Biomedical subjects
Publications and source records attributed to F Piedalue.
Healthcare professionals are trying to facilitate the use of evidence-based decision making for individual patients and patient populations they are privileged to serve. The authors describe an evidence-based multidisciplinary clinical practice model developed at the University of Colorado Hospital along with a clinical example of how the model was used to improve quality and decrease costs.
BACKGROUND: Inhaled nitric oxide (NO) is a promising therapy that may be valuable in the control of pulmonary hypertension in cardiac surgical patients. Patients with valvular heart disease have remodeling of the pulmonary vascular bed that contributes to pulmonary hypertension. The purpose of this study was to compare the efficacy of inhaled NO in cardiac surgical patients with pulmonary hypertension with and without valvular heart disease. METHODS: The effect of inhaled NO (40 ppm) on pulmonary hemodynamics in patients with pulmonary hypertension (mean pulmonary artery pressure > or = 30 mm Hg) was studied in the operating room after cardiac operation. Fifteen patients with valvular heart disease comprised the study group; 25 patients undergoing aortocoronary bypass grafting were controls. RESULTS: In patients undergoing aortocoronary bypass grafting, inhaled NO produced a 24% decrease in mean pulmonary artery pressure (33 +/- 1 to 25 +/- 1 mm Hg; p < 0.05), a 36% decrease in pulmonary vascular resistance (375 +/- 30 to 250 +/- 30 dyne.s.cm-5; p < 0.05), and no change in systemic arterial blood pressure. On the other hand, patients with pulmonary hypertension from valvular heart disease did not respond to inhaled NO: mean pulmonary artery pressure was 39 +/- 3 mm Hg and pulmonary vascular resistance was 620 +/- 30 dyne.s.cm-5 before, during, and after NO. CONCLUSIONS: Among cardiac surgical patients with pulmonary hypertension, the response to inhaled NO is variable. Despite the promise of inhaled NO as a pulmonary vasodilator in cardiac surgical patients, these data suggest that alternative therapies are needed to control pulmonary hypertension in patients with pulmonary hypertension from valvular heart disease.
OBJECTIVES: Inhaled nitric oxide is a promising therapy to control pulmonary hypertension. However, pulmonary hypertension caused by valvular heart disease is often refractory to inhaled nitric oxide. The objective of this study was to determine whether the combination of inhaled nitric oxide plus dipyridamole will cause a response in patients with pulmonary hypertension undergoing cardiac operations who had not responded to inhaled nitric oxide alone. METHODS: Responses in 10 patients (62 +/- 7 years) with pulmonary hypertension caused by aortic or mitral valvular disease (mean pulmonary artery pressure, > or = 30 mm Hg) were studied in the operating room after valve replacement. The effect of inhaled nitric oxide alone (40 ppm) on pulmonary vascular resistance, mean pulmonary artery pressure, cardiac output, and mean arterial pressure was determined. Inhaled nitric oxide administration was then stopped and patients were given dipyridamole (0.2 mg/kg intravenously); the effect of inhaled nitric oxide plus dipyridamole was then examined. RESULTS: Dipyridamole effected a response in patients who had not responded to nitric oxide. Pulmonary vascular resistance and mean pulmonary artery pressure were significantly reduced and cardiac output was increased without change in mean arterial pressure. CONCLUSIONS: Patients with refractory pulmonary hypertension in whom inhaled nitric oxide alone fails to cause a response may respond to combined therapy of inhaled nitric oxide plus dipyridamole. This therapy may be particularly valuable in patients with dysfunction of the right side of the heart as a result of pulmonary hypertension because of its effective lowering of right ventricular afterload.
Increased pulmonary vascular resistance may greatly complicate the perioperative management of cardiac surgical patients. Inhaled nitric oxide may be a promising new therapy to selectively lower pulmonary vascular resistance. The purpose of this study was to examine the effects of inhaled nitric oxide on pulmonary and systemic hemodynamics in cardiac surgical patients. Twenty patients (age 57 +/- 6 years) were studied in the operating room after weaning from cardiopulmonary bypass. Mean pulmonary artery pressure, pulmonary vascular resistance, systemic vascular resistance, and mean aortic pressure were determined at four points of data collection: before nitric oxide, with 20 ppm nitric oxide, with 40 ppm nitric oxide, and after nitric oxide. Statistical analysis was by analysis of variance; significance was accepted for p < 0.05. Inhaled nitric oxide produced selective pulmonary vasorelaxation. Pulmonary vascular resistance was lowered from 343 +/- 30 before nitric oxide to 233 +/- 25 dynes.sec-1.cm-5 with 20 ppm nitric oxide. Pulmonary vascular resistance was not further lowered by 40 ppm nitric oxide (p < 0.05). Mean pulmonary arterial pressure was 29 +/- 1 mm Hg before nitric oxide and was lowered to 22 +/- 1 mm Hg by 20 ppm nitric oxide and 21 +/- 1 mm Hg by 40 ppm nitric oxide (p < 0.05). Both pulmonary vascular resistance and mean pulmonary arterial pressure returned to baseline after withdrawal of inhaled nitric oxide. Inhaled nitric oxide produced no changes in either systemic vascular resistance or mean aortic pressure. We conclude that nitric oxide may be used as an effective pulmonary vasodilator after cardiac operations. It may be particularly valuable for selectively lowering right ventricular afterload in patients with right ventricular dysfunction.
OBJECTIVE: The purpose of this study was to determine the effect of inhaled nitric oxide (NO) on oxygenation, hemodynamics, and ventilation in patients with adult respiratory distress syndrome (ARDS). METHODS: Sixteen trials of inhaled NO were performed in 14 ARDS patients (age 42.9 +/- 6) who had significant pulmonary hypertension (mean pulmonary artery pressure > 30 mm Hg). Patients were monitored with arterial and pulmonary artery catheters. Volume ventilation was performed by a strict protocol. Data were collected at baseline and 30 minutes after 20 and 40 ppm NO. RESULTS: Overall, the Pao2/FIO2 ratio increased from 69.5 +/- 3.9 to 100.8 +/- 9.5 at 20 ppm, a 42.9 +/- 8.7% increase, and to 97.7 +/- 13.1 at 40 ppm, a 44.1 +/- 14.2% increase over baseline (p = 0.001). However, 5/16 trials demonstrated minimal improvement (Pao2/FIO2 ratio increase < 20%), 5 moderate improvement (20-50%), and 6 marked improvement (> 50%). Overall the mean pulmonary artery pressure (MPAP) decreased from 41.1 +/- 1.8 mm Hg to 34.3 +/- 1.3 at 20 ppm and 33.5 +/- 1.8 mm Hg at 40 ppm, a 15.0 +/- 3.7% decrease, p = 0.002. However, 5/16 trials demonstrated minimal improvement (MPAP decrease < 10%), 7 moderate improvement (10-20%), and 4 marked improvement (> 20%). At 40 ppm NO, 4 patients with moderate improvement in MPAP at 20 ppm NO had marked improvement. There were no changes in systemic oxygen delivery and consumption, intrapulmonary shunt, or lung compliance at 20 or 40 ppm (p > 0.05). Following collection of these data, prolonged NO inhalation (2-20 ppm) was done in 10 of 14 patients for 4.5 +/- 0.7 days (range 1-10 days). Overall, there were 7 deaths (mortality 50%). In patients receiving prolonged NO, there were 3 deaths (mortality 30%). All 4 patients who failed to respond to inhaled NO subsequently died (mortality 100%). CONCLUSIONS: Inhaled NO improves oxygenation and pulmonary hemodynamics in patients with ARDS. However, the improvement to NO is variable.