Strategy for patients with hypertensive heart disease

11

Strategy for patients with hypertensive heart disease JORGE DAGNINO CEDRIC PRYS-ROBERTS

Hypertension can be a major risk factor for anaesthesia and surgery either independently or because of its association with cardiovascular disease in general, and ischaemic heart disease in particular. Many aspects of the anaesthetic management of these patients are still the subject of debate, largely due to the scarcity of controlled studies. Several recent reviews have covered different aspects of hypertension in relation to anaesthesia (Prys-Roberts and Meloche, 1980; Prys-Roberts, 1983, 1984; Dagnino and Prys-Roberts, 1986) so we will focus particularly on those issues that are controversial, and on new developments. DEFINITION OF HYPERTENSION

There are many difficulties in trying to define hypertension. Blood pressure levels in the population have a unimodal distribution and the risks associated Table 1. Classification of blood pressure. From Report of the Joint National

Committee on Detection, Evaluation, and Treatment of High Blood Pressure (1984). Blood pressure (ram Hg)

Category*

Diastolic <85 85-89 90-104 105-114 >115

Normal High normal Mild hypertension Moderate hypertension Severe hypertension

Systolic (when DBP < 90 mm Hg) <140 140--159 > 160

Normal BP Borderline isolated systolic hypertension Isolated systolic hypertension

* A classification of borderline isolated systolic hypertension (SBP > 160 mm Hg) takes precedence over a classification of high normal blood pressure (DBP 85--89mm Hg) when both occur in the same individual. A high normal blood pressure classification(DBP 85-89 mm Hg) takes precedence over a classification of normal blood pressure (SBP < 140 mm Hg).

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with high blood pressure also increase in proportion, at all levels of blood pressure (Pickering, 1972). This means that the border between normotension and hypertension is necessarily arbitrary. In 1984, a Joint National Committee in the United States recommended multiple measurements on at least two separate occasions and, for use in persons aged 18 years or older, set the dividing line at 140 and/or 90 mm Hg. These definitions also take into account the epidemiological and pathophysiological significance of systolic pressure as can be seen in Table 1.

HYPERTENSION AS A RISK FACTOR

Hypertension meets most criteria as a direct cause of serious cardiovascular disease. The relative impact is greatest for stroke and least for peripheral artery disease, but ischaemic heart disease is the most common sequel. This association is complex and while hypertension is the most powerful independent factor, its impact is greatly modified by its interaction with other major contributors for ischaemic heart disease such as obesity, diabetes, hyperlipidaemia or dyslipidaemia and smoking (Kannel, 1986; Wood, 1988). The risk of each clinical manifestation of ischaemic heart disease, myocardial infarction, angina or sudden death, is increased in proportion to the severity of hypertension, but in patients with mild hypertension increased risks are concentrated in those with coexistent risk factors (Kannel, 1987). Some commonly held beliefs that have been shown to be untrue by the Framingham study (Kannel, 1986, 1987) are that high blood pressure is normal or even necessary in the elderly, that hypertension is less significant in women and that occasional high readings or systolic hypertension have little significance: 1.

2. 3.

4.

Whatever the variety of hypertension, systolic or diastolic, the absolute risk and the risk gradient in the elderly are the same when compared with a younger population. Cardiovascular mortality is tripled in the elderly hypertensive compared with a normotensive patient of the same age. Despite a lower absolute risk, there is no evidence that women tolerate hypertension well at any age. Labile elevations are considered less serious than fixed elevations, but most epidemiological studies have used single blood pressure determinations and for any given average pressure the risk of cardiovascular events is unaffected by the degree of blood pressure variability. In most studies the level of diastolic arterial pressure has been used for diagnostic, prognostic and therapeutic decisions. The fact is that most risks of hypertension are as closely or even better related to levels of systolic arterial pressure. In elderly patients systolic pressure is probably a better predictor particularly in women. This is not surprising as systolic arterial pressure is a major factor in determining cardiac work and maximum shear forces in blood vessels.

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TARGET ORGAN INVOLVEMENT Organ damage caused by a sustained high arterial pressure is mostly apparent in the heart, brain and kidneys. Consequences in the heart relate to ischaemic heart disease, left ventricular hypertrophy (LVH) and heart failure. Damage to the brain is manifested by transient ischaemic attacks, focal neurological deficits or stroke. A progressive decrease in function reveals renal involvement. During the major part of the evolution of hypertension, target organ involvement is silent and not easily detectable. Unfortunately, more than half of the cardiovascular clinical sequelae will occur before there is evidence of target organ involvement. Once present it is an ominous sign: within five years of the appearance of cardiac failure or LVH more than half of the patients will be dead (Kannel, 1986). Mortality from ischaemic heart disease in general, and from sudden death in particular, is increased three- fourfold with the appearance of electrocardiographic (ECG) evidence of LVH. In fact ECG voltage changes indicative of LVH, together with a strain pattern, carry the same prognostic significance as a silent myocardial infarction (Kannel, 1987). Stroke, other neurological syndromes and renal failure also represent a late stage of the disease and are much less common than ischaemic heart disease. It is clear then that treatment should not wait for the appearance of such signs or symptoms, and also that its absence can be very misleading as to the real magnitude and significance of organ damage. AETIOLOGY In about 90-95% of patients with high blood pressure no specific cause can be determined. This constitutes primary or essential hypertension. Although the pathophysiological mechanisms remain unclear, the principal environmental causes of high blood pressure have been identified. A genetic tendency to blood pressure elevation only operates in the presence of appropriate environmental stimuli. The most important factors which maintain a low blood pressure are the absence of excess body fat, low alcohol consumption, regular physical activity and some other dietary factors (vegetarian diet, low sodium, high potassium). These together appear to determine the level at which blood pressure regulatory mechanisms are set to respond to more transient stimuli such as physical and mental activity, emotional responses and stress (Beilin, 1988). A specific cause or disease can be demonstrated in about 6-8% of patients as causing high blood pressure, constituting what is called secondary hypertension (Table 2). Most cases of secondary hypertension are renal in origin, either parenchymal or renovascular (3-5% prevalence in the general population) or secondary to the use of oral contraceptives (2--4%). Other causes are much less frequent: primary aldosteronism (0.3 %), phaeochromocytoma (< 0.1%) or Cushing's syndrome (< 0.1%), while all other causes of secondary hypertension together reach a 0.2% incidence in the general

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Table 2. Classification of arterial hypertension. After Williams and Braunwald (1987).

Systolic hypertension with wide pulse pressure A B

Decreased compliance of aorta (arteriosclerosis) Increased stroke volume: aortic regurgitation, thyrotoxicosis, fever, arteriovenous fistula, patent ductus.

II Systolic and diastolic hypertension A Renal: renovascular stenosis, chronic pyelonephritis, acute and chronic glomerulonephritis. B Endocrine: oral contraceptives, adrenocortical hyperfunction, phaeochromocytoma. C Neurogenic: spinal cord section, psychogenic, increased intracranial pressure. D Miscellaneous: coarctation of aorta, increased intravascular volume, hypercalcaemia. E Unknown aetiology: essential hypertension, toxaemia of pregnancy, acute intermittent porphyria.

population and not more than 1% in a specialty clinic (Williams and Braunwald, 1987).

HAEMODYNAMICS Hypertension is an heterogeneous disorder, and several haemodynamic patterns have been described in patients with essential hypertension (Messerli et al, 1986; Frohlich, 1987). While these may be just simple variations of a single entity, there is growing support for the concept that they may represent separate diseases. Haemodynamic differences may appear according to aetiological type, and may also change according to the severity or evolution phase of the hypertensive disease.

