Isolated systolic hypertension: pressure on the anaesthetist?

Ever since Ambard & Beaujard [1], and later Volhard and Fahr [2], using Korotkoff sounds with Riva-Rocci's newly developed technique of sphygmomanometry [3], linked the consequences of renal (Bright's) disease with high blood pressure, human hypertension has been classified and stratified according to diastolic blood pressure levels [4]. These reflect the high systemic vascular resistance, or more correctly the modulus of aortic input impedance at zero frequency, which is characteristic of most forms of primary and secondary hypertension. A series of studies concerning anaesthesia in relation to hypertension [5–9] were stimulated by widely perceived problems, in the 60s and onwards, of hypertensive patients presenting for anaesthesia and surgery. It was common then to find patients with diastolic pressures higher than 120 mmHg being presented for routine anaesthesia and surgery without adequate pre-operative assessment. Based on these studies, I advocated that patients with uncontrolled or poorly controlled hypertension ideally should not be submitted to elective surgery until their blood pressure had been brought under control. In 1979, an article by Goldman & Caldera [10] seemed to contradict this approach. However, in an accompanying editorial [11] I drew attention to a substantial difference between their studies and mine. Notably, that 96% of their uncontrolled or poorly controlled hypertensive patients had diastolic pressures between 90 and 110 mmHg, and that only five had diastolic pressures over 110 mmHg but below 120 mmHg. By contrast, in all my studies, patients with uncontrolled or poorly controlled hypertension were defined as having diastolic pressures in excess of 120 mmHg. Despite these differences, I agreed with Goldman's conclusion that ‘…elective surgery in the absence of ideal antihypertensive therapy need not subject patients to an added clinical risk provided (my italics) a) diastolic pressure is stable and not higher than 110 mmHg, and b) intraoperative and recovery room blood pressures are closely monitored and treated to prevent hypertensive or hypotensive episodes.’ Three recent publications have highlighted the importance of isolated systolic hypertension (ISH), and of systolic and pulse pressure as independent predictors of cardiovascular risk especially in the elderly [12–14]. Al-Khalid raised the question in correspondence in this journal [15] as to whether anaesthesia and surgery should be delayed in patients with ISH. Neither the problem nor its solution in relation to anaesthesia is new. During the first 10 years (1969–79) of studying hypertension in relation to anaesthesia, I gradually realised that there were a number of patients with untreated systolic hypertension who could not be recruited into the various studies described above. This was because their diastolic pressures did not even fulfil the criterion for mild untreated hypertension (diastolic pressure > 95 mmHg). Most of these were elderly patients presenting for central (aortic or carotid) and peripheral vascular surgery. In the early eighties, I identified a relationship between ISH and arteriosclerosis, its relevance, and its management during and after anaesthesia [16–19]. I was partly influenced by the findings of Kannel and his colleagues in the Framingham study [20] and others [21] who, 20 years ago, identified ISH as a significant risk factor for stroke in elderly patients with rigid arterial disease (arteriosclerosis). I was also influenced by my own observations that patients with this condition would show dramatic increases of systolic arterial pressure (from 150–160 mmHg to 200 mmHg and more) during and after anaesthesia and surgery, with only minor changes of diastolic pressure [18]. So, what has changed in our understanding of high blood pressure? Three interrelated conditions coexist to greater or lesser extents in middle-aged to elderly patients: hypertension (primary or secondary), atheromatous vascular disease and arteriosclerosis. The latter two are often lumped together into a ‘portmanteau’ condition of atherosclerosis. However, although the two conditions can coexist, it is important to consider them separately, from a pathophysiological point of view, in order to understand the implications of their existence in patients who may require anaesthesia and surgery. Atheromatous vascular disease is a pathological process of deposition of atheromatous plaques in the intimal surfaces of arteries, with the consequence that as the plaques increase in size, they obstruct the relevant artery, decreasing the flow both at rest and under conditions of increased flow demand. Plaques in major coronary arteries cause angina as a major symptom of acute myocardial ischaemia; their disruption and embolisation distally in the distribution of the relevant artery cause total occlusion which if untreated result in myocardial infarction – death of tissue. Plaques in and around the carotid sinus (artery) either dislodge minor emboli which cause transient ischaemic attacks, or major emboli which cause frank strokes. Serious atheromatous vascular disease does not cause either diastolic or systolic hypertension, but there is good evidence that when the two conditions coexist they aggravate and accelerate their relative progress. In my own studies cited above, acute myocardial ischaemia, observeable as ST segment depression in specific chest ECG leads, was the