CVS: Angina and Acute Coronary Syndrome

Question 1

Describe coronary circulation and its special requirements

Answer 1

Special Requirements: Needs a high supply of O2
Can increase O2 supply in proportion to increased demand/cardiac work
e.g. exercise increases heart rate and contractility

Question 2

Give the structural special features of coronary circulation

Answer 2

High capillary density and large SA greatly increase O2 unloading to myocardium

These reduce diffusion distance of O2 to myocyte

Question 3

Give functional special features of coronary circulation

Answer 3

During normal activity: High blood flow. Sparse symp-mediated vasoconstriction + high NO released promotes vasodilatation
High O2 extraction (75%) - average body is 25%

During increased demand: vasodilators produced from active cardiac muscle e.g. adenosine, K+, acidosis produce local vasodilation, so higher BF
Circulating adrenaline acts on B2-adrenoceptors on coronary arteries to cause vasodilation

Question 4

What restricts coronary blood flow?

Answer 4

In systole, ventricular pa is = or > aorta, causing poor coronary perfusion
During diastole, aortic pa> ventricular pa. This opens the window for coronary blood flow.
Mechanical factors reducing coronary flow :
Shortening diastole, e.g. high HR
Increased ventricular end-diastolic pressure, e.g. in volume-overload heart failure
Reduced diastolic arterial pressure, e.g. hypotension

Question 5

Human coronary arteries are functional end-arteries. What does this mean?

Answer 5

Low numbers of cross-branching collateral vessels (Arterio-arterial anastomoses). Blood flow cannot be easily diverted to ischemic areas

Question 6

Give an example of when functional end arteries can cause ischaemia

Answer 6

Total occlusion of left anterior descending coronary artery leads to ischemia.

This causes ischemic tissue, acidosis, pain (stimulation of C-fibres). This leads to impaired contractility –> sympathetic activation –> arrhythmias –> cell death (necrosis)

Bc coronary arteries are functional end-arteries, it means other arteries cannot divert blood to the affected area

Question 7

What is Angina Pectoris?

Answer 7

Pain, crushing sensation in the chest which radiates to neck, arms, jaw. Shortness of breath, dizziness
3 forms: Stable, Variant, and Unstable (from Acute Coronary Syndrome)
Causes:
ischemia: increased O2 and nutrient demands of cardiac tissue not met due to coronary artery occlusion
Increased demand comes from increased HR, left ventricular contractility, wall stress like in exercise, hypertension (afterload), left ventricular dilatation (HF)

Question 8

Use diagrams to explain why stable angina becomes a problem with exercise

Answer 8

Question 9

Describe stable versus variant angina

Answer 9

Stable (Exertional, typical)
Predictable – symptoms appear after certain activity demand reached
Relief with nitrates (e.g. GTN spray)
ECG: exercise stress test produces symptoms and ST depression
Coronary angiography used to see any partial occlusion

Variant (Vasospastic, Prinzmetal)
Uncommon, caused by vasospasm, occurs at rest, not linked to coronary artery occlusion
Vasospasm occurs due to excessive responses to vasoconstrictors, endothelium dysfunction (e.g. less NO produced)

Question 10

How do you manage angina?

Answer 10

Question 11

Describe Acute coronary Syndrome and what its linked to

Answer 11

Life-threatening emergency linked to unstable angina:
NSTEMI (non-ST segment elevation myocardial infarction)
STEMI (ST segment elevation myocardial infarction)
Sudden decrease in flow of blood through a coronary artery
Initiated by atheroma rupture which produces a thrombus in a coronary artery, reducing BF
Unpredictable, sudden, lasts for >30 min, not relieved by GTN spray

ECGs: NSTEMI or STEMI
Troponins T and I often raised in NSTEMI and STEMI bc they’re released in cardiac cell death.

Question 12

What is an NSTEMI?

Answer 12

Question 13

What is a STEMI?

Answer 13

In total/severe occlusion of a coronary artery hay full wall thickness ischemia which does not depolarize. This leads to injury current and elevation of ST segment on ECG:

Question 14

Describe pharmacological therapy for unstable angina and NSTEMI

Answer 14

Pharmacological therapy

• Morphine to treat pain
• Anti-platelet - aspirin, clopidogrel
• Anti-thrombin - heparins, NOACs
• Long term - b-blockers, CCBs, statins, ACEi

Question 15

Describe the 2 types of revascularisation processes

Answer 15

PCI: less invasive, balloon catheter inflated in area of blockage to increase luminal size

But, restenosis can occur (vsmc migration into the area causing blockage)

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

Question 16

Describe the management of STEMI (acute myocardial infarction)

Answer 16

Pharmacological therapy

• Morphine
• Anti-platelet, aspirin, heparins
• Thrombolytics, eg streptokinase, cause fibrinolysis, break down fibrin-clot, increase reperfusion zone
• Long-term: b-blockers, CCBs, statins, ACEi reduce demands

Is revascularisation needed? Yes: PCI or CABG treatment within 2 hrs of symptom onset

Question 17

What are life threatening complications w STEMI?

Answer 17

• Cardiac failure
• Rupture of ventricular septal leads to blood leakage between ventricles
• Arrhythmias