Ecg interpretation reading 20031

Wednesday, 12 April 2023 1

ECG INTERPRETATION & READING


1. ANATOMY AND PHYSIOLOGY OF THE HEART

2. ECG 3. SINUS ARRHYTHMIAS 4. JUNCTIONAL ARRHYTHMIA 5. ATRIAL ARRHYTHMIAS 6. VENTRICULAR ARRHYTHMIAS7. CONDUCTION ARRHYTHMIAS 8. MISCELLANEOUS 9. EXAM

COURSE OUT LINES


objectives


At the end of this session you will be able to:

-Review the anatomy and physiology of the heart.-Define ECG correctly .-Identify the components of ECG paper

- Recognize the positions of ECG leads.-Define normal sinus rhythm P,Q,R,S,T.-Calculate the heart rate using ECG paper.-Recognize the types of cardiac arrhythmias

according to ECG interpretations.-List the main characteristics of each type according

to ECG. -List main causes of each cardiac arrhythmias.


OUT LINE

-Anatomy and physiology of the heart.

-ECG interpretation.

-Sinus Rhythm.

-Cardiac Arrhythmias.

*Sinus bready cardia. *Sinus tachy cardia. *Sinus arrhythmia.

*Sinus arrest.


OUT LINE

*Wendering Pace Maker. *Arrhythmias of atria. *Atrial Entopic Beat. *Atrial fibrillation. *Atrial Fluttur. *Supraventricular Tachy cardia. *Accelerated Juntional Rhythm.


OUT LINE

*Ventricular Arrhythmia. *Ventricular Ectopic Beat. *Ventricular Tachy cardia. *Ventricular Fibrillation. *Ventricular Standstill. *Idiovenricular Rhthytm. *Accelerated Idioventricular Rhthym.


OUT LINE *Atrioventricular Blocks. -First Degree AV Block. -Second Degree AV Block. -Second Degree AV Mobitz-1. - Second Degree AV Mobitz-2. *Complete Heart Block. *Bandle Branch Block. *Rt Bandle Branch Block.


OUT LINE

*Lt Bandle Branch Block.

*Rt Atrial Hypertrophy.

*Lt Atrial Hypertrophy.

*Rt Ventricular Hypertrophy.

*Lt Ventricular Hypertrophy.

*Dextro cardia.

Anatomy and physiology of the heart



LOCATION OF THE HEART



The heart lies in the mediastinum , about two thirds of the mass lies to the left of the body’s midline & the pointed end of the heart is the apex , which directed anteriorly & inferiorly & to the left .

And the broad portion of the heart opposite to the apex is the base , which is directed superiorly , posteriorly & to the right .



The heart has two surfaces & two boarders. the anterior surface which is deep to the sternum

and ribs , the inferior surface , the part between the apex

and the right border of the heart and rest on the diaphragm ,

the right border , faces the right lung & extends from the inferior surface to the base ,

the left border( pulmonary border ) , faces left lung & extends from the apex to the base .


Coverings of the Heart: Anatomy

Pericardium – a double-walled sac around the heart composed of:• A superficial fibrous pericardium

• A deep two-layer serous pericardium• The parietal layer lines the internal surface of the

fibrous pericardium

• The visceral layer or epicardium lines the surface of the heart

• They are separated by the fluid-filled pericardial cavity

Coverings of the Heart: Physiology

The pericardium:• Protects and anchors the heart

• Prevents overfilling of the heart with blood

• Allows for the heart to work in a relatively friction-free environment

Pericardial Layers of the Heart

Figure 18.2


1- The heart is a hollow, cone-shaped muscular organ situated in the space between lungs(mediastinum) , its about 12 cm in length & about 9 cm in width & 6cm in thickness .

2- It weighs about 300gms and about the size of owner clenched fist .

3- Its consist of three layers endocardium that lines the interior surface of the heart and valves (endothelial tissue)

Cardiac layers


Cardiac layers “endocardiumendocardium””


Cardiac layers “endocardium“endocardium””


Myocardium the middle layer of the heart that consist of striated muscle fibers atrial, ventricular , specialized muscle fibers

Epicardium which consist of mesothelial cells it covers the external surface of the heart

4- the heart consist of 4 chambers two atria ,two

ventricles . 5- consist of 4 valves 2 atrioventricular valves & 2

semilunar valves

Cardiac layers

Vessels returning blood to the heart include:

Superior and inferior venae cavaeRight and left pulmonary veins

Vessels conveying blood away from the heart include:Pulmonary trunk, which splits into right and left

pulmonary arteriesAscending aorta (three branches) –

brachiocephalic, left common carotid, and subclavian arteries

External Heart: Major Vessels of the Heart (Anterior View)

Arteries – right and left coronary (in atrioventricular groove), marginal, circumflex, and anterior interventricular arteries

