Health Human Disease Blog

The interaction between myosin and actin, coupled with ATP produced by oxidative phosphorylation, is thought to be the basis for the contraction of each myofibril and therefore the contraction of the whole muscle. Each myofibril exhibits a property called contractility (or inotropic state) that represents the ability of the fiber to develop contractile force. The force exhibited by the fiber is influenced not only by its contractile state but also by its initial length, or preload, according to the Starling curve (Fig. 1-7). This concept can be expanded from the single fiber to describe the function of the entire ventricle. Thus, the abscissa, formerly preload or fiber length, becomes left ventricular filling pressure or volume (i.e., the amount of stretch on the myocardial fibers in diastole); and the ordinate, formerly tension, becomes stroke volume or stroke work (i.e., the ability of the heart to generate tension). Note that as diastolic pressure increases, the normal heart is able to increase its stroke volume, up to a point. This relationship is referred to as a ventricular function curve and, given identical states of contractility and afterload (see below), defines the amount of work that a heart is able to perform. Several factors determine left ventricular filling The term afterload describes the “impedance” or resistance against which the heart must contract. Like preload, afterload also can refer either to a single myofibril or to the heart as a whole. The afterload is approximated by the arterial pressure, the major determinant of the impedance to left ventricular contraction. In the intact heart, the afterload determines the amount of blood the heart can pump given a fixed preload and fixed state of contractility; that is, the higher the workload against which the heart must function, the less blood it can eject, and vice versa. Therefore, the ventricular function curve will be shifted up and to the left with decreasing afterload and shifted down and to the right with increasing afterload. Shifts in ventricular function with changes in afterload are minimal in normal ventricles but prominent in failing ventricles.
Heart rate is another determinant of cardiac performance. Even though an increased demand for cardiac output increases contractility and stroke volume via sympathetic nervous system activa­tion, the most important response to sympathetic stimulation serving to increase cardiac output is the rise in heart rate (cardiac output = stroke volume x heart rate). A decrease in the cardiac output or blood pressure increases sympathetic and decreases parasympathetic discharge via barore-ceptor mechanisms to increase heart rate. Likewise, an elevated blood pressure will activate the carotid baroreceptors, augment vagal activity, and slow the heart rate.
Four phases of the cardiac cycle can be identified upon initiation of ventricular myocardial contraction (Fig. 1-8). (1) During “isovolumic contraction,” the intramyocardial pressure rises with no ejection of blood or change in ventricular volume. (2) When left ventricular pressure reaches that of the aorta, the aortic valve opens and blood is ejected from the contracting ventricle. (3) As the ventricle relaxes and left ventricular pressure decreases, the aortic valve closes, and “isovolumic relaxation” occurs. (4) Upon sufficient decrease in left ventricular pressure, the mitral valve opens and ventricular filling from the atrium occurs. The ventricle fills most rapidly in early diastole and again in late diastole when the atrium contracts. Loss of atrial contraction (e.g., atrial fibrillation or AV dissociation) can impair ventricular filling, especially into a noncompliant (”stiff”) vehicle.
Normal intracardiac pressures are shown in Figure 11. Atrial pressure curves are composed of the a wave, which is generated by atrial contraction, and the v wave, which is an early diastolic peak caused by filling of the atrium from the peripheral veins. The x descent follows the a wave and the y descent follows the v wave. A small deflection, the c wave, occurs after the a wave in early systole and probably represents bulging of the tricuspid valve apparatus into the right atrium during early systole. Ventricular pressures are described by a peak systolic pressure and an enddiastolic pressure, which is the ventricular pressure immediately before the onset of systole. Note that the minimum left ventricular pressure occurs in early diastole. Aortic and pulmonary artery pressures are represented by a peak systolic and a minimum diastolic value.
Cardiac output is a measure of the amount of blood flow in liters/minute. The cardiac index is the cardiac output divided by the body surface area and is normally 2.8 to 4.2 L/min/sq m. Cardiac output can be measured by either indicator dilution or the Fick technique (see Chapter 2). The pulmonary and systemic vascular resistances are also important parameters of circulatory function. Resistance is defined as the difference in pressure across a capillary bed divided by the flow across that capillary bed, usually the cardiac output: R = (Pi - P2)/ilow (Fig. 1-3). For example, the pulmonary vascular resistance is the difference between the mean pulmonary arterial pressure and mean pulmonary venous pressure, divided by the pulmonary blood flow. Similarly, systemic vascular resistance is the difference between mean arterial pressure and mean right atrial pressure, divided by the systemic cardiac output. Note that an increase in arterial pressure may occur without necessarily causing an increase in vascular resistance. For example, if both pulmonary arterial and venous pressures are elevated to the same degree, pulmonary vascular resistance will be unchanged; if pulmonary blood flow and pulmonary arterial pressure increase while pulmonary venous pressure remains the same, resistance will be unchanged.
The most widely used parameter for quantitat-ing overall ventricular function is the ejection fraction, defined as the diastolic volume minus the systolic volume (stroke volume), divided by Simultaneous ECG, pressures obtained from the left atrium, left ventricle, and aorta, and the jugular pulse during one cardiac cycle. For simplification, right-sided heart pressures have been omitted. Normal right atrial pressure closely parallels that of the left atrium, and right ventricular and pulmonary artery pressures time closely with their corresponding leftsided heart counterparts, only being reduced in magnitude. The normal mitral and aortic valve closure precedes tricuspid and pulmonic closure, respectively, whereas valve opening reverses this order. The jugular venous pulse lags behind the right atrial pressure.
During the course of one cardiac cycle, note that the electrical events (ECG) initiate and therefore precede the mechanical (pressure) events and that the latter precede the auscultatory events (heart sounds) they themselves produce. Shortly after the P wave, the atria contract to produce the a wave; a fourth heart sound may succeed the latter. The QRS complex initiates ventricular systole, followed shortly by left ventricular contraction and the rapid build-up of left ventricular (LV) pressure. Almost immediately LV pressure exceeds left atrial (LA) pressure to close the mitral valve and produce the first heart sounds. When LV pressure exceeds aortic pressure, the aortic valve opens (AVO), and when aortic pressure is once again greater than LV pressure, the aortic valve closes to produce the second heart sound and terminate ventricular ejection. The decreasing LV pressure drops below LA pressure to open the mitral valve (MVO), and a period of rapid ventricular filling commences. During this time a third heart sound may be heard. The jugular pulse is explained under the discussion of the venous pulse.
the diastolic volume: (DV-SV)/DV. These vol­umes may be estimated from either invasive (e.g., left ventriculography) or noninvasive (e.g., echocardiography or radionuclide ventriculography) tests. The ejection fraction may be a useful gross evaluation of ventricular function, but there are situations (for example, when a large left ventricular aneurysm is present) in which the ejection fraction can give a misleading impression of overall ventricular function.