Guidelines Summary
Advanced cardiac life support
Updated cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) guidelines were issued in 2015 by the following organizations [60, 61, 62] :
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American Heart Association (AHA)
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European Resuscitation Council (ERC)
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The International Liaison Committee on Resuscitation (ILCOR)
The following summarizes the AHA adult cardiac arrest algorithm for ventricular fibrillation (VF) or pulseless ventricular tachycardia (pVT) [60] :
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Activate the emergency response system.
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Initiate cardiopulmonary resuscitation (CPR) and give oxygen when available.
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Verify the patient is in VF as soon as possible (ie, automated external defibrillator [AED] and quick look with paddles).
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Defibrillate once: Use a device specific recommendations (ie, 120-200 J for biphasic waveform; 360 J for monophasic waveform); if unknown, use the maximum available.
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Resume CPR immediately without pulse check and continue for 5 cycles. One cycle of CPR equals 30 compressions and 2 breaths; 5 cycles of CPR should take roughly 2 minutes (compression rate 100 per minute). Do not check for rhythm/pulse until 5 cycles of CPR are completed.
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During CPR, minimize interruptions while securing intravenous (IV) access and performing endotracheal intubation. Once the patient is intubated, continue CPR at 100 compressions per minute without pauses for respirations, and administer respirations at 10 breaths per minute.
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Check rhythm after 2 minutes of CPR.
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Repeat a single defibrillation if rhythm check still reveals VF/pVT. Selection of fixed versus escalating energy for subsequent shocks is based on the specific manufacturer’s instructions. For a manual defibrillator capable of escalating energies, higher energy for the second and subsequent shocks may be considered.
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Resume CPR for 2 minutes immediately after defibrillation.
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Continuously repeat the cycle of (1) rhythm check, (2) defibrillation, and (3) 2 minutes of CPR.
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Administer a vasopressor: Give a vasopressor during CPR before or after the shock when IV or intraosseous (IO) access is available. Administer epinephrine 1 mg every 3-5 minutes.
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Administer antidysrhythmics: Give antidysrhythmic agents during CPR before or after the shock. Administer amiodarone 300 mg IV/IO once; then, consider administering an additional 150 mg once.
In addition, correct the following if necessary and/or possible:
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Hypovolemia
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Hypoxia
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Hydrogen ion (acidosis): Consider bicarbonate therapy.
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Hyperkalemia/hypokalemia and metabolic disorders
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Hypoglycemia: Check fingerstick or administer glucose.
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Hypothermia: Check core rectal temperature.
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Toxins
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Tamponade, cardiac: Check with ultrasonography.
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Tension pneumothorax: Consider needle thoracostomy.
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Thrombosis, coronary or pulmonary: Consider thrombolytic therapy if suspected.
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Trauma
According to the AHA, if all the following factors are present, termination of resuscitation in out-of-hospital cardiac arrest (OHCA) may be considered [60] :
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Arrest was not witnessed by emergency medical services (EMS) personnel
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No return of spontaneous circulation (ROSC) prior to transport
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No AED shock delivered prior to transport
In addition, in intubated patients, failure to achieve an end-tidal carbon dioxide (ETCO2) over 10 mm Hg by waveform capnography after 20 minutes of CPR may be considered as one component of a multimodal approach to decide when to end resuscitative efforts. However, no studies of nonintubated patients have been reviewed and ETCO2 should not be used as an indication to end resuscitative efforts.
Defibrillation
AHA recommendations for defibrillation include the following [60] :
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Use defibrillators (using biphasic truncated exponential [BTE], rectilinear biphasic [RLB], or monophasic waveforms) to treat atrial and ventricular arrhythmias. (Class I)
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Defibrillators using biphasic waveforms (BTE or RLB) are preferred. (Class IIa)
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Use a single-shock strategy (as opposed to stacked shocks) for defibrillation. (Class IIa)
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The benefit is unclear for using a multimodal defibrillator in manual instead of automatic mode. (Class IIb)
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The value is unclear regarding VF waveform analysis to guide management of defibrillation. (Class IIb)
Overall, the ERC and ILCOR guidelines concur with those of the AHA, [61, 62] but the ERC includes an additional recommendation for self-adhesive defibrillation pads which are preferred over manual paddles and should always be used when they are available. [62]
Adjuncts for airway control and ventilation
The AHA guidelines provide the following recommendations for airway control and ventilation [60, 81] :
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Advanced airway placement in cardiac arrest should not delay initial CPR and defibrillation for VF arrest. (Class I)
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If advanced airway placement will interrupt chest compressions, consider deferring insertion of the airway until the patient fails to respond to the initial CPR and defibrillation attempts or demonstrates ROSC. (Class IIb)
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The routine use of cricoid pressure in cardiac arrest is not recommended. (Class III)
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Either a bag-mask device or an advanced airway may be used for oxygenation and ventilation during CPR in both the in-hospital and out-of-hospital setting. (Class IIb) The choice of bag-mask device versus advanced airway insertion should be determined by the skill and experience of the provider.
