- Email: [email protected]
Minimal and deep sedation during ablation of ventricular tachycardia
International Journal of Cardiology 172 (2014) 161–164
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Minimal and deep sedation during ablation of ventricular tachycardia Alexander Wutzler a,⁎, Amélie Mueller a, Lena Loehr a, Martin Huemer a, Abdul Shokor Parwani a, Philipp Attanasio a, Florian Blaschke a, Christian Storm b, Leif-Hendrik Boldt a, Wilhelm Haverkamp a a b
Department of Cardiology, Charité — Universitaetsmedizin Berlin, Campus Virchow-Klinikum, Berlin, Germany Department of Intensive Care Medicine, Charité — Universitaetsmedizin Berlin, Campus Virchow-Klinikum, Berlin, Germany
a r t i c l e
i n f o
Article history: Received 29 October 2013 Received in revised form 17 December 2013 Accepted 31 December 2013 Available online 8 January 2014 Keywords: Ablation Deep sedation Minimal sedation Ventricular tachycardia
a b s t r a c t Background: Catheter ablation is a curative treatment option for ventricular premature contractions (VPC) and ventricular tachycardia (VT). Procedures require different sedation levels, depending on duration, ablation approach and patient characteristics. The aim of our study was to evaluate feasibility of minimal and deep sedation for ablation of VPC/VT. Methods: Patients underwent catheter ablation of VPC/VT under minimal or deep sedation. Events of hypotension, hypoxia, bradycardia, procedural complications and VT inducibility were compared between the groups. Results: 120 patients were included. In 42 patients (53.6 ± 17.1 years, 47.6% male) ablation was performed under minimal sedation with midazolam, and in 78 patients (54.2 ± 17.5 years, 67.9% male) ablation was performed under deep sedation with propofol/midazolam. There were significantly fewer patients with idiopathic VT (62.8 vs. 88.1%, p = 0.011) in the deep sedation group, LVEF was significantly lower (47 ± 14.4 vs. 53.1 ± 11.7) and the procedure duration was significantly longer (201.9 ± 85.9 vs. 137.9 ± 98.7). No significant differences in procedural complications or sedation related events (hypotension: 0 vs. 3.8%, p = 0.2, no hypoxia, no bradycardia) were detected. Conclusions: Minimal sedation and deep sedation are both feasible during VPC/VT ablation procedures. Propofol does not increase complications even in a collective with pre-existing impairment of LVEF. Adequate monitoring and trained personnel should be present. © 2014 Elsevier Ireland Ltd. All rights reserved.
1. Introduction Catheter ablation is an established and potentially curative treatment option for different types of ventricular tachycardia (VT) and ventricular premature contractions (VPC) [1]. Procedures may be painful and patient immobilization is required during radiofrequency delivery to provide sufficient catheter–tissue contact and to maintain validation of electroanatomic mapping systems. Therefore, procedures are performed under variable levels of sedation and analgesia from minimal sedation to general anesthesia (GA) [1–4]. General anesthesia is used in a large number of procedures. Although GA provides the most sufficient control of movement and pain, it has certain disadvantages. Of those, reduced VT inducibility, excessive hypotension during VT and (when combined with muscle relaxants) reduced sensitivity of high-output phrenic nerve mapping are particularly relevant [1,2]. Alternative strategies include minimal or moderate sedation during shorter procedures for idiopathic VT/VPC and deep sedation [2,3,5].
⁎ Corresponding author at: Department of Cardiology, Charité - Universitätsmedizin Berlin, Campus Virchow-Klinikum, Augustenburger Platz 1, 13353 Berlin, Germany. Tel.: +49 30 450 665411; fax: +49 30 450 553 994. E-mail address: [email protected] (A. Wutzler). 0167-5273/$ – see front matter © 2014 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2013.12.175
While propofol based deep sedation is a common practice in a wide range of electrophysiological procedures, it is challenging during VT ablation [5–7]. The risk of airway complications and the necessity of rapid change of sedation level for cardioversion of unstable VT require well trained personnel and adequate monitoring [3]. Besides that, propofol may alter myocardial conduction velocities [8] and VT inducibility [9] and it can lead to hypokalemia, especially after prolonged infusion [10]. Hypokalemia and alteration of other serum electrolytes could promote – particularly during the electrophysiological study and the attempt to induce ventricular tachycardia – unspecific malignant ventricular arrhythmias like polymorphic fast VT and ventricular fibrillation (VF). Compared to deep sedation, minimal sedation with midazolam carries a reduced risk of airway complications or hemodynamic impairment. On the other hand, procedural discomfort may be increased during minimal sedation and patient movements may be more likely. Furthermore, a rapid change of sedation level is even more challenging in patients under minimal sedation and may result in a deeper sedation level than intended and respiratory or cardiovascular complications. Analgesia and sedation for electrophysiological procedures have become an emerging research field with high clinical relevance [7,8,11,12]. Despite the growing importance of catheter ablation in the treatment of VT [13,14] and an increasing number of procedures worldwide, only very few studies are available on procedural sedation and analgesia
162
A. Wutzler et al. / International Journal of Cardiology 172 (2014) 161–164
during VT ablation. The aim of our study was to evaluate the feasibility of minimal and deep sedation during VT ablation. The main purpose was to evaluate procedural changes of oxygenation and hemodynamic parameters as well as the occurrence of sedation related adverse events under either sedation regimen. Incidence of complications and procedural changes were compared between the two sedation strategies. 2. Methods 2.1. Patients Consecutive patients presented to our center for catheter ablation of idiopathic or ischemic VT or VPC, in whom procedures were performed under minimal or deep sedation were enrolled from 2007 to 2013. The choice of sedation regimen (minimal vs. deep sedation) was at the discretion of the operating physician based on patient's concomitant disorders, type of VT and expected procedure duration. Study data were analyzed offline by an investigator who was not involved in the choice of anesthetic. Resting electrocardiogram (ECG), transesophageal or transthoracic echocardiography, physical examination and standard blood test were performed prior to ablation. All patients gave informed consent. The study was approved by the ethical committee of the Charité — Universitätsmedizin Berlin.
pressure and peripheral oxygen saturation at the discretion of the treating physician, but at least 4 h. Blood gas analysis was repeated at the discretion of the physician in charge. Patients were assigned to two study groups, according to the sedation strategy that was used: patients that underwent ablation under minimal sedation were assigned to group 1, and patients under deep sedation to group 2. Procedural complications, as well as episodes of hypotension, hypoxia, acidosis and bradycardia that required immediate correction were recorded and compared between the groups. Acidosis was treated at a pH b 7.2. Hypoxia was treated if oxygen saturation was b90% for 30 s or longer. Hypotension was treated if systolic blood pressure was b80 mm Hg (except from short drop in blood pressure during programmed ventricular stimulation with immediate recovery after cessation of stimulation). Bradycardia was treated at a heart rate b40 beats per minute. 2.4. Statistical analysis For comparison of categorical variables among groups, χ2 tests were used. Independent sample t test (normally distributed data) or Mann–Whitney u test (skewed data) was used to compare sedation and procedure related parameters. All analyses were performed using SPSS software version 20.0 (SPSS Inc., Chicago, IL, USA). Data are presented as absolute numbers and percentages for categorical variables or mean ± standard deviation (SD) for continuous variables. A p value of b0.05 was considered statistically significant.
