Journal of Asthma

ISSN: 0277-0903 (Print) 1532-4303 (Online) Journal homepage: http://www.tandfonline.com/loi/ijas20

Effect of 4% Lidocaine Inhalation in Bronchial Asthma Gulla Surya Prakash, Surender K. Sharma & J. N. Pande To cite this article: Gulla Surya Prakash, Surender K. Sharma & J. N. Pande (1990) Effect of 4% Lidocaine Inhalation in Bronchial Asthma, Journal of Asthma, 27:2, 81-85 To link to this article: http://dx.doi.org/10.3109/02770909009073301

Published online: 02 Jul 2009.

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Journal of Asthma, 27(2) 8 1-85 ( 1 990)

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ORIGINAL ARTICLES Effect of 4% Lidocaine Inhalation in Bronchial Asthma Gulla Surya Prakash, Surender K. Sharma, and J. N. Pande Department of Medicine All India Institute of Medical Sciences New Delhi, 110029 India

ABSTRACT The effect of 4% lidocaine inhalation was studied in a singfe-blind fashion in 18 patients with chronic stable asthma. inhalation of normal saline solution was used as placebo. None of the parameters except flow rate at 50% of vital capacity showed any statistically significant change from baseline values. Vs0 at 15 min was significantly lower (p < 0.05) after 4% lidocaine inhalation. Considering more than 10% change from the baseline value as significant, 8 of 15 patients showed decrease in airway resistance (Raw) and 7 of the 15 patients showed an increase in specific airway conductance (SGaw) after 15 min of inhalation. However, V50 (8/18 patients), flow rate at 25% vital capacity [i/25(6/15 patients], and forced expiratory flow rate at 25-75'10 of the vital capacity (FEF,,,,) (5/15 patients) showed a decrease after 15 min of 4% lidocaine inhalation. No change in pulmonary function was noted after 30 min of lidocaine inhalation. It i s concluded from this study that lidocaine produces a small bronchodilatory effect on the large airways and a bronchoconstrictor effect on the small airways after 15 min of inhalation, but this effect i s not statistically significant. It can be safely used as topical agent for bronchoscopy in patients with bronchial asthma.

(\iso)

Address correspondence to Dr. S.K. Sharma.

81 Copyright 0 1990 by Marcel Dekker, Inc.

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INTRODUCTION Asthma is a heterogenous condition in its causes, in the mechanism of production of its clinical symptoms, and in the severity of these symptoms. Although various groups of drugs are available, the search for new pharmacological approaches for the relief of bronchospasm continues, because any one, or all, of the agents hitherto in use may fail to produce the desired response. We have studied the effect of inhaled lidocaine on the airway dynamics of a group of individuals with bronchial asthma having moderately severe airflow limitation. Lidocaine is a local anesthetic and is likely to block the neural output from various receptors located in the airways. The importance of neural mechanisms in initiating and perpetuating bronchospasm in bronchial asthma is well established. The few findings reported in the literature regarding the effects of lidocaine are controversial and inconclusive. Moreover, many patients with bronchial asthma are subjected to bronchoscopy for other suspected lesions and the influence of lidocaine aerosols used for surface anesthesia in these subjects on the airway dynamics is unknown. MATERIAL AND METHODS Eleven adult women and 7 adult men with bronchial asthma aged 15-40years (26f 5.8) gave informed consent to participate in the trial. Children were not included in this study. All subjects were nonsmokers. No patient was on wrticosteroid treatment. All bronchodilator drugs were stopped 24 h before the study. The baseline pulmonary function tests were performed on each patient on constant volume body plethysmograph (Morgan, UK). Flow rates were measured with the help of Fleich No. 3 pneumotachograph with a linear response up to 12 literds. The pressure difference across the pneumotach was measured with the help of a Validyne differential pressure transducer. Flow rate was subjected to trapezoidal integration by the computer using commercial software in order to obtain the volume changes. Flow volume curves

