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Journal of Obstrectic Anaesthesia and Critical Care
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Year : 2014  |  Volume : 4  |  Issue : 2  |  Page : 87-88

Ketamine as bronchodilator in a parturient with bi-directional cardiac shunt undergoing cesarean section

Department of Anaesthesiology and Critical Care Gauhati Medical College and Hospital, Guwahati, Assam, India

Date of Web Publication1-Nov-2014

Correspondence Address:
Priyam Saikia
Gauhati Medical College and Hospital, Guwahati - 781 032, Assam
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2249-4472.143880

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How to cite this article:
Saikia P, De RR, Gogoi SK, Thakuria NC. Ketamine as bronchodilator in a parturient with bi-directional cardiac shunt undergoing cesarean section . J Obstet Anaesth Crit Care 2014;4:87-8

How to cite this URL:
Saikia P, De RR, Gogoi SK, Thakuria NC. Ketamine as bronchodilator in a parturient with bi-directional cardiac shunt undergoing cesarean section . J Obstet Anaesth Crit Care [serial online] 2014 [cited 2023 Feb 5];4:87-8. Available from: https://www.joacc.com/text.asp?2014/4/2/87/143880


Provision of anesthesia care to patients with preexisting pulmonary arterial hypertension (PAH) is a challenging task. [1] Avoidance of factors that can cause further increase in pulmonary vascular resistance (PVR) during anesthesia is a major goal. [1]

A 25-year-old lady weighing 39 kg, diagnosed with ventricular septal defect (VSD) of 20 mm in size with bidirectional shunt (left to right > right to left) and severe PAH was scheduled for emergency caesarean section due to fetal bradycardia. Her heart rate (HR) and blood pressure (BP) were 109 min−1 and 138/90 mmHg, respectively. Breath sounds on auscultation before anesthesia were normal. After preoxygenation, rapid sequence induction was achieved with fentanyl 40 μgm, thiopentone 125 mg, and succinylcholine 60 mg intravenously (IV). With maintenance of Sellick's maneuver, tracheal intubation (Cormack and Lehane Grade II) was done with direct laryngoscopy in a single attempt. Subsequent neuromuscular blockade was maintained with vecuronium. Her end-tidal carbon dioxide (EtCO 2 ) was 22 mmHg with tidal volume (TV) of 375 ml and respiratory rate (RR) of 12 min−1 . This low EtCO 2 was presumed to be due to decreased pulmonary blood flow because of the preexisting bidirectional shunt, so surgery was allowed to start. About 5 min into the surgery, before the delivery of the baby, her peak airway pressure (Ppeak) increased to 50 cm H 2 O from the baseline of 22 cm H 2 O. Inadequate anesthesia, mucous plugging of the airway, esophageal/endobronchial intubation, obstructed tube/circuit, bronchospasm, anaphylaxis, pulmonary aspiration/edema, and pneumothorax were considered as the differential diagnoses for her presentation. [2] We do not have fiber optic bronchoscope at our obstetric operation theater, and thus, endotracheal tube (ETT) placement was reconfirmed with chest auscultation, which revealed bilateral grossly diminished breath sound with wheeze. A quick check of the breathing apparatus did not reveal any kink/obstruction. The capnogram showed an expiratory upstroke. She was immediately disconnected from the ventilator, and her lungs were ventilated with 100% O 2 with a Bain's circuit. There was a marked decrease in compliance with failure of the reservoir bag to reinflate at the end of expiration even with O 2 flow of 10 Lmin−1 . Suctioning of airway revealed a patent ETT and no aspirate. Therefore, bronchospasm was considered. Although the end-tidal halothane concentration was 0.6%, her anesthesia was deepened with titrated IV doses of propofol in 10 mg aliquots and 40 μgm fentanyl. 200 mg hydrocortisone IV and 8 puffs (100μg/puff, metered dose inhaler) salbutamol administered. Salbutamol was repeated thrice (each 5 min apart and in a similar dose) but the bronchospasm persisted. Ventilator settings were changed to deliver a TV of 420 ml, inspiratory to expiratory ratio of 1:3.5, and RR of 14/min; flow volume curve was monitored to detect air trapping (Philips Intellivue 40 Monitor, Germany). Her bronchospasm did not show any response to these measures, and she developed ventricular bigeminy (VB) rhythm around 15 min into the crisis. Preexisting cardiac disease, hypoxia, hypercarbia, use of inhalational anesthetic, hypokalemia are among various causes known to produce VB. [3] Her SpO 2 was 100% and the result of the arterial blood gas taken just before development of VB was awaited. In the meantime, we discontinued halothane and increased the TV. Her arterial blood gas revealed pH 7.26, PaCO 2 55 mmHg, PaO 2 373 mmHg (fiO 2−1), and HCO 3 24.3 mEq/L and standard base excess −2.7 mEq/L. We presumed that hypercarbia and preexisting cardiac status may have led to the development of VB. Considering the preexisting cardiac disease, we decided to administer 60 mg lignocaine IV, even though her HR and BP were within 30% of baseline. Her cardiac rhythm reverted back to sinus rhythm, but bronchospasm persisted. The hemodynamic parameters were stable and there was no other evidence of anaphylaxis. [2] Considering the adverse effect of bronchospasm and hypercarbia on PVR, we administered 20 mg ketamine IV. [1],[4] Within 5 min, her lung compliance improved and there was improvement of monitored spirometry variables. At the end of surgery, her trachea was extubated, and she was shifted to the intensive care unit. She was discharged with a healthy baby on the 4 th postoperative day.

