Cardio2- EKG and Arrhythmias

  1. ____________ may increase voltage or prolong the P-wave.
    Atrial dilatation or disease
  2. What effects might ventricular hypertrophy (concentric or eccentric) have on the ECG? (3)
    increase voltages, wider QRS complex, change in the frontal axis
  3. Describe the difference between primary and secondary T wave abnormalities.
    primary T wave abnormalities occur with a normal QRS, from hyperkalemia hypotension/ischemia, etc; secondary T wave abnormalities occur due to an abnormality in the QRS, which is what we really care about diagnostically
  4. Increased height/ voltage/ taller P waves are consistent with __________.
    right atrial dilation (P pulmonale)
  5. Wider than normal P waves are consistent with ___________.
    left atrial dilation (P mitrale)
  6. What would eccentric LV hypertrophy look like on ECG?
    increased voltages of QRS with normal frontal axis (morphology)
  7. What are potential causes of increased QRS voltages and normal shape? (4)
    DCM, LV volume overload (such as PDA, MR, AR)
  8. Which 2 leads normally have the largest (most positive) QRS complexes?
    Leads II and aVF
  9. What causes increased QRS duration/ wider QRS complexes?
    left bundle branch block (b/c myocardial spread from cell to cell is ay slower than if it goes through the BB), LV hypertrophy, LV myocardial disease
  10. What is left axis deviation?
    instead of leads II and aVF being the most positive, leads I and aVL dominate (frontal axis has shifted to the left cranial quadrant)
  11. What are potential causes of left axis deviation? (3)
    normal variation, concentric LV hypertrophy, left anterior fascicular block
  12. What are potential causes of right axis deviation? (4)
    RV hypertrophy due to pulmonic stenosis, atrial septal defect, pulmonary hypertension, or RV conduction delay
  13. What is right axis deviation?
    instead of leads II and aVF being the most positive, leads III and aVR dominate
  14. What are the key ECG features of RV hypertrophy? (3)
    right axis deviation, prominent S wave in lead I, often an S wave in leads I, II and III (so-called S1,2,3 pattern)
  15. What does an S wave in lead I indicate?
    that means the terminal activation is going to the right, which is abnormal
  16. What are primary changes in repolarization (ST interval)? (4)
    ischemia, hypoxia, pericarditis, hyperkalemia
  17. What ECG changes are associated with hyperkalemia? (2)
    absent P waves (sodium channels don't open b/c have passed necessary voltage, atrial muscle inexcitable), tented T waves
  18. "Rescue" complex from subsidiary pacemaker cells.
    escape beat
  19. Impulse arising outside of the SA node.
    ectopia
  20. Delay or interruption of current flow.
    Block
  21. Rapid, disorganized electrical activity affecting atria or ventricles; disorganized electrical activation and ineffective myocardial contraction.
    Fibrillation
  22. Absence of electrical and mechanical activity.
    Asystole
  23. What are potential hemodynamic consequences of arrhythmias? (5)
    reduced cardiac function, decreased BP, reduced tissue perfusion, limited exercise capacity, syncope
  24. What are potential electrical consequences of arrhythmias? (3)
    myocardial fibrillation, asystole, sudden cardiac death
  25. What are the general causes of arrhythmias? (5)
    cardiac diseases (structural diseases, heart failure, ischemia, primary electrical disorders), metabolic/ endocrine disorders, autonomic nervous system, drugs/toxins, usual suspects (GDV, splenic disease, etc)
  26. Describe normal sinus rhythm.
    normal HR, every P is followed by a QRS, every QRS is preceeded by a P, and the rhythm is very regular
  27. Describe sinus arrhythmia.
    normal rate and irregular rhythm, varying sinus node discharge rate causes cyclical mild variation in HR; occurs due to varying amounts of vagal tone to SA node (often associated with respiration)
  28. Describe wandering pacemaker.
    varying vagal influence to the SA node, causing the node to fire from different foci, which may alter P wave morphology
