"- At least one documented episode of SpO₂ < 80%, ensuring accuracy of measurement.

• At least one episode of systolic arterial blood pressure (SAB) < 65 mmHg.
• SAB < 90 mmHg sustained for a duration of 30 minutes.
• Initiation of norepinephrine therapy.
• Escalation of pre-existing norepinephrine infusion dose.
• Administration of >15 mL/kg crystalloid fluids to achieve SAB > 90 mmHg.
• Occurrence of cardiac arrest." The occurrence of any of the above-mentioned events within the first 30 minutes following the initiation of the intervention will be considered as cardiovascular collapse.

The hemodynamic effects of propofol and ketamine are well-documented in the general patient population, yet the incidence and characteristics of cardiovascular collapse induced by these agents in critically ill patients remain underexplored. Cardiovascular collapse, a severe and potentially life-threatening event, may arise due to the unique physiological stressors present in the critical care setting, including pre-existing hemodynamic instability, comorbidities, and the administration of high-risk pharmacological agents. Despite the theoretical understanding of these drugs' pharmacodynamics, there is limited evidence assessing their differential impact on cardiovascular function in this vulnerable population.

This study aims to contribute novel insights to the literature by exploring the association between these widely used sedative-hypnotic agents and the development of cardiovascular collapse. While propofol is known for its potent vasodilatory and myocardial depressive effects,

• At least one documented episode of SpO₂ < 80%, ensuring accuracy of measurement.
• At least one episode of systolic arterial blood pressure (SAB) < 65 mmHg.
• SAB < 90 mmHg sustained for a duration of 30 minutes.
• Initiation of norepinephrine therapy.
• Escalation of pre-existing norepinephrine infusion dose.
• Administration of >15 mL/kg crystalloid fluids to achieve SAB > 90 mmHg.
• Occurrence of cardiac arrest.