Table of Contents  
CASE REPORT
Year : 2016  |  Volume : 9  |  Issue : 1  |  Page : 121-123  

Sudden onset of atrial fibrillation during neck dissection: Vagal atrial fibrillation


Department of Anaesthesiology, TNMC and BYL Nair Ch. Hospital, Mumbai, Maharashtra, India

Date of Web Publication22-Dec-2015

Correspondence Address:
Anjana Sahu
No. 69, C-Block, Jagjivanram Hospital Campus, Maratha Mandir Road, Mumbai Central, Mumbai - 400 008, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0975-2870.167985

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  Abstract 

Intraoperative vagal stimulation can lead to onset of atrial fibrillation (AF). The role of vagus mediated AF is not very much acknowledged. We report a case of AF during handling of great vessels in the neck region. After ruling out other causes of AF, we concluded that this sudden occurrence of AF could be a case of vagus nerve stimulation. In our case report, we also discuss the role of cholinergic activity in the development of AF and its treatment.

Keywords: Atrial fibrillation, free flap surgery, vagal atrial fibrillation


How to cite this article:
Sahu A, Kumar IH, Rahulgade PK, Awarde RG. Sudden onset of atrial fibrillation during neck dissection: Vagal atrial fibrillation . Med J DY Patil Univ 2016;9:121-3

How to cite this URL:
Sahu A, Kumar IH, Rahulgade PK, Awarde RG. Sudden onset of atrial fibrillation during neck dissection: Vagal atrial fibrillation . Med J DY Patil Univ [serial online] 2016 [cited 2020 Aug 8];9:121-3. Available from: http://www.mjdrdypu.org/text.asp?2016/9/1/121/167985


  Introduction Top


Atrial fibrillation (AF) is the most common arrhythmia occurring in the postoperative period. The incidence of intraoperative occurrence is less. It is a cardiac condition but may have many extracardiac etiologies. [1] We are reporting the incidence of AF during free flap reconstruction in head and neck surgery due to vagus nerve stimulation. Vagal stimulation causes bradyarrhythmias, but it is now well-known that vagal stimulation can cause AF. [2],[3] Hence, clinical vigilance is necessary during the handling of great vessels in the neck area. This case report also highlights the vagal mechanism leading to the onset of AF and its treatment.


  Case Report Top


A 63-year-old female weighing 40 kg presented with swelling of the right cheek. She was diagnosed with the squamous cell carcinoma of cheek and was scheduled for wide local excision of the mass with right hemimandibulectomy with radical neck dissection and reconstruction with anterolateral thigh free flap. Her biochemical routine investigations were within normal limit. Her electrocardiogram (ECG), two-dimensional-echocardiography, chest X-ray were normal. On airway examination, her mouth opening was one and half fingerbreadth and Mallampati airway Class IV with a normal range of neck movement.

After obtaining and confirming written informed consent and nil by mouth status, patient was connected to the multiparameter monitor-ECG, peripheral oxygen saturation (SpO 2 ), noninvasive blood pressure (BP), end-tidal carbon dioxide (EtCO 2 ). Wide bore 18G venous line was secured on right upper limb. Intravenous (IV) glycopyrrolate 0.2 mg and IV dexamethasone 8 mg were given. Fluid ringer lactate was started. A peripherally inserted central catheter was placed via right cubital basilic vein for central venous pressure (CVP) monitoring. Her heart rate (HR) was 78/min, regular rhythm, pulse was normovolemic, and BP was 128/74 mmHg. Patient was premedicated with IV midazolam 0.02 mg/kg and IV fentanyl 2 µg/kg. Patient was induced with IV propofol 1.5 mg/kg and after confirming mask ventilation, muscle relaxant IV succinylcholine 2 mg/kg was given. Nasal intubation was done with North Pole 7.5 size preformed RAE cuffed endotracheal tube. The patient was maintained on oxygen and air with FiO 2 0.5 and isoflurane (0.9-1%). Muscle relaxation was achieved with IV vecuronium with loading dose 0.08 mg/kg and intermittent maintenance dose of 0.02 mg/kg. Our anesthetic goals were to maintain the EtCO 2 in the range of 30-35 mmHg, BP above 100 mmHg, urine output 0.5-1 ml/h with adequate fluid infusion and normothermia using a convective warmer.

