Cardiac contraction is the process by which the heart muscle (myocardium) generates force to squeeze blood out of the chambers and into the circulation. It is triggered by an electrical impulse from the heart’s conduction system, which causes a rapid change in the electrical charge across the surface of each muscle cell (the action potential). This triggers the release of calcium ions inside the cell, which bind to proteins in the contractile machinery and cause the muscle fibres to slide together, shortening the cell and generating force.
Contraction of the ventricles (systole) ejects blood into the pulmonary and systemic circulations; relaxation (diastole) allows the chambers to refill. The amount of blood ejected per beat is the stroke volume, and the fraction of blood ejected from the left ventricle expressed as a percentage is the ejection fraction. In a healthy heart at rest, approximately 55 to 70% of the blood in the left ventricle is ejected with each beat.
The strength of contraction (contractility) is influenced by several factors. Preload (the degree of stretch in the ventricular wall before contraction, determined by how much blood fills the ventricle) affects contractile force via the Frank-Starling mechanism: the more the heart is filled, the more forcefully it contracts, up to a point. Afterload (the resistance the ventricle must overcome to eject blood, largely determined by blood pressure and valve resistance) also influences the volume ejected. Heart rate affects the amount of calcium available for contraction, with faster rates generally increasing force at moderate speeds.
After cardiac arrest, the heart muscle is often transiently stunned (myocardial stunning), causing reduced contractility even after circulation is restored. This reversible dysfunction typically improves over 24 to 72 hours. Where contractility is severely impaired, inotropic drugs (such as dobutamine) can be given to temporarily strengthen contraction while the heart recovers.
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