pt 2 The Cardiac Cycle and Cardiac Workload

What are the main phases of the cardiac cycle?

• Ventricular filling

• Atrial contraction

• Isovolumetric ventricular contraction

• Ventricular ejection

• Isovolumetric ventricular relaxation

When do contraction and relaxation occur in the cardiac cycle?

• SYSTOLE → contraction

• DIASTOLE → relaxation

What is stroke volume?

• Volume of blood ejected by a ventricle per contraction

What is contractility?

• Change in stroke volume without change in resting ventricular fibre length (no change in preload)

• Mechanism extrinsic to the heart

What is preload?

• Degree of ventricular stretch due to end-diastolic pressure

• Depends on EDV (end-diastolic volume)

• Changes in stroke volume with resting fibre length change (intrinsic mechanism)

What are the two mechanisms regulating cardiac workload?

• Heterometric (Intrinsic)

• Homeometric (Extrinsic)

explain starlings law of the heart: Heterometric (Intrinsic)

• The force of ventricular contraction is proportional to the initial fibre length during diastole.

• An increase in blood returning to the heart increases the filling pressure and end-diastolic volume (EDV).

• This stretches the ventricular muscle, producing a more forceful contraction.

Starling’s Law – effect of low preload on contraction?

• Force of contraction ∝ number of cross bridges possible

• Almost empty chamber (low preload): actin and myosin overlap is not optimal

• Result → reduced ability to contract

Starling’s Law – effect of high preload (full ventricle) on contraction?

• Full ventricle (high preload): ventricular muscle stretched

• Optimum cross-bridge formation between actin and myosin

• Troponin C affinity for Ca²⁺ increases

• Result → maximal force of contraction

Starling’s Law – effect of overfull heart (heart failure) on contraction?

• Overfull heart: actin and myosin physically separated

• Cross-bridge formation prevented

• Result → reduced force of contraction

How does sympathetic nerve stimulation affect cardiac workload via homeometric (extrinsic) mechanisms?

• Increase in stroke volume without change in initial fibre length

• Increase in contractility

• Positive inotropic effect

What effect do catecholamines have on cardiac workload via homeometric (extrinsic) mechanisms?

• Produces a more forceful contraction

• Contraction is shorter in duration

How does blood pressure change through the cardiovascular system?

• Left ventricle pressure: ~4–5 mmHg during diastole → ~120 mmHg during systole

• Aorta and arteries: systolic pressure maintained by thick arterial walls

• Diastolic pressure: stays higher than ventricle due to elastic recoil and aortic valve closure

• Along vessels: pressure decreases due to friction against vessel walls

• Veins: wide diameter, thin walls → pressure drops to ~4–5 mmHg

What controls mean arterial pressure (MAP)?

• Main determinants:

  • Cardiac output (CO)

  • Total peripheral resistance (TPR)

• Arterioles can change diameter → rapidly modify MAP

• Formula: MAP = CO × TPR

How does the parasympathetic nervous system control MAP?

• Parasympathetic neurons synapse on SA & AV nodes

• Reduce heart rate → decreases cardiac output

• Helps maintain normal MAP

How does sympathetic stimulation of the heart affect MAP?

• Sympathetic neurons synapse on SA node

• Increase heart rate and force of contraction → ↑ cardiac output

• Contributes to higher MAP

How does sympathetic stimulation of vessels affect MAP?

• Sympathetic neurons cause arteriolar vasoconstriction → ↑ TPR → ↑ MAP

• Venoconstriction shunts blood into arteries → further ↑ blood pressure