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.