Our study brings out the following two important findings: (1) on patients with COPD disconnected from mechanical ventilation and showing no sign of respiratory failure within two hours, the values of Vmin, VtAR, P01, pH, Pa02, and PaC02 did not provide any clue as to the final success or failure of medium-term weaning (ten hours); and (2) due to the low value of the Pdimax, the Pdi/Pdimax ratio was higher on the group that failed to be weaned within ten hours. In addition, that same group showed a negative Pga in 16/19 trials, which never occurred in the other group.
In a previous paper, we showed that the patients who had to be reconnected to mechanical ventilation within ten hours showed no initial difference in their breathing pattern compared with the others. Only later, and particularly after two hours, did changes occur that suggested a quicker deterioration of the pulmonary mechanical condition. On the present study, the differences between our groups after two hours were not really significant except for a shorter TVTtot ratio (p<0.01), a result probably due to a central type adaptation to compensate for the imposed extraload. On the contrary, the signs of diaphragmatic dysfunction occur earlier and are easily exposed, but their meaning is less clear.
The Pdi, ie, the difference between abdominal and pleural pressures, is a measure of diaphragmatic efficiency but needs a good technique in order to avoid misinterpretation; the Pga may be increased by the contraction of abdominal muscles: we took great care of our patients’ total relaxation during measurements, and only the inspiratory values of Pga and Pdi were recorded. Besides, evaluation of results is quite difficult in COPD patients because of airway obstruction and distension. Obstruction causes a lapse between swings in Ppl and Pga and measuring Pdi as the difference between the maximal values gives a wrong result. The error was lessened in our study as we recorded Pdi in real-time and measurements were made simultaneously. Distention reduces Pdi because of a flattening diaphragm with shortened fibers, so that it works on an ineffective portion of its length-tension curve. Therefore, Pdi may be underestimated, not only because of its volume-dependent character, but also because of the shape of the diaphragm. Moreover, Pdi varies over a wide range among individuals, a variation not related to fatigue but to a strong recruitment of the intercostal and accessory inspiratory muscles. For that reason, the Pdi was brought to the level of the Pdimax evaluated during a maximal inspiratory maneuver (Mueller), the patient receiving, on a monitor, visual feedback of the effort developed. This method turned out to be the surest and the most easily reproducible.
In our study, the group who had to be connected again to mechanical ventilation within ten hours showed a low Pdi and a still lower Pdimax; the values were even lower at the end of the weaning period, which may be due to such factors as decrease in central respiratory drive, diaphragm atrophy, hyperinflation, or alteration of the contractility. All publications about pharmacy and diseases you may find if you check out the website of Canadian Neighbor Pharmacy.
A central depression cannot be held responsible because of the high level of P01 recorded in both groups. Besides, this has been confirmed by other workers studying acute respiratory failure in the COPD patient. Diaphragm atrophy may arise in patients submitted to prolonged mechanical ventilation. That may account for the initial reduction of Pdimax, and therefore, the increased ratio of Pdi/ Pdimax, but however true for certain patients, this could not explain the differences between our two groups which were not that different in regard to the average duration of mechanical ventilation and the nutritional status. Moreover, a given patient may change groups within 24 hours, and his diaphragm condition would probably not undergo a drastic change in so short a delay.
A different level of pulmonary hyperinflation for each group would be a much more plausible theory but difficult to confirm without a direct measurement of the functional residual capacity. Intermittent positive pressure ventilation is, in itself, a cause of hyperinflation which may be aggravated by weaning, especially in COPD patients for whom hyperinflation is a preexisting condition. Several of our findings in group A may certainly be due to a more important distention than in group B. Therefore, the decrease in Pdimax could be an indicator of a bad condition of the diaphragmatic function, the diaphragm having to work more (increase of Pdi/Pdimax) with less efficiency (decrease of Pdi). Then, the bad condition of the diaphragm function was a major element causing fatigue and might as such account for the failure of the weaning trial in group A.
We cannot confirm here the alteration of diaphragmatic contractility during weaning with our methods. Indeed, diaphragmatic contractility is defined as the Pdi produced in response to a given level of stimulation, which may be measured by the Pdi/fre-quency curve recorded at different levels of phrenic stimulation. However, several authors have demonstrated the electromyographic evidence of inspiratory muscle fatigue using the ratio HI/LO of the rectified and integrated signals in patients who foiled to wean from the ventilator. Moreover, Roussos et al have shown that a Pdi greater than 40 percent of the Pdimax cannot be tolerated indefinitely without fatigue. Our findings agree with a diaphragmatic fatigue existing as early as two hours after the beginning of the weaning period because the patients in group A exhibited a significantly higher Pdi/Pdimax ratio, not related to an increased Pdi (on the contrary, it was lower than group Bs) but rather a lower Pdimax. Whatever the reason why the Pdimax decreased after two hours in group A (hyperinflation and/or alteration of diaphragm contractility), the resulting increase in the ratio Pdi/Pdimax caused the diaphragm to be much less fetigue-resist-ant. Nevertheless, fatigue would account much more easily than hyperinflation alone for the level of Pga recorded in group A. Regarding Pga overestimating Pab, our findings indicate a constant and often remarkable, negative abdominal pressure during inspiration, probably a symptom of abdominal paradoxic motion, which when undetected at the time of measurements, will show about an hour later. This paradoxic motion usually means poor prognosis in regards to the outcome of weaning. Thus, in a study where the diaphragmatic EMG was recorded during the weaning trial, the decrease in the ratio HI/LO was accompanied or followed by a paradoxic motion during inspiration, a clinical sign of fatigue.
After a two-hour weaning period, the blood gas parameters were not significantly different in the two groups, but group A showed a progressive respiratory acidemia and hypoxemia. The etiologic factors were probably multiple: increase in dead-space ventilation, heterogeneity of ventilation/perfusion ratio, and increase in production of carbon dioxide. Then, hypoxemia, hypercapnia, and acidosis joined their deleterious effects on diaphragmatic contractility, and fatigue was accentuated.
In conclusion, the failure of medium-term weaning trial in the COPD patient shows a definite diaphragmatic dysfunction two hours after the beginning of the weaning period. Neither the respiratory pattern nor the blood gas data allows a clear distinction between these patients and those who will stand the weaning trial over the ten following hours. Our data give no clue as to the origin of the dysfunction. It might
be diaphragmatic fatigue eased and worsened by a drastic hyperinflation, classic in these patients. For all cases, the recording, two hours after the beginning of the weaning trial, of a null or negative Pga during inspiration (together or without an abdominal paradoxic motion) or of a Pdi/Pdimax ratio over 40 percent, is undoubtedly of poor prognosis as regards the medium term outcome of weaning.