AAFP Board Review: Managing

Dysrhythmias Vu Tran, M.D.

July 22, 2014

LSUFP-Alexandria

Objectives Outlined by AAFP

• Differentiate the diagnosis and management of type I (Wenkebach) and type II (Mobitz) AV heart block.

• Analyze the diagnosis and management of common forms of supraventricular arrhythmias.

• Summarize the diagnosis and management of sinus node disease.

• Outline the diagnosis and management of ventricular tachycardia.

EKG Boxes

Review EKG ComponentsComplexes

P‐waves:Atrial depolarization

• Upright : I, II, V4‐V6, aVF• Inverted: aVR

QRS complexes:Ventricular depolarization

• Small Q‐waves: I, aVL, V5, V6

• Transition V3/V4• Q‐waves are common in

lead IIIT‐wavesVentricular repolarization

Intervals

PR: time from atrial to ventricular depolarization (<0.20 sec or < ONE BIG BOX)

QRS: Ventricular depolarization (<0.12 or < 3 SMALL BOX.

QT: Total time from depolarization to repolarization (<1/2 RR Interval)Corrected: Bazett’s formula: QTC = QT / √ RR

AV Block

• Abnormally prolonged AV conduction time or failure of conduction of one or more atrial impulses

• 1 degree AV block

• AV conduction delay

• 2 degree AV block

• Type 1‐ Wenckebach

• Type 2- Mobitz

• 3 degree AV block

• Complete

First Degree AV Block

• Prolonged PR interval >0.20 sec with every atrial impulse reaching the ventricles

• Better termed “AV delay”

• Commonly associated with higher degrees of physical conditioning

• Not a contraindication to the use of β-blockers or non-dihydropyridine CCBs (or any other anti-hypertensives)

Second Degree AV Block

• Allows some atrial depolarization to conduct to the ventricles, while some atrial depolarizations are blocked, leaving lone P-waves without and associated QRS.

• Refractory periods of the AV nodal tissue are abnormally prolonged

• Two types:• Type I: Wenckebach

• Type II: Mobitz

Second Degree: Type I (Wenkebach)

• PR gradually lengthens with each cycle until the last P-wave in the series does not produce a QRS.

• Repeated short series can produce “group beating” that looks like couplets of premature beats.

• Is sometimes caused by parasympathetic excess (inhibits AV node) or drugs that mimic or induce parasympathetic effects, i.e. Atropine.

• “Dropped QRS”

Second Degree: Type I AV Block

Second Degree: Type II (Mobitz)

• Almost always represents disease of the distal conduction system, the His-Purkinje system

• May progress to third-degree heart block, with no emerging escape rhythm

• Constant PR‐intervals in all conducted beats

• Commonly associated with bundle branch blocks

• Treatment: permanent pacemaker

Second Degree: Type II AV Block

3rd Degree AV Block

• Complete block that prevents atrial depolarizations from reaching the ventricles.

• If block is high in the AV node, the fastest-pacing focus below the block escapes to pace the ventricles at its inherent rate.

• If block destroys the whole AV node or is below the AV node, that leaves only ventricular foci to pace at it’s inherent slow pace.

• Two independent rhythms can therefore be seen on an EKG, a so called AV dissociation.

• Treatment is pace-maker.

Complete AV Block

Supraventricular Tachycardia (SVTs)

• All atrial foci and all junctional foci are above the ventricles.

• Starts suddenly and ends suddenly

• Usually starts in the 3rd or 4th decade of life

• Also common in teenage women

• Anxiety, SOB, chest pressure, numbness, dizziness, etc.

• Treatment: Adenosine/Cardioversion if unstable. If stable then can do vagal maneuvers, adenosine, Verapamil/Diltiazem, Beta-blockers.• Beta-blockers and nonhydropyiridine CCB can cause hypotension and/or

bradycardia

Major Types of SVTs

• AV Nodal Re-Entry Tachycardia (AVNRT)

• Atrial Tachycardia

• Multifocal Atrial Tachycardia (MAT)

• Atrial Flutter

• Atrial Fibrillation

Narrow Complex Tachycardias

• <120 milliseconds, reflects rapid activation of the ventricles via the normal His-Purkinje system, which in turn suggests that the arrhythmia originates above or within the His bundle (ie, a supraventricular tachycardia).

• The site of origin may be in the sinus node, the atria, the atrioventricular (AV) node, the His bundle, or some combination of these sites.

• Constant PR interval.

