Arrhythmias

Front 1

What are pacemakers?

Back 1

Ectopic electrical signal sent to heart; used for certain bradyarrhythmias

Front 2

Indications of using a pacemaker -

Back 2

• Indications: Mobitz II AV block, 3° AV block, symptomatic bradycardias
• Not indicated: asymptomatic bradycardias that are unlikely to cause danger

Front 3

Etiology of some arrhythmias -

Back 3

Structural disease: may cause abnormalities in impulse conduction
• Scars: resulting from ischemia, cardiac injury. Scars are composed of fibrotic tissue, which does not conduct impulses, and viable tissue, which does. This mish-mash of variably conducting tissue may result in an anterograde block or a re-entry loop.
• Congenital abnormal connections: conducting tissue where there should not be any, either within the AV node (microcircuit re-entry), or outside the valves on the wall of the myocardium (macrocircuit re-entry)

Front 4

Long QT syndrome -

Back 4

This heritable condition gives a long QT due to prolonged ventricular repolarization, and anything that prolongs QT can lead to torsades de point → sudden cardiac death.

# of diff forms of QT - some auto. dom, some auto recc

Not everybody who has gene has EKG finding
Not everyone with EKG findings have problem

Front 5

Brugada sydnrome -

Back 5

persistent ST elevations in V1-V3
RBBB ECG pattern.
Causes sudden cardiac death
Young Asian males are more affected.

Front 6

Hypertrophic cardiomyopathy -

Back 6

hypertrophy results in stretching of conduction fibers & disorganization, which can lead to lethal arrhythmias

Front 7

RVOT -

Back 7

LBBB seen with wide complex QRS tachycardia (ie ventricular tachycardia).

Generally asymptomatic and not dangerous, but must be differentiated from other dangerous ventricular tachycardia’s -> can appear in nL heart; not lethal

Tx with meds and ablation

Front 8

RV dysplasia -

Back 8

RV cardiomyopathy
Hallmark on EKG - Inverted T wave lead 1-3

Look for fatty infiltration of RV
Dx: MRI, not biopsy

Front 9

What is sinus bradycardia?

Back 9

sinus means atria beat before ventricles (P wave precedes QRS wave)

Front 10

What is sick sinus syndrome?

Back 10

SA node dysfunction resulting in sinus brady, pause, arrest

Front 11

What is tachybrady syndrome?

Back 11

subset of SSS, with alternating sinus brady & tachy

Front 12

What is vasovagal reaction?

Back 12

pain, anxiety, stress → sympathetic/parasympathetic response
o Increase in parasympathetic vagus nerve → bradycardia
o Decrease in sympathetic tone → vasodilation leading to hypotension

Front 13

Reasons for iatrogenic sinus bradycardia?

Back 13

o Drugs: β-blockers, CCBs, parasympathomimetics, digoxin, antiarrhythmics
o Procedures: damage to conducting system can occur during cardiac catheterization, EP studies, other surgery → scar tissue does not conduct impulses

Front 14

Reasons for ischemic mediated bradycardia?

Back 14

infarct of coronary artery may cause ischemia to SA and AV nodes
o RCA: usually supplies both SA and AV nodes
o LAD: may supply SA node, depending on anatomy

Front 15

1st degree AV block -

Back 15

delay across the AV node reflected as PR interval > 0.2s, but every atrial impulse still results in a ventricular beat (1:1 conduction)

Front 16

2nd degree AV block (Wenckeback's) type 1 -

Back 16

PR interval progressively prolongs and then QRS wave drops out
o Block is located in the AV node
Not usually indicated for pacemaker

Front 17

2nd degree Morbitz type II AV block -

Back 17

QRS wave drops out without a graduation of PR interval
o Block is located in His Bundle
Usually indicated for pacemaker

Front 18

3rd degree AV block -

Back 18

no association between atrial impulses and ventricular beats
o Block is located in either AV node or His Bundle

Front 19

• Premature ventricular contraction (PVC

Back 19

ectopic beat arising from ventricle, seen as a wide complex QRS not preceded by a P wave

Front 20

Etiology, presentation and tx of PVC -

Back 20

o Etiology: hypoxia, electrolyte abnormality, hyperthyroidism, stimulants
o Presentation: usually asymptomatic, may feel palpitations
o Treatment: β-blockers if symptomatic, ICD is repetitive PVCs (risk of VFib)

Front 21

Ventricular tachycardia -

Back 21

tachycardia originating below bundle of His, defined as a rapid firing of 3+ PVCs in a row at a rate above 100 bpm

Front 22

Etiology. presentation, treatment of VT -

Back 22

o Etiology: CAD, MI, cardiomyopathies, congenital heart defect, congenital QT
o Presentation: asymptomatic if nonsustained. Sustained VT (>30 seconds) usually symptomatic with palpitations, hypotension, angina, syncope; may lead to VFib
o Treatment: antiarrhythmics and/or cardioversion & ICD placement

Front 23

What is Torsades de point?
Etiology
Presentation
Treatment

Back 23

a type of ventricular tachycardia characterized by polymorphous QRS complexes in a shifting sinusoidal pattern, preceded by a prolonged QT

o Etiology: QT syndrome, class III antiarrhythmics, TCAs, hypocalcemia/kalemia/magnesemis, structural heart disease, ischemia
o Presentation: palpitations, dizziness, syncope, sudden death
o Treatment: Mg+ provides cardiac stabilization, address underlying disorder

Front 24

What is ventricular fibrillation?

