Arrhythmias Mustafa Salehmohamed, D.O.. DEFINITIONS An arrhythmia is defined as any rhythm other...

ArrhythmiasArrhythmias

Mustafa

Salehmohamed, D.O.

DEFINITIONSDEFINITIONS

An arrhythmia is defined as any rhythm other than normal sinus rhythm

Arrhythmias can be categorized as supraventricular or ventricular

Supraventricular arrhythmias can be further divided into tachyarrhythmias or bradyarrhythmias

SUPRAVENTRICULAR

ARRHYTHMIAS

SUPRAVENTRICULAR ARRHYTHMIAS

Any arrhythmia arising above the bifurcation of the His bundle is classified as supraventricular.

The QRS complex morphology either can be normal or may be wide owing to bundle-branch or fascicular block (aberrant conduction) or conduction over an accessory pathway (anomalous conduction or pre-excitation).

Supraventricular cardiac arrhythmias can be further sub-categorized into tachyarrhythmias or bradyarrhythmias.

TACHYARRHYTHMIAS

Sinus tachycardia is defined as a rapid sinus rhythm with a HR > 100bpm

Tachyarrhythmia is defined as an arrhythmia with a HR > 100bpm

Supraventricular tachyarrhythmias can occur either as isolated premature complexes or in the form of nonsustained or sustained tachycardias

PREMATURE ATRIAL CONTRACTIONSPREMATURE ATRIAL CONTRACTIONS

Premature atrial contractions (PACs) can arise from any part of the right or left atrium

The P wave morphology depends on the origin but differs from sinus rhythm

Frequent in normal persons and rarely cause symptoms

They are associated with respiratory disease, particularly in the presence of pulmonary hypertension

PREMATURE ATRIAL CONTRACTIONSPREMATURE ATRIAL CONTRACTIONS

Other precipitating factors include coffee, tea, alcohol, sympathomimetic cold remedies

If an etiology cannot be determined and treatment is necessary, a Beta -blocker can be given

AtrialAtrialTachycardiasTachycardias

Atrial FlutterAtrial Flutter

Atrial flutter is much less common than Atrial Fibrillation (AF)

Its hemodynamic consequences and management are similar to that of AF

It is due to a large reentrant circuit (several centimeters) that involves the low lateral right atrium

DiagnosisDiagnosis

ECG shows flutter waves, which (depending on rate) may look like discrete P waves or merge to form a classic sawtooth pattern

The atrial rate is 250 to 350 beats/min The ventricular rate depends on the AV conduction but typically is 150 to 220 beats/min

QRS complexes usually are normal Atrioventricular block may be consistent (2:1, 4:1, or

rarely 3:1 or 5:1) or may vary

Signs and SymptomsSigns and Symptoms

Symptoms depend principally on the resultant ventricular rate

If the rate is modest (< 120 beats/min) and regular (eg, stable 2:1 atrioventricular conduction), there may be no symptoms

Higher heart rates produce palpitations, and compromised cardiac output may produce dizziness and syncope

TreatmentTreatment

Medical therapy more likely to slow down ventricular response than to restore NSR

Medications used :• Digoxin

• Verapamil (works faster than digoxin but can cause hypotension

• Beta-blockers

• Class I drugs ( use with other drugs)

• IV Ibutilide (risk of developing Torsades)

TreatmentTreatment

If 1:1 conduction occurs with life-threatening rapid ventricular response rates (> 220 beats/min), immediate DC electroversion is indicated

Radiofrequency ablation (RFA) is emerging as an important approach for medically refractory atrial flutter.

The success rate is about 85% Some patients develop AF after the procedure

Atrial FibrillationAtrial Fibrillation


Atrial fibrillation (AF) is the most common sustained arrhythmia in adults

More than 2 million individuals in the United States have AF

With more than 160,000 new cases diagnosed every year

The incidence of AF increases with advancing age

Atrial fibrillation Atrial fibrillation accounts for 1/3 of all accounts for 1/3 of all

patient discharges patient discharges with arrhythmia as with arrhythmia as principal diagnosis.principal diagnosis.

2% VF

Data source: Baily D. J Am Coll Cardiol. 1992;19(3):41A.

