THE 5 step METHOD

1
EKGs by Wafer
Cardiac Muscle Characteristics 1. Conductivity 2.
Contractility 3. Excitability 4. Automaticity 5.
Refractoriness
EKG is Electrical Representation of Mechanical
Events
First Things First
Electrical Conduction System of the Heart 1. SA
node (rt atrium) beats 60 - 100 2. AV node (rt
atrium base _at_ septum) beats 40 -60 3. Bundle
Branches 4. Perkinje fibers
Leads 1. Similar to taking pictures of the heart
at different angles 2. 12 lead available from
standard EKG (I, II, III, AVR, AVL, AVF, six
precordial leads across the chest V1 - V6 3.
Continuous single lead monitoring usually lead
II. 4. Different leads give views of electrical
activity, thus morphology of tracings vary with
lead. 5. 3 leads attached for standard
monitoring RA, LA, LL (Einthoven Triangle)
EKG Graphic Paper 1. 25 mm/sec speed (can slow
to 50 mm/sec) 2. 1mm square .04 sec 3. 5 mm
squares .20 sec (darker lines) 4. 5 - 5 mm
squares 1 sec 5. 6 second increments marked by
hash marks on top of graphic paper
THE 5 step METHOD 1. Rate 2. Rhythm 3. P - R
interval 4. QRS 5. Take a Guess !
Rate Determination 1. Count R waves in 6 sec
strip X 10 2. Count of 5 mm boxes between R
waves and divide into 300 3. Count small boxes
(1 mm) divide into 1500
Traditional Major Classes of Arrhythmia's 1.
Sinus - impulse originates in SA node, these
rhythms have P waves 2. Junctional - impulse
originates _at_ AV node, P waves backwards or
hidden 3. Ventricular - no idd P waves
Wafers Major Classes of Arrhythmia's 1. Too
Slow 2. Too Fast
2
EKGs by Wafer
2 - Slow
2 - Slow
Normal Sinus Rhythm 1. 60 - 100 2. Regular 3.
lt.20 ms (5 little boxes) 4. lt .12 5. NSR
Sick Sinus Syndrome, Sinus Arrest, Sinus Block
a complex of conditions where there is short or
prolonged failure of the SA node to initiate an
impulse 1. Norm or slow 2. Irreg near pauses 3.
WNL 4. WNL TX Depends on Sx, withhold dig,
atropine
Sinus Brady 1. slow 2. reg 3. lt .20 4. WNL TX
None or Atropine if pt. Symptomatic
1O HB 1. slow 2. reg 3. gt.20 4. WNL TX
none or atropine or hold digoxin
3O- Complete HB (Most serious) 1. Slow 2.
Irreg 3. No relationship of Ps to Rs 4. Usually
wide TX Isuprel, Pacing,
Heart
Junctional Rhythm 1. 40 - 60 2. reg 3. lt.12 or
absent 4. WNL TX none, Tx underlying cause
2OHB Type I 1. slow 2. irreg 3. P-R inter
gradually lengthens till QRS dropped 4. WNL
occas dropped TX may be transient, depends on
SX, Atropine, withhold digoxin,consider pacing
2O HB - Type II (more serious) 1. Slow 2.
Regular P - P, R - R 3. P-R gt.2 4. Norm
consistently dropped 21 ratio, etc. TX
consider cause SX atropine, hold digoxin,
pacing
Blocks
Asystole Loss of all electrical activity
looks like straight or wavy line TX CPR, ACLS
3
EKGs by Wafer
2 - Fast
2 - Fast
Normal Sinus Rhythm 1. 60 - 100 2. Regular 3.
lt.20 ms (5 little boxes) 4. lt .12 5. NSR
Ventricular Tachycardia 1. gt100 2. Appears
reg 3. No P waves 4. Wide and picket
fence TX Determine if pt. has pulse, follow
ACLS protocol
Sinus Tachycardia 1. gt 100 2. reg 3. WNL, but P
may be fused with T wave 4. WNL TX Depends on
cause, possible sedation
PVCs (also consider PACs PJCs) 1. QRS complex
wide bizzare 2. QRS gt .12 3. R wave opposite
from T wave 4. Compensatory pause 5. No idd P
wave 6. associated terms unifocal, multifocal,
bigemy, trigemy, couplet, short run of V-tach TX
depends on frequency pt Sx. Lidocaine or
pronestyl
Atrial Fibrillation 1. WNL or gt100 2. irreg 3.
No distinguishable P waves 4. WNL TX depends on
ventricular reponse pt. Sx. For fast
ventricular response Cardizem, digoxin,
quinidine, cardioversion Must consider risk for
stroke, admin anticoagulant.
Ventricular Fibrillation 1. indistinguishable 2.
irreg 3. No idd P waves 4. No idd QRSs,
appears as a coarse or fine wavy line. TX CPR,
ACLS protocol
Junctional Tachycardia 1. 70 - 150 2. reg 3. lt
.12 or absent 4. WNL TX Dig or cardioversion
Atrial
Flutter 1. WNL or Slow 2. reg 3. sawtooth P
waves 4. WNL Ratio of Ps to QRSs reported (21
or 31, etc.) TX Depends on ventricular
response and pt. Sx.
4

• Pearls
• The EKG can be completely normal in AMI
• Larger ST elevations more leads involved
  more extensive damage

Time is Muscle
The 3 Is of Coronary Events

• Ischemia
• mismatch between blood/O2 supply O2 demand
• Time lt 20 minutes
• ECG changes ST seg depression T wave Changes
  (ie. inverted or peaked)
• angina pain that resolves with reduction of O2
  demand (rest or reduced heart rate from beta
  blockers) or increasing O2 delivery (vasodilation
  w/NTG or O2 application).

• Injury
• total artery occlusion that result in damage to
  myocardium with altered function
• Onset time 20 - 40 minutes
• ECG changes ST segment elevation
• classic AMI pain (substernal, crushing,
  unrelieved by rest, radiates to neck, arm jaw)
• Salvage can occur if blood flow restore thru
  rapid reperfusion. (TPA PTCA)

• 
  Infarction
• cell death
• Onset time gt 1 - 2 hours (minutes - hours after
  cell death)
• ECG changes Abnormal Q waves (gt 0.4 sec wide
  gt 25 gt height than R wave)
• Q waves dead tissue thus EKGs must be compared
  to previous EKGs