Coronary Circulation Flashcards

1
Q

How many people does coronary artery disease kill annually in the UK?

A

66,000 people

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2
Q

Special requirements of coronary circulation?

A
  • High basal supply of O2 – 20x resting skeletal muscle

- Increase O2 supply in proportion to increased cardiac work

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3
Q

Special structural features of coronary circulation?

A
  • High capillary density

- Large SA for O2 transfer

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4
Q

How to reduce diffusion distance to myocyte?

A
  • High capillary density

- Large SA for O2 transfer

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5
Q

Why reduce diffusion distance to myocyte?

A

t ∝ X² – so transport O2 is fast

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6
Q

Fibre diameter in skeletal vs cardiac muscle?

A

50μm vs 18μm

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7
Q

Special functional features of coronary circulation during rest?

A
  • High blood flow - 10x the flow per weight of rest of body
  • Sparse sympathetic-mediated vasoconstriction
  • High NO released : vasodilatation
  • High O2 extraction (75%) - body is 25%
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8
Q

Special functional features of coronary circulation during exercise?

A

-Coronary blood flow increases in proportion to demands
-Production of vasodilators : adenosine, K+, acidosis
‘out-compete’ sympathetic vasoconstriction during exercise
-Circulating A dilates coronary vessels due to β2-adrenoceptors

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9
Q

Why has only 25% O2 been extracted from tissues in circulation?

A
  • arterial blood has an O2 content of 200
  • mixed venous blood has O2 content of 150
  • so 25% of O2 extracted from tissues in the circulation
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10
Q

Why has 75% O2 been extracted from arterial blood in coronary circulation?

A
  • arterial blood has an O2 content of 200
  • coronary sinus flow has O2 content of 50
  • so 75% of O2 removed from arterial blood entering coronary circulation
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11
Q

Why should you increase blood flow with increased demand?

A
  • extraction is near max during normal activity
  • so need more O2
  • so increase BF
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12
Q

What’s metabolic hyperaemia?

A

increased BF by myocardium metabolism generating metabolites –> vasodilatation

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13
Q

How’s adenosine produced + released?

A

by ATP metabolism + released from cardiac myocytes

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14
Q

eg of metabolites produced for vasodilation?

A

adenosine, PCO2, H+, K+ levels

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15
Q

Special problems of coronary circulation?

A
  • Systole obstructs coronary blood flow

- Ischemic heart disease

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16
Q

When does coronary blood flow occur?

A

during diastole

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17
Q

What’s sudden obstruction?

A

acute thrombosis, Acute Coronary Syndrome (ACS), COMPLETE BLOCK, no O2 delivery –> MI

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18
Q

What’s slow obstruction?

A

atheroma (sub-endothelium lipid plaques) –> chronic narrowing of lumen, less O2 delivery –> angina

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19
Q

Why’s there no coronary perfusion during systole?

A

Pressure in ventricles is = or > aorta

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20
Q

Mechanical factors reducing coronary flow?

A

Shortening diastole, e.g. high heart rate
Increased ventricular end-diastolic pressure, e.g. volume-overload heart failure
Reduced diastolic arterial pressure, e.g. hypotension, aortic regurgitation

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21
Q

Mechanical factors reducing coronary flow?

A
  • Shortening diastole : high HR
  • Increased ventricular end-diastolic pressure : volume-overload HF
  • Reduced diastolic arterial pressure : hypotension, aortic regurgitation
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22
Q

Problem with coronary artery being functional end-arteries?

A
  • no arterio-arterial anastomoses
  • if 1 coronary artery blocked then area it supplies dies since only 1 supply
  • zone of necrosis (infarction)
  • other arteries can’t divert blood to zone of necrosis
23
Q

Define arterio-arterial anastomoses

A

cross-branching collateral vessels

24
Q

What happens if there’s total occlusion of left anterior descending coronary artery?

A
  • ischemic area – MI
  • ischemic tissue
  • acidosis
  • pain (stimulation of C-fibres)
  • impaired contractility
  • sympathetic activation
  • arrhythmias
  • necrosis
25
Q

Symptoms of angina pectoris?

A
  • Strangulation of the chest
  • Pain, crushing sensation in the chest
  • Radiates to neck, arms, jaw
  • Shortness of breath, dizziness
26
Q

3 forms of angina pectoris?

A

Stable, Variant, Unstable

27
Q

Causes of angina pectoris?

