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A Physiology > 2.12A. Coronary circulation and its control. > Flashcards

2.12A. Coronary circulation and its control. Flashcards

1
Q

I. Basic anatomy of heart vessels

A

Entire blood supply to the myocardium derives from right and left coronary arteries
- Originate at the root of aorta
- RCA -> right ventricle and atrium
- LCA -> left ventricle and atrium
- Venous blood drains into the right atrium through coronary sinus or directly into the cardiac chambers through thebesian veins

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2
Q

I. Basic anatomy of heart vessels

A

Entire blood supply to the myocardium derives from right and left coronary arteries
- Originate at the root of aorta
- RCA -> right ventricle and atrium
- LCA -> left ventricle and atrium
- Venous blood drains into the right atrium through coronary sinus or directly into the cardiac chambers through thebesian veins

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3
Q

II. Coronary circulation
1. What is the mechanism of coronary circulation?

A

Blood flow in the coronary circulation is controlled almost entirely by local metabolites, with SYM innervation only playing a minor role.

Blood vessels are compressed during the contractive force of systole, causing ischemia (periodic occlusions). After the occlusion, reactive hyperemia occurs and increases blood flow + oxygen delivery to compensate

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4
Q

II. Coronary circulation
2. What are the Most important local metabolite factor?

A

hypoxia + adenosine

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5
Q

III. Coronary blood flow
1. Definition of coronary blood flow (Qc)

A

Coronary blood flow (Qc)
- Amount of blood the heart gets in a minute

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6
Q

III. Coronary blood flow
2. What is the value of Coronary blood flow?

A
  • Qc = 200 – 250 mL blood/ min (5% of CO = 5,6L/min)
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7
Q

III. Coronary blood flow
3. What is AVDO2?

A
  • AVDO2 = how efficiently the heart extracts O2 from the blood (difference between arterial and venous O2 content)
  • AVDO2 = 110mL O2/L blood
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8
Q

III. Coronary blood flow
4. What is the value of AVDO2?

A

AVDO2 = 110mL O2/L blood

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9
Q

III. Coronary blood flow
5. What happen to the blood flow if we get more O2?

A

increase blood flow (Qc)

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10
Q

III. Coronary blood flow
6. What is AVDO2 during exercise?

A

AVDO2 during exercise
=> 900 – 1200 mL/min (extraction already at maximum at rest -> need to ↑ blood flow to heart)

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11
Q

III. Coronary blood flow
7. What is the driving force of coronary blood flow?

A

Perfusion pressure (created by the heart) is the driving force of the coronary circulation
(compress blood vessel
-> diameter decreases
-> blood resistance increases)

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11
Q

III. Coronary blood flow
7. What is the driving force of coronary blood flow?

A

Perfusion pressure (created by the heart) is the driving force of the coronary circulation
(compress blood vessel
-> diameter decreases
-> blood resistance increases)

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12
Q

IV. Coronary blood flow during cardiac cycle
1. Describe coronary blood flow in LCA during cardiac cycle

A

1st phase of systole:
- Tension in wall increases = AO valve closed
- Condition bad for LCA -> Increased pressure in myocardium compresses the coronary blood vessels
- Increase follows PA -> Increase in Qc = increase in perfusion pressure during systole
- Diastole -> wall tension decreases (heart relaxed)
- Resistance decreases
-> huge increase in blood flow in coronary circulatory

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13
Q

IV. Coronary blood flow during cardiac cycle
2. Describe coronary blood flow in RCA during cardiac cycle

A
  • Smaller valves compared to LCA (lower wall tension)
  • Pressure in LV not so high, coronary blood flow does not drop to 0
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14
Q

IV. Coronary blood flow during cardiac cycle
2. Describe coronary blood flow during Diastole of cardiac cycle

A
  • Heart can rest
  • Fed by blood supply
  • 80% of coronary circulation occurs during diastole
    -> HR increased (less optimal for QC)
    -> duration of diastole decreased
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15
Q

V. Regulation of blood flow
1. What are the 3 types of regulations of coronary circulation?

A

myogenic, metabolic, neural controls
(During exercise, blood flow can increase to max 5x and this is due to increased heart work)

16
Q

V. Regulation of blood flow
2A. Describe Myogenic mechanism

A

Autoregulation (Bayliss effect)
- little change in Qc as perfusion pressure changes (from 60 to 160mmHg)
- Heart itself will regulate its own blood flow
- Pa↑ -> vasoconstriction (less perfusion) -> R↑ (constant blood flow)
- Pa↓ -> vasodilation (more blood flow) -> R↓

17
Q

V. Regulation of blood flow
2B. What is the Bayliss effect?

A
  • Pressure ↑ -> wall tension↑ -> non-selective cation channels, depolarization, activate VDCC -> Ca2+↑ -> vasoconstriction
  • Pressure ↓ -> wall tension↓ -> same effects -> vasodilation
18
Q

V. Regulation of blood flow - Metabolic regulation
3A. What are the Factors that cause vasodilation?

A
  1. CO↑ (exercise) -> metabolism ↑ + O2-consumption↑
  2. Metabolic changes -> K+-channel activators (HCN, VDCC)
  3. Metabolism↑ -> NO (produced by endothelial cells) -> vascular SM relaxation -> vasodilation
19
Q

V. Regulation of blood flow - Metabolic regulation
3B. How can increasing CO↑ (exercise) participate in metabolic control>

A

CO↑ (exercise) -> metabolism ↑ + O2-consumption↑
-> Since ↑O2-consumption, we have different metabolic effects:
1. pO2↓, pCO2↑
2. [H+]↑ (pH↓)
4. [K+]↑
5. [adenosine]↑ - ATP metabolism
=> all lead to vasodilation (R↓ => Qc↑)

20
Q

V. Regulation of blood flow - Metabolic regulation
3C. How can Metabolic changes participate in metabolic control?

A

Metabolic changes -> K+-channel activators (HCN, VDCC)
-> SM hyperpolarization
-> Ca2+-channel activation
-> [Ca2+]IC↓
-> vasodilation (relaxation)

  • ↓[Ca2+] also comes from the increased cAMP due to adenosine
21
Q

V. Regulation of blood flow - Metabolic regulation
3C. How can Metabolism↑ participate in metabolic control?

A

Metabolism↑ -> NO (produced by endothelial cells) -> vascular SM relaxation -> vasodilation
- This is a positive feedback mechanism, because vasodilation -> ↑QC -> shear stress on endothelial cells↑ -> NO release↑ -> vasodilation again

22
Q

V. Regulation of blood flow - Neural regulation
1. What are the sympathetic effects in neural regulation?

A

1.Direct effects:
- α1-AR -> vasoconstriction
- β2-AR -> vasodilation

  1. indirect effect:
    - Sympathetic stimulation leads to ↑HR = ↑CO -> metabolism↑ -> vasodilation -> ↑QC
23
Q

VI. Pathophysiology of coronary blood flow
-> Describe

A
  1. Abrupt occlusion -> necrosis (myocardial infarct)
  2. Gradual occlusion (slow narrowing of vessels)
    -> new blood vessel formation occurs
    => Is a better form of occlusion

A Physiology (88 decks)

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