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Case Presentation: A 49-year-old woman with a medical history of epilepsy presented to the ED 1 h after a single, 15-min, witnessed, tonic-clonic seizure. Over the preceding 6 months, she had experienced five similar seizures of shorter duration. There were no recent changes to her phenytoin dose nor had she started any new medications. The patient had traveled to Jamaica 3 weeks before presentation, where she smoked marijuana once but otherwise had not used illicit substances nor had she used tobacco or alcohol. She states she felt well during and after the trip until this presentation. While being evaluated by the neurology service, the patient complained of sudden-onset chest pain and cough with associated hypoxemia. She denied changes in her sleep habits, she had not experienced any fevers, and she had no changes in her exercise tolerance. The patient was admitted to the general medicine floor for further workup., (Copyright © 2018 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.)

Background: Brain natriuretic peptide (BNP) is useful in diagnosing congestive heart failure (CHF) in patients presenting in the emergency department with acute dyspnea. We prospectively tested the utility of BNP for discriminating ARDS vs cardiogenic pulmonary edema (CPE)., Methods: We enrolled ICU patients with acute hypoxemic respiratory failure and bilateral pulmonary infiltrates who were undergoing right-heart catheterization (RHC) to aid in diagnosis. Patients with acute coronary syndrome, end-stage renal disease, recent coronary artery bypass graft surgery, or preexisting left ventricular ejection fraction /= 1,200 pg/mL, BNP had a specificity of 92% for CPE. Higher levels of BNP were associated with a decreased odds for ARDS (odds ratio, 0.4 per log increase; p = 0.007) after adjustment for age, history of CHF, and right atrial pressure. BNP was associated with in-hospital mortality (p = 0.03) irrespective of the final diagnosis and independent of APACHE (acute physiology and chronic health evaluation) II score., Conclusion: In ICU patients with hypoxemic respiratory failure, BNP appears useful in excluding CPE and identifying patients with a high probability of ARDS, and was associated with mortality in patients with both ARDS and CPE. Larger studies are necessary to validate these findings.

Objective: To review the clinical associations between peritoneal dialysis (PD) and cough., Methodology: A literature review was performed on PubMed for articles published between 1983 and 2004 using the search terms "dialysis" and "cough.", Results/conclusions: Patients receiving PD are more likely to develop a cough than other patients with end-stage renal disease who are receiving hemodialysis. Although both groups of patients frequently receive medications, such as angiotensin-converting enzyme inhibitors and beta-adrenergic blocking agents, that can trigger cough and both may be at increased risk for fluid overload and pulmonary edema, the increased risk associated with PD appears to relate to gastroesophageal reflux, likely from the peritoneal dialysate.

Negative pressure pulmonary edema, a well-recognized phenomenon, is the formation of pulmonary edema following an acute upper airway obstruction (UAO). To our knowledge, diffuse alveolar hemorrhage has not been reported previously as a complication of an UAO. We describe a case of negative pressure pulmonary hemorrhage, and we propose that its etiology is stress failure, the mechanical disruption of the alveolar-capillary membrane.

A prospective cohort study of 129 consecutive patients developing pulmonary infiltrates in the surgical ICU was conducted to determine the predictors and outcome of pulmonary infiltrates. Most common etiologies of pulmonary infiltrates were pneumonia (30%), pulmonary edema (29%), acute lung injury (15%), and atelectasis (13%). Enteral nutrition was associated with a significantly lower incidence of acute lung injury as compared with pneumonia (22% vs 58%, p = 0.012). Patients with liver disease were significantly more likely to have pulmonary infiltrates due to acute lung injury as compared with other etiologies (p = 0.02). Clinical pulmonary infection score (Pugin score) > 6 virtually excluded acute lung injury, pulmonary edema, or atelectasis as etiologies of pulmonary infiltrates. Nosocomial Haemophilus/pneumococcal pneumonia occurred significantly earlier in the ICU as compared with Gram-negative (p = 0.05) or methicillin-resistant Staphylococcus aureus pneumonia (p = 0.01). Pneumonia in trauma patients was significantly more likely to be due to Haemophilus/pneumococcus as compared with all other ICU patients (54% vs 0%, p = 0.0004). These data have implications for treatment of patients with nosocomial pneumonia in the ICU.

Study Objective: To determine whether quantitative measurement of end-tidal carbon dioxide (ETCO2) can differentiate between cardiac and obstructive causes of respiratory distress., Design: Prospective observational study., Setting: Emergency department (ED) of a tertiary care hospital., Patients: Adult patients who presented to the ED with moderate-to-severe dyspnea. Patients were excluded if they were unable to cooperate with the performance of peak expiratory flow rate (PEFR) or ETCO2 tests, were younger than 18 years of age, or had received prehospital intervention for their respiratory distress., Interventions: Physicians obtained an ETCO2 level and PEFR prior to ED pharmacologic intervention. A hand-held capnometer with digital read-out was used to obtain the ETCO2 level. The patient's age, sex, initial vital signs, breath sounds and medication history, the presence or absence of diaphoresis and/or orthopnea, the duration of symptoms, the chest radiograph interpretation, and final diagnosis were also recorded., Measurements and Results: Forty-two patients were eligible for inclusion in the analysis. The mean ETCO2 level was 31.1+/-9.4 mm Hg; the mean PEFR was 161.3+/-53.1 L/min. The ETCO2 levels for pulmonary edema/congestive heart failure (CHF) patients differed significantly from those of asthma/COPD patients (27.1+/-7.8 mm Hg vs 33.4+/-9.6 mm Hg; p=0.0375). However, no single ETCO2 level was found to be a reliable predictor of diagnosis., Conclusion: ETCO2 levels for pulmonary edema/CHF patients differ significantly from those of asthma/COPD patients. However, no single ETCO2 level reliably differentiates between the two disease processes.

