Intercurrent Disease and Anaesthesia
Many patients presenting for anaesthesia and surgery suffer from intercurrent disease and are often receiving a variety of medications. Many are elderly with limited physiological reserve, and may also be suffering from more advanced intercurrent disease. All these factors influence the conduct of anaesthesia and surgery and must be considered when assessing and managing a patient perioperatively.
It is increasingly recognized that physiological reserve is an important predictor of outcome from major surgery. Cardiopulmonary exercise (CPEX) testing is a useful tool to allow preoperative assessment of cardiovascular and respiratory reserve and the ability to withstand the stresses of major surgery. More simply, or where CPEX testing is unavailable, the capacity of the cardiorespiratory system to respond adequately to perioperative stress can be estimated in terms of metabolic equivalents (METs). If a patient has no major cardiac risk factors (see below) and can achieve more than 4 METs of activity without significant cardiorespiratory symptoms then the perioperative risk of an adverse cardiac event is low (Table 18.1). It may be possible to improve cardiorespiratory reserve before surgery in some patients. Knowledge of physiological reserve will guide the choice of anaesthetic technique, the level of monitoring used and the requirement for Level 2 or Level 3 care postoperatively.
|MET Score||Approximate Level of Activity|
|1||Dress, walk indoors|
|2||Light housework, slow walk|
|4||Climb one flight of stairs, run a short distance|
|6||Moderate sport, e.g. golf, doubles tennis or dancing|
|10||Strenuous sports or exercise|
Adapted from Fleisher LA, Beckman JA, Brown KA et al 2007 ACC/AHA guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 50:1707–1732.
This determines the level of physiological stress which the patient will experience. High-risk operations (cardiac morbidity > 5%) include aortic and other major vascular procedures; intermediate risk procedures include intraperitoneal, intrathoracic, major orthopaedic or urological surgeries, and also procedures anticipated to be prolonged and to involve significant fluid shifts and blood loss (Table 18.2). Following discussion with the patient and surgeon, it may be appropriate in some cases to consider alternatives to surgery or a less major operation if the patient is considered at too high a risk. In some cases the appropriate decision is not to undergo surgery.
|Risk Stratification||Procedure Examples|
|Vascular (reported cardiac risk|
often more than 5%)
|Aortic and other major vascular surgery|
Peripheral vascular surgery
|Intermediate (reported cardiac|
risk generally 1% to 5%)
|Intraperitoneal and intrathoracic surgery|
Head and neck surgery
|Low † (reported cardiac risk|
generally less than 1%)
Adapted from Fleisher LA, Beckman JA, Brown KA et al 2007 ACC/AHA guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 50:1707–1732.
All patients presenting for surgery should have a full clinical history and examination. Past medical history, including previous anaesthesia, regular medications and allergies (including food) are important. Previous anaesthetic records should be reviewed where available. Appropriate targeted investigations may then be planned.
The presence of coronary, cerebral or peripheral vascular disease defines a group of patients at increased risk from anaesthesia and surgery, manifesting as postoperative cardiovascular events such as myocardial ischaemia and infarction, arrhythmias, cardiac failure and in some cases death. Major surgery causes physiological stress leading to increased sympathetic activity, cardiac work and oxygen demand. Activation of coagulation and associated reduction in fibrinolysis leads to a prothrombotic state which predisposes to coronary thrombosis in some at-risk patients.
The presence of uncompensated left ventricular failure and a low left ventricular ejection fraction are also defined as active cardiac conditions. This is a result partly of the close association with coronary vascular disease and is also due to the resultant reduction in cardiac reserve. These should be assessed and treated before any non-emergency surgery.
Diabetes mellitus, a history of stroke, previous or treated heart failure and impaired renal function (creatinine > 177 μmol L− 1) are independent risk factors associated with perioperative myocardial ischaemia and infarction. The extent of preoperative testing required is dictated by the patient’s functional status and the type of intended surgery.
The Lee revised cardiac risk index for patients undergoing non-cardiac surgery identifies several intermediate risk factors (Table 18.3). The presence of two or more of these factors has been shown to identify patients with moderate (7%) and high (10%) risk of cardiac complications. There is evidence that this increased risk may continue for 6 months following surgery.
Active cardiac condition:
Unstable coronary syndrome (MI within 30 days, PCI within last 6 weeks)
Decompensated heart failure
Severe valvular disease
Intermediate Factors according to the Revised Cardiac Risk Index:
History of heart disease
History of compensated or prior heart failure
History of cerebrovascular disease
Adapted from Fleisher LA, Beckman JA, Brown KA et al 2007 ACC/AHA guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 50:1707–1732.
