Inhalation of nitric oxide as a life-saving therapy in a patient after pulmonary embolectomy

Schenk, Peter; Pernerstorfer, Thomas; Mittermayer, C; Kranz, Anna; Frömmel, Michael; Bı̂rsan, Tudor; Ratheiser, Klaus

doi:10.1093/bja/82.3.444

Cited by 10 publications

(4 citation statements)

References 17 publications

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“…A large variety of case reports have been published on the use of iNO, ranging from iNO administered to patients with RV failure (including PE-induced) as primary indication; as bridge to embolectomy or thrombolysis; with acute-on-chronic PE; during PE-induced cardiac arrest; on extra-corporal membrane oxygenation (ECMO) support or in case of contraindication to thrombolysis. 92–98 Some cases describe the use of iNO to treat increased PAP after embolectomy of acute PE 99–101 though not all with impressive hemodynamic responses. 102 iNO has been used in children and even infants with PE without success.…”

Section: Resultsmentioning

confidence: 99%

“…18 PE cases with mostly positive effects [92][93][94]96,108 Five cases in combination with thrombolysis, thrombectomy or embolectomy 97,[99][100][101][102] Five cases of post-operative PE 98 Note: Summary of review of the NO-sGC-cGMP pathway to induce pulmonary vasodilation in acute pulmonary embolism. Divided by treatment option, animal or clinical data and guideline recommendation.…”

Section: No-sgc-cgmp Pathwaymentioning

confidence: 99%

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Pulmonary vasodilation in acute pulmonary embolism – a systematic review

et al. 2020

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Acute pulmonary embolism is the third most common cause of cardiovascular death. Pulmonary embolism increases right ventricular afterload, which causes right ventricular failure, circulatory collapse and death. Most treatments focus on removal of the mechanical obstruction caused by the embolism, but pulmonary vasoconstriction is a significant contributor to the increased right ventricular afterload and is often left untreated. Pulmonary thromboembolism causes mechanical obstruction of the pulmonary vasculature coupled with a complex interaction between humoral factors from the activated platelets, endothelial effects, reflexes and hypoxia to cause pulmonary vasoconstriction that worsens right ventricular afterload. Vasoconstrictors include serotonin, thromboxane, prostaglandins and endothelins, counterbalanced by vasodilators such as nitric oxide and prostacyclins. Exogenous administration of pulmonary vasodilators in acute pulmonary embolism seems attractive but all come with a risk of systemic vasodilation or worsening of pulmonary ventilation-perfusion mismatch. In animal models of acute pulmonary embolism, modulators of the nitric oxide-cyclic guanosine monophosphate-protein kinase G pathway, endothelin pathway and prostaglandin pathway have been investigated. But only a small number of clinical case reports and prospective clinical trials exist. The aim of this review is to give an overview of the causes of pulmonary embolism-induced pulmonary vasoconstriction and of experimental and human investigations of pulmonary vasodilation in acute pulmonary embolism.

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Section: Resultsmentioning

confidence: 99%

Section: No-sgc-cgmp Pathwaymentioning

confidence: 99%

Pulmonary vasodilation in acute pulmonary embolism – a systematic review

et al. 2020

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“…A few case reports have shown its beneficial effect in patients with acute pulmonary embolism in association with medical therapy (5,11) and after surgical embolectomy (12,13). Effects included a decrease in pulmonary artery pressures, increased cardiac output, and improved blood oxygenation (5,12,13). Three studies found value in the use of iNO as a selective pulmonary vasodilator after thromboendarterectomy for chronic pulmonary embolism, particularly in a setting of reperfusion edema (10,14,15).…”

Section: Discussionmentioning

confidence: 99%

Inhaled Nitric Oxide as an Adjunct to Suction Thrombectomy for Pulmonary Embolism

Faintuch

Lang

Cohen

et al. 2004

Journal of Vascular and Interventional Radiology

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“…[8][9][10] Sporadic case reports have described the use of INO in patients with PE, most commonly following surgical thromboembolectomy. [11][12][13][14][15][16][17][18] We present a case series of patients who received INO as salvage therapy following massive PE.…”

Section: Introductionmentioning

confidence: 99%

Inhaled Nitric Oxide as Salvage Therapy in Massive Pulmonary Embolism: A Case Series

et al. 2012

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Inhaled nitric oxide (INO) has been shown to preferentially lower resistance in the pulmonary vasculature. The relative selectiveness of INO in accomplishing this effect makes it an attractive drug to administer as salvage therapy in patients with acute right ventricular failure secondary to pulmonary embolism. We describe 4 cases in which INO was used as a temporizing agent to decrease right ventricular after-load following massive near-fatal pulmonary embolism. All 4 patients survived to hospital discharge. Key words: massive pulmonary embolism; acute cor pulmonale; right heart failure; inhaled nitric oxide. [Respir Care 2012;57(3):444 -448. © 2012 Daedalus Enterprises]

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Inhalation of nitric oxide as a life-saving therapy in a patient after pulmonary embolectomy

Cited by 10 publications

References 17 publications

Pulmonary vasodilation in acute pulmonary embolism – a systematic review

Pulmonary vasodilation in acute pulmonary embolism – a systematic review

Inhaled Nitric Oxide as an Adjunct to Suction Thrombectomy for Pulmonary Embolism

Inhaled Nitric Oxide as Salvage Therapy in Massive Pulmonary Embolism: A Case Series

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