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arrhythmias

Basil

arrhythmias

Properties of cardiac cells

Automaticity• Ability to initiate an impulse spontaneously and

continuously.

Excitability.• Ability to be electrically stimulated.

Conductivity• Ability to transmit an impulse along a membrane in

an orderly manner.

Contractility• Ability to respond mechanically to an impulse.

Pacemakers of the Heart

• SA Node - Dominant pacemaker with an intrinsic rate of 60 - 100 beats/minute.

• AV Node - Back-up pacemaker with an intrinsic rate of 40 - 60 beats/minute.

• Ventricular cells - Back-up pacemaker with an intrinsic rate of 20 - 45 bpm.

Impulse Conduction & the ECG

Sinoatrial node

AV node

Bundle of His

Bundle Branches

Purkinje fibers

The “PQRST”

• P wave - Atrial depolarization

• T wave - Ventricular repolarization

• QRS - Ventricular depolarization

The PR Interval

Atrial depolarization

+

delay in AV junction

(AV node/Bundle of His)

(delay allows time for the atria to contract before the ventricles contract)

The ECG Paper

• Horizontally– One small box - 0.04 s– One large box - 0.20 s

• Vertically– One large box - 0.5 mV

ECG Composed of Waves And Complexes

P- WAVE QT- INTERVAL

QRS- COMPLEX PR- INTERVAL

T- WAVE ST- SEGMENT

Criteria's of a normal heart rhythm

1. Presence of one upright and consistent-appearing P wave before each QRS complex.

2. P-R interval between 0.12-0.20 seconds

3. A consistent appearing QRS complex of less than 0.12 seconds.

4. Consistent R-R interval

5. A heart rate between 60-100 beats/minute

6. The ST segment should be isoelectrical

Arrhythmias

• It is a disturbance in the rhythmic patterns of the heart. Results from abnormal impulse initiation, abnormal conduction or both mechanism together.

Four Steps to Identify Arrhythmias

1- Begin by labeling the P wave, QRS complex, T wave, PR interval, and QT interval.

2- Calculate the atrial and ventricular heart rates.

3- Determine if the rhythm is regular or irregular.

4- Evaluate the waveform of the ECG in detail for additional clues:

Mechanisms Of Arrhythmias

Arrhythmias result from

1-Abnormal impulse initiation and

2-Abnormal impulse conduction.

Mechanisms Of Arrhythmias

The major mechanisms of arrhythmias are

ABNORMAL IMPULSE INITIATION

Enhanced normal automaticity

Abnormal automaticity

Triggered activity due to afterdepolarization

ABNORMAL IMPULSE CONDUCTION

Conduction blocks

Reentry

1

2

Enhanced normal automaticity

• Automaticity is defined as the ability of a cell to independently initiate an action potential.

Classification Of Arrhythmias

• Disorders of Impulse Generation

• Disorders of Impulse Conduction

II. Disorder of impulse conduction

• S.A. Block

• First degree AV Block

• Second Degree A.V.Block» Mobitz type I

» Mobitz type II

• Third Degree or Complete A.V Block

Common causes

• Underline cardiac disease

• Sympathetic stimulation

• Vagal stimulation

• Electrolyte imbalance

• Hypoxia

Mechanism responsible for phase 4 depolarization

1. Decreased outward permeability to potassium

2. Increased inward permeability to sodium

3. Reduced sodium pump activity

4. Increased inward permeability to calcium

Rhythms Originating in SA Node

SINUS BRADYCARDIA

• It is characterized by atrial and ventricular rates of less than 60 beats/minutes.

• It occur gradually or suddenly for a brief period.

• It is usually a benign dysrhythmias and is common among general population

• It is commonly seen in athletes and also be associated with sleep

Sinus BradycardiaCAUSES Stimulation

Carotid Sinus MassageIncreased vagal tone

vomiting suctioning severe pain extreme emotions

Decreased sympathetic toneIntra Occular PressureValsalva maneuver

Disease ProcessMIUremiaRaised ICPAnorexia NervosaHypothermia Hypothyroidism

• Right and left Vagus nerve fibers of the parasympathetic nerve system plays an important role in the rate of impulse formation, the speed of conduction and the strength of cardiac contraction.

• Stimulation of the Vagus nerve causes a decrease rate of firing of the SA node, slowed impulse conduction of the AV node, and decreased force of cardiac muscle contraction.

• Stimulation of the sympathetic nerve system that supply the heart has essentially the opposite effect on the heart.

Valsalva maneuver

• The Valsalva maneuver or Valsalva manoeuvre is performed by moderately forceful attempted exhalation against a closed airway, usually done by closing one's mouth and pinching one's nose shut.

