TACHYARRYTHMIAS

Dr RAVI KANTH

DEFINITION

ANATOMY OF CONDUCTION

ELECTROPHYSIOLOGY

DIAGNOSTIC APPROACH

TREATMENT MODALITIES

DESCRIPTION ABOUT INDIVIDUAL ARRYTHMIAS 2

DEFINITION Any disturbance of the heart's rhythm,

regular or irregular, resulting by convention in a rate over 100 beats/min .

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CONDUCTION SYSTEM OF THE HEART AND ELECTROCARDIOGRAPHY

Conduction System of the Heart• SA node: sinoatrial node. The pacemaker.

– Specialized cardiac muscle cells.– Generate spontaneous action potentials (autorhythmic tissue). – Action potentials pass to atrial muscle cells and to the AV node

• AV node: atrioventricular node.– Action potentials conducted more slowly here than in any other

part of system. – Ensures ventricles receive signal to contract after atria have

contracted• AV bundle: passes through hole in cardiac skeleton to reach

interventricular septum• Right and left bundle branches: extend beneath

endocardium to apices of right and left ventricles• Purkinje fibers:

– Large diameter cardiac muscle cells with few myofibrils. – Many gap junctions. – Conduct action potential to ventricular muscle cells (myocardium)

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Conducting System of Heart

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IMPULSE CONDUCTION THROUGH THE HEART

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ACTION POTENTIAL Duration – 200- 400 msec Regulated by activity of time & voltage

dependent ionic currents Ionic currents maintained by

Ionic channels –passively conduct ions along electrochemical gradient

Pumps, transporters – transport ions against gradients

Exchangers- electrgenically exchange species AP are regionally distinct

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Electrical Properties of Myocardial Fibers

1. Rising phase of action potential • Due to opening of fast Na+ channels

2. Plateau phase • Closure of sodium channels• Opening of calcium channels• Slight increase in K+ permeability• Prevents summation and thus tetanus of

cardiac muscle3. Repolarization phase

• Calcium channels closed• Increased K+ permeability

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Heart Physiology: Intrinsic Conduction System

• Autorhythmic cells:– Initiate action potentials – Have unstable resting potentials

called pacemaker potentials– Use calcium influx (rather than

sodium) for rising phase of the action potential

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DEPOLARIZATION OF SA NODE SA node - no stable resting membrane potential Pacemaker potential

gradual depolarization from -60 mV, slow influx of Na+

Action potential occurs at threshold of -40 mV depolarizing phase to 0 mV

fast Ca2+ channels open, (Ca2+ in) repolarizing phase

K+ channels open, (K+ out) at -60 mV K+ channels close, pacemaker potential starts over

Each depolarization creates one heartbeat SA node at rest fires at 0.8 sec, about 75 bpm

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Pacemaker and Action Potentials of the Heart

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DEPOLARIZATION AND IMPULSE CONDUCTION Depolarization in

SA node precedes depolarization in atria, AV node, ventricles

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ELECTROCARDIOGRAM

P wave Depolarization of atria Followed by

contraction QRS complex

3 waves (Q, R, & S) Depolarization of

ventricles Followed by

contraction T wave

Repolarization of ventricles

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ELECTROCARDIOGRAM

P-Q intervalTime atria

depolarize & remain depolarized

Q-T intervalTime ventricles

depolarize & remain depolarized

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ELECTROCARDIOGRAM Intervals show timing of cardiac cycle

P-P = one cardiac cycle P-Q = time for atrial depolarization Q-T = time for ventricular depolarization T-P = time for relaxation

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MECHANISMS OF ARRYTHMOGENESIS Some tacyarythmias start by one mechanism

& gets perpetuated by another mechanism Some caused by one mechanism can

precipitate another episode caused by different mechanism

Mechanisms are Disorders of impulse formation Disorders of impulse conduction both

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DISORDERS OF IMPULSE FORMATION Characterised by

Inappropriate discharge rate of normal pacemaker

Inappropriate discharge of ectopic pacemaker

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Abnormal automaticity Arise from cells that have reduced maximum

diastolic potentials Don’t need prior stimulationTriggered activity Initiated by after depolarisations Induced by one or more preceding action

potentials

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After depolarisations are of two types Early after depolarisation- occurs during

phase 2 & phase 3 Delayed after depolarisation- occurs

during phase 4 All depolariations doesn’t reach threshold

potential but if they reach they trigger another after depolarisation & thus perpetuate

