Hypotension

3 Hypotension DAVID A. SCOTT MICHAEL J. DAVIES

Hypotension is a word commonly used but poorly defined In a general sense hypotension can be defined as the blood pressure at which organ perfusion is inadequate, the problem is that there is considerable difficulty defining this level in normal patients and in patients with occlusive vascular disease The literature is full of different definitions. Many define hypotension as a change below a certain level of systolic blood pressure, usually 90 or 100 mmHg (Mangano et al, 1990; Davies et al, 1992), or a percentage change of 20 or 30% from a baseline level (Haggmark et al, 1989; Haku et al, 1989; Slogoff and Keats, 1989; Shah et al, 1990; Smith et al, 1991). The duration of change varies from 3 to 10 minutes (Haku et al, 1989; Mangano et al, 1990; MAP

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Clinical Anaesthesiology--

Vol. 7, No. 2, June 1993 ISBN 0-7020--1734--5

237 Copyright 9 1993, by Bailli~reTindall All rights of reproduction in any form reserved

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Davies et al, 1992). Clearly all these definitions are arbitrary and perhaps a more reasonable practical definition should be a fall in blood pressure to a level at which the anaesthetist would consider treatment necessary after assessing the relevant clinical situation. Blood pressure levels have traditionally been used as an assessment of organ perfusion because it is easy to measure. The correlation is, however, questionable, as Reinhardt (1988) showed when comparing blood pressure and oxygen transport (Figure 1). Fortunately, the brain, heart and kidney are protected by autoregulation, in which blood flow remains constant despite large changes of blood pressure. Cerebral and coronary blood flow remain constant down to a mean blood pressure of 60 mmHg and renal blood flow does not fall until mean arterial pressure falls below 70 mmHg (Hainsworth, 1985; McDowall, 1985). These statements about mean arterial pressures and flow only apply when autoregulation is intact and when arteries are not stenosed. The prevalence of arteriosclerosis in our patients is such that we cannot always assume that the arteries are not critically stenosed or that autoregulation is unimpaired by anaesthesia. This chapter will consider unexpected hypotension in the perioperative setting and not in other medical situations. Blood pressure is affected by the following factors (Reves, 1984): BP = CO • SVR CO = SV • H R where BP SVR HR CO SV

= = = = =

Blood pressure Systemic vascular resistance Heart rate Cardiac output Stroke volume.

Hypotension results from a change of one or more of these factors and thus our plan for diagnosis and treatment will be based on these fundamental considerations.

CAUSES OF INTRAOPERATIVE HYPOTENSION

Blood pressure is the end-result of the interaction between the heart (as cardiac output) and the vascular system (as vasomotor and venomotor tone). The relationship between the heart and the vascular system is intimately involved with the circulating fluid volume status. In addition to this, further complexity is added by vascular disease states such as atherosclerosis (decreasing arterial elasticity) or physical problems such as altered blood viscosity. In essence, the ultimate causes of intraoperative hypotension are low cardiac output and/or low systemic vascular resistance. The following discussion outlines some of the causes of intraoperative hypotension and specific treatments where relevant. It must be remembered, however, that in clinical practice a given causative factor may influence all components of the cardiovascular system in some way. Figure 2

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Figure 2, Mechanisms causing hypotension, with common examples listed,

summarizes the mechanisms which induce hypotension and includes some of the more common causes for each. Low systemic vascular resistance Systemic vascular resistance (SVR) is a measure of the resistance to the outflow of blood from the arterial tree. It is determined largely by the calibre of the arteriolar resistance vessels, unless factors such as critical atherosclerotic stenosis of more proximal arteries are more limiting in diseased vascular beds. In addition to arteriolar tone, blood viscosity is the other major factor that influences SVR measured in vivo. SVR comprises a large component of the resistance to ejection of blood from the ventricle at each beat (the afterload), although by no means the only component. For a given level of SVR, the blood pressure measured will be determined by the cardiac

240

D. A. SCOTT AND M. J, DAVIES Table 1. Intraoperative causes of low systemic vascular resistance.

Patient factors Vagal and vasomotor reactions A u t o n o m i c nervous system pathology

Patient medications Other Anaesthetic factors Sympatheticnervous systemimpairment Direct vasodilatation Surgical factors Autonomic reflex stimulation Postischaemic 'washout' Embolism (gas, etc.) Vasodilator chemicals Post cardiopulmonarybypass Other factors Endotoxin release Blood transfusionreaction Anaphylaxis Hyperthermia Histamine release Endogenous vasodilators

output and the elastance of the arterial tree. A classification of causes for low systemic vascular resistance is listed in Table 1. Although many of the factors that cause a low SVR may alter other components in the cardiovascular system as well (such as causing venodilatation or direct cardiac effects), this section will be confined to arteriolar effects. Patient factors

There are some patients in whom it is possible to identify an increased likelihood of intraoperative hypotension occurring. A past history of 'vasovagal' attacks may indicate a tendency to abnormal vagal or sympathetic vasodilator outflow ([32 or cholinergic fibres to skin and muscle) (Keane et al, 1991). This is most likely to be a problem while the patient is conscious, i.e. before induction of anaesthesia or during an operation under regional anaesthesia. Even though a patient is supine and unlikely to lose consciousness, he or she may still become hypotensive from such a cause. Other patients at risk include those with autonomic neuropathy, such as long-term diabetics (Charlson et al, 1990; Tarkkila and Kaukinen, 1991), patients with peripheral vascular disease and the elderly, and those with abnormal baroreceptor responsiveness, as in chronic hypertensives (Racle et al, 1989). In a study of 38 patients having elective eye surgery, 17 of whom were diabetic (15 requiring insulin), the diabetic patients required vasopressors in 35% of cases compared with 5% of the non-diabetic group (Burgos et al, 1989). Preoperative testing for autonomic dysfunction was strongly predic-

