Prolonged post-hyperventilation apnea in two young adults with hyperventilation syndrome

Abstract

BackgroundThe prognosis of hyperventilation syndrome (HVS) is generally good. However, it is important to proceed with care when treating HVS because cases of death following hyperventilation have been reported. This paper was done to demonstrate the clinical risk of post-hyperventilation apnea (PHA) in patients with HVS.Case presentationWe treated two patients with HVS who suffered from PHA. The first, a 21-year-old woman, had a maximum duration of PHA of about 3.5 minutes and an oxygen saturation (SpO2) level of 60%. The second patient, a 22-year-old woman, had a maximum duration of PHA of about 3 minutes and an SpO2 level of 66%. Both patients had loss of consciousness and cyanosis. Because there is no widely accepted regimen for treating patients with prolonged PHA related to HVS, we administered artificial ventilation to both patients using a bag mask and both recovered without any after effects.ConclusionThese cases show that some patients with HVS develop prolonged PHA or severe hypoxia, which has been shown to lead to death in some cases. Proper treatment must be given to patients with HVS who develop PHA to protect against this possibility. If prolonged PHA or severe hypoxemia arises, respiratory assistance using a bag mask must be done immediately.

Respiratory dysfunction progresses with age in Kcna1‐null mice, a model of sudden unexpected death in epilepsy

“…Kcna1 À/À mice experience chronic oxygen desaturation, frequent seizures, and A-H, which have been shown to be associated with elevated CO 2 (hypercapnia) and hypoxia. [25][26][27][28] This suggests that chemoresponsive instability may occur in patients prior to SUDEP and if it occurs early, hyperventilation-induced apnea may provide a novel marker of SUDEP risk. 9 A similar breathing sequence of increased breathing rate followed by apnea was detected in Kcna1 À/À mice.…”

“…Hyperventilation-induced apnea has been reported to occur in people with central apnea or respiratory failure. [25][26][27][28] This suggests that chemoresponsive instability may occur in patients prior to SUDEP and if it occurs early, hyperventilation-induced apnea may provide a novel marker of SUDEP risk. F I G U R E 6 Kcna1 mRNA and protein are not present in lung, and do not participate in airway smooth muscle reactivity to MCh.…”

Progressive cardiorespiratory dysfunction in Kv1.1 knockout mice may provide temporal biomarkers of pending sudden unexpected death in epilepsy (SUDEP): The contribution of orexin

“…In the clinical study by Ryvlin et al, the final GTCS‐induced rapid breathing—a response that should trigger blood gas stability, recovery, and survival—triggered apnea, bradycardia, terminal apnea, and asystole . Rapid breathing–induced apnea is a pathological respiratory response attributed in part to blood gas instability, and it occurs in people with central idiopathic apnea, a condition also associated with early mortality . Preclinical SUDEP studies report that after a severe seizure, a fraction of KO mice experience rapid breathing–induced apnea; however, it is not known whether these mice were at low or high risk for sudden death .…”

“…4 Rapid breathing-induced apnea is a pathological respiratory response attributed in part to blood gas instability, and it occurs in people with central idiopathic apnea, a condition also associated with early mortality. 49,50 Preclinical SUDEP studies report that after a severe seizure, a fraction of KO mice experience rapid breathing-induced apnea; however, it is not known whether these mice were at low or high risk for sudden death. 16,20 Herein, we report that this response phenotype was more common in high-risk SD 55 KO mice.…”

Spasmophilia in the Cardiological Outpatient Department: A Retrospective Study of 228 Sub-saharan Africans over 5 Years

“…Apnea and loss of consciousness in patients with HVS have been reported by Munemoto [14], Inagaki [15] and MacDonald [16] and were related to post hyperventilation apnea (PHA). In most cases, patients spontaneously recover from PHA within one or two minutes without any clinical problems, but cases with prolonged PHA was reported as an example of near fatal instance of PHA [16].…”