Cardiac rhythm disturbance

CARDIAC RHYTHM DISTURBANCE

MAGDI AWAD SASI

MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 20131

Normal Sinus Rhythm

Implies normal sequence of conduction originating in the sinus node and proceeding to the ventricles via the AV node and His-Purkinje system

EKG Characteristics Regular narrow-complex rhythm

Rate 60-100 bpm

Each QRS complex is proceeded by a P wave

P wave is upright in lead II amp downgoing in lead Avr

P wave should be present lead 2v1 positive deflection single one p followed

by one QRS fixed shape within normal 25 width and 25 height (2x2) fixed P-R within normal max 02 sec

Rhythm Of The Heart

The Heart is Like an Orchestra

It has a conducting system that is directed by a conductor

This conductor is the ldquoNatural Pacemakerrdquo of the Heart

Conducting System

- SA node (Primary Pacemaker)

- AV node

- Bundle of His

- Purkinje Fibers

bull Sino-Atrial node (SA Node)

-Origination and dissemination of electrical signals to BOTH atria

-Causes BOTH atria to contract

bull Atrioventricular Node (AV Node)

-Transmits signal to ventricles by going through interventricular septum

-Causes intentional delay to allow atria to complete pumping

bull His Purkinje System MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013

-Electrical signal flows through the His-Purkinje system and causes the ventricles to contract SIMULTANEOUSLY

Normal ECG

Normal EKG1 Regular Rate ndash-----heart rate of 60-100 bpm 2 Regular Rhythm ndash P ndash QRS ndash T ndash P ndash QRS ndash T ndash P ndash QRS ndash

T - etc3 The height of the wave ndash related to the mass of the

muscle generating the wave- The ventricles have more mass than the atria

- large ventricles (ventricular hypertrophy) agrave more muscle creating a stronger signal when the ventricles contract

P wave is smaller than QRS complex

taller QRS complex

ATRIAL FIBRILLATION AF results from random chaotic depolarization of the atria leading to an irregularly irregular tachycardia with irregular ventricular response Atrial rate usually 400-700 beatminutes but ventricular rate is limited by the refractory period at the AV node so ventricular rate ranges from 140-170 beatminutesIn about one-third of patients with this arrhythmia the patient is not aware of so-called lsquoasymptomatic AFrsquoThe prevalence of AF increases with age from lt05 at 40ndash50 years to 5ndash15 at 80 years

Pathophysiology1048708No organized atrial electrical activity leads to loss of atrial contraction1048708 Leads to loss of atrial kick with resultant decrease in ventricular filling1048708 This loss of contraction can lead to stagnation of blood in atrium and can promote thrombus formation1048708 This thrombus can then be dislodged into the systemic circulation when AF converts to sinus rhythm leading to thromboembolic complications

Mechanisms of atrial fibrillation (AF)ndash

Inducing ectopic firing A - Enhanced automaticity B- EADs C- DADs EAD indicates early after depolarizations DAD delayed after depolarization RyR ryanodine receptor and AP action potential

Epidemiology1048708 most common arrhythmia encountered in clinical practice Affects more than 23 million Americans1048708 Approximately 15-25 of all strokes in US can be attributed to AF1048708 Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia occurring in 1ndash2 of the general population Over 6 million Europeans suffer from this arrhythmia and its prevalence is estimated to at least double in the next 50 years as the population ages1048708 The lifetime risk of developing AF is sim25 in those who have reached the age of 40year1048708 AF account for one-third of all admissions for cardiac arrhythmias1048708 Left ventricular (LV) function is often impaired by the irregular fast ventricular rate and by loss of atrial contractile function and increased end-diastolic LV filling pressure Both rate control and maintenance of sinus rhythm can improve LV function in AF patientsMAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013

Classification10487081048708 Paroxysmal AF Episodes that lasts less than 7 days Terminate spontaneously10487081048708 Persistent AF Episodes lasting more than 7 days Require either pharmacologic or electrical intervention to terminate10487081048708 Permanent AF Continuous AF that has failed cardioversion10487081048708 Lone AF In individuals without structural or cardiac disease Low risk for thromboembolism

