Angina and Acute Coronary Syndrome

Question 1

CORONARY CIRCULATION:
What are the special requirements of this circulation?

What are the structural features of this circulation?

Answer 1

• Requires a high basal (resting) supply of O2. ↑O2 supply is proportional to ↑Demand.
• • High capillary density
  • Large surface area for O2 transfer

Both shorten the diffusion pathway and make O2 transport fast.

Question 2

What are the functional features of this circulation during normal activity and increased demand?

Answer 2

During normal activity:
• There’s high blood flow and lots of NO release = Resting Vasodilation.
• Also, there’s a high O2 extraction.

During increased demand:
• Coronary blood flow increases in proportion to increased demand
• Metabolism produces K, H, Adenosine etc. and produces vasodilation (Metabolic Hyperaemia) - dominates over sympathetic vasoconstriction.
• Circulating Adr dilates the coronary vessels - due to abundance of β2-receptors

Question 3

Why does blood flow increase when their increased cardiac demand?

Answer 3

O2 unloading is already high during normal activity, so to increase Oxygen unloading during high activity, blood flow must be increased - this is why myocardial cells produce metabolic substances that cause vasodilation (Metabolic Hyperaemia).

Question 4

What are the special problems of this circulation?

Answer 4

1. Systole obstructs coronary blood flow - blood flow can only occur during diastole.
2. Ischaemic Heart Disease (IHD):
   • Coronary arteries are end-arteries - ↓perfusion can cause major problems
   • Heart is very susceptible to sudden/slow obstructions - Sudden obstructions include acute thrombosis, acute coronary syndrome, and MI. Slow obstructions include atheroma lumen narrowing - causes angina

Question 5

What are the 3 mechanical features that reduce coronary flow?

Why can’t blood be diverted to ischaemic areas?

LOOK AT DIAGRAM!

Answer 5

• 1. Shortening diastole - during high HR
     
     2. ↑Ventricular EDV
     3. ↓Diastolic arterial pressure - from hypotension, aortic regurgitation
• There’s very little cross-branching of the arteries.

Question 6

What is Angina?

What is it caused by?

What are the 3 types of Angina?

Answer 6

• Strangulation of chest - crushing pain in the chest that radiates to neck, arms and jaw. It also includes shortness of breath and dizziness.
• Ischaemia as to myocardial demands not being met - due to partial occlusion of coronary arteries. This increased demand is due to an ↑HR, ↑LV contractility, and ↑Wall stress/Afterload.

These causes of increased demand are triggered by exercise, HT, and LV dilation.

• Stable, Varient, Unstable

Question 7

Why do symptoms of Stable angina increase during activity?

LOOK AT DIAGRAMS!

Answer 7

In a normal heart: During normal activity, the total resistance is quite high, but during exercise, the metabolic vasodilation of coronary arterioles increase blood flow and reduces total resistance.

In a bad heart: With stenosis in an artery, there’s a high resistance at rest, so metabolic vasodilation occurs to meet demands. Then, during exercise, further vasodilation tries to occur to reduce resistance but fails to do so. Total resistance stays high due and demands can’t be met - causing Angina.

Question 8

How do you diagnose Stable angina?

How is Stable angina treated?

How do you diagnose Variant angina?

How is Stable and Variant angina managed?

Answer 8

• Predictable as symptoms appear after heart is exerted. There will be ST DEPRESSION and a Coronary Angiography can be done to confirm diagnosis.
• Quickly relieved with Nitrates e.g. GTN.
• Uncommon, caused by vasospasm and occurs at rest. Due to excessive vasoconstriction and endothelium dysfunction - less NO produced.
• CCBs, B-blockers and Nitrates to manage.
  Aspirin, Statins, Lifestyle used to minimise risk factors.

Question 9

What is Acute Coronary Syndrome (ACS)?

What causes it?

What is the presentation of an ACS?

How is it investigated?

Answer 9

• Unstable Angina, NSTEMI, STEMI
• Sudden decrease in coronary blood flow, initiated by rupture of an atherosclerotic plaque - produces a thrombus.
• Unpredictable, sudden, lasts for >30 mins, and NOT RELIEVED BY GTN spray
• ECGs for NSTEMI or STEMI
  TnI and TnT levels - elevated in NSTEMI and STEMI, but not Unstable angina

Question 10

Explain an NSTEMI and STEMI

LOOK AT PICTURES!

Answer 10

NSTEMI:
Partial occlusion of coronary arteries will lead to a small ischaemic area that won’t depolarise - leads to injury current and ST DEPRESSION.

STEMI:
Total occlusion of coronary arteries will lead to full wall thickness ischaemia that won’t depolarise - leads to injury current and ST ELEVATION.

Question 11

Management of NSTEMI and Unstable angina:
What pharmacological drugs can be given?

What are the ways in which the vessels can be revascularised?

LOOK AT PICTURES!

Answer 11

• • Morphine
  • Anti-platelets - Aspirin
  • Anti-thrombin - Heparin
  • Long-term drugs - β-blockers, CCBs, Statins, ACEi
• CABG (coronary artery bypass grafting) - done if 3 main coronary arteries are diseased or if LAD is occluded. This is where new vessel is used to bypass the occlusion.

PCI/stent can be used if 1/2 arteries are diseased. This is where a ballon catheter is inflated in the blocked area to ↑lumen diameter.

Question 12

Management of STEMI:
What pharmacological drugs can be given?

What is the treatment for it?

What are the life-threatening complications?

Answer 12

• • Morphine
  • Anti-platelets - Aspirin
  • Thrombolytic drugs - tPA
  • Long term drugs - β-blockers, CCBs, Statins, ACEi, Anti-arrhythmics
• Revascularisation within 2 hours of symptom onset.
• Heart failure, Rupture of ventricular septal, leading to blood leakage between chambers - causes arrhythmias.