Why does intubation cause bradycardia




















This was to be carried out under general anaesthesia. She gave a history of a myomectomy under general anaesthesia in , which was uneventful, and asthma for the last 25 yr. She was given 5 mg diazepam by mouth before going to the operating theatre.

Sinus rhythm was present throughout the episode. Immediately after direct laryngoscopy by the surgeon, the heart rate suddenly decreased to 28 beats min —1. Despite withdrawal of the laryngoscope, bradycardia persisted.

Atropine 0. A further dose of atropine 0. Hypotension persisted and was treated with infusion of ml of hydroxyethyl starch. Arterial blood gas and serum electrolyte measurements were normal. After 12 min the patient became cadiovascularly stable.

The operation was postponed, and the patient recovered without sequelae. Subsequent cardiac examination was normal. Six months later the same patient returned for treatment of nasal polyps, by nasal endoscopy. Her hoarseness had resolved with medical therapy. For the second operation, she was given diazepam 5 mg by mouth.

After tracheal intubation, the heart rate decreased. After ephedrine 10 mg i. The remainder of the surgery and anaesthesia was uneventful. The pacemaker was withdrawn the day after surgery. Inadequate CO can lead to cardiovascular collapse and decreased tissue perfusion of vital organs such as the brain, heart, gut, and kidneys. Signs may be immediately obvious hypotension, cardiac rhythm change on the monitor from poorly perfused coronaries or more subtle skin mottling, change in capillary refill.

Unless you have started high-dose vasopressors, hypotension and decreased perfusion is likely caused by changes in VR or HR. Patient-specific factors will help guide your workup.

In this case, your management will depend on underlying rhythm, presence of a pulse, and evidence of ischemia. Problem — adequate sedation.

In some cases, your patients may narrowly dodge adverse outcomes during RSI, only to develop hemodynamic collapse when post-intubation sedation is initiated. While it is critical to be on the lookout for this complication of sedation packages, do not be lured into thinking your patient must do without sedation.

Be creative! It may be necessary to avoid protocoled sedation packages that will endanger your patient. Be sure to talk to your nurse and develop a plan before you leave the room.

Ketamine may be a good resource. While commonly used as an RSI medication, ketamine can also be used in the sedation package. This may be a strategy that you need to discuss with nursing and pharmacy staff at your hospital first. Fentanyl is also your friend for these patients.

It has a quick onset and short duration of action, allowing you to pause if MAPs are looking low. Fluid boluses and even drip pressors may be a necessary adjunct to keeping your patient adequately sedated as opposed to leaving the sedation off to avoid pressors, with a thrashing and miserable patient. Conclusion While definitive evidence has yet to be supplied, preventative measures, high clinical suspicion, and patient-specific adaptations of intubation technique and care are likely to minimize the degree and frequency of post-intubation hemodynamic instability.

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Biomed Tech Berl ; 56 4 : - Previous Next. Back to top. In this issue. Respiratory Care Vol. Download PDF. Article Alerts. Email Article. Thank you for your interest in spreading the word on American Association for Respiratory Care. Your Personal Message. The patient was taken out of suspension and cardiopulmonary resuscitation was initiated per ACLS protocol for approximately five minutes.

Asystole converted to sinus tachycardia. Postcardiac arrest electrocardiogram, arterial blood gas, chemistry panel, and cardiac enzymes were obtained and within normal limits. The patient was awakened and extubated uneventfully. Cardiac arrest following intubation is rare, especially intraoperatively following endotracheal tube exchange [ 4 ]. On thorough review of this case, it is believed that the asystole occurred secondary to several contributions: strong vagal reflex, suspension laryngoscopy, vagotonic drugs fentanyl , and reinsertion of the endotracheal tube causing stimulation of the larynx and trachea.

A strong vagal reflex is more commonly seen in the pediatric population which has implemented the use of atropine as a premedication [ 5 ]. The belief is that during laryngoscopy, an arrest of the sinoatrial node occurs with a simultaneous impulse via the atrioventricular node leading to bradycardia and asystole.

This patient displayed strong vagal tone throughout the case. Patients intubated under suspension laryngoscopy can have a more pronounced vagal response to the stimulation than direct laryngoscopy. When utilizing suspension, as opposed to the Macintosh curved blade, the undersurface of the epiglottis is stimulated.

This portion of the airway is innervated by the internal branch of the superior laryngeal nerve derived from the vagus nerve. Stimulation of this can promote bradycardia.

Identifying patients who may benefit from premedication with a vagolytic drug such as atropine can prevent adversity. Patients intubated via suspension laryngoscopy may warrant prophylactic vagolytics. The threshold for administration of a vagolytic while a patient is in suspension should be lower especially if the surgeon is operating on the glottis. This case highlights the importance of continued vigilance even following the initial manipulation of the airway by both direct laryngoscopy and suspension laryngoscopy.

Glassman et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.



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