Causes

ACardiac causes-

Cardiomyopathy

Rheumatic heart disease-mitral stenosisregurgitation aortic regurgitaton

Coronary heart disease

Atrial septal defect

Hypertension

BNon cardiac causes

Thyrotoxicosis

Obesity Diabetes mellitus

Chronic obstructive pulmonary disease Sleep apnea

Pulmonary embolism pneumonialung cancer

CLINICAL FEATURES

Asymptomatic discover that they have atrial fibrillation at a doctorrsquos appointment Even without symptoms atrial fibrillation is a serious medical condition

Others present with acute left ventricular failure symptoms if the atrial contraction is mandatory for cardiac cycle in conditions with high end intraventricular diastolic pressure ie aortic stenosis HOCM hypertension or mitral stenosis

Others present with dyspnea palpitation syncopy chest pain or according to underlying cause symptomatic presentation

Chest discomfort or pain Fainting or light-headedness Fatigue shortness of breath or weakness

Risk Factors

To help prevent atrial fibrillation some risk factors may be controlled or modified

Controllable Risk Factors High cholesterol High blood pressure Heart disease Smoking Excess weight Caffeine

Alcohol abuse Lack of exercise Some medications Sleep apnea

Non-controllable Risk Factors Family history Advancing age Heart disorders from birth

Atrial Fibrillation Clinical ProblemsEmbolism and stroke (presumably due to LA clot)Acute hospitalization with onset of symptomsAnticoagulation especially in older patients (gt 75 yr)Congestive heart failure

o Loss of AV synchronyo Loss of atrial ldquokickrdquoo Rate-related cardiomyopathy due to rapid ventricular response

Rate-related atrial myopathy and dilatationChronic symptoms and reduced sense of well-being

ECG10487081048708 Results from random chaotic depolarization of the atria10487081048708 No organized electrical activity10487081048708 No real P waves10487081048708 Irregular ventricular rhythm10487081048708 Ventricular rate may be fast or slow

The Major Goals in treating Atrial Fibrillation are

Relieve AF symptoms and improve patientrsquos quality of life Prevent blood clots to decrease the risk of stroke Control the heart rate to allow the ventricles enough time to fill with

blood Restore the heart rhythm to allow the atria and ventricles to work

together more efficiently

TREATMENT

afibUnstabl

e Urgent Cardiovert

stable

Rate controlAnticoagulationConversion to and maintenance of sinus rhythm

IF A PATIENT PRESENTS WITH AFANSWER 4 QS1 Is heshe haemodynamically stable2 Weather to control the rate or rhythm 3 What is the underlying cause 4 Is there an indication for anticoagulation

Urgent cardioversion W defibrillator if hemodynamic instability hypotension angina heart failure confusion due to low cardiac output no urineIf cardioverting ensure R-wave synchronization with electrical cardioversion to prevent ldquoR-on-Trdquo shock which can induce Ventricular fibrillation There is also a role in the management of recent or new onset AF for elective cardioversion when the patient is hemodynamically stable and one wishes to try to bring them out of the arrhythmia if AF IS ACUTE AND LESS THAN 72 HRSOR TO BE ON WARFARIN FOR 4 WEEKS TO RAISE INR 2 TIMES NORMAL AND TO DO CARDIOVERSION

RHYTHM COTROL- Synchronized DC cardioversion and pharmacologic cardioversion gt 48 hours or lt48 hrs with mitral stenosis or history of emboli ndash you

must anticoagulate 3-4 weeks of INR at 2-3 Unless ndash TEE has excluded thrombi If unstable ndashDC cardioversion If stable and correction of underlying problem does not help ndash either

choiceMAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013

Rate vs rhythm Control Anticoagulate

A DC cardioversion ndash 75-93 successful Depends on atrial size and duration of AF

B Drugs ndash 30-60 successfullt7 days ndash dofetilide flecainide ibutilide propafenone gt7 days ndash dofetilide

AGENT III Amiodarone Ibutilide Dofetilide Sotalol IC Flecainide Propafenone IA Procainamide

