Systole and diastole are each subdivided into two further phases, resulting in a total of four phases of heart action. Pressure and volume in the ventricles and atria change in a characteristic manner due to contraction and relaxation processes, with the pressure in the left ventricle changing the most and the pressure in the atria the least.
During isovolumetric contraction and relaxation, all heart valves are closed.
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There are no periods in which all heart valves are open! The action potentials of the pacemaker centers are transmitted to the cells of the myocardium via the cardiac conduction system , thereby depolarizing the cells electromechanical coupling. As a result, voltage-activated calcium channels open, causing calcium ions to flow into the cardiomyocytes. Calcium binds to regulatory proteins of myofilaments troponin and allows interaction of actin and myosin.
The muscle cell contracts. The exact course of the molecular interaction of actin and myosin filament sliding theory is dealt with in the basics of muscle tissue. Membrane of SR. Plateau phase myocardium. All are located in the cell membrane. Depolarization myocardium. Upstroke and depolarization.
Early repolarization. Resting phase. Pacemaker cells have no stable resting membrane potential. Their special hyperpolarization -activated cation channels funny channels ensure a spontaneous new depolarization at the end of each repolarization and are responsible for automaticity of the heart conduction system!
In sympathetic stimulation, more I f channels open, increasing the heart rate. Upstroke and depolarization of a pacemaker cell are caused by the opening of voltage-activated L-type calcium channels. In other muscle cells and neurons , upstroke and depolarization are caused by fast sodium channels! The duration of action potentials differs in the various structures of the conduction system and increases from the sinus node to the Purkinje fibers!
To ensure the proper length of time for chamber emptying during systole and refilling during diastole before the next contraction, and to prevent tetany of cardiac muscle , it is imperative that every contraction of the myocardium is followed by a sufficiently long period of relaxation.
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Therefore, a heart muscle cell is not re-excitable for a short time after depolarization , which is known as the refractory period. Due to the very long action potential of cardiomyocytes — ms , the first excited cardiomyocytes are still refractory while the last are still excited. On the one hand, this prevents circulatory excitations and, on the other hand, gives the cardiomyocytes enough time to contract and relax, without being disturbed by re-excitation!
The firing frequency of the SA node is faster than that of other pacemaker sites e. The SA node activates these sites before they can activate themselves known as overdrive suppression. The plateau phase of the myocardial action potential is longer than the actual contraction. This allows the heart muscle to relax after each contraction and prevents a permanent contraction so-called tetany!
Cells in the relative refractory and supernormal period are particularly susceptible to arrhythmias e. During cardioversion, shock delivery needs to be synchronized with an R wave on ECG indicating depolarization and needs to be avoided during the relative and supernormal refractory periods T waves , indicating repolarization!
The heart can generate excitement on its own due to its pacemaker cells, but it must adapt its work to daily life requirements.
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Adaptation to short-term changes is provided by the Frank-Starling mechanism. Long-term changes in cardiac activity are regulated by the autonomic nervous system. The electrical activity of the heart can be recorded by electrocardiography. While an increase in preload leads to an increase in stroke volume , an increase in afterload leads to a decrease in stroke volume!
The autonomic nervous system is able to regulate the heart action in the long term. Sympathetic fibers innervate both the atria and ventricles. Parasympathetic fibers only innervate the atria.
The sympathetic nerve can therefore even alter the contraction force of the chambers inotropy. Persistent epinephrine surges and long-lasting sympathetic activity can damage blood vessel endothelium , increase blood pressure, and raise the risk of heart attacks and strokes. In the long term, however, these mechanisms increase cardiac work and lead to heart failure , which is why they are targeted by many drugs. Myocardial oxygen demand increases with an increase in the HR, myocardial contractility , afterload , and diameter of the ventricle.
Heart sounds are sounds that are generated during physiological heart action. Additional heart sounds may be heard in the context of pathological processes e. These pathological heart sounds are referred to as heart murmurs. Both heart sounds and heart murmurs can be heard using a stethoscope at characteristic points on the chest. For more information, please see auscultatory locations , heart sounds , abnormal heart sounds , and heart murmurs in the learning card on cardiac examination.
To regulate organ perfusion, it is necessary to adapt circulatory parameters, such as pressure, volume status, and pH, with sensors and then process this information in a central regulatory center. The regulation center in the medulla oblongata acts on various effectors to control the blood flow in the short and long term. If the baroreceptors of the carotid sinus are too sensitive, even small stimuli such as turning the head or the pressure of a shirt collar can lead to excessive blood pressure reduction and even fainting.
This is referred to as carotid sinus syndrome. The renin-angiotensin-aldosterone system plays a key role in long-term blood pressure regulation and therefore is an ideal target when it comes to lowering a patient's blood pressure. While beta blockers decrease renin release by the kidneys , the conversion of angiotensin I to angiotensin II by angiotensin-converting enzyme ACE can be influenced by so-called ACE inhibitors e. The effect of angiotensin II on receptors of target cells can be inhibited by AT1 receptor antagonists e.
In case of inadequate perfusion of organs and disturbed microcirculation e. To maintain adequate brain and heart perfusion, the blood supply to the extremities muscle, skin , the GI tract , and other internal organs is decreased centralization of blood flow by autoregulatory mechanisms. Additionally, vasoconstriction of precapillary resistance vessels raises systemic vascular resistance and reduces hydrostatic pressure in capillaries , increasing reabsorption of interstitial fluids into vessels.
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