2.2. Ablation procedures Patients were in a fasting state for at least 6 h. Patients with idiopathic VT/VPC or VT/ VPC associated with structural heart disease were included. Ablation procedures were performed using venous, transseptal, retrograde arterial and epicardial approaches or a combination of the aforementioned as appropriate. A 3-D-mapping system was used for ablation of ischemic ventricular tachycardia, epicardial approaches and in the majority of idiopathic VT/VPC procedures. Origin of the arrhythmia and the approach used for mapping and ablation were recorded. Number and type of complications were recorded. The procedural endpoint was defined as non-inducibility of VT/VPC with programmed electrical stimulation and administration of adrenergic agents (Metaproterenol, Epinephrine or Isoproterenol). In patients with unstable ischemic VT, substrate modification was performed during sinus rhythm with local abnormal ventricular activities (LAVA) as ablation target. Inducibility of VT was tested with programmed ventricular stimulation. If cardioversion was necessary due to hemodynamically unstable VT, manual painful stimulation was used to assess sedation level. In case of a positive response to painful stimulus, patients received a 2 mg propofol bolus prior to cardioversion. 2.3. Sedation, analgesia and monitoring Three different strategies are used in our center: 1. minimal sedation, 2. deep sedation and 3. general anesthesia as defined by the American Society of Anaesthesiologists [15]. Patients who underwent procedures under GA were excluded from the study. The remaining patients were either treated according to the minimal or the deep sedation protocol. 2.3.1. Minimal sedation Minimal sedation was achieved with midazolam (initial dose 0.03 mg/kg, repeated doses as needed). Additionally, the opioid analgesic piritramide was administered in repeated doses of 1–2 mg as needed to provide analgesia during radiofrequency (RF) application. 2.3.2. Deep sedation Deep sedation was achieved with continuous propofol infusion with a syringe pump at a dose of 4 mg/kg/h, following an initial midazolam dose (midazolam 0.03–0.05 mg/kg). Additionally, the opioid analgesic piritramide was administered in repeated doses of 2–3 mg as needed to provide analgesia, with a maximum cumulative dose of 15 mg. An oropharyngeal airway was applied in all patients when deep sedation was reached. Arterial blood gas was drawn usually before and at the end of the procedure and additionally at the discretion of the operating physician. All patients received oxygen via nasal cannula (2–8 l/min) with a target SaO2 of N95%. SaO2, and ECG and blood pressure were monitored continuously. Arterial blood pressure was monitored either via invasive intra-arterial blood pressure measurement or via automatically non-invasive measurement in three-minute intervals. Invasive blood pressure measurement was performed in patients with impaired left ventricular function or with known severe hemodynamic compromise under VT. All patients were breathing spontaneously throughout the procedure. Sedation level was continuously monitored by the operating physician and two registered nurses. Drugs were administered by a registered nurse under direct supervision of the electrophysiologist. All procedures were performed by a fully trained electrophysiologist and an electrophysiology fellow. All physicians had been trained in intensive-care medicine, airway management and application of anesthetic drugs. Physicians and nurses were trained in advanced cardiac life support. Additionally, procedures were supervised by a physician of the Department of Cardiology, who is holding a degree in intensive care medicine and emergency medicine. Anesthesiologist standby was available on a 24hour basis from the intensive care unit. After the procedure, patients were allowed to recover from anesthesia and were transferred to an intermediate care unit with continuous monitoring of ECG, blood
3. Results A total of 120 patients were included in the study. Forty-two patients (mean age 53.6 ± 17.1 years, 47.6% men) underwent ablation procedures under minimal sedation and 78 patients (mean age 54.2 ± 17.5 years, 67.9% men) received procedural deep sedation. Patient's baseline characteristics and medication are listed in Table 1. There were significantly more men in the deep sedation group (67.9 vs. 47.6%, p = 0.03). Furthermore, significantly fewer patients in the deep sedation group underwent ablation for idiopathic VT (62.8 vs. 88.1%, p = 0.011). The mean left ventricular ejection fraction (LVEF)
Table 1 Patients' baseline characteristics. ACEI = angiotensin converting enzyme inhibitor, ARB = angiotensin receptor blocker, ASA = American Society of Anesthesiologists, BP = blood pressure, CAD = coronary artery disease, COPD = chronic obstructive pulmonary disease, LVEF = left ventricular ejection fraction, SDH = structural heart disease, VT = ventricular tachycardia.
Age (years) (SD) Male (%) BMI (SD) Idiopathic VT (%) Hypertension (%) CAD (%) Diabetes mellitus (%) COPD (%) Chronic kidney disease ASA physical status (%) I II III ≥IV LVEF (%) (SD) Systolic BP (mm Hg) (SD) Diastolic BP (mm Hg) (SD) Beta-adrenergic blocker Digitalis Amiodarone ACEI ARB Calcium-channel blocker Sodium-channel blocker Diuretic Statin Aspirin Oral anticoagulant a
Statistically significant.
Group 1 Minimal sedation (n = 42)
Group 2 Deep sedation (n = 78)
p value
53.6 (17.1) 20 (47.6) 27.6 (7.2) 37 (88.1) 23 (54.8) 11 (26.2) 2 (4.7) 5 (11.9) 6 (14.3)
54.2 (17.5) 53 (67.9) 26.7 (4.4) 49 (62.8) 40 (52.3) 26 (33.3) 12 (15.4) 6 (7.7) 17 (21.8)
0.84 0.03a 0.42 0.011a 0.67 0.42 0.08 0.46 0.25
3 (7.1) 32 (76.2) 7 (16.7) 0 53.1 (11.7) 123.4 (18.9) 70.1 (12.3) 29 (69) 0 (0) 5 (11.9) 14 9 (21.4) 2 (4.7) 2 (4.7) 13 (31) 17 (40.5) 18 (42.9) 7 (16.7)
1 (1.3) 51 (65.4) 26 (33.3) 0 47 (14.4) 121.6 (17.4) 72.2 (13.5) 55 (70.5) 1 (1.3) 28 (36.4) 29 (37.2) 21 (26.9) 6 (7.7) 3 (3.8) 27 (34.6) 27 (34.6) 34 (43.6) 24 (30.8)
0.88 0.22 0.51 – 0.014a 0.73 0.59 0.79 0.46 0.004a 0.64 0.48 0.53 0.8 0.65 0.56 0.89 0.09
A. Wutzler et al. / International Journal of Cardiology 172 (2014) 161–164
was significantly lower in the deep sedation group (47 ± 14.4 vs. 53.1 ± 11.7%, p = 0.014). Significantly more patients in the deep sedation group were treated with amiodarone at baseline (36.4 vs. 11.9%, p = 0.004). The procedure duration was significantly longer in the deep sedation group (201.9 ± 85.9 vs. 137.9 ± 98.7 min, p b 0.001). RF delivery time was also significantly longer in the deep sedation group (19.24 ± 15.94 vs. 9.38 ± 7.14 min, p b 0.001). Only a minimal drop in systolic and diastolic blood pressure throughout the procedure was registered. There were no significant differences in the mean change of systolic blood pressure (−4.3 ± 21.7 vs. −7.9 ± 21.8 for minimal and deep sedation respectively, p = 0.62) or diastolic blood pressure (−5.5 ± 12 vs. − 7.8 ± 18 for minimal and deep sedation respectively, p = 0.68) between the study groups. Procedural parameters and ablation site are depicted in Table 2. Four complications of catheter ablation were registered: three cases of pericardial effusion or tamponade and one case of femoral vascular complication. In three patients, an episode of hypotension occurred that required treatment. One of those patients also had pericardial tamponade due to perforation of the right ventricle. The patient underwent surgical treatment and was discharged without further sequel. Before the patient was transferred to the operating room, a total of 15 mg of etilefrine was administered to treat hypotension. In the other two patients, an episode hypotension occurred in the absence of pericardial effusion or tamponade during normal sinus rhythm. Hypotension was successfully treated with two boluses of etilefrine 0.03 mg/kg and a reduction of propofol dose in each case. No further complications occurred in the two patients. One patient experienced VF after a fast VT degenerated to VF. VF was successfully treated by immediate biphasic defibrillation (200 J). The patient's serum potassium was 3.8 mmol/l. After termination of VT, mapping and ablation were continued without further adverse events. None of the patients received continuous catecholamine-infusion to maintain hemodynamic function. No ventricular assist devices were used in this study. No case of hypoxia or acidosis occurred. In one patient in the minimal sedation group and 3 patients in the deep sedation group induction of target arrhythmia was not achieved (p = 0.67). Substrate mapping and ablation were performed during sinus rhythm in these patients (See Table 3.) 4. Discussion We here present the results of a single-center study on procedural feasibility of midazolam based minimal sedation and propofol/ Table 2 Procedural parameters compared between the study groups. LV = left ventricle, LVOT = left ventricular outflow tract, RF = radiofrequency, RV = right ventricle, RVOT = right ventricular outflow tract.
