Transcript AAFP Board Review: Managing Dysrhythmias

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 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
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
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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 HisPurkinje system
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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)
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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
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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
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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
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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
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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
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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
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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). Moderateor 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: 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 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 lowerextremity 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 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
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.
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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.