Fetal Circulation and Persistent Pulmonary Hypertension of Newborn

2004 ◽  
pp. 197-197
Author(s):  
G Konduri
Keyword(s):  
Pulmonary Hypertension ◽  
Persistent Pulmonary Hypertension ◽  
Fetal Circulation

Persistent Pulmonary Hypertension of the Newborn

1991 ◽  
Vol 7 (S1) ◽  
pp. 66-69
Author(s):  
George Lister
Keyword(s):  
Pulmonary Hypertension ◽  
Diaphragmatic Hernia ◽  
Vascular Development ◽  
Clinical Syndrome ◽  
Persistent Pulmonary Hypertension ◽  
Maternal Infection ◽  
Fetal Circulation ◽  
Cns Disease ◽  
Persistent Fetal Circulation

Persistent pulmonary hypertension of the newborn or persistent fetal circulation is a clinical syndrome that is usually apparent within the first 2 days after birth because of the presence of hypoxemia (2;12;19). The syndrome was first described in an abstract by Gersony, Due, and Sinclair (6) in 1969. Two infants were reported who had “RV decompensation, cyanosis and clear lung fields… in the absence of recognizable cardiac, pulmonary, hematologic or CNS disease.” The syndrome has been associated with aspiration of meconium, diaphragmatic hernia, asphyxia, hemorrhage, shock, and maternal infection (4;18). In other cases, there is no clear antecedent event. Despite considerable interest in the problem and a wealth of research related to pulmonary vasoregulation and vascular development in the fetus and newborn, the etiology of the syndrome remains obscure 20 years since its recognition.

scholarly journals Anaesthesia for Antenatal Diagnosed Duodenal Atresia with Undiagnosed Persistent Pulmonary Hypertension of Neonate

2021 ◽  
Vol 18 (4) ◽  
pp. 792-794
Author(s):  
Rupesh Kumar Yadav ◽  
Bidur Kumar Dhungel ◽  
Pawan Kumar Hamal ◽  
Nabin Pokhrel ◽  
Manoj Kumar Shrestha
Keyword(s):  
Pulmonary Hypertension ◽  
Supportive Care ◽  
Respiratory Symptom ◽  
Duodenal Atresia ◽  
Persistent Pulmonary Hypertension ◽  
Pulmonary Vasculature ◽  
Severe Hypoxemia ◽  
Adult Type ◽  
Flip Flop ◽  
Fetal Circulation

Conversion of fetal circulation to adult-type occurs immediately after birth but neonates with problems in the development of pulmonary vasculature are prone to revert back to fetal circulation. This phenomenon is known as flip-flop circulation which may be induced perioperatively and as such anesthesiologist are central to its management. We report a case of term neonate planned for repair of duodenal atresia that despite having no respiratory symptom preoperatively developed severe hypoxemia under anesthesia that was even unresponsive to 100% oxygen. The intraoperative hemodynamics of the neonate was managed along with supportive care successfully. A postoperative echocardiogram confirmed the evidence of persistent pulmonary hypertension of the newborn.Keywords: Duodenal atresia; flip flop circulation; neonates; persistent pulmonary hypertension of newborn

scholarly journals Persistent Pulmonary Hypertension of the Newborn: Analysis of 181 cases over one Year

2018 ◽  
Vol 11 (1) ◽  
pp. 17-22
Author(s):  
Nurun Nahar Fatema
Keyword(s):  
Pulmonary Hypertension ◽  
Septal Defect ◽  
Ductus Arteriosus ◽  
Treatment Protocol ◽  
Persistent Pulmonary Hypertension ◽  
Systolic Pulmonary Artery Pressure ◽  
Fetal Circulation ◽  
Mortality And Morbidity ◽  
High Flow Oxygen ◽  
Minimum Age

Background: Persistent pulmonary hypertension (PPHN) is the persistence of the high pulmonary arterial pressure after birth which is a characteristic of the fetal circulation. PPHN is associated with substantial infant mortality and morbidity. Various treatment protocol are used according to the need of the patient. This study aimed to see the spectrum of the disease and its outcome in Bangladesh.Methods: 181 newborn babies were diagnosed as persistent pulmonary hypertension or persistent fetal circulation. After establishing diagnosis, all cases were kept in NICU and various management plans were prescribed according to necessity of a specific case. Repeat echocardiography was done after 72 hours to see the response of treatment. Residual congenital cardiac lesions were managed later on.Results: Most of the patient (69.06%) was diagnosed at first week of life. Minimum age of the patient was 1 day and maximum age 23 days. Among 181 cases 109 (66.22%) were male and 72(39.77%) were female. Associated congenital lesions like atrial septal defect was found in 52 (28.72%) cases, patent ductus arteriosus (PDA) was found in 14 (7.73%) cases and ventricular septal defect (VSD) was found in 2 (1.10%) cases. Combination of ASD & PDA was found in 75 (44.33%) cases. Systolic pulmonary artery pressure was more than 60 mmHg in 103 (56.91%) cases, more than 50 mmHg in 53 (29.28%) cases and more than 30 mmHg in 25 (13.81%) cases. Most of the patient (100%) received high flow oxygen therapy along with anti failure (66.30%) and sildenafil 98 (54.14%) therapy as per requirement of the patient. Complete cure was achieved in 95.58% cases and mortality was only 1.10%.Conclusion: These data showed a very impressive outcome of the PPHN in Bangladeshi Newborn even with minimally invasive management.Cardiovasc. j. 2018; 11(1): 17-22

