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American Nurse Today September 2008 S UDDEN CARDIAC DEATH kills350,000 to 400,000 Americans a year. That accounts for half of alldeaths from coronary artery disease(CAD), the leading cause of deathin the United States.Frequently, a dangerous arrhyth-mia, such as ventricular tachycardia(VT) or ventricular fibrillation (VF),precedes sudden cardiac death. Infact, VT precedes sudden cardiacdeath in more than 70% of patients.If you can detect VT and VF ear-ly on and provide prompt cardio-pulmonary resuscitation (CPR) anddefibrillation, your chances of pre- venting sudden cardiac death aregood. Hearts electrical system Before discussing ventricular ar-rhythmias, lets review how thehearts electrical conduction sys-tem works. The systems mainfunction is to transmit electricalimpulses from the sinoatrial (SA)node to the atria and ventricles,causing them to contract. Locatedhigh in the wall of the right atri-um, the SA node is the hearts nat-ural pacemaker. It normally fires60 to

100 times per minute, andeach impulse results in one heart-beat. (See The path of cardiacconduction .)The electrical impulse passesthrough both atria to the atrioven-

L EARNING O BJECTIVES 1. Identify the causes of ventricu-lar arrhythmias.2. Relate the hearts electricalconduction to components of the normal electrocardiogram.3. Differentiate the types of ven-tricular tachycardia (VT).4. Describe the management of ventricular arrhythmias.

CE 1.8contacthours Recognizing ventriculararrhythmias and preventing suddencardiacdeath Be prepared to stopthese dangerousarrhythmias. By Rose M. Coughlin, MSN, RN, ACNS-BC

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September 2008 American Nurse Today tricular (AV) node at the junctionof the atria and ventricles. If theSA node stops firing, the AV nodeinitiates the impulses, but the ratedrops to 40 to 60 times perminute.From the AV node, the impulsetravels through the bundle of Hisand down the right and left bun-dle branches into the Purkinje net- work of the ventricles, depolariz-ing the ventricular muscle. If theSA and AV nodes fail, the ventri-cles initiate the impulses but canonly manage 20 to 40 impulsesper minute. An electrocardiogram (ECG) re-flects the complete wave of depo-larization as it travels from the SAnode to the Purkinje network. Reading an electrocardiogram The key components of an ECG arethe P wave, PR interval, QRS com-plex, and T wave, as shown. Normal electrocardiogram The P wave represents atrial de-polarization and is the first deflec-tion from the isoelectric line. The P wave should appear rounded anduniform.The PR interval represents thetime needed for an impulse to trav-el through the atria and pause atthe AV node. This pause allows the ventricles to fill with blood beforecontracting. The PR interval extendsfrom the beginning of the P waveto the beginning of the QRS com-plex and normally is 0.12 to 0.20second. Remember that each smallsquare on the ECG paper repre-sents 0.04 second. Five smallsquares make up a large block of 0.20 second, and 30 large blocksequal 6 seconds.The QRS complex represents ventricular depolarization. The Q wave is the first negative deflection;the R wave is the first positive de-flection; and the S wave is the neg-ative deflection after the R wave. All three arent present in every ECG lead. The normal QRS width is0.06 to 0.12 second.The T wave represents ventricularrepolarization. It follows the QRScomplex and is normally in thesame direction. The T wave is usual-ly rounded and slightly asymmetric.The isoelectric line representsabsence of electrical activity. When a ventricular pacemakertakes control With VT, the myocardium becomesextremely irritable, and a ventricu-lar pacemaker in the bundlebranches, Purkinje network, or ventricular myocardium takes con-trol of the conduction system. Theimpulses override the higher pace-maker sites. When impulses originate in the ventricles, the electrical currentgoes backwards through the ven-tricles, greatly reducing the heartsefficiency. Because the ventriclesare the lowest sites in the conduc-tion system, there are no fail-safemechanisms if the heart rate dropstoo low. Causes of ventriculararrhythmias The most common cause of VT is The path of cardiac conduction Normally, an electrical impulse starts at the sinoatrial node, spreads through

the atria, reach-es the atrioventricular node, and then spreads through the ventricles via the His-Purkinjenetwork. Courtesy ofThe Cleveland Clinic, Cleveland, Ohio PulmonaryarteryPulmonaryveinsAortaAtrioventricularnodeHis-Purkinjenetwork Sinoatrial nodeBundleof His PwavePRintervalQRS complex Twaveisoelectricline }

