EKG INTERPRETATION
Smitha Raju MSN, RN
Adjunct Professor,
Broward College
Objectives of this 2 day Program
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Review of Cardiac Anatomy and Physiology
Review the Conduction System of the Heart
EKG Rhythm Analysis
Sinus Rhythms
Atrial Arrhythmias
Junctional Arrhythmias
Ventricular Arrhythmias
AV Blocks
Pacemaker Rhythms
Myocardial Infarction
Anatomy and Physiology
60 i00
gatekeeperDelays
to
impulsesfromsa
venticual
contractventricuals
pacemaker
five impulses
myocardio cell
fondract relax
Depolarization
Electrical Conduction
polarization
Electrical Impulses that Originate From:
SA Node: 60-100bpm
AV Node: 40-60bpm
Bundle Branches: 20-40bpm
Ventricular: 20-40bpm
cardiac cycle one
contraction
one relaxation
contra
relax
Electrocardiogram (EKG)
Graphic record of the heart’s electrical activity, its
conduction of impulses; a record of the electrical
events that precede the contractions of the heart
• Normal ECG is composed of the following:
• P wave—represents depolarization of the atria
• QRS complex—represents depolarization of the
ventricles and repolarization of the atria
• T wave—represents repolarization of the ventricles;
may also have a
• U wave that represents repolarization of the purkinji
fibers.
ECG Paper
6sec
strip 30large
boxes
ECG Paper
1 Small Box
5 Small Boxes
15 Boxes of .20
30 Boxes of .20
= .04 sec
= .20 sec
= 3 sec
= 6 sec
ometric I ne
ng p
l
ECG Waveforms
P wave
Represents depolarization of the atria
SA node impulse usually causes a positive deflection
on the ECG paper
Above the
Should be smooth and round
Isometric
line
ECG Waveforms
PR interval
Represents time from beginning of P wave
to beginning of QRS complex
Normal measurement .12-.20 seconds( 3-5boxes)
thetime it takes
For SAnote tothe
AUnode p rinterval
ECG Waveforms
QRS complex
Represent depolarization of the ventricles
Measured in time from the beginning of the ‘Q’ wave
to the end of ’S’ wave
see
Imits- 0.12 secs)
Normal measurement < 0.10seconds (0.8
(2-3 boxes)
QRS > 0.12 sec is called a Bundle Branch Block
ECG Waveforms
T Wave
Represents ventricular repolarization
Absolute Refractory Period
Watch OUT
ECG Waveforms
QT Interval
Starts from the beginning of the ‘Q’ Wave to the end
of the ‘T’ Wave
Represents electrical depolarization and repolarization
of the right and left ventricles
Prolong ‘QT’ will lead to ventricular tachyarrythmias.
Normal measurement 0.36 – 0.44 sec
812518
indicates
point
If
Isometric Line
MI if not
Flatt
ECG Interpretation
3 Methods are Used to Calculate Heart Rate
6 Second Method- Count the number of ‘R’
waves in a 6 second strip (30 large boxes) and
multiply by 10. This method can be used for both
regular and irregular rhythms
Large Boxes Method- Count the number of
large boxes between two consecutive ‘R’ waves and
÷ into 300
Sequence Method- Determine ventricular rate
by selecting an ‘R’ wave that falls on dark vertical
line. Number the next 6 dark lines: 300, 150, 100,
75, 60, 50.
For regular H.R.
For Irregular HR
Sequence Method
Find an R wave that peaks on a heavy black line and assign the numbers
Follow the following steps in
order to identify the Rhythm:
Analyzing
a Rhythm
Strip
• ‘P’ wave must be present: Look at the
shape.
• ‘P’ must be present for each QRS.
