CARDIAC ARRHYTHMIAS
Gobezie T
§1

Definition
 Arrhythmias = loss of heart rhythm
 Occurs when the electrical impulses in the heart that
coordinate heartbeats don't function properly
 Causes the heart to beat too fast, too slow or
irregularly
 Can be broadly grouped into bradyarrhythmias and
tachyarrhythmias.
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Normal conduction of the heart
 Sinoatrial node
 Atrioventricular node
 Bundle of His
 Purkinje fibers 3

Types of Arrhythmias
BRADYARRHYTHMIA
S
(<60bpm)
 Sinus bradycardia
 Sinoatrial (SA) block
 Sinus pause
 Sinus arrest (slow
junctional rhythm)
TACHYARRYTHMIAS
(>100bpm)
 Supraventricular Arrhythmias
Sinus tachycardia
Atrial flutter
Atrial fibrillation
Automatic (ectopic) atrial tachycardia
Multifocal atrial tachycardia
Junctional tachycardia
Atrioventricular nodal re-entrant
tachycardias
Atrioventricular reciprocating tachycardias
 Ventricular Arrhythmias
Premature ventricular beats
Ventricular tachycardia
Ventricular fibrillation
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Pathogenesis
 3 basic mechanisms:
 enhanced or suppressed automaticity
• Due to
• Ischemia, scarring, electrolyte disturbances, medications, advancing
age, excess catecholamine activity
 triggered activity
• Attempt to depolarize before or after the cell is fully repolarized
• torsades de pointes- initiated by early after-depolarization
• ventricular arrhythmias caused by digitalis toxicity- delayed after-
depolarization
 re-entry
• Most common
• Supraventricular and monomorphic ventricular tachycardia
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Risk Factors
Coronary artery disease
High blood pressure
Diabetes
Smoking
High cholesterol
Obesity
Excessive alcohol use
Drug abuse
Stress
Family history of heart disease
Advancing age
Certain medications, dietary
supplements and herbal remedies
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Signs and symptoms
 Most common signs &
symptoms:
 Palpitation
 A slow heartbeat
 An irregular heartbeat
 Feeling pauses between
heartbeats
 More serious signs &
symptoms:
 Anxiety
 Weakness, dizziness, and
lightheadedness
 Fainting or nearly fainting
 Sweating
 Shortness of breath
 Chest pain (angina)
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CLASS I: SODIUM CHANNEL BLOCKING DRUGS
 IA - lengthen APD (Action Potential Duration)- (longer QT
interval)
 Moderate slowing of phase 0 (medium Na blockade)
 used for supraventricular & ventricular arrhythmias
 Disopyramide, Quinidine, Procainamide
 IB - Shorten APD
 Minimal slowing of phase 0 (least Na blockade)
therefore shorter QT interval
Used primarily in ventricular arrhythmias
 Lidocaine, Mexiletene, Tocainide, Phenytoin
 IC - no effect APD
 Maximal slowing of phase 0 (greatest Na blockade)
 Effective for both ventricular & supraventricular
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CLASS II: BETA-BLOCKING AGENTS
 ↓ AV nodal conduction
 ↑ PR interval & prolong AV nodal refractoriness
 In the SA node, they reduce automaticity
 Reduce adrenergic activity
 In the atria and ventricles, they reduce contractility
 reduce calcium entry (during fast and slow potentials) and
depress phase 4 depolarization (in slow potentials only)
 Propranolol, Esmolol, Metoprolol, Sotalol
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CLASS III: POTASSIUM CHANNEL BLOCKERS
 Prolong effective refractory period by prolonging
Action Potential
 ↑↑ Refractory Period with little or no effect on
conduction velocity & automaticity
 Amiodarone & Dronedarone (dAlso has sodium, calcium,
and B-blocking actions)
 Ibutilide & Dofetilide (pure Kr blockers)
 Sotalol (also B blocker)
 Bretylium
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CLASS IV: CALCIUM CHANNEL BLOCKERS
 Blocks cardiac calcium currents
 velocity of AV nodal conduction decreases,
•↑ PR interval
 increase refractory period
• esp. in Ca2+ dependent tissues (i.e. AV node)
• Antidysrhythmic benefits derive from suppressing AV
nodal conduction
 Verapamil, Diltiazem
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Supraventricular arrhythmias
 Originate from above the bifurcation (branching) of the
bundle of His
 Include
 Atrial fibrilation
 Atrial flutter
 Paroxysmal sinus tachycardia
 Etopic atrial tachycardia
 Paroxysmal supraventricular tachycardias (PSVT)

