Randomised trial of cardiotocography alone or with ST waveform analysis for intrapartum monitoring

Westgate, Jenny A.; Harris, Maureen I.; Curnow, John; Greene, Kate

doi:10.1016/0140-6736(92)90465-f

Cited by 87 publications

(53 citation statements)

References 20 publications

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“…During bradycardia, there were variable changes in the ECG wave forms. Several previous clinical and experimental studies have observed increases in the T wave during acute fetal hypoxemia and asphyxia (16,17). These changes have been attributed to anaerobic myocardial metabolism (18).…”

Section: Discussionmentioning

confidence: 98%

Repeated Episodes of Umbilical Cord Occlusion in Fetal Sheep Lead to Preferential Damage to the Striatum and Sensitize the Heart to Further Insults

et al. 1995

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The effect of repeated episodes of asphyxia on the fetal cardiovascular system and CNS was examined. The umbilical cord was occluded for 5 min, four times, at 30-min intervals in 11 chronically instrumented fetal sheep (118-126 d). Fetal electrocorticogram (ECoG), cortical impedance, ECG, heart rate, and blood pressure were continuously recorded for 3 d, after which neuronal loss was determined histologically. Each occlusion resulted in fetal hypoxemia and bradycardia accompanied by increased TIQRS ratio. Progressively severe hypotension and lactic acidosis developed during successive occlusions. The ECoG was depressed and cortical impedance increased with each occlusion. During the final occlusion, blood pressure fell to 3.5 -C 1 kPa and heart rate to 93 + 9 bpm, TIQRS ratio increased to 0.44 + 0.3, and lactate rose to 7.2 2 1.2 mMIL. Three animals died from cardiac fibrillation during recirculation after the third or fourth occlusion. After the asphyxial episodes, blood pressure and heart rate returned to normal, and the T wave was inverted for 310 + 155 min. Lactate returned to baseline within 24 h. The ECoG remained depressed for 90 + 35 min, and intermittent Prenatal asphyxia is thought to be a cause of intrauterine death or impaired postnatal neurologic development in survivors. However, specific cause and effect relationships have been difficult to establish in the human fetus because of inadequate means of monitoring fetal events. W e have previously shown that repeated episodes of cerebral ischemia in the fetal sheep alter the degree and distribution of brain injury compared with single insults (1). In particular, these repeated insults result in the loss of striatal neurons.Intermittent partial umbilical cord occlusion has been reported to cause cerebral white matter injury in fetal sheep (2). Others seizures developed at 3.3 -C 1.4 h after the last occlusion. Neuronal loss was primarily found in the striatum. The extent of neuronal loss correlated with the degree of hypotension, increase in T/QRS ratio, duration of postasphyxial ECoG depression, and number of seizures. These results indicate that transient asphyxial episodes compromise the ability of the heart to tolerate additional insults and further suggest that neuronal loss is a consequence of cardiovascular compromise secondary to asphyxia. Therefore, repetitive asphyxial episodes may lead to intrauterine death or striatal damage in survivors. (Pediatr Res 37: 707-713, 1995) Abbreviations ECoG, electrocorticogram CI, cortical impedance HR, heart rate MAP, mean arterial blood pressure GABA, y-amino butyric acid have shown increasing acidosis and electrocardiographic evidence of asphyxia during repeated umbilical cord occlusions (3). However, the relationship between cardiac function, cerebral function, and neuronal loss after recurrent episodes of fetal asphyxia is not clear. W e have previously shown that systemic asphyxia induced by umbilical cord occlusion in fetal sheep results in hippocampal injury, the severity of which is related to th...

