Year : 2011 | Volume
: 5 | Issue : 3 | Page : 339--341
Role of clonidine in perioperative acute atrial fibrillation
Vishal Garg, KN Prasad
Department of Anaesthesiology, Kasturba Medical College, Manipal, Karnataka, India
Department of Anaesthesiology, Kasturba Medical College, Manipal, Karnataka - 576 104
We report a case of acute onset atrial fibrillation (AF) that presented for emergency surgery where rate control and sinus rhythm were successfully achieved using clonidine. Patient had acute AF with high blood pressure. Metoprolol failed to decrease the ventricular rate and blood pressure but with clonidine, we could achieve both the goals. Also, rhythm reverted to a sinus rhythm and continued to be in sinus rhythm after administering clonidine.
|How to cite this article:|
Garg V, Prasad K N. Role of clonidine in perioperative acute atrial fibrillation.Saudi J Anaesth 2011;5:339-341
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Garg V, Prasad K N. Role of clonidine in perioperative acute atrial fibrillation. Saudi J Anaesth [serial online] 2011 [cited 2022 Oct 7 ];5:339-341
Available from: https://www.saudija.org/text.asp?2011/5/3/339/84119
Atrial fibrillation (AF) is one of the commonest arrhythmias seen in perioperative period. It can present in a paroxysmal, persistent, or a chronic form. Paroxysmal AF is self-terminating, whereas persistent AF requires electrical or chemical cardioversion to establish sinus rhythm. Chronic AF is long-standing persistent AF where cardioversion was not successful or has not been attempted. The management of AF includes removal of any precipitating factors and treatment of the arrhythmia itself. Electrical cardioversion is the preferred method in hemodynamically unstable patient, whereas several pharmacological methods are described in literature for rate control and achieving sinus rhythm in hemodynamically stable patients. Clonidine is not routinely used for AF. We discuss our experience of using clonidine in a patient with acute AF.
A 64-year-old female patient presented for an emergency laparotomy in view of mesenteric vein thrombosis. Apart from being hypertensive, patient did not have any other comorbid illnesses and had a moderate effort tolerance. Preoperative investigations revealed hemoglobin - 8.2 gm%, total leukocyte count - 18 400 mm -3 , platelet count - 516 000 mm -3 , and ESR - 47. Renal and liver function tests were within normal limits. 12-lead ECG on admission showed sinus tachycardia with a rate of 110 per minute and no other significant changes. Chest radiograph showed clear lung fields and no other abnormality. Echocardiogram done 2 years ago was essentially normal. Patient was received in preoperative area about 16 hours after the admission, and on examination, she was conscious, cooperative, and oriented. She complained of severe pain abdomen. On general physical examination, patient was pale, had irregularly irregular pulse with a rate of 160 per minute, and good volume. Patient had a rapid, shallow breathing pattern with a respiratory rate of about 35 breaths per minute. Abdomen was grossly distended with guarding and rigidity on palpation. Patient was shifted to the operating room and baseline monitoring which included 5-lead ECG, noninvasive blood pressure, and SpO 2 was commenced. ECG on the monitor showed AF with a heart rate of 180 to 190 per minute. Apex pulse deficit was 30 to 35/min. AF was confirmed with a 12-lead ECG. Blood pressure was 200/120 mmHg and room air saturation was 92%. Arterial blood gas on room air showed pH of 7.425; pO 2 , 56 mmHg, pCO 2 , 30.3 mmHg, and HCO 3 , 19.4 meq.l -1 . We repeated serum sodium and potassium, which were 135 meq.l -1 and 4.3 meq.l -1 , respectively. Oxygen was started through face mask at 6 l/min flow which improved SpO 2 to 97%. Meanwhile, central venous catheter was secured and first recording of central venous pressure was recorded to be 24 mmHg. This ruled out any hypovolemia. We decided to use metoprolol to control the rate and the blood pressure. Invasive blood pressure monitoring was commenced and 4 mg (0.1 mg.kg -1 ) of i.v. metoprolol was given. This reduced the heart rate to about 160 per minute and pulse rate came down to 140 per minute. There was no change in blood pressure, which continued to be in the range of 180 to 210 mmHg systolic even after 15 minutes of administering metoprolol. 