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DAD’S Result from activation of calcium sensitive

inward current due to increase in intra cellular ca concentrations

Acquired or inherited abnormalities in Sarcoplasmic reticulum properties CA release channels SR calcium binding proteins

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EAD’S AP prolongation may increase ca influx

through l-type ca channels during cardiac cycle , causing excessive ca accumulation in SR & spontaneous SR ca release

Increased intracellular ca cause depolarisation by activation of ca dependent cl currents ,NA +/CA + exchanger provoking EAD,S

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Re-entry Two types

Anatomical re-entry Functional reentryANATOMICAL REENTRYCharacters

-2 or more pathways with different electropohysiological properties-impulse blocked in one pathway-impulse conducts slowly in alternate pathway &returns in pathway initially blocked in reversed direction to re exite tissue proximal to site of block

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For re entry to occur anatomical length of circuit should be greater than reentrant wave length

Conditions that depress conduction velocity & refractory period promote development of re entry[λ = c.v x rp]

Sustained reentry occurs due to excitable gap between activating head & recovery tail.

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Fuctional reentry Occur in fibres that exhibit functionally

different EP properties caused by local differences in transmembrane AP

functional heterogenities can be fixed or change dynamically

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Mechanisms of termination are When conduction & recovery characters of

circuit change When activating head of wave collides with

tail

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DETERMINANTS OF AMPLITUDES OF AFTER DEPOLARISATIONSintervention Effect on

amplitude of EAD’S

Effect on amplitude of DAD’S

Long cycles ↑ ↓Long AP duration ↑ ↑Reduced membrane potential

↑ ↓

Na channel blockers No effect ↓Ca channel blockers ↓ ↓catecholamines ↑ ↑

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APPROACH TO TACHYARRYTHMIAS

HISTORY• Mode of

onset• Mode of

termination• Drug

history• Dietary

history• H/o

systemic illness

• Family history

PHYSICAL EXAMINATION

• Symptoms• Signs

NON INVASIVE INVESTIGATIONS• 12 lead ECG• Holter

monitor• Patient

activated event monitor

• Implanted loop ECG monitor

• HUT• Exercise ECG• 2D ECHO

INVASIVE INVESTIGATIONS

• Electrophysiological studies

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HISTORY

MODE OF ONSET Occuring in the setting of exercise and stress – caused by

catecholamine sensitive automatic or triggered activity At rest – may be caused by vagal initiation (AF) Lightheadedness, syncope in setting of tightly fitting collar,

turning head- suggests carotid hypersensitivity

• MODE OF TERMINATION• If terminated by vagal manevoure – suggests AV node as integral part of

tachyarrythmias

May help determine diagnosis or further guide to diagnostic tests

• DRUG HISTORY• nasal decongestants• Beta blockers• Drugs prolonging QT interval. 36

DIETARY HISTORY Alcoholic intake Food containing Ephedrine

H/O SYSTEMIC ILLNESS COPD Thyrotoxicosis Pericarditis Congestive heart failure

FAMILY HISTORY HOCM Long QT syndromes Myotonic dystrophies

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PHYSICAL EXAMINATIONMORE HELPFUL IF DONE DURING SYMPTOMATIC PERIOD HR

>100 Regularly irregular Irregularly irregular

JVP Increased JVP Cannon waves

Heart sounds Variable heart sounds murmurs

BP -- Variable Physical manoeveurs– Can have diagnostic and therapeutic

value. Valsalva/Carotid sinus massage - terminate or slow tachyarrythmias that depend on AV node. 38

12 LEAD ECG

Primary tool in arrhythmia analysis 3 steps in diagnosing tachyarrythmia.

Step 1 – determine if QRS complex is narrow or wide. Step 2 – determine if QRS complex is regular or irregular. Step 3 -- look for p waves and relation to QRS complex.

Major branch point in DD is QRS duration. QRS < .12 – always almost SVT QRS >.12 – often VT

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24 hr Holter monitoring - for patients with daily symptoms

Patient activated event monitor – for patients with intermittent symptoms

Implanted loop ECG monitor – for patients with infrequent severe symptoms

Exercise ECG - to determine myocardial ischemia -For analysis of morphology of QT

interval. HUT – used in patients with recurrent syncope

Syncope with injuries in absence of heart disease

2D ECHO – for cardiac chamber size and function.To rule out valvular diseases.

