Ischeamic heart disease problems

Question 1

What is prinzmetals angina?

Answer 1

• Coronary artery spasm

Question 2

Why does prinzmetals angina worse lying down?

Answer 2

Symptoms worse lying down since:
- Inc. VR = Inc. RV and LV filling
= Greater load and O2 demand
= Impaired LV function = greater pulmonary congestion
= Anginal pain and work of breathing increase (pulmonary congestion)

Question 3

Why is prinzmetals angina worse at night?

Answer 3

Circadian variation in endothelial function and ANS
- i.e PNS active at rest / at night so possibly -> Ach -> Vasospasm

Question 4

Why do people with IHD faint when getting up?

Answer 4

Postural hypotension
- VR reduced when standing
- Reduced preload
- Reduced CO
= Reduced MAP
= Reduced cerebral perfusion

Question 5

Why does ACh provoke vasospasm in some segments of the coronary arteries:

Answer 5

Normally ACh->m3(endo)->NO

BUT in Endothelial dysfunction/absent endo
= ACh acts directly on VSM = inc.iCa = Contraction

Smoking damages endo

Question 6

How does nitroglycerine reverse coronary vasospasm?

Answer 6

Nitroglycerine increases NO levels - acts directly on VSM

Question 7

What causes ST elevation?

Answer 7

Elevated because difference in dipole b/w ischeamic region and rest of repolarising tissue

Question 8

When is ST elevated vs depressed?

Answer 8

Elevated: Transmural ischeamia

Depressed: Non-transmural ischeamia

Question 9

How does nifidipine help patients with angina?

Answer 9

Ca channel inhibitor

• Relaxes and prevents coronary artery spasm
  = Dilates arteries and arterioles in normal and ischeamic regions (potent inhibitor of coronary art. spams), increases myocardial oxygen delivery in patients with coronary art. spasm.
• Reduces oxygen utilisation
  = Reduces arterial pressure at rest, decreased TPR (lowers afterload and preload) reducing myocardial work and oxygen demands.

Question 10

Why would you not just use nitroglycerine in pretzmans agina?

Answer 10

Very short acting, tolerance issues

Question 11

What are the key risk factors for IHD?

Answer 11

• Obesity
• Hypertension
• Smoking
• High stress
• Dyslipidaemia
• Family hx

Question 12

What is coronary reserve?

Answer 12

Normally 5x resting (ability to increase flow)

Question 13

What causes chest discomfort in IHD?

Answer 13

• Chemical, mechanical stimuli (K, H, Adenosine)
• Sympathetic afferents / spinothalamic
• Referral to somatic segments of chest and arms

Question 14

If angina is triggered by exertion, why can it persist in the absence of effort?

Answer 14

• Endo dyfs, inappropriate vascular response (vasospasm)
• Neurohormonal i.e stress - Inc. HR, vascular tone
• Increased iCa -> Incomplete relaxation, decreased diastolic compliance (Extravascular compression of coronary vessels (impairs diastolic flow))

Question 15

Write some notes on the diastolic pressure time index for subendocardial blood flow:

Answer 15

• Decreased perfusion pressure
• Decreased diastolic interval
• Increased LV diastolic pressure

= Coronary supply limitation

Question 16

How does metoprolol help with chest discomfort in IHD?

Answer 16

• Beta adrenergic receptor blocker
• Limits inotropic state and HR increases
• Keeps myocardial O2 demand within coronary reserve capacity.

Question 17

How does nitrate spray relieve chest pain in IHD?

Answer 17

• Converted to NO
  = Coronary dilation
  = Systemic vasodilation -> Reduced afterload, preload, = reduced O2 demand
• Peripheral pooling -> Decreased cardiac filling and diastolic pressure
  = Increased coronary reserve (Via decreased extravascular compression)

Question 18

How can metoprolol result in muscle fatigue and sleep disturbance?

Answer 18

• CO doesnt meet needs.
• K and H accumulate = afferent stimulation and muscle fatigue.
• Sleep disturbance is well known S/E

Question 19

What other tests might be appropriate for IHD patients?

Answer 19

• Exercise ECG
• Stress Echo
• Angiography

Question 20

What other drug interventions might be appropriate for IHD?

Answer 20

• Statin
• Revascularisaiton

Question 21

How can atheroma plaque rupture lead to vessel occlusion?

Answer 21

Mechanical -> Distal embolization and mechanical plugging

Vasoconstrictive -> Thrombus -> Serotonin release = vasoconstriction

Question 22

What are the reciprocal changes of ECG following MI?

Answer 22

Acute = ST elevation

Reciprocal changes:
- ST depression
- Peaked T waves
- Absent Qs

Question 23

What leads will you see a posterior MI?

Answer 23

• Large R wave with ST depression in V1, V2

Question 24

What leads will you see a lateral MI?

Answer 24

• Huge Qs in lateral leads 1 and AVL (Circumflex art)

Question 25

What leads will you see a inferior MI?

Answer 25

Huge Qs in inferior leads 2,3, and AVF

R or L coronary art.

Question 26

What leads will you see an anterior MI?

Answer 26

Huge Q’s in V1,2,3,4 (Anterior descending coronary artery)

Question 27

What causes low systolic pressure in MIs?

Answer 27

Impaired contractile performance, pump failure (Cardiogenic shock)

Question 28

What are the potential causes of resp. difficulties in MI?

Answer 28

• Decreased CO
• Reduced O2 supply to body
• Increased Left atrial pressure (poor pump), increased pulm vein pressure, stiff lungs

Question 29

How do you access myocardial damage?

Answer 29

• Imaging -> EF
• Chemistry, trop levels

Question 30

How are cardiac troponins markers of damage in MI?

Answer 30

• Highly specific and not found in healthy persons
• Diagnostic and prognostic