Arrhythmia Review

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ariadne9
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Arrhythmia Review
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2013-07-17 15:55:18
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BC NU 494
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Arrhythmia Review
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  1. What is the intrinsic rate of the SA node?
    60-80 bpm
  2. What is the intrinsic rate of the AVJ?
    40-60 bpm
  3. What is the intrinsic rate of the ventricles?
    20-40 bpm
  4. PR interval length
    0.16-0.2
  5. QRS interval length
    0.06-0.1
  6. What formula is used to correct QT for HR?
    • Bazzetts formula
    • QT / square root of the RR interval
  7. T or F, the QT interval should be greater than half of the preceeding R-R interval when the HR  is between 65-90 bpm?
    F, it should be LESS than half
  8. Is the QRS complex positive or negative in leads I thru III?
    Positive
  9. Where are lead I's positive and negative electrodes?
    • + LA
    • - RA
  10. Where are lead II's positive and negative electrodes located?
    • + LL
    • - RA
  11. Where are lead III's positive and negative electrodes?
    • + LL
    • - LA
  12. Possible causes of ST
    hypovolemia, fever, exercise, SNS stimulation, hyperthyroidism
  13. Sinus arrhythmia
    • -normal variation due to alterations in ANS tone
    • -associated with the respiratory cycle
    • -HR increases with inspiration and decreases with expiration
    • -common in kids and young adults
    • -when seen in geri its it may be a precursor to sick sinus syndrome
  14. Sinus pause or sinus arrest
    • -sinus node does not conduct or initiate an impulse
    • -due to an automaticity or conduction issue
    • -causes: increased vagal tone, infarction, drugs (BB or CCB)
  15. What would cause the P wave to be inverted?
    -an impulse that originates near the AVJ
  16. Do PACs usually have compensatory or non compensatory pauses?
    Non-compensatory
  17. What is a compensatory pause?
    The QRS before the premature beat to the QRS after equals 2 R-R intervals
  18. What is a non-compensatory pause?
    The QRS before the premature beat to the QRS after equals less than 2 R-R intervals
  19. Why does a non-compensatory pause occur with a PAC?
    The premature depolarization of the atria by the PAC results in subsequent premature depolarization of the SA node which causes it to reset itself earlier than expected
  20. Why does a compensatory pause usually occur with PVCs?
    The SA node is not depolarized by the premature beat and thus is not reset and so the underlying rhythm appears at the expected time after the pause
  21. With a PAC is the QRS usually of normal duration?
    Yes
  22. PAC with aberrant conduction
    If it occurs very early then the impulse reaches the bundle branches before repolarization is complete.  The R bundle is slower to repolarize than the L bundle, so they are depolarized sequentially and the QRS is wide and measures >0.12 seconds.
  23. How can you distinguish between a PVC and a PAC with aberrant conduction?
    PAC usually has a non-compensatory pause
  24. Non-conducted PAC
    • The ectopic atrial focus occurs so early that the AV node is still refractory and so the impulse is not conducted to the ventricles.
    • Get a P wave with no QRS.
  25. Causes of PACs
    nicotine, stress, caffeine, ETOH
  26. Paroxysmal atrial tachycardia
    • -ectopic PM in the atria produces a rapid regular atrial rhythm
    • -rate 150-250 bpm
    • -occurs in bursts (hence paroxysmal)
    • -may not be able to differentiate between T and P waves
    • -QRS complex is narrow
  27. PAT causes
    • -same as PACs
    • -also due to COPD and digoxin toxicity
  28. Effects of PAT
    • -decreased CO as ventricular filling is impaired
    • -possible palpitations
    • -increased myocardial O2 consumption
  29. PAT treatment for an unstable pt
    cardioversion
  30. PAT treatment for a stable pt
    • -sedation
    • -vagal maneuvers
    • -adenosine
    • -dig, BB, CCB (pt with normal cardiac function)
    • -ablation
  31. wandering atrial pacemaker
    • -P has different morphologies due to different foci
    • -HR is usually normal but can be slow or irregular
  32. frequent cause of wandering atrial pacemaker
    increased vagal stimulation of the SA node, this slows the rate of SA node depolarization and gives an opportunity for ectopic PM to kick in
  33. is wandering atrial pacemaker clinically significant?
    • No, it's common in young healthy pts and athletes, especially with sleep.
    • No treatment required.
