Severe transmyocardial ischemia in a patient with tension pneumothorax

Objective: To report tension pneumothorax (TP) as a cause of severe myocard ial 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, uns uccessful percutaneous central venous catheterization. Interventions: Blood pressure, electrocardiogram (ECG), chest radiograph, a nd echocardiography during and after shock. Measurements and Main Results: On admission the patient was in profound sta te 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 tho racostomy resulted in reexpansion of the lung followed by instantaneous hem odynamic and respiratory improvement as well as nearly complete resolution of the ECG changes. Peak value of the creatine phosphokinase was 4140 U/L w ithout significant elevation of the MB isoenzyme at any time. Moreover, the initial hypokinesia of the posterior and lateral left ventricular wall res olved 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 a nd T-wave configuration in EGG indicative of transmyocardial ischemia. Gene ral symptoms, namely hypotension, tachycardia, and hypoxemia, are likewise typical for cardiogenic shock attributable to myocardial infarction. Yet an y therapeutic measure directed toward revascularization, such as thrombolys is or even percutaneous transluminal coronary angioplasty, would have had d evastating consequences. Therefore, thorough physical examination of our pa tient was pivotal in disclosing the true origin of profound shock.