Does decreased peripheral resistance increase cardiac output?

Answer 1

Decreased peripheral resistance can increase cardiac output, yes, but it is not necessarily a 1 to 1 relationship.

Cardiac output is a complex mechanism - cardiac output depends on stroke volume and heart rate. Heart rate is easy to understand, but stroke volume is a little trickier. Stroke volume depends on three things: contractility of the cardiac muscle, preload - or the filling of the heart, and afterload.

Contractility is partially determined by preload, how healthy the cardiac muscle is, and the effects of circulating bioamines, such as epinephrine, norepinephrine, dopamine, as well a any medications being taken that may affect contractility, such as beta blockers. Increased contractility causes a harder "squeeze," increasing the stroke volume on a beat by beat basis. Infarction of a portion of the wall decreases the amount of cardiac muscle present, decreasing the ability to contract, but also decreasing the ability to fill the ventricle, since scar tissue does not stretch like healthy muscle. Excessive hypertrophy (such as that caused by prolonged hypertension or hypertrophic cardiomyopathy), while helpful to a point in increasing contractility, will eventually impede filling of the ventricle by preventing the "stretch" before contraction and decrease the cardiac output.

Preload is basically how filled the ventricle is before it contracts. Decreased filling, obviously, decreases the stroke volume, thereby decreasing the cardiac output. The cardiac myocyte works best when slightly overstretched. This optimally apposes the actin and myosin myofilaments and produces the best power for contraction, which is the purpose of the atrial contraction - it provides just that little bit of extra fill before the AV valves close and optimizes the preload on the heart. Too much preload, however, is bad, as the myofibrils can be overstretched and then are less effective. This is all nicely explained by the Starling curve.

Afterload is basically what you asked about. It is partially determined by peripheral vascular resistance, but other factors interact as well. You have to remember that the vascular system is not a rigid tube, it is a living thing. As such, other obstacles can, and do, occur. For instance, aortic sclerosis is the most common cause of heart murmur in adults. The narrowing of the aortic valve and its impedence to blood flow increases the afterload on the heart, thereby decreasing the stroke volume. Septal hypertrophy, as seen in hypertrophic cardiomyopathy, can cause an intermittent occlusion or partial occlusion of the aortic outflow tract, increasing afterload, especially during high flow states and high heart rates.