Veins – small cardiac, anterior cardiac, and great cardiac veins

External Heart: Vessels that Supply/Drain the Heart (Anterior View)

External Heart: Anterior View

Figure 18.4b

Vessels returning blood to the heart include:

Right and left pulmonary veins

Superior and inferior venae cavae

Vessels conveying blood away from the heart include:Aorta

Right and left pulmonary arteries

External Heart: Major Vessels of the Heart (Posterior View)

Arteries – right coronary artery (in atrioventricular groove) and the posterior interventricular artery (in interventricular groove)

Veins – great cardiac vein, posterior vein to left ventricle, coronary sinus, and middle cardiac vein

External Heart: Vessels that Supply/Drain the Heart (Posterior View)

External Heart: Posterior View

Figure 18.4d


Gross Anatomy of Heart: Frontal Section

Atria of the Heart

Atria are the receiving chambers of the heart

Each atrium has a protruding auricle Pectinate muscles mark atrial walls Blood enters right atria from superior and

inferior venae cavae and coronary sinus Blood enters left atria from pulmonary

veins

Ventricles of the Heart

Ventricles are the discharging chambers of the heart

Papillary muscles and trabeculae carneae muscles mark ventricular walls

Right ventricle pumps blood into the pulmonary trunk

Left ventricle pumps blood into the aorta

Pathway of Blood Through the Heart and Lungs

Figure 18.5

Pathway of Blood Through the Heart and Lungs

Right atrium tricuspid valve right ventricle

Right ventricle pulmonary semilunar valve pulmonary arteries lungs

Lungs pulmonary veins left atrium Left atrium bicuspid valve left ventricle Left ventricle aortic semilunar valve

aorta Aorta systemic circulation

Coronary Circulation

Coronary circulation is the functional blood supply to the heart muscle itself

Collateral routes ensure blood delivery to heart even if major vessels are occluded

Coronary Circulation: Arterial Supply

Figure 18.7a

Coronary Circulation: Venous Supply

Figure 18.7b

Heart Valves Heart valves ensure unidirectional blood flow

through the heart Atrioventricular (AV) valves lie between the

atria and the ventricles AV valves prevent backflow into the atria

when ventricles contract Chordae tendineae anchor AV valves to

papillary muscles

Heart Valves

Aortic semilunar valve lies between the left ventricle and the aorta

Pulmonary semilunar valve lies between the right ventricle and pulmonary trunk

Semilunar valves prevent backflow of blood into the ventricles

Heart Valves

Figure 18.8a, b

Heart Valves

Figure 18.8c, d


The electrophysiological characteristics of cardiac muscle that maintain the heart rate and rhythm consist of :

1- EXCITABILITY : the ability of the cardiac muscle to respond to an electrical stimulus . In the resting state the inside –ve & outside +ve both are equal .

CARDIAC PHYSIOLOGY


2- AUTOMATICITY : the ability of cardiac muscle cells to reach a threshold potential & to be able to generate an action potential without the need for external stimulation

3- CONDUCTIVITY : the ability of cardiac

muscle to transmit electrical impulses from SA node through the AV node ,bundle of his, rt & lt bundle branch ,and purkinji fiber

CARDIAC PHYSIOLOGY



4- REFRACTORINESS : the ability of cardiac muscle cell to maintain a steady rhythm by blocking the effect of stronger than normal stimuli which would initiate a further contraction by the heart

5- CONTRACTILITY : the ability of cardiac muscle cells to respond to stimulation by shortening its fibers to produce an efficient pumping action

CARDIAC PHYSIOLOGY


Action potential





CHARACTERISTICS OF THE PACEMAKER POTENTIAL

RECALL: PHASE 4 PACEMAKER POTENTIAL OBSERVED HERE. FREQUENCY DEPENDS ON: THRESHOLD, MAX. REPOLARIZATION

POTENTIALS AND SLOPE OF THE PREPOTENTIAL


The action potential consist of two phases the depolarization & repolarization .

at rest the cell membrane potential equal ( -85 to -95 ) millivolts ,but in stimulation the membrane potential become positive around + 20 millivolts .

the cause of the cell’s membrane alteration state is due to opening of 2 types of channels .

ACTION POTENTIAL


1- FAST SODIUM CHANNEL : that allow for a large amount of sodium ions to diffuse rapidly across the membrane into the cell causing the cell to become positive or depolarize ( phase 0 ) , phase 1 the spike at the tip of phase 0 , heralds the end of depolarization & the beginning of early repolarization when the sodium channels begin to close .

ACTION POTENTIAL


2- SLOW CALCIUM CHANNEL : they remain open for long period of time , being positively charged , these ions prolong the period of time in which the inside cell remains positive ( phase 2 , plateau ) .

