Coronary Circulation Flashcards
How many people does coronary artery disease kill annually in the UK?
66,000 people
Special requirements of coronary circulation?
- High basal supply of O2 – 20x resting skeletal muscle
- Increase O2 supply in proportion to increased cardiac work
Special structural features of coronary circulation?
- High capillary density
- Large SA for O2 transfer
How to reduce diffusion distance to myocyte?
- High capillary density
- Large SA for O2 transfer
Why reduce diffusion distance to myocyte?
t ∝ X² – so transport O2 is fast
Fibre diameter in skeletal vs cardiac muscle?
50μm vs 18μm
Special functional features of coronary circulation during rest?
- 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%
Special functional features of coronary circulation during exercise?
-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
Why has only 25% O2 been extracted from tissues in circulation?
- 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
Why has 75% O2 been extracted from arterial blood in coronary circulation?
- 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
Why should you increase blood flow with increased demand?
- extraction is near max during normal activity
- so need more O2
- so increase BF
What’s metabolic hyperaemia?
increased BF by myocardium metabolism generating metabolites –> vasodilatation
How’s adenosine produced + released?
by ATP metabolism + released from cardiac myocytes
eg of metabolites produced for vasodilation?
adenosine, PCO2, H+, K+ levels
Special problems of coronary circulation?
- Systole obstructs coronary blood flow
- Ischemic heart disease
When does coronary blood flow occur?
during diastole
What’s sudden obstruction?
acute thrombosis, Acute Coronary Syndrome (ACS), COMPLETE BLOCK, no O2 delivery –> MI
What’s slow obstruction?
atheroma (sub-endothelium lipid plaques) –> chronic narrowing of lumen, less O2 delivery –> angina
Why’s there no coronary perfusion during systole?
Pressure in ventricles is = or > aorta
Mechanical factors reducing coronary flow?
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
Mechanical factors reducing coronary flow?
- Shortening diastole : high HR
- Increased ventricular end-diastolic pressure : volume-overload HF
- Reduced diastolic arterial pressure : hypotension, aortic regurgitation
Problem with coronary artery being functional end-arteries?
- 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
Define arterio-arterial anastomoses
cross-branching collateral vessels
What happens if there’s total occlusion of left anterior descending coronary artery?
- ischemic area – MI
- ischemic tissue
- acidosis
- pain (stimulation of C-fibres)
- impaired contractility
- sympathetic activation
- arrhythmias
- necrosis
Symptoms of angina pectoris?
- Strangulation of the chest
- Pain, crushing sensation in the chest
- Radiates to neck, arms, jaw
- Shortness of breath, dizziness
3 forms of angina pectoris?
Stable, Variant, Unstable
Causes of angina pectoris?
ischemia due to O2 + nutrient demands of cardiac tissue not being met due to partial occlusion of coronary arteries
Causes of increased demand?
increased HR, left ventricular contractility, wall stress
Why’s exercise a trigger of angina pectoris?
increased HR, contractility, hypertension (afterload), left ventricular dilatation (HF)
Define stenosis
partial occlusion due to plaque formation
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
Describe stable angina
exertional, typical, predictable – symptoms appear after certain demand reached
How to relieve stable angina?
Relief with nitrates (GTN spray)
ECG of stable angina?
exercise stress test produces symptoms + ST depression
Investigations for stable angina?
exercise stress test for ECG, coronary angiography
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)
Management of stable/variant angina?
CCB, β-blockers, nitrates,
Reduce risk factors – lifestyle, aspirin, statins
Types of acute coronary syndrome conditions?
- Unstable angina
- NSTEMI (non-ST segment elevation myocardial infarction)
- STEMI (ST segment elevation myocardial infarction)
Describe how acute coronary syndrome occurs?
- rupture of atherosclerotic plaque
- thrombus
- sudden decrease in BF via a coronary artery
Presentation of acute coronary syndrome?
unpredictable, sudden, lasts for >30 min, not relieved by GTN spray. EMERGENCY!!
Investigation of acute coronary syndrome?
- ECGs – NSTEMI or STEMI
- Measure troponins T, I (raised in NSTEMI + STEMI)
Why’s there an isoelectric line in healthy tissue?
ventricles uniformly depolarized - no current detected on ECG
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
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
Pharmacological therapy for unstable angina or MSTEMI?
Morphine
Anti-platelet : aspirin, clopidogrel
Anti-thrombin : heparins, NOACs
Long term : β-blockers, CCBs, statins, ACEi
When do you give revascularisation for unstable angina or MSTEMI?
If at moderate/high risk, symptoms persist, angiography shows occlusions
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
When do you give percutaneous coronary intervention (PCI, stents) for unstable angina or MSTEMI?
1 or 2 arteries diseased
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
Describe coronary artery bypass grafting (CABG)?
Invasive, patient on cardiopulmonary bypass, heart stopped, again potential restenosis issues, less with mammary artery
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
When do you give revascularisation for STEMI?
Preferred treatment within 2 hours of symptom onset
Life-threatening complications of STEMI?
- Cardiac failure (use of intra-aortic balloon)
- Rupture of ventricular septal –> blood leakage between ventricles
- Arrhythmias
