For any given inotropic state, ventricular performance will be significantly affected by the degree of ventricular stretch as determined by ventricular end-diastolic volumes (EDV).
The general relationship, as shown above, is the Frank-Starling mechanism.

Several factors influence end diastolic volumes, beginning with total blood volume.

• Significant volume depletion leads to decreased cardiac output with preload and end-diastolic volumes declining.

• Venous tone

• Skeletal muscle activity

Atrial contraction:

• Atrial contraction (atrial kick) enhances ventricular filling.

• In the hypertrophic ventricle (with reduced compliance) appropriately time atrial contraction may be especially important in achieving adequate levels of ventricular filling.
   

Inotropic state (myocardial contractility): Factors that influence the inotropic state affect ventricular performance at a given ventricular end-diastolic volume. These factors change the concentration of Ca2+ at the myofilaments and include in part

• Adrenergic nerve activity

• Circulating catecholamines

• Exogenously administered agents:

  • cardiac glycosides

  • dopamine/dobutamine

  • caffeine

  • isoproterenol

  •  theophylline

  • calcium

Exogenously administered agents: Drugs that decrease ventricular performance:

• procainamide

• disopyramide

• calcium channel blockers

• alcohol

• barbiturates

• local and general anesthetics

Physiological Depressants:  hypoxia, hypercapnia, ischemia, and acidosis.

Loss of ventricular muscle mass:

Ventricular afterload:

• Afterload is the stress developed in the wall of the ventricle during ejection and depends on aortic pressure and ventricular dimensions.

• Myocardial fiber tension is determined by the product of the intracavity ventricular pressure and radius divided by wall thickness (Laplace's law).

• Therefore, for the same level of aortic pressure, afterload increases with ventricular dilation.

• Left ventricular stroke volume is inversely proportional to afterload.

• In the failing heart with limited or no preload reserve (increasing preload in a normal heart increase contractility), afterload determines ventricular performance.

• When afterload increases (increase in vasoconstriction) in the failing heart, cardiac output may be reduced further even while oxygen demand increases.

• Vasodilators may improve myocardial performance by reducing ventricular afterload

Exercise:

• With exercise, venous return is significantly increased and results in enhanced ventricular filling and preload.
  Increases in cardiac adrenergic activity and increases in circulating levels of catecholamines increase heart rate and enhance the myocardial contractility.

• Arterial pressure does not increase substantially since vasodilatation in exercising muscles offset the increase in cardiac output.