What will be the 1 line treatment for the MI

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Reading File

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Here is the classic 1-line (mnemonic-based) treatment for Myocardial Infarction (MI):

1-Line Treatment for MI

MONA (or MONAB)

Letter	Drug	Purpose
M	Morphine	Relieves pain and anxiety; reduces preload
O	Oxygen	Correct hypoxia (SpO2 < 94%)
N	Nitrates (Nitroglycerin)	Vasodilation; reduces preload and ischemic pain
A	Aspirin	Antiplatelet - inhibits thrombus extension
B	Beta-blocker	Reduces heart rate, myocardial oxygen demand

"Morphine, Oxygen, Nitrates, and Aspirin are the main components of initial therapy for myocardial infarction." - Miller's Anesthesia, 10e

"Morphine, supplemental oxygen, nitroglycerin, and aspirin (MONA) are the initial therapeutic maneuvers for those being investigated for AMI." - Schwartz's Principles of Surgery, 11e

Important Notes

Aspirin should be given first among all agents (300 mg loading dose, chewed).
Morphine is now used cautiously - evidence suggests it may reduce the efficacy of P2Y12 inhibitors (e.g., clopidogrel) by slowing gastric absorption.
Oxygen is only recommended if SpO2 < 94% - routine high-flow O2 may be harmful in normoxic patients.
Nitrates are contraindicated if the patient has taken a PDE-5 inhibitor (e.g., sildenafil) within 24-48 hours, or in right ventricular (inferior) MI.

Definitive Treatment

The 1-line treatment is a bridge to reperfusion:

STEMI - Primary PCI (percutaneous coronary intervention) within 90 minutes, or thrombolysis if PCI is unavailable.
NSTEMI/UA - Medical management + PCI within 24-72 hours based on risk stratification.

What are STEMI vs NSTEMI differences and management?

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Here is a thorough comparison of STEMI vs NSTEMI - their differences and management - drawn from Harrison's, Washington Manual, and Rosen's Emergency Medicine.

STEMI vs NSTEMI - Differences & Management

1. Core Definitions

Feature	STEMI	NSTEMI
Full name	ST-Elevation MI	Non-ST-Elevation MI
Coronary occlusion	Complete (total occlusion)	Partial (subtotal occlusion)
Infarct depth	Transmural (full thickness)	Subendocardial (partial thickness)
ECG	ST elevation in ≥2 contiguous leads	ST depression, T-wave inversion, or normal ECG
Troponin	Elevated (high)	Elevated (can be mildly elevated)
Q waves	Usually develop	Usually absent
Urgency	Immediate emergency	Urgent but less immediate

2. Pathophysiology

	STEMI	NSTEMI
Mechanism	Atherosclerotic plaque rupture → complete thrombotic occlusion of epicardial artery	Plaque rupture → partial occlusion or transient occlusion; or demand ischemia
Collateral flow	Usually absent (sudden total occlusion)	May be present
Thrombus	Fibrin-rich, occlusive ("red thrombus")	Platelet-rich, non-occlusive ("white thrombus")

"STEMI is caused by acute, total occlusion of an epicardial coronary artery, most often due to atherosclerotic plaque rupture/erosion and subsequent thrombus formation... thrombotic occlusion is complete such that there is total transmural ischemia/infarct." - Washington Manual of Medical Therapeutics

3. ECG Criteria

STEMI ECG Criteria

Men >40 yrs: ST elevation ≥2 mm in V2-V3, ≥1 mm in all other leads
Men <40 yrs: ST elevation ≥2.5 mm in V2-V3
Women: ST elevation ≥1.5 mm in V2-V3, ≥1 mm in all other leads
New LBBB = equivalent to STEMI (suggests large anterior wall MI)
Reciprocal ST depression in opposite leads increases specificity

NSTEMI ECG Findings

ST depression ≥0.5 mm in V2-V3, ≥1 mm in all other leads
T-wave inversions (biphasic or deep >5 mm in V2-V4 = Wellens syndrome - critical LAD lesion)
ST elevation in aVR + ST depression in multiple leads = left main or multivessel disease
~50% of NSTEMI patients have significant ECG changes; ECG can also be normal

4. Mortality & Prognosis

	STEMI	NSTEMI
In-hospital mortality	Higher (6-10%; untreated >30%)	Lower (short-term)
Long-term (1 year) mortality	Similar to NSTEMI	Similar to STEMI
Complications	VF (50% of deaths, often within 1st hour), papillary muscle rupture, VSD, free wall rupture (mortality 90%)	More comorbidities; women have worse outcomes

