Contractility is a measure of the form of contraction of ventricle at a given preload.
A greater and forceful contraction will eject more fraction of blood from ventricle and this will increase the stroke volume.
Sympathetic nervous system (beta1 adrenergic receptors) and para sympathetic nervous system (muscarinic M2 cholinergic receptors) on the ventricular myocytes regulate the contractility of the ventricle.Beta blockers act by antagonising the sympathetic input into the myocardium.
Based on the action, it will reduce contraction and leads to anti hypertensive effects. Stroke volume, oxygen demand and cardiac output will be reduced too.
Contractility also increased by increasing the contraction of intracellular calcium. This can be achieved by the action of digitalis which decreased the extracellular calcium
Contractility can also decrease by systolic dysfunction, hypercapnia, hypoxia, acidosis and calcium channel blockade.
A greater and forceful contraction will eject more fraction of blood from ventricle and this will increase the stroke volume.
Sympathetic nervous system (beta1 adrenergic receptors) and para sympathetic nervous system (muscarinic M2 cholinergic receptors) on the ventricular myocytes regulate the contractility of the ventricle.Beta blockers act by antagonising the sympathetic input into the myocardium.
Based on the action, it will reduce contraction and leads to anti hypertensive effects. Stroke volume, oxygen demand and cardiac output will be reduced too.
Contractility also increased by increasing the contraction of intracellular calcium. This can be achieved by the action of digitalis which decreased the extracellular calcium
Contractility can also decrease by systolic dysfunction, hypercapnia, hypoxia, acidosis and calcium channel blockade.