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2013-07-14 16:35:24
BC CRNA Cardio Arrhythmias

Online lecture summer 2013
Show Answers:

  1. What is the rate of the atria?
  2. What is the rate of the AV junction?
  3. What is the rate of the ventricles?
  4. What is the normal PR interval?
  5. What is the normal QRS?
  6. What is the normal QT interval?
    • -QT interval will vary with HR so there is a formula called the Bazett's formula to correct QT.
    • -The correct QT is the QT is measured and divided by the sq root of the RR interval
    • Generally the QT should be less than ½ of the preceding RR when the HR is in the range of 65-90.
    • -Corrected QT = QTc =(QT /√R-R interval)
    • -It can also vary in different leads, use 12 lead EKG. Use the longest calculated as the official QT interval
  7. What is the rate for NSR?
  8. What is the rate for S. Brady?
  9. What is the rate for S.Tach
  10. What is the rate for Atrial Tachycardia?
  11. What is the rate for A. Flutter?
  12. What is the rate for A. Fib?
  13. How do figure out the rate from a rhythm strip?
    Basically if you can find an R wave that falls directly on a think black line of the EKG consider that you’re starting point, the next black line is 300 and then 150, 100, 75, 60, 50 until you get to the next R wave, this provides at least an approximation of the rate.
  14. What is overdrive suppression?
    • Overdrive suppression is characteristic of the conduction system.
    • That means any automaticity center will overdrive (suppress) all of the others with a slower intrinsic rate so the higher rate will always win.
    • (SA node rate of 60-100 will win over Ventricular node rate of 20-40)
  15. Describe the six basic steps in interpreting a rhythm
    • 1. Regular or not?
    • 2. Atrial rate
    • 3. Ventricular rate
    • 4. P wave morphology
    • 5. PR interval (Duration, Fixed or variable?)
    • 6. QRS morphology
  16. The QT interval is important. What could cause a prolonged QT?
    • Associated with CHF, ischemic heart disease, prinzmetal angina, rheumatic fever, Cerebral vascular disease, subarachnoid hemmorhage, hypocalcemia, hypothermia, mitral valve prolapse and a number of drugs.
    • Drugs include: procainamide, Quinidine, Amiodorone, and the 5HT3 antagnonists.
  17. How can a prolonged QT effect the rhythm?
    Prolonged QT is associated with delayed repolarization and re-entrant arrhythmias and the subsequent development of torsades.
  18. What does the size of the QRS (narrow vs. wide) tell us?
    • Narrow QRS, origin of the complex is supraventricular.
    • If there is a wide QRS, meaning greater than 0.10 or 0.12 seconds, it originated in the ventricle or above the ventricle with some sort of aberrantly conducted supraventricular impulse.
  19. What does an inverted P wave mean?
    The impulse originated in the AV node instead of the SA node
  20. Why do we look for a consistent relationship between the P wave and the QRS? (Regular PR interval)
    • Ensures the P wave depolarization is responsible for QRS complex (depolarization of the ventricle)
    • 1:1 conduction can be assumed if the PR interval is fixed
  21. Describe NSR (Rhythm, rate, P, PR, and QRS)
    • Rhythm: Regular
    • Rate: 60-100
    • P: normal
    • PR: normal
    • QRS: normal
  22. Describe S. Brady (Rhythm, rate, P, PR, and QRS)
    • Rhythm: Regular
    • Rate: 40-60
    • P: Normal
    • PR: Normal
    • QRS: Normal
  23. Describe S. Tach (Rhythm, rate, P, PR, and QRS)
    • Rhythm: Regular
    • Rate: 100-180
    • P: Normal
    • PR: Normal
    • QRS: Normal
    • Very common. The intervals are normal and the QRS complex is normal and follows the P wave
  24. Describe S. Arrhythmia (Rhythm, rate, P, PR, and QRS)
    • Rhythm: Irregular
    • Rate: 60-100 or <60
    • P: Normal
    • PR: Normal
    • QRS: Normal
  25. Describe S. Block (Rhythm, rate, P, PR, and QRS)
    • Rhythm: Basic rhythm, usually regular
    • Rate: 60-100 or <60
    • P: Sinus Ps, basic rhythm
    • PR: normal w/basic rhythm
    • QRS: Normal w/basic rhythm
  26. Describe Sinus Arrest (Rhythm, rate, P, PR, and QRS)
    • Rhythm: Basic rhythm, usually regular
    • Rate: 60-100 or <60
    • P: Sinus Ps with basic rhythm
    • PR: normal w/basic rhythm
    • QRS: normal w/basic rhythm
  27. What are some common etiologies for S. Tach? What is the treatment?
    fever, exercise, hypovolemia, SNS stimulation, & hyperthyroidism

    Tx: dependent on the cause
  28. S. Arrhythmia is a normal phenomenon thought to be caused by ________.
    What is it associated with?
    • variations in tone in the ANS.
    • Commonly associated w/phases of respiration. HR tends to increase gradually w/inspiration and decrease gradually w/expiration.
  29. In what population is S. Arrhythmia common? Do you need to treat it?
    • It’s very common to be found in kids & young adults.
    • Geriatric pt it is unrelated to phases of respiration and may be a precursor to sick sinus syndrome.
    • No tx required unless HD compromise
  30. What is Sinus pause or Sinus arrest?
    What are the two types?
    • there a sudden failure of the SA node to initiate or conduct an impulse
    • 2 types: sinus arrest and sinus exit block. Although they are different (pathophysiologies differ), they are really hard to distinguish and the significance and tx is the same.
    • Both originate in SA node and are characterized by a sudden pause in the sinus rhythm.
  31. Sinus arrest is a disorder of automaticity. What does this mean?
    • Sinus arrest is d/t a failure of SA node to initiate the impulse.
    • This then throws off the timing of the SA node so the underlying rhythm when it does resume, doesn’t do so on time after the pause.
  32. Sinus exit block is a conduction problem (instead of an automaticity problem like S. arrest). Describe this
    • The impulse is initiated by the sinus node but it’s then blocked so there is a block in the conduction through the atria.
    • With sinus exit block the underlying rhythm will resume on time because the SA node isn’t interrupted
  33. What can cause S. Pause or S. Arrest?
    Both of these can be caused by increased vagal tone, ischemia, or infarction and certain drugs like digoxin, BB, or Ca+ channel blockers.
  34. What is a premature atrial contraction?
    • Early beat from some ectopic site in the atria. It interrupts the normal rhythm (usually sinus) and it discharges before the next sinus beat is due.
    • May be a single ectopic focus or multiple foci and the shape of the P wave depends on where the ectopic focus is in the atria.
    • If near the AV junction, the P wave may inverted.
  35. What are the key features of a premature atrial contraction?
    • An underlying rhythm that’s usually regular, only becomes irregular with premature beats.
    • The P wave of the PAC is both premature and abnormal in terms of it’s morphology, it’s size, shape, and direction.
    • Commonly appears small, upright and pointed but it may be inverted.
    • Occasionally the abnormal P wave can be hidden in the prior T wave and this will distort the T wave.
    • PR interval is usually normal but can be prolonged. Naturally if the P wave is hidden in the T wave then it’s not really measurable.
