Ebook ECG short rapid review for non-Cardiologists (edition 2.1): Part 2

(BQ) Part 2 book ECG short rapid review for non-Cardiologists presents the following contents: Ventricular arrythmias, heart blocks, myocardial infarction, junctional arrythmias, premature ventricular contractions, miscellaneous, P&Q wave relationships.

CHAPTER 4 : VENTRICU LAR ARRYTHMIAS

IDIOVENTRICULAR RHYTHM

If the ventricle does not receive triggering signals , the ventricular myocardium itself becomes the pacemaker (escape rhythm) This is called Idioventricular Rhythm Ventricular signals are transmitted cell-to-cell between cardiomyocytes and not by the conduction system, creating wide sometimes bizarre QRS complexes(> 0.12 sec)

QRS : Wide (>0.10 sec) Bizzare type appearance

Idioventricular rhythms occur when all of the heart’s other pacemakers fail to function or when

supraventricular impulses can’t reach the ventricles because of a block in the conduction system

Ventricular arrhythmias originate in the ventricles below the bundle of His and fires at the rate of 20-40 bpm Idioventricular rhytm may also be called as agonal

rhythm If the rate is >40 bpm, it is called accelerated idioventricular rhythm The rate of 20-40 is the

"intrinsic automaticity" of the ventricular myocardium Bizzare appearance : The T wave and the QRS complex deflect in opposite directions because of the difference in the action potential during ventricular depolarization and repolarization P wave is absent because

depolarization of atria does not occur

The arrhythmias may accompany third-degree heart block or be caused by anything which damages AV node like infarction or blocks it like digoxin

ACCELETATED IDIOVENTRICULAR RHYTHM Same as Idioventricular rhytm , only difference is , heart rate Here it’s 40-100 bpm , while in IVR it’s been 20-40

QRS : Wide (>10 sec) , Bizzare appearance

Idioventricular rhythms appear when supraventricular pacing sites are depressed or absent If the heart rate

become slow , diminished cardiac output is expected History is helpful for identifying the underlying etiology for AIVR Most patients with AIVR presents with chest pain or shortness of breath (symptoms related to

myocardial ischemia with history of myocardial

reperfusion with drugs or coronary artery

interventions.) ,Plus Peripheral edema, cyanosis,

clubbing, (With the history of cardiomyopathy,

myocarditis, and congenital heart diseases )

Treatment : Idioventricular rhythm should never be treated with lidocaine or other antiarrhythmics that

would suppress that safety mechanism

If the symptoms develops , immediate treatment

required to increase his heart rate, improve cardiac output and establish a normal rhythm Treat the

Underlying Cause

In life-threatening situations in which time is critical, a transcutaneous pacemaker may be used to regulate heart rate

VENTRICULAR TACHYCARDIA (MONOMORPHIC) Ventricular tachycardia refers to any rhythm faster than

100 beats per minute, with 3 or more irregular beats in a row, arising distal to the bundle of His In Monomorphic type , The shape, size and amplitude of QRS complex will

be same

Rate : 100-250 bpm

Rhythm : Regular

P waves : None or not associated with the QRS

PR interval : None

QRS : Wide (>0.10sec) , Bizzare appearance

It is important for a physician to confirm the presence or absence of pulses because monomorphic VT may be perfusing or non perfusing Sustained SVTs requiring immediate treatment to prevent death, monomorphic VT will probably deteriote into VF or unstable VT if

sustained and not treated

Ventricular tachycardia usually results from increased myocardial irritability, which may be triggered by

enhanced automaticity or reentry within the Purkinje system or by PVCs

Conditions that can cause ventricular tachycardia

include:

 Myocardial ischemia & Infarction

 Coronary artery disease

 Valvular heart disease

 Heart failure, Cardiomyopathy

 Hypokalemia

 Drugs like digoxin , procainamide, quinidine or cocaine

VENTRICULAR TACHYCARDIA (POLYMORPHIC) The difference between monomorphic and polymorphic

is the presence of different type of complexes in

QRS : Wide (>0.10sec) , Bizzare appearance

Electrolyte abnormality is a possible etiology behind this Patient in VT will present with Palpitation,

lightheadedness, and syncope (from diminished cerebral perfusion) Chest pain (due to ischemia or to the rhythm itself Anxiety usually present Some patients describe a sensation of neck fullness, which may be related to increased central venous pressure and cannon a waves