34% Atrial

Fibrillation

18% Unspecified

6% PSVT

6% PVCs

4% Atrial Flutter

9% SSS

8% Conduction

Disease3% SCD

10% VT

Prevalence of Atrial Fibrillation in the U.S.

Estimated prevalence of atrial fibrillation in the United States.8

EtiologyEtiology

Ischemic Heart Disease Hypertensive Heart Disease Rheumatic Valvular Disease Cardiomyopathy Non-rheumatic Valvular Disease Congenital Hear Disease CHF Pericarditis WPW

EtiologyEtiology

Thyrotoxicosis Pulmonary Embolism Chronic Lung Disease Pneumonia Neoplastic disease Post- operative states Normal heart affected by: alcohol, stress, drugs, excessive

caffeine, hypoxia, hypokalemia, hypoglycemia, infection

Atrial Fibrillation Atrial Fibrillation Morbidity and MortalityMorbidity and Mortality

Two fold increase in CV mortality

The most important consequence of AF are thrombo-embolic events

and stroke

AF is one of the most potent risk factors for stroke

4 – 6 fold increase risk of stroke/15 fold with h/o RHD

Persistent rapid ventricular rate associated with AF may lead to

tachycardia induced cardiomyopathy (reversible)

Limitation in functional capacity from symptoms of palpitations,

fatigue, dyspnea, angina, or CHF

DiagnosisDiagnosis

During AF, the atria have disorganized, rapid, irregular electrical activity exceeding 400 beats per minute

The ventricular response is also irregular and variable (irregularly irregular)

EKG: Absence of visible discreet P waves, or the presence of irregular fibrillation waves and an irregular ventricular response

DiagnosisDiagnosis

History – precipitating factors such as alcohol, caffeine,

sympathomimetic drugs

Laboratory studies: Electrolytes, TFTs, substance abuse-

toxicity screens

Echocardiogram

Holter (indicating arrhythmia: SVT, A. Flutter, Bradycardia

induced)

EST ( R/O ischemia)

Signs and SymptomsSigns and Symptoms

Palpitations Chest DiscomfortSigns of CHF - 2° to loss of atrial kick or

due to rapid rateWeakness, faintness, and breathlessnessSymptoms and signs of systemic emboli

(eg, stroke due to thrombus formation in the fibrillating atrium)


Paroxysmal

Chronic (chronic paroxysmal)

Acute (onset within 24 – 48 hrs)

Lone (younger than 60, no HTN no CVD

no Pulmonary disease)

TreatmentTreatment

Treatment goals are management of any underlying (causative) disorder, control of the ventricular response rate, restoration of sinus rhythm, and prevention of emboli

Rate control vs. Rhythm control

Medications for Rate ControlMedications for Rate Control

DigoxinBeta – blockersCalcium channel blockers (diltiazem,

verapimil)Short-term control of ventricular rate in

preparation for DC cardioversion is usually done with a beta -blocker or verapamil to avoid postconversion digoxin arrhythmias.

CardioversionCardioversion

Chemical Cardioversion• Class Ia and Ic Anti-arrhythmic Drugs (AEDs)• Amiodarone

in recent studies, prophylaxis with amiodarone before cardiac surgery has been found to decrease the occurrence of atrial fibrillation

Aasbo, J et al. Amiodarone prophylaxis reduces major cardiovascular morbidity and length of stay after cardiac surgery: a meta analysis. Ann Intern Med 143: 2005.

Pharmacologic CardioversionPharmacologic Cardioversion Class Ia agents

• procainamide (Procanbid)• quinidine (Quinidex, Quinaglute)• disopyramide (Norpace)

Class Ic agents• flecainide (Tambocor)• propafenone (Rhythmol)

Class III agents• amiodarone (Cordarone) - acute efficacy 16%-71%• sotalol (Betapace)• ibutilide - efficacy for flutter (63%), fib (31%)• dofetilide (Tikosyn)

CardioversionCardioversion

Electric cardioversion – method of choice for the hemodynamically Electric cardioversion – method of choice for the hemodynamically

compromisedcompromised

• Evaluate need for anticoagulationEvaluate need for anticoagulation

• R/O drug toxicityR/O drug toxicity

• AnesthesiaAnesthesia

• Synchronized 50 – 200 joules shockSynchronized 50 – 200 joules shock

Control of ventricular rateControl of ventricular rate

• AV nodal ablation with PPMAV nodal ablation with PPM

• Pulmonary vein ablation (maintenance)Pulmonary vein ablation (maintenance)