Back 24

multiple foci of ventricles fire randomly leading to quivering ventricles and no CO, seen as erratic QRS complexes

Front 25

Etiology/Presentation/Tx of Vfib -

Back 25

o Etiology: ischemic heart disease, torsades, combination of Afib + WPW
o Presentation: syncope, no blood pressure, pulselessness, death
o Treatment: immediate defibrillation and CPR → advanced cardiac life support

Front 26

What are SVTs and 3 main causes of it -

Back 26

SVTs: tachycardias that originate above the ventricles, occurring as a result of the following -

1. Increased/abnormal automaticity
2. Triggered activity (EAD/DAD)
3. Re-entry

Front 27

Explain increased/abnL automaticity -

Back 27

change in activity within the atria due to…
a. Increased sympathetic stimulation of SA node
b. Cells outside SA node start to spontaneously depolarize
c. Change in resting membrane potential (ie from ischemia, electrolyte abnormalities) making it easier to depolarize

Front 28

Explain triggered activity

Back 28

abnormal depolarization triggered by a previous beat
a. Early after depolarization: depolarization before repolarization is complete
i. Increase in time of repolarization (extended opening of Ca channels during phase 2, or opening of Na channels during phase 3)
ii. Due to ischemia, hypokalemia, catecholamine excess, mechanical injury
b. Delayed after depolarization: depolarization after repolarization, but before a normal AP normally occurs (phase 4)
i. Excess Ca within the SR of cell resulting in spontaneous depolarization
ii. Due to digitalis toxicity, hypokalemia, hypercalcemia, catecholamines

Front 29

Explain re-entry -

Back 29

accessory pathway exists, where impulses can travel retrograde and back around to original pathway; requires unidirectional block with slow conduction in other pathway to allow enough recovery time for reentry
a. Micro-reentrant: occur within the AV node = AV Nodal reentrant tachycardia
b. Macro-reentrant: outside the AV node = AV reentrant tachycardia

Front 30

What is Afib?

Back 30

most common arrhythmia
• Description: multiple foci in atria fire continuously and in a chaotic pattern, resulting in a quivering atria & irregular rapid ventricle. Impulses commonly originate around the pulmonary veins. Classified as paroxysmal or continuous/refractory.
o ECG: no P waves, irregularly irregular QRS waves

Front 31

Etiology of Afib -

Back 31

HTN, valve disease, CAD, thyrotoxicosis, EtOH (holiday heart syndrome), pericardial disease, COPD, pheochromocytoma, sick sinus syndrome
• Presentation: range from asymptomatic to dyspnea, fatigue, palpitations; irregularly irregular rhythm on physical exam
o Complications: stroke, other embolic disease, angina, hypotension, syncope

Front 32

Treatment of Afib -

Back 32

rate control & anticoagulation >>> rhythm control & symptoms
o Rate: β-blockers or calcium channel blockers
o Anticoagulation: aspirin for low risk, warfarin for high risk (CHADS score)
o Rhythm: consider anti-arrhythmics, usually amiodarone
o Symptoms usually controlled with rate control, but some still feel symptomatic
• Cardioversion: shock the heart back into sinus rhythm (Note: unless the patient has been on therapeutic warfarin therapy, must do Echo to rule out ventricular thrombus)
• Ablation: ablate around the pulmonary veins; usually last ditch effort

Front 33

Atrial flutter -

Back 33

• Description: single automaticity focus in atria fires at 250-350 bpm, with atrial impulses being transmitted to the ventricles in a predictable pattern (2:1 or 3:1 conduction)
o ECG: sawtooth pattern (atrial contractions)

Front 34

Etiology/presentation/treatment of Afib -

Back 34

• Etiology: CAD, CHF, valvular disease, COPD
• Presentation: fatigue, palpitations, embolic disease (similar to A fib)
• Treatment: similar to A fib, except ablation is more effective

Front 35

Wolff-Parkinson-White disease -

Back 35

• Description: accessory pathway from atria to ventricles called the Bundle of Kent, located in the atrioventricular valvular rings. Pathway does not share the rate controlling properties of the AV node, allowing early depolarization of part of the ventricle
o ECG: short PR interval, delta wave, widened QRS

Front 36

Etiology, presentation, treatment of WPW -

Back 36

• Etiology: congenital
• Presentation: asymptomatic to syncope, palpitations
o Atrial premature beat may lead to orthodromic reciprocating tachycardia (reentry loop through accessory pathway, without a delta wave) or antidromic AVRT
o Atrial fibrillation with WPW can lead to ventricular fibrillation & sudden death
• Treatment: risk stratification – look for risk of atrial tachyarrhythmias on top of WPW, which predisposes to sudden death
o Ablation: very successful
o Avoid drugs that slow AV conduction because that may increase conduction through the accessory pathway

Front 37

Atrioventricular & AV Nodal re-entrant tachycardia -

Back 37

• Description: (1) Sinus beat conducted down both the fast & slow pathways. (2) Premature atrial contraction shoots out of the atria, but the fast pathway is still refractory, giving a unidirectional block. (3) Conduction through the slow pathway results in retrograde conduction via the fast pathway.
o AVRT: pathways located around the valves
o AVNRT: pathways within the AV node
o ECG: note upside down P wave (above); may have narrow or wide QRS depending on which pathways is depolarizing the ventricles

Front 38

Atrioventricular & AV Nodal re-entrant tachycardia etiology -

Back 38

• Etiology: ischemic heart disease, digoxin toxicity, caffeine/alcohol may exacerbate
• Presentation: may feel palpitations, generally not dangerous

Front 39

Atrioventricular & AV Nodal re-entrant tachycardia treatment -

Back 39

(1) Maneuvers (Valsalva, carotid massage, breath holding, head immersion in cold water) to stimulate vagus delay of AV conduction. (2) Adenosine decreases AV nodal activity. (3) Electric cardioversion.
• Ablation if episodes are recurrent and symptomatic