(Phase 3) represent the closure of the slow channels resulting in rapid repolarization . calcium , sodium & potassium ions efflux returning the cell to its negative state .

ACTION POTENTIAL


The space between (phase 2 & 3) represent the S-T segment , phase 3 represent T wave , (phase 0& 1) represent the QRS complex .

In resting period the potassium ion return back into the cell to equilibrium with sodium ion out side the cell represent phase 4 & on ECG the isoelectric line.

ACTION POTENTIAL


CARDIAC CYCLE


1- depolarization of the SA node causes atrial depolarization marked by the P wave on ECG .

2- atrial depolarization causes atrial systole , as the atria contract , they exert pressure on the blood within , which forces blood through the open AV valves into the ventricles .

CARDIAC CYCLE


3- atrial systole contributes a final 25 ml of blood to the volume already in each ventricle ( about 105 ml ) , the end of atrial systole also called the end of ventricular diastole , thus each ventricle contains about 130 ml at the end of relaxation period ( diastole ) .

4- the QRS complex on the ECG marks the onset of ventricular depolarization .

CARDIAC CYCLE


5- ventricular depolarization causes ventricular systole , as ventricular systole begins , pressure rises inside the ventricles & pushes blood up against the AV valves forcing them shut , both the SL & AV valves are closed this is the period of isovolemetric contraction .

CARDIAC CYCLE


6- continued contraction of the ventricles causes pressure in the chambers to rise sharply , when left ventricular pressure surpasses aortic pressure at about 80 mmHg & right ventricular pressure rises above the pressure in the pulmonary trunk about 20 mmHg both SL valves open . At this point ejection of blood from heart begins , the pressure in the left ventricle continues to rise to about 120 mmHg , and right ventricle to about 30 mmHg .

CARDIAC CYCLE


7- the left ventricle ejects about 70 ml of blood into the aorta , and the right ventricle ejects the same volume of blood into pulmonary trunk . The volume remaining in each ventricle at the end of systole is about 60 ml .

8- the T wave in the ECG marks the onset of ventricular repolarization

CARDIAC CYCLE


9- ventricular repolarization causes ventricular diastole , as the ventricles relax pressure within the chambers falls & the blood within the aorta & pulmonary trunk begins to flow backward toward the region of low pressure in the ventricles , back flowing blood catches in the valve cusps & closes the SL valves , the aortic valve closes at a pressure of about 100 mmHg , rebound of blood off the closed valve produces the dicrotic wave on the aortic pressure curve .

CARDIAC CYCLE


After the SL valves close there is a brief interval when the ventricular blood volume doesn’t change because all 4 valves are closed , this is the period of isovolemetric relaxation .

10- as the ventricles continue to relax , the pressure falls quickly , when the ventricular pressure falls below the atrial pressure the AV valves open and ventricular filling begins

CARDIAC CYCLE


The major part of ventricular filling occurs just after the AV valves open, at the end of relaxation period the ventricles are about 3 quarters full .

CARDIAC CYCLE


It is the means by which the electrical potential generated by the cardiac cells during cardiac cycle can be graphically recorded by using an electrocardiography machine

ECG


ECG PAPER


Vertically each large square = 0.5 mv , so each small square = 0.1 mv .

horizontally each small square = 0.04 second , so each large square = 0.2 second .

ECG PAPER


LEADS AND THEIR POSITIONS


The Cardiac Axis

- Normally: between - 30 to + 90 - Left axis deviation > -30- Right axis deviation > +90

Calculated by:

Take the sum of R-{Q+S} in leads I, II, III

CompareLead ILead IILead III

Normal+++

LAD+--

RAD--/++






1- BIPOLAR LEADS:

L1: has the +ve electrode attached to Lt arm & -ve to Rt arm

L2 :+ve to Lt leg & - ve to Rt arm

L3 : +ve to Lt leg & - ve to Lt arm



2- UNI POLAR :

a - Augmented :

AVR : the +ve electrode on the Rt arm

AVL : the +ve electrode on the Lt arm

AVF : the +ve electrode on the Lt leg

b – chest :

V1- rt side of the sternum 4th intercostal space



V2 – Lt side of the sternum on the 4th intercostals space

V3 – mid way between V2 & V4

V4 - mid clavicle line 5th intercostal space V5 - anterior axillary line, horizontal to V4

V6 – mid axillary line,horizontal to V5 &V6




P wave : atrial depolarization the 1st up right wave

round in shape the amplitude not more than 2.5mm & up to 0.12 second in duration .

Q wave : the 1st down ward deflection below isoelectric line following the p wave , if present its depth not exceeds one third R wave ( 2mm)

R wave : the 2nd upward deflection

S wave : the 2nd downward deflection

EXPLAINING P,Q,R,S&T


QRS complex : ventricular depolarization normal

measure is 0.08-0.12 second & up to 0.20mv in amplitude.