Atrial Fibrillation ManagementAtrial Fibrillation Management

Rate control versus rhythm control

• Advantage of maintaining NSR

• Adverse effects of antiarrhythmics

• After cardioversion even with antiarrhythmic therapy-50%

develop recurrent A.F after cardioversion

• Atrial Fibrillation Follow-up Investigation of Rhythm

Management (AFFIRM) : Anticoagulation advantageous

AFFIRMAFFIRM Atrial Fibrillation Follow-up Investigation of

Rhythm Management

Hypothesis: Effect on mortality of antiarrhythmic therapy to maintain sinus rhythm vs.

ventricular rate control alone, in the presence of anticoagulation

Primary endpoint: Total mortality

Secondary endpoint: Disabling CVACost of therapyQuality of life

NHLBI AFFIRM Investigators. Am J Cardiol. 1997;79:1198-1202.

Atrial FibrillationAtrial FibrillationManagement of the Risk of StrokeManagement of the Risk of Stroke

15 – 20% of ischemic strokes arise from emboli in the cardiac

chambers and valves

AF accounts for 45% of embolic strokes

Majority of emboli arise in the LAA

Other sources of emboli: LV thrombus Mitral valve disease (including

MVP and annular calcification), PFO Atrial septal aneurysm, and

complex aortic atheromatous plaques

Cerebrovascular disease may also be a cause of stroke

Transesophageal Echocardiogram Showing Thrombus

In this transesophageal echocardiogram, a thrombus (arrow) can be seen in the left atrial appendage (LAA).

Echocardiogram of Fibrillating Left Atrium

The smokelike echoes, or spontaneous echo contrast, in this transesophageal echocardiogram of a fibrillating left atrium are associated with prethrombotic conditions.

Protruding Atheroma in Descending Aorta

Protruding atheroma (arrows) in the descending aorta (DESC AO) is evident in this transesophageal echocardiogram.


Anticoagulation with warfarin is twice as effective as

with Aspirin

SPAF III: compared warfarin vs. combination of low

dose warfarin and aspirin - in high risk AF patients

the combination was not as effective as warfarin.

Recommendations for Anticoagulation in AFRecommendations for Anticoagulation in AF Low risk patient (younger than 65) – do not need anticoagulation

Patients above 65 years who have AF should be anticoagulated. ACP

recommendation – INR 2.0 – 3.0 (reduces risk by 2/3)

Warfarin considered in younger patients with risk factors (previous TIA, HTN,

CHF, Diabetes, CAD. MS, Thyrotoxicosis)

Patients, who are high risk for bleeding – give ASA 325 mg/d

Patients 65 – 75 years with no risk – balance the the low risk of stroke with

side effects of therapy

Patients 75 years should receive oral anticoagulant


Contraindications to AnticoagulationContraindications to Anticoagulation

Hemorrhage tendencies

Recent intra-cranial hemorrhage or neurosurgery

Recent hemorrhagic trauma

Recurrent or active bleeding

Diastolic BP>105

Other considerations

Risk of falling

Poor compliance with f/u

Uncontrolled siezure disorder

Atrial Fibrillation Management Atrial Fibrillation Management Cardioversion and the Risk ofCardioversion and the Risk of

ThromboembolismThromboembolism Risk of thromboembolism at cardioversion 0-5.6%

Dislodgement of a preexisting thrombus upon the return of the atrial

electrical and mechanical function (up to 4 weeks)

Formation and later dislodgment of newly formed thrombi, when

patient returns to NSR but atria in mechanical standstill

10-15% of patients with acute AF have thrombi on TEE

Most cardioversion related thrombi do not occur at cardioversion, but

are delayed for hours or weeks

Atrial Fibrillation Anticoagulation In Patients Atrial Fibrillation Anticoagulation In Patients Undergoing CardioversionUndergoing Cardioversion

Those with A.F. longer than 2 days or of unknown duration should receive anticoagulation

Warfarin should be given 3 weeks before cardioversion and 4 weeks after cardioversion

Anticoagulation beyond 4 weeks should be considered in patients with cardiomyopathy h/o previous ambolus or mitral valve disease

TEE role in cardioversion • Useful in r/o thrombus and facilitating early cardioversion by using

short term anticoagulation

• Acute trial: compared TEE directed approach with brief anticoagulation to conventional

Treatment Protocol in ACUTE Study

Treatment protocol used in Assessment of Cardioversion Using TEE (ACUTE) multicenter pilot study. The study involved 126 patients randomized into one of two treatment groups: the TEE guided group (62 patients) and the conventional-treatment group (64 patients).