• Variations of the maneuver can be used either in medical examination as a test of cardiac function and autonomic nervous control of the heart, or to "clear" the ears and sinuses (that is, to equalize pressure between them) when ambient pressure changes, as in diving, hyperbaric oxygen therapy, or aviation.

• The technique is named after Antonio Maria Valsalva

The normal physiological response consists of 4 phases

• Initial pressure rise: On application of expiratory force, pressure rises inside the chest forcing blood out of the pulmonary circulation into the left atrium. This causes a mild rise in stroke volume.

• Reduced venous return and compensation: Return of systemic blood to the heart is impeded by the pressure inside the chest. The output of the heart is reduced and stroke volume falls. This occurs from 5 to about 14 seconds in the illustration. The fall in stroke volume reflexively causes blood vessels to constrict with some rise in pressure (15 to 20 seconds).

• This compensation can be quite marked with pressure returning to near or even above normal, but the cardiac output and blood flow to the body remains low. During this time the pulse rate increases.

• Pressure release: The pressure on the chest is released, allowing the pulmonary vessels and the aorta to re-expand causing a further initial slight fall in stroke volume (20 to 23 seconds) due to decreased left ventricular return and increased aortic volume, respectively. Venous blood can once more enter the chest and the heart, cardiac output begins to increase.

• Return of cardiac output: Blood return to the heart is enhanced by the effect of entry of blood which had been dammed back, causing a rapid increase in cardiac output (24 seconds on). The stroke volume usually rises above normal before returning to a normal level. With return of blood pressure, the pulse rate returns towards normal.

Drugs

Digitalis

Morphine sulfate

Sedatives

Beta-Blockers

Ca-Channel Blockers

Amiodarone

30 bpm• Rate?• Regularity? regular

normal

0.10 s

• P waves?

• PR interval? 0.12 s• QRS duration?

Interpretation? Sinus Bradycardia

Sinus Bradycardia

• Deviation from NSR

- Rate < 60 bpm

Sinus Bradycardia

• Etiology: SA node is depolarizing slower than normal, impulse is conducted normally (i.e. normal PR and QRS interval).

Management

Inj Atropine Sulphate is administered if presented with hypotension, restless, chest pain, other signs of hemodynamic changes

Decrease the Vagal stimulation

Avoid drugs which causes Bradycardia

Transcutaneous pacing

Dopamine

Epinephrine

Isoproterenol

Sinus Tachycardia

• It is characterized by an atrial and ventricular

rate of 100 beats/minute or more.

• Generally the upper limit of sinus tachycardia

is 160 beats/ minute.

Sinus Tachycardia

Causes

• Increased Sympathetic Stimulation Exercise Emotions/ excitement Fever Fear Acute painAny condition that require a higher

basal metabolism

Causes……..

• Hyper metabolic States

• Blood Loss

• Consumption of alcohol, caffeine and tobacco.

• Drugs like

Atropine

Dopamine

Dobutamine

Nor epinephrine

amphetamines

• It can be a short term compensatory response to heart failure, anemia, hypovolemia, and hypotension.

• Hyperthyroidism

Causes……..

Sinus Tachycardia

130 bpm• Rate?• Regularity? regular

normal

0.08 s

• P waves?

• PR interval? 0.16 s• QRS duration?

Interpretation? Sinus Tachycardia

Sinus Tachycardia

• Deviation from NSR

- Rate > 100 bpm

Sinus Tachycardia

• Etiology: SA node is depolarizing faster than normal, impulse is conducted normally.

• Remember: sinus tachycardia is a response to physical or psychological stress, not a primary arrhythmia.

Management

• Treatment is directed at the cause

• Digitalis

• Beta-blockers

• Diltiazem

• Carotid Sinus Massage

Sinus Arrest/Sinus Pause

• Sinus node automaticity is depressed

• Impulses are not formed when expected

• No P wave or no QRS complex is generated

• Patient may feel palpitation from the increased stroke volume that accompanies the next beet after the pause.

Etiology

• Vagal Stimulation

• Hypoxia

• Myocardial ischemia

• Injury to SA node

• Carotid sinus sensitivity

• MI

• Drugs:- Digitalis, Beta-Blocker and Ca-Channel Blockers

ECG Characteristics

• Rate- Normal unless sinus node fails to form impulse

• Rhythm-Irregular

• P_waves- present when SA Node Initiates

• PR interval –normal if P waves present

• QRS –present, absent when arrest

Management

• Treatment is directed to the Cause

• Discontinue/withheld offending drugs

• Minimize Vagal Stimulation

• Inj Atropine sulphate

• Insertion of a permanent pacemaker

Sick Sinus Syndrome

• The term sick sinus syndrome is used to describe the rhythm in which there is marked sinus bradycardia, sinus pause or periods of sinus arrest alternating with paroxysms of rapid atrial arrhythmias.

