End-diastolic pressure-volume

FIGURE 54.5 Schematic diagram of left ventricular pressure-volume loops (a) End-systolic pressure-volume relation (ESPVR), end-diastolic pressure-volume relation (EDPVR) and stroke work. The three P-V loops show the effects of changes in preload and afterload, (b) Time-varying elastance approximation of ventricular pump function (see text). 

Diuretics and angiotensin-converting enzyme (ACE) inhibitors decrease cardiac output, dLYP/d, and end-diastolic pressure-volume relationships in normals but change these parameters, little, in heart failure patients. Studies in normals depend principally on decreasing preload, and effects on patients with diseases that increase preload would be/may be ntissed. 

JANICKI If you look at Shirato s data and if you look at the end diastolic point, they, more or less, fall on the exponential curve, even though the curves he gives, which are from the end of rapid filling to end diastole, are shifted. But they still end up on what looks like the end diastolic pressure-volume relationship. 

A-F This straight line represents the ESPVR. If a ventricle is taken and filled to volume a , it will generate pressure A at the end of systole. When filled to volume b it will generate pressure B and so on. Each ventricle will have a curve specific to its overall function but a standard example is shown below. Changes in contractility can alter the gradient of the line, a-f This curve represents the ED PVR. When the ventricle is filled to volume a it will, by definition, have an end-diastolic pressure a . When filled to volume b it will have a pressure b and so on. The line offers some information about diastolic function and is altered by changes in compliance, distensibility and relaxation of the ventricle. 

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. 

Adjust left ventricular balloon volume to produce an initial LV end-diastolic pressure (LVEDP) of 10 mmHg. Keep this balloon volume constant throughout the experiment. 

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... 

In their theoretical studies, Bogen et al (1980) assumed an initially spherical membrane model for the infarcted LV. Employing a finite element method, it was possible to obtain end diastolic and end systolic pressure-volume curves. From these P-V curves, the effects of infarct size and infarct stiffness on the... 

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...

The end diastolic aortic pressure = 85 mmHg The end diastolic LV volume = 101ml. 

Hemoglobin cotent = 0.15 gm/ml Arterial PO2 = 100 mmHg End diastolic aortic pressure = 85 mmHg End diastolic LV volume = 101 ml... 

Changes in the filling pressure of the ventricle (preload) move the end-diastolic point along the unique end-diastoHc pressure-volume relation (EDPVR), which represents the passive filling mechanics of the chamber that are determined primarily by the thick-walled geometry and nonlinear elasticity of the resting... 

Notes CO cardiac output VR venous return HR heart rate SV stroke volume EDV end-diastolic volume ESV end-systolic volume O blood flow AP pressure gradient R resistance r vessel radius P systolic pressure Piiastoik- diastolic pressure MAP mean arterial pressure TPR total peripheral resistance, P venous pressure Era- right atrial pressure Rv venous resistance. 

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. 

Cardiovascular Heart weight, wall thickness, left ventricular (LV) and right ventricular (RV) end-diastolic and end-systolic lumen volumes (EDV and ESV, respectively), cardiac output (CO), heart rate, and LV diastolic filling pressure Magnetic resonance imaging Dog Opie189... 

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. 

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. 

Hypertrophic cardiomyopathy (HCM) is a prototype for DHF The grossly thickened myocardium, structural changes, and interstitial fibrosis severely alter the passive elastic properties of the myocardium. Patients with HCM and LV outflow obstruction are sensitive to small changes in volume such that a small decrease in filling pressure can lead to a decrease in LV end-diastolic volume and a dramatic fall in stroke volume and cardiac output. 

Increased levels of angiotensin II The pericardium may have a constraining effect as LV filling pressure and end-diastolic volume increase. 

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