“Cannon A” waves are related to right atrial contraction against a closed tricuspid valve (Jugular Venous Pressure Graph is Discussed later on) Dyspnea (due to increased pulmonary venous pressures when left atrial contraction

against a closed mitral valve) Ventricular Tachycardia can convert into Ventricular Fibrillation if not treated V fib is a medical emergency

It is important to confirm the presence or absence of pulses because polymorphic VT may be perfusing or non perfusing

Treatment of VT: They are Treated aggressively by Anti

arrythmimc drugs Coronary revascularization is

indicated to reduce the risk of SCD in patients with VF when there is presence of direct evidence of acute

myocardial ischemia Amiodarone or lidocaine are usually used

VENTRICULAR FIBRILLATION

Is when ventricles fire rapidly and asynchronously at rate more than 300.Most common cause of death in cardiac ER Massive hypoperfusion will occur throughout the body

Ventricular fibrillation is defined when Ventricles beat

The ventricular rate, P wave, PR interval, QRS complex, T wave, and QT interval cannot be determined

Patient will present with Prodrome of symptoms of chest pain, fatigue, palpitations, and other nonspecific

complaints (50% patients visit in 4 week before death) ,

A history of Left Ventricular impairment (LV ejection fraction < 30-35%) is the single greatest risk factor for sudden death from VF

Otherwise , symptoms depend upon the underlying cause of V-Fib : Coronary artery Disease , Hypertrohpic

or dilated cardiomyopathy , valvular pathology ,

Myocarditis , Congenital Heart Disease (All this

pathology are discussed in Pathology Section)

Treatment : if pulseless , treat with immediate

defibrillation followed by epinephrine , vasopressin , amiodarone or lidocaine

If pulse is present treat with amiodarone and

synchronized cardioversion

TORSADE DE POINTES Characterized by a gradual change in the amplitude and twisting of the QRS complexes around the isoelectric line

Rate : 200-250 bpm

Rhythm : Irregular

P waves : None

PR interval : None

QRS : Wide (>0.10sec) , Bizzare appearance

The main causes of Torsades are Drugs that prolong QT interval and electrolyte abnormalities such as

Hypomagnessemia

This rhythm is unusual variant of polymorphic VT with the normal or long QT intervals It may deteriotes to Ventricular fibrillation or asystole Patient usually present with recurrent episodes of palpitations,

dizziness, and syncope; however, sudden cardiac death can occur with the first episode Nausea, cold sweats, shortness of breath, and chest pain also may occur but are nonspecific and can be produced by any form of tachyarrhythmia

HALLMARK : QRS complexes that rotate about the

baseline, deflecting downward and upward for several

beats

Treatment : Magnesium (Decreases the influx of calcium, thus lowering the amplitude of Action Potentials ) Beta-1 Agonist Drugs (to increase Heart rate and

decrease Prolonged QT interval)

If torsades convert into V-Fib – Direct Current

Cardioversion is required

PULSELESS ELECTRICAL ACTIVITY

When you try to measure pulse ,you will not detect them , but , when you will perform ECG , identifiable electrical

rhythms are produced

Rate , Rhythm , P waves PR interval ,QRS - All reflects the underlying rhythm

Rhythm may be sinus , atrial , juinctional , or ventricular

in origin PEA is also called as electromechanical

dissociation

In pulseless electrical activity, the heart muscle loses its ability to contract even though electrical activity is preserved As a result, the patient goes into cardiac arrest

On an electrocardiogram, you’ll see evidence of

organized electrical activity, but you won’t be able to palpate a pulse or measure the blood pressure

This condition requires rapid identification and

treatment

Causes include :

 Hypovolemia , Hypoxia,

 Acidosis, Tension pneumothorax,

 Cardiac tamponade, massive pulmonary

embolism

 Hypothermia, hyperkalemia,

 Overdose of drugs such as tricyclic

antidepressants , calcium channel blockers , digoxin

Treatment : Cardiopulmonary resuscitation is the

immediate treatment, along with epinephrine Atropine may be given to patients with bradycardia Subsequent treatment focuses on identifying and correcting the underlying cause

ASYSTOLE Electical activity in the ventricles is completely absent –

A straight line

Rate, Rhythm, P waves, PR interval, QRS : None

Always confirm asystole by checking the ECG in two different leads Also search to identify underlying

ventricular fibrillation

This most commonly occur from a prolonged period of cardiac arrest without effective resuscitation Seek to identify the underlying cause as in PEA

