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• W2017447628 abstract "For as long as blood pressure (BP) has been measured, we have known that it varies hugely from minute to minute. This was observed during the first invasive recordings made by Stephen Hales in 17331 and during the first noninvasive recordings by Riva Rocci in 1896.2 It may therefore seem paradoxical that in all the guidelines for the diagnosis and treatment of hypertension there have been precise thresholds for BP, above which we become concerned and advise treatment, and below which we tell the patient not to worry. The acceptance of such thresholds implicitly assumes two axioms, both of which in reality rest on very shaky ground. The first is that the threshold level identifies the point at which risk increases markedly, even though it is well recognized that the relationship between BP and risk is a continuously graded one. The second is that we can characterize an individual patient's BP level with sufficient precision to be able to distinguish whether it is just above or below the threshold level—again, a highly questionable assumption. Now that we can measure BP in different ways—such as in the clinic, using self-monitoring, or ambulatory monitoring—all three of which give different numbers, we are faced with the question: Which measure of BP should we use to characterize our patients' BP level? We assume that the measurements we use for decision-making in clinical practice are a valid surrogate measure for the patient's “true” BP, which we conceive as being the measure that will give us the best prediction of risk, or that most closely represents the prevailing level of BP over prolonged periods of time. These two conceptualizations of the true BP are not necessarily the same—because, for example, it is theoretically possible that the spikes of BP are what cause the damage. The search for the true BP has a long history. In 1922 Addis3 recognized the fallibility of clinic BP measurement and introduced the term “basal BP,” which he defined as the pressure measured in the morning after waking, but before getting up. This idea was further developed by Sir Horace Smirk,4, 5 who maintained that the “basal” pressure was the true pressure, on which which were superimposed the effects of activity and emotion (the supplemental pressure),which together made up the casual (or clinic)pressure. In a series of studies, he showed that the basal pressure might be 20–30 mm Hg lower than the casual pressure in normal subjects and 50 mm Hg or more lower in hypertensives. His idea was that the basal pressure gave the best prediction of risk. Smirk described two methods for measuring a patient's basal pressure. The first one was performed by having the patient rest supine for 2-4 hours while the physician took a series of readings and took the lowest two or three at the end of this time as the basal pressure. The full version was a much more elaborate process that required hospitalizing the patient, who would be given pentobarbital on the night before the measurement to ensure a good sleep. On the following morning, the patient was allowed to use a bedpan, but stayed in bed, and was given another shot of pentobarbital. If the measurement was not to be made in the room where the patient slept, the bed would be wheeled into “a warm single room, and the patient asked to remain quietly at rest. The observer now enters the room, greets the patient but does not converse, and proceeds to measure the BP at half-minute intervals for 20 to 30 minutes….The average of the two lowest BPs is taken as the basal BP.” It is perhaps not surprising that these methods did not find wide use—but a number of important studies were based on them. Kilpatrick6 studied patients convalescing in the hospital and measured their casual and basal pressures repeatedly over 7 days. He found that the basal pressure was much more reproducible than the casual pressure. Smirk was also aware of the BP-elevating effect of the physician. In a 1944 paper which he coauthored with Alam,7 he wrote: Much of the difference between casual and basal BP is of mental origin, as is indicated by the following observations. In four patients with essential hypertension the BP was reduced to its basal value by rest and habituation to the presence of an observer, called observer 1…. Observer 2 then entered the room, conversed with the patient, and measured the BP…. The BP readings obtained by observer 2 were in all cases nearer to the casual than to the basal pressure. It was immaterial in this investigation which of the authors played the part of observer 2. Smirk considered that the basal pressure was very close to the sleeping BP. In one of his studies,8 in which BPs were recorded with the patients supine for 30 minutes, he observed that some patients fell asleep during the procedure, with little additional decrease in BP; he also advocated the use of barbiturates to ensure proper relaxation of the patient. Smirk and colleagues5 reported on the 5-year survival of 299 patients, all of whom had their basal BP measured while hospitalized. They found a definite relationship between the height of the casual BP and mortality, but this was all due to the effects of the basal pressure; they were unable to show any influence of the supplemental pressure on survival. They also found no consistent correlation between the basal and supplemental pressures. A second study by Simpson and Gilchrist9 analyzed the survival of 299 patients who were hospitalized for hypertension in the days before effective antihypertensive drugs were available. They related survival to three measures of diastolic pressure (systolic pressure was not considered): the initial readings when first seen; the average level recorded on Days 5-11 of the hospitalization; and the lowest pressure recorded during barbiturate-induced sleep. Prediction of survival was clearly better for the latter two measures, and the authors concluded that “the amylobarbitone sedation test had succeeded in picking out a much larger number of patients with a good prognosis.” Their analysis was largely descriptive, since Cox survival analysis had not been invented. In 1964 Smirk10 published a paper on the mortality rates of 270 treated and 199 untreated hypertensive patients followed for 5 years. The untreated patients were those who had declined treatment—a decision that was perhaps not surprising, since the benefits of treatment were unproven, and treatment involved “a 7-hour daily session of drug administration and BP measurement 5 days a week for about 3 weeks.”10 