Volume Filling diastolic

A new ventricle model was developed using isolated canine heart experiments [37,46]. Experiments began with measurement of isovolumic ventricular pressure [37]. For each experiment, the isolated left ventricle was filled with an initial volume (end-diastolic) and the aorta was clamped to prevent outflow of blood. The ventricle was stimulated and the generated ventricular pressure was measured and recorded. The ventricle was then filled to a new end-diastolic volume (EDV) and the experiment repeated. As in the famous experiments of Otto Frank [21], isovolumic pressure is directly related to filling. 

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. 

The line plotted on a pressure-volume graph that describes the relationship between filling status and diastolic pressure for an individual ventricle (EDPVR). 

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. 

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... 

Myocardial hypertrophy The heart increases in size, and the chambers dilate. Initially, stretching of the heart muscle leads to a stronger contraction of the heart. However, excessive elongation of the fibers results in weaker contractions. This type of failure is termed systolic failure and is a result of a ventricle unable to pump effectively. Less commonly, patients with CHF may have diastolic dysfunction—a term applied when the ventricles ability to relax and accept blood is impaired by structural changes, such as hypertrophy. The thickening of the ventricular wall and subsequent decrease in ventricular volume decreases the ability of heart muscle to relax. In this case, the ventricle does not fill adequately, and the inadequacy of cardiac output is termed diastolic heart failure. 

In CHF, the impaired contractile function of the heart is exacerbated by compensatory increases in both preload and afterload. Preload is the volume of blood that fills the ventricle during diastole. Elevated preload causes overfilling of the heart, which increases the workload. Afterload is the pressure that must be overcome for the heart to pump blood into the arterial system. Elevated afterload causes the heart to work harder to pump blood into the arterial system. Vasodilators are useful in reducing excessive preload and afterload. Dilation of venous blood vessels leads to a decrease in cardiac preload by increasing venous capacitance arterial dilators reduce systemic arteriolar resistance and decrease afterload. 

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. 

Organic nitrates (A) increase blood flow, hence 02 supply, because diastolic wall tension (preload) declines as venous return to the heart is diminished. Thus, the nitrates enable myocardial flow resistance to be reduced even in the presence of coronary sclerosis with angina pectoris. In angina due to coronary spasm, arterial dilation overcomes the vasospasm and restores myocardial perfusion to normal. 02 demand falls because of the ensuing decrease in the two variables that determine systolic wall tension (afterload) ventricular filling volume and aortic blood pressure. 

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. 

Abnormalities in filling are also associated with changes in chamber stiffness that occur in HCM. This stiffness may be the result of myocardial fibrosis, cellular disorganization, or increased myocardial mass. The decreased distensibility leads to an abnormally steep slope of the diastolic pressure-volume curve such that an increase in LV volume results in a disproportionate increase in diastolic pressure. 

Most patients with EiCM who have been treated with a CCB have received verapamil, although others also have been used. Intravenous verapamil has been noted to reduce the outflow tract gradient in patients with obstructive HCM. The mechanism may be a decrease in systolic function, as well as an increase in LV volumes owing to an enhanced LV diastolic filling. 

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... 

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