Limited Left Ventricular Response to Volume Overload in the Neonatal Period: a Comparative Study with the Adult Animal

Romero, Tomás; Friedman, William F.

doi:10.1203/00006450-197908000-00008

Cited by 154 publications

(63 citation statements)

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“…The saline infusion in preterm lambs with closed ductus produced a significant increase in stroke volume. The response differed from that observed in lamb fetuses at the same gestational age (8)(9)(10)(11)(12), but was similar to that seen in full-term newborn (6) and I-wk-old lambs (3)(4)(5)7). Although a Frank-Starling relationship has been demonstrated in the fetal lamb (28), challenging the fetus with a volume load only modestly increases stroke volume above baseline measurements (8)(9)(10)(11)(12).…”

Section: Discussionmentioning

confidence: 53%

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

et al. 1987

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ABSTRACT. A model of patent ductus arteriosus in premature lambs was created to examine the lamb's ability to handle the volume load imposed by a patent ductus arteriosus and to determine the lamb's ability to handle any additional volume load. Fifteen preterm lambs I133 -C 2 ( 2 SD) days gestation, term 145 days], whose ductal diameter could be regulated with a mechanical occluder, were studied to determine the independent effects of ductus patency and a saline volume load (50 ml/kg over 3 min) on left ventricular output and its distribution. During a saline infusion, preterm lambs with a closed ductus could only increase their stroke volume by 40% above baseline stroke volume. When challenged with a saline infusion, lambs with an open ductus still were able to increase their stroke volume significantly; the maximal increase in stroke volume during the saline load with the ductus open was 70% above baseline stroke volume. W e hypothesize that the associated reduced left ventricular afterload plays a significant role in the preterm lamb's ability to increase its stroke volume when challenged with a patent ductus arteriosus. Even with a patent ductus arteriosus, the lamb still has the ability to handle additional volume loads. (Pediatr Res 22: 531-535, 1987) Abbreviations PDA, patent ductus arteriosus LV, left ventricle QLV, left ventricular output Q pulmonary, pulmonary blood flow Q ductus, ductus arteriosus blood flow Q systemic, systemic blood flow R pulmonary, pulmonary vascular resistance R systemic, systemic vascular resistance R ductus, ductus arteriosus resistance R total, total resistance Hbg, hemoglobin GI, gastrointestinalThe PDA represents a significant stress on the premature cardiovascular system. The extent of this stress depends both on the magnitude of the left to right shunt through the PDA and on the ability of the cardiovascular system to adjust to that shunt. Full-term newborn lambs respond to volume loading with a limited increase in stroke volume, compared with adult sheep. The left ventricle of the full-term newborn lamb is capable of developing greater force than the left ventricle of the preterm lamb (with closed ductus) at comparable filling volume and resistance (6). Several studies have shown that the fetal lamb has a limited ability to increase its stroke volume above its baseline value during an acute volume load (8-12).The limited ability of the developing left ventricle to increase its output during a volume load is caused by some degree of myocardial immaturity (13) as well as by the high resting output needed to supply the demand for oxygen after delivery (14). The high resting level of performance demanded of the newborn heart may exhaust any reserve pumping capacity. The purpose of our study was both to examine the premature lamb's ability to handle the volume load imposed by a PDA and to see how the presence of a PDA alters the lamb's ability to tolerate any additional volume load. METHODSPreparafion. Fifteen mixed breed western time-dated pregnant ewes at 128-133 days ge...

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Section: Discussionmentioning

confidence: 53%

“…Perhaps this increase in contractility when the ductus is open persists during the volume infusion and plays a role in the increased output observed during that condition. However, other studies in adult and newborn animals have not demonstrated an increase in left ventricular contractility during a volume infusion (5,6,30).…”

Section: Discussionmentioning

confidence: 97%

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

et al. 1987

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“…1A). Furthermore, the neonatal LV has a smaller twist amplitude coupled with slower and delayed untwisting when compared with older children and adults (23), which may reduce the contribution of LV untwisting/suction to early diastolic filling.Invasive animal studies that have explored the functional maturation of the neonatal LV within the first weeks of life (4, 27, 30), including its response to preload (2,19,28), also support the current assumption that the neonatal LV may have relatively less diastolic reserve when faced with altered loading conditions. The impact of atrial tachycardia on neonatal LV function, a common finding in the critically ill neonate, and a state that is poorly tolerated by the more mature heart with diastolic dysfunction in part as tachycardia reduces diastolic filling time (36), has been minimally examined.…”

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confidence: 90%

Postnatal neonatal myocardial adaptation is associated with loss of tolerance to tachycardia: a simultaneous invasive and noninvasive assessment

