Cardiac Physiology

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Chapter 3 Cardiac Physiology

A thorough knowledge of the principles of cardiovascular physiology is the foundation for the practice of cardiovascular anesthesia. It serves as the basis of understanding the pathophysiologic mechanisms of cardiac disease as well as the patient’s pharmacologic and surgical management.

To assess the physiologic basis for cardiac dysfunction, a systematic inspection of the elements that determine cardiac output (CO) is required. These intrinsic factors—heart rate (HR)/rhythm, preload, contractility, and afterload—are codependent such that abnormality in one often results in altered function in the others. This complex interaction is intrinsically designed to regulate beat-to-beat changes in the cardiovascular system, thereby adapting to changes in physiologic demands.

Heart rate, preload, afterload, and contractility determine CO, which, in turn, when combined with peripheral arterial resistance, determines arterial pressure for organ perfusion. Similarly, the arterial system contributes to ventricular afterload, and these interactions influence mechanoreceptors in the carotid artery and aortic arch, providing feedback signals to higher levels in the central nervous system (medullary and vasomotor center). These centers then modulate venous return, HR, contractility, and arterial resistance (Fig. 3-1).

The heart’s primary function is to deliver sufficient oxygenated blood to meet the metabolic requirements of the peripheral tissues. Under normal circumstances, the heart acts as a servant by varying the CO in accordance with total tissue needs. Tissue needs may vary with exercise, heart disease, trauma, surgery, or administration of drugs. Although tissue needs regulate circulatory requirements, the heart can become a limiting factor, particularly in patients with cardiac disease. In this regard, it is important to differentiate circulatory function from cardiac and myocardial function.

The focus of this chapter is on the heart’s function as a pump. The various determinants of its pumping function are reviewed and, where applicable, newer clinical measurements of ventricular function are discussed.

CARDIAC CYCLE

The cardiac cycle of the left ventricle (LV) begins as excitation of the myocardium, which results in a sequence of mechanical events that lead to a pressure gradient being developed, ejection of the stroke volume (SV), and forward flow of blood through the body. These phases can be discussed based on the electrical activity, intracardiac pressures, intracardiac volumes, opening and closing of the cardiac valves, or the flow of blood into the peripheral circulation. Most practical of these is the relationship of pressure to volume over the course of the cycle. In this regard, systole represents the rapid increase in intracardiac pressure followed by the rapid decrease in volume. Diastole, on the other hand, represents first a rapid decrease in pressure followed by an increase in volume. An alternative to this approach is to exclude any temporal element and to study the relation of pressure to volume in the framework of a pressure-volume diagram (Fig. 3-2). In this diagram, the pressure is typically displayed on the vertical axis and the volume on the horizontal axis. This yields a pressure-volume loop of four distinct phases over the course of one contraction: isovolumic contraction, ventricular ejection (rapid and slow), isovolumic relaxation, and filling (rapid and diastasis).

Phases of the Cardiac Cycle

Ejection Phase

As soon as the developed pressure exceeds that of the resting pressure of the aorta or pulmonary artery, the semilunar valves open and the ejection phase begins. The actual opening of the valves is due to the movement of blood across the valve leaflets caused by the pressure gradient. The ejection phase leads to a marked decrease in ventricular volume and a slight increase in pressure initially that rapidly decreases to the dicrotic notch pressure. The equalization of the pressure gradient between the ventricular and aortic pressures signals the end of the ejection phase and allows closure of the semilunar valves. This is the point of smallest ventricular size and volume, also known as the end-systolic volume (ESV). This ESV is greatly dependent on the contractile state of the ventricle and the properties of the vascular system.

The relationship among muscle force, velocity, and length is not readily applied to the clinical setting, owing to the extreme difficulty of obtaining measurements in intact hearts. In clinical practice, these difficulties lead to use of the end-diastolic volume (EDV) and ESV, which are relatively easy to measure. The difference between these two is the SV:

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In addition, by using the SV equation divided by the EDV, ejection fraction (EF) can be obtained:

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EF is a well-known estimation of global cardiac function that is used worldwide. It allows application of the Starling principle in the study of cardiac function based on changes in EDV as they relate to SV. The use of transesophageal echocardiography (TEE) has greatly enhanced the clinician’s ability to directly visualize EDV and ESV using biplane apical and single-plane ellipsoidal methods.2

DIASTOLIC FUNCTION

Diastology, or the study of diastolic function, has become the most important focus of cardiac physiology in the past few years. Diastolic dysfunction has been seen in 40% to 50% of patients with congestive heart failure (CHF) despite normal systolic function.3 This led to a shift in thinking about cardiac function not only as the typical systolic factors of contractile force, ejection of SV, and generation of CO but also as diastolic factors. The use of transthoracic echocardiography (TTE) and TEE has greatly improved this knowledge of diastole by showing the actual real-time activities in the heart, as related to filling pressures, shape, and relaxation. It is now possible to relate diastolic dysfunction, which is increased impedance to ventricular filling, to structural and pathologic causes of CHF (Table 3-1).

