Limits to blood pressure

Systolic pressure

The extent to which blood pressure rises during systolic ejection reflects how much the energy of ejection is able to compress the arterial contents downstream of the left ventricle. The size of the stroke volume is, therefore, one obvious factor that will influence the level of systolic blood pressure (SBP). Anything that reduces stroke volume will reduce SBP (Fig. 4.1A,B). In normal individuals, the most usual situations in which this occurs is when cardiac filling falls because of an increase in heart rate or reduced venous return, typically during postural change.

Figure 4.1 Effects on pulsatile aortic blood pressure (red) of varying left ventricular function. (A) Typical normal relationship between blood pressure and (from top downwards) ventricular volume, ventricular pressure and ECG. In (B), heart rate has increased without changed ventricular mechanical function; this reduces SBP due to reduced ventricular filling. In (C), the same heart rate increase is accompanied by shortening of the ventricular action potential, improving ventricular filling and returning SBP towards the control value. (D) The full physiological response to tachycardia, with action potential shortening, increased myocardial contractility and aortic stiffening: now, SBP is elevated above control, reflecting the increased stroke volume. Note that while tachycardia elevates DBP because of the reduced time for arterial run-off, this effect remains virtually the same regardless of stroke volume.

The linkage of stroke volume to SBP means that this pressure can in normal individuals be used to assess cardiac workload, most commonly by calculating the product of heart rate and SBP, termed the rate–pressure product. By contrast, in hearts where the atrioventricular valves do not seal fully so that there is back-flow of a proportion of the stroke volume or the semilunar valves do not open fully so that ejection of blood is delayed, then stroke volume and SBP are reduced but intraventricular pressure is increased. Under these circumstances, SBP can no longer be used as an index of cardiac work; in fact, there is likely to be an inverse relationship between the two.

Under most circumstances, not all of the energy developed by the myocardium during ejection is translated into pressure, because the proximal part of the aorta is distensible (compliant) rather than being a rigid tube and a proportion of ejection energy is, therefore, stored as potential energy as the aortic wall is stretched. The functional value of this is that once ejection is complete, aortic elastic recoil will continue to exert intravascular pressure and provide a means of converting the purely pulsatile cardiac ejection into continuous flow through the peripheral circulation.

Generalised sympathetic nervous system activation elevates SBP, due to a variety of factors. First, increased cardiac muscle contractility reduces end-systolic ventricular volume and increases stroke volume. Second, an increased action potential conduction velocity through the ventricular myocardium leads to faster compression of the contents and, therefore, to a higher velocity of ejection. In addition, the smooth muscle in the proximal aorta receives a sympathetic innervation and contraction of these muscle cells reduces aortic compliance. This stiffening allows all of the energy of ejection to be used in pressure generation. Finally, sympathetic vasoconstrictor drive to veins stiffens these and mobilizes blood normally stored in the venous reservoir back into active circulation, aiding cardiac filling and further increasing stroke volume. The additive effects of these factors are illustrated in Figures 4.1C and D.

Diastolic pressure

As diastolic blood pressure (DBP) represents the lowest value to which pressure falls in the arteries before the next systolic ejection, it must be influenced by the period over which the pressure can fall, so heart rate itself is also a major determinant of DBP, with tachycardia predictably causing a pressure rise (Fig. 4.1). Heart rate changes will also affect SBP if pulse pressure remains constant but, in practice, the consequences of heart rate alteration for ventricular filling time and, therefore, for stroke volume tends to minimize SBP changes.

The second main influence on DBP is the rate at which intra-arterial pressure falls after systolic ejection ceases; that is, how fast the pressurized blood flows out through the resistance of the peripheral blood vessels. Thus, the total peripheral resistance is a major determinant of DBP and changes in DBP can in many situations be used as an index of peripheral resistance changes. While all vascular beds and all segments of the vasculature contribute to the overall resistance of the system, most of the peripheral resistance occurs in the largest regional vascular beds, those supplying the digestive tract and associated tissues (the splanchnic circulation), the skeletal muscles, the skin and the kidneys, and almost all is localized to the arteriolar segment of the vasculature. In Chapter 5 (p. 50) we will see why the arterioles produce so much more resistance to flow than do other parts of the vascular tree.

Figure 4.2 adds the effects of sympathetic activation on cardiac generation of blood pressure to our flow chart of the exercise response.

