[CHANGES IN THE ELECTRICAL ACTIVITY OF RESPIRATORY MUSCLES IN CATS DURING COUGHING].
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Maximal force developed by the diaphragm at functional residual capacity is a useful index to establish muscle weakness; however, great disparity in its reproducibility can be observed among reports in the literature. We evaluated five maneuvers to measure maximal transdiaphragmatic pressure (Pdimax) in order to establish best reproducibility and value. Thirty-five naïve subjects, including 10 normal subjects (group 1), 12 patients with chronic obstructive pulmonary disease (group 2), and 13 patients with restrictive pulmonary disease (group 3), were studied. Each subject performed five separate maneuvers in random order that were repeated until reproducible values were obtained. The maneuvers were Mueller with (A) and without mouthpiece (B), abdominal expulsive effort with open glottis (C), two-step (maneuver C combined with Mueller effort) (D), and feedback [two-step with visual feedback of pleural (Ppl) and abdominal (Pab) pressure] (E). The greatest reproducible Pdimax values were obtained with maneuver E (P less than 0.01) (group 1: 180 +/- 14 cmH2O). The second best maneuvers were A, B, and D (group 1: 154 +/- 25 cmH2O). Maneuver C produced the lowest values. For all maneuvers, group 1 produced higher values than groups 2 and 3 (P less than 0.001), which were similar. The Ppl to Pdi ratio was 0.6 in maneuvers A and B, 0.4 in D and E, and 0.2 in C. We conclude that visual feedback of Ppl and Pab helped the subjects to elicit maximal diaphragmatic effort in a reproducible fashion. It is likely that the great variability of values in Pdimax previously reported are the result of inadequate techniques.
The role of the respiratory muscles in the evolution of experimental low cardiac output and lactic acidosis was studied in 2 groups of dogs. One group (6 dogs) was paralyzed and artificially ventilated, and the other (6 dogs) was breathing spontaneously. Shock was induced by cardiac tamponade; cardiac output during shock amounted to 25 to 35% of control values in both groups. All the spontaneously breathing dogs died from ventilatory failure (mean time, 2 h), whereas the artificially ventilated dogs were still alive 3 h after the onset of cardiogenic shock. At any given time after the onset of shock, arterial pH was significantly lower in the spontaneously breathing dogs than in the artificially ventilated ones. This was due to a greater increase in arterial blood lactate in the spontaneously breathing dogs than in the artificially ventilated ones (9.47 +/- 2.7 versus 4.74 +/- 56 mmoles/L at 2 h, respectively). Greater glycogen depletion associated with higher muscle lactate concentrations were found in the respiratory muscles of the spontaneously breathing dogs when compared with that in the artificially ventilated ones. It is concluded that artificial ventilation in cardiogenic shock decreases substantially the severity of lactic acidosis and prolongs survival.
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The effect of methacholine-induced bronchoconstriction on the electrical activity of respiratory muscles during expiration was studied in 12 anesthetized spontaneously breathing dogs. Before and after aerosols of methacholine, diaphragm, parasternal intercostal, internal intercostal, and external oblique electromyograms were recorded during 100% O2 breathing and CO2 rebreathing. While breathing 100% O2, five dogs showed prolonged electrical activity of the diaphragm and parasternal intercostals in early expiration, postinspiratory inspiratory activity (PIIA). Aerosols of methacholine increased pulmonary resistance, decreased tidal volume, and elevated arterial PCO2. During bronchoconstriction, when PCO2 was varied by CO2 rebreathing, PIIA was shorter at low levels of PCO2, and external oblique and internal intercostal were higher at all levels of PCO2. Vagotomy shortened PIIA in dogs with prolonged PIIA. After vagotomy, methacholine had no effects on PIIA but continued to increase external oblique and internal intercostal activity at all levels of PCO2. These findings indicate that bronchoconstriction influences PIIA through a vagal reflex but augments expiratory activity, at least in part, by extravagal mechanisms.