Narrow Complex Tachycardias

• Options to quickly slow AV conduction include: Vagal maneuvers: Valsalva, unilateral carotid massage

IV adenosine: 6 mg bolus; follow with 12 mg if ineffective

IV ß-blocker: metoprolol 5 mg

IV diltiazem: 15-30 mg bolus

Ventricular response in sinus tachycardia and atrial flutter gradually slows; ventricular response in SVT abruptly converts to sinus rhythm.

Digoxin also slows AV conduction, but because it requires loading over hours, it is not quickly effective.

Premature Atrial Contractions

• Ectopic P‐waves occur earlier in the cardiac cycle than P‐waves of sinus origin

• P‐wave configuration different than sinus P‐wave

• PR‐interval often normal, but can vary slightly

• Pause following the PAC is longer than that of the regular rhythm

• May initiate SVT or atrial tachyarrythmias

Atrial Tachycardia

• Consecutive PACs

• Can be reentrant or related to enhanced automaticity

• P‐wave configuration different from sinus

• Atrial rate often 160 – 200 bpm, AV block may be present at faster atrial rates

• Treatment Beta blockers

Diltiazem

Antiarrhythmics

Ablation

• Confused with afib, aflutter

Multifocal Atrial Tachycardia

• MAT is an irregular narrow-complex rhythm with 3 or more P waves of variable morphology.

• Most common in patients with lung disease; can occur post-MI or with hypokalemia or hypomagnesemia.

• Rate may be reduced by using IV verapamil.

• Differences from wandering atrial pacemaker (WAP): significantly increased rate and almost invariable association with severe pulmonary disease.

Varying P-wave morphologies

Atrial Flutter

• Atrial rate usually 200 – 400 bpm

• Sawtooth pattern

• Diagnostic criteria: Flutter cycle is precisely regular

Flutter waves usually related to QRS complex

Lack of isoelectric baseline

• Meds don’t work real well: Amiodarone an option, but can exacerbate arrhythmias as well as cause other toxicities (liver, lungs, and eyes are well known.)

• Cardioversion

• Ablation

• Needs anticoagulation

“Sawtooth” Pattern of Atrial Flutter

Atrial Fibrillation

• Most common sustained arrhythmia, especially as people age

• Diagnostic criteria: Absence of P‐waves

Baseline may have very fine deflections, or very course deflections

Atrial rate 400 – 650 bpm

Irregularly‐irregular

• Calculate CHADS2 Score for risk of embolization. CHADS2 score relates to non-valvular AF.

Not considered are: valvular heart disease, prior peripheral embolism, intracardiac thrombus, or hyperthyroidism.

Risk of Embolization: CHADS2 Score

• Congestive heart failure = 1 point

• Hypertension = 1 point

• Age > 75 = 1 point

• Diabetes = 1 point

• Prior Stroke or TIA = 2 points

• Score: 0 Low risk; ASA therapy

1 Moderate risk; ASA or warfarin therapy

> 2 Moderate-high risk; warfarin therapy

Afib Treatment

• Cardioversion for patients with active ischemia, significant hypotension, or severe heart failure. If present for greater than 48 hrs, then will need 4 weeks PO anticoagulation. TEE to screen for thrombi if needed before 4 weeks. Continue anticoagulation at least 4 weeks after cardioversion.

• Beta-blockers and non-dihydropyridine CCB preferred as first line treatment.

• Digoxin second line treatment or adjunct.

• Goal of less than 110 bpm.

Comparisons Between Atrial Tachycardias

Sinus Node Disease

• Dysfunction of the SA node that is often secondary to senescence of the node and the surrounding atrial myocardium. Can also be caused by superimposed drug effect, hypothyroidism, or CAD of the right or circumflex coronary artery.

• Can result in persistent sinus brady/tachy, tachy-brady syndrome, or episodic sinus arrest.

•  If the patient is receiving medications that can provoke sinus bradyarrhythmias (eg, beta-blockers, angiotensin-converting enzyme [ACE] inhibitors), the medications should be stopped if possible.

Treatment of Sinus Node Disease

• Treatment directed at symptoms. Acute treatment consists of atropine (0.04 mg/kg intravenously every 2-4 h) and/or isoproterenol (0.05-0.5 mcg/kg/min intravenously). Control usually involves a pacemaker.

• In patients with bradyarrhythmias-tachyarrhythmias, the tachyarrhythmias may be controlled with digoxin, propranolol, or quinidine. However, these patients should be monitored closely with frequent Holter monitoring to ensure that the bradyarrhythmias are not exacerbated or causing symptoms (eg, dizziness, syncope, CHF); if this is the case, permanent pacemaker therapy is also required.