Procedure duration (min) (SD) RF delivery time (min) (SD) Propofol dose (mg/h) (SD) Midazolam dose (mg) (SD) Piritramide dose (mg) (SD) Change of systolic BP (mm Hg) (SD) Change of diastolic BP (mm Hg) (SD) Ablation site RVOT LVOT Mitral annulus Aortic cusp LV RV Epicardial approach a
Statistically significant.
Group 1 Minimal sedation
Group 2 Deep sedation
p-Value
137.9 (98.7) 9.38 (7.14) – 5.5 (2.7) 5.9 (3) −4.3 (21.7) −5.5 (12)
201.9 (85.9) 19.24 (15.94) 638.1 (469.2) 6 (3) 6.1 (3.6) −7.9 (21.8) −7.8 (18)
b0.001a b0.001a – 0.43 0.86 0.62 0.68
26 9 – – 7 – –
29 16 3 1 29 – 10
163
Table 3 Procedural complications and episodes of hypotension, hypoxia, acidosis and bradycardia compared between the groups. Severe acidosis: pH b 7.2; hypoxia: oxygen saturation b90% for 30 s or longer; hypotension: systolic blood pressure b80 mm Hg; bradycardia: heart rate b40 beats per minute.
Hypotension (%) Hypoxia (%) Acidosis (%) Bradycardia (%) Pericardial effusion/tamponade (%) Femoral vascular complication (%) Ventricular fibrillation (%) Non-inducibility at baseline (%)
Group 1 Minimal sedation
Group 2 Deep sedation
p-Value
0 0 0 0 0 0 1 (2.4) 1 (2.4)
3 (3.8) 0 0 0 3 (3.8) 1 (1.3) 0 3 (3.8)
0.2 – – – 0.2 0.46 0.17 0.67
midazolam based deep sedation during ablation of ventricular tachycardia. We used an observational non-randomized design reporting the current practice in a real-life collective at a university hospital arrhythmia center. To the best of our knowledge, this is the largest study on sedation during VT ablation and the first study addressing minimal and deep sedation. Common practice at our center is that procedures in patients with severe hemodynamic compromise at baseline, electrical storm, severe life-threatening comorbidities or acute illness are performed with GA by an anesthesiology team or an intensive care team. Procedures that target idiopathic VT/PVC, such as tachycardia originating from right ventricular outflow tract in young patients in the absence of structural heart disease, or (occasionally) stable patients with scar related VT are performed under minimal sedation. Procedures in stable patients that are expected to have a longer duration or that require more painful and challenging techniques, such as transseptal or epicardial access and biventricular mapping, are performed under deep sedation. However, occasionally the sedation level is changed during an ongoing procedure, e.g. if the duration is longer than expected or transseptal puncture is necessary. The proportion of procedures where sedation level was changed from minimal to deep sedation was b10% in our study collective. Those procedures were considered as procedures with the use of deep sedation for the analysis of this study. There were significant differences between the study groups at baseline, all of which are reflecting the aforementioned practice: patients in the deep sedation group were more likely to have a VT related to structural heart disease, where more complex mapping and ablation procedures are expected. Accordingly, the LVEF was significantly lower in this group and significantly more patients were treated with amiodarone. On the other hand, those patients were still ASA class ≥ III and the LVEF in this group was only moderately impaired (47 ± 14.4%), so that the patients were classified eligible for deep sedation. The results show a significantly longer procedure duration in the deep sedation group, reflecting the more challenging procedures in those patients. However, despite the unfavorable patient characteristics and the more complex procedures (including 12.8% epicardial ablations), none of the study parameters nor the number of complications was significantly different between the groups. The overall complication rate was low (3.3% complications in the study collective) and stayed within the range of previous studies that found up to 8% complications in VT procedures [1]. Three events of hypotension occurred; no case of prolonged hypoxia, acidosis or bradycardia was seen. None of the cases required advanced airway management or continuous vasopressor infusion. The use of minimal or deep sedation during ablation of different types of arrhythmia has been reported before [6–8] and can be performed considerably safe even in patients with relevant comorbidities [6–8,16]. However, in contrast to most cases of supraventricular tachycardia and atrial fibrillation, VT is accompanied with severe hemodynamic impairment. During VPC and VT ablation procedures, repeated
164
A. Wutzler et al. / International Journal of Cardiology 172 (2014) 161–164
ventricular stimulation is necessary for induction of the tachycardia or for pace mapping [1,3–5]. Furthermore, catheter mapping during ongoing VT is often used to identify the region of origin [1,3–5]. The latter approach requires the maintenance of VT over minutes, sometimes repeated VT induction over hours if necessary. VT is common in patients with impaired LVEF and/or ventricular scar area, which increases the risk of relevant hypotension and hypoxemia during ongoing VT or rapid ventricular stimulation. Mild hemodynamic compromise and bradycardia have been reported under propofol [6,17]. Therefore, severe hemodynamic impairment subsequent to the combination of propofol infusion and VT may lead to sedation related complications. However, we only observed two brief episodes of hypotension in the deep sedation group, which responded immediately to etilefrine. One patient in the minimal sedation group experienced VF after VT induction. Although treatment was unproblematic in this case, VF is a serious arrhythmia and may be difficult to treat in patients with preexisting hemodynamic compromise or electrolyte disturbances. Especially hypokalemia has been associated with different types of cardiac arrhythmia including sustained VT/VF [18,19]. Although the serum potassium level of the patient in our study was within normal ranges (3.8 mmol/l), it was relatively low. Other monitoring parameters (blood pressure, SaO2) were also within the normal range, the patient was free from drugs that prolong the qt-interval. Therefore we were not able to identify a specific trigger for the degeneration of VT to VF in this patient. Noteworthy, the patient was in the minimal sedation group, so no effect of propofol can be stated. Inducibility of the target arrhythmia was not significantly different between the groups. In general, the use of anesthetic agents may alter inducibility [9], but no specific effect of propofol was found in our study. Our results are in accordance with a previous study by Ramoul et al., who observed no complication during moderate sedation for epicardial VT ablation [2] and with a case report, reporting the feasibility of remifentanil–midazolam sedation during VT ablation [3]. In summary, our results suggest that catheter ablation of VT with the use of minimal or deep sedation is feasible and considerably safe. In a collective of patients with impaired LVEF undergoing relatively long and complex procedures including epicardial ablation, deep sedation did not result in relevant airway complications or hypotension requiring prolonged vasopressor infusion. Furthermore, for a collective of patients with preserved LVEF undergoing procedures with a shorter duration, minimal sedation seems appropriate. However, adequate monitoring should be provided and experienced personnel should be present to immediately detect changes in sedation level, hypotension or hypoxia. 