11/9 Cardiac Arrhythmias - Coromilas Flashcards
types of arrhythmias
2 large categories & subtypes
bradyarrythmias
- SA node dysfx
- atrioventricular block
tachyarrhythmias
- supraventricular arrhythmias
sinus bradycardia in normals
mech
etiology
clinical presentation
tx
mechanism: decr automaticity in SA node
etiology:
- incr PSNS tone
- medications
clinical presentation:
- fatigue, dizziness, or asymptomatic
- trained athletes
- beta blockers, Ca blockers
tx: n/a (or treat underlying cause if symptomatic)
sinus bradycardia in disease
mech
etiology
clinical presentation
tx
mechanism: decr automaticity in SA node
etiology:
- age, atrial fibrosis, SCN5A mutation
- Sick Sinus Syndrome
clinical presentation:
- fatigue, dizziness, or asymptomatic
tx: pacemaker if symptomatic
brady-tachy syndrome
often with atrial fibrillation!
req pacemaker
extended PR interval
most likely reason?
prob slowing in AV node!
approx 1/2 to 2/3 of PR interval comprises atria→bundleofHis transmission
first degree AV block
mech
etiology
clinical presentation
tx
prolonged PR interval (>240ms)
mechanism: slowed conduction in AV node
etiology:
- incr PSNS tone
- medications
- MI
- chronic degen disease of conduction system
clinical presentation:
- patients on beta blockers, Ca channel blockers, digitalis
- age
- usually asymptomatic!
tx: non or adjust meds
Mobitz type I
(2nd degree AV block)
P waves in regular, normal rate
one of those P waves occasionally does not conduct
Mobitz Type I (vs type II): prolonged PR interval
- usually benign (vs. Mobitz type II, which is not)
aka Wenckebach
mechanism: impaired conduction in AV node with intermittent block
etiology:
- incr PSNS tone
- medications
- inferior MI
- congenital AV block
- myocarditis
clinical presentation:
- beta blockers, Ca channel blockers, digitalis
- palpitations
- dizziness
- could be asymptomatic
tx: usually reversible removing medication or with time
Wenckebach 2nd degree AV block
PP interval steady
PR interval increases, then resets
RR interval decreases, then gets long (with skipped beat)
Mobitz type III
(2nd degree AV block)
P waves in regular, normal rate
one of those P waves occasionally does not conduct
Mobitz Type I (vs type II): NO prolonged PR interval
mechanism: intermittent conduction block distal to AV node (in bundle of His)
etiology:
- permanent structural damage in His-Purkinje system
- extensive anterior MI
- chronic degen in HisPurkinje system
clinical presentation:
- syncope (Stokes-Adams), dizziness
- prolonged HV interval
tx: pacemaker
diff between Mobitz I and Mobitz II
Mobitz I
- progressively prolonged PR interval (followed by dropped QRS)
- usually benign
Mobitz II
- no prolonged PR interval (but is still followed by dropped QRS)
- affects conduction system, so potential to get much worse
complete heart block
(3rd degree)
AV dissociation (atria and ventricles dissociated from each other)
mechanism: complete failure of conduction between atria and ventricles
etiology:
- block below level of AV node (His-Purkinje system)
- extensive anterior MI
- chronic degen in His-Purkinje system
clinical presentation:
- syncope, lightheadedness
- assoc with BBB
tx: pacemaker
escape rhythms in sinus arrest
junctional escape = 50 bpm
ventricular escape = 21 bpm
mechanism: normal automaticity of latent pacemakers
precipitating factors:
- decr sinus node automaticity
- impaired AV conduction
clinical presentation:
- sinus arrest
- complete heart block
- dizziness
- syncope
- asymptomatic
tx: pacemaker
tachycardia:
supraventricular arrhythmias
sinus node
- sinus tachycardia
atria
- atrial premature complexes
- atrial tachycardia
- atrial flutter
- atrial fibrillation
AV node
- junctional premature depolarizations (complexes)
- AVNRT or AVRT (nodal reentry tachy or reciprocating tachy)
sinus tachycardia
mechanism
increased automaticity of SA node
etiology
- incr SNS tone
clinical presentation
- exercise/excitement
- fever, pain
- low CO, CHF
- anemia
- hyperthyroidism
treatment
underlying cause
APC
atrial premature complexes
mechanism
- abnormal automaticity
- delayed afterdepolarizations
- reentry (less likely)
etiology
- incr SNS tone, stretch, fibrosis
clinical presentation
- may occur in healthy or diseased hearts
- caffeine, alcohol
- adrenergic stimulation
- palpitations
- asymptomatic
atrial tachycardia
P wave in front of each QRS
