Preload

Technically the end-diastolic pressure of either the left or right ventricles; simplified as the blood volume supplied to the left or right ventricles; note that the more volume or preload, the greater the myocardial stretch and forceful the contraction; increased preload most often results in increased cardiac output.

The blood supply to the ventricle is often referred to as preload. Technically, the definition of preload is the volume or pressure in the ventricle at the end of diastole. Note that atrial kick offers much to preload, especially for those getting on in years (contributing up to 35% of cardiac output). Preload is connected to stroke volume and cardiac output via the Frank-Starling law.

Related to stroke volume is the term ‘ejection fraction’. An ejection fraction is determined by an echocardiogram or via a pulmonary artery catheter. Ejection fraction is the percentage of volume ejected from the left ventricle. The left ventricle has about 100 ml of blood just before contraction. Of this 100 ml, about 50-80 ml is normally ejected from the heart with each beat (stroke volume). Therefore, about 50 to 80 percent of blood is ejected. This is a normal ejection fraction.

Most of us have heard of the Frank-Starling phenomenon (often referred to as Starling’s Law – Frank has somehow been left out over the years). Frank and then Starling demonstrated that as cardiac muscle fibers stretch, contraction becomes more forceful. In other words, the more the stretch of the heart’s chambers, the more forceful the contraction (and indeed the greater the stroke volume).

What causes the heart’s chambers to stretch? Blood filling into the chambers increase pressures causing fibers to stretch. Whether you refer to increased pressure or volume in a chamber as the cause of the stretch is probably not important. The key is that either way, you are referring to preload. More preload causes more cardiac fiber stretch and increased contractility.

Please refer to Figure 2.3: The Frank-Starling curve. The resting healthy heart depicts the varying contractility of the myocardium with respect to changes in ventricular end diastolic pressure (preload).

The slope of each curve is the key to this graph. Compare the healthy resting heart to the curves of both the diseased heart and the heart during strenuous activity. Notice how the effect of sympathetic stimulation (i.e. norepinephrine) during exercise results in a magnified effect of preload on contractility.

Compare the preload/contractility curve of the healthy heart with that of the diseased heart. While the healthy heart curves peak with a preload of about 12 mm of Hg, the diseased heart requires increased pressures to maximize contractility. The diseased heart depends more on preload than the healthy heart to drive an effective contraction.

Note that the higher the preload, the higher the myocardial workload. Therefore, high preload states (i.e. fluid overload) can make matters worse during ischemic episodes. And ischemia is one precursor to the development of serious dysrhythmias.

Figure 2.3 Frank-Starling Curve

Figure 2.3 depicts the relationship between ventricular end diastolic pressure and contractility for a resting healthy heart, a resting diseased heart and a healthy heart during strenuous activity.

Several points are evident here:

  1. in general, the force of contraction (contractility) increases as the pressure within the ventricles increase (increases in pressure and volume increase both cardiac fiber stretch and contractility);
  2. during strenuous activity, catecholamine release increases the force of contraction;
  3. for the diseased heart (i.e. cardiomyopathies), the force of contraction is impaired;
  4. increases in chamber pressure do not produce significant changes in contractility for the diseased heart; and
  5. there is a limit to the affect of ventricular end-diastolic pressures (VEDP) on contractility. With high VEDP, contractility begins to fall. In other words, with high VEDP, contractility and stroke volumes tend to decrease.

1. Six Second ECG Guidebook (2012), T Barill, p. 32, 40, 203, 206

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