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Abstract |
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Lung inflation causes cardiovascular suppression via an increase in intrathoracic pressure and neural mechanisms. To examine the mechanisms involved, we mea-sured the heart rate (HR) and arterial blood pressure (AP) responses to lung inflation before and after spraying the bronchi with lidocaine to suppress airway reflex. Thirty women participated in the study. One group (n = 20, Group BT) had their tracheas intubated by using double-lumen tubes. The other group (n = 10, Group TT) received an ordinary endotracheal tube. They were all studied under general anesthesia by using nitrous oxide, isoflurane, and muscle relaxation after a thiopental induction. In each patient, airway pressure was increased for 3 s, and changes in HR and AP were measured. Lung inflation was repeated after 5 mL of 4% lidocaine had been sprayed into the main bronchi unilaterally in Group BT or bilaterally in Group TT. There were no significant differences in cardiovascular responses between left and right lung inflation with the pressure at 20 and 30 cm H2O. Both lungs inflated at 20 cm H2O caused an increase in HR with a significantly greater decrease in AP than with unilateral inflation. Anesthesia of the bronchi abolished the HR increase, but not the AP decrease. Lung inflation at 30 cm H2O caused significant decreases in HR and AP which were not affected with topical anesthesia. These results indicate that the cardiovascular responses elicited by lung inflation in anesthetized humans are predominantly the direct effect of the increase in intrathoracic pressure, although sympathetic afferent activity induced via stimulation of mechanoreceptors in the airways contributes.
Implications: Localized airway anesthesia with lidocaine is unlikely to suppress the cardiovascular responses to lung inflation. This suggests that a limited number of neurogenic mechanisms are involved in the cardiovascular responses to lung inflation in anesthetized humans.
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Introduction |
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It is well recognized that mechanical and chemical stimulation of the respiratory tract can elicit potent respiratory-cardiac reflex responses under anesthesia. Mechanical stimulation, such as direct laryngoscopy, endotracheal intubation, and suctioning (1,2), and chemical stimulation, such as with pungent volatile anesthetics, can cause tachycardia and hypertension with associated sympathetic activation (3,4). Stimulation of receptors other than those in the upper airways also modulates the cardiovascular system: inflation of the lungs, for instance, affects heart rate and arterial blood pressure via receptors in the bronchi and lungs (5). However, the physiological importance of airway-cardiovascular excitatory and inhibitory reflexes is not yet clear, and indeed such reflexes could be detrimental during anesthesia. Producing airway anesthesia by the use of a local anesthetic is one medical intervention that could be used to suppress such potent cardiovascular responses. Because the distribution of airway receptors is uneven (6), the evoked responses could differ in intensity, depending on the section of the airway stimulated. Moreover, because most airway receptors are located just beneath the epithelium (7), it should be possible to block them by topical application or infiltration of local anesthetics. Topical application of bupivacaine has been confirmed, by monitoring afferent traffic in pulmonary nerves, to block most, if not all, airway receptors in animals (8) and humans (9). Although lung inflation also causes cardiovascular responses by a direct mechanical effect secondary to the increase in intrathoracic pressure, it is not clear how significant such direct cardiovascular effects are by comparison with the reflex effects associated with airway receptor stimulation, much less whether airway anesthesia has any effect on the cardiovascular response to lung inflation.
For this reason, we designed our study, in anesthetized patients, to examine whether airway anesthesia produced by topical administration of lidocaine has significant effects on the cardiovascular responses to inflation of the lungs. We hoped to gain an insight into the significance of the contribution made by receptor-mediated effects to the airway-cardiovascular responses in anesthetized humans.
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Methods |
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Thirty female patients (aged 20–65 yr, ASA physical status I) gave oral, informed consent to their participation in the study after we received approval from the Human Investigation Committee of our institution. Each patient was scheduled for elective gynecological surgery, such as hysterectomy or oophorectomy. None of the patients had either a past or present cardiorespiratory disorder. Premedication with oral diazepam 10 mg and famotidine 20 mg was given 90 min before their arrival in the operating room.
