Critical care medicine
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We studied pulmonary function in 7 infants age 3-16 months who were dependent upon mechanical ventilation due to bronchopulmonary dysplasia (BPD). Raised lower expiratory airway resistance (RAe), low dynamic lung compliance (CL) and rapid respiratory frequency (f) characterized the breathing pattern in these infants. End-tidal carbon dioxide tension (PECO2) was elevated in spite of abnormally high minute ventilation (VE). ⋯ Recovery from chronic respiratory failure in 4 infants occurred between age 1.2-2.5 years. The infants recovered concomitant with the ability to sustain a high VE in spite of persistently elevated RA and low CL. All of the surviving infants, although developmentally delayed, have the potential for home care with further growth and development.
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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.
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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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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.