ECG Interpretation

and Dysrhythmias
Karen L. O’Brien
MSN, RN
JAN 07
Electrocardiogram (ECG)
 Graphic representation of the heart’s
electrical activity
 Wave forms produced by movement of ions
into and out of the cardiac cell membranes
 Commonly use Lead II and MCL: show P
waves and QRS clearly
Cardiac Cell at REST

(negative)
(positive)

Na+
K+
Cardiac Cell: Depolarization

(positive) (negative)
K+

Na+
Na+
Cardiac Cell: Repolarization

( decrease positive) (negative)

K+

Na+
CL-

Ca++ (slow)
Cardiac Cell: Resting
Membrane

( negative) (positive)
K+Pump

K+
Na+Pump
Cardiac Cells
 Properties:
 Automaticity-create an impulse
 Excitability-cardiac muscle to respond to stimulus
 Conductivity-receive impulse and conduct to
adjoining cells
 Contractility-muscle cells shorten in response to
impulse
 40-60 bpm

60-100 bpm

20-40 bpm

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ECG Paper
 Standard speed 25mm/sec
 Vertical axis is amplitude/voltage
 Horizontal axis is time
 Use squares to determine HR and intervals
between ECG complexes
ECG Waveform
P Waves
 Impulse initiated in SA node, pass thru atria
 Atrial depolarization and contraction
 Characteristics:
 Should be present
 Usually round
 Upright deflection from baseline
 1:1 ratio with QRS complex
P-R Interval
 Beginning of P wave to beginning of QRS
complex
 Time impulse takes to spread thru atria, AV
node, Bundle of His, to the Bundle Branches
 Isoelectric
 Duration: 0.12 - 0.20 seconds
QRS Complex
 Ventricular depolarization and ventricular
contraction
 Duration: 0.06 - 0.10 sec
 3 distinct waves
 Q-wave:
 first downward deflection, below baseline
 Usually small, < 0.04 sec duration
 Wider/deeper than normal indicates pathology-infarct
 May or may not show early, serial ECGs
QRS Complex
 R-wave:
 Upward deflection, above baseline
 Triangular
 S-wave:
 Upward deflection, back toward base line
 R and S: simultaneous depolarization of R and L
ventricles
T Wave
 Ventricular repolarization, recovery
 If stimulated before repolarized completely d/t
ectopic impulse, lethal dysrhythmia can
occur-vulnerable period of cardiac cycle
 Characteristic:
 Round, upright, usually asymmetric
 No > 5mm tall
 Elevated: high K+, MI, or ischemia
S-T Segment
 Time between ventricular depolarization and
the beginning of ventricular repolarization
 From end of QRS complex to beginning of T
wave
 Characteristics:
 Isoelectric (not > 1mm above or below )
 Elevation: acute MI
 Depression: low K+, or ischemia
Q-T Interval
 Time for entire electrical
depolarization/repolarization of ventricles
 Beginning of QRS complex to end of T wave
 Usually 0.36 – 0.44 sec
 Duration varies with age, gender and heart rate
 Medication and electrolyte imbalances can prolong,
lengthens relative refractory period, increased
vulnerability
 QTc: corrected for HR, more accurate
Interpretation of ECG
 Calculate HR
 Count the number of complexes in 6-sec period
then multiply by 10.
 Atrial rate: count P waves
 Ventricular rate: count R waves
 More than 50% of complex in the 6-sec interval,
count as full complex
Interpretation of ECG
 Assess rhythm
 How regular do the complexes occur
 Artial: determine regularity of P waves
 Ventricular: determine regularity of R waves, R-R
intervals
 Examine P waves
 If P waves present and precede each QRS
complex, then the impulse originated in the SA
node
 Sinus rhythm
Interpretation of ECG
 Measure P-R interval
 End of P to beginning of QRS
 Should be 0.12 - 0.20 sec