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tive for the occurrence of intraoperative hypotension. Bedside tests for autonomic nervous system function include the quantitation of sinus arrhythmia (Murray et al, 1975) and heart rate and blood pressure responses to Valsalva's manoeuvre or postural changes. It has long been noted that patient medications may interact with anaesthetic and surgical techniques to cause intraoperative hypotension by lowering SVR. The current commonly used antihypertensives which affect SVR include calcium antagonists, a-adrenergic blockers (e.g. labetalol, prazosin) and angiotensin converting enzyme (ACE) inhibitors. Hypotension associated with the use of these drugs can usually be countered with suitable agonists. Calcium intravenously reverses the negative inotropic effects of calcium antagonists, but not the effects on cardiac conduction (Harrimen et al, 1979). Unfortunately the effect of calcium is quite short lived, and it is also a venous irritant, so adrenergic agonists are probably more appropriate in most circumstances. Inhalational agents may also react, with calcium antagonists to affect cardiac conduction (see below). ACE inhibitors have been associated with profound refractory intraoperative hypotension in some case reports (Selby et al, 1989) and these effects can extend into the postoperative period (Russell and Jones, 1989). Also of concern is the situation when a patient taking ACE inhibitors receives plasma protein solution (i.e. stable plasma protein solution (SPPS)) as a plasma volume expander. The high levels of prekallikrein activator (PKA) in some preparations of this solution may lead to excessive endogenous bradykinin production, which causes potent direct vasodilatation (Young, 1990; Schiff, 1992). The combination of ACE inhibitor therapy and propofol use has also been associated with significant hypotension (Littler et al, 1989). Despite earlier opinions regarding the lack of interaction of ACE inhibitors with anaesthesia, it may be appropriate to withhold a patient's dose of ACE inhibitor on the day of surgery if blood pressure changes are of concern. Interestingly, in a number of the case reports of ACE inhibitorassociated hypotension, bradycardia was also a feature. Treatment is nonspecific, such as atropine and/or a vasopressor if needed in addition to volume loading. However, even aggressive therapy may not be very effective. Psychotropic drugs such as monoamine oxidase inhibitors may interact with certain anaesthetic agents to cause hypertension or hypotension. Traditional advice has been to withdraw these drugs at least 2 weeks preoperatively, but this approach has been recently questioned (Wells and Bjorkstein, 1989). Patients who have taken sufficient doses of exogenous steroids for a period of time may have suppression of stress-related endogenous steroid release and this may result in intraoperative or postoperative hypotension due to vasodilatation which is resistant to normal vasopressor therapy. Some of the newer high-dose inhaled steroids (e.g. beclomethasone in Becloforte) cause adrenal suppression if more than 1500 Ixg (six puffs) are taken per day. The real significance of ongoing or recent steroid therapy and surgical stress is unclear, but although the risk of perioperative collapse may be small it is probably worthwhile providing steroid 'cover' for a patient who has had

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steroid therapy within the previous 6-9 months (Roizen, 1986). Unfortunately, there are no straightforward tests for adrenocortical reserve. Minor surgical cases are best managed by the patient having the usual oral steroid early on the day of surgery, while more major cases will need 3 or more days of reducing dose steroid cover, starting with 200-300mg of hydrocortisone during the day of operation. If hypotension does develop in a steroid-dependent patient it will usually be due to a more common cause such as hypovolaemia, but if adrenocortical insufficiency is suspected then 100 mg of intravenous hydrocortisone should be given, and fluid and electrolyte support undertaken, including monitoring for hypoglycaemia. Other, less common patient-related causes for a low intraoperative SVR include rare endocrine causes such as carcinoid syndrome.

Anaesthetic factors Anaesthesia-related factors which may cause a fall in SVR are outlined in Table 2. A common cause of anaesthesia-induced vasodilatation is the sympathectomy induced by a regional block such as a subarachnoid or epidural anaesthetic. The effects are especially marked in the hypovolaemic patient Table 2. Anaesthetic factors capable of causing low systemic vascular resistance intraoperatively. Sympathetic nervous system blockade Regional block Spinal Coeliac/lumbar plexus Pharmacological Endogenous SNS outflow withdrawal Direct vasodilatation Pharmacological Volatile agents, especially isoflurane Vasodilator agents, e.g. sodium nitroprusside, glyceryl trinitrate Adverse drug effects, e.g. histamine release

(see below) or when other compensatory responses are obtunded, e.g. a high block (>T4 spinal level). Hypotension has been reported to occur in 16.4% of patients receiving subarachnoid anaesthesia in a prospective study of 1881 patients (Tarkkila and Kaukinen, 1991). It was found to be associated with increasing age and high sensory levels of anaesthesia. The peak incidence of hypotension occurred on average 19 minutes after lignocaine and 39 minutes after bupivacaine. The incidence of hypotension with spinal anaesthesia is probably higher than this, however, and Coe and Revan~is (1990) found a 60% incidence in elderly patients, which was not reduced by crystalloid preloading at up to 16 ml/kg. It is worth noting that there is evidence that hypotension induced by spinal anaesthesia is not always associated with decreased tissue perfusion and may be well tolerated even by chronically hypertensive patients (Sharrock et al, 1991). Other regional