Study Objective: To assess whether pressure support ventilation (PSV) could be used as an alternative ventilatory mode to assist-control (A/C) ventilation in the treatment of respiratory failure., Design: A short-term (4-h) prospective study in which the beneficial effect of PSV on respiratory mechanics, gas exchange, arterial oxygenation, cardiovascular hemodynamics, and oxygen consumption was compared with A/C ventilation., Setting: ICU of a community hospital., Patients: Forty-five patients (mean age, 62.8 [11.8] years) with respiratory failure secondary to COPD, restrictive disorders, or neuromuscular disease requiring mechanical ventilatory support in the ICU were selected for study., Interventions: The mean duration of mechanical ventilation before the study was 7.16 (8.64) days. Patients were switched to the PSV mode of the mechanical ventilator for a period of 4 h after which conventional A/C ventilation was resumed., Results: Patients supported with PSV compared with A/C ventilation showed significantly higher tidal volume, minute ventilation, and inspiratory time in association with significantly lower pressure in the airway and I:E ratio. With regard to gas exchange data, an increase in dead space/tidal volume ratio (VD/VT), decrease in PaO2, and statistically but not clinically significant alteration of arterial oxygenation indexes were noted. However, when patients with COPD, restrictive disorders, and neuromuscular disease were compared, significant changes in arterial oxygenation parameters were found only in patients with restrictive disorders. There were significant decreases in heart rate, systolic pulmonary artery pressure, and pulmonary capillary wedge pressure when PSV was applied. Oxygen transport and oxygen consumption were unchanged., Conclusions: PSV could be a possible alternative to A/C ventilation in patients with respiratory failure. PSV caused an increase in VD/VT in association with a significantly lower pressure in the airway and I:E ratio. Randomized studies are needed to define the long-term benefits of both respiratory modes and the conditions in which PSV may be a valuable alternative to A/C ventilation.

A 43-year-old woman had two episodes of lung edema at moderate altitudes. She had taken slimming pills containing fenfluramine hydrochloride and diethylpropion hydrochloride. At sea level, catheterization of the right side of the heart showed a mean pulmonary artery pressure of 16 mm Hg, which increased to 34 mm Hg with mild exercise in a supine position. An extensive workup failed to identify a cardiac or a pulmonary cause of pulmonary hypertension. This patient experienced mild primary pulmonary hypertension related to the intake of anorexigens, which was revealed by high-altitude pulmonary edema.

The effect of recombinant human interleukin 1B (IL-1B) and recombinant human gamma interferon (IFN-g), when given prophylactically, in a mouse model of septic acute lung injury was studied. Mice were treated with various doses of IL-1B and IFN-g for 3 consecutive days prior to administration of lipopolysaccharide of Escherichia coli (1 mg/kg given intraperitoneally). To determine the histologic changes occurring after prophylactic administration of such cytokines, a scoring system was assessed. A significant reduction of edema and neutrophil accumulation into the lungs of mice was observed, especially at doses of 100 U per mouse and 10,000 U per mouse of IL-1B and IFN-g, respectively. Prophylactic administration of IL-1B or IFN-g caused histologic changes, including marked reduction of edema and neutrophil accumulation in the interstitial and alveolar spaces. Combined prophylactic administration of IL-1B and IFN-g provoked a marked decrease of neutrophil accumulation into the lungs, but was not accompanied by significant reduction of edema or hemorrhage. These results provide evidence for the beneficial role of IL-1B and IFN-g in the abnormality of septic acute lung injury by reducing inflammatory lesions.

The management of patients with respiratory failure from cardiogenic pulmonary edema may require intubation and mechanical ventilation. This provides both ventilatory assistance as well as the beneficial hemodynamic effects of positive intrathoracic pressure. As the need for ventilation is usually short term, noninvasive ventilatory support may be adequate. We report the use of biphasic positive airway pressure by nasal mask (BiPAP system) to successfully manage two patients with respiratory failure due to pulmonary edema.

Severe pulmonary edema occurred in a patient during the third trimester of two consecutive pregnancies, 17 months apart. Noncardiac origin of the pulmonary edema was demonstrated by normal pulmonary capillary wedge pressures, normal roentgenographic cardiac dimensions with absence of effusions, normal echocardiographic ejection fraction, and elevated thermodilution cardiac outputs; moderate reduction in serum albumin levels may have contributed. In the setting of pregnancy-induced hypertension, the development of ARDS on each occasion suggests a pathophysiologic link.