• The term brady- tachy syndrome is commonly used to describe the same arrhythmias.

Causes

• Inflammatory cardiac disease. • Cardiomyopathy • Sclerodegenerative process involving both the

SA and AV node• Drugs

beta-blockers

calcium-channel blockers

digitalis, amiodarone, and adenosine.

Etiologies of Sick Sinus Syndrome

More Common

Sinus node fibrosisAtherosclerosis of the SA arteryCongenital heart diseaseExcessive vagal toneDrugs

Less Common

Familial SSS (due to mutations in SCN5A)Infiltrative diseasesPericarditisLyme diseaseHypothyroidismRheumatic fever

ECG characteristics

• Rate :varies from bradycardiac to tachycardiac rates depending on sinus node function and presence of atrial tachy dysrhythmias

• Rhythm: irregular

• P waves : normal during sinus rhythm

• PR interval : may be normal depend upon the state of AV conduction

• QRS complex: usually normal

Sinus bradycardia (rate of ~43 bpm) with a sinus pause

Abrupt termination of atrial flutter with variable AV block, followed by sinus arrest with a junctional escape beat.

Clinical manifestations

• Patients are usually elderly and present with lightheadedness and/or syncope,

• but it can also manifest as

• angina,

• dyspnea,

• and palpitations.

Treatment

• Ing.Atropine sulphate for brady arrhythmias

• Atntiarrhyhmics like quinidine or procainamide

• Permanent pacemaker insertion

Rhythms originating in atria

Atrial Tachycardia

It is rapid atrial rhythm at a rate of 120 to 250 b/min. It is due to rapid firing of an ectopic foci present in the atria

Atrial tachycardia frequently occurs in paroxysms.

Possible mechanisms of atrial Tachy arrhythmias.

• Two groups of fundamentally different mechanisms are responsible for producing Tachy arrhythmias

• 1- those mechanisms based on some form of abnormal impulse formation

• 2- based on a disorder of impulse conduction, leading to circulating excitation or reentry.

Pathophysiology

• The spontaneous depolarization in the fibers in the center of the sinus node is normally the fastest, and therefore this depolarization brings these fibers to a discharge before others. Thus under normal conditions, automaticity of the dominant pacemaker in the center of the sinus node suppress the subsidiary pacemakers in the atria.

• Abnormal impulse formation may be defined as the generation of impulses by fibers other than the dominant pacemaker fibers in the centre of the sinus node regardless of whether the abnormal impulse is generated spontaneously or induced by foregoing normal or abnormal activities.

• Normal impulse formation is the occurrence of a spontaneous depolarization before the onset of an action potential, the so- called diastolic depolarization.

• If depolarization occurs either during repolarization or under special conditions directly after repolarization the term abnormal impulse formation may be used.

• There are some muscle fibers in the right atrium close to the crista terminalis that have a some characteristics of purkinje fibers (ie. Relatively low resting potential and develops spontaneous depolarization under certain conditions)

Etiology

• RHD• COPD • Mitral valve Disease • Acute MI• Digitalis Toxicity • Caffeine• Tobacco• Alcohol

ECG Characteristics

• Rate- 140-250/min,

• Rhythm- regular unless there is block

• P-wave- differ in configuration

• PR interval- may be shorter and difficult to measure

• QRS- Usually normal

Signs and Symptoms

• Palpitation

• Light headedness

• Angina

• Syncope

Management

• Sedation to terminate the rate

• Carotid sinus massage

• Cardioversion if severe symptoms occurs

• Beta-blockers

• Radiofrequency catheter ablation of the ectopic focus

Atrial Flutter

A rapid well-organized contraction of the atrium at a rate of 200-350 contractions per minute which is fired by ectopic foci present in the atria.

Atrial flutter can be classified in to two types type-1 which is the commonest one has an atrial rate of 240-340 beats/ minute

Causes

• Mitral valve disease

• Pulmonary embolism

• Thoracic surgery

• Myocardial hypoxia

• Electrolyte disturbances

• Hypercalcaemia

ECG Characteristics

• Rate- Atrial 250 to 350b/min

Ventricular 150 to 200b/min

• Rhythm- Atrial Rhythm is regular

Ventricular may be irregular

• P waves- saw tooth appearance

• QRS- usually normal

• PR Interval not measurable

ATRIAL FLUTTER

2:1 Atrial flutter

Signs and Symptoms

• Palpitation

• Chest pain

• Dizziness

• Blurred vision

Management

• Carotid Sinus Massage

• Digitalis

• Ca Channel Blockers

• Beta Blockers

• Synchronized Cardioversion if 1:1

ATRIAL FIBRILLATION

• Atrial fibrillation is an extremely rapid and disorganized pattern of depolarization in the atria where the rate is 400 to 600b/min.

