1c:I[419806,["/_next/static/chunks/bb923814e1f4d2e9.js","/_next/static/chunks/dd3ee9f5b7716ca6.js","/_next/static/chunks/4204a0ae82542ca8.js","/_next/static/chunks/30036bedc5269936.js","/_next/static/chunks/6e1aa89a642f40be.js","/_next/static/chunks/cd5e572bc3e4eb92.js","/_next/static/chunks/8ffd0b71567920d8.js","/_next/static/chunks/67ea6dfd21f16c5f.js","/_next/static/chunks/24eb4379f68013fd.js","/_next/static/chunks/b8cd775ffdf935bd.js","/_next/static/chunks/983103cd9eb7b428.js","/_next/static/chunks/d4ac9dcf27f6ff52.js","/_next/static/chunks/294b9525248c8e5f.js"],"default"] 1d:T459,The symptom patterns of the hyperventilation syndrome have been recognized for many years.^1-5Some workers have reported abnormal lowering or inversion of the T-wave and, less frequently, depression of the ST segment in the routine electrocardiogram of many patients with this syndrome or with anxiety and emotional instability.^6-13These changes are readily reproduced by voluntary hyperventilation. Several others have observed similar changes of the T-wave in the electrocardiogram of certain normal persons during voluntary hyperventilation.^14,15 The purpose of this report is (1) to describe the electrocardiographic abnormalities during voluntary hyperventilation in 20 patients with the hyperventilation syndrome and the effects of inhalation of CO₂and administration of various drugs in these changes; (2) to present the changes of serum electrolytes, respiratory gases, and pH of the blood in these patients during hyperventilation, with or without inhalation of CO₂; (3) to postulate a possible mechanism for the electrocardiographic changes, and (4)1e:T458,Subjects voluntarily hyperventilated for 10 breaths. A dynamic end-tidal forcing technique manipulated inspired gases to hold end-tidal CO2-O2 tensions at normal values during the voluntary ventilation period and the postvoluntary ventilation recovery period when the subjects returned to spontaneous breathing. Six of the seven subjects studied exhibited a hyperpnea during the recovery period. Although intersubject and intrasubject variations were evident, the average response for 30 experiments in the six subjects was characterized by an initial drop to 32% of the hyperventilation magnitude followed by an exponential-like decrease with a time constant of 22 s. This recovery period response is consistent with theoretical properties of neural network and physical oscillators where there is a persistence in the amplitude response after the removal of the stimulus. Thus, such oscillator properties may govern the respiratory center behavior in man. Furthermore, since isocapnic voluntary ventilation increases cardiac output, the recovery period response may be a consequence of cardiodynamic hyperpnea.

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