Adenosine Infusion Improves Oxygenation in Term Infants With Respiratory Failure

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.

Download Full-text

Duration of sweep gas off trial for weaning from venovenous extracorporeal membrane oxygenation

Therapeutic Advances in Respiratory Disease ◽

10.1177/1753466619888131 ◽

2019 ◽

Vol 13 ◽

pp. 175346661988813 ◽

Cited By ~ 1

Author(s):

Soo Jin Na ◽

Hee Jung Choi ◽

Chi Ryang Chung ◽

Yang Hyun Cho ◽

Kiick Sung ◽

...

Keyword(s):

Extracorporeal Membrane Oxygenation ◽

Gas Flow ◽

Blood Gases ◽

Arterial Blood Gases ◽

Time Points ◽

Membrane Oxygenation ◽

Arterial Blood ◽

Institutional Experience ◽

Venovenous Extracorporeal Membrane Oxygenation ◽

Venovenous Ecmo

Background: No data are available on the duration of time needed to assess the adequacy of lung function after stopping sweep gas for weaning of venovenous extracorporeal membrane oxygenation (ECMO). The objective of this study was to investigate changes in arterial blood gases (ABGs) during sweep gas off trials in patients receiving venovenous ECMO. Methods: Data on patients receiving venovenous ECMO, with a weaning trial at least once, were collected prospectively from January 2012 through December 2017. Serial changes in ABGs during sweep gas off trial and clinical outcomes after weaning from venovenous ECMO were evaluated. Results: Over the study period, 192 sweep gas off trials occurred in 93 patients: 115 (60%) failed and 77 (40%) were successful. During the trial, significant changes in blood gases were observed within 1 h in all patients. When serial ABGs were compared according to trial off results, there were no significant differences in the pH, PaCO2, and HCO3− trends across time points between successful and failed trials. However, PaO2 (70.6 versus 93.4 mmHg), SaO2 (91.9 versus 95.2%), and PaO2/FiO2 ratio (164.0 versus 233.4) were significantly lower in failed trials than successful trials within 1 h after stopping sweep gas. After 2 h of trial off, no significant change in blood gases was observed until the end of the trial. Conclusions: No change in blood gases was observed 2 h after stopping sweep gas in patients receiving venovenous ECMO. Based on our institutional experience, however, we suggest monitoring for 2 h or more after stopping sweep gas flow to assess if patients are ready for decannulation. The reviews of this paper are available via the supplemental material section.

Download Full-text

Establishment and Evaluation of a Rat Model of Extracorporeal Membrane Oxygenation (ECMO) Thrombosis Using a 3D-printed Mock Oxygenator

10.21203/rs.3.rs-139858/v1 ◽

2021 ◽

Author(s):

Nao Umei ◽

Angela Lai ◽

Jennifer Miller ◽

Suji Shin ◽

Kalliope Georgette Roberts ◽

...

Keyword(s):

Blood Flow ◽

Extracorporeal Membrane Oxygenation ◽

Flow Resistance ◽

Blood Gases ◽

Membrane Oxygenation ◽

Arterial Blood ◽

Anticoagulation Agents ◽

Normal Mean ◽

3D Printed ◽

Large Animals

Abstract Background: Extracorporeal membrane oxygenation (ECMO) research using large animals requires a significant amount of resources, slowing down the development of new means of ECMO anticoagulation. Therefore, this study developed and evaluated a new rat ECMO model using a 3D-printed mock oxygenator.Methods: The circuit consisted of tubing, a 3D-printed mock oxygenator, and a roller pump. The mock oxygenator was designed to simulate the geometry and blood flow patterns of the fiber bundle in full-scale oxygenators but with a low (2.5 mL) priming volume. Rats were placed on arteriovenous ECMO at a 1.9 mL/min flow rate at two different heparin doses (n = 3 each): low (15 IU/kg/h for eight hours) versus high (50 IU/kg/h for one hour followed by 25 IU/kg/h for seven hours). The experiment continued for eight hours or until the mock oxygenator failed. The mock oxygenator was considered to have failed when its blood flow resistance reached three times its baseline resistance.Results: During ECMO, rats maintained near-normal mean arterial pressure and arterial blood gases with minimal hemodilution. The mock oxygenator thrombus weight was significantly different (p < 0.05) between the low (0.02 ± 0.006 g) and high (0.003 ± 0.001 g) heparin delivery groups, and blood flow resistance was also larger in the low anticoagulation group.Conclusions: This model is a simple, inexpensive system for investigating new anticoagulation agents for ECMO and provides low and high levels of anticoagulation that can serve as control groups for future studies.

Download Full-text

A Protocol that Mandates Postoxygenator and Arterial Blood Gases to Confirm Brain Death on Venoarterial Extracorporeal Membrane Oxygenation

ASAIO Journal ◽

10.1097/mat.0000000000001086 ◽

2020 ◽

Vol 66 (2) ◽

pp. e23-e28 ◽

Cited By ~ 3

Author(s):

Joshua F. Ihle ◽

Aidan J. C. Burrell ◽

Steve J. Philpot ◽

David V. Pilcher ◽

Deirdre A. Murphy ◽

...

