Afterload is a concept of the work or pressure needed by the ventricle to eject blood out of the semilunar valve. The most common influence on afterload is the vascular tone or resistance to blood flow. But other factors, such as stenosis of the semilunar valve or viscosity of blood, may also affect afterload. Clinically, the vascular resistance is monitored and manipulated with drugs to increase or decrease afterload.
Vascular tone is a reflection of the diameter of the vascular lumen through which blood is pumped. Imagine blowing through straws. If the lumen of the straw is wider, it will be easier to blow through the straw. If the lumen is smaller, then it takes more work to blow through the straw. If you had to breathe through a narrow straw continuously, you would get tired over time. Similarly, when the ventricle has to pump blood through narrow arteries, it has to work harder to eject the blood through the vessels. The narrowness of the arteries is partially due to vascular muscle tension causing constriction of the vessel. This vascular tension is referred to as resistance to blood flow.
Vascular resistance is influenced physiologically by different factors. The sympathetic nervous system can either dilate or constrict blood vessels. When stimulated, alpha adrenergic receptor sites in the arteries will constrict arteries making their lumens narrower. Drugs like norepinephrine, phenylephrine, epinephrine, and dopamine have positive alpha-adrenergic properties which stimulate alpha-adrenergic receptor sites and cause vasoconstriction increasing vascular resistance. Other sympathetic agents stimulate beta2-adrenergic receptor sites in the vascular walls causing vasodilation and reduced vascular resistance. Drugs with beta2-adrenergic properties include isoproterenol and dobutamine.
The parasympathetic nervous system (PNS) can indirectly influence the vascular resistance. When stimulated, PNS releases acetylcholine which can facilitate the release of nitric oxide, a vasodilator.
Another vasoconstricting physiologic mechanism is the renin-angiotensin homeostatic system. When kidneys experience a drop in blood perfusion, they release renin, which converts angiotensinogen into angiotensin I. Then angiotensin converting enzyme (ACE) converts angiotensin I into angiotensin II, a potent vasoconstrictor. Angiotensin II also stimulates the release of aldosterone, a hormone that promotes the reabsorption of sodium and water through the kidneys.
Pathophysiological conditions that increase vascular resistance include hypertension, aortic stenosis, and polycythemia. Pathophysiological conditions that decrease vascular resistance include the distributive forms of shock such as neurogenic shock, anaphylactic shock, and more commonly septic shock.
Afterload is measured clinically by computations for systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR). Pulmonary vascular resistance is the afterload assessment for the right ventricle. Systemic vascular resistance is the afterload assessment for the left ventricle.
| SVR | = |
MAP – CVP CO |
× | 80 |
| PVR | = |
MPAP – PAOP CO |
× | 80 |
| Normal SVR = 800 – 1400 dynes/sec/cm-5 | ||||
| Normal PVR = 100 – 250 dynes/sec/cm-5 | ||||