Central versus peripheral cannulation of extracorporeal membrane oxygenation support during double lung transplant for pulmonary hypertension

Objective. Adenosine infusion causes selective pulmonary vasodilation in fetal and neonatal lambs with pulmonary hypertension. We investigated the effects of a continuous infusion of adenosine on oxygenation in term infants with persistent pulmonary hypertension of newborn (PPHN). Design. A randomized, placebo-controlled, masked trial comparing the efficacy of intravenous infusion of adenosine to normal saline infusion over a 24-hour period. Setting. Inborn and outborn level III neonatal intensive care units at a university medical center. Participants. Eighteen term infants with PPHN and arterial postductal Po2 of 60 to 100 Torr on inspired O2 concentration of 100% and optimal hyperventilation (PaCo2 <30 Torr) were enrolled into the study. Study infants were randomly assigned to receive a placebo infusion of normal saline, or adenosine infusion in doses of 25 to 50 µg/kg/min over a 24-hour period. Results. Nine infants each received adenosine or placebo. The two groups did not differ in birth weight, gestational age, or blood gases and ventilator requirements at the time of entry into the study. Four of nine infants in the adenosine group and none of the placebo group had a significant improvement in oxygenation, defined as an increase in postductal PaO2 of ≥20 Torr from preinfusion baseline. The mean PaO2 in the adenosine group increased from 69 ± 19 at baseline to 94 ± 15 during 50 µg/kg/min infusion rate of adenosine and did not change significantly in the placebo group. Arterial blood pressure and heart rate did not change during the study in either group. The need for extracorporeal membrane oxygenation, incidence of bronchopulmonary dysplasia, and mortality were not different in the two groups. Conclusion. Data from this pilot study indicate that adenosine infusion at a dose of 50 µg/kg/min improves PaO2 in infants with PPHN without causing hypotension or tachycardia. Larger trials are needed to determine its effects on mortality and/or need for extracorporeal membrane oxygenation in infants with PPHN.

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Extracorporeal Membrane Oxygenation for End-Stage Interstitial Lung Disease With Secondary Pulmonary Hypertension at Rest and Exercise

ASAIO Journal ◽

10.1097/mat.0000000000000646 ◽

2018 ◽

Vol 64 (2) ◽

pp. 203-210 ◽

Cited By ~ 5

Author(s):

Scott Chicotka ◽

Daniel Burkhoff ◽

Marc L. Dickstein ◽

Matthew Bacchetta

Keyword(s):

Pulmonary Hypertension ◽

Interstitial Lung Disease ◽

Extracorporeal Membrane Oxygenation ◽

Lung Disease ◽

Membrane Oxygenation ◽

Secondary Pulmonary Hypertension ◽

End Stage ◽

Rest And Exercise

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The Wythenshawe Hybrid Circuit for lung transplantation: a previously undescribed circuit for lung transplant

Perfusion ◽

10.1177/0267659119868664 ◽

2019 ◽

Vol 35 (3) ◽

pp. 197-201

Author(s):

Andrew Brazier ◽

Edward Seville ◽

Wesley Hesford ◽

Bryce Pate ◽

Paul Exton ◽

...

Keyword(s):

Cardiopulmonary Bypass ◽

Extracorporeal Membrane Oxygenation ◽

Lung Transplantation ◽

Lung Transplant ◽

Transfusion Requirement ◽

Safety Net ◽

Membrane Oxygenation ◽

Hybrid Circuit

Extracorporeal membrane oxygenation is a safe modality of cardiorespiratory support for lung transplantation, with a reduction in coagulopathy and transfusion requirement when compared with cardiopulmonary bypass. In some scenarios, in lung transplantation, there are advantages to the use of cardiopulmonary bypass, which allows cardiac decompression, filtering of embolic air, easy addition and removal of volume, and a means to immediately reintroduce lost blood into circulation. We describe a novel circuit which allows safe and easy switch between modalities without prolonged interruption of flow. This circuit offers a safety net during surgery to minimise the risks influencing the use of extracorporeal membrane oxygenation.