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ELECTROPHYSIOLOGICAL STUDIES For diagnostic purposes For therapeutic purposes

COMPONENTS OF TEST Measuement of conduction under resting , stress

conditions and maneuvers

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SITE OF ORIGIN

Atrial SA node Atrial muscle

Junctional AV node His bundle Kent bundle

Bundle branches Purkinje fibres Ventricular muscle

SUPRAVENTRICULAR VENTRICULAR

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Atrial Fibrillation Paroxysmal

supraventriculartachycardias(PSVT)-AV nodal reentry tachycardia (AVNRT)

-AV junctional tachycardia-AV reentry tachycardia (AVRT)-WPW-AV reentry over concealed bypass tract–Atrial Tachycardia

VPC’S VT Ventricular flutter Ventricular

fibrillation Brugada syndrome

Supraventricular arryhthmias Ventricular arryhthmias

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WIDE QRS TACHY CARDIA

Ventricular tachycardia

SVT with BBB Antidromic AV re –

entry tachycardia

Torsades de – pointes

LBBB with AF or Atrial flutter with variable block

WPW with AF or AFL with variable block

WITH REGULAR RHYTHM

WITH IRREGULAR RHYTHM

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DIFFERENTIAL DIAGNOSIS OF WIDE QRS TACHYCARDIA

Initiation with premature P wave

Changes in P-P interval precedes R – R interval changes

Slowing or termination by vagal maneuvers

Initiation with premature QRS complex

Changes in R – R interval precedes P – P interval

AV – dissociation Fusion ,capture beats QRS duration-

RBBB type V1 morphology - >140 msLBBB type V1 - > 160 ms

Delayed activation –LBBB - R- wave > 40 msRBBB- onset of R- wave to nadir of S – wave > 100 ms

Concordance of QRS complexes in all precordial leads

SVT VT

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ANTIARRYHTHMIC DRUGS

Class IA. This includes drugs that reduce V.max (rate of rise of

action potential upstroke [phase 0]) and prolong action potential duration

Eg-quinidine, procainamide, disopyramide.Class IB. This class of drugs does not reduce V.max and shortens

action potential duration—Eg-mexiletine, phenytoin, and lidocaine.

Class IC. This class of drugs can reduce V.max, primarily slow

conduction, and prolong refractoriness minimallEg-flecainide, propafenone, and moricizine.

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Class II. These drugs block beta-adrenergic receptors.

Eg- propranolol, timolol, and metoprolol.Class III. This class of drugs predominantly blocks

potassium channels (such as IKr) and prolongs repolarization. Eg-sotalol, amiodarone, and bretylium.

Class IV. This class of drugs predominantly blocks the

slow calcium channel (ICa.L)—Eg-verapamil, diltiazem, nifedipine,

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SINUS TACHYCARDIA PHYSIOLOGICAL

fever anxiety anemia sepsis hyperthyroidism congetive heart failure hypoxemia

INAPPROPRIATE viral – post viral dysautonomia

TREATMENT

Treat underlying cause

Beta blockers

Increase hydration Beta blockers Catheter

ablation/pacing

PHYSIOLOGICAL INAPPROPRIATE

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APC’S – Incidence increases with age ECG – Premature & abnormal P wave Short PR interval Precedes normal QRS complex Compensatory pause is incompleteTREATMENT – No treatment needed If severely symptomatic – Β-blocker, Catheter ablation .

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FOCAL ATRIAL TACHYCARDIAS

Can not be initaiated by programmed atrial stimulation

First P wave same as othr P waves

Response to adenosine –AV block seen

-- slow or terminate

Initiated by programmed stimulation

First P wave different from others

Response to adenosine

-AV block seen -cant slow or

terminate

Automatic AT Focal reenterant AT

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ECG – P wave distinct from sinus P wave PR interval shorter than RP intervalTREATMENT

Rate control Rhytm control Anticoagulation if LA diameter > 5cm Catheter ablative theraphy DC version

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MULTIFOCAL ATRIAL TACHYCARDIA – Mostly seen in patients of pulmonary disease ECG – Atrial & ventricular rate – 100 – 150 bts / min > 3 distinct P wave morphology > 3 distinct PR intervalTREATMENT – Treat underlying pulmonary disease CCB’s , amiodarone