Figure 4.2 Expansion of Figure 3.4, with the factors discussed in this chapter denoted in red.

Mean versus phasic arterial pressure

As indicated above, the phasic limits of blood pressure can provide valuable information on the behaviour of specific components of the circulatory system. The pulsatile nature of pressure in large arteries is, however, irrelevant to perfusion of the peripheral tissues, since virtually all pulsatility is damped out by the time blood enters the capillaries. Also, calculation of parameters such as peripheral resistance requires an averaged value for pressure. The concept of mean arterial pressure is, therefore, essential to quantitative evaluation of circulatory function.

Central and peripheral arterial pressures

The concept of arterial pressure generation from cardiac ejection and the factors determining systolic and diastolic limits as discussed above relate specifically to pressure just outside the semilunar valves. In the systemic circulation, however, additional factors become significant in pressure determination the further one moves away from the heart down the system of distributing arteries, with the result that absolute values recorded from, for example, arteries in the arm or leg, are no longer a precise reflection of the pressures in the aortic arch.

A finite resistance to flow is imposed by the vessel walls, so that mean BP falls progressively along the arterial tree. If this were not the case, there would be no pressure gradient and no flow could occur. For the same reason, DBP falls to a similar extent. Nonetheless, this longitudinal resistance to flow is quite small in large arteries so that the mean BP and DBP fall by only around 5 mmHg between the aortic arch and the brachial artery at the elbow.

By contrast, SBP in the brachial and other peripheral conducting arteries may be up to 10–15 mmHg higher than in the aortic arch. This change is due in part to reflection of pressure when the descending pressure wave meets the much higher resistance of the microcirculation. As well, the more peripheral arteries lack the high compliance of the thoracic aorta, so the energy of cardiac contraction is no longer partially dissipated in volume changes of the vessels.

Palpation

The sudden rise in intra-arterial pressure associated with systole can be detected with the fingertips in a number of arteries that lie just below the skin surface. The most commonly used site is the radial artery at the wrist. If an occlusive cuff is inflated around the arm, the pulsation disappears once the cuff is inflated above SBP and reappears during deflation when cuff pressure falls below SBP. This is a rapid method for determining SBP. It can provide no information on DBP and so cannot be used for calculation of mean BP.

Auscultation

Auscultation (from the Latin ausculatatus = to listen to) is the traditional method by which blood pressure is detected using a stethoscope or a microphone applied to the skin over an artery, distal to an occlusive cuff. While it is routine to apply the cuff to the upper arm and the detector to the brachial artery at the elbow, this technique can also be used to measure pressure in the patellar artery at the knee.

The technique relies on the luminal diameter of an artery being narrowed along the section underneath an inflated occlusive cuff and that this diameter suddenly increases at the downstream edge of the cuff. Flow velocity is increased through the narrowed section of the vessel. The combination of this increased velocity and the larger diameter vessel just downstream of the cuff transforms the flow profile to a turbulent one just in this region. At occlusive pressures above SBP there is of course no forward flow and so no turbulence. At pressures below SBP, however, intra-arterial pressure exceeds the cuff pressure for a portion of each cardiac cycle, producing periods of noisy turbulent flow separated by silence. These noises are known as Korotkow sounds.

During inspiration, the increased cardiac filling and consequent increased stroke volume associated with negative intrathoracic pressure causes a rise in SBP. In younger individuals, this is reinforced by the tachycardic phase of sinus arrhythmia. Appreciable respiratory fluctuations in SBP are seen even during quiet respiration, and are more pronounced at low respiratory frequencies because the longer period of low intrathoracic pressure allows greater cardiac filling (Fig. 4.3). In order to measure SBP accurately, it is obviously important that the cuff is inflated to a pressure that is above the highest SBP value. The standard recommendation is for inflation to a value around 20 mmHg higher than that at which the palpated radial pulse disappears, but this advice does not take account of the respiratory phase at which the pulse is detected. For accurate results, it is a sensible precaution to measure several palpated SBP values over a complete respiratory cycle and then to use an inflation pressure for auscultation around 20 mmHg above the maximum recorded.

Figure 4.3 Fluctuations in SBP during quiet breathing in a healthy, 24-year-old woman. The phase of inspiration can be identified by the progressive tachycardia. (A) With slow respiration at 7 breaths/min, the increased cardiac filling and stroke volume associated with inspiration increases SBP by up to 50 mmHg. (B) At a respiratory frequency of 15 breaths/min in the same subject, the duration of negative intrathoracic pressure is shortened and the amplitude of SBP fluctuation is reduced correspondingly.