4.1. Limitations There are limitations of our study that should be acknowledged. We did not randomize the patients. Instead, patients were assigned to the minimal or deep sedation group based on clinical considerations. Certain key factors (type of VT, LVEF, amiodarone use) differed significantly between the groups at baseline. However, our study focused on sedation related endpoints. In contrast to a study that would have compared e.g. ablation success, endpoints in our study (hypotension, hypoxia) are less dependent on the type or origin of the VT or long term amiodarone use. Of course a reduced LVEF can increase the risk of events of hypotension or hypoxia. In our study the deep sedation group was treated with propofol and therefore was at higher risk of hypotension. Yet, despite the lower LVEF and the propofol treatment the drop in blood pressure
during the procedure was not significantly higher in this group. Only two patients (2.5%) in the deep sedation group experienced sedation related hypotension, which immediately responded to an etilefrine bolus in both cases. None of the endpoints differed significantly between the groups, suggesting the feasibility of both approaches during VT ablation.
4.2. Conclusion Minimal sedation and deep sedation are both feasible and considerably safe during VPC/VT ablation procedures. Deep sedation can be carried out during longer procedures with expected patient discomfort (e.g. epicardial ablation). Minimal sedation may be sufficient for shorter procedures (e.g. idiopathic VPC/VT). Adequate monitoring and trained personnel should be present to maintain patient safety.
References [1] Aliot EM, Stevenson WG, Almendral-Garrote JM, et al. EHRA/HRS expert consensus on catheter ablation of ventricular arrhythmias: developed in a partnership with the European Heart Rhythm Association (EHRA), a registered branch of the European Society of Cardiology (ESC), and the Heart Rhythm Society (HRS); in collaboration with the American College of Cardiology (ACC) and the American Heart Association (AHA). Europace 2009;11(6):771–817. [2] Ramoul K, Tafer N, Sacher F, et al. Conscious sedation with sufentanil and midazolam for epicardial VT ablation. J Innov Card Rhythm Manage 2012;3:849–53. [3] Mandel JE, Hutchinson MD, Marchlinski FE. Remifentanil–midazolam sedation provides hemodynamic stability and comfort during epicardial ablation of ventricular tachycardia. J Cardiovasc Electrophysiol 2011;22(4):464–6. [4] Miller MA, Dukkipati SR, Mittnacht AJ, et al. Activation and entrainment mapping of hemodynamically unstable ventricular tachycardia using a percutaneous left ventricular assist device. J Am Coll Cardiol 2011;58(13):1363–71. [5] Wasmer K, Köbe J, Dechering DG, et al. Ventricular arrhythmias from the mitral annulus: patient characteristics, electrophysiological findings, ablation, and prognosis. Heart Rhythm 2013;10(6):783–8. [6] Wutzler A, Rolf S, Huemer M, et al. Safety aspects of deep sedation during catheter ablation of atrial fibrillation. Pacing Clin Electrophysiol 2012;35:38–43. [7] Kottkamp H, Hindricks G, Eitel C, et al. Deep sedation for catheter ablation of atrial fibrillation: a prospective study in 650 consecutive patients. J Cardiovasc Electrophysiol 2011;22(12):1339–43. [8] Wutzler A, Huemer M, Boldt LH, et al. Effects of deep sedation on cardiac electrophysiology in patients undergoing radiofrequency ablation of supraventricular tachycardia: impact of propofol and ketamine. Europace 2013;15(12):1019–24. [9] Mulpuru SK, Patel DV, Wilbur SL, Vasavada BC, Furqan T. Electrical storm and termination with propofol therapy: a case report. Int J Cardiol 2008;128:e6–8. [10] Fogarty DJ, McCleane GJ. Propofol and serum potassium. Anaesthesia 1992;47:63–4. [11] Sabbatani P, Mantovan R. Electrical cardioversion of atrial fibrillation: evaluation of sedation safety with midazolam by means of EtCO2 and IPI algorithm analysis. Int J Cardiol 2013;30(169):430–2. [12] Looi KL, Lee AS, Cole K, et al. Conscious sedation and analgesia use in cardiac device implantation. Int J Cardiol 2013;20(168):561–3. [13] Reddy VY, Reynolds MR, Neuzil P, et al. Prophylactic catheter ablation for the prevention of defibrillator therapy. N Engl J Med 2007;357(26):2657–65. [14] Kuck KH, Schaumann A, Eckardt L, et al. Catheter ablation of stable ventricular tachycardia before defibrillator implantation in patients with coronary heart disease (VTACH): a multicentre randomised controlled trial. Lancet 2010;375(9708):31–40. [15] American Society of Anesthesiologists (ASA). Standards for basic anesthetic monitoring. Continuum of depth of sedation: definition of general anesthesia and levels of sedation/analgesia. http://www.asahq.org/For-Members/Standards-Guidelinesand-Statements.aspx; 2009. [16] Wutzler A, Loehr L, Huemer M, et al. Deep sedation during catheter ablation for atrial fibrillation in elderly patients. J Interv Card Electrophysiol 2013;38(2):115–21. [17] Newstead B, Bradburn S, Appelboam A, et al. Propofol for adult procedural sedation in a UK emergency department: safety profile in 1008 cases. Br J Anaesth 2013;111(4):651–5. [18] Krijthe BP, Heeringa J, Kors JA, et al. Serum potassium levels and the risk of atrial fibrillation: the Rotterdam study. Int J Cardiol 2013;168(6):5411–5. [19] Michaud GF, Sticherling C, Tada H, et al. Relationship between serum potassium concentration and risk of recurrent ventricular tachycardia or ventricular fibrillation. J Cardiovasc Electrophysiol 2001;12(10):1109–12.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Minimal and deep sedation during ablation of ventricular tachycardia Alexander Wutzler a,⁎, Amélie Mueller a, Lena Loehr a, Martin Huemer a, Abdul Shokor Parwani a, Philipp Attanasio a, Florian Blaschke a, Christian Storm b, Leif-Hendrik Boldt a, Wilhelm Haverkamp a a b
Department of Cardiology, Charité — Universitaetsmedizin Berlin, Campus Virchow-Klinikum, Berlin, Germany Department of Intensive Care Medicine, Charité — Universitaetsmedizin Berlin, Campus Virchow-Klinikum, Berlin, Germany
a r t i c l e
i n f o
Article history: Received 29 October 2013 Received in revised form 17 December 2013 Accepted 31 December 2013 Available online 8 January 2014 Keywords: Ablation Deep sedation Minimal sedation Ventricular tachycardia
