Preload, HF, and Cardiac Output

by Lnursing Lnursing (New) New


So I'm reading up about heart failure for my NCLEX exam. One of the goals of care is to increase cardiac output in order to increase perfusion to vital organs such as the kidneys. Another goal is to decrease preload (or venous return) because the heart of overfilled. To decrease preload, diuretics can be given. This is where I am confused. This might be a dumb question, but I feel like these two goals are contradictory. If one were to decrease preload via diuretics, wouldn't this decrease cardiac output as well and then decrease perfusion to the kidneys? Wouldn't this be counterintuitive? Clarification would be great!


Edited by Lnursing

Rose_Queen, BSN, MSN, RN

Specializes in OR, education. Has 17 years experience. 5 Articles; 11,078 Posts

Perfusion, not profusion. Volume is only one part of cardiac output. Cardiac output depends on stroke volume and heart rate.

From Diuretics and Heart Failure (emphasis mine):

[h=3]Mechanism of action[/h]The pulmonary and peripheral edema seen in CHF are the result of multiple physiologic disturbances. Decreased cardiac output leads to relative renal hypoperfusion that stimulates neurohormonal activation of the renin-angiotensin-aldosterone axis. Sodium and free water retention occur, resulting in an increase in both volume and pressure in capacitance vessels. Hydrostatic pressure elevation leads to fluid extravasation into peripheral tissues as well as the lungs.

The Frank-Starling law describes the mechanism whereby a normal heart under a physiologic range of filling pressures increases stroke volume proportionally with an increase in preload. In contrast, in acute decompensated heart failure, a myopathic heart subjected to very elevated filling pressures is not able to effectively increase stroke volume. Acute elevation of left ventricular preload (end-diastolic pressure) directly leads to elevated left atrial pressures and pulmonary edema. Diuretics reduce intravascular volume, leading to a decrease in central venous pressure, right and left heart filling pressures, and pulmonary vascular pressures. Venous capacitance increases, and intrapulmonary fluid returns to the circulation. The left ventricular volume is smaller, and cardiac output typically increases. In the setting of mitral regurgitation, the reduced left ventricular volume improves mitral leaflet coaptation and decreases the regurgitant volume.