Left ventricular end-diastolic volume

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. 

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. 

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. 

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. 

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. 

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-... 

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. 

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... 

In addition to improving symptoms, randomized clinical trials have also shown that conventionally indicated patients derive objective evidence of beneficial structural changes (often referred to as reverse remodeling) in response to CRT. Resynchronization reduces left ventricular end-systolic (10,18-19) and end-diastolic volumes (10,22,23), and increases left ventricular ejection fraction (10,21,23). The improvements in ejection fraction ranged from 2% to 7% and are noteworthy given that the baseline ejection fractions in these trials were in the range... 

ACE inhibitors are more potent arterial than venous dilators. In response to ACE inhibition, mean arterial pressure (MAP) may decrease or be unchanged the change in MAP will be determined by the stroke volume response to afterload reduction. Heart rate typically is unchanged, even when there is a decrease in systemic arterial pressure, a response that hkely refiects a decrease in sympathetic tone in response to ACE inhibition. The decrease in left ventricular afterload results in increased stroke volume and cardiac output. Venodilation results in decreases in right and left heart filling pressures and end-diastolic volumes. 

Holt [1] described the method of injecting an indicator into the left ventricular during diastole and measuring the stepwise decrease in aortic concentration with successive beats (Figure 13.5). From this concentration-time record, end-diastolic volume, stroke volume, and ejection fraction can be calculated. No assumption need be made about the geometric shape of the ventricle. The following describes the theory of this fundamental method. 

Equation (2) states that, given an end-diastolic volume 5V is inversely proportional to (the line coursing from the lower left to upper right corner of the bottom panel of Figure 1). This rectilinear relation is denoted the ventricular end-systolic pressure-stroke volume relationship (VPSVR) . 

Figure 1. Schematic explanation of coupling the left ventricular contraction with the systemic arterial tree. In the middle left panels, left ventricular contraction is represented by its end-systolic pressure-volume relationship. Given a particular end diastolic volume (EDV), this relationship can be converted into ventricular end-systolic pressure P s) stroke volume (5Vj relationship, which is shown by the rectilinear curve coursing from the lower left to upper right corner in the graph at the bottom. In the right middle panel, the aortic input impedance property is represented by a rectilinear arterial end-systolic pressure fF, )-stroke volume SV) relationship curve (Eq. (5)). See the text for the explanation of this representation. This arterial Pes-SV relationship is transcribed in the bottom panel in superposition with the ventricular Pe -SV relationship. The intersection of the two Pes-SV relationship curves indicates the end-systolic pressure and stroke volume which should result from coupling a left ventricle with the given EDV and the slope parameter with a systemic arterial tree with the slope parameter...

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