Crit Care Nurse 2006 Oct; 26(5): 13-20
Cover Article
CE Article
Mapping Ventricular Tachycardia
Jody Zak, RN, BSN
Jody Zak has more than 30 years of nursing experience and currently works in the electrophysiology laboratory at the University of Maryland Medical Center in Baltimore.
To purchase electronic or print reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 809-2273 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints{at}aacn.org.
* This article has been designated for CE credit. A closed-book, multiple-choice examination follows this article, which tests your knowledge of the following objectives:- Discuss the advantages and limitations of radiofrequency ablation as a therapy for patients at high risk of sudden death caused by ventricular arrhythmias
- Describe appropriate nursing interventions before, during, and after radiofrequency ablation for patients undergoing the procedure
- Identify the signs and symptoms of common complications of radiofrequency ablation and proper nursing care related to each one
Corresponding author: Jody Zak, RN, BSN, Electrophysiology Lab, Cardiac EP Service, 22 South Greene St., N3W77, Baltimore, Md 21201 (e-mail: jzak{at}medicine.umaryland.edu).
Implantable cardioverter defibrillators (ICDs) have become the standard treatment for patients at high risk of sudden death due to ventricular arrhythmias. Because implantation of an ICD is not a cure, the risk of recurrence of arrhythmia is not reduced, and frequent sequential ICD shocks can cause patients marked discomfort.1 This discomfort accounts for decreased acceptance of the device and a decreased quality of life among patients.2 Although pharmacological treatment of ventricular tachycardia can help reduce recurrences of sustained arrhythmia, antiarrhythmic drugs have been associated with low efficacy, proarrhythmic actions, and frequent toxic effects or long-term adverse effects.3 These problems associated with pharmacological therapies have prompted a search for alternative approaches to decrease recurrence of potentially lethal ventricular dys-rhythmias. One of these approaches involves ablation of the arrhythmogenic myocardial focus.
With radiofrequency ablation, alternating current is delivered in low voltage (typically 40 V) for 30 to 60 seconds to cause controlled thermal injury of the contacted myocardial tissue. This current is delivered between a catheter tip and an indifferent electrode (ground patch). The lesion created is discrete and its location is precisely defined, with minimal risk of damage to adjacent structures. Irreversible injury occurs when the myocardial tissue reaches a temperature of 48°C to 50°C.4
Radiofrequency ablation has revolutionized therapy of most forms of supraventricular tachycardia and ventricular tachycardia in patients without structural heart disease by providing arrhythmia cure in almost 90% of cases.5 These types of tachycardia are due to an arrhythmia focus that occurs in a fixed location, providing a precise target and making the tachycardia more amenable to treatment by ablation. Most cases of ventricular tachycardia in patients without heart disease originate from 1 of 2 locations: the right ventricular outflow tract or the left ventricle. However, ventricular tachycardia in patients without structural heart disease is uncommon,6 accounting for less than 10% of all patients with ventricular tachycardia.7
Treatment of ventricular tachycardia in patients with structural heart disease has not been nearly as successful. Use of ablation to treat ventricular tachycardia in such patients is a valuable adjunct to treatment with ICDs, mainly to decrease recurrence of the clinical arrhythmias and the frequency of ICD shocks. Most sustained monomorphic ventricular tachycardias are caused by reentry involving a region of ventricular scar. The scar is most often caused by an old myocardial infarction, but right ventricular dysplasia, sarcoidosis, Chagas disease, other nonischemic cardiomyopathies, and scar related to surgical repair can also cause reentry.6
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Anatomy of a Scar
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In the weeks after a myocardial infarction, the healing infarct undergoes structural changes. Fibrosis creates areas of conduction block and also increases separation of myocyte bundles, slowing conduction through myocyte pathways in the border of the infarct.8 These pathways can support reentry circuits, leading to monomorphic ventricular tachycardia. The best target for ablation of scarred tissue causing tachycardia is usually within these zones of slow conduction.4
The reentry circuits associated with ventricular scar can be difficult to define. The situation is further complicated by the presence of multiple reentry circuits, giving rise to multiple different monomorphic ventricular tachycardias. The approach to ablation depends on the stability and number of ventricular tachycardias targeted for ablation and the location of the ventricular scar.9 Limitations of ventricular tachycardia ablation to date have included imprecise mapping tools, limited efficacy, multiple sites of origination of arrhythmia, unstable hemodynamic status during the arrhythmia, and unpredictable changes in the myocardial scar tissue.5
In the rest of this article, I discuss using advanced mapping techniques to better localize the origin of the ventricular tachycardia in order to improve applicability and effectiveness of ablation in treating this arrhythmia. I also review nursing care before, during, and after the procedure and essential monitoring requirements, risks, and complications.
