To the Editor:—

I was interested to read the case report by Stuth et al.  1about negative-pressure pulmonary edema. The pathogenesis of negative-pressure pulmonary edema is multifactorial and associated commonly with sustained negative intrapleural pressure. 2It develops rapidly after the event. Although hiccups produce sharp and intermittent negative intrapleural pressure that is nonsustained, they produced pulmonary edema in this case. The authors have discussed the possibility of other causes of noncardiogenic pulmonary edema (NCPE). However, the possibility of cardiogenic pulmonary edema (CPE) was not discussed. Could this be a case of pulmonary edema resulting from an acute cardiac event?

This patient developed severe hypertension followed by a nonpalpable pulse and possibly hypotension. This hypertension could have been the result of a response to laryngoscopy and endotracheal intubation. High blood pressure could have contributed to the development of acute left ventricular failure and pulmonary edema. After left ventricular failure, the patient’s blood pressure dropped, and, thus, the pulse could not be palpated.

There are few other findings in this case report that indicate that this could be a case of CPE. Using chest radiography, the authors found a central pattern distribution of pulmonary edema. Centrally distributed pulmonary edema could be suggestive of cardiogenic origin. 3A radiograph may show a normal-sized heart in the presence of acute left ventricular failure. It has been stated that radiograph film proves to be of little help, partly because of the portable nature of the film and suboptimal interpretative quality. 3Thus, the absence of cardiomegaly by no means excludes cardiogenic pulmonary edema. 3 

An echocardiogram shows normal left ventricular systolic and diastolic function in NCPE. 3The intraoperative echocardiogram of this patient showed good biventricular function but probably abnormal ventricular function. The resolution of all of the intraoperative echocardiogram abnormalities during follow-up also may imply an intraoperative cardiac event.

The most specific method for differentiating NCPE from CPE is the demonstration of increased alveolar–capillary permeability, which is characteristic of NCPE. 3Alternatively, pulmonary capillary wedge pressure measurement could be useful to differentiate CPE from NCPE. These investigations may not always be feasible, and they may not be necessary when the diagnosis is obvious.

I believe that this patient developed acute pulmonary edema secondary to acute left ventricular failure. The physiologic mechanism ofhiccups is the stimulation of the epipharynx. 4This patient was drooling. It could be that the saliva stimulating the epipharynx of the partially anesthetized patient produced hiccups. Could this be prevented by an anticholinergic premedication?

Stuth EAE, Stucke AG, Berens RJ: Negative-pressure pulmonary edema in a child with hiccups during Induction. A nesthesiology 2000; 93: 282–4
Lang SA, Duncan PG, Shephard DAE, Ha HC: Pulmonary oedema associated with airway obstruction. Can J Anaesth 1990; 37: 210–8
Meyer TE, Gaasch WH: Acute congestive heart failure and pulmonary edema, Cardiac Intensive Care. Edited by Brown DL. Philadelphia, WB Saunders, 1998, pp 375–90
Oshima T, Sakamoto M, Arita H: Hiccuplike response elicited by mechanical stimulation of dorsal epipharynx of cats. J Appl Physiol 1994; 76: 1888–95