Contractility

Myocardial contractility is the intrinsic ability of the heart to contract independent of preload and afterload. Changes in the ability to produce force during contraction result from different degrees of binding between myosin (thick) and actin (thin) filaments. The degree of binding that occurs depends on concentration of calcium ions in the cell; in an intact heart, it is usually the action of the sympathetic nervous system (through catecholamines) that determines the concentration of calcium ions in the cytosol of cardiac muscle cells. All factors that cause an increase in contractility work by causing an increase in intracellular [Ca⁺⁺] during contraction.

Inotropy

Contractility is synonymous with inotropy and may be altered through the administration of inotropic agents. Drugs such as catecholamines (norepinephrine and epinephrine) that enhance contractility are considered to have a positive inotropic effect.

Model as a contributing factor

Under one existing model , the five factors of myocardial performance are considered to be

• Heart rate
• Conduction velocity
• Preload
• Afterload
• Contractility

By this model, if myocardial performance changes while preload, afterload, heart rate, and conduction velocity are all held constant, then the change in performance must be due to a change in contractility. However, changes in contractility alone generally do not occur. Other examples:

• An increase in sympathetic stimulation to the heart increases contractility and heart rate.
• An increase in contractility tends to increase stroke volume and thus a secondary increase in preload.
• An increase in preload results in an increased force of contraction by Starling's law of the heart; this does not require a change in contractility.
• An increase in afterload will increase contractility (through the Anrep effect).^[1]
• An increase in heart rate will increase contractility (through the Bowditch effect).^[1]

References