Cardiovascular and Pulmonary Physiology

Published on 13/02/2015 by admin

Filed under Cardiovascular

Last modified 13/02/2015

Print this page

This article have been viewed 1530 times

Chapter 4

Cardiovascular and Pulmonary Physiology

Elizabeth Dean

This chapter reviews basic cardiovascular and pulmonary physiology. A thorough understanding of normal physiology provides a basis for understanding the deficits in cardiovascular and pulmonary function (in the context of limitation of activity and social participation, as well as structure and function) and the adaptations to changing physiological and pathophysiological demands. This knowledge provides the foundation for conducting a thorough assessment and prescribing treatment.1–8

The mechanical activity of the heart is precisely regulated in accordance with the electrical activity of the heart to effect optimal cardiac output to the organs of the body.9,10 The electrical activity of the heart, based on electrocardiography, in both health and pathology, is described in detail in Chapter 12. The electrical and mechanical events of the cardiac cycle and their coupling (electromechanical coupling) are summarized in Figure 4-1. These events include the spread of the wave of electrical excitation throughout the myocardium; the resulting sequence of contraction of the atria and ventricles, followed by dynamic changes in blood pressure and volume in the heart chambers; the heart sounds; and the timing of these events. The cardiac cycle takes 0.8 second in a heart beating at 75 beats per minute. Ventricular systole or ejection takes about one-third of this time. Its onset and termination are marked, respectively, by the closing and opening of the atrioventricular valves (mitral and tricuspid). Diastole, or the period between successive ventricular systoles, in which the ventricles fill with blood, takes two-thirds of the 0.8 second of each cardiac cycle.

Fig. 4-1 Summary of electrical and mechanical events of the heart. A, Atrial systole. B, Isovolumetric contraction. C, Ejection. D, Isovolumetric relaxation. E, Rapid inflow, diastasis, and active rapid filling. Note the relationship between ventricular pressure and volume: a, closure of the atrioventricular valves; b, opening of the semilunar valves; c, closure of the semilunar valves; d, opening of the atrioventricular valves.

Phases of Systole and Diastole

Ventricular systole normally has three phases: the isovolumetric contraction period, the rapid ejection period, and the slower ejection period. Ventricular diastole also has three phases: the passive rapid-filling phase, the slower filling phase (diastasis), and the active rapid-filling phase.

Cardiac Reflexes

The heart behaves automatically and is therefore termed a functional syncytium. Three primary reflexes enable the heart to increase stroke volume and cardiac output with moment-to-moment changes in myocardial demand.

The first reflex is the Starling effect, which refers to the increased force of contraction that occurs with increased venous return (preload). The second reflex, the Anrep effect, refers to the increase in ventricular contractile force as a result of an increase in aortic pressure (afterload). The third reflex, the Bowdich effect, refers to the corresponding increase in heart rate when myocardial contractile force increases. The integrated function of these three reflexes ensures that cardiac output adjusts as demands on the heart change (i.e., in healthy individuals, primarily in response to exercise, body position, and emotional stress).

Volume and Pressure Changes

Changes in the ventricular volume curve and aortic pressure wave reflect changes in atrial and ventricular pressures during systole and diastole. The sequence of events appears in a flow chart in Figure 4-2. Pressure gradients within the heart are responsible for the opening and closing of the valves. Coordinated valve opening and closure are important to promote the forward movement of blood and prevent mechanical inefficiency of the heart pump resulting from valvular regurgitation of blood during ventricular contraction. Regurgitation of blood in the retrograde direction gives rise to heart murmurs that are audible on auscultation of the heart.

Fig. 4-2 The sequence of pressure changes in the heart during the cardiac cycle.

Heart Sounds

The heart sounds are described as a low-pitched, long-duration sound (S₁) followed by a higher pitched, slower duration sound (S₂) that resembles the phonic sounds of LUB-dub. S₁ is associated with the closure of the atrioventricular valves. S₂ is associated with the closure of the semilunar valves. In inspiration, the aortic valve closes several milliseconds before the pulmonic valve, resulting in a splitting of the second heart sound, S₂. During inspiration, intrathoracic pressure becomes more negative, and venous return and right heart volume increase; hence pulmonary ejection is prolonged in this situation, and closure of the pulmonary valve is delayed. Other variations in splitting of S₂ occur with pathology. The presence of a third (S₃) or fourth (S₄) heart sound is usually considered abnormal. S₃ is usually associated with the passive rapid-filling phase and S₄ with the active rapid-filling phase.