The patient is in cardiopulmonary arrest Without rapid initiation of CPR (Cardio-pulmonary Resuscitation) and appropriate treatment, the situation quickly becomes irreversible

Anything that causes inadequate blood flow to the heart may lead to asystole

The immediate treatment for asystole is CPR

CHAPTER 4 : HEART BLOCKS

ATRIOVENTRICULAR BLOCKS (FIRST DEGREE

BLOCK)

It is the prolongation of the PR interval on an

electrocardiogram (ECG) to more than 200 msec

Rate : Depends on the underlying rhythm

First-degree AV block occurs when impulses from the atria are consistently delayed during conduction through the AV node Conduction eventually occurs , it just takes longer than normal just the underlying cause will be treated, not the conduction disturbance itself

Patient is usually asymptomatic at REST Markedly prolonged PR interval may reduce exercise tolerance in some patients with left ventricular systolic dysfunction Syncope may result from transient high-degree AV block, especially in those with infranodal block and wide QRS complex Other symptoms might be present depending upon the causes of AV Block

Causes of AV block :

Temporary block : Myocardial infarction (MI), usually inferior wall MI , Digoxin toxicity ,Calcium Channel and Beta blockers , Cardiac surgery

Permanent block : Changes associated with aging , Congenital abnormalities , MI, usually anteroseptal MI , Cardiomyopathy , Cardiac surgery

Treatment :

Asymptomatics : No treatment ,

Symptomatics : If PR interval > 300 msec, Placement of a dual-chamber pacemaker, medications (eg, atropine, isoproterenol) can be used in anticipation of insertion of

a cardiac pacemaker

Warning : Avoid B-blockers and CCBs (both slowers the

conduction)

2ND DEGREE AV BLOCK : MOBITZ TYPE I P-R interval becomes progressively longer and then one P wave will be block , resulting in no QRS production Note that – P wave is formed and later on normal cycle

QRS : Normal (Absent during block)

Ischemia involving right coronary artery is one potential cause Because RCA supplies AV node in 80% of Patients Hallmark : increasing PR interval with successive beat and sudden drop and cycle repeats

Usually asymptomatic, a patient with type I degree AV block may show signs and symptoms of decreased cardiac output, such as light-headedness or hypotension

second-Symptoms may be especially pronounced if the

ventricular rate is slow

Treatment :

 For asymptomatics – No Rx

 For symptomatics : Atropine may improve AV

node conduction

 For long term relief : Temporary Pacemaker

2ND DEGREE AV BLOCK : MOBITZ TYPE II

Conduction ratio (P waves to QRS complexes) is

commonly 2:1 , 3:1, or 4:1 QRR complexes are usually wide because this block

usually involves bot right and left bundle branch block

Rate : Atrial rate (60-100bpm) , Faster than the

ventricular rate (because they are blocked)

Rhythm : Atrial regular, and ventricular : Irregular

P Waves : Normal , more P waves than QRS complexes

PR interval : Normal or prolonged but constant

QRS : Usually wide

Resulting Bradycardia can compromise cadiac output

and lead to complete AV block This rhythm often

occurs with cardiac ischemia or an MI

Occasional impulses from the SA node fail to conduct to

the ventricles so a drop beat will be seen

In 2:1 second-degree atrioventricular (AV) block, every other QRS complex is dropped, so there are always two P waves for every QRS complex

Aim in treatment use to be

 Increase cardiac output by increasing heart rate

to prevent underperfusion of organs Atropine, dopamine, or epinephrine may be given for symptomatic bradycardia

 Pacemaker

 Discontinue digoxin, if it’s the cause of the arrhythmia

3RD DEGREE AV BLOCK Electrical block is at or below the AV node , and so , conduction between the atria and ventricle is absent 3rddegree heart block is also called as complete heart block

Rate : Atrial (60-100bpm) , Ventricular : 40-60 bpm if escape focus is junctional , <40 bpm if escape focus is ventricular

Rhythm : Usually regular , but atria and ventricles contracts independently

P Waves : Normal , may be superimposed on QRS

complexes or T waves

PR interval : Varies greatly

QRS : Normal , if ventricles are activated by junctional escape focus , wide if escape focus is ventricular

It is most commonly a congenital condition This block

may also be caused by :