"Although the short-term mortality of STEMI is greater than that of NSTEMI, the long-term mortality is similar." - Washington Manual

5. Management

STEMI Management - TIME IS MUSCLE

Step 1: Immediate (within minutes)

MONA(B): Morphine, Oxygen (if SpO2 <94%), Nitroglycerin, Aspirin 162-325 mg (chewed), Beta-blocker
12-lead ECG within 10 minutes of arrival
IV access, continuous monitoring, defibrillator ready

Step 2: Reperfusion - the cornerstone of STEMI treatment

Strategy	Timing	When to Use
Primary PCI (1st choice)	Door-to-balloon ≤90 min (or ≤120 min if transfer needed)	PCI-capable center available
Thrombolysis (fibrinolysis)	Within 30 min of arrival ("door-to-needle")	No PCI available within 120 min; no contraindications
Rescue PCI	After failed thrombolysis	If thrombolysis unsuccessful
CABG	Acute setting only	Failed PCI, ongoing ischemia with large territory at risk, mechanical complications

Antiplatelet & Anticoagulation for STEMI

Drug	Dose	Notes
Aspirin	162-325 mg loading	Non-enteric-coated, chewed
Clopidogrel	600 mg load, 75-150 mg/d	Caution in elderly
Prasugrel	60 mg load, 10 mg/d	Avoid if >75 yrs, <60 kg, or h/o stroke/TIA
Ticagrelor	180 mg load, 90 mg BD	ASA dose ≤100 mg; mortality benefit vs clopidogrel
UFH	60 units/kg IV bolus, then 12 units/kg/h	Max bolus 4000 units; all PCI patients
Enoxaparin (LMWH)	30 mg IV + 1 mg/kg SC BD	Reduce dose in age >75 yrs
Bivalirudin	0.75 mg/kg IV bolus, then 1.75 mg/kg/h	PCI validated

NSTEMI Management - Risk-Stratify First

Step 1: Medical Stabilization (all patients)

Aspirin + P2Y12 inhibitor (dual antiplatelet therapy)
Anticoagulation: UFH, LMWH, fondaparinux, or bivalirudin
Anti-ischemic: Nitrates, beta-blockers, oxygen if hypoxemic
Continuous ECG monitoring, serial troponins

Step 2: Risk Stratification - Choose Invasive Strategy by Timing

Risk Category	Timing of PCI	Criteria
Immediate/urgent (<2 hrs)	Emergency PCI	Refractory angina, hemodynamic instability/shock, sustained VT/VF, worsening HF or MR
Early invasive (<24 hrs)	Urgent PCI	TIMI score ≥3, dynamic ECG changes, elevated troponin, new ST depression
Delayed invasive (24-72 hrs)	Elective PCI	Intermediate risk features
Ischemia-driven (conservative)	Only if symptoms recur or stress test positive	Low-risk patients, no recurrent ischemia

"Those with NSTEMI do not require immediate PCI... All patients should receive aggressive antithrombotic, antiplatelet, and ischemic medical therapy no matter the final revascularization strategy." - Rosen's Emergency Medicine / Washington Manual

TIMI Risk Score for NSTEMI/UA (1 point each):

Age ≥65 yrs
≥3 CAD risk factors
Known CAD (stenosis ≥50%)
ASA use in past 7 days
Severe angina (≥2 episodes in 24 hrs)
ST deviation ≥0.5 mm
Positive cardiac marker

Score 0-2 = low risk; 3-4 = intermediate; 5-7 = high risk

6. Summary Comparison Table

Feature	STEMI	NSTEMI
Occlusion	Complete	Partial
ECG	ST elevation / new LBBB	ST depression / T-wave changes / normal
Troponin	Elevated	Elevated (can be lower)
Q waves	Yes (often)	Rare
Reperfusion	Immediate (PCI ≤90 min or thrombolysis)	Risk-stratified (PCI within 2-72 hrs)
Thrombolysis	YES (if no PCI)	Contraindicated
Short-term mortality	Higher	Lower
Long-term mortality	Similar	Similar
Antiplatelet	Dual (ASA + P2Y12)	Dual (ASA + P2Y12)
Anticoagulation	UFH / LMWH / bivalirudin	UFH / LMWH / fondaparinux

Key clinical pearl: Thrombolytics are used in STEMI when PCI is unavailable, but are never used in NSTEMI - because the partial occlusion in NSTEMI involves a platelet-rich clot that is poorly responsive to fibrinolysis and thrombolytics may paradoxically worsen outcomes.

Sources: Washington Manual of Medical Therapeutics; Harrison's Principles of Internal Medicine 22e; Rosen's Emergency Medicine

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