100 μg fentanyl (2.5 μg.kg -1 ) was given to relieve pain and 40 μg clonidine (1 μg.kg -1 ) was administered intravenously to lower the blood pressure and also to reduce the analgesic and anesthetic requirement subsequently. Blood pressure reduced up to 140 to 150 mmHg systolic and heart rate came down to 120/ min with a pulse rate of 100/min. With this, we decided to induce anesthesia; rapid sequence induction was done with thiopentone and succinylcholine and subsequent analgesia was provided with morphine infusion in a dose of 1 mg/hr, which was continued in postoperative period for analgesia. There was no hemodynamic response to intubation. Anesthesia was maintained with isoflurane in air and oxygen. After 5 minutes into the surgery, we noticed that the rhythm reverted to sinus with a rate of 80/min and blood pressure stabilized between 110 and 120 mmHg systolic. Approximately 2 l of ascitic fluid was drained once abdomen was opened. This improved the lung dynamics and with fiO 2 of 0.4, SpO 2 was maintained between 98 and 99%. Central venous pressure came down to 14 mm Hg after opening the abdomen and it was maintained between 12 and 15 mmHg throughout the procedure. A segment of bowel was found to be gangrenous, which was resected and anastomosed by the surgeons. Urine output was adequate throughout the procedure that lasted for 4 hours and rhythm continued to be sinus throughout with no hemodynamic instability. Trachea was extubated at the end of the procedure as there was no indication for need of postoperative ventilation and patient was awake after reversing the residual neuromuscular blockade and tapering off the anesthetic. Patient was shifted to intensive care unit for monitoring. Postoperative period was uneventful and there were no further episodes of AF.
AF is one of the common arrhythmias seen in a surgical patient. The management includes removal of the precipitating factor and treatment of the arrhythmia itself. Direct current cardioversion is the mainstay of treatment in unstable patients, whereas various pharmacological methods are described in the literature for rhythm control and rate control. Clonidine is not routinely used drug for AF. In the above mentioned case, we had an interesting situation where AF was of recent onset since the ECG recorded at the time of admission to the hospital was normal and the blood pressure was very high. We had ruled out most of the acute precipitating factors of AF, such as hypoxia, hypovolemia, acid-base abnormalities, and electrolyte imbalance. Since the patient was hemodynamically stable, we decided to use metoprolol, considering that it would help in rate control and also would decrease the blood pressure. There was no significant change in either the heart rate or the blood pressure even after 15 minutes of administering the drug. Multitude factors could have been the cause of this acute AF, chief among them being abdominal pain and thereby aggravating the hypertension, we decided to tackle both the pain and hypertension with clonidine along with fentanyl. We also considered other advantages of using clonidine in such a scenario, which would include anxiolysis, improved perioperative hemodynamic stability in patients with mild or moderate arterial hypertension with a reduction of the anesthetic requirement,  decreased laryngoscopy response,  and decreased requirement of intraoperative and postoperative narcotic analgesia.  We could have used amiodarone for rhythm control but decided against it in view of the various other advantages associated with clonidine. The heart rate and blood pressure came down within reasonable limits after few minutes of administering clonidine, but the rhythm was still AF. We induced anesthesia at this juncture and after five minutes into the surgery, the rhythm reverted to a sinus rhythm with a normal heart rate and blood pressure. There was no rhythm disturbance thereafter. We believe that the reason for termination of AF could have been due to combined effect of clonidine, along with opioid analgesia. On literature search, we found that Roth et al. had reported use of clonidine in patients with acute AF and concluded that low-dose clonidine was an easy, efficient, and effective treatment for patients with rapid AF who were hemodynamically stable. Six of the nine patients in whom clonidine was used, rhythm reverted to normal sinus rhythm in the study done by Roth et al. In another study done by Simpson et al. where they assessed the role of clonidine in new onset rapid AF, they concluded that clonidine was effective in controlling ventricular rate in new onset AF. Though it may not be appropriate to attribute the termination of AF in this patient due to clonidine alone, the role of clonidine in achieving an acceptable heart rate and possibly sinus rhythm cannot be undermined.
In conclusion, clonidine can be a useful drug to be used in a situation with acute AF and hemodynamically stable patient.
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