 Coronary artery disease an anterior or inferior wall MI, degenerative changes in the heart

 Drugs like Digoxin toxicity, calcium channel blockers, beta-adrenergic blockers, or surgical injury

Patients are symptomatics, symptoms include severe fatigue, dyspnea, chest pain, lightheadedness, changes in mental status, and loss of consciousness

You may note hypotension, pallor, diaphoresis,

bradycardia, and a variation in the intensity of the pulse Therapy aims to improve the ventricular rate

Treatment : Atropine , Dopamine , Epinephrine,

temporary pacing For permanent block requires

permanent pacemaker

SINOATRIAL BLOCK (SA BLOCK)

There is drop of beat , but , after beat drop , cycle

continues with normal rate and rhythm

Rate : Normal to slow , depends upon the duration and frequency of SA block

Rhythm : Irregular whenever SA blocks occur , Regular after that

P waves : Absent during drop beat, but once cycle continues it will be normal

PR interval : Depends upon the duration of drop beat , afterward , it will be normal

QRS : Depends upon the duration of drop beat ,

afterward , it will be normal

Cardiac output can decrease during drop beat usually asymptomatic , but if last longer , syncope or dizziness

can occur SA Blocks must not be confuse with – A) Mobitz type l AV Block (discussed next) where there is prolongation of PR intervation with every successive beat and then beat is dropped B) P waves are present , ventricular beat is dropped Here , PR interval remains same after all beats and problem is with SA node

Patients are usually asymptomatics , while In some people they can cause fainting, altered mental status, chest pain, hypoperfusion, and signs of shock

Treatment : Not required for asymptomatics , but in emergent situation use Atropine or Transuctaneous Pacing

RIGHT & LEFT BUNDLE BRANCH BLOCKS

Notches in the QRS complex are classics of BBB

Rate : Depends upon the rate of underlying rhythm Rhythm : Regular

P Waves : Normal

PR interval : Normal

QRS : Usually wide (>0.10 sec) with a notched

appearance

Commonly , BBB occur in Coronary artery Disease Potential complication of an Myocardial Infarction is a bundle-branch block

Right bundle-branch block

RBBB occurs with such conditions as anterior wall MI, CAD, cardiomyopathy, cor pulmonale, and pulmonary embolism

Left bundle-branch block

Left bundle-branch block (LBBB) never occurs normally This block is usually caused by hypertensive heart disease, aortic stenosis, degenerative changes of the conduction system, or Coronary artery disease

Left anterior fascicular block is a cardiac condition

distinguished from left bundle branch block It is caused

by only the anterior half of the left bundle branch being

defective It is manifest on the ECG by left axis

 It also associated with hypertensive heart

disease, aortic valvular disease,

cardiomyopathies, and degenerative fibrotic disease of the cardiac skeleton

Left posterior fascicular block (LPFB) is a condition

where the left posterior fascicle, i.e the backside part of the left cardiac bundle, does not conduct the electrical impulses from the atrioventricular node The electricity then has to go through the other fascicle, and thus is a

frontal right axis deviation seen on the ECG

BBB are usually normal , even some people are born with this , but , in Some people it describes the underlying defect (Causes mentioned above)

Treatment is not required for asymptomatics , Treat according to the underlying cause In severe Cases Pacemaker might be required

CHAPTER 5 : MYOCARDIAL INFARCTION

Acute myocardial infarction : Pain is the most common

presenting symptom in patients with AMI The pain is typically felt substernally or in the epigastrium It’s often described as – Crushing or Stabbing or Burning pain Pain may also irradiate to left arm and/or jaw (because the sympathetic fibres from T1-T2 will supply both heart and left arm, jaw) , sudden onset of shortness of breath , fatigue or adrenergic symptoms

Pain is not controlled by Nitroglycerin

Serum Cardiac markers will be released into the blood due to Cell lysis/death Markers will not be present in blood if myocardiocyte does not die (example : in Angina Pectoralis)

 Troponin I (Specific marker)- Rises by first 4

hours and remain elevated for 7-10 days.(usually drawn every 8 hours three times till MI is ruled out)

 Creatine Kinase-MB peaks about 20 hours after

AMI

 LDH (Lactate dehydrogenase) is marker of

reinfarction within 7 days

On ECG , Total occlusion of artery will result in ST

elevation (depression means ischemia , elevation means injury)

