ventricular arrhythmias

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ventricular arrhythmias pdf

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ventricular arrhythmias and preventing Recognizing sudden cardiac death Be prepared to stop these dangerous arrhythmias. By Rose M. Coughlin, MSN, RN, APRN-BC S UDDEN CARDIAC DEATH kills Heart’s electrical system 350,000 to 400,000 Americans a year. That accounts for half of all deaths from coronary artery disease (CAD), the leading cause of death in the United States. Frequently, a dangerous arrhyth- mia, such as ventricular tachycardia (VT) or ventricular fibrillation (VF), precedes sudden cardiac death. In fact, VT precedes sudden cardiac death in more than 70% of patients. If you can detect VT and VF ear- ly on and provide prompt cardio- pulmonary resuscitation (CPR) and defibrillation, your chances of pre- venting sudden cardiac death are good. 38 American Nurse Today Volume 2, Issue 5 CE 1.8 contact hours L EARNING O BJECTIVES 1. Identify the causes of ventricu- lar arrhythmias. 2. Relate the heart’s electrical conduction to components of the normal electrocardiogram. 3. Differentiate the types of ven- tricular tachycardia (VT). 4. Describe the management of ventricular arrhythmias. Before discussing ventricular ar- rhythmias, let’s review how the heart’s electrical conduction sys- tem works. The system’s main function is to transmit electrical impulses from the sinoatrial (SA) node to the atria and ventricles, causing them to contract. Located high in the wall of the right atri- um, the SA node is the heart’s nat- ural pacemaker. It normally fires 60 to 100 times per minute, and each impulse results in one heart- beat. (See The path of cardiac conduction.) The electrical impulse passes through both atria to the atrioven-
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The path of cardiac conduction tricular (AV) node at the junction of the atria and ventricles. If the SA node stops firing, the AV node initiates the impulses, but the rate drops to 40 to 60 times per minute. From the AV node, the impulse travels through the bundle of His and down the right and left bun- dle branches into the Purkinje net- work of the ventricles, depolariz- ing the ventricular muscle. If the SA and AV nodes fail, the ventri- cles initiate the impulses but can only manage 20 to 40 impulses per minute. An electrocardiogram (ECG) re- flects the complete wave of depo- larization as it travels from the SA node to the Purkinje network. 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-Purkinje network. Aorta Pulmonary artery Pulmonary veins Sinoatrial node Reading an electrocardiogram The key components of an ECG are the P wave, PR interval, QRS com- plex, and T wave, as shown. QRS complex P wave PR interval T wave isoelectric line Atrioventricular node Bundle of His His-Purkinje network 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 and uniform. The PR interval represents the time needed for an impulse to trav- el through the atria and pause at the AV node. This pause allows the ventricles to fill with blood before contracting. The PR interval extends from the beginning of the P wave to the beginning of the QRS com- plex and normally is 0.12 to 0.20 second. Remember that each small square on the ECG paper repre- sents 0.04 second. Five small squares make up a large block of 0.20 second, and 30 large blocks equal 6 seconds. The QRS complex represents ventricular depolarization. The Q } Courtesy of The Cleveland Clinic, Cleveland, Ohio 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 aren’t present in every ECG lead. The normal QRS width is 0.06 to 0.12 second. The T wave represents ventricular repolarization. It follows the QRS complex and is normally in the same direction. The T wave is usual- ly rounded and slightly asymmetric. The isoelectric line represents absence of electrical activity. lar pacemaker in the bundle branches, Purkinje network, or ventricular myocardium takes con- trol of the conduction system. The impulses override the higher pace- maker sites. When impulses originate in the ventricles, the electrical current goes backwards through the ven- tricles, greatly reducing the heart’s efficiency. Because the ventricles are the lowest sites in the conduc- tion system, there are no fail-safe mechanisms if the heart rate drops too low. When a ventricular pacemaker takes control With VT, the myocardium becomes extremely irritable, and a ventricu- Causes of ventricular arrhythmias The most common cause of VT is May 2007 American Nurse Today 39
