How a Patent Ductus Arteriosus Effects the Premature Lamb's Ability To Handle Additional Volume Loads

Clyman, Ronald I.; Roman, Christine; Heymann, Michaël; Mauray, Françoise

doi:10.1203/00006450-198711000-00012

Cited by 25 publications

(21 citation statements)

References 38 publications

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“…We suggest that the neonatal LV is capable of generating adequate contraction under the lower afterload condition during the patency of the ductus arteriosus. Clyman et al (1987) hypothesized that an associated reduction in the LV afterload played a significant role in the increase of stroke volume in newborn lambs with a patent ductus arteriosus after birth, and our present results seems to support his hypothesis. Blood pressure is thought to be lowest at birth and increase gradually by the first 2 weeks of life (Kitterman et al 1969;Earley et al 1980), and these findings are consistent with our result.…”

Section: Discussiqnsupporting

confidence: 82%

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Left Ventricular Contractile State of Early Human Neonates with Patent Ductus Arteriosus.

Harada

Shiota

Tamura

et al. 1994

Tohoku J. Exp. Med.

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A. and TAKADA, G. Left Ventricular Contractile State of Early Human Neonates with Patent Ductus Arteriosus. Tohoku J. Exp. Med., 1994, 172 (2), 155-161 Using echocardiographic technique, we studied the left ventricular (LV) contractile state in 32 full-term infants within 24 hr after birth. They were divided into 2 groups based on the timing of the examinations; the group 1(n -17), < 3 hr after birth; the group 2 (n=15), > 3 and <24 hr after birth, and the additional examinations were performed on day 5. The patency of the ductus arteriosus and its internal diameter were determined by pulsed Doppler and two-dimensional echocardiography. The left atrial to aortic root ratio was obtained from M-mode echocardiography, and the LV contractile state was estimated by the relationship between heart rate-corrected velocity of circumferential fiber shortening (mVcfc) and end-systolic meridional wall stress (ESS). The ductus arteriosus was open in all cases of group 1 and in 83% of the cases of group 2, but the ductal diameter and the left atrial to aortic root ratio significantly decreased in group 2. The relationship between mVcfc and ESS showed no significant differences between 2 groups and the control. Afterload, represented as ESS, was significantly lower in group 1 than the control. We suggest that the low afterload condition helps the adequate LV contraction even under the increased preload through the left-to-right ductus arteriosus shunting after birth. left ventricle; patent ductus arteriosus; neonate; end-systolic meridional wall stress During the transition from fetal to neonatal circulation, the left-to-right ductus arteriosus shunting acts as a preload to the left ventricle (LV). In animal research on newborn lambs, some investigators demonstrated the less capacity of LV response to an increased preload (Klopfenstein and Rudolph 1978;Romero and Friedman 1979;Baylen et al. 1985), whereas, others demonstrated the capa-

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Section: Discussiqnsupporting

confidence: 82%

“…bility of LV to handle the increased volume load through the ductus arteriosus shunting (Baylen et al 1986;Clyman et al 1987). In human neonates, the LV contractile state during a patency of the ductus arteriosus has not been fully evaluated.…”

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confidence: 99%

Left Ventricular Contractile State of Early Human Neonates with Patent Ductus Arteriosus.

Harada

Shiota

Tamura

et al. 1994

Tohoku J. Exp. Med.

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“…That myocardial contractility may be impaired in preterm infants (15,27) raises the possibility that ductal steal in the first postnatal day may lead to decreased systemic perfusion. However, high-volume ductal shunting occurs into a pulmonary circulation of low resistance, and there is some suggestion from animal studies that even the immature myocardium is able to significantly increase LVO when afterload is low (28). In addition, ductal shunting leads to increased venous return to the left atrium, increasing preload to the left ventricle.…”

Section: Discussionmentioning

confidence: 99%

“…Eighty infants with median (range) gestation 28 (24)(25)(26)(27)(28)(29)(30) wk and birth weight 1060 (510 -1900) g were studied. Forty (50%) infants were male and 76 (95%) had been exposed to antenatal steroids.…”

Section: Resultsmentioning

confidence: 99%

Does Retrograde Diastolic Flow in the Descending Aorta Signify Impaired Systemic Perfusion in Preterm Infants?

et al. 2008

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High-volume systemic-to-pulmonary ductal shunting occurs frequently in preterm infants and is indicated by diastolic flow reversal in the descending aorta (DAo). We studied the relationship between ductal diameter, diastolic DAo reversal, and left ventricular output (LVO); and superior vena caval (SVC) flow (upper body perfusion) and DAo flow (lower body perfusion) in preterm (Ͻ31 wk) infants. Echocardiographic assessments were performed at 5, 12, 24, and 48 h postnatal age (80 infants, median gestation 28 wk, 1060 g). Incidence of ductal patency fell from 100% at 5 h to 72% at 48 h; incidence of pure systemic-to-pulmonary shunting increased from 66% to 95% of infants with patent ducts. In infants with duct diameter greater than the median, 35-48% of infants had DAo flow reversal. In infants with duct diameter greater than median, DAo reversal was associated with 23-29% increases in LVO at 5-48 h, and 35% decreases in DAo flow volume at 24 -48 h, but no differences in SVC flow. In conclusion, a large duct with left-to-right shunting is common in preterm infants. Retrograde DAo flow is a marker of high-volume shunt, evidenced by increased LVO. Preterm infants with high-volume ductal shunt may have preserved upper body perfusion but reduced lower body perfusion. T he clinical significance of shunting through the patent ductus arteriosus in the premature newborn infant remains uncertain (1-4). It is clear that prolonged patency of the ductus arteriosus is seen in preterm infants with respiratory distress (5), and can be associated with significant volume of systemic-to-pulmonary shunting (6). In addition, prolonged ductal patency is associated with a variety of adverse outcomes in preterm infants (7). However, a causative association between ductal shunting and adverse outcome has not been established (8,9), and clinical trials of therapeutic intervention have not demonstrated reductions in morbidity (1). There is increasing awareness that ductal patency may not be a primary pathologic entity but rather an epiphenomenon of prematurity itself (10).Circulatory impact of ductal shunt depends on the volume of shunt and the ability of the myocardium to produce a compensatory increase in left ventricular output (LVO). It has previously been suggested that in the first postnatal days shunt volume through the ductus would be low due to the relatively balanced pulmonary and systemic arterial pressures at this time (11). However, there is now substantial evidence that pulmonary pressure in surfactant treated infants falls rapidly after birth (12,13). High-volume ductal shunt, as evidenced by reversal of blood flow during diastole in the descending aorta (DAo), has been seen as early as 7 h after birth (8), and may occur days before clinical signs appear (5).LVO has been shown to increase with increased ductal shunting in many preterm infants (14). However, it is possible that the immature myocardium has a limited ability to increase output in the first postnatal day (15). The combination of high-volume ductal shunt...

