ECG Booklet.pdf

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sic Principles of ECG Booklet

frina Hany,S.Kp/Brawijayaniversity

Basic Principles ofElectrocardiography

Nursing Program, Medicine Faculty

Brawijaya University 2004

References

Atwood,Stanton, Storey (1996). Pengenalan DasarDisritmia Jantung. Yogyakarta : Gajah MadaUniversity Press.

Emergency Nurses Chapter (2001). Basic ECGCourse. 3rd edition. Singapore : Singapore NursesAssociation

Ginger & Melvin Ochs (1997). Recognition &Interpretation : ECG RHYTHMS. 3rd edition.USA: Appleton & Lange.

Thaler (2000). Satu-satunya BUKU EKG yangAnda Perlukan. Edisi 2. Jakarta : Hipokrates.
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Learning Objectives

General Objectives

After studying this subject in about

2 x 3 x 50 menit, the students expected

to be able to use ECG machine

and interpret the ECG result.

Composition :

15 Pre test90 Presentation & Discussion

15 Post test

Specific Objectives1. Fundamentals of EKG (20)

a. Introduction

b. Hearts conducting system

c. EKG Machine

d. EKG Waveform Analysis

2. Obtaining 12 leads EKG (20)

a. About 12-Lead EKG

b. Recording 12-Lead EKG

c. Troubleshooting (problems&solutions)

d. Care & Cleaning

3. Interpreting Basic EKG (50)

a. 5 Steps of Arrhythmia Interpretation

b. Classification of Arrythmias

c. Recognition & Treatment
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Fundamentals of EKG

Introduction

Hearts conducting system

EKG Machine

EKG Waveform Analysis

During the late 1800's and early 1900's, Dutchphysiologist Willem Einthoven developed the earlyelectrocardiogram. He won the Nobel prize for itsinvention in 1924.

Hubert Mann first uses the electrocardiogram todescribe electrocardiographic changes associatedwith a heart attack in 1920.

Electrocardiography- graphic recording of theelectrical activity (potentials) produced by theconduction system and the myocardium of theheart during it depolarization / repolarizationcycle.
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Hearts Conducting System(Ginger & Melvin Och, 1997)

Normally electrical impulses that causesrythmic contraction of heart muscles arises inthe SA Node as the intrinsic pacemakerof theheart. From the SA Node, impulse spreads overthe atrial muscles causing atrial contraction.The impulse is also conducted to the AV Node& it takes 0.03 sec to travel from SA to AVNode. From AV Node the electrical impulse is

conducted to ventricular muscles via thebundle of his, the bundle branches & thepurkinje fibres. The bundle branches & thepurkinje fibres are collectively calledtheventricular conduction system

Fundamentals of ECG
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A heart controlled by the SA Node is said to be

in normal sinus rhythm. The SA Node underinfluence of the autonomic nervous system

(Sympathetic which increases the heart rate via

B1 adrenergic receptors; Parasympathetic which

slows the heart rate via vagus nerve)

The rhythm originates from SA Node because

the SA Node depolarizes more frequently (60-

100 beats/min) than AV Node (40-60 b/m) &

ventricular conducting system (30-40 b/m), sothe AV Node & ventricular conducting system

are captured by the sinus impulse and driven

at 60-100 b/m

Fundamentals of ECG

The electrical impulse from the SA node isconducted through the AV node because theatria & ventricles are separated by a fibrousconnective tissue ring that has poorconductivity. The AV node provides a pathfor the impulse to proceed from the atria toventricles.

The AV node together with bundle of Hismake up theAV junctional tissue. The AVJunc Tissue has its own intrinsic pacemakeractivity at 40-60 b/m. if SA node are injured,the AV Junc Tissue can take over control ofthe heart rate & rhythm

Fundamentals of ECG
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EKG Machine(Ginger & Melvin Och, 1997)

An EKG machine is a highly sensitivevoltmeter that measures voltage differencebetween two points on the body surface

The voltage difference comes fromdepolarization and repolarization of cardiacmuscle cells

An EKG machine has a positive and anegative terminal

Single, Multi Channel

Fundamentals of ECG

Electrophysiology(Ginger & Melvin Och, 1997)

Normal electrical activity of the heart

Polarization the phase of readiness. The muscles is relaxedand the cardiac cells are ready to receive an electrical impulse

Depolarization the phase of contraction. The cardiac cells havetransmitted an electrical impulse, causing the cardiac muscle to

contract. Repolarization the recovery phase. The muscles are returning

to a relaxed state.

