Pathophysiology of MI
Electrical conducting system
Pharmacology
Pathophysiology of arrhythmias
BONUS !!!
100

What are the kinds of MI

  • ST elevation myocardial infarction (STEMI)
  • non-ST elevation myocardial infarction (NSTEMI)
  • unstable angina
100

Where does the electrical impulses in the heart begin

SAN

100

What is the MOA of class II antiarrhythmics (50 Pts)

Give 1 example (50)

Beta blockers

Beta-adrenergic receptor antagonists  Inhibits sympathetic stimulation - Block the effects of adrenaline  Reduce heart rate, cardiac output, and blood pressure

Propranolol
Atenolol
Bisoprolol
Metoprolol  

100

n What is an ectopic pacemaker

An ectopic pacemaker is an excitable group of cells that causes a premature heart beat outside the normally functioning SA node of the heart.

100

What is the management of an MI

MONA:

  • Morphine
  • Oxygen
  • Nitrates
  • Aspirin
200

Name 5 symptoms of an MI

chest pain.

dyspnoea

sweating

nausea 

vomiting

200

Why are signals in the AVN delayed

Because the AV node has a longer refractory period than the rest of the conduction system, it takes longer for the electrical impulse to travel from the AV node to the AV bundle due to the smaller number of gap junctions between the cells.

 This delay allows time for the atria to fully contract and push blood into the ventricles before they contract.

200

What is the MOA of class V antiarrhythmics (150 Pts)

Give 1 example (50)

Atypical eg Digoxin

Cardiac slowing and reduced rate of conduction through AV node 

Increased force of contractions 

Disturbance of rhythm and increased ectopic pacemaker activity

200

What would you notice on ECG with ventricular arrhythmias

They are almost always wide QRS complex arrhythmias.

200

How does a PCI work

In this procedure the blocked arteries are opened up using a balloon (angioplasty) following which a stent may be deployed to prevent the artery occluding again in the future. This is done via a catheter inserted into either the radial or femoral artery

300

How would you investigate for an MI

  • ECG
  • cardiac markers e.g. troponin
300

Action potential is conducted to the myocardiocytes through what kind of cell junction 

Intercalated discs

300

What is the MOA of class IV antiarrhythmics (250 Pts)

Give 1 example (50)

L-TYPE CALCIUM CHANNEL BLOCKER

MoA: Slows the movement of calcium into the heart and blood vessel walls 

Reduces heart rate, force of contraction, and blood pressure 

Examples: Nifedipine, Diltiazem, Amlodipine, Verapamil

 

300

What is ventricular fibrillation and how can it lead to death

Ventricular fibrillation is the chaotic depolarisation of the ventricles. This results in an arrested cardiac pump function and immediate death

300

n  Where & when is ventricular tachycardia more likely to happen

Often origin around old scar tissue in the heart e.g. after an MI

400

Difference between a STEMI & NSTEMI

Pathology (200 pts)

ECG (200 pts)

STEMI results from complete and prolonged occlusion of an epicardial coronary blood vessel and is defined based on ECG criteria while NSTEMI is a type of heart attack that usually happens with coronary artery narrowing, transient occlusion, or microembolization of thrombus and/or atheromatous material - i.e., partial or temporary occlusion.

STEMI-ST elevation and NSTEMI - normal ECG or minor T wave changes (inversions) & minor ST depression

400

Why does repolarisation take a while in cardiac muscle

Repolarisation takes a while in cardiac muscle to prevent the muscles from going into tetanus (prolonged contraction).

400

What is the MOA of class III antiarrhythmics (350 Pts)

Give 1 example (50)

Potassium channel blocker
Extends the refractory period and delays repolarisation                                                  Blocks transmission of abnormal signals and terminates arrhythmia 

Amiodarone
Sotalol
Ibutilide
Bretylium

400

What is ventricular tachycardia and how can it lead to death

- A sequence of three or more ventricular beats 

Cardiac output is strongly reduced during VT resulting in hypotension and loss of consciousness. Can deteriorate into ventricular fibrillation.

400

List the 5 secondary prevention drugs for an MI (80 pts each)

  • aspirin
  • a second antiplatelet if appropriate (e.g. clopidogrel)
  • a beta-blocker
  • an ACE inhibitor
  • a statin
500

Describe the pathophysiology causing an MI

  • initial endothelial dysfunction is triggered by a number of factors such as smoking, hypertension and hyperglycaemia
  • this results in a number of changes to the endothelium including pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability
  • fatty infiltration of the subendothelial space by low-density lipoprotein (LDL) particles
  • monocytes migrate from the blood and differentiate into macrophages. These macrophages then phagocytose oxidized LDL, slowly turning into large 'foam cells'. As these macrophages die the result can further propagate the inflammatory process.
  • smooth muscle proliferation and migration from the tunica media into the intima results in formation of a fibrous capsule covering the fatty plaque.
500

Name the sequence that electrical signals travel in the heart

SAN

AVN

bundle of His

left and right and bundle 

Purkinje fibres which are spread throughout the ventricles

The impulses cause the ventricles to contract from base up

500

What is the MOA of class Ia antiarrhythmics (150 Pts)

What is the MOA of class Ib antiarrhythmics (150 pts)

What is the MOA of class Ic antiarrhythmics (150 pts)

Give 1 example of each (50 pts)

Class I - Agents that interfere with the sodium channel Ia - Lengthens the action potential eg Quinidine, Procainamide, Disopyramide 

Ib - Shortens the action potential eg lidocaine, phenytoin

 Ic - No significant effect on action potential eg Flecainide, Encainide, Propafenone 

500

What is ventricular flutter and how can it lead to death

Ventricular flutter is mostly caused by re-entry with a frequency of 300 bpm. The ventricles depolarise in a circular pattern, which prevents good function. Most often this results in a minimal cardiac output and subsequent ischemia. Often deteriorates into ventricular fibrillation.

500

What are the 2 systems for breaking bad news (250 pts each)

SPIKES 

 Setting up  Perception  Invitation  Knowledge  Emotions  Strategy and summary

ABCDE

  Advanced preparation  Building a relationship  Communicate well  Deal with patient reactions  Encourage and validate emotions