A 59-year-old man with a medical history of schizophrenia, severe hearing loss, and drug addiction, without known allergies, on chronic medication with clozapine (100 mg once daily) and amisulpiride (50 mg once daily), presented to the emergency department with severe dyspnea. Upon admission to the emergency room, the patient was diaphoretic, tachypneic, and exhibited accessory muscle use (intercostal retraction and abdominal breathing). Clinical signs included a blood pressure of 117/71 mmHg (mean blood pressure 86 mmHg), heart rate of 110 beats per minute (bpm), and a peripheral oxygen saturation of 70% while on a 28% Venturi mask. Arterial blood gas analysis confirmed severe hypoxemia with a PaO₂/FiO₂ ratio of 178 mmHg, alongside metabolic acidosis (pH 7.263, HCO₃ 15.9 mEq/L, and lactate 4.34 mmol/L). According to the Berlin criteria, the patient’s clinical presentation and oxygenation index were consistent with moderate acute respiratory distress syndrome (ARDS). However, the possibility of acute cardiogenic pulmonary edema was also considered, particularly in the context of a potential TS secondary to substance use. To investigate potential infectious triggers, two sets of blood cultures and a urine culture were collected upon admission, all of which subsequently yielded negative results.

Due to impending respiratory failure from ARDS, non-invasive mechanical ventilation (NIMV) was initiated. A trial of NIMV was attempted initially to manage the severe hypoxemia and the potential cardiogenic component of the pulmonary edema, while avoiding immediate sedation in a patient with psychomotor agitation. The NIMV was started in spontaneous/timed (S/T) mode with an inspiratory positive airway pressure (IPAP) of 16, expiratory positive airway pressure (EPAP) of 6, and FiO₂ of 100%. The chest X-ray showed a diffuse bilateral reticulonodular pattern (Figure 1), consistent with the patient's ARDS presentation.

The patient admitted to having consumed the K4 drug by inhalation hours before the onset of symptoms. However, the exact timing and potential concomitant use of other substances could not be determined. Furthermore, his rapid and progressive cognitive decline upon admission precluded a detailed medical history, leaving his long-term drug use and previous exposure to K4 unknown.

The Poison Information Center (CIAV) was contacted, and information about the synthetic cannabinoid and its potential complications, particularly cardiac ones, was provided.

Laboratory analysis showed a leukocytosis of 24.8 × 10⁹/L with neutrophilia of 21.56 × 10⁹/L, a high-sensitivity troponin I (hsTnI) of 2695.0 ng/L, and N-terminal pro-brain natriuretic peptide (NT-proBNP) of 13732 pg/mL, with no other significant changes (Tables 1-2).

The electrocardiogram revealed a left anterior fascicular block, T-wave inversion in the precordial leads, and a prolonged QTc interval (Figure 2).

Echocardiogram revealed severe left ventricular dysfunction with mid-apical akinesia of all walls and basal hypercontractility. Considering the severity of the clinical picture, the echocardiogram was performed at the patient's bedside in the emergency room, so no images were recorded. No baseline echocardiograms were available, as the patient had no prior cardiovascular history.

While in the emergency department, the patient's respiratory failure worsened, requiring invasive mechanical ventilation. He also developed marked hypotension in the context of cardiogenic shock, which required vasopressor support with norepinephrine.

Cardiac catheterization showed no evidence of coronary artery disease (Figure 3).

The patient was admitted to the Coronary Intensive Care Unit (CICU) for targeted treatment and further investigation. However, on the second day of hospitalization, despite transient clinical improvement, he experienced a cardiac arrest with asystole. Advanced life support was initiated, but the clinical situation could not be reversed, and he ultimately passed away.