Cardiac contraction cycle

Changes in mitochondrial calcium concentration during the cardiac contraction cycle. Cardiovasc. Res. 27, 1800-1809. 

Although blood pressure control follows Ohm s law and seems to be simple, it underlies a complex circuit of interrelated systems. Hence, numerous physiologic systems that have pleiotropic effects and interact in complex fashion have been found to modulate blood pressure. Because of their number and complexity it is beyond the scope of the current account to cover all mechanisms and feedback circuits involved in blood pressure control. Rather, an overview of the clinically most relevant ones is presented. These systems include the heart, the blood vessels, the extracellular volume, the kidneys, the nervous system, a variety of humoral factors, and molecular events at the cellular level. They are intertwined to maintain adequate tissue perfusion and nutrition. Normal blood pressure control can be related to cardiac output and the total peripheral resistance. The stroke volume and the heart rate determine cardiac output. Each cycle of cardiac contraction propels a bolus of about 70 ml blood into the systemic arterial system. As one example of the interaction of these multiple systems, the stroke volume is dependent in part on intravascular volume regulated by the kidneys as well as on myocardial contractility. The latter is, in turn, a complex function involving sympathetic and parasympathetic control of heart rate intrinsic activity of the cardiac conduction system complex membrane transport and cellular events requiring influx of calcium, which lead to myocardial fibre shortening and relaxation and affects the humoral substances (e.g., catecholamines) in stimulation heart rate and myocardial fibre tension. 

Arterial BP is the measnred pressnre in the arterial wall in millimeters of mercury. Two arterial BP values are typically measured, systolic BP (SBP) and diastolic BP (DBP). SBP is achieved during cardiac contraction and represents the peak valne. DBP is achieved after contraction when the cardiac chambers are filling and represents the nadir value. The difference between SBP and DBP is called the pulse pressure and indicates arterial wall tension. Mean arterial pressnre (MAP) is the average pressure throughout the cardiac cycle of contraction. It is sometimes used clinically to represent overall arterial BP. During a cardiac cycle, two-thirds of the time is spent in diastole and one-third in systole. Therefore, the MAP can be estimated by using the following equation ... 

Ryanodine receptors are a family of intracellular Ca release channels that were originally identified in the sarcoplasmic reticulum of skeletal muscle cells. Three members of the family were distinguished, RyR2 ryanodine receptors in the cardiac muscle. RyRl (in the skeletal muscle) and RyR2 function as Ca release chaimels from the sarcoplasmic reticulum intracellular calcium store and play a crucial role in the exdtation-contraction cycle. They bind and calmodulin and become phosphorylated by various protein kinases including Ca /calmodulin- and cAMP-dependent kinases (Lokuta etal. 1995, Mayrleitner etal. 1995). 

Additional information about regional cardiac contraction, like the dynamic fibre shortening and fibre orientation are measured with help of radiopaque markers which are inserted in the cardiac walls at different places. The spatial positions of the markers throughout the cardiac cycle and thus also cardiac dimensions are determined with help of a biplane X-ray system. 

It is the purpose of the present study to develop a general model of the LV which relates the mechanical determinants of cardiac contraction to the spatial myocardial energetics and the local coronary perfusion during the cardiac cycle. It is hoped that the model will help in the understanding and the quantification of... 

The Cardiac Cycle. The heart (Eig. lb) performs its function as a pump as a result of a rhythmical spread of a wave of excitation (depolarization) that excites the atrial and ventricular muscle masses to contract sequentially. Maximum pump efficiency occurs when the atrial or ventricular muscle masses contract synchronously (see Eig. 1). The wave of excitation begins with the generation of electrical impulses within the SA node and spreads through the atria. The SA node is referred to as the pacemaker of the heart and exhibits automaticity, ie, it depolarizes and repolarizes spontaneously. The wave then excites sequentially the AV node the bundle of His, ie, the penetrating portion of the AV node the bundle branches, ie, the branching portions of the AV node the terminal Purkinje fibers and finally the ventricular myocardium. After the wave of excitation depolarizes these various stmetures of the heart, repolarization occurs so that each of the stmetures is ready for the next wave of excitation. Until repolarization occurs the stmetures are said to be refractory to excitation. During repolarization of the atria and ventricles, the muscles relax, allowing the chambers of the heart to fill with blood that is to be expelled with the next wave of excitation and resultant contraction. This process repeats itself 60—100 times or beats per minute... 

Another noteworthy anatomical feature of the arteries is the presence of elastic connective tissue. When the heart contracts and ejects the blood, a portion of the stroke volume flows toward the capillaries. However, much of the stroke volume ejected during systole is retained in the distensible arteries. When the heart relaxes, the arteries recoil and exert pressure on the blood within them, forcing this "stored" blood to flow forward. In this way, a steady flow of blood toward the capillaries is maintained throughout the entire cardiac cycle. 

Cardiac function may be evaluated by the determination of left (or right) ventricular ejection fraction (VEF). In this procedure, regions of interest are defined at the end diastolic and end systolic phases of heart beat. The ejection fraction is defined as the ratio of tracer (blood) in the heart in the contracted (systolic) versus the relaxed (diastolic) phases of the heart cycle with appropriate corrections for decay and gamma camera dead time. The value obtained provides a measure of the ability of the heart to pump blood through the lungs (RVEF) or the body (LVEF). A criticism of Ir-191m for this application has been that the half-life (4.96s) is too short to allow effective visualization and quantitation of left ventricular function in adults, particularly those with delayed transit times. A recent... 

Then x variable plays in Zeeman s model the role of length of a fibre of the cardiac muscle while the b variable corresponds to the electrochemical control (contraction of the cardiac muscle is triggered by a biochemically generated electric impulse). A stable stationary point E may occur near the point B which is infinitely sensitive to perturbations. To transfer the system from the stable stationary point E to B, a perturbation of the system is required if E is located close to B the perturbation can be small. The mechanism of switching the heart from the state of equilibrium E (lack of heartbeat) to the state of action involves removing the system from the state E to B by way of stimulation, for example by an electric impulse. On reaching the state B the model system imitates the heartbeat — this is the trajectory BB CC E. A subsequent cycle requires the repeated stimulation at the point E. 

Electrical activity in the heart can be picked up by electrodes placed on the skin and recorded as the familiar electrocardiogram (ECG). The ECG is a record of the sum of all action potentials in the heart as it contracts. Action potentials are generated by depolarization followed by repolarization of the cardiac muscle cell membrane. Depolarization is initiated by an influx of sodium ions into the cardiac muscle cells, followed by an influx of calcium ions. Repolarization is brought about by efflux of potassium ions. The phases of a cardiac action potential are shown in Eigure 4.3 where the depolarization is the change in resting membrane potential of cardiac muscle cells from —90 mV to 4-20 mV. This is due to influx of sodium ions followed by influx of calcium ions. Contraction of the myocardium follows depolarization. The refractory period is the time interval when a second contraction cannot occur and repolarization is the recovery of the resting potential due to efflux of potassium ions. After this the cycle repeats itself. 

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