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| Pathophysiology of persistent pulmonary hypertension of newborn (PPHN). Acute pulmonary hypertension is the commonest adverse adaptation during cardiovascular transition after birth. PVR, pulmonary vascular resistance; PBF, pulmonary blood flow; MAS, meconium aspiration syndrome; RDS, respiratory distress syndrome; CDH, congenital diaphragmatic hernia. 

| Pathophysiology of persistent pulmonary hypertension of newborn (PPHN). Acute pulmonary hypertension is the commonest adverse adaptation during cardiovascular transition after birth. PVR, pulmonary vascular resistance; PBF, pulmonary blood flow; MAS, meconium aspiration syndrome; RDS, respiratory distress syndrome; CDH, congenital diaphragmatic hernia. 

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The hemodynamic changes during the first few breaths after birth are probably the most significant and drastic adaptation in the human life. These changes are critical for a smooth transition of fetal to neonatal circulation. With the cord clamping, lungs take over as the source of oxygenation from placenta. A smooth transition of circulation is a...

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... most immediate and adverse adaptation of transitional circulation occurs from persistent high PVR leading to continued right to left or bidirectional shunting across ductus arteriosus and/or via foramen ovale. Because of the increased PVR, PBF is decreased leading low oxygen saturation levels, increased oxygen requirement and ventilator support. This leads to decreased pulmonary venous return, and hence, decreased LV preload and low systemic blood flow (LV cardiac output). The decrease in perfusion of organs leads to increase in lactate, acidosis and hypoxia which are the most potent pulmonary vasoconstrictors. This further increases PVR, and it becomes a vicious cycle leading to acute pulmonary hypertension (commonly referred as persistent pulmonary hypertension of newborn or PPHN) (9, 10) ( Figure ...
Context 2
... decrease in perfusion of organs leads to increase in lactate, acidosis and hypoxia which are the most potent pulmonary vasoconstrictors. This further increases PVR, and it becomes a vicious cycle leading to acute pulmonary hypertension (commonly referred as persistent pulmonary hypertension of newborn or PPHN) (9, 10) ( Figure 2). ...

