Arrhythmias: Disorders of Impulse Conduction Flashcards

1
Q

What is an AV block? What are some extra-cardiac and intra-cardiac causes?

A

impulse conduction disturbance caused by a delay/failure of transmission at the AV node

  • EXTRA-CARDIAC = drugs, electrolytes, thyroid, vagus
  • INTRA-CARDIAC = ischemia, myocarditis, neoplasia, trauma, genetics, idiopathic
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2
Q

Heart blocks:

A
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3
Q

What is a 1st degree AV block? What are 3 ECG findings?

A

prolonged AV nodal conduction time —> AV node conducts slower than normal through the AV junction and bundle of His

  1. normal rate, rhythm, P waves, and QRS complexes
  2. prolonged PR interval (>0.13s in dogs, >0.09s in cats)
  3. 1:1 conduction - a P wave for every QRS
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4
Q

What is occurring in this ECG?

A

first degree AV block

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5
Q

What are some physiologic and pathologic causes of first-degree AV blocks?

A

PHYSIOLOGIC = increased vagal tone —> respiratory disease, GI disease, ocular disease, nervous system disease (vagus nerve/pathway)

PATHOLOGIC = structural AV node disease (degenerative changes in older patients - fibrosis, inflammation, neoplasia, infection, infarction, trauma, hypothyroidism), drug-induced

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6
Q

What treatment is indicated for 1st degree AV blocks?

A

usually asymptomatics

  • evaluate for structural cardiac disease
  • monitor for disease progression
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7
Q

What are 2nd degree AV blocks? What are 3 ECG findings?

A

when atrial depolarization intermittently fails to conduct through the AV node to the ventricles (lonely P wave)

  1. more P waves than QRS complexes
  2. some P waves still conduct through
  3. PR intervals can be variable
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8
Q

What is a Mobitz Type I AV block? What is seen on ECG?

A

(Wenckebach) progressive PR interval prolongation until atrial impulse fails to conduct through the AV node —> no more than 2:1 P waves to QRS

PR intervals gradually elongate until a P wave is completely blocked

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9
Q

What are Mobitz Type I AV blocks associated with? What treatment is recommended?

A
  • high vagal tone
  • drug-mediated
  • physiologic > pathologic

treat underlying cause for increased vagal tone or reverse drug eliciting AV block —> responds to Atropine

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10
Q

What is occurring in this ECG?

A

Mobitz Type I AV block (Wenckebach)

  • PR intervals gradually elongate until a P wave is completely blocked
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11
Q

What is a Mobitz Type II AV block? What is seen on ECGs?

A

random failure of impulse conduction through the AV node with no PR change and more than 2:1 P wave to QRS conduction

PR intervals are consistent, but some P waves don’t conduct

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12
Q

What is the clinical significance of Mobitz Type II AV blocks? What is it commonly exacerbated by? What treatment is recommended?

A

pathologic > physiologic - structural disease of the AV node is usually present and symptoms vary with severity of the block

high vagal tone or anesthesia

may respond to Atropine, pacemaker

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13
Q

What is occurring in this ECG?

A

Mobitz Type II AV block

  • consistent PR intervals, P wave conduction fails at second arrow
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14
Q

What indicates a low grade vs. high grade Mobitz Type II AV blocks?

A

LOW GRADE = few QRS blocked, ~2:1 P waves to QRS complexes, typically random without a specific pattern

HIGH GRADE = multiple missed QRS ~3:1 AV block

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15
Q

Mobitz Type I vs. Type II

A

2nd degree AV block

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16
Q

What is a 3rd degree AV block?

A

atrial depolarization completely fails to conduct through the AV node to the ventricles (AV node no longer functional) —> some other part of the conduction system takes over as a pacemaker

  • junctional or ventricular escape rhythms at regular intervals, as they are self-pacing
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17
Q

What 2 findings on ECG are indicative of 3rd degree AV blocks?