  34. Multifocal atrial tachycardia
    -what is it?
    -in what pts is it often seen in?
    • -wandering atrial PM with a rate > 100 bpm
    • -seen with severe COPD- the associated PH puts strain on the RV and RA
  35. Multifocal atrial tachycardia treatment
    • -vagal maneuvers
    • -adenosine
    • -BB, CCB, amio
    • -NOT cardioversion
  36. atrial flutter
    • -ectopic PM in atria with rate of 250-350 bpm
    • -sawtooth P waves are called F waves
    • -about half of the atrial impulses are conducted to the ventricles, usually in even ratios (2:1, 4:1)
    • -regular or irregular
  37. atrial flutter treatment- normal heart
    • -dilt or other CCB or BB
    • -IV heparin and r/o atrial clot with TEE
    • -then cardioversion within 24 hours followed by 4 weeks of anti-coagulation
  38. atrial flutter treatment- impaired heart
    • -dilt, amio, or dig
    • -cardioversion
  39. When can cardioversion be performed in relation to anti-coagulation and duration of abnormal rhythm?
    • -If abnormal rhythm is less than 48 hours in duration, then CV can be performed without initial anti-coagulation
    • -If abnormal rhythm duration is > 48 hours, then need to anti-coagulate for 3 weeks, then CV can be performed, pt must con't anti-coags for 4 weeks after
  40. class III anti-arrhythmic
    ex: amio
    • -blocks K+ channels and prolongs depolarization
    • -increases duration of AP
    • -increases duration of refractory period
    • -decreases excitability
  41. class II anti-arrhythmic
    ex: BB
    decreases rate of spontaneous phase 4 depolarization
  42. class IV anti-arrhythmic
    ex: CCB
    inhibits the slow Ca++ channels
  43. AFib
    • -atria fire at a faster rate > 350-400 bpm
    • -atria just quiver
    • -no P waves, called small F (fib) waves
    • -irregular
  44. controlled AF
    rate < 100 bpm
  45. What is the 2nd most common rhythm after NSR?
    AF
  46. AF causes
    • self-limiting:
    • -excess ETOH (holiday heart)
    • -stress
    • -drugs
    • chronic:
    • -valvular disease (especially MV)
    • -HTN, CAD, PE, hyperthyroid, common after cardiac surgery
  47. AF treatment
    same as Aflutter: rate control, rhythm conversion, anti-coagulation
  48. T or F, AF may not convert with any therapy so the treatment revolves around rate control and anti-coagulation?
    T
  49. Wolff-Parkinson White syndrome
    -what is it?
    -cause?
    • -prototypical pre-excitation syndrome
    • -due to a congenital malformation where strands of conducting myocardial tissue form between the atria and ventricles and form an accessory pathway called "bundle of kent"
  50. WPW defining characteristics on EKG
    • -QRS is distorted by a delta wave (slurred upstroke)
    • -short PR interval because conduction going thru accessory pathway is faster than thru AV node
    • -rate 60-100 bpm
  51. Why is AF so problematic in pts with WPW?
    • -pts with WPW have no greater incidence of AF 
    • -risk of RVR due to accessory pathway
  52. Treatment of AF in pts with WPW
    • std treatment: rate control, anti-coag, rhythm conversion
    • -CV and amio are recommended
    • -pts with normal heart can also get flecainide or procainamide
    • -adenosine, BB, and CCB are CLASS 3 (harmful) in pts with WPW
  53. 3 regions of the AVJ
    -which of these areas contain PM cells?
    • upper- atrial nodal, has PM cells
    • middle- nodal
    • lower- nodal His, has PM cells
  54. What does the AVJ do if the SA node fails or if its rate falls below a certain range?
    • -takes on role of secondary PM
    • -inherent rate of 40-60 bpm 
    • -rhythm originating here is a junctional rhythm (rate 40-60 bpm)
