The Science Journal of the American Association for Respiratory Care

2001 OPEN FORUM Abstracts

NitricOxide For Pulmonary Hypertension Associated With ARDS

Kenneth MillerRRT, MEd, Lawerence Mann, RRT, Mark Cipolle MD, PhD, RandolphWojick MD, Martin Tyson DO, Stephanie Brown, RRT. Lehigh Valley Hospital, Allentown,Pa 18105

Introduction:Nitric oxide (NO) is a major regulator of vascular smooth muscle tone. Whenadministered via inhalation, NO relaxes pulmonary vascular smooth muscle andis activated without altering the systemic bed. In adults with respiratory distresssyndrome (ARDS) NO reduced pulmonary arterial pressure and increased oxygenationsecondary to a decrease in intra-pulmonary shunting and reduced the pulmonaryvascular resistance (PVR)1. The clinical utilization of NO has beenquestioned in the adult population secondary to recent clinical studies2.

Case Study: A28 year-old male hit by a car sustained multiple long fractures along with possiblechest trauma. Also there was a question of gastric aspiration at the traumascene. On admission he was quickly intubated and ventilated secondary to respiratoryinsufficiency. Initial arterial blood gas on volume targeted ventilation with100% O2 was PH 7.19 PaC02 66 torr and Pa02192 torr. Multiple ventilator parameter changes were made to resolve the respiratoryacidosis but the Pa02/FI02 ratio (P/F ratio) dropped toless than 100. Hemodynamic instability was noted and was treated with largevolume replacement. Bedside flexible bronchoscopy was performed secondary toperiods of oxygen desaturation and to determine degree of gastric aspirationwithout any change in the clinical course. During the next several hours, themode of ventilation was changed to Pressure Control Ventilation (PCV) with increasinglevels of PEEP. The P/F ratio remained less than 100. Chest x-ray revealed bilateralinfiltrates with noted increased pulmonary vascularity. The patient was placedon the Volumetric Diffusive Ventilator (VDR) and PEEP recruitment maneuverswere attempted to improve the P/F ratio. Modest increase in the P/F ratio wasnoted. Hemodynamic parameters remained unstable with a sustained period of tachycardiaalong with periods of hypotension. A 2-D echogram demonstrated a severe hypokineticright ventricle with normal left ventricular function. Pulmonary embolus wasruled out via arterial-gram study. PVR elevated to 430dynes/sec/cm and intropicsupport with dopamine 3mg/kg/min and dobutrex 5mcg/kg/min were administeredto maintain a cardiac output greater than 2 L/m. PVR increased to 523dynes/sec/cmand P/F ratio deteriorated to 50. Prostaglandin therapy was started at .1 mcg/kg/minand the PVR dropped to 302dynes/sec/cm. Large volume loading was necessary tomaintain an adequate cardiac output above 2 L/m. PVR rose above 350. At thispoint in the clinical course secondary to elevated PVR and poor oxygenationthe decision was made to administer Nitric Oxide(NO) at 20ppm via PCV. Priorto NO administration the PEEP was 24cm H20 with a FIO2 of75%. After 10 hours after the start of NO the PVR dropped to 182dynes/sec/cmand cardiac output rose to 3 L/m. P/F ratio increased above 200. FIO2and PEEP were reduced to pedestrian parameters. The NO was weaned off over thenext two days along with intropic support. The PVR remained less than 150dynes/sec/cmand P/F ratio greater than 300. Weaning of the ventilator continued to volumetargeted ventilation with minimum FI02 and PEEP settings. Post NOadministration hemodynamics and oxygenation continued to be stable.

Conclusion: Theutilization of Nitric Oxide in the adult patient population has been the subjectof much study and debate. Our case presentation demonstrates that there existclinical scenarios that may respond favorably to its administration. There co-existsthe potential for cardiac and respiratory improvement in patients with dualdecompensation. In these type of patients NO should be considered if many ofconventional modalities have failed to produce the desired clinical end-points.

1. Rossiant R, FalkeKJ, Zapol WM. Inhaled nitric oxide for the adult respiratory distress syndrome.N Eng J Med 1993;328:399-405.

2. Micheal J, BartonR, Saffle J, Hinson D, etc. Inhaled Nitric Oxide versus Conventional Therapy.Amer J Resp Critical Care Med 1998:157:1372-1380.

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