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blocks such as coeliac or lumbar plexus blocks influence blood pressure by sympathectomy. Cervical plexus and other higher level blocks may cause hypotension by obtunding cardiovascular compensatory responses. Most anaesthetic agents cause direct vasodilatation to some extent. Of the intravenous agents, propofol is a more potent vasodilator than thiopentone (Harris et al, 1988), although neither is usually a problem in uncompromised patients. Propofol induces quite significant hypotension in hypovolaemic patients after a bolus intravenous induction. The mechanism of hypotension due to thiopentone is largely vasodilatation and myocardial depression, whereas propofol appears to cause inhibition of sympathetic activity and obtunds baroreceptor responses (Ebert et al, 1992). Ketamine has very little vasodilating effect, and the increase in central SNS sympathetic nervous system (SNS) outflow usually offsets any myocardial depression. The use of high-dose opiates generally results in a small degree of vasodilatation during induction but this is balanced by preserving myocardial function, enabling blood pressure to be maintained. The addition of benzodiazepines, however, may result in marked hypotension with an opiate-based induction technique (Tomicheck et al, 1983). Of the inhalational agents, nitrous oxide has the weakest vasodilating effect. Isoflurane is known to produce moderate to marked direct vasodilatation over 1 minimum alveolar concentration (MAC), usually offset by reflex heart rate increases, a-Adrenergic agonists have been reported to be effective in reversing the vasodilating effects of isoflurane. Halothane, while causing less vasodilatation, is vagotonic and results in more hypotension for a given MAC level. Enflurane lies somewhere between these two, although it and halothane are capable of significant myocardial depression which can have a significant effect on blood pressure and cardiac output (Quail, 1989). The induction of general anaesthesia p e r se causes a reduction in central SNS outflow from the awake state, which aggravates hypotension in the compromised patient. In patients with diabetic autonomic neuropathy, the most pronounced hypotensive events occurred in the period between induction of general anaesthesia and the surgical incision (Tarkkila and Kaukinen, 1991). There are many drugs which specifically induce vasodilatation, but of relevance to this discussion are those which result in unexpected vasodilatation and hypotension, through some adverse effect. The extreme example of an anaphylactic (or anaphylactoid) reaction results in a wide range of vasoactive mediators being released into the circulation which, amongst other effects, cause capillary leak and profound vasodilatation--largely Via a histamine mediated Hi-receptor effect. The most effective treatment for these reactions is incremental intravenous doses of adrenaline (0.1 mg aliquots) until the blood pressure responds, supplemented by fluid loading to compensate for the capillary leak. Adrenaline may have to be given over the next few hours by a slow infusion in order to maintain blood pressure. Lesser degrees of histamine release occur with basic drugs such as dtubocurarine, atracurium and protamine and are usually transient in nature. Slowing the rate of intravenous administration of these drugs can minimize their hypotensive effects.

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Surgical factors The manipulations of surgery may also cause vasodilation (Table 3). Stimuli to vagal afferents cause central inhibition of the vasomotor centre as well as stimulation of the dorsal motor nucleus of the vagus. Thus reflex hypotension from stimuli such as extraocular muscle traction, mesenteric traction or cervical dilatation is likely to have a vasodilatory as well as a bradycardiac component. Operations around the carotid sinus (eg carotid endarterectomy) may also cause hypotension, which may or may not be accompanied by a significant bradycardia. Table 3. Surgical factors capable of causing low systemic vascular resistance intraoperatively. Autonomic reflex stimulation Mesenteric traction Carotid artery dissection Postischaemic 'washout' Reactive hyperaemia Metabolite washout on tourniquet or arterial clamp release Vasodilator chemicals Papaverine Methylmethacrylate

Hypotension on tourniquet release following lower limb surgery is not uncommon, especially if there has been a long ischaemic time and the patient is hypovolaemic at the time. Vasodilator (and myocardial depressant) metabolites are washed out from the ischaemic limb (Stathopoulou et al, 1992), which is itself widely vasodilated (due to reactive hyperaemia). In aortic surgery, the release of the aortic cross-clamp can result in profound and prolonged hypotension. Adequate volume loading of these patients is essential before controlled declamping. Acid metabolites (e.g. lactate) are in high concentrations initially, especially after supracoeliac cross-clamping, so a dose of sodium bicarbonate (50-100 mmol i.v. ) immediately before limb and visceral reperfusion is useful to reduce their immediate systemic effects. Hypotension after cardiopulmonary bypass is often associated with low SVRs. This is partly due to the effects of changing from non-pulsatile to pulsatile perfusion, and also from the lowered viscosity of haemodiluted blood. Other factors include the patient's temperature at the time of weaning. The radial artery pressure is often at least 10% lower than the brachial or aortic root pressures at the time of weaning from bypass (Bazaral et al, 1990). Although the explanation for this is often given as 'vasospasm', it is more likely that it is due to an extremely low vascular resistance in the hand (Urzua, 1990). In any case, the discrepancy usually resolves within 20 to 30 minutes post-bypass. At various stages during an operation, vasodilator compounds may enter the circulation from the operative site. Methylmethacrylate monomer (Duncan, 1989), is a vasodilator and myocardial depressant which may be absorbed during cementing of joint prostheses, especially if the cement is

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not sufficiently 'cured' before placement. It is probable, however, that a large number of episodes of hypotension on insertion of the femoral prosthesis are due to air or fat embolism (see below). Papaverine injected into or around arteries to reduce vasospasm may also be absorbed and cause transient hypotension.

Other factors There are many other factors which need to be considered as causes for a low SVR. These include hyperthermia from any cause, including endotoxins and sepsis, pyrogen release and malignant hyperpyrexia. Reactions to blood and blood product administration may confuse the treatment of hypotension if a transfusion reaction should occur. Serious consequences may result if, for example, incompatible blood continues to be administered in order to treat the hypotension for which it is the cause. As mentioned earlier, acute and profound hypotension may be due to an anaphylactic or anaphylactoid reaction.

