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3 Blood Pressure and Its Measurement Chapter 3 / Blood Pressure and Its Measurement 49 3 Blood Pressure and Its Measurement CONTENTS PHYSIOLOGY OF BLOOD FLOW AND BLOOD PRESSURE PHYSIOLOGY OF BLOOD PRESSURE MEASUREMENT POINTS TO REMEMBER WHEN MEASURING BLOOD PRESSURE FACTORS THAT AFFECT BLOOD PRESSURE READINGS INTERPRETATION OF BLOOD PRESSURE MEASUREMENTS USE OF BLOOD PRESSURE MEASUREMENT IN SPECIAL CLINICAL SITUATIONS REFERENCES PHYSIOLOGY OF BLOOD FLOW AND BLOOD PRESSURE The purpose of the arterial system is to provide oxygenated blood to the tissues by converting the intermittent cardiac output into a continuous capillary flow and this is achieved by the structural organization of the arterial system. The blood flow in a vessel is basically determined by two factors: 1. The pressure difference between the two ends of the vessel, which provides the driving force for the flow 2. The impediment to flow, which is essentially the vascular resistance This can be expressed by the following formula: 6P Q = R where Q is the flow, 6P is the pressure difference, and R is the resistance. The pressure head in the aorta and the large arteries is provided by the pumping action of the left ventricle ejecting blood with each systole. The arterial pressure peaks in systole and tends to fall during diastole. Briefly, the peak systolic pressure achieved is determined by (see Chapter 2): 1. The momentum of ejection (the stroke volume, the velocity of ejection, which in turn are related to the contractility of the ventricle and the afterload) 2. The distensibility of the proximal arterial system 3. The timing and amplitude of the reflected pressure wave When the arterial system is stiff, as in the elderly, for the same amount of stroke output, the peak systolic pressure achieved will be higher. The poor distensibility causes a greater peak pressure. In addition, a stiff arterial system results in faster transmission and reflection of the pressure wave, thereby adding to the peak pressure. The narrow and peaked pressure seen in the more peripheral muscular arteries is the effect of such reflection. The level to which the arterial pressure will fall during diastole is primarily 49 50 Cardiac Physical Examination dependent on the state of the peripheral resistance, which controls the runoff. Conditions with low peripheral resistance and vasodilatation will cause the diastolic pressure to fall to low levels. The mean arterial pressure is the average of all the pressures obtained over an entire duration of a cardiac cycle. Since diastole is longer than systole, the mean pressure is estimated as the sum of 60% diastolic pressure and 40% systolic pressure. More accurate measurement will be derived by integrating the area under a recorded pressure curve. The pulse pressure, which is the difference between the systolic and the diastolic pres- sure, reflects not only the stroke volume but also the state of the peripheral resistance. Conditions associated with a large stroke volume and low peripheral resistance will be expected to give rise to a large pulse pressure, and this will be reflected in the amplitude of the arterial pulse by palpation. While the control of the cardiac output is usually determined by local tissue flow under physiological states, the control of the arterial pressure is independent of these and is regulated through a complex system, which involves nervous reflexes and neurohu- moral mechanisms for short-term needs (such as “flight,” “fright,” and “fight” type reactions or in situations like those following acute loss of blood volume) and neuroen- docrine, renin–angiotensin–aldosterone system, and renal mechanisms for long-term adaptation. These control systems in the normal as well as their alterations in hyperten- sion and in heart failure are well discussed in standard texts for physiology and medicine. In this chapter our focus will be mainly on measurement of blood pressure by the sphyg- momanometer and its use in special clinical situations. PHYSIOLOGY OF BLOOD PRESSURE MEASUREMENT The indirect measurement of blood pressure by the sphygmomanometer involves the application of a controlled lateral pressure by an inflatable cuff to occlude the artery by compression, thereby stopping the flow. The detection of the resumption of flow during slow deflation allows the determination of the pressure. The cuff is normally applied to the arm over the brachial artery. When the cuff pressure exceeds the systolic pressure, the brachial artery is fully occluded and the flow ceases. When the cuff is deflated to pressures just below the systolic peak, the flow begins to resume with each cardiac systole. The jet of blood coming through the partially occluded vessel is associated with tapping-type sounds, which can be recognized using a stethoscope placed over the bra- chial artery just distal to the cuff. These sounds, termed the Korotkoff sounds, help in identifying the systolic and the diastolic pressures in the artery. The detection of the first