Preload

Preload refers to the volume of blood present in the heart at the end of diastole (before the onset of contraction).

Measuring preload

Preload is measured as either the pressure in the ventricle at end diastole or the volume of blood in the ventricle at end diastole. Note that pressure and volume are intricately related.

Effect of preload on myocardial performance

Preload alters cardiac performance by way of the Frank Starling Law of the heart.

This law states that as preload is increased, the contractility of the heart is increased to increase stroke volume.

The mechanism for the action of the Frank Starling Law is as follows: the increased stretch of cardiac fibers at the onset of systole induces an increase in contractility by way of increasing the sensitivity of troponin-C for the existing amount of cytosolic calcium.

Factors affecting preload

Preload = volume of blood returning to the heart + the volume of blood left over from the last contraction (recall that approximately 50% of the blood in the ventricle is ejected during each contraction).

Factors that increase preload:

• Venoconstriction
• Increased blood volume
• Reduced ejection of blood from the ventricle due to reduced contractility so that more blood is left over at the end of the last contraction.
• Increased blood volume due to valvular insufficiencies.

Factors that reduce preload:

• Venodilation
• Blood loss with reduced circulating blood volume
• An increase in the volume of blood ejected at the time of the last contraction

How might an abnormality of preload manifest?

If preload is too high we usually observe signs of congestion. The increase in volume and therefore pressure in the ventricle causes an increase in pressure in all the chambers and vessels that drain into the ventricle with the elevated preload.

• If preload is abnormally elevated in the left ventricle, elevated pressures will develop in the left atrium, pulmonary veins, and pulmonary capillary bed, which may be followed by elevated pressures in the pulmonary arteries, right ventricle, right atrium, vena cavae, and veins that drain into the vena cavae. When the flux of fluid from the vasculature exceeds the ability of the lymphatics to accommodate, then fluid accumulates.
  • The elevated hydrostatic pressure in the pulmonary capillary bed will promote the efflux of fluid into the pulmonary interstitium with pulmonary edema developing.
  • The elevated pressures in the right atrium will promote the collection of fluid in the pleural space (pleural effusion), in the abdominal cavity (ascites or abdominal effusion), or collection of fluid in the other organs such as the skin (subcutaneous edema) or edema of other organs.
• If preload is abnormally elevated in the right ventricle, elevated pressures will develop in the right ventricle, right atrium, vena cavae, and veins that drain into the vena cavae.
  • The elevated pressures in the right atrium will promote the collection of fluid in the pleural space (pleural effusion), in the abdominal cavity (ascites or abdominal effusion), or collection of fluid in the other organs such as the skin (subcutaneous edema) or edema of other organs.

If preload is too low we observe signs of reduced blood volume or perfusion. The reduction in volume and therefore pressure in the ventricle causes a reduced contractility (Frank Starling Law) and a reduced CO.

• If preload is abnormally reduced in the left ventricle, hypotension will develop and reduced organ perfusion will occur with signs related to the organs involved.
• If preload is abnormally reduced in the right ventricle, pulmonary artery hypotension will develop with reduced filling of the left heart and reduced organ perfusion will occur with signs related to the organs involved.

Effect of the autonomic nervous system on preload

Sympathetic stimulation causes venoconstriction with increased venous return to the heart (increased preload). Reduction of venous stimulation or parasympathetic stimulation causes venodilation with reduced venous return to the heart (reduced preload).