T wave : ventricular repolarization , rounded upright, not exceeds 0.2 sec of duration & 5mm of amplitude.

PR interval : the interval between the beginning of p wave and the beginning of R wave it measures between ( 0.12-0.2) sec



ST segment : the isoelectric line between the end of QRS and the beginning of T wave

QT interval : the interval between the beginning of Q wave and the end of T wave , it measures ( 0.32 – 0.40 ) second




We have many ways to measure the heart rate

1- to count number of small boxes between 2 R waves , then to divide 1500 by number of small boxes .

2- to count number of large boxes between 2 R waves , then divide 300 by number of large boxes .

MEASUREMENT OF HEART RATE


Number of small boxes = 20, and the number of large boxes = 4 if you divide 1500/20 or 300/4 you will the same result 75bpm





SINUS RHYTHM PATH WAY


Characteristics of normal sinus rhythm

1- RHYTHM : regular p-p & r-r intervals

2- RATE : vary between 60-100 bpm .

3- P WAVE : present ,normal configuration

4- PR INTERVAL :vary between 0.12-0.2 second

SINUS RHYTHM


5- QRS COMPLEX : vary between 0.06-0.12 second

6- ST SEGMENT: isoelectric

7- T WAVE : normal ( symmetric , rounded )

8- CONDUCTION : normal conduction from SA node , each P followed by QRS & T wave .

SINUS RHYTHM


SINUS RHYTHM


SA NODE ABNORMALITY PATH WAY


Occurs when the SA node discharge an impulses regularly at a rate less than 60 bpm , the complexes and intervals remain within normal time duration

SINUS BRADY CARDIA


SINUS BRADY CARDIA


1- RHYTHM : regular 2- RATE : less than 55 bpm .3- P WAVE : normal (up right ,rounded )4- PR INTERVAL : normal 5- QRS COMPLEX : normal 6- ST SEGMENT: isoelectric 7- T WAVE : normal ( symmetric , rounded ) 8-CONDUCTION : normal electrical path

way

SINUS BRADY CARDIA


CAUSES :

1- vagal stimulation

2- increased intra cranial pressure

3- myocardial infarction

4- use of beta blockers

SINUS BRADY CARDIA


Occurs when the SA node discharges an impulses in a rate of more than 100 bpm , some times the rate can be as high as 180 bpm

SINUS tachy CARDIA


SINUS tachy CARDIA


1- RHYTHM : regular

2- RATE : more than 100bpm .

3- P WAVE : normal (up right ,rounded )

4- PR INTERVAL : normal

5- QRS COMPLEX : normal duration



8- CONDUCTION : normal electrical path way

SINUS TACHYCARDIA


CAUSES :

1-fever

2- anxiety

3-hypo volemia

4- congestive heart failure

SINUS TACHY CARDIA


The rate usually increase with inspiration & decrease with expiration .

During expiration the parasympathetic vagal tone activated , so the heart rate decreased .

During inspiration the stretch receptors in the lung stimulate the cardioinhibitary centers in the medulla via fibers in the vagus nerve , so the heart rate increased .

SINUS ARRHYTHMIA


SINUS ARRHYTHMIA


1- RHYTHM : rate increased with inspiration ,decreased with expiration

2- RATE : varies between 50 -100 bpm .3- P WAVE : normal (up right ,rounded )4- PR INTERVAL : normal 5- QRS COMPLEX : normal duration 6- ST SEGMENT: isoelectric 7- T WAVE : normal ( symmetric , rounded ) 8-CONDUCTION : normal electrical path way

SINUS ARRHYTHMIA


CAUSES :

During inspiration venous blood returning to the heart increases and vagal tone decreases resulting on tachy cardia & vice versa

SINUS ARRHYTHMIA


When the SA node fails to initiate an impulse at a specific time resulting in an absence of a PQRST complexes for at least one complete cardiac cycle some times up to three consecutive cycles , all complexes and intervals within normal limits

SINUS ARREST


SINUS ARREST


1- RHYTHM : regular disturb only by missed beat 2- RATE : normal except for missed beat .