Low cardiac output There are a large number of factors which influence cardiac output; these are summarized in Table 4. Disturbances of heart rate and rhythm and reduction in stroke volume due to inadequate venous return are common causes of intraoperative hypotension.

Dysrhythmias Sinus bradycardia is a common event in certain types of surgery and anaesthesia, and may be triggered by excessive vagal stimulation (e.g. mesenteric traction, cervical dilatation, extraocular muscle traction) or by an imbalance of vagal and sympathetic outflow (e.g. high thoracic epidural) (Doyle and Mark, 1990). There has also been increasing concern over the last few years about the occurrence of sudden bradycardia and even asystole, especially during spinal anaesthesia (Caplan et al, 1988). Although oversedation and hypoxia have been proposed as predisposing factors, such bradycardic events continue to occur even in otherwise healthy, minimally sedated patients with records of normal continuous pulse oximetry (Mackey et al, 1989). Bradycardia occurred in 8.9% of patients studied by Tarkkila and Kaukinen (1991), including one episode which rapidly progressed to asystole. They found that the risk of bradycardia was greater with high sensory levels and younger patients. Arndt et al (1985) has suggested that a significant component of the sudden cardiac arrest in these patients is due to vagally mediated splanchnic vessel dilatation which results in acute preload reduction due to blood pooling. Bradycardia is particularly compromising to cardiac output when there is limitation to increasing the stroke volume, such as in left ventricular hypertrophy or valvular incompetence. It is clear that vigilant monitoring of heart rate is essential during spinal anaesthesia and that any downward trend must be watched closely, with a low threshold for intervention.

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Table 4. Factors capable of causing low cardiac output intraoperatively. Dysrhythmias

Sinus bradycardia Nodal rhythm Supraventricular tachycardia Atrial fibrillation Ventricular tachycardia Other Stroke volume reduction

Contractility impairment Ischaemia Drug effects Cardiomyopathy Other Left ventricle filling/ejection limitation Tamponade Valvular stenosis Acute mitral regurgitation Other Preload reduction Hypovolaemia (absolute) Blood loss ECF extravasation ECF deficit Vcnodilation Impaired venous return Caval compression Pregnancy Posture Raised intraabdominal pressure Direct pressure (packs/retractors) Central venous restriction High intrathoracic pressure Gas embolism

The contribution of synchronized atrial contraction to ventricular filling is well understood. It is particularly important in situations of decreased ventricular compliance, such as left ventricular hypertrophy, where atrial ejection may contribute up to 40% of the end-diastolic volume (Atlee, 1987). Hence, even the loss of P waves on the E C G because of a nodal rhythm may result in clinically significant hypotension in certain patients. Pancuronium in combination with halothane is known to be associated with an increased risk of heart block and nodal rhythm. The combination of : calcium antagonists and inhalational agents (notably halothane and enflurane) has been associated with atrioventricular conduction problems, including prolongation of the P - R interval and nodal rhythms (Reves et al, 1982; Hantler et al, 1987). Withdrawal of the volatile agent m a y be effective with time, or an infusion of isoprenaline can be used if a m o r e immediate response is needed. As noted earlier, calcium administration is ineffective in the m a n a g e m e n t of this problem.

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Tachyarrhythmias are also of consequence because of inadequate time for cardiac filling, and also increased risk of ischaemic ventricular dysfunction due in part to decreased coronary perfusion. Sinus tachycardia may result in decreased cardiac output if it is severe, or if there is a flow limitation to filling or ejection, as in mitral or aortic valvular stenosis.

Stroke volume reduction Cardiac output also falls as a result of stroke volume reduction, secondary to either decreased ejection fraction or inadequate ventricular end-diastolic volume. Myocardial contractility is impaired by drugs, toxins, myocardial ischaemia or with cardiomyopathy. Drugs are the most common cause of contractility impairment intraoperatively. The depressant effects of most anaesthetic agents are well known. The older volatile agents such as halothane and enflurane cause the majority of their hypotensive effects by direct myocardial depression, compared with isoflurane which decreases blood pressure mainly by vasodilatation. There is a reduction in myocardial (and cerebral) oxygen requirement associated with these agents (Quail, 1989) and, as a result, the decrease in tissue perfusion is often well tolerated at mild levels. The effect of these agents, as with the intravenous agents, is reversible as the drug levels fall. A more permanent effect is caused by some chemotherapeutic agents such as Adriamycin. A permanent reduction in stroke volume may result from treatment with doses over 550 mg/m2. This is a cumulative lifetime dose, and because cardiomyopathy may take weeks to develop after dosing, a preoperative echocardiogram is useful for patients at risk. If myocardial ischaemia is widespread it may be the primary cause of intraoperative hypotension. Often, however, ischaemia is secondary to the decreased coronary perfusion pressure associated with the hypotensive episode. Treatment of ischaemia in the presence of hypotension presents conflicting objectives. If the cause is a tachyarrhythmia then normalization of the rhythm may be effective. It is probably of more benefit to raise the coronary perfusion pressure to more normal levels with vasopressor agents than to administer agents such as glyceryl trinitrate, although glyceryl trinitrate may still be of value as a co-infusion to decrease preload and enhance diastolic relaxation (a positive lusitropic effect) (Thys and Kaplan, 1989). Many toxic factors (e.g. myocardial depressant factor) are released into the circulation on reperfusion of ischaemic tissue, such as the legs after tourniquet use or aortic surgery. Although the effect on the heart is generally short lived, it occurs at the same time as peripheral vasodilatation and makes pressure support at this time quite difficult to manage. Methylmethacrylate monomer from uncured orthopaedic cement also induces transient myocardial depression (see below). When cardiac failure is causing problems of low cardiac output despite adequate filling, and the cause is not readily reversible, then a positive inotropic agent such as adrenaline, dopamine or dobutamine may be useful. Pulmonary artery catheterization and full haemodynamic monitoring is necessary for optimal management of such patients. Although isoprenaline