a b s t r a c t Background: Catheter ablation is a curative treatment option for ventricular premature contractions (VPC) and ventricular tachycardia (VT). Procedures require different sedation levels, depending on duration, ablation approach and patient characteristics. The aim of our study was to evaluate feasibility of minimal and deep sedation for ablation of VPC/VT. Methods: Patients underwent catheter ablation of VPC/VT under minimal or deep sedation. Events of hypotension, hypoxia, bradycardia, procedural complications and VT inducibility were compared between the groups. Results: 120 patients were included. In 42 patients (53.6 ± 17.1 years, 47.6% male) ablation was performed under minimal sedation with midazolam, and in 78 patients (54.2 ± 17.5 years, 67.9% male) ablation was performed under deep sedation with propofol/midazolam. There were significantly fewer patients with idiopathic VT (62.8 vs. 88.1%, p = 0.011) in the deep sedation group, LVEF was significantly lower (47 ± 14.4 vs. 53.1 ± 11.7) and the procedure duration was significantly longer (201.9 ± 85.9 vs. 137.9 ± 98.7). No significant differences in procedural complications or sedation related events (hypotension: 0 vs. 3.8%, p = 0.2, no hypoxia, no bradycardia) were detected. Conclusions: Minimal sedation and deep sedation are both feasible during VPC/VT ablation procedures. Propofol does not increase complications even in a collective with pre-existing impairment of LVEF. Adequate monitoring and trained personnel should be present. © 2014 Elsevier Ireland Ltd. All rights reserved.
1. Introduction Catheter ablation is an established and potentially curative treatment option for different types of ventricular tachycardia (VT) and ventricular premature contractions (VPC) [1]. Procedures may be painful and patient immobilization is required during radiofrequency delivery to provide sufficient catheter–tissue contact and to maintain validation of electroanatomic mapping systems. Therefore, procedures are performed under variable levels of sedation and analgesia from minimal sedation to general anesthesia (GA) [1–4]. General anesthesia is used in a large number of procedures. Although GA provides the most sufficient control of movement and pain, it has certain disadvantages. Of those, reduced VT inducibility, excessive hypotension during VT and (when combined with muscle relaxants) reduced sensitivity of high-output phrenic nerve mapping are particularly relevant [1,2]. Alternative strategies include minimal or moderate sedation during shorter procedures for idiopathic VT/VPC and deep sedation [2,3,5].
⁎ Corresponding author at: Department of Cardiology, Charité - Universitätsmedizin Berlin, Campus Virchow-Klinikum, Augustenburger Platz 1, 13353 Berlin, Germany. Tel.: +49 30 450 665411; fax: +49 30 450 553 994. E-mail address: [email protected] (A. Wutzler). 0167-5273/$ – see front matter © 2014 Elsevier Ireland Ltd. All rights reserved. http://dx.doi.org/10.1016/j.ijcard.2013.12.175
While propofol based deep sedation is a common practice in a wide range of electrophysiological procedures, it is challenging during VT ablation [5–7]. The risk of airway complications and the necessity of rapid change of sedation level for cardioversion of unstable VT require well trained personnel and adequate monitoring [3]. Besides that, propofol may alter myocardial conduction velocities [8] and VT inducibility [9] and it can lead to hypokalemia, especially after prolonged infusion [10]. Hypokalemia and alteration of other serum electrolytes could promote – particularly during the electrophysiological study and the attempt to induce ventricular tachycardia – unspecific malignant ventricular arrhythmias like polymorphic fast VT and ventricular fibrillation (VF). Compared to deep sedation, minimal sedation with midazolam carries a reduced risk of airway complications or hemodynamic impairment. On the other hand, procedural discomfort may be increased during minimal sedation and patient movements may be more likely. Furthermore, a rapid change of sedation level is even more challenging in patients under minimal sedation and may result in a deeper sedation level than intended and respiratory or cardiovascular complications. Analgesia and sedation for electrophysiological procedures have become an emerging research field with high clinical relevance [7,8,11,12]. Despite the growing importance of catheter ablation in the treatment of VT [13,14] and an increasing number of procedures worldwide, only very few studies are available on procedural sedation and analgesia
162
A. Wutzler et al. / International Journal of Cardiology 172 (2014) 161–164
during VT ablation. The aim of our study was to evaluate the feasibility of minimal and deep sedation during VT ablation. The main purpose was to evaluate procedural changes of oxygenation and hemodynamic parameters as well as the occurrence of sedation related adverse events under either sedation regimen. Incidence of complications and procedural changes were compared between the two sedation strategies. 2. Methods 2.1. Patients Consecutive patients presented to our center for catheter ablation of idiopathic or ischemic VT or VPC, in whom procedures were performed under minimal or deep sedation were enrolled from 2007 to 2013. The choice of sedation regimen (minimal vs. deep sedation) was at the discretion of the operating physician based on patient's concomitant disorders, type of VT and expected procedure duration. Study data were analyzed offline by an investigator who was not involved in the choice of anesthetic. Resting electrocardiogram (ECG), transesophageal or transthoracic echocardiography, physical examination and standard blood test were performed prior to ablation. All patients gave informed consent. The study was approved by the ethical committee of the Charité — Universitätsmedizin Berlin.
pressure and peripheral oxygen saturation at the discretion of the treating physician, but at least 4 h. Blood gas analysis was repeated at the discretion of the physician in charge. Patients were assigned to two study groups, according to the sedation strategy that was used: patients that underwent ablation under minimal sedation were assigned to group 1, and patients under deep sedation to group 2. Procedural complications, as well as episodes of hypotension, hypoxia, acidosis and bradycardia that required immediate correction were recorded and compared between the groups. Acidosis was treated at a pH b 7.2. Hypoxia was treated if oxygen saturation was b90% for 30 s or longer. Hypotension was treated if systolic blood pressure was b80 mm Hg (except from short drop in blood pressure during programmed ventricular stimulation with immediate recovery after cessation of stimulation). Bradycardia was treated at a heart rate b40 beats per minute. 2.4. Statistical analysis For comparison of categorical variables among groups, χ2 tests were used. Independent sample t test (normally distributed data) or Mann–Whitney u test (skewed data) was used to compare sedation and procedure related parameters. All analyses were performed using SPSS software version 20.0 (SPSS Inc., Chicago, IL, USA). Data are presented as absolute numbers and percentages for categorical variables or mean ± standard deviation (SD) for continuous variables. A p value of b0.05 was considered statistically significant.