• Rhythm Regular? R-R distance must be
constant
• Determine PR interval: Must be 0.12 0.20 sec
• Determine QRS interval: Must be < or
equal to 0.10 sec
• Determine the Heart Rate:
• Atrial Heart Rate: Count # of P waves
and X 10
• Ventricular Rate: Count # of R waves
and X 10
• Normal Heart Rate: 60 – 100 bpm
Sinus Rhythms
Normal Sinus Rhythm
Sinus Arrhythmia
Sinus Bradycardia Heart rate low r hythem normal
Sinus Tachycardia Heart rate high rhythmnormal
Sinus Arrest vythm pause
Practice
P Present : Yes
P Before QRS: Yes
Rhythm Regular: Yes
PR Interval: 4 small boxes = 0.16sec Normal is .12 - .20sec
QRS Interval: 2 small boxes = .08sec Normal is < or = .10sec
Atrial Rate = 8 ‘P’ waves 8X10 = 80
Ventricular Rate = 8 ‘R’ waves 8X10 = 80
Normal HR is 60 – 100bpm
Rhythm is NSR
NSR Rhythm
Sinus Bradycardia Rhythm
Sinus Bradycardia
—- Normal in sleep; aerobically trained athlete
— Causes: Drug abuse, digoxin toxicity, CHF, hypothyroidism,
hypothermia, hypokalemia/hyperkalemia
SYMPTOMS
— Hypotension
— Pale, cool skin
— Weakness
— Angina
— Dizziness or syncope; shortness of breath
— Confusion or disorientation
— Shortness of breath
— Treatment- if symptomatic, atropine or pacer
ppacemaker
Sinus Tachycardia Rhythm
SINUS TACHYCARDIA
• Rate >100: Sinus Tachycardia
50
between
•Causes-Anemia, bleeding, fever,
dehydration, infection, anxiety, hypoxia,
shock, pain, caffeine, drugs
•Treatment-eliminate cause
Sinus Dysrhythmias (Arrhythmia) (SA)
— Rate 60-100
— Irregular rhythm- increases with inspiration, decreases with
expiration
— P, QRS,T wave normal
— Cause- children, drugs (Morphine sulphate), MI
— Treatment- none
Sinus Arrest
•See pauses
•May see ectopic beats (PAC s PVC s)*don t treat
•Due to MI
•Treatment
Atropine
Isoproterenol (Isuprel)
Pacemaker
Isoproterenol-synthetic sympathomimetic amine
Analyzing a Rhythm Strip
DON’T Treat the Monitor Treat the Patient!!!
Assess patient: Symptomatic or Asymptomatic
Is Heart Rate Brady or Tachy?
Assess patient: Stable vs Unstable
Treat Stable Patients with Meds
Treat Unstable Patients with Electricity
*******KNOW YOUR DRUGS!!!!!
OR
Practice
Sinus
sinus
Taihy
sinus
ythias
Sinus
Brady
Atrial Arrhythmias
Premature Atrial Contraction
(PAC)
Supraventricular Tachycardia paroxysmal
(SVT)
atrial tachy
Atrial Flutter
Atrial Fibrillation
Premature Atrial Contraction
PAC
P wave abnormally shaped-contraction originates from ectopic focus in
atrium other than SA Node
PR interval shorter-travels abnormal pathway (distorted P waves)
QRS normal
Cause-age, MI, CHF, stimulants, dig, electrolyte imbalance; valvular
disease; hypoxia
Treatment- remove stimulants; watch for SVT, depends upon cause;
isolated not significant; B-adrenergic blockers
Supraventricular Tachycardia
No p waves
SVT Toomoth impulses
Pat waves
together
SVT/PSVT
PSVT is Paroxysmal Supraventricular Tachycardia
Rate is usually greater than 150bpm
Causes: Alcohol or caffeine use, dig tox,hepatic failure,
Hypokalemia, resp.illness
V fib just give an electric 250 360jew
in emerengy
Treatment
Vagal Maneuvers baredown cough kneeto chest
Meds-Adenosine Iv
6mg
Unstable Patient: Cardioversion reset the rhythm
Shockduring Qrscomplex 20 150jewls
wait 2 mins 12mg
wait 2min 12mg
much
too
Atriffing
Atrial Fibrillation
printed'd
i
8
Pwaves now f waves
Atrial Flutter
more
seriousthan
A
fiberate
high
fraternal
regular
gun
Complication
Atrial Fibrillation stroke PE
Causes of Atrial Fibrillation:
Hypertension
Heart surgery
Viral infections
Stress due to pneumonia
Sleep apnea
Drugs: Stimulants
controlthat
Mt
Lung diseases
Heart Failure
Abnormal Heart Valves
Metabolic Imbalances
Myocardial Infarction
Heart Defects
É
carsonDrip
j
Treatment: Beta Blockers and Calcium Channel Blockers
É Unstable Patient: Cardioversion Anticoagulants bc of clots
Heprin
drip
blood gets
Drwill get
clots
cause
Atrium
May
in
trapped
you a target goal
for the heart rate
TED
Practice
scope to the O
to see if thereis
any clots inthere
A fib
SVT
A
flutter
Supraventricular Rhythm
•
•
•
Junctional Rhythm (40-60bpm)
Accelerated Junctional Rhythm(>60-100bpm
Junctional Tachycardia(>100BPM)
Junctional Rhythm (Supraventricular Rhythm)
Dysrhythmia that originates in area of AV node
— AV node is pacemaker- slow rhythm (40-60) but
regular impulse goes to atria from AV nodebackward); SA node failed to fire or impulse
delayed or blocked at AV node
—P wave patterns
—Absent or hidden; Short < .0.12 or negative or PR
interval; P wave precedes QRS inverted in II, III, and
AVF or P wave hidden in QRS or P wave follows QRS
—QRS normal
.