appearance of Korotkoff sounds (Phase I) as the cuff is being deflated corresponds to the systolic pressure, and the disappearance of Korotkoff sounds with further deflation of the cuff corresponds to the diastolic pressure. Korotkoff sounds generally become muffled first when the cuff is being deflated before they totally disappear. It is always advisable to take the diastolic pressure to the level at which the sounds disappear because it is less likely to introduce errors (1). The Mechanism of Origin of Korotkoff Sounds The exact mechanism of origin of Korotkoff sounds is not completely established. They have been thought to result from turbulence of flow coming through the partially occluded artery. This is thought to be supported by the following: they become muffled (Phase IV) and eventually disappear (Phase V) generally when the flow resumes in Chapter 3 / Blood Pressure and Its Measurement 51 diastole, i.e., when the cuff is deflated below the diastolic pressure, allowing the artery to be open throughout the cardiac cycle. In addition, before they become muffled and completely disappear, they may sound like a short bruit (initially as soft bruit in Phase II and louder bruit as in Phase III). However, they do not always sound like murmurs and often present as sharp sounds. The Waterhammer theory was suggested (not to be confused with the water-hammer pulse in aortic regurgitation) to explain the presence of distinct sounds (2). The sounds are thought to be produced by the deceleration of high-velocity flow coming through the vessel as it opens up from an occluded state against the stationary column of blood distal to the occlusion. The intensity of the sounds, however, may vary, being loud and persistent to low diastolic pressures or throughout diastole in certain situations such as in aortic regurgitation, in children, and in pregnancy. In aortic regurgitation, the stroke volume tends to be large with increased velocity of ejection. Children generally have hyperkinetic circulation, and pregnant women tend to have a high cardiac output with increased sym- pathetic tone. On the other hand, Korotkoff sounds tend to be poor in low-output states. When an oversized cuff is used it may lead to underestimation of the systolic blood pressure. It has been shown that the state of the distal vasculature in the limb where the blood pressure is being measured affects the intensity of the Korotkoff sounds. Vasodi- latation makes the sounds louder, and vasoconstriction softer (3,4). When the peripheral resistance in the arm distal to the cuff was changed by interventions such as heating, cooling, and induction of reactive hyperemia, the amplitude of the Korotkoff sounds appeared to change. Thus, these effects may lead to either over- or underestimation of both systolic and diastolic pressures (5). In fact, when the Korotkoff sounds are poorly heard, they are best augmented by raising the arm (decreasing venous distension) and having the patient open and close his or her fist on the side where the pressure is being measured a few times (6,7). This is thought to increase the forearm flow. Others have proposed that the pressure pulse wave itself may be the source of the Korotkoff sounds. The sounds may be attributed to “shock waves” where the flow velocity of blood in the narrowed segment may exceed the pulse wave propagation velocity and give rise to vibrations in the audible frequency range. This would be analo- gous to the sonic boom heard when the speed of a jet plane reaches and surpasses the speed of sound. It is also possible that the Korotkoff sounds are related to energy (vibrations) that results from sudden termination of the pressure pulse wave at the site of the inflated cuff, which leads to partial occlusion of the vessel, causing this to become a terminating site favoring reflection. Between the systolic peak and the diastolic pressures during which time the Korotkoff sounds are present there is a considerable degree of termination and reflection together with beginning onward transmission of the pressure pulse wave. Once the cuff pressure is lowered below the diastolic pressure, there is no more termi- nation or reflection at the site of the cuff application and the pressure pulse is further transmitted along the artery. Therefore, there is no sound to be heard. This may be supported by the fact that when an oversized cuff is used, it may lead to underestimation of the systolic blood pressure. In conditions where the Korotkoff sounds are loud and last longer to low levels of diastolic pressure such as aortic regurgitation, there is a more rapid and higher launching momentum to the pressure pulse wave because of the large stroke volume, which is ejected with a rapid velocity. Thus, there may be more energy for dissipation at the termination sites. In significant aortic regurgitation, one often feels 52 Cardiac Physical Examination “pistol shots” over the femoral arteries, which are also often sites of reflection because of bifurcation.
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