Arrhythmias: Disorders of Impulse Conduction Flashcards
What is an AV block? What are some extra-cardiac and intra-cardiac causes?
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
Heart blocks:
What is a 1st degree AV block? What are 3 ECG findings?
prolonged AV nodal conduction time —> AV node conducts slower than normal through the AV junction and bundle of His
- normal rate, rhythm, P waves, and QRS complexes
- prolonged PR interval (>0.13s in dogs, >0.09s in cats)
- 1:1 conduction - a P wave for every QRS
What is occurring in this ECG?
first degree AV block
What are some physiologic and pathologic causes of first-degree AV blocks?
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
What treatment is indicated for 1st degree AV blocks?
usually asymptomatics
- evaluate for structural cardiac disease
- monitor for disease progression
What are 2nd degree AV blocks? What are 3 ECG findings?
when atrial depolarization intermittently fails to conduct through the AV node to the ventricles (lonely P wave)
- more P waves than QRS complexes
- some P waves still conduct through
- PR intervals can be variable
What is a Mobitz Type I AV block? What is seen on ECG?
(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
What are Mobitz Type I AV blocks associated with? What treatment is recommended?
- high vagal tone
- drug-mediated
- physiologic > pathologic
treat underlying cause for increased vagal tone or reverse drug eliciting AV block —> responds to Atropine
What is occurring in this ECG?
Mobitz Type I AV block (Wenckebach)
- PR intervals gradually elongate until a P wave is completely blocked
What is a Mobitz Type II AV block? What is seen on ECGs?
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
What is the clinical significance of Mobitz Type II AV blocks? What is it commonly exacerbated by? What treatment is recommended?
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
What is occurring in this ECG?
Mobitz Type II AV block
- consistent PR intervals, P wave conduction fails at second arrow
What indicates a low grade vs. high grade Mobitz Type II AV blocks?
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
Mobitz Type I vs. Type II
2nd degree AV block
What is a 3rd degree AV block?
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
What 2 findings on ECG are indicative of 3rd degree AV blocks?
- atrial rate (120-160 bpm) and ventricular rates (40-60 bpm) are regular, but not associated with each other
- wide QRS complex if ventricular OR narrow QRS complex if junctional
Junctional escape vs. ventricular escapes; 3rd degree AV block:
- 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)
What is occurring in these ECGs?
3rd degree AV block
- no relation between P and QRS
- wider escape beats = ventricular
What is occurring in this ECG?
3rd degree AV block
- sinus rate = 120 bpm
- ventricular rate = 40 bpm
- wide QRS = ventricular
What is occurring in this ECG?
3rd degree AV block
- sinus rate = 150 bpm
- ventricular rate = 50 bpm
- narrow QRS = junctional
What is occurring in this ECG?
3rd degree AV block
- no correltion between P waves and QRS complexes
- no constant PR interval
- wide QRS = ventricular
What clinical signs are associated with 3rd degree AV blocks? What treatment is indicated? What 2 are contraindicated?
- collapse, syncope, fainting
- sudden death
- backward failure - CHF
- forward failure - GI weakness, collapse, lethargy, azotemi
pacemaker
- Lidocaine
- Atropine - does not respond
How does the left bundle separate?
into 2 fascicles —> anterior fascicle and posterior fascicle
AV blocks:
What are fascicular/bundle branch blocks? How is the rest of the heart affected?
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
What is seen on ECGs with right bundle branch blocks?
- normal P waves and PR intervals
- negative QRS complex
What is occurring in this ECG?
right bundle branch block
- negative QRS
What must be ruled out if a right bundle branch block is seen?
right ventricular disease
- enlargement of right heart
- infection (Chagas)
- neoplasia
- infarction
- fibrosis
- trauma
- normal variant
no hemodynamic consequences common
What is seen in these ECGs?
right bundle branch block
- deep S
- prolonged and negative QRS
- decreased R
What is occurring in this ECG?
right bundle branch block
- P wave present!
- small R
- deep S
- long and negative QRS
What is indicative of left BBB/fascicular disease on ECGs? What causes this?
wide positive QRS complex preceded by a P wave
conduction delay in the left ventricle, making LV activated later in the electrical cycle
What needs to be ruled out in cases of left BBB/fascicular disease?