Table 3-1 Conditions Involving Diastolic Heart Failure*

Conditions Mechanisms of Diastolic Dysfunction
Mitral or tricuspid stenosis Increased resistance to atrial emptying
Constrictive pericarditis Increased resistance to ventricular inflow, with decreased ventricular diastolic capacity
Restrictive cardiomyopathies (amyloidosis, hemochromatosis, diffuse fibrosis) Increased resistance to ventricular inflow
Obliterative cardiomyopathy (endocardial fibroelastosis, Loeffler’s syndrome) Increased resistance to ventricular inflow
Ischemic heart disease Postinfarction scarring and hypertrophy (remodeling)
Flash pulmonary edema, dyspnea during angina Diastolic calcium overload
Impaired myocardial relaxation Increased resistance to ventricular inflow
Hypertrophic heart disease (hypertrophic cardiomyopathy, chronic hypertension, aortic stenosis)

Volume overload (aortic or mitral regurgitation, arteriovenous fistula)

Dilated cardiomyopathy

* Diastolic heart failure is increased resistance to filling of one or both cardiac ventricles.

From Grossmvan W: Diastolic dysfunction in congestive heart failure. N Engl J Med 325:1557, 1991.

Determinants of Diastolic Function

Myocardial Relaxation

Relaxation of the myocardium is the first step in the physiologic process of diastole. It begins during the end of the previous systolic contraction and is intimately related to systolic forces. It is also key in the determination of the length and amount of earlypassive ventricular filling. Relaxation relies heavily on the use of energy and adenosine triphosphate (ATP) to drive the calcium from the cell into the sarcoplasmic reticulum. This energy-dependent process is controlled by myriad regulatory proteins and by numerous clinical factors. Failure of relaxation leads to rapid Ca2+ overload, particularly at increased levels of stimulating frequency.

Relating Echocardiography to Diastolic Function

The relationship between the stages of diastolic function and findings on both TEE and TTE has greatly enhanced the study and importance of diastolic function (Box 3-1). Using TTE and TEE in combination with Doppler techniques has made it possible via indirect means to obtain LV filling patterns.5 The most commonly accepted means of analyzing the flow patterns are via the Doppler transmitral flow and the pulmonary vein flow. Newer modes of measurement using tissue Doppler and color M-mode are leading to further insights into diastolic function.

Transmitral flow patterns are the first method, which is performed by placing a pulsed-wave Doppler signal in the area between the leaflet tips of the mitral valve. Two waves are obtained: first the E wave, which represents the early passive flow across the mitral valve; and second, the A wave, which represents atrial systole (Fig. 3-3). The small area of no flow between the E and A waves represents the diastasis.By comparing the ratios of these two waves it is possible to form a view of diastolic function. The ratios change with disease and age to yield several patterns, which represent different stages of failure. In early diastolic failure, the E/A wave ratio becomes less than 1, and the waves reverse with the E wave being shorter than the A wave; this is known as the delayed relaxation pattern. As failure progresses, the waves become pseudonormalized; that is, the E/A ratio reverts to the normal pattern of greater than 1. The final stage of failure as seen via the mitral valve shows a high, rapidly decelerating E wave with a small A wave; this pattern is known as the restrictive pattern. The use of these patterns on Doppler imaging allows for the staging of diastolic failure from a mild form to a more severe form.6,7

SYSTOLIC FUNCTION

Systolic function is the period existing between closure of the mitral valve and the start of contraction to the end of ejection of blood from the heart. The primary purpose of systole is the ejection of blood into the circulation via the generation of a pressure gradient. Systolic function has been used to determine outcome and therapeutic effectiveness for years.

Stroke Volume

The SV is the amount of blood ejected by the ventricle with each single contraction. The determinants of SV are preload, afterload, and contractility. Although these variables have a very clear meaning in reference to isolated muscles, their exact significance is much more ambiguous in the intact heart.

