ecg interpretation

BASIC ECG INTERPRETATION

ECG - is a series of waves and deflections recording the heart’s electrical activity from a certain “view.”

Heart Conduction

Electrical Conduction Rate

• SA node • Rate: 60 – 100 bpm

• AV node • act as back-up pacemaker• Rate: 40 – 60 bpm

• Purkinje Fiber • can act as back-up pacemaker

• Rate: 20 – 40 bpm

Breakdown of ECG strip

P wave: (SA node fires)

• Atrial depolarization

• Normal shape: upright & round

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Components of the Cardiac Cycle

P-R interval (PRI)• impulse travels from the SA node to the atria

• P wave followed by isoelectric line

• From the beginning of P wave to the beginning of Q wave

QRS Complex

• ventricular depolarization

• Impulse from the Bundle of HIS throughout the ventricular muscles

T wave• Ventricular repolarization

• Resting phase of the cardiac cycle

• upright & round

U wave• Purkenji fiber repolarization

• Etiology:• hypokalemia

Electrode application

• White to right• Red to ribs• Black over the red.

LEAD II

• Produces positive deflection

• Commonly used for routine monitoring

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STEPS IN ANALYSING ECG

Step I: rhythm• Regular

• irregular

Step II: Rate

• Normal: 60 – 100 bpm

• Bradycardia: < 60 bpm

• Tachycardia: > 100 bpm

HEART RATE CALCULATION

Method I

•For regular rhythm:• Count the number of large boxes between 2 R waves and that number is divided into 300.

• Remember: • .20 sec/large box = 5 large boxes/sec.• 60 sec/min x 5 = 300 large boxes/min.

What is the rate?

Rate: 300 / 4 = 75 bpm

Method II• For fast heart rate:

• count the number of small boxes between two R waves and that number is divided into 1500

• Remember: • 5 small boxes/large box• 300 large boxes/min• 300 x 5 = 1500

What is the rate?

Rate: 1500 / 10 = 150 bpm

Method III• For irregular rhythm:

• Count the R waves in 6 sec strip (between 3 hash marks) and multiply it by 10.

• Remember: 5 large boxes / sec

Method IV:• Find the R wave that fall on a large box line. Level the next large box line a rate of 300 – 150 - 100 – 75 – 60 – 50 – 43 – 37 – 33 & 30, until the next R wave.

Step 3 P wave• configuration: round and upright • Location: precedes QRS complex• Duration: .06 -.11 sec. (1.5 – 2.5 small boxes)• Amplitude: up to 2.5mm

• To ask:• Are P wave present?• Do they look the same?• Is there P before every QRS?

Other P wave configurations

Step 4: PR interval• From the start of Atrial depolarization to the beginning of

ventricular depolarization

• Location: beginning of P wave to beginning of Q wave

• Duration: .12 - .20 sec

• Amplitude: not measured

• Configuration: P wave followed by isoelectric line

• To ask?• Are all P-R intervals consistent?

P-R interval (PRI)

Step 5: QRS complex• Ventricular depolarization / atrial repolarization• Location: follows P-R interval• Amplitude: varies with lead• Duration: .04 -.12 (1-3 small boxes)• Configuration: varies with lead

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to ask?Are there QRS? Do they look the same?Do they come after the P wave?Are the R – R intervals equal?

Configuration

T wave• Ventricular repolarization• Location: after S wave• Amplitude: 5 mm or less• Duration: not measured• Configuration:

• Normal: rounded & upright• Inverted• Flat• Peaked

ST segment• End of ventricular depolarization to the beginning of

ventricular repolarization• Location: end of S wave to beginning of T wave• Amplitude: isoelectric• Duration: not measured• Configuration: nearly isoelectric

Configuration • Isoelectric• Elevated (> 1 – 2 mm)

• Sign of acute MI• Depressed (> .5 mm)

• Sign of ischemia

QT interval• Location: beginning of Q wave to end of T wave• Amplitude: not measured• Duration: < ½ the distance of the R-R interval• Configuration: not measured

U wave• Purkinje fiber repolarization• Location: follows T wave or may not be present• Amplitude: not measured• Duration: not measured• Configuration: rounded & upright

ARTIFACTS

• First Rhythm Strip to Identify 31.