A

ischemia due to O2 + nutrient demands of cardiac tissue not being met due to partial occlusion of coronary arteries

28
Q

Causes of increased demand?

A

increased HR, left ventricular contractility, wall stress

29
Q

Why’s exercise a trigger of angina pectoris?

A

increased HR, contractility, hypertension (afterload), left ventricular dilatation (HF)

30
Q

Define stenosis

A

partial occlusion due to plaque formation

31
Q

How does stable angina develop during exercise?

A
  • exercise
  • arterioles further dilate to reduce resistance
  • but total resistance still too high due to stenosis
  • O2 demand not met
  • angina develops
32
Q

Describe stable angina

A

exertional, typical, predictable – symptoms appear after certain demand reached

33
Q

How to relieve stable angina?

A

Relief with nitrates (GTN spray)

34
Q

ECG of stable angina?

A

exercise stress test produces symptoms + ST depression

35
Q

Investigations for stable angina?

A

exercise stress test for ECG, coronary angiography

36
Q

Describe variant angina?

A
  • Vasospastic, Prinzmetal’s, uncommon - caused by vasospasm, occurs at rest
  • Not linked to coronary artery occlusion
  • Excessive responses to vasoconstrictors, endothelium dysfunction (less NO produced)
37
Q

Management of stable/variant angina?

A

CCB, β-blockers, nitrates,

Reduce risk factors – lifestyle, aspirin, statins

38
Q

Types of acute coronary syndrome conditions?

A
  • Unstable angina
  • NSTEMI (non-ST segment elevation myocardial infarction)
  • STEMI (ST segment elevation myocardial infarction)
39
Q

Describe how acute coronary syndrome occurs?

A
  • rupture of atherosclerotic plaque
  • thrombus
  • sudden decrease in BF via a coronary artery
40
Q

Presentation of acute coronary syndrome?

A

unpredictable, sudden, lasts for >30 min, not relieved by GTN spray. EMERGENCY!!

41
Q

Investigation of acute coronary syndrome?

A
  • ECGs – NSTEMI or STEMI

- Measure troponins T, I (raised in NSTEMI + STEMI)

42
Q

Why’s there an isoelectric line in healthy tissue?

A

ventricles uniformly depolarized - no current detected on ECG

43
Q

Why’s there depression of ST segment on ECG?

A
  • partial/less severe occlusion of coronary arteries
  • small area of ischemia which doesn’t depolarize
  • injury current
44
Q

Why’s there elevation of ST segment on ECG?

A
  • total/severe occlusion of coronary arteries
  • full wall thickness ischemia which does’t depolarize
  • injury current
45
Q

Pharmacological therapy for unstable angina or MSTEMI?

A

Morphine
Anti-platelet : aspirin, clopidogrel
Anti-thrombin : heparins, NOACs
Long term : β-blockers, CCBs, statins, ACEi

46
Q

When do you give revascularisation for unstable angina or MSTEMI?

A

If at moderate/high risk, symptoms persist, angiography shows occlusions

47
Q

When do you give coronary artery bypass grafting (CABG) for unstable angina or MSTEMI ?

A

3 main coronary arteries diseased, or main left CA occluded, occlusion position not appropriate for PCI

48
Q

When do you give percutaneous coronary intervention (PCI, stents) for unstable angina or MSTEMI?

A

1 or 2 arteries diseased

49
Q

Describe percutaneous coronary intervention (PCI)?

A
  • Less invasive, balloon catheter inflated in area of blockage, increase luminal
  • Restenosis can occur, thickening of internal area of vessel causing blockage
50
Q

Describe coronary artery bypass grafting (CABG)?

A

Invasive, patient on cardiopulmonary bypass, heart stopped, again potential restenosis issues, less with mammary artery

51
Q

Pharmacological therapy for STEMI?

A

Morphine
Anti-platelet : aspirin, heparins
Thrombolytics : streptokinase, tissue plasminogen activators
Cause fibrinolysis, break down fibrin-clot, increase reperfusion zone
Long term : β-blockers, anti-arrhythmics, CCBs, statins, ACEi

52
Q

When do you give revascularisation for STEMI?

A

Preferred treatment within 2 hours of symptom onset

53
Q

Life-threatening complications of STEMI?

A
  • Cardiac failure (use of intra-aortic balloon)
  • Rupture of ventricular septal –> blood leakage between ventricles
  • Arrhythmias