My professor explained a situation where a vasodilator was infused into a patient. He said that if you infuse a vasodilator, Pdiastolic decreases, which causes SVR to decrease, which decreases MAP and increases afterload. This logic does NOT make sense to me AT ALL and I don't understand why afterload increases.
Can I instead think of it in the following way? Infuse a vasodilator > the blood vessels in the body will dilate > SVR decreases > MAP decreases (since MAP = CO x SVR)?
But if MAP decreases, the pressure in the aorta (or pulmonary artery) is decreased. Doesn't this mean that afterload decreases (since the pressure that the heart must generate in order to open the aortic valve or pulmonic valve is decreased) and, consequently, stroke volume increases?
Then I become confused all over again because if stroke volume increases, shouldn't MAP increase as well (according to MAP = CO x SVR)? MAN I feel like I go in circles when it comes to cardiology...
These questions entail the crux of cardiovascular physiology and this blurb will do it no justice. Arterial pressure, as its name entails, is the pressure inside the arterial vessels (rather than venous or other vessel types). Arterial pressure changes with respect to the heart's contractions, meaning that arterial pressure changes depending on whether the heart is in contraction (systole) or when the heart is relaxed (diastole). Mean arterial pressure (MAP) is the average of this rise and fall in pressure over time and can be calculated by integrating pressure tracings and dividing them over time. Graphically, if we instead assume that a diastole->systole->diastole contraction cycle causes a rise and drop in pressure tracings such that it looks similarly in shape to a triangle, MAP is half of the area of this triangle, and thus about the pressure 1/3 of the way up the height of the triangle. Pretty cool.
Anyway, arterial pressure is a pressure directly dependent upon two
physical factors: arterial blood volume and arterial compliance (a measure of vessel distensibility defined as the change in arterial blood volume over the change in arterial pressure, dV/dP). How these two elements directly affect arterial pressure (ie MAP) is by thinking that the heart injects a certain amount of blood volume into the arterial vessels, which then works to increase the pressure inside the arteries. This increase in pressure is offset if the arteries can expand in luminal size and accommodate this increase in blood volume, and is a characteristic of healthy (high compliance) patients. Another way to think about this is by trying to stuff water in plastic tubing of varying rigidity: it is much easier to stuff water in a more elastic tube filled with water than to stuff water in a more rigid tube also partially filled with water. This exact pressure with which you must overcome to stuff more water into is called "afterload" and is why, after all of the water injected by the heart is emptied into the aorta and the heart begins to relax, afterload=MAP. The relationship also helps explain why high compliance individuals are healthier than low compliance individuals, because if certain vessels are less distensible, they can therefore accommodate less blood volume inside them before there is a sharp increase in arterial pressure. If there is now an increase in arterial pressure, the heart has to pump harder against this greater vasculature pressure (again, since MAP=afterload). The heart overcomes this afterload by increasing its contractility through a number of certain ways, one of which is by increasing cardiac muscle, explaining why patients with low compliance can present with "enlarged hearts".
Now, remember how I said that MAP is a function of two
physical factors (arterial blood volume and arterial compliance)? Well, these two physical factors are an effect of earlier
physiological factors: cardiac output (essentially the volume of blood pumped by the heart per contraction, CO=heart rate times stroke volume) and peripheral resistance (ie total peripheral resistance, TPR or also systemic vascular resistance, SVR). The physiological factors influence the physical factors which directly influence arterial pressure. Since CO is a measure of the volume of blood pumped by the heart, increasing the heart's CO increases arterial volume, which then increases arterial blood pressure, demonstrating how CO affects MAP. Regarding TPR, one way to overcome this increase in blood pressure/volume is ensuring more blood leaves the arterial system and passes into the venous or lymphatic system, decreasing arterial pressure. This is done by decreasing peripheral resistance and allowing more flow from the arteries into the veins (where increases in blood volume have less of an effect on blood pressure because they can expand more). This also explains why veins are also termed "capacitance" vessels because they can "hold" blood volume similar to how capacitors can hold charge in physics. Remember the equations for series and parallel circuits? I hope you do since they are the exact equations used in cardio phys (electrical current is blood flow and voltage is pressure difference).
Vasodilators, the most important endogenous mediator being nitric oxide (NO), function by increasing blood vessel lumen size in the peripherals, decreasing the
resistance that prevents the blood in the arteries from passing into the veins. Since blood is leaving the arterial system more readily, there is less blood in the arteries with which the heart must pump against, decreasing systolic pressure (and MAP) and thus decreasing afterload. At a certain point, decreased resistance allows more blood to enter the venous system, which results in more blood returning to the heart. If more blood returns to the heart, this increase in preload causes more blood to be ejected per contraction, resulting in an increase in stroke volume. Increases in stroke volume would eventually cause an increase in afterload when enough blood has been transferred into the aorta such that there is now a substantial amount in the arterial system. This is the only way you can experience an increase in afterload with vasodilator administration, I believe. I would be interested in your professor's explanation.