main cause of peri-operative morbidity in patients with uncontrolled or poorly controlled hypertension. The commonest causes of such changes were hypertension and tachycardia in response to laryngoscopy and tracheal intubation [6]. Arteriosclerosis is a process of vascular ageing, characterised by fracturing of the elastic laminae with a loss of elastin in the arterial wall and, as the process progresses, a deposition of collagen and glycosaminoglycans and, eventually, calcium. These changes were recognised by Bramwell and Hill [22] in 1924 to result in increased arterial wall stiffness, also associated with increased pulse wave velocity [23] and aortic characteristic impedance [24]. In young humans, systolic pressure is substantially higher in peripheral arteries than in the aorta as a result of wave reflection which augments the pressure wave close to the reflection sites in smaller arteries [25]. As arteries ‘stiffen’ with age and/or hypertension, the increasing pulse wave velocity causes an increase in central systolic pressure, pulse pressure, and the rate of change of pressure (aortic dP/dt) which, in turn, have a deleterious degenerative effect on the walls of arteries, and the left ventricle. Patients who develop hypertension in their 40s and 50s also age, and the established phase of hypertension becomes progressively influenced by structural adaptation in the heart and arteries with increased collagen formation [24], implying an acceleration of cardiovascular ageing. Increased characteristic impedance representing increased wall stiffness, especially at the aortic level, tends to further elevate the end-systolic afterload for an already compromised left ventricle [25, 26]. It was believed for some time that these combined processes in elderly patients would make it more difficult to reverse the hypertension and its effects even with prolonged drug therapy [27, 28]. More recently, certain classes of antihypertensive drugs, notably ACE inhibitors and angiotensin II type 1 receptor (AT1) antagonists, have been shown to reverse left ventricular (LVH) and arteriolar hypertrophy, and the associated ventricular remodelling [29], in addition to decreasing blood pressure. Ramipril, an ACE inhibitor, was shown in the HYCAR (Hypertrophie Cardiaque et Ramipril) study to induce regression of LVH in humans, even in doses which did not affect blood pressure [30]. Losartan (potassium), a specific competitive AT1 receptor inhibitor, exerts similar effects independently of its blood pressure lowering effects [31], and has been shown to be an effective antihypertensive agent in randomised double-blind trials with placebo [32, 33]. Five other AT1 receptor inhibitors (candesartan, eprosartan, irbesartan, telmisartan, valsartan) are now available in the UK. Monatepil, a novel calcium channel antagonist with α1-adrenoceptor antagonist activity, has also been shown to have anti-atherosclerotic and plasma lipid-lowering activity [34, 35]. There is now substantial evidence from well-controlled trials that patients with ISH are at risk from heart failure [36] and stroke [20, 21, 37, 38] and benefit significantly from therapy designed to decrease their systolic pressure [39, 40]. The latest guidelines of the British Hypertension Society [41] and the Joint National Committee [3] give a target blood pressure of 140/85 mmHg in non-diabetic patients, and 140/80 mmHg in diabetic patients. Both guidelines state that there are compelling indications for either a low-dose diuretic or a long-acting dihydropyridine calcium antagonist as the preferred first-line therapy in ISH, as these were the only classes of drug which have been shown to decrease stroke and total cardiovascular events in large randomised controlled trials. There is some evidence that β-adrenoceptor antagonists may not be the optimal first-line therapy in the elderly patient [42], although drugs with specific vasodilator activity (e.g. dilevalol) have been proposed [24]. Other antihypertensive drugs, especially those in the newer classes, such as imidazoline receptor agonists (e.g. moxonidine) [43], angiotensin AT1 receptor inhibitors (see above) or α1-adrenoceptor antagonists (e.g. doxazosin) [44], may be suitable for the elderly hypertensive but randomised controlled trials are awaited. Elderly patients may present for anaesthesia and surgery with ISH. Systolic pressure is raised to a variable degree in supine resting patients, usually to about 160–170 mmHg [16–18], but diastolic pressures are lower than 90 mmHg [18–45]. Any factor that increases the stroke volume, such as exercise, apprehension, or sympathetic nervous activation by noxious stimulation, results in a disproportionate increase in systolic and pulse pressure. Patients can be classified as: A, those with arteriosclerosis but no history of primary or secondary diastolic hypertension – not receiving antihypertensive drugs; B, those receiving antihypertensive drugs specifically for the treatment of ISH; C, those receiving antihypertensive drugs for the treatment of established primary or secondary diastolic hypertension. By the criteria used in previous guidelines [10, 11, 17], Group A would be considered not to be hypertensive, whereas Groups B and C would comprise patients whose hypertension was adequately controlled on drugs which have a predominant vasodilator effect. However, there are many patients whose systolic pressures on admission to hospital for surgery, at the pre-operative visit, and in the