RHYTHM CONTROLADVANTAGES

Avoids electrical and anatomical remodeling Improves hemodynamics Enhanced exercise capacity Symptom relief Improves Quality Of Life Restores atrial transport Reduces thromboembolic events

DISADVANTAGES Ventricular proarrhythmia Increased mortality Drug-induced bradyarrhythmias Adverse effects Recurrences are likely

AF Antiarrhythmic Therapybull Treatment goalsndash darr frequency of recurrencesndash darr duration of recurrencesndash darr severity of recurrencesndash Not to abolish every episodebull Safety is primary concern

bull Minimize risk of proarrhythmia

After cardioversionOnly 20-30 percent of patients stay in sinus for gt1 yearWhen to Consider Antiarrythmics

Donrsquot in patients with AF less than 1 year no atrial enlargement reversible cause

Consider it in patients with high risk of recurrence Risks generally outweigh benefits Amiodirone ndash good but high toxicity profile used in patients with

bad heart disease (significant systolic dysfunction hypertension with LVH)

Toxicity ndash pulmonary photosensitivity thyroid dysfxn corneal deposits ECG changes Liver dysfunction

RATE CONTROLo Essential in all patientso Persistent tachycardic rates can induce cardiomyopathy and heart failureo Occasional follow-up holter monitor to ascertain rate control o Achieved by slowing AV conduction (beta blockers CCB dig amiodarone)o Digoxin only in hypotension and Heart Failureo Amiodirone ndash rarely but effective

Agents Beta Blocker Metoprolol and Propranolol (ICU=esmolol ) Non-dihydropyridine CA blockers verapamil amp Diltiazem (ICU=diltiazem ) Digoxin Goal Rest 60-80 bpm and Activity 80-110 IV Amiodarone (in the ICU setting) Electrical ablation

RATE CONTROL Which Agent to choose

SBP90-110

SBP 100 to 120

SBP gt120

Estimated risk of stroke is determined with a CHADS2 score and therapy determined with this scale of 1-6 (CHF HTN Age DM Secondary prevention)

0 get ASA because of 05year wo coumadin 1-2 intermediate risk gt or = 3 warfarin PS ndash ASA usually added to warfarin

Anticoagulation during reversion to NSR AF gt48 hrs or unknown

Anticoagulate for gt3 weeks INR 2-3 Or TEE to evaluate for clots in LA Appendage ndash if no clots ndash convert

After anticoagulate for 4 weeks with warfarin ndash ldquostunned atriumrdquoConsider chronic anticoagulation for those with high risk for reversion

DIGOXINLoad 05mg IV6 hrs later 025mg IV6 hrs later 025 mg IVMaintenance 0125 mg daily

B-BlockerInitial Metoprolol 5mg IVP q5min x3dosesPrn metoprolol 5mg IV q6hr prnMaintenance Metoprolol 25 mg po BID (max 100mg BID)

Ca2+ BlockersInitial and prn Diltiazem 10mg IVP q6hrsMaintenance Diltiazem 30mg PO q6hs

Multifocal Atrial Tachycardia (MAT) bull Multiple ectopic focuses fire in the atria all of which are conducted

normally to the ventriclesMAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013

bull QRS complexes are almost identical to the sinus beatsbull Rate is usually between 100 and 200 beats per minutebull The rhythm is always IRREGULARbull P-waves of different morphologies (shapes) may be seen if the rhythm is

slowbull If the rate lt 100 bpm the rhythm may be referred to as

ldquowandering pacemakerrdquobull Commonly seen in pulmonary disease acute cardiorespiratory problems

and CHFbull Treatments

1 Ca++ channel blockers2 B blockers3 potassium4magnesium

bull supportive therapy for underlying causes (antiarrhythmic drugs are often ineffective)