A
  1. atrial rate (120-160 bpm) and ventricular rates (40-60 bpm) are regular, but not associated with each other
  2. wide QRS complex if ventricular OR narrow QRS complex if junctional
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18
Q

Junctional escape vs. ventricular escapes; 3rd degree AV block:

A
  • JUNCTIONAL = conduction block at AV node, pacemaker from His bundle, narrow QRS complexes
  • VENTRICULAR = conduction block below His and bundle branches, pacemaker from Purkinje fibers, wide QRS complexes (takes longer to reach = wider)
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19
Q

What is occurring in these ECGs?

A

3rd degree AV block

  • no relation between P and QRS
  • wider escape beats = ventricular
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20
Q

What is occurring in this ECG?

A

3rd degree AV block

  • sinus rate = 120 bpm
  • ventricular rate = 40 bpm
  • wide QRS = ventricular
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21
Q

What is occurring in this ECG?

A

3rd degree AV block

  • sinus rate = 150 bpm
  • ventricular rate = 50 bpm
  • narrow QRS = junctional
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22
Q

What is occurring in this ECG?

A

3rd degree AV block

  • no correltion between P waves and QRS complexes
  • no constant PR interval
  • wide QRS = ventricular
23
Q

What clinical signs are associated with 3rd degree AV blocks? What treatment is indicated? What 2 are contraindicated?

A
  • collapse, syncope, fainting
  • sudden death
  • backward failure - CHF
  • forward failure - GI weakness, collapse, lethargy, azotemi

pacemaker

  1. Lidocaine
  2. Atropine - does not respond
24
Q

How does the left bundle separate?

A

into 2 fascicles —> anterior fascicle and posterior fascicle

24
Q

AV blocks:

A
25
Q

What are fascicular/bundle branch blocks? How is the rest of the heart affected?

A

delayed or blocked conduction in one of the bundle branches resulting in widened QRS complexes

  • SA and AV nods are still functional (normal atria!)= normal P waves and PR intervals
  • ventricles are activated non-simultaneously
  • not normal, r/o structural disease
26
Q

What is seen on ECGs with right bundle branch blocks?

A
  • normal P waves and PR intervals
  • negative QRS complex
27
Q

What is occurring in this ECG?

A

right bundle branch block

  • negative QRS
28
Q

What must be ruled out if a right bundle branch block is seen?

A

right ventricular disease

  • enlargement of right heart
  • infection (Chagas)
  • neoplasia
  • infarction
  • fibrosis
  • trauma
  • normal variant

no hemodynamic consequences common

29
Q

What is seen in these ECGs?

A

right bundle branch block

  • deep S
  • prolonged and negative QRS
  • decreased R
30
Q

What is occurring in this ECG?

A

right bundle branch block

  • P wave present!
  • small R
  • deep S
  • long and negative QRS
31
Q

What is indicative of left BBB/fascicular disease on ECGs? What causes this?

A

wide positive QRS complex preceded by a P wave

conduction delay in the left ventricle, making LV activated later in the electrical cycle

32
Q

What needs to be ruled out in cases of left BBB/fascicular disease?

A

LV disease

  • eccentric hypertrophy - DCM, CVD
  • concentric hypertrophy - SAS, HCM, HOCM, hyperthyroidism, infiltrative disease, systemic hypertension
  • VPC
33
Q

What is occurring in this ECG?

A

left bundle branch block

  • normal P wave
  • wide positive QRS
  • normal height and CO
34
Q

What is occurring in these ECGs?

A

left bundle branch block

  • normal P wave
  • wide, positive QRS
35
Q

What is the major difference in VPCs and bundle branch blocks?

A

bundle branch blocks are associated with normal P waves

36
Q

Fascicular/BBB:

A
37
Q

What is sinus sick syndrome? What causes it?

A

(sinus nodal dysfunction) - SA nodal dysfunction with periods of severe sinus block, intermittent sinus arrest/AV blocks or cardiac standstill when the AV pacemaker does not take over

AV node pathology - scar tissue

38
Q

What are 5 ECG findings in cases of sinus sick syndrome?

A
  1. severe and persistent sinus bradycardia (not from drugs!)
  2. sinus block occurs with or without escape rhythm
  3. bradycardia-tachycardia syndrome = severe sinus bradycardia alternates with ectopic supraventricular tachycardias
  4. long pause after APC
  5. AV junctional rhythm or slow Afib
39
Q

What are some higher risk breeds that develop sinus sick syndrome? How do they typically present? What is required for definitive diagnosis?