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D. A. SCOTI" A N D M. J. DAVIES

is a potent inotrope, the rapid heart rates and reduced SVR induced by its [3-adrenergic effects make it unsuitable for use in the majority of situations. Left ventricular filling may be limited by external or internal factors. Cardiac output becomes rate dependent for most situations where physical filling restrictions exist. Chronic constrictive pericarditis decreases the margin of safety for contractility reduction by anaesthetic agents which would decrease the ejection fraction. In acute pericardial tamponade, filling pressures rise on both sides of the heart and heart rate rises. It is important to maintain preload and heart rate in this situation until the pericardium can be drained. Mitral valve stenosis limits the rate and force of left ventricular filling and is best managed by maintaining sinus rhythm (although these patients are often in atrial fibrillation) at a slow-normal rate, and keeping preload up. Inadequate filling is the main mechanism for decreased cardiac output with rapid atrial fibrillation and other tachyarrhythmias and so slowing of the rate with an agent like verapamil will often improve blood pressure and cardiac output, even though the drug has negative inotropic and vasodilatory properties. Aortic stenosis limits left ventricular ejection and results in a high pressure gradient between the ventricle and the aorta. Hypotension occurring in patients with severe degrees of aortic stenosis must be avoided, and treated promptly if it occurs, in order to prevent ischaemic contractile failure and cardiac arrest. Tachycardia may also precipitate hypotension in these patients, who need slow-normal rates. Preload reduction is most commonly caused by hypovolaemia or venous pooling. The presence of hypovolaemia makes patients very susceptible to changes in cardiovascular status. It should be corrected before epidural or subarachnoid anaesthesia or the use of any vasodilator drugs, especially in obstetric practice (Douglas, 1991). Reflex tachycardia may accompany hypotension induced by hypovolaemia, and may be quite marked in young adults. In older patients, those with some degree of autonomic neuropathy or those on [3-blocking medications tachycardia may not be present, and the degree of hypotension may be more severe. Hypovolaemia is one of the most common causes of moderate to severe hypotension intraoperatively, either alone or in conjunction with other aggravating factors. Knowledge of the nature of fluid loss or deficit is important in determining the correct fluid replacement. Blood loss may be easy to quantify if it is accurately scavenged, but concealed haemorrhage, as in multiple trauma patients, may be hard to estimate. Changes in measured haemoglobin concentration after acute haemorrhage will not accurately reflect the actual blood loss until the patient becomes euvolaemic, either through the passage of time with endogenous correction or with intravenous fluid replacement. Many procedures lend themselves to autologous blood salvage, cell washing and reinfusion. This is a great help in coping with red cell loss and avoiding homologous blood transfusion, but it must be remembered that the reinfused blood contains saline-suspended red cells only and so after massive blood loss, additional clotting factors (in the form of fresh frozen plasma) and platelets will have to be given. Haemorrhage in the presence of a high epidural or subarachnoid block is poorly tolerated. This is largely due to the

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disabling of haemodynamic compensatory mechanisms, including splanchnic arteriolar and venomotor tone, the importance of which has only recently been fully appreciated (Jordan and Miller, 1991). Deficits in the circulating fluid volume may also result from electrolyte and water loss (as in excessive diuresis, evaporative losses, etc.) or shifts of fluid through 'leaky' capillary beds. Cardiopulmonary bypass is associated with a marked capillary leak, and the phenomenon of 'third-space' fluid shifts accompanies most major surgery, especially intraabdominal procedures. Estimates of third-space losses extend up to 30ml kg -1 h - l f o r major bowel surgery. These losses need to be replaced with an appropriate amount of isotonic electrolyte solution, such as lactated Ringer's solution (Hartmann's solution). Replacement of blood volume loss with non-blood solutions is often desirable if a moderate degree of haemodilution can be tolerated. An acceptable minimal level of haemoglobin seems to be around 7 g/dl, which offsets the reduced oxygen content of the blood with reduced viscosity (Consensus Conference, 1988). The heart must be capable of increasing its cardiac output to cope with tissue demands, however, and so patients with severe ischaemic heart disease, cardiac failure or aortic stenosis should be maintained at a higher level of haemoglobin. Crystalloid solutions may be given, usually in a ratio of 3 ml crystalloid to replace 1 ml blood loss. This results in a euvolaemic state in the circulating blood volume after approximately 1 hour because the crystalloids distribute themselves to the extracellular fluid (ECF) with a half-life of around 20 minutes. The significance of this is that, although some tissue oedema occurs, more importantly the final equilibration will result in less than one-quarter of the given fluid remaining in the circulation, and any diuresis evoked by the lower colloid pressure will further reduce this contribution. Thus a patient who was adequately volume replaced early in a case may have a circulating fluid deficit and be hypotensive some hours later, despite having no further losses. Colloid solutions such as albumin (expensive), polygeline (half-life approximately 3 hours) or hydroxyethyl starch (half-life approximately 18 hours) are often used as alternatives to limit the amount of oedema, preserve colloid osmotic pressure and increase the duration of effect. The crystalloid versus colloid debate has been often argued (Davies, 1989), but the best strategy is probably to combine the two and replace ECF deficits with crystalloid and large blood losses with a colloid and homologous or autologous blood. Venodilatation causes reduced preload and will result in systemic hypotension if compensatory mechanisms are impaired. Drugs that cause direct venodilatation and arteriolar dilatation, such as glyceryl trinitrate, will lower venous pressure as well as arterial pressure, so the tissue perfusion pressure gradient will be better preserved than with a predominant arteriolar dilator such as sodium nitroprusside. The reduced preload caused by withdrawal of sympathetic venomotor tone with intraspinal regional blockade is a major component of the hypotension associated with lumbar epidural or spinal anaesthetic techniques. Management with volume loading may be effective, but if a vasopressor is required then one which exerts a distributive effect by increasing venous tone is desirable (Table 5). Phenylephrine and