were recorded in triplicate and the best of three curves with the higheet flow rate was used for the final analysis of the record. The intrathoracic gas volume was determined using body plethysomography according to the method of Dubois et al. (1).Airway resistance and specific conductance were measured with the subject panting at a frequency of 1Hz.All results were stored on floppy discs. Arterial blood was taken anaerobically while breathing room air under resting conditions, stored at 4"C, and analyzed within 30 min after collection for PO,, PCO,, and pH using Clark's Seviringhaus, and Glass pH electrodes, respectively. The assembly used was that of radiometer model ABL3. Each patient was randomly allocated to recieve either 2 ml of 0.9% saline solution or 2' ml of 4% lidocaine solution administered as aerosol via face mask from a nebulizer. The study with saline (control)and 4% of lidocaine was done on the same patient on separate days. The nebulizer instrument used was the aerolyzer electric inhaler CFIR which produces a n airflow of 14 literdmin and nebulizes 2 ml of lidocaine solution in 8 min. More than 90%of particles produced were between 0.5 and 5 bm in diameter. Pulse rate and blood pressure were recorded before during, and every 15 min after administration of aerosols. Pulmonary function tests were performed in each patient at 15 and 30 min after completion of nebulization. In case of normal saline inhalation, the pulmonary function tests were performed only at 15 min. Postnebulization arterial blood samples were taken at 15 rnin for blood gas analysis. The postnebulization results were compared with the baseline values. Paired Student's t-test was applied to calculate the significance of change in various parameters of lung functions before and after inhalation. Unpaired Student's t-test was applied to determine the difference in various resting parameters on the saline day and lidocaine day. RESULTS Baseline values of pulmonary functions of 18 patients with bronchial asthma on normal saline day and 4% lidocaine day are shown

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Lidocaine Inhalation in Asthma

83

in Table 1. None of the resting parameters showed any statistically significant difference on the two occasions. Various parameters of pulmonary function 15 and 30 min after inhalation of 4% lidocaine are shown in Tables 2 and 3. V50showed a statistically significant decrease (p < 0.05) from baseline aRer 15 rnin of 4% lidocaine inhalation. Other parameters of pulmonary function did not show any statistically signxicant change from the baseline values. None of the parameters of pulmonary function showed any statistically significant change from baseline values after 30 min of lidocaine inhalation. None of the parameters of pulmonary function showed any statistically significant change from baseline values after 15 min of normal saline inhalation. Furthermore, when there was a 10% increase or decrease in various parameters of lung function from baseline values, Raw decreased in 8 of 15 patients and SGaw increased in 7 of 15 patients after 15 min of 4% lidocaine inhalation. V5j50 decreased in 8 of 18 patients, V25decreased in 6 of 15 patients, decreased in 5 of 15 patients. and FEF26-,59b These changes are shown in Table 4. None of the parameters showed any significant change after 30 min of lidocaine inhalation. Fifteen min after normal saline inhalation,

Raw increased in 8 of 14 patients and SGaw decreased in 6 of 14 patients, V 5 0 increased in 6 of 16 patients. There was no statistically significant correlation between AFEV, (L) (pretreatment FEV, (L) - posttreatment FEV, (L)), and ASGaw (S-l cm H,O-l) (pretreatment SGaw - posttreatment SGaw) after 15 and 30 min of lidocaine inhalation. Arterial carbon dioxide tension (Pam,) showed a statistically significant fall (p < 0.05) after 15 rnin of normal saline inhalation (32.7 f 4.5) compared with baseline value (33.8 f 4.2). Arterial oxygen tension (PaO,) however, remained unchanged. There was no statistically significant change in either PaO, or Pam, after 15 min of lidocaine inhalation as compared to the baseline values. No alteration was found in pulse rate or blood pressure during the period of study with either normal saline or lidocaine inhalation. No patient complained of giddiness,tightness in the chest, or breathlessness during either normal saline or 4% lidocaine inhalation.

DISCU SSlON We carried out this study to evaluate the effect of 4% lidocaine inhalation on airway

Table 1. Baseline Values of Pulmonary Functions of 18 Patients with Bronchial Asthma on Two Occasions ~~~~

~

PARAMETER

1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

11. 12. 13. 14. 15. 16.