    • Although the QRS is premature, the duration is normal. The QT is normal (~0.10 sec).
  36. Pause associated w/PAC is usually not _____
    • compensatory
    • Meaning that the measurement from the R wave of the complex before the PAC to the R wave of the complex after the PAC is less than the sum of two R –R intervals of the underlying rhythm.
    • This is because premature depolarization of the atria by the PAC results in subsequent premature depolarization of the SA Node causing the SA node to reset itself a little earlier than expected
  37. Occasionally the PAC will occur w/a compensatory pause, what does this mean?
    • is equal to the sum of two R-R intervals (but this is usually seen w/a PVC)
    • With a compensatory pause the SA node isn’t depolarized by the PAC and it’s timing isn’t reset.
    • Underlying rhythm appears expected after the pause.
    • Rarely the PAC can occur w/a pause that is longer than compensatory.
  38. What is a PAC with Aberrant conduction?
    • Usually w/ PAC the QRS complex resembles the normal QRS and there is normal duration (~0.10 seconds) but if the PAC occurs very early then the impulse can reach the bundle branches before repolarization is complete.
    • The R BB is usually slower to repolarize than the L. Consequently the L BB and LV are depolarized before the R BB and the RV in a sequential depolarization.
    • Because of this delayed conduction the QRS appears wide and measures 0.12 sec or more. So PACs with this wide QRS complex are called aberrantly conducted PACs because the conduction through the ventricles is abnormal. Can appear like PVCs and it’s impt to distinguish between the two.
  39. The importance with ANY rhythm assessment
    is ..........
    whether it’s HD significant!
  40. When does a non-conducted PAC occur?
    • Results when an ectopic atrial focus occurs so early that the AV node is still refractory so the impulse isn’t conducted to the ventricles.
    • With this there is premature P wave but there is no associated QRS complex. The P wave is abnormal in size, shape, or direction.
  41. The non-conducted PAC is the most common cause of ___________________________
    • unexpected pauses in irregular sinus rhythm
    • The difference between this and a sinus arrest or a sinus block is that a non-conducted PAC will still show a P wave but the P wave can be hidden (look for it in the T wave of the prior beat)
  42. What is the cause and tx for PACs?
    • Causes of PACs: stress, caffeine, nicotine, and alcohol.
    • The TX is the same for all PACs, eliminate the cause.
  43. What is paroxymal Atrial Tachycardia (aka paroxymal supraventricular tachycardia)
    • ectopic pacemaker in the atria produces a rapid regular atrial rhythm with a rate
    • between about 150-250bpm. 
    • Paroxysmal because it often happens in bursts. Commonly will start with a PAC.
    • P waves associated with this atrial tachycardia are normal and often difficult to see because buried in preceding T wave. The T and the P essentially appear as a single deflection and are then sometimes referred to as the T P wave.
    • Unless AV Block is also present each P wave is followed by a QRS.
    • The PR interval is often not measureable (P wave buried in T) QRS complex itself is normal
  44. Paroxymal Atrial Tachycardia can occur in pts w/healthy hearts as well as those w/ disease. What are the triggers?
    • Same triggers as those w/PACs hold true here as well (Stress, caffeine, alcohol, nicotine)
    • Other causes: COPD and digoxin toxicity.
    • Patients may experience palpitations which may cause further anxiety and stress
  45. What can be a problem during Paroxymal Atrial Tachycardia?
    • ventricular filling during diastole is impaired if the rate is fast enough so CO decreases.
    • Fast rate will also increase myocardial Oxygen consumption.
  46. Treatment of paroxymal atrial tachycardia is aimed at rate control and rhythm conversion. How do you treat the stable patient?
    • Sedation can be tried (help w/associated anxiety)
    • Vagal maneuvers (carotid sinus massage and the valsalva maneuver).
    • If these fail then Adenosine 6mg. Followed in 2 min by 12mg (can be repeated 1x if not effected)
  47. Treatment of paroyxmal atrial tachycardia is aimed at rate control and rhythm conversion. If the patient is unstable, how do you treat it?
    cardioversion is the 1st line
  48. Your stable patient is in paroxymal atrial tachycardia and did not respond to vagal maneuvers or Adenosine. What do you try next?
    • Pt w/normal cardiac func can be tx w/Ca+ channel blocker, BB, or Digoxin. All increase block at AV node slowing the ventricular rate and often terminating the rhythm.
    • Cardioversion comes next w/the stable patient.
  49. When would you treat paroyxmal atrial tachycardia with Amiodarone or Procainamide?
    Antiarrhythmic like Amiodarone or Procainamide should be considered only when an AV block or a cardioversion fails
  50. Your patient with LV dysunction is in paroxymal atrial tachycardia. Can you use BB or CCB?
    • No, they are avoided d/t negative inotropic effects
    • The exception here is Diltializam. It exhibits less depression of contractility.
    • Digoxin can also be used but the onset is slower, as we know.
    • Best to avoid combining all the possibilities (BB, Ca+ channel blocker, and anti arrhythmics) because of the additive hypotensive bradycardia and pro arrhythmic effects of these drugs in combination
  51. What do you do for paroyxmal atrial tachycardia that is refractory and unresponsive to drug therapy?
    Radio frequency ablation of ectopic focus or re-entry circuit may be necessary for refractory PAT that is unresponsive to drug therapy
  52. What is wandering atrial pacemaker?
    • Occurs when pacemaker site shifts back and forth between the Sinus node, other atrial sites, and sometimes the AV node.
    • P waves change in shape this happens and this rhythm is thought to be the result of multiple pacemaker sites competing with each other for control over the heart.
    • Necessary to identify 3 different P wave morphologies in order to call it wandering Atrial Pacemaker.
    • HR is usually normal, can be slow. The rhythm can be regular or irregular.
    • The PR interval may depend on the pacemaker site and the QRS is normal in duration
  53. What causes wandering atrial pacemaker?
    • In most cases it’s caused by increased vagal stimulation on the SA node.
    • This slows the rate of SA node depolarization and provides an opportunity for an ectopic pacemaker to kick in.
    • Normal in young healthy hearts, esp. in athletes, and during sleep
  54. How do you treat wandering atrial pacemaker?
    • It isn’t usually clinically significant and tx isn’t indicated.
    • Having pt cough may decrease vagal tone and encourage sinus rhythm.
  55. What is multifocal atrial tachycardia?
    • wandering pacemaker with a rate greater than 100.
    • Most commonly seen in patients w/severe COPD because assocaited pulmonary HTN puts a strain on the RV and the RA.
    • Tx for multifocal atrial tachycardia includes vagal maneuvers and adenosine followed by betablockade followed by Ca+ channel blockers and amiodarone.
    • Cardioversion isn’t utlized for this.
  56. What is A. Flutter?
    • Begins in an ectopic pacemaker in atria that typically fires at a rate of between 250-350 or 400 bpm.
    • Produces saw tooth wave form called flutter waves (F waves)
    • There is essentially no isoelectric line between the flutter waves.
    • T wave is partially or completely obscured by the flutter waves.
    • QRS is usually narrow as long as conduction through the ventricle is normal.