Multifocal Atrial TachycardiaMultifocal Atrial Tachycardia

Presents similarly to AF but arise not by multiple interlacing wavelets of reentry (as in AF) but by focal pacemaker abnormalities

The term multifocal atrial tachycardia implies several different P wave morphologies (at least 3 different morphologies)

Atrial rates range between 100 and 250 beats per minute, and the ventricular response depends on the status of AV conduction

A 1:1 P wave-to-QRS complex ratio is common with rates less than 200 beats per minute, whereas at higher rates various degrees of block (e.g., 3:2, 2:1, 3:1) are common

Multifocal Atrial TachycardiaMultifocal Atrial Tachycardia

Causes• Chronic Obstructive Lung Disease• Any other underlying pulmonary disorders can

cause MAT• Can be exacerbated by theophylline

TreatmentTreatment

Treat underlying diseaseSimilar treatment as AFHowever beta-blockers contraindicated in

those whose MAT is caused by lung diseaseDigoxin is not as useful and may even

exacerbate the tachycardiaUse calcium channel blockers

Regular Atrial TachycardiasRegular Atrial Tachycardias 1) Sinus Tachycardia: physiologic or pathologic increase of sinus rate >

100 bpm. Treat the condition causing the tachycardia, not the tachycardia itself. However, in cases of acute MI sinus tachycardia must be controlled to

prevent myocardial ischemia (beta blockers or Ca-channel blockers)

2) Paroxysmal Atrial Tachycardia: sudden onset, a normal heart, HR 150-250 bpm.

P waves may be not visible because buried in the QRS complex or the T wave

Therapy: quiet setting and comfort the patient to reduce sympathetic discharge. Increase vagal tone by carotid sinus massage or valsalva maneuver. Medical therapy: Beta-blocker, Ca channel blocker, digoxin, adenosine. If angina, hypotension, or CHF then consider cardioversion.

Supraventricular TachycardiasSupraventricular Tachycardias

Atrial Tachycardia Atrial Fibrillation/flutter AV nodal reentry (micro) tachycardia AV reentry tachycardia (macro) - WPW Syndrome or concealed

accessory pathway

If the patient is very symptomatic or breaks through drugs, consider catheter ablation

Supraventricular Tachycardias

Supraventricular TachycardiaSupraventricular Tachycardia Atrioventricular Nodal Reentry TachycardiaAtrioventricular Nodal Reentry Tachycardia

(AVNRT)(AVNRT)

The most common type of paroxysmal SVT (PSVT)

AVNRT accounts for 50 – 60% of PSVT

AVNRT present later than SVT related to accessory

pathways (frequently after 20 years of age)

Tachycardia Induction-Reentry

During sinus rhythm, antegrade conduction occurs through both the fast pathway and the slow pathway. However, the fast-pathway conduction predominates and the atrioventricular conduction time is short. If a premature atrial beat blocks in the antegrade fast pathway, atrioventricular (AV) conduction proceeds via the slow pathway. Then, if the fast pathway recovers quickly enough to permit retrograde conduction, atrial echoes or typical slow-fast atrioventricular nodal reentrant tachycardia (AVNRT) occurs. This simplified diagram demonstrates only one method of tachycardia induction and implies the requisite tachycardia circuit is confined to the compact AV node.

Supraventricular TachycardiaSupraventricular Tachycardia AVNRT Diagnosis AVNRT Diagnosis

• The typical HR ranges 150 – 250 bpm

• Palpitation, light headedness and near-syncope may accompany the

paroxysm.

