regulation of cardiac output

What component of the cardiac output is affected by sympathetic + parasympathetic system? 

Cardiac output: heart rate X stroke volume 

	Sympathetic	Parasympathetic
Heart rate	Y	Y
Stroke volume	Y	N

What effect does the sympathetic + parasympathetic systems have on cardiac output

chronotropic ( changing heart rate ) + inotropic effects ( activating/ deactivating voltage gated ion channels ) 

Chronotropic effect of sympathetic + parasympathetic systems

HR	Sympathetic	Parasympathetic
Effect on depolarisation	Reduce slow inward Na+ + Ca2+  → faster	Increases slow influx Na+ + Ca2+  → slower
Effect on hyperpolarisation	Increases K+ efflux  → More	Decreases K+ efflux  → less
Overall effect	Shorter  time to reach threshold of AP	Longer time to reach threshold

Inotropic effect of sympathetic + parasympathetic systems

Stroke volume( influenced by muscular contraction + influences cardiac ouput )

2 methods of influencing stroke volume 

1. Direct excitatory innervation of myocardium → stronger contraction → larger stroke volume → extrinsic control 

2. Indirect control: stimulate adrenal medulla to produce adrenaline → veins constrict more → increases venous return → higher ventricular filling → higher end-diastole volume → larger stroke volume result of length tension relationship ( Frank-starling law ) → intrinsic control

What is the Frank-Starling Law? 

Venous return ↑ → end diastolic volume  ↑ 

1. Fibre length of cardiac muscles < optimal length for developing maximal tension 

2.  ↑ end diastolic volume stretches fibres → achieve optimal tension 

3. High tension → stronger contraction → more blood squeezed out

Effect of extrinsic + intrinsic control on stroke volume + end diastolic volume

 

Extrinsic control shifts curve to left → same end diastolic volume → ↑ stroke volume 

Intrinsic control shifts the curve upwards by ↑ end diastolic volume 

What does the graph look like in heart failure + how it is compensated ? 

The graph is shifted downwards + to the right / stroke volume decreases at normal EDV 

Compensation: 

1. Sympathetic stimulation → ↑ contractility ( increased velocity of cardiac muscle fibre shortening )→ curve shifted to left 

2. Increase in blood volume → end diastolic volume ↑ / muscle fibre length ↑ → achieve normal stroke volume

How is the heart kept pumping? 

Oxygen supply: from coronary circulation in diastole bc 

1. Coronary arteries is partially blocked by open aortic valve since it branches off aorta close to aortic valve 

2. Major branches of coronary arteries are compressed by contracting myocardium \

In exercise: matching of oxygen supply to cardiac muscle 

→ increase blood flow through vasodilation bc adenosine 

→ impairment occurs in coronary heart disease → atherosclerosis develops in arteries by hypertension + hyperlipidemia + hyperglycemia → partial/ full obstructions → angina + ischemic heart disease → death of muscle wall