Anesthesia and Sedation Strategies in Electrophysiology: General Concepts




© Springer International Publishing Switzerland 2017
Basavana G. Goudra and Preet Mohinder Singh (eds.)Out of Operating Room Anesthesia10.1007/978-3-319-39150-2_12


12. Anesthesia and Sedation Strategies in Electrophysiology: General Concepts



Anjan Trikha , Bharathram Vasudevan  and Anuradha Borle 


(1)
Department of Anaesthesiology, Pain Medicine and Critical Care, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, Delhi, India

 



 

Anjan Trikha (Corresponding author)



 

Bharathram Vasudevan



 

Anuradha Borle



Abstract

Numerous procedures are carried out in the cardiac electrophysiology laboratory including catheter ablation for various arrhythmias and implantation of devices such as pacemakers and implantable cardioverter-defibrillators (ICD). Patients undergoing these procedures pose unique challenges to the anesthetist as they have serious cardiovascular conditions like unstable arrhythmias, coronary artery disease and poor cardiac function, often with left ventricular ejection fraction less than 35 %. Many of these procedures can be carried out under local anesthesia with conscious sedation administered by a trained nurse. However, monitored anesthesia care with varying levels of sedation provided by trained anesthesia personnel is preferable in patients with multiple comorbidities and severe cardiac conditions. General anesthesia is needed for patient populations such as pediatric patients, those with poor functional status who cannot lie on their back and for complex catheter ablation procedures which require minimal patient movement for prolonged durations. Midazolam and fentanyl are the commonly used agents for conscious sedation. Propofol, etomidate or ketamine are commonly used for deeper sedation or general anesthesia. The effects of anesthetic drugs on the cardiac conduction system should be kept in mind as they can interfere with identifying arrhythmias during electrophysiological studies.


Keywords
AnesthesiaSedationMonitored anesthesia careCardiac electrophysiologyCatheter ablationAtrial fibrillationPacemakerImplantable cardioverter-defibrillatorCardiac resynchronization therapyMidazolamFentanylPropofolKetamineEtomidateHigh frequency jet ventilation



Introduction


The number of procedures being carried out in the cardiac electrophysiology laboratory (EP lab) has increased tremendously in the past few decades. They have grown from simple diagnostic electrophysiology studies for cardiac conduction abnormalities to complex therapeutic procedures offering treatment for a variety of cardiac conditions. For instance, more than 12,500 implantable cardioverter-defibrillators (ICD) are implanted every month in the United States of America [1]. Many of the procedures in the EP lab can be done under local infiltration anesthesia with minimal sedation that is usually administered by non-anesthesia personnel. Certain complex procedures and patient populations require deep sedation or general anesthesia and the expertise of an anesthesiologist. The focus of this chapter is to provide a general overview of anesthesia and sedation strategies employed in the EP laboratory.


Arrhythmias and EP Lab Procedures


An in-depth knowledge of the mechanisms of arrhythmias and various procedures done in the EP laboratory are crucial for safe and effective anesthetic management for the procedure. The types of interventions done in any EP lab can be divided into two –


  1. 1.


    Device based interventions and

     

  2. 2.


    Catheter based interventions

     


Device Based Interventions


Device based interventions include implantation of pacemakers, implantable cardioverter-defibrillators and lately biventricular pacing gadgets for cardiac resynchronization therapy (CRT) with or without implantable cardioverter-defibrillator. Permanent pacemakers are indicated for symptomatic bradycardia in patients with sick sinus syndrome, atrioventricular block, bifascicular or trifascicular blocks, carotid sinus hypersensitivity and neurally mediated bradycardia [2]. ICD is indicated for both primary prevention and secondary prevention of sudden cardiac death. Patients with previous history of cardiac arrest due to ventricular fibrillation or sustained ventricular tachycardia require an ICD as a secondary prevention measure. ICD implantation for primary prevention is indicated in patients at risk for sudden cardiac death and sustained ventricular tachyarrhythmias (e.g. – patients with previous myocardial infarction and ischemic cardiomyopathy with left ventricular ejection fraction (LVEF) less than 35 %). CRT involves biventricular pacing to improve coordination and increase ejection fraction in patients with poor left ventricular function (LVEF less than 35 %) and QRS duration more than 0.12 s. CRT can also be combined with an ICD to prevent sudden cardiac death in such patients. Readers are referred to the ‘appropriate use’ criteria published by the American College of Cardiology Foundation in association with other related societies for knowing the exact indications for placement of these devices [3]. Implantation of these devices is done by transvenous route (usually subclavian vein) and the generator is placed in a subcutaneous pocket in the infra-clavicular region.


