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John B Downs

Publications and source records attributed to John B Downs.

7 recordsLinked to original sources
PubMed2004

Supplemental oxygen impairs detection of hypoventilation by pulse oximetry.

STUDY OBJECTIVE: This two-part study was designed to determine the effect of supplemental oxygen on the detection of hypoventilation, evidenced by a decline in oxygen saturation (Spo(2)) with pulse oximetry. DESIGN: Phase 1 was a prospective, patient-controlled, clinical trial. Phase 2 was a prospective, randomized, clinical trial. SETTING: Phase 1 took place in the operating room. Phase 2 took place in the postanesthesia care unit (PACU). PATIENTS: In phase 1, 45 patients underwent abdominal, gynecologic, urologic, and lower-extremity vascular operations. In phase 2, 288 patients were recovering from anesthesia. INTERVENTIONS: In phase 1, modeling of deliberate hypoventilation entailed decreasing by 50% the minute ventilation of patients receiving general anesthesia. Patients breathing a fraction of inspired oxygen (Fio(2)) of 0.21 (n = 25) underwent hypoventilation for up to 5 min. Patients with an Fio(2) of 0.25 (n = 10) or 0.30 (n = 10) underwent hypoventilation for 10 min. In phase 2, spontaneously breathing patients were randomized to breathe room air (n = 155) or to receive supplemental oxygen (n = 133) on arrival in the PACU. MEASUREMENTS AND RESULTS: In phase 1, end-tidal carbon dioxide and Spo(2) were measured during deliberate hypoventilation. A decrease in Spo(2) occurred only in patients who breathed room air. No decline occurred in patients with Fio(2) levels of 0.25 and 0.30. In phase 2, Spo(2) was recorded every min for up to 40 min in the PACU. Arterial desaturation (Spo(2) < 90%) was fourfold higher in patients who breathed room air than in patients who breathed supplemental oxygen (9.0% vs 2.3%, p = 0.02). CONCLUSION: Hypoventilation can be detected reliably by pulse oximetry only when patients breathe room air. In patients with spontaneous ventilation, supplemental oxygen often masked the ability to detect abnormalities in respiratory function in the PACU. Without the need for capnography and arterial blood gas analysis, pulse oximetry is a useful tool to assess ventilatory abnormalities, but only in the absence of supplemental inspired oxygen.

Aged↗
PubMed2003

Chest wall disruption with and without acute lung injury: effects of continuous positive airway pressure therapy on ventilation and perfusion relationships.

OBJECTIVE: We investigated the evolution of lung injury in an animal model with multiple rib fractures, both with and without acute lung injury, and the influence of spontaneous breathing with continuous positive airway pressure (CPAP) therapy on the relative distributions of alveolar ventilation ([OV0312]a) and perfusion ([OV0422]). DESIGN: Prospective, randomized laboratory investigation using an established porcine model with instrumentation for measurement of ventilation/perfusion distribution, pulmonary mechanics and gas exchange, and cardiovascular variables. SETTING: University experimental research laboratory. SUBJECTS: Twenty-nine domestic swine. INTERVENTIONS: Anesthetized pigs were assigned randomly to undergo chest wall dissection alone or chest wall dissection and bilateral fractures of ribs with or without oleic acid-induced acute lung injury. MEASUREMENTS AND MAIN RESULTS: Gas exchange was evaluated by blood gas analysis and multiple inert gas elimination technique. After baseline data were collected, subsequent data were collected at 60 and 120 mins after experimental injuries, and at 180 mins, which was 60 mins after titration of CPAP therapy. The range of CPAP was 4-22 cm H2O. Shunt ([OV0312]a/[OV0422] < 0.005), venous admixture [OV0312]a/[OV0422] < 0.1), and functional deadspace ([OV0312]a/[OV0422] > 10) before injury were similar among all animals and ranged from 3.4% to 4.5%, 4.2% to 5.0%, and 54.4% to 56.5%, respectively. There were no changes, throughout the study, in lung regions with low [OV0312]a/[OV0422] (0.005 < [OV0312]a/[OV0422] </= 0.1) in any group of animals. Shunt of control animals increased to 10.5 +/- 8.8% (p <.05) at 60 mins but demonstrated no further changes in [OV0312]a/[OV0422] at subsequent measurements. Shunt also increased after animals underwent bilateral rib fractures without (12.7%, p <.05) and with (19.9%, p <.05) acute lung injury; however, it decreased in both groups after the application of CPAP (4.6% and 6.6%, respectively, p <.05). All changes in venous admixture directly reflected the change in shunt at all intervals. Functional deadspace was unaffected by chest wall dissection, rib fractures, or subsequent lung injury but decreased after CPAP therapy in all animals. CONCLUSIONS: Acute lung injury exacerbated the right-to-left intrapulmonary shunt seen within the first hour after disruption of the chest wall. Application of CPAP decreased shunt, improved matching of [OV0312]a/[OV0422], and reduced the requirement for supplemental oxygen, without any significant impairment in cardiovascular function.

