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Arrhythmias

MELISSA DEAN, BSN-BC


Objectives

1. Review pathophysiology basics


2. Familiarize yourself with arrhythmias
3. Causes of arrhythmias
4. Types of arrhythmias
5. Risks associated with arrhythmias
6. Diagnostics
7. Treatments
8. Monitoring
9. Patient teaching
Arrhythmias

▪ Tachyarrhythmia
▪ Bradyarrhythmia
▪ Symptomatic
▪ Asymptomatic
Symptomatic

▪ Palpitations
▪ Weakness
▪ ALOC
▪ Heart failure
▪ Sudden death
▪ Diaphoresis
▪ Palpitations
Electrical – conduction – structural

▪ Myocardial ischemia ▪ Thyroid disorder


▪ Chronic HF ▪ Renal failure
▪ Imbolism
▪ Electrolyte disturbances
▪ Cardiac tamponade
▪ Drugs
▪ Hypoxemia
▪ Caffeine
▪ HTN
▪ Valvular disease
▪ Ethanol
▪ Hypoxemia ▪ Anxiety
Pathophysiology

▪ Basic review
▪ Action potential
▪ Sodium potassium pump
▪ Polarization cycle
▪ Anatomy of the pacemakers
▪ Cardiac conduction
Action potential

▪ Phase 0
▪ Depolarization
▪ Influx of Na+

▪ Phase 1
▪ Initial repolarization (rapid)
▪ Inactivation of inward Na+
▪ Activation of outward K+

▪ Phase 2
▪ Plateau
▪ Outward K+
▪ Influx Ca2+

▪ Phase 3
▪ Repolarization
▪ K+ influx

▪ Phase 4
▪ Gradual depolarization
▪ Na+ leakage into intracellular space
▪ Decrease efflux of K+
▪ Increase in Na+ permeability
Cardiac conduction

▪ Specialized cells
▪ Send messages that cause
contraction

▪ SA node - sinoatrial
▪ AV node - atrioventricular
▪ Bundle of His
▪ Bundle branches
▪ Purkinje fibers
Cardiac conduction

▪ Pacemakers ▪ SA node
▪ SA and AV nodes ▪ Impulse origin
▪ Regulates
▪ Regulated by the autonomic
▪ Both atria – left and right
nervous system ▪ AV node
▪ Neural impulses not needed to
maintain
▪ Heart will beat without nervous ▪ AV node
connection
▪ Regulates
▪ Sympathetic/parasympathetic ▪ Both ventricles – left and right
▪ Regulates heart rate ▪ Septum
▪ Delays conduction
▪ Boosts ventricular filling
Cardiac conduction

▪ Bundle of His
▪ Muscle fibers
▪ Also called AV bundle

▪ Bundle branches
▪ Left
▪ Right

▪ Purkinje fibers
Cardiac conduction

Heart Conduction
Arrhythmias causes

▪ Disorders ▪ Automaticity
▪ Impulse formation ▪ Spontaneous depolarization
▪ Impulse conduction ▪ Three factors
▪ Diastolic depolarization
▪ Ectopic pacemakers ▪ Rate of depolarization
▪ Level of threshold potential
▪ Impulse conduction = action
▪ Reentry
potential
▪ Impulse
▪ Blocked or slowed
▪ Activation of refractory tissue
▪ Functional block
▪ Change in conduction velocity ▪ Other causes
▪ Change in refractory period ▪ MI, HF, HTN, thyroid, electrolytes, drugs,
caffeine and ethanol.
Types

▪ Supraventricular
▪ Tachy or brady
▪ Regular or irregular
▪ Types
▪ Sinus tach
▪ PSVT
▪ Sinus brady
▪ AF/Afl
▪ Atrial tach
▪ PAC
▪ WPW
Types

▪ AV nodal arrhythmia
▪ Delayed or absent SA conduction
▪ Types
▪ Nonparoxysmal AV junctional
tachycardia
▪ Junctional escape
▪ PAV junctional complexes
▪ AV dissociation
▪ First degree heart block
▪ Second degree heart block
▪ Mobitz I
▪ Mobitz II
▪ Third degree heart block (complete)
Types

▪ Ventricular
▪ Ventricles or bundle of His
▪ Usually symptomatic
▪ Immediate intervention
▪ Types
▪ PVC
▪ VT
▪ VF
▪ TdP (long QT) or LQTS
Arrhythmia increases risk

▪ CHF
▪ Sudden cardiac death
▪ Stroke
▪ Syncope
▪ Organ damage
▪ Poor perfusion
Cardiac tests