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CAD. Other cardiac causes include myocardial infarction (MI), car- diomyopathy, valvular heart dis- ease, and mitral valve prolapse. Patients are at higher risk for ven- tricular arrhythmias after having an MI because of a significant reduc- tion in left ventricular systolic function. VT may result from metabolic ab- normalities, such as acidosis, hypox- emia, hyperkalemia, hypokalemia, and hypomagnesemia. And VT may be caused by certain drugs, such as caffeine, cocaine, alcohol, digoxin, theophylline, antipsychotics, tricyclic antidepressants, and antiarrhythmics with proarrhythmic potential such as flecainide, dofetilide, sotalol, and quinidine. Tips for differentiating SVT with aberrancy from VT Ventricular rhythm is usually regular in both supraventricular tachycardia (SVT) with aberrancy and ventricular tachycardia (VT), but these other characteristics may 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 or heart failure. • Circulatory collapse is more common with VT than with SVT, although patients can maintain a normal blood pressure with VT. • Atrioventricular dissociation, which can appear as independent P waves march- ing through the QRS complexes, strongly suggests VT. • If the QRS complex is more than 0.14 second with right bundle-branch block or more 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 with aberrancy is likely. • If an upright QRS complex has a taller-left-peak pattern in lead V 1 , the diagnosis is likely VT. Recognizing ventricular arrhythmias With VT, an ectopic pacemaker in the ventricles initiates a heart rate between 110 and 250 beats per minute (bpm). On the ECG, the QRS complexes are abnormally wide and bizarre and more than 0.12 second. The forms of VT are classified by the configurations of the QRS com- plex. In monomorphic VT, the QRS complexes are the same or almost the same shape, size, and direction, as shown. Torsades de pointes VF, a medical emergency, is an erratic, disorganized firing of impuls- es from the ventricles. The ventricles quiver and are unable to contract or pump blood to the body. VF may be coarse or fine, as shown. Coarse fibrillation Fine fibrillation Ventricular fibrillation Monomorphic ventricular tachycardia In polymorphic VT, the QRS complexes markedly differ in shape, size, and direction from beat to beat. Torsades de pointes (mean- ing twisting around a point) is a form of polymorphic VT, character- ized by QRS complexes that gradu- ally change back and forth from one shape, size, and direction to another over a series of beats, as shown. 40 American Nurse Today Understanding sustained and nonsustained ventricular tachycardia VT may be sustained or nonsus- tained. Sustained VT lasts longer than 30 seconds and may require termination because the rapid rate doesn’t allow the heart to fill with blood, causing hemodynamic compromise. Nonsustained VT consists of three or more beats at a rate of at least 120 bpm lasting less than 30 seconds and terminat- ing spontaneously without causing hemodynamic compromise. Nonsustained VT is common, and usually patients don’t have symptoms. Some patients do de- velop palpitations, syncope, or lightheadedness. Patients with nonsustained VT may have struc- tural heart disease, such as CAD, dilated cardiomyopathy, or valvu- lar heart disease and should have further evaluation. The risk of sudden cardiac death in patients with preserved left ventricular function is doubled when nonsustained VT occurs more than 1 week after an MI. The risk of death is the greatest in the first 6 months after an MI and persists for up to 2 years. The risk of death is five times greater in patients with left ventricular dys- function, defined as an ejection fraction 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 patient’s beta-blocker dosage. A patient with recurrent, nonsustained VT may also need a } } Volume 2, Issue 5
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Diagnostic ECG features of VT, VF, and SVT Signs and Symptoms of Hypoglycemia S Class I antiarrhythmic, such as mexiletine, propafenone, or fle- cainide, or a Class III antiarrhyth- mic, such as amiodarone or sotalol. The American College of Cardi- ology–American Heart Association guidelines recommend placing an implantable cardioverter defibrilla- tor (ICD) in certain patients, such as those with prior CAD, MI, left ventricular dysfunction (defined as an ejection fraction of 35% or less), and inducible VF, nonsus- tained VT or sustained VT at elec- trophysiologic study that is not suppressible by a Class I antiar- rhythmic drug. Arrhythmia Ventricular tachycardia Heart rate (beats per