ATRIAL FIBRILLATION AND ATRIAL
FLUTTER
 Atrial fibrillation and atrial flutter are common
supraventricular tachycardias.
 Atrial fibrillation is characterized by extremely rapid (atrial
rate of 400–600 beats/min) and disorganized atrial
activation
 Atrial flutter occurs less frequently than AF, This
arrhythmia is characterized by rapid (270 to 330 atrial
beats/min) but regular atrial activation.
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ATRIAL FIBRILLATION/FLUTTER
 Causes/Etiology:
 Cardiac: atrial septal defect, Previous cardiac surgery,
HTN, Coronary arterial disease, cardiomyopathy, mitral
valve disease, Pericarditis
 Systemic: alcohol, CVA, chronic pulmonary disease,
electrolyte abnormalities, fever, hypothermia,
Hyperthyroidism, Sleep apnea, Alcohol abuse, Smoking,
Excessive caffeine consumption.
 Patients with AF are at risk for thrombotic stroke
 risk increases following restoration of normal sinus rhythm,
• or in patients with other comorbidities (HF, cardiomyopathy,
congenital heart disease, thyrotoxicosis)
 Pathophysiology: Predominant mechanism is reentry, usually

Diagnosis
 ECG shows irregularly irregular supraventricular rhythm
with no discernible, consistent atrial activity (P waves);
ventricular response usually 120–180 beats/min.
Desired Outcomes
 Prevent thromboembolic complications.
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ATRIAL FIBRILLATION/FLUTTER
Management
Treatment (Desired Outcomes)
 Relieve symptoms
Slowing ventricular rate: (Digoxin, BBs, CCBs)
Restoring normal sinus rhythm
Chemical cardioconversion: (ibutilide, propafenone,
flecainide)
Electrical: (DCC) Hemodynamically unstable patients
 Preventing AF recurrences
Class IA, IC, III antiarrhythmic agents for maintenance of sinus
rhythm
 Reduce risk of stroke

Atrial Fibrillation and Atrial Flutter
Acute Treatment
 with signs and/or symptoms of hemodynamic instability
(e.g., severe hypotension, angina, or pulmonary edema,
qualifies as a medical emergency
 DCC is indicated as first-line therapy in an attempt to
immediately restore sinus rhythm (without regard to the risk
of thromboembolism).
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ATRIAL FIBRILLATION AND ATRIAL
FLUTTER
Acute Treatment
 If patients are hemodynamically stable, there is no
emergent need to restore sinus rhythm.
 Instead, the focus should be directed toward controlling
the patient’s ventricular rate.
 Achieving adequate ventricular rate control is a treatment
goal for all patients with AF.
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ATRIAL FIBRILLATION AND ATRIAL FLUTTER
Acute Treatment
 Initial therapy, drugs that slow conduction and ↑
refractoriness in the AV node (e.g., βBs,
nondihydropyridine CCBs, or digoxin).
 use of digoxin for achieving ventricular rate control,
especially in patients with normal LV systolic function
(left ventricular ejection fraction [LVEF] >40%) not
recommended.
its relatively slow onset & its inability to control heart rate during
exercise.
 digoxin , ineffective for controlling ventricular rate under
conditions of ↑ed sympathetic tone (i.e., surgery,
thyrotoxicosis)
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ATRIAL FIBRILLATION AND ATRIAL
FLUTTER
Acute Treatment
IV βBs (propranolol, metoprolol, esmolol),
diltiazem, or verapamil is preferred
a relatively quick onset and can effectively control the
ventricular rate at rest and during exercise.
 β- blockers are also effective for controlling ventricular rate
under conditions of increased sympathetic tone.
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ATRIAL FIBRILLATION AND ATRIAL
FLUTTER
Acute Treatment
 Drug selection to control ventricular rate in the acute
setting should be primarily based on the patient’s LV
function.
 In patients with normal LV function (LVEF >40%), IV
βBs, diltiazem, or verapamil is recommended as first-
line therapy
 If LVEF ≤40%, IV diltiazem or verapamil should be
avoided because of their potent negative inotropic
effects. 22