Late-Onset Hearing Loss

PEDIATRICS ◽  
1989 ◽  
Vol 83 (5) ◽  
pp. 807-808
Author(s):  
TOM NIELD ◽  
ANGELA D. RAMOS ◽  
DAVID WARBURTON
Keyword(s):  
Mechanical Ventilation ◽  
Pulmonary Hypertension ◽  
Hearing Loss ◽  
Respiratory Failure ◽  
Chronic Lung Disease ◽  
Late Onset ◽  
Prolonged Mechanical Ventilation ◽  
Persistent Pulmonary Hypertension ◽  
Fetal Circulation ◽  
Delayed Onset

The findings of Hendricks-Munoz and Walton concerning the incidence of sensorineural hearing loss in infants with persistent pulmonary hypertension (persistent fetal circulation) substantiate our findings that, in some cases, the loss appears to be of delayed onset and progressive. We would, however, like to point out that delayed-onset sensorineural loss is not limited to infants with persistent pulmonary hypertension, because four of the 11 infants we reported did not have persistent pulmonary hypertension. Therefore, serial audiologic evaluations should also be done for any infant with significant respiratory failure requiring prolonged mechanical ventilation with resultant chronic lung disease.

Congenital Alveolar Capillary Dysplasia: Rare Cause of Persistent Pulmonary Hypertension

1997 ◽  
Vol 17 (6) ◽  
pp. 959-975 ◽  
Author(s):  
Sibylle Haraida ◽  
Hannelore Lochbuhler ◽  
A. Heger ◽  
A. Nerlich ◽  
J. Diebold ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Persistent Pulmonary Hypertension ◽  
Alveolar Capillary Dysplasia ◽  
Alveolar Capillary

scholarly journals Inhaled Nitric Oxide at Birth Reduces Pulmonary Vascular Resistance and Improves Oxygenation in Preterm Lambs

Children ◽  
2021 ◽  
Vol 8 (5) ◽  
pp. 378
Author(s):  
Satyan Lakshminrusimha ◽  
Sylvia F. Gugino ◽  
Krishnamurthy Sekar ◽  
Stephen Wedgwood ◽  
Carmon Koenigsknecht ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Pulmonary Vascular Resistance ◽  
Preterm Infants ◽  
Vascular Resistance ◽  
Inhaled Nitric Oxide ◽  
Persistent Pulmonary Hypertension ◽  
Inhaled No ◽  
Birth Preterm

Resuscitation with 21% O2 may not achieve target oxygenation in preterm infants and in neonates with persistent pulmonary hypertension of the newborn (PPHN). Inhaled nitric oxide (iNO) at birth can reduce pulmonary vascular resistance (PVR) and improve PaO2. We studied the effect of iNO on oxygenation and changes in PVR in preterm lambs with and without PPHN during resuscitation and stabilization at birth. Preterm lambs with and without PPHN (induced by antenatal ductal ligation) were delivered at 134 d gestation (term is 147–150 d). Lambs without PPHN were ventilated with 21% O2, titrated O2 to maintain target oxygenation or 21% O2 + iNO (20 ppm) at birth for 30 min. Preterm lambs with PPHN were ventilated with 50% O2, titrated O2 or 50% O2 + iNO. Resuscitation with 21% O2 in preterm lambs and 50%O2 in PPHN lambs did not achieve target oxygenation. Inhaled NO significantly decreased PVR in all lambs and increased PaO2 in preterm lambs ventilated with 21% O2 similar to that achieved by titrated O2 (41 ± 9% at 30 min). Inhaled NO increased PaO2 to 45 ± 13, 45 ± 20 and 76 ± 11 mmHg with 50% O2, titrated O2 up to 100% and 50% O2 + iNO, respectively, in PPHN lambs. We concluded that iNO at birth reduces PVR and FiO2 required to achieve target PaO2.

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