Primary hypertension An elevated systemic vascular resistance together with a normal or subnormal cardiac output has been considered to be the prevalent pattern in established essential hypertension. In long-standing hypertension the systemic vascular resistance is even higher while cardiac output tends to decrease. By contrast, cardiac output can be markedly increased with a normal systemic vascular resistance in young patients with borderline or labile hypertension (LundJohansen, 1980; Conway, 1984). In patients with moderate hypertension there is often an increase in pulmonary artery pressure and vascular resistance. There is also involvement of the right ventricle, with a reduced ejection fraction, and an increased responsiveness of the pulmonary circulation to adrenergic stimuli (Guazzi et al, 1987). Renal blood flow tends to be decreased although glomerular filtration rate is normal due to an increased filtration fraction. Renal vascular resistance is increased more than the elevation in total systemic vascular resistance (SVR), particularly at high blood pressure. With advancement of the disease there is a progressive reduction of renal flow. Plasma and blood volumes are normal or slightly reduced (Conway,

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1984), although in the preoperative hypertensive patient greater reduction in plasma and blood volumes may be found. Cardiopulmonary blood volume is normal or increased, indicating a shift from the periphery probably as a consequence of reduced venous compliance (Lund-Johansen, 1980). The response of hypertensive patients to exercise, an increase in cardiac output and a decrease in systemic vascular resistance, is diminished in comparison with that in normotensive subjects. Stroke volume is subnormal, probably reflecting the decreased compliance of the left ventricle. In late or severe hypertension, cardiac output after exercise is markedly lower than in age-matched controls (Conway, 1984).

Systolic hypertension Systolic and diastolic arterial pressures are determined independently, though with close dynamic interrelations. Peak systolic pressure is determined by stroke volume, the speed of left ventricular contraction, aortic distensibility and systolic run-off to the periphery. The main determinants of diastolic pressure are arteriolar resistance, arterial distensibility and the duration of diastole. During systole a normal aorta can store up to half the stroke volume while elastic recoil permits flow through the resistance vessels to continue during diastole. The most common form of systolic hypertension is that associated with a reduced aortic compliance seen in elderly patients. With a rigid aorta the same stroke volume will determine a higher systolic pressure while the absence of elastic recoil will determine a lower diastolic arterial pressure, unless the SVR is increased. Thus any patient with systolic hypertension and a normal cardiac output, heart rate and diastolic pressure, must have an increased SVR. Systolic hypertension due solely to loss of aortic compliance (arteriosclerosis) must be accompanied by a lower than normal diastolic pressure (Saltzberg et al, 1988). Even small changes in stroke volume can produce major changes in pressure in patients with advanced arteriosclerosis. Also, an acute increase in output impedance may precipitate acute left ventricular failure due to a prolongation of the ejection time, increased systolic wall stress and oxygen consumption of the left ventricle. Such a situation frequently occurs during anaesthesia following laryngoscopy and endotracheal intubation or after aortic cross-clamping. An increased velocity of ventricular ejection is responsible for systolic hypertension in young patients while arterial compliance is normal.

Secondary hypertension Hypertension produced by renal disease is the result of volume expansion, due to altered renal handling of sodium and water, or of activation of the renin-angiotensin system. Classification into parenchymal and vascular renal hypertension follows these two mechanisms although it is now clear that both may interact in some patients.

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Most patients with renovascular hypertension will have high SVR, normal or slightly elevated cardiac output and normal blood volume. Blood volume tends to be higher than normal in renal parenchymal disease, but may be reduced in severe renovascular hypertension. In primary aldosteronism there is also a relationship between aldosteroneinduced sodium retention and hypertension, although functional changes in the arterial wall, related to altered sodium permeability and leading to vasoconstriction, have also been implicated (Bravo, 1987). STRUCTURAL ADAPTATION Whatever the aetiology, a sustained elevation of blood pressure leads to structural changes in the heart and arteries that have great importance in the evolution and consequences of hypertension. They are of immediate concern to the anaesthetist because of their bearing on the haemodynamic responses of these patients during anaesthesia and surgery. Also, it is these structural alterations and eventual damage to target-organs, rather than the elevated blood pressure per se, that account for the morbidity and mortality associated with hypertension. The cardiovascular changes of hypertension can be classified as

1. Damage, which occurs when the adaptive changes described below either have not taken place or are insufficient to cope with the effects of an increased pressure. Hypertensive encephalopathy and fibrinoid necrosis of malignant hypertension are examples of such damage. 2. Adaptation, representing the response of muscle cells to the increased work imposed by a raised arterial pressure, occurs primarily in the walls of arteries and of the left ventricle, but has also been demonstrated in veins and in the pulmonary circulation. Adaptation involves increased synthesis of elastin and collagen by smooth muscle cells that undergo hypertrophy and hyperplasia in response to increased pressure and also, probably, to neurohumoral trophic influences (Folkow, 1987). The structural changes in resistance vessels result in an increased reactivity in that even minor changes in muscle tone may produce large changes in resistance (Folkow, 1978). This has been termed vascular structural adaptation or structural autoregulation, which can be seen as a second protective mechanism to maintain pressure at the capillary bed. The first is the functional autoregulation that precapillary resistance vessels display in response to acute pressure elevations. The increased wall to inner radius ratio (w/ri) due to smooth muscle hypertrophy and hyperplasia, makes the wall stronger and less distensible, and also produces exaggerated luminal changes for any given degree of muscle activity change. The encroachment on the inner radius means that resistance to flow is increased even at complete muscular relaxation. These magnifying effects may be exaggerated in the presence of subintimal atheromatosis. Figure 1 depicts schematically the difference in position and slope of the

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HYPERTENSIVE HEART DISEASE

10'1

H

N

8

(D

~" 6'

;4 32

E

'1.~, O

"

O >.

to 2

t==

J

I;=

N

14

I0

I"5

2"0

25

Shortening smooth muscle (%) Figure 1. Effects of structural adaptation on systemic resistance changes, in response to the degree of smooth muscle shortening, in a hypertensive (H) arteriole compared with a normotensive (N) vessel. In A, regression of structural changes produce a displacement of the response curve. B shows the effect of acute treatment, with vasodilation but no anatomic regression.

curves of normotensive and hypertensive populations, showing resistance changes in relation to smooth muscle length variations9 Both groups have the same degree of arterial smooth muscle shortening under resting conditions, but the resistance to flow is greater in hypertensives than in normotensives. It is also apparent that equal changes in tone or muscle fibre length, shortening or elongation, will produce very different changes in resistance to flow. It is therefore not surprising that hypertensive patients respond to vasoconstrictor stimuli such as pain, drugs, or manoeuvres such as laryngoscopy and intubation, with a greater increase in arterial pressure than a normotensive patient. The same can be said of changes in the opposite direction, with the same degree of vasodilation producing proportionally greater decreases in systemic vascular resistance. These structural changes appear very early in the evolution of hypertensive disease and their progressive accentuation can facilitate persistence of elevated blood pressure9 These changes are also the basis of the

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displacement, towards a higher range, of autoregulation curves of cerebral and renal flows seen in hypertensive patients (Barry and Lassen, 1984). Treatment of hypertension can lead to partial regression of these structural changes (Folkow, 1978, 1987). Regression is more sluggish and less complete when the proportion of connective tissue and interstitial deposits in relation to smooth muscle hypertrophy is greater. Treatment of patients with longstanding hypertension and advanced age will produce less reversion than treatment in younger patients. Regression is seen with antihypertensive drugs that decrease, or at least do not increase, adrenergic tone. The greater the success in inducing regression of anatomical changes, the greater the displacement towards the normotensive resistance response curve as shown in A in Figure 1. As a consequence, there will be less amplification of vascular responses to diverse stimuli, and the renal and cerebral autoregulation curves will be shifted toward a lower pressure range (Barry and Lassen, 1984). Short treatments or just a small regression of structural changes will only produce a displacement along the same hypertensive response curve. This means a lower resistance at rest, due to vasodilation, but the same increased reactivity to further vasodilation and especially to vasoconstrictive stimuli (B in Figure 1). Autoregulation curves of renal and cerebral circulation continue to be shifted to the right so that acute decreases in blood pressure are more apt to cause a diminution of flow to these territories. The changes in coronary microcirculation are similar to those seen in other locations. This fact along with the particular vulnerability of the subendocardium, help explain the frequency of ischaemia during anaesthesia in hypertensive patients. An additional mechanism which may explain the elevated systemic resistance is a diminished number of arterioles, a phenomenon called arterial rarefaction (Chen et al, 1981).

