Articles: respiratory-distress-syndrome.
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57 preterm and 1 term infant suffering from severe idiopathic respiratory distress syndrome with respiratory insufficiency were mechanically ventilated with an inspiratory-time of at least 1.5 sec and an inspiratory:expiratory ratio of always less than 1:2. Consequently the respiratory frequencies were below 14/min (low frequency ventilation). ⋯ None showed radiological evidence of bronchopulmonary dysplasia. This fact together with a relatively low incidence of pneumothorax (6.8%) suggests that this method if compared with conventional ventilation is less likely to cause persistent lung damage.
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Critical care medicine · Sep 1980
Pathogenesis of respiratory failure (ARDS) after hemorrhage and trauma: I. Cardiorespiratory patterns preceding the development of ARDS.
To evaluate clinical and physiologic determinants of adult respiratory distress syndrome (ARDS), we studied 152 consecutively monitored patients with trauma and hemorrhage: 60 developed ARDS. The cardiorespiratory patterns of hemorrhage and trauma patients who did not develop ARDS were compared to those who subsequently did develop ARDS, but before the time of their ARDS. Comparisons also were made in the patients with trauma and those with hemorrhage, as well as in those who survived and those who did not. ⋯ Description of the temporal cardiorespiratory patterns before the clinical appearance of ARDS showed the progressive appearance of these deficits beginning 36 h before the hypoxemia was observed. The data are consistent with the concept that ARDS after hemorrhage and trauma is preceded by hypovolemia, reduced myocardial performance, inadequate O2 delivery, and inadequate O2 extraction needed to maintain VO2 at the elevated levels demanded by the increased metabolic requirements of the injured patients. Thus, the so-called shock lung is a complication of shock associated with hypovolemia, hypoxemia, and inadequate cardiac compensatory responses to increasesd O2 demands.
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Critical care medicine · Sep 1980
Pathogenesis of respiratory failure (ARDS) after hemorrhage and trauma: II. Cardiorespiratory patterns after development of ARDS.
Hemodynamic and oxygen transport variables were studied in a series of 60 patients who sustained adult respiratory distress syndrome (ARDS) from hemorrhage and trauma; measurements were made during the period of their ARDS and in survivors after their recovery from ARDS. In general, cardiac index (CI) and myocardial performance were increased over normal values; they were greater in trauma patients than in hemorrhage patients and greater in the survivors than in nonsurvivors. The mean pulmonary artery pressure (MPAP) and pulmonary vascular resistance index (PVRI) were high in all groups. ⋯ Thus, the patient with post-traumatic ARDS has circulatory and metabolic needs which are greater than normal values defined by values from healthy unstressed volunteers and also somewhat greater than hemorrhage and trauma patients without ARDS. Optimal blood volume, hemodynamic and oxygen transport values defined by the survivor's values as well as the standard respiratory care are recommended as goals for preventive or ealy therapy of these patients. Volume therapy should be given provided it does not elevate the pulmonary arterial wedge pressure (WP) above 18 mm Hg to avoid overloading the pulmonary vascular bed and causing pulmonary edema.
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Pulmonary hypertension gives an indication of poor prognosis in adult respiratory distress syndrome (ARDS) complicating sepsis. In this study, we examined the role of the platelet and the vasoactive amine, serontonin, in pulmonary hypertension accompanying septic ARDS. The lack of any significant difference in platelet number (delta + 3.9 +/- 8.4, X 10(3)/mm3) or serum serotonin (delta - 0.03 +/- 0.06 nm/mm3) across the pulmonary vascular bed (pulmonary artery minus pulmonary vein), would suggest that platelet sequestration and/or release of serotonin is not a major factor in septic ARDS. However, we did note a direct positive relationship between serum serotonin (Ss) and the pulmonary artery diastolic minus pulmonary capillary wedge pressure (PAd-PCWP) gradient (r = 0.64, p < 0.01) implying that serum serotonin may be related to pulmonary hypertension in septic ARDS.