Atrial Flutter

bull A single ectopic macroreentrant focuses fire in the atria causing the

ldquoflutteringrdquo baseline Classic inverted ldquosawtoothrdquo flutter waves

bull AV node cannot transmit all impulses (atrial rate 250 ndash350 per minute) bull ventricular rhythm may be regular or irregular and range from 150

ndash170 beats minutebull A-fibrillation and A-flutter rhythm may alternate ndash these rhythms may

also alternate with SVTrsquosbull May be seen in CAD (especially following surgery) VHD history of

hypertension LVH CHFbull Treatmentbull DC cardioversion if patient is unstable

bull Drugs (goal rate control) Ca++ channel blockers to delay AV conduction

bull Amiodarone to delay AV conduction + prolong myocardial AP (refractoriness of myocardium)

bull The danger of thromboembolic events is also high in A-flutter

Paroxysmal (of sudden onset) Supraventricular Tachycardia (PSVT) MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013

bull A single reentrant ectopic focuses fires in and around the AV node all of which are conducted normally to the ventricles (usually initiated by a PAC)

bull QRS complexes are almost identical to the sinus beatsbull Rate is usually between 150 and 250 beats per minutebull The rhythm is always REGULARbull Possible symptoms

palpitations angina anxiety polyuruia syncope bull Prolonged runs of PSVT may result in atrial fibrillation or atrial flutterbull May be terminated by carotid massage

bull carotid pressure - baroreceptor firing rate ndashto increase vagal tone by valsalva maneuver gag reflex eye ball massage

Treatment Ablation of focus Adenosine (delay AV conduction) Ca++ Channel blockers

AV nodal reentrant tachycardia (AVNRT)AV reentrant tachycardia (AVRT)

ndash Orthodromic ndash Antidromic

A premature ventricular contraction (PVC) also known as a premature ventricular complex ventricular premature contraction (or complex or complexes) (VPC) ventricular premature beat (VPB) or extrasystole is a relatively common event where the heartbeat is initiated by the heart ventricles rather than by the sinoatrial node the normal heartbeat initiator The electrical events of the heart detected by the electrocardiogram allow a PVC to be easily distinguished from a normal heart beatPVC- bizarre wide not preceded by P wave QRS reverse T wave

PVCs may be unifocal multifocal or multiformed Multifocal PVCs have different sites of origin which means their coupling intervals (measured from the previous QRS complexes) are usually different Multiformed PVCs are common in digitalis intoxication

PVCs may occur as isolated single events or as couplets triplets and salvos (4-6 PVCs in a row) also called brief ventricular tachycardiarsquos

PVCs may occur early in the cycle (R-on-T phenomenon) after the T wave or late in the cycle - often fusing with the next QRS (fusion beat) R-on-T PVCs may be especially dangerous in an acute ischemic situation because the ventricles may be more vulnerable to ventricular tachycardia or fibrillation

Late (end-diastolic) PVCs are illustrated with varying degrees of fusion For fusion to occur the sinus P wave must have made it to the ventricles to start the activation sequence but before ventricular activation is completed the late PVC occurs The resultant QRS looks a bit like the normal QRS and a bit like the PVC ie a fusion QRS

What is the risk of VPCSIt depends on

a Frequency of VPCSb Form of VPCS_ uniform multiform salvos

VPCS IN ACUTE SYNDROMES 1 Myocarditispercarditis 2 Myocardial reperfusion-PRINZEMATALS ANGINA THROMBOLYSIS IN MI BALLON DEFLATION IN PTCA

c Transient ischemic eventsVentricular tachycardia (V-Tach or VT) is a tachycardia or fast heart rhythm that originates in one of the ventricles of the heart This is a potentially life-threatening arrhythmia because it may lead to ventricular fibrillation a systoles and sudden death VT is defined as three or more consecutive ventricular ectopic impulses at a rate 120minutes or greaterBy ECG rapid broad often bizarre QRS complexes with T waves usually opposite in direction to the main QRS deflection and with rate 140 min or moreVT can be defined by duration or ECG patternVentricular tachycardia can be classified based on its morphology A Monomorphic ventricular tachycardia means that the appearance of all the beats match each other in each lead of a surface electrocardiogram (ECG)

B Polymorphic ventricular tachycardia on the other hand has beat-to-beat variations in morphology This most commonly appears as a cyclical progressive change in cardiac axis previously referred to by its French name torsades de pointes (twisting of the points) However currently the term torsades de pointes is reserved for polymorphic VT occurring in the context of a prolonged resting QT interval