ARTIFACTS

Four Common Causes: • Patient Movement • Loose or defective electrodes • Improper grounding • Faulty ECG apparatus

SINUS RHYTHMS

Mechanism: Rhythm originates in the SA node

1.

• ECG characteristics• Rhythm: regular• Rate: normal (60 – 100 bpm)• P wave: normal / 1 per QRS complex• PR interval: normal (.12 - .20 sec)• QRS complex: normal (.04 - .12 sec)• ST segment: not elevated or depressed• T wave: normal

Normal sinus rhythm• Etiology: Normal cardiac function

• Clinical Tip: A normal ECG does not exclude heart disease.

• Mechanism:

• depressed automaticity of the SA node with normal conduction

2.

• ECG characteristics:• all normal• rate - < 60

Sinus BradycardiaEtiology:

• sleeping; young, athletic individuals• Excessive vagal tone (straining, vomiting, intubation)• Sick sinus syndrome, MI • Digoxin toxicity, Sedative• Hyperkalemia• Trauma to conductive system

Clinical signs: low CO low perfusion lethargy, mental status change, anxiety, poor capillary refill, mottled skin, low UO syncope

BradycardiaNursing action: (if symptomatic)• Document rhythm & notify MD • Apply O2 & consider atropine• Prepare for external pacing• If with PVCs – don’t treat with lidocaine (this is the heart’s

attempt to improve perfusion)• Atropine SO4

• 0.5 mg IV (may repeat in 3-5 min)• Maximum dose: 3 mg• Do not give < 0.5 mg may worsen the bradycardia• Do not push slow

Mechanism: • increased automaticity of the SA node with normal conduction

3.

• ECG characteristics: • all normal• Rate: 101 – 160 bpm• P wave: normal or merge to T wave

Sinus tachycardiaEtiology: • a natural response to environmental stimuli – pain, fever, exercise,

emotion, dehydration• Drugs, caffeine, alcohol, Hyperthyroidism, shock, CHF, hypoxia

Clinical signs:• Increased workload of the heart decrease CO low perfusion

angina, SOB, anxiety, hypotension, low UO

Nursing action: if symptomatic• Document rhythm & notify MD• Apply O2• Treat underlying cause• May consider vagal maneuver

• cough, bear down, blow through straw • try blowing plunger off the syringe

Mechanism:

reflux vagal tone inhibition associated with respiration. (rate increases with inspiration & drops with exhalation)

4.

ECG characteristics:• Rhythm: irregular• Others: All normal

Sinus ArrhythmiaEtiology:

• Normal phenomenon with inspiration (esp, in infant)• Digitalis toxicity, MI, increased ICP• Fever, anxiety, shock

Nursing action:• Document rhythm & notify MD if symptomatic• No treatment

• Mechanism:

• Signal to SA node is not generated or it fails to leave the SA node

5.

• Sinus pause / block - Basic rhythm resumes after a pause

• ECG Characteristics:• Rhythm: irreg• Rate: normal or < 60 • Other waves: Normal except during pause or arrest

Sinus arrest – basic rhythm does not resume after a pause

6.

Sinus pause/arrest/block• Etiology:

• High vagal tone or increased vagal stimulation• Drug toxicity (esp. digoxin)• MI, s/p cardiac surgery, SA node trauma• lupus, metabolic disorders

• Clinical signs:• If HR is <50 decreased CO hypotension, changes in mental

status and fatigue

• Nursing Action if symptomatic• Document the rhythm • Apply O2• Consider atropine• Consider pacemaker

ATRIAL DYSRHYTHMIAS

(PAC)Mechanism: (early P) premature beat originate from the Atria • 7.

ECG characteristics:• Rhythm: irreg during the beat• Rate: varies• P wave: different from normal P wave• PRI: varies during the beat• QRS com / ST seg: Normal• T wave: may be distorted during the beat

Premature Atrial Contraction (PAC)• Etiology:

• Stress, stimulants, alcohol, overeating• Electrolyte imbalance, drug toxicity (digoxin)• Pericarditis, MI, ischemia, COPD

• Clinical signs:• >10 PACs = CHF• Palpitations

• Nursing Action:• Document• Treat underlying cause

AF• Mechanism:

• Atrial quiver with ventricular response (> 100 = RVR (rapid) / 60 =100 – CVR (controlled)) blood clots

8.