rate: 100-150bpm
mechanism:
- abnormal automaticity
- delayed afterdepol
- reentry
etiology:
- incr SNS tone
- stretch, scar, prior surgery
clinical presentation:
- may occur in healthy or diseased hearts
- caffeine, alcohol
- adrenergic stim
- palpitations
- dizziness
tx:
- beta blockers, Ca channel blockers
- class IC or III antiarrhythmic drugs
- ablation
atrial flutter
atrial rate is v high, approx 300bpm
ventricular rate doesn’t match up (slower, maybe 75bpm)
SAWTOOTH PATTERN
mechanism
- reentry along tricuspid valve annulus
- typical: counterclockwise, sawtooth pattern
etiology
- areas of scar
- prior surgery
- dx of AF
- no heart disease
clinical presentation
- palpitations, dyspnea, chest discomfort, SVT at 150bpm
treatment
- beta blockers, Ca channel blockers to slow conduction across AV node/decrease ventricular rate
- cardioversion
- ablation
atrial fibrillation
continuous noise in EKG
no discrete P waves
irregularly irregular pattern
mechanism: reentry, focal PV origin
- multiple wandering atrial circuits
- paroxysmal? pulmo vein triggers
precipitating factors:
- LA enlargement
- LA fibrosis
- scarring
- PV triggers
clinical presentation:
- palpitation
- CVA
- heart failure
treatment:
- rate control: beta blockers, Ca channel blockers, digitalis
- rhythm control: cardioversion, class IC, class III, ablation
afib chronic treatment
- anticoagulation
- rate control
- (beta blockers, Ca blockers) to slow conduction across AV node and decr ventricular rate
- rhythm control
- class IC or class III antiarrhythmic drugs
- ablation
PSVT
paroxysmal supraventricular tachycardia
- AV nodal reentrant tachycardia
- AV reentrant tachycardia
- atrial trachycardia (focal or reentrant)
PSVT
AV nodal reentrant tachycardia
mechanism: reentry
etiology: dual AV nodal pathways
clinical presentation:
- teens, young adults, but can also present late
- rates usually approx 190bpm (140-250)
- palpitations, dizziness, dyspnea, chest pain
treatment:
- vagal maneuvers
- adenosine
- ablation
- pharma: Ca channel blockers, beta blockers
typically dont see a P wave!
PSVT
AV reentrant tachycardia
mechanism: reentry
etiology: bypass tract (manifest, as in WPW, or concealed)
clinical presentation:
- teens, young adults, but can also present late
- rates usually approx 220bpm (140-250)
- palpitations, dizziness, dyspnea, chest pain
treatment:
- vagal maneuvers
- adenosine
- ablation
- pharma: class Ic, class III
narrow complex
PSVT
AF and ventricular pre-excitation
mechanism: rapid conduction across bypass tract
etiology: bypass tract (manifest, as in WPW)
clinical presentation:
- hypotension
- syncope
- cardiac arrest
- SCD
treatment:
- cardioversion
- class IA - IV procainamide
- AVOID Ca blockers, beta blockers, digoxin
narrow complex
review:
supraventricular tachyarrhythmias
ventricular arrhythmias
- VPC: ventricular premature complexes
- ventricular tachycardia
- monomorphic
- polymorphic
- Torsades de Pointes VT
- ventricular fibrillation
ventricular premature complexes
from here on, look at slides for info.
Torsades de Pointes VT
mechanism: EADs (long QT)
etiology:
- class III AAD or other drugs with Class III effects
- congenital Long QT Syndrome
clinical presetation:
- palpitation
- dizziness
- syncope
- SCD
acute tx:
- IV magnesium
- defibrillation
- IV lidocaine
- remove precipitating drug
- pacing
- isoproternol
genetic mutations and ventricular arrhythmias
- long QT syndrome
- Brugada syndrome
- familiar catecholaminergic polymorphic VT
- arrhythmogenic RV cardiomyopathy
congenital long QT syndromes
LQT1 (KCNQ1): triggered by activities like swimming
- beta blockers: +++ effective
LQT2 (KCNQ1): susceptible to auditory stim
- beta blockers: ++ effective
LQT3 (SCN5A): usually at night/rest
- beta blockers: +/- neutral
LQT1,2,3syndromes account for 95% of genes identified and 75% of all LQT
Brugada Syndrome
3 types
familial catecholaminergic polymorphic VT
mechanism:
- mutation in genes coding for calcium handling proteins (RyR2)
- DAD
clinical presentation:
- stress induced syncope or SCD in pt with normal ECG and no structural heart disease
treatment:
- beta blockers
- ICD
arrhythmogenic RV cardiomyopathy
- genetically determined
- mutations in desmosomal proteins
- progressive replacement of RV myocardium with fatty/fibrous tissue
ventricular arrhythmias of RV origin