2.2. Ablation procedures Patients were in a fasting state for at least 6 h. Patients with idiopathic VT/VPC or VT/ VPC associated with structural heart disease were included. Ablation procedures were performed using venous, transseptal, retrograde arterial and epicardial approaches or a combination of the aforementioned as appropriate. A 3-D-mapping system was used for ablation of ischemic ventricular tachycardia, epicardial approaches and in the majority of idiopathic VT/VPC procedures. Origin of the arrhythmia and the approach used for mapping and ablation were recorded. Number and type of complications were recorded. The procedural endpoint was defined as non-inducibility of VT/VPC with programmed electrical stimulation and administration of adrenergic agents (Metaproterenol, Epinephrine or Isoproterenol). In patients with unstable ischemic VT, substrate modification was performed during sinus rhythm with local abnormal ventricular activities (LAVA) as ablation target. Inducibility of VT was tested with programmed ventricular stimulation. If cardioversion was necessary due to hemodynamically unstable VT, manual painful stimulation was used to assess sedation level. In case of a positive response to painful stimulus, patients received a 2 mg propofol bolus prior to cardioversion. 2.3. Sedation, analgesia and monitoring Three different strategies are used in our center: 1. minimal sedation, 2. deep sedation and 3. general anesthesia as defined by the American Society of Anaesthesiologists [15]. Patients who underwent procedures under GA were excluded from the study. The remaining patients were either treated according to the minimal or the deep sedation protocol. 2.3.1. Minimal sedation Minimal sedation was achieved with midazolam (initial dose 0.03 mg/kg, repeated doses as needed). Additionally, the opioid analgesic piritramide was administered in repeated doses of 1–2 mg as needed to provide analgesia during radiofrequency (RF) application. 2.3.2. Deep sedation Deep sedation was achieved with continuous propofol infusion with a syringe pump at a dose of 4 mg/kg/h, following an initial midazolam dose (midazolam 0.03–0.05 mg/kg). Additionally, the opioid analgesic piritramide was administered in repeated doses of 2–3 mg as needed to provide analgesia, with a maximum cumulative dose of 15 mg. An oropharyngeal airway was applied in all patients when deep sedation was reached. Arterial blood gas was drawn usually before and at the end of the procedure and additionally at the discretion of the operating physician. All patients received oxygen via nasal cannula (2–8 l/min) with a target SaO2 of N95%. SaO2, and ECG and blood pressure were monitored continuously. Arterial blood pressure was monitored either via invasive intra-arterial blood pressure measurement or via automatically non-invasive measurement in three-minute intervals. Invasive blood pressure measurement was performed in patients with impaired left ventricular function or with known severe hemodynamic compromise under VT. All patients were breathing spontaneously throughout the procedure. Sedation level was continuously monitored by the operating physician and two registered nurses. Drugs were administered by a registered nurse under direct supervision of the electrophysiologist. All procedures were performed by a fully trained electrophysiologist and an electrophysiology fellow. All physicians had been trained in intensive-care medicine, airway management and application of anesthetic drugs. Physicians and nurses were trained in advanced cardiac life support. Additionally, procedures were supervised by a physician of the Department of Cardiology, who is holding a degree in intensive care medicine and emergency medicine. Anesthesiologist standby was available on a 24hour basis from the intensive care unit. After the procedure, patients were allowed to recover from anesthesia and were transferred to an intermediate care unit with continuous monitoring of ECG, blood
3. Results A total of 120 patients were included in the study. Forty-two patients (mean age 53.6 ± 17.1 years, 47.6% men) underwent ablation procedures under minimal sedation and 78 patients (mean age 54.2 ± 17.5 years, 67.9% men) received procedural deep sedation. Patient's baseline characteristics and medication are listed in Table 1. There were significantly more men in the deep sedation group (67.9 vs. 47.6%, p = 0.03). Furthermore, significantly fewer patients in the deep sedation group underwent ablation for idiopathic VT (62.8 vs. 88.1%, p = 0.011). The mean left ventricular ejection fraction (LVEF)
Table 1 Patients' baseline characteristics. ACEI = angiotensin converting enzyme inhibitor, ARB = angiotensin receptor blocker, ASA = American Society of Anesthesiologists, BP = blood pressure, CAD = coronary artery disease, COPD = chronic obstructive pulmonary disease, LVEF = left ventricular ejection fraction, SDH = structural heart disease, VT = ventricular tachycardia.
Age (years) (SD) Male (%) BMI (SD) Idiopathic VT (%) Hypertension (%) CAD (%) Diabetes mellitus (%) COPD (%) Chronic kidney disease ASA physical status (%) I II III ≥IV LVEF (%) (SD) Systolic BP (mm Hg) (SD) Diastolic BP (mm Hg) (SD) Beta-adrenergic blocker Digitalis Amiodarone ACEI ARB Calcium-channel blocker Sodium-channel blocker Diuretic Statin Aspirin Oral anticoagulant a
Statistically significant.
Group 1 Minimal sedation (n = 42)
Group 2 Deep sedation (n = 78)
p value
53.6 (17.1) 20 (47.6) 27.6 (7.2) 37 (88.1) 23 (54.8) 11 (26.2) 2 (4.7) 5 (11.9) 6 (14.3)
54.2 (17.5) 53 (67.9) 26.7 (4.4) 49 (62.8) 40 (52.3) 26 (33.3) 12 (15.4) 6 (7.7) 17 (21.8)
0.84 0.03a 0.42 0.011a 0.67 0.42 0.08 0.46 0.25
3 (7.1) 32 (76.2) 7 (16.7) 0 53.1 (11.7) 123.4 (18.9) 70.1 (12.3) 29 (69) 0 (0) 5 (11.9) 14 9 (21.4) 2 (4.7) 2 (4.7) 13 (31) 17 (40.5) 18 (42.9) 7 (16.7)
1 (1.3) 51 (65.4) 26 (33.3) 0 47 (14.4) 121.6 (17.4) 72.2 (13.5) 55 (70.5) 1 (1.3) 28 (36.4) 29 (37.2) 21 (26.9) 6 (7.7) 3 (3.8) 27 (34.6) 27 (34.6) 34 (43.6) 24 (30.8)
0.88 0.22 0.51 – 0.014a 0.73 0.59 0.79 0.46 0.004a 0.64 0.48 0.53 0.8 0.65 0.56 0.89 0.09
A. Wutzler et al. / International Journal of Cardiology 172 (2014) 161–164
was significantly lower in the deep sedation group (47 ± 14.4 vs. 53.1 ± 11.7%, p = 0.014). Significantly more patients in the deep sedation group were treated with amiodarone at baseline (36.4 vs. 11.9%, p = 0.004). The procedure duration was significantly longer in the deep sedation group (201.9 ± 85.9 vs. 137.9 ± 98.7 min, p b 0.001). RF delivery time was also significantly longer in the deep sedation group (19.24 ± 15.94 vs. 9.38 ± 7.14 min, p b 0.001). Only a minimal drop in systolic and diastolic blood pressure throughout the procedure was registered. There were no significant differences in the mean change of systolic blood pressure (−4.3 ± 21.7 vs. −7.9 ± 21.8 for minimal and deep sedation respectively, p = 0.62) or diastolic blood pressure (−5.5 ± 12 vs. − 7.8 ± 18 for minimal and deep sedation respectively, p = 0.68) between the study groups. Procedural parameters and ablation site are depicted in Table 2. Four complications of catheter ablation were registered: three cases of pericardial effusion or tamponade and one case of femoral vascular complication. In three patients, an episode of hypotension occurred that required treatment. One of those patients also had pericardial tamponade due to perforation of the right ventricle. The patient underwent surgical treatment and was discharged without further sequel. Before the patient was transferred to the operating room, a total of 15 mg of etilefrine was administered to treat hypotension. In the other two patients, an episode hypotension occurred in the absence of pericardial effusion or tamponade during normal sinus rhythm. Hypotension was successfully treated with two boluses of etilefrine 0.03 mg/kg and a reduction of propofol dose in each case. No further complications occurred in the two patients. One patient experienced VF after a fast VT degenerated to VF. VF was successfully treated by immediate biphasic defibrillation (200 J). The patient's serum potassium was 3.8 mmol/l. After termination of VT, mapping and ablation were continued without further adverse events. None of the patients received continuous catecholamine-infusion to maintain hemodynamic function. No ventricular assist devices were used in this study. No case of hypoxia or acidosis occurred. In one patient in the minimal sedation group and 3 patients in the deep sedation group induction of target arrhythmia was not achieved (p = 0.67). Substrate mapping and ablation were performed during sinus rhythm in these patients (See Table 3.) 4. Discussion We here present the results of a single-center study on procedural feasibility of midazolam based minimal sedation and propofol/ Table 2 Procedural parameters compared between the study groups. LV = left ventricle, LVOT = left ventricular outflow tract, RF = radiofrequency, RV = right ventricle, RVOT = right ventricular outflow tract.
