Function

Providing sufficient cardiac output to maintain blood flow to other organ systems is the primary function of the left ventricle. Cardiac output is the result of systolic contraction of the left ventricle, which can be influenced by preload, afterload, and contractility.

Cardiac output (CO) is defined as the amount of blood that is pumped out of the heart in a given time. Heart rate (HR) is the number of heartbeats in a given time, often recorded as beats per minute (bpm). Stroke volume (SV) is the volume of blood ejected in a single ventricular contraction. Cardiac output can be calculated using the following equations:

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Cardiac output cannot be measured clinically, so ejection fraction is a commonly used index to estimate heart contractility. Left ventricular ejection fraction (LVEF) is the volume of blood pumped out of the heart during systole relative to the volume in the left ventricle at the end of diastole. LVEF is calculated using the following equation:

Factors Affecting Cardiac Output

Preload is the load on ventricular muscle during diastole. The load is caused by the volume of blood that fills the ventricle as it rests between contractions. Higher preload volumes generally increase contractility through the Frank-Starling mechanism. This mechanism occurs when the preload volume lengthens the myocyte sarcomere length closer to the optimal overlap of actin and myosin.

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Afterload is the pressure that the left ventricle must push against during each contraction. Conditions like hypertension, atherosclerosis, and aortic stenosis all require the left ventricle to work harder to overcome the elevated afterload pressure. If this occurs chronically, the left ventricle will undergo hypertrophic adaptations which can lead to pathology.

Contractility is the inotropic state of the heart muscle. The intracellular calcium levels greatly influence heart contractility with higher levels inducing a stronger contraction. Medications like digoxin are given to increase heart contractility via myocyte contractile performance and electrophysiological variables do so by raising intracellular calcium levels. These medications are therapeutic for those who suffer from chronic left ventricular dysfunction. Therapy can normalize action potential characteristics and result in improved left ventricular pump function in the setting of left ventricular failure. [6]

Evaluation of left ventricular function is the result of three indices: end-diastolic left ventricular chamber size, LVEF, and mean velocity of circumferential fiber shortening (MVCFc), which reflects heart muscle performance. All of these indices of measurements are preload and afterload-dependent and, therefore, can influence contractility, or relative inotropic sensitivity. [7]

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