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November 1992

Acute Intracranial Lesions and Respiratory Sinus Arrhythmia

Author Affiliations

From the Neuromedical/Neurosurgical Intensive Care Unit, Massachusetts General Hospital, Boston, and the Neurology Division, St Elizabeth's Hospital, Boston, Mass. Dr Frank is now with the Departments of Neurosurgery and Neurology, The Cleveland (Ohio) Clinic Foundation.

Arch Neurol. 1992;49(11):1200-1203. doi:10.1001/archneur.1992.00530350122028

• We studied the effects of acute intracranial lesions on the respiratory sinus arrhythmia (RSA) with the use of computerized measurements of the ratio of expiratory to inspiratory R-R intervals. The RSA was reduced below the 95th percentile for age in 20 of 27 patients, an average of 2 days after an acute event. Only four patients, without neurological deficits, had a normal RSA. Two patients, with signs of secondary brain-stem compression from a mass, had an increased RSA, without the bradycardia that is usually associated with Cushing's response. Twenty-three patients had their respiratory rate controlled by positive pressure ventilation during testing, and our preliminary findings suggested that this was not responsible for reducing the RSA. Acute intracranial lesions cause a diminished RSA, perhaps by reducing supratentorial influences on vagal cardioinhibitory activity. In contrast, once signs of secondary brain-stem compression occur, the RSA is greatly increased while the heart rate remains unchanged, offering a possible method of noninvasive monitoring for this complication.

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