Keyword(s):

Extracorporeal Membrane Oxygenation ◽

Brain Death ◽

Blood Gases ◽

Arterial Blood Gases ◽

Membrane Oxygenation ◽

Arterial Blood ◽

Venoarterial Extracorporeal Membrane Oxygenation

Download Full-text

Establishment and evaluation of a rat model of extracorporeal membrane oxygenation (ECMO) thrombosis using a 3D-printed mock-oxygenator

Journal of Translational Medicine ◽

10.1186/s12967-021-02847-w ◽

2021 ◽

Vol 19 (1) ◽

Author(s):

Nao Umei ◽

Angela Lai ◽

Jennifer Miller ◽

Suji Shin ◽

Kalliope Roberts ◽

...

Keyword(s):

Blood Flow ◽

Extracorporeal Membrane Oxygenation ◽

Flow Resistance ◽

Blood Gases ◽

Membrane Oxygenation ◽

Arterial Blood ◽

Anticoagulation Agents ◽

Normal Mean ◽

3D Printed ◽

Large Animals

Abstract Background Extracorporeal membrane oxygenation (ECMO) research using large animals requires a significant amount of resources, slowing down the development of new means of ECMO anticoagulation. Therefore, this study developed and evaluated a new rat ECMO model using a 3D-printed mock-oxygenator. Methods The circuit consisted of tubing, a 3D-printed mock-oxygenator, and a roller pump. The mock-oxygenator was designed to simulate the geometry and blood flow patterns of the fiber bundle in full-scale oxygenators but with a low (2.5 mL) priming volume. Rats were placed on arteriovenous ECMO at a 1.9 mL/min flow rate at two different heparin doses (n = 3 each): low (15 IU/kg/h for eight hours) versus high (50 IU/kg/h for one hour followed by 25 IU/kg/h for seven hours). The experiment continued for eight hours or until the mock-oxygenator failed. The mock-oxygenator was considered to have failed when its blood flow resistance reached three times its baseline resistance. Results During ECMO, rats maintained near-normal mean arterial pressure and arterial blood gases with minimal hemodilution. The mock-oxygenator thrombus weight was significantly different (p < 0.05) between the low (0.02 ± 0.006 g) and high (0.003 ± 0.001 g) heparin delivery groups, and blood flow resistance was also larger in the low anticoagulation group. Conclusions This model is a simple, inexpensive system for investigating new anticoagulation agents for ECMO and provides low and high levels of anticoagulation that can serve as control groups for future studies.

Download Full-text

10-Year Experience with Postoperatively-Extended Intraoperative Extracorporeal Membrane Oxygenation in Lung Transplantation for Patients with Severe Pulmonary Hypertension

The Journal of Heart and Lung Transplantation ◽

10.1016/j.healun.2021.01.928 ◽

2021 ◽

Vol 40 (4) ◽

pp. S330

Author(s):

M. Franz ◽

K. Aburahma ◽

T. Siemeni ◽

M. Avsar ◽

D. Bobylev ◽

...

Keyword(s):

Pulmonary Hypertension ◽

Extracorporeal Membrane Oxygenation ◽

Lung Transplantation ◽

Severe Pulmonary Hypertension ◽

Membrane Oxygenation

Download Full-text

Transportation of patients on extracorporeal membrane oxygenation: a tertiary medical center experience and systematic review of the literature

Annals of Intensive Care ◽

10.1186/s13613-016-0232-7 ◽

2017 ◽

Vol 7 (1) ◽

Cited By ~ 15

Author(s):

Pedro Vitale Mendes ◽

Cesar de Albuquerque Gallo ◽

Bruno Adler Maccagnan Pinheiro Besen ◽

Adriana Sayuri Hirota ◽

Raquel de Oliveira Nardi ◽

...

Keyword(s):

Systematic Review ◽

Extracorporeal Membrane Oxygenation ◽

Medical Center ◽

Transportation Of Patients ◽

Review Of The Literature ◽

Membrane Oxygenation

Download Full-text

Newborns With Acute Respiratory Distress: Diagnosis and Management

Pediatrics in Review ◽

10.1542/pir.9.9.279 ◽

1988 ◽

Vol 9 (9) ◽

pp. 279-285

Author(s):

Richard L. Schreiner ◽

Niceta C. Bradburn

Keyword(s):

Pulmonary Hypertension ◽

Respiratory Distress ◽

Newborn Infant ◽

Blood Gases ◽

Indirect Measurement ◽

Chest Roentgenogram ◽

Inborn Errors ◽

Severe Respiratory Distress ◽

Glucose Determination ◽

Arterial Blood

If respiratory distress develops in the newborn after he or she has been normal for more than a few hours, bacterial sepsis, inborn errors of metabolism, cardiac disorders, and intracranial hemorrhage should be suspected. It is virtually impossible to determine whether an infant with mild respiratory distress in the first few hours of life will have rapid resolution of disease or progress to severe respiratory distress. That is, it is difficult to differentiate among transient tachypnea of the newborn, sepsis, and pulmonary hypertension in the infant with mild respiratory distress in the first few hours of life. Transient tachypnea is a diagnosis that can only be made with certainty after the infant's respiratory distress has resolved. The newborn infant with mild respiratory distress of more than a few hours' duration requires a minimum number of laboratory tests including chest roentgenogram, hematocrit or hemoglobin, blood glucose determination, direct or indirect measurement of arterial blood gases, and blood cultures. The liberal use of oxygen in the near-term, term, or post-term vigorous but cyanotic infant in the delivery room may decrease the incidence and/or severity of respiratory distress due to pulmonary hypertension. A newborn infant with respiratory distress for more than a few hours should be considered a candidate for infection.

Download Full-text

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

Download Full-text

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).

Download Full-text