Ventricular Tachycardia (VT): Mechanism to Management

By Andrew P. Mardell and Derek V. Exner, M.D.

Ventricular tachycardia (VT) for the most part has been the harbinger of bad news for many patients and a predictor of death, particularly for patients with a history of structural heart disease, and most commonly for those with a prior myocardial infarction (MI). VT can be a precursor of ventricular fibrillation (VF) and is a cause for concern. This article reviews the mechanisms of various forms of VT, key electrocardiographic (ECG) criteria for diagnosing VT, and managing VT in the prehospital setting.

ECG DIAGNOSIS

A difficult problem for the practitioner, VT can cause life-threatening situations requiring rapid evaluation, diagnosis, and treatment. Patients with this rhythm may be either hemodynamically stable (strong and perfusing pulse or mentating with a stable blood pressure) or unstable (pulseless or showing signs of cardiogenic shock, such as cold, pale, and clammy skin or a decreased level of consciousness). Both patient presentations require a different response. Ventricular tachycardia can degenerate rapidly with severe hemodynamic compromise to polymorphic VT or ventricular fibrillation (VF). VF must be treated rapidly to prevent death. The rule of thumb: A wide complex tachycardia in a patient with known heart disease is almost always the result of VT rather than supraventricular tachycardia (SVT). Thus, treat any unknown wide complex rhythm as VT.

Ventricular tachycardia may also be classified as monomorphic (originating from a single focus or re-entrant circuit and has identical QRS complexes) or polymorphic. Polymorphic VT may appear with an irregular rhythm with varying QRS amplitudes and morphologies.

Defining VT can be related to its mechanism.¹ VT is defined as three or more beats of ventricular origin (wide QRS complex) in succession at a rate greater than 100 beats per minute (bpm). There are no normal-looking narrow QRS beats, and it is usually quite regular. If the rhythm continues for more than 30 seconds, it is termed sustained VT. Less than 30 seconds of this tachycardia is called non-sustained VT.

Some other clues to help diagnose VT come from looking at the atria. If we presume that VT is present and that part of the ventricle is driving the ventricular activation, then we could surmise that the atria would continue their normal activity under the direction of the sinus node (which is not affected by the VT). So we might see P waves that are dissociated (not related to rate and rhythm) from ventricular depolarization. This is called atrioventricular or AV dissociation. You might find P waves occurring at any time in relation to the QRS complex (see Figure 1).²

Figure 1. ECG of VT Proven with Capture and Fusion Beats and Dissociated P Waves

This suggests that atria are not conducting to the ventricle. Source: Courtesy of Andrew P. Mardell.

Just as a ventricular impulse can occasionally travel retrograde or backward through the AV node to the atrium, so, too, can an atrial impulse travel antegrade or forward down the AV conduction system to the ventricle and cause depolarization if the ventricle is not refractory. A narrow-looking (normal) beat will occur in the midst of the regular wide complex tachycardia; this is called a capture beat. The capture beat will occur prior to the next expected VT beat. It is also likely that AV conduction may occur simultaneously with ventricular depolarization. An impulse traveling down through the AV conduction system might simultaneously cause depolarization of part of the ventricular myocardium while the ventricle may be depolarized at a different location. This leads to a QRS complex that is intermediate between the fully ventricular and fully AV conducted beat, called a fusion beat (see Figure 1).³

Conduction from the atria to the ventricles is usually prevented because the AV node or ventricular conduction system is refractory because of ventricular depolarization, meaning that because the preceding beat has recently conducted, the AV node or ventricular conduction system is not ready to depolarize again because of a mandatory rest period called repolarization. Sometimes retrograde conduction from the ventricles to atria can occur. If this were to happen, there would be a relationship between the QRS complex and the retrograde P wave. This phenomenon makes distinguishing VT from supraventricular tachycardia (SVT) more difficult (Figure 2). (3)

Figure 2. ECG of VT Proven with Capture and Fusion Beats

Source: Courtesy of Andrew P. Mardell.

