Core EM - Emergency Medicine Podcast

Episode 220: Post-ROSC Care

Core EM - Emergency Medicine Podcast

Show Notes

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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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

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