Catheter Based Interventions


These include the diagnostic electrophysiological studies and catheter ablations done for various tachyarrhythmias. The arrhythmias amenable to catheter ablation include atrioventricular reentrant tachycardia (AVRT), atrioventricular nodal reentrant tachycardia (AVNRT), Wolff-Parkinson-White syndrome, atrial tachycardia, atrial flutter, atrial fibrillation (AF) and ventricular tachycardia (VT). Catheter ablation is offered for patients with symptomatic and recurrent tachyarrhythmias not responding to medical treatment or recurrent VT requiring multiple ICD generated shocks if the same has been implanted earlier [46]. It may also be indicated as the first-line of treatment in some arrhythmias with high cure rates after ablation. Catheter ablations have been associated with better outcomes and improved quality of life [6].

Cardiac electrophysiologic mapping refers to the determination of spatial and temporal distribution of electrical activity of heart to find the specific mechanism of arrhythmias and to identify the target location for ablation. EP testing involves placement of electrode catheters at multiple predetermined positions inside the heart and programmed pacing is done to obtain intra-cardiac localized electrograms. Classical locations for placement of catheters are in the right atrium, near the bundle of His, in the right ventricle and the coronary sinus. The sequence of activation at these different positions and time delay between the recorded electrograms help in the exact diagnosis and localization of the target area. Various strategies of mapping are employed that include activation mapping, entrainment mapping, pace mapping and substrate mapping. During such procedures, arrhythmias may be induced by programmed electrical stimulation, burst pacing or pharmacological methods (catecholamine infusion). Conventional mapping techniques uses fluoroscopy to position the electrode catheters. Newer non-fluoroscopic catheter navigational systems (such as CARTO and Ensite NAVx) provide three-dimensional electroanatomical mapping of the heart chambers and help in catheter localization and navigation by using electromagnetic and impedance based technologies respectively. They provide the advantage of three dimensional modeling and also a decrease in fluoroscopy times [7].

Catheter ablation at the identified site is performed usually using radiofrequency energy delivered by a catheter tip to the endocardial surface which causes a burn by resistive heating. Some arrhythmias have a known anatomical cause and the ablation energy is directed to this site – e.g. atrial flutter arises from a reentrant mechanism at the cavo-tricuspid isthmus between the inferior vena cava and tricuspid valve.

To avoid excessive tissue damage with radiofrequency ablation, saline irrigation to cool the catheter tip has been used but this can lead to fluid overload in susceptible patients [8]. Cryothermal energy to produce cryo-ablation has also been used, although less frequently. The advantage of cryo-ablation is the ability to produce reversible test lesions by controlling the temperature and a reduced risk of thromboembolism [9].


Anesthetic Drugs and Cardiac Electrophysiology


The ideal anesthetic agent for cardiac electrophysiology procedures should not interfere with the ability to identify arrhythmias during an electrophysiological procedure. While all anesthetic agents can affect the cardiac conduction system, a balanced anesthesia technique has been shown not to interfere in the ability to identify aberrant pathways during open surgical ablation [10]. The anesthetic agents commonly used in the EP laboratory with their relevant pharmacokinetic and pharmacodynamic properties are discussed below.



  • Propofol is an alkyl phenol exerting its hypnotic effects through GABA and NMDA receptors. It is commonly used for sedation as well as induction and maintenance of general anesthesia. Propofol is a profound cardiovascular depressant. It causes hypotension after an induction dose due to reduction in systemic vascular resistance and also associated myocardial depression. However, it is not accompanied by an increase in heart rate due to probable inhibition of baroreceptor reflex. The effects may lead to hemodynamic instability especially in patients with poor LV function (candidates for CRT) and in elderly population. Small titrated doses of propofol have been found to be safe in these patients. The onset time is prolonged in patients with heart failure due to longer circulation times and the administration of a repeat bolus should be delayed. Though various studies have shown that propofol does not affect conduction at sinus node, AV node or through accessory pathways, it has been reported to interfere with the induction of supraventricular tachycardia especially in children, which should be kept in mind during electrophysiological studies [1114].


  • Etomidate is an imidazole derivative acting on the GABA receptor. It is cardiovascular stable drug and is an attractive choice for induction of anesthesia in patients with cardiovascular instability. It causes lesser depression of respiratory drive than propofol and may be advantageous in situations requiring short GA with minimal airway manipulation. Two main disadvantages of etomidate include the high incidence of myoclonus and prolonged adrenal suppression after long term infusions. Myoclonus can interfere with the ECG recording which is undesirable in cardiac electrophysiological studies [15, 16]. Pretreatment with midazolam has been shown to reduce the incidence of myoclonus [17, 18].


