The fetal heart monitor tracing in pregnancies complicated by a spontaneous umbilical cord hematoma.

The objective of this study is to present and describe the fetal heart rate appearance in pregnancies complicated by an antenatal spontaneous umbilical cord hematoma that resulted in a live birth. Three cases of antenatal spontaneous umbilical cord hematoma are described. All three patients presented with a complaint of decreased fetal movement. The fetal heart monitor tracings on admission are depicted and discussed. In all three cases, the fetal heart rate pattern showed decreased variability with an absence of accelerations. Decelerations were noted but were identified in 25% or less of the contractions and primarily with contractions that exceeded 90 s. Absent accelerations with minimal to absent variability, if caused by uteroplacental insufficiency, usually develop in the presence of recurrent decelerations. Absent accelerations with minimal to absent variability in the absence of recurrent decelerations may suggest other causes including aneuploidy or congenital cardiac or neurologic anomalies. Though rare, spontaneous umbilical cord hematoma can be added to the differential.

Pulmonary hypertension induced with an intra-arterial balloon: an alternate mechanism.

The Laks catheter is a triple-lumen balloon catheter used to distend the canine main pulmonary artery while recording right ventricular pressure and the arterial pressure distal to the balloon. A rise in arterial pressure reported to occur during distension has been attributed to vasoconstriction rather than passive obstruction by the balloon. We tested this in six anesthetized dogs by inflating the Laks catheter-balloon while recording pressure distal to the balloon from the Laks catheter as well as from additional catheters in right and left pulmonary arteries placed retrogradely through lobar branches following thoracotomy. We found that balloon inflation increased pressures in the arterial port of the Laks catheter and in the left pulmonary artery catheter but reduced it in the right pulmonary artery. Tightening a snare around the right pulmonary artery had the same effects on pressures. Similar results were obtained while cardiac output was controlled by left ventricular bypass perfusion in four dogs. We conclude that the Laks catheter-balloon obstructs flow to the right lung and that the arterial pressure rise recorded in it during balloon inflation cannot be distinguished from that caused by occlusion of the right pulmonary artery.

Reversal of reflex pulmonary vasoconstriction induced by main pulmonary arterial distension.

Distension of the main pulmonary artery (MPA) induces pulmonary hypertension, most probably by neurogenic reflex pulmonary vasoconstriction, although constriction of the pulmonary vessels has not actually been demonstrated. In previous studies in dogs with increased pulmonary vascular resistance produced by airway hypoxia, exogenous arachidonic acid has led to the production of pulmonary vasodilator prostaglandins. Hence, in the present study, we investigated the effect of arachidonic acid in seven intact anesthetized dogs after pulmonary vascular resistance was increased by MPA distention. After steady-state pulmonary hypertension was established, arachidonic acid (1.0 mg/min) was infused into the right ventricle for 16 min; 15-20 min later a 16-mg bolus of arachidonic acid was injected. MPA distension was maintained throughout the study. Although the infusion of arachidonic acid significantly lowered the elevated pulmonary vascular resistance induced by MPA distension, the pulmonary vascular resistance returned to control levels only after the bolus injection of arachidonic acid. Notably, the bolus injection caused a biphasic response which first increased the pulmonary vascular resistance transiently before lowering it to control levels. In dogs with resting levels of pulmonary vascular resistance, administration of arachidonic acid in the same manner did not alter the pulmonary vascular resistance. It is concluded that MPA distension does indeed cause reflex pulmonary vasoconstriction which can be reversed by vasodilator metabolites of arachidonic acid. Even though this reflex may help maintain high pulmonary vascular resistance in the fetus, its function in the adult is obscure.

Ventilatory control during experimental maldistribution of VA/Q in the dog.