Each patient was randomly assigned to one of two groups on the basis of the airway management and subsequent stimulation they received. One group (Group BT, n = 20) received endobronchial intubation and one-lung inflation, and the other group (Group TT, n = 10) received endotracheal intubation and two-lung inflation. Recordings of the electrocardiograms, arterial blood pressure (AP; by sphygmomanometry), and SpO2 of arterial hemoglobin (by pulse oximetry) were established in each patient. Also in each patient, general anesthesia was induced with IV thiopental 5 mg/kg, and either a double-lumen endobronchial tube (Bronchocath®; Mallinckrodt, St. Louis, MO) for the left bronchus (Group BT) or an endotracheal tube (Lo-Pro®; Mallinckrodt) was put in place with the aid of IV vecuronium 0.1 mg/kg. Ventilation to maintain normocapnia was confirmed with ETCO2 (by capnography). Light general anesthesia was maintained by inhaled nitrous oxide (67%) in oxygen accompanied by <0.5 minimum alveolar anesthetic concentration (MAC) of isoflurane (
0.6% in end-tidal concentration). Each patient’s radial artery was cannulated for the direct measurement of AP.
After at least 10 min of stable hemodynamic conditions, baseline heart rate (HR) and AP were recorded as the mean of 5 cardiac contractions. Inflation of either one-lung (Group BT) or two-lung (Group TT) followed to raise airway pressure and keep it at 20 or 30 cm H2O for 3 s. The consequent changes in HR and AP were then recorded. In Group BT, the contralateral lung was exposed to atmospheric pressure by releasing the connection to the anesthetic circuit. The same stimulus was given in triplicate to all patients, and the average of the three consecutive responses was taken as the result. Each patient underwent lung inflation at the intervals of 3 min; lung inflation at 20 cm H2O was applied first, then inflation at 30 cm H2O was applied at the same intervals.
Anesthesia of one of three different portions of the respiratory tract was produced by spraying 5 mL of 4% lidocaine solution as described below. One of the authors sprayed the appropriate portion of the airways with the lidocaine solution via a specially designed spray tube; this tube was 550 mm long and had multiple microholes over a length of 35 mm at the tip (No. 10 x 550 mm–R100; Hakko, Tokyo, Japan). The spray was applied to the unilateral main bronchus (either left or right, Group BT), or bilateral main bronchi (Group TT). It was applied under direct visual control with the aid of a fiberoptic bronchoscope. Group BT was divided into two subgroups: those whose right bronchus was sprayed with lidocaine (Group BTRt; n = 10), and those whose left bronchus was sprayed (Group BTLt; n = 10). Lung inflation was repeated (by using the same protocols as before) 10–15 min after lidocaine application.
In summary, Group BTRt received one-lung inflation (both right and left) at 20 cm H2O for 3 s, 3 times at the intervals of 3 min to record consequent changes in HR and AP, followed by one-lung inflation at 30 cm H2O in the same manner. Then the right main bronchus was sprayed with 5 mL of 4% lidocaine solution, and one-lung inflation was repeated in the same protocols. In Group BTLt, the topical lidocaine spray was applied to the left main bronchus, and one-lung inflation was given before and after the spray in the same way as Group BTRt. Group TT received a series of two-lung inflation in the same protocols as the other two groups before and after the topical lidocaine spray to the bilateral main bronchi.
Results were reported as mean ± SEM, unless otherwise stated. A two-way factorial analysis of variance was applied to test the effects of both lidocaine application and airway pressure, followed by Fisher’s protected least significant difference test for post hoc comparisons between groups. To assess differences produced by lidocaine administration in a given group, a paired Student’s t-test was used after a repeated measures analysis of variance. P values < 0.05 were considered statistically significant.
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Results |
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The patients’ demographic data showed no significant differences among the groups (Table 1). The data of arterial blood gas tensions and electrolytes 5 min after the topical lidocaine application was within the normal range in both groups.
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Unilateral Topical Lidocaine, One-Lung Inflation at 20 cm H2O
When airway pressure was increased to 20 cm H2O, inflation of either right- or left-one-lung had a similar effect on HR, which decreased in each case (Fig. 1). Airway anesthesia by using 4% lidocaine did not affect the HR responses to one-lung inflation. Lung inflation caused biphasic changes in AP (an initial increase followed by a larger decrease), and topical anesthesia of either contralateral or ipsilateral bronchus to one-lung inflation had no effect on these AP responses.