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... As of the third trimester, DA becomes progressively more sensitive to constrictive factors, such as prostaglandin synthetase inhibitors. [1][2][3] Intrauterine closure of the DA usually occurs after 31 weeks of gestation. Although its incidence is unknown, it is a rare event, ranging from 0.17% to 1.4%. ...
... In the first week of life alterations of RV performance are common, particularly in various pathophysiological states related to transition from fetal to postnatal circulation. Traditionally, RV function was assessed qualitatively by visual inspection of its size, wall thickness, and systolic function [3]. With the advancement of functional echocardiography as an adjunct to the clinical evaluation of the hemodynamic status of newborns, there is a tendency to move from the qualitative to quantitative assessment of cardiac function in newborns. ...
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... The coincidental decrease in SV and CO with an increase in TPRI and no significant increase in BP would seem to indicate that the reason for the drop in CO is secondary to increased TPRI. This is probably related to the neonate's disconnection from the placenta as well as the release of various vasoactive factors [44]. These vasoactive substances stabilise at various time points, which may account for the varying effects on SV, CO, BP, HR and TPR [45]. ...
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... Although the diagnosis of PPHN is first evoked in the presence of clinical signs such as respiratory or hemodynamic instability in a characteristic context (such as those mentioned above), it is confirmed by bedside structural and functional echocardiography [4] performed by trained neonatal intensivists [5]. Therefore, it is helpful to first rule out any underlying congenital heart defect [6] (such as total anomalous pulmonary venous return or transposition of the great arteries), establish the diagnosis of PPHN, and then assess the hemodynamic status (hypovolemic or obstructive shock). Recent papers by experts such as Storme [3] recommend an acute analysis of extrapulmonary shunts and management similar to that for duct-dependent congenital heart disease for severe PPHN. ...
... This prospective cohort study was performed in the NICU of a tertiary university center in Toulouse, France. All neonates less than 28 days old with an obvious clinical and echocardiographic diagnosis of PPHN (respiratory and hemodynamic instability was compulsory, one echocardiographic sign among those usually described [6] was required, as detailed in Table 1) were prospectively enrolled from April 2012 to April 2013. Congenital heart diseases were excluded. ...
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... The coincidental decrease in SV and CO with an increase in TPRI and no significant increase in BP would seem to indicate that the reason for the drop in CO is secondary to increased TPRI. This is probably related to the neonate's disconnection from the placenta as well as the release of various vasoactive factors [44]. These vasoactive substances stabilise at various time points, which may account for the varying effects on SV, CO, BP, HR and TPR [45]. ...
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... This is in contrast to all previous studies using echocardiography that measured SV at the LV outflow track (LVOT). However, measurement at the LVOT is not suitable to estimate effective CO in neonates because it is affected by physiologic intracardiac shunts (40). In contrast, SVCf is unaffected by shunts and reflects flow to the CNS. ...
... We have shown excellent and good-to-excellent intra-and interobserver agreements with this method; therefore, we think that the repeatability of our index and standard reference methods is not influencing our results. Finally, being pragmatic, echocardiography is the most useful method that can estimate CO in preterm infants and neonates for whom invasive monitoring, such as pulmonary artery catheterization or transpulmonary thermodilution, is either unreliable, impractical, or even dangerous (40,43,44). ...
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... It is assessed using color Doppler and direction of blood flow across ductus arteriosus is normally left to right, from the aorta (high systemic pressure) to the pulmonary artery (low pulmonary pressure) but it can be right to left or bi-directional when there is high pulmonary vascular resistance or when there is anatomical cause (due to certain CHDs). With conventional setting left to right shunt is seen as red jet while right to left shunt is seen as blue (21). A right-to-left shunt across the PDA is more difficult to see because color Doppler will show it as a blue jet, blood going toward aorta from pulmonary end, similar to branch pulmonary arteries. ...
... Color compare or simultaneous mode can be very helpful in such situation. Bi-directional flow is often seen during transitional circulation or when the pulmonary artery pressures are equal to systemic pressures (21). Shunt direction can also be assessed using pulse or continuous wave Doppler where left to right shunt is seen above the baseline (blood coming toward the probe) while right to left shunt is seen below the baseline (blood going away from the probe) (15,21) (Figure 4). ...
... Bi-directional flow is often seen during transitional circulation or when the pulmonary artery pressures are equal to systemic pressures (21). Shunt direction can also be assessed using pulse or continuous wave Doppler where left to right shunt is seen above the baseline (blood coming toward the probe) while right to left shunt is seen below the baseline (blood going away from the probe) (15,21) (Figure 4). ...
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... Premature infants and infants with underlying congenital heart disease and diaphragmatic hernia may have altered transitional physiology. [23] Transitional circulation is vulnerable. Inadvertent rise of pulmonary vascular resistance during the perioperative period may reopen ductus arteriosus and foramen ovale in neonates and young infants and may bring back transitional circulation to persistent foetal circulation. ...
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Children are at increased risk of perioperative respiratory and cardiovascular complications because of their unique respiratory and cardiovascular physiology compared to adults. Anaesthesia can exaggerate respiratory deterioration in young children because of their inability to control respiration and inherent susceptibility to rapid desaturation, airway obstruction, early respiratory fatigue and lung atelectasis. Premature infants (less than 60 weeks of postconceptional age) can be exposed to the danger of prolonged apnoea and consequent worsening of respiratory function. The transitional phase of circulation is vulnerable to revert to persistent foetal circulation in neonates. Myocardium and autonomic control of the heart is immature and different in neonates and infants compared to older children and adults and are predisposed to inadvertent life-threatening haemodynamic changes during the perioperative period. In this review article, we discuss respiratory and cardiovascular physiology in neonates, infants and younger children and their differences with older children and adults. We mainly focus on transitional physiology of both respiratory and cardiovascular system in newborns and infants and the deleterious changes that may occur during anaesthesia or perioperatively.