minute) 110 to 250 Rhythm P waves PR interval QRS complexes • Wide, bizarre, > 0.12 second • No recog- nizable complexes or low- amplitude complexes Usually • Absent None regular but or can be dissociated slightly from QRS irregular complexes Irregular, chaotic • None None Ventricular fibrillation Not discernible Supra- ventricular tachycardia 160 to 240 Regular Finding the cause of wide QRS-complex tachycardia A wide QRS-complex tachycardia has a QRS complex of more than 0.12 second and a ventricular rate of more than 110 bpm. Ventricu- lar conduction is abnormally slow either because the arrhythmia originates in the ventricles out- side of the normal conduction system (ventricular tachycardia) or because there are abnormali- ties in the His-Purkinje system (supraventricular tachycardia with aberrancy). A supraventricular tachycardia (SVT) originates above the ventri- cles, in the atria, or in the bundle of His. If the His-Pukinje system is normal, the QRS complex will be normal, so it’s easy to tell the difference between SVT and VT. However, an abnormal system produces aberrancy and creates a wide QRS complex. When this oc- curs, distinguishing VT from SVT can be tricky. When a differential diagnosis can’t be made, treatment proceeds as if the patient has VT. The reason? Treating a patient with VT as if he has SVT can lead to hemodynamic instability. To identify the arrhythmia caus- ing wide QRS-complex tachycar- dia, consider such factors as the patient’s age, cardiac history, and physical examination findings. • Usually not visible; often buried in the QRS complex Usually • Usually not narrow discernible (< 0.12 second) • May be wide if aberrant conduction occurs • All QRS complexes look alike (See Tips for differentiating SVT with aberrancy from VT.) Always report the rhythm to the cardiolo- gist as soon as possible because he has the expertise to identify and manage the rhythm. A medical history of angina, MI, coronary artery bypass graft- ing, valvular heart disease, or heart failure strongly suggests VT. The presence or absence of he- modynamic instability doesn’t sug- gest the rhythm diagnosis; howev- er, if a patient is hemodynamically unstable, the rhythm should be treated as VT. The main tool for identifying arrhythmias is the 12-lead ECG. (See Diagnostic ECG features of VT, VF, and SVT.) Atrioventricular dissociation, fusion, and capture beats suggest, but don’t confirm, VT. The following rhythm strips show the characteristics of SVT and VT. The characteristics of SVT with aberrancy include a rapid, regular heart rate; P waves that are usually not visible because they are buried in the QRS com- plex, a PR interval that isn’t dis- cernible, and QRS complexes that look alike and are usually wide (greater than 0.12 second). Note that the onset of wide QRS-complex tachycardia in lead V 1 shows a triphasic pattern, which suggests a diagnosis of SVT with aberrant ventricular conduction or right bundle-branch block. Wide QRS-complex supraventricular tachycardia with aberrancy The characteristics of VT also include 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 QRS complexes 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. May 2007 American Nurse Today 41
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ACLS pulseless arrest algorithm Reprinted with permission. Handbook of Emergency Cardiovascular Care for Healthcare Providers. ©2006, American Heart Association. Key to abbreviations AED automated external defibrillator BLS basic life support CPR cardiopulmonary resuscitation 42 American Nurse Today IV/IO J PEA U intravenous/intraosseous joules pulseless electrical activity units VT VF ventricular tachycardia ventricular fibrillation Volume 2, Issue 5
ventricular arrhythmias - page 6
Wide QRS-complex ventricular tachycardia Treating ventricular arrhythmias To treat pulseless arrest from VF or pulseless VT, use the 2005 Advanced Cardiac Life Support (ACLS) guide- lines. (See ACLS pulseless arrest algo- rithm.) Initiate CPR immediately and defibrillation as soon as a defibrilla- tor is available. Note that a rhythm check is done only after 5 cycles or 2 minutes of CPR. The rationale is to minimize interruptions in chest com- pressions and the time between compressions and shock delivery. After an I.V. line is established, a vasopressor will be given. The preferred antiarrhythmic is amio- darone, although lidocaine can be given. Don’t forget to investigate the cause of the arrhythmia. For example, draw blood for arterial blood gas analysis and other blood tests to check for hypoxia, acido- sis, and hypoglycemia. recurrence, especially as