Also see information about afteroad in Pharmacy Profession Forum at http://forum.tomhsiung.com/pharmacy-research-study-and-policy/physiology-and-pathophysiology/699-preload-and-afterload.html#post1130
Afterload in the intact heart reflects the resistance that the ventricle must overcome to empty its contents. It is more formally defined as the ventricular wall stress that develops during systolic ejection. Wall stress (σ), like pressure, is expressed as force per unit area and, for the left ventricle, may be estimated from Laplace relationship:
σ = (P x r)/(2 x h) [Laplace Equation]
where P is ventricular pressure, r is ventricular chamber radius, and h is ventricular wall thickness. Thus, ventricular wall stress rises in response to a higher pressure load (e.g., hypertension) or an increased chamber size (e.g., a dilated left ventricle). Conversely, as would be expected from Laplace relationship, an increase in wall thickness (h) serves a compensatory role in reducing wall stress, because the force is distributed over a greater mass per unit surface area of ventricular muscle.
Components of Afterload
The forces that contribute to ventricular afterload can be identified by their relationship to the variables in the Laplace equation. The component forces of ventricular afterload include end-diastolic volume (EDV/preload), pleural pressure, vascular impedance, and peripheral vascular resistance.
Since afterload is a transmural wall tension, it will be influenced by the pleural pressure surrounding the heart. Therefore, negative pressure surrouding the heart will impede ventricular emptying by opposing the inward movement of the ventricular wall during systole. This effect is responsible for the transient decrease in systolic blood pressure that occurs during the insiratory phase of spontaneous breathing. When the inspiratory drop in systolic pressure is greater than 15 mm Hg, the condition is called "pulsus paradoxus" (which is a misnomer, since the response is not paradoxical, but is an exaggeration of the normal response).
Conversely, positive pressures surrounding the heart will promote ventricular emptying by facilitating the inward movement of the ventricular wall during systole. When intrathoracic pressure rises during a positive-pressure breath, there is a transient rise in systolic blood pressure, reflecting an increase in the stroke output of the heart. The inspiratory rise in blood pressure during mechanical ventilation is known as "reverse pulsus paradoxus". The "unloading" effect of positive intrathoracic pressure is the basis for the use of positive-pressure breathing as a "ventricular assist" maneuver for patients with advanced heart failure.
Vascular impedance is the force that opposes the rate of change in pressure and flow, and it is expressed primarily in the large, proximal arteries, where pulsatile flow is predominant. Impedance in the ascending aorta is considered the principal afterload force for the left ventricle, and impedance in the main pulmonary arteries is considered the principal afterload force for the right ventricle. Vascular impedance is a dynamic force that changes frequently during a single cardiac cycle, and it is not easily measured in the clinical setting.
(Systemic) vascular resistance is the force that opposes non-pulsatile or steady flow, and is expressed primarily in small, terminal blood vessels, where non-pulsative flow is predominant. About 75% of the vascular resistance is in arterioles and capillaries. In the beginning of arterioles, although the blood pressure is still pulsatile, the vascular smooth muscles have autoregulation function so the blood flow is steady. Becasue the flow is steady, the mean arterial pressure had been created to equal the "average" arterial pressure during a cardac cycle, under which the amount of blood flow per time is the same. So the relationship between SVR, MAP, and CO is:
SVR = (MAP – RAP) / CO
Similarly, the relationship between PVR, PAP, and CO is:
PVR = (PAP – LAP) / CO
However, SVR and PVR are not considered to be accurate representations of the resistance to flow in the pulmonary and systemic circulations. Because vascular impedance is not easily measured, vascular resistance is often used as a clinical measure of ventricular afterload. But animal studies have shown a poor correlation between direct measures of ventricular wall tension (true afterload) and the calculated vascular resistance. This is consistent with the notion that vascular impedance is the principal afterload force for ventricular emptying. However, the contribution of vascular resistance to afterload cannot be determined with the SVR and PVR because these parameters do not represent the actual resistance to flow in the circulatory system.
Determinants of Myocardial Oxygen Consumption
Myocyte contraciton is the primary factor determining myocardial oxygen consumption (MVO2) above basal levels. Therefore, factors that enhance tension development by the caridac muscle cells, the rate of tension development, or the number of tension generating cycles per unit time will increase MVO2. For example, doubling heart rate approximately doubles MVO2 because ventricular myocytes are generating twice the number of tension cycles per minute. Increasing inotropy also increases MVO2 because the rate of tension development is increased as well as the magnitude of tension, both of which result in increased ATP hydrolysis and oxygen consumption. Increasing afterload, because it increases tension development, also increases MVO2. Increasing preload (e.g., ventricular end-diastolic volume) also increases MVO2; however, the increase is much less than what might be expected because of the LaPlace relationship.
The LaPlace relationship has been discussed above. If we substitute ventricular end-diastolic volume/EDV for ventricular radius, we get below new LaPlace equation:
This relationship indicates that a 100% increase in venticular volume (V) incrases wall tension (T) by only 26%. In contrast, increasing intraventricular pressure (P) by 100% increases wall tension by 100%. For this reason, wall tension, and therefore MVO2, is far less sensitive to changes in ventricular volume than pressure.