Analysis of Variance↗
PubMed2003

Has oxygen administration delayed appropriate respiratory care? Fallacies regarding oxygen therapy.

Modern clinical use of supplemental oxygen supposes that: (1) exposure to F(IO)(2) < or = 60% is without adverse effects, (2) an individual at risk of developing arterial hypoxemia can be protected by administering high F(IO)(2), and (3) routine administration of supplemental oxygen is useful, harmless, and clinically indicated. There is now substantial evidence that none of those 3 suppositions are correct, and, on the contrary, supplemental oxygen is actually detrimental to many of the patients who receive it. Supplemental oxygen is much overused and its use should be limited to the few conditions and situations in which it is truly effective, useful, and non-detrimental.

Attitude of Health Personnel↗
PubMed2002

Effect of low isoflurane concentrations on the ventilation-perfusion distribution in injured canine lungs.

BACKGROUND: Rapid recovery and weaning from ventilatory support and cardiovascular stability are suggested advantages of isoflurane inhalation, in concentrations ranging from 0.1 to 0.6 vol%, for long-term sedation in mechanical ventilated patients. This study was designed to determine whether isoflurane in low concentrations impairs pulmonary gas exchange by increasing ventilation and perfusion (V(A)/Q) mismatch during lung injury. METHODS: Fourteen anesthetized dogs received in random order 0, 0.25, or 0.5 vol% end-tidal isoflurane before and after induction of lung injury with oleic acid. Gas exchange was assessed by blood gas analysis and by estimating the V(A)/Q distributions using the multiple inert gas elimination technique. RESULTS: Administration of oleic acid produced a lung injury with severe V(A)/Q mismatch and 38 +/- 4% intrapulmonary shunting of blood. During lung injury, isoflurane accounted for a dose-related increase in blood flow to shunt units from 38 +/- 4 to 42 +/- 3 (0.25 vol%) and 48 +/- 4% (0.5 vol%) (P < 0.05), dispersion pulmonary blood flow distribution from 0.94 +/- 0.07 to 1.01 +/- 0.09 (0.25 vol%) and 1.11 +/- 0.11% (0.5 vol%) (P < 0.05), and a decrease in perfusion of normal V(A)/Q units from 58 +/- 5 to 55 +/- 4 (0.25 vol%) and 50 +/- 4% (0.5 vol%) (P < 0.05) (mean +/- SE). Isoflurane decreased arterial oxygen partial pressure from 72 +/- 4 to 62 +/- 4 mmHg (0.25 vol%) and 56 +/- 4 mmHg (0.5 vol%) (P < 0.05) and oxygen delivery from 573 +/- 21 to 529 +/- 19 ml. kg. min (0.25 vol%) and 505 +/- 22 ml. kg. min (0.5 vol%) (P < 0.05). Gas exchange, perfusion of shunt and normal V(A)/Q units, and pulmonary blood flow distribution was similar in absence of lung injury with and without isoflurane. Isoflurane 0.5 vol% lowered cardiac output during all conditions (P < 0.05). CONCLUSIONS Inhalation of low concentrations of isoflurane contributed to increased V(A)/Q mismatch and decreased systemic blood flow and oxygen delivery in mechanically ventilated animals with injured lungs.

Algorithms↗