Another way to classify ventricular tachycardias is the duration of the episodes 1 Non-sustained V T__ the fast rhythm self-terminates within 30 seconds2 Sustained VT the rhythm lasts more than 30 seconds (even if it terminates on its own after 30 seconds) VT CAN BE

d Bigiminy trigiminye Couplet tripletf Salvos-uniform morphology VT-3 to 5 vectopics

Descriptors to consider when considering ventricular tachycardia Sustained (lasting gt30 sec) vs nonsustained Monomorphic (uniform morphology) vs polymorphic vs Torsade-dp

Torsade-de-pointes a polymorphic ventricular tachycardia associated with the long-QT syndromes characterized by phasic variations in the polarity of the QRS complexes around the baseline Ventricular rate is often gt200bpm and ventricular fibrillation is a consequence

Presence of AV dissociation (independent atrial activity) vs retrograde atrial capture Presence of fusion QRS complexes (Dressler beats) which occur when supraventricular beats (usually sinus) get into the ventricles during the ectopic activation sequence

What is the riskDepends on

i Structural heart diseaseii Ejection fracture

Symptomspalpitation SOB chest syncope

DD OF WIDE QRS TACCHYCARDIASVT with LBBBSVT with RBBBWolf Parkinson white syndromeHyperkalemiaAF with preexcitationPacemaker mediated tachycardiaSVT with aberrant conduction

Ventricular fibrillation is life-threateningVentricular fibrillation (v-fib for short) is the most serious cardiac rhythm disturbance The lower chambers quiver and the heart cant pump any blood causing cardiac arrest

How it worksThe hearts electrical activity becomes disordered When this happens the hearts lower (pumping) chambers contract in a rapid unsynchronized way (The ventricles flutter rather than beat) The heart pumps little or no blood Collapse and sudden cardiac arrest follows -- this is a medical emergency

Signs of cardiac arrest

Sudden loss of responsiveness (no response to tapping on shoulders) No normal breathing (the victim does not take a normal breath when you

tilt the head up and check for at least five seconds) Pulse less Apnea Centrally cyanosed convulsion This is sudden cardiac arrest (SCA) -- which requires immediate medical

help (CPR and defibrillation)

Treatment Ventricular fibrillation can be stopped with a defibrillator which gives an electrical shock to the heart

HEART BLOCK------------------------First-degree AV blockbull First-degree (AV) block is defined as a fixed prolonged PR interval

exceeding 021 seconds with all atrial impulses conductedCAUSESE

1 Athletic training2 Vascular--Acute MI3 Drugs

bull Calcium channel blockers bull Beta-blockers bull Digoxin bull Amiodarone

4 Valvular-- Mitral or aortic valve annulus calcification Rheumatic fever

5 Infectious disease

bull Infective endocarditis

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

6Collagen vascular disease

bull Rheumatoid arthritis

bull systemic lupus erythematous

bull scleroderma

7Fetuses of pregnant women who are anti-SSARo positive

8Infiltrative diseases such as amyloidosis or sarcoidosis

9Myotonic dystrophy

SYMPTOMS

bull Asymptomatic at rest

bull Markedly prolonged PR interval may reduce exercise tolerance in patients with left ventricular systolic dysfunction

bull Syncope may result from transient high-degree AV block and in those with infranodal block and wide QRS complex

bull The intensity of the first heart sound (S1) is decreased in patients with first-degree AV block

bull Patients with first-degree AV block may have a short soft blowing diastolic murmur heard at the cardiac apex The diastolic murmur is thought to be related to antegrade flow through closing mitral valve leaflets that are stiffer than normal

TREATMENT

bull Patients with asymptomatic first-degree AV block----no treatment

bull In patients with symptomatic first-degree AV block medications with potential for AV block must be discontinued if possible

bull Permanent electronic pacemakers may be indicated in those with the following

1 Severe bradycardia

2 Syncope associated with infranodal block

3 Left ventricular systolic dysfunction when a shorter AV delay has been shown to improve hemodynamic condition

bull Medications

COMPLCATIONS

bull Progression to higher degrees of AV blockMAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013

bull Reduction in left ventricular stroke volume and cardiac output

bull Pseudo-pacemaker syndrome

PROGNOSIS

bull Isolated first-degree AV block carries no increased risk of mortality

bull Patients with first-degree AV block and infranodal blocks have increased risk of progression to complete AV block