Left ventricular hypertrophy Structural adaptation also occurs in the wall of the left ventricle as a very early response to increased arterial blood pressure. Cardiac hypertrophy is not a single homogeneous entity (Tarazi and Levy, 1982; Laragh, 1988) and different types can have different aetiologies, functional and prognostic significance. Hyperviscosity is a very important factor in the process of LVH (Devereux, 1987). Prevalence of echocardiographic LVH in mild to moderate hypertensives can be as high as 48% (Devereux, 1987). Impairment of diastolic filling is an early sign of left ventricular hypertrophy appearing before the first anatomical signs or even before systolic functional signs (Fouad, 1987). Electrocardiographic signs of left atrial enlargement are early indicators of probable LVH reflecting abnormalities of left atrial emptying due to early LV diastolic dysfunction (Frohlich, 1987).

Haemodynamic consequences of L VH The thicker LV wall leads to a diminished diastolic compliance so that the heart with LVH is more dependent on an increased filling volume to maintain performance. This is not always readily apparent but appears

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during exercise as an increase in pulmonary wedge pressure (Conway, 1984). It agrees too with the central relocation of circulating volume seen in hypertensive patients (Lund-Johansen, 1980). While mechanical performance is initially well maintained, or is even better in the presence of an increased SVR, there is a time-dependent deterioration during the evolution of hypertension (Tarazi and Levy, 1982). This deterioration is related to the dilation of the cavity of the left ventricle and/or to the appearance of myocardial ischaemia. Thus, at least until hypertension becomes severe, this compensatory mechanism enables the heart to maintain cardiac output in the presence of an increased afterload, at rest or exercise. Recent studies suggest that in the majority of mild hypertensive patients the heart plays a secondary role undergoing adaptive hypertrophy in proportion to the increased blood pressure, whereas in a minority of such patients the increased myocardial contractility may be of pathogenic importance, allowing an increased cardiac output without hypertrophy. Among some patients with sustained moderate to severe hypertension the situation may be different in that functional changes of a supernormal cardiac performance, manifested by high LV ejection fraction, was found to be associated with an over-compensatory concentric LVH and subnormal wall stresses at rest (Devereux, 1987). Fewer than 10% of hypertensive patients with abnormal LV functional reserve can be identified by echocardiographic evidence of impaired contractility at rest. In the remainder, LV dysfunction is only revealed by exercise stress and its incidence can be as high as 75% when hypertension is associated with obesity (Devereux, 1987). Hypertrophy is associated with normal or slightly reduced resting coronary flow per gram of myocardium. However, coronary flow reserve, which gives information about what might happen during maximal stress, is specifically reduced in hypertensive LVH (Strauer, 1988). Treatment has also been shown to induce regression ~f LVH. This regression is not consistent with reduction in blood pressure but is related to the types of drugs used for treatment. It occurs with most adrenergic inhibitors, angiotensin converting enzyme inhibitors, probably most calcium-channel blocking agents and beta-adrenoceptor antagonists. In contrast, diuretics and direct vasodilators do not induce regression of LVH (Frohlich, 1987). Although LVH clearly increases the risk of morbidity and mortality, reduction of this risk has not been shown with treatment-induced regression of LVH. There is still no agreement if this regression is beneficial and concern has been expressed that it might even be deleterious (Tarazi and Levy, 1982; Tarazi and Frohlich, 1987). TREATMENT OF HYPERTENSION

It is clear that treatment of moderate or severe hypertension reduces total morbidity and mortality associated with high blood pressure. However, the

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lowest level in the mild hypertension range for which antihypertensive drugs are recommended is still open to debate (Borhani, 1987). Clinical trials have shown convincingly the efficacy in reducing the occurrence of stroke, cardiac failure and renal insufficiency. The effect is not so clear in reducing ischaemic heart disease (IHD) and treatment does not restore cumulative mortality of treated hypertensive patients to that in the non-hypertensive population. For many years the reduction of blood pressure was the obvious major objective of treatment and led to the development of the stepped-care approach in which first line drugs, usually a diuretic or a beta-adrenergic antagonist, were initially indicated and then second- or third-line drugs were added if no reduction in blood pressure was observed. The increased variety and efficacy of antihypertensive drugs, along with a better understanding of their effects and side-effects, has led progressively to a more individualized kind of approach (Messerli et al, 1986). This calls for additional considerations when choosing a specific drug for a particular patient, tailoring the known pharmacological effects of the antihypertensive agent to the pathophysiological profile of the patient. Current attitudes seem to be changing towards this individualized therapy according to type of hypertension, associated risk factors or diseases, age, sex, race and target organ involvement. The action of antihypertensive drugs on renal function is receiving increasing attention because different drug effects will determine efficacy and perhaps long-term use (Hollenberg, 1987). A desirable profile is that of an increased renal blood flow without producing sodium retention. This profile is shared by calcium-channel blocking agents, converting enzyme inhibitors and nadolol alone among the beta-adrenoceptor antagonists. New agents of this class with direct vasodilating properties have not yet been adequately evaluated in this respect. Antihypertensive treatment in relation to anaesthesia has been reviewed (Prys-Roberts, 1990) so that only major interactions or adverse effects seen in the perioperative period will be mentioned here (Table 3). Table 3. Comparative incidence of postoperative myocardial infarction or reinfarction between normotensive (NT) and hypertensive (HT)* patients. Author(s) Steen et al (1978) Eerola et al (1980) von Knorring (1981) Rao et al (1983) Retrospectivet Prospectivet

Total number infarctions

% incidence NT HT

p

36 6 50

4.7 2.7 15.3

9.4 10.8 29.7

<0.05 <0.1 <0.05

28 14

0.9 0.2

2.9 0.4

ns ns

* Steen et al defined HT as those requiring treatment and Eerola et al as blood pressure > 160/110. No definitions were specified in the other studies. t Incidence of reinfarction also differs when comparing NT with angina against HT with angina: percentages were 2.8% versus 23% (p < 0.005) and 1.0% versus 2.1% (ns) in the retrospective and prospective series, respectively.

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ANAESTHESIA AND HYPERTENSION

Controversies about the perioperative risk of hypertensive patients have revolved around two major questions (i) Is the hypertensive at greater risk than the normotensive patient?; and (ii) Is the untreated or poorly controlled hypertensive at a greater risk than the treated and well controlled hypertensive? Hypertensives versus normotensives

Many studies can be, and have been, cited for or against hypertension as a significant and independent risk factor for anaesthesia and surgery. Populations studied, definitions, methods and presentation of results are so varied that comparisons are difficult. Perhaps the surgical risk in relation to blood pressure also has a continuous distribution, increasing with augmenting blood pressure. What seems even more important is that trying to define perioperative risks and practices based solely on blood pressure levels is a mistake because more relevant factors may be missed. There is little probability that an adequate epidemiological study will be undertaken to elucidate this question in its full range, in part because of cost if not for other reasons. Population estimates of risk will not be of much help in individual estimations or management decisions unless specific factors are determined. Table 3 shows a comparison between normotensives and hypertensives in relation to the incidence of postoperative myocardial infarction or reinfarction. Incidence in hypertensive patients was almost consistently double that observed in normotensives, although the differences were not always statistically significant, probably because of the small numbers involved. Given this higher incidence and the fact that mortality after myocardial infarction is higher in hypertensives than in normotensives (Kannel et al, 1980) one would expect a higher mortality amongst the former but this remains to be proven. Even mild hypertension with no target organ involvement carries an increased risk, arguably a small increase, requiring greater care, vigilance and knowledge. Severe hypertensive patients, with extensive organ damage, represent the other end of this spectrum and require the highest standards of care to limit morbidity and mortality. Untreated or treated