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).
FIGURE 18.1 Cardiac evaluation and care algorithm for noncardiac surgery based on active clinical conditions, known cardiovascular disease, or cardiac risk factors for patients 50 years of age or greater. *See Table 18.3 for active cardiac conditions. † See Table 18.1 for estimated MET level equivalent. ‡ Clinical risk factors include ischaemic heart disease, compensated or prior heart failure, diabetes mellitus, renal insufficiency, and cerebrovascular disease (Table 18.3). §Consider perioperative beta blockade for populations in which this has been shown to reduce cardiac morbidity/mortality. ACC/AHA indicates American College of Cardiology/American Heart Association. HR, heart rate; LOE, level of evidence; and MET, metabolic equivalent. (Adapted from Fleisher LA, Beckman JA, Brown KA et al 2007 ACC/AHA guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 50:1707–1732.)
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).
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.
FIGURE 18.2 Recommended timing of noncardiac surgery following percutaneous coronary intervention (PCI) depends on whether a stent was placed and the type of stent used. (Adapted from Fleisher LA, Beckman JA, Brown KA et al 2007 ACC/AHA guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery. J Am Coll Cardiol 50:1707–1732.)
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.
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).
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.
There are two main areas to be addressed. Pre-existing cardiovascular disease should be treated and management optimized where necessary. In addition, there may be interventions which, appropriately initiated in patients at risk, may improve outcome.
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.
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.
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.
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.
Use of neuraxial blockade. This has been associated with reduced perioperative myocardial ischaemia and infarction. However, this must be balanced against the sympathetic block and associated hypotension. This 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, e.g. severe aortic stenosis (see below).
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 (see Fig. 16.2).
Other minimally invasive cardiac output monitors are now available and may prove useful as intraoperative monitors. Examples include devices which derive cardiac output and other variables from the arterial pressure waveform using internal algorithms. Some devices (FloTrac/Vigileo or LiDCO) use a standard arterial catheter whereas others (PiCCO) require a dedicated thermistor tipped catheter in a proximal (femoral or axillary artery).
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.
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?
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.
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.
Preoperative arrhythmias should be treated before surgery. The patient should be screened for predisposing factors such as ischaemic or valvular heart disease and electrolyte and endocrine abnormalities. In atrial fibrillation, the ventricular rate should be controlled preoperatively if possible.
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.
Physiological abnormalities should be corrected, as specific antiarrhythmic therapy may be ineffective in the presence of uncorrected hypoxaemia, hypovolaemia or electrolyte abnormalities. Treatment of these should be concurrent with specific management of the arrhythmia.
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.
Atrial fibrillation. This is the commonest supraventricular arrhythmia seen intraoperatively. Often, a return to sinus rhythm cannot be achieved until the underlying precipitants are resolved. Improvements in oxygenation, volume status and analgesia may all improve the situation. However, ventricular rate control may also require treatment with either amiodarone or digoxin. Beta blockers or verapamil may also be used to slow ventricular rate. When surgery is complete, anticoagulation should be considered to avoid the embolic complications of atrial fibrillation.
AV node/AV re-entry tachycardia and atrial tachycardia. Vagal manoeuvres, e.g. carotid sinus massage, may be tried, as can intravenous adenosine. Adenosine transiently slows AV conduction and may convert supraventricular tachycardia (SVT) to sinus rhythm. Alternatively, it may aid diagnosis by revealing flutter or fibrillation waves. A rapid i.v. bolus of 6 mg is given, followed by 12 mg a maximum of three times at 2-min intervals. Adenosine is contraindicated in patients with asthma, second- or third-degree heart block, patients receiving carbamazepine or dipyridamole and patients with a denervated heart, e.g. after cardiac transplant. Care must be taken with its use if the patient has Wolff-Parkinson-White syndrome. Verapamil, β-blockers and amiodarone may control the ventricular rate. Intravenous verapamil should never be given to a β-blocked patient.
Ventricular tachycardia. Synchronized DC cardioversion is the treatment of choice. Alternatively, amiodarone (300 mg i.v. over 20-60 min, followed by an infusion of 900 mg over 24 h) may be given if the arrhythmia is well tolerated. Lidocaine 1 mg kg− 1 may be used as an alternative if amiodarone is not available, but should not be given if amiodarone has been given already.
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).
Preoperative assessment: the pacemaker clinic should be contacted to find out the indication for pacemaker insertion, its history and mode of action noted, and any evidence of malfunction sought. The underlying rhythm and rate should be determined and the consequences in case of pacemaker malfunction failure known to determine the need for backup support.