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Mapping
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A number of mapping techniques have been developed to assist in the accurate localization of the reentrant circuit and detect critical regions for ablation. QRS morphology of ventricular tachycardia can be used as a starting point for localizing the source of the arrhythmia when the ventricles are structurally normal but can be misleading and less reliable in patients who have structural damage due to infarction or scarring.6,9 The QRS morphology of focal-origin ventricular tachycardia is largely determined by the location of the focus of the arrhythmia.9 Ventricular tachycardias associated with scarring have a QRS morphology indicative of the exit location of the reentry circuit9 (Table 1
).
Previous mapping techniques include activation-sequence, pace-mapping, and entrainment approaches. These approaches are often used during the tachycardia by means of a steerable mapping catheter. Activation mapping involves maneuvering the ablation catheter to a site where the tip records electrical activity generated earlier than at any other endocardial site.4
For patients with unstable or noninducible ventricular tachycardia, pace mapping during sinus rhythm is done at sites around the infarct region in an attempt to produce a QRS morphology similar to that of the spontaneous ventricular tachycardia.4 Entrainment mapping involves pacing from the ablation catheter during induced tachycardia at a slightly faster rate and evaluating the response of the tachycardia and QRS morphology to confirm location within the reentry circuit. This approach is most applicable if the ventricular tachycardia is easily induced, sustained, and hemodynamically stable.9
However, many patients with sustained monomorphic ventricular tachycardia, particularly patients with multiple infarctions or nonischemic cardiomyopathy, have marked left ventricular dysfunction and may not be able to maintain a stable hemodynamic status during the ventricular tachycardia to allow necessary mapping.
With the development of more advanced mapping systems, "substrate mapping" has been added to previous mapping techniques. Such mapping allows identification of the reentrant area during stable sinus rhythm, a step that minimizes mapping during ventricular tachycardia. Use of an anatomically based approach during sinus rhythm might extend the applicability of ablative therapy. Such an approach could also reduce procedural time, subsequent radiation exposure, and the number of radiofrequency lesions. Theoretically, limiting the number of radiofrequency lesions to the minimum required for success is desirable, because the risk of damage to functioning myocardium and the creation of potentially thrombogenic endocardial lesions are minimized.10
In fewer than 5 years, several advanced mapping systems have been developed, including noncontact mapping (Ensite 3000, Endocardial Solutions, St Paul, Minn), basket catheters, CARTO-XP (Biosense-Webster, Diamond Bar, Calif ), and the Real-Time Position Management System (Boston Scientific, Natick, Mass). The Real-Time Position Management System allows electroanatomical mapping by means of a combination of electrophysiological measurements and anatomical information derived from ultrasound imaging.11 Selection of appropriate target sites is based on a combination of these 2 functions. In this system, an ultrasound ranging technique enables multiple distance measurements between 2 reference catheters positioned in the coronary sinus and the right ventricle and a mapping catheter positioned in the left ventricle. Each catheter is equipped with ultrasound transducers. Areas showing recordings of low-voltage electro-grams are used to detect scarred myocardium. A diminished bipolar electrogram amplitude of less than 1.5 mV is considered a marker of scarred myocardium; dense scar has a voltage of less than 0.5 mV.12 Plots of electrogram amplitude, referred to as voltage maps, clearly delineate the infarcted region (see Figure).
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Anteroseptal view of septal scar. In this voltage map, an ablation catheter is positioned in a septal scar zone in an area color-coded red. The red indicates a voltage <0.5 mV, correlating with dense scar. The corresponding electrogram is shown in the right panel.
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By moving the ablation catheter from point to point around the ventricle, the electrogram signals can be displayed as color gradients. Normal amplitude areas (>1.5 mV) are indicated by purple; progressively lower amplitude regions are indicated by blue, green, yellow, and red. Dense scar is color-coded red. These areas can then be targeted for ablation.