Two SVTs that have 1:1 wide complex conduction with retrograde P waves are antidromic AV reciprocating tachycardia (AVRT) and AV nodal reentrant tachycardia with aberrant conduction (AVNRT). Antidromic AVRT occurs in the presence of an accessory (alternate) pathway between the atrium and ventricle. Forward (antegrade) conduction through the accessory pathway occurs, leading to a widened QRS complex with backward (retrograde) conduction through the AV node, causing retrograde P waves. AVNRT with aberrant conduction occurs when a reentrant circuit in the AV node propagates impulses both antegrade through an abnormal His-Purkinje system (thus the wide QRS) and also retrograde throughout the atria, creating retrograde P waves. These two rhythms may be indistinguishable from VT with 1:1 ventriculo-atrial conduction. Atrial flutter with 1:1 AV conduction can also be aberrantly conducted, causing a wide QRS complex tachycardia that mimics VT.

Typically, suppressing the AV node (or slowing AV nodal conduction) with medications (i.e., adenosine), carotid sinus massage, or vagal maneuvre(s) will slow conduction enough to terminate the SVT or at least render a diagnosis of SVT vs. VT.

No absolute ECG criteria exist to prove VT; however, several criteria suggest VT, such as the following:

A heart rate >100 beats per minute (usually 150-200).
Wide QRS complexes (>140 ms).
The presence of atrioventricular (AV) dissociation.
Fusion beats.
Capture beats.⁴

It is important to recognize that a wide complex tachycardia in a patient with structural heart disease (e.g., prior MI or heart failure) is almost always the result of VT rather than SVT. If there is any doubt as to whether a wide complex tachycardia is VT or SVT, treat it as VT. A failure to do so may result in significantly adverse outcomes for the patient, including death.

VT MECHANISM

All cardiac arrhythmias result from one of the three following primary mechanisms—abnormal automaticity, reentry, or triggered activity—and are mediated by localized or generalized changes in the cardiac action potential.⁵

Automatic arrhythmias are often seen in patients who are acutely ill with associated metabolic abnormalities. They also commonly occur in the setting of myocardial ischemia or an MI. Rapid and spontaneous early action potentials are the result of abnormal automaticity and thus inappropriate tachycardia. Treating the underlying cause of metabolic derangement or ischemia is the most effective treatment of this mechanism of VT.

Triggered activity is a fairly rare mechanism for VT and is broken into two subgroups: pause-dependent VT and catechol-dependent VT. These two fairly distinct clinical syndromes tend to create a type of polymorphic VT that is also called torsades de pointes.

Pause-dependent torsades de pointes occurs when an extra action potential comes earlier in the normal cardiac action potential, also called early afterdepolarizations (EADs). These are seen when conditions exist to prolong the normal cardiac action potential, such as electrolyte imbalance (hypokalemia and hypomagnesemia) and with the use of drugs (primarily antiarrhythmic agents).

Acute treatment is primarily to reduce the duration of the action potentials, to eliminate pauses (with drugs or pacing) or both. Discontinue immediately and avoid drugs that prolong the QT interval (see www.qtdrugs.org). Reversing electrolyte abnormalities, particularly low magnesium levels, is important. Emergency treatment consists of preventing the pauses that trigger VT. This is most often accomplished by pacing the atrium or ventricles (at rates of 80 to 120 bpm) or occasionally by using intravenous isoproterenol infusion.

Catecholamine-dependent VT is caused by extra action potentials that come late in the normal cardiac action potential and are called delayed afterdepolarizations (DADs). DADs occur in the setting of digitalis toxicity, cardiac ischemia, and in certain patients who have a congenital form of QT interval prolongation. This is usually found in patients with high sympathetic tone. In other words, the arrhythmia occurs during times of extreme emotional stress, during exercise, or with the use of sympathomimetics from relatively benign caffeine to more potent agents such as methamphetamine or cocaine. Often, the ECG at rest is normal but with exercise develops a prolonged QT interval. DADs are thought to be mediated by calcium channels, so treatment usually consists of beta blockers or calcium channel blockers.

