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.

Does mean blood pressure change with heart rate?

As mean pressure represents the average value throughout the cardiac cycle and the shape of the pulse wave means that the pressure is closer to DBP than to SBP for much of the cycle, the mean cannot simply be taken as half way between the two limits. For practical purposes it is assumed to lie approximately one-third (actually 1/e) of the way up the pressure waveform and so can be calculated as:

or

With increasing heart rate, the shape of the BP wave changes so that the flatter late diastolic portion disappears and the waveform becomes more triangular. There is some experimental evidence suggesting that under these circumstances mean BP may be better approximated by DBP + 2/5PP (Robinson et al 1988).