Atrial fibrillation Showing multiple ectopicsFiring erratically

Causes

• Coronary Artery Diseases• Atrial enlargement • Valve diseases • Sick sinus syndrome• Pericarditis• Lung disease • Congenital heart defects• Thyrotoxicosis

ECG Characteristics

• Rate- atrial- 400 to 600b/min

ventricular- 110 to160b/min

• Rhythm- irregular

• P wave- not present. Atrial activity is chaotic.

• PR Interval- not measurable

• QRS- Usually normal

ATRIAL FIBRILLATION

Management

• Cardioversion if Hemodynamically unstable

• Inj Dilitiazem

Verapmil

Beta-blockers

• Anticoagulation if fibrillation is chronic

Complication

• Mural Thrombi

• Pulmonary Emboli

• CHF

VENTRICULAR ARRHYTHMIAS

• PREMATURE VENTRICULAR CONTRACTION

• VENTRICULAR TACHYCARDIA

• VENTRICULAR FIBRILLATION

Premature Ventricular Contraction

• Premature contraction that is generated by the ectopic foci present in the ventricles. Which fires independently.

Premature ventricular contraction

Etiology

• Ischemia or MI

• Hypoxia

• Hypokalemia

• Digitalis toxicity

• Acidosis

• Hyper metabolic states

P V C s• UNIFOCAL

• MULTIFOCAL

• BIGEMINY

• TRIGEMINY

• COUPLETS

• TRIPLETS

• After each normal QRS complex there is one Ectopic appear

• After two QRS complex which are from normal sinus rhythm then the ectopic foci fires called Trigeminy

• When 2 ectopic appears sequentially in a row or pairs called Couplets

• When 3 ectopic occurs sequentially in one row is called Triplets

ECG Characteristics

• Rate- 60-100b/min

• Rhythm- Irregular

• P-waves usually present in sinus rhythm not related to PVC

• QRS- wide and bizarre, greater than 0.12sec

Management

• Treatment is directed to the cause

• If PVCs are associated with heart disease can be treated

• Inj lidocaine bolus followed by titrated drip

Ventricular Tachycardia

• It is repetitive firing of the ventricular ectopic foci at a rate more than 100 to 200b/min, which may cause the heart to beat inefficiently.

Etiology

• Ischemia

• Acute MI

• Hypoxia

• Hypokalemia

• Digitalis toxicity

• Acidosis

• Hypermetabolic states

ECG Characteristics

• Rate- ventricular rate 100 to 200b/min

• Rhythm- usually regular

• P-waves present if S.A.Node fires

may be buried in QRS or T

• PR Interval- not measurable

• QRS- wide, bizarre and greater than 0.12sec

V-TACH

Management

• Cardioversion • Defibrillation can be done when the

patient is pulseless• Inj Lidocaine bolus and drip as

maintenance dose• Antiarrhythmic like inj Amidarone

or inj MgSo4• Resuscitative measures to kept ready

Ventricular Fibrillation

• An erratic, disorganized firing of impulses from the ventricles.

Etiology

• Myocardial Infarction

• V-Tach

• Drug toxicity

• Electrocution

• Drowning

ECG Characteristics

• Rate- rapid, uncoordinated, ineffective

• Rhythm- Chaotic, irregular

• P waves- not seen

• PR interval- none

• QRS – no formed QRS complex

Management

• Defibrillation

• CPR must be performed

• Anti-arrhythmic like

inj Lidocaine

inj Procainmide

inj MgSo4 most commonly used

• Beta-Blockers

Disorders of impulse Conduction

• S.A. Block

• First degree AV Block

• Second Degree A.V.Block» Mobitz type I

» Mobitz type II

• Third Degree or Complete A.V Block

• Bundle Branch Block» RBBB

» LBBB

First Degree A.V.Block

• It is defined as prolonged AV conduction time of supraventricular impulses into the ventricles.

Etiology

• Congestive Heart Disease

• Rheumatic Heart Disease

• Vagal Stimulation

• Digitalis

• Beta-Blockers

• Ca-channel Blockers

ECG Characteristics

• Rate- 60 to 100b/min

• Rhythm- Regular

• P waves- normal, precede every QRS

• PR Interval- Greater than 0.20 sec

• QRS complex- usually normal

Management

• Usually does not require treatment

• It should be observed for progression

Second Degree A.V.Block

• It occurs when one atrial impulse at a time fails to be conducted to the ventricles.

