Left ventricular end-diastolic pressure

Fig. 6.3 Hemodynamic profile of CAS 1609 on anesthetised dog (0.3mgkg 1 i.v.) systolic blood pressure (BPs), diastolic blood pressure (BPd), left ventricular end diastolic pressure (LVEDP), diastolic pulmonary artery pressure (PAPd), heart rate (HR), left ventricular...

Pharmacology The principal pharmacological action of nitrates is relaxation of the vascular smooth muscle and consequent dilation of peripheral arteries and especially the veins. Dilation of the veins promotes peripheral pooling of blood and decreases venous return to the heart, thereby reducing left ventricular end-diastolic pressure and pulmonary capillary wedge pressure (preload). Arteriolar relaxation reduces systemic vascular resistance, systolic arterial pressure, and mean arterial pressure (afterload). Dilation of the coronary arteries also occurs. The relative importance of preload reduction, afterload reduction, and coronary dilation remains undefined. 

Concomitant use of calcium channel blockers (atenolol) Bradycardia and heart block can occur and the left ventricular end diastolic pressure can rise when beta-blockers are administered with verapamil or diltiazem. Patients with preexisting conduction abnormalities or left ventricular dysfunction are particularly susceptible. Recent acute Ml (sotalol) Sotalol can be used safely and effectively in the long-term treatment of life-threatening ventricular arrhythmias following an Ml. However, experience in the use of sotalol to treat cardiac arrhythmias in the early phase of recovery from acute Ml is limited and at least at high initial doses is not reassuring. 

Since Kantrovitz et al. described the concept of counterpulsation in 1968 [3], the lABP has been the mainstay for temporarily augmenting the cardiac output and improving hemodynamics in acutely decompensated refractory HF [4, 5]. lABP use has been shown to reduce heart rate, left ventricular end-diastolic pressure, mean left atrial pressure, afterload, and myocardial oxygen consumption by at least 20-30%. The lABP also modestly increases coronary perfusion pressure and decreases the right atrial pressure, pulmonary artery pressure, and pulmonary vascular resistance [6]. 

The effects of phenytoin on the cardiovascular system vary with the dose, the mode and rate of administration, and any cardiovascular pathology. Rapid administration can produce transient hypotension that is the combined result of peripheral vasodilation and depression of myocardial contractility. These effects are due to direct actions of phenytoin on the vascular bed and ventricular myocardium. If large doses are given slowly, dose-related decreases in left ventricular force, rate of force development, and cardiac output can be observed, along with an increase in left ventricular end-diastolic pressure. 

Usual IV doses of verapamil are not associated with marked alterations in arterial blood pressure, peripheral vascular resistance, heart rate, left ventricular end-diastolic pressure, or contractility. 

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... 

Injection into the left ventricle or the proximal aorta is likely to produce more marked effects. Cardiac rate, stroke volume, and cardiac output increase. There is a rise in right and left atrial pressures and left ventricular end-diastolic pressure. The pulmonary arterial pressure is also increased. The blood volume expands and peripheral blood flow increases and then decreases as systemic resistance falls. The hematocrit falls and venous pressure gradually rises. As the systemic arterial pressure falls, the heart rate increases. These responses are largely due to the injection of strongly hypertonic solutions, which promote a rapid expansion of the plasma volume water shifts from the extravascular fluid spaces to the blood and moves out of the erythrocytes, which shrink and become crenated. Blood viscosity rises, but plasma viscosity does not increase significantly. The erythrocytes give up potassium to the plasma and this might contribute to the observed reduction in peripheral vascular resistance. 

There is a theoretical contraindication to nicorandil in patients with cardiogenic shock, acute left ventricular failure with low fiUing pressure, and hypotension. A sublingual dose of 20 mg in patients with coronary artery disease and normal left ventricular function was associated with a 12% fall in left ventricular end-systolic pressure, a 3% fall in left ventricular end-diastolic pressure, accentuated diastohc filhng, a 13% reduction in mean aortic pressure, and a reduced cardiac output at rest (9,30). However, cardiac output may be augmented by up to 60% in patients with congestive cardiac failure or... 

The effects of berbamine of the isolated and perfused working heart of the guinea pig was studied. The alkaloid was observed to depress the function of the isolated working heart in a dose-dependent manner. The alkaloid (3 mol/l) decreased the left ventricular pressure, aortic pressure -dP/dtmax, aortic blood flow and coronary blood flow, and increased left ventricular end-diastolic pressure. At a concentration of 100 mol/l, ventricular asystole was produced, but there was no influence on atrial contraction. Berbamine was also observed to antagonize epinephrine-induced arrhythmias [202]. 

Right ventricular function frequently is impaired, presumably as a result of preservation injury and elevated pulmonary vascular resistance. A restrictive hemodynamic pattern may be present initially, but it usually improves over the 6 weeks following transplantation. Donor-recipient size mismatch may contribute to early posttransplantation hemodynamic abnormalities characterized by higher right and left ventricular end-diastolic pressures. Supraventricular arrhythmias in the early posttransplant period usually are transient and may result from overvigorous use of catecholamines or milrinone later, they should raise suspicion for acute rejection. 

Tocainide produces a small degree of depression on left ventricular function and left ventricular end diastolic pressure. 

Effects on the myocardium are not significant in normal individuals. In patients with coronary artery disease but no acute medical problems, 8-15 mg morphine administered intravenously produces a decrease in oxygen consumption, left ventricular end-diastolic pressure, and cardiac work effects on cardiac index usually are slight. In patients with acute myocardial infarction, the cardiovascular responses to morphine may be more variable than in normal subjects, and hypotension may be more pronounced. 

The protective effects of the Mn(ii)-based SOD mimics against myocardial ischemia/reperfusion injury in the isolated rabbit heart and monkey heart have been investigated. Kilgore et subjected Langendorff perfused, isolated rabbit hearts to a 30 minute period of global ischemia followed by a 45 minute period of reperfusion. Upon reperfusion, an increase in left ventricular end-diastolic pressure occurred, which was attenuated when the hearts were perfused with 20/.iM SC-52608. Perfusion of SC-52608 also inhibited the release of creatine kinase and intracellular potassium, and reduced the extent of antibody binding to the intracellular protein myosin which occurs upon reperfusion of the ischemic heart. These studies indicated that SC-52608 is cardioprotective to the reperfused, ischemic isolated rabbit heart. 

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