Central Hemodynamic and Regional Blood Flow Changes in the Newborn with Right Ventricular Hypertension

Belik, Jaques; Baron, Ken; Light, R. Bruce

doi:10.1203/00006450-198912000-00004

Cited by 8 publications

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“…Progressive increase in PVR without a parenchymal lung disease is shown to result in a significant fall in systemic arterial pressure in adults and newborns, apparently through decreased left ventricular output (21,22). Our present and earlier findings however indicate that the vascular hypertensive response in meconium-contaminated newborn lungs is not connected with significant changes in cardiac output or systemic arterial pressure (2,23).…”

Section: Discussioncontrasting

confidence: 47%

Asphyxia Aggravates Systemic Hypotension But Not Pulmonary Hypertension in Piglets with Meconium Aspiration

et al. 2003

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Meconium aspiration and birth asphyxia are both separately connected to significant pulmonary and systemic hemodynamic changes in newborns, but, although these insults frequently coexist, their combined effects on the neonatal circulation are still controversial. To determine the pulmonary and systemic circulatory changes induced by pulmonary meconium contamination with concurrent asphyxia, 41 anesthetized and ventilated newborn piglets (10 -12 d) were studied for 6 h. Eleven piglets were instilled with a bolus of human meconium intratracheally, and 10 piglets had meconium instillation with immediate induction of an asphyxic insult. Eight piglets had only asphyxia and 12 ventilated piglets served as controls. Meconium instillation (with and without asphyxia) resulted in a sustained decrease in the oxygenation, which remained, however, on the control level in the asphyxic group. Although meconium insufflation (with and without asphyxia) increased pulmonary artery pressure and vascular resistance progressively during the study period, the meconium-induced hypertensive effect was actually diminished by additional asphyxia. Asphyxia alone did not have any effect on these pulmonary hemodynamic parameters. On the other hand, whereas systemic arterial pressure and vascular resistance remained on the control level after meconium instillation alone, asphyxia (with and without pulmonary meconium insult) resulted in a sustained fall in systemic pressure already by 4 h. Our data thus indicate that although the coexisting asphyxia seems to moderate the meconium aspiration-induced pulmonary hypertensive response, this additional asphyxic insult does not affect the associated hypoxemia, but rather significantly exacerbates systemic hypotension. Abbreviations CO, cardiac output CVP, central venous pressure HR, heart rate MABP, mean arterial blood pressure MAS, meconium aspiration syndrome MPAP, mean pulmonary artery pressure PVR, pulmonary vascular resistance PWP, pulmonary wedge pressure SVR, systemic vascular resistance Aspiration of meconium-stained amniotic fluid frequently produces a severe respiratory failure in term and postterm infants. The clinical MAS has high morbidity and mortality, often linked with the presence of pulmonary hypertension (1-5). The pathophysiology and predisposing factors of the pulmonary hypertensive reaction in MAS are, however, complex and poorly defined. Although abnormal pulmonary arteriolar hypertrophy resulting from intrauterine hypoxia is supposed to play an etiologic role in some fatal cases of hypertensive MAS (6), experimental data indicate that acute intrapulmonary meconium contamination per se is able to cause, in a concentration-dependent manner, progressive pulmonary hypertensive response (2, 7). Alike, there are clinical data suggesting that meconium aspiration and its associated complications, rather than the structural vascular changes, are primarily responsible for the elevated pulmonary vasomotor tone and hypoxemic respiratory failure in newborns (8, 9). Because eventual disturb...

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Section: Discussioncontrasting

confidence: 47%

Asphyxia Aggravates Systemic Hypotension But Not Pulmonary Hypertension in Piglets with Meconium Aspiration

et al. 2003

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“…Further, an increase in PsA has been shown to lead to an increase in cardiac output in adult animals with RVH (4,5), likely as a result of reestablishment of adequate right ventricular coronary perfusion compromised by the increase in right ventricular intracavitary pressure (4). However, in our newborn pig model of RVH, myocardial blood flow to the right ventricular free wall is actually.increased much above baseline values (2). In addition, although Qp increased along with increasing PsA, and this was associated with a 20% increase in mean right ventricular myocardial blood flow, this increase in coronary blood flow did not achieve statistical significance and changes in myocardial flow did not correlate with changes in Qp.…”

Section: Discussionmentioning

confidence: 64%

“…In the newborn pig, we have previously shown that RVH is associated with a significant decrease in PSA and cardiac output (1,2). The factors responsible for the reduction in cardiac output during RVH are presently unclear, but previously reported data suggest that the reduction is related to the changes in PSA (3-6).…”

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confidence: 90%

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The Effect of an Increase in Systemic Arterial Pressure in the Newborn with Right Ventricular Hypertension

