Ventilatory Mechanics in Pulmonary Edema in Man1

Sharp, John T.; Griffith, Geraint T.; Bunnell, Ivan L.; Greene, David G.

doi:10.1172/jci103577

Cited by 118 publications

(36 citation statements)

References 7 publications

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“…There was a progressive decrease in the slope of the inspiratory limb of the static pressure volume curve with increasing time at altitude. This is the type of change in lung compliance that has been reported in cases of pulmonary edema; however, our compliances were still 4-5 times greater than those reported for patients in pulmonary edema (26).…”

Section: Discussioncontrasting

confidence: 58%

Pulmonary Artery Pressure and Alveolar Gas Exchange in Man during Acclimatization to 12,470 ft

Kronenberg¹,

Šafář²,

Leej³

et al. 1971

J. Clin. Invest.

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A B S T R A C T Pulmonary hemodynamics and Rotta, Canepa, Hurtado, Velasquez, and Chavez in 1956 (1) and has been confirmed many times since, both in acclimatized natives (2, 3) and in newcomers (4). The relationship of this pulmonary hypertension to the development of high altitude pulmonary edema (HAPE) is uncertain, but pulmonary artery pressure is higher during episodes of HAPE than during control observations in the same individuals (5), and persons who have had such episodes previously have higher pulmonary artery pressures when reexposed to altitude than nonsusceptible individuals under the same conditions (6). Although it is recognized that the peak incidence of HAPE occurs 1-3 days after entry to high altitude (7), it has not been established whether pulmonary arterial pressure rises in a progressive fashion over the same time course. A progressive rise in pulmonary arterial pressure during a 6 wk period at 12,700 ft has been reported in steers, apparently associated with the right heart failure termed "brisket disease" (8), but was not observed in lambs in a matched experiment (9). Therefore, we decided to investigate in ourselves the time course of the pulmonary arterial pressure both at rest and during exercise at 12,470 ft and to examine other aspects of cardiovascular function over the same time span. We also explored the possibility suggested by Haab, Held, Ernst, and Farhi (10) and Reeves, Halpin, Cohn, and Daoud (11) that hypoxia widens the alveolar to arterial 02 difference.

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Section: Discussioncontrasting

confidence: 58%

Pulmonary Artery Pressure and Alveolar Gas Exchange in Man during Acclimatization to 12,470 ft

Kronenberg¹,

Šafář²,

Leej³

et al. 1971

J. Clin. Invest.

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“…Regional changes in compliance or resistance due to gravitational forces could explain the development of frequency dependence of airway resistance (29). Lung compliance decreases with pulmonary congestion and this decrease is probably greater in dependent zones where pathological changes are more marked (22,31). However, the degree of change reported in the dependent areas (6, 32) is probably not large enough to explain the degree of frequency dependence of pulmonary resistance observed in our subjects.…”

Section: Resultsmentioning

confidence: 65%

“…One patient showed no radiological evidence of left ventricular failure, two patients had minimal changes, five had moderate changes, and two had severe changes. The correlation of the clinical classification with FEV, (1,6,22). An original and more striking finding was the transient development of frequency dependence of RT (Table III, Fig.…”

Section: Resultsmentioning

confidence: 99%

Interrelation between Alterations in Pulmonary Mechanics and hemodynamics in Acute Myocardial Infarction

Interiano¹,

Hyde²,

Hodges³

et al. 1973

J. Clin. Invest.

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A B S T R A C T Pulmonary mechanics were evaluated in 30 patients with acute myocardial infarction by measuring forced expiratory flow rates and total pulmonary resistance (RT) with the oscillometric method at the resonant frequency of the chest (6-8) cycle/s). During the first 3 days after infarction, forced expiratory volume (FEV) and forced mid-expiratory flow rate (FEF25 75%) were 69% and 60% of predicted values, respectively. 10 or more wk later these values were 95% and 91%. Initially, RT was 52% greater than predicted, but was only 4% greater 10 or more wk later. In 11 patients RT was measured at both resonant frequency and at 3 cycle/s. Five of these patients had no clinical signs of heart failure, but nine had abnormally high values of pulmonary artery pressure, "wedge" pressure and pulmonary extravascular water volume. All of these patients recovered. Initially, RT at resonance was 50% and RT at 3 cycle/s was 130% greater than predicted values. 2-3 wk later these figures were -3% and + 6% of those predicted, respectively. At 10 wk or more, significant frequency dependence of RT had disappeared (RT at 3 cycle/s was 7% greater than RT at resonance). Isoproterenol inhalation in six patients caused no change in flow rates, RT at resonance, or RT at 3 cycle/s. RT

