Course Content
Module 1: Basic ECMO
Module I: Extracorporeal Membrane Oxygenation Basics (ECMO Basics) This module covers the foundational knowledge of ECMO, including circuit physiology, components, and basic ECMO management. Duration: 3 Weeks (Course weeks 1 to 3) Week 1: Introduction to ECMO Week 2: ECMO Physiology & Circuit Management Week 3: ECMO Complications and Troubleshooting Module I Pretest: 30 MCQs
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Module II: Veno-venous Extracorporeal Membrane Oxygenation (VV ECMO)
This module focuses on the use of VV ECMO in patients with respiratory failure. Topics include ARDS management, VV ECMO cannulation strategies, and VV ECMO troubleshooting. Duration: 3 Weeks (Course weeks 4 to 6) Module II Pretest: 30 MCQs Week 4: VV ECMO Fundamentals Start Date: July 20, 2025 a. Respiratory failure and ARDS management (Ahmed Magdey) b. Evidence for VV ECMO use and landmark trials (Hesham Faisal) c. VV ECMO cannulation techniques and pros and cons of different VV ECMO configuration choices (Moustafa Esam) d. ECMO Retrieval and Patient Transport on ECMO (Ahmed Labib)
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Module III: Veno-arterial Extracorporeal Membrane Oxygenation (VA ECMO)
This module focuses on VA ECMO for cardiogenic shock, including cannulation strategies, LV unloading, and advanced applications. Duration: 3 Weeks (Course weeks 7 to 9) Module II Pretest: 30 MCQs
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Extra Corporeal Membrane Oxygenation (ECMO) and Mechanical Circulatory Support (MCS) course (Copy 4)

Cardiogenic Shock — Summary (Dr. Aws Alherbish)

Definition & Key Concepts

  • Syndrome: Cardiac disorder → low cardiac outputend-organ hypoperfusion.

  • Clinical triad: Hypotension (SBP <90), cardiac index <1.8, elevated filling pressures (e.g., LVEDP ~18).

  • Time-critical: First 30 min = assessment; by 60–90 min = logistics (cath lab/CCU/transfer); next 6–12 h = resuscitation/escalation; by 24 h = trajectory/need for MCS.

Classification Frameworks

  • SHOCK categories: AMI-CS (STEMI/NSTEMI), HF-CS (de novo vs acute-on-chronic cardiomyopathy), post-cardiotomy CS, secondary CS (myocarditis, tachycardia-induced, etc.).

  • SCAI stages: C (stable on inotropes), D (deteriorating), E (extremis).

  • Phenotypes:

    • 1 (Dry–Cold): Non-congested hypoperfusion—lower mortality.

    • 2 (Wet–Cold): Cardiorenal—higher mortality.

    • 3 (Cardiometabolic): Shock liver/severe acidosis—highest mortality.

Pathophysiology & Hemodynamics

  • Vicious circles: Low CO → vasoconstriction/↑afterload, ischemia, sympathetic surge.

  • Goals: Restore perfusion, reduce congestion, decrease myocardial work.

  • Key metrics: LVOT VTI (SV surrogate; <10 cm concerning), cardiac power output (MAP × CO).

  • Forrester lens: Assess perfusion and congestion to guide therapy.

Initial Assessment (≤30 min)

  • Focused Hx/Exam: Perfusion (cold, mental status, urine), congestion (JVP/edema), vitals.

  • Rapid tests: ECG (rule STEMI), POCUS/echo (LV/RV, volume, lungs), CXR; monitor outputs.

  • If pre-arrest: Prioritize stabilization (PLR over fluid bolus, vasoactive boluses, early echo); correct acidosis, calcium, electrolytes.

Management Pillars

  • Etiology-directed: Early revascularization for AMI-CS (primary mortality benefit).

  • Pharmacologic:

    • Pressors/inotropes: Start norepinephrine; add dobutamine or milrinone as needed; avoid dopamine (arrhythmias/ischemia).

    • Begin diuretics once hemodynamically safer (congestion).

    • Aggressive metabolic correction (acidosis, Ca/K/Na).

  • Procedural: PCI/CABG; MCS (IABP less used; Impella or VA-ECMO based on needs).

    • Device choice by urgency, flow requirement, lung involvement, RV, valves/thrombus, access.

    • ECMO ↑afterload; consider LV venting (e.g., Impella).

  • Ancillary: Ventilation (NIV/intubation), antibiotics if infected, delirium control, transfusion targets ~70–80 g/L per clinician judgment.

MCS Strategy & Outcomes

  • Team-based decision: Heart failure, interventional, surgery, intensivist.

  • Candidacy: Age/frailty, comorbidities, and clear exit strategy (recovery, PCI, LVAD, transplant).

  • Timing: Not too early (before pharma failure) or too late (irreversible organ injury).

  • Destinations: Recovery, durable LVAD, heart transplant, or death.

  • Mortality: Still ~40–50%; risk rises with ≥3 vasoactive agents.

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