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Right Ventricular Function in Acute Respiratory Distress Syndrome: Impact on Outcome, Respiratory Strategy and Use of Veno-Venous Extracorporeal Membrane Oxygenation

Frontiers in Physiology ◽

10.3389/fphys.2021.797252 ◽

2022 ◽

Vol 12 ◽

Author(s):

Matthieu Petit ◽

Edouard Jullien ◽

Antoine Vieillard-Baron

Keyword(s):

Pulmonary Hypertension ◽

Extracorporeal Membrane Oxygenation ◽

Right Ventricle ◽

Pulmonary Circulation ◽

Distress Syndrome ◽

Cor Pulmonale ◽

Prone Positioning ◽

Acute Cor Pulmonale ◽

Membrane Oxygenation ◽

The Right

Acute respiratory distress syndrome (ARDS) is characterized by protein-rich alveolar edema, reduced lung compliance and severe hypoxemia. Despite some evidence of improvements in mortality over recent decades, ARDS remains a major public health problem with 30% 28-day mortality in recent cohorts. Pulmonary vascular dysfunction is one of the pivot points of the pathophysiology of ARDS, resulting in a certain degree of pulmonary hypertension, higher levels of which are associated with morbidity and mortality. Pulmonary hypertension develops as a result of endothelial dysfunction, pulmonary vascular occlusion, increased vascular tone, extrinsic vessel occlusion, and vascular remodeling. This increase in right ventricular (RV) afterload causes uncoupling between the pulmonary circulation and RV function. Without any contractile reserve, the right ventricle has no adaptive reserve mechanism other than dilatation, which is responsible for left ventricular compression, leading to circulatory failure and worsening of oxygen delivery. This state, also called severe acute cor pulmonale (ACP), is responsible for excess mortality. Strategies designed to protect the pulmonary circulation and the right ventricle in ARDS should be the cornerstones of the care and support of patients with the severest disease, in order to improve prognosis, pending stronger evidence. Acute cor pulmonale is associated with higher driving pressure (≥18 cmH2O), hypercapnia (PaCO2 ≥ 48 mmHg), and hypoxemia (PaO2/FiO2 < 150 mmHg). RV protection should focus on these three preventable factors identified in the last decade. Prone positioning, the setting of positive end-expiratory pressure, and inhaled nitric oxide (INO) can also unload the right ventricle, restore better coupling between the right ventricle and the pulmonary circulation, and correct circulatory failure. When all these strategies are insufficient, extracorporeal membrane oxygenation (ECMO), which improves decarboxylation and oxygenation and enables ultra-protective ventilation by decreasing driving pressure, should be discussed in seeking better control of RV afterload. This review reports the pathophysiology of pulmonary hypertension in ARDS, describes right heart function, and proposes an RV protective approach, ranging from ventilatory settings and prone positioning to INO and selection of patients potentially eligible for veno-venous extracorporeal membrane oxygenation (VV ECMO).

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Inhaled Nitric Oxide Trials: "Vive la différence!"

PEDIATRICS ◽

10.1542/peds.97.3.438 ◽

1996 ◽

Vol 97 (3) ◽

pp. 438-438

Author(s):

DENNIS DAVIDSON

Keyword(s):

Nitric Oxide ◽

Clinical Trials ◽

Pulmonary Hypertension ◽

Optimal Design ◽

Extracorporeal Membrane Oxygenation ◽

Rescue Therapy ◽

Underlying Disease ◽

Inhaled Nitric Oxide ◽

Persistent Pulmonary Hypertension ◽

Membrane Oxygenation

The commentary by Drs Abman and Kinsella entitled "Inhaled Nitric Oxide for Persistent Pulmonary Hypertension of the Newborn: The Physiology Matters!" provides one important and valid viewpoint concerning the optimal design of clinical trials in this area of neonatology. The approach that they advocate involves individualized and meticulous care of persistent pulmonary hypertension of the newborn (PPHN) patients depending on their underlying disease, using whatever conventional or rescue therapy (before extracorporeal membrane oxygenation [ECMO] is needed to support the patient, while testing the efficacy of inhaled nitric oxide (I-NO).

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