Second-degree block

Mobitz type I (Wenckebach) AV block

Mobitz type II AV block

Mobiz type 1

It is a progressive prolongation of P-Rinterval with the RR interval shortening before the blocked beat this phenomenon is almost always due to abnormal conduction within the AV node (one P in ECG except in one place BW 2QRSs)CAUSES

It may occur in normal individuals with heightened vagal tone

1 Drug effect (especially digitalis calcium channel blockers β-blockers or other sympatholytic agents) often superimposed on organic disease

2 These disturbances also occur transiently or chronically due to A Ischemia B InfarctionC Inflammatory processesD fibrosisE CalcificationF Infiltration

The prognosis is usually good since reliable alternative pacemakers arise from the AV junction below the level of block if higher degrees of block occurTHE MOST IMPORTANT AETIOLOGY TO BE RO IS STEMI (INFERIOR WALL)

Mobitz type II AV block MAGDI AWAD SASI CARDIAC RHYTHM DISTURBANCE 2013

There are intermittently nonconducted atrial beats not preceded by lengthening AV conduction It is usually due to block within the His bundle system

The distance of P waves from QRS complexes is fixed but only one P wave pass through AV node and result in QRS It is called 21 block- 2 P waves or 31 block 3 P waves

Mobitz type II block is almost always due to organic disease involving the infranodal conduction system In the event of progression to complete heart block alternative pacemakers are not reliable Thus prophylactic ventricular pacing is required

SUMMARYFIRST DEGREE- ONE P FIXED PROLONGED PR INTERVAL MORE THAN 5 SQSECOND DEGREE MOBIZ 1 - PROGRESSIVE PROLONGATION OF PR INTERVAL ONE P EXCEPT IN ONE PLACE 2 P WITH ONE QRS REVERSIBLE BENIGN CONDITION ACUTE INFERIOR MI MOBIZ 2 - MANY FIXED P WAVES FIXED NUMBER AND DISTANCES 31 BLOCK 41 BLOCK ONE P ONLY PRODUCE ONE QRS PACEMAKER IS THE TREATMENTACUTE STEMI CAN CAUSE ALL TYPES OF BLOCKANY PATIENT PRESENTED WITH HEART BLOCK SHOULD ALARM US TO LOOK FOR DRUGS AND POSSIBILITY OF ACUTE CORONARY SYNDROMES

Complete heart blockComplete (third-degree) heart block is a more advanced form of block often due to a lesion distal to the His bundle and associated with bilateral bundle branch block The QRS is wide and the ventricular rate is slower usually less than50 beatsmin Transmission of atrial impulses through the AV node is completely blocked and a ventricular pacemaker maintains a slow regular ventricular rate usually less than 45 beatsmin Exercise does not increase the rate(( LBBB + RBBB+ 1ST DEGREE HAERT BLOCK=CHB )) SYMPTOMS Patients may be asymptomatic or may complain of low cardiac output symptoms- fatigue sweating dizziness lose of effort weakness or dyspnea ifthe rate is less than 35 beatsmin symptoms may occur at higher rates if the left ventricle cannot increase its stroke outputThe patient may be in shock if it is caused by acute myocardial infarction During periods of transition from partial to complete heart block some patients have ventricular asystole that lasts several seconds to minutes Syncope occursabruptly

SIGNSThe first heart sound varies in intensity Wide pulse pressure Changing systolic BP level Cannon venous pulsations in the neck are also present

TreatmentThe indications for permanent pacing have been discussedSymptomatic bradyarrhythmias asymptomatic Mobitz II AV block or complete heart block

Risk Factors

Normal Sinus Rhythm

Implies normal sequence of conduction originating in the sinus node and proceeding to the ventricles via the AV node and His-Purkinje system