  57. What gives the saw tooth appearance of A. Flutter?
    Typically atrial flutter wave consists of an initial negative component followed by a positive component so results in sort of a v shape wave. Giving the classic saw tooth appearance.
  58. In A flutter the AV node is bombarded by these rapid atrial impulses but will only conduct some of them. At least____ of them are blocked to protect the ventricles from excessive rates.
    • 1/2
    • Typically the AV node conducts impulses in specific ratios (like 2:1 or 4:1).
    • Even ratios are more common than odd ratios.
    • If the ratio is constant the rhythm is regular. But it becomes irregular if the ratio varies. The ventricular rate then would be different from the atrial rate
  59. How do you treat A. Flutter?
    • Directed at rate control and rhythm conversion.
    • For the patient with a normal heart the rate can be blocked w/Diltiazem or another Ca+ channel blocker or a betablocker
  60. How do you tx A. Flutter in the impaired heart?
    Digoxin or Diltiazem or amiodarone

    (Amio is class III antiarrthymic that blocks the K+ channels and prolongs depolarization so it increases the duration of A.P. also increases the duration of the refractory period and decreases the excitability.)
  61. When can you cardiovert A. Flutter without initial anticoagulation?
    • Can only be done without initial cogaulation, if the rhythm is 48hrs or less in duration.
    • If the duration of A flutter is more than 48hrs the patient must be first anticoagulated for 3 weeks, only then can cardioversion be accomplished.
    • Pt has to continue anticoagulation for another 4 weeks following cardioversion.
    • Also an option in pt w/normal heart to give IV Heparin and perform a TEE to R/O an atrial clot. DC cardioversion can then be done within 24hrs again followed up with anticoagulation for 4 weeks
  62. What is A. Fib?
    • Occurs when the ectopic pacemaker now fires at a greater rate (more than 350-400bpm)
    • Atria quivers rather than contracts so the resulting wave is called fibriltory wave (f wave).
    • These may appear either course or fine and the fine waves might be so small that the line appears flat between the QRS complexes.
    • The QRS is usually normal because the conduction through the ventricles is usually normal.
    • AV node is gate keeper and blocks most of the impulses to protect the ventricles.Ventricular rate is typically grossly irregular or irregular. As there is no fixed ratio of conduction through the AV node.
  63. When is A fib considered controlled?
    A fib is regarded as controlled Afib if the ventricular rate is less than 100.
  64. _______ is the most common rhythm, second only to NSR
    A fib
  65. What patient population gets A. fib?
    • Normal individuals as well as people with heart disease.
    • Normal people: usually temporary and may be associated with emotional distress, excessive alcohol consumption (holiday heart syndrome) In this case it will usually revert to NSR or it’s easily converted w/drugs alone.
    • In other patients may be chronic and can persist indefinitely
  66. What causes chronic A. fib?
    Chronic A. Fib is common in valvular disease, particularly Mitral disease. Also associated w/HTN, CAD, Pulmonary emboli, and hyperthyroidism. It’s very common after heart surgery
  67. What are the clinical consequences of A. fib? (Similar to those of A. flutter)
    • Increase in HR will influence oxygen demand and CO.
    • Because the atria don’t contract, atrial kick is lost this further decreases CO.
    • Patient w/cardiac disease and particularly the elderly are dependent on atrial kick for ventricular filling.
    • The quivering atria are also prone to clot formation from the pooling of blood. As we know theses clots can dislodge into the pulmonary circulation, and cause pulmonary emboli or they can enter systemic circulation and cause a CVA, an MI or an occlusion of circulation to some other vital organ
  68. How do you tx A. fib?
    • Rate control, anticoagulation, and rhythm conversion.
    • Protocols are the same as those w/A. Flutter.
    • The HD unstable patient needs to be cardioverted immediately regardless of the duration of the arrhythmia. Pt w/chronic A. Fib may not convert w/any therapy so treatment revolves around rate control and anticoagulation.
  69. What causes Wolff-Parkinson-White Syndrome?
    congenital malformation where strands of conducting myocardial tissue forms between the atria and the ventricles. When this persists after birth the strands can form an accessory pathway called the bundle of kent.
  70. What are the defining characteristics on the EKG in WPW?
    • QRS complex is distorted by a delta wave. Means the upward deflection of the QRS complex is slurred.
    • The rate is usually between 60-100 and the rhythm is usually sinus except during pre-excitation tachycardia.
    • The PR interval is shorter since conduction going through the accessory pathway is faster than that going through the AV node. P waves appear normal and the QRS has the classic distortion.
  71. The patient w/ WPW may not ever have clinical s/s. Pt also have same annual incidence of atrial fibrillation as age and gender match populations. So what is the concern/problem?
    • onset of Afib poses the risk of rapid ventricular response by the accessory pathways.
    • Consequently the rapid ventricular response leads to all the s/s of stable and unstable tachycardias
  72. How do you tx the patient w/WPW in A fib?
    • Begins w/patient assessment in terms of CV stability and knowing how long the A fib has been present.
    • Focus is on controlling the rate and the rhythm along with anticoagulation.
    • For both normal and impaired heart, cardioversion and amiodarone is recommended for rate control.
    • Pt w/normal heart can receive flecanide or procainamide for rate control.
    • In order to convert the rhythm the patient w/the normal heart may benefit from amiodorone or a cardioversion if the duration is less than 48hrs. (Same issue w/coag apply)
  73. Can you use adenosine in a patient w/WPW?
    • NO!!!!
    • Adenosine, BB, Ca+ channel blockers, and Digoxin are class 3 meaning they can be harmful in treating Atrial fib. in patients with WPW syndrome
  74. What is junctional rhythm?
    • AV junctional rhythms originate in the AV junction.
    • Inherit firing of the junctional pacemaker cells the rate is 40-60bpm, so a rhythm originating in this area at this rate is called a junctional rhythm.
    • Junctional rhythm is the NORMAL response of the AV junction is the sinus rhythm falls below the AV junctional rate or if the sinus impulse fails to reach the AV junction.
  75. AV junction itself consists of the AV node as well as the HIS bundle. Area includes what THREE regions? (talked about during junctional rhythm part of lecture)
    • Atrial nodal upper junction
    • the nodal middle junction
    • the nodal HIS or lower junction.
  76. What area of the AV junction contains pacemaker cells.
    Upper and the lower regions contain pacemaker cells which can spontaneously generate the impulses and take on the role of the secondary pacemaker site if the sinus node fails or if it slows below it’s normal range
  77. What does the middle area of the AV junction do?
    Middle junctional areas slows impulses going from the atria to the ventricles.This region itself doesn’t contain pacemakers cells.
  78. If the junctional rhythm is 45bpm, is it junctional bradycardia?
    No, it's junctional rhythm if the rate is between 40-60.
  79. Other arrhythmias originating in the junction include:
    • premature junctional contractions
    • accelerated junctional rhythm
    • Junctional tachycardia
    • Junctional bradycardia

    Electrophysiological mechanisms thought to be responsible for the junctional arrhythmias are altered automaticity, triggered activity, or a re-entry circuit
  80. (Junctional) When the AV node is functioning as the pacemaker of the heart the electrical impulse produces a wave of depolarization that’s backward (retrograde) into the atria as well as antegrade into the ventricles. The location of the P wave relative to the QRS complex depends on....