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American Nurse Today September 2008 CAD. Other cardiac causes includemyocardial infarction (MI), car-diomyopathy, and valvular heartdisease. Patients are at higher riskfor ventricular arrhythmias afterhaving an MI because of a signifi-cant reduction in left ventricularsystolic function. VT may result from metabolicabnormalities, such as acidosis,hypoxemia, hyperkalemia, hypo-kalemia, and hypomagnesemia. And VT may be caused by certaindrugs, such as caffeine, cocaine,alcohol, digoxin, theophylline,antipsychotics, tricyclic antidepres-sants, and antiarrhythmics withproarrhythmic potential such asflecainide, dofetilide, sotalol, andquinidine. Recognizing ventriculararrhythmias With VT, an ectopic pacemaker inthe ventricles initiates a heart ratebetween 110 and 250 beats perminute (bpm). On the ECG, theQRS complexes are abnormally wide and bizarre and more than0.12 second.The forms of VT are classified by the configurations of the QRS com-plex. In monomorphic VT, the QRScomplexes are the same or almostthe same shape, size, and direction,as shown. Monomorphic ventricular tachycardia

In polymorphic VT, the QRScomplexes markedly differ inshape, size, and direction from beatto beat. Torsades de pointes (mean-ing twisting around a point ) is aform of polymorphic VT, character-ized by QRS complexes that gradu-ally change back and forth fromone shape, size, and direction toanother over a series of beats, asshown. Torsades de pointes VF, a medical emergency, is anerratic, disorganized firing of impuls-es from the ventricles. The ventriclesquiver and are unable to contract orpump blood to the body. VF may be coarse or fine, as shown. Ventricular fibrillation Understanding sustained andnonsustained ventriculartachycardia VT may be sustained or nonsus-tained. Sustained VT lasts longerthan 30 seconds and may requiretermination because the rapid ratedoesnt allow the heart to fill withblood, causing hemodynamiccompromise. Nonsustained VTconsists of three or more beats ata rate of at least 120 bpm lastingless than 30 seconds and terminat-ing spontaneously without causinghemodynamic compromise.Nonsustained VT is common,and usually patients dont havesymptoms. Some patients do de- velop palpitations, syncope, orlightheadedness. Patients withnonsustained VT may have struc-tural heart disease, such as CAD,dilated cardiomyopathy, or valvu-lar heart disease and should havefurther evaluation.The risk of sudden cardiacdeath in patients with preservedleft ventricular function is doubled when nonsustained VT occursmore than 1 week after an MI.The risk of death is the greatest inthe first 6 months after an MI andpersists for up to 2 years. The riskof death is five times greater inpatients with left ventricular dys-function, defined as an ejectionfraction of less than 40%.The initial treatment of nonsus-tained VT includes correcting elec-trolyte imbalances, removing exac-erbating factors (such as hypoxia,dehydration, and drugs), and ad-justing the patients beta-blockerdosage. A patient with recurrent,nonsustained VT may also need a Tips for differentiating SVT with aberrancy fromVT Ventricular rhythm is usually regular in both supraventricular tachycardia (SVT)with aberrancy and ventricular tachycardia (VT), but these other characteristicsmay help you distinguish these two arrhythmias. VT is four times more common than SVT with aberrancy. VT is more common in patients who have a history of myocardial infarction orheart failure. Circulatory collapse is more common withVT than with SVT, although patientscan maintain a normal blood pressure withVT. Atrioventricular dissociation, which can appear as independent P waves march-ing through the QRS complexes, strongly suggestsVT. If the QRS complex is more than 0.14 second with right bundle-branch block ormore than 0.16 second with left bundle-branch block,VT is more likely. If the wide QRS-complex tachycardia has a triphasic pattern in lead V 1 , SVT withaberrancy is likely. If an upright QRS complex has a taller-left-peak pattern in lead V