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Ablation
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Ablations can be done on either an outpatient basis or while the patient is hospitalized for incessant ventricular tachycardia. If an ablation is done on an outpatient basis, pre-procedural instructions including no food or drink after midnight, the need for a designated driver, required laboratory tests, and medication instructions are given (Table 2). Procedures generally last 3 to 4 hours, and patients are monitored for 4 hours after sheath removal to allow adequate recovery from sedation and stabilization of vascular access sites. Patients may be discharged after the 4-hour recovery or may be admitted to the hospital overnight for closer observation.
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During the Procedure
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During the procedure, patients are sedated by using a moderate sedation protocol with a combination of midazolam and fentanyl citrate. Diphenhydramine may be added. Heart rate, blood pressure, pulse oximetry readings, and carbon dioxide levels are monitored every 5 minutes. The response to sedation is assessed by using the Richmond Agitation Sedation Scale.13 Multiple venous sheaths are typically placed in the femoral veins for positioning electrode catheters high in the right atrium, the right ventricular apex, the bundle of His, and the coronary sinus.
The left side of the heart can be accessed in 1 of 2 ways: a transseptal approach or a retrograde approach. An arterial catheter is placed in the femoral artery for retrograde approach and continuous monitoring of blood pressure. Because platelet activation, thrombin formation, and fibrinolytic activation can occur after ablation, systemic anticoagulation with intravenous heparin is necessary while catheters are present in the left side of the heart.14 Anticoagulation status is monitored by measuring activated clotting time. The time is determined 10 minutes after every heparin bolus and then every 30 minutes to maintain a value greater than 250 seconds while catheters are in the left side of the heart.
Electroanatomical mapping of the left ventricle is performed by using 2 reference catheters, the ablation catheter, and the Real-Time Position Management mapping system. The 2 reference catheters are placed via the right femoral vein and positioned in the right ventricular apex and either the coronary sinus or high in the right atrium. An 8- or 10-mm-tip ablation catheter is positioned in the left ventricle. Radiofrequency lesions are created in sinus rhythm or during hemodynamically stable ventricular tachycardia around the scar at the border zone or at critical points in the scar that are required for ventricular tachycardia. An 8- or 10-mm ablation catheter is used to create the larger deeper lesions needed to eliminate reentry circuits, which may occupy several square centimeters or more and may involve the endocardium, the myocardium, and even the epicardium.15
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Complications
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The potential risks and benefits of the procedure are discussed in detail with each patient before the procedure while informed consent is being obtained. Procedure-related mortality rate for ablation of ventricular tachycardia associated with heart disease is 1% to 2.7%.6,9 The risk for major complications, including stroke, transient ischemic attack, myocardial infarction, cardiac perforation requiring treatment, or heart block is 5% to 8%.6,15,16 During follow-up, approximately 10% of the patients die of progressive heart failure.6,9,17 This risk of death is not unexpected in patients with markedly depressed function of the left ventricle.17 Other risks are those associated with vascular access (2%–4%), including bleeding, infection, hematoma, and vascular injury. Cardiac trauma, infarction, and valvular damage (1%–2%) have been reported.18 The frequency of valvular complications is slightly higher with left-sided ablations in which the retrograde aortic approach is used.19 Thromboembolism, including stroke, systemic embolism, and pulmonary embolism (<1%) are possible.18 Radiofrequency catheter ablation may require extended fluoroscopic exposure, resulting in elevated radiation risk, including skin burns and risk of malignant neoplasms.20
Segal et al21 found 6 major procedural complications (15%) in the 40 patients studied. These included cardiogenic shock after ventricular fibrillation and 5 complications after transseptal puncture, including cerebrovascular accident, hemothorax, and pericardial tamponade. Other complications included transient ischemic attack after a direct-current shock, complete heart block, and a false aneurysm in the femoral artery.21
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After the Procedure
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Nursing care after ablation to treat ventricular tachycardia involves frequent monitoring of vital signs and groin sites, with checks every 15 minutes for the first hour, then checks twice every 30 minutes, and then checks twice every hour. The patient is transferred to the holding area or inpatient room when the recovery score on the Aldrete scale22 is 8 or greater. A decrease in blood pressure is treated initially with intravenous fluids and may be related to sedation, a vagal response to sheath removal, or hypovolemia. Sustained decreased blood pressure that does not respond to fluids, especially if chest pain occurs is followed up by using emergent echocardiography to rule out pericardial effusion.