One of the main conclusions of the paper, which included 37 tables and few statistics, was that basal BP was a better predictor of prognosis than casual pressure. These studies thus provided some quite impressive evidence that the basal pressure is both more stable and a better predictor of risk than the casual pressure. What killed the concept was the sheer impracticability of measuring the basal pressure. At the time when these studies were performed (mostly in the 1940s and 1950s), the only reliable technique for measuring BP was a trained observer using a mercury sphygmomanometer. Now, of course, all that has changed, and obtaining multiple readings in situations where the patient is relatively relaxed, and not in the presence of a physician, is an easy task. We can do this by using all three of the currently used methods for measuring BP in clinical practice. In the clinic setting there are devices available which will automatically take multiple readings without a human observer being present; self-monitoring at home also provides the opportunity to provide readings away from any medical setting, and ambulatory monitoring gives the opportunity to describe BP over the whole 24 hours, including sleep. So to what extent do these newer measures of BP relate to the concept of the basal pressure? Although there are many fewer studies than with self and ambulatory monitoring, there is evidence that automated clinic readings are consistently lower and more reproducible than casual readings. In one study of 22 patients,11 the average clinic BP levels for four different types of measurement were: 174/92 mm Hg by a specialist physician; 166/89 mm Hg by the family physician; 158/90 mm Hg by a research technician; and 155/88 mm Hg for an automated recorder. The automated readings were closest to the daytime ambulatory BP average (146/82mm Hg). Somewhat surprisingly, home readings are generally similar to daytime ambulatory readings, although if the patient goes to work the latter will be higher.12 One study has attempted to compare the basal pressure with home and daytime ambulatory pressure in subjects with borderline hypertension, using the modified Smirk protocol (resting supine for 30 minutes) on 3 separate days.13 The averages(for Day 1)were 159/99 mm Hg for the clinic, 148/94 mm Hg for the home, 142/90 mm Hg for basal, and 139/88 mm Hg for the ambulatory readings. There were no significant differences between the home, basal, and ambulatory pressures. Today we talk about the white coat effect (defined as the difference between the clinic and daytime ambulatory or home readings), which is analogous to Smirk's supplemental pressure, and which, like the supplemental pressure, has been found to have no prognostic significance.14 There are differences, however, because the supplemental pressure is always positive, whereas the white coat effect can be positive or negative.15 The two measures of BP that have been most extensively used to describe the true pressure are the average daytime level and the 24-hour level. There is increasing interest in the nighttime pressure, which can be evaluated either as the absolute level, or the relative change from the daytime value (dipping). In a recent article in this series,16 I discussed the prognostic significance of nocturnal dipping and suggested that the evidence is not sufficiently strong to make clinical recommendations for the evaluation of dipping status because its prognostic significance is unclear. The issue here is whether, as Smirk proposed, the true BP can be equated with the sleeping pressure. His version of the basal pressure was probably higher than the true sleep pressure for three reasons. First, in the few subjects who did fall asleep during the measurement, the BP was actually lower when they fell asleep8; second, it is most unlikely that they went into stage 4 sleep, when the pressure is at its lowest; and third, most of the measurements of basal pressure were made soon after waking, when the BP is relatively high. Although the jury is still out on which component of the 24-hour BP profile gives the best prediction of risk, the trend in prospective studies (most notably the Systolic Hypertension in Europe [Syst-Eur]17 and Pressioni Monitorate e Loro Associazioni [PAMELA]18 studies)is that the nighttime pressure may be the best predictor. If this is indeed the case, it raises the interesting question of why this should be. There are at least two general possibilities: one is statistical—the nighttime pressure is a more reliable surrogate marker of the true BP; the other is physiological—there is something about the state of the circulation at night that makes it more susceptible to vascular damage. If the first explanation is correct, we would expect the nighttime BP to be more reproducible than the daytime pressure, on the grounds that activity during the day tends to vary more than at night. Some years ago, we showed that the reproducibility of the daytime BP could be improved if the subject's activities were standardized.19 However, one of the problems with the nighttime BP is that there is a potential source of error in people who sleep on their sides because the arm with the cuff will be either above or below the heart level.20 In addition, the number of readings taken during the night is typically less than during the day. Both of these would tend to reduce the statistical value of the nighttime pressures. The finding that a high nighttime pressure is the best predictor is also hard to reconcile with numerous studies showing that most cardiovascular events show a pronounced diurnal rhythm and occur less frequently during the night than during the day.21 The second explanation, that a high nighttime pressure causes vascular damage, also has problems, although it has been argued that the renal glomerulus may be vulnerable if there is dilation of the afferent arterioles during the night.22 Thus, this new emphasis on the significance of the nighttime BP raises more questions than it answers—we simply don't know why it should have superior predictive value. It is a humbling thought that more than 50 years after Smirk introduced the concept that the basal pressure is the true pressure, an idea that was largely forgotten in the interim, he was perhaps right after all." @default.
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• W2017447628 date "2005-07-01" @default.
• W2017447628 modified "2023-10-17" @default.
• W2017447628 title "What Is the True Blood Pressure? Smirk Revisited" @default.
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