Cardiac Function

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The Cardiac Cycle

As a departure point, we begin this section by considering the sequence of events that occur at the organ level during the course of a single heartbeat, or cardiac cycle Fig. 3-1, Plate 27). Before mechanical activity begins, an electric signal is delivered to the myocardium (see Chaps. 11 and 23). Electrical signaling is accomplished by specialized conduction system tissue that controls heart rate (HR) by responding to a variety of influences (especially sympathetic and parasympathetic stimulation), provides a normal sequence of activation of the heart chambers that in turn maximizes efficient contraction and filling, and at the cellular level, initiates the biochemical processes that underlie contraction. With respect to HR, conduction system cells have the general property of undergoing spontaneous electrical depolarization and thereby functioning as pacemakers that control the rate of beating. The sinus node, located in the right atrium (RA) near the superior vena caval junction, is the component of the conduction system that has the fastest rate of spontaneous depolarization and therefore provides normal control of HR. It is under the direct influence of the autonomic nervous and neuroendocrine systems, which modulate beat-to-beat and longer-term variations in HR.

At the body surface, activity of the specialized conduction system and spread of the electric impulse is represented by the electrocardiogram (ECG), which is caused by electrical potential differences generated by the heart (see Chap. 11). At the cellular level, electrical excitation consists of transmission of a membrane-based depolarizing and then repolarizing current called the action potential (AP) that is propagated through the cardiac chambers via the specialized conduction system, ultimately reaching individual atrial and ventricular myocytes.

The electric signal (AP) begins in the sinoatrial node and then traverses specialized conduction tissue in both atria, spreading to atrial myocytes and causing atrial contraction (the P wave of the ECG). The atrial conduction system tissue then converges at the atrioventricular node region, consisting of the atrioventricular node itself and the more distal His bundle. These structures are located in the junctional tissue where interatrial and interventricular septa meet. The atrioventricular node is an area of relatively slow conduction that is responsible for most of the normal delay between atrial and ventricular contraction (the PR interval of the ECG). A properly timed delay maximizes the booster pump function of the atria and also protects the ventricles from excessively rapid stimulation. From the His bundle, electrical excitation spreads through large, intraventricular fascicles, the left and right bundles. The left bundle branches into two smaller branches, the left anterior and posterior fascicles. Both bundle-branch systems then ramify within the ventricular myocardium. The smallest branches of the specialized conduction tissue are Purkinje system fibers. The electric signal is transmitted from the Purkinje fibers to individual ventricular myocytes, which contract following a series of cellular events described below. Depolarization of ventricular myocardium accounts for the QRS complex of the ECG. Within the myocardium, the AP spreads from myocyte to myocyte through specialized structures called intercalated disks, which contain low-resistance gap junctions across which current flows preferentially. The left ventricle (LV), most massive of the cardiac chambers, is the largest source of electrical potential differences. Electrical activation of the LV begins in the interventricular septum, spreads toward the anteroapical region, and reaches the posterobasal portion last. Activation of the right ventricle (RV) begins slightly after the LV.

This pattern of normal electrical activation causes a coordinated sequence of contraction and relaxation of the cardiac chambers, resulting in ejection of blood by the ventricles into the aorta and pulmonary artery (PA), followed by relaxation and filling. The fact that interference with the normal electrical activation sequence almost always adversely affects cardiac function is strong evidence that normal activation is also the most efficient.

By convention, the mechanical cycle (see Fig. 3-1) is considered to begin at ventricular end diastole (ED), the instant just before systole, when the ventricles begin to actively generate tension as signaled by a sudden, rapid rise in intraventricular pressure. Soon after ventricular systolic pressure begins to rise, it exceeds atrial pressure, at which time the mitral and tricuspid valves close. Ventricular pressures then continue to rise rapidly until aortic (Ao) and PA pressures are exceeded, resulting in opening of the Ao and pulmonic valves and onset of the period of ejection of blood into the systemic and pulmonary circulations. Between mitral/tricuspid valve closure and Ao/pulmonic valve opening, ventricular volume is constant. This phase of the cycle is termed isovolumic or isovolumetric contraction. As ejection proceeds, ventricular and Ao/PA pressures rise and then fall together. The Ao and pulmonic valves close, and ejection ends when ventricular pressure falls below Ao and PA pressure. This event is signaled by the dicrotic notch of the respective arterial pressures. In the LV, a period then ensues during which pressure continues to fall rapidly until it drops below left atrial (LA) pressure, when the mitral valve opens. Since Ao and mitral valves are closed during this period, volume is constant, and it is termed isovolumic or isovolumetric relaxation. Although pulmonic valve closure and tricuspid valve opening are shown as separated significantly in time in Fig. 3-1, the point at which RV pressure falls below PA pressure is actually so low (slightly above the point at which it falls below RA pressure) that the RV isovolumic relaxation period is almost nonexistent.3

