Physiologic determinants of cardiac output

Published on 13/02/2015 by admin

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Last modified 13/02/2015

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Physiologic determinants of cardiac output

Amorn Vijitpavan, MD

Cardiac output (CO) is the quantity of blood that the heart pumps per minute. CO in a normal 70-kg individual with a heart rate (HR) of 70 to 80 beats/min is 5 to 6 L/min, but it decreases by approximately 25% when the individual is resting in the supine position and may increase approximately eightfold with exertion. The cardiac index (CI) normalizes a person’s CO for body surface area (BSA):

< ?xml:namespace prefix = "mml" />CI (L·min–1·m–2)=CO/BSA

A normal CI varies between 2.5 and 3.5·L·min^-1·m^-2. The two major determinants of CO are stroke volume (SV) and HR:

CO (L/min)=SV×HR

Heart rate

The HR is determined primarily by the rate of spontaneous phase 4 depolarization of the sinoatrial (SA) node pacemaker cells, which are influenced by neural and humeral mechanisms. In children, HR is critically important for maintenance of CO, whereas in adults, both HR and SV contribute significantly to CO. In addition to an increase in CO from an increase in HR (as one would expect from the formula CO = HR × SV), an increase in HR increases contractility (positive inotropic effect); however, a HR exceeding 170 beats/min reduces CO because of decreased ventricular filling time.

Stroke volume

The SV is the amount of blood ejected by the ventricle with each contraction. A normal SV is 70 to 80 mL. Determinants of SV include preload, afterload, and contractility.

Preload

Preload is directly proportional to end-diastolic myocardial fiber length, often represented as end-diastolic volume (EDV, with a normal value of ∼120 mL). During normal cardiac muscle contraction, the sarcomere length is relatively short, but if EDV increases, the length of the sarcomere increases, and during subsequent contractions, more force is generated, the maximum rate of pressure development (dP/dt) increases, and SV increases proportionately (Figure 34-1).

Figure 34-1 The Starling curve. As left ventricular end-diastolic volume (stretch of myofibrils) increases, myocardial contractility (stroke volume) increases.

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