How does increased afterload affect cardiac output (CO)?

Increased afterload refers to the resistance the heart must overcome to eject blood during systole. When afterload is elevated, such as in conditions like hypertension or aortic stenosis, the heart faces greater resistance. This heightened workload can lead to several physiological changes.

First, when afterload increases, the heart may not be able to eject the same volume of blood with each contraction. The increased resistance causes a decrease in stroke volume, which is the amount of blood pumped in one beat. Cardiac output is a product of stroke volume and heart rate, so a decrease in stroke volume typically results in a decrease in overall cardiac output, assuming heart rate does not significantly increase to compensate for the loss.

Further, prolonged increased afterload can lead to changes in myocardial function. The heart muscle may become fatigued or oversensitized, particularly if the condition persists, ultimately impairing its ability to pump effectively. This is why increased afterload is associated with lower cardiac output.

Thus, an increase in afterload negatively impacts cardiac output by making it more difficult for the heart to eject blood effectively during each contraction.