The time when ventricular pressure falls below atrial pressure signals the onset of the ventricular filling period. (There is disagreement as to the best conceptual definition of the onset ofdiastole. One is that contraction and relaxation should be viewed as linked events. Diastole therefore does not begin until relaxation is complete. As will be seen, ventricular filling begins before relaxation ends. A second is that diastole begins when ventricular filling commences. A third is that diastole begins when the ventricular myocardium begins to relax, i.e., at about the time ventricular systolic pressure begins to fall. Each definition has merit, and there is no need to take sides in the debate.) Immediately after the atrioventricular (AV) valves open, there is rapid inflow of blood into the ventricles. The latter is caused by an AV pressure gradient (typically several millimeters of mercury) that develops immediately after the AV pressure crossover (Fig. 3-2). Ventricular pressure normally declines by at least several millimeters of mercury immediately after the onset of filling and then rises rapidly after reaching its minimum value. Following this initial rapid filling phase, ventricular pressure plateaus, the AV gradient diminishes markedly, and filling slows and actually may come to a complete halt (diastasis). Slow filling is immediately succeeded by the final filling event, contraction of the atria, which results in a second increase in the AV gradient and injection of an additional bolus of blood into the ventricle. The increase in pressure caused by atrial contraction is the a wave. Because of its brief duration, it has relatively little effect on mean atrial pressure. Thus normal atrial pump function augments ventricular filling with little risk of an excessive increase in atrial pressure and attendant circulatory congestion. With a normal PR interval, ventricular contraction begins during atrial relaxation.

Atrial And Ventricular Pressures

Figure 3-2: Mitral flow recorded with a Doppler probe in the mitral annulus and simultaneous LA (LAP) and LV (LVP) pressures in a dog. Note initial gradient immediately after LV pressure crosses LA pressure. As shown here, when recorded with high-fidelity manometers, this is typically followed by a brief reversal of the gradient and then, following the slow-filling phase, by atrial contraction and a second increase in the gradient. Note rapid, early transmitral mitral flow (E wave) and smaller contribution of atrial contraction (A wave). The record also reveals a middiastolic increase in flow (L wave) that is occasionally observed. (From Yellin EL, Nikolic SD. Diastolic suction and the dynamics of LV filling. In: Gaasch WH, LeWinter MM, eds. LV Diastolic Dysfunction and Heart Failure. Philadelphia: Lea & Febiger, 1994:92. Reproduced with permission of the publisher.)

Figure 3-2: Mitral flow recorded with a Doppler probe in the mitral annulus and simultaneous LA (LAP) and LV (LVP) pressures in a dog. Note initial gradient immediately after LV pressure crosses LA pressure. As shown here, when recorded with high-fidelity manometers, this is typically followed by a brief reversal of the gradient and then, following the slow-filling phase, by atrial contraction and a second increase in the gradient. Note rapid, early transmitral mitral flow (E wave) and smaller contribution of atrial contraction (A wave). The record also reveals a middiastolic increase in flow (L wave) that is occasionally observed. (From Yellin EL, Nikolic SD. Diastolic suction and the dynamics of LV filling. In: Gaasch WH, LeWinter MM, eds. LV Diastolic Dysfunction and Heart Failure. Philadelphia: Lea & Febiger, 1994:92. Reproduced with permission of the publisher.)

Ventricular volume changes as a function of time are similar on the right and the left sides, except for the virtual absence of isovolumic relaxation on the right (see Q+iH; Fig. 3-1). Systolic pressure waveforms, of course, differ. The thick-walled LV generates a much higher pressure than the RV, reflecting the highresistance systemic vascular bed. Pressure waveforms during filling are qualitatively similar in both ventricles but normally on the order of a few to as many as 7 to 8 mmHg higher in the left, reflecting the less distensible, thicker-walled LV chamber. Table 3-1 is a listing of hemodynamic values in normal adult human subjects.

Table 3-1: Hemodynamic Values in Normal Recumbent Adults

Measurement

Range

Mean

Cardiac index, liters/min per m2

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