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For healthcare providers trained in their use, either an supraglottic airway (SGA) device or an endotracheal tube (ETT) may be used as the initial advanced airway during CPR. (Class IIb)
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Providers who perform endotracheal intubation should undergo frequent retraining (Class I)
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To facilitate delivery of ventilations with a bag-mask device, oropharyngeal airways can be used in unconscious (unresponsive) patients with no cough or gag reflex and should be inserted only by trained personnel. (Class IIa)
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In the presence of known or suspected basal skull fracture or severe coagulopathy, an oral airway is preferred. (Class IIa)
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Continuous waveform capnography in addition to clinical assessment is the most reliable method of confirming and monitoring correct placement of an ETT. (Class I)
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If continuous waveform capnometry is not available, a nonwaveform CO 2 detector, esophageal detector device, or ultrasonography used by an experienced operator is a reasonable alternative. (Class IIa)
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After placement of an advanced airway, it is reasonable for the provider to deliver 1 breath every 6 seconds (10 breaths/min) while continuous chest compressions are performed. (Class IIb)
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Automatic transport ventilators (ATVs) can be useful for ventilation of adult patients in noncardiac arrest who have an advanced airway in place in both out-of-hospital and in-hospital settings. (Class IIb)
There are no significant differences in the recommendations from the ERC or ILCOR. [61, 62]
Medication management
The 2015 AHA guidelines offers the following recommendations for the administration of drugs during cardiac arrest [60] :
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Amiodarone may be considered for VF or pVT that is unresponsive to CPR, defibrillation, and a vasopressor therapy; lidocaine may be considered as an alternative. (Class IIb)
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Routine use of magnesium for VF/pVT is not recommended in adult patients. (Class III)
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Inadequate evidence exists to support routine use of lidocaine. However, the initiation or continuation of lidocaine may be considered immediately after ROSC from cardiac arrest due to VF/pVT. (Class IIb)
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Inadequate evidence exists to support the routine use of a beta blocker after cardiac arrest. However, the initiation or continuation of a beta blocker may be considered after hospitalization from cardiac arrest due to VF/pVT. (Class IIb)
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Atropine during pulseless electrical activity (PEA) or asystole is unlikely to have a therapeutic benefit. (Class IIb)
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There is insufficient evidence for or against the routine initiation or continuation of other antiarrhythmic medications after ROSC from cardiac arrest.
