| Article Access Statistics|
| Viewed||808 |
| Printed||28 |
| Emailed||0 |
| PDF Downloaded||178 |
| Comments ||[Add] |
Click on image for details.
|Year : 2022
: 25 | Issue : 4 | Page
|The use of ketamine as an induction agent for anesthesia in pulmonary thromboendarterectomy surgery: A case series
Kiran Salaunkey1, David Jenkins2, Andrew Roscoe3
1 Department of Anaesthesia, Royal Papworth Hospital, Cambridge, UK
2 Department of Cardiac Surgery, Royal Papworth Hospital, Cambridge, UK
3 Department of Anaesthesiology, Singapore General Hospital; Department of Cardiothoracic Anaesthesia, National Heart Centre, Singapore, Singapore
Click here for correspondence address and
|Date of Submission||22-Feb-2021|
|Date of Decision||08-Jun-2022|
|Date of Acceptance||09-Jun-2022|
|Date of Web Publication||10-Oct-2022|
| Abstract|| |
Pulmonary thromboendarterectomy (PTE) surgery is the treatment of choice for patients with chronic thromboembolic pulmonary hypertension (CTEPH). The induction of anesthesia in patients with severe pulmonary hypertension (PHT) can be challenging, with a risk of cardiovascular collapse. The administration of ketamine in patients with PHT is controversial, with some recommendations contraindicating its use. However, ketamine has been used safely in children with severe PHT. We present a retrospective case series of adult patients with severe PHT presenting for PTE surgery, using intravenous ketamine as a co-induction anesthetic agent.
Keywords: Cardiac anesthesia, chronic thromboembolic pulmonary hypertension, ketamine, pulmonary hypertension, pulmonary thromboendarterectomy
|How to cite this article:|
Salaunkey K, Jenkins D, Roscoe A. The use of ketamine as an induction agent for anesthesia in pulmonary thromboendarterectomy surgery: A case series. Ann Card Anaesth 2022;25:528-30
|How to cite this URL:|
Salaunkey K, Jenkins D, Roscoe A. The use of ketamine as an induction agent for anesthesia in pulmonary thromboendarterectomy surgery: A case series. Ann Card Anaesth [serial online] 2022 [cited 2022 Dec 2];25:528-30. Available from: https://www.annals.in/text.asp?2022/25/4/528/358123
| Introduction|| |
Pulmonary thromboendarterectomy (PTE) is the treatment of choice for patients with chronic thromboembolic pulmonary hypertension (CTEPH). The induction of anesthesia in patients with severe pulmonary hypertension (PHT) can be challenging, with a risk of cardiovascular collapse. The use of ketamine in PHT is controversial with some recommendations advocating the avoidance of ketamine due to its effect of the increasing mean pulmonary artery pressure (mPAP) and pulmonary vascular resistance (PVR)., However, ketamine has been used safely in children with PHT., We report a retrospective case series of CTEPH patients with severe PHT, who successfully underwent PTE surgery using intravenous ketamine as a co-induction anesthetic agent.
| Case Histories|| |
The local research and ethics committee's approval was obtained to review the patient records. A retrospective review of the prospectively captured data for the patients undergoing PTE surgery over 2 years was undertaken. Thirty-one patients underwent PTE surgery with preoperative PVR >10 wood units (WU) and received ketamine at the induction of anesthesia. The patient demographics and preoperative data are presented in [Table 1].
Before the induction of anesthesia, in addition to standard routine monitoring, all the patients had peripheral intravenous access, radial artery invasive blood pressure monitoring, and near-infrared spectroscopy cerebral oximetry monitoring. A central venous catheter, pulmonary artery catheter (PAC), and femoral artery invasive blood pressure monitor were inserted after the induction of anesthesia, as per standard institutional practice.
The induction of anesthesia was achieved with intravenous midazolam (0.05 mg/kg), fentanyl (2–4 μg/kg), ketamine (0.75–1 mg/kg), and pancuronium (0.15–0.2 mg/kg).
After endotracheal intubation, the patients were ventilated with oxygen/air mixture with a fraction of inspired oxygen 0.6–0.8, tidal volume 6–7 mL/kg, positive end-expiratory pressure 5 cmH2O, and respiratory rate 12–18 per min, adjusted to target arterial pCO2 35–40 mmHg. The maintenance of anesthesia was achieved using an intravenous propofol infusion at 60–75 μg/kg/min. A second dose of fentanyl (2–4 μg/kg) was administered immediately prior to the start of the surgery.
No patient suffered a cardiovascular collapse after the induction of anesthesia. All the patients were hemodynamically stable and no patients required inotropic or vasopressor support through to the initiation of cardiopulmonary bypass (CPB).
