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# BASIC ECG INTERPRETATION

ECG - is a series of waves and deflections recording the hearts electrical activity from a certain view.

Heart Conduction

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

## Components of the Cardiac Cycle

P wave: (SA node fires)
Atrial depolarization Normal shape:

## 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.

monitoring

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

Remember:

## 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

## Rate: 1500 / 10 = 150 bpm

Method III
For irregular rhythm:

## 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?

## 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

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: < 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

31.

ARTIFACTS

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:

conduction 2.

## ECG characteristics: all normal rate - < 60

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

3.

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

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

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

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

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 BLOCKS
It is a delay or failure of the impulse across 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 Wenckebach Type 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 (0.060.10 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.

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

## 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

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.

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: 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

27.

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

## Accelerated Idioventricular rhythm

28.

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.

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

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.