What Is the Contraction Phase of the Heart Called
In people at rest, the heart beats about once a second. With each beat, the heart undergoes a series of four hemodynamic events represented by changes in pressures and volumes (E Fig. 47-4), as well as by the electrical activity represented by the ECG. When the heart muscle at the terminal diastole is relaxed, the ventricular pressure is at its resting level (terminal diastolic pressure) and the ventricular volumes are at their maximum value (final diastolic volume). The aortic pressure decreases as the blood expelled into the aorta during the previous ventricular contraction flows into the peripheral circulation. Atrial contraction provides a final boost to the ventricular volume immediately before the ventricular systole. Ventricular contraction increases the pressure in the ventricle; If this pressure exceeds the pressure in the atrium, the mitral valve closes. However, as the ventricular pressure remains lower than the aortic pressure, the aortic valve remains closed and, during this first phase of the cardiac cycle, the isovoluminous contraction phase, no blood enters or leaves the ventricle. During systole, the ventricular pressure eventually exceeds the aortic pressure, at which point the aortic valve opens, blood is expelled into the aorta, and the ventricular volume decreases during the sputum phase of the cycle. At the end of the systole, when the contraction is maximum, the ejection ends and the ventricular volumes are the lowest (endsystolic volume). The volume of blood expelled, called stroke volume (SV), is defined as the difference between terminal and final systolic diastolic volumes.
The ejection fraction (EF), defined as the percentage of final diastolic volume (PDE) expelled during contraction (EF = 100 × SV/EDP), is an index of cardiac function. The next phase of the cycle occurs when the heart muscle relaxes, the ventricular pressure is lower than the aortic pressure, and the aortic valve is closed. During this isovolume relaxation phase, the ventricular volumes remain constant, as the mitral and aortic valves are closed. When the ventricular pressure falls below the atrial pressure, the mitral and tricuspid valves open, and during the filling phase, blood flows from the atria into the ventricles. The “new” epidemiology of diastolic dysfunction of VLT was discussed in Chapter 6 of this volume. Diastolic heart failure is now recognized as a major national health problem, especially in older adults who have a high incidence of LV hypertrophy (LVH). Despite a normal VL injection fraction (LVEF), these patients have symptomatic heart failure and have morbidity and mortality almost equal to those of patients with reduced systolic function. Patients with diastolic heart failure also have a risk of first-onset atrial fibrillation and a higher incidence of stroke. Although LVEF is normal in diastolic heart failure, the ventricular contractile mechanics have been modified to prolong the period of isovolume contraction and relaxation, so that the diastolic filling period becomes shorter and may be insufficient. In systolic and diastolic heart failure, the degree of diastolic dysfunction is a powerful predictor of prognosis. The first cardiac tone or S1 or the “lub” sound 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” sound 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 end of the ECG T-wave. Cardiac cycle events for the left ventricle, which show changes in left atrial pressure, left ventricular pressure and volume, as well as aortic pressure. Point A, the opening of the valve AV. Point B, ear contraction. Point C, valve closure AV. Point D, opening of crescent valves. Point E, closing the semi-lunar flap.
Eventually, the ventricular pressure becomes lower than the ear pressure and the atrioventricular valves open. This leads to a filling of the ventricles with blood, which is often called rapid filling of the ventricles. It makes up most of the blood that is in the ventricle before it contracts. A small volume of blood flows directly from the vena cava into the ventricles. Towards the end of the ventricular diastole, the blood remaining in the atria is pumped into the ventricle. The total volume of blood present in the ventricle at the end of the diastole is called terminal diastolic volume or preload. Ventricular systole refers to the period of contraction of the ventricles. The electrical impulse arrives at the atrioventricular node (AV node) shortly after depolarization of the atria. There is a small delay at the AV node that allows the atria to complete the contraction before the ventricles are depolarized. The action potential descends to the AV node, the bundle of His, and then to the left and right branches of the bundle (conductive fibers that pass through the interventricular septum and branches to supply the ventricles).
