A 64-year-old woman with a history of asthma presented in cardiac arrest from a presumed severe asthma exacerbation. She underwent prehospital endotracheal intubation. Her initial cardiac rhythm was asystole, and she was treated with epinephrine, atropine, and transported to the hospital.
Chest x-ray. WA = pneumopericardium, WDA = extensive subcutaneous emphysema
On arrival to the emergency department (ED), the patient was in cardiopulmonary arrest. Most notable on initial physical examination was the presence of severe widespread swelling from subcutaneous emphysema that involved her entire head, face, and extended through her torso down to the lower extremities. She had extremely high airway pressures evident by difficult manual bag ventilation.
This patient had status asthmaticus.
Hypoxia and acidosis from the inability to ventilate likely resulted in the cardiac arrest.
A tension pneumothorax could have resulted in poor cardiac function and decreased venous return with a cardiac tamponade-like syndrome.
The patient was treated aggressively with nebulized albuterol, IV methylprednisolone, and IV epinephrine and sodium bicarbonate. Bilateral needle thoracostomies for possible tension pneumothorax were performed with no rush of air and no improvement in either ventilation or hemodynamics. She was ventilated at a rate of 6 breaths/min to allow for her markedly prolonged expiratory phase, and attempts at manual compression of her chest were made. A supine portable chest radiograph demonstrated severe subcutaneous emphysema as well as a significant pneumopericardium. The mediastinum was narrow and appeared compressed. A subxiphoid pericardiocentesis was performed with a large rush of air heard and palpated through the needle. Within a minute of the pericardiocentesis, the patient regained a stable pulse. Bilateral thoracostomies were then performed, and the patient was admitted to the intensive care unit.
Despite return of spontaneous circulation, the patient had suffered diffuse anoxic brain injury, and subsequently died.
Asthma exacerbations lead to a prolonged expiratory phase, and it is vitally important to decrease the ventilator rate to avoid dynamic hyperinflation.
Manual thoracic compression to assist exhalation may be helpful.
Cardiac arrest from asthma is typically from hypoxia and respiratory acidosis. Tension pneumothorax is another common etiology for asthma-related cardiac arrest.
Tension pneumopericardium has been most frequently reported from penetrating and blunt trauma, barotrauma caused by mechanical ventilation, and iatrogenic complications from various invasive procedures. Pneumomediastinum from asthma occurs relatively frequently, but tension pneumopericardium with hemodynamic compromise from asthma is distinctly rare.
RM. Cardiac tamponade due to pneumopericardium. Thorax.
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