| Abstract |
Clinically important bronchospasm in anesthetic practice is relatively rare. However,
laryngoscopy and endotracheal intubation are associated with stimulation of
mechanoreceptors in the nose, larynx or airways precipitating reflex bronchospasm and
mucus production, which might cause an increase of airway resistance up to 40%.
Previous studies have shown that volatile anesthetics may decrease lung resistance
and elastance by several mechanisms, including direct relaxation of airway smooth muscle,
inhibition of the release of chemical mediators and augmentation of β‐adrenergic tone. The
bronchodilatory action of halothane, isoflurane and sevoflurane has been documented in
both animal and clinical studies. The majority of animal studies report that these agents
effectively relax constricted bronchial muscles. Studies in humans have also concluded that
isoflurane and sevoflurane, at clinically relevant concentrations, are associated with a
decrease of respiratory resistance.
Data on desflurane are inconsistent. Several animal studies have demonstrated
desflurane’s capacity to dilate proximal and distal bronchial musculature to a greater extent
than halothane. On the other hand, clinical studies failed to show the bronchodilatory
properties of this agent and showed significant variability on desflurane’s action on
respiratory resistance with a tendency to aggravate bronchoconstriction. It is apparent that
the likelihood of bronchospasm in patients with pulmonary disease, but also in patients
with normal lungs, becomes a major concern during desflurane anesthesia.
In order to clarify desflurane’s effect on respiratory resistance an experimental study
in a laboratory lung model and a randomized clinical trial were performed. The aim of the
experimental study was to compare the effect of different concentrations of isoflurane,
sevoflurane, and desflurane on the measured pulmonary resistance under experimental
conditions in a laboratory lung model with fixed resistance. The working hypothesis was
that the volatile agents with high density would increase the density of their mixture with
25% oxygen in air and would lead to an increased pulmonary resistance. This effect should
ΠΤΗΤΙΚΑ ΑΝΑΙΣΘΗΤΙΚΑ & ΜΗΧΑΝΙΚΕΣ ΙΔΙΟΤΗΤΕΣ ΑΝΑΠΝΕΥΣΤΙΚΟΥ
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be greater at the higher volatile concentrations. The results of the study confirmed the
initial hypothesis and concluded that the high density of volatile anesthetics significantly
increased airway resistance. This phenomenon was more pronounced with the less potent
agents that are delivered in equivalent high concentrations. Studies of the effects of these
agents on airway resistance should take into account that a percent of these effects may
result from the altered density of the inspired gas mixture.
The aim of the clinical study was twofold. First, to investigate the effects of desflurane
on total inspiratory resistance (Rrs) and its components during 30 min administration at
1.0 and 1.5 MAC in patients without pulmonary disease undergoing general anesthesia.
Second, to verify the bronchodilating effect of isoflurane and sevoflurane at 1.0 and 1.5 MAC
in healthy patients and to compare them to desflurane. The results of the study
documented that from the commonly used volatile anesthetics in clinical practice no agent
can surpass the others regarding their effect on respiratory resistance, when administered
at concentrations of 1.0 MAC for a period of 30 min. The higher concentrations of
desflurane at 1.5 MAC caused an increase of total respiratory resistance, an effect that
clearly should be taken into account in patients with hyperesponsive airways. This effect of
the 1.5 MAC concentrations of desflurane could be attributed to possible improvement of
the time‐constant inhomogeneities within the lung. Further studies are needed to confirm
whether more prolonged administration of high concentrations of desflurane could have a
favourable effect on the component of resistance attributed to tissue viscoelastic properties
and alveolar time‐constant inequality. In addition, further studies are needed to clarify
whether anesthesia depth itself, regardless of the anesthetic agent used, intravenous or
volatile, affects the resistance of the respiratory system.
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Επίδραση των πτητικών αναισθητικών στις μηχανικές ιδιότητες των πνευμόνων