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ATRIAL FIBRILLATION Most common sustained arrhythmia Disorganised , rapid and irregular atrial activation and

ventricular responses Atrial rate – 400- 600 bpm Ventricular rate – 120-150 bpm

CLASSIFICATION Recurrent Paroxysmal Persistent Permanent

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CAUSES RHD Ischaemic heart disease Hypertension Constrictive pericarditis Hyperthyroidism Acute alcoholism Vascular,abdominal and thoracic surgery Anemia Acute vagotonic episode Lone atrial fibrillation ( no structural heart disease)

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ECG Atrial deflections are irregular and chaotic – ragged baseline Ventricular rate is irregular In longstanding cases, baseline almost straight with minimal

undulation .

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TREATMENT

Control ventricular rate Betablockers Ca channel blockers Digoxin

Anticoagulation When AF >12hrs and

risk factors for stroke present.

Maintain INR – 2 to 3 Warfarin

DC cardioversion – 200 J Pharmacological

To terminate - Amiodarone , Procainamide iv To maintain restored sinus rhytm – beta

blockers ,class Ic drugs. Emergency

If AF >24 - 48hrs TEE done to r/o atrial thrombus Heparin given with warfarin until INR > 1.8 Anticoagulate for 1 month after restoration of

sinus rythm Elective

Anticoagulate for atleast 3 weeks before cardioversion.

RATE CONTROL TERMINATION OF AFACUTE

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CHRONIC

Beta blockers Ca channel blockers Digoxin His bundle / AV junction

ablation with implantation of activity sensor pacemaker

Anti coagulation Surgical ablation of left

atrial appendage

Catheter ablation – of atrial muscle sleeves entering pulmonary veins

Surgical ablation – COX – MAZE procedure

RATE CONTROL TERMINATION OF AF

SURVIVAL OUTCOME Restoration of sinus rhytm not superior to rate control with anticogulation as evidenced by AFFIRM and RACE trials 65

ATRIAL FLUTTERatrial rate = 250-350 cycles/min Ventricle rate is closer to 150, 100 or 75

beats/min 2:1, 3:1 and 4:1F waves“sawtooth” shape

ATRIAL FLUTTER

Reentrant type arrhythmia

ATRIAL FLUTTER Treatment

DC – version 50 – 100 j Anticoagulation If asymptomatic –

- rate control -rhythm control - catheter ablation

AV NOAL RE ENTERANT TACHYCARDIA – Most common Mostly in women Repetitive activation down slow pathway &

up fast pathway results in tachycardiaECG – Rate – 120 – 150 P waves negative Narrow QRS complexes P wave not visible or distorts QRS complex

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TREATMENT – ACUTE Vagal maneuvers Adenosine – 6 – 12 mg iv B – blockers ,CCB’s DC - version -100- 200 j

PREVENTION B-blockers , CCB’s Catheter ablation – slow pathway

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AV JUNCTIONAL RHYTHM Rate – 40 – 50 Accelerated AVJR – 50 – 100TREATMENT

Stop digoxin B – blockers Catheter ablation

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WPW SYNDROMEECG

Short PR interval.

Short or long RP interval.

Delta waves Narrow QRS

complex.

SITES OF BYPASS TRACTS

Left lateral Right lateral Posteroseptal Anteroseptal

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A comment on PSVT in patient with WPW:

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MAIN SITES OF BYPASS

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COMPLICATIONS Reciprocating tachycardia

Orthodromic – AV reentry – conduction to ventricle via AV node and reentry via AP.Antidromic - conduction to ventricle via AP and reentry via His purkinje system – mimics VT

Atrial fibrillation50% predisposed

-fast ventricular rate results in hemodynamic compromise. 83

TREATMENTACUTE

Orthodromic tachycardiaVagal stimulationAdenosineCCB sBetablockers

AFDC cardioversionProcainamideIbutelideDigoxin avoided

CHRONIC

Beta blockers CCB s Class Ia or Ic drugsCATHETER

ABLATION Indications --

recurrent symptomatic SVTs HR >200

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AIVR

>3 or more consecutive VPCs VR >40 and <120 Benign rhytm CAUSES

Idiopathic Acute MI Acute myocarditis Digoxin intoxication Postoperative cardiac surgery Cocaine intoxication

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TREATMENT If hemodynamic compromise occurs

atropine Atrial pacing

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PREMATURE VENTRICULAR COMLEXES Broad QRS > 120ms T wave is large ,opposite in direction to QRS No preceding p waves Compensatory or noncompensatory pause Fixed or variable coupling interval.

