Diastolic filling pressure

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... 

Preload Preload (diastolic filling pressure) is a function of blood volume and venous tone. Because venous tone is mainly controlled by sympathetic outflow, activities that increase sympathetic activity usually increase preload. 

Stable angina pectoris Decreased myocardial oxygen consumption -decreased LV end-diastolic dimension -decreased LV filling pressure -decreased LV systolic pressure -decreased PVR Increased coronary blood flow -epicardial coronary artery dilation -stenotic segment dilation -coronary collateral vessel dilation -increased subendocardial perfusion... 

Systolic dysfunction Improved hemodynamic performance -decreased end-diastolic dimension -decrease filling pressure -decreased systolic pressure -decreased SVR -decreased mitral regurgitation Arterial vasodilation... 

The intramyocardial pressure, i.e., systolic squeeze, compresses the capillary bed. Myocardial blood flow is halted during systole and occurs almost entirely during diastole. Diastolic wall tension ("preload ) depends on ventricular volume and filling pressure. The organic nitrates reduce preload by decreasing venous return to the heart. 

Calcium accumulation and overload secondary to ischemia impair ventricular relaxation as well as contraction. This is apparently a result of impaired calcium uptake after systole from the myofilaments, leading to a less negative decline in the pressure in the ventricle over time. Impaired relaxation is associated with enhanced diastolic stiffness, decreased rate of wall thinning, and slowed pressure decay, producing an upward shift in the ventricular pressure-volume relationship put more simply, MVO2 is likely to be increased secondary to increased wall tension. Impairment of both diastolic and systolic function leads to elevation of the filling pressure of the left ventricle. 

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. 

Minoxidil has particularly adverse consequences in hypertensive patients who have left ventricular hypertrophy and diastolic dysfunction. Such poorly compliant ventricles respond subopti-mally to increased volume loads, with a resulting increase in left ventricular filling pressure. This likely contributes to the increased pulmonary artery pressure seen with minoxidil therapy in hypertensive patients and is compounded by the drug-induced retention of salt and water. Cardiac failure can result from minoxidil therapy in such patients the potential for this complication can be reduced but not prevented by effective diuretic therapy. Pericardial effusion is an uncommon but serious complication of minoxidil. Although more commonly described in patients with cardiac failure and renal failure, pericardial effusion can occur in patients with normal cardiovascular and renal function. Mild and asymptomatic pericardial effusion is not an indication for discontinuing minoxidil, but the situation should be monitored closely to avoid progression to tamponade. Effusions usually clear when the drug is discontinued but can recur if treatment with minoxidil is resumed. 

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. 

Preload Filling pressure of the heart determines end-diastolic fiber length and tension... 

Ventricular function curve The graph that relates cardiac output, stroke volume, etc, to filling pressure or end-diastolic fiber length also known as the Prank-Starling curve... 

During diastolic filling (A to B), ventricular pressure is below atrial and aortic pressures, so the mitral valve (between the left atrium and the left ventricle) is open, and the aortic valve (between the left ventricle and the aorta) is closed. Blood therefore flows from the atrium into the ventricle, based on the pressure gradient and the inertances and resistances of the inlet. Note that the pressure gradient will decrease as the ventricle fills due to the passive compliance of the chamber and the drop in pressure in the atrium. 

The retrospective analysis of 35 cases of large persistent AL pleural effusions versus 120 AL cardiomyopathy patients without effusions offers perspective on the role of cardiac dysfunction and elevated filling pressures on amyloid pleural effusions. No differences in multiple echocardiographic parameters (interventricular septal thickness, left ventricular ejection fraction, or sensitive measures of diastolic function) could be identified between the pleural effusions group and the effusion-free cardiomyopathy group (21). Ironically, nephrotic range proteinuria and hypoalbuminemia were more prevalent in the... 

The literature includes eight case reports of pulmonary hypertension in AL amyloidosis attributed to pulmonary vascular amyloid deposition (Table 2). Autopsies confirmed pulmonary artery amyloid deposits in four out of four cases. The prevalence of restrictive cardiomyopathy and diastolic dysfunction in AL patients predisposes them to secondary forms of pulmonary vascular disease. Direct measurements of pulmonary artery pressures (PAP) were obtained in five cases (3 pulmonary arteriograms, 2 right heart catheterizations) however, only two reports include direct measures of left atrial filling pressures. Echocardio-graphic estimates of elevated right ventricular systolic pressures and normal diastolic function were reported in all cases. 

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... 

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