    • the speed of the antegrade and retrograde conduction.
    • If the electrical impulse from the AV junction depolarizes the atria first and then depolarizes the ventricle, the p wave will be in front on the QRS.
    • If the electrical impulse from the AV junction depolarizes the ventricles first and then depolarizes the atria, the p wave will be after the QRS.
    • If the electrical impulse from the AV junction depolarizes both atria and ventricle simultaneously the P wave will be hidden by the QRS.
  81. ________ stimulation of the atria is just opposite to the direction of atrial depolarization when NSR is present and produces negative P waves rather than upright in lead II
    Retrograde (seen in Junctional rhythm)
  82. What is a premature junctional contraction?
    • Like PAC (early beat) but now it originates in ectopic pacemaker in the AV junction.
    • It has an abnormal P wave and a normal QRS and is usually followed by a non-compensatory pause.
    • Because atrial depolarization occurs in a retrograde fashion the p wave will be negative or inverted in Lead II and will occur immediately before or after the QRS complex or will be hidden in the QRS
    • PR interval will be short (0.10 seconds or less)
    •  (PACs the PR is not short!)
  83. Which is more common, PACs or PJCs?
  84. Causes of Premature Junctional Contractions
    • digoxin toxicity, enhanced automaticity of the AV junction, CAD, HF and valvular disease.
    • Can occur without a definable cause.
    • Tx usually not required
  85. Occasionally a premature junctional contraction occurs late rather than early and if it occurs late, this is called a ________________
    • junctional escape beat
    • More likely to occur d/t increased vagal effect on the SA node rather than d/t enhanced automaticity. Junctional escape beats are common after a pause in the underlying rhythm (they are protective to maintain the HR)
    • No tx is necessary, important to ID underlying cause and tx that.
  86. What is accelerated junctional rhythm
    • Originates in AV junction and has a rate of 60-100 bpm.
    • The accelerated means it exceeds the normal rate of the junction (which is 40-60) but not fast enough to be junctional tachycardia.
    • Retrograde atrial stimulation cause the P waves to be inverted in Lead II.
    • Can come before or after QRS or be buried within it.
    • The PR interval is short and QRS is normal
  87. Only difference between junctional rhythm and junctional tachycardia is _______
    the rate
  88. What can cause acclerated junctional rhythm?
    • enhanced automaticity from digoxin toxicity
    • can be from damage to AV node from inferior myocardial infarction.
    • HF, acute rheumatic fever, myocarditis, valvular heart disease, and following cardiac surgery particularly valvular surgery
  89. What happens to CO in junctional rhythm?
    loss of atrial kick can cause a decrease in CO
  90. How do you treat junctional rhythm?
    aim at underlying cause and tx for low CO if that’s present
  91. What is junctional tachycardia?
    • Narrow complex tachycardia.
    • The rate is 100-180bpm.
    • PR interval not measurable unless the P wave comes before the QRS. P wave can appear in any location (before, after, or in QRS)
  92. What are common causes of junctional tachycardia?
    • Digoxin toxicity
    • acute coronary syndromes
  93. How do you treat junctional tachycardia?
    • Therapy that’s recommended if dx is unknown is vagal stimulation or adenosine.
    • And then followed by tx w/BB, Ca+ channel blockers and amio in the patient w/reserved heart function.
    • If Heart function is impaired. Amio is tx. In any case cardioversion should be done.
  94. What types of rhythms don't respond to cardioversion?
    • Automatic rhythms.
    • Multifocal or ectopic atrial tachycardia, Sinus tachycardia, junction tachycardia junctional tachycardia don’t respond to cardioversion often require tx of underlying problem although they may be responsive to both Ca+ channel blocker and Betablockers.
  95. Synchronized cardioversion is not effective for tx of _____________________ and shouldn’t be used again to what’s considered to be class 3 (unacceptable no documented benefit and they may be harmful
    supraventricular arrhythmias
  96. What is first degree AV block?
    • Is when the sinus impulses normally conducted to the AV node but then it’s delayed longer than usual before being conducted to the ventricles.
    • This is results in a prolonged PR interval greater than 0.2 seconds.
    • But we do see a regular rhythm on EKG. One P wave is followed by a QRS but the PR interval although consistent in duration is long
  97. What are causes of 1st degree AV block?
    • Anatomically this disorder is located at the level of the AV node and it’s really not a serious form of HB.
    • May be d/t to drug therapy like digoxin, BB, CCB, Amio.
    • May also be d/t increased vagal tone, hyperkalemia, acute rheumatic fever or myocarditis.
    • It could be d/t an MI particularly an inferior MI.
    • Degeneration of the conducting pathways from age or some sort of idiopathic cause
  98. How do you treat 1st degree AV block?
    • No symptoms and needs no tx.
    • Should be monitored because it can progress to higher levels of block.
    • Meds should be reviewed and causes looked for.
    • Meds changed if indicated
  99. What is 2nd degree AV block? (Mobitz Type 1  or Wenckebach)
    • Characterized by some of the sinus impulses to be conducted to the ventricles.
    • So the sinus impulse is normally conducted to the AV node but each successive impulse has more and more difficulty passing through the AV node until finally an impulse doesn’t pass through and isn't conducted.
    • P waves that occur at regular intervals and PR intervals that progressively lengthen from beat to beat until a p wave appears that is not followed by a QRS.
    • Results in irregular ventricular rhythm but normal narrow QRS.
    • After each dropped beat the cycle repeats itself. The grouping of beats separated by pauses is a distinguishing characteristic of Mobitz 1.
  100. 2nd degree AV block (Mobitz Type 1) can be confused w/non conducted PACs. Why and how do you differentiate between them?
    • Both rhythms have p waves that aren’t followed by a QRS (followed by a pause).
    • To differentiate between the two, you need to look at the configuration of the P waves and measure the P wave irregularity.
    • The non-conducted PAC will have an abnormal P wave and will occur prematurely. In mobitz type 1, the P wave configuration remains the same as the sinus beats and the P wave occurs on schedule, not early
  101. What are the causes of 2nd degree AV block (Mobitz Type 1)
    • Mobitz Type 1 is common after an acute MI but is usually temporary and resolves spontaneously.
    • Other causes: drugs (Dig, BB, CCB, or Amio), increased vagal tone, hyperkalemia, acute rheumatic fever, and myocarditis.
    • Can also be seen as a normal variant for athletes at rest because they tend to have a physiologic increase in vagal tone.
  102. How do you treat 2nd degree AV block (Mobitz Type 1)?
    • Rarely a serious form of heart block but it can progress to higher of HB.
    • Pt are usually symptomatic unless the ventricular rate is slow.
    • If HD status is compromise, d/t bradycardia, atropine may help to improve conduction.
    • If it becomes really problematic, transcutaneous pacing may also be helpful, and if severe consider the catecholamines, Dopa, Epi or Isuprel.
  103. What is second degree AV block Mobitz Type II?
    • There is the failure of the sinus impulses to be conducted to the ventricles but here there is more than 1 P wave before each QRS. (2, 3 or more) with only one impulse being conducted to the ventricles.
