Supraventricular tachycardia with edema, ascites, and hydrops in fetal sheep

Stevens, Dennis C.; Hilliard, Janet K.; Schreiner, Richard L.; Hurwitz, Roger A.; Murrell, Richard; Mirkin, L. David; Bonderman, Pauline; Nolen, Phyllis A

doi:10.1016/0002-9378(82)90737-2

Cited by 36 publications

(8 citation statements)

References 11 publications

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“…We and other investigators have consis tently produced hydrops by increasing the central venous pressure (CVP) in fetal sheep by rapidly pacing the atrium [1][2][3]. Presum ably, the increased CVP raises the microvascular filtration pressure and causes more fluid to be filtered out of the circulation into the interstitium, contributing to edema formation [1].…”

Section: Introductionmentioning

confidence: 99%

“…We contend that edema occurs only when the fluid filtra tion rate exceeds the rate of removal of fluid by the lymphatic system. Accordingly, edema occurs under three conditions: (1) the amount of fluid filtered is so excessive that the lym phatic system is overwhelmed; (2) the lym phatic vessel function itself is impaired, or (3) there is a combination of the two condi tions [4], Experiments by Brace [5] and us [6] have shown that the rate of fetal thoracic duct lymph flow is a function of outflow pressure. In vivo CVP approximates the outflow pres sure of the thoracic duct.…”

Section: Introductionmentioning

confidence: 99%

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Thoracic Duct Lymph Flow in Fetal Sheep with Increased Venous Pressure from Electrically Induced Tachycardia

Gest

Bair²,

Straten³

1993

Neonatology

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The intent of this study was to investigate thoracic duct lymph flow, as it is related to the development of hydrops fetalis during rapid atrial pacing. We studied 6 fetal sheep at 128 ± 6 days of gestation who had chronically placed thoracic duct catheters, aortic and superior vena cava catheters, and atrial pacing electrodes. Atrial pacing at 317 beats/min caused an elevation in central venous pressure from a baseline value of 3 Torr to 7 Torr without affecting pH, arterial blood gas tensions, aortic blood pressure, total protein concentration, or colloid osmotic pressure, although there was a small rise in hematocrit. The thoracic duct lymph flow rate at baseline was 41 ± 6 ml/h. After atrial pacing for 6 h, the lymph flow rate as measured over at least three consecutive 10-min intervals, and presumably the transvascular fluid filtration rate, increased to 67 ± 7 ml/h if it was collected at an outflow pressure of 3 Torr, equal to the venous pressure prior to the onset of atrial pacing. However, if the lymph was collected instead at an outflow pressure of 7 Torr, equal to the actual venous pressure measured with rapid atrial pacing, then the lymph flow rate diminished to 48 ± 5 ml/h. This difference in lymph flow secondary to the increase in venous pressure could account for a maximum of 19 ml/h of edema that accumulates in fetal interstitium and body cavities with atrial pacing. We conclude that the increased venous pressure measured after rapid atrial pacing for 6 h not only increases the transvascular fluid filtration rate, but it also impairs the return of lymph flow to the circulation.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Thoracic Duct Lymph Flow in Fetal Sheep with Increased Venous Pressure from Electrically Induced Tachycardia

Gest

Bair²,

Straten³

1993

Neonatology

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“…Stevens et al [4] induced continuous, su praventricular tachycardia (300 beats/min) by atrial pacing in fetal sheep for 72-216 h. All animals developed signs of congestive heart failure, including ascites, cardiomegaly, cyanotic myocardium, hepatomegaly and generalized edema, and 6 died in útero. There was also a decrease in arterial PO2 and pH and an increase in PCO2, consistent with a failing heart and decreased cardiac output.…”

Section: Discussionmentioning

confidence: 99%

“…Intrauterine supraventricular tachycardia is an infrequent but serious complication of pregnancy, with fetal congestive heart failure developing in 60% of cases [3], Fetal sheep with chronic supraventricular tachycardia induced by pacing developed edema, ascites and hydrops after 72-216 h [4], In pregnan cy, one cause of intrauterine tachycardia is the use of beta-adrenergic tocolytics to stop premature labor. Fetal tachycardia (rates greater than 160 beats/min) has been re ported in 35% of patients treated with isoxsuprine [5] and in 6% treated with the beta-2 selective agent ritodrine [6], Although re lated perinatal morbidity is uncommon, fe tal distress, stillbirths and congestive heart failure have been reported [6][7][8],…”

Section: Introductionmentioning

confidence: 99%

Effects of Isoproterenol-Induced Tachycardia on Myocardial Blood Flow and Glycogen in the Fetal Lamb