The surgeon did the tracheostomy as part of the procedure with 8.5 mm cuffed tracheostomy tube. The growth was excised along with right hemimandible, and the right neck dissection was done and prepared for the graft. When surgeon was preparing the internal jugular vein for venous anastomosis, the sudden change in the ECG rhythm was observed on the monitor. Transient bradycardia (HR 52-60) followed by atrial premature ectopics, supraventricular tachycardia, junctional ectopics, and the final picture of sustained AF. Monitor showed HR 130-150/min, SpO 2 100%, EtCO 2 14, and BP 63/36 mmHg, and there were missed beats on radial palpation with the rate of 52-54/min irregularly irregular. Soon we informed the surgeons and the arterial blood gas (ABG) sample sent, showed pH 7.5, and normal values of electrolytes. BP was managed with fluid and two aliquots of IV ephedrine 6 mg each. Manual ventilation with 100% O 2 started to maintain EtCO 2 above 20. One unit of blood was transfused slowly as the blood loss exceeded the allowable limit. CVP was 8-10 cm H 2 O [Figure 1]. Arterial line was secured, and invasive BP monitoring was started. ABG sample was sent again which showed normal study with normal electrolytes. To control the rate IV esmolol 10 mg was given over 10 min. To control the rhythm IV amiodarone 150 mg administered over 10 min and infusion at 1 mg/min for 6 h.
Figure 1: Intraoperative electrocardiogram showing rhythm of atrial fibrillation

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Flap vessels were anastomosed to the facial artery (end to end) and the right internal jugular vein (end to side). Subcutaneous low molecular weight heparin was given intraoperatively to prevent thrombosis as an anticoagulant and was continued postoperatively. Surgery was continued for 4 more hours. The patient was not reversed and shifted to Postanesthesia Care Unit (PACU) with a tracheostomy tube in situ. In the PACU, she was put on a ventilator. IV amiodarone infusion continued at 0.5 mg/h for 18 h (total duration of amiodarone infusion was 24 h). In the initial postoperative period the 12 lead ECG showed AF the rhythm became normal after 6 h of shifting to PACU. Postoperative chest X-ray and serial ABGs were normal. The postoperative course was uneventful. She was put on tablet amiodarone 100 mg TDS for 15 days. She was gradually weaned off from the ventilator on day 2. She was shifted to the ward on day 3 with a tracheostomy tube in situ.


  Discussion Top


AF is an excessively rapid and irregular atrial focus with no p-wave appearing on ECG. This is described as irregularly irregular rhythm and may be associated with pulse deficit. QRS complex is normal, and the atrial rate varies from 300 to 350. The major intraoperative causes are surgical manipulation of atrium, pulmonary embolism (PE), electrolyte imbalance (sodium, potassium, calcium, and magnesium), vagal manipulation, age more than 60 years, [4] malignancy, [5] and mechanical irritation of pulmonary vein due to pressure over left atrium in case of esophagitis, hiatus hernia. [1] Cardiac causes are hypertension, valvular heart disease, coronary artery disease, cardiac failure. [5]

Therefore to find out the cause of intraoperative AF, we should keep in mind all the possible conditions. In our case, the risk factors were firstly the site of operation where all the great vessels and neural plexuses were exposed hence vulnerable for venous air embolism (VAE) and vagal manipulations. secondly there was an age factor >60 years and thirdly presence of malignancy. Among these, the most common is PE. Geibel et al. found sinus tachycardia and atrial arrhythmias in 83% of patients with a confirmed diagnosis of PE. [6] The intraoperative manifestations in PE are tachycardia, hypotension, decrease in SpO 2 , sudden fall of EtCO 2 , and arrhythmias while in VAE presence of wheeze and mill wheel murmur in addition of these symptoms ABG analysis in PE is hypoxemia, respiratory alkalosis, and hypocarbia. Systemic arterial hypoxemia is the most sensitive manifestation of PE.

In our case, we ruled out the possibility of PE and VAE as there was no decrease in SpO 2 at any point of time, serial ABGs showed no alkalosis, acidosis, hypoxia, and hypercarbia: Though there was transient decrease in EtCO 2 , (due to sudden decrease in cardiac output due to AF), no wheeze and no murmur on auscultation. Electrolyte imbalance was also ruled out as the cause of AF. Patient's temperature was well-maintained. The possibility of central venous catheter-induced arrhythmia was also ruled out in confirming the position of the catheter tip by postoperative chest X-ray. As the site of operation was the head and neck area and the time of onset of AF coincided with the preparation of internal jugular vein for the venous anastomosis. Hence it would have been a possibility that the vagus nerve manipulation stimulated the cholinergic fibers at the right atrium and vagal AF resulted. The autonomic nervous system plays an important role in the occurrence of AF. [2],[5] Cardiac parasympathetic stimulations are mediated through the vagus nerve and increased parasympathetic tone may cause vagal AF. Coumel [2] described the terms, adrenergic and vagal AF. Adrenergic AF occurs in patient with structural heart disease while vagal AF without underlying heart disease. Vagal AF is often preceded by bradycardia. I KACh is an inwardly rectified K+ current carried by G-protein regulated inward rectifier K+ channels (GIRK) and activated by muscarinic acetylcholine receptors (M 2 AChRs). [7] This is the main mediator of vagal activity. In SAN, I KACh causes membrane hyperpolarization and slowing of pacemaker activity. In atrial myocytes, I KACh causes atrial repolarization and shortens the action potential duration (APD), which facilitates re-entry and tachyarrhythmias. The M 2 AChRs inhibit gap junction communication, which causes a decrease in conduction velocity in the atrium and facilitate re-entry and tachyarrhythmia. It increases spatial dispersion in atrial refractoriness, and APD. The APD/effective refractory period shortening and their increased heterogeneity facilitate reentry and tachyarrhythmia. [8] One study suggested that vagal stimulation shortens fibrillatory cycle length in pulmonary veins and triggered AF. [9]