3- P WAVE : normal (up right ,rounded )

4- PR INTERVAL : normal




8- CONDUCTION : normal electrical path way

SINUS ARREST


CAUSES :

1- inferior MI

2- increased vagal tone

3- digoxin toxicity

SINUS ARREST


The site of the wandering pacemaker originates from at least three different sites in the cardiac muscles , its position may shift to another irritable foci in the atria and the AV junction , the size and the shape of the P wave vary depending on the site of origin for that particular cycle

WANDERING PACEMAKER


WANDERING PACEMAKER


1- RHYTHM : vary according to the site of initial impulse

2- RATE : varies from normal to low upon the site

3- P WAVE : varies in shape and direction

4- PR INTERVAL : vary depending on atrial origin

WANDERING PACEMAKER





8- CONDUCTION : normal electrical path way after passing the AV junction

WANDERING PACEMAKER


CAUSES :

1- digitalis toxicity

2- MI

WANDERING PACEMAKER


ARRHYTHMIAS OF ATRIA


Occur when an ectopic atrial focus discharge an impulse before the next anticipated sinus node activation , these ectopic Ps have a bizarre appearance and can be pointed , inverted or notched

ATRIAL ECTOPIC BEAT


ATRIAL ECTOPIC BEAT


1- RHYTHM : regular except for ectopic beat

2- RATE : normal except for ectopic beat

3- P WAVE :normal ,pointed in atrial ectopic beat

4- PR INTERVAL : normal except for ectopic beat


ATRIAL ECTOPIC BEAT




8- CONDUCTION : normal electrical path way after passing the AV junction

ATRIAL ECTOPIC BEAT


CAUSES :

1- IHD

2-electrolytes imbalance

3-CHF

ATRIAL ECTOPIC BEAT


Occurs when multiple irritable focuses in both atria

started to initiate impulses that resulting in chaotic , irregular excitation of the atrium .

Its characterized by the appearance of numerous irregular fibrillatory waves on the rhythm strip , the ventricular wave also irregular depending on the conduction of the atrial impulses conduction through the AV junction .

ATRIAL FIBRILLATION

ATRIAL FIBRILLATION


1- RHYTHM: irregular for both atrium & ventricles .

2- RATE : atrial ( 400-500 )bpm , ventricular ( 80 -180 ) bpm ( varies upon conduction .

3- PR INTERVAL : absent .4- QRS COMPLEX : normal shape & duration 5- CONDUCTION : bizarre atrial conduction ,

normal conduction after AV junction .

ATRIAL FIBRILLATION


CAUSES :

1- anterior myocardial infarction .

2- inferior myocardial infarction .

3- valvular heart disease .

ATRIAL FIBRILLATION


occurs when there is a rapid but regular excitation from an ectopic focus in the atrium at rate of 300 bpm . The ventricular waves are regular , the ratio between atrial and ventricular rate varies between ( 2:1 & 3:1& 4:1 ) .

ATRIAL FLUTTER

250-350 bpm

75-150 bpm

2:1 or higher block


ATRIAL FLUTTER

always think "atrial flutter with 2:1 block" whenever there is a regular supraventricular tachycardia @ ~150 bpm!

ATRIAL FLUTTER


1- RHYTHM : atrial rhythm is regular ,ventricular rhythm regular & depend on the conduction .

2- RATE : atrial 288 bpm , ventricular 96 bpm . Ratio 3: 1 .

3- P WAVE : saw-tooth ; no true p waves , only flutter or F waves .

4- PR INTERVAL : absent .

ATRIAL FLUTTER


5- QRS COMPLEX : normal shape & duration .

6- T WAVE : difficult to define .

7- CONDUCTION : ectopic atrial foci , impulses follow normal path way after AV junction .

ATRIAL FLUTTER


CAUSES :

1- atrial enlargement .

2- hyper thyroidism .



ATRIAL FLUTTER


During an episode of SVT the heart beat is not controlled by SA node , another part of the heart overrides this role with faster impulses .

The source of the impulse is some where above

ventricles , but the impulse then spread to the ventricles so the heart beats faster than normal .

SUPRAVENTRICULAR TACHYCARDIA




1- RATE: between (140 – 200) bpm .

2- RHYTHM : R-R interval regular .

3- P WAVE : absent .

4- P-R INTERVAL : absent .



5- QRS COMPLEX : narrow < 0.06 second .

6- T WAVE : peaked T wave .

7- CONDUCTION : the ventricles is stimulated from some where in the atria .



CAUSES :

1- hypothyroidism .

2- anxiety .

3- pericarditis .

4- heart failure .

5- structural abnormality .



This type occurs when SA node & the atria

are unable to discharge an impulse to depolarize both atria & ventricles , therefore an ectopic focus in the surrounding junctional tissue take the responsibility as apace maker at a rate of ( 40-60 ) bpm .

The P wave may be absent, inverted & next QRS complex ; depends upon its origin .

JUNCTIONAL RHYTHM


JUNCTIONAL RHYTHM


JUNCTIONAL RHYTHM


1- RHYTHM : regular .2- RATE : 50 bpm , ( 40 – 60 ) bpm .3- P WAVE : Absent .4- QRS COMPLEX : normal configuration &

duration . 5- T WAVE : normal .6- CONUCTION : the atria is stimulated by the

junctional tissue after activation after or with the activation of the ventricles .