Reentry is the most common mechanism for VT. Conditions present to cause automatic ventricular arrhythmias are usually temporary (i.e., cardiac ischemia); however, the substrate necessary for reentrant arrhythmias is usually permanent. Reentrant circuits in the ventricle usually arise after scar formation in the ventricular myocardium. Scar formation usually follows myocardial infarction (MI), cardiomyopathy, or myocarditis and results in a permanent reentrant circuit. Structural congenital disorders such as right ventricular dysplasia, the tetralogy of Fallot, and other cardiac surgical scars can also create reentrant scar formation. Reentrant VT is the main cause for “late” sudden cardiac deaths following MI (from 24 hours to several years after an acute event). Given that scar formation must be present for this reentrant mechanism to exist, it is rare for these patients to have normally structural hearts. Antiarrhythmic drugs have limited effect on automatic and triggered VT; however, they directly affect the mechanism for reentrant VT.

The key to understanding how drugs affect reentrant arrhythmias is that reentry requires a critical relationship between the refractory periods and the conduction velocities of the two limbs of the reentrant circuit. Antiarrhythmic drugs make reentrant arrhythmias less likely to occur by altering the refractory periods and conduction velocities. For this reason, antiarrhythmic drugs may make the reentrant circuit more likely to conduct and sustain the arrhythmia or less likely to occur. When the arrhythmia is more likely to sustain or initiate, it is considered proarrhythmic. All antiarrhythmic drugs have the potential to be proarrhythmic in the reentrant setting.⁶

EMERGENCY MANAGEMENT OF VT

As noted, a wide complex tachycardia in a patient with known heart disease is almost always the result of VT rather than SVT. Thus, treat an unknown wide complex rhythm as VT.

Interpret the ECG and rhythm information within the context of the patient assessment. Errors in treatment are likely to occur if practitioners base treatment decisions solely on rhythm interpretation and neglect other clinical information. VT is a common cause of sudden cardiac death. Establish cardiac monitoring as soon as possible for all patients who collapse suddenly or have signs of ischemia or infarction. The fastest way to do this is to apply “quick look” pads/paddles using a defibrillator for rapid rhythm interpretation.

The American Heart Association (AHA) outlines key treatment principles in managing ventricular tachycardia.⁷ First, if a tachycardia patient is unstable based on signs and symptoms, prepare for immediate synchronized cardioversion. If the patient is stable, determine if the tachycardia is narrow complex or wide complex, then adjust therapy as required. You need to understand drug and electrical treatment for unstable or immediately life-threatening arrhythmias. Finally, know when to call for expert advice for complex rhythm interpretation, drugs, or management decisions.

Because it may be difficult to distinguish SVT from VT, assume that wide complex tachycardias are ventricular in origin. Determining whether the rhythm is regular or irregular will be the next step in deciding the treatment option in the stable patient. If the rhythm is regular in the stable patient and you suspect VT, consider the following treatment options:

a) Amiodarone 150 mg over 10 minutes. Repeat as needed to a maximum of 2.2 g over two hours.

b) Prepare for elective synchronized cardioversion (+/- sedation if the patient is stable and based on local protocols).

If you suspect SVT with aberrancy, consider the following:

a) Adenosine 6 mg rapid IV push. If no conversion, give 12 mg IV push; you may repeat a 12 mg dose once.

Irregular wide-complex tachycardias can be difficult to diagnose, and you may need expert consultation. Atrial fibrillation with aberrancy is commonly found.

a) Consider rate control with calcium channel blockers (i.e., dilitiazem) or beta blockers (i.e., metoprolol). Use caution when using beta blockers in patients with pulmonary disease or HF.

If you suspect pre-excited atrial fibrillation (AF with Wolf-Parkinson-White disease):

a) Avoid AV nodal blocking agents such as adenosine, digoxin, diltiazem, and verapamil.

b) Consider antiarrythmics (i.e., amiodarone 150 mg IV over 10 minutes).

With torsades de pointes, give magnesium (load with 1-2 grams over 5-60 minutes followed by an infusion). Use caution, as rapid infusion of any of these drugs (except adenosine, which should be given rapidly) can cause hypotension.

PHARMACOLOGY IN MANAGING VT

The ideal antiarrhythmic drug should decrease the number of ectopic driven beats and decrease mortality. This is not always the case; some antiarrhythmic drugs had higher mortality rates compared to placebo. All antiarrhythmic drugs act by altering ion fluxes within excitable tissues in the myocardium. The three ions of primary importance are sodium (Na+), calcium (Ca++), and potassium (K+). Antiarrhythmic drugs have various mechanisms of action, and some classes and specific drugs within each class are effective only with certain types of arrhythmias. There are various classification models; however, the Vaughn-Williams system is the most frequently used and easy to understand.