Three members of one family, a father and two sons, inflicted with Marfan syndrome, suffered multiple bilateral episodes of spontaneous pneumothorax that required repeated drainage procedures. The youngest patient also had an episode of unilateral expansion pulmonary edema; he underwent sequential pleural abrasions. Familial pneumothorax is very uncommon, and its association with Marfan syndrome is an exception.

A case of Brucella pneumonitis and myocarditis complicated by acute pulmonary edema is presented. The clinical, laboratory and roentgenographic findings are discussed.

Cheyne-Stokes respiration is characterized by crescendo-decrescendo fluctuations in tidal volume and respiratory rate interrupted by central apneas. It has long been associated with cardiac disease and has often been cited as a poor prognostic indicator, yet the incidence and immediate significance of CSR in the setting of acute cardiogenic PE is not well defined. Therefore, we studied 95 patients who required MVS because of PE. Breathing patterns were monitored by continuous respiratory inductive plethysmography for a minimum of 12 hours of spontaneous respiration after recovery from PE; CSR was noted in 42 patients (44 percent). There were no significant differences between patients with PE and CSR and those with only PE in regard to LVEF (mean +/- SD, 36 +/- 18 percent vs 33 +/- 16 percent; p = 0.55), reinstitution of MVS within 48 hours (4.8 percent vs 17.0 percent; p = 0.065), or in-hospital mortality (16.7 percent vs 26.4 percent; p = 0.255). We conclude that CSR is a relatively common breathing pattern in patients who required MVS because of cardiogenic PE and does not portend a poor immediate prognosis in this population.

Severe heroin-induced pulmonary edema occurred in three previously healthy young men. Adequate arterial PO2 could only be achieved with the use of positive endexpiratory pressure (PEEP). Recovery was characterized by the gradual clearing of the pulmonary infiltrates and a gradual lessening of the severe restrictive ventilatory defects over many weeks. Concomitant aspiration of gastric acid was thought to be the explanation for the severity of these cases. In cases such as these, initial vigorous therapy, including PEEP for hypoxia, corticosteroids for possible aspiration and volume replacement for hypotension, is recommended.

In a retrospective study of 304 patients with acute transmural myocardial infarction admitted to the coronary care unit, 22 percent (67 patients) exhibited low voltage on their electrocardiograms within 72 hours of admission. The course of hospitalization of these patients was compared with an equal number of consecutive patients with transmural infarctions and normal electrocardiographic voltages. Among the patients with low voltage, there was a significantly higher incidence of previous infarction or present extensive infarction, congestive heart failure, and cardiogenic shock. This group of patients also demonstrated a markedly higher mortality. This study substantiates the clinical impression that acute myocardial infarction complicated by a low-voltage ECG implies a poor prognosis. It is speculated that this electrocardiographic pattern may reflect decreased ventricular performance as a result of widespread myocardial damage.

In chronic pulmonary emboli, lung perfusion may be maintained by either recanalization of occluded pulmonary artery segments or collateral bronchial circulation. We present a case of noncardiogenic pulmonary edema superimposed on chronic pulmonary emboli, in which the occluded segments of lung were spared from pulmonary edema, but not from neutrophil infiltration. This case demonstrates that chronic emboli may lead to roentgenographic sparing in noncardiogenic pulmonary edema, similar to that previously reported in acute pulmonary emboli superimposed on noncardiogenic edema.

Respiratory failure of different origins often requires therapy with mechanical ventilation and positive end-expiratory pressure (PEEP). These supports are occasionally inadequate if the damage to one lung is significantly more pronounced than that to the other lung. Technical means exist to ventilate each lung independently or to provide a different PEEP to each lung. The findings from nine patients in whom one of these techniques was applied are presented, and advantages and disadvantages are discussed.

We studied a 58-year-old woman during an acute episode of cardiac pulmonary edema complicated by carbon dioxide (CO2) retention. As pulmonary wedge pressure became greater, metabolic production of CO2 increased by 38 ml/min and minute ventilation by 1.53 L; by contrast, alveolar ventilation remained unchanged due to a concomitant rise in physiologic dead space and, as a result, arterial CO2 tension increased up to 61 mm Hg. With treatment, all these variables returned to baseline values. Subsequent measurement of mouth occlusion pressure (p 0.1) during a CO2 rebreathing trial showed that neuromuscular inspiratory drive response to CO2 was preserved, but that ventilatory response was markedly reduced, presumably because of the severe restrictive and obstructive ventilatory defect and of the loss of inspiratory muscle force demonstrated in the patient. We conclude that CO2 retention in cardiac pulmonary edema involves a combination of: (1) increased CO2 production, (2) rise in physiologic dead space, and (3) severe respiratory mechanical impairment.

While travelling across the intermountain West at an altitude of approximately 2,300 m, a 35-year-old man developed symptoms of HAPE. Delay in diagnosis and treatment was nearly lethal. Subsequent evaluation demonstrated unilateral pulmonary artery occlusion, presumably resulting from antecedent granulomatous mediastinitis. This case report supports the concept of evaluating anyone developing HAPE at relatively low altitude for an underlying predisposition.