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Standard-dose epinephrine (1 mg every 3-5 minutes) may be reasonable for patients in cardiac arrest. (Class IIb); high-dose epinephrine is not recommended for routine use in cardiac arrest. (Class III)
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It may be reasonable to administer epinephrine as soon as feasible after the onset of cardiac arrest due to an initial nonshockable rhythm. (Class IIb)
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Vasopressin has been removed from the adult cardiac arrest algorithm as it offers no advantage in combination with epinephrine nor as a substitute for standard-dose epinephrine. (Class IIb for both)
Evaluation and Medical Management
Evaluation
Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death were published jointly in 2006 by the American College of Cardiology (ACC), the American Heart Association (AHA), and the European Society of Cardiology (ESC). [40] In 2015, the European Society of Cardiology (ESC) released an updated guideline. [82]
The guidelines recommend assessment of family members of victims of sudden unexplained death syndrome (SUDS) or sudden arrhythmic death syndrome (SADS). Recommendations for the evaluation of suspected or known ventricular arrhythmias are summarized in the table below. [82]
Table 1. Evaluation of Suspected or Known Ventricular Arrhythmias (Open Table in a new window)
Recommendation | Class |
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Resting 12-lead electrocardiography (ECG) in all patients | Class I |
12-lead ambulatory ECG to evaluate QT-interval changes or ST changes |
Class I |
Cardiac event recorders when symptoms are sporadic to rule out transient arrhythmias | Class I |
Implantable loop recorders when symptoms are sporadic and suspected to be related to arrhythmias and when a symptom–rhythm correlation cannot be established by conventional diagnostic techniques |
Class I |
Exercise stress testing in adult patients who have an intermediate or greater probability of having coronary artery disease (CAD) to provoke ischemic changes or ventricular arrhythmia (VA) |
Class I |
Exercise stress testing in patients with known or suspected exercise-induced VA | Class I |
Echocardiography in all patients | Class I |
Pharmacologic stress testing plus imaging modality study to detect silent ischemia in patients with VAs who have an intermediate probability of having CAD and are physically unable to perform a symptom-limited exercise test |
Class I |
Cardiac magnetic resonance imaging (cMRI) or computed tomography (CT) scanning in patients with VAs when echocardiography does not provide accurate assessment of left- and right-ventricular function and/or evaluation of structural changes |
Class IIa |
Electrophysiologic study in patients with CAD with remote myocardial infarction with symptoms suggestive of ventricular tachyarrhythmias, including palpitations, presyncope, and syncope. |
Class I |
Coronary angiography to establish or exclude significant obstructive CAD in patients with life-threatening VAs or in survivors of sudden cardiac death, who have an intermediate or greater probability of having CAD by age and symptoms |
Class IIa |
Medical management
The 2015 ESC guidelines note that the selection of appropriate therapy is focused on the associated medical conditions that may contribute to and/or exacerbate the arrhythmia, the risk posed by the arrhythmia, and the risk–benefit aspects of potential therapy. [82] Management involves appropriate antiarrhythmic therapy with drugs, implantable devices, ablation, or surgery. Beta blockers are recommended as the first line of treatment for management of ventricular arrhythmias and prevention of sudden cardiac death. [82]
Cardioverter-Defibrillator Therapy
Implantable cardioverter-defibrillator therapy
A 2013 published report of the American College of Cardiology Foundation, Heart Rhythm Society, American Heart Association, American Society of Echocardiography, Heart Failure Society of America, Society for Cardiovascular Angiography and Interventions, Society of Cardiovascular Computed Tomography, and Society for Cardiovascular Magnetic Resonance (ACCF/HRS/AHA/ASE/HFSA/SCAI/SCCT/SCMR) provided the following appropriate use criteria for implantable cardioverter-defibrillator (ICD) therapy. [4]
ICD therapy is used for secondary prevention in the following groups [4] :
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Most patients with hemodynamically unstable ventricular tachycardia (VT)
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Most patients with prior myocardial infarction (MI) and hemodynamically stable sustained VT
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Most cardiomyopathy patients with unexplained syncop
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Most patients with genetic sudden death syndromes when unexplained syncope is noted
The 2015 ESC guidelines include the following recommendations for ICD for secondary prevention [82] :
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Patients hemodynamically unstable VT in the absence of reversible causes or within 48 hours after an MI who are receiving chronic optimal medical therapy and have a reasonable expectation of survival longer than1 year. (Class I)
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Patients with recurrent sustained VT (not within 48 hours after an MI) who are receiving chronic optimal medical therapy, have a normal left ventricular ejection fraction (LVEF) and have a reasonable expectation of survival with good functional status for longer than 1 year. (Class IIa)
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Amiodarone may be considered when an ICD is not available, is contraindicated for concurrent medical reasons, or is refused by the patient. (Class IIb)
Wearable cardioverter-defibrillator therapy
The 2016 AHA recommendations for wearable cardioverter-defibrillator (WCD) therapy are summarized below [83] :
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A WCD is reasonable when there is a clear indication for an implanted/permanent device accompanied by a transient contraindication or interruption in ICD care (ie, infection). (Class IIa)