The Vaughn-Williams system primarily breaks down antiarrhythmics according to their mechanism of action and the ions they affect as shown below.⁸

Class I drugs act by blocking the fast inward sodium channels and are subdivided into three categories based on their potency toward blocking sodium channels and effects on repolarization.

Subclass IA has high/intermediate potency as sodium channel blockers and may prolong repolarization (in other words, prolong the QT interval). These include quinidine, procainamide, and disopyrimide.
Subclass IB has the lowest potency as sodium channel blockers and may shorten repolarization (or decrease the QT interval). These include lidocaine and mexilitine.
Subclass IC has the highest potency as sodium channel blockers (prolongs QRS complex) and has little effect on repolarization. These include flecainide and propafenone.

Class II drugs act indirectly by blocking beta-adrenergic receptors, which may slow sinus rhythm and prolong conduction through the AV node (demonstrated by prolonging the PR interval). Examples of these include metoprolol, propranolol, esmolol, and acebutolol.

Class III drugs prolong repolarization and thereby increase refractoriness and prolong the QT interval. They have no affect on QRS and little effect on the rate of depolarization.

Block fast outward K+ currents are amiodarone, sotalol, dofetilide, and dronedarone.
Block slow inward Na+ currents is ibutilide.

Class IV drugs are relatively selective AV nodal L-type calcium-channel blockers that slow sinus rhythm and AV nodal conduction, thus prolonging the PR interval. Examples of these include verapamil and diltiazem. It is important to note that dihydropyridine types of calcium-channel blockers (i.e., hydralazine) have minimal effect on the AV node. Of course, there are drugs that don’t fit into any classification system such as digoxin, adenosine, and magnesium, but they have unique and important properties.

Specifically in managing VT, the Class I, II, and III drugs may be useful, depending on the mechanism of action of the VT. For instance, slowing the rate of conduction, as may be seen with Class II drugs, may not be beneficial for patients with pause-dependent VT; prolonging repolarization and lengthening the QT interval might not be beneficial in patients with drug-induced long QT syndrome (LQTS).

Note that antiarrhythmics are not usually indicated for patients with premature ventricular complexes (PVCs). However, patients who have short couplets of torsades de pointes, also called torsadelets, are prone to suddenly developing sustained torsades de pointes, which can degenerate to VF rapidly.

Patients who have VT and remote history of MI can be treated with amiodarone, Class III and Class I agents. VF can be treated with lidocaine (a Class I agent), amiodarone (Class III), or other Class I agents such as procainamide. Torsades de pointes should acutely be treated with magnesium sulfate or less importantly isoproterenol and chronically with Class II (beta blocking) agents.

Remember that drugs within a class do not necessarily have similar clinical effects. Almost all of the currently available antiarrhythmics have at least three mechanisms of action depending on the pharmacokinetics of the drug. The metabolites of these drugs contribute significantly to the antiarrhythmic actions or side effect. Typically, an empiric approach is used to determine the most appropriate antiarrhythmic to use in the stable patient.

Following is a review of a few important antiarrhythmic drugs that you might see in practice.

Amiodarone is a Class III agent that is used frequently for both stable and unstable atrial and ventricular arrhythmias. Though amiodarone is formally classified as a Class III antiarrhythmic, it has multiple actions and is more appropriately considered a “broad spectrum” antiarrhythmic. (8)

Although it prolongs QT interval, its potential to cause proarrhythmias (torsades) is significantly lower than other Class III agents, and it is one of the few antiarrhythmic agents to have consistently decreased mortality in many clinical trials.

It is approved for use in refractory life-threatening ventricular arrhythmias, but its therapeutic role has been expanding to include a variety of arrhythmias ranging from supraventricular to ventricular. Used intravenously, amiodarone is superior to lidocaine and other agents for the treatment of ventricular fibrillation (2005 ECC/AHA guidelines), and it is also used orally to suppress a variety of arrhythmias, even in combination with implantable cardioverter defibrillator (ICD) therapy.