TYPES BIGEMINY TRIGEMINY QUADRIGEMINY COUPLET TRIPLET MONOMORPHIC POLYMORPHIC

Incidence >60% of healthy males during 24hr Holter

>80% post MI Benign ectopics disappear on exercise Pts –normal life span.

CLINICAL SIGNIFICANCE LOWNs grading system of VPCs Determines prognostic significance after MI As grade advances, there is increased risk of

SCD

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GRADES VPCs0 none1 <30/hr2 >30/hr3 multiform

4A 2 consecutive4B >3 consecutive5 R on T phenomenon

MANAGEMENTIn Normal heart Asym- No treatment Sym - betablockersStructural heart disease betablockers Class IA, III drugs

VENTRICULAR TACHYCARDIA

VT consists of at least three or more consecutive VPCs at a rate of 100bpm.

Types- -Nonsustained <30s -sustained > 30s

Rhythm- Regular / slightly irregular Rate 70 to 250 / min

ECG DIAGNOSIS QRS duration RBBB > 140 ms LBBB > 160 ms Wellens et al QRS >140ms good indicator of VT QRS 120- 140 ms only 50% have VT

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VT with RBBB (Wellens & Gulamhusein)

FUSION & CAPTURE BEATS 33 % cases of VT Diagnosis of VT is certain Seen in VT of lower rates(< 160) Capture beat- sinus beat Fusion beat- hybrid beat due to both atrial &

ventricular activation.

VT IN PATIENTS WITH CORONARY ARTERY DISEASE

Non-sustained VT (NSVT) -67% Sustained VT 3.5% VF – 4.1% VT + VF – 2.7 %Mortality VT - 18.6% VT + VF – 44% 1 yr mortality 7% Without VT is 3 %

CLINICAL PRESENTATION Symptoms are variable Depend upon rate of VT & degree of LV

dysfunction Syncope / presyncope / dizziness Palpitations Sudden death

TREATMENT OF VT

HEMODYNAMIC COMPROMISE --

DC – version asynchronously 200j , repeat with ↑energy if no response

IV lidocaine, amiodarone

DC –version synchronously with R wave

IV lidocaine , procainamide , amiodarone

Polymorphic VT Monomorphic VT

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NO HEMODYNAMIC COMPROMISE

Correction of k+ & mg

Removal of offending drug

B – blocker iv Treat acute ischemia Pacing Catheter ablation Quinidine,procainam

ide for BRUGADA syndrome

Lidocaine , procainamide , amiodarone

Catheter ablation

Polymorphic VT Monomorphic VT

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•B-BLOCKERSFocal out flow tract VT

•VERAPAMILSeptal VT

•ICD’S VT with structural

heart disease 114

SPECIFIC TYPES OF VTARRHYTHMOGENIC RT

VENTRICULAR DYSPLASIA(0.4%)

LBBB contour with right axis deviation during VT

ICRBBB ,T waves inverted over the right precordial leads

Type of Cardiomyopathy, possibly familial, with hypokinetic thin walled RV

Abnormality in Chr 1 & Chr 10 -apoptosis

Imp cause of VT in children & young adults with normal hearts

Rt heart failure or asymptomatic rt ventricular enlargement can be present with normal pulmonary vasculature

Males predominate Pathology- Fatty & fibrofatty infiltration

OR myocardial atrophy

Preferentially affects rt ventricular inflow & outflow tracts & the apex

ECG- T wave inversion in V1 to V3, Terminal notch in QRS called “epsilon” wave can be present due to slowed intra ventricular conduction

ICDs are preferable to pharmacological Radio frequency catheter ablation is often

not successful

LEFT SEPTAL VT Arises in the left posterior septum, often

preceded by a fascicular potential. It is sometimes called Fascicular

tachycardia Cause – Re-entry Mgm – Verapamil or Diltiazem Oral verapamil is less effective than iv

verapamil

LEFT SEPTAL VT(FASCICULAR VT) Seen in normal heart. 70% males ,15-40 yrs Resting ECG normal

VT – RBBB pattern with left superior axis QRS < 140 ms

Left septal ventricular tachycardia. This tachycardia is characterized by a right bundle branch block contour. the axis is rightward.

