Objective: To report tension pneumothorax (TP) as a cause of severe myocardial ischemia.
Design: Clinical case report.
Setting: Medical intensive care unit of a university hospital.
Patients: One patient with severe shock attributable to right TP after unsuccessful percutaneous central venous catheterization.
Interventions: Blood pressure, electrocardiogram (ECG), chest radiograph, and echocardiography during and after shock.
Measurements and main results: On admission the patient was in profound state of shock (heart rate 140 beats/min, blood pressure 65/30 mm Hg). Twelve-lead ECG showed pronounced ST segment elevation in leads II, III, aVF, and V4-V6. Chest radiograph revealed right TP with complete displacement of the mediastinum and the heart to the left side. Immediate right-sided tube thoracostomy resulted in reexpansion of the lung followed by instantaneous hemodynamic and respiratory improvement as well as nearly complete resolution of the ECG changes. Peak value of the creatine phosphokinase was 4140 U/L without significant elevation of the MB isoenzyme at any time. Moreover, the initial hypokinesia of the posterior and lateral left ventricular wall resolved completely, as demonstrated by echocardiography.
Conclusion: The specific condition of TP may lead to impaired systolic and diastolic coronary artery blood flow affecting ventricular repolarization and T-wave configuration in ECG indicative of transmyocardial ischemia. General symptoms, namely hypotension, tachycardia, and hypoxemia, are likewise typical for cardiogenic shock attributable to myocardial infarction. Yet any therapeutic measure directed toward revascularization, such as thrombolysis or even percutaneous transluminal coronary angioplasty, would have had devastating consequences. Therefore, thorough physical examination of our patient was pivotal in disclosing the true origin of profound shock.