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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. Undulating 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. Key words: fetal anemia, pre-mortem heart rate pattern, pseudo-sinusoidal heart rate pattern, sinusoidal heart rate pattern.
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. Undulating 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. Key words: fetal anemia, pre-mortem heart rate pattern, pseudo-sinusoidal heart rate pattern, sinusoidal heart rate pattern.
On 52 occasions 24 Rh immunized women were monitored with a nonstress test (NST) prior to fetal blood sampling. Cardiotocographic characteristics were recorded for each NST. Fetal blood was analysed for hemoglobin and hematocrit. Fetal hemoglobin and hematocrit were positively correlated to long-term variability, acceleration amplitude and negatively correlated to deceleration amplitude (linear regression analysis; p less than 0.05). Decelerations were almost without exception associated with low concentrations of hemoglobin and hematocrit. In fetuses of 32 weeks' gestation or more, a loss of variability (less than or equal to 5 bpm) was associated with severe anemia. Hemoglobin and hematocrit were significantly lower in the group with a pathological NST (n = 15) compared with the group with a normal NST (n = 37) (Mann-Whitney U test; p less than 0.05). The predictive value of a pathological test was 13/15 concerning hemoglobin and hematocrit; whereas, the predictive value of a normal test was poor. A pathological NST, especially when decelerative, is a good predictor of fetal anemia, but a normal NST is no guarantee for a normal blood status.
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