  55. In junctional rhythm, why can the P wave be inverted, in the QRS, or after the QRS?
    • -With the AV node as the heart's PM, the depolarization spreads backward (to the atria)  and forward (to the ventricles)
    • -P wave inverted due to retrograde conduciton
    • -P wave in QRS if atria and vent are depolarized simultaneously
    • -P wave after QRS if vent are depolarized before ventricles
  56. PJC
    • -like a PAC
    • -an early ectopic beat from the AVJ
    • -followed by non-compensatory pause usually
    • -P wave can be in QRS or after or inverted
    • -short PR interval of <0.1 sec
    • -normal P wave and QRS
    • -treat underlying cause
  57. PJC causes
    • -dig toxicity
    • -enhanced automaticity in the AVJ
    • -CAD
    • -HF
    • -valve disease
  58. accel junctional rhythm
    • -rate 60-100 bpm
    • -originates in AVJ
    • -only difference between accel junctional and junctional is the rate
  59. accel junctional rhythm treatment
    • -treat underlying cause
    • -treat low CO if present
  60. junctional tachycardia
    • -rate 100-180 bpm
    • -same P wave variances as in junctional rhythm
  61. common causes of junctional tachycardia
    dig toxicity and ACS
  62. junctional tachycardia treatment
    • -treat cause
    • -if cause unknown then vagal stim or adenosine
    • -preserved heart function: amio, BB, CCB
    • -impaired heart function: just amio
    • -NO CV!! (class 3)
  63. Is cardioversion indicated for automatic rhythms like ST, JT, multifocal AT? 
    No, they require treatment of the underlying problem.  They may be responsive to BB and CCB.  
  64. 1st degree AVB
    • -sinus impulse is normally conducted to the AV node but then is delayed longer than usual before being conducted to the ventricles
    • -PR > 0.2 secs
    • -PR interval is constant
    • -rhythm is regular
  65. Causes of 1st degree AVB
    • -drugs
    • -hyperkalemia
    • -acute rheumatic fever
    • -myocarditis
    • -MI (especially inferior)
    • -degeneration of conduction pathways from age
    • -idiopathic
    • -increased vagal tone
  66. Should we be concerned about 1st degree AVB?
    No, it's asymptomatic and requires no treatment, however it may progress to more serious types of AVB.  Causes should be looked for.
  67. Mobitz I (Wenkebach)
    • -failure of some sinus impulses to be transmitted to the ventricles
    • -each successive impulse has more difficulty passing thru the AV node until finally an impulse is not conducted
    • -PR interval widens, eventually a P wave appears that is not followed by a QRS
    • -irregular ventricular rhythm
    • -"group beating"
  68. How do you differentiate between a non conducted P wave (PAC) and Mobitz I?
    In Mobitz I the P-P intervals will remain constant

    With a non-conducted P wave the P wave will occur early and will have a different morphology
  69. What is the treatment for Mobitz I?
    Often asymptomatic unless rate becomes very slow.  If there is HD compromise due to bradycardia then atropine may help to improve conduction, TC pacing, catecholamines may also be used (dopamine).  
  70. Mobitz II
    • -failure of some sinus impulses to be transmitted to the ventricles
    • -there's more than 1 P wave before each QRS, finally 1 is conducted to the ventricles
    • -PR interval is constant
    • -conduction ratio can vary (2:1, 3:1)
    • -QRS width can vary
  71. In Mobitz II, what determines if the QRS complex is narrow or wide?
    • It depends on where the conduction disturbance is.  
    • -QRS is narrow if the disturbance is in the bundle of His
    • -QRS is wide if the disturbance is in the bundle branches
  72. Causes of Mobitz II
    • -anterior MI
    • -degeneration of the conduction system due to age
    • -acute myocarditis
    • -NOT a result of increased vagal tone or dig toxicity
  73. Which is more serious, Mobitz I or II?
    Mobitz II, as the conduction disturbance is lower in the conduction system, making it easier for it to progress to complete heart block or ventricular standstill with little or no warning
