CIRCULATORY PHYSIOLOGY



The interaction between and actin, coupled with ATP produced by oxidative , is thought to be the basis for the contraction of each and therefore the contraction of the whole muscle. Each 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 , 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 , becomes left ventricular filling pressure or volume (i.e., the amount of stretch on the in diastole); and the ordinate, formerly tension, becomes or (i.e., the ability of the heart to generate tension). Note that as diastolic pressure increases, the normal heart is able to increase its , up to a point. This relationship is referred to as a curve and, given identical states of contractility and afterload (see below), defines the amount of work that a heart is able to perform. determine left ventricular filling The term afterload describes the “” or resistance against which the heart must contract. Like preload, afterload also can refer either to a single or to the heart as a whole. The afterload is approximated by the , the major determinant of the to left . 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 against which the heart must function, the less blood it can eject, and vice versa. Therefore, the curve will be shifted up and to the left with decreasing afterload and shifted down and to the right with increasing afterload. Shifts in 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 increases contractility and via sympathetic nervous system activa­tion, the most important to sympathetic stimulation serving to increase is the rise in heart rate ( = x heart rate). A decrease in the 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 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 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.
is a measure of the amount of blood flow in liters/minute. The cardiac index is the divided by the body surface area and is normally 2.8 to 4.2 L/min/sq m. 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 : R = (Pi - P2)/ilow (Fig. 1-3). For example, the is the difference between the mean pulmonary and mean pulmonary venous pressure, divided by the pulmonary blood flow. Similarly, is the difference between mean and mean right atrial pressure, divided by the systemic . Note that an increase in 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, will be unchanged; if pulmonary blood flow and pulmonary increase while pulmonary venous pressure remains the same, resistance will be unchanged.
The most widely used parameter for quantitat-ing overall is the ejection fraction, defined as the diastolic volume minus the systolic volume (), divided by Simultaneous ECG, pressures obtained from the left atrium, left ventricle, and aorta, and the jugular pulse during one . 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 , 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 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 , 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 .




Tags: , , , , , , , , , , , , , , , , , , ,

myofibril

Page 1 of 212»