Tweed

Davies²,

Alexander³

et al. 1987

Neonatology

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In utero tachycardia is a cause of fetal congestive heart failure and fetal hydrops. We investigated the effects of isoproterenol-induced tachycardia (IIT) on cardiac output and its distribution, on myocardial blood flow and intramyocardial blood flow distribution as well as on regional myocardial glycogen in 8 chronically prepared, near-term fetal lambs and 3 control twins (for myocardial glycogen only). Blood flows were measured by the radioactive microsphere method, myocardial glycogen by an enzymatic method. In animals with IIT (heart rate 200–280), cardiac output (excluding lung flow) increased from 0.399 to 0.544 ml/g/tissue/min (+36%), blood flow to the carcass increased from 0.19 to 0.32 ml/g/tissue/min (+68%) and myocardium increased from 2.31 to 7.72 ml/g/tissue/min (+234%), while kidney blood flow decreased from 1.34 to 0.72 ml/g/tissue/min (––46%). The normal intramyocardial blood flow distribution and predominance of flow to the endocardium of both ventricles was preserved during IIT. In the three sets of twins, glycogen was lower in the right (RV) and left (LV) ventricular walls of each animal stressed by IIT (mean RV = 0.19, mean LV = 0.44) than of its unstressed twin (mean RV = 0.75, mean LV = 0.70). Furthermore, a metabolic acidemia (mean pH 7.21, mean BE -8.4) developed in the stressed animals. Although we were unable to demonstrate regional myocardial ischemia at the maximal fetal heart rates achieved by isoproterenol infusion, our data suggest that metabolic acidemia and myocardial glycogen depletion are consequences of severe inotropic and chronotropic stress in the fetal lamb.

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“…22 Reduction of fetal arterial blood pressure and ventricular output might reduce cerebral blood flow; however, this study did not measure carotid artery flow or calculate cerebral vascular resistance to support this conclusion. Vascular resistance could be significantly reduced in the fetus with rapid pacing; Stevens et al 18 showed an increased PaCO 2 and a decreased PaO 2 with supraventricular tachycardia. Increased arterial PaCO 2 can induce a significant cerebral vasodilatation; thus, cerebral blood flow might not be affected in fe-tuses with reduced aortic pressure.…”

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confidence: 99%

Left Atrial Tachyarrhythmia in Fetal Lambs

Shiraishi

Kikuchi

Hoshina

et al. 2002

Pacing Clinical Electrophis

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To evaluate the hemodynamic effect of rapid left atrial pacing on fetal circulation, a fetal supraventricular tachyarrhythmia model was made and the aortic pressure, central venous pressure, and left and right ventricular outputs were measured in ten fetal lambs. Under maternal anesthesia, the uterus was opened, and under local anesthesia, catheters were inserted into thefetal superior vena cava and ascending aorta through a neck incision. Pacing leads were then sutured onto the fetal left atrial appendage via left thoracotomy. Ventricular output was estimated using echocardiography by a transuterine approach. Fetal hemodynamics were observed without pacing (control), and at the pacing rates of 200, 300, 350, and 400/min. The aortic pressure decreased when the left atrium was paced at 300/min or more and the central venous pressure increased when the left atrium was paced at 350/min or more. The left and right ventricular outputs decreased when the left atrium was paced at 350/min or more. The left ventricular output was 215+/-54 mL/kg per minute at control, 205+/-60 mL/kg minute when paced at 200/min, 178+/-58 mL/kg per minute when paced at 300/min, but decreased to 164+/-44 mL/kg per minute when paced at 350/min and to 149+/-57 mL/kg per minute when paced at 400/min. The right ventricular output was 338+/-66 mL/kg per minute at control, 336+/-95 mL/kg per minute when paced at 200/min, 273+/-91 mL/kg per minute when paced at 300/min, but decreased to 256+/-80 mL/kg per minute when paced at 350/min and to 202+/-76 mL/kg per minute when paced at 400/min. Fetal circulatory failure was initially confirmed when the left atrium was paced at 300/min in this left atrial tachyarrhythmia model.

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Supraventricular tachycardia with edema, ascites, and hydrops in fetal sheep

Cited by 36 publications

References 11 publications

Thoracic Duct Lymph Flow in Fetal Sheep with Increased Venous Pressure from Electrically Induced Tachycardia

Thoracic Duct Lymph Flow in Fetal Sheep with Increased Venous Pressure from Electrically Induced Tachycardia

Effects of Isoproterenol-Induced Tachycardia on Myocardial Blood Flow and Glycogen in the Fetal Lamb

Left Atrial Tachyarrhythmia in Fetal Lambs

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