    • P waves are identical and occur irregularly. The PR interval of the conducted beats may be normal or prolonged but they are constant.
    • The ventricular rhythm is usually regular unless the AV conduction varies, alternating like 2:1, 3:1, 4:1 and so on.
    • The location of the conducting disturbance is below the AV node in the bundle of HIS and the bundle branches as a result the QRS complexes may be narrow if  it’s located in the bundle of HIS or wide if located in the bundle branches. (The most common location is the bundle branches)
  104. If there is 2:1 conduction it can be hard to tell if the 2nd degree AV block is Type 1 or Type 2. How can you tell which it is?
    • A 2:1 conduction can also occur w/Mobitz 1, can be difficult to determine if the block is Mobitz 1 or 2 if this occurs.
    • So if you’re examining a strip with  2:1 conduction and an AV block, consistent PR intervals and a narrow QRS, there are interpreted as Mobitz 2 but with a little notation that clinical correlation is necessary to make a definitive diagnosis
  105. What causes 2nd degree AV block Mobtiz Type II?
    • Mobitz 2 is commonly associated with an anterior wall MI.
    • Other causes include: acute myocarditis and degeneration of the conduction system (suually d/t age). It’s less common but more serious as the anatomic location is lower in the conduction system so it would be easier for this type of Mobitz (2) to progress to 3rd degree HB or ventricular stand still with little to no warning.

    *Unlike Mobitz 1, not the result of vagal tone or digoxin toxicity.*
  106. How do you treat Mobitz Type II?
    • Mobitz type II is anatomically lower in the conduction system and could progress into 3rd degree HB so a temporary transvenous or transcutaneous pacemaker is indicated.
    • Atropine should be used with great caution, if at all, because with atropine it will increase SA node discharge but it won’t improve conduction through the AV node. Acceleration of the SA node may result in paraoxymal slowing of the ventricular rate.
    • If there is significant hypotension, Dopamine or Epi is indicated and perm. Pacemaker may be necessary.
  107. What is 3rd degree AV Block (complete HB)?
    • Complete absence of conduction between the atria and the ventricles.
    • Atria and ventricles beat independently to each other and there is not relationship between the activities so AV dissociation. The atria are paced by the SA node (60-100) but the ventricles are either paced by the AV junction escape pacemaker (40-60) or at the ventricles (30-40 or less)
    • The P wave marched through the QRS and the PR intervals vary widely. The width of the QRS and the ventricular rate depends on the location of the anatomic block.
  108. What are the causes of 3rd Degree AV Block?
    • May be temporary or d/t specific causes.
    • Temporary, reversible, 3rd degree AV block is usually associated w/narrow QRS complexes and can result from inferior MI, ischemic heart disease, increased vagal tone, drug effects (digoxin, BB, CCB, and amio). Hyperkalemia, acute rheumatic fever, or myocarditis.
    • Chronic or permanent is usually associated with a wide QRS complex, and can be d/t an acute anterior MI or chronic degeneration in the conducting system as seen in the elderly. Chronic block is not due to either vagal tone or drug toxicity.
  109. Is 3rd degree AV block serious?
    • This is a serious and life threatening arrhythmia and progress to ventricular standstill with little to no warning.
    • S/s can range from a patient being asymptomatic, particularly in elderly patient with age degeneration, to hypotension, syncope or chest pain from decreased CO (secondary to the slow rate and loss of atrial kick).
    • The syncope that’s associated with this is called Stoke’s Adam’s attacks or Stoke’s syncope
  110. How do you treat 3rd degree AV block?
    • Transcutaneous pacing is indicated while the patient is being prepared for a transvenous wire.
    • Atropine may work in narrow QRs complex complete HB but has little to no effect for the wide QRS  complex CHB at the BB level.
    • For significant Hypotension, Dopa and Epi are indicaated and a permanent pacemaker is needed for unresolved block
  111. What is BBB?
    • Refers to some sort of disruption of the electrical impulse through either the L or R branch of the bundle of HIS.
    • Normally the ventricles depolarize simultaneously and usually the process is completed in 0.1sec or less.
    • BBB the ventricles depolarizes sequentially so the conduction through one of the ventricles is slower resulting in a wide QRS complex so 0.2 sec or more.
  112. How can you differentiate between R and L BBB?
    To differentiate between a R and L BBB you need to look at a 12 lead EKG to know whether it’s a R or a L but presence of a BBB can be determined from a rhythm strip
  113. What are the causes of R. BBB?
    • R BBB may be present in pts w/heart disease.
    • CAD is most common cause but also hypertensive heart disease, cardiomyopathy, acute anteroseptal MI, acute pulmonary embolism and also a congenital R Bundle.
    • And also chronic degeneration of the conducting system.
    • It can also occur in healthy people.
    • May be temporary or permanent.
    • Sometimes only appears if rate exceeds a certain critical value (rate related BBB).
  114. What causes L. BBB?
    • Unlike RBBB, L BBB is usually d/t heart disease but it may also be temporary or permanent.
    • Common causes include the cardiac diseases noted for RBBB
  115. How do you treat BBB?
    • Specific tx isn’t usually needed for BBB alone, pacing may be indicated if a new BBB develops secondary to an acute MI, RBBB is associated with a block of a fasicle of the L bundle.
    • If RBBB or LBBB is complicated by AV block, esp in setting of an acute MI.
  116. What is a premature ventricular contraction?
    • Premature ectopic impulse originating in the ventricle.
    • Unlike PACs, or premature junctional contractions, these don’t travel down normal conducting pathways but rather through the ventricular muscle so the ventricles depolarize sequentially (wide QRS)
    • A P wave isn’t associated with a PVC. But there may be P waves associated with an underlying sinus rhythm and these may appear before the PVC or after it in the ST segment or T wave.
    • The wide QRS is often notched, and different in appearance from the normal QRS.
    • The ST and T wave slope in the opposite direction from the main deflection of the QRS complex in the PVCs
  117. With PVC, depolarization is abnormal and so is repolarization. Describe the pause associated with a PVC
    • It's compensatory (meaning the measurement between the R wave before the PVC to the R wave in the complex after the PVC is equal to the sum of two R-R intervals from the underlying rhythm).
    • The compensatory pause happens because the SA node isn’t depolarized by the ectopic ventricular beat and so the discharge timing of the SA node remains unchanged and the basic underlying rhythm resumes on time after the PVC.
    • Rarely the sinus node will be depolarized by the PVC  and this will reset the discharge time resulting in a non-compensatory pause.
  118. We know patterns can occur w/PVCs like:_____________ and they can be unifocal or multifocal.
    bigeminy, trigeminy or couplets.
  119. What is an interpolated PVC?
    • A PVC that gets sandwiched between two normally conducted sinus beats greatly disturbing the underlying rhythm is called an interpolated PVC.
    • In this case the compensatory pause usually associated with a PVC is absent.
  120. What is the R on the T phenomenon that can occur w/a PVC?
    • Refers to a PVC that occurs during the vulnerable period of ventricular repolarization.
    • So on or near the peak of the T wave, during this period the ventricular fibers have repolarized enough so that they can respond to a strong stimulus.
