Inhaled Nitric Oxide Delivery by Anesthesia Machines

Ceccarelli, Patrizia; Bigatello, Luca M.; Hess, Dean; Kwo, Jean; Melendez, Luis

doi:10.1213/00000539-200002000-00045

Cited by 8 publications

(2 citation statements)

References 10 publications

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“…NO and epoprostenol are selective pulmonary vasodilators that are most often used in noncardiac surgery. 162–165 NO can be delivered at a dose of 1 to 80 ppm, although most centers use maximum doses of 20 to 40 ppm. 166 Inhaled epoprostenol (iEPO) is the aerosolized formulation of epoprostenol solution and is commonly delivered in doses between 10 and 50 ng·kg −1 ·min −1 .…”

Section: Intraoperative Management Of Phmentioning

confidence: 99%

Evaluation and Management of Pulmonary Hypertension in Noncardiac Surgery: A Scientific Statement From the American Heart Association

Rajagopal¹,

Ruetzler²,

Ghadimi³

et al. 2023

Circulation

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Pulmonary hypertension, defined as an elevation in blood pressure in the pulmonary arteries, is associated with an increased risk of death. The prevalence of pulmonary hypertension is increasing, with an aging population, a rising prevalence of heart and lung disease, and improved pulmonary hypertension survival with targeted therapies. Patients with pulmonary hypertension frequently require noncardiac surgery, although pulmonary hypertension is associated with excess perioperative morbidity and death. This scientific statement provides guidance on the evaluation and management of pulmonary hypertension in patients undergoing noncardiac surgery. We advocate for a multistep process focused on (1) classification of pulmonary hypertension group to define the underlying pathology; (2) preoperative risk assessment that will guide surgical decision-making; (3) pulmonary hypertension optimization before surgery to reduce perioperative risk; (4) intraoperative management of pulmonary hypertension to avoid right ventricular dysfunction and to maintain cardiac output; and (5) postoperative management of pulmonary hypertension to ensure recovery from surgery. Last, this scientific statement highlights the paucity of evidence to support perioperative pulmonary hypertension management and identifies areas of uncertainty and opportunities for future investigation.

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Section: Intraoperative Management Of Phmentioning

confidence: 99%

Evaluation and Management of Pulmonary Hypertension in Noncardiac Surgery: A Scientific Statement From the American Heart Association

Rajagopal¹,

Ruetzler²,

Ghadimi³

et al. 2023

Circulation

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“…Nitrous continues to be a useful inhaled anesthetic, whereas inhaled nitric can be a life-saving pulmonary vasodilator [11]. The rhyming problem will become a crisis soon, when many anesthesia machines will be able to deliver both oxides of nitrogen [12]. [6].…”

Section: Introductionmentioning

confidence: 99%

Nitrous or nitric? Same difference. Molecular formulas in the 1840s

Alston

2007

Journal of Clinical Anesthesia

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Is There a Place for Inhaled Nitric Oxide in the Therapy of Acute Pulmonary Embolism?

Tanus‐Santos

Theodorakis

2002

Am J Respir Med

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Acute pulmonary embolism (PE) is a serious complication resulting from the migration of emboli to the lungs. Although deep venous thrombi are the most common source of emboli to the lungs, other important sources include air, amniotic fluid, fat and bone marrow. Regardless of the specific source of the emboli, very little progress has been made in the pharmacological management of this high mortality condition. Because the prognosis is linked to the degree of elevation of pulmonary vascular resistance, any therapeutic intervention to improve the hemodynamics would probably increase the low survival rate of this critical condition. Inhaled nitric oxide (iNO) has been widely tested and used in cases of pulmonary hypertension of different causes. In the last few years some authors have described beneficial effects of iNO in animal models of acute PE and in anecdotal cases of massive PE. The primary cause of death in massive PE that is caused by deep venous thrombi, gas or amniotic fluid, is acute right heart failure and circulatory shock. Increased pulmonary vascular resistance following acute PE is the cumulative result of mechanical obstruction of pulmonary vessels and pulmonary arteriolar constriction (attributable to a neurogenic reflex and to the release of vasoconstrictors). As such, the vasodilator effects of iNO could actively oppose the pulmonary hypertension following PE. This hypothesis is consistently supported by experimental studies in different animal models of PE, which demonstrated that iNO decreased (by 10 to 20%) the pulmonary artery pressure without improving pulmonary gas exchange. Although maximal vasodilatory effects are probably achieved by less than 5 parts per million iNO, which is a relatively low concentration, no dose-response study has been published so far. In addition to the animal studies, a few anecdotal reports in the literature suggest that iNO may improve the hemodynamics during acute PE. However, no prospective, controlled, randomized clinical trial addressing this issue has been conducted to date. Future investigations addressing the effects of iNO combined with other drugs such as vasoconstrictors and inhibitors of phosphodiesterase III or V, may increase the responsiveness to iNO in acute PE.

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Inhaled Nitric Oxide Delivery by Anesthesia Machines

Cited by 8 publications

References 10 publications

Evaluation and Management of Pulmonary Hypertension in Noncardiac Surgery: A Scientific Statement From the American Heart Association

Evaluation and Management of Pulmonary Hypertension in Noncardiac Surgery: A Scientific Statement From the American Heart Association

Nitrous or nitric? Same difference. Molecular formulas in the 1840s

Is There a Place for Inhaled Nitric Oxide in the Therapy of Acute Pulmonary Embolism?

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