**The cardiac muscle cells have K inside and Na outside the cells.When polarized cell is stimulated by an electrical impulse, Kmoves outside the cell and Na moves inside.

Fundamentals of ECG
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Voltage

Time

.1 mv

.5 mv

.04 seconds .20 seconds

Paper speed =

25mm / second

paper

Fundamentals of ECG

1 mm = 1mV

1 small box = 0.040 sec

5 small boxes = 0.20 sec

15 small boxes = 3 sec

30 small boxes = 6 sec

300 small boxes = 1 min

ECG Waveform Analysis

Consist of :

1. Isoelectric Line Picture 12. ECG Waves * P Picture 1 & 2

* QRS

* T* U

3. ECG Intervals * P-R Picture 1 & 2

* QRS4. ST Segment Picture 25. J Point Picture 2

Fundamentals of ECG
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Picture1 Picture 2

Fundamentals of ECG

EKG Intervals

P wave

QRS Complex

T wave P wave

P-R

Interval

Q-T

Interval

P-R Interval = A-V Conduction Time

Q-T Interval = Ventricular Contraction

Time

R-R Interval = Cardiac Cycle Time

Heart Rate = 1/R-R Interval

Fundamentals of ECG

One Cardiac Cycle
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P Wave represents the electrical activity of the original

impulse from the SA node and its subsequent spread tothe atria. If the P wave is absent or abnormal in shape, itmeans the impulse originates from outside of the SA node.Normal duration is 0.04 to 0.11 second (maximum about 3small squares)

PR Intervals is measured from the beginning of the Pwave to the beginning of the QRS complex. It representsthe time taken for the impulse to travel from the SA node

to the AV node and the ventricles. Normal duration is 0.12to 0.20 second (3 to 5 small squares)

Fundamentals of ECG

Emergency Nursing Chapter, 2001

QRS Complex represents the time taken for the impulse to travel

from the Bundle of His to the Purkinje fibres, wich results in the

contraction of the ventricles. Duration is less than 0.12 second (3

small squares). The complex consists of an initial downward

deflection Q wave, an upward deflection R wave and second

downward deflection S wave. The configuration of the QRS

complex varies from lead to lead and there are several patterns.

ST Segment begins at the end of the S wave and terminates at the

upstroke of the T wave. The J point (junction point) marks where the

S wave ends the ST segment begins. The segment is elevated in

acute injury of AMI and depressed in ischemic states

Fundamentals of ECG

Emergency Nursing Chapter, 2001


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frina Hany,S.Kp/Brawijayaniversity 1

T Wave represents the recovery phase after ventricular

contraction. Tall, peaked or tented T waves indicate myocardialinjury or hyperkalemia. Inverted T waves may mean myocardial

ischemia.

QT Interval represents the depolarization& repolarization of the

ventricles. Abnormal duration indicates myocardial problems

U Wave represents the recovery period of the Purkinje fibres. It

is not present on all ECG waveforms. A prominent u wave may

indicated hypercalemia, hypokalemia or digoxin overdose.

Emergency Nurses Chapter, 2001

Fundamentals of ECG

Characteristics of a Normal Sinus Rhythm

Regular rhythm

Heart rate 60 to 100 per minute

P wave precedes every QRS complex. All P waves are similar inshape and size

All QRS complexes are similar in shape and size

Normal PR interval

T waves are after the QRS complexes All waves and interval are normal in duration and position

An Arrhytmia is an abnormal rhythm I.e. either the rate or thecontour/position of any individual wave is abnormal

Fundamentals of ECG
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Obtaining 12 Lead EKG

About 12-Lead EKG

Recording 12-Lead EKG

Troubleshooting (Problems& Solution)

Care & Cleaning

12-Lead ECG

The 12 EKG leads measure theelectrical activity of the heart from 12different directions

Bipolar Leads (augmented vector):Lead I, Lead II, Lead III

Unipolar Leads: aVR, aVL, aVF

Precordial Leads: V1, V2, V3, V4, V5, V6

Obtaining 12-lead ECG
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Recording the 12-Leads ECG(Emergency Nurses Chapter, 2001)

