Sinusoidal heart rate pattern: Reappraisal of its definition and clinical significance

Objectives: To address the clinical significance of sinusoidal heart rate (SHR) pattern and review its occurrence, define its characteristics, and explain its physiopathology. Background: In 1972, Manseau et al. and Kubli et al. described an undulating wave form alternating with a flat or smooth baseline fetal heart rate (FHR) in severely affected, Rh-sensitized and dying fetuses. This FHR pattern was called 'sinusoidal' because of its sine waveform. Subsequently, Modanlou et al. described SHR pattern associated with fetal to maternal hemorrhage causing severe fetal anemia and hydrops fetalis. Both Manseau et al. and Kubli et al. stated that this particular FHR pattern, whatever its pathogenesis, was an extremely significant finding that implied severe fetal jeopardy and impending fetal death. Underlating FHR pattern: Undulating FHR pattern may be due to the following: (1) true SHR pattern; (2) drugs; (3) pre-mortem FHR pattern; (4) pseudo-SHR pattern; and (5) equivocal FHR patterns. Fetal conditions associated with SHR pattern: SHR pattern has been reported with the following fetal conditions: (1) severe fetal anemia of several etiologies; (2) effects of drugs, particularly narcotics; (3) fetal asphyxia/hypoxia; (4) fetal infection; (5) fetal cardiac anomalies; (6) fetal sleep cycles; and (7) sucking and rhythmic movements of fetal mouth. Definition of true SHR pattern: Modanlou and Freeman proposed the following definition for the interpretation of true SHR pattern: (a) stable baseline FHR of 120-160 bpm; (b) amplitude of 5-15 bpm, rarely greater; (c) frequency of 2-5 cycles per minute; (d) fixed or flat short-term variability; (e) oscillation of the sinusoidal wave from above and below a baseline; and (f) no areas of normal FHR variability or reactivity. Physiopathology: Since its early recognition, the physiopathology of SHR became a matter of debate. Murata et al. noted a rise of arginine vasopressin levels in the blood of posthemorrhagic/anemic fetal lamb. Further works by the same authors revealed that with chemical or surgical vagotomy, arginine vasopressin infusion produced SHR pattern, thus providing the role of autonomic nervous system dysfunction combined with the increase in arginine vasopressin as the etiology. Conclusion: SHR is a rare occurrence. A true SHR is an ominous sign of fetal jeopardy needing immediate intervention. The correct diagnosis of true SHR pattern should also include fetal biophysical profile and the absence of drugs such as narcotics

Biochemical and molecular endothelin responses to morphine sulfate infusion in conscious newborn piglets

The biochemical and molecular endothelin-1 (ET-1)responses to high dose morphine sulfate infusion were studied in conscious newborn piglets(n = 6) that received a loading dose of 100 µg/kg over 5 min followed by acontinuous i.v. infusion dose of 100 µg·kg–1·h–1 for 4 h. The controlgroup (n = 6) received equivalent volume loading and infusion doses of 5% dextrose.Blood samples were drawn serially from the femoral artery and sagittal sinus vein before (0),during (30 min, 1, 2, 3, and 4 h), and post (1 and 2 h) infusion. Five micrograms oftotal RNA obtained from brainstem tissue homogenates was analyzed by reverse transcriptase –polymerase chain reaction (RT-PCR). The amounts of mRNA encoding ET-1, and endothelinreceptor subtypes ETA and ETB, were semiquantitated using densitometricscanning. Morphine infusion resulted in elevated respiratory rate and mean arterial bloodpressure, with no effect on arterial pH, PO2, and O2saturation. Compared with the control group, morphine induced significant elevations in plasmaET-1 levels following the bolus dose (systemic: 13.2 ± 3.6 vs. 8.6 ± 2.2 pg/mL, p &lt; 0.05;sagittal sinus vein: 13.7 ± 3.4 vs. 8.2 ± 0.9 pg/mL, p &lt; 0.01). These effects lasted up to2 h after discontinuation of morphine infusion (systemic: 14.5 ± 3.4 to 18.7 ± 5.7 pg/mL vs.7.5 ± 0.8 to 9.4 ± 3.2 pg/mL, p &lt; 0.05 to p &lt; 0.01; sagittal sinus vein: 14.8 ± 2.7to 17.6 ± 2.8 pg/mL vs. 7.5 ± 1.4 to 9.4 ± 3.4 pg/mL, p &lt; 0.05 to p &lt; 0.01). TheRT-PCR assay showed a twofold (p &lt; 0.02) upregulation in ET-1 and a threefold(p &lt; 0.007) upregulation in ETA receptor mRNA expression in the brainstemof morphine-treated animals. In contrast, there was a threefold (p &lt; 0.0001)downregulation of the ETB receptor mRNA expression. The rapid and sustainedelevations in systemic arterial and sagittal sinus venous ET-1 levels suggest a role for ET-1 in themorphine-induced excitatory responses observed in newborn piglets. Upregulation ofETA receptors and downregulation of ETB receptors in the brainstem withhigh doses of morphine may indicate possible effects on cerebral vascular tone. Key words: morphine sulfate, endothelin-1, reverse transcriptase –polymerase chain reaction. </jats:p

Neonatal Manifestations of Maternal Phencyclidine (PCP) Abuse

Two cases concerning newborn infants whose mothers used phencyclidine (PCP) during pregnancy are described. The neonatal symptoms of maternal PCP abuse were jitteriness, hypertonicity, vomiting, and one case of diarrhea. In both infants, PCP was detected in the urine during the first few days of life. Both infants were successfully treated with phenobarbital but they continued to remain jittery and slightly hypertonic following discontinuation of the therapy. In one case the infant was noted to be microcephalic. In the neonate, the symptoms of maternal PCP abuse are similar to the symptoms of narcotic withdrawal. The diagnosis of PCP effects in the neonate can be confirmed by urinalysis for the drug. The teratogenicity of PCP remains a possibility. The metabolism and treatment of PCP effects in the newborn need further clarification.</jats:p