Procedure duration (min) (SD) RF delivery time (min) (SD) Propofol dose (mg/h) (SD) Midazolam dose (mg) (SD) Piritramide dose (mg) (SD) Change of systolic BP (mm Hg) (SD) Change of diastolic BP (mm Hg) (SD) Ablation site RVOT LVOT Mitral annulus Aortic cusp LV RV Epicardial approach a
Statistically significant.
Group 1 Minimal sedation
Group 2 Deep sedation
p-Value
137.9 (98.7) 9.38 (7.14) – 5.5 (2.7) 5.9 (3) −4.3 (21.7) −5.5 (12)
201.9 (85.9) 19.24 (15.94) 638.1 (469.2) 6 (3) 6.1 (3.6) −7.9 (21.8) −7.8 (18)
b0.001a b0.001a – 0.43 0.86 0.62 0.68
26 9 – – 7 – –
29 16 3 1 29 – 10
163
Table 3 Procedural complications and episodes of hypotension, hypoxia, acidosis and bradycardia compared between the groups. Severe acidosis: pH b 7.2; hypoxia: oxygen saturation b90% for 30 s or longer; hypotension: systolic blood pressure b80 mm Hg; bradycardia: heart rate b40 beats per minute.
Hypotension (%) Hypoxia (%) Acidosis (%) Bradycardia (%) Pericardial effusion/tamponade (%) Femoral vascular complication (%) Ventricular fibrillation (%) Non-inducibility at baseline (%)
Group 1 Minimal sedation
Group 2 Deep sedation
p-Value
0 0 0 0 0 0 1 (2.4) 1 (2.4)
3 (3.8) 0 0 0 3 (3.8) 1 (1.3) 0 3 (3.8)
0.2 – – – 0.2 0.46 0.17 0.67
midazolam based deep sedation during ablation of ventricular tachycardia. We used an observational non-randomized design reporting the current practice in a real-life collective at a university hospital arrhythmia center. To the best of our knowledge, this is the largest study on sedation during VT ablation and the first study addressing minimal and deep sedation. Common practice at our center is that procedures in patients with severe hemodynamic compromise at baseline, electrical storm, severe life-threatening comorbidities or acute illness are performed with GA by an anesthesiology team or an intensive care team. Procedures that target idiopathic VT/PVC, such as tachycardia originating from right ventricular outflow tract in young patients in the absence of structural heart disease, or (occasionally) stable patients with scar related VT are performed under minimal sedation. Procedures in stable patients that are expected to have a longer duration or that require more painful and challenging techniques, such as transseptal or epicardial access and biventricular mapping, are performed under deep sedation. However, occasionally the sedation level is changed during an ongoing procedure, e.g. if the duration is longer than expected or transseptal puncture is necessary. The proportion of procedures where sedation level was changed from minimal to deep sedation was b10% in our study collective. Those procedures were considered as procedures with the use of deep sedation for the analysis of this study. There were significant differences between the study groups at baseline, all of which are reflecting the aforementioned practice: patients in the deep sedation group were more likely to have a VT related to structural heart disease, where more complex mapping and ablation procedures are expected. Accordingly, the LVEF was significantly lower in this group and significantly more patients were treated with amiodarone. On the other hand, those patients were still ASA class ≥ III and the LVEF in this group was only moderately impaired (47 ± 14.4%), so that the patients were classified eligible for deep sedation. The results show a significantly longer procedure duration in the deep sedation group, reflecting the more challenging procedures in those patients. However, despite the unfavorable patient characteristics and the more complex procedures (including 12.8% epicardial ablations), none of the study parameters nor the number of complications was significantly different between the groups. The overall complication rate was low (3.3% complications in the study collective) and stayed within the range of previous studies that found up to 8% complications in VT procedures [1]. Three events of hypotension occurred; no case of prolonged hypoxia, acidosis or bradycardia was seen. None of the cases required advanced airway management or continuous vasopressor infusion. The use of minimal or deep sedation during ablation of different types of arrhythmia has been reported before [6–8] and can be performed considerably safe even in patients with relevant comorbidities [6–8,16]. However, in contrast to most cases of supraventricular tachycardia and atrial fibrillation, VT is accompanied with severe hemodynamic impairment. During VPC and VT ablation procedures, repeated
164
A. Wutzler et al. / International Journal of Cardiology 172 (2014) 161–164
ventricular stimulation is necessary for induction of the tachycardia or for pace mapping [1,3–5]. Furthermore, catheter mapping during ongoing VT is often used to identify the region of origin [1,3–5]. The latter approach requires the maintenance of VT over minutes, sometimes repeated VT induction over hours if necessary. VT is common in patients with impaired LVEF and/or ventricular scar area, which increases the risk of relevant hypotension and hypoxemia during ongoing VT or rapid ventricular stimulation. Mild hemodynamic compromise and bradycardia have been reported under propofol [6,17]. Therefore, severe hemodynamic impairment subsequent to the combination of propofol infusion and VT may lead to sedation related complications. However, we only observed two brief episodes of hypotension in the deep sedation group, which responded immediately to etilefrine. One patient in the minimal sedation group experienced VF after VT induction. Although treatment was unproblematic in this case, VF is a serious arrhythmia and may be difficult to treat in patients with preexisting hemodynamic compromise or electrolyte disturbances. Especially hypokalemia has been associated with different types of cardiac arrhythmia including sustained VT/VF [18,19]. Although the serum potassium level of the patient in our study was within normal ranges (3.8 mmol/l), it was relatively low. Other monitoring parameters (blood pressure, SaO2) were also within the normal range, the patient was free from drugs that prolong the qt-interval. Therefore we were not able to identify a specific trigger for the degeneration of VT to VF in this patient. Noteworthy, the patient was in the minimal sedation group, so no effect of propofol can be stated. Inducibility of the target arrhythmia was not significantly different between the groups. In general, the use of anesthetic agents may alter inducibility [9], but no