Respiratory Physiology for the Intensivist by Robert Vender

Author:Robert Vender [Vender, Robert]
Language: eng
Format: azw3
Published: 2016-08-18T04:00:00+00:00

Regardless of the mechanism or cause of inspiratory muscle fatigue, the clinical result is a similar breathing pattern—that is, rapid, shallow breathing, which pattern in clinical practice is termed the rapid, shallow breathing index (RSBI). The RSBI, defined as RR (breaths/minute)/Vt (measured in liters), has been shown to assist in assessing clinical weanabilty for ICU patients in whom liberation from mechanical ventilation is being considered. In general, a RSBI greater than 105 is an accurate predictor of failure to successfully wean and extubate (Yang 1991).

Patients with severe COPD, especially during periods of acute exacerbations or at times of invasive mechanical ventilation, clearly exemplify these principles. Patients with severe COPD, given the systemic complications associated with this chronic disease, both because of overall skeletal muscle dysfunction, including the diaphragm, plus the marked degrees of hyperinflation, which reduce the pressure-generating capacity of the diaphragm by altering the ideal length-tension relationship, are set up for fatigue and subsequent respiratory failure at times of increased mechanical loads as occurs with acute exacerbation of COPD (AECOPD). Studies have shown, even in stable COPD patients, reduced muscle-generating capacity with Pgimax, Pplmax, and Pdimax values of 25 percent, 62 percent, and 49 percent of normal control values, respectively, compared to nondiseased, healthy volunteers (Marin 1999). In a group of intubated COPD patients who failed weaning, reductions in both Pdi and Pdimax were observed with the resultant ratio of these two values above the 40 percent fatiguing threshold in comparison to patients who were successfully liberated from mechanical ventilation: Pdi (cmH2O) = 12.6 +/− 5.8 versus 15.8 +/− 3.36; Pdimax (cmH2O) = 34.2 +/− 24.1 versus 50.5 +/− 16.1; Pdi/Pdimax = 0.456 +/− 0.08 versus 0.330 +/− 0.09 respectively, shown in Table 10.2 (Pourriat 1986). Of note, both groups of COPD patients have similar indices of central respiratory drive, thus reinforcing the fact that muscle function—and not CNS respiratory drive suppression—is the predominate mechanism of weaning failure; that is, P0.1 (cmH2O) = 8.21 +/− 4.4 versus 6.22 +/− 2.67, respectively. Of interest, patients with asthma are exposed to airway obstruction and hyperinflation only intermittently, unlike patients with COPD, whereby the inspiratory load is constant, yet similar muscle-related physiological principles apply.

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