Junctional Dysrhythmias
Accelerated Junctional
Rhythm
Rate is 60-100
Junctional Tachycardia
Rate is Greater Than 100bpm
Junctional Dysrhythmia
Cause:
— Digitalis/Digoxin toxicity-Digibind
— MI
— Cardiac Surgery(Valve Replacement)
— Treatment
— Treat underlying cause
— Accelerated junctional rhythm and junctional tachycardia caused by
digoxin toxicity; digoxin is held
— b- blockers, calcium channel blockers, and amiodarone for rate control
for junctional tachycardia not caused by digoxin toxicity
— Cardioversion is contraindicated
49
Types of Heart Blocks
First Degree AV Block
Second-Degree AV Block (Mobitz Type I) or
Wenckebach
Second-Degree AV Block (Mobitz Type II)
Third Degree AV Block (Complete)
reflex in the PR inteval
more
than 0.2sec largebox
First Degree AV Block
First Degree AV Block
—Cause-dig toxicity, MI, CAD, vagal stimulation;
hyperthyroidism, beta- adrenergic drugs; calcium channel
blockers
—Usually asymptomatic
—Treatment
—none but watch for further blockage
— Check medications.
— Continue to monitor.
Second-Degree AV Block
(Mobitz Type I) or Wenckebach
Second Degree AV Block
more P s than QRS s
• A. Mobitz I (Wenckebach)
• Cause- MI, drug toxicity
• Treatment- watch for type II and 3rd degree
Second-Degree AV Block
(Mobitz Type II)
Second-Degree AV Block,
Type 2 (Mobitz II)
• Clinical significance
• Often progresses to third-degree AV block ; associated with poor
prognosis
• Reduced HR often results in dec. CO with subsequent hypotension and
myocardial ischemia
Second-Degree AV Block,
Type 2 (Mobitz II)
— Clinical associations
—Rheumatic heart disease
—CAD
—Anterior MI
—Digitalis toxicity
— Treatment
—If symptomatic (e.g., hypotension, angina) before permanent
pacemaker can be inserted, temporary transvenous or
transcutaneous pacemaker
—Permanent pacemaker
Copyright © 2011, 2007 by Mosby,
Inc., an affiliate of Elsevier Inc.
60
Third Degree AV Block
(Complete)
3rd Degree AV Block
• Atria and ventricles beat independently (ventricular rhythm is
escape rhythm
• Atrial rate- 60-100
• Slow ventricular rate 20-40
• No PR interval
• Wide or normal QRS (depends on where block is)
• Cause- severe heart disease, systemic diseases; meds as digoxin,
beta-adrenergic blockers, calcium channels blockers
• Complications- dec. CO, ischemia, HF, shock, bradycardia,
syncope, possible asystole
Third-Degree AV Heart Block
(Complete Heart Block)
• Treatment
• If symptomatic, transcutaneous pacemaker until a temporary
transvenous pacemaker can be inserted
• Drugs (e.g., atropine, epinephrine): Temporary
measure to increase HR and support BP until
temporary pacing is initiated
• Permanent pacemaker as soon as possible
64
PRACTICE QUESTION
PRACTICE QUESTION
SECOND DEGREE AV BLOCK, TYPE I WENCKEBACH
FIRST DEGREE AV BLOCK
Second degree AV Block MOBITZ II
THIRD DEGREE AV BLOCK
SECOND DEGREE AV BLOCK, TYPE I WENCKEBACH
THIRD DEGREE AV BLOCK
Second degree AV Block MOBITZ II
First degree AV Block
Bundle Branch Blocks
• Left BBB
• Right BBB
• QRS.12 or greater
• Rabbit ears- RR - Right bundle branch block
• Devil’s ear-RR- LBB Block
• No change in rhythm
Types of Ventricular Rhythms
most Dangerous
Premature Ventricular Complexes
Ventricular Tachycardia
Torsades de Pointes
Ventricular Fibrillation
Asystole
Pulseless Electrical Activity (PEA)
expat
Premature Ventricular
Complexes (PVCs)
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extrawfoutpwave
Premature Ventricular
Contractions (PVC s)-ectopic
• Cause- 90% with MI, stimulants, dig, electrolyte imbalance
• Treatment- O2, lidocaine, procainamide (Pronestyl),
*amiodarone, *abalation
side
warning
elegygyatences
for
jaded
Definitions
Bigeminy- (PVC) every other complex
Trigeminy-(PVC) every 3rd complex
Couplet- pair of abnormal beats
Treat if:
• >5 PVC s a minute
II
It
if
code
we
Ventricular Tachycardia
• V-tach is caused by a disruption in the normal electrical impulses that
control the ventricular contraction
• Abnormal electrical signals in the ventricles cause the heart to beat
faster than normal
Symptoms
• Palpitation/chest pain
• Syncope/Dizziness
• Weak/no pulse
• Shortness of breath
Ventricular Tachycardia
Ventricular Tachycardia (VT)
• Can be stable- pulse or unstable –no pulse
• Cause- electrolyte imbalance, MI, CAD, dig
• Life- threatening, decreased CO, watch for V-fib
• Symptomatic or Asymptomatic Sustained VT must be
treated! Or It will lead to Ventricular Fibrillation
• Treatment:
•
Stable with a pulse = Meds
•
Unstable with a pulse = Cardioversion
•
Unstable without a pulse = Defibrillate
Remember VT without a pulse is a life-threatening situation.