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P < 0.05 versus before lidocaine administration.Unilateral Topical Lidocaine, One-Lung Inflation at 30 cm H2O
When the tests involved an increase in airway pressure to 30 cm H2O, the evoked changes in HR and AP were mostly larger, but qualitatively similar to those seen at 20 cm H2O (Fig. 2). Application of the lidocaine spray, to either the ipsilateral or contralateral airway, did not affect the cardiovascular responses to lung inflation. The decreases in AP after left-one-lung inflation were significantly larger than those after right-one-lung inflation (P
0.0391); this discrepancy tended to remain after airway anesthesia.
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Bilateral Topical Lidocaine, Two-Lung Inflation at 20 cm H2O
In contrast to one-lung inflation, two-lung inflation (Group TT) caused a HR increase. The change in HR for Group TT was significantly different from that seen in the other groups (P
0.0063). Airway anesthesia by using 4% lidocaine reversed the HR response to lung inflation to a bradycardia, so that the change in HR values before and after lidocaine administration in Group TT showed a significant difference (P = 0.011). The change in AP in Group TT was significantly greater than those seen in the other groups (P 0.0046).
Bilateral Topical Lidocaine, Two-Lung Inflation at 30 cm H2O
Two-lung inflation at 30 cm H2O caused a smaller tachycardia than that seen at 20 cm H2O. The change in HR values were not significantly different among the groups, though the change in AP was significantly larger for Group TT than for the other groups (P 0.0007).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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In this study, most of the responses to lung inflation induced a decrease in HR and an initial, small increase followed by a larger decrease in AP. The one exception was the response to bilateral inflation at 20 cm H2O; this included a tachycardia rather than a bradycardia. The evoked changes in AP were larger on two-lung inflation than on one-lung inflation, and corresponding responses were larger at 30 than at 20 cm H2O of airway pressure. The latter was also observed in the bradycardia elicited by one-lung inflation, but not of the tachycardia elicited by two-lung inflation. Topical anesthesia of the peripheral bronchi did not significantly alter the cardiovascular responses to lung inflation, except for the tachycardia evoked by two-lung inflation at 20 cm H2O of airway pressure (which was reversed by bilateral anesthesia of the bronchi).
Although the physiological importance of airway-cardiovascular reflexes is not yet clearly understood, it is well known that airway manipulations can elicit potent cardiovascular responses in both awake and anesthetized humans (1,2,4,10). There are three main kinds of sensory receptors in the respiratory tract and lungs: rapidly adapting chemo- and mechanoreceptors (RARs) with small-diameter myelinated fibers, slowly adapting stretch receptors (SARs) with large-diameter myelinated fibers, and receptors with nonmyelinated nerve fibers, including pulmonary C fibers (11–13). Although there may be considerable species differences among the cardiovascular responses to mechanical and chemical stimuli (6), it is generally assumed that lower down the airway, the receptor population becomes (a) more chemosensitive and less mechanosensitive, and (b) slower to adapt to repeated stimuli, at least in animals (14). Lung inflation could affect the cardiovascular system through either a neurally mediated reflex arising from the airways, or via intrathoracic pressure changes (which would reduce venous return), or both. Lung inflation may activate SARs with afferents running in the vagus nerve in animals (11–13). In humans, lung inflation has also been reported to increase the activity of pulmonary stretch receptors, whose afferents are assumed to run in the vagus nerve (15), and the cardiovascular responses are similar to those seen in dogs (5,16).