A second possible complication is bleeding or hematoma at the groin site. Any further bleeding at the groin site requires direct manual pressure for an additional 5 to 10 minutes. Patients must maintain bed rest for at least 4 hours with the head of the bed elevated to no greater than 30°. The urinary catheter is left in place until bed rest restrictions are removed.
A change in level of consciousness, including restlessness and confusion, must always be investigated. An initial change in level of consciousness may be related to sedation, which can be reversed with naloxone or flumazenil. However, continued changes may require computed tomography of the head to rule out stroke or intracerebral bleeding.
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Results
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Studies have indicated an immediate success rate, defined as noninducibility of the target ventricular tachycardia at the end of ablation, of 63% to 93%.15,23 O’Callaghan et al15 found that 5 years after ablation, total mortality was 51%, and probability of freedom from all ventricular tachyarrhythmias was 28%. Segal et al21 found that of the 57.9% of areas targeted for ablation, 87.2% were successfully ablated. However, only 42.5% of patients remained free from ventricular tachycardia/fibrillation 3 years after ablation.21 Therefore, immediate procedural success should not be accepted as definitive therapy, and further studies must be done to improve understanding of methods for performing ablations to treat ventricular tachycardia.
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Conclusions
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Radiofrequency catheter ablation offers potential control of arrhythmia without the adverse effects of antiarrhythmic drugs. To date, applicability had been limited for patients with multiple hemodynamically unstable or unmappable ventricular tachycardias. The development of advanced mapping systems has expanded the array of options for clinicians in the treatment of ventricular tachycardia. Ablation can be lifesaving for patients with incessant ventricular tachycardia and can decrease frequent episodes of ventricular tachycardia that cause an ICD to deliver repeated shocks.
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References
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- Bella PD, Trevisi N. Catheter ablation: is it good for all post infarct ventricular tachycardias? Eur Heart J. 2002;23:1645–1647.[Free Full Text]
- Sears SF, Todaro TF, Urizar G, et al. Assessing the psychosocial impact of the ICD: a national survey of implantable cardioverter defibrillator health care providers. Pacing Clin Electrophysiol. 2000;23:939–945.[Medline]
- O’Donnell D, Bourke JP, Anilkumar R, Simeonidou E, Furniss SS. Radiofrequency ablation for post infarction ventricular tachycardia: report of a single centre experience of 112 cases. Eur Heart J. 2002;23:1699–1705.[Abstract/Free Full Text]
- Murgatroyd F, Krahn A. Mapping and Catheter Ablation Handbook of Cardiac Electrophysiology: A Practical Guide to Invasive EP Studies and Catheter Ablation. London, England: ReMEDICA Publishing Ltd; 2002:178–216.
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- Soejima K, Stevenson WG. Ventricular tachycardia associated with myocardial infarct scar: a spectrum of therapies for a single patient. Circulation. 2002;106:176–179.[Free Full Text]
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- Sessler CN, Gosnell MS, Grap MJ, et al. The Richmond Agitation-Sedation Scale: validity and reliability in adult intensive care patients. Am J Respir Crit Care Med. 2002;166:1338–1344.[Abstract/Free Full Text]
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- Della Bella P, DePonti R, Uriarte JAS, et al. Catheter ablation and antiarrhythmic drugs for haemodynamically tolerated post-infarction ventricular tachycardia: long-term outcome in relation to acute electrophysiological findings. Eur Heart J. 2002;23:414–424.[Abstract/Free Full Text]
- Ganz L. Catheter ablation of cardiac arrhythmias: overview and technical aspects. Available at: http://www.utdol.com. Accessed December 16, 2004.
- Olsson A, Darpo B, Bergfeldt L, Rosenqvist M. Frequency and long term follow up of valvar insufficiency caused by retrograde aortic radiofrequency catheter ablation procedures. Heart. 1999;81:292–296.[Abstract/Free Full Text]
- Koenig TR, Wolff D, Mettler FA, Wagner LK. Skin injuries from fluoroscopically guided procedures, I: characteristics of radiation injury. AJR Am J Roentgenol. 2001;177:3–11.[Free Full Text]
- Segal O, Chow A, Markides V, Schilling RJ, Peters NS, Davies DW. Long-term results after ablation of infarct-related ventricular tachycardia. Heart Rhythm. 2005;2:474–482.[Medline]
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Anatomy of a Scar
Mapping
