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High Flow Oxygen and Low Dose Inhaled Nitric Oxide in a Case of Severe Pulmonary Hypertension and Obstructive Shock
October 2011, Vol 140, No. 4_MeetingAbstracts
Case Reports: Monday, October 24, 2011 | October 2011
High Flow Oxygen and Low Dose Inhaled Nitric Oxide in a Case of Severe Pulmonary Hypertension and Obstructive Shock Joseph Huang, MD; David Fridman, MD Chest. 2011;140(4_MeetingAbstracts):63A. doi:10.1378/chest.1117113
Abstract INTRODUCTION: Inhaled nitric oxide (iNO2) is an effective pulmonary vasodilator in treatment of pulmonary hypertension. Prior studies demonstrated a decrease in pulmonary arterial pressure and pulmonary vascular resistance and increase in cardiac output at a dosage between 20-80ppm. However, the effect of lower dosage in conjunction with high flow oxygen has not been well-studied. CASE PRESENTATION: A 63 year-old woman with obese hypoventilation syndrome, severe pulmonary hypertension, patent foramen ovale with right-to-left shunt, coronary artery disease with RCA/LAD stents, and diabetes was admitted for diarrhea. She was transferred to MICU for oxygen desaturation to 88% on 5L nasal cannula, hypotension, and decrease urinary output. Her right heart catheterization prior to admission showed pulmonary arterial pressure of 95/22mm and mean pulmonary arterial pressure (MPAP) of 56mm Hg on 100% FiO2. The MPAP improved to 42-45mg with 20-40ppm of iNo2. Her cardiac index was 2.0 L/min/m2 on 100% FiO2 and improved to 3.2 L/min/m2 on 20-40ppm of iNO2. Upon arrival to MICU, her vitals were pulse 74, blood pressure 82/65, respiration rate 24, and O2 saturation of 95% on 4 liters nasal cannula. A right internal jugular triple lumen catheter was inserted and showed elevated CVP of 19-20mm Hg. Physical exam showed morbid obesity, right sided S3 gallop, clear lungs, and 2+ bilateral leg edema. Laboratory findings were significant for HCO3 18, Cr 1.6, NT-BNP 771, ABG 7.31/36/62/18 at room air, and SvO2 42%. CXR showed mild cardiomegaly without focal consolidation or pulmonary edema. The patient was started on dobutamine and norepinephrine for obstructive shock. 20ppm of iNO2 with 4L O2 was initiated and CVP improved from 19-20mm Hg to 11-14mm Hg, which rebounded to 1820mm Hg when the iNO2 was accidentally turned off. iNO2 was reinstated and subsequently weaned down to 10ppm on hospital day 3 and high flow oxygen at 30L/min with 60% FiO2 was added on hospital day 4. iNO was weaned off slowly at 1.5ppm/day and high flow O2 was titrated down to 4L nasal cannula over 9 days. Sildenafil was restarted at 20mg po bid and titrated up to 40mg tid by the time iNO2 was completely weaned off. DISCUSSION: The treatment of pulmonary hypertension involves targeting various mechanisms of the pathophysiology, including pulmonary vasoconstriction, endothelial and smooth muscle cell proliferation, and thrombosis. These pathophysiological parameters involve the endothelin, nitric oxide, and prostacyclin pathways. Prior to FDA approval of iloprost, inhaled NO2 was the only available inhaled therapy for pulmonary hypertension. It is a vasodilator restricted to pulmonary vasculature without affecting the systemic circulation. In a pilot study involving patients with pulmonary hypertension and right heart failure, iNO2 increased cardiac output and stroke volume and decreased pulmonary vascular resistance at a mean dosage of 35ppm without affecting systemic arterial pressure1. Another study demonstrated similar findings as well as decreased flow through PFO at a dosage of 80ppm2. Other studies demonstrated similar findings at a dosage of 40ppm. These studies suggest
that iNO2 is effective in treating pulmonary hypertension with hemodynamic instability by selectively targeting pulmonary vasculature and decreasing right ventricular afterload, resulting in overall improvement in cardiac output.