    • Stimulation of a ventricle at this time, can easily precipitate ventricular tachycardia or ventricular fibrillation
  121. What causes PVCs? What is the treatment?
    • Like PACs, PVCs are common, even more so as we age. Can occur in individuals w/healthy heart as well as those w/heart disease.
    • They can be caused by enhanced automaticity, an increase in catechols (ex: alcohol, caffeine, nicotine, ingestion) as well as ischemia/infarction, cardiomyopathy, hypoxia, drugs, and electrolyte imbalance (particularly hypokalemia & hypomagnesiumia)
    • Tx directed at underlying cause.
  122. Occasionally a ventricular beat may occur late instead of early and as we said when we were talking about the junctional beats, these are called _____________.
    • ventricular escape beats
    • Escape beats are more likely to occur because of increased vagal tone on SA node rather than because of increased automaticity.
    • They are common after a pause in normal rhythm.
    • Again it’s a protective mechanism, so no tx for an escape beat is indicated.
  123. What is VTach?
    • Originating at an ectopic focus in the ventricles and discharging at a rate of 140-250bpm.
    • The EKG shows a series of wide (more than 1.2 sec) QRS complexes with no observable P waves or atrial activity.
    • Sinus node is still firing independently but the P waves are usually hidden in the QRS complex.
    • Usually the QRS complexes are all identical, meaning monomorphic. If they differ they are referred to as polymorphic.
    • The T waves are large and in opposite direction of the QRS.
  124. Clinically the patient with monomorphic VT may be asymptomatic. If there is a pulse and pt condition is stable, tx includes any one these following antiarrhythmics
    • Amio
    • Lidocaine  
    • Procainamide
  125. Amiodarone is first line tx for Vtach w/a pulse. What is the dosing and the adverse effects?
    • 150mg IV bolus over 10min Followed by 1mg/min infusion over 6 hrs.
    • Then 0.5mg/min infusion over 18hrs. Max of 2.2 gm of amiodarone can be given in boluses of 150mg IV for recurrent or resistant V Tach. Major adverse effects of amio are bradycardia and hypotension.
    • Amiodarone can also induce Torsades.
  126. Lidocain is another tx for Vtach w/a pulse. What is the dosing and adverse effects?
    • 1-1.5mg/kg bolus.
    • Followed by ½ the initial dose every 5-10min for a max of 3mg/kg.
    • Maintenance infusion rate is 1-4 mg/min.
    • Recurrence of V-tach during infusion calls for small bolus of 0.5mg/kg and upping the infusion rate.
    • After 24hr the dose should be decreased or blood levels monitored.
    • Signs of Lidocaine toxicity: slurred speech, altered LOC, muscle twitching, seizures, bradycardia.
  127. Procainamide can also be used for tx of Vtach w/a pulse. What is the dosing?
    • Given in an infusion of 20-30 mg/min until the arrhythmia is suppressed or significant hypotension occurs or QRS complex doubles it’s pre-tx width or finally, a total dose of 17mg/kg is given.
    • Maintenance infusion rate is the same as Lidocaine: 1-4mg/min
  128. What happens if you give Procainamide too fast?
    • Rapid administration of procainamide will exacerbate hypotension.
    • Also prolongs the QT interval
  129. How and when do you cardiovert for Vtach w/pulse
    If the rhythm is unresponsive to drug therapy, cardioversion is indicated beginning at 100 joules and increasing w/subsequent attempts.
  130. Vtach w/pulse, if the patient has an EF less than ___% the recommended guidelines are amio or lido and cardioversion if drug therapy is unsuccessful.
  131. Tx of polymorphic V-tach is similar to monomorphic Vtach except
    you should look at most recent 12 lead EKG to check the QT interval. If this is prolonged, then you want to follow the algorithm for torsades.
  132. Ventricular flutter is a form of V-Tach, describe this.
    where the ventricular rate is so fast that the QRS complexes have a saw tooth appearance the pt becomes HD compromised acutely bc there is a virtually no CO it’s usually former to Vfib.
  133. What is Torsades de pointes?
    • unique subtype of polymorphic Vtach. The term means twisting of the points.
    • With this the direction of the QRS complexes seem to rotate, pointing down for a series of beats then twisting and pointing up.
    • The QRS complexes show a spindal node pattern where the amplitude of the QRS increases and decreases in a normal pattern and this creates the spindal.
    • The initial deflection at the start of one spindle (meaning negative) will be followed by the opposite (positive) deflection of the start of the next spindle.
  134. In torsades de pointes, the ventricular rate is fast or slow?
    The ventricular rate is quite fast, much faster than monomorphic V-tach and the patient becomes HD unstable quickly. Torsades is often an immediate precursor to Vfib
  135. When does torsades de pointes classically occur?
    • in setting of delayed ventricular repolarization.
    • So a prolonged QT interval or in the presence of prominent U waves.
    • Prolonged QT can be d/t meds: Procainamide, Quinidine, Phenothiazines, Tricylics, can be d/t electrolyte imbalances like hypokalemia, hypomagnesiumia, or hypocalcemia.
    • Can also occur d/t bradycardia. Liquid protein diet or low QT syndrome. And we know our 5HT3 blockers are also implicated.
  136. Why is recognition of torsades de pointes essential?
    • Recognition is essential because tx differs from that of monomorphic VT.
    • The meds used to tx monomorphic VT can cause Torsades so if these are given, they make the situation worse
  137. What is the treatment for Torsades de pointes?
    • Tx for torsades includes correcting any underlying causes.
    • Magnesium given as 1-2gm in 50ml of D5W over 5min, followed by a maintenance infusion of 0.5-1gm/hr.
    • This needs to be given slowly because rapid administration of magnesium can cause hypotension and asystole.
    • Overdrive pacing may be helpful if underlying cause is bradycardia. Cardioversion will convert the rhythm but torsades will likely reoccur unless the precipitating factors are corrected. Cardioversion may be used while other measures like Mg and overdrive pacing are being done.
    • Finally drug therapy w/Isuprel (which is essentially pharmacologic overdrive pacing), phenytoin or Lidocaine may also be used in selective cases.
  138. What is Vfib?
    • Rhythm is chaotic and disorganized.
    • The ventricles don’t beat rather they quiver. Half hazard depolarization of the muscle fibers.
    • P waves and QRS complexes are absent if the fibrillatory waves are large it’s called coarse VF and if they are small it’s fine VF.
  139. Which is more likely to be reversed, coarse or fine vfib?
    Coarse VF is more likely to be reversed than fine VF
  140. What is the most common cause of sudden death in patient with an acute MI?
    VFib. V fib Can occur from any type of heart disease
  141. What is the treatment for Vfib?
    Tx involves following ACLS protocols including defibrillation at 200J, 300J, 360J, CPR, vasopressin 40u IV or Epi 1mg IV every5min.
  142. __________is class 2b (Fair to good evidence provides support that the drug is acceptable and useful) for sharp refractory VF or pulseless VT.
    • Amiodarone
    • Lidocaine is class indeterminate meaning there is insufficient evidence to determine support of it’s use but appears to be no harm but may be no benefit for using Lidocaine.