SALINE DAY

FVC (L) FEV, (L) FEV,/FVC(%) PEF (Us)

Vso (Us)

FEF25-75 (us) v25 (Us) Raw (cmHzO/Us) SGaw (5 - 1cm H,OTLC (L) svc (L) RV (L) FRC (L) RViTLC ('10) PaO, (mmHg) PaC0, (mmHg)

')

2.610 1.593 64.153 3.725 1.538 1.327 0.618 4.735 0.069 4.586 2.540 2.042 3.163 41.909 79.41 33.146

All data are presented as mean f SD. None of the parameters showed any significant difference.

f 0.518 f 0.490 f 16.025

1.562 f 0.985 f 0.714 f 0.340 f 2.168 f 0.046 f 1.069 f 0.413 f 1.183 f 0.927 f 15.655 f 12.76 3.92 f

*

LIDOCAINE DAY

2.689 f 0.650 1.638 f 0.517 63.769 f 14.226 3.969 f 1.697 1.660 f 1.029 0.68 1.315 0.589 f 0.322 3.994 f 1.447 0.067 f 0.039 4.89 f 0.774 2.557 f 0.346 2.328 f 0.765 2.942 f 0.676 46.909 f 8.949 79.5 f 10.76 33.353 f 4.26

*

Prakash et al.

04

Table 2. Pulmonary Functions Parameters After 15 min of 4% Lidocaine Inhalation PARAMETER

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1. 2. 3. 4. 5.

PRETREATMENT

Fvc (L) FEVl (L) FEV,/FVC(%) PEF (Us) Vso (us)a

6. V25 (US) 7. FEF25-,5 (US) 8. Raw (cmHzO/Us) 9. SCaw (S-lcmH2O-') 10. TLC (L) 11. svc (L) 12. RV (L) 13. FRC (L) 14. RVnLC (%) 15. Pa02 (mmHg) 16. PaC02 (mmHg)

aj/50at 15 min was statistically significantly lower (p change. All data are presented as mean f SD.

2.73 1.68 62.63 3.84 1.6 0.54 1.22 4.36 0.06 4.95 2.74 2.21 2.93 43.87 79.42 33.98

0.660 0.54 14.04 1.57 0.94 f 0.29 f 0.64 f 1.98 f 0.04 f 0.84 f 0.46 f 0.78 f 0.68 f 10.15 f 9.91 f 4.13 f f f f f

POSTTREATMENT

2.75 f 0.63 1.66 f 0.52 62.19 f 13.15 3.67 f 1.4 1.44 f 0.89 0.50 f 0.23 1.15 f 0.60 4.95 f 2.38 0.07 f 0.06 4.92 f 0.97 2.81 f 0.61 2.10 f 0.96 3.09 f 0.79 41.47 f 13.71 76.73 f 12.55 32.67 f 4.96

c 0.05); none of the other parameters showed any statistical significant

dynamics and gas exchange in patients with bronchial asthma and also to evaluate the safety of lidocaine inhalation as a topical anaesthetic in asthmatic subjects as results of the previous studies are variable and inconclusive (2-5). In general, no significant change was observed in various parameters of pulmonary functions except v50; which showed a significant decrease 15 min after 4% lidocaine inhalation. The inhalation apparatus used in this study produced particles which were less than 5 pm in diameter and the majority of these particles, by virtue of their size, penetrate into the smaller airways. This is evidenced in this study by a significant decrease in V after 15 min of 4% lidocaine 69 inhalation, whch signifies the effect of drug

on the small airways. The size of the particle makes it unlikely that a significant amount of deposition occurred in the nose and pharynx. There is no significant change in arterial blood gases after 4% lidocaine inhalation compared with baseline values. Miller et al. (2)showed significant decrease (p < 0.01) in FEF,,,,, and an increase (p < 0.01) in SRaw in 14 subjects with reversible obstructive lung disease immediately after 1% lidocaine inhalation. Clinically they also found worsening of symptoms in 3 of 14 patients. Weiss and Patwardhan (3) showed a bimodal response to 4% lidocaine aerosol administration following an initial reduction of approximately 20% in indices of expiratory airflow in all patients.