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Section: Discussionmentioning

confidence: 98%

Repeated Episodes of Umbilical Cord Occlusion in Fetal Sheep Lead to Preferential Damage to the Striatum and Sensitize the Heart to Further Insults

et al. 1995

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“…It is thus important to identify compromised infants as early as possible in labor. The presence of elevation of the ST segment of the fetal ECG, typically measured relative to the QRS complex (the T/QRS ratio), is a marker for the development of fetal metabolic acidosis in clinical and experimental studies (1,2,19,35,43). The relationship between ST segment changes and fetal compromise is complex (40); however, there is some evidence that preexisting hypoxia can enhance the rise in T/QRS ratio and affect ST waveform shape during subsequent insults (39, 45).…”

mentioning

confidence: 99%

Preexisting hypoxia is associated with a delayed but more sustained rise in T/QRS ratio during prolonged umbilical cord occlusion in near-term fetal sheep

Wibbens

Westgate²,

Haan³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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There is limited information about whether preexisting fetal hypoxia alters hemodynamic responses and changes in T/QRS ratio and ST waveform shape during subsequent severe asphyxia. Chronically instrumented near-term sheep fetuses (124 +/- 1 days) were identified as either normoxic Pa(O(2)) > 17 mmHg (n = 9) or hypoxic Pa(O(2)) < or = 17 mmHg (n = 5); then they received complete occlusion of the umbilical cord for 15 min. Umbilical cord occlusion led to sustained bradycardia, severe acidosis, and transient hypertension followed by profound hypotension in both groups. Preexisting hypoxia did not affect changes in mean arterial blood pressure but was associated with a more rapid initial fall in femoral blood flow and vascular conductance and with transiently higher fetal heart rate at 2 min and from 9 to 11 min of occlusion compared with previously normoxic fetuses. Occlusion was associated with a significant but transient rise in T/QRS ratio; preexisting hypoxia was associated with a significant delay in this rise (maxima 3.7 +/- 0.4 vs. 6.2 +/- 0.5 min), but a slower rate of fall. There was a similar elevation in troponin-T levels 6 h after occlusion in the two groups [median (range) 0.43 (0.08, 1.32) vs. 0.55 (0.16, 2.32) microg/l, not significant]. In conclusion, mild preexisting hypoxia in normally grown singleton fetal sheep is associated with more rapid centralization of circulation after umbilical cord occlusion and delayed elevation of the ST waveform and slower fall, suggesting that chronic hypoxia alters myocardial dynamics during asphyxia.

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“…Additional studies are required to evaluate whether ultrasonographic assessment of the left ventricular contraction pattern could provide diagnostic information in utero [7]. During labor fetal ECG and ST waveform anal- ysis may help to identify LQTS and imminent potentially lethal arrhythmias [12]. In the presence of unexplained irregular fetal heart rate, LQTS should be considered as a possible underlying disorder.…”

Section: Discussionmentioning

confidence: 99%

Perinatal manifestations of idiopathic long QT syndrome

et al. 1996

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A neonate who had presented with sustained irregular heart rate during labor was found to have QT prolongation and repetitive polymorphic ventricular tachycardia (torsades de pointes) postnatally. Propranolol and propafenone successfully controlled the ventricular arrhythmias. Follow-up electrocardiograms and Holter records show persistent QT prolongation, bizarre T waves, and intermittent episodes of T wave alternans. On propranolol monotherapy the boy is thriving and completely free of ventricular arrhythmias. In the rare case of long QT syndrome in the neonate, early detection and therapy are mandatory to prevent ventricular arrhythmias and sudden death.

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Randomised trial of cardiotocography alone or with ST waveform analysis for intrapartum monitoring

Cited by 87 publications

References 20 publications

Repeated Episodes of Umbilical Cord Occlusion in Fetal Sheep Lead to Preferential Damage to the Striatum and Sensitize the Heart to Further Insults

Repeated Episodes of Umbilical Cord Occlusion in Fetal Sheep Lead to Preferential Damage to the Striatum and Sensitize the Heart to Further Insults

Preexisting hypoxia is associated with a delayed but more sustained rise in T/QRS ratio during prolonged umbilical cord occlusion in near-term fetal sheep

Perinatal manifestations of idiopathic long QT syndrome

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