Explanation Tell the patient that the doctor has ordered an

ECG and explain the procedure Emphasize that the test takes about a few

minutes and that its a safe and painless way toevaluate cardiac function Answer the patients question, and offer

reassurance. Preparing him well helps alleviateand promote co-operation


Prepping the Patient Ask the patient to lie supine in the center of the bed

with his arms at his sides

If he cant tolerate lying flat, raise the head of thebed to semi-Fowlers position

Ensure privacy, and expose the patients arms, legs,and chest

Selection of the Electrode Sites Choose spots that are flat and fleshy, not muscular

or bony

Clean excess oil or ather substances from the skin toenhance electrode contact. Rememberthe betterthe electrode contact, the better the recording

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Steps in recording the ECG

Know your machine

Set the ECG paper speed selector to 25mm/second.If necessary, enter the patients identification data.Then calibrate or standardize the machine accordingto the manufacturers instructions.

Plug the cord of the ECG machine into a groundedoutlet. If the machine operates on a charged battery,it may not need to be plugged in.

Place one or all of the electrodes on the patientschest, based on the type of machine youre using.

Make sure all the leads are securely attached, andthen turn on the machine.


Instruct the patient to relax, lie still, and breathenormally. Ask him not to talk during the recording toprevent distortion of the ECG tracing.

Press the AUTO button and record the ECG. Ifyoure performing a right chest lead ECG, select theapproriate button for recording.

Observe the quality of the tracing. When themachine finishes the recording, turn it off.

Remove the electrodes and clean the patients skin.

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Documentation

Date Time

Doctors name

Nurses name

Special circumstances : vital sign, clientscondition


Troubleshooting

Problem Cause Solution

Power line AC

interference

Poor electrode contact.

Dry or dirty electrodes

Abrade skin. Use new electrodes.

Reapply electrodes.

Power line ACinterference Lead wires may be pickingup interference from

poorly grounded

equipment near the patient

Route lead wires along limbs and awayfrom other equipment. Fix or move poorly

grounded equipment

Power line AC

interference

Patient cable is too

close to the cardiograph

or other power cords

Move cardiograph away from the

patient. Unplug the cardiograph and

operate on battery only. Move other

equipment away from the patient

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Wanderingbaseline

Electrodemovement. Poor

electrode contact

and skin

preparation

Be sure that the leadwires are not pulling on

the electrodes. Reapply

electrodes. Press the

filterkey

Patient movement Reassure and relax the

patient

Respiratoryinterference Move lead wires awayfrom areas with the

greatest respiratory

motion



Tremor or muscle

artifact

Poor electrode

placement. Poor

electrode contact.

Patient is cold

Clean the electrode

site. Be sure the

limb electrodes are

placed on flat, non-

muscular areas.

Warm the patient

Tense,uncomfortable

patient

Reassure and relaxthe patient. Press

the filterkey

Tremors Attach the limb

electrodes near the

trunk. Pressthe

filterkey

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Emergency Nurses Chapter, 2001


Intermittent or

jittery waveform

Poor electrode

contact. Dry

electrodes

Clean the electrode

site. Reapply

electrodes

Faulty lead wires Replace faulty

patient cable

Poor print quality Dirty printhead or

ink has finished

Clean printhead or

change the ECG

stylus


Interpreting Basic ECG

5 Steps of Arrhythmia Interpretation

Classification of Arrythmias Recognition & Treatment

Acute Myocard Infarct
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5 Steps of Arrhythmia

InterpretationStep 1 : Calculate the Heart

Rate

Using the two simplest methods : 10-times / 20-times

method

= Number of R-waves in a 6second strip multiply by 10

= Number of R waves in 3

second strip multiply by 20= 1500 divided by the number ofsmall boxes between consecutiveR-waves


Dividing Methods

Use only if the rhythm is regular.Divide 300 with the big boxesbetween 2 R waves.

If there are also small boxes, addthe small boxes to the big boxes.Divide 300 with the combination

Step 2 : Measure the regularity of

the R wavesUsing methods :

Pen/pencil and paper method

Caliper method

Step 3 : Examine the P waves Present before all QRS

Normal configuration

Similar size & shape

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Step 4 : Measure the PR interval Number of small squares between the start of P

wave and the beginning of QRS complex not morethan 5.

Step 5 : Evaluate the QRS complex Number of small squares from the beginning to

the end of the complex not more than 3.