 Measure QRS duration

 Should be 0.06 - 0.10 sec
Normal Sinus Rhythm-NRS
 Rate: 60-100 bpm
 Rhythm: regular atrial and ventricular
 P wave: before each QRS, 1:1 with each
QRS, round, upright
 P-R interval: 0.12 - 0.20 sec, constant
 QRS complex: 0.06 - 0.10 sec, constant
Ventricular rate/rhythm 60 bpm/regular
Atrial rate/rhythm 60 bpm/regular
PR interval 0.20 sec
QRS duration 0.06 sec
Identification Sinus rhythm
Sinus Tachycardia
 HR = 100-150
 Regular rhythm, P waves, QRS
 Exercise, fever, pain, decreased BP, anxiety,
CHF, hyperthyroid, caffiene, theophylline
 S/S: Decreased BP, dizziness, angina
(increased myocardial O2 consumption)
 TX: IF NEEDED -treat underlying cause, B-
blockers
Ventricular rate/rhythm 130 bpm/regular
Atrial rate/rhythm 130 bpm/regular
PR interval 0.14 to 0.16 sec
QRS duration 0.06 to 0.08 sec
Identification Sinus tachycardia
Sinus Bradycardia
 HR = 40-60 bpm
 Rhythm regular, P wave, QRS
 Normal in athletes, during sleep
 Seen with decreased ventilation, valsalva
maneuver, increased ICP, hypothermia,
hypothyroid, inferior wall MI, hypothyroid
 TX: IF NEEDED -Atropine, pacemaker
Ventricular rate/rhythm 58 bpm/regular
Atrial rate/rhythm 58 bpm/regular
PR interval 0.20 sec
QRS duration 0.08 sec
Identification Sinus bradycardia
Premature Ventricular
Contraction (PVC)
 Originates from ectopic focus in the ventricle
 Premature QRS
 HR regular except for PVC
 No P wave before PVC, no P-R interval
 QRS complex: wide and bizarre
 Name underlying rhythm
 Seen with stimulants (caffeine), ETOH,
aminophylline, epinephrine, digoxin, emotional
stress, decreased K+, fever, hypoxia, post-MI,
exercise
Premature Ventricular
Contraction (PVC)
 TX: lidocaine, procainamide, treat underlying cause
 Frequent may decrease CO, leading to angina and
heart failure
 Bigeminy: every other beat is PVC
 Trigeminy: every third beat is PVC
 Multi-focal: occur from different ectopic foci, different
wide bizarre shapes- need to treat
 Couplets: two in a row- need to treat
 3 or more = V-TACH!!!!
 6 or more, call MD, treat!!!!
Ventricular rate/rhythm 107 bpm (sinus beats)/
Regular except for the events
Atrial rate/rhythm 107 bpm (sinus beats)/
Regular except for the events
PR interval 0.20 sec (sinus beats)
QRS duration 0.08 sec (sinus beats)
Identification Sinus tachycardia with uniform PVCs
Ventricular rate/rhythm 30 bpm (sinus beats)/regular except for events
Atrial rate/rhythm 30 bpm (sinus beats)/regular except for events
PR interval 0.12 to 0.16 sec (sinus beats)
QRS duration 0.06 sec (sinus beats)
Identification Sinus bradycardia with ventricular bigeminy, inverted T
waves, horizontal ST-segments
Ventricular rate/rhythm 125 bpm/essentially regular except for
events
Atrial rate/rhythm 125 bpm/essentially regular except for
events
PR interval 0.12 sec (sinus beats)
QRS duration 0.06 sec (sinus beats)
Identification Sinus tachycardia with multiform PVCs
Ventricular rate/rhythm 94 (sinus beats)/irregular
Atrial rate/rhythm 94 (sinus beats)/irregular
PR interval 0.16 sec (sinus beats)
QRS duration 0.08 sec (sinus beats)
Identification Sinus rhythm with an episode
of couplets and a run of VT
Atrial Fibrillation
 Disorganized atrial activity, ineffective
contractions, “quivering”
 Atrial HR >400 bpm
 Ventricular rate varies:
 Uncontrolled: rate >100 bpm
 Controlled: rate 60-100 bpm
 Slow: rate < 60 bpm
 Ventricular rhythm grossly irregular
Atrial Fibrillation
 Wavy baseline, no visible P waves, no PR interval
 QRS normal
 Seen with heart disease, CHF, CAD, pericarditis,
rheumatic disease, alcoholism, cardiomyopathy,
infection, gastroenteritis, stress, PE, after cardiac
surgery
 Decreased CO, clot formation d/t incomplete
emptying of atria, SOB esp with exertion
 TX: Cardioversion, B-Blockers, digoxin, Calcium
channel blockers, anticoagulation
Ventricular rate/rhythm 79 bpm/regular
Atrial rate/rhythm Unable to determine
PR interval Unable to determine
QRS duration 0.08 sec
Identification Atrial fibrillation (controlled)
Ventricular Tachycardia (VT)
 LIFE-THREATENING!!!!!
 HR = 100-250 bpm
 Rhythm regular
 No P wave seen, no PR interval
 QRS complex wide and bizarre
 3 or more PVCs in a row, ventricle acting as
pacermaker
 Severely compromised CO
 Can deteriorate into Ventricular Fibrillation-a
lethal dysrhythmia!!!
Ventricular Tachycardia (VT)
 Seen with Acute MI, CAD, K+ imbalances,
cardiomyopathy, mitral valve prolapse
 Severe decrease in CO d/t decreased
ventricular filling and lack of atrial contraction
 Can lead to pulmonary edema, decreased
blood flow to brain, shock
 Manifested by: change in LOC, chest pain,
hypotension, SOB
Ventricular Tachycardia (VT)
 Stable VT: left ventricular function-O2, IV
access,procainamide, lidocaine, or amiodarone