To determine the role of the peripheral chemoreceptors in mediating the hyperpnea associated with acute, nonocclusive inflation of a balloon in the main pulmonary artery of the conscious dog, we performed balloon inflations in awake and lightly anesthetized (chloralose-urethan) dogs before and after a) bilateral carotid body resection (CBR), b) cervical vagotomy (V), and c) after both CBR and V. In the intact awake state, balloon inflation increased VE from a mean of 4.91 to 7.16 1/min, usually within 1.5-2.0 min. Mean arterial PO2 decreased from 82 to 71 Torr and end-tidal PCO2 was reduced by 6 Torr. Arterial PCO2 and pH were unchanged in the steady state (as evidenced by discrete blood samples), even in those dogs in which VE increased up to 7.5 1/min. However, an indwelling PCO2 electrode in the femoral artery demonstrated a consistent transient elevation of arterial PCO2 prior to the steady state regulation. Vagotomy alone did not impair the ability to regulate PCO2 during balloon inflation. In some cases with CBR alone, arterial PCO2 was regulated at control levels in the steady state, but the transient increase during the early phase of balloon inflation was more marked (mean increase, 2 Torr). We conclude that the peripheral chemoreceptors are responsible for a significant component of the dynamic ventilatory behavior during this early phase (1.5-2.0 min) of acute maldistribution of VA/Q.

Pulmonary arterial hypertension induced by distention of the main pulmonary artery in conscious newborn, young, and adult sheep.

Distention of the main pulmonary artery by balloon inflation in sheep results in presumably reflex elevation of pulmonary arterial pressure and resistance distal to the balloon. This response to main pulmonary artery distention is significantly greater in newborn lambs than in older lambs or adult sheep. In several of the newborn lambs, pulmonary artery pressure was raised to suprasystemic levels. Further, in some of the newborn animals, these increases in pulmonary artery pressure and resistance were sustained after deflation of teh balloon for periods up to 2 hr. The functional significance of this pulmonary hypertension reflex was not elucidated. However, the data strongly suggest that this reflex may contribute to the maintenance of high pulmonary vascular resistance during fetal and early neonatal life.

Experimental pulmonary hypertension produced by surgical and chemical denervation of the pulmonary vasculature.

The purpose of this study was to investigate the hypothesis that balloon distention of the main pulmonary artery (MPA) induces pulmonary hypertension that is produced by a neural reflex and to investigate the possible efferent components of its reflex arc. Using a specially designed triple-lumen balloon catheter, positioned under fluoroscopy in the MPA, the hemodynamic responses to MPA distention were studied before and after the following: surgical denervation of the bifurcation of the MPA, chemical sympathectomy (6-hydroxydopamine), 100 percent oxygen breathing, and vagotomy. Our findings suggest that the experimental pulmonary hypertension caused by distention of the MPA is produced by excitation of stretch receptors in or near the bifurcation of the MPA and that the efferent limb of this reflex is predominantly mediated via the adrenergic nervous system.

Main pulmonary artery distention: a potential mechanism for acute pulmonary hypertension in the human newborn infant.

Balloon-induced distention of the main pulmonary artery causes acute pulmonary hypertension and reflex pulmonary vasoconstriction in animals. Pulmonary artery pressure responses caused by MPA balloon inflation were measured in ten human newborn infants with cardiac failure (n = 5) or persistent fetal circulation (n = 5). During balloon inflation distal mean PAP increased significantly while cardiac rate remained unchanged. MPA distention caused greater increases of PAP in those infants with lower resting PAP. The greatest balloon-induced increases of PAP were observed in infants recovering from PFC. The existence of a pulmonary artery reflex and its possible role in the regulation of the human fetal and neonatal pulmonary circulation is discussed.

Acute pulmonary artery hypertension produced by distention of the main pulmonary artery in the conscious dog.

In order to delineate further the function of the main pulmonary artery as a receptor site, a specially designed Laks triple-lumen balloon catheter was inserted transvenously and positioned in the main pulmonary artery. In six conscious nonsedated dogs, inflation of a balloon in the main pulmonary artery produced acute reversible pulmonary arterial hypertension; the pressure beyond the balloon increased from a mean of 21/6 mm Hg to 43/14 mm Hg (P less than 0,001). This observed pulmonary hypertension occurred at an amount of balloon inflation which produced an increase in right ventricular systolic pressure (P less than 0.001), but no significant change occurred in cardiac output (P greater than 0.05) or right ventricular end-diastolic pressure (P greater than 0.1). Left atrial and pulmonary artery wedge pressures did not change or decreased slightly (P greater than 0.1 and P greater than 0.1, respectively). The calculated pulmonary vascular resistance increased (P less than 0.001), while the calculated systemic vascular resistance did not chang (P greater than 0.04). Therefore, we postulate that distention of the main pulmonary artery in the conscious dog reflexly produces constriction of pulmonary arterioles, and possibly venules, due to excitation of receptors probably located in the wall of the pulmonary artery or possibly the right side of the heart, or both.