In Subtotal occlusion or transient occlusion , there will

be adequate collateral circulation , then ST segment elevation does not occur Most patients who present with

ST segment elevation , eventually develop Q wave on

ECG (which will indicate as a marker of previous MI)

Causes of MI :

Ischemic Angina, reinfarction, infarct extension

Mechanical Heart failure, cardiogenic shock, mitral valve dysfunction, aneurysms, cardiac

Rupture

Arrhythmic Atrial or ventricular arrhythmias, sinus or atrioventricular node dysfunction

Embolic Central nervous system or peripheral embolization

Inflammatory Pericarditis

Differentials for MI : Gastroesophageal reflux disease &

Peptic ulcer disease (pain related to certain food ,

relieved by antacids) , Stable angina (Pain on exertion ,

ST segment depression) , Unstable angina (pain at rest,

ST segment depression ) , Esophageal problems ,

Pericarditis (Diffuse ST-segment elevation) , Pleuritis, Prinzmental angina (pain at rest, ST ELEVATION)

Post MI Complications :

Cardiac arrest : This most commonly occurs due to

patients developing ventricular fibrillation and is the most common cause of death following a MI Patients are managed with defibrillation

Cardiogenic shock : If a large part of the ventricular

myocardium is damaged in the infarction the ejection fraction of the heart may decrease to the point that the

patient develops cardiogenic shock This is difficult to treat Other causes of cardiogenic shock include the 'mechanical' complications such as left ventricular free wall rupture as listed below Patients may require inotropic support and/or an intra-aortic balloon pump

Chronic heart failure: As described above, if the patient

survives the acute phase their ventricular myocardium may be dysfunctional resulting in chronic heart failure Loop diuretics such as furosemide will decrease fluid overload Both ACE-inhibitors and beta-blockers have been shown to improve the long-term prognosis of patients with chronic heart failure

Tachyarrhythmias : Ventricular fibrillation, as

mentioned above, is the most common cause of death following a MI Other common arrhythmias including ventricular tachycardia

Bradyarrhythmias : Atrioventricular block is more

common following inferior myocardial infarctions

Pericarditis : Pericarditis in the first 48 hours following

a transmural MI is common (c 10% of patients) The pain is typical for pericarditis (worse on lying flat etc), a pericardial rub may be heard and a pericardial effusion may be demonstrated with an echocardiogram

Dressler's syndrome tends to occur around 2-6 weeks

following a MI The underlying pathophysiology is thought to be an autoimmune reaction against antigenic proteins formed as the myocardium recovers It is

characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR It is treated with NSAIDs

Left ventricular aneurysm : The ischemic damage

sustained may weaken the myocardium resulting in aneurysm formation This is typically associated with persistent ST elevation and left ventricular failure Thrombus may form within the aneurysm increasing the risk of stroke Patients are therefore anticoagulated

Left ventricular free wall rupture : This is seen in

around 3% of MIs and occurs around 1-2 weeks

afterwards Patients present with acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds) Urgent

pericardiocentesis and thoracotomy are required

Ventricular septal defect : Rupture of the

interventricular septum usually occurs in the first week and is seen in around 1-2% of patients Features: acute heart failure associated with a pan-systolic murmur An echocardiogram is diagnostic and will exclude acute mitral regurgitation which presents in a similar fashion Urgent surgical correction is needed

Acute mitral regurgitation : More common with

infero-posterior infarction and may be due to ischemia or rupture of the papillary muscle An early-to-mid systolic murmur is typically heard Patients are treated with vasodilator therapy but often require emergency surgical repair

ECG CHANGE FROM DAY 1 TO YEAR LATER

ST SEGMENT CHANGES FROM ISCHEMIA TO MI

ST Segment elevates as heart progresses toward

infarction

Treatment : Medical therapy with aspirin, heparin,

nitrates, and beta blockers is indicated in patients who have had a myocardial infarction and have ongoing ischemic symptoms Calcium channel blockers are

contraindicated for acute coronary syndrome , but as drug of choice in Prinzmetal angina

An intra-aortic balloon pump (IABP) should be

inserted promptly in patients with hemodynamic

instability or severe LV systolic dysfunction Coronary angiography should be performed in patients who are

stabilized with medical therapy, but emergency

angiography may be undertaken in unstable patients Revascularization, percutaneous or surgical, is

associated with improved prognosis

ST SEGMENT ELEVATION & DEPRESSION

A normal ST segment represents early ventricular

repolarization Displacement of the ST segment can be caused by various conditions listed below :