The safety of amiodarone for chronic therapy is controversial because of its variable and complex pharmacokinetics and many adverse effects, some of which can be lethal. Without loading doses, it can take several weeks to months to achieve steady-state plasma levels. Similarly, it can take many months to clear the drug, with an elimination half-life ranging from 26 to 107 days (mean of 53 days). The most common serious long-term adverse effects are pulmonary fibrosis and interstitial pneumonitis (in two to 15 percent of patients on chronic amiodarone), which is fatal in 10 percent of these patients. The pneumonitis is reversible if the drug is stopped early on; thus, clinical assessment and chest X-rays are required every six to 12 months.

For life-threatening ventricular arrhythmias, the IV loading dose for amiodarone is 150 mg over 10 minutes (15mg/min); this is followed by 360 mg over the next six hours (1 mg/min), then 540 mg for the next 18 hours (0.5 mg/min). After the first 24 hours, there should be a continuous infusion at 0.5 mg/min (720 mg/24 hrs). This will meet the recommended 1,000 mg in the first 24 hours. (7)

An easy tip to quickly prepare the initial rapid-loading dose is to place 3 ml (150 mg) of IV amiodarone in 100 ml D5W. This will be a concentration of 1.5 mg/ml. Amiodarone has not been studied in children.

Lidocaine is a widely used antiarrhythmic and local anesthetic drug. It is only used intravenously for treating arrhythmias because of its metabolism. Mexilitine is lidocaine’s orally active agent. Both are used to treat acute, life-threatening ventricular arrhythmias.

Although lidocaine has long been the first choice for treating ventricular arrhythmias, the AHA Emergency Cardiovascular Care 2005 guidelines for cardiopulmonary resuscitation recommend IV amiodarone before lidocaine for treatment of VF or pulseless VT. (7) Mexilitine does not prolong QT interval and can be used in patients with a history of torsades or drug-induced LQTS.

Severe interactions can occur with co-administration of other antiarrhythmic agents, especially amiodarone. The most frequent side effects are CNS, including tinnitus, seizures, occasionally hallucinations, drowsiness, and coma.

Give a loading dose of lidocaine when initiating treatment. Loading dose is 1 mg/kg (usually between 50 and 100 mg) at a rate of 25-50 mg/min and may be repeated after five minutes, if required. Follow the loading dose with an infusion (due to the very short duration of action) at 1-4 mg/min (20-50 mcg/kg/min) to a total dose of 300 mg/hr. (7)

Pediatric load is also 1 mg/kg/min to a maximum of 3 mg/kg and should be followed by continuous infusion at 30 mcg/min (range 20-50 mcg/min) or 0.03 mg/kg/min with a rate of infusion not to exceed the adult dose of 4 mg/min. (7)

Decrease infusion rates in geriatric patients and patients with heart failure and hepatic dysfunction to avoid lidocaine toxicity. Refer to manufacturer specific product information.

Lidocaine is contraindicated in patients with heart block.

Procainamide.Procainamide (Class IB) is another antiarrhythmic being used more frequently in practice. Effective against both supraventricular and ventricular arrhythmias (including atrial arrhythmias associated with WPW syndrome or AVRT), it can be administered IV and orally. Oral procainamide is no longer marketed in the United States.

Its major metabolite, N-acetylprocainamide (NAPA), has predominantly Class III antiarrhythmic actions. Fast acetylators (approximately 50 percent of the population) quickly convert procainamide to NAPA. When procainamide is given orally, both procainamide and NAPA can contribute to the antiarrhythmic effects and toxicities; initial dosing should be conservative, and monitoring of plasma concentrations is recommended.

Up to 40 percent of patients discontinue therapy within six months because of side effects. Between 15 and 20 percent of patients develop a lupus-like syndrome, which usually begins as mild arthralgia but can be fatal if allowed to progress. These symptoms reverse when therapy is stopped, but patients need to be warned of the symptoms so therapy can be aborted before serious problems develop.