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“…13,14 Because of these changes, PEEP may improve oxygenation recruiting alveoli and redistributing fluid, thereby increasing end-expiratory lung volume. 2,15 Myocardial function may also improve because of reduced left ventricular afterload resulting from increased intrathoracic pressure.…”

Section: Discussionmentioning

confidence: 99%

Effect of Nasal Continuous Positive Airway Pressure on Pulmonary Edema Complicating Acute Myocardial Infarction

Takeda¹,

Nejima²,

Takano³

et al. 1998

Jpn Circ J

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ardiogenic pulmonary edema, which is a common complication of acute myocardial infarction, remains a serious clinical problem. 1 If pulmonary edema results in hypoxemia, mechanical ventilation with positive end-expiratory pressure (PEEP) is required. Mechanical ventilation, however, has associated morbidity. The potential benefits of continuous positive airway pressure (CPAP) ventilation include an improvement in oxygenation, a decrease in respiratory work, and a decrease in left ventricular afterload. [2][3][4][5] If CPAP using a mask is utilized in patients with cardiogenic pulmonary edema, the number of patients that later require mechanical ventilation by means of endotracheal intubation can be reduced, while oxygenation and respiratory rate are improved. 6 Further, we have reported that nasal CPAP led to an early decrease in plasma endothelin-1 (ET-1) concentrations in patients with severe cardiogenic pulmonary edema. 7 In practice, however, there are no generally accepted criteria for the initiation of mechanical ventilation in patients with pulmonary edema in the setting of acute myocardial infarction. Accordingly, the primary goal of the present study was to determine the effects of different methods of respiratory management on the hemodynamics, oxygenation, and outcome in patients who developed respiratory failure due to severe cardiogenic pulmonary edema after acute myocardial infarction. Patients and MethodsThis study was approved by the Committee on Human Patients. Because of the severity of cardiogenic pulmonary edema, no patient was able to give valid informed consent at entry into the study. Therefore, information was provided to the patient's next of kin and their consent was obtained prior to study entry. During the 1-year study period, we prospectively studied 31 of 147 patients with acute myocardial infarction admitted to the coronary care unit (CCU) of our hospital. Of these, one patient with left ventricular free wall rupture and another with ventricular septal perforation were excluded. The remaining patients consisted of 29 adults with respiratory failure due to severe cardiogenic pulmonary edema. All patients with cardiogenic pulmonary edema who had clinical evidence of respiratory distress and a PaO2 below 80 mmHg while receiving 50% oxygen by tight-fitting mask were enrolled.Cardiogenic pulmonary edema was diagnosed if a patient had dyspnea of sudden onset, typical findings on Effect of Nasal Continuous Positive Airway Pressure on Pulmonary Edema Complicating Acute Myocardial InfarctionJpn Circ J 1998; 62: 553 -558 Shinhiro Takeda, MD; Jun Nejima, MD; Teruo Takano, MD; Kazuhiro Nakanishi, MD; Morimasa Takayama, MD; Atsuhiro Sakamoto, MD*; Ryo Ogawa, MD* Cardiogenic pulmonary edema is a frequent cause of reparatory failure. We investigated the effects of nasal continuous positive airway pressure (CPAP) in patients with severe pulmonary edema associated with acute myocardial infarction. Twenty-nine consecutive patients were divided into 3 groups: firstly, 7 intubated patients who rece...

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Ventilatory Mechanics in Pulmonary Edema in Man1

Cited by 118 publications

References 7 publications

Pulmonary Artery Pressure and Alveolar Gas Exchange in Man during Acclimatization to 12,470 ft

Pulmonary Artery Pressure and Alveolar Gas Exchange in Man during Acclimatization to 12,470 ft

Interrelation between Alterations in Pulmonary Mechanics and hemodynamics in Acute Myocardial Infarction

Effect of Nasal Continuous Positive Airway Pressure on Pulmonary Edema Complicating Acute Myocardial Infarction

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