Ventricular end diastolic

A pulmonary artery (Swan-Ganz) catheter can be used to determine central venous pressure (CVP) pulmonary artery pressure CO and pulmonary artery occlusive pressure (PAOP), an approximate measure of the left ventricular end-diastolic volume and a major determinant of left ventricular preload. 

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...

This trace shows the volume of the left ventricle throughout the cycle. The important point is the atrial kick seen at point a. Loss of this kick in atrial fibrillation and other conditions can adversely affect cardiac function through impaired LV filling. The maximal volume occurs at the end of diastolic filling and is labelled the left ventricular end-diastolic volume (LVEDV). In the same way, the minimum volume is the left ventricular end-systolic volume (LVESV). The difference between these two values must, therefore, be the stroke volume (SV), which is usually 70 ml as demonstrated above. The ejection fraction (EF) is the SV as a percentage of the LVEDV and is around 60% in the diagram above. 

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... 

The usual cause of pulmonary edema is acute left ventricular failure. The sequelae of events after left heart failure roughly follow the pattern of reduced stroke volume, leading to increased end-systolic and diastolic volume, which elevates left ventricular end-diastolic pres-... 

Abbreviations BM-MNC, bone marrow mononuclear cell CABO, coronary artery bypass grafting CPC, circulating progenitor cells LV. left ventricle LVED. left ventricular end-diastolic diameter LVEDV, left ventricular end-diastolic volume LVEF, left ventricular ejection fraction NYHA, New York Heart Association SKMB, skeletal myoblast. 

However, if the ventricle is overly stretched, the effect of ventricular contraction is diminished. Q is the normal operating point to increased cardiac output. Decreased sympathetic reflexes and vascular tone cause decrease in ventricular end-diastolic pressure (B toQ). 

Ventricular end-diastolic pressure increases ( to Q ) in an effort to maintain an adequate cardiac output. 

The increased ventricular end-diastolic pressure causes symptoms of congestion, for example, dyspnea. 

Left ventricular end-diastolic (LVEDP) and peak systolic pressure (mm Hg)... 

GTN is a nitrate. This class of drugs are potent vasodilators. At therapeutic doses the main effect of nitrates is to act on vascular smooth muscle to dilate the veins, thus reducing central venous pressure (preload) and ventricular end-diastolic volume. The overall effect is to lower myocardial contraction, wall stress and oxygen demand, thereby relieving the angina. Nitrates also promote vasodilation of the coronary blood vessels. 

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]. 

Adverse Effects. The side effects of topical minoxidil are mainly local, caused by skin irritation and contact dermatitis. Systemic side effects are uncommon because of limited percutaneous absorption, but diffuse hypertrichosis of the face and limbs has been reported with the 5% solution and was attributed to systemic absorption of the drug (84). Although topical minoxidil does not change blood pressure in healthy subjects, it increases heart rate by 3-5 beats/min and slightly increases the left ventricular end-diastolic volume, cardiac output, and left ventricular mass (85). These effects are not considered clinically significant, and the potential for cardiovascular side effects is very low. 

Restrictive cardiomyopathy is primarily an abnormality of diastolic function that results in impaired filling and increases in ventricular end-diastolic pressures with normal or decreased diastolic volume. It is associated with normal systolic function early in the course of the disease but a decrease in systolic function later in the disease... 

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. 

Preload—Along with afterload, it is an important determinant of cardiac output. It is the degree of stretch of the myocardial fibers (sarcomeres) at the end of diastole. As the sarcomeres are stretched, the force of contraction increases. Preload is approximated by the left ventricular end diastolic volume or pressure. 

AF atrial fibrillation CHF congestive heart failure ICD implantable cardioverter defibrillator LBBB left bundle branch block LVEDD left ventricular end diastolic dimension LVEF left ventricular ejection fraction 6MHWD 6-minute hall walk distance NSR normal sinus rhythm QoL quality of life TDI tissue Doppler imaging. 

The nitrates/nitrites have multiple physiological effects. NTG, which has been in use for well over a century and is probably the most studied, is considered the prototype. It is an arterial and venous dilator. However, venous dilation is more pronounced at low nitrate levels, resulting in a pooling of blood in the veins. The ensuing decrease in venous return reduces ventricular volume, preload, which in turn reduces left ventricular end diastolic... 

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