• ECG Characteristics:• Rhythm: irreg• Rate: Atria: 350-600 / Ventricle: varies• P wave: none ( F wave)• QRS comp: Normal• Others: not measurable

Atrial Fibrillation• Etiology:

• Atrial enlargement due to AV valve disorders• Hpn, CAD, COPD, CHF, MI• Hypoxia, drugs, digitoxicity, tobacco

• Clinical signs:• Irregular pulse, palpitation, anxiety, SOB CHF shock

• Nursing Action:• Document rhythm & inform MD• Apply O2• Possible Synchronize cardioversion• Anticoagulant therapy

• Mechanism:• Extremely rapid atrial rate (saw-tooth configuration)

9.

• ECG characteristics:• Rhythm: irreg / regular• Rate: Atria: 250-350 / ventricle: varies• QRS comp: Normal• Others: not measurable

Atrial Flutter• Etiology:

• Related to underlying heart disease • Hyperthyroidism, alcoholism

• Clinical signs:• decreased CO hypotension, mental status change,

fatigue, CHF, SOB

• Nursing Action if symptomatic:• Document rhythm & notify MD• Apply O2• Vagal maneuver

• If tachycardic – consider synchronize cardioversion

PAT / SVT

• Mechanism: impulse originate above the ventricle, due to rapid rate loss of atrial kick

• 10.

• ECG characteristics:• Rhythm: regular• Rate: 140 – 250 bpm• P wave: hidden in T wave• QRS comp: normal• PRI: not measurable

Paroxysmal Atrial tachycardia (PAT) / Supraventricular tachycardia• Etiology• Heart diseases, emotional stress• Regular atrial rhythm• Digitalis toxicity

• Clinical sign: loss of atrial kick decrease CO decreased perfusion myocardia ischemia

• Nursing Action:• Treat the cause• Valsalva maneuver or carotid massage

JUNCTIONAL DYSRHYTHMIAS

Junctional rhythm / junctional escape rhythm

• Mechanism:• Rhythm originate from AV junctional tissue (maybe an escape rhythm,

enhanced automaticity of the AV node that override the SA node)

11.

• ECG characteristics:• Rate: 40 – 60 bpm• P wave: inverted or none or retrograde • PRI: shortened• QRS comp: normal• Others – normal unless distorted by the P wave

Accelerated junctional rhythm:

12.

• Rate: 61 – 100 bpm

• Nursing action: same as junctional rhytm

Junctional tachycardia

13.

• Rate: 101 – 180 bpm

Junctional rhythm• Etiology:

• SA node failure due to vagal stimulation, IHD, valve surgery, Rheumatic fever, hypoxia, drug toxicity (digitalis, quinidine)

• Usually no symptoms• Low CO due to slower HR and loss of atrial kick syncope,

hypotension & other CNS symptoms

• Nursing Action:• Document rhythm & notify MD• Apply O2• Treat underlying cause• Consider atropine• Consider pacemaker

• Mechanism: conduction defect at the bundle branches• Shows RSR wave or notched QRS complex “rabbit ear”

14.

• ECG characteristics:• QRS comp: >.20 sec.• ST segment: maybe depressed• T wave: maybe inverted• Others: normal

Bundle branch Block (BBB)• Etiology:

• MI, ischemia, chronic conduction disorder

• Clinical sign• None

• Nursing Action:• Document rhythm and notify MD if new onset• Be aware that left BBB causes bizarre ST segment that may mask

signs of acute MI

AV HEART BLOCKSIt is a delay or failure of the impulse across the AV node

• the sinus impulse is conducted normally to the AV node

but there is a delay before being conducted to the ventricles

15.

• ECG characteristics:• All normal except for Prolonged PRI (>.20 sec)

• Etiology:• Drugs – quinidine, digitalis, beta blockers, calcium channel

blockers, procainamide• Acute inferior wall MI, Increase vagal tone, Hyperkalemia

• Tx: none

SECOND DEGREE AV BLOCK Type I – Mobitz I or WenckebachType II – Mobitz II

• 1 or more impulses are unable to travel through the AV junction

16.