The second question has been even more controversial. It is clear that antihypertensive treatment can reduce the risks of hypertension over the long course. There is also consensus that severe, untreated hypertensive patients have greater variations in blood pressure and a greater incidence of myocardial ischaemia and dysrhythmias than treated patients when subjected to anaesthesia, mechanical ventilation and surgery (Prys-Roberts et al, 197 la,b, 1972; Goldman and Caldera, 1979). A group of moderate mild untreated hypertensives responded to lumbar epidural anaesthesia with greater and unpredictable decreases in blood pressure than a comparable group of treated

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hypertensives (Dagnino and Prys-Roberts, 1984). A recent study (Stone et al, 1988) showed that even mild untreated hypertensive patients are likely to show frequent episodes of myocardial ischaemia during intubation and emergence from anaesthesia. Goldman and Caldera's (1979) study is often cited as proof that hypertensives are at no added risk compared with normotensives, nor untreated hypertensives compared with treated patients. Although this study contributed important insights to the care of the hypertensive patient, these suggestions were neither supported by the results nor by the authors' conclusions. They state in the first paragraph of their discussion, Our single study from one hospital should not settle this controversy because our patients with persistent hypertension had only mildly to moderately increased values, because our series is not as large as an epidemiologic study might ideally be, and because a randomized trial would be preferable to our prospective cohort approach.

Indeed only five of 196 hypertensive patients in the study (2.6%) had diastolic pressures over 111 mm Hg, treated hypertensives had more target organ involvement than untreated patients and the small numbers studied invalidate a positive conclusion in relation to complications. At least 3200 patients, divided into two equal groups, would have been needed to state that the fivefold difference in cardiovascular deaths between normotensives (0.2%) and hypertensives (1%) was not significant, while simultaneously controlling the possibility of a type II error at a 10% level (Feinstein, 1977). Hypertensives showed a greater lability in blood pressure, especially the untreated and inadequately treated groups (IV and V). Mean decrease from preoperative values to lowest intraoperative systolic pressure values was greater in groups IV and V but similar between normotensives and treated hypertensives. There was an insignificant difference in the need for measures to increase blood pressure when comparing normotensives (20%) and hypertensive patients (30%). We think that the main conclusion of this study should be cited as 'Ideally, all hypertensive patients should be identified and adequately treated prior to hospitalization'--perhaps adding 'because this reduces their risk', rather than the more usual 'elective operations in the absence of ideal hypertensive control need not subject patients to an added clinical risk provided: (i) diastolic blood pressure is stable and not higher than l l 0 m m Hg; (ii) intraoperative and recovery room pressures are closely monitored and treated to prevent hypertensive or hypotensive episodes'. Although this last statement is a sensible suggestion to diminish the logistical problem posed by discovering untreated patients the day before surgery, it is not the logical conclusion of their results. This study should not be cited as evidence that hypertensive patients have no added risk when compared with their normotensive counterparts. PREOPERATIVE EVALUATION

The anaesthetist should be prepared to be actively involved in many decisions

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taken in this period as they can greatly influence intraoperative and postoperative events and management. Planning the preoperative evaluation and management by seeking an answer to the following questions is helpful: 1. Is hypertension primary or secondary?

There are several important anaesthetic considerations involved in the answer to this question. Probably the most significant relates to the opportune diagnosis of phaeochromocytoma, as anaesthesia and surgery without previous diagnosis and preparation can lead to a high morbidity and mortality (St John Sutton et al, 1981; Hull, 1986). Recognition of poor renal function associated with hypertension of renal vascular or parenchymal origin might be important in reducing the incidence of new postoperative renal failure (Goldman and Caldera, 1979). Clues for suspecting secondary hypertension are often cited as: hypertension starting before 35 years of age or after 55 years of age, sudden deterioration in a previously well controlled hypertensive and intractable hypertension. 2. How severe is hypertension?

This includes determination of blood pressure levels and their variability. Several readings should be done to determine minimal and maximal values. Supine and standing measurements should be made to evaluate baroreceptor function and blood volume. High admission blood pressure may well predict patients that will have large increases in blood pressure intraoperatively (Bedford and Feinstein, 1980). Pseudohypertension, though rare, should be suspected in patients with very high readings and with little or no symptoms or signs of target organ involvement. Osler's manoeuvre can help in the diagnosis: pseudohypertension should be suspected if the radial or brachial artery pulse continues to be palpated after increasing sphygmomanometer pressure just above the systolic reading (Messerli et al, 1985). In pseudohypertension, indirect measurement of arterial pressure will differ considerably from intra-arterial recordings. 3. Are target organs involved?

Estimation of risk and proper management cannot be made if a serious attempt to answer this question is not done. By far the most significant finding is the presence of ischaemic heart disease (IHD). It must be remembered that even critical obstructive lesions of a major coronary artery may be asymptomatic especially at rest. Therefore a high degree of suspicion is necessary especially in patients with limited physical activity. Myocardial infarction may also occur unrecognized in a high proportion of patients, particularly in the elderly or diabetic patients (Kannel, 1987). The presence or absence of other risk factors for ischaemic heart disease should be noted as their combination makes IHD probable.

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Cerebrovascular disease can present as stroke, focal neurologic deficits or transient ischaemic attacks. Symptoms and signs will depend on the vessel involved; their presence may pass unnoticed unless specifically searched for. A careful history and physical examination in a hypertensive patient should include the optic fundus as it can provide an estimate of the extent of vascular involvement. The presence of haemorrhages, exudates and particularly papilloedema points to severe or even malignant hypertension. In these cases elective surgery should be postponed and urgent treatment started. A 12-lead ECG will serve as a baseline and indicate specific alterations. Hypertensive subjects with other risk factors for IHD who present with ECG signs of LVH, intraventricular conduction blocks or repolarization abnormalities should be considered to have a compromised coronary circulation (Kannel et al, 1987). Particular attention should be paid to evidence of previous transmural (Q wave) infarction, its extent, and history; and of non Q-wave infarction (predominantly subendocardial) characterized by deeply inverted T waves in four or five of the chest leads. Evolutive ECG signs of myocardial ischaemia should also mean postponement of elective surgery for appropriate consultation. The ECG and chest X-ray are not sensitive means for the diagnosis of LVH. M-mode echocardiography is probably the most cost-effective method available and should be routine in preoperative hypertensive patients if available. There is also a considerable epidemiologic risk associated with even mild echocardiographic LVH (Devereux, 1987). For the evaluation of left ventricular function and myocardial ischaemia, twodimensional echocardiography or nuclear imaging techniques are emerging as clinical tools. Serum potassium determinations should be done in all patients under diuretic treatment and perhaps before all major surgery. Hypokalaemia related to diuretic use has been the subject of much debate in relation to the possibility of an increased incidence of ventricular dysrhythmias and sudden death during long-term treatment with these agents (Freis, 1987). There is also debate as to the significance and management of preoperative hypokalaemia. Accepted practice has been to postpone surgery in these patients or to initiate aggressive replacement therapy when surgery could not be postponed. Recent studies have challenged this approach after finding intraoperative dysrhythmias to be related to severity of heart disease and chronic digoxin therapy but not to preoperative potassium levels or diuretic therapy (Vitez et al, 1985; Hirsch et al, 1988). It must be remembered that aggressive potassium replacement is costly and can be hazardous. Hypocapnia should be avoided in patients with hypokalaemia, as should the administration of beta-adrenoceptor agonists. Urea and creatinine determinations should be routine in elderly hypertensives and in all those with long-standing or severe hypertension. These are rather late markers of renal impairment. An otherwise unexplained hyperuricaemia has been suggested to be early evidence of renal dysfunction in hypertensives (Messerli et al, 1980). A creatinine clearance should be obtained before all major operations.

