 mg 6-hourly i.v. They should be cared for in a high dependency or critical care area. Antibiotics are advisable to cover the possibility that infection has provoked the crisis. In cases of primary adrenal failure, mineralocorticoid replacement with fludrocortisone is required. If emergency surgery is required in acute adrenal failure, all precautions necessary for anaesthetizing the shocked patient should be taken (see Ch 37).

Congenital Adrenal Hyperplasia (Adrenogenital Syndrome): This is associated with overproduction of androgens as a result of deficiency of the hydroxylase enzyme required for production of cortisol. Hydrocortisone treatment overcomes adrenal insufficiency and, by suppressing ACTH production, decreases androgen accumulation. Augmented steroid cover is required for surgery in these patients.

Phaeochromocytoma: This is discussed in Chapter 31.

 reduced central drive, e.g. because of an impaired conscious level

 motor neuropathy, e.g. Guillain–Barré syndrome, motor neurone disease

 neuromuscular dysfunction, e.g. myasthenia gravis

 muscle weakness, e.g. muscular dystrophies

 rigidity, e.g. Parkinson’s disease.

Preoperative assessment:

Anaesthetic Management:

ECT is frequently undertaken in isolated units. However, the availability of monitoring, anaesthetic assistance and recovery facilities should be of an equivalent standard to those required for surgical patients.

Tricyclic Antidepressants: Tricyclic antidepressants, e.g. amitriptyline and dothiepin, inhibit reuptake of noradrenaline into the presynaptic nerve terminals. These drugs have the following side-effects:

Monoamine Oxidase Inhibitors:

Selective Serotonin Reuptake Inhibitors: These selectively inhibit serotonin reuptake, e.g. fluoxetine, sertraline. They have fewer cardiac and anticholinergic effects than tricyclic antidepressants and may cause CNS toxicity in conjunction with tramadol.

Phenothiazines: This is a broad group of drugs and their therapeutic actions and side-effects vary considerably, e.g. chlorpromazine, thioridazine, prochlorperazine:

Lithium: Lithium inhibits release and increases reuptake of noradrenaline:

 consideration of general versus regional anaesthesia

 how to secure and maintain the patient’s airway if a general anaesthetic is required

 vascular access

 steroid replacement where indicated

 positioning for surgery

 analgesia for a group of patients who may have significant preoperative pain and may be on regular opioids and other analgesics.

 Autonomic dysfunction, leading to attenuated baroreceptor reflexes and susceptibility to hypotension, impaired temperature regulation and impaired gut motility.

 Cognitive impairment, resulting in a reduced capacity to cope with new situations and increased likelihood of confusional states. This effect may be compounded by sensory deprivation associated with impaired hearing and vision.

 There is a loss of atrial pacemaker cells, resulting in an increasing tendency to develop atrial fibrillation.

 Maximum heart rate decreases and the elderly are increasingly dependent on increased stroke volume to increase cardiac output. This renders them more sensitive to hypovolaemia and reduced preload.

 Peripheral vascular resistance is increased as a result of loss of blood vessel compliance, and compensatory left ventricular hypertrophy is common.

 Catecholamine receptors are downregulated, resulting in a less predictable response to adrenergic agents used therapeutically.

 Closing volume increases and encroaches on tidal volume such that, when supine, significant shunting, hypoxaemia and later atelectasis may occur.

 Obstructive sleep apnoea is more common with associated episodes of desaturation and these episodes may be potentiated by opioid analgesia.

 Silent regurgitation and aspiration of gastric contents occurs more commonly.

 There is a progressive loss of functioning glomeruli and a resultant reduction in the ability to excrete or conserve sodium and water.