Intraventricular flow-pressure

According to Laplace s law, a reduction in ventricular pressure and heart size results in a decrease in the myocardial wall tension that is required to develop a given intraventricular pressure and therefore decreases oxygen requirement. Since blood flow to the subendocardium occurs primarily in diastole, the reduction in left ventricular end diastolic pressure induced by nitroglycerin reduces extravascular compression around the subendocardial vessels and favors redistribution of... 

Direct effects on the heart are determined largely by Bi receptors, although B2 and to a lesser extent a receptors are also involved, especially in heart failure. Beta-receptor activation results in increased calcium influx in cardiac cells. This has both electrical and mechanical consequences. Pacemaker activity—both normal (sinoatrial node) and abnormal (eg, Purkinje fibers)—is increased (positive chronotropic effect). Conduction velocity in the atrioventricular node is increased (positive dromotropic effect), and the refractory period is decreased. Intrinsic contractility is increased (positive inotropic effect), and relaxation is accelerated. As a result, the twitch response of isolated cardiac muscle is increased in tension but abbreviated in duration. In the intact heart, intraventricular pressure rises and falls more rapidly, and ejection time is decreased. These direct effects are easily demonstrated in the absence of reflexes evoked by changes in blood pressure, eg, in isolated myocardial preparations and in patients with ganglionic blockade. In the presence of normal reflex activity, the direct effects on heart rate may be dominated by a reflex response to blood pressure changes. Physiologic stimulation of the heart by catecholamines tends to increase coronary blood flow. 

There are two proposed theories describing the mechanism of blood flow during CPR. The first theory, known as the cardiac pump theory, states that the active compression of the heart between the sternum and vertebrae creates an artificial systole in which intraventricular pressure increases, the atrioventricular valves close, the aortic valve opens, and blood is forced out of the ventricles. When ventricular compression ends, the decline in intraventricular pressure causes the mitral and tricuspid valves to open, and ventricular filling begins. The second, more recent theory is the thoracic pump theory. 

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