CONCLUSIONS: The concomitant administration of high flow oxygen and iNO2 in the treatment of pulmonary hypertension has not been well studied. Our patient’s obstructive shock physiology improved at a dosage of iNO much less than what had been published previously. We postulate that the addition of high flow oxygen may drastically decrease the iNO2 requirement and the combination of high flow oxygen and low dose iNO2 may be as effect as iNO2 alone at a higher dose. Reference #1 Sangeeta B, Christensen J, O’Connor M et al. Response to Inhaled Nitric Oxide in Patients with Acute Right Heart Failure. Am J Respir Crit Med 1999; 159: 571-579. Reference #2 Inglessis I, Shin J, Lepore J et al. Hemodynamic Effect of Inhaled Nitric Oxide in Right Ventricular Myocardial Infarction and Cardiogenic Shock. J Am Coll Cardiol. 2004 Aug 18;44(4):793-8. Reference #3 Hoeper MM, Olschewski H, Ghofrani HA et al. A comparison of the acute hemodynamic effects of inhaled nitric oxide and aerosolized iloprost in primary pulmonary hypertension. German PPH study group. J Am Coll Cardiol. 2000 Jan;35(1):176-82 DISCLOSURE: The following authors have nothing to disclose: Joseph Huang, David Fridman No Product/Research Disclosure Information 07:15 AM - 08:45 AM
Case Reports: Monday, October 24, 2011 | October 2011
High Flow Oxygen and Low Dose Inhaled Nitric Oxide in a Case of Severe Pulmonary Hypertension and Obstructive Shock Joseph Huang, MD; David Fridman, MD Chest. 2011;140(4_MeetingAbstracts):63A. doi:10.1378/chest.1117113
Abstract INTRODUCTION: Inhaled nitric oxide (iNO2) is an effective pulmonary vasodilator in treatment of pulmonary hypertension. Prior studies demonstrated a decrease in pulmonary arterial pressure and pulmonary vascular resistance and increase in cardiac output at a dosage between 20-80ppm. However, the effect of lower dosage in conjunction with high flow oxygen has not been well-studied. CASE PRESENTATION: A 63 year-old woman with obese hypoventilation syndrome, severe pulmonary hypertension, patent foramen ovale with right-to-left shunt, coronary artery disease with RCA/LAD stents, and diabetes was admitted for diarrhea. She was transferred to MICU for oxygen desaturation to 88% on 5L nasal cannula, hypotension, and decrease urinary output. Her right heart catheterization prior to admission showed pulmonary arterial pressure of 95/22mm and mean pulmonary arterial pressure (MPAP) of 56mm Hg on 100% FiO2. The MPAP improved to 42-45mg with 20-40ppm of iNo2. Her cardiac index was 2.0 L/min/m2 on 100% FiO2 and improved to 3.2 L/min/m2 on 20-40ppm of iNO2. Upon arrival to MICU, her vitals were pulse 74, blood pressure 82/65, respiration rate 24, and O2 saturation of 95% on 4 liters nasal cannula. A right internal jugular triple lumen catheter was inserted and showed elevated CVP of 19-20mm Hg. Physical exam showed morbid obesity, right sided S3 gallop, clear lungs, and 2+ bilateral leg edema. Laboratory findings were significant for HCO3 18, Cr 1.6, NT-BNP 771, ABG 7.31/36/62/18 at room air, and SvO2 42%. CXR showed mild cardiomegaly without focal consolidation or pulmonary edema. The patient was started on dobutamine and norepinephrine for obstructive shock. 20ppm of iNO2 with 4L O2 was initiated and CVP improved from 19-20mm Hg to 11-14mm Hg, which rebounded to 1820mm Hg when the iNO2 was accidentally turned off. iNO2 was reinstated and subsequently weaned down to 10ppm on hospital day 3 and high flow oxygen at 30L/min with 60% FiO2 was added on hospital day 4. iNO was weaned off slowly at 1.5ppm/day and high flow O2 was titrated down to 4L nasal cannula over 9 days. Sildenafil was restarted at 20mg po bid and titrated up to 40mg tid by the time iNO2 was completely weaned off. DISCUSSION: The treatment of pulmonary hypertension involves targeting various mechanisms of the pathophysiology, including pulmonary vasoconstriction, endothelial and smooth muscle cell proliferation, and thrombosis. These pathophysiological parameters involve the endothelin, nitric oxide, and prostacyclin pathways. Prior to FDA approval of iloprost, inhaled NO2 was the only available inhaled therapy for pulmonary hypertension. It is a vasodilator restricted to pulmonary vasculature without affecting the systemic circulation. In a pilot study involving patients with pulmonary hypertension and right heart failure, iNO2 increased cardiac output and stroke volume and decreased pulmonary vascular resistance at a mean dosage of 35ppm without affecting systemic arterial pressure1. Another study demonstrated similar findings as well as decreased flow through PFO at a dosage of 80ppm2. Other studies demonstrated similar findings at a dosage of 40ppm. These studies suggest
that iNO2 is effective in treating pulmonary hypertension with hemodynamic instability by selectively targeting pulmonary vasculature and decreasing right ventricular afterload, resulting in overall improvement in cardiac output.
CONCLUSIONS: The concomitant administration of high flow oxygen and iNO2 in the treatment of pulmonary hypertension has not been well studied. Our patient’s obstructive shock physiology improved at a dosage of iNO much less than what had been published previously. We postulate that the addition of high flow oxygen may drastically decrease the iNO2 requirement and the combination of high flow oxygen and low dose iNO2 may be as effect as iNO2 alone at a higher dose. Reference #1 Sangeeta B, Christensen J, O’Connor M et al. Response to Inhaled Nitric Oxide in Patients with Acute Right Heart Failure. Am J Respir Crit Med 1999; 159: 571-579. Reference #2 Inglessis I, Shin J, Lepore J et al. Hemodynamic Effect of Inhaled Nitric Oxide in Right Ventricular Myocardial Infarction and Cardiogenic Shock. J Am Coll Cardiol. 2004 Aug 18;44(4):793-8. Reference #3 Hoeper MM, Olschewski H, Ghofrani HA et al. A comparison of the acute hemodynamic effects of inhaled nitric oxide and aerosolized iloprost in primary pulmonary hypertension. German PPH study group. J Am Coll Cardiol. 2000 Jan;35(1):176-82 DISCLOSURE: The following authors have nothing to disclose: Joseph Huang, David Fridman No Product/Research Disclosure Information 07:15 AM - 08:45 AM