During these two phases, many different events are observed and we will describe them in the following sections. The heart rhythm consists of two phases: diastole and systole. The cardiac cycle is continuous. Filling of the ventricle (diastole) is followed by ventricular contraction (systole) to ensure sufficient cardiac output both during rest and during exercise to meet the body`s metabolic needs. Systole and diastole influence each other intimately to achieve this goal. Normal elastic recoil after left ventricular contraction (LV) promotes early filling of the ventricle, with late diastolic atrial contraction ensuring that myocardial sarcomas are stretched enough to optimize contractile strength. Exercise tests the health of this integrated system by shortening the time of myocardial filling and infusion, and a normally functioning cardiac electrical system is also needed for optimal performance. Atrial relaxation (atrial diastole) occurs when the ventricle contracts (ventricular systole). However, before ventricular contraction begins, the spread of the action potential of the atrium into the AV canal is briefly delayed.
This AV delay ensures that the blood has enough time to get out of the atrium and the full ventricular filling. Ventricular contraction pushes blood into the discharge tract beyond an open bulboventricular valve (BV). The cardiac cycle is completed when the ventricle relaxes (ventricular diastole). The cardiac cycle, completed by Lewis58 but first designed by Wiggers,59 provides important information about the timing of events (Fig. 22.16). The three basic events related to the left ventricle are HV contraction, HV relaxation and HV filling (Table 22.3). Similar mechanical events occur in the right ventricle. Heart murmurs and sounds caused by turbulence or vibration in the heart and vascular system can be innocent or pathological.
It is important to understand the timing of events in the cardiac cycle as a prerequisite for understanding heart murmurs. The relationship between the normal cardiac cycle and that of cardiac sounds is illustrated in Fig. 8.2. The cardiac cycle is defined as a sequence of alternating contraction and relaxation of the atria and ventricles to pump blood through the body. It begins at the beginning of one heartbeat and ends at the beginning of another. The process begins as early as the 4th week of pregnancy, when the heart contracts for the first time. When the myocyte [Ca2+]i decreases due to the absorption of SR Ca2+, Ca2+ dissociates troponin C, thus preventing further bridges.4 As this state of relaxation progresses, the rate of ejection of LV blood into the aorta (sputum reduction phase) decreases. During this phase, blood flow from the left ventricle to the aorta decreases rapidly, but is maintained by aortic recoil – the wind boiler effect.4 When the pressure in the aorta significantly exceeds the descending LV pressure, the aortic valve closes, creating the first component of the second sound, A2 (the second component, P2, results from the closure of the pulmonary valve, because pulmonary arterial pressure exceeds RV pressure). After that, the ventricle continues to relax. As the mitral valve is always closed during this phase after aortic occlusion, the LV volume cannot change (isolumonic relaxation). The rate of pressure drop during isovolumic relaxation is related to the extent of systolic shortening during the previous contraction, similar to a spring pressed under its unloaded sagging length.60 When the LV pressure falls below that of the left atrium, the mitral valve opens (usually silent) and the filling phase of the cardiac cycle begins again (Fig. 22.16).
Another independent representation of cardiac cycle time is obtained by recording instant ventricular pressure and volume (Figure 11). During ventricular filling, pressure and volume increase non-linearly (phase I). The instantaneous slope of the pressure-volume (P-V) curve during filling (dP/dV) is diastolic stiffness, and its inversion (dV/dP) is conformity. As the volume of the chamber increases, the ventricle becomes more rigid. In a normal ventricle, surgical adherence is high because the ventricle acts on the flat part of its diastolic P-V curve. During isovolumetric contraction (phase II), the pressure increases and the volume remains constant. During sputum (phase III), the pressure rises and falls until the minimum ventricular size is reached. The maximum pressure-to-volume ratio (maximum stiffness or elasticity of the active chamber) usually occurs at the end of ejection. This is followed by isovolumetric relaxation (phase IV), and when the left ventricular pressure falls below the left ear pressure, ventricular filling begins. Thus, the end diastole is located in the lower right corner of the loop and the end sysstole in the upper left corner of the loop. Left ventricular P-V diagrams can illustrate the effects of changes in preload, postload, and inotropic state in the intact ventricle (see below).
The first heart tone or S1 or “lubricating noise” is caused by the closure of the atrioventricular valves. This occurs at the beginning of the ventricular systole. It can be displayed graphically at the point after the first ventricular pressure wave. This coincides with the “a” wave of the ear pressure wave and the “R” wave of the ECG. The second heart tone or S2 or the “dub” tone is caused by the closure of the crescent valves. This occurs at the beginning of the diastole, during the isovolumetric relaxation phase. It coincides with the “incisura” of the aortic pressure curve and the terminal end of the ECG T-wave. These four phases of the cardiac cycle can be determined by a pressure-volume diagram (E-Fig. 47-5), which represents the instantaneous ventricular pressure relative to the volume to calculate the pressure-volume loop. Similar effects occur on the left and right sides of the heart, but with higher pressures on the left (Table 47-1). The autonomic sinuatrial node initiates an action potential that spreads throughout the atrial myocardium. Electrical depolarization leads to a simultaneous contraction of the atria, as a result of which residual blood is pushed from the upper chambers into the lower chambers of the heart.
Ear contraction causes a further increase in ear pressure. The heart has a remarkable ability to absorb an increased volume of blood that enters the heart. In fact, the increase in the final diastolic volume also leads to an increase in cardiac output. This principle was described by two renowned physiologists and was therefore called the Frank-Starling mechanism of the heart. The underlying principle is that the heart pumps all the blood that returns to it through the veins within physiological limits. Typical changes in blood pressure and flow during the cardiac cycle occur in large veins such as vena cava (Fig. 1.17). Such pressure and flow oscillations can sometimes be transmitted to more peripheral vessels.
There are three positive pressure waves (a, c, v) in the central veins that correspond to the pressure changes in the atria. This wave is caused by an atrial contraction at the terminal diastole. The buoyancy of the C wave is related to the increase in pressure when the tricuspid valve is closed and inflates during isovolumetric ventricular contraction. The subsequent downward impact (x descent) results from the pressure drop during atrial relaxation caused by the traction of the tricuspid valve ring towards the end of the heart during ventricular contraction, which tends to increase the right ear volume. Iv-wave buoyancy results from a passive increase in atrial pressure during the late ventricular systole, when the tricuspid valve is closed and the atrium fills with blood from the peripheral veins. The downward shock of the V-wave is caused by the pressure drop that occurs when blood quickly leaves the atria and fills the ventricles, shortly after the tricuspid valve is opened, at the beginning of the ventricular diastole, called the Y-descent. Early ventricular filling begins with Y-shaped descent. Changes in blood pressure and flow in the large central veins associated with cardiac cycle events are usually not evident in the peripheral veins of the extremities. This is probably the result of attenuation associated with high stretching (adherence) of the veins, as well as compression of the veins by intra-abdominal pressure and mechanical compression in the thoracic entrance.
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