Quick question about sympathetic discharge to the heart?

[sameeralord]

Hello everyone,

Vasomotor centre for example, increases heart rate and increases blood vessel constriction and raises total peripheral resistance. The end result is increase in stroke volume. My question is if blood pressure is raised too much by constricting blood vessels, wouldn't that make it hard for the ventricles to pump blood and decrease stroke volume. Thanks

 

[SW VandeCarr]

Hello everyone,

Vasomotor centre for example, increases heart rate and increases blood vessel constriction and raises total peripheral resistance. The end result is increase in stroke volume. My question is if blood pressure is raised too much by constricting blood vessels, wouldn't that make it hard for the ventricles to pump blood and decrease stroke volume. Thanks

Correct except that the end result is increased cardiac output, but not necessarily increased stroke volume. Increased total peripheral resistance (TPR) due to sympathetic vasomotor action will increase mean arterial pressure (MAP) and tend to reduce stroke volume (SV) particularly if there is aortic disease resulting in stiffening (atherosclerosis). Cardiac output (Q) can be maintained by the corresponding increase in heart rate (HR) which also results from sympathetic activity (Q=HR x SV). Other factors are also involved such as end diastolic volume(EDV) and ejection fraction which is SV/EDV. In healthy persons this ratio is large, but with heart failure (due to myocardial disease and/or increased TPR) it can drop to 50% or lower.

Reliance on sympathetic activity to deal with physical demands is not the most efficient or healthiest physiological mode. With regular vigorous exercise, resting EDV and SV increase allowing good tissue perfusion at rest with low MAP and low HR. With physical stress, increase in HR alone can often meet the tissue demand and increased MAP is due mostly to increased Q, not increased TPR.

EDIT: The situation with SV and sympathetic activity can be complicated by increased venous return and increased EDV, so SV can increase even if TPR is increased. It just depends on how much and the general state of cardiovascular health.

 

[sameeralord]

Correct except that the end result is increased cardiac output, but not necessarily increased stroke volume. Increased total peripheral resistance (TPR) due to sympathetic vasomotor action will increase mean arterial pressure (MAP) and tend to reduce stroke volume (SV) particularly if there is aortic disease resulting in stiffening (atherosclerosis). Cardiac output (Q) can be maintained by the corresponding increase in heart rate (HR) which also results from sympathetic activity (Q=HR x SV). Other factors are also involved such as end diastolic volume(EDV) and ejection fraction which is SV/EDV. In healthy persons this ratio is large, but with heart failure (due to myocardial disease and/or increased TPR) it can drop to 50% or lower.

Reliance on sympathetic activity to deal with physical demands is not the most efficient or healthiest physiological mode. With regular vigorous exercise, resting EDV and SV increase allowing good tissue perfusion at rest with low MAP and low HR. With physical stress, increase in HR alone can often meet the tissue demand and increased MAP is due mostly to increased Q, not increased TPR.

EDIT: The situation with SV and sympathetic activity can be complicated by increased venous return and increased EDV, so SV can increase even if TPR is increased. It just depends on how much and the general state of cardiovascular health.

Thanks. Nice detailed answer

 

[SW VandeCarr]

Thanks. Nice detailed answer

It's one of my favorite subjects. Btw, I forgot to mention that SV can be affected indirectly by sympathetic activity in another way. As HR increases, left ventricular filling time (LVFT) decreases which can result in lower EDV (depending on filling rate, a function of total pulmonary resistance) and thereby lower SV unless the ejection fraction is increased. So there's no simple correlation between sympathetic activity and SV.