Cardiac function refers to the contraction of cardiac muscle, which works as a pump to send blood throughout the circulatory system to provide adequate blood flow to organs and tissues. The heart achieves this by contracting its muscular through the aortic valve, into the aorta, and throughout the body. To accomplish this, the heart must maintain systolic and diastolic blood pressure and cardiac output (amount of blood ejected from the heart in one minute). Each time the heart beats, a volume of blood is ejected. This stroke volume (SV), times the number of beats per minute (heart rate [HR]), equals the cardiac output (CO). Normal, resting CO differs among individuals of different size. The resting CO of someone who weighs 240 pounds is greater than the cardiac output found in a person who weighs 120 pounds. Thus, measured values for CO are expressed as a flow (liters per minute [L/min]) per body surface area (m2). When cardiac output is expressed in this way, it is termed cardiac index and has the units of L/min/m2. The surface area is estimated from calculations based on body weight and height (body surface area = 0.007184 x W0.425x H0.725). Cardiac index normally ranges from 2.6 to 4.2 L/min/m2.
There are numerous measures that can assess cardiac function. More extensive analyses include simple and noninvasive to more complicated and invasive tests of cardiac function. Noninvasive tests include chest x-ray analysis, electrocardiography (ECG), and echocardiography. Invasive tests include cardiac catheterization, Thallium scanning, and for patients with coronary artery disease, pharmacologic or exercise stress ECG, pharmacologic or exercise stress myocardial perfusion imaging (MPI), electron beam computed tomography (EBCT), and positron emission tomography (PET). These techniques allow for the determination of global cardiac muscle function analyses, volumetric analyses (calculation of left ventricular functional parameters like end-diastole volumes and ejection fraction), and regional wall motion abnormalities. In addition, the function of the heart as a pump can be determined by the force of ventricular muscles during systole and is directly affected by the preload and contractility of the heart. Preload is the load on the cardiac muscle during diastole (relaxation). This preload (enddiastolic volume) alters the ability of the heart to change its force of contraction and therefore increases stroke volume. This response to changes in venous return is called the Frank-Starling mechanism. Contractility can also be increased with an increase in calcium release into the cell. This can occur in response to catecholamines (epinephrine and norepinephrine), which are released by the sympathetic nervous system. Cardiac activation is often a result of sympathetic activation from the central nervous system.
Blood pressure indirectly provides a measure of cardiac function. As blood is pumped out of the left ventricle into the arteries, pressure is generated. The mean arterial pressure (MAP; the average pressure within an artery over a complete cycle of one heartbeat) is determined by the CO, systemic vascular resistance (SVR), and central venous pressure (CVP): MAP = (CO × SVR) + CVP. At normal resting heart rates, MAP can be approximated by the following equation: MAP = DBP +1/3(SBP-DBP). MAP can indicate a level of cardiac function at rest.
In sport and exercise psychology, measures of cardiac function provide specific information regarding the effects of stress, both physical and psychological, on cardiac function. Elevations in cardiac function in physically healthy individuals indicate sympathetic nervous system activation. This can occur in response to perceived threat in a competitive challenge or in response to meeting the physical demands of movement. In addition, measures of cardiac function are often used to identify the physiological demand or intensity of an activity. This can be done to ensure that the activity is appropriate and safe and to examine changes in cardiac function following physical training, treatment, or an intervention.
References:
- Berntson, G. G., Quigley, K. S., & Lozano, D. (2007).Cardiovascular psychophysiology. In J. T. Cacioppo, L. G.Tassinary, & G. G. Berntson (Eds.), Handbook of psychophysiology (3rd ed., pp. 60–92). New York: Cambridge University Press.
- Boutcher, S. H., & Hamer, M. (2006). Psychobiological reactivity, physical activity, and cardiovascular health. In E. O. Acevedo & P. Ekkekakis (Eds.), Psychobiology of physical activity (pp. 161–176). Champaign, IL: Human Kinetics.
- Klabunde, R. E. (2012). Cardiovascular physiology concepts (2nd ed., pp. 60–99). Baltimore, MD: Lippincott, Williams & Wilkins.
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