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 .

Components of the Cardiac Cycle P wave: (SA node fires) • Atrial depolarization • Normal shape: upright & round . .

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 • .

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 .

• Remember: • . • 60 sec/min x 5 = 300 large boxes/min.20 sec/large box = 5 large boxes/sec.Method I • For regular rhythm: • Count the number of large boxes between 2 R waves and that number is divided into 300. .

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 .

• Remember: 5 large boxes / sec .Method III • For irregular rhythm: • Count the R waves in 6 sec strip (between 3 hash marks) and multiply it by 10.

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

06 -.5mm .5 – 2. (1.5 small boxes) • Amplitude: up to 2.11 sec.Step 3 P wave • configuration: round and upright • Location: precedes QRS complex • Duration: .

• 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 •

• 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 .

5 mm) • Sign of ischemia .Configuration • Isoelectric • Elevated (> 1 – 2 mm) • Sign of acute MI • Depressed (> .

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

Normal sinus rhythm • Etiology: Normal cardiac function • Clinical Tip: A normal ECG does not exclude heart disease. .

< 60 .• Mechanism: • depressed automaticity of the SA node with normal conduction 2. • ECG characteristics: • all normal • rate .

athletic individuals • Excessive vagal tone (straining.Sinus Bradycardia Etiology: • sleeping. vomiting. Sedative • Hyperkalemia • Trauma to conductive system Clinical signs:  low CO  low perfusion  lethargy. poor capillary refill. mental status change. mottled skin. intubation) • Sick sinus syndrome. anxiety. young. MI • Digoxin toxicity. low UO  syncope .

Bradycardia Nursing 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  may worsen the bradycardia • Do not push slow .5 mg IV (may repeat in 3-5 min) • Maximum dose: 3 mg • Do not give < 0.

• ECG characteristics: • all normal • Rate: 101 – 160 bpm • P wave: normal or merge to T wave .Mechanism: • increased automaticity of the SA node with normal conduction 3.

Sinus tachycardia
Etiology: • 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 Arrhythmia
Etiology: • 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.

SA node trauma • lupus.Sinus pause/arrest/block • Etiology: • High vagal tone or increased vagal stimulation • Drug toxicity (esp. changes in mental status and fatigue • Nursing Action if symptomatic • Document the rhythm • Apply O2 • Consider atropine • Consider pacemaker . metabolic disorders • Clinical signs: • If HR is <50  decreased CO  hypotension. digoxin) • MI. s/p cardiac surgery.

ATRIAL DYSRHYTHMIAS .

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

overeating • Electrolyte imbalance. MI.Premature Atrial Contraction (PAC) • Etiology: • Stress. ischemia. COPD • Clinical signs: • >10 PACs = CHF • Palpitations • Nursing Action: • Document • Treat underlying cause . alcohol. drug toxicity (digoxin) • Pericarditis. stimulants.

• ECG Characteristics: • Rhythm: irreg • Rate: Atria: 350-600 / Ventricle: varies • P wave: none ( F wave) • QRS comp: Normal • Others: not measurable .AF • Mechanism: • Atrial quiver with ventricular response (> 100 = RVR (rapid) / 60 =100 – CVR (controlled))  blood clots 8.

CHF. anxiety. drugs. digitoxicity.Atrial Fibrillation • Etiology: • Atrial enlargement due to AV valve disorders • Hpn. CAD. COPD. MI • Hypoxia. tobacco • Clinical signs: • Irregular pulse. palpitation. 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 .

mental status change. SOB • Nursing Action if symptomatic: • Document rhythm & notify MD • Apply O2 • Vagal maneuver • If tachycardic – consider synchronize cardioversion . alcoholism • Clinical signs: •  decreased CO  hypotension. fatigue.Atrial Flutter • Etiology: • Related to underlying heart disease • Hyperthyroidism. CHF.

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 .PAT / SVT • Mechanism: impulse originate above the ventricle.

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 .Paroxysmal Atrial tachycardia (PAT) / Supraventricular tachycardia • Etiology • Heart diseases.

JUNCTIONAL DYSRHYTHMIAS .

• 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 .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.

