Regulation Of Cardiac Output

The primary function of the heart is to impart energy to blood to generate and sustain an arterial blood pressure sufficient to adequately perfuse organs. The heart achieves this by contracting its muscular walls around a closed chamber to generate sufficient pressure to propel blood from the left ventricle, through the aortic valve, and into the aorta. Each time the left ventricle contracts, a volume of blood is ejected into the aorta. This stroke volume (SV), multiplied by the number of beats per minute (heart rate, HR), equals the cardiac output (CO) (Equation 4-1).

Therefore, changes in either stroke volume or heart rate alter cardiac output.

The units for cardiac output are expressed as either mL/min or liters/min. The units for stroke volume are milliliters/beat (mL/beat), and the units for heart rate are beats/min. In a resting adult, cardiac output typically ranges from 5-6 L/min. Sometimes cardiac output is expressed as a cardiac index, which is the cardiac output divided by the estimated body surface area (BSA) in square meters. Several different formulas can be used to estimate BSA. One formula is BSA (m2) equals the square root of the (height [cm] times weight [kg] divided by 3600); BSA = (cm ■ kg/3600)1/2 (Mosteller formula). Calculating the cardiac index normalizes cardiac output to individuals of different size. A normal range for cardiac index is 2.6 to 4.2 L/min/m2.

Influence of Heart Rate on Cardiac Output

Although cardiac output is determined by both heart rate and stroke volume, changes in heart rate are generally more important quantitatively in producing changes in cardiac output. For example, heart rate may increase by 100% to 200% during exercise, whereas stroke volume may increase by less than 50%. These changes in heart rate are brought about primarily by changes in sympathetic and parasympathetic nerve activity at the sinoatrial node.

Changes in heart rate alone inversely affect stroke volume. For example, doubling heart rate from 70-140 beats/minute by pacemaker stimulation alone does not double cardiac output because stroke volume falls nearly proportionately. This occurs because the ventricular filling time decreases as the length of diastole shortens. However, when physiological mechanisms during exercise cause the heart rate to double, cardiac output more than doubles because stroke volume actually increases. This

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