• True syncope unusual

• Neck pounding (connon waves) is pathognomonic of AVNRT

AVNRT Acute ManagementAVNRT Acute Management

Vagal maneuver (carotid Sinus Massage, valsalva

maneuver)

Adenosine (6 mg, 12mg, 12mg, 18mg)

Verapamil 5 – 10 mg I.V.P

If hypotension, angina or CHF is precipitated by AVNRT –

DC cardioversion (25 – 50 joules)

AVNRT AVNRT Chronic Pharmacologic ManagementChronic Pharmacologic Management

Long term pharmacological approach is still reasonable Digoxin – sometimes effective Beta-blockers - when arrhythmia induction is catecholamines

dependent Verapamil (240 mg qd) - may cause constipation, fatigue, flushing,

edema Diltiazem Class I agents (quinidine, flecainide) Amiodarone (Tissue toxicity) Catheter – RF ablation (success rate 94 – 100%, complete AV Block

2 – 4%)

Wolff – Parkinson – White Syndrome Wolff – Parkinson – White Syndrome and Concealed Accessory Pathwayand Concealed Accessory Pathway

Normal AV conduction is limited antegrade conduction to a single pathway through the AVN

Presence of an alternative pathway of AV conduction creates the potential for reentry

tachycardia

The most prominent manifestation of an accessory pathway is the wolff-parkinson – white

(WPW) syndrome

In WPW the accessary pathway can be located at various regions of the AV ring (most

common – left free wall of the mitral annulus)

In WPW a sinus beat will travel both through the accessory pathway (conducts like muscle,

no decremental conduction) and the AVN – HIS – Purkinji- system, creating a fusion beat.

The EKG presentation: short PR, Delta wave (may mimic a Q wave)

WPW- Left Free Wall Accessory Pathway

(a) Activation of the ventricles via an accessory pathway precedes earliest activation through the His-Purkinje system and results in a slurring of the QRS onset called a delta wave. (b) A more subtle delta wave is produced when there is minimal preexcitation, as shown in this example of a left free wall accessory pathway. Delta waves can be mistaken for infarction Q waves. For example, a posteroseptal accessory pathway produces a delta wave that mimics an inferior MI (a). (b) ECG changes related to early activation at the base of the LV free wall include the negative delta wave in lead aVl and the large R wave in V1, which can be mistaken for a posterolateral wall MI.

WPW Clinical PresentationWPW Clinical Presentation

Begin in teenage years – early adulthood

(pregnancy may precipitate).

Symptoms: Palpitations with or without dizziness,

syncope, SOB, weakness or chest pain. Sometimes

diuresis.

WPW Electrocardiographic FindingsWPW Electrocardiographic Findings

Tachyarrhythmia associated with the WPW can be of

several types

• Orthodromic reentry tachycardia

Most common (QRS narrow, no short PR, no delta)

• Antidromic reentry tachycardia

• Atrial fibrillation, may produce very rapid tachycardia with

QRS complexes that may cause syncope or S.D.

ECG During Reentrant Tachycardia

Electrocardiograms taken during episodes of reentrant tachycardia in a patient with the WPW syndrome reveal both antidromic and orthodromic tachyarrhythmias. (a) During an antidromic episode, the QRS complex is wide, resembling the morphology seen in VT. The

impulse then travels retrogradely up the AV node to the atria before reentering the ventricle via the accessory pathway. (b) In the orthodromic reentrant tachycardia, the QRS complex is narrow in all leads. The ventricle is activated strictly via the AV node, followed

by retrograde propagation of the impulse via the accessory pathway to the atria.

WPW ManagementWPW Management Asymptomatic patient

• need for invasive evaluation unclear. Competitive athletes and Pilots probably should be evaluated.

Acute Management: • Vagal maneuver • Procainamide• DC Cardoversion

Long-term Management• Flecainide (N. CAD, Normal LVF)• Amiodarone• Catheter Ablation

Concealed Accessory PathwayConcealed Accessory Pathway

An accessory pathway that conduct only in the

retrograde direction

Antegrade conduction only via normal pathway –

therefore preexcitation not present (no short PR, no

Dela waves) during NSR

Can participate in a reentry circuit. (AVRT)

Ventricular ArrhythmiasVentricular Arrhythmias

These are arrhythmias with broad QRS complexes (>120 ms in duration)• Ventricular tachycardia (VT)

Torsades de pointesPolymorphic VTAccelerated idioventricular rhythm

• Ventricular flutter/ fibrillation (VF)

Ventricular TachycardiaVentricular Tachycardia

Sustained ventricular tachycardia is defined as VT that persists for >30 s

VT generally accompanies some form of structural heart disease, most commonly chronic ischemic heart disease associated with a prior myocardial infarction.