JUNCTIONAL RHYTHM


CAUSES :

1- acute myocardial infarction .

2- digoxin toxicity .

JUNCTIONAL RHYTHM


This occur when the junctioal tissue discharges impulses at a rate of ( 60 – 100 ) bpm .

the P wave may be absent , inverted or after QRS complex.

ACCELARATED JUNCTIONAL RHYTHM




1- RHYTHM : regular .2- RATE : 83 bpm .3- P WAVE : after QRS complex .4- QRS COMPLEX : normal configuration &

duration .5- T WAVE : Normal .6- CONDUCTION : atria activated after the

ventricles so P wave comes after QRS complex .



CAUSES :

1- congestive heart failure .

2- cardiogenic shock .

NOTE : this type of arrhythmia start & end gradually .



VENTRICULAR ARRHYTHMIAS


Occurs when an ectopic focus discharging an

impulse ahead of the next anticipated sinus node beat .

the ectopic beat consist of QRS & T waves that are opposite together in their directions , if QRS positive direction the P in negative direction .

The ectopic beat may occur after T wave or on the top of T wave .

VENTRICULAR ECTOPIC BEAT




Multi focal means that the ectopic beat has more than one foci , that discharge many shapes of QRS & T .



That means that 2 consequences impulses discharged prior to the next anticipated sinus rhythm impulse .





Bigemini : the ectopic beat occurs every other one beat .



Trigemini : the ectopic beat occurs every other 2 sinus beats .

Sequential : when more than 3 consequences ectopic beats occur .



Occurs when the VEB occurs on the top of previous sinus rhythm T wave which dangerous because may lead to torsades de pointes .



occurs when there is no time for compensatory pause for the SA node after the occurrence of VEB .



1- RHYTHM : depends on the underlying rhythm, in regular rhythm the ectopic beat causes irregularity .

2- RATE : depends on underlying rhythm , but VEB can occur any time .

3- P WAVE : in ectopic beat its not identifiable or hidden in QRS because of force of ventricular depolarization .



4- P-R INTERVAL : normal ( 0.12-0.2 ) if underlying rhythm is sinus .

5- QRS COMPLEX :always widened & distorted with no preceding P wave , the duration is greater than 0.12 second , and some times pointed in the opposite direction in comparing with the sinus complexes . If the QRS in normal appearance & duration the origin is situated near the bundle of his but if wide & bizarre the focus is situated in the purkinji fiber .



6- T WAVE : usually deflected in the opposite

direction of the QRS complex of the VEB .

7- CONDUCTION : the atria may not be depolarized , the ventricles are stimulated by their own pace maker .

HINT : following the VEB there is a complete compensatory pause allowing the SA node to regain control as a pace maker .



CAUSES :


2- electrolytes imbalance .

3- ingestion of stimulants ( tea , coffee ) .



VENTRICULAR TACHYCARDIA

Develops when there is more than 3 consequences VEBs and the heart rate exceeds 100 bpm , such activity is due to enhanced automaticity and re-entry within the purkinji fibers . P wave not visible because its hidden in the QRS complex .

Ventricular Tachycarida




A- start of spindle increase QRS amplitude

B-end of spindle & start of node .

C- end of node & start of next spindle . Note the positive initial deflection .

TORSADES DE POINTES


1- RHYTHM :regular .2- RATE : ventricular 180 bpm , it range is ( 100-

200) bpm .3- P WAVE : not present , or hidden in the QRS

complex .4- P-R INTERVAL : not present .5- QRS COMPLEX : uniform configuration .6- CONDUCTION : the ventricles are directly

stimulated by an ectopic focus within the purkinji fibers network .



CAUSES :

1-hypokalemia .

2-cardiomyopathy .

3-acute myocardial infarctions .



chaotic un coordinated ventricular depolarization , usually initiated by the R wave of a VEB striking the peak of the T wave of preceding beat . Because of chaotic activity the muscle mass on quivers & cardiac out put falls rapidly .


Ventricular fibrillation


VENTRICULAR FIBRILLATION

Ventricular fibrillation

Top emergency!! Most common cause is acute MI.


1- RHYTHM : irregular , chaotic .

2- RATE : cannot be determined .



5- QRS COMPLEX : replaced by f wave .

6- CONDUCTION : un coordinated ventricular depolarization .



CAUSES :

1- R on T phenomenon .


3- hypokalemia .

4- hypothermia .

5- sever acidosis or alkalosis .



Occurs when the electrical impulses from the SA node doesn’t reach the ventricles , in this situation the ventricles muscles take the role as apace maker and widened QRS may appear .

VENTRICULAR STANDSTILL




1- RHYTHM : no ventricular activity , the atrial activity appear .

