Cardiac output (CO) is dependent on the product of two variables, heart rate (HR) and stroke volume (SV), or the volume pumped by the heart with each contraction. The relationship between CO, HR, and SV can be summarized by the following equation: CO = SV × HR. While the intrinsic HR is dependent on the depolarization of the sinoatrial (SA) node, SV is dependent on three factors: ventricular preload, aortic afterload, and the strength of the myocardial contraction.
Left ventricular filling determines the left ventricular end-diastolic volume (LVEDV), which is generally directly proportional to left ventricular preload and CO. The Frank–Starling Law describes the relationship between LVEDV and CO. According to the Starling Law, CO increases with increasing left ventricular preload until the left ventricle reaches excessive end-diastolic volumes. With excessive end-diastolic volumes, the CO does not change and may actually decrease. The Frank–Starling Law is further described schematically in Figure 150-1.
Relationships between the output of the right and left ventricles and mean pressure in the right and left atria, respectively. At any given level of cardiac output, mean left atrial pressure (eg, point C) exceeds mean right atrial pressure (point A).
(Reproduced with permission from Koeppen BM, Stanton BA, Berne RM, Berne and Levy Physiology, 6th ed. Philadelphia, PA: Mosby/Elsevier; 2010.)
Factors Affecting Frank–Starling Physiology
Left ventricular preload and therefore, LVEDV are directly affected by changes in the filling of the left ventricle. Left ventricular filling, in turn, is affected by changes in intravascular volume as well as venous tone.
Factors leading to an increase in LVEDV and CO, thus shifting the Starling curve up and left, include:
volume expansion of the intravascular compartment (with administration of crystalloid, colloid, or blood components);
avoiding increases in the intrathoracic pressure (from positive pressure ventilation or tension pneumothorax) or increases in the pericardial pressure (from effusions or tamponade physiology); and
augmenting venous tone and venous return to the heart.
In contrast, factors leading to a decrease in LVEDV and CO, thus shifting the Starling curve down and right, include:
volume contraction of the intravascular space;
increases in the intrathoracic pressure (from positive pressure ventilation or tension pneumothorax) or increases in the pericardial pressure (from tamponade physiology); and
decreases in venous tone and venous return to the heart.
In addition to the effect of LVEDV on the shift of the Starling curve, left ventricular contractility is an additionally important factor with a profound impact on myocardial physiology. Myocardial contractility (inotropy) is influenced by the rate of myocardial fiber shortening (dependent on the concentration of intracellular calcium) as well as by neural and pharmacological factors. Sympathetic adrenergic ...