Accelerated junctional rhythm: 12. • Rate: 61 – 100 bpm • Nursing action: same as junctional rhytm .

Junctional tachycardia 13. • Rate: 101 – 180 bpm .

quinidine) • Usually no symptoms • Low CO due to slower HR and loss of atrial kick  syncope.Junctional rhythm • Etiology: • SA node failure due to vagal stimulation. hypoxia. Rheumatic fever. hypotension & other CNS symptoms • Nursing Action: • Document rhythm & notify MD • Apply O2 • Treat underlying cause • Consider atropine • Consider pacemaker . drug toxicity (digitalis. IHD. valve surgery.

• ECG characteristics: • QRS comp: >.• Mechanism: conduction defect at the bundle branches • Shows RSR wave or notched QRS complex “rabbit ear” 14. • ST segment: maybe depressed • T wave: maybe inverted • Others: normal .20 sec.

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 .Bundle branch Block (BBB) • Etiology: • MI.

AV HEART BLOCKS It is a delay or failure of the impulse across the AV node .

20 sec) .• 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 (>.

• Etiology: • Drugs – quinidine. digitalis. Increase vagal tone. calcium channel blockers. procainamide • Acute inferior wall MI. beta blockers. Hyperkalemia • Tx: none .

SECOND DEGREE AV BLOCK Type I – Mobitz I or Wenckebach Type II – Mobitz II .

• 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) .• 1 or more impulses are unable to travel through the AV junction 16.

and • calcium channel blockers. digoxin. Ischemia involving the right coronary artery is another cause.Mobitz I • ♥ Clinical Tip: This rhythm may be caused by medication such as beta blockers. .

• ECG characteristics: • P wave – 2 or more P wave for every QRS complex • PRI – normal or prolonged • QRS: normal or wide .Mechanism: • Damage of the AV junction below the bundle of HIS  SA or AV beat cannot depolarize the ventricle 17.

CAD. ischemia.Mobitz II • Etiology: • AMI. degenerative dis of conductive system • Drug toxicity . s/p cardiac surgery.

• There is no correlation between the conduction of the atria & ventricle 18. .

Complete heart block • Rate: Atrial: 60–100 bpm. but atria and ventricles act independently • P Waves: Normal (upright and uniform). ventricular: 40–60 bpm • Rhythm: Usually regular. may be superimposed on QRS complexes or T waves • PR Interval: Varies greatly • QRS: normal .

VENTRICULAR RHYTHM .

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

PVCs: bigeminy 20. .

.PVCs: trigeminy 21.

.22.

23. .

.PVCs: quadrigeminy 24.

PVCs: couplets 25. .

tobacco. alcohol. • 1st line – lidocaine followed by procainamide. CHF.Premature Ventricular Contraction (PVC) • Causes: • Hypokalemia. hypocalcemia • Caffeine. Hypoxia • Tx. bretylium • 6 PVCs/min is pathologic . exercise • Drug toxiciy • MI.

• ■ The QT interval is normal or long.• QRS complexes in polymorphic VT vary in shape and amplitude. • 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). 26. 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 .

bizarre appearance ♥ Clinical Tip: Idioventricular rhythms appear when supraventricular pacing sites are • depressed or absent. .10 sec).Accelerated Idioventricular rhythm 28. Diminished cardiac output is expected if the heart rate is slow. • • • • • • Rate: 41–100 bpm Rhythm: Regular P Waves: None PR Interval: None QRS: Wide (0.

10 sec). • ■ This rhythm is an unusual variant of polymorphic VT with normal or long QT intervals.Torsade de pointes • The QRS reverses polarity and the strip shows a spindle effect. Rate: 200–250 bpm • Rhythm: Irregular • P Waves: None • PR Interval: None • QRS: Wide (0. bizarre appearance . 29.

.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.

• Rate: Indeterminate • Rhythm: Chaotic • P Waves: None • PR Interval: None • QRS: None .• Chaotic electrical activity occurs with no ventricular depolarization or contraction. 30.

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

. Also. • search to identify underlying ventricular fibrillation. • • • • • • 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.• Electrical activity in the ventricles is completely absent.

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