There could be many reasons why airway anesthesia did not completely block the cardiovascular responses to lung inflation. For example, because we used a small spray tube for administrating the lidocaine solution, the spray may not have effectively blocked the receptors throughout the entire area of the peripheral bronchi and lungs that was exposed to high pressure during lung inflation. It is true that aerosolized particles can be distributed throughout the airways, including the alveoli (17), and bupivacaine aerosols seem to almost completely block airway receptors in dogs and humans (9). In addition, because SARs are located within the bronchial and lobar bronchial muscles (13), whereas RARs are located only in areas of lung parenchyma supplied by bronchi and bronchioles and are concentrated in the more proximal airways (18), it can be assumed that topical lidocaine applied by using the present method would block RARs more easily than SARs. Because the tachycardia that was evoked by two-lung inflation at 20 cm H2O was blocked (indeed reversed) by airway anesthesia (Fig. 1), it presumably was of a reflex nature, although we cannot tell from the present data whether the reflex originated from RARs, SARs, or lung stretch receptors. The finding that use of the higher airway pressure (30 cm H2O) reduced, rather than enhanced, the evoked tachycardia may indicate that the higher level of lung inflation produced direct effects on the heart powerful enough to overwhelm the comparatively small reflex effect. Although we cannot exclude the possibility that complete anesthesia of the peripheral respiratory tracts would affect the lung inflation-induced cardiovascular changes, our results suggest that, in anesthetized humans, neurally-mediated mechanisms are not significantly involved in the decrease in AP and HR that occurs in response to lung inflation.
Because the inflation pressures of 20 and 30 cm H2O were quite high, and because local airway anesthesia failed to affect the depressor effects, it is possible that the reduction in venous return and the direct cardiac compression associated with lung inflation overwhelmed any reflex cardiovascular responses induced by the inflation. Indeed, the actual changes associated with lung inflation differ depending on the hemodynamic and volumetric status in anesthetized humans (19) and the anesthetic state in dogs (16). The major drawback of our study might be that we did not provide any methods to assess venous return and cardiac output, such as a pulmonary catheter with a thermistor or echocardiography. Continuous monitoring and recording of venous return (central venous pressure) and cardiac output in conjunction with HR and AP would have clarified the mechanical effects of lung inflation on the cardiovascular system. As a consequence of this limitation, it is difficult to deduce the relative contributions of mechanically mediated and neurally mediated mechanisms of the decrease in AP and HR in response to lung inflation in anesthetized humans.
Topically administered local anesthetic is known to have systemic effects because of its appearance in the blood after local absorption. Lidocaine given IV in humans suppresses the cough reflex at a plasma concentration of 6 µg/mL (20), and it also suppresses the neuronal responses to noxious stimuli (21). Indeed, IV lidocaine can affect the sensitivity of the baroreflex reflex arch (22). Nevertheless, the cardiovascular responses to lung inflation were essentially similar before and after topical lidocaine, which suggests that those responses at least were not affected to any great extent by such potential systemic effects of local anesthetic administered into the airways.
In addition to the possible systemic effect of lidocaine, there could be several factors affecting the neurally mediated circulatory responses to airway stimulation during anesthesia. Use of 0.5 MAC isoflurane, as in our study, has been reported to preserve baroreflex sensitivity in humans (23) and to maintain HR with only minimal changes (24), but at 1 MAC, isoflurane causes considerable depression of the vascular responses to lung inflation in dogs (16). Although the effect of 0.5 MAC isoflurane on the reflex cardiovascular responses to airway stimulation may be small or negligible, some reflex responses to lung inflation could have been suppressed by the small concentration of isoflurane and, therefore, may not have been seen at all in our study.
In conclusion, the present study, in anesthetized humans, indicates that sympathetic afferent activity induced via stimulation of mechanoreceptors in the airways contributes in part to the cardiovascular responses to inflation of the lungs. The apparently sympathetically mediated responses (tachycardia) induced by lung inflation was blocked by topical application of lidocaine to the airway, but nonsympathetic effects of lung inflation (bradycardia and hypotension) were not. In fact, decreases in HR and AP, which occurred regardless of whether airway pressure was increased to 20 or 30 cm H2O and whether one lung or both lungs were inflated, seem likely to be results of a direct mechanical effect rather than any airway-circulatory reflex. Thus, they would not be expected to be significantly affected by airway anesthesia, although the possibility remains that we achieved an incomplete blockade of the peripheral airway receptors, perhaps leaving intact reflex responses arising from SARs exposed to a high intrathoracic pressure.
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Footnotes |
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This work was presented in part at annual meeting of the American Society of Anesthesiologists, Atlanta, GA 1995.
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References |
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