  143. What is ventricular standstill?
    • Absence of all electrical activity in the ventricles.
    • If P waves are present, then some type of advance AV block (Mobitz 2 or 3rd degree) likely proceeded the arrhythmia.
  144. What is the cause and treatment for ventricular standstill?
    • This may occur from acidosis hypoxia, hyperkalemia, hypothermia or drug overdose.
    • The only tx is to ID and tx underlying cause, CPR, Epi and transcutaneous pacing and atropine may be tried.
  145. What are some indications for a pacemaker?
    • SA node dysfunction
    • AV node dysfunction (mobitz type 2 and 3rd degree)
    • Chronic bifascicular block
    • Post MI
    • Hypersensitive carotid sinus syndrome
    • Arrhythmia avoidance
  146. SA node dysfunction is an indication for a pacemaker including.............
    symptomatic bradycardia with frequent pauses and syncope and hx of sinus node dysfunction
  147. Why would a pacemaker be indicated post MI?
    Residual problems like a mobitz type 2 or 3rd degree, alternating BBB, or a prior ST elevation MI
  148. Hypersensitive carotid sinus syndrome & Neurocardiogenic syndrome are indications for a pacemaker. What is this?
    This may be syncope caused by spontaneous carotid stimulation inducing asystole for greater than 30sec. It could be syncope without clear provocative events and with a hypersensitive cardio inhibitory response of 3sec or longer
  149. What type of arrhythmia avoidance would indicate the need for a pacemaker?
    Recurrent SVT proven to be prevented with pacing or pause dependent VT (long QT syndrome)
  150. When is an AICD indicated?
    • VT or VF (esp w/syncope or heat disease)
    • Low EF (less than 35%)
    • Cardiomyopathy (possibly indicated with: dilated cardiomyopathy, hypertrophic cardiomyopathy)
    • Long QT(possibly indicated)
  151. What do the first 3 letters in the pacemaker mode mean?
    • First letter = chamber being paced
    • A = atria
    • V = ventricles
    • D = dual
    • Second letter = chamber being sensed
    • A = atria
    • V = ventricles
    • D = dual
    • 0 = none
    • Third letter = response to sensing
    • I = inhibition
    • T = triggered
    • D = dual
  152. How does a pacemaker work?
    • Lithium iodine battery that generates impulse or output.
    • The impulse goes from the battery through leads and excites the endocardial cells creating a wave of depolarization in the myocardium.
    • The circuitry modulates the amount of frequency and the amount of current flow and also senses the spontaneous electrical activity in the heart
  153. What does the 4th letter in the pacemaker settings mean?
    • Originally developed to describe programmable functions but it’s now used to designate the presence of rate adaptive abilities in which the pace rate will vary with the metabolic need.
    • An R indicates the pacer contains a sensor other than sinus rhythm that can modulate the interval between the lower and the upper rates
  154. What does the 5th letter in the pacemaker settings mean?
    • presence of anti-tachycardia capabilities
    • most of these capabilities are implanted into automatic implantable defibrillators.
  155. What are the most common modes of pacemakers?
    • VVI and DDD
    • In most dual chamber pacing modes the atrial output is inhibited when atrial signal is sensed and if no intrinsic ventricular activity is sensed by the end of whatever is programmed as the AV interval, a ventricular output is generated but if ventricular activity is sensed then ventricular output is also inhibited.
  156. What is VVI mode on the pacemaker?
    • V pace, V sense and the response to sensing in the ventricle is inhibition.
    • This is what’s used w/transvenous wire in temporary pacing
  157. What is DDD mode on the pacemaker?
    both chambers are sensed and paced, when an impulse sensed in either chamber the result may be paced or inhibition depending on the chamber.
  158. In ventricular pacing, what does ventricular capture refer to?
    • Ventricular capture is seen here referred to the fact that the ventricle has responded (depolarized) in response to a paced stimulus.
    • See pacing spike before QRS.
    • With a pacemaker there is sequential rather than simultaneous depolarization of the ventricles so one ventricle usually is depolarized before the other resulting in a wide QRS complex.
  159. What is a fusion beat?
    • There are ventricular paced beats followed by a native beat which is followed by a fusion beat.
    • A fusion beat is when the pacemaker fires at the same time as the normal electrical impulse.
    • Both impulses get to the ventricle at the same time and the fusion beat is the result.
    • QRS looks somewhat like the paced beat but has some of the characteristics of the normal beat as well.
  160. What is loss of capture?
    • Meaning the ventricles didn’t respond to the pacing stimulus (pacing spike).
    • This is common in temporary pacemakers and usually d/t a problem with the interface of the catheter and the endocardium.
    • Tip of the electrode has to be in contact with the endocardium for depolarization to occur so if it becomes dislodged there will be loss of capture.
    • There is also cause if the tip is near an area of infarction (won’t conduct)
    • Also may be absence of enough current to cause a ventricular response.
  161. What is threshold?
    • The minimum amount of current required for capture is called the threshold.
    • This is determined during the insertion of the pacemaker.
    • The milliamps is usually set at 2x the threshold.
    • Threshold may increase d/t the development of scar tissue or inflammation and this could lead to loss of capture.
  162. What is undersensing?
    • Happens when the pulse generator doesn’t sense the native beats so the EKG shows the pacing spike that comes earlier than it should after a normal or a paced beat.
    • If pacemaker is working properly (W/regard to sensing) it will sense the beat and won’t fire a stimulus until the time indicated again determined by the automatic interval setting.
    • Undersensing can occur from problems w/contact w/the electrode in the endocardium and also if the sensitivity is set too low.
    • Also the pacemaker could be set in the asynchronous mode meaning the sensing capability has been turned off.
  163. The patient should carry and ID card that documents the type and # of the device. If not, how can you find this information out?
    CXR can also reveal the device ID # and can be referenced.
  164. Intraop there are sources of magnetic electro interference with various devices with pacemakers and ACIDs that can cause it to malfunction. Name them
    • Unipolar cautery
    • Radiofrequency ablation
    • Lithotripsy
    • MRI
    • Radiation therapy
  165. What happens if you place a magnet over the pacer?
    the pacer will typically convert to a VVO mode w/a heart rate of about 80-100bpm. The ICD will be disabled (Defib capability disabled w/magnet applied)
  166. Almost all pacemakers are supplied by
    Medtronic and Boston Scientific.
  167. Is a single recommendation approach for periop management of an CIED appropriate?
    • Single recommendation is inappropriate
    • Periop management must be individualized to the pt, the type of pacer, and the procedure being performed
  168. What type of communication is necessary for periop management of a CIED?
    • Operative team should communicate with CIED team (physicians and others who monitor the functioning of the device for the particular patient)
    • The surgical or procedural team need to communicate w/the CIED to ID the type of procedure and likely risk of elecromagnetic interference.
  169. TRUE or FALSE. For periop managment of a CIED, information needed is usually available in CIED team records but a small number of patients will need new CIED team consultation
    TRUE! CIED team gives prescription of peri-op management of the device. Most pt prescription may be made from review of records they have in clinic. Small % of pt may require a consult from specialist if info can’t be found
  170. Is it ok for Medtronic or Boston Scientific to be part of the periop prescription since they make the CIED?
  171. For CIED, the significance and extent of abnormal behavior of these devices seen in EMI is dependent on
    • the strength, duration, and the type of interference.