The PTE surgery was conducted as previously described with the patients having predominantly type II and type III disease resected. After rewarming, the patients were weaned from CPB. The first-line inotropic support administered was dopamine (5 μg/kg/min). A central venous pressure of 50% of the baseline was targeted to achieve optimal volemic status. Additional vasoactive agents were administered depending upon the thermodilution cardiac output studies performed using the PAC. In addition to dopamine, four patients required noradrenaline support. One patient required vasopressin in addition to both dopamine and noradrenaline. One patient suffered a surgical tear of the pulmonary artery and was initially supported with central veno-arterial extracorporeal membrane oxygenation after discontinuation of CPB. At the end of the surgery, all the patients were transferred to the intensive care unit and followed a standard hemodynamic and ventilatory postoperative weaning protocol. The postoperative hemodynamic data and patient outcomes are presented in [Table 2].
|Table 2: Intraoperative data, postoperative hemodynamic data, and patient outcomes|
Click here to view
Data are presented as mean (± standard deviation) for normally the distributed data, as median (interquartile range [IQR]) for the ordinal data, and number (percentage) for the categorical data.
| Discussion|| |
The induction of anesthesia in patients with severe PHT can result in right ventricular (RV) failure, cardiovascular collapse, and cardiac arrest. The basic hemodynamic goals include avoiding RV ischemia by maintaining systemic blood pressure and RV perfusion pressure; preserving RV contractility by avoiding negative inotropic agents; optimizing preload and preventing RV overdistension; and reducing RV afterload by implementing measures to decrease PVR: avoidance of hypoxemia, hypercarbia, acidemia, and hypothermia.
The use of ketamine in patients with PHT is contentious. The earlier studies demonstrating an increase in mPAP and PVR on the administration of intravenous ketamine were performed on spontaneously breathing patients with normal baseline PVR, receiving doses of 2 mg/kg or greater., The later studies, with controlled ventilation in children with baseline PHT, showed no effect of ketamine on PVR., The co-induction of anesthesia using a combination of ketamine with a benzodiazepine and opioid has been shown to be hemodynamically stable, with no significant increase in PVR, in adult patients undergoing coronary artery bypass graft surgery. The preservation of a sympathetic tone by ketamine at the induction of anesthesia is advantageous in maintaining the Systemic Vascular Resistance (SVR) and RV perfusion pressure, and some authors recommend it as the agent of choice in severe PHT.
Although our cases series is not able to directly show the precise effect of ketamine on PVR in severe PHT, the hemodynamic stability of the patients after the induction of anesthesia suggests that ketamine was not detrimental to patient outcome. We have shown that ketamine in a dose less than 1 mg/kg can be used safely as a co-induction agent in adult patients with severe PHT presenting for PTE surgery, and the presence of severe PHT should not preclude its use.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Jenkins D, Madani M, Fadel E, D'Armini AM, Mayer E. Pulmonary endarterectomy in the management of chronic thromboembolic pulmonary hypertension. Eur Respir Rev 2017;26:160111.
Schisler T, Marquez JM, Hilmi I, Subramaniam K. Pulmonary hypertensive crisis on induction of anesthesia. Semin Cardiothorac Vasc Anesth 2017;21:105-13.
Strumpher J, Jacobsohn E. Pulmonary hypertension and right ventricular dysfunction: Physiology and perioperative management. J Cardiothorac Vasc Anesth 2011;25:687-704.
Aguirre MA, Lynch I, Hardman B. Perioperative management of pulmonary hypertension and right ventricular failure during noncardiac surgery. Adv Anesth 2018;36:201-30.
Williams GD, Philip BM, Chu LF, Boltz MG, Kamra K, Terwey H, et al
. Ketamine does not increase pulmonary vascular resistance in children with pulmonary hypertension undergoing sevoflurane anesthesia and spontaneous ventilation. Anesth Analg 2007;105:1578-84.
Friesen RH, Twite MD, Nichols CS, Cardwell KA, Pan Z, Darst JR, et al
. Hemodynamic response to ketamine in children with pulmonary hypertension. Paedriatr Anaesth 2016;26:102-8.
Sarkar MS, Desai PM. Pulmonary hypertension and cardiac anesthesia: Anesthesiologist's perspective. Ann Card Anaesth 2018;21:116-22.
] [Full text]
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.
Tweed WA, Minuck M, Mymin D. Circulatory responses to ketamine anesthesia. Anesthesiology 1972;37:613-9.
Gooding JM, Dimick AR, Tavakoli M, Corssen G. A physiologic analysis of cardiopulmonary responses to ketamine anesthesia in noncardiac patients. Anesth Analg 1977;56:813-6.
Hickey PR, Hansen DD, Cramolini GM, Vincent RN, Lang P. Pulmonary and systemic hemodynamic responses to ketamine in infants with normal and elevated pulmonary vascular resistance. Anesthesiology 1985;62:287-93.
Raza SM, Masters RW, Zsigmond EK. Haemodynamic stability with midazolam-ketamine-sufentanil analgesia in cardiac surgical patients. Can J Anaesth 1989;36:617-23.
Department of Anaesthesiology, Singapore General Hospital, Outram Road
Source of Support: None, Conflict of Interest: None
[Table 1], [Table 2]