Conclusion


Classification of ArrhythmiaEmergency Nursing Chapter, 2001

According to :

Site of arrhythmia Mechanism of disorder

Seriousness of the arrhythmia

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Major Sites Sinus arrhythmia Atrial arrhythmia AV node arrhythmia Ventricular arrhythmia

Major Mechanisms Tachycardia (HR > 100 beats per minute) Bradycardia (HR < 60 beats per minute) Premature beats Flutter

Fibrilation Defects in conduction e.g. heart block


Recognition & TreatmentGinger & Melvin Och, 1997

Thaler, 2000

Normal Sinus Rhythm

Sinus Arrhythmias

Atrial Arrhythmias Heart Blocks

Ventricular Arrhythmias

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Normal Sinus Rhythm (NSR)

Description

This is the normal heart rhythm. It originates in the SA node and follows the appropriate

conduction pathways. The rate is normal, and the rhythm is regular. Every beat has a P wave,

and every P wave is followed by a ventricular response.

EKG Criteria

Rate: 60-100 bpm.

Rhythm: Regular. A normal variant called Sinus Arrythmia changes rhythm in response to

respiration. This is seen most often in young healthy people.Pacemaker: Each beat originates in the SA node.

P wave: look the same, all originate from the same locus (SA node)

PRI: 120-200 msec

QRS: 80-120 msec, narrow unless effected by underlying anomoly


SINUS BRADYCARDIA

Description

Sinus bradycardia originates in the SA node. It has reduced rate generally from a reduction in

sympathetic input, or excessive vagal (parasympathetic) tone. This rhythm may accompany

inferior MI's, hypoxia, hypothermia, or drug reactions. At moderately slow rates, the patient may

be asymptomatic. At slower rates, they may become hypotensive and present with symptoms

consistant with decreased perfusion: dizziness, syncope, shock like signs and symptoms.

Treatment is aimed at increasing the heart rate. Therapies include atropine, transcutaneous and

transvenous pacing, epinephrine, dopamine, isoproterenol .

EKG Criteria

Rate:


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SINUS TACHYCARDIA

Description

This arrythmia originates from the SA node. It is defined as a sinus rhythm exceeding 100 bpm.

Sinus tach is a normal rhythm which occurs in response to increased oxygen demand. This

occurs with exercise, infection, hypovolemia, hypoxia, myocardial infarct, and in response to

stimulant drugs, The rate usually has a gradual onset and elimination. Treatment is not usually

needed, but is aimed at treating the underlying condition.

EKG Criteria

Rate: >100 bpm.

Rhythm: Regular, generally.

Pacemaker: SA node.

P wave: Present and normal, may be buried in T waves in rapid tracings.

PRI: 120-200 msec., generally closer to 120 msec.

QRS: Normal.


PREMATURE ATRIAL COMPLEXES(PAC)

Description

These complexes originate in the atria. They often originate from ectopic pacemaker sites within

the atria which results in an abnormal P wave. The complex occurs before the normal beat is

expected, hence the prematurity. It is followed by a pause. There are many causes including:

increased sympathetic input, exogenous stimulants, drug interactions, AMI, cardiac ischemia,

idiopathic. These complexes can indicate increased automaticity. They may lead to re-entry

rhythms.

EKG Criteria

Rate: Underlying rhythm.

Rhythm: Irregular with PACs.

Pacemaker: Ectopic atrial pacemaker outside SA node.

P wave: Ectopic P wave present, generally different than normal SA P wave.

PRI: Generall normal range 120-200 msec, but differ from underlying rhythm.

QRS: Same as underlying rhythm.

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SUPRAVENTRICULAR TACHYCARDIA (SVT)

Description

There are several different types of SVT depending on the site of reentry (accessory pathway,

atrioventricular node or atrium). This rapid rhythm starts and stops suddenly. Treatment includes

vagal maneuvers, antiarrhythmia medication, radio-frequency ablation or surgical modification of

site of reentry.

EKG Criteria

Rate: 140 - 220 bpm

Rhythm: RegularPacemaker: Reentry circuit

Accessory pathway: Normal or short (if down accessory pathway)

A-V nodal reentry: Hidden in or at end of QRS

PRI: Depends on location of circuit

QRS: Normal if accessory pathway used - prolonged (>120 msec) with delta wave


ATRIAL FLUTTER

Description

Atrial flutter is characterized by "sawtooth" atrial activity and a conduction ratio to the ventricles of

2:1 to 8:1. It is caused by a reentrant circuit located in the right atrium. It may occur when the

atria are enlar ged in chronic obstructive lung disease, mitral or tricuspid disease, pericarditis orpost-operatively. Definitive treatment is direct-current cardioversion, surgical or catheter ablation.