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4. Is the patient in the best possible condition to undergo surgery? There is little or no disagreement that surgery should, ideally, be postponed when the patient has suffered an acute myocardial infarction within the last 6 months. For surgery that should not be delayed that long, a period of 8-10 weeks should be considered. Even earlier than that, treadmill testing performed 3 weeks after an uncomplicated myocardial infarction can aid in discriminating high-risk from low-risk patients (De Busk et al, 1983). Heart failure is an ominous sign in surgical patients and every effort should be made to compensate these patients before surgery. In the hypertensive patient this means optimizing antihypertensive therapy. A useful test of cardiac function can be carried out immediately before induction: administration of 250 ml of a crystalloid solution usually rises central venous pressure by no more than 3 mm Hg; a rise of more than 5 mm Hg, especially if it stays elevated after stopping the infusion, may indicate a compromised ventricular function (Prys-Roberts and Meloche, 1980).

PERIOPERATIVE MANAGEMENT Treated patients Most controversies over the anaesthetic management of hypertensive patients have revolved around the perioperative handling of antihypertensive therapy. Although this can no longer be regarded as controversial, several points are worth emphasizing or deserve some comments. It is now widely accepted that the hypertensive patient should ideally reach surgery with well-controlled blood pressure and that antihypertensive therapy should be maintained up to and including the day of surgery, and restarted as soon as possible. For the most part, interactions between antihypertensive drugs and anaesthetic agents are predictable and easily managed provided they are readily recognized (Craig and Bose, 1984). Table 4 shows a list of antihypertensive drugs along with possible inter, actions or adverse effects during the perioperative period. Three circumstances deserve further comment.

Monoamine oxidase inhibitors Although no longer widely used as antihypertensive drugs, accepted practice has been to withdraw monoamine oxidase inhibitors (MAOI) 2 weeksbefore surgery, with or without substitution. Recent evidence seems to indicate that interactions are for the most part predictable and infrequent so that the dangers of MAOI therapy, in relation to the surgical patient, may well have been overstated. Current recommendation is that patients taking MAOI should continue to do so before elective surgery. Morphine is the narcotic analgesic of choice while pethidine must never be given to these patients (EI-Ganzouri et al, 1985; Stack et al, 1988).

276

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Clonidine Abrupt stoppage of antihypertensive drugs can be hazardous. One problem is hypertension in the postoperative period as their effect wears off. This is a minor problem, predictable by pharmacokinetic and pharmacodynamic knowledge, and easily managed. Another problem is a withdrawal syndrome; although this has been described in association with the majority of antihypertensive agents, most concerns have involved cloriidine and beta-adrenergic antagonists. Awareness of their existence, pathophysiology and diagnostic features is important in their prevention and/or management. Clonidine withdrawal is due to an increased peripheral sympathetic nervous system activity, it occurs 24--48 hours after cessation of therapy although it can start earlier and it may be present postoperatively as an hypertensive crisis in up to 20% of patients (Kaukinen et al, 1978). Fear of clonidine withdrawal led to recommendations that this drug should be discontinued or substituted in the preoperative period. Advent of new antihypertensive drugs for parenteral use along with the realization that clonidine might have a number of advantageous effects in the perioperative period (Kaukinen et al, 1978; Flacke et al, 1987; Ghignone et al, 1987, 1988) has changed this attitude. Care should be taken to administer the last dose of clonidine close to the time of surgery. Availability of transdermal administration of clonidine might be a useful adjunct for the management of these and other hypertensive patients although it must be realized that therapeutic blood levels are not reached before 48-72 hours (Lowenthal et al, 1988).

Beta-adrenergic antagonists There is ample evidence that beta-adrenoceptor antagonists have no major deleterious interactions with the majority of anaesthetic drugs and procedures (Prys-Roberts et al, 1973; Roberts JG, 1980; Prys-Roberts, 1982). Among the halogenated agents, enflurane, at high concentration, is probably less well tolerated than halothane or isoflurane in beta-blocked patients. It must also be appreciated that hypercapnia, hypoxia, anaemia and hypovolaemia may be more deleterious in these patients so that their occurrence should be carefully prevented. Consideration should also be given to the fact that vasoactive drugs in the beta-blocked patient can change their pharmacologic profile, as blockade of their beta-agonist effects may leave their alphaadrenergic actions unbalanced (Tarnow and Komar, 1988). There is now consensus in maintaining adequate beta-blockade before and during surgery in hypertensive patients and especially in patients with ischaemic heart disease. Not so generally appreciated, is that maintenance of beta-blockade during the postoperative period might be even more important. Withdrawal symptoms usually occur 48-72 hours after cessation of therapy, but stress during the postoperative period might make symptoms appear earlier and perhaps more frequently and more seriously. Chronic beta-blockade leads to an increase in the number of beta-adrenergic receptors. This causes an augmented responsiveness to beta-adrenergic stimulation which is probably the basis of the withdrawal syndrome (Frishman, 1987).

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It has been stated that tissue half-life of beta-adrenergic antagonists is quite prolonged so that it is not necessary to restart postoperative administration until the day after surgery. Most patients will tolerate this without harm but not those with ischaemic heart disease. Oka et al (1980) found that even a 10-hour cessation of propranolol therapy was accompanied by an increased reactivity after intubation, and that continuation of propranolol therapy in the postoperative period decreased the incidence of dysrhythmias in patients undergoing coronary surgery. Preoperative administration and postoperative continuation of metoprolol therapy was also associated with a reduction of perioperative myocardial infarction and dysrhythmias in patients undergoing abdominal aortic aneurysm repair (Pasternak et al, 1987). Even with a long-acting drug like atenolol it is usually necessary to administer additional doses in the postoperative period when the degree of beta-adrenoceptor blockade is assessed with isoprenaline dose-response curves (Prys-Roberts and Dagnino, 1985; Dagnino and Prys-Roberts, 1986). Demonstration that intraoperative ischaemia is associated with an increased ificidence of postoperative myocardial infarction (Slogoff and Keats, 1985) has led to increased efforts to limit ischaemic episodes. There is also evidence that repeated episodes of short periods of ischaemia can lead to necrosis in the experimental model (Geft et al, 1982). The use of preoperative beta-adrenoceptor antagonists to diminish haemodynamic lability and myocardial ischaemia in hypertensive patients has been advocated for more than 15 years (Prys-Roberts et al, 1973) and recently shown to be useful for mild hypertensives too (Stone et al, 1988). Reduction of ECG myocardial ischaemia was striking in both studies: from 38% to 4% in the former and from 28% to 2% in the latter. Chronic treatment with calcium channel blockers does not reduce the incidence of myocardial ischaemia (Chung et al, 1988; Slogoff and Keats, 1988). Patients being treated with a combination of a calcium-channel blocker and a beta-adrenergic antagonist usually receive low doses of both so that consideration should be given to increase the dose of the betaadrenergic antagonist preoperatively.

