A. Brancatisano

Cardiorespiratory consequences of expiratory chest wall compression during mechanical ventilation and severe hyperinflation.

To measure and compare the effects of manual expiratory compression of either the rib cage or abdomen on cardiac output, end-expiratory lung volume, and other cardiorespiratory variables in an animal model that mimics the severe pulmonary hyperinflation and hemodynamic impairment occurring in patients with severe acute asthma during mechanical ventilation. Design:Prospective, randomized, crossover trial. Setting:Research laboratory. Subjects:Seven cross-bred, anesthetized, supine dogs. Interventions:The following sequence was employed: a) spontaneous breathing without pulmonary hyperinflation; b) positive-pressure ventilation with severe pulmonary hyperinflation (produced by an external variable expiratory flow resistor); c) ∼7 mins of manual expiratory compression of either the rib cage or abdomen during positive-pressure ventilation-hyperinflation. This sequence was then repeated, incorporating the alternative type of expiratory compression. Measurements and Main Results:Cardiac output (measured by thermodilution), aortic pressure, pleural (esophageal) pressure, and changes in end-expiratory lung volume were measured. The decrease in cardiac output due to mechanical ventilation with pulmonary hyperinflation was exacerbated by rib cage compression (p < .001; spontaneous breathing 2.9 ± 0.2 L/min, hyperinflation 1.5 ± 0.1 L/min, and rib cage compression 1.0 ± 0.1 [SEM] L/min). However, the positive-pressure ventilation-hyperinflation-induced decrease in cardiac output was attenuated by abdominal compression (p < .001; spontaneous breathing 3.3 ± 0.2 L/min, hyperinflation 1.4 ± 0.1 L/min, and abdominal compression 2.1 ± 0.1 L/min). Mean aortic pressure returned to prehyperinflation levels during abdominal compression (p < .001; spontaneous breathing 126 ± 2 mm Hg, hyperinflation 75 ± 5 mm Hg, and abdominal compression 120 ± 3 mm Hg). Both types of compression were similarly effective (p > .75) in increasing mean expiratory pleural pressure, so that end-expiratory lung volume ‘was similarly (p > .25) reduced (0.45 ± 0.05 and 0.40 ± 0.05 L for rib cage and abdominal compressions, respectively) in this non-air flow, limiting animal model. Conclusions:The cardiorespiratory effects of manually compressing the rib cage or abdomen during expiration in this animal study suggest that these techniques should be carefully evaluated in mechanically ventilated patients with severe acute asthma. (Crit Care Med 1993; 21: 1908–1914)

Mechanisms of oronasal airflow partitioning in dogs

We examined the integrated (MTA) electromyographic activity (EMG) of the hyoepiglotticus (HE) muscle and the soft palate muscles (SPM) during CO2 administration in 6 anaesthetised prone, mouth open dogs. As ventilation increased nasal flow (VN) as a percentage of total flow (VT), i.e. VN/VT%, decreased. Breath-by-breath peak inspiratory and peak expiratory HE EMG activity was strongly and inversely correlated with VN/VT% (both r > 0.8, p < 0.001), whereas the correlation between SPM MTA EMG activity and VN/VT% was highly variable. Severing of the HE muscles halved the rate at which VN/VT% was reduced with respect to increasing ventilation while electrical stimulation of HE muscle contraction resulted in a fall in VN/VT% to near zero levels. Active control of epiglottic position appears to be an important mechanism controlling the patency of the epiglottic-soft palate seal and thus the oronasal partitioning of airflow in dogs.

Electromyographic activity of the hyoepiglotticus muscle in dogs.

We examined the respiratory-related electromyographic (EMG) activity of the hyoepiglotticus muscle using fine wire bipolar electrodes, inserted perorally in five anaesthetised (IV chloralose) tracheostomised dogs studied in the prone, mouth open position. The integrated HE EMG was measured in arbitrary units (a.u.) during resting breathing via the upper airway, and on a breath-by-breath basis during progressive increases in respiratory drive induced by infusion of CO2 into the inspired gas. The HE demonstrated inspiratory activity which increased linearly in relation to ventilation (r = 0.85 +/- 0.06, p < 0.001) due to an increase in both phasic (8.8 +/- 1.8 to 32.4 +/- 9.2 a.u.) and tonic (0.2 +/- 0.1 to 26.3 +/- 13.3 a.u.) activity (both p < 0.05). In addition, HE EMG developed substantial phasic expiratory activity (1.3 +/- 1.1 to 13.8 +/- 4.4 a.u., p < 0.05). We conclude that the canine HE exhibits inspiratory and expiratory related activity which is augmented during increased respiratory drive. These findings imply active control of epiglottic position during breathing in dogs.

Influence of hyoepiglotticus muscle contraction on canine upper airway geometry

We examined the effect of hyoepiglotticus (HE) muscle contraction on epiglottic position in 4 anaesthetised (IV choralose, pentobarbitone sodium) tracheostomised, mechanically ventilated dogs studied in the prone mouth open position. Computerised axial tomography (coronal plane) was used to measure the vertical distance between the tip of the epiglottis (E) and (1) the soft palate (SP) (i.e. E-SP distance) and (2) the dorsal wall of the nasopharynx (N) (i.e. E-N distance). Duplicate runs of graded electrical stimulation of the HE muscle, using bilateral bipolar fine wire electrodes, were performed in each animal and resulted in a progressive increase in both the E-SP distance (baseline of 0.5 +/- 0.5 to a maximum of 13.1 +/- 2.3 mm, mean +/- SE) and the E-N distance (29.1 +/- 2.0 to a maximum of 42.2 +/- 2.7 mm, both p < 0.02). We conclude that HE contraction moves the epiglottis ventrally away from the soft palate thus opening and enlarging the oral pathway for airflow.

Control of epiglottic position in dogs: role of negative upper airway pressure.

We investigated the influence of negative upper airway pressure (NUAP) on hyoepiglotticus and genioglossus muscle electromyographic (EMG) activity in anaesthetised (sodium pentobarbitone/ chloralose) dogs breathing via a tracheostomy. Changes in pressure were not transmitted through the entire upper airway, thus confirming airway occlusion during NUAP. When NUAP was applied at the larynx, peak inspiratory and tonic EMG activity of the genioglossus and HE both increased significantly (p < 0.05) and reached a plateau at NUAP of -10 to -20 cmH2O. Nasal NUAP at any level failed to influence either genioglossus or HE EMG activity. Following bilateral section of the internal branches of the superior laryngeal nerves (SLNin), resting levels of HE and genioglossus EMG activity decreased to virtually zero. Moreover, NUAP applied at the larynx now failed to recruit EMG activity for either muscle. These findings suggest active control of epiglottic position in dogs during NUAP.