Sustained VT may also be associated with nonischemic cardiomyopathies, metabolic disorders, drug toxicity, or prolonged QT syndrome, and it occurs occasionally in the absence of heart disease or other predisposing factors


Nonsustained VT (three beats to 30 s) is also associated with cardiac disease but occurs in its absence more often than the sustained arrhythmia.

While nonsustained VT usually does not produce symptoms, sustained VT is almost always symptomatic

It is often associated with marked hemodynamic compromise and/or the development of myocardial ischemia


The most important clinical predictor of VT is the presence of structural heart disease

The observation of intermittent cannon a waves and varying first heart sounds suggests AV dissociation and is diagnostic of VT

In a majority of cases, the diagnosis can and should be made by close examination of the 12-lead ECG


The ECG diagnosis of VT is suggested by a wide-complex QRS tachycardia at a rate exceeding 100 beats/min.

The QRS configuration during any episode of VT may be uniform (monomorphic) or it may vary from beat to beat (polymorphic).


Treatment• Immediate treatment of hypotensive VT requires synchronized DC

shock

• Drug treatment of VT is lidocaine 100 mg IV given over 2 min with a further 50 mg IV 5 min later if the arrhythmia has not reverted

• A second antiarrhythmic drug (flecainide, encainide, propafenone, procainamide, disopyramide, mexiletine, tocainide) may be used if DC cardioversion (or programmed stimulation) is unavailable or if the patient is not hemodynamically compromised and has shown no adverse response to lidocaine


All patients with sustained VT should be investigated by invasive electrophysiology and therapy selected accordingly

Long-term prophylaxis of VT may be achieved by any class Ia, Ib, Ic, II, or III drug

Calcium channel blockers – specifically diltiazem and verapimil are contraindicated because of reports of hemodynamic collapse and fatalities

Torsades de PointesTorsades de Pointes

Torsade de pointes or twisting of the points, causes symptoms and death in patients with the rare congenital long QT syndromes

Its importance in everyday practice is its provocation by drugs (especially antiarrhythmics, which are contraindicated in its further management) or electrolyte imbalance.

Management is to stop all cardioactive drugs (eg, antidepressants, antiarrhythmics, phenothiazines), normalize electrolytes (particularly K and Mg), and stabilize cardiac electrophysiology, if necessary by atrial overdrive pacing

Ventricular FibrillationVentricular Fibrillation

A rapid irregular ventricular rhythm due to multiple reentrant activity associated with essentially zero cardiac output

Causes :• Ischemic heart disease

• Severe hypoxia

• Electrical accidents

• Antiarrhythmic drugs

• WPW with rapid Afib

• After reperfusion therapy


Clinical picture• Shock• Syncope• Sudden Death


Treatment• Fatal unless patient defibrillated• Patients with recurrent VF benefit from

Automated Implantable Cardioverter Defibrillator( AICD)

Transvenous Cardioverter-Defibrillator

The transvenous implantable cardioverter-defibrillator is usually installed in the pectoral region. A transvenous defibrillating lead is inserted into the subclavian vein and advanced into the apex of the right ventricle. When a persistent ventricular tachyarrhythmia with a rate faster than the programmed rate cutoff is detected by the rate-sensing electrode in the lead's tip, the device charges and delivers a high-voltage shock between the right ventricular defibrillating elec-trode and the metal casing of the defibrillator, which serves as the return electrode (anode) for defibrillating shocks.

Congenital Long QT SyndromeCongenital Long QT Syndrome Usually present as syncope (cardiac arrest – rare)

Recurrent rapid episodes of polymorphic VT

Many youngsters are incorrectly diagnosed with grand mal seizures

The arrhythmia is triggered by an adrenergic surge (physical, emotional or auditory stimulus)

Family h/o S.D or syncope

QTC of longer than 0.46 sec in man and 0.48 sec in woman is abnormal

Jervell – large – Nielson – autosomal recessive with deafness

Romano – ward – autosomal dominant with no deafness

50% of affected experience SD or syncope by age 12.

