The risk factors and prognostic implication of acute pulmonary edema in resuscitated cardiac arrest patients

Abstract

ObjectivePulmonary edema is frequently observed after a successful resuscitation in out-of-hospital cardiac arrest (OHCA) patients. Currently, its risk factors and prognostic implications are mostly unknown.MethodsAdult OHCA patients with a presumed cardiac etiology who achieved sustained return of spontaneous circulation (ROSC) in emergency department were retrospectively analyzed. The patients were grouped according to the severity of consolidation on their initial chest X-ray (group I, no consolidation; group II, patchy consolidations; group III, consolidation involving an entire lobe; group IV, total white-out of any lung). The primary objective was to identify the risk factors of developing severe pulmonary edema (group III or IV). The secondary objective was to evaluate the association between long-term prognosis and the severity of pulmonary edema.ResultsOne hundred and seven patients were included. Total duration of cardiopulmonary resuscitation (CPR) and initial pCO2 level were both independent predictors of developing severe pulmonary edema with their odds ratio (OR) being 1.02 (95% confidence interval [CI], 1.00 to 1.04; per 1 minute) and 1.04 (95% CI, 1.01 to 1.07; per 1 mmHg), respectively. The long term prognosis was significantly poor in patients with severe pulmonary edema with a OR for good outcome (6-month cerebral performance category 1 or 2) being 0.22 (95% CI, 0.06 to 0.79) in group III and 0.16 (95% CI, 0.04 to 0.63) in group IV compared to group I.ConclusionThe duration of CPR and initial pCO2 level were both independent predictors for the development of severe pulmonary edema after resuscitation in emergency department. The severity of the pulmonary edema was significantly associated with long-term outcome.

The relationship between low survival and acute increase of tumor necrosis factor α expression in the lung in a rat model of asphyxial cardiac arrest

“…This inflammation involves activation of leukocytes, secretions of cytokines, leukocytes adhesions to microvascular endothelium, and leukocytes extravasation, which develop tissue damage in final [ 2 6 21 22 ]. In addition, immune cells are rapidly activated upon reperfusion and induce direct tissue injury or augment inflammation via production of pro-inflammatory cytokines.…”

“…The release of various proinflammatory cytokines such as TNF-α can lead to entrapment of neutrophils in the pulmonary capillaries. Elevated plasma levels of TNF-α, interleukin (IL)-6, IL-8 are strongly correlated with pulmonary dysfunction [ 10 21 22 ]. Those cytokines cause generation of polymorphonuclear cells and their entrapment in pulmonary capillaries, and eventually result in cell swelling, plasma and protein extravasation into the interstitial tissue, release of proteolytic enzymes, congestion of alveoli with plasma, erythrocytes and inflammatory debris which alter capillary permeability [ 6 23 ].…”

Effect of mild hypothermia on lung injury after cardiac arrest in swine based on lung ultrasound

“…In this study, ELWI, PVPI, and PO 2 /FiO 2 changed significantly in the TH and NT groups compared to the control group after resuscitation, indicating the presence of lung injury after cardiac arrest in both of the former groups. Previous studies have shown that lung injury is common after resuscitation [21, 22]. The mechanism of lung injury after cardiac arrest is unclear for a variety of reasons; first, pulmonary hemorrhage and edema may be initiated by the alveolar capillary membrane rupture caused by chest compressions; second, oxidative stress induced by the generation of intracellular free radicals may aggravate the damage to membrane function and lead to ischemia-reperfusion injury; third, aspirated gastric juices and oropharyngeal secretions during chest compressions can also cause lung damage [23, 24].…”

Quantitative CT assessment of lung injury after successful cardiopulmonary resuscitation in a porcine cardiac arrest model of different downtimes

“…GGO is considered to be a manifestation of pulmonary edema, which is usually found in pulmonary tissues of hemodynamic dysfunction, toxic injury, or embolism (27,28). Pulmonary edema is a very common pathological characteristic of lung injury following CPR, and severe pulmonary edema is a major cause of failing lung function, which is correlated with a poor long-term prognosis (29,30). In our study, GGO was found in the QCT images in all animals of both VF groups at 6 hours after ROSC, and histopathological results confirmed that the GGO area in QCT scans was pulmonary edema.…”