EKG Characteristics Regular narrow-complex rhythm

Rate 60-100 bpm

Each QRS complex is proceeded by a P wave

P wave is upright in lead II amp downgoing in lead Avr

P wave should be present lead 2v1 positive deflection single one p followed

Rhythm Of The Heart

Conducting System

- AV node

- Bundle of His

- Purkinje Fibers

Normal ECG

taller QRS complex

Causes

ACardiac causes-

Cardiomyopathy

Hypertension

BNon cardiac causes

Thyrotoxicosis

CLINICAL FEATURES

Risk Factors

TREATMENT

afibUnstabl

e Urgent Cardiovert

stable

SBP90-110

SBP 100 to 120

SBP gt120

Atrial Flutter

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

Rhythm Of The Heart

Conducting System

- AV node

- Bundle of His

- Purkinje Fibers

Normal ECG

taller QRS complex

Causes

ACardiac causes-

Cardiomyopathy

Hypertension

BNon cardiac causes

Thyrotoxicosis

CLINICAL FEATURES

Risk Factors

TREATMENT

afibUnstabl

e Urgent Cardiovert

stable

SBP90-110

SBP 100 to 120

SBP gt120

Atrial Flutter

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

Normal ECG

taller QRS complex

Causes

ACardiac causes-

Cardiomyopathy

Hypertension

BNon cardiac causes

Thyrotoxicosis

CLINICAL FEATURES

Risk Factors

TREATMENT

afibUnstabl

e Urgent Cardiovert

stable

SBP90-110

SBP 100 to 120

SBP gt120

Atrial Flutter

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

Causes

ACardiac causes-

Cardiomyopathy

Hypertension

BNon cardiac causes

Thyrotoxicosis

CLINICAL FEATURES

Risk Factors

TREATMENT

afibUnstabl

e Urgent Cardiovert

stable

SBP90-110

SBP 100 to 120

SBP gt120

Atrial Flutter

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

Causes

ACardiac causes-

Cardiomyopathy

Hypertension

BNon cardiac causes

Thyrotoxicosis

CLINICAL FEATURES

Risk Factors

TREATMENT

afibUnstabl

e Urgent Cardiovert

stable

SBP90-110

SBP 100 to 120

SBP gt120

Atrial Flutter

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

Causes

ACardiac causes-

Cardiomyopathy

Hypertension

BNon cardiac causes

Thyrotoxicosis

CLINICAL FEATURES

Risk Factors

TREATMENT

afibUnstabl

e Urgent Cardiovert

stable

SBP90-110

SBP 100 to 120

SBP gt120

Atrial Flutter

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

Causes

ACardiac causes-

Cardiomyopathy

Hypertension

BNon cardiac causes

Thyrotoxicosis

CLINICAL FEATURES

Risk Factors

TREATMENT

afibUnstabl

e Urgent Cardiovert

stable

SBP90-110

SBP 100 to 120

SBP gt120

Atrial Flutter

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

Hypertension

BNon cardiac causes

Thyrotoxicosis

CLINICAL FEATURES

Risk Factors

TREATMENT

afibUnstabl

e Urgent Cardiovert

stable

SBP90-110

SBP 100 to 120

SBP gt120

Atrial Flutter

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

TREATMENT

afibUnstabl

e Urgent Cardiovert

stable

SBP90-110

SBP 100 to 120

SBP gt120

Atrial Flutter

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

TREATMENT

afibUnstabl

e Urgent Cardiovert

stable

SBP90-110

SBP 100 to 120

SBP gt120

Atrial Flutter

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

stable

SBP90-110

SBP 100 to 120

SBP gt120

Atrial Flutter

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

SBP90-110

SBP 100 to 120

SBP gt120

Atrial Flutter

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

SBP90-110

SBP 100 to 120

SBP gt120

Atrial Flutter

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

Atrial Flutter

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

Atrial Flutter

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

Atrial Flutter

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

bull Diphtheria

bull Chagas disease

bull Lyme disease

bull Tuberculosis

bull scleroderma

9Myotonic dystrophy

SYMPTOMS

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

TREATMENT

bull Medications

COMPLCATIONS

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

PROGNOSIS

Second-degree block

Mobiz type 1

Risk Factors

Mobiz type 1

Risk Factors

Health & Medicine

Cardiac rhythm disturbance