anaesthetic room before induction, are found to lie in the range 160–210 mmHg while still fulfilling the criterion for a diastolic pressure at or below 90 mmHg. These are clearly patients with ISH! At other times when they are less apprehensive and not under stress, they usually have systolic pressures around the 140–160 mmHg level. Such patients may have pre-existing silent myocardial ischaemia (asymptomatic ST segment depression representing subendocardial ischaemia), and a linear relationship has been shown between increasing admission systolic pressure and the risk of postoperative silent myocardial ischaemia [46]. What action should the anaesthetist take when patients with ISH present at the pre-operative visit? Figure 1 shows a modification of a flow diagram that I published in 1983 [17]. Although drug therapies have changed in the intervening period, the decision-making process is no less valid today than it was then. The main modification concerns the patient with ISH in the left lower part of the diagram. The only justification for postponing surgery is to create an opportunity to improve the patient's medical condition to an extent that would reasonably be expected to decrease risk factors substantially. In relation to hypertension, this would be a patient with a diastolic pressure greater than 120 mmHg, untreated, and with no previous assessment of cardiovascular status. Other than the risk of postoperative silent ischaemia [46], there is at present little evidence that the magnitude of systolic pressure is a risk factor per se in relation to anaesthesia. Other associated risk factors, especially left ventricular hypertrophy, congestive cardiac failure or specific left ventricular failure, must be taken into account [47–49]. Additional screening may include echocardiography, Holter monitoring and radionuclide ventriculography [48]. In the absence of major indications of intercurrent disease or risk factors, one is left to consider alternative strategies for the patient with ISH. Flow diagram for the management of hypertensive patients presenting for anaesthesia and surgery. The diagram is a modification of one published in Prys-Roberts [17]. Should the patient arriving in hospital the day before surgery be given specific drugs to modify their cardiovascular status before anaesthesia and surgery? Elective administration of a β-adrenoceptor antagonist was proposed for untreated hypertensive patients 28 years ago [8]; the idea was resurrected in 1988 [50], and the question has been reconsidered recently [51, 52], and such drugs have been shown to be beneficial specifically for the elderly [53]. By contrast, patients receiving ACE inhibitors [54, 55] and angiotensin AT1 receptor inhibitors [56, 57] have shown greater degrees of arterial hypotension following induction of anaesthesia compared to patients receiving other antihypertensive drugs. Although the authors recommend withdrawing these two classes of drugs on the day before surgery, some thought needs to be given to the marked bradycardia which accompanied, and indeed may have been the cause of, the arterial hypotension in these studies [55–57]. What criteria should be applied to patients presenting for day-case surgery? There is no evidence available which would preclude the application of the decision-making process shown in Fig. 1 to such patients. Most texts on day-case surgery would be consistent with this process (based on diastolic pressure) but do not consider the problem of ISH. During induction and maintenance of anaesthesia, elderly patients in general, and ISH patients in particular, show substantial decreases of systolic pressure associated with decreased stroke volume and little change in systemic vascular resistance [18]. Much of this effect is the result of sudden venodilatation in response to induction agents, with consequent impairment of right and left ventricular filling leading to a decrease in stroke volume. The effect is difficult to avoid even if induction is achieved slowly, and occurs as a result of loss of consciousness and decreased sympathetic control of the venous system [58]. The hypotension can be largely offset by tilting the patient head down for a few minutes after induction. Small (1–2 mg) doses of methoxamine are also effective as the drug acts primarily as a venoconstrictor in this dose range. Both methods are much quicker and more effective than giving the patient a volume load of 500–1000 ml of crystalloid. Ephedrine has been suggested as a prophylactic measure [56, 57, 59]. Another major cause of hypotension on induction in this group of patients is the combined central vagotonic effects of opioids and propofol which usually results in a modest bradycardia, but can cause severe bradycardia. The best prophylactic is intravenous glycopyrronium before induction. Establishing mid-thoracic epidural block awake before induction of anaesthesia can cause marked decrease in arterial pressure in patients with ISH [18] compared with a relative lack of effect of either lumbar or thoracic block in treated or untreated hypertensive patients [9]. Isolated systolic hypertension is but part of the wide spectrum of hypertension, common in elderly patients, and deserving of both awareness and further research by both physicians and anaesthetists. There is little evidence to warrant the postponement of surgery in such patients unless there is associated evidence of other risk factors which could be improved by such postponement.