Primary causes of ST segment depression

 Myocardial ischemia

 Left ventricular Hypertrophy

 Intraventricular conduction defects

 Medication (eg digitalis)

 Reciprocal changes in leads opposite the area of acute injury

Primary Causes of ST Elevation :

ST elevation > 1mm in the limb leads and >2mm in the chest leads indicates an evolving acute MI until there is proof to the contrary

 Early repolarization (normal variant in young adults)

 Pericarditis

 Ventricular aneurysm

 Pulmonary embolism

 Intracranial Hemmorrhage

Lead aVR is a non diagnostic lead and does not show any

change in an MI

An MI may not be limited to just one region of the heart , for example, if there are changes in leads V3 , V4

(anterior) and in l , aVL , V5 & V6 (lateral) , the resulting

MI is called as anterolateral infarction

INFERIOR WALL MI

Results from occlusion of the right coronary artery –

Posterior descending branch

ECG Changes : ST segment elevation in leads ll , lll , and

aVF

Be alert for symptomatic sinus bradycardia , AV blocks , hypotension and hypopersion which can lead this MI

ANTERIOR WALL MI

Occlusion of the left coronary artery – Left anterior descending branch

ECG changes : ST segment elevation with tall T waves &

taller than normal R waves in lead V3 & V4

LATERAL WALL MI

Occlusion of left coronary artery – Circumflex branch

ECG Changes : ST segment elevation in leads l, aVL , V5 &

V6 Lateral MI is often associated with anterior or inferior wall MI Be alert for the changes that may indicate cardiogenic shock or congestive heart failure

CHAPTER 6 : JUNCTIONAL ARRYTHMIAS

JUNCTIONAL RHYTHM The atria and SA node do not perform their normal pacemaking function A junctional escape rhythm begins

Rate : 40-60 bpm

Rhythm : Regular

P Waves : Absent , inverted , buried or retrograde

PR interval : None , short or retrograde

QRS : Normal

Junctional arrhythmias originate in the atrioventricular (AV) junction—the area around the AV node and the bundle of His

The arrhythmias occur when the sinoatrial (SA) node, a higher pacemaker, is suppressed and fails to conduct impulses or when a block occurs in conduction

Electrical impulses may then be initiated by pacemaker cells in the AV junction AV node fires at the rate of 40-60 bpm

Treatment : For asymptomatic : No treatments In patients with complete AV block, high-grade AV block, or symptomatic sick sinus syndrome (ie, sinus node

dysfunction), a permanent pacemaker may be needed

ACCELERATED JUNCTIONAL RHYTHM

Rate : 60-100 bpm

Rhythm : Regular

P waves : Absent , inverted , buried or retrograde

PR interval : None , Short or retrograde

QRS : Normal

Moniter the patient , not just the ECG , for clinical

improvement

An accelerated junctional rhythm is caused by an

irritable focus in the AV junction that speeds up to take over as the heart’s pacemaker (AV dissociation)

The atria are depolarized by means of retrograde

conduction, and the ventricles are depolarized normally The accelerated rate is usually between 60 and 100 beats/minute

Conditions Responsible for AJR are :

 Digoxin toxicity

 Hypokalemia

 Inferior or posterior wall MI

 Rheumatic heart disease

 Valvular heart disease

Treatment : Same as in Junctional Rhythm

JUNCTIONAL ESCAPE BEATS

A junctional escape beat is a delayed heartbeat

originating not from the atrium but from an ectopic focus somewhere in the AV junction An escape complex comes later than the next expected sinus complex

Rate : Depends on the rate of underlying rhythm

Rhythm : Irregular , whenever an escape beat occurs

P waves : None , inverted , buried , or retrograde in the escape beat

PR interval : None , short , or retrograde

QRS : Normal

A junctional escape rhythm is a string of beats that

occurs after a conduction delay from the atria AV node junction firing rate is 40 to 60 beats/minute

A junctional escape rhythm can be caused by any

condition that disturbs SA node function or enhances AV junction automaticity

Causes of the arrhythmia include:

 Sick sinus syndrome

 Vagal stimulation , Digoxin toxicity

 Inferior wall MI

 Rheumatic heart disease

Junctional rhythms (if a bradycardia), can cause

decreased cardiac output Therefore, the person may