The main intraoperative hazards are electromagnetic interference, which may reprogramme the pacemaker, cause inappropriate inhibition or trigger a defibrillator discharge, or damage the pacemaker circuitry.
Due to the complexity of programming available, it is no longer acceptable practice to use a magnet to return the pacemaker to a fixed rate mode. Magnets should not be used, as they have an unpredictable effect on programming.
Some pacemakers have a rate modulation facility. This implies that they can vary the rate of pacing with the patient’s activity detected usually by muscle activity or respiratory activity so that heart rate may be increased with exercise. In general, rate modulation features should be inactivated before anaesthesia and surgery as shivering and muscle fasciculation may be misinterpreted and lead to inappropriate increases in heart rate.
Central venous or pulmonary artery catheters may dislodge pacing leads, particularly if the pacemaker has only recently been inserted. Consideration should be given to use of the femoral vein for central venous access and to alternative monitors of cardiac output.
Pacemakers should be routinely checked postoperatively either before discharge or via an early appointment at the pacemaker clinic. Electromagnetic interference may unpredictably reprogramme the pacemaker or cause damage to it.
Diathermy: bipolar diathermy should be used if possible. If unipolar diathermy is used, the diathermy and ground plate should be as far from the pacemaker as possible and the current pathway should be placed at right angles to the pacing wire(s).
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.
In both aortic and mitral stenosis, there is a low fixed cardiac output which leaves no reserve to compensate for changes in heart rate or vascular resistance. Regurgitant lesions are usually better tolerated.
As with ischaemic heart disease, specific intervention such as valve replacement or valvuloplasty is indicated before non-cardiac surgery only if the valvular lesion merits intervention anyway. Clearly, in an emergency situation, this is not an option.
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
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 elderly 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 heart size on chest X-ray is normal until late in the disease, while symptoms of angina, effort syncope and left ventricular failure indicate advanced disease.
Left ventricular systolic function is usually good but the hypertrophied ventricle has reduced compliance. Tachycardia and arrhythmias which compromise ventricular filling are poorly tolerated and should be avoided. Normally, 30% 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.
This is usually a manifestation of rheumatic heart disease. Characteristic features include atrial fibrillation, arterial embolism, pulmonary oedema, pulmonary hypertension and right heart failure. Acute pulmonary oedema may be precipitated by the onset of atrial fibrillation.
Patients with mitral stenosis who present for surgery are frequently receiving digoxin, diuretics and anticoagulants. Preoperative control of atrial fibrillation, treatment of pulmonary oedema and management of anticoagulant therapy (see Ch 13) are necessary. During anaesthesia, control of heart rate is important. Tachycardia reduces diastolic ventricular filling and thus cardiac output, while bradycardia also results in decreased cardiac output because stroke output is limited. As with aortic stenosis, drugs which produce vasodilatation may cause severe hypotension. As a result of pre-existing pulmonary hypertension, patients are particularly vulnerable to hypoxaemia. Both hypoxaemia and acidosis are potent pulmonary vasoconstrictors and may produce acute right ventricular failure. Thus, opioid analgesics should be prescribed cautiously, and airway obstruction avoided.
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.
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 beat 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. Careful monitoring is required, and in severe cases a pulmonary artery catheter may be useful to aid management.
Acute mitral regurgitation usually results from infective endocarditis, or myocardial infarction with papillary muscle dysfunction or ruptured chordae tendineae. Acute 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 pressure. The degree of regurgitation may be limited by reducing the size of the left ventricle and the impedance to left ventricular ejection. Thus, inotropic agents and vasodilators may be useful, while vasopressors should be avoided. A slight increase in heart rate is desirable unless there is concomitant stenosis.
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 intravenous 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 risk.
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. HOCM is also a cause of sudden cardiac death caused by arrhythmias.
Successful anaesthetic management of the patient with respiratory disease is dependent on accurate assessment of the nature and extent of functional impairment and an appreciation of the effects of surgery and anaesthesia on pulmonary function.
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 within 3 months of the date of surgery necessitates augmented cover for the perioperative period and may cause hypokalaemia and hyperglycaemia. Bronchodilators should be continued during the perioperative period. Patients with cor pulmonale may be receiving digoxin and diuretics.
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 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, e.g. a supervised walk up stairs.
ECG: This may indicate right atrial enlargement or right ventricular hypertrophy (P pulmonale in II; dominant R wave in III, V1–3). Associated ischaemic heart disease is common, and ECG abnormalities may confirm this (Fig. 18.1).
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.
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.