  • Ketamine, a NMDA receptor antagonist is an indirectly acting sympathomimetic leading to an increase in blood pressure, heart rate and cardiac output. This leads to increased myocardial oxygen demand which may have deleterious effects in cardiac patients with coronary artery disease or pulmonary hypertension. Ketamine also causes psychomimetic effects leading to emergence phenomenon postoperatively. These hemodynamic and psychomimetic effects of ketamine can be attenuated with prior administration of midazolam or dexmedetomidine [19]. It should also be noted that in critically ill patients with catecholamine depletion, ketamine can lead to myocardial depression by its direct effect on the heart. The advantages of using ketamine for sedation include profound analgesia and its minimal effects on respiratory drive. Wutzler et al. found that the hemodynamic effects of ketamine were beneficial compared to propofol in patients undergoing radiofrequency ablation for supraventricular tachycardia with pre-existing bradycardia and hypotension [20].


  • Benzodiazepenes are commonly used for sedation and anxiolysis. Midazolam is especially suited for intravenous procedural sedation because of its faster onset and shorter duration of action. It does not cause significant cardiovascular instability though it can decrease peripheral vascular resistance and cardiac output more than other benzodiazepenes. It has no effect on cardiac conduction system. Exaggerated sedation and cardiovascular responses can be seen in the elderly and requires appropriate titration [7]. Midazolam can sometimes cause paradoxical agitation which can be treated with flumazenil or propofol [21, 22].

Short acting opioids such as fentanyl, alfentanil, sufentanil and remifentanil are also used for sedation and analgesia in these groups of patients. Fentanyl and midazolam combination is one of the most commonly used sedation technique in procedures carried out in EP labs. They have a synergistic effect when used along with other sedatives or induction agents. High dose opioid based anaesthesia has been associated with hemodynamically stable intraoperative period when compared to other intravenous or inhalational anesthetics. Opioids can cause bradycardia at high doses due to a direct membrane action or via opioid receptors [23]. They have also been associated with QTc prolongation and remifentanil has been reported to cause slowing of conduction in sino-atrial and AV node during electrophysiological studies in children [24].

Dexmedetomidine is a highly selective alpha-2 agonist and is often used for sedation and monitored anesthesia care with minimal effects on respiration. During cardiac electrophysiologic procedures, it has been shown to produce slowing in both sino-atrial and AV node function which can be deleterious in patients at risk for AV nodal block and bradycardia [25, 26]. Also it can lead to sympatholysis which can interfere with the induction of arrhythmias during the electrophysiological study thereby hampering diagnosis and treatment.

Neuromuscular blocking agents are rarely used in the EP lab as most procedures are done under sedation and muscle relaxants might interfere with the ability to test the phrenic nerve which may be injured during catheter ablation procedures. They also affect the cardiac conduction system. Succinylcholine can lead to both brady and rarely tachyarrhythmias. It can also lead to elevation of serum potassium which may alter the electrophysiological responses. Pancuronium can lead to tachycardia due to its vagolytic properties. Atracurium and mivacurium can cause hypotension and reflex tachycardia by histamine release. Vecuronium can cause bradycardia when combined with potent opioids while rocuronium is relatively cardiovascular stable [7, 23].

All inhalational anaesthetics can affect the conduction system of heart. Volatile agents, especially halothane sensitize the myocardium to the arrhythmogenic action of catecholamines thereby leading to abnormal automaticity and this can cause premature contractions and arrhythmias [23]. All volatile agents also lead to prolongation of QTc which may lead to induction of torsades de pointes [27]. A study comparing isoflurane and propofol in children undergoing ablation procedure for supraventricular tachycardia found no clinically significant interference by either of the agents, while another report found significant prolongation of accessory pathway refractory period with sevofurane when compared with propofol in children [13, 28].

Finally, the context-sensitive half-life of propofol and opioids after prolonged infusions should be kept in mind and the dose should be titrated accordingly. Context-sensitive half-life is the time taken for the plasma drug concentration to decrease by 50 % after discontinuation of an infusion. It depends on the duration of infusion (‘context’ = duration) and the half-life of the drug increases with an increase in duration of the infusion except for drugs with very short elimination half times (e.g. Remifentanil).

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Aug 26, 2017 | Posted by in Uncategorized | Comments Off on Anesthesia and Sedation Strategies in Electrophysiology: General Concepts
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