Associazione Nazionale Medici Cardiologi Ospedalieri




Munaretto Laura Pordenone(Pordenone) – Azienda Sanitaria Universitaria Giuliano-Isontina, Dipartimento Cardiotoracovascolare | Della Mattia Alessio Pordenone(Pordenone) – Azienda Sanitaria Friuli Occidentale, S.C. Cardiologia | Marson Gloria Pordenone(Pordenone) – Azienda Sanitaria Friuli Occidentale S.C Anestesia-RIanimazione e Terapia Intensiva


A 64-year-old male with a history of paroxysmal atrial fibrillation, alcohol abuse, and tonic-clonic epileptic seizures post traumatic brain injury, treated with Valproic acid, was admitted unconscious. In the ICU, a comatose state from crush syndrome-induced oligo-anuric AKI necessitated sedation.

Upon sedation discontinuation, a tonic-clonic seizure occurred. Deep sedation was reintroduced for burst suppression using Propofol and Valproic acid, with dosage adjusted based on serial monitoring of Valproate levels, reaching Propofol levels up to 3.6 mg/kg/h extended during the entire duration of hospitalization.

Initially hypertensive, there was a worsening of the general condition with hemodynamic instability and the need for incremental dosage of vasopressor support with Norepinephrine and Vasopressin.

The subsequent night episodes of non-sustained ventricular tachycardia (TVNS) occurred, followed by in-hospital cardiac arrest due to pulseless ventricular tachycardia (PTV) treated with DC shock with immediate return of spontaneous circulation (ROSC) and a shift to wide QRS complex atrial fibrillation (AF) and repolarization changes compatible with a coved-shaped type pattern (Fig.1). Hemodynamic instability persisted leading to progressive evolution towards refractory hypotension until cardiac arrest (ACC) and subsequent death.


The incidence of Propofol Infusion Syndrome (PRIS) is unknown but carries a 18-30% mortality rate. Critical illness, especially neurological injury, may predispose to PRIS triggered by Propofol, dose, and duration dependent (≥4 mg/kg/hr for ≥48 hours). PRIS results from mitochondrial dysfunction, inhibiting Carnitine Palmitoyl Transferase I (CPT I), disrupting fatty acid beta-oxidation, leading to reduced ATP levels, and systemic fatty acid accumulation. Stress exacerbates a metabolic shift to free fatty acids, intensified by inotropic and vasopressor drugs, causing arrhythmias and systemic and myocardic necrosis.

PRIS manifests as metabolic acidosis, severe rhabdomyolysis, AKI, and hyperkalemia. Myocardial injury is evident in ECG changes, including a Brugada-like pattern and coved-type ST-segment elevations, arrhythmias, and cardiovascular collapse. Timely recognition is crucial, and management involves Propofol discontinuation, hemodynamic support, hemodialysis, and, in refractory cases, ExtraCorporeal Membrane Oxygenation (ECMO). Prevention is paramount.