Prolonged QT Interval Corrected for Heart Rate During Diabetic Ketoacidosis in Children: Psychological Stress Could Be Another Explanation

AbstractThere is a consensus that sudden infant death syndrome, the leading cause of mortality in the first year of life, is multifactorial. Most of the cases are probably due to respiratory or cardiac disorders. It has been proposed that some cases of sudden infant death might result from ventricular fibrillation triggered by a sudden increase in sympathetic activity affecting the heart with reduced electrical stability. This impairment can be due to an insufficient or delayed development of cardiac vagal innervation, with the resultant lack of its protective effect that has been demonstrated to be present since the third week of life. Clinical studies suggest that some of the sudden infant death victims may have a reduced heart rate variability that could be interpreted as a decreased parasympathetic activity to the heart. On the other hand, a reduced cardiac electrical stability may be provoked by a developmental imbalance in sympathetic innervation such to create a dominance of left-sided nerves. We have demonstrated that an imbalance of this type experimentally induced in puppies increases the susceptibility to ventricular fibrillation and prolongs QT interval. In order to demonstrate a significant relationship between prolonged QT interval and sudden infant death, we performed a large prospective study on 18,832 neonates. QT interval corrected for heart rate (QTc) measured from an electrocardiogram on the fourth day of life, was within the normal limits in nine victims from known causes, while it was exceeding the mean by two standard deviations (>433 msec) in six of 12 sudden infant death victims. If these data are confirmed by a larger multicenter study started in Italy, it will be possible to identify some of the sudden infant death victims by the observation of a prolonged QT interval on the electrocardiogram. In this case a preventive strategy based on a time-limited administration of beta adrenergic blocking agents to the infants at risk, might reduce the incidence of sudden infant death.

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Changes in left ventricular electromechanical relations during targeted hypothermia

Intensive Care Medicine Experimental ◽

10.1186/s40635-020-00363-7 ◽

2020 ◽

Vol 8 (1) ◽

Author(s):

Kristin Wisløff-Aase ◽

Viesturs Kerans ◽

Kristina Haugaa ◽

Per Steinar Halvorsen ◽

Helge Skulstad ◽

...

Keyword(s):

Heart Rate ◽

Qt Interval ◽

Clinical Importance ◽

Left Ventricular ◽

Peak Strain ◽

Time To Peak ◽

Mechanical Dispersion ◽

Dispersion Of Repolarization ◽

Aortic Valve Closure ◽

Prolonged Qt Interval

Abstract Background Targeted hypothermia, as used after cardiac arrest, increases electrical and mechanical systolic duration. Differences in duration of electrical and mechanical systole are correlated to ventricular arrhythmias. The electromechanical window (EMW) becomes negative when the electrical systole outlasts the mechanical systole. Prolonged electrical systole corresponds to prolonged QT interval, and is associated with increased dispersion of repolarization and mechanical dispersion. These three factors predispose for arrhythmias. The electromechanical relations during targeted hypothermia are unknown. We wanted to explore the electromechanical relations during hypothermia at 33 °C. We hypothesized that targeted hypothermia would increase electrical and mechanical systolic duration without more profound EMW negativity, nor an increase in dispersion of repolarization and mechanical dispersion. Methods In a porcine model (n = 14), we registered electrocardiogram (ECG) and echocardiographic recordings during 38 °C and 33 °C, at spontaneous and atrial paced heart rate 100 beats/min. EMW was calculated by subtracting electrical systole; QT interval, from the corresponding mechanical systole; QRS onset to aortic valve closure. Dispersion of repolarization was measured as time from peak to end of the ECG T wave. Mechanical dispersion was calculated by strain echocardiography as standard deviation of time to peak strain. Results Electrical systole increased during hypothermia at spontaneous heart rate (p < 0.001) and heart rate 100 beats/min (p = 0.005). Mechanical systolic duration was prolonged and outlasted electrical systole independently of heart rate (p < 0.001). EMW changed from negative to positive value (− 20 ± 19 to 27 ± 34 ms, p = 0.001). The positivity was even more pronounced at heart rate 100 beats/min (− 25 ± 26 to 41 ± 18 ms, p < 0.001). Dispersion of repolarization decreased (p = 0.027 and p = 0.003), while mechanical dispersion did not differ (p = 0.078 and p = 0.297). Conclusion Targeted hypothermia increased electrical and mechanical systolic duration, the electromechanical window became positive, dispersion of repolarization was slightly reduced and mechanical dispersion was unchanged. These alterations may have clinical importance. Further clinical studies are required to clarify whether corresponding electromechanical alterations are accommodating in humans.

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