Belik

Baron

1990

Pediatr Res

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ABSTRACT. To evaluate the effect of an elevation in systemic arterial pressure upon pulmonary blood flow and arterial oxygenation during right ventricular hypertension (RVH), we acutely studied 13 1-d-old piglets. Catheters were positioned in the pulmonary artery, both atria, and the aorta for hemodynamic measurements. An electromagnetic probe was positioned in the main pulmonary artery for pulmonary blood flow measurement. Systemic and regional blood flow were measured with the radiolabeled microsphere technique. A balloon-mounted catheter was advanced in the aorta and maintained at the lower thoracic level. After induction of RVH (pulmonary artery banding), a significant decrease in arterial 0 2 pressure from 54.4 f 1.6 to 10.6 2 0.4 kPa (p < 0.01), a 30% reduction in systemic arterial pressure, and a 44% decrease in pulmonary blood flow were observed. During RVH, partial inflation of the aortic balloon to restore the systemic arterial pressure to its initial value led to an increase in arterial O2 pressure to 23.5 2 3.1 kPa ( p < 0.01). Full inflation of the balloon further increased the arterial O2 pressure to 32.6 f 2.9 kPa ( p < 0.01). Aortic balloon inflation increased pulmonary blood flow in 11 and systemic O2 delivery in nine of the 13 animals. RVH was associated with a significant increase in cerebral and right ventricular myocardial free-wall blood flow and a decrease in renal and bowel blood flow and O2 delivery (p < 0.01). Aortic balloon inflation during RVH did not change either the cerebral or myocardial free-wall blood flow, but further significantly decreased renal and bowel blood flow and O2 delivery. In conclusion, an elevation in systemic arterial pressure significantly reduces foramen ovale shunt and increases pulmonary blood flow and systemic O2 delivery in the newborn pig with RVH. This finding may prove useful in the clinical management of hypoxemic infants with persistent pulmonary hypertension syndrome. (Pediatr Res 28: 603-608, 1990 PPHN, persistent pulmonary hypertension syndrome Pao2, arterial O2 pressureIn the newborn pig, we have previously shown that RVH is associated with a significant decrease in PSA and cardiac output (1,2). The factors responsible for the reduction in cardiac output during RVH are presently unclear, but previously reported data suggest that the reduction is related to the changes in PSA (3-6). Meadow et al. (3)reported that after group B streptococcusinduced pulmonary hypertension in the piglet, a significant increase in Qp can be achieved by elevating the PSA Although not evaluated in their experimental animals, Meadow et al. also suggested that a selective elevation of the PsA during pulmonary hypertension could also impede right to left shunt at the foramen ovale and thus improve oxygenation (3). Furthermore, in adult animals with RVH and decreased Qp, an elevation in PSA increases cardiac output (4-6).In infants, the PPHN syndromeis associated with hypoxemia related not only to the decreased Qp, but also to the magnitude of the right to left shunt across ...

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“…This syndrome is characterized by sustained elevation of PVR (15), causing extrapulmonary right-to-left shunting of blood across the DA and foramen ovale and severe hypoxemia (15). PPHN is also usually associated with low systemic pressure and low cardiac output because of increased right ventricular afterload and myocardial dysfunction (5,6). PPHN contributes to significant morbidity and mortality, indicating a need for further study of its pathogenesis and management (35).…”

mentioning

confidence: 99%

Pulmonary vascular effects of sildenafil on the development of chronic pulmonary hypertension in the ovine fetus

Larrue¹,

Jaillard²,

Lorthioir³

et al. 2005

American Journal of Physiology-Lung Cellular and Molecular Phys

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We investigated the pulmonary vascular effects of prophylactic use of sildenafil, a specific phosphodiesterase-5 inhibitor, in late-gestation fetal lambs with chronic pulmonary hypertension. Fetal lambs were operated on at 129 +/- 1 days gestation (term = 147 days). Ductus arteriosus (DA) was compressed for 8 days to cause chronic pulmonary hypertension. Fetuses were treated with sildenafil (24 mg/day) or saline. Pulmonary vascular responses to increase in shear stress and in fetal PaO2 were studied at, respectively, day 4 and 6. Percent wall thickness of small pulmonary arteries (%WT) and the right ventricle-to-left ventricle plus septum ratio (RVH) were measured after completion of the study. In the control group, DA compression increased PA pressure (48 +/- 5 to 72 +/- 8 mmHg, P < 0.01) and pulmonary vascular resistance (PVR) (0.62 +/- 0.08 to 1.15 +/- 0.11 mmHg x ml(-1) x min(-1), P < 0.05). Similar increase in PAP was observed in the sildenafil group, but PVR did not change significantly (0.54 +/- 0.06 to 0.64 +/- 0.09 mmHg x ml(-1) x min(-1)). Acute DA compression, after brief decompression, elevated PVR 25% in controls and decreased PVR 35% in the sildenafil group. Increased fetal PaO2 did not change PVR in controls but decreased PVR 60% in the sildenafil group. %WT and RVH were not different between groups. Prophylactic sildenafil treatment prevents the rise in pulmonary vascular tone and altered vasoreactivity caused by DA compression in fetal lambs. These results support the hypothesis that elevated PDE5 activity is involved in the consequences of chronic pulmonary hypertension in the perinatal lung.

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Central Hemodynamic and Regional Blood Flow Changes in the Newborn with Right Ventricular Hypertension

Cited by 8 publications

References 0 publications

Asphyxia Aggravates Systemic Hypotension But Not Pulmonary Hypertension in Piglets with Meconium Aspiration

Asphyxia Aggravates Systemic Hypotension But Not Pulmonary Hypertension in Piglets with Meconium Aspiration

The Effect of an Increase in Systemic Arterial Pressure in the Newborn with Right Ventricular Hypertension

Pulmonary vascular effects of sildenafil on the development of chronic pulmonary hypertension in the ovine fetus

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