1 , the diagnosisis likelyVT. Coarse fibrillation Fine fibrillation } }

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September 2008 American Nurse Today Class I antiarrhythmic, such asmexiletine, propafenone, or fle-cainide, or a Class III antiarrhyth-mic, such as amiodarone or sotalol.The American College of Cardi-ologyAmerican Heart Associationguidelines recommend placing animplantable cardioverter defibrilla-tor (ICD) in certain patients, suchas those with prior CAD, MI, left ventricular dysfunction (defined asan ejection fraction of 35% orless), and inducible VF, nonsus-tained VT or sustained VT at elec-trophysiologic study that is notsuppressible by a Class I antiar-rhythmic drug. Finding the cause of wideQRS-complex tachycardia A wide QRS-complex tachycardiahas a QRS complex of more than0.12 second and a ventricular rateof more than 110 bpm. Ventricu-lar conduction is abnormally sloweither because the arrhythmiaoriginates in the ventricles out-side of the normal conductionsystem (ventricular tachycardia)or because there are abnormali-ties in the His-Purkinje system(supraventricular tachycardia withaberrancy). A supraventricular tachycardia(SVT) originates above the ventri-cles, in the atria, or in the bundleof His. If the His-Pukinje system isnormal, the QRS complex will benormal, so its easy to tell thedifference between SVT and VT.However, an abnormal systemproduces aberrancy and creates a wide QRS complex. When this oc-curs, distinguishing VT from SVTcan be tricky. When a differentialdiagnosis cant be made, treatmentproceeds as if the patient has VT.The reason? Treating a patient with VT as if he has SVT can leadto

hemodynamic instability.To identify the arrhythmia caus-ing wide QRS-complex tachycar-dia, consider such factors as thepatients age, cardiac history, andphysical examination findings.(See Tips for differentiating SVT with aberrancy from VT .) Alwaysreport the rhythm to the cardiolo-gist as soon as possible becausehe has the expertise to identify and manage the rhythm. A medical history of angina,MI, coronary artery bypass graft-ing, valvular heart disease, orheart failure strongly suggests VT.The presence or absence of he-modynamic instability doesnt sug-gest the rhythm diagnosis; howev-er, if a patient is hemodynamically unstable, the rhythm should betreated as VT.The main tool for identifyingarrhythmias is the 12-lead ECG.(See Diagnostic ECG features of VT, VF, and SVT. ) Atrioventriculardissociation, fusion, and capturebeats suggest, but dont confirm, VT. The following rhythm stripsshow the characteristics of SVTand VT. The characteristics of SVT with aberrancy include a rapid,regular heart rate; P waves thatare usually not visible becausethey are buried in the QRS com-plex, a PR interval that isnt dis-cernible, and QRS complexes thatlook alike and are usually wide(greater than 0.12 second). Notethat the onset of wide QRS-complextachycardia in lead V 1 shows atriphasic pattern, which suggests adiagnosis of SVT with aberrant ventricular conduction or rightbundle-branch block. Wide QRS-complex supraventricular tachycardia with aberrancy The characteristics of VT alsoinclude a rapid, regular heart rate,but the P waves are absent or dis-sociated from the QRS complexes,so there is no PR interval, and QRScomplexes are wide and bizarre(more than 0.12 second). The up-right QRS complex with a taller-left-peak pattern in lead V 1 indi-cates a diagnosis of VT. S Heart rate(beats per PR QRSArrhythmia minute) Rhythm P waves interval complexes Ventricular 110 to 250 Usually Absent None Wide,tachycardia regular but or bizarre,can be dissociated > 0.12slightly from QRS secondirregular complexesVentricular Not Irregular, None None No recog-fibrillation discernible chaotic nizablecomplexesor low-amplitudecomplexesSupra- 160 to 240 Regular Usually Usually Usuallyventricular not not narrowtachycardia visible; discernible (< 0.12often second)buried May bein the wide if QRS aberrantcomplex conductionoccurs All QRScomplexeslook alike Signs and Symptoms of Hypoglycemia

Diagnostic ECG features of VT, VF, and SVT

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