Abd A G, Braun N M, Baskin M I, O'Sullivan M M, Alkaitis D A
St. Luke's-Roosevelt Hospital Center, New York, New York.
Ann Intern Med. 1989 Dec 1;111(11):881-6. doi: 10.7326/0003-4819-111-11-881.
Of 1225 patients undergoing open heart surgery over an 18-month period, 13 had diaphragmatic dysfunction due to phrenic nerve injury; 11 of these had internal mammary artery grafting. Nine had diaphragmatic dysfunction on the same side as the internal mammary artery graft side (7 bilateral and 2 unilateral) as determined by fluoroscopy during phrenic nerve stimulation. Although topical cardiac hypothermia has been the prevailing mechanism for diaphragmatic dysfunction due to phrenic nerve injury after open-heart surgery, dissection of the internal mammary artery with electrocautery, traction, or vascular compromise to the phrenic nerve, or a combination, could be additional factors. Rocking bed ventilation was instituted to facilitate passive diaphragmatic movement and airway decannulation and was continued at home until the phrenic nerve or nerves recovered. These patients were followed up clinically and with serial measurements of vital capacity, respiratory muscle strength, phrenic nerve latency, and fluoroscopy to determine recovery rate. Phrenic nerve recovery occurred from 4 to 27 months after surgery. This recovery was heralded by the patients' ability to assume the supine position without dyspnea when use of the rocking bed was discontinued. Unilateral diaphragmatic recovery was sufficient for the restoration of symptom-free supine posture.