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A WCD is reasonable as a bridge to more definitive therapy, such as cardiac transplantation. (Class IIa)
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A WCD may be reasonable when there is concern about a heightened risk of sudden cardiac death (SCD) that may resolve over time or with treatment of LV dysfunction. (Class IIb)
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A WCD may be appropriate as bridging therapy in situations associated with an increased risk of death in which ICDs have been shown to reduce SCD but not overall survival. (Class IIb)
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A WCD should not be used when the nonarrhythmic risk is expected to significantly exceed the arrhythmic risk, particularly in patients who are not expected to survive longer than 6 months. (Class III)
Catecholaminergic Polymorphic Ventricular Tachycardia
In its 2013 expert consensus statement on inherited primary arrhythmia syndromes, the Heart Rhythm Society/European Heart Rhythm Association/Asia Pacific Heart Rhythm Society (HRS/EHRA/APHRS) indicated catecholaminergic polymorphic ventricular tachycardia (CPVT) can be diagnosed when any for the following criteria are met [84] :
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Structurally normal heart, normal electrocardiogram (ECG), and unexplained exercise or catecholamine-induced bidirectional VT or polymorphic ventricular premature beats (VPBs) or VT in an individual younger than 40 years
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Presence of a pathogenic mutation
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Family history of CPVT with a normal heart, exercise-induced premature ventricular contractions or bidirectional/polymorphic VT
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Structurally normal heart and coronary arteries, normal ECG, and unexplained exercise or catecholamine-induced bidirectional VT or polymorphic VPBs or VT in an individual older than 40 years
Management recommendations include [84] :
Class I
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Limit or avoid competitive sports, strenuous exercise, and/or stressful environments
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Beta blockers for all symptomatic patients
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Placement of an implantable cardioverter-defibrillator for patients who experience cardiac arrest, recurrent syncope, or polymorphic/bidirectional VT despite optimal medical management, and/or left cardiac sympathetic denervation (LCSD)
Class IIa
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Flecainide in addition to beta blockers in patients who experience recurrent syncope or polymorphic/bidirectional VT while on beta blockers
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Beta blockers for carriers of a pathogenic CPVT mutation without clinical manifestations (concealed mutation-positive patients).
Class IIb
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Consider LCSD in patients who experience recurrent syncope or polymorphic/bidirectional VT/several appropriate ICD shocks while on beta blockers and in patients for whom beta blockers are contraindicated.
Class III
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ICD is not indicated as a stand-alone therapy in an asymptomatic CPVT patients.
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Programmed electrical stimulation is not indicated.
In general, the 2015 ESC guidelines concur with the recommendations above as well as include the following additional guidance [82] :
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Flecainide should be considered in addition to beta blockers in patients with an ICD to reduce appropriate ICD shocks. (Class IIa)
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This electrocardiogram (ECG) shows rapid monomorphic ventricular tachycardia (VT), 280 beats/min, associated with hemodynamic collapse. The tracing was obtained from a patient with severe ischemic cardiomyopathy during an electrophysiologic study. A single external shock subsequently converted VT to sinus rhythm. The patient had an atrial rate of 72 beats/min (measured with intracardiac electrodes; not shown). Although ventriculoatrial dissociation (faster V rate than A rate) is diagnostic of VT, surface ECG findings (dissociated P waves, fusion or capture beats) are present in only about 20% of cases. In this tracing, the ventricular rate is simply too fast for P waves to be observed. VT at 240-300 beats/min is often termed ventricular flutter.
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This electrocardiogram shows slow monomorphic ventricular tachycardia (VT), 121 beats/min, from a patient with an old inferior wall myocardial infarction and well-preserved left ventricular (LV) function (ejection fraction, 55%). The patient presented with symptoms of palpitation and neck fullness. Note the ventriculoatrial dissociation, which is most obvious in leads V2 and V3. Slower VT rates and preserved LV function are associated with better long-term prognosis.
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At first glance, this tracing suggests rapid polymorphic ventricular tachycardia. It is actually sinus rhythm with premature atrial complex and a superimposed lead motion artifact. Hidden sinus beats can be observed by using calipers to march backward from the final two QRS complexes. This artifact can be generated easily with rapid arm motion (eg, brushing teeth) during telemetry monitoring.
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Torsade de pointes. Image A: This is polymorphic ventricular tachycardia associated with resting QT-interval prolongation. In this case, it was caused by the class III antiarrhythmic agent sotalol. This rhythm is also observed in families with mutations affecting certain cardiac ion channels. Image B: Torsade de pointes, a form of ventricular tachycardia. Courtesy of Science Source/BSIP.
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Preexcited atrial fibrillation. The patient has an accessory atrioventricular connection. Atrial fibrillation has been induced. Conduction over an accessory pathway results in a wide QRS complex, mimicking ventricular tachycardia.
