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ECG - is a series of waves and deflections recording the hearts 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

Resting phase of the

cardiac cycle
upright & round

U wave
Purkenji fiber

Etiology: hypokalemia

Electrode application
White to right Red to ribs Black over the red.


Produces positive deflection Commonly used for routine



Step I: rhythm


Step II:


Normal: 60 100 bpm

Bradycardia: < 60 bpm Tachycardia: > 100 bpm


Method I
For regular rhythm:
Count the number of large boxes between

2 R waves and that number is divided into 300.


.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

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

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


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


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: < 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

First Rhythm Strip to Identify



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


Mechanism: Rhythm originates in the SA node


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



depressed automaticity of the SA node with normal

conduction 2.

ECG characteristics: all normal rate - < 60

Sinus Bradycardia
Etiology: 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

Nursing action: (if symptomatic)
Document rhythm & notify MD
Apply O2 & consider atropine Prepare for external pacing If with PVCs dont treat with lidocaine (this is the hearts

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


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

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


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


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


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)


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

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


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

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

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


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

Mechanism: impulse originate above the ventricle, due to rapid

rate loss of atrial kick


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


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 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)


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:


Rate: 61 100 bpm Nursing action: same as junctional rhytm

Junctional tachycardia

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


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

It 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


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


Type I Mobitz I or Wenckebach Type II Mobitz II

1 or more impulses are unable to travel through the AV


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 (0.060.10 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.

Damage of the AV junction below the bundle of HIS SA or AV

beat cannot depolarize the ventricle


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 & ventricle 18.

Complete heart block

Rate: Atrial: 60100 bpm; ventricular: 4060 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


Ectopic beats that originate in the ventricle abnormal QRS complex.


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


PVCs: trigeminy




PVCs: quadrigeminy


PVCs: couplets


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


The QT interval is normal or long. Rate: 100250 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


Rate: 2040 bpm Rhythm: Regular P Waves: None PR Interval: None QRS: Wide (0.10 sec), bizarre appearance

Accelerated Idioventricular rhythm


Rate: 41100 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: 200250 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.

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.