Arrhythmias

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Arrhythmias

• Medicine Clerkship Lecture
• By
• John Liuzzo, M.D., Ph.D.

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Case 1

• A 59 y/o man collapses without warning while
  eating dinner. A family member initiates
  cardiopulmonary respiration and within 5 minutes
  paramedics arrive. After a quick look at his
  rhythm using the defibrillator paddles, they
  administer one 200-Joule shock. On arrival in the
  ER he is unconscious and intubated, and requires
  mechanical intubation. A telemetry monitor shows
  sinus tachycardia. The family states that the
  patient did not take any drugs, either illicit or
  prescribed, before the event.
• 1) What is the most likely rhythm documented by
  the paramedics?
• 2) What is the most likely heart disease in this
  patient?

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Case 1 (cont)

• The resuscitated patient is admitted to the
  hospital, where ECG reveals evidence of an old
  anterior myocardial infarction. An acute MI is
  ruled out on the basis of cardiac enzyme levels.
  Over the course of 24 hours, the patient recovers
  fully neurologically. Cardiac catherization
  reveals single-vessel coronary disease (100
  obstruction of the left anterior descending
  artery) and an anteroapical aneurysm. An exercise
  test reveals good tolerance and no evidence of
  myocardial ischemia or arrythmias with exercise.
  A 24 hour Holter monitor shows an average of 30
  PVCs per hour, but no ventricular tachycardia.
• 3) What is the most likely acute cause of the
  arrythmia in this patient?
• 4) How should this patients condition be managed?
• 5) If electrophysiological studies reveal no
  abnormal rhythms, you should?

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Outline

• Atrial tachyarrythmias
• - Regular Sinus tachycardia
• Paroxysmal Atrial
  Tachycardia
• Atrial Flutter with
  constant conduction
• - Irregular Atrial Fibrillation
• Multifocal Atrial
  Tachycardia
• Atrial Flutter with
  irregular conduction
• Bradyarrhythmias
• Sinus bradycardia
• Sinus Pause
• AV Block
• Ventricular tachyarrhythmias
• Premature ventricular
  contraction
• Ventricular
  tachycardia
• Ventricular
  fibrillation

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Introduction

• Sustained atrial tachyarrhythmias usually permit
  adequate cardiac output
• Sustained ventricular arrhythmias often cause
  collapse or death

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Atrial Tachyarrythmias

• Two categories regular cardiac rhythms and
  irregular rhythms
• In general, atrial tachyarrythmias do not
  interfere with inter- or intra-ventricular
  conduction
• The QRS remains narrow in form
• Occasionally, atrial arrythmias cause aberrant
  ventricular conduction with a wide QRS complex.

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Regular Atrial Tachycardias

• 1) Sinus Tachycardia physiologic or pathologic
  increase of sinus rate gt 100 bpm.
• Treat the condition causing the tachycardia, not
  the tachycardia itself.
• However, in cases of acute MI sinus tachycardia
  must be controlled to prevent myocardial ishemia
  (beta blockers or Ca-channel blockers)
• 2) Paroxysmal Atrial Tachycardia sudden onset, a
  normal heart, HR 150-250 bpm.
• P waves not visible because buried in the QRS
  complex or the T wave
• Therapy quiet setting and comfort the patient to
  reduce sympathetic discharge. Increase vagal tone
  by carotid sinus massage or valsalva maneuver.
  Medical therapy Beta-blocker, Ca channel
  blocker, digoxin, adenosine. If angina,
  hypotension, or CHF then consider countershock.

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Regular atrial tachycardia (cont)

• 3) Atrial Flutter with constant conduction
  occurs in patients with some sort of heart
  disease (e.g. CAD, pericarditis, valvular
  disease, cardiomyopathy)
• Atrial rate of 240-400 bpm. Usually conducted to
  the ventricle with block so that ventricular rate
  is a fraction of the atrial rate
• On ECG produces a classic saw tooth pattern
• Therapy IV digoxin, beta-blocker, or Ca-channel
  blocker may convert the arrythmia to NSR. Use to
  control the ventricular response which helps
  maintain hemodynamic stability (to 31 or 41
  block)
• If medical therapy does not convert to NSR,
  atrial flutter usually convert itself over time,
  either to Atrial fibrillation or NSR
• Use direct current cardioversion if pt is
  hemodynamically unstable

