The Ventilatory Response to Carbon Dioxide in Mitral Disease

Respiratory effects of intravenous lobeline in normal subjects and in patients with mitral stenosis.

“…These results resemble the diminished respiratory response of patients with mitral stenosis following CO2 breathing (Pauli et al, 1960;Bruderman et al, 1965). While CO2 breathing induces hyperventilation by a combined stimulatory effect on the respiratory centre and the peripheral chemoreceptors (Heymans et al, 1930), lobeline in small doses, as used in our experiments, produces hyperventilation through stimulation of the peripheral chemoreceptors only (Liljestrand, 1951).…”

“…Reduced responsiveness of the respiratory centre (Pauli, Noe, and Coates, 1960) and/or altered mechnical properties of the lungs are assumed to be responsible for this change (Bruderman, Braun, and Rogel, 1965). The ventilatory response to CO2 inhalation is mediated partly through peripheral chemoreceptors (Heymans, Bouckaert, and Dautrebande, 1930), and the possibility of decreased activity of these receptors in the presence of mitral stenosis has not been investigated.…”

The Mechanism of Cheyne-Stokes Respiration*

“…However, the mild to moderate hypocapnea which has been observed has led to the suggestion that there may be a primary respiratory mechanism that causes cyclic respiration, with hyperexcitability of the center(s) causing intermittent hypocapnea and apnea. One should recall that a mild degree of hypocapnea is found in individuals with chronic circulatory impairment associated with pulmonary venous congestion (18). Since congestive heart failure of some degree with increased pulmonary venous pressure was the hallmark of the patients in the present study, one would expect a lowered average Paco2 in these patients even if cyclic respiration were not present.…”

Effect of Co2 Inhalation on Ventilation and Mechanics of Breathing in Mitral Disease

“…Diminished ventilatory response to CO2 stimulation, as in the emphysematous patients, was also described in patients with mitral valvular disease (Pauli et al, 1960). This similarity was found in spite of the difference in the resting arterial CO2 levels in these two groups of patients.…”

“…This rise is achieved mainly by an increase in tidal volume. Plotting different levels of arterial or alveolar CO2 tensions against corresponding levels of total ventilation results in a stimulus response curve which is linear within the range of physiological stimulation and response (Alexander et al, 1955;Pauli, et al, 1960) (Fig. 3).…”