ATRIAL FIBRILLATION AND ATRIAL
FLUTTER
Acute Treatment
 If Exacerbation of HF symptoms, IV administration of
either digoxin or amiodarone should be used as first-
line therapy to achieve ventricular rate control.
 IV amiodarone can also be used in patients who are
refractory to or have C/Is to βBs, nondihydropyridine CCBs,
and digoxin
 But use of amiodarone for controlling ventricular rate may
also stimulate the conversion of AF to sinus rhythm, and
place the patient at risk for a thromboembolic event.
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ATRIAL FIBRILLATION AND ATRIAL
FLUTTER
chronic management
 Because a rhythm control strategy does not confer any
advantage over a rate-control strategy in the management
of AF
 Now it remains acceptable to allow patients to remain in
AF, while being chronically treated with AV nodal-blocking
agents to achieve adequate ventricular rate control (e.g.,
HR <80 beats/min at rest and <100 beats/min during
exercise).
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ATRIAL FIBRILLATION AND ATRIAL
FLUTTER
chronic management
 The selection of an AV nodal-blocking agent to control ventricular
rate in the chronic setting primarily based on the patient’s LV
function.
 normal LV function
 In patients with normal LV function (LVEF >40%), oral βBs,
diltiazem, or verapamil are preferred over digoxin because of
their relatively quick onset and maintained efficacy during
exercise.
 When adequate ventricular rate control cannot be achieved with
one of these agents, the addition of digoxin may provide an
additive lowering of the heart rate.
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ATRIAL FIBRILLATION AND ATRIAL
FLUTTER
chronic management
 LV dysfunction
 Verapamil and diltiazem should not be used (LVEF ≤40%).
 βBs (i.e., metoprolol, carvedilol, or bisoprolol) and digoxin are
preferred, as these agents are also concomitantly used to treat
chronic HF;
 if possible, βBs should be considered over digoxin in this situation
because of their survival benefits in patients with LV systolic
dysfunction.
 If patients are having an episode of decompensated
HF, digoxin is preferred first-line therapy
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AF……ANTICOAGULATION
 In those patients in whom it is decided to restore sinus
rhythm, one must consider that this very act (regardless of
whether an electrical or pharmacologic method is chosen)
places the patient at risk for a thromboembolic event.
 the return of sinus rhythm restores effective contraction in
the atria, which may dislodge poorly adherent thrombi.
 Administering antithrombotic therapy prior to cardioversion
not only prevents clot growth & formation of new thrombi
but also allows existing thrombi to become organized &
well-adherent to the atrial wall. 27

AF…..ANTICOAGULATION THERAPY
Indicated for
 CVA Prevention in Atrial fibrillation
 Preparation for atrial fibrillation cardioversion
Atrial fibrillation < 48 hours
Consider Heparin (UFH, lMWH) while considering cardioversion
Consider early atrial fibrillation cardioversion
Atrial fibrillation >48 hours
Warfarin – 3 weeks before cardioversion
Consider atrial fibrillation cardioversion
Continue warfarin for 4 weeks after cardioversion
 Dosing
 Target INR 2-3
 Tight INR control is important
INR 1.5-1.9 with 2 fold risk of severe CVA
INR 1.5-1.9 with 3 fold risk of mortality