Adult dosing for IV procainamide is 20 mg/min for 25-30 minutes as a loading dose followed by a continuous infusion at 20-80 mcg/kg/min (maximum 2 grams/day). This drug can also be given IM for long-term management of arrhythmias. The pediatric loading dose is 3-6 mg/kg/dose for 5 minutes followed by a continuous infusion at 20-80 mcg/kg/min (maximum 2 grams/day). (7)

The following antiarrhythmics have been found to be more proarrhythmic than others (depending on the dose) and should be considered when patients present with unexplained syncope. Torsades de pointes (or drug-induced LQTS) is documented with the use of quinidine, sotolol, amiodarone (long QT is common; however, torsades is rare), ibutilide, and dofetilide. The Cardiac Arrhythmia Suppression Trial (CAST) found that flecainide was also proarrhythmic.

ADVANCED CARDIAC LIFE SUPPORT FOR PULSELESS VT OR VF

The following is a review of the 2005 American Heart Association guidelines for the management of pulseless VT or VF. (7) The SCREAM acronym can be used to remember the sequence of care as follows:

Shock. 200 joule (J) biphasic shock (use same or higher energy for subsequent shocks). Shock every two minutes if indicated.

CPR. After shock, immediately begin chest compressions followed by respirations (30:2) for two minutes. Do not check rhythm or pulse.

Rhythm. Rhythm check after two minutes of CPR (and after every two minutes of CPR after that), and shock if indicated. Check pulse only if an organized or nonshockable rhythm is present. Implement the Secondary ABCD Survey. Continue this algorithm if indicated. Give drugs during CPR before or after shocking. Minimize interruptions in chest compressions to <10 seconds. Consider Differential Diagnosis.

Epinephrine. 1.0 mg IV/IO q 3-5 minutes or vasopressin 40 units IV/IO once, in place of the first and second doses of epinephrine.

Antiarrhythmic Medications. Consider antiarrhythmics [Any Legitimate Medication (ALM) is the acronym]:

Amiodarone 300 mg IV/IO, may repeat once at 150 mg in 3-5 min if VT/VF persists or;
Lidocaine (if amiodarone unavailable) 1-1.5 mg/kg IV/IO, may repeat x2, q 5-10 minutes (3 mg/kg max load) if VT/VF persists or;
Magnesium sulphate 1-2 G IV/IO diluted in 10 ml D5W (5-20 minutes push) for torsades de pointes or suspected/known hypomagnesemia.

As mentioned, a wide complex tachycardia in a patient with known heart disease is almost always because of VT rather than SVT. It is safer to treat a wide complex tachycardia as VT to prevent serious harm to the patient.

LONG-TERM MANAGEMENT AND THE FUTURE

Although this article focuses on the emergent and prehospital management of VT, long-term VT management is important. Antiarrhythmic drugs must be initiated and up titrated in an area where continuous ECG monitoring is available and there is rapid access to resuscitation equipment and personnel. (8)

Patients with VT and structurally abnormal hearts should also be assessed for implantation of an implantable cardioverter defibrillator (ICD), as well as patients who experience sudden cardiac death and for which a reversible cause is not found [i.e., MI resulting in revascularization with thrombolytics, percutaneous coronary angioplasty (PCI), or coronary artery bypass grafting (CABG) or drug use].⁹ ICD therapy also will treat bradyarrhythmias (pacing) and slower VT episodes with painless anti-tachycardia pacing (ATP). ATP works by overdrive pacing the ventricle so that the tissue becomes refractory in the reentrant circuit, thus terminating the electrical propagation around the scar. This works in most cases.

However, if it does not, or if it speeds up to a dangerous rate or starts off at a high rate (such as VF), then the device will give the patient an internal shock. Practitioners can safely be in contact with a patient experiencing a shock from his ICD. A magnet placed over the ICD (usually found in the left upper chest) will turn off the ability to detect VT/VF temporarily while the magnet is in contact with the ICD.¹⁰ This is helpful if you want to manage a stable VT with medications and prevent an ICD shock or if there is a malfunction with the ICD or intracardiac leads. The patient should always have continuous ECG monitoring while the ICD is disabled. Standard cardioversion and defibrillation can be carried out in patients who have an ICD or pacemaker as long as the defibrillation pads are at least 2.5 cm (one inch) away from the device.¹¹ Anterior-posterior pad placement will be the most effective for this (one pad over right scapula and the other just below the left nipple). The AHA suggests that if the ICD is delivering shocks, allow 30 to 60 seconds for the ICD to complete the treatment cycle before delivering a shock.