A
  • Miniature Schnauzer (~6 y/o)
  • WHWT
  • Cocker Spaniel
  • Dachshund
  • NOT seen in cats

syncopal events (can look like seizures)

Holter monitor

40
Q

Sick sinus syndome, tachy-brady syndrome:

A
41
Q

What is occurring in these ECGs?

A

sinus sick syndrome

  • tachy-brady syndrome
  • arrest
42
Q

What treatment is required in sick sinus syndrome? What is not commonly used?

A

permanent pacemaker implantation

anticholinergic medications —> unreliable, may exacerbate arrhythmias

43
Q

What is electrical alternans? What are 3 causes?

A

low voltage/amplitude complexes

  1. obesity
  2. pleural or pericardial effusions = swinging heart in pericardial sac
  3. pneumothorax
44
Q

What is seen on ECGs in cases of electrical alternans?

A

alternating QRS amplitude seen in any or all leads with no additional changes to the conduction pathways of the heart

45
Q

What are the major treatments for tachyarrhythmias and bradyarrhythmias?

A

TACHY = anti-arrhythmic therapy immediately

BRADY = permanent pacemaker

46
Q

What is a major exception in the treatment of bradyarrhythmias?

A

hyperkalemia —> may respond to theophylline

  • first goal is to decrease K
47
Q

What are the 2 major indications of treating tachyarrhythmias?

A
  1. hemodynamic consequences - severe tachycardia, decreased cardiac function, hypotension, heart failure, syncope/collapse
  2. electrical instability - can lead to sudden death, complex ventricular arrhythmias, systolic dysfunction, Boxers/Dobermans
48
Q

What is the goal of treating arrhythmias? In hospital? At home?

A

prevent syncope and sudden cardiac death —> does NOT completely alleviate risk of sudden cardiac death even with chronic threatment

  • IN-HOSPITAL = unstable patients —> alleviate clinical signs, control or convert hemodynamically relevant arrhythmias
  • HOME = stable patients —> reduce clinical signs
49
Q

What are the 4 classes of antiarrhythmic drugs? How do they work?

A
  1. SODIUM CHANNEL BLOCKERS - slows conduction in atrial and ventricular tissues by stabilizing membranes and prologing repolarization (Lidocaine, Mexiletine, Procainamide)
  2. BETA-BLOCKERS - slows conduction in SA and AV nodes, reduces excitability of all cells (Atenolol, Esmolol, Carvedilol, Propranolol)
  3. POTASSIUM CHANNEL BLOCKERS - prolongs repolarization in all cells (Sotalol, Amiodarone)
  4. CALCIUM CHANNEL BLOCKERS - slows conduction in SA and AV nodes (Diltiazem, Verapamil)
50
Q

What is the goal of treating supraventricular tachycardias? What are the 4 most common options?

A

(Afib, Atach) - HR control, not return to normal rhythm

  1. vagal maneuver
  2. Digoxin - increases AV node function (good for CHF); check levels weekly, hypokalemia predisposes to toxicity
  3. Diltiazem - good for cats, increases AV node function, better control of rate control
  4. Atenolol - can decrease cardiac output, which completely compromises patients with CHF
51
Q

What is the goal of treating ventricular tachycardias? What are the 3 most common options?

A

only treating symptomatic patients or those with malignant arrhythmias (degeneration to ventricular fib/flutter)

  1. Lidocaine (Class I agents) - does not prolong lifespan, controls number of irregular beats to decrease symptoms (Mexiletine or Procainamide are better long-term)
  2. Atenolol - commonly combined with Mexiletine for Boxers in Vtach
  3. Sotalol - minimal side effects
52
Q

What is the goal of treating bradycardias? How are sick sinus syndrome and AV blocks treated?

A

only treating patients that absolutely need it —> treatment not necessarily needed if patient is asymptomatic

  • SINUS SICK SYNDROME - combination of tachy/brady makes treatment difficult, usually require a pacemaker to prevent bradycardia and aggressive treatment of tachycardia
  • AV BLOCKS - may respond to Atropine, Theophylline, pacemakers for 3rd degree that is commonly not responsive to therapy