AF……ANTICOAGULATION
 patients become at ↑ed risk of thrombus formation and a
subsequent embolic event particularly if duration of AF
exceeds 48 hours.
 patients with AF for longer than 48 hours or an unknown
duration should receive warfarin (target INR 2.5; range: 2.0
to 3.0) for at least 3 weeks prior to cardioversion.
 After restoration of sinus rhythm, full atrial contraction
returns gradually to a maximum contractile force over a 3-
to 4-week period.
 warfarin continued for at least 4 weeks after effective
cardioversion and return of sinus rhythm 29

ATRIAL FIBRILLATION AND ATRIAL
FLUTTER
chronic management
 methods of restoring sinus rhythm in patients with AF or
atrial flutter:
pharmacologic cardioversion and
 DCC.
 The disadvantages of pharmacologic cardioversion are the
risk of significant side effects
the inconvenience of drug–drug interactions (e.g.,
digoxin–amiodarone), and
drugs are generally less effective when compared to
DCC.
 The advantages of DCC are that it is quick and more often
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ATRIAL FIBRILLATION AND ATRIAL
FLUTTER
chronic management
 Pharmacologic cardioversion appears to be most effective
when initiated within 7 days after the onset of AF
 Single, oral loading doses of propafenone (600 mg) or
flecainide (300 mg) are effective for conversion of
recent onset AF and provide a simple regimen.
 A method called the “pill-in- the-pocket” approach was
recently endorsed by the treatment guidelines.
 In patients with AF that is longer than 7 days in duration,
only dofetilide, amiodarone, and ibutilide have proven
efficacy for cardioversion.
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ATRIAL FIBRILLATION AND ATRIAL
FLUTTER
chronic management
 Selection of an antiarrhythmic drug should be based on whether the
patient has structural heart disease (SHD) (e.g., LV dysfunction,
coronary artery disease, valvular heart disease, LV hypertrophy)
 In the absence of any structural heart disease, the use of a single,
oral loading dose of flecainide or propafenone is a reasonable
approach for cardioversion
 In patients with underlying SHD, these antiarrhythmics should be
avoided , and amiodarone or dofetilide should be used instead.
 amiodarone can be administered safely on an outpatient basis
because of its low proarrhythmic potential, dofetilide can only be
initiated in the hospital.
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TABLE Guidelines for Selecting AADs for Maintenance of Sinus Rhythm
in Patients with Recurrent Paroxysmal (Persistent) AF
No structural heart disease
 1st line: flecainide, propafenone, or sotalol
 2nd line: amiodarone, dofetilide, or dronedarone (catheter ablation be
considered as alternative to AAD)
Heart failure
 1st line: amiodarone or dofetilide
 2nd line: catheter ablation
Coronary artery diseasea
 1st line: sotalol (to be used only if patients have normal LV systolic
function)
 2nd line: amiodarone, dofetilide, or dronedaroneb (catheter ablation
alternative to AAD)
Hypertension
 Presence of significant LVH: 1st line: amiodarone; 2nd line: catheter
ablation
 Absence of significant LVH:

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Fig 1. Algorithm for tt of atrial fibrillation (AF) & atrial
flutter.

Chronic antithrombotic therapy
 Chronic antithrombotic therapy recommendations based on
stroke risk (Fig. 2).
 High risk (chA2DS2-VASc score ≥2): warfarin (INR 2–
3), apixaban, dabigatran, edoxaban, or rivaroxaban.
 Intermediate risk (chA2DS2-VASc score of 1): oral
anticoagulant (warfarin [INR target range 2–3], apixaban,
dabigatran, edoxaban, or rivaroxaban), aspirin 75–325
mg/day, or no antithrombotic therapy.
 Low risk (chA2DS2-VASc score of 0): no antithrombotic
therapy.
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Stroke risk stratification in AF patients
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Fig 2. Algorithm for prevention of thromboembolism in
AF
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