specific effect of propofol was found in our study. Our results are in accordance with a previous study by Ramoul et al., who observed no complication during moderate sedation for epicardial VT ablation [2] and with a case report, reporting the feasibility of remifentanil–midazolam sedation during VT ablation [3]. In summary, our results suggest that catheter ablation of VT with the use of minimal or deep sedation is feasible and considerably safe. In a collective of patients with impaired LVEF undergoing relatively long and complex procedures including epicardial ablation, deep sedation did not result in relevant airway complications or hypotension requiring prolonged vasopressor infusion. Furthermore, for a collective of patients with preserved LVEF undergoing procedures with a shorter duration, minimal sedation seems appropriate. However, adequate monitoring should be provided and experienced personnel should be present to immediately detect changes in sedation level, hypotension or hypoxia. 4.1. Limitations There are limitations of our study that should be acknowledged. We did not randomize the patients. Instead, patients were assigned to the minimal or deep sedation group based on clinical considerations. Certain key factors (type of VT, LVEF, amiodarone use) differed significantly between the groups at baseline. However, our study focused on sedation related endpoints. In contrast to a study that would have compared e.g. ablation success, endpoints in our study (hypotension, hypoxia) are less dependent on the type or origin of the VT or long term amiodarone use. Of course a reduced LVEF can increase the risk of events of hypotension or hypoxia. In our study the deep sedation group was treated with propofol and therefore was at higher risk of hypotension. Yet, despite the lower LVEF and the propofol treatment the drop in blood pressure
during the procedure was not significantly higher in this group. Only two patients (2.5%) in the deep sedation group experienced sedation related hypotension, which immediately responded to an etilefrine bolus in both cases. None of the endpoints differed significantly between the groups, suggesting the feasibility of both approaches during VT ablation.
4.2. Conclusion Minimal sedation and deep sedation are both feasible and considerably safe during VPC/VT ablation procedures. Deep sedation can be carried out during longer procedures with expected patient discomfort (e.g. epicardial ablation). Minimal sedation may be sufficient for shorter procedures (e.g. idiopathic VPC/VT). Adequate monitoring and trained personnel should be present to maintain patient safety.
References [1] Aliot EM, Stevenson WG, Almendral-Garrote JM, et al. EHRA/HRS expert consensus on catheter ablation of ventricular arrhythmias: developed in a partnership with the European Heart Rhythm Association (EHRA), a registered branch of the European Society of Cardiology (ESC), and the Heart Rhythm Society (HRS); in collaboration with the American College of Cardiology (ACC) and the American Heart Association (AHA). Europace 2009;11(6):771–817. [2] Ramoul K, Tafer N, Sacher F, et al. Conscious sedation with sufentanil and midazolam for epicardial VT ablation. J Innov Card Rhythm Manage 2012;3:849–53. [3] Mandel JE, Hutchinson MD, Marchlinski FE. Remifentanil–midazolam sedation provides hemodynamic stability and comfort during epicardial ablation of ventricular tachycardia. J Cardiovasc Electrophysiol 2011;22(4):464–6. [4] Miller MA, Dukkipati SR, Mittnacht AJ, et al. Activation and entrainment mapping of hemodynamically unstable ventricular tachycardia using a percutaneous left ventricular assist device. J Am Coll Cardiol 2011;58(13):1363–71. [5] Wasmer K, Köbe J, Dechering DG, et al. Ventricular arrhythmias from the mitral annulus: patient characteristics, electrophysiological findings, ablation, and prognosis. Heart Rhythm 2013;10(6):783–8. [6] Wutzler A, Rolf S, Huemer M, et al. Safety aspects of deep sedation during catheter ablation of atrial fibrillation. Pacing Clin Electrophysiol 2012;35:38–43. [7] Kottkamp H, Hindricks G, Eitel C, et al. Deep sedation for catheter ablation of atrial fibrillation: a prospective study in 650 consecutive patients. J Cardiovasc Electrophysiol 2011;22(12):1339–43. [8] Wutzler A, Huemer M, Boldt LH, et al. Effects of deep sedation on cardiac electrophysiology in patients undergoing radiofrequency ablation of supraventricular tachycardia: impact of propofol and ketamine. Europace 2013;15(12):1019–24. [9] Mulpuru SK, Patel DV, Wilbur SL, Vasavada BC, Furqan T. Electrical storm and termination with propofol therapy: a case report. Int J Cardiol 2008;128:e6–8. [10] Fogarty DJ, McCleane GJ. Propofol and serum potassium. Anaesthesia 1992;47:63–4. [11] Sabbatani P, Mantovan R. Electrical cardioversion of atrial fibrillation: evaluation of sedation safety with midazolam by means of EtCO2 and IPI algorithm analysis. Int J Cardiol 2013;30(169):430–2. [12] Looi KL, Lee AS, Cole K, et al. Conscious sedation and analgesia use in cardiac device implantation. Int J Cardiol 2013;20(168):561–3. [13] Reddy VY, Reynolds MR, Neuzil P, et al. Prophylactic catheter ablation for the prevention of defibrillator therapy. N Engl J Med 2007;357(26):2657–65. [14] Kuck KH, Schaumann A, Eckardt L, et al. Catheter ablation of stable ventricular tachycardia before defibrillator implantation in patients with coronary heart disease (VTACH): a multicentre randomised controlled trial. Lancet 2010;375(9708):31–40. [15] American Society of Anesthesiologists (ASA). Standards for basic anesthetic monitoring. Continuum of depth of sedation: definition of general anesthesia and levels of sedation/analgesia. http://www.asahq.org/For-Members/Standards-Guidelinesand-Statements.aspx; 2009. [16] Wutzler A, Loehr L, Huemer M, et al. Deep sedation during catheter ablation for atrial fibrillation in elderly patients. J Interv Card Electrophysiol 2013;38(2):115–21. [17] Newstead B, Bradburn S, Appelboam A, et al. Propofol for adult procedural sedation in a UK emergency department: safety profile in 1008 cases. Br J Anaesth 2013;111(4):651–5. [18] Krijthe BP, Heeringa J, Kors JA, et al. Serum potassium levels and the risk of atrial fibrillation: the Rotterdam study. Int J Cardiol 2013;168(6):5411–5. [19] Michaud GF, Sticherling C, Tada H, et al. Relationship between serum potassium concentration and risk of recurrent ventricular tachycardia or ventricular fibrillation. J Cardiovasc Electrophysiol 2001;12(10):1109–12.