    • How this effects the patient depends on the patients own rate and rhythm and the manufacturers specific algorithms designed to minimize problems.
  172. For us, the type of electromagnetic interference we're concerned about is usually the
    • bovie or electrosurgery.
    • Uses focused electrical current to cut or coagulate tissue.
    • Current can be delivered in a bipolar or a monopolar configuration w/varied waveforms in order to get whatever the desired effect on the tissue is.
  173. Which interferes more with CIEDs, monopolar or bipolar cautery?
  174. What is bipolar cautery
    Bipolar cautery is used typically ophthalmic and microsurgery and involves the use of electrical forces where each limb of the force is an electrode.
  175. What is monopolar cautery?
    • Most surgeries use monopolar cautery and with this the electrical is applied with a small active electrode that represents a pen.
    • The pen electrode is applied to the operative site and then flows through the patients body to a large surface area return electrode (typically referred to as the bovie pad)
  176. What kinds of problems exist with cautery and CIEDs?
    • With bipolar (forces type) bipolar electrocautery, really doesn’t cause any electromagnetic interference unless it would be applied directly the device which would be unlikely to happen.
    • But EMI from monopolar cautery is the most common problem seen during surgical procedures and again can include inhibition of the device, triggering a needed tachyarrhythmia therapy, and even resetting of the pulse generator.
  177. How can we minimize problems with EMI from cautery and CIEDs?
    • By taking certain precautions.
    • It’s been shown that if the distance between current path of the electrocautery unit and the pulse generator is greater than 6inches then interaction and damage is unlikely.
    • So for example if surgery is to be preformed on the L arm (which is the side of the implanted device) and the return electrode should be placed on the same arm rather than on the plank which would expose the device to the full energy of the bovie.
    • Also electrosurgery or the bovie monopolar cautery applied below the umbilicus is much less likely to cause any interference than when it’s applied above the umbilicus. Since there is more distance between the cautery and the device particularly when the bovie thigh or the gluteal area which is typically where it’s placed. So using monopolar cautery for surgery involving the upper abdomen the chest, the arms, the head, and neck will prevent a greater risk for oversensing and damage to the system.
  178. Another thing that helps to prevent any problems with EMI from cautery and CIEDs is if a surgeon minimizes the length of monopolar electrocautery bursts to _________.
    5sec or less
  179. Oversensing can be a problem with a CIED periop. Why?
    Can get inhibition of pacing and false tachyarrhythmia detection
  180. What essential information must we give the CIED team?
    • Type of procedure
    • Anatomic location of procedure
    • Type of cautery & location of application (of monopolar bouvie pad and where surgeon will be using monopolar unit)?
    • Other sources of EMI (Diagnostic, Radiation, Cardioversion, ECT, Lithotripsy)
    • Post-op plan
  181. TRUE or FALSE. If patient has implantable defibrillator, inactivation is not a universal requirement for all procedures. Likewise, rendering pacemakers asynchronous in pacemaker dependent patients is not a universal requirement for all procedures
  182. Will placing a magnet over an ACID generator render pacemaker function in an AICD asynchronous?

    • If the pacemaker needs to be protected from inhibition, they can be made asynchronous by programming or by placing a magnet over the pulse generator.
    • Likewise with an AICD, arrhythmias detection can be suspended by placing a magnet of the pulse generator if the pulse generator is accessible
  183. When would rendering a pacemaker asynchronous be preferable?
    • Rendering a pacemaker asynchronous in a pacemaker dependent patient is preferable for most procedures above the umbilicus.
    • In pacemaker patients no reprogramming is usually needed if the electrosurgical stimulus is applied below the level of the umbilicus
    • Likewise inactivation of an AICD is recommended for all procedures using monopoloar electrosurgery or radiofrequency ablation above the umbilicus
  184. When should patients with pacemakers having elective surgery have had a device check?
    All patients with pacemakers undergoing elective surgery should have had a device check as part of routine care within the past 12M that identifies all the required elements that we need to know about.
  185. All patients with an AICD undergoing elective surgery should have had the device check as part of routine care within the past ___
  186. You're patient (who has a CIED) is about to go home, what should you MAKE SURE of?
    That if the device was turned off, it has been turned back on!
  187. What EKG changes will you see with hypokalemia?
    • Flattened or inverted T waves
    • Increased U waves
    • Slight depression of ST segment
    • Increased amplitude of P wave
    • Premature beats and sustained tachyarrhythmias
    • Prolonged QT interval
  188. What EKG changes will you see with hyperkalemia
    • Increased amplitude & peaked T waves
    • Prolonged PR interval (also in Hypokalemia)
    • Prolonged QRS interval
    • Flattened P wave
  189. What EKG changes will you see w/hypo and hyper calcemia?
    • Hypocalcemia:Prolonged QT interval
    • Hypercalcemia: Shortened QT interval
  190. What is the effect of Class I anti-arrhythmics? Give an example
    • Inhibit fast sodium channels (Phase 0-the upstroke)
    • 1A: Quinidine
    • 1B: Lidocaine
    • 1C: Flecainide
  191. What is the effect of Class II anti-arrhythmics? Give an example
    • ↓ rate of spontaneous phase 4 depolarization
    • Beta Blockers
  192. What is the effect of Class III anti-arrhythmics? Give an example
    • Block potassium channels
    • Amiodarone
  193. What is the effect of Class IV anti-arrhythmics? Give an example
    • Block calcium channels
    • Ca+ Channel Blockers
  194. Sub endocardial MI shows ST depression or elevation?
    ST depression and/or T wave inversion
  195. transmural MI shows ST elevation or depression?
    ST elevation
  196. What is the myocardial infarction triad?
    • Ischemia
    • Transient T wave inversion & ST depression 2° altered repolarization of ischemic cells

    • Injury
    • ST segment deviates from baseline
    • Subendocardial = ST depression
    • Transmural = ST elevation

    • Infarction (Necrosis)
    • Q waves (significant)
    • 1 mm wide (1 small square)
    • 1/3 the height of the QRS
    • Avoid lead AVR (Q’s unreliable)
  197. Anterior MI involves which coronary artery and what would you see on the EKG?
    • LAD
    • Q’s & ST elevation in leads V1, V2, V3, V4
  198. Lateral MI involves what coronary artery and what would you see on the EKG?
    • Cirumflex
    • Q’s & ST elevation in leads I & AVL
  199. Inferior MI involves what coronary artery and what would you see on the EKG?
    • RCA dominant in most individuals supplying the posterior descending artery
    • Q’s & ST elevation in leads II, III, & AVF
  200. Posterior MI involves what coronary artery and what would you see on the EKG?
    • RCA dominant in most (85%) individuals, in 8% the supply is from the circumflex & the rest are “co-dominant”
    • Large R’s & ST depression in leads V1 – V3, possible Q in V6
  201. MI Localization, Always check V1 & V2 for…
    • ST elevation & Q waves (anterior infarct)
    • ST depression & large R waves (posterior infarct)