C/F – palpitations, syncope Not associated with sudden death

Treatment- Verapamil . RF ablation 85-100% Prognosis – good

CATECHOLAMINERGIC POLYMORPHIC VT

Uncommon form of inherited VT Occurs in children & adolescents

without any overt structural heart disease

Adenosine sensitive Pts present with syncope or aborted

sudden death with highly reproducible stress induced VT that is often bidirectional

QT interval – Normal Family history present in 30%

During exercise typical responses, initial sinus tachycardia & ventricular extrasystoles followed by monomorphic or bidirectional VT, which eventually leads to polymorphic VT as exercise continues

Mgm – Beta blockers & ICDs Lt cervicothoraic sympathetic

ganglionectomy

BRUGADA SYNDROME

30-40% of idiopathic VF AD, M:F 8:1 2-4th decade Distinct form of idiopathic VT,V fib RBBB & ST segment elevation in anterior

precordial leads No evidence of structural heart disease Mutation in gene responsible for sodium

channel

Acceleration of Na channel recovery or nonfunctional channels

Common in apparently healthy south east Asians – 40-60%

Precise mechanism is not known Can be reproduced by sodium channel

blockers ICDs are the only effective treatment to

prevent sudden deaths

LONG QT SYNDROMES Normal QT males - 440 ms females – 470ms Congenital Jervell Lange-Neilsen syndrome- AR with

deafness Ramano-Ward syndrome - AD with normal

hearing Defect in Na, K channels.

LQTS ECG PATTERNS

AcquiredDrugs Antiarrhythmic Phenothiazines Antihistaminics Antimalarials,pentamidine Tricyclic antidepressants Ketoconazoles Erythromycin cisapride Hypokalemia Hypomagnesemia

C/F Syncope, dizziness,sudden deathTreatment Underlying condition Betablockers ICD

CARDIOMYOPATHIESDILATED CARDIOMYOPATHY

Focus basal septum Mutiple macrorentry ICDs -life threatening ventricular

arrhythmias Comparing amiodarone v/s ICD,

improved survival was found with ICD In case bundle branch re-entry is the

basis, ablate the RBB

HYPERTROPHIC CARDIOMYOPATHY

Risk of sudden death is increased by presence of syncope, family h/o, sudden death in 1st degree relative, septal thickness >3cms or presence of non sustained VT in 24 hr recordings

Infrequent episodes of non sustained VT have low mortality

Amiodarone – Useful symptomatic non sustained VT but not in improving survival

MITRAL VALVE PROLAPSE

VT in MVP has good prognosis although sudden death can occur

Treated with betablockers.

CHD Can occur in pts some years after repair Sustained VT can be caused by re entry at

the site of surgery Mgm- resection or catheter ablation of the

area

VENTRICULAR FLUTTER Severe derangement of heart beat Macro-reentrant Sine wave appearance, with large

regular oscillations (150-300 Bpm) Distinct QRS ,ST T are absent Difficult to distinguish between rapid

VT & V.flutter

VENTRICULAR FIBRILLATION Grossly irregular ,undulation of varying

amplitudes, contours with rates >300 /min Starts with VT Distinct QRS ,ST T are absent Multiple wavelets of reentry 75% of sudden death after MI have VF.

MANAGEMENT

TORSADES DE POINTES

VT characterized by QRS complexes of changing amplitude

that appear to twist around the isoelectric line & occur at rates of 200 to 250 /min

Prolonged ventricular repolarization with QT intervals generally exceeding 500 msec

U wave can also become prominent& merge with T wave

Torsades de Pointes can terminate with progressive prolongation in cycle length with distinctly formed QRS complexes & culminate into basal rhythm, ventricular standstill, or VFib

Common causes Potassium depletion Congenital LQTS Antiarrhythmic drugs IA,IC,III c/f Palpitations, syncope, death Women are at a greater risk

Management IV magnesium Temporary ventricular or atrial pacing+

ICD Lidocaine, mexiletine or phenytoin can

be tried K channel activating drugs pinacidil,

cromakalim Cause of long QT should be treated

REFERENCES BRAUNWALD ‘S HEART DISEASE 8 th ed HARRISONS INTERNAL MEDICINE 17 th ed HURST ‘S HEART DISEASES SHAMMROTH ECG MARRIOTS ECG MEDICINE UPDATE

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