Prophylactic use of carotid sheath infiltration with local anesthetic decreases the incidence of arrhythmias. Treatment of intraoperative AF includes, beta-blocker, calcium channel blocker, but they are more effective in case of structural heart disease with adrenergic AF. Electrical cardioversion should be considered if patient is hemodynamically unstable. The primary goal is to control the ventricular rate to achieve hemodynamic stability and then the restoration of sinus rhythm. Antiarrhythmics Class I flecainide, quinidine, and disopyramide are useful in treating vagal AF. [10] Administration of anti-arrhythmic Class III amiodarone has been used for rate control and cardioversion. It eliminates the difference in I KACh densities between left atrial (LA) and right atrial (RA), but I KACh is still higher in LA and RA appendage. This decreased dispersion of I KACh densities may be the reason of amiodarone efficacy in AF. [10] Radiofrequency ablation of the vagus nerve is also a useful technique in treating AF. In near future, selective GIRK blockers may help in treating vagal AF. The published data for the treatment of vagal AF are still limited.


  Conclusion Top


Head and neck site for any kind of operation is always challenging to the anesthesiologist. The presence of great vessels and nerves makes it more vulnerable. VAE is always a concern though it is rare. Vagal manipulations can cause AF and have a detrimental effect. Longstanding AF can lead to episodes of thromboembolism, stroke, and heart failure with fatal prognosis. Timely recognition of rhythm and appropriate treatment can prevent such life-threatening events.

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Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Stöllberger C, Gatterer E, Finsterer J. Central and peripheral vagal nerve involvement in atrial fibrillation. Eur Heart J 2009;30:1012.  Back to cited text no. 1
    
2.
Coumel P. Paroxysmal atrial fibrillation: A disorder of autonomic tone? Eur Heart J 1994;15(Suppl A):9-16.  Back to cited text no. 2
    
3.
Srinivasan B, Awasthi A. Transient atrial fibrillation after the implantation of a vagus nerve stimulator. Epilepsia 2004;45:1645.  Back to cited text no. 3
    
4.
Furberg CD, Psaty BM, Manolio TA, Gardin JM, Smith VE, Rautaharju PM. Prevalence of atrial fibrillation in elderly subjects (the Cardiovascular Health Study). Am J Cardiol 1994;74:236-41.  Back to cited text no. 4
    
5.
de Vos CB, Nieuwlaat R, Crijns HJ, Camm AJ, LeHeuzey JY, Kirchhof CJ, et al. Autonomic trigger patterns and anti-arrhythmic treatment of paroxysmal atrial fibrillation: Data from the Euro Heart Survey. Eur Heart J 2008;29:632-9.  Back to cited text no. 5
    
6.
Geibel A, Zehender M, Kasper W, Olschewski M, Klima C, Konstantinides SV. Prognostic value of the ECG on admission in patients with acute major pulmonary embolism. Eur Respir J 2005;25:843-8.  Back to cited text no. 6
    
7.
Sarmast F, Kolli A, Zaitsev A, Parisian K, Dhamoon AS, Guha PK, et al. Cholinergic atrial fibrillation: I(K,ACh) gradients determine unequal left/right atrial frequencies and rotor dynamics. Cardiovasc Res 2003;59:863-73.  Back to cited text no. 7
    
8.
Liu L, Nattel S. Differing sympathetic and vagal effects on atrial fibrillation in dogs: Role of refractoriness heterogeneity. Am J Physiol 1997;273:H805-16.  Back to cited text no. 8
    
9.
Zimmermann M, Kalusche D. Fluctuation in autonomic tone is a major determinant of sustained atrial arrhythmias in patients with focal ectopy originating from the pulmonary veins. J Cardiovasc Electrophysiol 2001;12:285-91.  Back to cited text no. 9
    
10.
Huang CX, Zhao QY, Liang JJ, Chen H, Yang B, Jiang H, et al. Differential densities of muscarinic acetylcholine receptor and I(K,ACh) in canine supraventricular tissues and the effect of amiodarone on cholinergic atrial fibrillation and I(K,ACh). Cardiology 2006;106:36-43.  Back to cited text no. 10
    


    Figures

  [Figure 1]


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