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Inhaled Nitric Oxide Use for Refractory Hypoxemia with Cardiogenic and Septic Shock
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A5271 - Inhaled Nitric Oxide Use for Refractory Hypoxemia with Cardiogenic and Septic Shock
Author Block: N. Dhawan, V. Jetty, J. Abayev, K. D'Souza, N. Saenger, D. E. Murphy; The Jewish Hospital, Cincinnati, OH, United States.
Inhaled Nitric Oxide (iNO) has proven benefit in patients with underlying pulmonary hypertension by selectively causing pulmonary vasodilation. Much of the research conducted in the acute setting has been in the pediatric population and more recently involving adults. Trials have focused on the management of acute respiratory distress syndrome (ARDS) and cardiogenic shock.
A 74-year-old male with a history of congestive heart failure (EF 45-50%), chronic kidney disease, interstitial lung disease (organizing pneumonia) and severe pulmonary hypertension (on chronic home oxygen, steroids, and sildenafil), presented with acute shortness of breath, profound hypoxemia, and shock requiring intubation. He had pink, frothy sputum and decreased air entry but an otherwise unremarkable physical exam. Chest x-ray showed a right middle lobe infiltrate, which blossomed into widespread right lung airspace disease, however, the left lung remained clear. He became hypotensive shortly after intubation and required maximum doses of norepinephrine and vasopressin to maintain systolic blood pressures of approximately 80 mmHg. His volume overload and acute renal failure were managed with furosemide and continuous renal replacement therapy. The shock was presumed to be cardiogenic and septic in origin. Pulmonary embolism was excluded due to chronic oral anticoagulation and a negative transthoracic echocardiogram for acute right heart strain. Despite medical management, his concurrent hypotension and significant ventilation-perfusion mismatch prevented his PaO2 from reaching higher than mid-70 mmHg. The iNO was started at 20ppm and his PaO2 increased from 69 mmHg to 298 mmHg in 90 minutes. His ventilator support decreased from 100% FiO2 to 60% on PEEP 15. He weaned off two vasopressors only requiring continued dopamine infusion. Despite this improvement, the family decided to withdraw care later that day.
iNO has been shown to improve cardiac output and oxygenation in patients with acute right heart failure and ARDS. However, no cases have shown iNO to be beneficial in acute lung injury in the setting of shock, both cardiogenic and septic, in addition acute renal failure. Multiple clinical trials have recorded an average increase in PaO2 of approximately 10 mmHg after initiation of iNO. Given these findings, our patient’s response was well beyond expectation. The iNO therapy provided us the chance to isolate his acute medical conditions to more effectively treat our patient’s condition. Further studies are needed to determine the efficacy of iNO in combined cardiogenic and septic shock.
Author Block: N. Dhawan, V. Jetty, J. Abayev, K. D'Souza, N. Saenger, D. E. Murphy; The Jewish Hospital, Cincinnati, OH, United States.
Inhaled Nitric Oxide (iNO) has proven benefit in patients with underlying pulmonary hypertension by selectively causing pulmonary vasodilation. Much of the research conducted in the acute setting has been in the pediatric population and more recently involving adults. Trials have focused on the management of acute respiratory distress syndrome (ARDS) and cardiogenic shock.
A 74-year-old male with a history of congestive heart failure (EF 45-50%), chronic kidney disease, interstitial lung disease (organizing pneumonia) and severe pulmonary hypertension (on chronic home oxygen, steroids, and sildenafil), presented with acute shortness of breath, profound hypoxemia, and shock requiring intubation. He had pink, frothy sputum and decreased air entry but an otherwise unremarkable physical exam. Chest x-ray showed a right middle lobe infiltrate, which blossomed into widespread right lung airspace disease, however, the left lung remained clear. He became hypotensive shortly after intubation and required maximum doses of norepinephrine and vasopressin to maintain systolic blood pressures of approximately 80 mmHg. His volume overload and acute renal failure were managed with furosemide and continuous renal replacement therapy. The shock was presumed to be cardiogenic and septic in origin. Pulmonary embolism was excluded due to chronic oral anticoagulation and a negative transthoracic echocardiogram for acute right heart strain. Despite medical management, his concurrent hypotension and significant ventilation-perfusion mismatch prevented his PaO2 from reaching higher than mid-70 mmHg. The iNO was started at 20ppm and his PaO2 increased from 69 mmHg to 298 mmHg in 90 minutes. His ventilator support decreased from 100% FiO2 to 60% on PEEP 15. He weaned off two vasopressors only requiring continued dopamine infusion. Despite this improvement, the family decided to withdraw care later that day.
iNO has been shown to improve cardiac output and oxygenation in patients with acute right heart failure and ARDS. However, no cases have shown iNO to be beneficial in acute lung injury in the setting of shock, both cardiogenic and septic, in addition acute renal failure. Multiple clinical trials have recorded an average increase in PaO2 of approximately 10 mmHg after initiation of iNO. Given these findings, our patient’s response was well beyond expectation. The iNO therapy provided us the chance to isolate his acute medical conditions to more effectively treat our patient’s condition. Further studies are needed to determine the efficacy of iNO in combined cardiogenic and septic shock.
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