Neostigmine induced coronary artery spasm: A case report and literature review.

Neostigmine is a cholinesterase inhibitor which does not cross the blood brain barrier and a commonly used for reversal of nondepolarizing muscle relaxants. In the following case report, we present a patient who developed coronary artery spasm, after the administration of repeated doses of neostigmine. Ours is the first case to demonstrate such a longstanding coronary artery vasospasm that lasted several hours in response to neostigmine, resulting in myocardial damage and left ventricular dysfunction. We would like to draw the attention of the anesthesiologists to this rare effect that may lead to perioperative cardiac complications.

Prediction of cardiogenic pulmonary edema onset by monitoring right lung impedance.

OBJECTIVE: To evaluate the ability of internal thoracic impedance (ITI) monitors to predict cardiogenic pulmonary edema in patients at risk. DESIGN AND SETTING: Prospective, controlled multicenter study. PATIENTS: We examined 328 consecutive patients admitted for cardiac conditions. Of these 265 patients aged 27-83 years with no clinical signs of pulmonary edema, extracardiac respiratory failure or pacemakers comprised the study cohort. INTERVENTION: Monitoring of the lung's electrical impedance was used for predicting cardiogenic pulmonary edema since accumulation of blood and fluid decreases impedance values. MEASUREMENTS AND RESULTS: Impedance of the lung is the main feature of ITI measured by the RS-207 monitor: decreased ITI prior to the clinical signs of cardiogenic pulmonary edema was used as the prediction criterion. The clinical signs used for confirmation of its prediction were dyspnea, cyanosis, pulmonary rales, crepitations, arterial hypoxemia, and radiographic evidence of pulmonary congestion in chest radiographs. Clinicians were blinded to the results of ITI measurements and radiologists were blinded to both ITI and clinical data. Thirty-seven patients developed cardiogenic pulmonary edema while being monitored. ITI decreased by more than 12% of baseline in all of them; this occurred at 30 min or longer (26 patients) and at 60 min or longer (11 patients) before the appearance of clinical signs. ITI fell by less then 10.1% of baseline in all 228 patients who did not develop the edema. CONCLUSION: Monitoring ITI is suitable for early prediction of cardiogenic pulmonary edema, before the appearance of the clinical signs.

Internal thoracic impedance monitoring: a novel method for the preclinical detection of acute heart failure.

BACKGROUND: Acute heart failure (AHF) evolves through two phases. In the first phase, there is interstitial congestion with no clinical sign of edema (preclinical phase); the second, during which lung alveoli begin to fill with fluid, manifests as clinically overt alveolar edema. Treatment of AHF at its preclinical phase can alleviate its clinical impact. Presently, there is no technique that detects the interstitial phase of AHF. We used a device based on a new method of lung bioimpedance measurement. The device measures internal thoracic impedance (ITI), which nearly equals inherent lung bioimpedance. This method can detect small changes in lung fluid that occur during the interstitial stage of AHF. AIM: The objective of this study was to assess the feasibility and efficacy of the said new method in detecting preclinical AHF. METHODS: Internal thoracic impedance and pertinent clinical parameters were monitored for 72 h in 403 patients hospitalized for an acute coronary syndrome without evidence of AHF at study entry. RESULTS: Seventy patients developed AHF during monitoring. Internal thoracic impedance decreased in these patients by 16.4% (95% CI=-12.2% to -20.6%; P<.0001) from the baseline level at 44+/-15.1 min prior to the onset of lung rales. The other 333 patients had no clinical sign of AHF, and their ITI declined only by 4.5% (95% CI=2.5% to -11.5%; P=.3) compared with the baseline level. CONCLUSION: The new method for ITI measurement is sufficiently sensitive in detecting AHF at its preclinical stage. An ITI decrease of more than 12% heralds the appearance of clinically overt AHF and, thus, allows earlier therapy.