1. AAFP Board Review: Managing Dysrhythmias
Vu Tran, M.D.
July 22, 2014
LSUFP-Alexandria

2. 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.

3. EKG Boxes

4. Review EKG Components Complexes Intervals 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 III
T‐waves
Ventricular 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

7. 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

8. 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)

9. 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

10. 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”

11. Second Degree: Type I AV Block

12. 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

13. Second Degree: Type II AV Block

14. 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.

15. Complete AV Block

17. 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

18. Major Types of SVTs AV Nodal Re-Entry Tachycardia (AVNRT)
Atrial Tachycardia
Multifocal Atrial Tachycardia (MAT)
Atrial Flutter
Atrial Fibrillation

19. 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.

20. 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: 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.

21. 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

23. 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

24. 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.

25. Varying P-wave morphologies

26. 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

27. “Sawtooth” Pattern of Atrial Flutter

28. 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.

29. 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

30. 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.

31. Comparisons Between Atrial Tachycardias

32. 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.

33. 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 ( 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.

36. 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.

37. 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 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.

38. 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.

39. Comparing Ventricular Tachycardias

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

41. Torsades = “Twisted Ribbon”

42. 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.

45. 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

46. 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.

47. 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

48. 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.

49. 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

50. 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.

51. 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

52. 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.

53. 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

55. Answer: D
The 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

56. 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

57. 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):

58. 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

60. 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

61. Question 8
A 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

62. 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): ) Colucci RA, Silver MJ, Shubrook J: Common types of supraventricular tachycardia: Diagnosis and management. Am Fam Physician 2010;82(8):

64. References Dubin, Dale (2000). Rapid Interpretation of EKG's (6th ed.)
Diagnostic Approach to Palpitations. Am Fam Physician. 2005 Feb 15;71(4):
Common Types of Supraventricular Tachycardia: Diagnosis and Management. Am Fam Physician. 2010 Oct 15;82(8):
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):
Management of Common Arrhythmias Part II. Am Fam Physician. 2002 Jun 15;65(12):