Peripheral Circulation

The purpose of the peripheral circulation, including the microcirculation at the tissue level, is to provide saturated oxygenated blood and remove partially desaturated blood. The microcirculation within each organ regulates the blood flow both exogenously, via the neurological system, and endogenously, via the humoral system, commensurate with the metabolic needs of that tissue bed (see Chapter 3). The four principal factors that determine the movement of fluid in the microcirculation are the following:

1. The capillary hydrostatic pressure from the blood pressure, which tends to move blood across the capillary membrane and out of the circulation into the interstitium

2. The capillary oncotic pressure from the proteins within the blood vessels, which tends to retain fluid in the circulation

3. The interstitial hydrostatic pressure, which tends to move fluid back into the circulation

4. The interstitial oncotic pressure, which tends to draw fluid out of the circulation and into the interstitium

The net forces acting on the capillary fluid are nearly in equilibrium, with a slight tendency for fluid to be filtered out of the systemic circulation into the interstitium. Box 4-1 illustrates the mean pressures that determine normal fluid dynamics across capillary membranes.

Box 4-1 Balance of Forces Moving Fluid into and out of the Capillary

Mean Forces Moving Fluid out of the Capillary

Mean capillary pressure	17.0 mm Hg
Negative interstitial pressure	6.3 mm Hg
Oncotic interstitial pressure	5.0 mm Hg
Total outward pressure	28.3 mm Hg

Mean Forces Moving Fluid into the Capillary

Plasma oncotic pressure	28.0 mm Hg
Total inward pressure	28.0 mm Hg

Net Outward Pressure

28.3 (outward pressure) − 28.0 (inward pressure) = 0.3 mm Hg

Transport of Oxygen

Once oxygen reaches the blood, it rapidly combines with hemoglobin to form oxyhemoglobin. A small proportion of oxygen is dissolved in the plasma. The use of the hemoglobin molecule as an oxygen carrier allows for greater availability and efficiency of oxygen delivery to the tissues in response to metabolic demand. Saturation of the oxygen-carrying sites on the hemoglobin molecule is curvilinearly related to the partial pressure of oxygen in the tissues. This relationship is called the oxyhemoglobin dissociation curve and is a sigmoid, or S-shaped, curve (Fig. 4-3). The hemoglobin of arterial blood is 99%, or almost completely saturated with oxygen. Under normal circumstances, arterial blood is mixed with a small proportion of venous blood from the coronary and pulmonary circulation, resulting in arterial saturation slightly less than 100%. The graph shows a range of partial pressures of oxygen that may exist in the tissues. At relatively high arterial oxygen pressures, the oxygen saturation is high. This reflects high association or low dissociation between oxygen and hemoglobin. Saturation does not fall significantly until the partial pressure of oxygen falls below 80 mm Hg. Even at PO₂ levels of 40 to 50 mm Hg, arterial saturation is still 75%. This suggests that the oxyhemoglobin dissociation system has an enormous capacity to meet the varying needs of different tissues without severely compromising arterial saturation. A PO₂ of less than 50%, for example, has a profound effect on arterial saturation. This demonstrates an adaptive response of hemoglobin dissociation to respond to low oxygen tissue pressures by greater dissociation of oxygen from hemoglobin as the need arises. As PO₂ improves with increased supply of oxygen or decreased demand, the affinity between oxygen and hemoglobin increases, and arterial saturation increases. Thus oxygen is not released unless there is a need for greater oxygen delivery to the tissues.

Fig. 4-3 The oxyhemoglobin dissociation curve.

Various conditions can increase or decrease hemoglobin’s affinity for oxygen and thereby cause a shift in the oxyhemoglobin dissociation curve (see Fig. 4-3). A shift to the right results in decreased oxygen affinity and greater dissociation of oxygen and hemoglobin. In this instance, for any given partial pressure of oxygen, there is a lower saturation than normal. This means that there is more oxygen available to the tissues. Shifts in the curve to the right occur with increasing concentration of hydrogen ions (i.e., decreasing pH), increasing PCO₂, increasing temperatures, and increasing levels of 2,3-DPG (diphosphoglycerate), a byproduct of red blood cell metabolism. West suggests that “a simple way to remember these shifts is that an exercising muscle (increased metabolic demand), is acid, hypercapnic and hot, and it benefits from increased unloading of oxygen from its capillaries.”⁸

A shift of the curve to the left results in increased oxygen affinity. Thus for any given partial pressure of oxygen, there is a higher saturation than normal. This means that there is less oxygen available to the tissues. This occurs in alkalemia, hypothermia, and decreased 2,3-DPG.

Anemia (reduced red blood cell count and hemoglobin) and polycythemia (excess red blood cell count and hemoglobin) produce changes in the oxygen content of the blood, as well as in its saturation. Anemia shifts the curve to the right and lowers the maximal saturation achievable. Polycythemia has the opposite effect. The curve is shifted to the left, and maximal saturation approaches 100%.