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“…Four of these infants were transferred to our unit from other hospitals for ductal ligation at the age of 21 (15)(16)(17)(18)(19)(20)(21)(22) d. Six additional patients were studied before a ductal L-R shunt was detectable, during symptomatic PDA, and after ligation. The time between ductal closure and LVO measurement (mean * SD) was 2 + 1.9 d. In infants with clinical signs such as systolic murmur, precordial pulsations, and bounding pulses, the PDA was verified by pulsed Doppler examination of the blood flow in the main pulmonary artery.…”

Section: Methodsmentioning

confidence: 99%

Stroke Volume and Left Ventricular Output in Preterm Infants with Patent Ductus Arteriosus

Lindner

Seidel

Versmold³

et al. 1990

Pediatr Res

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ABSTRACT. To assess the effect of patent ductus arteriosus (PDA) on left ventricular output (LVO) we studied stroke volume (SV), LVO, and heart rate (HR) in 21 very low birth wt preterm neonates with clinically symptomatic PDA before and after surgical ligation. Six additional infants were also studied before PDA with left-to-right shunt was detectable by the pulsed Doppler technique. Gestational age (median and range) was 28 (24-32) wk. SV was measured by duplex Doppler and M-mode echocardiography, and LVO was calculated as product of SV and HR. LVO was 419 (305-562) mL/min/kg during symptomatic PDA. It decreased to 246 (191-292) mL/min/ kg after ligation (n = 21, p < 0.001). SV was 2.69 (1.98-4.10) mL/kg during symptomatic PDA decreasing to 1.63(1.22-1.98) mL/kg after ductal closure (n = 21,p < 0.001).HR did not change after ductal closure. In the six infants with three examinations, LVO and SV were normal before detectable ductal left-to-right shunt and after ligation, but LVO was increased by 59.5 2 23% (mean + SD) ( p < 0.05), and SV by 60 + 32% (p < 0.05) during symptomatic PDA. In conclusion, preterm neonates with RDS, requiring mechanical ventilation, increased LVO during symptomatic PDA by increasing their SV, and not by changing their HR. (Pediatr Res 27: 278-281, 1990) Abbreviations AoBFV, aortic blood flow velocity (cm/s) HR, heart rate (bpm) LVO, left ventricular output (mL/min. kg) L-R, left-to-right mBP, mean systemic blood pressure PDA, patent ductus arteriosus RDS, respiratory distress syndrome GA, gestational age SV, stroke vol (mL/kg) LVO is determined by SV and HR. It is well known that neonates can regulate LVO by changing their HR. It has also been stated that newborn infants, because of their low contractile reserve, can increase LVO only by increasing their HR (1, 2). Inasmuch as noninvasive assessment of LVO in neonates by Doppler echocardiography became an established method (3), several reports on LVO in neonates have been published (4-6), but only little information is available on intraindividual changes of SV in preterm neonates (7). PDA, a common problem in Received February 10, 1989; accepted October 19, 1989 preterm neonates with RDS, should be associated with an increased LVO, if PDA is hemodynamically significant. We therefore studied the intraindividual changes of SV, HR, LVO, and mBP in preterm infants with RDS and symptomatic PDA. MATERIALS AND METHODSWe studied 21 preterm neonates with a symptomatic PDA before and after surgical ligation. Four of these infants were transferred to our unit from other hospitals for ductal ligation at the age of 21 (15-22) d. Six additional patients were studied before a ductal L-R shunt was detectable, during symptomatic PDA, and after ligation. The time between ductal closure and LVO measurement (mean * SD) was 2 + 1.9 d. In infants with clinical signs such as systolic murmur, precordial pulsations, and bounding pulses, the PDA was verified by pulsed Doppler examination of the blood flow in the main pulmonary artery. The PDA was considere...

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How a Patent Ductus Arteriosus Effects the Premature Lamb's Ability To Handle Additional Volume Loads

Cited by 25 publications

References 38 publications

Left Ventricular Contractile State of Early Human Neonates with Patent Ductus Arteriosus.

Left Ventricular Contractile State of Early Human Neonates with Patent Ductus Arteriosus.

Does Retrograde Diastolic Flow in the Descending Aorta Signify Impaired Systemic Perfusion in Preterm Infants?

Stroke Volume and Left Ventricular Output in Preterm Infants with Patent Ductus Arteriosus

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