EKG Criteria

Rate: 250 - 350 bpm (atrium)

Rhythm:Atrial rate regular, ventricular conduction 2:1 to 8:1

Pacemaker: Reentrant circuit rhythm located in the right atrium

P wave: Saw-tooth or picket fence

PRI: Constant onset



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ATRIAL FIBRILLATION

Description

This is the most common sustained cardiac arrhythmia. It is characterized by an undulating baseline

replacing P waves and an irregularly irregular ventricular response. This arrhythmia occurs with

hypertension, ischemic, mitral, myocardial and pericardi al disease, thyrotoxicosis, aging and sometimes

occurs in normals. Treatment includes anticoagulation, drugs to slow ventricular conduction and/or

cardioversion

EKG Criteria

Undulating baseline replaces P waves

Rhythm: Irregularly irregular


FIRST DEGREE AV BLOCK

Description

Conduction disturbances are characterized as first degree, second degree Mobitz 1, second

degree Mobitz II and complete heart block. The normal P-R interval is 120 - 200 msec. First

degree AV block is a constant and prolonged PR interval. Possible etiologies include insult to AV

node, hypoxemia, myocardial infarction, digitalis toxicity, ischemia of the conduction system and

increased vagal tone but is also seen in normals.

EKG Criteria

Rhythm: Regular

PRI: >200 msec



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SECOND DEGREE AV BLOCK

MOBITZ I (WENKEBACH)

Description

Wenkebach is characterized by progressive delay at the AV node until the impulse is completely

blocked. Etiologies are the same as cause first degree AV block and is also seen in normals. This

conduction abnormality does usually not progress to higher degree heart blocks.

EKG Criteria

Rhythm: Irregular

PRI: Progressive lengthening of PRI until dropped beat. A clue to Wenckebach is that the QRS's

appear to occur in groups.


SECOND DEGREE AV BLOCKMOBITZ II

DescriptionThis is a higher degree of conduction block then Mobitz I and may progress to complete AV

block. AV conduction appears normal until suddenly there is no AV conduction following one P

wave. This may occur in a pattern (every 2nd, 3rd or 4th complex) or may occur randomly. This is

intermittent block at the AV node and may progress to complete heart block.

EKG Criteria

PRI: Constant on conducted complexes until a sudden block of AV conduction. That is, a P wave

is abruptly not followed by a QRS



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PREMATURE VENTRICULAR CONTRACTIONS (PVC)

DescriptionA PVC is a depolarization that arises in either ventricle before the next expected sinus beat. The

normal sequence of depolarization is altered because the impulse originates in the ventricle. The two

ventricules depolarize sequentially insteat of simultaneously. Conduction moves more slowely than

through the specialized conduction pathways, this results in a widened QRS complex (greater than

0.12 sec). PVCs may occur as isolated complexes ormay occur in pairs, triplets, or in a repeating

sequence with normal QRS complexes. Three or more PVCs in a row is considered a run of

Ventricular Tachycardia. If it lasts for more than 30 seconds it is designated sustained VT. Treatment:

Rarely treated unless symptomatic. PVCs may indicate acute mycardial ischemia requiring rapid

intervention including oxygen, NTG, morphine, thrombolytic. Treating with lidocaine will cease the

PVC, but won't address the ischemic cause.

EKG CriteriaRhythm: Irregular

QRS: Is not normal looking. Broadened, greater than 0.12 seconds. P waves are usually obscured by

the QRS, ST segment, or T wave of the OVC. The P wave may sometimes be seen as notching during

the ST segment or T wave.

BIGEMINY PVCs

Description

PVC's may occur in patterns. When each normal complex is followed by a PVC forming groupsof 2, the term "ventricular bigeminy" is used.

EKG Criteria

QRS: Normal QRS complex followed by premature wide bizarre complex (PVC) in patterns of 2



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VENTRICULAR TACHYCARDIA

Description

Ventricular Tachycardia (VT) is defined as three or more beats of ventricular origin in succession at a

rate greater than 100 beats per minute. There are no normal (narrow) looking QRS complexes.

