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Study Objective: We evaluate the incidence of complications associated with the use of nitrates in patients presenting with acute pulmonary edema and concomitant moderate or severe aortic stenosis compared with patients without aortic stenosis. Nitrates are contraindicated in severe aortic stenosis because of the theoretical yet unproven risk of precipitating profound hypotension., Methods: A cohort design with retrospective chart review study was conducted at two Canadian hospitals. Patients with aortic stenosis (moderate or severe) and without aortic stenosis were included if they presented with acute cardiogenic pulmonary edema, received intravenous or sublingual nitroglycerin, and had an echocardiography report available. The primary outcome was clinically relevant hypotension, defined as hypotension leading to any of the following predefined events: nitroglycerin discontinuation, intravenous fluid bolus, vasopressor use, or cardiac arrest. The secondary outcome was sustained hypotension, defined as a systolic blood pressure less than 90 mm Hg and lasting greater than or equal to 30 minutes., Results: The cohort consisted of 195 episodes of acute pulmonary edema, representing 65 episodes with severe aortic stenosis (N=65) and an equal number of matched episodes with moderate aortic stenosis (N=65) and no aortic stenosis (N=65). Nitroglycerin was administered intravenously only in 70% of cases, intravenously and sublingually in 25%, and sublingually only in the remaining 5%. After adjustment for sex, initial systolic blood pressure, furosemide dose, and use of noninvasive ventilation, moderate and severe aortic stenosis were not associated with clinically relevant hypotension after receipt of nitroglycerin (adjusted odds ratio [OR] 0.97, 95% confidence interval [CI] 0.40 to 2.37 for moderate aortic stenosis; adjusted OR 0.99, 95% CI 0.41 to 2.41 for severe aortic stenosis). The incidence of clinically relevant hypotension was 26.2% for moderate and severe aortic stenosis and 23.1% in the no aortic stenosis reference group. The secondary outcome of sustained hypotension occurred in 29.2% of patients with severe aortic stenosis, 16.9% with moderate aortic stenosis, and 13.8% in the no aortic stenosis group (adjusted OR for severe aortic stenosis 2.34; 95% CI 0.91 to 6.01)., Conclusion: In this retrospective study, neither moderate nor severe aortic stenosis was associated with a greater risk of clinically relevant hypotension requiring intervention when nitroglycerin was used for acute pulmonary edema. Future studies should investigate safety and efficacy of nitroglycerin for patients with aortic stenosis because this study was limited by a small sample size and design limitations. Cautious use of nitroglycerin in patients with moderate or severe aortic stenosis and presenting with acute pulmonary edema may be a safer strategy than traditionally thought., (Copyright © 2015 American College of Emergency Physicians. Published by Elsevier Inc. All rights reserved.)

We report 2 infants with severe bronchopulmonary dysplasia in whom left ventricular diastolic dysfunction contributed to clinical abnormalities, including pulmonary hypertension and recurrent pulmonary edema. We speculate that close monitoring for left ventricular diastolic dysfunction may assist with clinical management and improve outcomes of infants with severe bronchopulmonary dysplasia.

Background: Cholesterol embolism (CE) is an increasingly common but often underdiagnosed medical problem. The recognition of clinical manifestations of CE is the first step toward a correct diagnosis., Objective: Our aim was to characterize the features of CE and the risk factors for fatal outcome., Methods: Clinical records of patients with clinical and histopathologic diagnoses of CE seen from January 1993 through March 2003 were reviewed., Results: Twenty-six male patients were identified. Mean age was 64 years (range, 48-88 years). All patients had two or more risk factors for atherosclerosis. All but one patient had preexisting symptomatic atherosclerotic disease. At least one precipitating factor was identified in 23 patients (88%). Diagnosis of CE at admission was made in 9 patients only (35%). Cutaneous lesions (88%) and renal failure (73%) were the most common clinical findings. Complications (dialysis, acute pulmonary edema, amputation, or gastrointestinal surgery) were present in 21 patients (81%), and 15 patients died (58%). Previous chronic renal failure was the only variable associated with mortality (relative risk: 4.54, 95% confidence interval 1.26-16.6; P = .02)., Limitations: The results were obtained from patients admitted to a university hospital. This fact may have selected a higher proportion of severe cases., Conclusions: CE was frequently misdiagnosed. Skin lesions were the most common clinical findings and skin biopsy provided histologic confirmation in most of the patients. Chronic renal failure was the only factor related to death.

Presented is the case of a 2 1/2-year-old with acute pulmonary edema associated with epiglottitis prior to intubation. The patient complained only of odynophagia and had one brief episode of apnea and flaccid posturing. Chest radiograph demonstrated pulmonary edema. A soft tissue radiograph of the neck confirmed the diagnosis of epiglottitis. The patient was managed successfully with prompt intubation, PEEP, and antibiotics. Pulmonary edema associated with epiglottitis may be more common than previously recognized. It may occur prior to or after intubation. When pulmonary edema is clinically evident, PEEP should be administered early.