• Rate: Depends on rate of underlying rhythm• Rhythm: Irregular• P Waves: Normal (upright and uniform)• PR Interval: Progressively longer until one P wave is blocked

and a QRS is dropped• QRS: Normal (0.06–0.10 sec)

Mobitz I• ♥ Clinical Tip: This rhythm may be caused by medication

such as beta blockers, digoxin, and• calcium channel blockers. Ischemia involving the right

coronary artery is another cause.

Mechanism:

• Damage of the AV junction below the bundle of HIS SA or AV beat cannot depolarize the ventricle

17.

• ECG characteristics:• P wave – 2 or more P wave for every QRS complex• PRI – normal or prolonged• QRS: normal or wide

Mobitz II• Etiology:

• AMI, ischemia, s/p cardiac surgery, CAD, degenerative dis of conductive system

• Drug toxicity

• There is no correlation between the conduction of the atria

& ventricle18.

Complete heart block• Rate: Atrial: 60–100 bpm; ventricular: 40–60 bpm • Rhythm: Usually regular, but atria and ventricles act

independently• P Waves: Normal (upright and uniform); may be

superimposed on QRS complexes or T waves• PR Interval: Varies greatly• QRS: normal

VENTRICULAR RHYTHM

(PVC)• Ectopic beats that originate in• the ventricle abnormal QRS complex.

19.

• ECG characteristics:• Rhythm: regular / becomes irreg with PVC• Rate: within normal• P wave: none associated with PVC• PRI: not measureable• QRS: wide & bizarre• T wave: in opposite direction of the wide QRS

PVCs: bigeminy

20.

PVCs: trigeminy

21.

22.

23.

PVCs: quadrigeminy

24.

PVCs: couplets

25.

Premature Ventricular Contraction (PVC)

• Causes:• Hypokalemia, hypocalcemia• Caffeine, tobacco, alcohol, exercise• Drug toxiciy• MI, CHF, Hypoxia

• Tx; • 1st line – lidocaine followed by procainamide, bretylium

• 6 PVCs/min is pathologic

• QRS complexes in polymorphic VT vary in shape and amplitude.

26.

• ■ The QT interval is normal or long.• Rate: 100–250 bpm• Rhythm: Regular or irregular• P Waves: None or not associated with the QRS• PR Interval: None• QRS: Wide (0.10 sec), bizarre appearance

Ventricular tachycardia (V-tach)• ♥ Clinical Tip: It is important to confirm the presence or

absence of pulses because• polymorphic VT may be perfusing or nonperfusing.

• ♥ Clinical Tip: Consider electrolyte abnormalities as a possible etiology.

idioventricular rhythm / agonal rhythm

27.

• Rate: 20–40 bpm• Rhythm: Regular• P Waves: None• PR Interval: None• QRS: Wide (0.10 sec), bizarre appearance

Accelerated Idioventricular rhythm

28.

• Rate: 41–100 bpm• Rhythm: Regular• P Waves: None• PR Interval: None• QRS: Wide (0.10 sec), bizarre appearance• ♥ Clinical Tip: Idioventricular rhythms appear when supraventricular pacing sites

are• depressed or absent. Diminished cardiac output is expected if the heart rate is

slow.

Torsade de pointes• The QRS reverses polarity and the strip shows a spindle effect.• ■ This rhythm is an unusual variant of polymorphic VT with normal or

long QT intervals.

29.

Rate: 200–250 bpm• Rhythm: Irregular• P Waves: None• PR Interval: None• QRS: Wide (0.10 sec), bizarre appearance

Torsade de pointes• In French the term means “twisting of the points.”• ♥ Clinical Tip: Torsade de pointes may deteriorate to VF

or asystole.• ♥ Clinical Tip: Frequent causes are drugs that prolong

QT interval and electrolyte• abnormalities such as hypomagnesemia.

• Chaotic electrical activity occurs with no ventricular

depolarization or contraction.

30.

• Rate: Indeterminate• Rhythm: Chaotic• P Waves: None• PR Interval: None• QRS: None

♥ Clinical Tip: • There is no pulse or cardiac output. • Rapid intervention is critical. • The longer the delay, the less the chance of conversion.

• ECGs

• Electrical activity in the ventricles is completely absent.

• Rate: None• Rhythm: None• P Waves: None• PR Interval: None• QRS: None• ♥ Clinical Tip: Always confirm asystole by checking the ECG in two

different leads. Also,• search to identify underlying ventricular fibrillation.

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