Consequences of VT depend on accompanying myocardial dysfunction. It may be well tolerated or

associated with life-threatening hemodynamic compromise. Treatment: If patient is stable, they are

initially treated with lidocaine, procainamide, or bretylium tosylate. Hemodynamically unstable VT (with

a pulse) is cardioverted at 200J, 300J, 360J as needed. VT without a pulse is treated like VF and

defibrillated.

EKG Criteria

No normal looking QRS complexes, often bizzare with notching. Width of QRS>0.12 sec. ST segment

and T wave are opposite polarity to the QRS. Sinus node may be depolarizing normally. There is

usually complete AV dissociation. P waves are sometimes seen between QRS complexes. They have

no impact on the QRS complexes.

Rate: Generally 100 to 220 bpm

Rhythm: Generally regular, on occassion can be modestly irregular.


VENTRICULAR FIBRILLATION

DescriptionVentricular Fibrillation is a rhythm in which multiple areas within the ventricles display marked variation in

depolarization and repolarization. There is no organized depolarization, therefore the ventricles do not

contract as a unit. The myocardium is quivering when visualized grossly. There is no cardiac output. This is

the most common arrythmia seen in cardiac arrest from ischemia or infarction. The rhythm is described as

coarse or fine VF. Coarse VF indicates recent onset of VF. Prolonged delay without defibrillation results in

fine VF and eventually asysyole. Resuscitation becomes more difficult as VF becomes finer. Treatment is

always immediate unsynchronized defibrillation at 200J, 300J, 360J for adult patients.

EKG CriteriaRate: Very rapid, too disorganized to count.

Rhythm: Irregular, waveform varies in size and shape

No normal QRS complexes.

Absent ST segments, P waves, T waves.



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ASYSTOLE

Description

Asystole represents the total absence of ventricular electrical activity. Since depolarization does not occur,

there is no ventricular contraction. This may occur as a primary event in cardiac arrest, or it may follow VF

or pulseless electrical activity (PEA). Ventricular asystole can occur also in patients with complete heart

block in whom there is no excape pacemaker. VF may masquerade as asystole; it is best always to check

two leads perpendicular to each other to make sure that asystole is not VF. Treatment for each arrythmia is

very different. Fine VF which may mimic asystole should be treated with defibrillation. But defibrillating

asystole is potentially harmful. Treatment: Epinephrine and Atropine are administered. Consider causes:

pulmonary embolism, acidosis, tension pneumothorax, cardiac tamponade, hyperkalemia, hypokalemia,

hypoxia, hypothermia, overdose, myocardial infarction.

EKG Criteria

Complete absence of ventricular electrical activity. Occasional P waves or erratic ventricular beats may be

seen. These patients will be pulseless. Treatment must be immediate if the patient is to have any chance at

resusctiation.

Rate: None

Rhythm: None


Myocardial Infarction

ECG will reflect thethree pathologicchanges of a MI :

Ischaemia

Injury Infarction/Necrotic



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Zone of Infarction / Necrotic Area of myocardial necrosis may develop within an hour of an infarct / a few

days later.

Irreversibel & permanent

Pathologic Q wave (1/3 R wave)


Zone of Injury

Marked by an elevated ST-segment

Result from prolonged lack of blood supply



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Zone of ischaemia Results from an interrupted blood supply

Represented by T-wave inversion or

J-point depression



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EVOLUTION OF AMI

Assessing AMI


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Conclusion

It is important for nurses not only to

record the patients ECG but also

interpret it to give the best treatment

for their patient based on his/her

problem
http://www.123greetings.com/encouragement_and_inspiration/encouragement/encourage9.htmlhttp://www.123greetings.com/encouragement_and_inspiration/encouragement/encourage9.htmlhttp://www.123greetings.com/encouragement_and_inspiration/encouragement/encourage9.htmlhttp://www.123greetings.com/encouragement_and_inspiration/encouragement/encourage9.htmlhttp://www.123greetings.com/encouragement_and_inspiration/encouragement/encourage9.htmlhttp://www.123greetings.com/encouragement_and_inspiration/encouragement/encourage9.htmlhttp://www.123greetings.com/encouragement_and_inspiration/encouragement/encourage9.htmlhttp://www.123greetings.com/encouragement_and_inspiration/recovery/recovery4.html


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ECG Booklet.pdf

Documents

Transcript of ECG Booklet.pdf