To assess the effects of chronic left ventricular (LV) dysfunction on intravascular pulmonary blood volume (PBV) and extravascular lung water (EVLW) lung fluid volumes, 56 dogs were evaluated by means of double-indicator dilution techniques. PBV and EVLW were measured in seven control dogs, in eight dogs 4 hours after the production of left heart dysfunction, and then in three additional groups of dogs (n = seven in each group) 7, 14, and 30 days after the production of LV dysfunction. Twenty dogs were excluded because we were unable to produce elevations in LV end-diastolic volume greater than 25 mm Hg. EVLW was measured using heat as the diffusible indicator, and electric shock was used to create heart block and myocardial scarring in order to produce LV dysfunction. Plasma volume was calculated prior to death by means of radioiodinated albumin. In the remaining animals, electric shock acutely and chronically elevated LV end-diastolic pressure (control 2.3 +/- 1.0 mm Hg; postshock pressures greater than 25 mm Hg). PBV increased initially after cardiac failure and remained so as time progressed, although it represented a smaller fraction of the plasma volume as time passed (11.2 +/- 2.1% control, 15.9 +/- 3.4% at 4 hours after failure, and 12.6 +/- 2.0% at 7 days; the former p less than 0.005 vs control, the latter p less than 0.01 vs control). EVLW increased as time progressed, in consort with small but progressive increases in left atrial pressure. Thus, we conclude that the effects of acute and chronic LV dysfunction on pulmonary circulation are significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)

The use of electrical energy for the immediate treatment of atrial and ventricular arrhythmias is practical and easily applied. The method, though simple, is the most effective method for terminating cardiac arrhythmias and is associated with only a low risk if properly employed. In symptomatic patients, the utilization of cardioversion reduces patient discomfort and complications which may occur while awaiting pharmacologic reversion of arrhythmia. At present, transthoracic defibrillation is the only practical method for terminating VF. Despite the safety of electrical reversion, proper precautions are necessary to prevent complications. In particular, the discharge of excessive energies, especially in the presence of digitalis toxicity, promises grave and life-threatening consequences. The use of antiarrhythmic medications is not supplanted by cardioversion and defibrillation. Rather, ongoing drug therapy is frequently necessary to prevent recurrence of arrhythmia.

Pulmonary extravascular volume or lung water (PEV), arterial blood gases, and cardiac hemodynamics were measured in 88 patients with acute myocardial infarction. A progressive increase in PEV and a decrease in arterial oxygen tension (PaO2) were observed from Class I (uncomplicated) patients to Class III (frank pulmonary edema) patients. Heart rate and pulmonary wedge pressure (Pw) rose and cardiac index declined with increasing severity of heart failure by clinical classification. There was a significant correlation between PEV and Pw independent of clinical class (r = 0.47, p less than 0.01). PaO2 had a negative correlation with Pw (r = -0.28, p less than 0.01) as well as PEV (r = -0.26, p less than 0.02). We conclude therefore that increased pulmonary hydrostatic pressure secondary to pulmonary venous hypertension in patients with acute myocardial infarction is a major determinant of interstitial edema. At higher values of PEV, PaO2 was lower. The mechanism of hypoxemia in the presence of excessive lung water may be due to multiple factors, including small airway dysfunction and intrapulmonary shunting.

At New York University Medical Center over the past 18 months, a distinctive and potentially lethal syndrome of fulminating noncardiogenic pulmonary edema has been observed in three patients following cardiopulmonary bypass. The clinical appearance is virtually identical to that produced by acute left ventricular failure, and the condition could have been diagnosed incorrectly in the past as myocardial infarction with left ventricular failure and pulmonary edema. Thus it is uncertain whether this is a new syndrome or whether it has long been present. Fulminating noncardiogenic pulmonary edema can be diagnosed by finding a low left atrial or pulmonary artery wedge pressure combined with a high protein content in the pulmonary edema fluid when compared to simultaneous measurements of the plasma protein level. As no other etiologic agent could be identified in our three patients, the probable cause seems to be an unknown type of allergic reaction to blood or blood products, manifested by acute pulmonary edema--the pulmonary capillary membranes being the first to be exposed to fluids administered intravenously. The significant point is that a nearly fatal degree of pulmonary congestion can be managed safely and effectively with corticosteroids, antihistamines, positive-pressure ventilation, diuretics, and albumin. Presently, two important questions remain: (1) Should fluids be restricted and balloon pump counterpulsation and vasopressors utilized to maintain systemic pressure? (2) How long after administration of steroids is it safe to give intravenous albumin? Meanwhile, both the mechanism and frequency of this syndrome remain unknown.

The case of a patient who developed severe acute respiratory failure during therapy for salicylate intoxication is described. The individual with aspirin overdose is at risk for this complication because of the potential for treatment modalities to cause or worsen lung edema initiated by the effects of salicylates on the pulmonary capillary bed.