Regulation of Cardiac Output: 2

Question 1

Sympathetic control of SV

Answer 1

Extrinsic: direct increase in
muscle contractility = SV
Intrinsic: indirectly causes increase in venous return, increased EDV = SV

Question 2

The Frank-Starling Law

Answer 2

The heart has the capacity to automatically adjust its output (Stroke Volume) to match its input (End Diastolic Volume)

Cardiac muscle fibre length is determined by the extent of venous filling:
• fibre length normally less than the optimal length for developing maximal tension
• an increase in EDV (through increased venous return) stretches fibre, moving it closer to optimal = increased tension
• increased tension leads to a stronger contraction, squeezes out more blood
Thus, as VR increases, EDV increases = more stretch = increased SV

Question 3

Extrinsic control: increasing contractility

Answer 3

curve shifts it to the left
y axis: increase in SV at same EDV

• Extrinsic control shifts the curve to the left: same EDV, more SV

Question 4

Together: Intrinsic + Extrinsic effects

Answer 4

even greater increase in SV

• Intrinsic effect shifts up curve through increased EDV
• Extrinsic effect shifts curve to the left through increased contractility

Question 5

Frank Starling law is important in heart failure

Answer 5

Heart Failure: Frank–Starling curve shifts downward and to

the right - SV decreases at normal EDV

Question 6

Frank Starling law is important in heart failure

- compensation

Answer 6

Compensation:
Sympathetic stimulation increases contractility, shifting curve to the left
Increase in blood volume increases EDV, increases muscle fibre length
= able to get normal S

Question 7

Summary: controlling cardiac output

- Parasympathetic innervation:

Answer 7

• inhibits SA and AV nodes, decreasing heart rate and increasing AV node delay
• inhibits atrial muscle, weakening atrial contraction

Question 8

Summary: controlling cardiac output

- Sympathetic innervation:

Answer 8

Sympathetic innervation:
imperialchinesemedicine.com.au
• stimulates SA and AV nodes, increasing heart rate and decreasing AV node delay
• excites conduction pathways, increasing conduction
• stimulates myocardium increasing atrial & ventricular
contractility and stroke volume
• causes venoconstriction increasing venous return & EDV

Question 9

Keeping the heart going: O2 and nutrients

Answer 9

Although filled with blood, cardiac muscle cannot get oxygen nutrients from the blood within its chambers
- Heart gets its own blood supply through the coronary circulation, but mostly during diastole because:
• the coronary arteries branch off the aorta close to aortic valve, but during contraction, the open aortic valve partially blocks their entrances
• the contracting myocardium compresses the major branches of the coronary arteries
• but, cardiac muscle very good at getting O2 out of blood, and can use multiple sources of energy

Question 10

Matching flow to cardiac needs

Answer 10

Coronary blood flow normally varies to keep pace with cardiac oxygen needs

• Cardiac muscle removes 65% of oxygen from blood even at rest (other tissues remove 25%), but has little capacity to increase this
• During exercise blood flow increases five-fold through vasodilation, due to local increases in adenosine

Question 11

Coronary artery disease: when needs aren’t met

Answer 11

Coronary artery disease refers to pathological changes within the artery walls that diminish blood flow
- Coronary artery
disease, particularly vessel wall the development of atherosclerosis, can occur due to hypertension, hyperlipidemia & hyperglycaemia

Question 12

Coronary artery disease

Answer 12

Atherosclerotic plaques in coronary arteries can cause partial or full obstructions, leading to angina, ischemic heart disease (inflammatory response) & myocardial infarction (heart actually dies) → death of muscle wall