 Unstable VT: poor left ventricular function-O2, IV

access, amiodarone, lidociane, followed by
Synchronized Cardioversion

 Pulseless VT: treat like V-Fib, start CPR-

DEFIBRILLATE ASAP!!!
Ventricular rate/rhythm 245 bpm/regular

Atrial rate/rhythm 245 bpm/regular

PR interval None
QRS duration 0.28 sec
Identification Monomorphic ventricular
tachycardia
Ventricular rate/rhythm 250 to 333 bpm/irregular
Atrial rate/rhythm Unable to determine
PR interval Unable to determine
QRS duration 0.16 sec
Identification Polymorphic VT
Ventricular Fibrillation
 LIFE-THREATENING!!!!!
 HR rapid and disorganized
 Multiple firing of ectopic foci
 Ventricle “quivering”
 Rhythm irregular chaotic
 No visible P waves, no P-R interval
 QRS wide, irregular oscillation of baseline
 No true QRS
Ventricular Fibrillation
 Seen with Acute MI, CAD, cardiomyopathy,
ventricular stimulation, electrical shock,
hypoxemia, HYPER-kalemia
 S/S: unconscious, apneic, pulseless
 TX:
 CPR, defibrillation, ACLS protocols
 Pressor agents: Epinephrine, Vasopressin
(increase CO)
 Antiarrhythmics- lidocaine, procainamide,
amiodarone
Ventricular rate/rhythm Unable to determine
Atrial rate/rhythm Unable to determine
PR interval Unable to determine
QRS duration Unable to determine
Identification Ventricular fibrillation (coarse)
Ventricular rate/rhythm Unable to determine
Atrial rate/rhythm None
PR interval None
QRS duration None
Identification Coarse ventricular fibrillation
Asystole
 LETHAL Arrhythmia!!!!
 Complete absence of ventricular electrical
activity, straight line
 No ventricular contraction= NO CO!!!
 Occasional P wave
 Seen with advanced cardiac disease, severe
conduction disturbance, end-stage CHF
 TX: CPR, ACLS, transcutaneous pacing,
intubation, epinephrine, atropine
Ventricular rate/rhythm None
Atrial rate/rhythm None
PR interval None
QRS duration None
Identification Asystole
Defibrillation
 Most effective way to terminate V-Fib
 Send direct current (DC) of electricity thru the
heart to depolarize the myocardial cells,
asynchronized
 Cells then repolarize allowing SA node to
resume role of pacemaker
 Works best if cells are NOT anoxic and/or
acidotic
Defibrillation
 Amount depends on biphasic or monophasic
 High doses of electricity can further damage
myocardium, start with lowest energy
 V-tach without pulse, V-fib
 Paddles placed one to right of sternum below
clavicle, other to left of apex of heart
 Use gel or protective pads-prevent burns
 Call “all clear” before discharging paddles
Cardioversion
 Synchronized shock
 Countershock is programmed
 Delivered during QRS complex
 Avoids vulnerable period of T wave (relative
refractory period)
 Lower energy delivered: 50-150 joules
 Pt can be given sedative
Implantable Cardioverter-
Defibrillator (ICD)
 Pulse generator implanted under the skin of chest
wall with leads placed thru subclavian vein into
endocardium
 HX of cardiac arrest, recurrent Sustained VT, at risk
for SCD
 Able to sense V-tach or V-Fib
 After 25 seconds, delivers 25 joule shock
 If unsuccessful, shock is repeated
 Some have antitachycardia and antibradycardia
capabilites
Antiarrhythmics Drugs
 Dysrhythmias d/t problems of automaticity,
conduction, or both
 Four classes of antiarrhythmics
 Based on how they affect the action potential
 Class I- IV
 Class I: membrane stabilizing
 Class II: depress depolarization
 Class III: prolong repolarization
 Class IV: depress depolarization and prolong repolarization
Class I: Sodium Channel
Blockers- 1A

 Membrane stabilizing
 Work on Sodium fast channels
 Block sodium channels, delay repolarization,
increase length of action potential
 Examples: procainamide, quinidine
 Uses: A-fib, PVCs, V-tach
Class IB
 Block sodium channels
 Accelerate repolarization, decrease length of
action potential
 Decrease ectopic foci stimulation in ventricles
 Examples: lidocaine
 Uses: Ventricular dysrhythmias only -
PVCs, V-tach, V-fib
 IV only, CNS toxicity
Class IC
 Stronger effect on blocking sodium channels
 Little effect on repolarization and action
potential
 Effects ventricular conduction, eliminate or
reduce ectopic foci in ventricles
 Examples: flecainide
 Uses: severe ventricular dysrhythmias (may
use in a-fib)
 Reserved for most severe
Class II: Beta Blockers

 Reduce SNS stimulation to heart

 Reduce transmission of impulses in the conduction
system, esp. SA node
 Reduces ectopic foci in atria, reduce ventricular rate,
decreases CO and BP
 Examples: atenolol, esmolol, metoprolol,
propranolol
 Uses: myocardial depressant for supraventricular
and ventricular dysrhythmias
Class III: Potassium Channel
Blockers
 Increase length of action potential, prolonging
repolarization
 Block alpha and beta adrenergic stimulation
 Examples: amiodarone, sotalol
 Uses: life-threatening V-tach or V-fib, also A-
fib resistant to other drugs
 Pulmonary toxicity: pneumonia-like,
pulmonary fibrosis
Class IV: Calcium Channel
Blockers
 Increase length of action potential, prolonging
repolarization
 Reduce AV node conduction, rapid ventricular
conduction with A-fib
 Calcium channel blockers
 Examples: diltiazem, verapamil
 Uses: supraventricular tachycardia, A-fib