AMI

Question 1

Myocardial Infarction (MI) – IBCC

Diagnosis

Answer 1

• Ischaemic symptoms
• Evolving ECG changes
• New RWMA on echo
• Dynamic rise/fall of troponin

Question 2

Types of MI

Answer 2

Type I – due to acute plaque rupture
* Blockage of coronary artery

Type II – due to demand ischaemia
* Usually patients with stable coronary stenosis
* Develop MI if ↑ demand beyond perfusion
* e.g. Anaemia, hypoxia; hypotension, hypertension; tachycardia, arrhythmia, sepsis

Type III – MI resulting in death
* Biomarker values are still unavailable

Type IV – MI related to PCI (percutaneous intervention)
* IVa → <48 hrs post PCI
* IVb → stent thrombosis
* IVc → stent stenosis

Type V – MI related to CABG

Question 3

Type I vs Type II-
Q. how to differentiate
Q. Significance of ECG changes in AMI

Answer 3

Type I vs Type II
* Troponin rise usually milder in Type II
* No characteristic RWMA
* Could see global hypokinesia

⸻

ECG Considerations
* No. of leads involved in ECG ∝ extent of myocardial injury
* Height of initial STE only modestly correlates with degree of ischaemia
* Acute resolution of STE correlates well with reperfusion

Question 4

Official definition of STEMI according to the American College of Cardiology/American Heart Association

Answer 4

=>“new ST segment elevation at the J point of >/= 1 mm in any two contiguous leads except leads V2 or V3, where the elevation must be 2 mm in men or 1.5 mm in women.

Question 5

ECG changes in MI

HAELIO

Answer 5

=> Anterior MI:
->Proximal LAD occlusion- Antero-lateral wall involved STE in V1-V6, I, AVL
->Mid LAD occlusion (after the septal branch), the diagonal branch(es) may or may not be involved–>
STE in V3 to V6 — and not the septal leads(V1,V2)
->Because the anatomical opposite of the precordial leads would be posterior leads, (not commonly checked) –> There may be No “reciprocal changes” during anterior or septal MIs EXCEPT in
“high lateral” MIs with STE in I and aVL –> can show reciprocal ST segment depression in leads II, III and aVF.

Question 6

Reciprocal changes in ECG

Answer 6

=>PAILS mnemonic m/c used tool for remembering reciprocal changes (ST depressions) in a 12-lead ECG.

=>ST elevation in a group of leads creates depression in the next letter’s corresponding leads, usually in a “next-in-line” sequence

Question 7

Inferior MI

Answer 7

=>ECG criteria:
* ST elevation ≥ 1 mm in ≥2 contiguous leads
* Leads involved: II, III, aVF

=>Reciprocal changes:
* ST depression in I and aVL
* Helps differentiate from pericarditis

=>Morphology:
* ST elevation often concave upwards
* Amplitude variable (mild → marked elevation)

Question 8

Posterior Wall MI

Answer 8

=>Postr wall- supplied by PDA-> branch of RCA in 80% cases( Rt dominant circulation)
* Hence, occlusion of RCA may result in Inferior/ Posterior/ Inferoposterior MI

=>ECG criteria to diagnose a posterior MI:
* ST segment depression (not elevation) in V1 to V4 (Reciprocal changes)
* Ratio of the R wave to the S wave in V1 or V2 is >1 (upside-down Q wave)
* STE in posterior leads (leads V7-V9)

continue in the same horizontal line->
V7 on the posterior axillary line,
V8 at the tip of the left scapula, and
V9 at the left paraspinal region.

