❤️ Chapter 50: Acute Myocarditis

Viral Inflammation of Myocardium · Fulminant vs Acute · Cardiogenic Shock · Inotropes · ECMO · IVIG · ACE Inhibitors · Beta-Blockers

❤️ Acute Myocarditis: Inflammation of Cardiac Myocytes — Often Viral

📊 Definition & Aetiology
Acute inflammation of cardiac myocytes. Most common cause: viral (enterovirus, adenovirus, parvovirus B19, influenza, EBV, CMV). Also toxins, hypersensitivity, connective tissue diseases.
🩸 Pathophysiology — 3 Phases
Phase 1: Direct viral myocyte injury → cardiac dilatation.
Phase 2: Autoimmune-mediated injury (days to weeks).
Phase 3: Dilated cardiomyopathy (DCM) if recovery incomplete.
📋 Clinical Classification
• Fulminant myocarditis: sudden onset, haemodynamic compromise, requires inotropes/ECMO, good outcome with recovery.
• Acute lymphocytic myocarditis: insidious onset, less severe, may progress to DCM.
🔬 Diagnosis
• ECHO: decreased EF, chamber dilatation, ± diastolic dysfunction
• ECG: sinus tachycardia, low voltage, ST/T changes, arrhythmias
• Labs: elevated troponin, CK-MB, BNP
• Gold standard: endomyocardial biopsy (Dallas criteria) — rarely done
💊 Management
• Supportive: oxygen, mechanical ventilation, sedation (decrease O2 demand)
• Inotropes: Adrenaline (hypotensive), Milrinone/Dobutamine (normotensive)
• Afterload reduction: ACE inhibitors, milrinone
• IVIG: 2 g/kg (limited evidence, may have role)
• Diuretics for fluid overload (after shock resolved)
⚙️ Mechanical Support & Prognosis
• VA-ECMO: bridge to recovery (fulminant myocarditis) — 1-2 weeks support
• VAD: bridge to transplant
• Prognosis: 1/3 recover fully, 1/3 develop DCM, 1/3 die or require transplant
📌 Fulminant vs Acute Myocarditis: Fulminant → abrupt onset, severe haemodynamic compromise, requires aggressive support (ECMO), paradoxically better outcome. Acute → insidious, less severe, higher risk of chronic DCM.

🩺 Step-by-Step: Management of Acute Myocarditis

1
Recognise myocarditis
Suspect in child with viral prodrome (URI, GI symptoms) followed by: tachycardia out of proportion to fever, gallop rhythm, hepatomegaly, poor perfusion, +/- chest pain, arrhythmias. May present as cardiogenic shock.
2
Initial stabilisation — ABCs
100% oxygen. If respiratory distress or shock, early intubation (reduces work of breathing, decreases O2 demand). Use ketamine for induction (avoid etomidate).
3
Haemodynamic support — cautious fluids, inotropes
Fluid bolus only if hypovolaemic (small 5-10 mL/kg). Hypotensive cardiogenic shock → Adrenaline 0.05-0.3 mcg/kg/min. Normotensive with low output → Milrinone or Dobutamine (inodilators).
4
Afterload reduction (once BP stable)
Add milrinone, nitroprusside, or oral ACE inhibitor (captopril/enalapril) after BP improves. Afterload reduction is cornerstone in systolic dysfunction.
5
Diastolic dysfunction management
If ECHO shows diastolic dysfunction (E/A reversal): use milrinone (lusitropy), avoid tachycardia, slow fluid administration, avoid high-dose adrenaline.
6
Specific therapies
• IVIG 2 g/kg over 10-12 hours (controversial, may benefit)
• Corticosteroids: NOT routinely indicated; consider if biopsy-proven giant cell or eosinophilic myocarditis
• Antiviral therapy if specific pathogen identified (rare)
7
Mechanical support (ECMO/VAD)
If shock persists despite maximal medical therapy → VA-ECMO. Fulminant myocarditis has excellent recovery potential with ECMO bridge (1-2 weeks). VAD for longer-term bridge to transplant.
8
Long-term heart failure management
After recovery: ACE inhibitors (enalapril/captopril), beta-blockers (carvedilol), diuretics as needed, ± digoxin. Follow ECHO for progression to DCM.