During deflation of the cuff, blood flow becomes almost continuous once the occlusive pressure falls to within a few mmHg of DBP, because of the flattened base of the pulse wave. This transition from intermittent to near-continuous flow is detected through the stethoscope as a change in the character of the Korotkow sounds from discrete tapping to a more blurred and somewhat softer noise, a change known as ‘muffling’, or Korotkow phase IV. Once cuff pressure falls below a value approximating DBP, the amount of vessel distortion is insufficient to cause turbulence in the presence of absolute blood flow velocities typical of normal resting cardiac output. Therefore, the cuff pressure at which Korotkow sounds disappear (Korotkow phase V) can be used as an approximation of DBP. This is convenient because the presence or absence of a sound is usually easier to assess than whether the character of the sound has changed, especially when there is a high level of background noise.

However, it is essential for the experimental scientist to remember that the association of Korotkow phase V with DBP is coincidental and based entirely on the absolute velocity of blood flow. If velocity increases because cardiac output is elevated (for example by exercise or pregnancy), or because the occluded artery is small in diameter (as occurs in children), then less compression of the artery will be sufficient to cause turbulence. Under these circumstances, Korotkow sounds may persist until cuff pressure is as much as 20–30 mmHg below DBP. By contrast, the cuff pressure at which muffling occurs has a constant and close relationship to DBP. For this reason, muffling and not disappearance of sounds must be used as the auscultatory criterion for DBP during exercise if serious errors are to be avoided. A stethoscope is essential in such circumstances: microphones are able to reliably recognize only the presence or absence of sounds.

Robinson et al (1988) proposed on the basis of comparisons of auscultatory and inter-arterial BP values that the standard formula DBP + 1/3PP does not provide accurate calculation of mean BP when auscultatory readings are used during heavy exercise; it was suggested that DBP + 1/2PP gave a closer approximation of true (that is, intra-arterial) mean pressure. However, the intra-arterial values in that study were significantly higher than those from auscultation and appeared likely to be an overestimate of the true pressure because of the cannula placement (see Intra-arterial catheters, below). If this probable error is discounted then there seems no good reason to assume that the standard formula is not accurate even at high work intensities.

A number of alternative methods for BP measurement are available and in some situations provide advantages over the auscultatory technique. These are summarized below. However, auscultation is the most generally appropriate for obtaining accurate values during whole-body exercise and, therefore, it is important that every exercise physiologist is expert in its use.

In a few individuals the Korotkow sounds disappear and then reappear in the middle of the pulse pressure range. The silent range of pressures is known as the ‘auscultatory gap’ (Korotkow phases II–III). In these individuals, the pressure at which sounds reappear might be mistaken for SBP, or the pressure at which they disappear might be mistaken for DBP. It is, therefore, a sensible precaution to always check the cuff pressure at which the palpated radial pulse disappears and reappears, before starting auscultatory measurement.

Oscillometry

This technique is used in the portable blood pressure monitoring kits commonly available from pharmacies and medical suppliers and in routine hospital units such as the Dinamap^TM. The occlusive cuff is usually inflated automatically to a preset value and deflates at a preset rate. The absolute pressure inside the cuff is monitored at a high frequency and an algorithm is used to determine which part of the pressure wave corresponds to particular pressure values.

The oscillometric technique has several potential advantages over auscultation. For one thing, the underlying theory obviates the potential problems of detecting and interpreting Korotkow sounds. As well, observer error is removed. Extensive studies of the pressure values recorded using auscultation by even highly trained personnel show that a surprisingly high number of people routinely round numbers up or down, sometimes to the nearest 10 mmHg. The automatic digital display provided by oscillometry avoids this potentially serious source of error. However, since they rely on small variations in cuff pressure for their operation, oscillometric devices are extremely sensitive to movement of the cuff relative to the skin. This means that they cannot be used unless the arm is completely stationary, precluding their use during whole-body exercise.