Untreated patients Any decision to postpone surgery should be taken only after consultation with the cardiologist or physician, and the surgeon. In patients hospitalized and scheduled for surgery, few would argue against postponing in patients with diastolic pressures over 110 m m Hg or those with evidence of advanced target organ damage. Patients with significant systolic arterial hypertension would also benefit by postponing surgery to bring their blood pressure under control (Schneider et al, 1979; Eerola et al, 1980; Assidao et al, 1982), but care must be taken to differentiate patients with arteriosclerosis (high systolic pressure, but diastolic pressure below normal ( 7 0 9 0 m m Hg) who cannot be assisted by drug therapy or delaying surgery. Other factors should also be considered: age, magnitude and site of surgery, target organ involvement, pulmonary disease, diabetes and obesity. If the decision is made to

HYPERTENSIVE HEART DISEASE

279

postpone surgery and start treatment, this should be done slowly to avoid sudden decreases in blood pressure that might compromise flow to vital organs. Treatment should probably be prolonged for several weeks or even months if full advantage of structural regression is to be obtained. Acute decreases in blood pressure or too short a treatment are not in the patient's best interest. In untreated patients with mild hypertension or those with moderate hypertension but with no evidence of target organ damage and in whom postponement is not desirable (Goldman and Caldera, 1979) premedication with clonidine (Flacke et al, 1987; Ghignone et al, 1987) or with a betaadrenergic antagonist (Prys-Roberts et al, 1973; Stone et al, 1988) should be considered.

Monitoring Adequate monitoring will permit prompt assessment of rapidly changing circulatory conditions so that appropriate measures can be taken before the development of irreversible complications. Non-invasive methods can be used in patients with well-controlled hypertension or those with mild or moderate untreated hypertension undergoing elective and uncomplicated surgery. The decision to use invasive monitoring should take into account the extension, type and duration of surgery along with blood pressure levels, their stability, and evidence of target organ involvement. Direct arterial pressure monitoring is warranted in severe hypertensive patients especially if untreated or uncontrolled, and in hypertensive patients with evidence of important target organ involvement or in those undergoing major surgery. Auscultatory methods can significantly under-estimate systolic arterial pressure and over-estimate diastolic pressures and the same has been shown to occur with automatic devices (Hutton et al, 1984; Gourdeau et al, 1986). In ECG, a V5 or an equivalent lead (CM5 or CS5) should be used routinely in all hypertensive patients whether they have evidence of ischaemic heart disease or not. Lead V5 will detect around 75% of the ischaemic episodes displayed in a 12-lead ECG, while DII will detect only 33 %. The combination of DII and V5 will detect 80%, V4 and V5 90%, and DII, V4 and V5, 96% of ischaemic episodes (London et al, 1988). Trans-oesophageal echocardiography has been used to document wall motion abnormalities that are far more common than ECG changes. There is still some debate as to whether this is because of a greater sensitivity of the method or because these abnormalities are not specific for ischaemia. Central venous pressure can be very helpful in guiding volume replacement. We have already mentioned the use of a fluid challenge test to assess the adequacy of overall cardiac function. It must be remembered that in patients with ischaemic heart disease and poor left ventricular function, central venous pressure is not a reliable estimate of the degree or even direction of changes in the left side of the heart. In these patients, and in those undergoing surgery during which major blood volume shifts are expected, insertion of a pulmonary artery catheter should be considered. Significant LVH plus major surgery or a history of left ventricular failure

280

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should be an indication too. It must be remembered that these patients have a higher wedge pressure due to the decreased left ventricular compliance. In patients under chronic treatment with beta-adrenoceptor antagonists, preoperative assessment of the degree of beta-adrenoceptor blockade using isoprenaline should be considered to guide replacement therapy during and after surgery (Dagnino and Prys-Roberts, 1985). ANAESTHESIA Given the number of factors which determine the cardiovascular changes during induction, maintenance and emergence from anaesthesia it is hardly surprising that we have little evidence that will permit selection of one agent or technique over others for the management of hypertensive patients. General anaesthesia

Induction

The induction sequence in the hypertensive patient is probably the most dangerous and unpredictable period. Hypotension after induction, due to a decrease in sympathetic outflow and the direct action of drugs, may be followed by hypertension and tachycardia as a consequence of sympathetic stimulation provoked by laryngoscopy and intubation (Prys-Roberts et al, 1971b). In hypertensive patients this response is associated with greater increases in noradrenaline and adrenaline concentrations than those observed in normotensives (Low et al, 1986). Management of such events is difficult and leads to conflicts: deep anaesthesia will blunt the response to laryngoscopy and intubation while light anaesthesia is needed to diminish the magnitude of hypotension after induction. Several strategies have been proposed to minimize these changes and their consequences. Moderate doses of synthetic opioids do not cause marked hypotension during induction of anaesthesia (Prys-Roberts, 1982) but will effectively blunt the haemodynamic and electrocardiographic changes during laryngoscopy and intubation. Their use is limited only by the possibility of postoperative ventilatory depression. Alfentanil (50 p.g/kg) has a shorter duration of action than fentanyl (10 ~g/kg) and should be preferred in shorter operations. Fentanyl in a dose of 8 p.g/kg, as an adjunct to thiopentone induction, has been shown to blunt hypertension and tachycardia (Martin et al, 1982). A nitroglycerine infusion plus a 3 ~.g/kg dose of fentanyl reduced the incidence of ischaemia, and was associated with less haemodynamic alterations when compared with 3 or 8 p.g/kg of fentanyl alone (Fusciardi et al, 1986). The use of beta-adrenergic antagonists, either chronic treatment or even a single preoperative dose, will blunt the haemodynamic response and decrease the incidence of dysrhythmias and myocardial ischaemia after intubation (PrysRoberts et al, 1973, 1982; Magnusson et al, 1986; Chung et al, 1988; Slogoff and Keats, 1988; Stone et al, 1988).

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281

Esmolol, a beta-adrenergic antagonist with an ultra-short half-life, has also been used to blunt haemodynamic responses during and after surgery (Frishman et al, 1988). The main advantage seems to be a rapid titration and disappearance of effects. This can be a disadvantage in a setting where continuous beta-blockade is nearly always desirable. Close attention to maintenance of a suitable infusion rate is then very important. Etomidate generally produces few cardiovascular effects in patients with ischaemic heart disease but its effects have not been evaluated directly in hypertensive patients. If used alone though, there exists the danger of a greater hypertensive response after laryngoscopy. Use of all other agents, with the exception of ketamine (which is probably contraindicated for most uses in hypertensive patients), leads to a certain degree of hypotension. Probably the most important factor in determining its magnitude is the speed of injection. A slow infusion scheme has been demonstrated to produce a smoother induction with less hypotension by avoiding the overshoot of the blood concentration inherent to the use of a bolus dose (Tackley et al, 1987; Roberts FL et al, 1988). Maintenance

There is no evidence which shows that any of the available anaesthetic agents or techniques are better than others. Halothane reduces blood pressure by a predominant effect on cardiac output while isoflurane reduces systemic vascular resistance. There is a current controversy on the potential deleterious effects of isoflurane on the coronary circulation or of its salutatory effects on the cerebral circulation. Care should be taken though in extrapolating effects of anaesthetic agents in normotensive patients to hypertensives, as they might be different (Seyde et al, 1987). Probably more important than the agent or agents selected is the careful adjustment of the anaesthetic depth to follow the degree of surgical stimulation so as to avoid tachycardia, hypertension and hypotension. Although no limits for blood pressure deviations have been proved to be safe or even adequate, probably upward or downward deviations of more than 20 or 30%, respectively, from normal preoperative values should not be tolerated for prolonged periods. Deviations of more than 40% (upward) or 50% (downward) call for immediate intervention. Heart rate should probably be controlled in a narrower band. Hypotension has long been recognized as a cause of morbidity during anaesthesia. The lower limit of cerebral and renal autoregulation curves are shifted upwards in hypertensive patients. Although there is uncertainty about the lower limit below which the reduced flow is unable to meet metabolic or functional demands, in all probability this level varies from one individual to another and from one part of the brain to another. The cause and mechanism of hypotension, the effects of localized vessel obstructions and the presence or absence of collateral circulation are important factors in determining net effects. Monitoring of the heart for signs of ischaemia and of urinary flow, as indirect evidence of adequate renal blood flow, are mandatory. Cerebral function monitoring has proven less practical and less reliable.

