Check name & date – make sure you’re reading the correct ECG

 

Calculate ventricular rate

  • count number of large boxes between consecutive QRS complexes
  • divide number into 300
  • if rate is 150, consider atrial flutter

 

# of boxes

1

2

3

4

5

6

7

8

Rate

300

150

100

75

60

50

43

37

 

P-waves

  • are they present?  II/V1 are best leads to check
  • are they regular?  If different morphology ® ectopic atrial rhythm
  • check axis; if abnormal ® ectopic atrial rhythm
  • LAE criteria

Ø      V1 – pronounced negative deflection ≥ 1 box (1°criteria)

Ø      II, III, aVF – broad ≥ 3 boxes, or notched (P-mitrale)

  • RAE criteria

Ø      II, III, aVF – tall, peaked ≥ 2.5 boxes (P-pulmonale)

Ø      V1 – may have prominent upward deflection

 

PR interval

  • should be 120-210
  • if prolonged (≥ 5 small boxes) ® block present

 

QRS complex

  • Width

Ø      if ≥ 120 msec (3 small boxes) ® RBBB, LBBB, NIVCD

Ø      if LBBB, then can’t call AMI unless new

·        Axis

Ø      normal if I & II both upright: -30º to +90º

Ø      LAD (> -30º - II is mostly negative) ® r/o LAFB

Ø      RAD (> +90º - I is mostly negative) ® r/o RVH, LPFB

·        Voltage

Ø      Should be ≥ 5 mm in limb leads; ≥ 7 mm in precordial leads

Ø      Low voltage ® COPD, pericardial effusion, obesity

Ø      LVH criteria

      • S (in V1 or V2) + R (in V5 or V6) > 35 mm
      • S + R (in any precordial leads) > 45 mm
      • R (in I or aVL) > 10 mm
      • LVH w/ pressure overload ® often has ST + T D’s (strain pattern)

Ø      RVH criteria

      • Tall R wave in V1, R/S ratio > 1 & inverted T
      • Other DDx for tall R in V1: post MI, RBBB, WPW

Ø      HOCM: S + R (in V3) > 50

·        Q waves: should be 1 small box wide; 25-30% or R-wave height

Ø      V5/V6 often have small Q waves (septal Qs)

·        R wave progression: R should be greater than S by V4; if not, consider anterior MI

 

I

aVR

V1

V4

 

II/III/aVF – inferior

 

II

aVL

V2

V5

 

V1/V2 – septal

V5/V6 – lateral

III

aVF

V3

V6

 

V3/V4 – anterior

I/aVL – high lateral

 

ST segment

·        elevation ® injury; depression ® ischemia

·        ST elevation with Q waves ® possible aneurysm

·        Diffused ST elevation ® pericarditis

·        Less likely to be ominous if concave up

                       

Less ominous

More ominous

 

T wave

  • inversion ® consider ischemia
  • peaked ® consider hyperkalemia

 

U wave

  • assoc w/ flattened T wave ® consider hypokalemia

 

 

BLOCKS

 

Consider bundle block if QRS > 120 msec

Intrinsicoid deflection time: time from onset of QRS to peak of complex ® greater on side of block

 

If not either, consider NIVCD

 

 

If RAD or extreme LAD, consider LPFB/LAFB

 

 

LPFB

LAFB

I/aVL

Small R

Small Q

II/aVF

Small Q

Small R

Axis

> 110º (RAD)

< -45º (X-LAD)

 

AV Blocks

  • 1º: prolonged PR > 200 msec
  • 2º: considered if grouped beating present

Ø      type I (Wenckebach): continually increasing PR interval until dropped QRS

o       largest increase in 2nd beat ® decreasing RR interval

Ø      type II: normal rhythm until dropped QRS, normal PR & RR interval

o       ominous sign ® may lead to 3º block & require pacing

  • 3º: complete AV dissociation

 

SA Blocks

·        consider if every P followed by QRS, but P has grouped beating

·        2º: if PP interval constant, then probably type II, otherwise type I (Wenckebach)

 

 

ARRHYTHMIAS

 

Re-entry arrhythmias (90%) – usually paroxysmal; requires 2 paths with unidirectional block

 