  29. What are the types of supraventricular arrhythmias? (4)
    PACs, atrial tachy, atrial flutter, atrial fib
  30. What is respiratory sinus arrhythmia?
    SA node speed during inspiration and slows during expiration due to changes in vagal tone
  31. Wandering pacemaker is completely normal in the setting of _____________.
    sinus arrhythmia
  32. How is sinus arrest defined?
    no atrial activity for a period exceeding two normal P to P intervals
  33. What are PACs?
    beats that occur earlier than the current R-R interval, but whose QRS complex appears nearly identical to the sinus QRS complexes
  34. What is considered atrial tachycardia?
    a string of more than 3 PACs in a row
  35. What is considered atrial flutter?
    sawtooth looking F waves in the baseline; contrast from afib because they are uniform and consistent (afib is disorganized and haphazard)
  36. Describe afib.
    highly chaotic and irregular, the AV node slows conduction, only allowing a random number of beats to be conducted and therefore, causing the irregular ventricular rhythm (sounds like tennis shoes in the dry on auscultation)
  37. Which patients benefit from rhythm control? (3)
    those with relentless tachycardia, atrial flutter, or afib
  38. How do you manage a dog with heart failure and an atrial arrhythmia?
    digoxin (the only positive inotrope of the 3 rate control drugs) + diltiazem
  39. Which type of rate control drug should NOT be used in a heart failure patient and why?
    beta blockers because they are negative inotropes
  40. How should you manage sinus tachycardia?
    identify underlying cause of increased sympathetic activity, manage hypotension or heart failure
  41. How do you manage sinus bradycardia?
    identify underlying reasons for high vagal tone, atropine or catecholamine if needed
  42. How do you manage sinus arrest- sick sinus syndrome?
    pacemaker
  43. How do you pharmacologically control how fast the ventricle beats?
    regulate the AV node because the atria control how fast the ventricles go
  44. In sinus arrest, the blame is with the _________; with atrial standstill, the blame is with the _________ because it is _________.
    sinus node; atrial muscle; inexcitable (usually due to hyperkalemia)
  45. _____________ determine ventricular rate.
    AV nodal conduction
  46. ____________ determines which fibrillation waves get through to cause a QRS complex.
    AV nodal conduction
  47. What drugs are used for heart rate control in animals with afib? (3)
    Digoxin, Diltiazem, Beta-blockers (-lol)
  48. How are persistent PACs managed sometimes?
    drugs that suppress automaticity or modify conduction (rhythm control)- sotalol, beta-blockers, amiodarone, flecainide
  49. What drug is used in horses to convert afib to normal sinus rhythm? What is the initial effect of this drug on the HR prior to conversion?
    quinidine (horses don't usually have associated structural heart disease, unlike dogs, which almost always have structural disease as the cause); initially causes sinus tachycardia because of increased AV nodal conduction
  50. Describe electrical cardioversion.
    electrical shock delivered to heart right at the R wave to convert the animal from afib back to normal sinus rhythm (horses and dogs)
  51. What is Tosades de pointes?
    ventricular arrhythmia in which the QRS complexesgo from positive to negative, like a ballerina turning on a point
  52. What are two life-threatening and lethal ventricular arrhythmias?
    ventricular fibrillation and ventricular standstill/asystole
  53. When is a QRS complex considered premature (VPCs)?
    it's very very close to the prior T wave and causes secondarily irregular following T wave [the QRS is wide and bizarre and P waves do not occur at a regular interval]
  54. Why is the QRS of VPCs "wide and bizarre"?
    the depolarization spreads out from the ectopic focus from cell to cell, which takes more time than through the his-purkinje system
  55. PCVs originating from the LV are usually __________ in lead II,while PCVs originating from the RV are usually _________ in lead II.