2- RATE : atrial regular .

3- P WAVE : present .


5- QRS COMPLEX : absent .

6- CONDUCTION : no conduction through the ventricles .



CAUSES :

1- complete heart block .

2- respiratory failure .





This arrhythmia occurs when all supra ventricular pace makers ( SA node , AV junction , bundle of his , bundle branch ) fail to elicit an electrical impulse ; the ventricles take over as a pace maker , firing at their own inherent rate of ( 30 – 40 ) bpm .

IDIOVENTRICULAR RHYTHM




1- RHYTHM : regular R-R interval .

2- RATE :(30-40) bpm .


4- QRS COMPLEX : wide & bizarre .

5- CONDUCTION : electrical impulses arises from the purkinji fibers or ventricular myocardium .



CAUSES :


2- medication effects like adrenaline .



This arrhythmia occurs when the SA node & AV junction fail to initiate impulse the ventricles take over the role as a pace maker at a rate about ( 50-100) bpm .

ACCELERATED IDIOVENTRICULAR RHYTHM




1- RATE : 60 bpm .

2- RHYTHM : regular R-R interval .


4- QRS COMPLEX : wide & bizarre .

5- T WAVE : caught up in ST segment .

6- CONDUCTION : pace maker site is in bundle branch , purkinji fibers or myocardium



CAUSES :

1- Acute myocardial infarctions .




ATRIOVENTRICULAR BLOCKS


Occurs when there is a delay in the transmission of electrical impulse through the AV node to the ventricles .

FIRST DEGREE AV BLOCK




1- RHYTHM : regular .

2- RATE : 45 bpm < 50bpm

3- P WAVE : normal .

4- P-R INTERVAL : 0.28 seconds

5- QRS COMPLEX : normal .

6- CONDUCTION : follow normal conduction pathway but there is a delay in the process .



CAUSES :





Occurs when conduction through the AV junction become progressively difficult with each successive impulse until finally a ventricular depolarization doesn’t occur .

SECOND DEGREE AV BLOCK MOBITZ-1




1-RATE :ventricular = 68 bpm , atrial = 75 bpm .

2- RHYTHM : atrial regular , but ventricular irregular .


4- P-R INTERVAL : lengthening with each successive beat .

5- QRS COMPLEX :normal .



6- CONDUCTION : some of the impulses from the atria are blocked . P-R interval gets progressively longer until one P wave is not followed by QRST .



CAUSES :

1-rehumatic fever .





In this arrhythmia 2 or more atrial impulses conducted normally , then the next impulse blocked without warning . Block may occur occasionally or at regular intervals . ( for every third beat ) ( 3:1) .





1- RATE : atrial 64 bpm , but ventricular depend on conduction .

2- RHYTHM : P-P interval regular , R-R interval irregular .


4- P-R INTERVAL : 0.16 sec , absent in missed beats .



5- QRS COMPLEX : normal, some dropped beats .

6- T WAVE : normal , some dropped as QRS

7- CONDUCTION : Third atrial impulse is blocked .



CAUSES :

1- degenerative changes in conduction system


3- coronary artery disease .



Occurs when the electrical impulses above the AV node are blocked , therefore no impulses conducted to the ventricles , if SA node blocked the junctional arises , if the block involve the junctional tissue , the idiodventricular rhythm arises .

COMPLETE HEART BLOCK




1-RATE : atrial rate ( 60-100) bpm, ventricular rate (30-40) bpm .

2- RHYTHM : P-P interval regular , R-R interval regular .


4- P-R INTERVAL : absent ( no relation between atria& ventricles )



5- QRS COMPLEX : depend on the site of pace maker , ( wide = purkinji fibers ) ( normal =junctional tissue )

6- T WAVE : absent .

7- CONDUCTION : the atria & ventricles have independent pacemaker ,so there is no relationship between both .



CAUSES :

1-inferior myocardial infarction .


3- degeneration of conduction system .


Myocardial Infarction

V1-V2 anteroseptal wall

V3-V4 anterior wall

V5-V6 anterolateral wall

II, III, aVF inferior wall

I, aVL lateral wall

V1-V2 posterior wall (reciprocal)

1 .Ischemia

Represented by symmetrical T wave inversion (upside down). The definitive leads for ischemia are: I, II, V2 - V6 .

2 .Injury Acute damage - look for elevated ST segments. (Pericarditis and cardiac aneurysm can also cause ST elevation; remember to correlate it with the patient) .

3 .Infarct Look for significant "pathologic" Q waves. To be significant, a Q wave must be at least one small box wide or one-third the entire QRS height. Remember, to be a Q wave, the initial deflection must be down; even a tiny initial upward deflection makes the apparent Q wave an R wave .