Table 3. Pulmonary Functions Parameters After 30 min of 4% Lidocaine Inhalation PARAMETER

~-~~~ ~

1. FVC (L) 2. FEVl IL) 3. FEV,/FVC(%) 4. PEF (Us) 5. FEF25-75 (US) 6. Raw (cmH20/L/s) 7. SCaw (S-lcmH,O-

PRETREATMENT ~~

2.68 1.83 67.4 4.0 1.41 3.66 0.07

POSTTREATMENT

~

f 0.63

f 0.55 f 12.44 rt 1.41 f 0.633 f 0.88 f 0.02

2.81 1.83 65.0 4.16 1.32 3.91 0.07

None of the parameters showed any statistically significant change after 30 min of 4% lidocaine inhalation. All data are presented as mean f SD.

*

0.61 f 0.54 f 14.91 1.28 f 0.65 5 1.12 f 0.03

*

Lidocaine Inhalation in Asthma

85

Table 4. Number of Patients Showing More Than 10% Change from Baseline Values After 15 and 30 min of 4% Lidocaine inhalation 15 MIN

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PARAMETER 1. Fvc (L) 2. FEV, (L) 3. FEV,/FEV(%) 4. PEF (Us) 5. V5(J (Us) 6. V25 (US) 7. FEF25-7, (US) 8. Raw (crnH20/Us) 9. SCaw (S-1crnH20-1) 10. TLC (L) 11. svc (L) 12. RV (L) 13. FRC (L) 14. RV/TLC (%) 15. Pa02 (rnmHg) 16. PaC02 (rnrnHg)

30 MIN

10% INCREASE

10% DECREASE

10% INCREASE

10% DECREASE

2

2

1

3 1

2 1 4

1 2 3 2

3 2 3

3 3 3

2 5 3 4 3 5

7 4 4 6 5 5 1

2

Fish and Peterman (4) showed deterioration in pulmonary functions immediately aRer 4% lidocaine inhalation. Salisburg et al. (5) studied the effect of topical lidocaine anesthesia in 7 patients with chronic obstructive pulmonary disease and 10 control subjects. They found a significant decrease (p < 0.05) in arterial oxygen tension in both patients and control subjects. In comparison to the above studies, we did not find any significant change in either airway dynamics or in arterial blood gases after 4% lidocaine inhalation in patients with moderate bronchial asthma. However, we have further analyzed the data and found a significant (10% change from the baseline value) decrease in Raw in 8 of 15 patients and a significant increase in SGaw in 7 of 15 patients after 15 min of lidocaine inhalation. This shows a significant improvement in the large airway function. However, we found significant deterioration in small airway function after 15 min of lidocaine inhalation. These changes in large airway and small airway functions are small and not statistically significant. Furthermore, none of the parameters showed any significant change after 30 min of lidocaine inhalation. We have not observed any symptomatic deterioration

8 8

6 5 8 5 3 1 7 3

0

6

2 4

in our patients. On the basis of the findings of this study, inhalation of 4% lidocaine can be safely recommended in patients with bronchial asthma who are undergoing procedures such as fiberoptic bronchoscopy etc., however, no studies are available in the literature on the efficacy of administration of lidocaine in patients with severe intractable asthma. Further studies are required to define this parameter.

REFERENCES 1. Dubois AB,Botelho SY, Bedell GN, Marshall R, Corm JH Jr: A rapid plethysmographicmethod for measuring thoracic gas volume. J Clin Invest 35:322,1956. 2. Miller WC,Robert AWE: Effect of nebulized lidocaine on reactive airways. A m Rev Respir Dis 111:739, 1975. 3. Weiss EB,Patwardhan, AV: "he response to lidocaine in bronchial asthma. Chest 72:429, 1977. 4. Fish JE, Peterman VI:Effect of inhaled lidocaine on airway function in asthmatic subjects. Respiration 37:201, 1979. 5. Salisburg BG, Metzgir LF, Altose MD, Stanley NN, Cherniac NS: Effect of fiberoptic bronchoscopy on respiratory performance in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 109:691, 1984.

Effect of 4% lidocaine inhalation in bronchial asthma.

The effect of 4% lidocaine inhalation was studied in a single-blind fashion in 18 patients with chronic stable asthma. Inhalation of normal saline sol...
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