Ventricular Arrythmias

• PVCs most common, often insignificant if no demonstrable heart disease. Can be unifocal or multifocal

• Causes of wide QRS Ventricular Ectopy

Bundle branch block

Aberrant Ventricular Conduction

Ventricular Pacing

• Patient most likely elderly and suffering from diminished coronary blood flow, reducing the oxygen supply to the ventricular foci.

Ventricular Tachycardia

• 3 or more consecutive ventricular beats

• Sustained (>30 seconds) or nonsustained (less than 30 seconds)

• Monomorphic or polymorphic

• Must differentiate from SVT with aberrancy• QRS complexin SVT, even if widened by aberrant ventricular conduction, is usually

0.14 secs or less in duration. Ventricular complexes in VT are very wide, 0.14 sec or greater.

• The SA node still paces but the wide complexes hide the P-waves. There is independent pacing of the ventricles, a type of AV dissociation.

• Causes: Hypoxia, electrolyte disturbance, ischemia, drug toxicity, heart failure, and prolonged QT interval.

Ventricular Tachycardia Treatments

• SMVT: Synchronized cardioversion if unstable. Stable patients can be given IV Amiodarone, Lidocaine, Procainamide, or Sotalol. If not terminated, second bolus may be given or external cardioversion may be perfomed.

• NSVT: symptoms treated with Beta Blocker as initial therapy. Alternatives include non-dihydropyridine CCB, particularly in patients with normal LVF or catheter ablation with frequent symptoms.

• Patients with NSVT with prior MI and LVEF less than 40% should have an EPS done. If positive, an implantable cardioverter-defibrillator should be placed.

Comparing Ventricular Tachycardias

Torsades de Pointe

• Means “twisting point,” with outline of the rhythm looking like a twisted ribbon. Amplitude of each successive complex gradually increases and then

gradually decreases.

Polymorphic VT, characterized by a cyclical progressive change in cardiac axis.

• Usually non-sustained; may evolve into ventricular fibrillation.

• Rate is 250-350 bpm.

• Caused by low potassium, low magnesium, medications that block potassium channels, or congenital abnormalities.

Torsades = “Twisted Ribbon”

Treatment of Torsades de Pointe

• Prompt defibrillation for unstable patients.

• IV magnesium sulfate is first line, good for treatment and prevention.

• Acquired LQT: Mg2SO4, Isoproterenol, Lidocaine, Phenytoin, Sodium Bicarbonate (quinidine related).

• Congenital: Beta blockers (Metoprolol), Mexiletine, permanent dual chamber pacemaker, left cardiac sympathetic denervation, or cardioverter-defibrillator.

Question 1

A 75-year-old African-American male with no previous history of cardiac problems complains of shortness of breath and a feeling of general weakness. His symptoms have developed over the past 24 hours. On physical examination you find a regular pulse with a rate of 160 beats/min. You note rales to the base of the scapula bilaterally, moderate jugular venous distention, and hepatojugular reflux. His blood pressure is 90/55 mm Hg; when he sits up he becomes weak and diaphoretic and complains of precordial pressure. An EKG reveals atrial flutter with 2:1 block. Management at this time should include

A) intravenous digoxin

B) intravenous verapamil (Calan, Isoptin)

C) amiodarone (Cordarone)

D) electrical cardioversion

E) insertion of a pacemaker

Answer: D

• This patient has stage 2 hypertension, and his history of stroke is a compelling indication to use specific classes of antihypertensives. For patients with a history of previous stroke, JNC-7 recommends using combination therapy with a diuretic and an ACE inhibitor to treat the hypertension, as this combination has been clinically shown to reduce the risk of recurrent stroke. Other classes of drugs have not been shown to be of benefit for secondary stroke prevention. Although blood pressure should not be lowered quickly in the setting of acute ischemic stroke, this patient is not having an acute stroke, so treatment of his hypertension is warranted.

• Ref: Ressel GW; NHLBI: NHLBI releases new high blood pressure guidelines. Am Fam Physician 2003;68(2):376, 379.

Question 2

• Which cardiac arrhythmia has been reported with high-dose methadone use?

• A) Atrial fibrillation

• B) Paroxysmal supraventricular tachycardia

• C) Third degree heart block

• D) Torsades de pointes

• E) Multifocal atrial tachycardia

Answer: D

The cardiac toxicity of methadone is primarily related to QT prolongation and torsades de pointes.

