Ventricular Tachycardia and Cardiovascular Collapse following Flexible Bronchoscopy: Lidocaine Cardiotoxicity

To the Editor:

Flexible bronchoscopy (FB) is commonly performed under mild sedation and lidocaine is the preferred drug for topical anesthesia during the procedure. Although the safety of lidocaine is well established, there are reports of lidocaine toxicity manifesting as seizures after bronchoscopy.¹ Cardiac toxicity from lidocaine is uncommon but has been reported after intravenous infusion² and nerve blocks.³ We recently encountered a near fatal complication following FB.

A 65-year-old male nonsmoker without any comorbidities was planned for bronchoalveolar lavage for evaluation of a right upper lobe cavitary lesion. After obtaining written informed consent, bronchoscopy was performed. No premedication was used and lidocaine was used for topical anesthesia. Five milliliters of 2% lidocaine gel (100 mg) intranasally and 5 sprays of 10% lidocaine to oropharynx (50 mg) were administered.

Following nasal bronchoscopic insertion, 9 mL lidocaine solution (2%) was instilled using spray-as-you-go method through the bronchoscope. The total lidocaine dose was 330 mg (6 mg/kg). Patient underwent airway inspection followed by bronchial washings from right upper lobe (apical segment). Patient was comfortable during the procedure with minimal cough and procedure duration was 10 minutes.

Twenty minutes later in the recovery room, patient became suddenly unresponsive and was found pulseless. Cardiopulmonary resuscitation was immediately initiated.

After 2 minutes, rhythm check demonstrated ventricular tachycardia (VT) (Fig. 1). After synchronized direct current cardioversion, it reverted to normal sinus rhythm.

FIGURE 1: Electrocardiogram following flexible bronchoscopy showing ventricular tachycardia.

Patient was endotracheally intubated and mechanical ventilation was initiated. Arterial blood gas analysis revealed pH 7.23, pCO₂ 56 mm Hg and pO₂ 96 mm Hg. Patient regained consciousness after 15 minutes and was transferred to the respiratory intensive care unit. Serum creatine phosphokinase-MB level was normal and troponin I (qualitative) was negative on serial estimation. A 2D-echocardiography did not reveal any structural cardiac abnormality and ejection fraction was 60%. Patient had 2 more episodes of VT over the next 4 hours which were reverted with cardioversion. Patient was extubated and remained stable for 3 days during which 24-hour Holter monitoring revealed occasional ventricular premature complexes. Patient developed pneumonia and hypoxemic respiratory failure during hospital stay and succumbed to ventilator associated pneumonia and septic shock 2 weeks later. The absence of chest pain, no ST elevation on electrocardiogram, no elevation of cardiac biomarkers and normal echocardiography ruled out an ischemic episode, while normal Holter monitoring excluded any possibility of intrinsic arrhythmia. Thus, we attribute the occurrence of ventricular tachycardia to lidocaine toxicity although the serum lidocaine levels could not be measured.

Lidocaine is also a commonly used antiarrhythmic for ventricular arrhythmias. Cardiac toxicity of lidocaine is potentiated by acidosis, hypercapnia and hypoxia. As seizures can lead to such a metabolic state, lidocaine induced seizures can potentially precipitate cardiotoxicity. It is recommended that lidocaine dose in bronchoscopy be limited to <8.2 mg/kg. The chances of toxicity increase with increasing serum levels and a serum concentration cutoff value of <5 mcg/mL is considered safe. The cardiovascular side effects of lidocaine include slowing of sinus conduction, QRS widening, hypotension, shock and asystole. Lidocaine toxicity is usually dose dependent and risk is increased in individuals with renal and hepatic dysfunction. It usually resolves spontaneously upon drug discontinuation. In our patient, the lidocaine dose was well below the recommended safe limit. Serum lidocaine levels may be unpredictable in patients undergoing bronchoscopy as a significant amount of drug is aspirated via bronchoscope channel during suctioning of bronchial secretions. In our patient, the requirement of suctioning during procedure was less due to minimal cough and bronchial secretions. This might have led to increased systemic absorption of drug leading to high serum levels. Second, due to underlying lung disease, FB might have led to bronchospasm causing respiratory acidosis which can precipitate cardiac toxicity of lidocaine even when dose administered is within safe limits. Also, any inflammatory process involving the airways can increase the systemic absorption of lidocaine that might have contributed to toxicity in our patient. In a study by Sutherland et al⁴ it was found that during bronchoscopy peak serum lidocaine levels are achieved at 30 to 40 minutes after starting the instillation. It coincides with the timing of VT in our patient suggesting it can be attributed to lidocaine. We could find one report of wide QRS complex and bradycardia during FB requiring temporary pacing which was attributable to lidocaine, though patient had recent cardiac surgery and an intrinsic cardiac cause could not be definitely ruled out.⁵ To the best of our knowledge, this is the first report of ventricular tachycardia following bronchoscopy likely due to lidocaine toxicity. This case highlights that during FB, dose of lidocaine administration should be closely monitored and kept to minimum especially in a patient vulnerable to its side effects.

Saurabh Mittal, MD, DM

Anant Mohan, MD

Karan Madan, MD, DM
Department of Pulmonary Medicine and Sleep Disorders All India Institute of Medical Sciences (AIIMS), New Delhi, India