▪ Blood work ▪ Stress test


▪ CBC, BMP, thyroid function, dig level,
claudication studies ▪ SPECT

▪ X – ray ▪ Elecrophysiology studies

▪ CT ▪ Angiography

▪ MRI ▪ Dopplers

▪ Electrocardiogram ▪ Vitals signs

▪ Echocardiogram
Common cardiac tests

▪ Electrocardiogram
▪ Basic 5 lead – basic info
▪ 12 lead
▪ Better view of all parts of the heart
▪ Can tell us
▪ Dysrhythmias
▪ Ischemia
▪ Cardiac enlargement
Common cardiac tests

▪ Stress test
▪ Echo
▪ EKG
▪ Induced by
▪ Medications
▪ Exercise
Treatments

▪ Medications
▪ AAD

▪ ICD
▪ Ablation
Medications

▪I
▪ Sodium channel blockers

▪ II
▪ b blockers

▪ III
▪ Potassium channel blockers

▪ IV
▪ Calcium channel blockers

▪ Others
▪ Digoxin
▪ Adenosine
▪ Atropine
I - Sodium channel blockers

▪ Ia
▪ Disopyramide
▪ Procainamide
▪ Quinidine
▪ Ib
▪ Lidocaine
▪ Mexiletine
▪ Ic
▪ Flecainide
▪ Propafenone
▪ Also II
I - Sodium channel blockers

▪ Rate of dissociation
▪ Ia – rate dependence
▪ Quinidine
▪ Procainamide
▪ Disopyramide
▪ Ib – fast on and off
▪ Lidocaine
▪ Mexiletine
▪ Ic – slow on and off
▪ Flecainide
▪ Propafenone
Quinidine – Ia

▪ Arrhythmia types ▪ AE
▪ Supraventricular ▪ Nausea
▪ Ventricular ▪ Vomiting
▪ Diarrhea
▪ Mechanism of action ▪ Proarrhythmia (TdP)
▪ Anticholinergic ▪ torsades de pointes
▪ SA node – increase discharge rate ▪ Thrombocytopenia
▪ AV node – increase conduction ▪ Hepatitis
▪ Slows conduction velocity (phase 0) ▪ Cinchonism
▪ Prolongs refractoriness (phase 3) ▪ HF
▪ Decreases automaticity (phase 4) ▪ Hemolytic enema

▪ Widens QRS, prolongs QT, prolongs ▪ Contraindicated


PR ▪ Digoxin
Procainamide – Ia

▪ Arrhythmia types
▪ Supraventricular
▪ AE
▪ Ventricular
▪ Lupus erythematosus
▪ Mechanism of action ▪ Bradycardia
▪ Not an anticholinergic ▪ AV block
▪ Slows conduction velocity (phase 0) ▪ Hypotension
▪ Prolongs refractoriness (phase 3) ▪ HF
▪ Decreases automaticity (phase 4 ▪ TdP

▪ Widens QRS, prolongs QT, ▪ Contraindicated


prolongs PR ▪ Renal impairment

▪ IV only
Disopyramide – Ia

▪ Arrhythmia types ▪ AE
▪ Supraventricular ▪ Anticholinergic
▪ Ventricular ▪ Dry mouth
▪ Urinary retention
▪ Mechanism of action
▪ Constipation
▪ Anticholinergic/negative inotropic
▪ Blurred vision
▪ Slows conduction velocity (phase 0)
▪ TdP
▪ Prolongs refractoriness (phase 3)
▪ Decreases automaticity (phase 4 ▪ Contraindicated
▪ HF or reduced EF
▪ Prolongs QRS, prolongs QT
▪ Depresses contractility
Lidocaine – Ib

▪ Arrhythmia types ▪ AE
▪ Ventricular ▪ CNS
▪ Decreases incidence of VF ▪ Dizziness
▪ Paresthesia
▪ Mechanism of action ▪ Disorientation
▪ Selective to ischemic tissue ▪ Tremor
▪ Suppresses ▪ Aggitation
▪ ectopic ventricular pacemakers ▪ Seizures
▪ Purkinje fibers ▪ Respiratory arrest
▪ Decreases conduction velocity (phase
0) ▪ Contraindicated
▪ Prolongs action potential ▪ Hepatic impairment
▪ Slows conduction ▪ Elderly
Mexiletine – Ib

▪ Arrhythmia types ▪ AE
▪ VT ▪ Nausea
▪ Vomiting
▪ Mechanism of action ▪ CNS
▪ Decreases conduction velocity (phase ▪ Dizziness
0) ▪ Confusion
▪ Ischemic tissue ▪ Ataxia
▪ Speech
▪ Prolongs QRS, prolongs QT ▪ Proarrhythmia

▪ Contraindicated
▪ Cardiogenic shock
▪ Preexisting second or third degree block
Flecainide – Ic