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noradrenaline both have potent, but short-lived, venomotor effects (Pincus and Magitsky, 1989). Ephedrine is slightly less effective as a venoconstrictor but the additional ~-sympathomimetic effects make it useful for management of hypotension associated with high blocks. With thoracic epidural anaesthesia, preload reduction is combined with cardiac sympathetic blockade, causing a decrease in baroreceptor-induced heart rate increases in response to hypotension and decreased contractility. Systemic hypotension is common in these patients despite fluid loading , especially when general anaesthesia is combined. In a study of 20 vascular surgical patients having thoracic epidural anaesthesia and general anaesthesia, ephedrine was compared with phenylephrine using transoesophageal echocardiography to assess myocardial performance for the same degree of blood pressure support (Samain et al, 1990). Heart rate was lowered with phenylephrine (50 _+8 beats/rain) and stroke volume was reduced (ejection fraction area = 51 + 14%). With ephedrine, however, heart rate was maintained (65 _+ 16 beats/min) and stroke volume was not decreased (ejection fraction area -- 60 _+ 13%). This suggests that ephedrine would be the vasopressor of choice in these patients because of preservation of heart rate and inotropy, thus maintaining cardiac output. Metaraminol has a more pronounced arteriolar constrictive effect than ephedrine, and it has a weak venomotor effect. With all the predominant o~-agonists there is a likelihood of a reflex reduction in heart rate in response to the induced rise in blood pressure. In patients who are already bradycardic (i.e. heart rate <60 beats/min) this may result in an elevated perfusion pressure but a decreased cardiac output, and hence decreased tissue perfusion. Ephedrine is also indicated for the treatment of hypotension during epidural anaesthesia in obstetrics (once appropriate volume loading has been completed) because it preserves uterine blood flow. It is important to consider impaired v e n o u s return as a cause of hypotension during surgery. Posture alone, such as placing patients in the reverse Trendelenburg position, reduces venous return. Postures such as the kneechest or lateral position with kidney-rest elevation may cause compression of the inferior vena cava. The inferior vena cava is susceptible to extrinsic compression from a number of other causes. The caval compression syndrome of late pregnancy, with uterine compression of the inferior vena cava when lying supine, can be averted by transporting these patients on their side and placing a wedge under their hip when on the operating table to maintain a 15~ lateral tilt during the procedure.

HYPOTENSION

251

High intraabdominal pressures will also compress the inferior vena cava, and the use of laparoscopic surgery requires the anaesthetist to be vigilant with regard to the amount of gas infused and the pressures obtained. Of course, any abdominal surgery may result in direct compression of the inferior vena cava with hands, packs, or retractors. Venous gas embolism may occur as a result of laparoscopic gas insufflation into a vessel or secondary to spontaneous aspiration into an open vein which is above the height of the right atrium. Classically, the sitting neurosurgical position places patients at risk from such a problem, but central venous catheter insertion, pelvic surgery and even varicose vein surgery have been associated with venous air embolism. Clinical manifestations include hypotension and tachycardia and diagnosis is usually made initially by clinical suspicion or the presence of a rapid fall in end-tidal carbon dioxide. Precordial Doppler monitoring and pulmonary artery pressure monitoring are also of value in diagnosis. The use of a precordial or oesophageal stethoscope may also detect the 'mill wheel' murmur of a large venous gas embolism. Management includes prevention of further gas entry (ceasing insufflation, placing a damp pack over the wound), positioning the patient to prevent passage of gas into the right ventricle (left lateral) if possible, and attempted aspiration of gas via a central venous catheter positioned in the right atrium. Supportive therapy may also be necessary. The use of positive end expiratory pressure (PEEP) has also been suggested in order to increase central venous pressure and thus decrease gas entry into the venous system. Venous embolism of amniotic fluid (during caesarian section) or fat (femoral shaft surgery) can cause acute cardiovascular collapse. Hypotension on insertion of the femoral prosthesis during hip surgery is often attributed to an effect of the methylmethacrylate monomer on the circulation, but there is evidence to suggest that venous fat or air embolism is quite common at this stage. Techniques for minimizing air pockets or venting the femoral shaft cavity during insertion may help decrease this effect (Evans et al, 1989). High intrathoracic pressure will obstruct venous return and may reduce cardiac output, resulting in hypotension. The extreme physiological example is Valsalva's manoeuvre which causes hypotension, leading to compensatory vasoconstriction and tachycardia when an intrathoracic pressure of more than 20 cmH20 is sustained for a period of time. High tidal volumes or the use of PEEP during mechanical ventilation may therefore result in hypotension, and inspiratory pressures should be checked after connection to a ventilator or after a change of posture to ensure they are not excessive. Hypovolaemia makes the effects of positive pressure ventilation even more obvious, Cyclic variations in blood pressure with respiration have long been noted, for example the pulsus paradoxus associated with severe asthma resulting in a fall in systolic pressure with large negative inspiratory pressures. During positive pressure ventilation there may also be a variation in systolic presure, with a transient increase in pressure during inspiration due to increased venous return to the left ventricle from the compressed pulmonary circulation and decreased afterload because of a decreased transmural pressure gradient for the left ventricle and aorta. This is followed

252

D. A. SCOTT AND M. J. DAVIES

later in the inspiratory cycle by a fall in systolic pressure due to impairment of venous return by the continued positive intrathoracic pressure. During expiration, right ventricular output is augmented by the increased peripheral venous return, but blood fills the pulmonary vessels initially and so systemic arterial pressure recovery is delayed. This effect is much more marked during hypovolaemia, and there have been recent attempts to quantitate these changes and use systolic pressure variations as an aid to assessment of volume and cardiac status (Pizov et al, 1990).