  74. Mobitz II treatment
    • -TV or TC pacing  
    • -atropine should be used cautiously
    • -dopamine or epi may be indicated if significant hypotension develops 
    • -possible permanent pacer
  75. Why should atropine be used cautiously in Mobitz II?
    It will increase firing of the SA node but will not improve conduction thru the AV node.  It may cause paradoxical slowing of the ventricular rate
  76. 3rd degree heart block
    • -AV dissociation
    • -no conduction btw atria and ventricles
    • -atria paced at usual rate of 60-100 bpm
    • -ventricles paced by AVJ escape PM at 40-60 bpm or by the ventricles themselves at 30-40 bpm 
    • -PR interval varies
    • -QRS width depends on location of anatomic block
  77. Causes of 3rd degree heart block
    temporary or reversible usually has narrow QRS and is due to: inferior MI, ischemic heart disease, increased vagal tone, drugs (dig, BB, CCB, amio), hyperkalemia, acute rheumatic fever, myocarditus

    chronic CHB usually has wide QRS and is due to: acute AMI, degeneration of the conduction system (in the elderly); NOT due to increased vagal tone or drug toxicity
  78. What is syncope associated with complete heart block called?
    stokes-adams
  79. Symptoms associated with complete heart block
    • -elderly may be asymptomatic
    • -syncope (decreased CO due to slow rate and loss of atrial kick)
    • -chest pain
    • -hypotension
  80. Treatment of 3rd degree heart block
    • -TC pacer while awaiting TV wire
    • -permanent pacer
    • -atropine may work in narrow complex CHB but not in a wide complex 
    • -dopa or epi for significant hypotension
  81. bundle branch block
    • -ventricles are not depolarized simultaneously due to obstruction in LBB, RBB, or bundle of His
    • -QRS > 0.12 sec
  82. Can BBB be diagnosed from a rhythm strip?
    Yes, but you need a 12 lead EKG to differentiate between L and R BBB
  83. RBBB causes
    • -heart disease (CAD, HTN, cardiomyopathy, acute anteroseptal MI)
    • -congenital
    • -chronic degeneration
    • -may be rate related
    • -may be temporary or permanent
  84. LBBB causes
    • -usually due to heart disease (similar causes as with RBBB)
    • -can be temporary or permanent
  85. BBB treatment
    • -A BBB alone does not require treatment.  
    • -Pacing may be indicated if it develops 2/2 an MI
  86. PVCs
    • -premature ectopic impulse originating in the ventricle
    • -unlike a PJC it doesn't travel thru normal conduction pathways but rather thru the ventricle muscles and hence they are depolarized sequentially causing a wide QRS
    • -QRS differs in appearance from normal QRS
  87. Do PVCs have compensatory pauses?
    Yes, so measuring from the QRS prior to the PVC to the QRS after the PVC = the sum of 2 R-R intervals of the underlying rhythm.  This is b/c the SA node is not depolarized by the PVC and so the normal rhythm resumes on time.  
  88. Interpolated PVC
    PVC sandwiched inbetween 2 regularly occurring SR beats without disturbing the regularity of the underlying rhythm.  A compensatory pause does NOT occur.  
  89. R on T
    PVC occurs during vulnerable period of ventricular repolarization, so on or near the peak of the T wave.  Stimulation of the ventricles at this time can precipitate VT or VF.  
  90. Are PVCs more common in the young or the old?
    They get more common as we age.  
  91. PVC causes
    • -enhanced automaticity
    • -ETOH, caffeine, nicotine
    • -cardiomyopathy
    • -electrolyte imbalances (decreased K and Mg)
    • -ischemia or infarction
    • -increased catecholamines
  92. PVC treatment
    treat the underlying cause
  93. ventricular escape beat
    • PVC that occurs late 
    • -occur due to increased vagal tone on the SA node not due to increased automaticity
    • -protective mechanism after a pause in the normal rhythm
    • -no treatment needed
  94. VT
    • -originates in an ectopic focus in the ventricle
    • -wide QRS
    • -no atrial activity
    • -rate 140-250 bpm
    • -monomorphic or polymorphic 
  95. Is the sinus node still firing in VT?
    Yes, but the P waves are hidden in the QRS
  96. Treatment of stable pt with VT and a pulse
    • any of the following:
    • 1) amio bolus and infusion
    • 2) lido bolus and infusion
    • 3) procainamide infusion

    if unresponsive to drugs CV starting at 100 J and increasing with subsequent attempts
  97. Amiodarone adverse effects
    hypotension, bradycardia, prolonged QT
  98. S/sx lido toxicity
    slurred speech, bradycardia, muscle twitching, seizure, altered LOC
  99. Procainamide adverse effects
    hypotension and prolonged QT
  100. Ventricular flutter
    • -a form of VT where the ventricular rate is so fast that the QRS has a sawtooth appearance
    • -there's no CO so hemodynamics become compromised quickly
  101. torsades
    • -a form of polymorphic VT
    • -direction of QRS complex rotates
    • -"twisting of the points"
    • -ventricular rate is faster than in monomorphic VT so HD instability occurs quickly
  102. torsades causes
    • -prolonged QT due to 5HT-3 blockers, phenathiazines, quinidine, tricyclics, procainamide, amio)
    • -electrolyte disturbances (decreased K, Mg, or Ca)
    • -bradycardia
    • -liquid protein diet
  103. torsades treatment
    • -meds used to treat monomorphic VT can cause torsades
    • -treat underlying causes
    • -Mg
    • -overdrive pacing
    • -CV but torsades will likely recur if precipitating factors are not corrected
    • -isopril (pharm overdrive pacing)
    • -lido or phenytoin in select cases
  104. VF
    • -ventricles just quiver
    • -haphazard depolarization of the ventricles
    • -no P or QRS
  105. coarse vs fine VF
    • coarse- large waves
    • fine- small waves
  106. which is more likely to be reversed: coarse or fine VF?
