Cardiac outputTotal peripheral resistanceBlood pressureControl of TPR, CO & BP


Three important concepts in cardiovascular physiology are cardiac output, peripheral resistance and blood pressure. Peripheral resistance is determined by the diameter of small arteries, while cardiac output is simply a measure of how much blood the heart pumps in a given time. Blood pressure is the product of both cardiac output and peripheral resistance. Therefore, blood pressure can be modified by changes in either cardiac output, peripheral resistance or both.

Cardiac output

Cardiac output is determined by the volume ejected from the ventricles and the rate that the heart is beating. Both of these variables can change in different circumstances. For example, stroke volume is influenced by the volume of blood returning from the body and lungs, due to an intrinsic property of the heart known as the Frank-Starling relationship. Heart rate, on the other hand, can be increased and decreased by the sympathetic and parasympathetic innervations of the heart, respectively. Don’t get too lost in the technical aspects for our purposes here though. You can think about CO as the number of people carried by buses from a bus stop. This will be determined by the size of the bus (mini-bus, single-decker or double-decker; equivalent to stroke volume) and the frequency with which buses arrive (equivalent to heart rate). Mathematically, cardiac output (CO) is the product of stroke volume (SV) and heart rate (HR):

Total Peripheral Resistance (TPR)

If the heart is the pump, then the arteries are the pipes that the heart pumps into, and their diameter determines how much resistance to flow there is. By the time blood has reached the capillaries and the veins, blood pressure has dropped enormously due to the effect of resistance (friction, essentially). As with airway-resistance the effect of a decrease in radius (r) affects resistance (R) to the power of 4:

Systemic vascular resistance increases enormously from the aorta (radius = 1.5 cm) to arterioles (radius = about 150 µm) where the biggest drop in pressure occurs. By the time blood returns to the heart from the systemic circulation, pressure (central venous pressure) is only about 3-8 mmHg:

Blood pressure

As we’ve seen above, blood pressure decreases down the vascular tree as arteries get smaller and smaller. When we talk about blood pressure as a clinical [measure], we really mean an estimate of the blood pressure in the larger arteries near the heart. This is usually measured in the brachial artery in the upper arm, which is level with the heart when sitting with arms at rest. Because blood flow is pulsatile (due to the contractions of the heart) in large arteries, the results of such a measurement are systolic and diastolic blood pressure readings. Mean (or average) arterial pressure (MAP) can be estimated from these two readings:

So, if BP is 120/80 mmHg, then MAP:

MAP is determined by CO and TPR, so if you happen to have measurements of those two variables you could calculate MAP quite easily:

However, in practice you are unlikely to know a patient’s TPR (although CO can be measured or estimated by various means).

The point of understanding the above equation is to see that MAP can be altered by the heart (CO) the vasculature (TPR) or both.

Injection of a vasoconstrictor (AKA vasopressor) will increase MAP primarily by increasing TPR. On the other hand, injection of a drug that slows the heart will reduce CO. Some clinically invaluable drugs affect both CO and TPR. For example, adrenaline constricts blood vessels and increases the rate and force of cardiac contractility. That’s a handy mixture in anaphylactic shock and other cardiovascular crises.

Control of TPR, CO and BP

The body controls BP by altering CO and TPR both on a minute to minute basis via baroreflex activation of the autonomic nervous system. The renin-angiotensin system (RAS) is a slower-acting, endocrine system that also affects TPR by causing vasoconstriction and blood volume (and hence CO) by affecting renal salt and water regulation. The two systems are not separate and interact at crucial points. For example, the RAS is activated by the sympathetic nervous system and the RAS accentuates the effects of sympathetic neurotransmission to blood vessels.

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