Mechanical Properties of the Heart
Adapted from Dr. Marc Dickstein's Lecture Notes

Pressure and Volume

It is important to understand what happens to LV pressure and volume throughout the cardiac cycle.

When pressure is plotted as a function of volume, a Pressure-Volume Loop is generated as shown in the above right panel. Note that Pressure and Volume circles the loop in the counter-clockwise direction.

What Determines How Much the Heart Pumps?

The primary goal of the heart is to circulate the right amount of blood to the tissues such that adequate amounts of oxygen are delivered. This "right amount" may fluctate greatly, and swiftly, depending on such things as metabolic rate (the amount of oxygen being used by the tissues). At rest, cardiac output (CO) is typically 70 ml/kg/min (around 5 liters/min for a 70 kg person). During exercise, cardiac output may increase upwards of 5-fold. So what are the mechanisms that allow for cardiac output to change?

1. Heart Rate. Let's say the heart rate at rest in a well-conditioned medical student is 50 beats per minute. That would mean that for each beat, the heart ejects 100 ml (Stroke Volume (SV)) of blood (to result in 5 liters being pumped each minute [CO=SV*HR]). All else being equal (i.e. SV stays at 100ml), raising the HR will raise the CO proportionally.
2. Preload. Preload refers to the stretch on the sarcomeres just prior to initiation of contraction (systole). The more blood there is in the chamber just prior to systole (i.e. at the end of diastole, termed end-diastole), the more the sarcomeres are stretched. The more they are stretched, the stronger is the contraction that occurs during systole, and the greater is the stroke volume. This is the Frank-Starling Relationship. You might ask, why should end-diastolic sarcomere length affect strength of contraction? Old answer: greater availability for actin-myosin cross-bridging. New answer: Length dependent activation of calcium channels. Both are right.
3. Afterload. Afterload refers to the forces that oppose ejection of blood out of the chamber. (sounds sinister!). Opposition to ejection is influenced by the state of the blood vessels (will be discussed in more detail in the blood flow in arteries section). Suffice it to say (for now) that the vessels can constrict or dilate, and thereby change the amount of total resistance to blood flow. This resistance influences afterload. Under normal conditions, the heart does not eject all of its contents; instead, it normally ejects approximately 2/3 of the blood that is in the chamber at end-diastole. (i.e. the Ejection Fraction is 67%). If afterload were increased, less of the blood in the ventricle would be ejected; conversely, if afterload were decreased, more of the blood in the ventricle would be ejected. All else being equal, raising afterload decreases SV, and lowering afterload increases SV.
4. Contractility. Contractility refers to the intrinsic strength of the ventricle, independent of loading condtions. If all else were kept constant, and contractility were increased (let's say by epinephrine release for example), then the ventricle would empty more of its contents during ejection; stroke volume (SV) would increase. All else being equal (i.e. preload and afterload unchaged), raising contractility increases SV, and lowering contractility decreases SV.