Contractility

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Myocardial Contractility is a term used in physiology to describe the performance of cardiac muscle.

Contractility is often defined as the intrinsic ability of a cardiac muscle fibre to contract at a given fibre length. 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.

The five determinants of myocardial performance are:

Heart rate
Conduction velocity
Preload
Afterload
Contractility

If myocardial performance changes while preload, afterload, heart rate, and conduction velocity are all constant, then the change in performance must be due to the change in contractility.

It might be thought that a better definition would be that Contractility is the property that represents the strength of myocardial contraction. However, this definition does not separate contractility from the other loading factors that affect the strength of myocardial contraction. In particular, an increase in preload results in an increased force of contraction - this is Starling's law of the heart - but this does not require a change in contractility.

Any substance that affects contractility is called an inotropic agent. For example, drugs such as catecholamines (norepinephrine and epinephrine) that enhance contractility are considered to have a positive inotropic effect.

The concept of Contractility was necessary to explain why some interventions (e.g. an adrenaline infusion) could cause an increase in myocardial performance even if, as could be shown in experiments, the preload, afterload and heart rate were all held constant. Experimental work controlling the other factors was necessary because a change in contractility is generally not an isolated effect.

For example:

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.

All factors that cause an increase in contractility work by causing an increase in intracellular [Ca⁺⁺] during contraction.