Question 9

ACS- Immediate Mx

Answer 9

Immediate Management of ACS
1) Cardiac monitoring

2) O₂ supplementation: only for breathless/hypoxic (aim sat > 90%)
* No benefit if O₂ sat normal (may be harmful in normoxic)

3) Antiplatelets:
* Aspirin: 150–325 mg chewed/dissolved, then maintenance
* Not enteric-coated release
* Reduces mortality (~5%)
* Clopidogrel -> addition of a P2Y12 inhibitor to aspirin significantly reduces platelet aggregation and incidence of recurrent MACE but with an increased risk of bleeding.
* DAPT (dual antiplatelet therapy): before PCI and lytics
4) Analgesia:
* Sublingual GTN spray: relieve chest pain
* Avoid if recent phosphodiesterase inhibitor use (↑ risk severe hypotension)
* Morphine (2-4mg iv bolus repeated 5-15min upto 10 mg or Fentanyl 25-50mcg every 5mins upto 100mcg) if persistent pain
* Avoid NSAIDs (↑ risk of reinfarction, mortality)
5) Reperfusion therapy:
* Ideally primary PCI (preferred if available <120 min)
If not posssible→ thrombolysis, then transfer to PCI-capable centre

AHA guidelines- 2025

Question 10

RVMI (Right Ventricular Myocardial Infarction)
Definition
&
Importance

Answer 10

->Definition:
* Refers to infarction of RV free wall
* Isolated RVMI rare (~3%)
* Usually occurs with inferior/posterior MI

• Importance:
  
  • Recognition is crucial (haemodynamic implications)
  • Requires urgent revascularisation
  • Associated with higher morbidity & risk of complications

Question 11

Clinical Findings

Answer 11

• Chest pain
• Classical triad of :
  -Clear lung fields (distinguishes from LV failure)
  -Raised JVP
  -Hypotension
• Severe hypotension after nitrates/morphine
• Refractory hypoxaemia may occur:
  
  • R→L shunt via patent foramen ovale
• **Bradycardia/AV block **may occur → slow/aggressive pacing may be required

Question 12

ECG signs of RV MI

Answer 12

=>Suspect and look for right ventricular (RV) infarction in all patients with inferior STEMI.

=>ECG diagnostic criteria
In patients with inferior STEMI, RV infarction is suggested by:
* ST elevation in V1
* ST elevation in V1 and ST depression in V2 (highly specific for RV infarction)
* Isoelectric ST segment in V1 with marked ST depression in V2
* ST elevation in III > II
* Diagnosis is confirmed by the presence of ST elevation in the right-sided leads (V3R-V6R)

=>V1 is the only standard ECG lead that looks directly at the right ventricle

=>Lead III is more rightward facing than lead II and hence more sensitive to the injury current produced by the right ventricle

=>Clinical Significance of RV Infarction
* RV infarction complicates up to 40% of inferior STEMIs (isolated RV infarction is extremely uncommon)
* Very preload sensitive (due to poor RV contractility) and can develop severe hypotension in response to nitrates or other preload-reducing agents.

=>Hypotension in right ventricular infarction is treated with fluid loading, and nitrates are contraindicated.
The ECG changes of RV infarction are subtle and easily missed!

Lead V4R is placed in the 5th ICS on the Rt mid-clavicular line.
It is the mirror image of the standard V4 lead and is used to identify right ventricular infarction, typically by moving the V4 electrode to the right side of the chest

Question 13

RVMI – Echocardiography

Answer 13

• RV dilatation, dysfunction
• McConnell’s sign: hypokinesis of RV free wall with preserved apex (classically PE, but not specific)
• Patent foramen ovale → hypoxaemia
• Dilated IVC
• RV infarction often seen with inferior MI

Question 14

Management of RVMI

Answer 14

1). Urgent Revascularisation
* Primary PCI or thrombolysis

2). Haemodynamics
* Avoid agents ↓ preload (e.g., GTN, diuretics)
* Avoid excess ↑ afterload (e.g., ↑ PEEP, hypoxia, acidosis)
* Judicious fluid administration may help (RV preload dependent)
* Too much fluid → RV distension + compress LV
* Use dynamic fluid monitoring
* CVP: 10–14 mmHg may be optimal
* Inhaled pulmonary vasodilators → ↓ afterload; ↑ forward CO

Question 15

Management of RVMI cont..