Ref: Death, narcotic overdose, and serious cardiac arrhythmias. FDA Alert, 2006.

Question 3

A 45-year-old male sees you for a routine annual visit and is found to have atrial fibrillation, with a ventricular rate of 70–75 beats/min. He is otherwise healthy, and a laboratory workup and echocardiogram are normal. Which one of the following would be the most appropriate management?

A) Aspirin, 325 mg daily

B) Warfarin (Coumadin), with a target INR of 2.0–3.0

C) Clopidogrel (Plavix), 75 mg daily

D) Amiodarone (Cordarone), 200 mg daily

E) Observation only

Answer: A

Atrial fibrillation is the most common arrhythmia, and its prevalence increases with age. The major risk with atrial fibrillation is stroke, and a patient’s risk can be determined by the CHADS score. CHADS 2 stands for Congestive heart failure, Hypertension, Age >75, Diabetes mellitus, and previous Stroke or transient ischemic attack. Each of these is worth 1 point except for stroke, which is worth 2 points. A patient with 4 or more points is at high risk, and 2–3 points indicates moderate risk. Having 1 point indicates low risk, and this patient has 0 points. Low-risk patients should be treated with aspirin, 81–325 mg daily (SOR B). Moderate- or high-risk patients should be treated with warfarin. Amiodarone is used for rate control, and clopidogrel is used for vascular events not related to atrial fibrillation.

Ref: Gutierrez C, Blanchard DG: Atrial fibrillation: Diagnosis and treatment. Am Fam Physician 2011;83(1):61-68.

Question 4

An 80-year-old female is being started on warfarin (Coumadin) for atrial fibrillation. According

to the American College of Chest Physicians guidelines, the initial dose in this patient should

NOT exceed

A) 2.5 mg

B) 5 mg

C) 7.5 mg

D) 10 mg

E) 12.5 mg

Answer: B

The American College of Chest Physicians recommends a starting warfarin dosage of 5 mg/day in elderly patients, or in patients who have conditions such as heart failure, liver disease, or a history of recent surgery. The INR should be used to guide adjustments in the dosage.

Ref: Ansell J, Hirsch J, Hylek E, et al: Pharmacology and management of the vitamin K antagonists. American College of Chest Physicians evidence-based clinical practice guidelines (8th edition). Chest 2008;133(6 Suppl):161S.

Question 5

An 80-year-old white male is admitted to the hospital with an acute myocardial infarction. He

is given an antiarrhythmic for ventricular ectopic beats. During monitoring in the coronary care

unit, he develops the rhythm shown on the EKG on the next slide. This rhythm is best described as

A) ventricular flutter

B) ventricular fibrillation

C) ventricular tachycardia

D) torsades de pointes

Answer: DThe EKG shown represents torsades de pointes. This special form of ventricular tachyarrhythmia is often regarded as an intermediary between ventricular tachycardia and ventricular fibrillation. Morphologically it is characterized by wide QRS complexes with apices that are sometimes positive and sometimes negative. It is generally restricted to polymorphous tachycardias associated with QT prolongation. Anything that produces or is associated with a prolonged QT interval can cause torsades de pointes, including drugs (quinidine, procainamide, disopyramide, phenothiazines), electrolyte disturbances, insecticide poisoning, subarachnoid hemorrhage, and congenital QT prolongation. Its great clinical importance lies in the fact that the usual anti-arrhythmic drugs are not only useless but contraindicated, because they can make matters worse. Ventricular flutter is the term used by some authorities to describe a rapid ventricular tachycardia producing a regular zigzag on EKG, without clearly formed QRS complexes. Ventricular tachycardia consists of at least three consecutive ectopic QRS complexes recurring at a rapid rate. They are usually regular. Ventricular fibrillation is characterized by the complete absence of properly formed ventricular complexes; the baseline wavers unevenly, with no clear-cut QRS deflections.

Ref: Bonow RO, Mann DL, Zipes DP, Libby P (eds): Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine, ed 9. Elsevier Saunders, 2011, pp 806-809.

Question 6

Which one of the following cardiac rhythm abnormalities is most common in patients with anorexia nervosa?

A) Atrial fibrillation

B) Ventricular fibrillation

C) Sinus bradycardia

D) Sinus tachycardia

E) Paroxysmal supraventricular tachycardia

Answer: C

Sinus bradycardia is almost universally present in patients with anorexia nervosa. It is hypothesized that this is due to vagal hyperactivity resulting from an attempt to decrease the amount of cardiac work by reducing cardiac output. It is also possible that the bradycardia can be accounted for by low serum T3 levels, a common finding in persons with chronic malnutrition. Sinus tachycardia may occur with re-feeding in patients with anorexia. Other arrhythmias may also occur but are less frequent.