the day of discharge approaches. To allay fears, use patient-centered care de- livery. Provide emotional support and patient teaching that includes family members. Patient and family teaching should include these topics, as ap- propriate: • pathophysiology of CAD and the risk of sudden cardiac death • CAD risk factor modification • ICD use and follow-up care • management of drug therapy • prescribed activity levels • importance of follow-up appoint- ments • use of 911. Most important, make sure the family knows how to perform CPR and use an automated external de- fibrillator. Alspach JG. Core Curriculum for Critical Care. 6 th ed. Philadelphia, Pa: W.B. Saunders Co; 2006. American Heart Association. (Winter 2006-2006). Highlights of the 2005 American Heart Associa- tion guidelines for cardiopulmonary resuscita- tion and emergency cardiovascular care. Curr Emerg Cardiovasc Care. 16(4):1-27. Available at: Accessed April 9, 2007. Brady WJ, Skiles J. Wide QRS complex tachycardia: ECG differential diagnosis. Am J Emerg Med. 1999;17(4):376-381. Field JM, Hazinski MF, Gilmore D, eds. Handbook of Emergency Cardiovascular Care for Healthcare Providers. Dallas, Tex: American Heart Association, Inc.; 2006. Hebbar AK, Hueston WJ. Management of com- mon arrhythmias: Part II: Ventricular arrhyth- mias and arrhythmias in special populations. Am Fam Physician. 2002;65(12):2491-2496. Huszar RJ. Basic Dysrhythmias: Interpreta- tion and Management. 3 rd ed. St. Louis: Mos- by, Inc; 2002. Kokolis S, Clark LT, Kokolis R, Kassotis J. Ven- tricular arrhythmias and sudden cardiac death. Prog Cardiovasc Dis. 2006;48(6):426-444. Lambiase P. Supraventricular or ventricular tachycardia? Br J Hosp Med. 2005;66(9):M28-29. Podrid PJ, Kowey PR. Cardiac Arrhythmia: Mechanisms, diagnosis and management. 2 nd ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2001. Tarditi DJ, Hollenberg SM. Cardiac arrhyth- mias in the intensive care unit. Semin Respir Crit Care Med. 2006;27(3):221-229. Woods SL, Sivarajan Froelicher ES, Underhill Motzer S, Bridges EJ. Cardiac Nursing. 5 th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2005. Your role Preventing sudden cardiac death starts with recognizing the dangerous ventricular arrhythmia that precedes it. The next step is providing prompt CPR and defibrillation, following the current ACLS guidelines. After these life-saving interventions, your role in preventing sudden cardiac death con- tinues as you identify the patient’s risk factors and teach the patient and his family how to stay alive. * Selected references ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. A report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines. Circulation. 2006;114:1088-1132. Teaching the patient After the ventricular arrhythmia has been corrected, assess the patient for risk factors for CAD. Carefully review the patient’s past medical history as well as current medica- tions. Obtaining a 12-lead ECG and baseline blood tests can help reveal risk factors. People who have experienced a sudden cardiac death event fear a Rose M. Coughlin, MSN, RN, APRN-BC, is a Clinical Nurse Specialist in the Cardiothoracic Stepdown Units at The Cleveland Clinic in Cleveland, Ohio. The author does not have any financial arrangements or affiliations with any corporations offering financial support or educational grants for continuing nursing education activities. Illustrations reprinted with the permis- sion of The Cleveland Clinic. CE POST-TEST — Recognizing ventricular arrhythmias and preventing sudden cardiac death Instructions To take the post-test for this article and earn contact hour credit, please go to Once you’ve suc- cessfully passed the post-test and completed the evaluation form, simply use your Visa or MasterCard to pay the processing fee. (Online: ANA members $15; nonmembers $20.) You’ll then be able to print out your certificate immediately. If you are unable to take the post-test online, complete the print form and mail it to the address at the bottom of the next page. (Mail-in test fee: ANA members $20; nonmembers $25.) Provider accreditation The American Nurses Association (ANA) is accredited as a provider of continuing nursing education by the American Nurs- es Credentialing Center’s Commission on Accreditation. ANA is approved by the California Board of Registered Nursing, Provider # CEP6178. Contact hours: 1.8. Expiration: 12/31/08. Purpose/goal: To provide registered nurses with information on how to identify and manage the patient with ventricular arrhythmias or VF. 43 May 2007 American Nurse Today
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