PQRST complex

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

Calculate ventricular rate

• count # of large boxes between identical points of consecutive QRS complexes

• divide number into 300 = ventricular rate

  • eg. if QRS complexes are 4 boxes apart, then rate = 75 bpm (300/4)

  • if rate is 150, consider atrial flutter

  • in example below, rate is between 60-75 bpm

  • if there are 3-5 boxes separating QRS complexes, then rate is normal (60-100 bpm)

• are they present?

  • II/V1 are best leads to check

  • if different morphology, then ectopic atrial rhythm

  • if abnormal axis, then ectopic atrial rhythm

• LAE criteria

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

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

• RAE criteria

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

  • V1 – may have prominent upward deflection

• should be 120-210

• if prolonged (≥ 5 small boxes), then block present

• if shortened, considered accessory pathway

Width

• if ≥ 120 msec (3 small boxes) → RBBB, LBBB, NIVCD

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

  • see Sgarbossa criteria

Axis

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

• LAD (> -30º - II is mostly negative), consider LAFB

• RAD (> +90º - I is mostly negative), consider RVH, LPFB

Voltage

• should be ≥ 5 mm in limb leads; ≥ 7 mm in precordial leads

• low voltage: COPD, pericardial effusion, obesity

• if severe and dagger like, consider hypertrophic cardiomyopathy

• HCM: S + R (in V3) > 50 mm

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)

RVH criteria

• Tall R wave in V1, R/S ratio > 1 & inverted T

• Other DDx for tall R in V1: post MI, RBBB, WPW

Q waves

• should be 1 small box wide; 25-30% of R-wave height

• 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

• elevation = injury; depression = ischemia

• elevation aVR assoc w/ left main artery disease

• ST elevation with Q waves = possible aneurysm

• diffused ST elevation = pericarditis

• less likely to be ominous if concave up

• T wave inversion: consider ischemia

• U wave: assoc w/ flattened T wave; consider hypokalemia

• II/III/aVF – inferior

• V1/V2 – septal

• V5/V6 – lateral

• V3/V4 – anterior

• I/aVL – high lateral

• rate dependent

• prolonged QT can lead to ventricular dysrhythmias, Torsade de Pointes

  • hypocalcemia, hypomagnesemia

  • mult drugs: antipsychotics, antiemetics, antiarrhythmics

  • usually prolonged if QT interval > half RR interval

• 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

LBBB

• RR' pattern left leads (I/V6)

• wide S in V1

RBBB

• RR' pattern right leads (V1)

• sloping S in V1

LAFP

• leads I/aVL: small R

• leads II/aVF: small Q

• axis: > 110º (RAD)

LPFB

• leads I/aVL: small Q

• leads II/aVF: small R

• axis: < -45º (extreme LAD)

AV Blocks

• 1º: prolonged PR > 200 msec

• 2º: considered if grouped beating present

  • type I (Wenckebach): continually increasing PR interval until dropped QRS; largest increase in 2nd beat; decreasing RR interval

  • type II: normal rhythm until dropped QRS, normal PR & RR interval; ominous sign - may lead to 3º AVB & 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)

• Re-entry: 90% of all arrhythmias

• usually paroxysmal; requires 2 paths with unidirectional block

Atrial fibrillation

• rate: 400-600

• morphology: irregular baseline; irregular V-response

• reaction to vagal tone: ↓ V-rate irregularly

Atrial flutter

• rate: 250-350

• morphology: saw tooth

  • seen best in leads II, III, aVF, V1

  • even division of A-rate

• reaction to vagal tone: ↓ V-rate in regular division

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

PSVT

• rate: 120-250

• morphology: regular, narrow complex tachycardia

  • negative P wave

  • 1:1 AV conduction

• reaction to vagal tone: stops arrhythmia paroxysmally

V-Tach

• rate: 120-250

• morphology: wide complex tachycardia

  • AV dissociation

• reaction to vagal tone: none

V-Fib

• rate: tachy

• morphology: ugly looking; multiple re-entry

• reaction to vagal tone: none

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

Amount of joules required to cardiovert (low to high):

• V-Tach

• PSVT

• A-Flutter

• A-Fib

• V-Fib

Ectopic atrial rhythm

• irregular P-wave morphology

• PR interval normal

Wandering atrial pacemaker (WAP)

• ≥ 3 P-wave morphology

• variable PR interval

Multifocal atrial tachycardia (MAT, MFAT)

• same as wandering atrial pacemaker with rate > 100

• most likely cause – COPD (80%)

Accelerated jxn rhythm

• no P wave

• narrow QRS

• rate > 60

• P wave may be 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

Atrial tachycardia

• atrial rate (P-waves) 120-200

• A-tach w/ block – dig toxic until proven otherwise

• 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

Left Main Coronary Artery Occlusion

• ST elevation in aVR > V1

• ST depression in inferior leads

Wellens’ Syndrome

• usually present when pain free

• biphasic or deep inverted T-waves in leads V2 & V3

• little or no cardiac enzyme elevation

• no pathologic precordial Q waves

• little or no ST-segment elevation

• no loss of precordial R waves

• critical LAD occlusion

• exercise stress test contraindicated

Brugada’s Syndrome

• ST elevation in leads V1-V3 w/ morphology resembling RBBB

• high risk for life-threatening ventricular tachyarrhythmias

• usually seen in mid/late 30s

• needs admission for EPS & poss AICD placement

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 ® Torsade de Pointes

Hypermagnesemia

• peaked T wave

• bradycardia

Hypomagnesemia

• flat T wave

• ST interval depression

• prolonged QT interval > Torsade de Pointes

Pericarditis

• diffused ST elevation over precordium

• PR depression, best seen in V1

• if pericardial effusion ® decreased voltage

• if pericardial effusion ® electrical alternans

COPD

• decreased voltage

• RAD

• RAA

• possible RBBB

Pulmonary embolism

• sinus tachycardia

• S1Q3T3 / S1S2S3

• new RBBB

ICH (SAH)

• prolonged QT interval

• inversed T wave