A further problematic characteristic is the fact that the automated inflation–deflation cycle cannot be overridden easily. If SBP is above the preset inflation ceiling then the cuff immediately deflates without taking a measurement. In experimental circumstances where SBP varies from moment to moment, for example in subjects with pronounced sinus arrhythmia or during laboratory stress tests, this may result in unacceptable loss of data. Alternatively, the inflation ceiling can be preset to a very high value. However, this prolongs the inflation time and is found by some subjects to be uncomfortable, leading to stress-induced hypertension.

Applanation tonometry

This technique employs high-frequency application of inwardly directed pressure over an artery, so as to continually exactly balance the intravascular pressure. The pressurizing and sensing devices are located together in a housing that is strapped on the skin, overlying either the radial artery at the wrist or a digital artery on a finger. As no process of cuff inflation or deflation is needed, a continuous beat-to-beat record of BP is obtained. This makes the technique an attractive one when SBP varies from moment to moment and for situations in which rapid changes in BP must be tracked. For example, a Valsalva manoeuvre (see Chapter 10, p. 120) lasts typically for only around 12 s. Over this time there are several significant changes in BP due to different mechanisms, all of which must be measured in order to assess the physiological response. None of these pressure changes could be detected by auscultation or oscillometry because the cuff inflation–deflation cycle takes in excess of 20 s.

Despite this advantage, applanation tonometry has its own limitations. One is that the positioning of the detecting head is critical, so the wrist or finger must be kept absolutely still. In the case of wrist devices, this makes it very difficult to maintain BP measurements during even light exercise. With finger devices, exercise can be performed as long as one hand can be kept motionless, but this obviously restricts both the type and the intensity of exercise undertaken. The finger presents a further problem with anything but short experiments. As the fingers are a major site for thermoregulatory heat exchange, the digital arteries are usually relatively vasoconstricted, which causes a significant fall in pressure from that in the larger, more central arteries. To obviate this error, devices that record from digital arteries include a heating element that ensures local vasodilatation. However, the effect of this can be painful when a finger is exposed for longer than around 30 min. So during prolonged study sessions it is necessary to periodically change fingers, resulting in inevitable gaps in the pressure record.

Intra-arterial catheters

Of all the above techniques, auscultation is the only one that can give reliable information during intense whole-body exercise. Even then, it has to be accepted that readings are possible only about every 60 s because of the need for slow cuff deflation in order to obtain accurate values. If more frequent readings are necessary, or when blood pressure must be monitored remotely (for instance from swimming subject), then the only alternative is to use direct intra-arterial cannulation. This is not a course to be taken lightly. The procedure requires medical expertise and sterile conditions, it involves some subject discomfort and there is always a small but finite risk of injury. Nonetheless, intra-arterial recording is routine in a number of exercise physiology facilities, most of which are attached to hospitals. Some information on the methodology used can be found in Wasserman et al (2004).

To interpret intra-arterial BP measurements accurately, it is important to know the position of the catheter tip and the direction in which this faces. The catheter is usually inserted retrogradely into the radial artery in the forearm or the femoral artery in the groin and, because of the rise in SBP with increasing distance away from the heart (see Central and peripheral pressures, p. 35), the absolute pressures recorded will depend on how far the cannula tip is advanced towards the central aorta. In addition, most catheters are open-tipped tubes, so when they are inserted retrogradely into an artery the open tip faces upstream. Under these circumstances, the pressure recorded is greater than the true intravascular hydrostatic pressure, because of the kinetic energy of blood flow pushing on the catheter lumen. The kinetic component is determined primarily by the velocity of blood flow and can be calculated as:

As flow velocity is greatest during the ejection phase of the cardiac cycle, P_kinetic affects SBP more than DBP. At a normal resting cardiac output, it adds around 4–8 mmHg to SBP, but the quadratic relationship to flow velocity means that the contribution rises rapidly as cardiac output rises. If, for example, P_kinetic added an additional 5 mmHg to SBP at rest, then a threefold rise in cardiac output should increase the kinetic contribution by 3² or ninefold, to 45 mmHg. This would introduce a serious source of error if intra-arterial values were compared quantitatively with those obtained by non-invasive techniques in the same subject.

When an end-opening catheter faces downstream, then the true intra-arterial pressure is underestimated by the P_kinetic value. This is not a problem with systemic BP measurement but can be important when measuring pulmonary BP, since the catheters for this purpose are inserted through a central vein and passed on through the right heart (see Chapter 8, p. 101). The only way in which the kinetic artefact can be obviated is to use a catheter that has its opening at right angles to the direction of blood flow.