It is classified into two• Mobitz type I• Mobitz type II

Type I Second degree A.V.Block

• It is a progressive increase in conduction times of consecutive atrial impulses into the ventricles until one impulse fail to conduct or is ‘dropped’

Etiology

• Aortic Valve Disease

• Congestive Heart Failure

• Inferior Wall MI

• ASD

• Drugs

• Mitral Valve Prolapse

ECG Characteristics• Rate- usually normal

• Rhythm- irregular unless 2:1 conduction present

• P waves- normal. Some p waves are not conducted to the ventricle, but only one at time fails.

• PR Interval- gradually lengthens in consecutive beats.

• QRS- normal unless BBB

IInd Degree type I

Management

• Treatment depends on the conduction ratio, ventricular rate

• If the ventricular rate slow give

inj Atropine Sulphate

• Removal of precipitating factor

• Temporary pacing can be done.

Type II Second degree A.V.Block

• It is sudden failure of conduction of an atrial impulse to the ventricles without progressive increase in conduction time.

ECG Characteristics

• Rate- normal• Rhythm- irregular • P waves- usually regular and

precede QRS. Periodically a P wave

is not followed by a QRS• PR interval- constant unless there

is block• QRS- usually normal

IInd Degree type II

Management

• Pacemaker therapy because it is often permanent and progress to complete block

Third Degree A.V. Block(Complete Block)

• It is complete failure of conduction of all atrial impulses to the ventricles.

Etiology

• Congestive Heart Disease

• MI

• Lenegre’s disease

• Cardiac Surgery

• Congenital Heart Disease

• Digitalis Toxicity

ECG Characteristics

• Rate- atrial normal, Ventricular rate is less that 45/min

• Rhythm- Regular

• P waves- independent

• PR Interval- no consistent PR interval

• QRS- Normal If ventricles controlled by Junctional pacemaker, may be wide

Management

• Onset is sudden or associated with MI pacing can be done without delay

• CPR should performed if the cardiac out put severly diminished

Ventricular Asystole

• It refers to the absence of any ventricular rhythm; there is no QRS complex, no pulse and no cardiac output.

Management

• Cardio Pulmonary Resuscitation

• Endotracheal Intubation immediately

• Obtain IV Access

• Confirm Asystole in more than one lead

• Consider immediate Transcutaneous Pacing

• Epinephrine 1 mg IV push q3-5 minutes

– Consider Vasopressin as alternative

• Atropine 1 mg IV q3-5 minutes

The P wave is caused by atrial depolarization. The P wave duration is normally less than 0.12 sec. The P wave is usually smooth and positive.

The QRS complex represents ventricular depolarization. The normal QRS interval range is from 0.04 sec - 0.12 sec, measured from the first deflection to the end of the QRS complex

The T wave due to ventricular repolarization The wave is normally rounded and positive.

• The PR interval is the beginning of the P wave to beginning of QRS complex. It is normally  0.12 - 0.20 seconds. (onset of atrial depolarization to onset of ventricular depolarization)

• The QT interval begins at the onset of the QRS complex and to the end of the T wave.

• The ST Segment represents the period of ventricular muscle contraction before repolarization.

• The ECG below illustrates primary ST-T wave abnormalities (leads I, II, aVR, V5, V6) in a patient with RBBB. ST-T wave abnormalities such as these may be related to ischemia, infarction, electrolyte abnormalities, medications, CNS disease, etc.

• In the above ECG the ST-T waves are "normal" for LBBB; i.e., they are secondary to the change in the ventricular depolarization sequence.

 Wolff-Parkinson-White Preexcitation

• Early ventricular activation in region of the accessory AV pathway•  Short PR interval (<0.12s) •  Initial slurring of QRS complex (delta wave) representing early ventricular

activation through normal ventricular muscle in region of the accessory pathway

•  Prolonged QRS duration (usually >0.10s) •  Secondary ST-T changes due to the altered ventricular activation sequence

The ectopic atrial rate is 150 bpm. Some of the ectopic P waves are easily seen and indicated by the arrows. Other P waves are burried in the T waves and not so easily identified. Atrial tachycardia with AV

block is often a sign of digitalis intoxication. 3:2 and 2:1 AV block is seen in this example.

Premature Atrial Contractions

When an irritable focus in the atria fires before the next sinus impulse is due

Premature atrial contractions

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