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Hypocapnia should also be avoided as it produces a marked increase in systemic vascular resistance and a decrease in cardiac output (Prys-Roberts et al, 1972). It can also lower serum potassium concentration (Edwards et al, 1977). The best method is to adjust the fresh gas flow into a circle system without soda-lime absorber, or a Bain System, so as to maintain a normal PCO 9

Myocardial ischaemia is a frequent complication during anaesthesia of hypertensive patients. Repeated episodes of even short duration can produce prolonged effects on left ventricular function (Braunwald and Kloner, 1982; Coriat et al, 1985) and are associated with an increased incidence of postoperative myocardial infarction (Slogoff and Keats, 1985). Careful haemodynamic management, preventing or rapidly treating episodes of hypertension, hypotension and especially tachycardia, are extremely important. A continuous infusion of nitroglycerine (Coriat et al, 1984) or of diltiazem (Godet et al, 1987) have been shown to decrease the incidence of perioperative myocardial ischaemia in patients with IHD, most of whom are hypertensive. Premedication with clonidine or beta-adrenergic antagonists are useful adjuncts to the anaesthetic management.

Fluid therapy One should use the same guidelines as in normal patients unless severe renal damage complicates hypertension. It must be stressed that preoperative renal dysfunction is the most important factor in the development of postoperative renal failure and that correct haemodynamic and fluid therapy are crucial in its prevention. There are no systematic studies evaluating fluid and electrolyte requirements in hypertensive patients during and after surgery. It must be remembered that while normal patients may tolerate fluid overloading, this could provoke acute left ventricular failure and pulmonary oedema in patients with a stiff left ventricle due to ventricular hypertrophy or ischaemia. Excessive fluid loading during anaesthesia could make hypertension in the postoperative period more frequent and perhaps more difficult to manage. Conversely, the hypertrophied left ventricle is less tolerant to decreases in filling pressures caused by venodilation or hypovolaemia. Correct management calls for judicious infusion of fluids together with the use of a vasopressor to augment venous tone. Non-surgical hypertensive patients have a normal or slightly reduced blood volume (Conway, 1984). Preoperative bed rest and starving is probably associated with a greater reduction in blood volume in hypertensive patients (Table 5). Blood volume and plasma volume of hypertensive patients were found to be 12-22% below normotensive controls matched for age, sex and body weight. Differences between the diuretictreated patients (13% reduction), beta-blocked patients (16% reduction) and untreated patients (22%) did not reach statistical significance. A direct and significant correlation was observed between blood or plasma volumes with the decrease in blood pressure after induction of anaesthesia to a steady-state level (Dagnino et al, unpublished data). Suggestions have been

283

HYPERTENSIVE HEART DISEASE

Table 5. Preoperative blood volumes (BV) and plasma volumes (PV) in a group of normo-

tensive patients (NT), and hypertensive patients being treated with diuretics (HT-D), betaadrenoceptor antagonists (HT-B) or untreated (HT-U).*

Group

n

Age (years)

Weight (kg)

Height (cm)

Bloodvolume (ml/kg)

Plasmavolume (ml/kg)

NT HT-D HT-B HT-U

10 8 9 5

52+5 50+5 52+7 50+7

65+10 61+ 9 61+ 7 64+ 9

165+9 160+5 163+8 166+7

73+10 64+ 9 62+ 2 58+ 4

46+5 40+6 38+1 36+2

* All valuesare means + SD. There were no differencesin relation to age, weightor height. Bloodvolumesand plasmavolumesof the hypertensivegroupsweresignificantlylowerthan in the normotensivegroup (p < 0.05, ANOVAand ScheffeF-test)but the differencesbetweenthe hypertensivegroups were not significant.

made to infuse volume before induction but this has not been evaluated. During anaesthesia though, infusion of dextran produced a significant increase in cardiac output but no increase in mean arterial pressure because systemic vascular resistance decreased, partly because of haemodilution (Prys-Roberts and Meloche, 1980).

Regional anaesthesia Concern over the response of hypertensive patients to regional anaesthesia, particularly when combined with general anaesthesia, has been frequently voiced. Known information in relation to spinal anaesthesia is based on studies performed in the fifties by physicians studying the effects of acute reductions of blood pressure on cerebral blood flow. No great details of anaesthetic management were given, but considerable and often unpredictable decreases of blood pressure, and CBF, were observed (Kety et al, 1950; Pugh and Wyndham, 1950). Treated patients with well-controlled hypertension, mostly with betaadrenergic antagonists, tolerated lumbar or thoracic epidural anaesthesia very well. Lumbar anaesthesia with lignocaine 1.5% up to a T7 level produced a moderate decrease (24%) of blood pressure in patients without fluid preloading. This decrease was entirely due to a reduction in systemic vascular resistance. A thoracic block from T4 to L1 produced an 18% decrease in blood pressure partly because of a modest reduction in cardiac output. By contrast patients with untreated hypertension exhibited a much greater (44%) and less predictable decrease in blood pressure. In three of the five untreated patients studied there was an abrupt decrease in heart rate and blood pressure along with signs of cerebral hypoperfusion (Dagnino and Prys-Roberts, 1984). Provided extensive monitoring is used, combined general and epidural anaesthesia can be used to provide a stable course with less intravenous or inhalational anaesthetic requirements. Postoperative pain relief can be provided through the epidural catheter using opioids alone or in combination with bupivacaine (Prys-Roberts, 1987).

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POSTOPERATIVE PERIOD

This period can be one of great blood pressure instability. Arousal, pain, hypothermia and shivering, hypoxia and bladder distension can combine to produce sudden and sustained increases in heart rate and blood pressure. Fluid shifts, drug effects and rewarming can lead to hypotension and oliguria. Initial management calls for exclusion or treatment of these common causes. Many drugs or combinations have been recommended for use in the postoperative period. Intranasal, sublingual or intravenous nifedipine (Adler et al, 1986; Davis et al, 1988) have been shown to be effective; reflex tachycardia often requires the addition of a beta-adrenergic antagonist. In patients with hypertension and ischaemic heart disease who received a nitroglycerine infusion during surgery, this can be continued into the postoperative period, increasing the dose if necessary. Labetalol infusions (5-10 mg/h) are particularly effective in controlling hypertension and tachycardia while maintaining postoperative betaadrenoceptor blockade in patients under chronic therapy with these agents (Dagnino and Prys-Roberts, 1985; Prys-Roberts and Dagnino, 1985; Chauvin et al, 1987; Leslie et al, 1987). Alternativelypropranolol (Smulyan et 30

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Figure 2. Replacement therapy in this patient was guided by repeated isoprenaline doseresponse curves performed before, during and until the second day after surgery. The patient was receiving atenolol 100rag and an atenolol infusion was started during surgery and continued until the next day when a labetalol infusion was begun. Displacement of the dose-response curves paralleled changes in plasma concentrations of atenolol. From Dagnino and Prys-Roberts, 1986, with permission.