CONFIRMED HYPOTENSION I 'q~l~"

Ensu~Oxygen.4drrmislra~on

E.C.G.

.

,MMED,ATE 1

SUPPORTIVE[ MEASURES J

~

Rx

A~IYA~e

I 9 Decreaseor CeaseMyocardialDepressanlDrugs I 9 IncreaseVenous Return: Elevate Legs or Head-down tilt 9 I.V. Fluid Bolus (if not oontraindicated) 9 Vasopressorsif Critical : F_.pheddne(esp. ff HR < 60) Mataraminol/ Phenylephrine Adrenaline 'if suspect Anaphylaxis) 9 EPIDURAL or SUBARACHNOID Block ?

I

CONSIDER 1 CONTEXT

I

CONSIDER I tYPOVOLAE~

- is timing appropriate to dosing ?

9 RecentDRUGADMINISTRATION ? 9 CheckforSURGICALCAUSES

- rate and degree of blood loss - obstructionto venous return - toumiquat/ vascular clamp release embolism/ toxins -

9 Recentconnectionto VENTILATOR ?

t

- cheo~ airway pressures

Figure 3. Intraoperative hypotension m a n a g e m e n t overview. @, return to start of algorithm.

HYPOTENSION

253

MANAGEMENT OF INTRAOPERATIVE HYPOTENSION The management of hypotensive episodes during anaesthesia is not always simply a matter of giving a dose of a vasopressor or a bolus of intravenous fluid. Deciding on the most appropriate course of action, or indeed whether any action is required, depends on knowledge and evaluation of the context in which the hypotensive episode is occurring. The context may relate to patient factors, anaesthetic factors and/or surgical factors. It will be assumed

BALANCE II 9FLUID Deficit Pre Operative

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HYPOTENSION

: C mVip( / J.VmPm

Heart Rate increase Urine Output decrease (ideally> 0.5 ml/kg/hr) Peripheral Vasoconstriction Systolic Pressure Variation with I.P.P.V.

s~ Tab;r 6

254

D. A. SCOTT A N D M. J. DAVIES

for the purposes of this discussion that a threshold has been crossed such that the state of the patient's blood pressure requires some active intervention. In the preceding section, a detailed listing of causes of hypotension during surgery and anaesthesia was provided, together with a description of the management of some specific situations. The use of a structured approach to the assessment of the cause for hypotension may seem superfluous in most instances, but in practice the above context-related factors are what are used in the initial clinical assessment of the most probable cause and hence the initial therapy. For example, a drop in blood pressure a few minutes after placement of a subarachnoid block would be most likely to be related to anaesthetic factors. The time-course and degree of the hypotensive event is also relevant, and in some circumstances supportive therapy may need to be initiated before a definitive assessment of a cause can be made and appropriate specific therapy given, e.g. the use of a vasopressor to support perfusion pressure until adequate volume replacement could be achieved. A flowchart for the management of intraoperative hypotension is provided in Figure 3. This chart deliberately differs in content and detail from that of Figure 2 and the tables in the preceding section. The purpose of the chart is to provide an algorithm for the clinical management of an intraoperative hypotensive event, reflecting the realities of clinical practice. Validation of the blood pressure reading will usually need to be done, especially if the monitoring device is a non-invasive (oscillotonometric) blood pressure machine. Extraneous movement of the patient or tubing or disturbances of cardiac rhythm may result in erroneous readings. Independent validation by manual sphygmomanometer is worthwhile before initiating significant therapy. Even intra-arterial cannulas will be inaccurate if the transducer height is incorrect or the signal becomes damped. As noted earlier, radial arterial pressures may read significantly lower than aortic or brachial arterial pressures after cardiopulmonary bypass. Heart rate and rhythm should be checked in the process of blood pressure validation. Dysrhythmias, especially bradycardia, are a common cause of hypotension, or contribute to it, and require specific treatment to correct a low cardiac output. At this time, the (correctly calibrated) ECG should be carefully examined for the loss of P waves (indicating a nodal rhythm) or ST segment depression or elevation (indicating myocardial ischaemia). Oxygen should be administered (if not already started), and oxygenation verified with pulse oximetry if possible. Unfortunately, distal perfusion is often impaired in cold or hypotensive patients and it may be difficult to obtain a good pulse amplitude for an accurate pulse oximeter reading. A patient with severe hypotension should be given as close to 100% oxygen as possible. Immediate blood pressure support may be required, especially if the blood pressure fall is precipitate or profound. An immediate response is also required if the patient has a critical need for blood pressure maintenance, such as in pregnancy, severe aortic valve or coronary artery disease, or during carotid artery surgery. At this stage, a rapid appraisal of the context may lead to specific therapy, e.g. obvious massive surgical blood loss, overdistended pneumoperitoneum, recent subarachnoid block, etc. Supportive