These fibers carry electrical impulses through their respective ventricular territories, resulting in ventricular contraction. It`s not uncommon to sometimes hear a third-heart or S3 tone. This is usually caused by a sudden surge of blood into the ventricles of the atria. It is therefore most often an average diastolic sound that occurs after S2. As ventricular preload increases, the ventricle swells and, more broadly, the myocardiocytes are also stretched. This stretching brings the actin and myosin components of the muscle fiber to a more optimal level. Therefore, muscle fibers contract with greater force to pump the extra blood. Note, however, that this principle is only valid up to an optimal point. Any additional stretching beyond this point dissociates the actin-myosin complex, making it difficult to contract. Mitral and tricuspid valves, also called atrioventricular or AV valves, open during the ventricular diastole to allow filling. Late in the filling period, the atria begin to contract (atrial sysstole) and force a final blood harvest into the ventricles under pressure – see the cycle diagram. Then, triggered by electrical signals from the sinus node, the ventricles begin to contract (ventricular systole), and when the back pressure against them increases, the AV valves are forced to close, which prevents blood volumes from entering or leaving the ventricles; This is called the isovolumic contraction stage.
 Stages 1 and 2 together – “relaxation isovole” plus influx (equivalent to “rapid discharge”, “diastasis” and “atrial sysstole”) – include the ventricular period of “diastole”, including the atrial systole, during which blood returning to the heart flows through the atria into the relaxed ventricles. Stages 3 and 4 together – “isovolumic contraction” plus “sputum” – are the ventricular period “systole”, which is the simultaneous pumping of blood supplies separated from the two ventricles, one to the pulmonary artery and the other to the aorta. Remarkably, towards the end of the “diastole”, the atria begin to contract, and then pump blood into the ventricles; This pressure delivery during ventricular relaxation (ventricular diastole) is called the atrial systemstole, also known as the atrial kick. [Citation needed] Figure 11. a) Left ventricular pressure-volume loop (P-V) whose segments correspond to cardiac cycle events: diastolic ventricular filling along the passive P-V curve (phase I), isovolumetric contraction (phase II), ventricular exclusion (phase III) and isovolumetric relaxation (phase IV). (b) the ventricle emits a final systolic volume determined by the highest isovolumetric P-V line; an isovolumetric contraction (large arrowheads) of different terminal diastolic volumes (preload). When the ventricle begins to contract, the pressure exceeds that of the corresponding atrium, which leads to the closure of the atrioventricular valves. At the same time, the pressure is not enough to open the crescent-shaped valves. Therefore, the ventricles are in a state of isovolumetric contraction – since the total volume (final diastolic volume) in the ventricle does not change. During auscultation, it is common for the clinician to ask the patient to take a deep breath. This procedure not only allows you to hear the airflow, but can also increase heart murmurs. Inhalation increases blood flow to the right side of the heart and can increase the amplitude of heart murmurs on the right side.
The drain partially restricts blood flow to the left side of the heart and can increase the brightness of the left heart. Figure 4 shows the correct location of the stethoscope bell to facilitate auscultation. In a healthy heart, all activities and rest during each individual heart cycle or heartbeat are initiated and orchestrated by signals from the heart`s electrical conduction system, which is the heart`s “wiring” that carries electrical impulses through the body of cardiomyocytes, the heart`s specialized muscle cells. These impulses eventually stimulate the heart muscle to contract, thereby expelling blood from the heart chambers into the arteries and cardiovascular system; And they provide a complex and persistent signal system that controls the rhythmic beat of heart muscle cells, especially the generation of complex impulses and muscle contractions in the ear chambers. The rhythmic sequence (or sinus rhythm) of this signal transmission through the heart is coordinated by two groups of specialized cells, the sinus node (AS), located in the upper wall of the right atrium, and the atrioventricular (AV) node, located in the lower wall of the right heart between the atrium and ventricle. .