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Ventilatory response to CO 2 in patients with epilepsy
Author(s) -
Sainju Rup K.,
Dragon Deidre N.,
Winnike Harold B.,
Nashelsky Marcus B.,
Granner Mark A.,
Gehlbach Brian K.,
Richerson George B.
Publication year - 2019
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/epi.14660
Subject(s) - medicine , anesthesia , hypercapnia , tidal volume , respiratory minute volume , ictal , respiratory rate , epilepsy , ventilation (architecture) , hypoventilation , respiratory system , heart rate , blood pressure , acidosis , mechanical engineering , psychiatry , engineering
Summary Objective Severe periictal respiratory depression is thought to be linked to risk of sudden unexpected death in epilepsy ( SUDEP ) but its determinants are largely unknown. Interindividual differences in the interictal ventilatory response to CO 2 (hypercapnic ventilatory response [ HCVR ] or central respiratory CO 2 chemosensitivity) may identify patients who are at increased risk for severe periictal hypoventilation. HCVR has not been studied previously in patients with epilepsy; therefore we evaluated a method to measure it at bedside in an epilepsy monitoring unit ( EMU ) and examined its relationship to postictal hypercapnia following generalized convulsive seizures ( GCS s). Methods Interictal HCVR was measured by a respiratory gas analyzer using a modified rebreathing technique. Minute ventilation ( V E ), tidal volume, respiratory rate, end tidal ( ET ) CO 2 and O 2 were recorded continuously. Dyspnea during the test was assessed using a validated scale. The HCVR slope (Δ V E /ΔETCO 2 ) for each subject was determined by linear regression. During the video–electroencephalography ( EEG ) study, subjects underwent continuous respiratory monitoring, including measurement of chest and abdominal movement, oronasal airflow, transcutaneous (tc) CO 2 , and capillary oxygen saturation ( SPO 2 ). Results Sixty‐eight subjects completed HCVR testing in 151 ± (standard deviation) 58 seconds, without any serious adverse events. HCVR slope ranged from −0.94 to 5.39 (median 1.71) L/min/mm Hg. HCVR slope correlated with the degree of unpleasantness and intensity of dyspnea and was inversely related to baseline ETCO 2 . Both the duration and magnitude of postictal tc CO 2 rise following GCS s were inversely correlated with HCVR slope. Significance Measurement of the HCVR is well tolerated and can be performed rapidly and safely at the bedside in the EMU . A subset of individuals has a very low sensitivity to CO 2 , and this group is more likely to have a prolonged increase in postictal CO 2 after GCS . Low interictal HCVR may increase the risk of severe respiratory depression and SUDEP after GCS and warrants further study.

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