Fortin-Pellerin

Khoo

Mills

et al. 2016

American Journal of Physiology-Heart and Circulatory Physiology

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Fortin-Pellerin E, Khoo NS, Mills L, Coe JY, Serrano-Lomelin J, Cheung PY, Hornberger LK. Postnatal neonatal myocardial adaptation is associated with loss of tolerance to tachycardia: a simultaneous invasive and noninvasive assessment. Am J Physiol Heart Circ Physiol 310: H598 -H607, 2016. First published December 30, 2015; doi:10.1152/ajpheart.00595.2015-Doppler studies at rest suggest left ventricular (LV) diastolic function rapidly improves from the neonate to infant. Whether this translates to its response to hemodynamic challenges is uncertain. We sought to explore the impact of early LV maturation on its ability to tolerate atrial tachycardia. As tachycardia reduces filling time, we hypothesized that the neonatal LV would be less tolerant of atrial tachycardia. Landrace cross piglets of two age groups (1-3 days; NPs; 14 -17 days, YPs; n ϭ 7/group) were instrumented for an atrial pacing protocol (from 200 to 300 beats/min) and assessed by invasive monitoring and echocardiography. NPs maintained their LV output and blood pressure, whereas YPs did not. Although negative dP/dt in NPs at baseline was lower than that of YPs (Ϫ1,599 Ϯ 83 vs. Ϫ2,470 Ϯ 226 mmHg/s, respectively, P ϭ 0.007), with increasing tachycardia negative dP/dt converged between groups and was not different. Both groups had similar preload reduction during tachycardia; however, NPs maintained shortening fraction while YPs decreased (NPs: 35.4 Ϯ 1.4 vs. 31.8 Ϯ 2.2%, P ϭ 0.35; YPs: 31.4 Ϯ 0.8 vs. 22.9 Ϯ 0.8%, P Ͻ 0.001). Contractility measures did not differ between groups. Peak LV twist and untwisting rate also did not differ; however, NPs tended to augment LV twist through increased apical rotation and YPs through increasing basal rotation (P ϭ 0.009). The NPs appear more tolerant of atrial tachycardia than the YPs. They have at least similar diastolic performance, enhanced systolic performance, and different LV twist mechanics, which may contribute to improved tachycardia tolerance of NPs. HEMODYNAMIC MANAGEMENT OF the critically ill term newborn is complex. Understanding the functional nature of the neonatal myocardium and how it evolves through the first few weeks and months after birth is key to optimizing care. Although many authors have provided their opinions regarding clinical management strategies (1, 12, 32), more translational and clinical studies are needed to provide insight into the functional capacity of the early postnatal heart. In particular, changes in diastolic reserve during the first few weeks and months of life in relation to the known disproportionate left ventricular (LV) growth (3, 27) have been poorly explored.In human infants, most of our understanding of the evolution of diastolic function has been derived from noninvasive Doppler-based studies (16,26,31). These investigations have suggested that the neonatal LV myocardium has less robust diastolic relaxation (16) with greater dependency on atrial contraction for filling, much like that of the diseased adult heart with diastolic dysfunction (15). In the first few mo...

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“…Consequently, its output need not be as high as that of the newborn left ventricle (1)(2)(3)(4). At birth, when oxygen demand increases dramatically and the systemic and pulmonary circulations separate, left ventricular output increases threefold (5)(6)(7)(8)(9)(10)(11)(12). However, studies performed in sheep suggest that the fetal left ventricle is incapable of increasing its output anywhere near levels seen in the newborn; maximal increases are less than 50% above control in response to increases in preload (13) or heart rate (14,15), or during {J-adrenergic stimulation (16).…”

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confidence: 99%

In Utero Ventilation Augments the Left Ventricular Response to Isoproterenol and Volume Loading in Fetal Sheep

et al. 1991

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The basis of this limitation in the ability of the fetal left ventricle to greatly increase output (systolic performance) is controversial. Several studies point to myocardial immaturity: incomplete development of sarcomeres (17-21), decreased functioning of {J-receptors (22, 23), and myofibrillar disarray (24,25) have all been implicated. Although fetal myocardium is certainly immature relative to that of the adult, none of these factors have been shown to change immediately at birth. In addition, many indices of systolic performance are increased in the newborn left ventricle relative to that of the adult (11,12), so that myocardial immaturity may not necessarily be associated with impaired ventricular function. It is remarkable that both the prematurely born animal (26-28) and human (29), which have not been exposed to prenatal hormone surges and labor to accelerate myocardial maturation, are capable of greatly increasing left ventricular output in response to a patent ductus arteriosus. In addition, recent studies of fetal sheep undergoing oxygen ventilation in utero have shown a doubling of left ventricular output (3,30), and other determinants of output such as septal compliance (31) have been shown to change in the perinatal period.Thus, left ventricular output may be limited in the fetus more because of its "circulatory environment" (the combination of a parallel circulation with central shunts, a dominant hypertrophied right ventricle that ejects more output and fills under similar pressures, a pulmonary vascular bed that is markedly constricted and that returns a very limited amount of blood to the left atrium and ventricle, and a highly compliant fetoplacental vascular bed that can absorb increases in volume that would otherwise increase left ventricular filling volume) than because of myocardial immaturity. For example, the fetal left ventricle has a very limited ability to increase output via the Frank-Starling mechanism (13), with a plateau occurring at 5-7 mm Hg. However, Hawkins et at.(32) have shown that some of this limitation is caused by a concomitant increase in afterload; if afterload is controlled, left ventricular output continues to rise at filling pressures of 10 mm Hg. In addition, high right ventricular filling and ejecting pressures may constrain left ventricular performance both in diastole and systole (33-36).We undertook the present study to determine whether the near-term (approximately 0.9 gestation) fetal left ventricle, functioning in a simulated "postnatal circulatory environment" (abolition of most central shunts with a small left to right shunt through the ductus arteriosus, a dominant left ventricle ejecting somewhat more blood than the right under higher filling pressures, a dilated pulmonary vascular bed returning a large amount of blood to the left atrium and ventricle, and a decrease in the fetoplacental vascular bed), is capable of increasing its output to levels similar to those seen in the newborn. We simulated the immediate postnatal circulatory environment in ute...

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Limited Left Ventricular Response to Volume Overload in the Neonatal Period: a Comparative Study with the Adult Animal

Abstract: Cardiac dimensions fetus cardiac function newborn cardiac output ventricular compliance

Cited by 154 publications

References 7 publications

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

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

Postnatal neonatal myocardial adaptation is associated with loss of tolerance to tachycardia: a simultaneous invasive and noninvasive assessment

In Utero Ventilation Augments the Left Ventricular Response to Isoproterenol and Volume Loading in Fetal Sheep

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