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PubMed1998

The development of hyperventilation in patients with chronic heart failure and Cheyne-Strokes respiration: a possible role of chronic hypoxia.

AIM: To analyze the relationship between daytime respiratory and cardiac function in patients with compensated chronic heart failure (CHF) with and without periodic breathing (PB) or Cheyne-Stokes respiration (CSR). PATIENTS: We studied 132 patients (female, 13%; mean age, 53+/-8 years; body mass index, 25.9+/-3.5 kg/m2; left ventricular ejection fraction <40%; 23% in New York Heart Association class I, 43% in class II, and 34% in class III-IV). METHODS: Measurement of pulmonary function and blood gases, hemodynamic evaluation, analysis of breathing profile, echocardiography, recording of ECG, beat-to-beat arterial oxygen saturation, and respiration during spontaneous breathing. RESULTS: Fifty-eight percent of patients showed PB or CSR. Patients with PB or CSR have greater cardiac function impairment. Mean values of lung volumes and PaO2 were similar in the three groups of patients considered. In contrast, patients with PB or CSR had an increased minute ventilation and reduced PaCO2 values. Interestingly, patients with PB or CSR had lower values of arterial content of O2 and systemic oxygen transport (SOT) than patients with a normal breathing pattern (SOT, 394+/-9.8, 347+/-9.6, 438+/-11 mL of O2/min/m2, respectively; analysis of variance p<0.001). Weak correlations were found among lung volumes, blood gases, and cardiac function parameters: ie, vital capacity was correlated inversely with pulmonary capillary wedge pressure (PCWP) (-0.25; p<0.05); PaCO2 with PCWP (r=0.26; p<0.05), lung-to-ear circulation time (LECT) (r=-0.4; p<0.05), SOT (r=-0.33; p<0.0001), and cardiac index (CI) (r=0.27; p=0.003). Multiple regression analyses showed that arterial PCO2 was significantly correlated with SOT, LECT, and CI (r=0.51; r2=0.26; p<0.000001); the correlation became stronger considering only CSR patients (r=0.64; r2=0.4; p<0.001). CONCLUSIONS: Our study shows that patients with daytime breathing disorders have chronic hypocapnia. A reduced SOT may be one of the stimuli determining increased minute ventilation in these patients.

Cheyne-Stokes Respiration↗
PubMed2002

Effects of hypocapnic hyperventilation on the response to hypoxia in normal subjects receiving intermittent positive-pressure ventilation.

OBJECTIVE: To confirm the hypothesis that the ventilatory response to hypoxia (VRH) may be abolished by hypocapnia. METHODS: We studied four healthy subjects during intermittent positive-pressure ventilation delivered through a nasal mask (nIPPV). Delivered minute ventilation (Ed) was progressively increased to lower end-tidal carbon dioxide pressure (PETCO(2)) below the apneic threshold. Then, at different hypocapnic levels, nitrogen was added to induce falls in oxygen saturation, a hypoxic run (N(2) run). For each N(2) run, the reappearance of a diaphragmatic muscle activity and/or an increase in effective minute ventilation (E) and/or deformations in mask-pressure tracings were considered as a VRH, whereas unchanged tracings signified absence of a VRH. For the N(2) runs eliciting a VRH, the threshold response to hypoxia (TRh) was defined as the transcutaneous oxygen saturation level that corresponds to the beginning of the ventilatory changes. RESULTS: Thirty-seven N(2) runs were performed (7 N(2) runs during wakefulness and 30 N(2) runs during sleep). For severe hypocapnia (PETCO(2) of 27.1 +/- 5.2 mm Hg), no VRH was noted, whereas a VRH was observed for N(2) runs performed at significantly higher PETCO(2) levels (PETCO(2) of 34.0 +/- 2.1 mm Hg, p < 0.001). Deep oxygen desaturation (up to 64%) never elicited a VRH when the PETCO(2) level was < 29.3 mm Hg, which was considered the carbon dioxide inhibition threshold. For the 16 N(2) runs inducing a VRH, no correlations were found between PETCO(2) and TRh and between TRh and both Ed and E. CONCLUSION: During nIPPV, VRH is highly dependent on the carbon dioxide level and can be definitely abolished for severe hypocapnia.

Adult↗