Risk factors for SD: congenital deafness, h/o syncope, VT/NSVT on holler, female gender

Any patient or family member with one risk factor should be treated with beta - blockers

Schwartz PJ. Curr Probl Cardiol. 1997;22:297-351. Smith WM. Ann Intern Med. 1980;93:578-584. Garson A Jr. Circulation. 1993;87:1866-1872.

Long QT SyndromeLong QT Syndrome

Idiopathic LQTS is a congenital disorder that may lead to unexplained syncope, seizures, and SCA

Patients either remain asymptomatic or are prone to symptomatic and potentially lethal arrhythmias

A positive family history of LQTS or SCA is present in 60% of LQTS patients

Due to the hereditary linkage, it is necessary to identify other family members at risk

Bradyarrhythmias

Sick Sinus Syndrome(SSS)Sick Sinus Syndrome(SSS)

A wide variety of abnormalities of sinus node function

It is an intrinsic defect of the sinoatrial nodeConsists of:

• Sinus bradycardia• Sinoatrial blocks• Sinus arrest

SSSSSS

Bradycardia-tachycardia syndrome is an important variant of sick sinus syndrome, in which atrial flutter and fibrillation alternate with prolonged asystolic periods

Signs and symptomsSigns and symptoms

AsymptomaticLethargySyncope FatigueCHFTachycardia phases are often perceived as

palpitations

TreatmentTreatment

Permanent Pacemaker Placement – dual chamber preferred

Beta- blockers for paroxysmal tachycardic component

Atrioventricular BlocksAtrioventricular Blocks

First degree heart blockSecond degree heart block

• Wenkebach ( Mobitz type I) block• Mobitz type II block

Third Degree or Complete heart block (CHB)

First degree blockFirst degree block

PR interval is greater than normal (usually > 0.20 sec) It is asymptomatic and may be physiologic. It is often seen

in well-trained athletes, the young, and those with high vagal tone

It is a common manifestation of digitalis effect (not necessarily toxicity)

First-degree heart block is asymptomatic and may be physiologic.

It is often seen in well-trained athletes, the young, and those with high vagal tone

Treatment is not mandated but further testing maybe

Second degree heart blockSecond degree heart block

Mobitz type I or Wenkebach• progressive PR prolongation, a QRS complex is

dropped with restoration of atrioventricular nodal conduction and a repetition of the sequence

• It is seen most often as a transient abnormality with inferior wall infarction or with drug intoxication, particularly digitalis, beta blockers, and occasionally calcium channel antagonists

• Most of the time patients are asymptomatic and only need to be observed

Second degree heart blockSecond degree heart block

Mobitz type II• PR interval is constant but there is an unexpected dropped

QRS complex• Mobitz type II block may occur in the setting of

anteroseptal infarction or in the primary or secondary sclerodegenerative or calcific disorders of the fibrous skeleton of the heart

• It is important to recognize this type of block because it has a high incidence of progression to complete heart block with an unstable, slow, lower escape pacemaker

• Therefore, pacemaker implantation is necessary in this condition

Third degree heart blockThird degree heart block

There is no electrical communication between the atria and the ventricles.

Heart rate is maintained by an escape junctional (atrioventricular node or His) or ventricular pacemaker

Signs/symptoms - lethargy, postural hypotension, breathlessness, syncope, dizziness, acute heart failure and asystole

Third degree heart blockThird degree heart block

Treatment is based on cause of CHB Digoxin as a cause- stop drug and cautious restarting at a

lower dose; may need temporary pacemaker in the interim With an inferior wall MI, use of atropine is usually

sufficient, since CHB resolve with healing With an anterior wall MI, damage is extensive requiring

emergent transvenous pacemaker insertion for a CHB Usually resolution of CHB does not occur following an

AWMI, warranting the need to insert a permanent pacemaker (DDD dual chamber pacemaker)

Arrhythmias Mustafa Salehmohamed, D.O.. DEFINITIONS An arrhythmia is defined as any rhythm other...

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