Air in the coronary circulation before and after hypotension. (Image source: Anesthesia & Analgesia)

Air in the coronary circulation before and after hypotension. (Image source: Anesthesia & Analgesia)

The patient experiences profound hypotension after induction: quick, what’s your differential diagnosis?  Let’s also say the patient has a secundum atrial septal defect (ASD) that’s to be closed in the cardiac catheterization lab.  Is your differential diagnosis any different now?

Dr. Dinesh Kumar, Department of Cardiac Thoracic & Vascular Anesthesia, Sri Chitra Tirunal Institute of Medical Science & Technology, Trivandrum, Kerala, India, and colleagues describe just such a patient.  Their summary is published in the 15 March 2014 issue of A&A Case Reports in the article “Paradoxical Air Embolism to Left Anterior Descending Artery During Induction of Anesthesia in a Patient with an Atrial Septal Defect.”

The patient was a 50-year-old female who had dyspnea on exertion and palpitations.  Two-dimensional transthoracic echocardiography (TTE) performed before the procedure showed a 28-mm ostium secundum ASD surrounded by a 5-mm rim of atrial tissue, and a left to right shunt.  Left ventricular ejection fraction was 58%, and RV systolic pressure was 45 mm Hg. Before the procedure, and prior to injection, all syringes, extension tubing, and 3-way connectors had been de-aired.

Anesthesia was induced with propofol 2 mg/kg, midazolam 0.1 mg/kg, fentanyl 4 μg/kg, and vecuronium 0.2 mg/kg. Anesthesia was maintained with isoflurane in oxygen and air, supplemented with intermittent doses of fentanyl and vecuronium.  Following trachea intubation the patient became profoundly hypotensive (60/40 mm Hg). This was accompanied by bradycardia (42 bpm), and ST elevations in leads I, II, AVI, and V2-5.  Atropine and phenylephrine injections didn’t help, so an epinephrine infusion was started.  TTE showed anterolateral wall hypokinesia with global dysfunction of the left ventricle.  The air / oxygen mixture was replaced with 100% oxygen.  Coronary angiography was performed and showed slow flow in the mid and distal left anterior descending artery, suggestive of coronary air embolism.  After 15 minutes, the appearance of air embolism had disappeared and vital signs had resolved, though regional wall motion abnormalities persisted.

The ASD was closed using a 38-mm device, yet the patient’s left ventricular end diastolic pressure (LVEDP) remained elevated despite administration of furosemide and continued resolution of her vital signs.  Given her acute coronary event and elevated LVEDP, the ASD closing device was removed.  The patient’s trachea was extubated after 12 hours, and inotropic drugs were discontinued after 24 hours.  One week later, mild hypokinesia of the lateral wall persisted.  Surgical closure of the ASD was performed 6 months later.

Though unusual, the reader might wonder why air in the coronary circulation does not happen more often in patients who have an ASD.  Given this case report, one should consider consider the possibility of coronary air embolus when a patient presents intraoperatively with profound refractory hypotension and ST elevation.