▪ Arrhythmia types ▪ Dose


▪ Exercise induced ventricular arrhythmias ▪ 300 mg loading

▪ Supraventricular ▪ AE
▪ A fib ▪ Proarrhythmia
▪ Aflutter ▪ Conduction disturbances
▪ Ventricular arrhythmias
▪ Mechanism of action ▪ Mortality

▪ Blocks sodium channels ▪ Blurred vision


▪ Dizziness
▪ Slows conduction
▪ Headache
▪ Purkinje fibers
▪ Tremor
▪ AV node ▪ Nausea
▪ Slows conduction velocity (phase 0) ▪ Vomiting

▪ Increases PR interval and QRS duration ▪ Contraindicated


▪ HF
▪ Restores SR in 75-90% of AF ▪ Negative inotropic effects
Propafenone – Ic

▪ Arrhythmia types ▪ Dose


▪ Ventricular ▪ 450-600 mg loading
▪ Not common use
▪ Supraventricular - AF ▪ AE
▪ Mechanism of action ▪ Contraindicated
▪ Blocks sodium channels
▪ Slows conduction
▪ Purkinje fibers
▪ AV node
▪ Slows conduction velocity (phase 0)
▪ Mild nonselective b-blocking effect

▪ Prolongs QRS, prolongs QT


II - b blockers

▪ Atenolol
▪ Esmolol
▪ Metoprolol
▪ Propranolol
II - b blockers

▪ Atenolol
▪ Esmolol
▪ Metoprolol
▪ Propranolol
II - b blockers

▪ Arrhythmia types ▪ Dose – varies based on med


▪ Ventricular
▪ Paroxysmal SVT
▪ AE
▪ Supraventricular ▪ Sinus bradycardia
▪ AF, Afl, ▪ Decreased contractility
▪ Bronchospasm
▪ Mechanism of action ▪ COPD
▪ Blocks conduction system
▪ HF
▪ Slows AV node conduction
▪ Hypotension
▪ Slows SA node rate
▪ Depression
▪ Slows ventricular rate
▪ Fatigue
▪ Decreases automatic of sinus node, Purkinje fibers.
▪ Impotence
▪ Decreases slope (phase IV)
▪ Prolongs refractoriness (phase III) ▪ Contraindicated
▪ Prolongs PR, shortens QT ▪ COPD
▪ Asthma
III - Potassium channel blockers

▪ Amiodarone
▪ Also I, II, and IV

▪ Dofetilide
▪ Dronedarone
▪ Also I, II, and IV

▪ Ibutilide
▪ Sotalol
▪ Also II
Amiodarone

▪ Arrhythmia types ▪ AE
▪ Supraventricular ▪ Lethargy
▪ Ventricular ▪ GI – N/V/C, decreased appetite, abdominal pain
▪ VT, VF ▪ CV – Bradycardia. heart block
▪ CNS – tremors, ataxia, neuropathy, fatigue, insomnia
▪ Mechanism of action ▪ Photosensitivity
▪ Characteristics of all classes ▪ Organ toxicity
▪ Primarily calcium channel ▪ Lungs, thyroid, eyes, liver, skin, heart, GI, and CNS
▪ Blocks the rapid, slows components of delayed rectifier
potassium current ▪ Contraindicated
▪ Blocks sodium channels ▪ Oral reduced bioavailability
▪ Non-selective b blocker ▪ Loading dose
▪ Reduces automaticity (phase IV) ▪ Poor clearance
▪ Reduces conduction velocity (phase 0) ▪ liver

▪ Prolongs refractoriness (phase III) ▪ Drug interactions


▪ Coumadin
▪ IV use acute arrhythmia ▪ Digoxin
▪ Simvastatin
▪ Prolongs QT ▪ Lovastatin
Dronedarone

▪ Arrhythmia types ▪ AE
▪ Paroxysmal and persistent AF ▪ N/V/D
▪ Organ toxicities
▪ Mechanism of action
▪ Hepatic, intestinal, lungs, kidney
▪ Characteristics of all classes
▪ Primarily calcium channel ▪ Contraindicated
▪ Shorter half-life than amiodarone ▪ Advanced HF
▪ Loading dose
▪ Permanent AF
▪ Prolongs QT ▪ Multiple drug interactions
▪ Digoxin, ketoconazole, rifampin
▪ Monitor renal function
Sotalol

▪ Arrhythmia types ▪ AE
▪ Supraventricular ▪ Fatigue
▪ Ventricular ▪ Dispnea
▪ Hypokalemia and hypomagnesmia
▪ Mechanism of action
▪ TdP
▪ Prolongs atrial and ventricular
refractoriness ▪ Contraindicated
▪ Prolongs ventricular polarization ▪ Other QT increasing meds
▪ Increases QT interval ▪ Impaired renal function
▪ HF
▪ Monitor closely
▪ Discontinue if QT exceeds 550 msec
▪ Tele x3 days
Dofetilide

