Control Of Cardiac Output

Front 1

Define how preload, after load, and contractility affect stroke volume.

Back 1

Increase in preload (the intrinsic quality of the heart to adjust stroke volume to match changes in venous return) and contractility will increase SV

Increase in afterload (pressure that the ventricles must contract against once the aortic valve opens -- mainly aortic pressure) will decrease SV immediately. however, EDV will increase thereby increasing the SV in subsequent contractions. This occurs because the decrease in SV means that more is stored in the ventricle for the next contraction. Assuming the same venous return, there should be a higher EDV than before.

Contractility: (force of contraction) as contractility increases, you get a higher ejection fraction and thus have a lower EDV. You also have an increased max systolic elastance. However, SV remains the same usually.

An increase in contractility means that at a given end diastolic pressure the SV will be greater.

Front 2

List the mechanisms by which the ANS controls contractility

Back 2

ANS decreases contractility

1) increase Ca2+ channel activation through Gs --> pKa increased
2) more rapid relaxation -- I subunit of troponin is phosphorylated which reduces affinity of troponin C to Ca2+
3) phosphorylation of Ca2+ SR pumps increase Ca sequestration, thereby shortening systole

Parasympathetic: the most important effect of vagal activation is the profound slowing of the HR. Because of the longer diastole, SV usually increases, although CO usually falls.

Front 3

Describe the factors that determine the internal and external work of the heart

Back 3

Internal Work (metabolic activities): includes maintenance of tissues, ion channels, cell metabolism, etc.

Rearrangement of muscle during contraction. This is determined primarily by wall stress (Law of LaPlace). Appreciate that less stress to the heart can be achieved in people with hypertension with a greater wall thickness. Also, realize that the heart is under more stress when the radius is increased while everything remains the same (typical of heart failure)

External Work: Work required to eject stroke volume. This can be quantified by calculating the area underneath the SV curve --> may be approximated by multiplying stroke volume by mean systolic pressure.

In general, the goal is to minimize the amount of work on the heart to eject a particular stroke volume. If the muscle demand to eject a SV is greater than the amount of O2 supplied by that SV, then angina, arrythmias, and MI or cell injury may occur.