Preload

definition

Preload is equal to the ventricular wall stress at end-diastole. It is determined by ventricular EDV, end-diastolic pressure (EDP), and wall thickness. To apply the preload principle to clinical practice, the following adjustments can be made:

The assumption that ventricular distensibility is normal is not a valid assumption in many patients with cardiac disease. With coronary artery disease or aortic disease, diastolic function is often altered so that small increases in ventricular volume can produce large changes in ventricular pressure.

measurement

The LVEDV is difficult to measure clinically, and measurements have only recently become possible with techniques such as echocardiography. TEE has been extensively used to measure LV areas as an approximation of LV volumes. Some studies have found a good correlation between areas and volumes and have also shown that in surgical patients EDV derived from a single plane is a significant determinant of SV.8

The LVEDP can be measured with placement of a catheter into the LA. The LA catheter is commonly inserted surgically through one of the pulmonary veins. The LAP provides a good approximation of LVEDP, provided the mitral valve is normal (Fig. 3-4). The most common technique for the estimation of LVEDP during cardiac surgery is the placement of a pulmonary artery (PA) catheter. The PCWP usually provides a good approximation of LVEDP. Marked alterations in airway pressure, such as occur during the use of high levels of positive end-expiratory pressure (PEEP), may disturb the relationship between the PCWP and LAP. Depending on the compliance of the pulmonary parenchyma, either part or all of the airway pressure may be transmitted to the PA catheter. This must be considered when evaluating LV filling pressure with the PA catheter in patients receiving mechanical ventilation and PEEP. When the catheter cannot be advanced into the wedge position, the PADP may be used to estimate the LVEDP. It is usually quite accurate unless the pulmonary vascular resistance (PVR) is markedly elevated. The CVP provides the poorest estimateof LVEDP, although it is frequently used in patients with good function of the RV and LV. When cardiac disease is characterized by disparate RV and LV functions, the CVP may be misleading as an indicator of LVEDP.

Afterload

Contractility

definition

The third determinant of SV is contractility. Contractility is an intrinsic property of the cardiac cell that defines the amount of work that the heart can perform at a given load. It is primarily determined by the availability of intracellular Ca2+. With depolarization of the cardiac cell, a small amount of Ca2+ enters the cell and triggers the release of additional Ca2+ from intracellular storage sites (sarcoplasmic reticulum). The Ca2+ binds to troponin, tropomyosin is displaced from the active binding site on actin, and actin-myosin crossbridges are formed. All agents with positive inotropic properties, such as the catecholamines, have in common that they increase intracellular Ca2+, whereas negative inotropes have the opposite effect (Table 3-2).9

Table 3-2 Factors Affecting Contractility

Factors Increasing Contractility

Factors Decreasing Contractility

determinants

The large number of methods developed to measure contractility in the intact heart suggests that it is difficult to measure. Indices of contractility can be classified according to the phase of the cardiac cycle during which they are obtained.

Load-Independent Indices.

Because traditional indices of contractility are load dependent, different approaches to the quantification of the contractile properties of the heart have been explored. In one such approach, Suga and colleagues10,11 studied instantaneous pressure and volume in the canine heart. The ratio of ventricular pressure over volume is the ventricular elastance, which varies throughout the cardiac cycle. For each cardiac cycle, these researchers defined the maximal value of this ratio as the end-systolic elastance (EES) and the point at which it was reached as the end-systolic point. They further noted that with rapid decreases in preload all consecutive end-systolic points were positioned on a single straight line, known as the end-systolic pressure-volume relation (ESPVR) (Fig. 3-5). The slope of this line (EES) is proportional to contractility; it is steeper at higher contractility and flatter at lower contractility.

RIGHT VENTRICULAR FUNCTION

The contractile pattern, as well as the afterload presented to each ventricle (i.e., RV vs. LV), results in marked physiologic differences between the ventricles (Box 3-3). In contrast to the LV, which has a relatively simple and unified mechanism of contraction (by coaxial shortening), RV contraction occurs in three distinct phases. Initially, the spiral muscles contract, resulting in a downward movement of the tricuspid valve and shortening of the longitudinal axis of the RV chamber. This is followed by movement of the RV free wall inward toward the intraventricular septum. Because the RV free wall has limited muscular power, alterations in or failure of the intraventricular septum to contract normally will disturb the systolic function of the RV to a much greater degree than does a loss of RV free wall contractility. Finally, the third phase of RV contraction occurs when LV contraction imposes a “wringer” action, further augmenting overall RV contraction.

Global RV function is exquisitely sensitive to the impedance offered by the pulmonary vasculature.12 In comparison with the LV, which maintains a constant output over a relatively wide range of afterloads, the RV output abruptly decreases with even small increases in afterload (Fig. 3-6). Under normal conditions of RV function, any increase in afterload is accompanied by a substantial decrease in RVEF. However, normal RV contractile function is usually maintained until the mean PAP is 40 mm Hg or greater. Conversely, the RV appears to be less preload dependent than the LV (i.e., for a given preload, a smaller increase in SV is seen in the RV).

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Figure 3-6 Varying effects of afterload and preload seen in ventricular function curves from the right and left ventricles. The RV output is more afterload dependent and less preload dependent than the LV output.

(From McFadden ER, Braunwald E: Cor pulmonale and pulmonary thromboembolism. In Braunwald E [ed]: Textbook of Cardiovascular Medicine. Philadelphia, WB Saunders, 1980, pp 1643−1680.)

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