Answer 15

3). Vasopressors
* β-adrenergic agonists:
* ↑ pulmonary vasodilation + RV contractility
* Dobutamine, milrinone (caution: hypotension risk)
* For ↓ BP with ↓ CO → noradrenaline (vasopressor + inotrope)
* Avoid pure α-agonists (e.g., phenylephrine)–> ↑ RV afterload

4) If Hypoxemia–>R/O PFO

5) Arrhythmias- poorly tolerated–>
Amiodarone / Cardioversion for tachyarrhythmias
+/- Pacing for bradyarrhythmias

Question 16

Complications Post-MI

Answer 16

1. Reinfarction (in-stent thrombosis)
2. Cardiac complications
   
   • Rupture of MI chordae tendinae
   • Ventricular septal defect
   • Free wall rupture
   • RV free wall rupture
3. Pericarditis
   
   • Post-MI pericarditis
4. Arrhythmias
   
   • AF / AFl
   • VT / VF
   • Heart block
5. Haemorrhage
   
   • e.g., retroperitoneal haemorrhage
   • Tamponade
6. Medication effects
   
   • β-blockers, ACEi, diuretics

Question 17

Cocaine induced MI

LITFL

Answer 17

• Cocaine -> sympathomimetic effects + sodium channel blocker
• Can induce acute coronary syndromes through Vasoconstriction, Atheroma rupture and/ or Dissection
• Accounts for 1/4th of AMI cases in age- 18-45yrs
• Risk of MI ⬆️es 24-fold in 1st hr post cocaine use
• Chest pain only +nt in 40%
• Dysnoea, Diaphoresis often +nt

=>MANAGEMENT

->Rule out aortic dissection

• Treat suspected acute coronary syndrome
• Aspirin / other anti platelets
• Nitroglycerine
• Calcium channel antagonists
• Coronary angiography +/- stenting – if ST elevation that persists after medical treatment

=>Avoid beta-blockers (including labetolol) due to risk of unopposed alpha-agonism

=>Thrombolytics are contraindicated if severe hypertension, seizures, intracerebral haemorrhage or aortic dissection

Question 18

Antiplatelet classification

Answer 18

=> Cyclooxygenase (COX-1) Inhibitors
Drugs: Aspirin (acetylsalicylic acid).
* Mechanism: Irreversibly inhibits the COX-1 enzyme, blocking the conversion of arachidonic acid to Thromboxane A2 which is a potent platelet activator and vasoconstrictor.
* Duration: Lasts for the lifetime of the platelet (7–10 days).

2). P2Y12 Adenosine Diphosphate (ADP) Receptor Antagonists
* Prevent platelet aggregation by blocking ADP receptor, which is crucial for activating the GP IIb/IIIa receptor.
->Irreversible (Thienopyridines): Clopidogrel, Prasugrel, Ticlopidine.
->Reversible: Ticagrelor, Cangrelor (IV).

3). Glycoprotein (GP) IIb/IIIa Receptor Antagonists
Drugs: Abciximab, Eptifibatide, Tirofiban.
->Mechanism: Block the final common pathway of platelet aggregation—the GP IIb/IIIa receptor—preventing the binding of fibrinogen and von Willebrand factor, thus preventing platelets from bridging together.
Route: Parenteral (IV) only.

4). Phosphodiesterase (PDE) Inhibitors
Drugs: Dipyridamole
Mechanism: Inhibits phosphodiesterase, leading to increased cyclic AMP (cAMP) levels within platelets. High cAMP inhibits platelet activation and aggregation.

5). Protease-Activated Receptor-1 (PAR-1) Antagonists
Drugs: Vorapaxar.
Mechanism: Reversibly binds to PAR-1, inhibiting thrombin-induced platelet activation.