|Year : 2020 | Volume
| Issue : 2 | Page : 153-155
Dexmedetomidine in a patient with unrepaired congenital cyanotic heart disease
Kumar Parag1, Nishith Govil2, Vinay Rai2, Abullais Raheeq Gowda3
1 Department of Cardiac Anesthesia, SGRRIM and HS, Dehradun, Uttarakhand, India
2 Department of Anesthesiology, SGRRIM and HS, Dehradun, Uttarakhand, India
3 Department of Anaesthesia, AIIMS, Rishikesh, Uttarakhand, India
|Date of Submission||26-Mar-2020|
|Date of Decision||19-Apr-2020|
|Date of Acceptance||11-May-2020|
|Date of Web Publication||19-Sep-2020|
Dr. Nishith Govil
Department of Anesthesiology, SGRRIM and HS, Dehradun - 248 001 Uttarakhand
Source of Support: None, Conflict of Interest: None
The challenges in a patient with unrepaired congenital cyanotic heart disease (CCHD) requiring controlled hypotension are to prevent a further increase in the right-to-left (R-L) shunt by maintaining systemic vascular resistance, controlling pulmonary vascular resistance (PVR), decreasing oxygen consumption, and preventing arrhythmia and hypovolemia. To the best of our knowledge, combination of ketamine and dexmedetomidine has not been used in a patient with unrepaired CCHD to keep hemodynamic stable, preventing reversal of shunt and arrhythmias while providing controlled hypotension. The rationale of using combination of intravenous ketamine and dexmedetomidine is to counteract sympathoinhibitory effects of dexmedetomidine with the cardiostimulatory effects of ketamine, thus maintaining a stable hemodynamic in cases with R-L shunt. Another benefit in CCHD is that dexmedetomidine decreases the incidence of arrhythmia intraoperatively and decreases dynamic response of the right ventricular outflow tract induced by pain, thus decreasing R-L shunt. Dexmedetomidine encourages protective mechanisms during hypoxia as in patients with CCHD by lowering anti-ischemic responses such as lactate production and a modest decrease in the PVR. Dexmedetomidine provides controlled hypotension and uneventful recovery due to its lowering of stress response of surgery and opioid sparing effect and decreases the incidence of emergence agitation and postoperative nausea and vomiting.
Keywords: Congenital cyanotic heart disease, dexmedetomidine, right-to-left shunt
|How to cite this article:|
Parag K, Govil N, Rai V, Gowda AR. Dexmedetomidine in a patient with unrepaired congenital cyanotic heart disease. Indian Anaesth Forum 2020;21:153-5
|How to cite this URL:|
Parag K, Govil N, Rai V, Gowda AR. Dexmedetomidine in a patient with unrepaired congenital cyanotic heart disease. Indian Anaesth Forum [serial online] 2020 [cited 2020 Oct 20];21:153-5. Available from: http://www.theiaforum.org/text.asp?2020/21/2/153/295382
| Introduction|| |
Dexmedetomidine has been approved for sedation in short procedures and has an established application for providing controlled hypotension. To the best of our knowledge, dexmedetomidine has not been used in surgery in a patient with unrepaired congenital cyanotic heart disease (CCHD) to keep hemodynamic stable, preventing reversal of shunt and arrhythmias while providing controlled hypotension.
| Case Report|| |
We submit a case report after taking written consent of the patient's parents for potential publication, on the successful anesthetic management of functional endoscopic sinus surgery with CCHD.
A 15-year-old male weighing 35 kg presented with persistent nasal obstruction and rhinorrhea for the past 2 months. Computed tomographic images showed nasal polyposis extending from the nasal cavity to sphenoid sinus [Figure 1]. The patient was a known case of CCHD since childhood and was advised surgery, but parents kept deferring. He was not on any medication and had symptoms of dyspnea on moderate exertion. On examination, he had peripheral and central cyanosis and Grade 3 clubbing. His heart rate was 110 beats per min (bpm), blood pressure (BP) was 110/78 mm of Hg, and SpO2 on room air was 84%. Cardiovascular system revealed a pansystolic murmur radiating all over the precordium. His hemoglobin was 14.5 g%, platelet count was 148,000 per mm3, and international normalized ratio (INR) was 1.38. Chest X-ray showed boot-shaped heart with clear pulmonary fields. Electrocardiogram showed right-axis deviation with sinus rhythm and right bundle branch block [Figure 2]. Echocardiography showed a subaortic ventricular septal defect with right-to-left (R-L) shunt, 40%–50% overriding of the aorta, and right ventricular hypertrophy. There was infundibular stenosis with well-developed pulmonary arteries, and biventricular function was within normal limits.
|Figure 1: Computed tomographic scan showing the extent of mass; (a) bowing of the posterior wall of the maxilla (thick white arrow) as seen in the axial section, (b) bone window in the axial cut, (c) coronal section showing extension (thin white arrow) into sphenoid sinus, (d) coronal section showing extension (thin white arrow) into infratemporal fossa|
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|Figure 2: Chest X-ray (anteroposterior view) and electrocardiogram of the patient showing changes suggestive of tetralogy of Fallot|
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Preoperatively, Ringer's lactate at 2 ml/kg/h, midazolam 2 mg intravenously (IV), and infective endocarditis prophylaxis were administered. Multichannel monitor attached with bispectral index and a 20G arterial cannula in the right radial artery was inserted for invasive BP monitoring before induction. Patients' mean arterial pressure (MAP) was 62 mmHg and baseline arterial blood gas (ABG) further confirmed shunting (pH 7.30, pO2 59.2 mmHg, pCO2 32.0 mmHg, SO2 89%, and HCO3 19.0 mmol/l).
