Core EM - Emergency Medicine Podcast

Episode 220: Post-ROSC Care


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We explore how to refine and optimize care in the vital minutes following ROSC.

Hosts:

Jonathan Elmer, MD, MS
Brian Gilberti, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Post-ROSC_care.mp3
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Show Notes
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Course Highlights:

  • Credit: 12.5 AMA PRA Category 1 Credits™
  • Curriculum: Comprehensive coverage of Core Emergency Medicine,  with 12 modules spanning from Critical Care to Pediatrics.
  • Cost:
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    • $250 for Non-NYU Learners
    • Click Here to Register and Begin Module 1
      I. Phase 1: Stabilization (Minutes 0–10)
      The “Rearrest” Window & Pathophysiology
      • High-Risk Period: Rearrest rates reach 30% within the first minutes post-ROSC.
      • Shock Incidence: Two-thirds of patients develop profound hypotension/shock as initial resuscitative efforts subside.
      • Catecholamine Washout: Super-physiologic “code-dose” epinephrine (1mg IV) typically wears off within ~3 minutes post-ROSC, leading to predictable hemodynamic collapse.
      • Secondary Injuries: Evaluate for “CPR-induced trauma” (blunt thoracic trauma, rib fractures, pneumothorax, liver/splenic lacerations).
      • Immediate Resuscitative Actions
        • Vascular Access:
          • Transition rapidly from IO to reliable IV access within 1–2 minutes.
          • Prioritize Intraosseous (IO) placement within 5 minutes if IV attempts fail; intra-arrest data suggests no significant difference in early outcomes.
          • Vasoactive “Bridge”:
            • Maintain a “bolus-dose” pressor at the bedside for immediate push-dose titration.
            • Options: Phenylephrine, dilute Epinephrine, or dilute Norepinephrine (titrated to effect rather than rigid dosing).
            • Physician-Specific Task: Arterial Line:
              • Goal: Placement within 5 minutes of ROSC.
              • Preferred Site: Femoral (by landmarks/blind if necessary) for speed; should be a <2-minute procedure.
              • Utility: Immediate detection of rearrest and beat-to-beat titration of vasopressors.
              • II. Phase 2: Diagnostic Workup (Minutes 10–40)
                Etiology Epidemiology
                • ACS Shift: Acute Coronary Syndrome (ACS) is the cause in only 6–10% of resuscitated survivors (lower than historical estimates).
                • Common Etiologies:
                • Respiratory: COPD, pneumonia, mucus plugging.
                  • Cardiac: Arrhythmia (cardiomyopathy/scar), RV failure (PE), or LV failure.
                  • Neurological: Intracranial hemorrhage (SAH/ICH), status epilepticus (4–5%).
                  • Metabolic: Dialysis-related disarray/hyperkalemia.
                  • Toxicology: Overdose accounts for ~10% of cases in urban centers.
                  • The “Broad Net” Strategy
                    • “Rainbow Labs”: Comprehensive panel including toxicology and serial biomarkers.
                    • Pan-Scan Protocol:
                      • Components: CT/CTA Head/Neck, Contrast CT Chest/Abdomen/Pelvis.
                      • Diagnostic Yield: 50% for clinically significant findings (causes or consequences of arrest).
                      • Contrast Risk: Negligible (1–2% increase in AKI risk) compared to the high diagnostic utility.
                      • Avoid Anchoring: Do not assume ischemic EKG changes are the cause; they are frequently a consequence of the global arrest-induced ischemia.
                      • III. Hemodynamic & Respiratory Targets
                        Mean Arterial Pressure (MAP)
                        • Autoregulation Shift: In acute brain injury/post-arrest, the lower limit of cerebral autoregulation shifts right, often requiring MAPs of 110–120 mmHg for adequate perfusion.
                        • Clinical Target: Aim for MAP >80 mmHg.
                        • The BOX Trial Nuance: While the BOX trial showed no difference between MAP 63 vs. 77, its cohort (Denmark) had exceptionally high survival rates (70% back to work) and short response times, which may not generalize to North American populations with lower shockable rhythm incidence.
                        • Permissive Hypertension: If the patient is “self-driving” to higher pressures, do not aggressively lower them, as this may be a physiologic demand for cerebral blood flow.
                        • Ventilation and Oxygenation
                          • PaCO2 Management:
                            • Target: High-normal to slightly hypercarbic (45–55 mmHg).
                            • Rationale: Avoid accidental hyperventilation (PaCO2 <30), which can cut cerebral blood flow by 50%.
                            • PaO2 Management: Maintain normoxia; avoid extreme hyperoxia, though trial data (BOX trial) suggests small variances (70 vs 90 mmHg) are likely neutral.
                            • IV. Neurological Prognostication & Communication
                              The “Stunned” Brain
                              • Anoxic Depolarization: Occurs within ~2 minutes of pulselessness as ATP-dependent ion pumps fail.
                              • Clinical Pitfall: Early neurological exams (absent pupils, no motor response) are unreliable in the first hours as they reflect global neuronal “stunning” rather than definitive permanent injury.
                              • Time Horizon: Meaningful recovery is measured in days/weeks, not minutes/hours.
                              • Family Engagement
                                • Presence: Bring family to the bedside immediately, including during procedures or continued resuscitation.
                                • Psychological Impact: Significantly reduces PTSD, anxiety, and depression in survivors’ families.
                                • Prognostic Honesty: Explicitly state “I don’t know” regarding etiology and outcome.
                                • Framing: Define “No News” as the best possible early outcome (preventing rearrest and stabilization).

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