Rapid change in pulmonary vascular hemodynamics with pulmonary edema during cardiopulmonary resuscitation

Previous studies have shown that pulmonary edema occurs in half of all pre-hospital cardiac arrest victims who cannot be successfully resuscitated and is a major cause of hypoxemia and poor lung compliance during resuscitation. Pulmonary vascular hypertension and elevation of pulmonary capillary wedge pressure have been observed during cardiac resuscitation in humans. To further define the time course of the pulmonary hemodynamic changes, pulmonary artery diastolic pressure (PAd) was measured on a computerized trend recorder prior to, during, and immediately after arrest in three adult patients. Prior to arrest, PADP was 20.9 +/- 3.1 mm Hg. The PADP rose in all three patients by an average of 30.6% after 5-10 minutes and 71.3% after 10-15 minutes of CPR. Peak PADP reached 35.8 +/- 5.1 mm Hg (difference from pre-arrest level significant, P less than 0.001). In both patients who were resuscitated successfully, the PADP returned to baseline within 5 minutes of effective spontaneous circulation. The finding that such hemodynamic changes occur rapidly during resuscitation and can reverse quickly with resumption of effective spontaneous circulation is consistent with the time course for the early development of pulmonary edema. Development of pulmonary edema many hours following successful resuscitation likely involves other mechanisms.     

Effects of body position on regional pulmonary blood flow during acute pulmonary edema in dogs: A positron emission tomography study

The effect of body position on regional pulmonary blood flow (rPBF) and lung water concentration (rLWC) was studied before and after canine oleic acid (OA)-induced acute lung injury. Regional measurements were made with positron emission tomography. Eleven supine and five prone dogs were studied. In supine animals, LWC increased significantly 60 minutes after OA, primarily in gravity-dependent dorsal lung regions, with a small but still significant additional change over the next 75 minutes. Despite some redistribution, a disproportionate amount of blood flow continued to go to regions with the greatest lung water accumulation. In the prone group, LWC and rPBF were more evenly distributed than in the supine animals, both before and after lung injury. Furthermore, in the prone position, and in contrast to the supine position, regions with the greatest LWC had the least fractional flow. Thus, the benefits of the prone position on oxygenation are related to both the spatial distribution of lung water accumulation and regional pulmonary blood flow.     

Noncardiogenic pulmonary edema during intrabiliary infusion of mono-octanoin

Mono-octanoin (glycerol-1-mono-octanoate) is a medium-chain diglyceride used to dissolve gallstones. We describe a patient in whom noncardiogenic pulmonary edema developed during intrabiliary infusion of monooctanoin. The temporal sequence suggests that the drug infusion initiated the lung injury.     

Absence of pulmonary edema during peritonitis and shock in rats

We evaluated the development of pulmonary edema early in the course of peritonitis and shock in rats. Peritonitis was established by cecal ligation and perforation. In a preliminary experiment, sepsis was induced in five animals and five animals served as sham-operated controls. Lungs harvested for gravimetric analysis at 6 hours revealed no significant difference in wet-dry/dry (W-D/D) ratios. In a second experiment, 15 rats were randomized to three groups: septic animals, septic animals infused with 5% albumin, and sham-operated animals. Thermodilution cardiac output and arterial blood gases were sequentially measured over a 6-hour interval. At 6 hours, the lungs were harvested for gravimetric analysis. Lung W-D/D and arterial oxygenation were not significantly different between the three groups. The W-D/D was 3.46 +/- 0.10 in sham-operated rats, 3.37 +/- 0.12 in septic rats, and 3.88 +/- 0.27 in albumin-infused septic rats. The alveolar-arterial oxygen difference at 6 hours was 10 +/- 2 mm Hg in sham-operated rats, 7 +/- 1 mm Hg in septic rats, and 13 +/- 6 mm Hg in albumin-infused septic rats. These data suggest that overt pulmonary edema and arterial hypoxemia may not occur early in septic shock when fluid infusion is not excessive.     