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Irregular Atrial Tachycardias

• 1) Atrial Fibrillation an irregularly irregular
  arrythmia in which there is no ordered
  contraction of the atria, but rather multiple
  discoordinate wave fronts of depolarization that
  send a large number of irregular impulses to
  depolarize the AV node
• ECG irregular impulses produce an irregular
  ventricular response, the rate of which depends
  on the number of impulses conducted
• Causes of atrial fibrillation include
• stress, fever, excessive alcohol
  intake, volume depletion, Wolf-Parkinson White
  syndrome, pericarditis, CAD, MI, pulmonary
  emboli, mitral valve disease, thyrotoxicosis, and
  idiopathic (lone) atrial fibrillation

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Atrial Fibrillation (cont)

• If the patient is hemodynamically unstable, or
  demonstrates increase in angina pectoris or
  worsening of CHF, immediate DC cardioversion is
  indicated
• If the patient is hemodynamically stable, focus
  on controlling the ventricular response, while
  simultaneously treating the cause of the
  arrythmia (use beta-blocker, Ca-channel blocker,
  or digoxin)
• Once the rate is controlled cardioversion may
  occur spontaneously or with anti-arrythmic drugs,
  or DC cardioversion
• If patient in atrial fibrillation gt 48 hours,
  then treat with anticoagulation for 3 weeks
  before attempted cardioversion because risk of
  intra-atrial thrombus is high after 48 hours

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Irregular Atrial Tachycardias (cont)

• 2) Multifocal Atrial Tachycardias there is
  synchronous atrial contraction, but the
  contraction arises from many sites in the atria,
  not from the sinus node
• In majority of MAT the patient has antecedent
  pulmonary disease
• On ECG the multi-sites of origin of atrial
  contraction produces many P wave configurations,
  and different R-R intervals
• Three or more different P wave morphologies are
  needed to make the diagnosis P-R interval may
  vary
• Therapy to improve the patients oxygenation,
  ventilation, and airway mechanics. If not
  effective, can use Ca-channel blockers

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Irregular Atrial Tachycardias (cont)

• 3) Atrial Flutter with irregular conduction
• there is varying block, e.g. 21 alternating with
  31 block, thus the rhythm is irregular
• Therapy is the same as atrial flutter with
  constant block

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Case 2

• A 62 y/o man, w/ hx of HTN, CAD, and CHF,
  presents to the E.D. with a c/o worsening SOB. He
  has been experiencing DOE (one block) for a long
  time, and usually sleeps on three pillows. Over
  the last few days the SOB reoccurs even with the
  slightest exertion. He is experiencing fatique
  and lightheadness and also has observed worsening
  of the swelling in his legs
• PMH hypertension, CAD, CHF, mitral valve
  stenosis
• Medications Enalapril 20 mg BID Metoprolol
  50 mg BID
• ECASA 325 mg QD
  Furosemide 40 mg PO QD
• Social Hx Smoking 2 ppd for 30 yrs
• Alcohol 3-4 drinks per week
  (red wine)
• Married, lives with wife,
  retired high school teacher
• Family Hx F-acute MI age 65 M-hypertension, DM

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Case 2 (cont)

• Physical Exam
• elderly WM, moderate respiratory distress
• Wt90kg, R24, BP150/70, P125, T98.6F, Pulse
  Ox93 on RA
• Neck elevated JVP
• Heart S1,S2 of variable intensity, S3 gallop
  present, irregularly irregular rhthym, II/VI
  holosystolic murmer heard best at apex with
  radiation to axilla
• Lungs bibasilar dullness, rales extending two
  thirds way up from the basal lung fields
  bilaterally
• Abd obese, otherwise nl exam
• Ext 2 pitting edema.
• ECG What will it show???

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Case 2 Study Questions

• 1) The patients presents with an exacerbation of
  CHF from new onset atrial fibrillation. Describe
  the pathogenesis of AF and what are the clinical
  conditions that may predispose to it?
• 2) What are the possible consequences of A. Fib
  that may occur in this patient. How does the
  atrial fibrillation lead to his CHF?
• 3) What are the major issues in management of
  patients with atrial fibrillation?