HYPOTENSION

255

measures are listed in Figure 3. The choice of vasopressor relates to the discussion earlier. If the hypotension is rapid and severe it may be due to an anaphylactic or anaphylactoid reaction, especially if associated with bronchospasm or flushing of the skin. In this case adrenaline is the drug of choice. If time and the degree of assistance permits, it is useful to take a blood sample during the acute phase for histamine and complement levels to aid in the later diagnosis of the episode. Context has already been mentioned. This is usually an unconscious assessment by the anaesthetist, but it is vital if a rapid diagnosis is to be made so that specific therapy is to be given. Check for common anaesthetic causes, including recent drug administration, the 'left on' vaporizer and hyperventilation with high inspiratory pressures. Looking over the drapes and checking on current surgical activity can be very rewarding. Knowledge of the patient's history and current medical status and drug therapy is also important. Hypotension induced by spinal anaesthesia may be prevented by gradual titration of the block (epidural or subarachnoid catheter) or fluid preloading. Although Coe and Revan~is (1990) found no benefit in elderly patients, fluid preloading is considered worthwhile in obstetric patients having spinal anaesthesia for caesarian section. The incidence of hypotension reported ranges from 0 to 45% of obstetric patients receiving differing types and volumes of fluid preloads, although there is no consensus regarding whether colloid is better than crystalloid (Murray et al, 1989). In general, a minimum of 1 litre preload of isotonic electrolyte solution would be considered appropriate. Hypovolaemia, either absolute or relative, is probably second only to the effects of anaesthetic drugs as a cause of intraoperative hypotension. Evaluation of the patient's fluid balance status, and appraisal of volume-related and perfusion-related clinical indicators should suggest hypovolaemia as a likely cause. The commonly used parameters such as heart rate or blood pressure may be misleading, and in young patients blood pressure changes occur late. Central venous pressure (CVP) monitoring is often used as a guide to volume status, but it is only monitoring preload to the right ventricle and so may not reflect left ventricular filling status in the presence of myocardial impairment. The presence of a pulmonary artery catheter avoids the limitations of CVP monitoring, making preload assessment much more accurate, and enables titration of therapy but it does not preclude other clinical observations nor the maintenance of accurate fluid balance assessments. The choice of which fluid to use for volume replacement depends on many factors, including the nature of the fluid deficit, the current rate and composition of fluid or blood loss, the circulatory status, recent fluid administration history and current haemoglobin levels. Having proceeded to this point, the majority of patients will have the cause of their hypotension correctly diagnosed and will be responding to appropriate therapy. There are some situations, however, where the response to appropriate therapy is inadequate or non-specific therapy is needed because of the lack of an identifiable aetiology. Refractory hypotension presents the difficult situation where, despite what seems to be adequate therapy and an appropriate amount of time for it

256

D . A . SCOTT AND M. J. DAVIES Table 6. Causes of refractory hypotension. Anaphylactic or anaphylactoid reaction Occult surgical cause Caval compression (see Table 4) Concealed haemorrhage Gas embolism Complicating Patient Factors Drug related Blockade of Autonomic Pathways e.g. [3-Blockers c~-Blockers ACE inhibitors Calcium channel blockers Exogenous steroid use Autonomic neuropathy Myocardial dysfunction Tension pneumothorax Myocardial tamponade Undiagnosed valvular stenosis Anaesthetic factors Extensive sympathetic block Drug administration error

to work, a patient's blood pressure still remains low. Table 6 lists some causes for refractory hypotension. Hypotension cannot be considered to be refractory unless it is clear that the heart rate and rhythm are appropriate. In this circumstance, a systematic search for supportive evidence for specific problems will help to narrow the list down. If possible, identification of the primary physiological disturbance will help to define the problem, and persistent severe hypotension requires more monitoring information, e.g. pulmonary artery and wedge pressures, cardiac output, intra-arterial pressure monitoring and blood gas, acid-base and electrolyte analysis.

CONCLUSIONS

Hypotension is a common intraoperative problem. It is usually apparent from the context of the situation what the cause is, and what is the most appropriate action to take. There are many preventive strategies which can be taken to reduce the occurrence of this problem, including adequate volume loading before and during regional anaesthesia or before aortic declamping, and avoidance of certain drug combinations. When the cause of intraoperative hypotension is not obvious, then an understanding of the possible physiological mechanisms involved is essential, and a review of patient, anaesthetic and surgical factors may lead to a diagnosis and specific therapy.

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257

SUMMARY H y p o t e n s i o n r e q u i r e s t r e a t m e n t w h e n o r g a n p e r f u s i o n is i n a d e q u a t e or at risk. T h e t h r e s h o l d for i n t e r v e n t i o n is t h e r e f o r e d e p e n d e n t o n a n u m b e r of e l e m e n t s , i n c l u d i n g the p a t i e n t ' s vascular status a n d the causative factors. H y p o t e n s i o n is caused by either a r e d u c t i o n in systemic vascular resistance or a decrease in cardiac o u t p u t , which in itself can b e d u e to i n a d e q u a t e stroke v o l u m e or a b n o r m a l rate or r h y t h m . T h e causes of these changes are discussed in the f r a m e w o r k of p a t i e n t , a n a e s t h e t i c a n d surgical factors. A g e n e r a l clinical a p p r o a c h to diagnosis a n d m a n a g e m e n t is discussed. T h e context of the s i t u a t i o n n e e d s to be i m m e d i a t e l y assessed, a n d will usually lead to a rapid d e t e r m i n a t i o n of the cause. A m o r e s t r u c t u r e d a p p r o a c h is r e q u i r e d in the case of refractory h y p o t e n s i o n w h e r e the cause is n o t obvious or the r e s p o n s e to t r e a t m e n t is i n a d e q u a t e .

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