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Curative ablation of ventricular tachycardia (VT). The patient had VT in the setting of ischemic cardiomyopathy. VT was induced in an electrophysiology laboratory, and an ablation catheter was placed at the critical zone of slow conduction within the VT circuit. Radiofrequency (RF) energy was applied to tissue through the catheter tip, and VT was terminated when the critical conducting tissue was destroyed.
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Ventricular pacing at 120 beats/min. Newer pacemakers use bipolar pacing. If a smaller pacing stimulus artifact is overlooked, an erroneous diagnosis of ventricular tachycardia may result. Because leads are most commonly placed in the right ventricular apex, paced beats will have a left bundle-branch block morphology with inferior axis. Causes of rapid pacing include (1) tracking of atrial tachycardia in DDD mode, (2) rapid pacing due to the rate response being activated, and (3) endless loop tachycardia. Application of a magnet to the pacemaker will disable sensing and allow further diagnosis. Sometimes “pacing spike detection” must be programmed “ON” in the electrocardiographic system to make the spike apparent.
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Supraventricular tachycardia with aberrancy. This tracing is from a patient with a structurally normal heart who has a normal resting electrocardiogram. This rhythm is orthodromic reciprocating tachycardia with rate-related left bundle-branch block. Note the relatively narrow RS intervals in the precordial leads.
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Termination of ventricular tachycardia (VT) with overdrive pacing. This patient has reentrant VT, which is terminated automatically by pacing from an implantable cardioverter-defibrillator.
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Posteroanterior view of a right ventricular endocardial activation map during ventricular tachycardia in a patient with a previous septal myocardial infarction. The earliest activation is recorded in red, and late activation as blue to magenta. Fragmented low-amplitude diastolic local electrograms were recorded adjacent to the earliest (red) breakout area, and local ablation in this scarred zone (red dots) resulted in termination and noninducibility of this previously incessant arrhythmia.
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This tracing depicts monomorphic ventricular tachycardia.
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This image demonstrates polymorphic ventricular tachycardia.
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This electrocardiogram is from a 32-year-old woman with recent-onset heart failure and syncope.
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This electrocardiogram is from a 48-year-old man with wide-complex tachycardia during a treadmill stress test. Any wide-complex tachycardia tracing should raise the possibility of ventricular tachycardia, but closer scrutiny confirms left bundle-branch block conduction of a supraventricular rhythm. By Brugada criteria, RS complexes are apparent in the precordium (V2-V4), and the interval from R-wave onset to the deepest part of the S wave is shorter than 100 ms in each of these leads. Ventriculoatrial dissociation is not seen. Vereckei criteria are based solely upon lead aVR, which shows no R wave, an initial q wave width shorter than 40 ms, and no initial notching in the q wave. The last Vereckei criterion examines the slope of the initial 40 ms of the QRS versus the terminal 40 ms of the QRS complex in lead aVR. In this case, the initial downward deflection in lead aVR is steeper than the terminal upward deflection, yielding Vi/Vt ratio above 1. All of these criteria are consistent with an aberrantly conducted supraventricular tachycardia. Gradual rate changes during this patient's treadmill study (not shown here) were consistent with a sinus tachycardia mechanism.
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The electrocardiogram shows a form of idiopathic ventricular tachycardia (VT) seen in the absence of structural heart disease. This rhythm arises from the left ventricular septum and often responds to verapamil. Upon superficial examination, it appears to be supraventricular tachycardia with bifascicular conduction block. Closer examination of lead V1 shows narrowing of fourth QRS complex, consistent with fusion between the wide QRS complex and the conducted atrial beat, confirming atrioventricular dissociation and a VT mechanism.
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A wide QRS complex tachycardia is evident on this electrocardiogram from a 64-year-old man with history of previous myocardial infarction (MI) and syncope. In patients with a prior MI, the most common mechanism of wide QRS complex tachycardia is ventricular tachycardia.
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This tracing depicts atrioventricular dissociation.
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Fusion beats, capture beats, and atrioventricular dissociation can be seen on this electrocardiogram.
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Note the retrograde P waves in this electrocardiogram.
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Retrograde P waves are also observed in this electrocardiogram.
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This electrocardiogram reveals torsade de pointes.
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Hematoxylin and eosin stain; intermediate power of a healed myocardial infarct. Note the areas of fibrosis (pale pink) dissecting between the myocytes (red).