After preoxygenation with 100% O2, SpO2 improved from 84% (room air) to 89%. The patient was induced with fentanyl 2 μg/kg IV over 5 min and ketamine 2 mg/kg and dexmedetomidine 1 μg/kg over 10 min. Oral intubation was done after injection rocuronium i mg/kg IV. This was followed by 5 mg IV intermittent boluses of injection rocuronium along with oxygen-nitrous oxide in 50:50 ratio and isoflurane 0.6% to 0.8% for maintenance of anesthesia. Dexmedetomidine infusion started at 20 μg/h and titrated to 35 μg/h to maintain the bispectral index (BIS) level 40–60 and MAP above 60 mmHg. The patient was kept normovolemic with Ringer's lactate at 80 ml/h; SpO2 was maintained at 85%–90% and MAP was 60 mmHg. Duration of the surgery was 2 h with 300 ml of blood loss. Dexmedetomidine was stopped 20 min before the conclusion of surgery, muscle relaxation reversed with neostigmine, and the patient extubated smoothly.
ABG after completion of surgery was pH 7.37, pO2 was 78.2 mmHg, and hemoglobin was 13 g%. In the postanesthesia care unit, the patient monitored for pain, sedation, or agitation for 24 h. Recovery was uneventful with no episodes of postoperative nausea and vomiting, hypotension, bradycardia, or any other respiratory complication until the time of patient discharge after 3 days.
| Discussion|| |
Challenges in these patients are to maintain controlled hypotension for blood-less surgical field, while preventing reversal of shunt. Anesthetic management is directed to prevent increase in the R-L shunt by maintaining systemic vascular resistance (SVR), preventing right ventricular outflow tract (RVOT) obstruction due to spasm, decreasing pulmonary vascular resistance (PVR), decreasing oxygen consumption, and preventing arrhythmia and hypovolemia. Another problem in CCHD patients is deranged coagulation profile and platelets dysfunction due to systemic hypoxia, and it is recommended to transfuse plasma and platelets in major cardiac and noncardiac surgery. We selected dexmedetomidine over other agents for controlled hypotension, considering its safety, efficacy, associated analgesia, and amnesia at clinical doses.
During induction, sympathoinhibitory effects of dexmedetomidine counteract the cardiostimulatory effects of ketamine, thus maintaining a stable hemodynamic in cases with R-L shunt. There is no significant rise or fall in hemodynamics with this drug combination. The beneficiary action of dexmedetomidine is due to its ability to block sympathetic stress response of surgery, decrease analgesic and anesthetic requirements, and decrease the incidence of arrhythmias. Adult CCHD patients are more prone for arrhythmia due to increasing right ventricular hypertrophy and dysfunction over time. Kamibayashi et al. and Guo et al. showed in animals model, that the direct myocardial preserving effect of dexmedetomidine is due to lowering of stress response, lowering of anti-ischemic responses and acting as antiarrhythmic agent during periods of hypoxia and preoxygenation.,
Mukhtar et al. have demonstrated that dexmedetomidine infusion blunts the endogenous catecholamine release in pediatric patients undergoing surgery for congenital heart disease. This attenuation of neuroendocrine response decreases the incidence of arrhythmia intraoperatively and dynamic response of RVOT, thus decreasing R-L shunt. Due to analgesic effect, it prevents sudden spasm of RVOT, which can be induced by pain. PVR is usually not relevant in the setting of RVOT obstruction because PVR is typically low in these patients; still increase of PVR will be avoided at all cost.
The undesired hemodynamic effects of dexmedetomidine in this case are hypotension and decrease in SVR. Mechanism of decrease in SVR by dexmedetomidine is complex. Activation of presynaptic α2 receptors on the sympathetic nerves and the central nervous system induces sympatholysis, whereas activation of the vascular postsynaptic receptors causes both vasoconstriction (activation of α2 receptors on the vascular smooth muscle cells) and vasodilatation (activation of α2 receptors on the endothelial cells). Decrease in SVR can cause increase in R-L shunt and may lead to fall in saturation. This can be countered by pressing both femoral arteries in the inguinal region firmly; thus, increasing SVR and increasing saturation or phenylephrine can be used in titrated doses to increase SVR.
| Conclusion|| |
Dexmedetomidine has desirable effects in unrepaired CCHD to provide controlled hypotension.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient's parents have given consent for images and other clinical information to be reported in the journal. The patient's parents understand that the names and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflict of interest.
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[Figure 1], [Figure 2]