Cardiac Physiology

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Chapter 3 Cardiac Physiology

Brian Johnson, MD, Maher Adi, MD, Michael G. Licina, MD, Zak Hillel, MD, Daniel Thys, MD, Roberta L. Hines, MD, Joel A. Kaplan, MD

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).

Figure 3-1 Interactions controlling the intact circulation. Changes in one or more of the determinants of cardiovascular performance directly affect the integrity of the circulation. Such interdependence must be considered when analyzing or treating hemodynamic disturbances.

(Modified from Braunwald E: Regulation of the Circulation, NEJM 290 (20): 1124–1129, 1974.)

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).

Figure 3-2 Phases of the cardiac cycle displayed in a pressure-volume diagram.

Phases of the Cardiac Cycle

Isovolumic Contraction Phase

This phase represents the first portion of systolic activity of the myocardial muscle. It occurs just after the QRS complex on the ECG, when individual myocardial fibers begin to shorten. As the contraction continues, the ventricular pressure increasesrapidly, exceeding atrial pressure and forcing the atrioventricular (AV) valve to close due to the reversed pressure gradient. While the AV valve closes, it also balloons up into the atrium and causes the chordal apparatus to tense, holding the coaptation point at its optimal position, thus preventing regurgitation. This now forms a sealed chamber (ventricle) because the AV valve has closed and the semilunar valves have yet to open. The ventricle continues to alter shape without changing its volume, thereby resulting in increased pressure. In awake canine hearts, the ventricle has been shown to change into an ellipse. This shape seems to be volume dependent, and at lower volumes the shape during contraction is spherical.¹

Early work by Frank has shown that tension (T) developed by cardiac muscle is determined by the initial length (L) or stretch of the muscle. In isolated muscles, the optimal tension developed is known as Lmax. At muscle lengths below or above Lmax, the developed tension is less than maximal.

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:

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

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

Isovolumic Relaxation Phase

The biochemical process of isovolumic relaxation begins to occur before the blood has even stopped flowing out of the ventricle and is an energy-consuming process. The term relaxation phase refers to the period immediately after closure of the semilunar valves. It is a phase in which the ventricle undergoes a rapid decrease in pressure and no change in volume, returning to the precontractile configuration.

Filling Phase (Diastolic Filling)

As the relaxation phase continues, the ventricular pressure continues to drop. At the same time, the atria are receiving blood flow from the pulmonary veins (left atrium [LA]) or the superior and inferior vena cava (right atrium [RA]), thus experiencing rises in pressure and volume. As the atrial pressure rises and ventricular pressure drops, a crossover point is reached where the AV valves open and blood flows down the pressure gradient into the ventricle. There are two phases to this flow: (1) a rapid phase based solely on the pressure gradient, and (2) a slower active phase based on the contraction of the atria (atrial kick). During this filling, the ventricular volume increases rapidly and yet the ventricular pressure changes very little, if at all, in the normal heart. This is measured by the end-diastolic pressure-volume relation (EDPVR), which describes ventricular distensibility and has a strong relationship to the compliance of the ventricle, extrinsic factors, and the determinants of ventricular relaxation. This process continues until the next electrical signal, which starts the contraction phase again.

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)	Impaired myocardial relaxation Diastolic calcium overload Increased resistance to ventricular inflow due to thick chamber walls, altered collagen matrix Activation of renin-angiotensin system

Volume overload (aortic or mitral regurgitation, arteriovenous fistula)

Increased diastolic volume relative to ventricular capacity

Myocardial hypertrophy, fibrosis

Dilated cardiomyopathy

Impaired myocardial relaxation

Diastolic calcium overload

Myocardial fibrosis or scar

* 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

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