    Coarse.  Fine VF is the most common cause of sudden cardiac death in pts after an acute MI
  107. VF treatment
    • CPR
    • defib at 200J- 300J- 360J
    • vasopressin
    • amio
    • lido (indeterminate class)
  108. ventricular standstill
    • -AKA asystole
    • -absence of all electrical activity in the ventricles
    • -may get just P waves (due to advanced AV block preceding)
  109. Ventricular standstill causes
    acidosis, hypoxia, hyperkalemia, hypothermia, drug OD
  110. Ventricular standstill treatment
    • -treat underlying cause
    • -CPR
    • -epi, TC pacing, and atropine may be tried
  111. Pacemaker indications
    • -SA or AV node dysfunction
    • -chronic bifascicular block
    • -post MI
    • -arrhythmia avoidance
    • -hypersensitive carotid sinus syndrome
  112. AICD indications
    • -VT or VF
    • -low EF (<35%)
    • -cardiomyopathy
    • -long QT
  113. How does a pacemaker work
    • -Lithium battery generates an impulse, goes from the battery to the wires and leads, stimulates the endocardial cells, and creates a wave a depolarization in myocardium.
    • -Circuitry senses spontaneous electrical activity in the heart.
  114. Pacemaker nomenclature
    • 1st letter- chamber paced
    • 2nd- chamber sensed
    • 3rd- response of the pacer to sensed signal (inhibit, trigger, or dual)
    • 4th- adaptive abilities (can vary with metabolic needs)
    • 5th- anti-tachycardia capabilities
  115. Why is there a wide QRS with a ventricular paced rhythm?
    The ventricles are not depolarized simultaneously.  Usually the RV is depolarized before the LV.  
  116. fusion beat
    • pacer fires at same time as normal electrical impulse, both impulses reach ventricle at
    • same time and a fusion beat is the result, thus QRS has characteristics of paced and
    • native beat
  117. loss of capture
    • -heart does not respond to pacer stimulus
    • -see a pacer spike with no P wave or QRS
  118. loss of capture causes
    • -tip of electrode is not in contact with endocardium 
    • -tip is in an area of infarct 
    • -inadequate electrical current
  119. threshold
    minimum amt of current required to stimulate the heart
  120. undersensing
    • -pacer does not sense native beats
    • -EKG shows a pacer spike that occurs earlier than it should 
  121. undersensing causes
    • -tip of electrode not in contact with endocardium
    • -sensitivity set too low
    • -PM in asynchronous mode meaning sensing is turned off
  122. What devices in the OR could cause issues with a PM or AICD?
    • -unipolar caudery
    • -RF ablation
    • -MRI
    • -lithotripsy
    • -radiation therapy
  123. CIED
    CV implantable electronic device
  124. How do we manage a pt intraop with a CIED?
    • -operative team and CIED team collaborate to determine best plan of action for the pt
    • -we need to tell the CEID team about the procedure type and anatomic location, type of cautery to be used, where we'd likely place the bovie pad, and exact location where the surgeon will be using the mono polar unit
  125. is bipolar or mono polar cautery more likely to cause issues with CEIDs?
    Monopolar as the current flows thru the pt's body to a bovie pad.

    Bipolar causes no electromagnetic interference unless it's placed directly on the device
  126. What effects can monopolar cautery have on a CEID?
    • -device inhibition
    • -reset of pulse generation
  127. What precautions can we take to minimize effects from the monopolar cautery on CEIDs?
    • -maintain a distance btw current path of bovie and
    • pulse generator of > 6 inches
    • -place bovie below umbilicus
    • -minimize length of use of cautery to 5
    • sec or less

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