Rate

Name

Morphology

Reaction to vagal tone

400-600

A-fib

Irregular baseline

Irregular V-response

↓ V-rate irregular

250-350

280-320

A-flutter

Saw tooth – seen best in leads II, III, aVF, V1

Even division of A-rate

↓ V-rate in regular division

* V-rate of 150 is A-flutter until proven otherwise

120-250

PSVT

Negative P wave

1:1 AV conduction

Regular canon A waves

Stop arrhythmia paroxysmally

120-250

VT

Wide complex tachycardia

AV dissociation

Irregular canon A waves

none

 

VF

Ugly looking

Multiple re-entry

None

 

Amount of joules required to cardiovert (low to high): VT, PSVT, A-flutter, A-fib, VF

 

WPW: accessory pathway → delta waves, decreased PR interval

May disappear with exercise

Can’t call LVH due to high delta waves

May appear as pseudo-infarct or ischemia in other leads

Will go into VF through accessory pathway if A-fib develops

Presence of accessory pathway may lead to re-entry arrhythmia

May look like PSVT if block is in accessory pathway

May look like VT if block is in AV node → really PSVT with aberrant conduction

\NEVER GIVE AV-BLOCKER TO WIDE COMPLEX TACHYCARDIA

(Adenosine OK – short half-life)

 

Ectopic arrhythmias (10%)

 

Name

Morphology

Ectopic atrial rhythm

Irregular P-wave morphology

PR interval normal

 

Wandering atrial pacemaker

≥ 3 P-wave morphology

variable PR interval

Accelerated jxn rhythm

Rate > 60

P wave may be absent or inverted with PR interval < 120

Consider digoxin toxicity

Junctional tachycardia

Same as accel jxn rhythm with rate > 100

Suspect if “atrial fibrillation” is regular

Likely digoxin toxicity

MAT (MFAT)

Same as wandering atrial pacemaker with rate > 100

Most likely cause – COPD (80%)

 

Atrial tachycardia

Atrial rate (P-waves) 120-200

A-tach with block – digoxin toxicity until proven otherwise

 

 

WIDE COMPLEX TACHYCARDIA

 

If unstable → cardiovert

Hypotension

Ischemia – angina, ST depression

Significant CHF

Altered mental status; syncope

Other signs of peripheral hypoperfusion – eg., mottled clammy skin

 

90% is VT; more likely if

  • Structural heart disease
  • LV dysfunction
  • Signs/symptoms of CHF
  • Irregular canon A-waves
  • Wide QRS interval > 140 msecs
  • Positive concordance
  • AV dissociation
  • Absence of RS in precordium

 

Brugada’s Criteria (Circulation 1991;83:1649)

·        Is there an absence of RS complex in all precordial leads?

·        Is interval from R to nadir of S > 100 msec in any precordial lead?

·        Is there AV dissociation?

·        Are there morphology criteria for VT in both V1 & V6?

If yes to any → VT
If no to all → SVT w/ aberrancy

 

SPECIAL CASES

 

Hyperkalemia

Peaked T wave

Wide QRS complex

Flat P wave

Lead into sine wave appearance

 

Hypokalemia

Flat T wave

U wave

 

Hypercalcemia

Shortened QT interval

 

Hypocalcemia

Prolonged QT interval – may lead to Torsade de Pointes

 

Hypermagnesemia

Peaked T wave

Bradycardia

 

Hypomagnesemia

Flat T wave

ST interval depression

Prolonged QT interval – may lead to Torsade de Pointes

 

Pericarditis

Diffused ST interval elevation over precordium

PR depression, best seen in V1

May have decreased voltage if pericardial effusion develops

May have electrical alternans if pericardial effusion develops

 

COPD

Decreased voltage

RAD

RAA

Possible RBBB

 

Pulmonary embolism

Sinus tachycardia

S1Q3T3/S1S2S3

New RBBB

 

ICH (SAH)

Prolonged QT interval

Inversed T wave

 

Quinidine effect

Wide QRS complex

Prolonged QT interval

ST interval depression

Notched P wave

U wave

 

Digoxin effect

Shortened QT interval

Downward curve of ST interval

Flat or inverse T wave

 

Digoxin toxicity

Atrial tachycardia with block

Junctional tachycardia

SA/AV block

Bi/trigeminy

VT/VF

 

TCA OD

Quinidine-like effects

Terminal R wave in aVR