• Cardiopulmonary resuscitation (CPR) and rapid defibrillation
• Epinephrine if defibrillation is unsuccessful
Polymorphic Ventricular Tachycardia-
Torsades de Pointes
French term that signifies the “twisting of the
points”.
May wax and wane in amplitude and may “flip”
or “twist” on its electrical axes.
Similar to ventricular tachycardia
Caused by hypomagnesemia or by
antiarrhythmic drugs
Alchot intoxicated
r
wing up alot
e
y s
imbalances
Torsades de Pointes
Magni un
Polymorphic Ventricular Tachycardia- Torsades de
Pointes ( twisting around a point )
Causes : hypo/hyperkalemia, HYPOMAGNESEMIA, TCA OD, and some
antidysrhythmic medications.
Treatment – Defibrillation at 200j, Mg 2gm IVP rapidly/drip 3mg/min, antiarrhythmic
drug, pacing
Ventricular Rhythms
Idioventricular Rhythm
When gross damage above the ventricles
The ventricular cells are generating the
impulses
Rate-20- 40
When is very slow is called Agonal Rhythm
Poor Cardiac Output
TX: Transcutaneous Pacing
Epinephrine, Dopamine,
Idioventricular Rhythm
Idioventricular Rhythm
Accelerated Idioventricular Rhythm
V. Fibrillation
tiffin
course
fir
Ventricular Fibrillation
• No P s
• No QRS s
• No CO
• Cause-MI, CAD, CMP, shock, altered K+, hypoxia, acidosis, and
drugs
• Treatment- code situation, ACLS, CPR, **defibrillate *cannot
cardiovert…no rhythm to cardiovert
Pulseless Electrical Activity(PEA)
NO PULSE
Treatment: Find the Cause: Find the H’s & T’s
Hypovolemia
Toxins Tamponade
Hypoxia
Tension Pneumothorax
Hydrogen ion (acidosis)
Thrombosis
Hyper-/hypokalemia
(Coronary or Pulmonary)
Hypothermia.
Asystole
Asystole
• Clinical significance
• Unresponsive, pulseless, and apneic state
• Prognosis for asystole is extremely poor.
• Treatment
• CPR with initiation of ACLS measures (e.g., intubation, transcutaneous
pacing, IV therapy with epinephrine and atropine)
100
Pacemaker Rhythms
Pacemaker Rhythms
Atrial Pacemaker
Spike before P wave
0
before
Spike QRS
Pacemaker Rhythms Ventricular Pacemakercomplex
EI
pwave
before
Spike
a QRS
Pacemaker Rhythms
AV Sequential Pacer
00
Myocardia Infarction (MI)
• An Myocardial Infarction or (MI) can be defined as irreversible myocardial
damage. It is caused by a blockage or narrowing of one or more coronary
arteries.
• Lack of Oxygen to the heart leads to myocardial death.
• 12-Lead EKG is used to identify the area of myocardial damage as well as
heart disease
STDMI (MYOCARDIAL ISCHEMIA)
12 Lead EKG
•A 12-lead electrocardiogram or EKG shows
the representation of the heart's electrical
activity recorded from electrodes on the
body surface.
•Bipolar Limb Leads - (I, II, III)
•Augmented Limb Leads – (aVR, aVL, aVF)
•Chest Leads – (V1 – V6)
White Right Arm
Blaik
Bipolar Leads
Lead I, II & III
e
i n m
Green Right Leg
red
Left leg
Brown Chest
Augmented Leads
AUGMENTED
OR
UNIPOLAR
LEADS, AVR,
AVL,AVF
Chest Leads
CHEST
PRECORDIALS:
V1-V6
Normal 12-Lead EKG
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