Ventricular preload

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. 

Rapid fluid resuscitation is the best initial therapeutic intervention for treatment of hypotension in sepsis. The goal is to maximize cardiac output by increasing the left ventricular preload, which will ultimately restore tissue perfusion. 

The primary direct result of an effective dose of nitroglycerin is marked relaxation of veins with increased venous capacitance and decreased ventricular preload. Pulmonary vascular pressures and heart size are significantly reduced. In the absence of heart failure,... 

Diuretics are the mainstay of heart failure management and are discussed in detail in Chapter 15. They have no direct effect on cardiac contractility their major mechanism of action in heart failure is to reduce venous pressure and ventricular preload. This results in reduction of salt and water retention and edema and its symptoms. The reduction of cardiac size, which leads to improved pump efficiency, is of major importance in systolic failure. Spironolactone and eplerenone, the aldosterone antagonist diuretics (see Chapter 15), have the additional benefit of decreasing morbidity and mortality in patients with severe heart failure who are also receiving ACE inhibitors and other standard therapy. One possible mechanism for this benefit lies in accumulating evidence that aldosterone may also cause myocardial and vascular fibrosis and baroreceptor dysfunction in addition to its renal effects. 

How it works Decreases myocardial oxygen demand reduces left ventricular preload and afterload dilates coronary arteries, improves collateral blood flow to ischemic areas within myocardium. IV Produces peripheral vasodilation. 

Septic patients have enormous fluid requirements as a result of peripheral vasodilation and capillary leakage. Rapid fluid resuscitation is the best initial therapeutic intervention for the treatment of hypotension in sepsis. The goal of fluid therapy is to maximize cardiac output by increasing the left ventricular preload, which ultimately will restore tissue perfusion. Fluid administration should be titrated to clinical end points such as heart rate, urine output, blood pressure, and mental status. An increased serum lactate level, a byproduct of cellular anaerobic metabolism, should normalize as the tissue perfusion improves. 

Pulmonary artery occlusion pressure—It is usually determined by a balloon-tipped Swan-Ganz catheter that is advanced into a distal branch of the pulmonary artery. Inflation of the balloon at the catheter tip occludes the pulmonary artery and allows measurement of the left atrial pressure which reflects the left ventricular diastolic pressure. Therefore, it is a measure of the left ventricular preload. 

Children with complex congenital heart disease and hypoplasia of either ventricle frequently receive a bidirectional superior cavopulmonary shunt as a palliative procedure in anticipation of further surgical operations to reinstate all systemic venous return directly to the pulmonary artery. Thus, pulmonary blood flow occurs passively through the lungs in the absence of a subpulmonary ventricle. The pulmonary vascular resistance may influence both pulmonary blood flow and adequate systemic ventricular preload. Following such a superior cavopulmonary shunt intense cyanosis may occur... 

As with all the alkyl nitrates, GTN accumulates in the venous side of the circulation more than the arterial side. This phenomenon probably explains why these dmgs reduce ventricular preload more than afterload (unlike the calcimn channel blockers). GTN is excreted via the kidneys as a mixture of mono- and dinitrates, probably as their glucuronides. 

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