Ketamine as a Sedative Agent in Type 2 Respiratory Failure Complicating Severe Bronchial Asthma with Cardiomegaly

Abstract

Background: When severe asthma progresses to type 2 respiratory failure together with cardiomegaly and circulatory instability, choosing an appropriate sedative becomes particularly difficult. An optimal agent in this scenario needs to maintain tissue perfusion, limit further suppression of breathing, and contribute to lowering airway resistance. These considerations make ketamine attractive, owing to its capacity to dilate the airways, its limited depressant effect on respiration at sedative doses, and its sympathomimetic action that can help sustain arterial pressure when hemodynamics are marginal.

Case: A 66-year-old man was admitted to the intensive care unit (ICU) with type 2 respiratory failure arising from bronchial asthma, together with cardiomegaly and pulmonary congestion. He arrived with a reduced level of consciousness, rapid breathing, wheeze in both lung fields, and unstable circulation. Blood gas sampling showed marked carbon dioxide retention with acidemia (pH 7.2; PaCO₂ 118.5 mmHg) and a raised lactate. Imaging and echocardiography pointed to an enlarged heart, a likely pulmonary infection, and diastolic impairment, with the left ventricular ejection fraction measured at 39%. After conventional sedation was replaced, a continuous ketamine infusion (0.5–1 mg/kg/h) was titrated to a Richmond Agitation–Sedation Scale (RASS) target of −2 to −3. Care was multimodal, combining lung-protective ventilation, bronchodilators, systemic steroids, antimicrobials, electrolyte correction, and vasopressor support. The patient improved steadily and was extubated by the fifth day without emergence phenomena or serious adverse events.

Discussion: Ketamine was chosen for its combined bronchodilatory action and sympathomimetic support of the circulation, which suited a patient with coexisting severe bronchospasm and hemodynamic instability. Improvement in ventilatory parameters and successful weaning paralleled the ketamine infusion, although the contribution of ketamine cannot be separated from the comprehensive supportive care provided. The reduced left ventricular function (EF 39%) warranted particular caution, since ketamine's sympathomimetic drive may raise myocardial oxygen demand, underscoring the need for close cardiovascular monitoring and careful, graded dose titration in this high-risk geriatric setting.

Conclusion: Ketamine may be considered as a sedative option in selected mechanically ventilated patients with severe asthma and type 2 respiratory failure, particularly when bronchospasm and hemodynamic instability coexist. Nevertheless, meticulous dose titration and vigilant cardiovascular surveillance are essential, especially where cardiac performance is already compromised.