Abstract: Case Reports |


Jason M. Golbin, DO, MS*; Ognjen Gajic, MD
Author and Funding Information

Mayo Clinic, Rochester, MN


Chest. 2007;132(4_MeetingAbstracts):731. doi:10.1378/chest.132.4_MeetingAbstracts.731
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INTRODUCTION:Recent literature demonstrates that mild therapeutic hypothermia after cardiac arrest due to ventricular fibrillation increases the rate of a favorable neurologic outcome and reduces mortality. However, there is a dearth of information on pulmonary complications resulting from the hypothermic technique.

CASE PRESENTATION:A forty year old female was brought by helicopter to our hospital for emergent coronary catheterization. Earlier, she had complained of left arm pain and indigestion while on the phone, and then became unconscious. Approximately 20 minutes later, she was found by EMS to be in ventricular fibrillation, and had received multiple defibrillations, amiodarone, tracheal intubation, and prolonged CPR. In the catheterization lab, the left anterior descending artery was found to be occluded and stented open with resumption of flow. Intra-aortic balloon pump was temporarily placed and the patient’s hemodynamics improved.In the coronary care unit, the patient was placed on a hypothermic cooling protocol using the Arctic Sun 2000 system. The patient was sedated, paralyzed, and was ventilated in an assist control mode. Initial arterial blood gas (ABG) values demonstrated PaO2=231 mmHg on FiO2=80%. Over the next 18 hours, the PaO2 gradually decreased despite an increase in FiO2. On FiO2 of 100%, the PaO2 was only 49 mmHg. Peak and plateau pressures were mildly elevated at 34 and 30 mmHg, respectively. Emergent echocardiography demonstrated mild global dilatation, ejection fraction of 25-30%, no significant pulmonary hypertension, and a negative bubble study for intra-cardiac shunt. Chest radiography demonstrated bilateral (b/l) lower lobe infiltrates and/or atelectasis. CT angiography was negative for pulmonary embolism, but did demonstrate b/l lower lobe atelectasis (Figure 1). Inspection bronchoscopy demonstrated no secretions or endobronchial lesions, and had no effect on oxygenation. Recruitment maneuver (increasing PEEP to achieve pressure control ventilation of 45/30 for sixty seconds) had a minimal effect. Repeated physical examination revealed the tight cooling pads of the Arctic Sun wrapped around the lower chest and abdomen. The pads were unstrapped and the neuromuscular blocking agent was discontinued. The oxygenation rapidly improved, with the PaO2 nearly doubling on a lower FiO2 (103 on 85% FiO2). The patient continued to improve, and was extubated uneventfully 24 hours later. She awoke with a minimal residual neurologic deficit and is undergoing rehabilitation.

DISCUSSIONS:This case represents the first published complication of hypoxemia resulting from compressive atelectasis due to the extrinsic compression of a cooling system used in post-cardiac arrest hypothermia. The Arctic Sun 2000 system induces hypothermia by using Energy Transfer Pads applied directly to the skin, which cover 40% of the body surface, including the lower chest, the abdomen, and both legs above the knee. Temperature controlled water is then circulated through the Pads, resulting in efficient heat exchange. In our protocol, the patient is cooled to 32 Celsius for 24 hours. This case emphasizes a number of important pulmonary and critical care lessons, including the differential diagnosis of unexplained hypoxemia and shunt in ventilated patients after cardiac arrest. Compression atelectasis occurs when the transmural pressure distending the alveolus is reduced to a level below the “closing volume” which allows it to collapse. Increased pressure on the chest wall or on the diaphragm, such as in obesity, increased intraabdominal pressure, or artificial extrinsic pressure as seen in this case, predisposes patients to atelectasis, and may result in profound intrapulmonary shunt.

CONCLUSION:In cases of unexplained hypoxemia after cardiac arrest, the differential diagnosis needs to include compressive atelectasis induced by tightly applied external cooling devices.

DISCLOSURE:Jason Golbin, No Financial Disclosure Information; No Product/Research Disclosure Information

Wednesday, October 24, 2007

2:00 PM - 3:30 PM


Hypothermia after Cardiac Arrest Study Group.NEJM2002;346:549-556. [CrossRef]
Duggan M and Kavanagh BP.Anesthesiology2005;102:838-854. [CrossRef]




Hypothermia after Cardiac Arrest Study Group.NEJM2002;346:549-556. [CrossRef]
Duggan M and Kavanagh BP.Anesthesiology2005;102:838-854. [CrossRef]
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