In Full thickness MI ( Q MI, ST elevation MI ): ST elevation = Injury . T inversion = Ischemia. Q wave = Infarction ( necrosis).

First few Minutes : Hyperacute T. First few Hours : ST Elevation. Hours to Days : ST goes down+ T inversion+ Q

appears+ Reciprocal changes go back to normal . Few Days ( OLD ): Everything back to norm and the

Q stays forever (10 years!!!).

Inferior Wall

II, III, aVF• View from Left Leg

• inferior wall of left ventricle

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Inferior Wall

Inferior Wall

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Posterior View• portion resting on diaphragm

• ST elevation suspect inferior injury

Lateral Wall

I and aVL• View from Left Arm

• lateral wall of left ventricle

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Lateral Wall

Lateral Wall

I, aVL, V5, V6• ST elevation suspect

lateral wall injury

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Anterior Wall

V3, V4• Left anterior chest

electrode on anterior chest

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Anterior Wall

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

V3, V4• ST segment

elevation suspect anterior wall injury

Septal Wall

V1, V2• Along sternal borders

• Look through right ventricle & see septal wall

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Septal

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

V1, V2• septum is left

ventricular tissue

Note ST segment elevation in leads V2-V3 (anteroseptal/anterior wall).

Acute injury in the anterior, anterolateral, and lateral wall (ST elevation in V2-V6, I and aVL).

Infarct in the antereoseptal and anterior wall (Q waves in V2-V4)there is also a probable inferior infarct (Q waves in II, III, and aVF).

Ischemia: Note symmetric T wave inversions in leads I, V2-V5.

Left ventricular and left atrial hypertrophy. S wave in V2 plus R wave in V5 > 35. The left atrial hypertrophy is noticaeable by a P wave that is long in lead II, with an increase in the negative terminal deflection in lead V1.

Right ventricular and right atrial hypertrophy. The R wave is greater than the S wave in V1 and the R wave gets progressively smaller from V1 to V6. Normally, the R wave should increase from V1 to V6. The right atrial hypertrophy is marked by peaked P waves in lead II and a large intitial positive deflection of the P wave in lead V1.

ST Segment Analysis

For each complex, determine whether the ST segment is elevated one millimeter or more above

the TP segment


BUNDLE BRANCH BLOCK


Occurs when the right ventricle is activated abnormally by the interventricular septum .

In RBBB the following take place 1- initial impulse activate interventricular

septum . 2- the left bundle branch stimulates the left

ventricle to depolarize , 3- the impulse is transmitted across the

septum below the level of block .

RIGHT BUNDLE BRANCH BLOCK




By using chest leads V1 & V6 you see :

1- rSR shape in V1 :

a- small R wave in V1

b- large S wave in V1

c- second large R wave in V1

2- Q wave in V6

3- prominent ( deep & wide ) S wave in V6 .




CAUSES :

1- right ventricular hypertrophy


3-pulmonary embolism .

4- cardiomyopathy .



Occurs when left ventricle is abnormally activated by impulses spreading through the interventricular septum by the right ventricle

LEFT BUNDLE BRANCH BLOCK




By using the chest leads V1 & V6 you will find the following :

1- inverted T wave .

2- RSR” in V6 .

3- no Q wave .

4- wide QRS > 0.12 second .




CAUSES :

1- valvular heart disease .

2- acute myocardial infarctions .

3- hypertension .



This abnormality occurs when the right atria become enlarged due to the following :

1- tricuspid valve stenosis .

2- pulmonary hypertention .

RIGHT ATRIAL HYPERTROPHY




CRITERIA :

differentiated by looking on P wave if amplitude > 2.5 mm in L2 .



Left atrial hypertrophy caused by mitral valve stenosis ( the valve between left atrium & left ventricle ) .

The criteria of left atrial hypertrophy is P wave duration > 0.12 second .

LEFT ATRIAL HYPERTROPHY


LEFT ATRIAL HYPERTROPHY


Right ventricular hypertrophy caused by pulmonary valve stenosis .

The criteria of ECG changes is skolo law that says :

if R wave in V1 + S wave in V6 > 35 mv that means the patient has right ventricular hypertrophy .

RIGHT VENTRICULAR HYPERTROPHY




Left ventricular hypertrophy caused by aortic

valve stenosis .

The criteria of determination of left ventricular hypertrophy is skolo law that says :

if S wave in V1 + R wave in V6 > 35 mv means that the patient has left ventricular hypertrophy .



That means the heart lies in the right area , this abnormality is only congenital.

The criteria of interpretation is L1 & AVR :

when L1 is in negative deflection & AVR in positive deflection .

DEXTROCARDIA


DEXTROCARDIA


QUESTIONS


THANK YOU

Date post:	26-May-2015
Category:	Health & Medicine
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Ecg interpretation reading 20031

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