HYPERTENSIVE HEART DISEASE

285

al, 1982; Villers et al, 1984), atenolol ( P r y s - R o b e r t s and D a g n i n o , 1985; D a g n i n o and P r y s - R o b e r t s , 1986) or esmolol (Frishman et al, 1988) infusions can be used for r e p l a c e m e n t t h e r a p y in patients with I H D in w h o m the alpha-blocking or h y p o t e n s i v e effect o f labetalol is n o t n e e d e d . In these cases the use of C D 2 5 , d e t e r m i n e d by a baseline p r e o p e r a t i v e isoprenaline d o s e r e s p o n s e curve, is particularly useful in guiding infusion rates (Figure 2). I n clinical practice, o n c e a f o u r point d o s e - r e s p o n s e curve has b e e n o b t a i n e d , o n l y a single isoprenaline dose (5-10 mg) two or three times daily is n e e d e d to guide r e p l a c e m e n t t h e r a p y in the p o s t o p e r a t i v e period. REFERENCES

Adler AG, Leahy JL & Cressman MD (1986) Management of perioperative hypertension using sublingual nifedipine. Experience in elderly patients undergoing eye surgery. Archives of Internal Medicine 146: 1927-1930. Assidao CB, Donegan JH, Whiteshell RC & Kalbfleisch JH (1982) Factors associated with perioperative complications during carotid endarterectomy. Anesthesia and Analgesia 61: 631-637. Barry DI & Lassen NA (1984) Cerebral blood flow autoregulation in hypertension and effects of antihypertensive drugs. Journal of Hypertension 2 (supplement 3): 519-526. Bedford RF & Feinstein B (1980) Hospital admission blood pressure: a predictor for hypertension following endotracheal intubation. Anesthesia and Analgesia 59: 367-370. Beilin LJ (1988) Epitaph to essential hypertension--a preventable disorder of known aetiology? Journal of Hypertension 6: 85-94. Borhani NO (1987) Left ventricular hypertrophy, arrhythmias and sudden death in systemic hypertension. American Journal of Cardiology 60: 131-181. Braunwald E & Kloner RA (1982) The stunned myocardium: prolonged, postischemie ventricular dysfunction. Circulation 66: 1146-1149. Bravo EL (1987) Clinical aspects of endocrine hypertension. Medical Clinics of North America 71: 907-920. Chauvin M, Deriaz H & Viars P (1987) Continuous i.v. infusion of labetalol for postoperative hypertension. Haemodynamic effects and plasma kinetics. British Journal of Anaesthesia 59: 1250-1256, Chen IIH, Prewitt RL & Dowell R (1981) Microvascular rarefaction in spontaneously hypertensive rat cremaster muscle. American Journal of Physiology 241: H306--H310. Chung F, Houston PL, Cheng DCH et al (1988) Calcium channel blockade does not offer adequate protection from perioperative myocardial ischemia. Anesthesiology 69: 343-347. Conway J (1984) Hemodynamic aspects of essential hypertension in humans. Physiological Reviews 64: 617-660. Coriat P, Daloz M, Bousseau D et al (1984) Prevention of intraoperative myocardial ischemia during non cardiac surgery with intravenous nitroglycerin. Anesthesiology 61: 193-196. Coriat P, Fauchet M, Bousseau D et al (1985) Left ventricular dysfunction after non-cardiac surgical procedures in patients with ischemic heart disease. Acta Anaesthesiologica Scandinavica 29: 804-810. Craig D & Bose D (1984) Drug interactions in anaesthesia: chronic antihypertensive therapy. Canadian Anaesthetists Society Journal 31: 580-588. Dagnino J & Prys-Roberts C (1984) Studies of anaesthesia in relation to hypertension. VI: Cardiovascular responses to extradural blockade of treated and untreated hypertensive patients. British Journal of Anaesthesia 56" 1065-1073. Dagnino J & Prys-Roberts C (1985) Assessment of [3-adrenoceptor blockade during anesthesia in humans: Use of isoproterenol dose-response curves. Anesthesia and Analgesia 64: 305-311. Dagnino J & Prys-Roberts C (1986) Anesthesia in the aged hypertensive patient. In Stephen CR & Assaf RAE (eds) GeriatricAnesthesia: Principles and Practice, pp 243-275. Boston: Butterworths.

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Davis ME, Jones CJH, Feneck RO & Walesby RK (1988) Intravenousnifedipinefor control of hypertension in patients after coronary artery bypass graft surgery. Journal of Cardiothoracic Anesthesia 2: 130-139. De Busk RF, Kraemer HC, Nash E et al (1983) Stepwise risk stratification soon after acute myocardial infarction. American Journal of Cardiology 52:1161-1166. Devereux RB (1987) Cardiac involvement in essential hypertension. Prevalence, pathophysiology and prognostic implications. Medical Clinics of North America 71: 813--826. Edwards R, Winnie AP & Ramamurthy S (1977) Acute hypocapneic hypokalemia: an iatrogenic anesthetic complication. Anesthesia and Analgesia 56: 786-792. Eerola M, Eerola R, Kaukinen S & Kaukinen L (1980) Risk factors in patients with verified preoperative myocardial infarction. Acta Anaesthesiologica Scandinavica 24: 219-223. EI-Ganzouri AR, Ivankovich AD, Braverman B & McCarthy R (1985) Monoamine oxidase inhibitors: should they be discontinued preoperatively? Anesthesia and Analgesia 64: 592-596. Feinstein AR (1977) Clinical biostatistics, pp. 328. St Louis: C.V. Mosby. Flacke JW, Bloor BC, Flacke WE et al (1987) Reduced narcotic requirement by clonidine with improved hemodynamic and adrenergic stability in patients undergoing coronary bypass surgery. Anesthesiology 67: 11-19. Folkow B (1978) Cardiovascular structural adaptation; its role in the initiation and maintenance of primary hypertension. Clinical Science and Molecular Medicine 59: 343s-354s. Folkow B (1987) Structure and function of the arteries in hypertension. American Heart Journal 114: 938-948. Fouad FM (1987) Left ventricular diastolic function in hypertensive patients. Orculation 75 (supplement I): 148-155. Freis ED (1987) Diuretic induced hypokalemia. The debate over its relationship to cardiac arrhythmias. Postgraduate Medicine 81: 123-129. Frishman WH (1987) Beta-adrenergic blocker withdrawal. American Journal of Cardiology 59: 26F-32F. Frishman WH, Murthy S & Strom JA (1988) Ultra-short-acting 13-adrenergicblockers. Medical Clinics of North America 72: 359-371. Frohlich ED (1987) Hemodynamic considerations in clinical hypertension. Medical Clinics of North America 71: 803--812. Fusciardi J, Godet G, Bernard JM et al (1986) Roles of Ientanyl and nitroglycerin in prevention of myocardial ischemia associated with laryngoscopy and tracheal intubation in patients undergoing operations of short duration. Anesthesia and Analgesia 65: 617-624. Geft IL, Fishbein MC, Ninomiya K et al (1982) Intermittent brief periods of ischemia have a cumulative effect and may cause myocardial necrosis. Circulation 66:1150-1153. Ghignone M, Calvillo O & Quintin L (1987) Anesthesia and hypertension: the effect of clouldine on perioperative hemodynamics and isofiurane requirements. Anesthesiology 67: 3-10.

Ghignone M, Noe C, Calvillo O & Quintin L (1988) Anesthesia for ophthalmic surgery in the elderly: the effects of clonidine on intraocular pressure, perioperative hemodynamics, and anesthetic requirement. Anesthesiology 68: 707-716. Godet G, Coriat P, Baron JF et al (1987) Prevention of intraoperative myocardial ischemia during noncardiac surgery with intravenous diltiazem: a randomized trial versus placebo. Anesthesiology 66: 241-245. Goldman L & Caldera DL (1979) Risks of general anesthesia and elective operation in the hypertensive patient. Anesthesiology 50: 285-292. Gourdeau M, Martin R, Lamarche Y & Tetreault L (1986) Oscillometry and direct blood pressure: a comparative clinical study during deliberate hypotension. Canadian Anaesthetists Society Journal 33: 300--307. Guazzi MD, De Cesare N, Fiorentini C et al (1987) The lesser circulation in patients with systemic hypertension. Orculation 75(supplement I): 156--162. Hirsch IA, Tomlinson DL, Slogoff S & Keats AS (1988) The overstated risk of preoperative hypokalemia. Anesthesia and Analgesia 67: 131-136. Hollenberg NK (1987) The kidney and antihypertensive therapy. American Journal of Cardiology 59: 76A-79A. Hull CJ (1986) Phaeochromocytoma. Diagnosis, preoperative preparation and anesthetic management. British Journal of Anaesthesia 58: 1453-1468.

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