Ref: Casiero D, Frishman WH: Cardiovascular complications of eating disorders. Cardiol Rev 2006;14(5):227–231. 2) Williams PM, Goodie J, Motsinger CD: Treating eating disorders in primary care. Am Fam Physician 2008;77(2):187-195.

Question 7

A 72-year-old female presents to the emergency department complaining of dizziness. She also reports palpitations since yesterday, with dyspnea on exertion. She does not have chest pain. On examination her blood pressure is 102/60 mm Hg, pulse rate 140 beats/min, respirations 16/min, and O2 saturation 94% on room air. She has tachycardia with no murmurs and her lungs are clear. The remainder of her examination is normal, including the absence of lower-extremity edema. Her EKG is shown on the next slide. Which one of the following is the best initial step in the management of her tachycardia?

A) Amiodarone (Cordarone)

B) Intravenous adenosine (Adenocard)

C) Intravenous metoprolol tartrate (Lopressor)

D) Immediate synchronized cardioversion

E) Unsynchronized cardioversion under conscious sedation

Answer: C

The EKG shows atrial fibrillation with a rapid ventricular rate. The patient is stable, so initial treatment should focus on rate control. Intravenous -blockers or nondihydropyridine calcium channel antagonists are preferred for initial therapy to control the rate. Amiodarone may be used for rhythm control but would not be the initial treatment of choice in this case. Cardioversion is not indicated unless the patient becomes unstable. Adenosine is not a recommended treatment for atrial fibrillation.

Ref: Fuster V, Rydén LE, Cannom DS, et al: ACC/AHA/ESC 2006 Guidelines for the Management of Patients with Atrial Fibrillation: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines

Question 8A 39-year-old male presents to the emergency department with a 2-hour history of chest discomfort, dyspnea, dizziness, and palpitations. He has no history of coronary artery disease. He states that he has had several similar episodes in the last year. On examination he has a temperature of 36.8°C (98.2°F), a respiratory rate of 25/min, a heart rate of 193 beats/min, a blood pressure of 134/82 mm Hg, and an O2 saturation of 96% on room air. The physical examination is otherwise normal. An EKG reveals a regular narrow QRS complex tachycardia with no visible P waves. He converts to normal sinus rhythm with intravenous adenosine (Adenocard). Which one of the following would be most useful in the long-term management of this patient’s condition?

A) Adenosine

B) Digoxin

C) Vagal maneuvers

D) Pacemaker placement

E) Radiofrequency ablation

Answer: E

This patient presents with a classic description of supraventricular tachycardia (SVT). The initial management of SVT centers around stopping the aberrant rhythm. In the hemodynamically stable patient initial measures should include vagal maneuvers, intravenous adenosine or verapamil, intravenous diltiazem or -blockade, intravenous antiarrhythmics, or cardioversion in refractory cases. While digoxin is occasionally useful in atrial fibrillation with a rapid ventricular rate, it is not recommended for SVT. Radiofrequency ablation is fast becoming the first-line therapy for all patients with recurrent SVT, not just those refractory to suppressive drug therapies. Observational studies have shown that this therapy results in improved quality of life and lower cost as compared to drug therapy.

Ref: King DE, Dickerson LM, Sack JL: Acute management of atrial fibrillation: Part 1. Rate and rhythm control. Am Fam Physician 2002;66(2):249-256. 2) Colucci RA, Silver MJ, Shubrook J: Common types of supraventricular tachycardia: Diagnosis and management. Am Fam Physician 2010;82(8):942-952.

References

• Dubin, Dale (2000). Rapid Interpretation of EKG's (6th ed.)

• Diagnostic Approach to Palpitations. Am Fam Physician. 2005 Feb 15;71(4):743-750.

• Common Types of Supraventricular Tachycardia: Diagnosis and Management. Am Fam Physician. 2010 Oct 15;82(8):942-952.

• AAFP Board Review 2012

• Up To Date

• Outpatient Approach to Palpitations. Am Fam Physician. 2011 Jul 1;84(1):63-69

• Management of Common Arrhythmias Part I Am Fam Physician. 2002 Jun 15;65(12):2479-2487.

• Management of Common Arrhythmias Part II. Am Fam Physician. 2002 Jun 15;65(12):2491-2497.