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Bradyarrhythmias

• Occurs when sinus node impulse generation is
  slowed or when normal impulses cannot be
  conducted to the ventricles because of AV nodal
  block or conduction system disease
• Only a concern when the patient has become
  symptomatic with presyncope or syncope from low
  cardiac output
• 1) Sinus bradycardia may be normal in trained
  athletes and requires no therapy
• If extreme sinus bradycardia (lt35 bpm) from sinus
  node dysfunction may cause symptoms
• 2) Sinus pause failure of the sinus node to
  generate an impulse on time
• Pauses may last for several seconds and cause
  syncope. Definitive therapy requires pacemaker
  implantation

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Bradyarrhythmias (cont)

• 3) AV block all the impulses generated from the
  sinus node are not conducted to the ventricle
• Types
• 2nd degree Mobitz Type I (Wenkebach) block
  progressive prolongation of P-R interval until a
  generated P wave is not conducted. This block
  usually occurs at the level of the AV node.
• 2nd degree Mobitz Type II block no prolongation
  of the P-R interval before the dropped beat.
  Often conduction in a 21 ratio is prolonged
  leading to symptomatic bradycardia. Block occurs
  in the AV node or in the His-Purkinje system
• 3rd degree Complete Heart Block No impulses are
  conducted, and the ventricular rate becomes
  dependent on spontaneous ventricular
  depolarizations. Severe symptomatic bradycardia
  with HR25-40 bpm
• Therapy Atropine, isoproterenol, transcutaneous
  pacing

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Ventricular Tachyarrythmias

• 1) Premature ventricular contractions heart
  beats arise from the ventricles, bypassing the
  His-Purkinje conduction system.
• On ECG, the His -Purkinje system is bypassed, the
  QRS configuration is widened and bizarre in
  appearance
• PVCs do not affect atrial depolarization, which
  proceeds normally and is dissociated with the
  PVC. The next sinus beat occurs at the same time
  it would have occurred if no PVC
• Therapy Most isolated PVCs are benign and should
  not be treated

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Ventricular Tachyarrythmias (cont)

• 2) Ventricular tachycardia a regular rhythm that
  occurs paroxysmally and is gt 120 bpm
• AV dissociation, allows the ventricular rhythm to
  proceed independently of the normal atrial rhythm
  and is the hallmark
• During V. Tach, cardiac relaxation is impaired,
  and together with loss of AV syncrony (loss of
  electrical coordination) leads to severely
  reduced cardiac output, producing hypotension
• Sustained V. Tach. Is usually a life-threatening
  arrythmia than can degenerate into ventricular
  fibrillation if untreated

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Ventricular tachycardia (cont)

• Physical Exam
• in many cases exam is precluded by
  decompensation
• If patient is relatively stable, cannon a waves
  can appear in the neck secondary to AV
  dissociation
• Observed when the tricuspid valve is closed and
  the right atrial contraction occurs during
  ventricular contraction
• Since the atrial blood cannot go forward against
  the closed tricuspid valve, backward flow
  produces a large bulge in the neck veins

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Ventricular tachycardia (cont)

• On ECG QRS is widened and bizarre in appearance
  (the His-Purkinje system is not utilized)
• no relationship between P wave and QRS complex
  (atria and ventricles operate independently)
• QRS may be monomorphic or polymorphic
• a polymorphic arrythmia revolving around a
  central point associated with prolonged QT
  interval is torsades de pointes
• Therapy DC cardioversion is urgently required in
  most cases since this arrythmia is unstable and
  life threatening
• In a stable patient, or while preparing for
  cardioversion, IV amioderone, lidocaine,
  vasopressin, or procainamide may return the
  patients rhythm to normal

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Ventricular Fibrillation

• Characterized by lack of ordered contraction of
  the ventricles therefore there is no cardiac
  output
• Ventricular fibrillation is synonymous with death
  unless conversion to an effective rhythm is
  accomplished
• Begin resuscitation (ventilation, compressions,
  drug and electrical therapy) immediately upon
  recognizing V. Fib