In certain cases, catheter and surgical ablation for VT is warranted.¹² This option is available for certain recurrent VTs. This is a rapidly evolving field. Frequently, ablation is the sole therapy for VT in patients without structural heart disease and is commonly combined with an ICD and/or antiarrhythmic drugs for scar-related VTs associated with structural heart disease.¹³

As patients continue to survive MIs because of advances in health promotion, disease prevention, improved access to EMS, advanced training in the prehospital arena, and improved invasive and pharmacological interventions, many might go on to present with VT. As the field progresses, it is important for fire department paramedical professionals to continually maintain skills, competencies, and knowledge in the area of arrhythmia management, specifically those that cause sudden cardiac death.

Endnotes

1. American College of Cardiology/American Heart Association Task Force on Clinical Data Standards (ACC/AHA/HRS Writing Committee to Develop Data Standards on Electrophysiology), Buxton AE et al. ACC/AHA/HRS 2006 key data elements and definitions for electrophysiological studies and procedures: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Data Standards. Circulation. Dec 2006; 114(23):2534-70.

2. Wellens HJ, Bar FW, Lie KI. The value of the electrocardiogram in the differential diagnosis of a tachycardia with a widened QRS complex. Am J Med. Jan 1978; 64(1):27-33.

3. American Heart Association. Ventricular tachycardia for healthcare professionals. 12 May 2008. http://www.americanheart.org/presenter.jhtml?identifier=64.

4. De Souza IS, Ward C. Ventricular tachycardia. Dec 17, 2008. eMedicine from webMD. http://emedicine.medscape.com/article/760963-overview.

5. Zipes, P, Jalife, J. Cardiac Electrophysiology: From Cell to Bedside, Second Edition. Philadelphia, PA: WB Saunders Company, 1995.

6. Myerberg RJ, Kessler KM, Bassett AL, Castellanos A. A biological approach to sudden cardiac death: Structure, function and cause. Am J Cardiol .1989; 63:1512-1516.

7. American Heart Association. 2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. Dec 2005; 112(24) Supplement I.

8. Fogoros RN. Antiarrhythmic drugs: A practical guide. Hoboken, NJ: Blackwell. 1997.

9. Woods SL, Froelicher, ES, Motzer SA, Bridges EJ. Cardiac Nursing. Philadelphia PA: Lippincott Williams and Wilkins. 2005.

10. Dawes, J, Mahabir, R, Hillier, K, Cassidy, M, de Haas, W, and Gillis, A. Electrosurgery in patients with pacemakers/implanted cardioverter defibrillators. Ann Plast Surg. Feb 2007; 58(2): 226-7.

11. American Heart Association. BLS for healthcare providers. Dallas TX, 2001.

12. Stevenson WG. Catheter ablation of monomorphic ventricular tachycardia. Curr Opin Cardiol. Jan 2005; 20(1):42-7.

13. Aliot, EM., Stevenson WG. et al. EHRA/HRS Expert Consensus on Catheter Ablation of Ventricular Arrhythmias. Heart Rhythm. Jun 2009; 6(6):887-933.

ANDREW P. MARDELL, RN, BScN, CNCC(C), is a lieutenant with the Rocky View County Fire Service near Calgary, Alberta, Canada. He is a clinical nurse educator with the cardiac arrhythmia service at Foothills Medical Centre in Calgary. He has experience in cardiology, critical care, emergency, trauma, and air medical services and is an educator for firefighters, paramedics, nurses, and physicians.

DEREK V. EXNER, MD, MPH, FRCPC, is an associate professor in the Libin Cardiovascular Institute of Alberta at the University of Calgary. He is a cardiologist (heart rhythm specialist) and clinical trials expert. He obtained his master’s degree in epidemiology and clinical trials from Johns Hopkins University before returning to Calgary in 2000. Exner has written more than 100 articles, book chapters, and abstracts related to cardiac device therapy and heart failure for publications including the New England Journal of Medicine, Journal of the American Medical Association, Circulation, and the Journal of the American College of Cardiology.