Hameeda Shaikh

Diaphragmatic neuromechanical coupling and mechanisms of hypercapnia during inspiratory loading.

We hypothesized that improved diaphragmatic neuromechanical coupling during inspiratory loading is not sufficient to prevent alveolar hypoventilation and task failure, and that the latter results primarily from central-output inhibition of the diaphragm and air hunger rather than contractile fatigue. Eighteen subjects underwent progressive inspiratory loading. By task failure all developed hypercapnia. Tidal transdiaphragmatic pressure (ΔPdi) and diaphragmatic electrical activity (ΔEAdi) increased during loading - the former more than the latter; thus, neuromechanical coupling (ΔPdi/ΔEAdi) increased during loading. Progressive increase in extra-diaphragmatic muscle contribution to tidal breathing, expiratory muscle recruitment, and decreased end-expiratory lung volume contributed to improved neuromechanical coupling. At task failure, subjects experienced intolerable breathing discomfort, at which point mean ΔEAdi was 74.9±4.9% of maximum, indicating that the primary mechanism of hypercapnia was submaximal diaphragmatic recruitment. Contractile fatigue was an inconsistent finding. In conclusion, hypercapnia during acute loading primarily resulted from central-output inhibition of the diaphragm suggesting that acute loading responses are controlled by the cortex rather than bulbopontine centers.

New device for nonvolitional evaluation of quadriceps force in ventilated patients: Assessment of Quadriceps Force

In mechanically ventilated patients, nonvolitional assessment of quadriceps weakness using femoral‐nerve stimulation (twitch force) while the leg rests on a right‐angle trapezoid or dangles from the bed edge is impractical. Accordingly, we developed a knee‐support apparatus for use in ventilated patients.

Eating on noninvasive ventilation

www.ccmjournal.org 737 Feeding patients while receiving noninvasive ventilation (NIV) is a challenge (1). Using the nasogastric tube can disrupt the patient-mask interface and cause an air leaks (2). Removal of the mask to allow for oral intake may not be tolerated in patients with respiratory distress. To these concerns, we must add our limited understanding of the interaction between breathing and swallowing in critically ill patients and the ever-present concern of inducing aspiration. Accordingly, many intensivists are reluctant to begin oral nutrition in patients requiring NIV (3). Withholding nutrition, however, is not without consequence. Malnutrition develops rapidly and is associated with poor outcomes (4). Furthermore, depriving patients of the enjoyment of food detracts from their quality of life. As use of NIV for acute respiratory failure has increased (1), determining how best to provide nutrition to these patients has become a topic of great clinical relevance. In this issue of Critical Care Medicine, Terzi et al (5) explore the interaction between nasally delivered NIV and the breathing-swallowing mechanism in 15 patients with chronic obstructive pulmonary disease (COPD) when the patients were able to breathe without ventilatory support for at least 2 hours. All of them were cared for in one ICU during an acute exacerbation of COPD. The investigators triggered swallowing placing water boluses in the mouth of patients. These boluses were given during each of two conditions: unassisted respiration and while on NIV. Compared with unassisted respiration, all patients demonstrated improved swallowing efficiency while on NIV, with fewer swallows needed to clear the fluid bolus, shorter swallowing time per bolus, and fewer breaths taken during the period of swallowing. Furthermore, while on NIV, fewer swallows were followed by inspiration, a condition which may promote prandial aspiration (6, 7). The first eight patients in the study frequently experienced patient-ventilator uncoupling in the form of swallow-induced ventilator triggering followed by autotriggering. To limit such uncoupling, the remaining seven patients were studied with a modified NIV machine that was provided with a patient-controlled off-switch pushbutton. As long as the patient pressed the off-switch pushbutton, the ventilator would stop delivering assisted breaths—but not for more than 18 seconds. When patients used the pushbutton, autotriggering was completely eliminated. Concurrently, 89% of these patients demonstrated a restoration of the normal breathing-swallowing pattern of “exhalation-swallow-exhalation” (6). In contrast, less than 80% of patients displayed this breathing pattern when ventilated with the conventional NIV machine and less than 40% of patients when breathing unassisted. The latter percentage is about half of that previously reported in clinically sable patients with COPD instructed to swallow semisolid food (6). Irrespective of the offswitch modification, all patients found swallowing more comfortable while on NIV than during unassisted respiration. By what mechanism did swallowing improve on NIV? One potential mechanism could be an NIV-induced increase in operating lung volumes (8). Increases in operating lung volumes have been associated with reduced swallow duration and a probable increase in subglottic pressure (8). And greater subglottic pressures can, in turn, reduce the risk of aspiration (9). Unfortunately, the French investigators (5) did not measure lung volumes during the swallowing maneuvers. Nevertheless, it is likely that lung volumes were larger during NIV than during unassisted breathing (10). A second potential explanation for improved swallowing with NIV could be the NIV-induced unloading of the respiratory muscles and the concomitant decrease in carbon dioxide tension (10). In healthy subjects, experimentally-induced hypercapnia and elastic loading increase respiratory frequency and disrupt the normal breathing-swallowing coordination (11, 12). This pattern is similar to what was observed by Terzi et al (5). When their patients were off NIV, there was an increase in arterial carbon dioxide tension and a likely increase in the mechanical load on the respiratory muscles (10). Similarly to what has been described in healthy subjects (11, 12), the increase in carbon dioxide tension and the likely increase in mechanical load on the respiratory muscles were accompanied by a rise in respiratory frequency and a disruption in the normal breathing-swallowing coordination. These variables improved during NIV. Could it be the respiratory rate alone is driving the uncoordinated breathing-swallowing interactions? This is unlikely for two reasons. First, breathing-swallowing interactions are preserved during exercise-induced tachypnea (13). Second, even in patients with COPD who are clinically Copyright