The intracardiac shunt in patients with VSD is initially from left to right. [5] The increased amount of blood ejected into the pulmonary circulation brings about a progressive change in the pulmonary vascular system leading to increase in PVR. [5] As the disease progresses, PVR approaches the systemic vascular resistance (SVR). [5] As both PVR and SVR are dynamic in nature, the direction of shunt changes from beat to beat and the shunt is then known as "bidirectional shunt". [5] Any increase in right to left shunt will lead to hypoxemia, and this reversal of shunt may precipitate right ventricular (RV) failure. Thus, it is very much necessary to maintain a fine balance between PVR and SVR in patients with bidirectional shunt. Catheter-based central neuraxial anesthetic technique is attractive in patients with PAH as they do not increase PVR and causes less hemodynamic perturbations if performed carefully. [1] Spinal anesthesia (without an intrathecal catheter) runs the risk of precipitous decrease in SVR, leading to disastrous complications. [1] Although general anesthesia with endotracheal intubation may increase PVR, it provides the benefit of safe oxygenation and definitive airway. [1] Although commonsense behests us to avoid manipulation of the airway in patients with hyperactive airway disease, no single technique of anesthesia has been documented as superior in patients with bronchospasm. [4] In fact, the anxiety and pain associated with a regional block may precipitate an attack of bronchospasm in susceptible individuals. [4] Considering the above-mentioned factors and the presence of fetal distress, we decided to proceed with general anesthesia with endotracheal intubation and mechanical ventilation. However unfortunately, the patient developed severe bronchospasm intraoperatively.

Among many other dreaded side effects, progressive bronchoconstriction may lead to increased PVR and RV afterload progressing to RV failure, hypoxemia and hypercarbia, and "pulmonary tamponade". [4] Management strategies of perioperative bronchospasm have been published recently. [2],[4] Though we could have used inhaled antimuscarinic agents (their combination with nebulized β2 -agonist produces greater bronchodilatation than a β2 -agonist alone), it was not available with us at that moment. [2] Moreover in another review, inhaled antimuscarinic agents are mentioned to be of limited value in acute asthmatic bronchospasm. [4] Although magnesium sulfate and nitroglycerine has been used in perioperative bronchospasm, we chose not to use them because of their propensity to cause vascular smooth muscle relaxation with the possibility of adverse effect on the shunt fraction and uterine contraction. [4],[6] We did not use adrenaline as there was no clinical evidence of anaphylaxis, and the hemodynamic of the patient was stable. [2] Randomized controlled trials do not provide enough evidence regarding the utility of ketamine in bronchospasm, but it has been used when other agents have failed. [7] Increased PVR has been reported with its use in adult patients with PAH but has been proposed to be safe in children with PAH. [1],[8] Inhaled salbutamol, which was used in this patient, is also known to improve PVR in patients with primary PAH. [9] Considering the overall clinical scenario, we presume that ketamine may be considered in cases of severe bronchospasm of nonallergic etiology when more conventional therapy fails even in settings of increased PVR. But the other factors that might have led to concurrent decrease in PVR should also be given due consideration. [1],[9]

  References Top

Gille J, Seyfarth HJ, Gerlach S, Malcharek M, Czeslick E, Sablotzki A. Perioperative anesthesiological management of patients with pulmonary hypertension. Anesthesiol Res Pract 2012;2012:356982.  Back to cited text no. 1
Dewachter P, Mouton-Faivre C, Emala CW, Beloucif S. Case scenario: Bronchospasm during anesthetic induction. Anesthesiology 2011;114:1200-10.  Back to cited text no. 2
Anand N, Anand M, Mathur AV, Maletha M, Ghildyal SK. Intra-operative ventricular bigeminy: Can retractor be a cause. J Anaesthesiol Clin Pharmacol 2010;26:569-70.  Back to cited text no. 3
[PUBMED]  Medknow Journal  
Woods BD, Sladen RN. Perioperative considerations for the patient with asthma and bronchospasm. Br J Anaesth 2009;103 Suppl 1:i57-65.  Back to cited text no. 4
Joyce JA. Update for nurse anesthetists. Eisenmenger syndrome: An anesthetic conundrum. AANA J 2006;74:233-9.  Back to cited text no. 5
Euser AG, Cipolla MJ. Magnesium sulfate for the treatment of eclampsia: A brief review. Stroke 2009;40:1169-75.  Back to cited text no. 6
Goyal S, Agrawal A. Ketamine in status asthmaticus: A review. Indian J Crit Care Med 2013;17:154-61.  Back to cited text no. 7
[PUBMED]  Medknow Journal  
Maxwell BG, Jackson E. Role of ketamine in the management of pulmonary hypertension and right ventricular failure. J Cardiothorac Vasc Anesth 2012;26:e24-5.  Back to cited text no. 8
Spiekerkoetter E, Fabel H, Hoeper MM. Effects of inhaled salbutamol in primary pulmonary hypertension. Eur Respir J 2002;20:524-8.  Back to cited text no. 9


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