LV disease
- eccentric hypertrophy - DCM, CVD
- concentric hypertrophy - SAS, HCM, HOCM, hyperthyroidism, infiltrative disease, systemic hypertension
- VPC
What is occurring in this ECG?
left bundle branch block
- normal P wave
- wide positive QRS
- normal height and CO
What is occurring in these ECGs?
left bundle branch block
- normal P wave
- wide, positive QRS
What is the major difference in VPCs and bundle branch blocks?
bundle branch blocks are associated with normal P waves
Fascicular/BBB:
What is sinus sick syndrome? What causes it?
(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
What are 5 ECG findings in cases of sinus sick syndrome?
- severe and persistent sinus bradycardia (not from drugs!)
- sinus block occurs with or without escape rhythm
- bradycardia-tachycardia syndrome = severe sinus bradycardia alternates with ectopic supraventricular tachycardias
- long pause after APC
- AV junctional rhythm or slow Afib
What are some higher risk breeds that develop sinus sick syndrome? How do they typically present? What is required for definitive diagnosis?
- Miniature Schnauzer (~6 y/o)
- WHWT
- Cocker Spaniel
- Dachshund
- NOT seen in cats
syncopal events (can look like seizures)
Holter monitor
Sick sinus syndome, tachy-brady syndrome:
What is occurring in these ECGs?
sinus sick syndrome
- tachy-brady syndrome
- arrest
What treatment is required in sick sinus syndrome? What is not commonly used?
permanent pacemaker implantation
anticholinergic medications —> unreliable, may exacerbate arrhythmias
What is electrical alternans? What are 3 causes?
low voltage/amplitude complexes
- obesity
- pleural or pericardial effusions = swinging heart in pericardial sac
- pneumothorax
What is seen on ECGs in cases of electrical alternans?
alternating QRS amplitude seen in any or all leads with no additional changes to the conduction pathways of the heart
What are the major treatments for tachyarrhythmias and bradyarrhythmias?
TACHY = anti-arrhythmic therapy immediately
BRADY = permanent pacemaker
What is a major exception in the treatment of bradyarrhythmias?
hyperkalemia —> may respond to theophylline
- first goal is to decrease K
What are the 2 major indications of treating tachyarrhythmias?
- hemodynamic consequences - severe tachycardia, decreased cardiac function, hypotension, heart failure, syncope/collapse
- electrical instability - can lead to sudden death, complex ventricular arrhythmias, systolic dysfunction, Boxers/Dobermans
What is the goal of treating arrhythmias? In hospital? At home?
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
What are the 4 classes of antiarrhythmic drugs? How do they work?
- SODIUM CHANNEL BLOCKERS - slows conduction in atrial and ventricular tissues by stabilizing membranes and prologing repolarization (Lidocaine, Mexiletine, Procainamide)
- BETA-BLOCKERS - slows conduction in SA and AV nodes, reduces excitability of all cells (Atenolol, Esmolol, Carvedilol, Propranolol)
- POTASSIUM CHANNEL BLOCKERS - prolongs repolarization in all cells (Sotalol, Amiodarone)
- CALCIUM CHANNEL BLOCKERS - slows conduction in SA and AV nodes (Diltiazem, Verapamil)
What is the goal of treating supraventricular tachycardias? What are the 4 most common options?
(Afib, Atach) - HR control, not return to normal rhythm
- vagal maneuver
- Digoxin - increases AV node function (good for CHF); check levels weekly, hypokalemia predisposes to toxicity
- Diltiazem - good for cats, increases AV node function, better control of rate control
- Atenolol - can decrease cardiac output, which completely compromises patients with CHF
What is the goal of treating ventricular tachycardias? What are the 3 most common options?
only treating symptomatic patients or those with malignant arrhythmias (degeneration to ventricular fib/flutter)
- Lidocaine (Class I agents) - does not prolong lifespan, controls number of irregular beats to decrease symptoms (Mexiletine or Procainamide are better long-term)
- Atenolol - commonly combined with Mexiletine for Boxers in Vtach
- Sotalol - minimal side effects
What is the goal of treating bradycardias? How are sick sinus syndrome and AV blocks treated?
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