▪ Arrhythmia types ▪ AE
▪ AF ▪ Ventricular arrhythmias
▪ AFl ▪ TdP
▪ Headache
▪ Mechanism of action
▪ Dizziness
▪ Selective potassium channel
▪ Prolongs action potential ▪ Contraindicated
▪ Affects atria more than ventricles ▪ Prolonged QT
▪ Drug interactions – ketoconazole,
▪ Prolongs QT HCTZ, Bactrim, megace, compazine
▪ Impaired renal function
IV - Calcium channel blockers

▪ Diltiazem
▪ Verapamil
Diltiazem and Verapamil

▪ Arrhythmia types ▪ Dose


▪ PSVT
▪ AE
▪ AF, Afl
▪ Bradycardia, flushing, headache,
▪ Mechanism of action edema, hypotension
▪ Inhibits inward movement of calcium ▪ Contraindicated
▪ Slows conduction ▪ HF
▪ Prolongs refractoriness ▪ Accessory pathway (WPW)
▪ Decreases automaticity SA, AV ▪ Increases ventricular rate
▪ Vasculary relaxation
▪ Verapamil more potent inotropic

▪ Prolongs QRS, prolongs QT


Others -

▪ Digoxin
▪ Adenosine
▪ Atropine Arrhythmia types
Digoxin

▪ Arrhythmia types ▪ Dose


▪ Loading dose can take 6-8 hours
▪ AF, Afl
▪ Takes a week without renal impairment
▪ Mechanism of action ▪ Monitor electrolytes

▪ Slow onset ▪ AE
▪ Slows electrical impulse through AV ▪ N/V/D
node ▪ Blurred vision
▪ Slows vent rate ▪ Dizziness
▪ Heart block

▪ Contraindicated
▪ Caution in renal failure
▪ Dig toxicity
▪ Narrow therapeutic index
Choices

▪ First line
▪ Diltiazem IV
▪ Verapamil IV
▪ Beta blocker IV
▪ Amiodarone IV

▪ Second line
▪ Dependent on arrhythmia and cause
▪ Long term PO meds
Monitoring

▪ 12 lead EKG
▪ Holter monitor
▪ Blood pressure
▪ Heart rate
▪ Echocardiograms
▪ Labs
▪ Electrolytes
▪ Serum drug levels
Education

▪ Taking medications
▪ Overdosing
▪ Underdosing
▪ Managing missed doses
▪ Side effects

▪ Monitoring blood pressure/pulse


▪ When not to take
▪ blood pressure

▪ Basics
▪ Name of med
▪ Dose
▪ Frequency
▪ Timing
▪ Reason
Education

▪ Symptoms
▪ Chest pain
▪ Lightheadedness
▪ Dizziness
▪ Syncope
▪ Palpitations
▪ Dyspnea
▪ Weight gain

▪ Keep follow ups


▪ Keep lab appointments
▪ When to seek help
Education

▪ Weight
▪ Hazardous activities
▪ Driving
▪ Power tools
▪ Climbing ladders

▪ Nutrition
▪ Alcohol
▪ Salt
▪ Caffeine
▪ Licorice (hypokalemia)
▪ St. Johns wart


1. Review pathophysiology basics
2. Familiarize yourself with arrhythmias
3. Causes of arrhythmias
4. Types of arrhythmias
5. Risks associated with arrhythmias
6. Diagnostics
7. Treatments
8. Monitoring questions?
9. Patient teaching
References

▪ Heart Rhythm Society - diseases and disorders. (2017). Retrieved from


http://www.hrsonline.org/Patient-Resources/Heart-Diseases-Diso
rders?gclid=CjwKEAjwqZ7GBRC1srKSv9TV_iwSJADKTjaDKpXCrDBMwY8l6v
Kjp80fDkAxBXY5flRcfpdb3_XBaxoCThrw_wcB
▪ McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. R. (2014).
Pathophysiology: The Biologic Basis for Disease in Adults and Children
(7th ed.). St. Louis, MO: Elsevier Mosby.
▪ RxList. (2017). Retrieved from http://www.rxlist.com
▪ Why Arrhythmia Matters. (2016). Retrieved from
http://www.heart.org/HEARTORG/Conditions/Arrhythmia/WhyArrhyth
miaMatters/Why-Arrhythmia-Matters_UCM_002023_Article.jsp#.WMqz
W_nyu00
▪ Poole Arcangelo, V., Peterson, A. W., Wilbur, V., & Reinhold, J. A.
(2017). . In Pharmacotherapeutics for Advanced Practice a Practical

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