A novel technique to follow fast PaO2 variations during experimental CPR

OBJECTIVE: An ultrafast responding fluorescent-quenching PO2 probe allows time-resolved, in vivo measurement of PO2. This study describes several validation experiments of this new device in vitro, and reports its first use during cardiopulmonary resuscitation in an animal model of cardiac arrest. METHODS: The influence of CO2, temperature and motion artefacts on the signal response of the PO2 probe was analysed in vitro by systematic variation of these values. Thereafter, with approval of the Review Board for the care and use of animals, CPR was performed in four pigs. The PaO2 course was recorded continuously at time resolution of <80 ms in the abdominal aorta using an uncoated fluorescence-quenching probe (Foxy AL-300, OceanOptics Inc., USA). RESULTS: In vitro experiments showed that signal intensity is dependent on CO2 concentration (DeltaPfaO2=4 mmHg/vol.% CO2) and temperature (DeltaPfaO2=16 mmHg/ degrees C), but it is robust with regards to probe motion. In the animal experiments, the uncoated fluorescence-quenching probe was calibrated by repeated simultaneous measurements with the Paratrend 7 sensor to correct the PfaO2 for a potential signal drift, PCO2 and temperature variations. In all animal experiments, the individual PaO2 courses were clearly related to therapeutic interventions and their haemodynamic effects during CPR and allowed recording of ultrafast PO2 changes with a time resolution of 80 ms. CONCLUSIONS: The results demonstrate the feasibility of ultrafast PO2 measurement during CPR and low-flow states. They also demonstrate very rapid systemic effects of CPR upon aortic PO2. Among many other useful applications, the information derived from this technique may help to define the optimum conditions for successful defibrillation and restoration of spontaneous circulation.     

Postobstructive pulmonary edema

Pulmonary edema is a potentially life-threatening complication of acute airway obstruction. It develops rapidly, without warning, in persons who are otherwise well. Two forms of postobstructive pulmonary edema (POPE) have been identified. POPE I follows sudden, severe upper airway obstruction. POPE II occurs following surgical relief of chronic upper airway obstruction. Treatment for both is supportive. Full and rapid recovery can be expected with appropriate management.     

Neurogenic pulmonary edema

Neurogenic pulmonary edema may be a consequence of a number of diverse central nervous system insults, including resection of an acoustic neuroma. Brainstem lesions in particular seem to cause neurogenic pulmonary edema. Diagnosis requires a high index of suspicion, especially in the case of respiratory decompensation following a seizure.     

Noncardiac pulmonary edema

ARDS is a severe disorder affecting over 150,000 patients per year in the United States alone. The syndrome has multiple etiologies that to a larger extent determine the 60% to 70% mortality associated with the process. In spite of intense research, there is still no specific therapy of proven benefit that we can offer patients. Supportive measures designed to keep the patient alive long enough to allow the pulmonary lesion to heal are the mainstay of therapy. These measures are constantly being improved and increasingly require invasive high technology. Even with advances in treating established ARDS, careful attention toward prevention and day-to-day management of ARDS patients will be required to reduce the excessive mortality.     

Laryngospasm-induced pulmonary edema

Laryngospasm is one of the more common forms of airway obstruction encountered by an anesthetist. Therapy usually is straightforward, with resolution of the obstruction normally occurring within minutes. In some cases, however, the patient's vigorous inspiratory efforts may lead to a rapidly deteriorating form of pulmonary edema. Two cases are presented that are quite typical of the development of this complication. The etiology, recognition and management of this form of non-cardiac pulmonary edema is discussed.     

Postobstructive pulmonary edema

Postobstructive pulmonary edema (POPE; also known as negative pressure pulmonary edema) is a potentially life-threatening complication in which pulmonary edema occurs shortly after the relief of an upper airway obstruction. The incidence of POPE has been reported to be as high as 1 in 1000 general anesthetic cases and commonly presents as acute respiratory distress that requires immediate intervention. This review examines the 2 subclasses of POPE and describes the etiologic factors, pathophysiology, clinical manifestations, diagnostic criteria, and treatment strategies associated with each. The aim of this review was to equip clinicians with the knowledge base necessary to identify patients at increased risk for POPE and to expeditiously diagnose and treat this potentially catastrophic complication.