    negative; positive
  56. What is sick sinus syndrome?
    disease of the SA node as well as the distal conducting system that results in periods of SA arrest without appropriate escape activity
  57. How do we TRY to assess PVCs? (6)
    frequency, timing (R on T), morphology, runs of Vtach, rate of Vtach, complexity
  58. What are oral drugs for the chronic therapy of ventricular and atrial arrhythmias?
    SPAAM: sotalol, procainamide, atenolol, amiodarone, mexiletine
  59. What is the usual in-hospital therapy for ventricular tachyarrhythmia?
    • First line: lidocaine
    • Second line: amiodarone, procainamide
    • Third line: esmolol
    • Supportive: potassium and magnesium salts
  60. Describe first degree AV block.
    prolonged PR interval but all P waves are conducted
  61. Describe second degree AV block.
    incomplete atrial-ventricular conduction- some P waves are blocked
  62. Describe third degree AV block.
    complete AV block- patient survives on an escape rhythm below the level of block
  63. Hyperkalemia causes __________.
    atrial standstill
  64. Bundle branch block occurs when...
    only a portion of the normal conduction system is blocked; the normal conduction system splits from the bundle of His into the left and right bundles, supplying the left and right ventricles respectively; if one of the bundles cannot conduct, then half of the heart is depolarized normally, while the other half is depolarized from cell to cell, causing the QRS to widen (takes longer)
  65. If the right bundle branch is blocked, the QRS will be...
    wider than normal and will be predominantly negative in lead II.
  66. If the left bundle branch is blocked, the QRS will be...
    wider than normal and positive in lead II.
  67. What is the clinical significance of an ECG with a normal frontal axis and very large R waves in lead II from a young dog with a continuous heart murmur?
    PDA causing LV dilatation to increase SV to feed the shunt and maintain normal CO
  68. What is the clinical significance of an ECG with a normal frontal axis, absent Q waves in lead II, and a very long QRS duration in a dog with DCM?
    LV eccentric hypertrophy; can lead to BBB
  69. What are causes of ST segment elevation and depression?
    • ST elevation: normal variant "early repolarization", ischemic heart disease, acute pericarditis, LV hypertrophy, LBBB, advanced hyperK+, hypothermia
    • ST depression: usually ischemia, normal variant/artifact, hyperventilation, ventricular hypertrophy, Digoxin, hypoK+, MV prolapse, CNS disease, secondary to arrhythmia
  70. J point depression occurs with ____________.
    sinus tachycardia
  71. What is sick sinus syndrome? How is it managed?
    disease of the SA node and distal conducting system that results in periods of SA arrest without appropriate escape activity; the only effective management is a pacemaker.
  72. Describe the clinical features of premature atrial complexes on ECG. (3)
    irregular rhythm, premature QRS initiated by a premature ectopic P wave, P waves have weird morphology
  73. Describe the clinical features of focal atrial tachycardia on ECG.
    ectopic atrial rhythm from outside the SA node
  74. Contrast defibrilliation from electrical cardioversion.
    defibrillation is when you have no QRS complexes and are going to die, so you shock/depolarize all of the cells of the heart at once to get them conducting again; cardioversion is when you give a shock right on the R wave to depolarize and allow the sinus node to resume normal function/rhythm
  75. Using afib as an example, explain the circumstances when you rate versus rhythm control.
    • We cannot use rhythm control in animal with structural heart disease (ie. almost ALL dogs with afib); conversely, horses do not usually have structural heart disease with a fib, so we manage them with quinidine first.
    • For SA with afib, we use rate control, such as Digoxin, Diltiazem, or beta-blockers.
  76. Which 3 drugs are commonly used to obtain rate control in SAs with atrial tachyarrhythmias? What is the mechanism of each drug?
    • Digoxin: increases vagal tone through sensitization of the baroreceptor reflex
    • Diltiazem: blocks Ca2+ entry into AV node
    • Beta-blockers: reduced Ca2+ entry across L-Ca2+ channels by decreasing sympathetic tone
  77. What is ventricular bigeminy?
    ectopic beats/VPCs occur after every sinus beat, causing alternating long and short heart beats
  78. What is ventricular tachycardia?
    a string of VPCs linked together
  79. Contrast monomorphic and polymorphic vtach.
    • monomorphic: accelerated idioventricular rhythm- "slow" vtach
    • polymorphic: very fast vtach that is varying in appearance; more serious
  80. What are the indications for pacemakers in dogs?
    high grade second degree AV block, complete AV block (third degree), sinus arrest/sick sinus syndrome
Author
Mawad
ID
317975
Card Set
Cardio2- EKG and Arrhythmias
Description
vetmed cardio2
Updated