Control of Breathing in Diseases of the Respiratory Tract and Lungs

Rěbuck, A. S.; Slutsky, A. S.

doi:10.1002/cphy.cp030224

Cited by 8 publications

(7 citation statements)

References 182 publications

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“…Inspiratory muscle effort is increased immediately after the chest wall and abdomen are strapped, and progressively increases during subsequent breaths as VT approaches control values (13,19,20). This increase in inspiratory effort returns VT and E to control values, with an increase in amplitude of respiratory muscle contraction and changes in shape of the phases of inspiratory muscle activity, without substantial changes in RR (13,14). The steady-state response is due to the physiologic coupling between VT and inspiratory muscle effort (29).…”

Section: Discussionmentioning

confidence: 94%

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Compensation for Increase in Respiratory Workload during Mechanical Ventilation

Grasso

Puntillo

Mascia

et al. 2000

Am J Respir Crit Care Med

108

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Variation in respiratory impedance may occur in mechanically ventilated patients. During pressure-targeted ventilatory support, this may lead to patient-ventilator asynchrony. We assessed the hypothesis that during pressure-support ventilation (PSV), preservation of minute ventilation (V E) consequent to added mechanical loads would result in an increase in respiratory rate (RR) due to the large reduction in tidal volume (VT). WITH proportional-assist ventilation (PAV), preservation of V E would occur through the preservation of VT, with a smaller effect on RR. We anticipated that this compensatory strategy would result in greater patient comfort and a reduce work of breathing. An increase in respiratory impedance was obtained by chest and abdominal binding in 10 patients during weaning from mechanical ventilation. V E remained constant in both ventilatory modes after chest and abdominal compression. During PSV, this maintenance of VE was obtained through a 58 +/- 3% increase in RR that compensated for a 29 +/- 2% reduction in VT. The magnitudes of the reduction in VT (10 +/- 3%) and of the increase in RR (14 +/- 2%) were smaller (p < 0. 001) during PAV. During both PSV and PAV, chest and abdominal compression caused increases in both the pressure-time product (PTP) of the diaphragm per minute (142.9 +/- 26.9 cm H(2)O. s/min, PSV, and 117.6 +/- 16.4 cm H(2)O. s/min, PAV) and per liter (13.4 +/- 2.5 cm H(2)O. s/L, PSV, and 9.6 +/- 0.7 cm H(2)O. s/L, PAV). These increments were greater (p < 0.001) during PSV than during PAV. The capability of keeping VT and V E constant through increases in inspiratory effort after increases in mechanical loads is relatively preserved only during PAV. The ventilatory response to an added respiratory load during PSV required greater muscle effort than during PAV.

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Section: Discussionmentioning

confidence: 94%

“…Respiratory loading has often been used to simulate changes in respiratory impedance (13,14) and to evaluate the consequences of such changes on ventilatory patterns and respiratory muscle performance (15). The aim of this study was to assess ventilatory responses to added mechanical loads during PSV and PAV in patients during the weaning period.…”

mentioning

confidence: 99%

Compensation for Increase in Respiratory Workload during Mechanical Ventilation

Grasso

Puntillo

Mascia

et al. 2000

Am J Respir Crit Care Med

108

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show abstract

“…Previous studies have shown the possibility of using this approach (Alarie 1981; Alarie and Schaper 1988;Alarie et al 1990). With an increase in knowledge of the control of respiration in normal conditions and diseases, as well as during stimulation of nerve endings at different levels of the respiratory tract or from recording of nerve impulses during stimulation of these nerve endings (Paintal 1981;Bartlett 1986;Coleridge and Coleridge 1986;Rebuck and Slutsky 1986;Von Euler 1986;Widdieombe and Tatar 1988;Lawson et al 1991;Boggs 1992;Matsumoto et al 1992), it is now possible to present a broader as well as a more quantitative approach as shown in Fig. l.…”

Section: Rationalementioning

confidence: 97%

“…c) The work of many investigators using a variety of animal species, primarily under anesthesia, and using a variety of injected or airborne chemicals to stimulate pulmonary vagal nerve endings and/or upper respiratory tract nerve endings (Paintal 1981;Bartlett 1986;Coleridge and Coleridge 1986;Rebuck and Slutsky 1986;Widdicombe and Tatar 1988).…”

Section: Rationalementioning

confidence: 99%

Characteristic modifications of the breathing pattern of mice to evaluate the effects of airborne chemicals on the respiratory tract

et al. 1993

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A system was developed for exposure of unanesthetized mice to airborne chemicals and for continuous measurement of their breathing pattern prior to, during and following exposure. By measuring inspiratory and expiratory airflows (VI and VE), and integration with time to yield tidal volume (VT), we obtained characteristic modifications to the normal breathing pattern. These permitted recognition that a specific portion of the respiratory tract was affected by the selected airborne chemicals. Following recognition, we also quantitated the degree of effect using one specific measurement in each case. An effect on the upper respiratory tract, induced by the sensory irritant, 2-chlorobenzylchloride, was quantitated by measuring a decrease in respiratory frequency. An effect on the conducting airways, induced by the airway constrictor, carbamylcholine, was quantitated by a decrease in VE at the mid-point of VT. An effect at the alveolar level, induced either by the vagal nerve ending stimulant, propranolol, or by the pulmonary irritant, machining fluid G, was quantitated by an increase in the length of a pause induced at the end of expiration. The system is easy to construct and operate and can be used to rapidly evaluate the effects of airborne chemicals on the respiratory tract.

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“…These episodes may be associated with significant hypoxaemia, an issue of great importance for critically ill patients. However, it should be mentioned that in the presence of active lung disease, input to the respiratory controller from nonchemical sources [51] may not permit chemical feedback to prevent respiratory alkalosis during sleep or under anaesthesia.…”

Section: Chemical Feedbackmentioning

confidence: 99%

Control of breathing in mechanically ventilated patients

Georgopoulos¹,

Roussos²

1996

Eur Respir J

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Thus, the response of ventilator to patient effort, and that of patient effort to ventilator-delivered breath are inevitably the two components of control of breathing during mechanical ventilation; the ventilatory output is the final expression of the interaction between these two components. As a result of this interaction, the various aspects of control of breathing of the respiratory system may be masked or modulated by mechanical ventilation, depending on several factors related both to patient and ventilator. This should be taken into consideration in the management of mechanically ventilated patients.

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Control of Breathing in Diseases of the Respiratory Tract and Lungs

Cited by 8 publications

References 182 publications

Compensation for Increase in Respiratory Workload during Mechanical Ventilation

Compensation for Increase in Respiratory Workload during Mechanical Ventilation

Characteristic modifications of the breathing pattern of mice to evaluate the effects of airborne chemicals on the respiratory tract

Control of breathing in mechanically ventilated patients

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