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CVS II > Coronary Circulation > Flashcards

Coronary Circulation Flashcards

(53 cards)

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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?

Study These Flashcards
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

Study These Flashcards
A

cross-branching collateral vessels

24
Q

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

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A
  • ischemic area – MI
  • ischemic tissue
  • acidosis
  • pain (stimulation of C-fibres)
  • impaired contractility
  • sympathetic activation
  • arrhythmias
  • necrosis
25
Symptoms of angina pectoris?
- Strangulation of the chest - Pain, crushing sensation in the chest - Radiates to neck, arms, jaw - Shortness of breath, dizziness
26
3 forms of angina pectoris?
Stable, Variant, Unstable
27
Causes of angina pectoris?
ischemia due to O2 + nutrient demands of cardiac tissue not being met due to partial occlusion of coronary arteries
28
Causes of increased demand?
increased HR, left ventricular contractility, wall stress
29
Why's exercise a trigger of angina pectoris?
increased HR, contractility, hypertension (afterload), left ventricular dilatation (HF)
30
Define stenosis
partial occlusion due to plaque formation
31
How does stable angina develop during exercise?
- exercise - arterioles further dilate to reduce resistance - but total resistance still too high due to stenosis - O2 demand not met - angina develops
32
Describe stable angina
exertional, typical, predictable – symptoms appear after certain demand reached
33
How to relieve stable angina?
Relief with nitrates (GTN spray)
34
ECG of stable angina?
exercise stress test produces symptoms + ST depression
35
Investigations for stable angina?
exercise stress test for ECG, coronary angiography
36
Describe variant angina?
- 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
Management of stable/variant angina?
CCB, β-blockers, nitrates, | Reduce risk factors – lifestyle, aspirin, statins
38
Types of acute coronary syndrome conditions?
- Unstable angina - NSTEMI (non-ST segment elevation myocardial infarction) - STEMI (ST segment elevation myocardial infarction)
39
Describe how acute coronary syndrome occurs?
- rupture of atherosclerotic plaque - thrombus - sudden decrease in BF via a coronary artery
40
Presentation of acute coronary syndrome?
unpredictable, sudden, lasts for >30 min, not relieved by GTN spray. EMERGENCY!!
41
Investigation of acute coronary syndrome?
- ECGs – NSTEMI or STEMI | - Measure troponins T, I (raised in NSTEMI + STEMI)
42
Why's there an isoelectric line in healthy tissue?
ventricles uniformly depolarized - no current detected on ECG
43
Why's there depression of ST segment on ECG?
- partial/less severe occlusion of coronary arteries - small area of ischemia which doesn't depolarize - injury current
44
Why's there elevation of ST segment on ECG?
- total/severe occlusion of coronary arteries - full wall thickness ischemia which does't depolarize - injury current
45
Pharmacological therapy for unstable angina or MSTEMI?
Morphine Anti-platelet : aspirin, clopidogrel Anti-thrombin : heparins, NOACs Long term : β-blockers, CCBs, statins, ACEi
46
When do you give revascularisation for unstable angina or MSTEMI?
If at moderate/high risk, symptoms persist, angiography shows occlusions
47
When do you give coronary artery bypass grafting (CABG) for unstable angina or MSTEMI ?
3 main coronary arteries diseased, or main left CA occluded, occlusion position not appropriate for PCI
48
When do you give percutaneous coronary intervention (PCI, stents) for unstable angina or MSTEMI?
1 or 2 arteries diseased
49
Describe percutaneous coronary intervention (PCI)?
- Less invasive, balloon catheter inflated in area of blockage, increase luminal - Restenosis can occur, thickening of internal area of vessel causing blockage
50
Describe coronary artery bypass grafting (CABG)?
Invasive, patient on cardiopulmonary bypass, heart stopped, again potential restenosis issues, less with mammary artery
51
Pharmacological therapy for STEMI?
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
When do you give revascularisation for STEMI?
Preferred treatment within 2 hours of symptom onset
53
Life-threatening complications of STEMI?
- Cardiac failure (use of intra-aortic balloon) - Rupture of ventricular septal --> blood leakage between ventricles - Arrhythmias

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