BASIC ECG INTERPRETATION

Marian Williams RN BN CEN CCRN CFRN

CTRN

Marian Williams RN

Heart Anatomy
Layers
Pericardium
Myocardium
Endocardium

Four Chambers
Atria
Left
Right

Ventricles
Left
Right
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Marian Williams RN

Heart Valves
Atrioventricular
Bicuspid
Tricuspid

Semi-lunar
Pulmonic
Aortic

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Marian Williams RN

Major Vessels
Superior Vena Cava
Inferior Vena Cava
Coronary Sinus
Aorta
Pulmonary Vein
Pulmonary Artery

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Heart Blood Flow

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Cardiac Cycle
Atrial Systole
Atrial Kick

Atrial Diastole
Ventricular

Systole
Ventricular

Diastole
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Marian Williams RN

Coronary Arteries
Right Coronary

Artery

Posterior Descending
SA Node (60%)
Right Atrium
Right Marginal
Right Ventricle
AV node (85%-90%)
Proximal portion
Bundle of His
Part of Left Bundle
Branch
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Marian Williams RN

Coronary Arteries
Left Coronary

Artery
Left Anterior

Descending
Anterior Left Ventricle
Right Bundle Branch
Part Lateral Left

Ventricle
Most Interventricular
Septum
Left Bundle Branch
Marian Williams RN

Coronary Arteries
Circumflex
Left Atrium
Lateral Left

Ventricle
InferiorLeft Ventricle
(15%)
Posterior-Left
Ventricle
SA Node (40%)
AV Node (10%-15%)

Marian Williams RN

Cardiac Muscle
Syncytium
Network of cells
Electrical impulses
Atrial
Ventricular

Sarcolemma
Membrane

enclosing cardiac
cell
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Cardiac Muscle
Sarcolemma
Holes in Sarcolemma
T-(transverse)

tubules
Go around muscle
cells
Conduct impulses

Sarcoplasmic

Reticulum
Series of tubules
Stores Calcium
Calcium moved from

sarcoplasm into
sarcoplasmic reticulum
by pumps
Marian Williams RN

Cardiac Muscle
Sarcomeres
Made of thick and

thin filaments
Thin
Troponin

Thick
Myosin

Contraction
Thin/thick

filaments slide over

each other
Marian Williams RN

Cardiac Muscle

Marian Williams RN

ION Concentrations
Extracellular
Sodium and

Chloride
Intracellular
Potassium

and Calcium

Cardiac Muscle
Channels
Openings (pores)

in cell membrane
Sodium Na+
Potassium K+
Calcium Ca++
Magnesium Mg+
+

Marian Williams RN

EFFECTS ON HEART
RATE
1. Baroreceptors

(Pressure)

Internal Carotids
Aortic Arches
Detects changes in

BP

2. Chemoreceptors
Internal Carotids
Aortic Arches
Changes in pH

(Hydrogen Ion,
Oxygen, Carbon
Dioxide)

Marian Williams RN

Autonomic Nervous
System
Parasympathetic
SA Node
Atrial Muscle
AV Node
Vagus Nerve
Acetycholine is

released and binds to

parasympathetic
receptors
Slows SA node rate
Slows AV Conduction
Decreases atrial
contraction strength

Marian Williams RN

Autonomic Nervous
System
Sympathetic
Electrical system
Atrium
Ventricles
Norepinephrine

release
Increased force of

contraction
Increased heart
rate
Increased BP
Marian Williams RN

Autonomic Nervous
System
Sympathetic

Receptor Sites
Alpha Receptors
Constriction of blood
vessels
Skin
Cerebral
Splanchnic
Beta 1 Receptors
Heart
Beta 2 Receptors
Lungs
Skeletal Muscle Blood
Cells

Marian Williams RN

Dopaminergic

Receptors

Coronary arteries
Renal Blood

Vessels
Mesenteric Blood
Vessels
Visceral Blood
Vessels

CARDIAC OUTPUT
Stroke Volume x

Heart Rate = CO (48 L/min)

Stroke Volume
approx. 70 ml/beat
Increased by:
Adrenal medulla
Norepinephrine;
Epinephrine
Pancreas
Insulin; Glucagon
Medications
Calcium; Digitalis;
Dopamine; Dobutamine
Marian Williams RN

CARDIAC OUTPUT
Decrease in Force

of Contraction
Severe hypoxia
Decreased pH
Elevated carbon

dioxide
Medications
Calcium channel
blockers, Beta
Blockers

Marian Williams RN

BLOOD PRESSURE
Definition
Force exerted by

circulating blood on
artery walls
Equals: Cardiac
output xs
peripheral vascular
resistance
CO x PVR

Marian Williams RN

STROKE VOLUME
Stroke Volume

determined by
Preload
Force exerted on

ventricles walls at end

of diastole
Increased volume
means increased
preload

Afterload
Pressure or resistance

against which the

ventricles must pump
to eject blood
Marian Williams RN

Marian Williams RN

STROKE VOLUME
Afterload

influenced by:
Arterial BP
Ability of arteries

to stretch
Arterial resistance

Marian Williams RN

STROKE VOLUME
Frank Starlings

Law
The greater the

volume of blood in
the heart during
diastole, the more
forceful the cardiac
contraction, the
more blood the
ventricle will pump
(to a point)
Marian Williams RN

CARDIAC CELLS
Two Types
Myocardial Cells
Mechanical
Can be electrically
stimulated
Cannot generate
electricity
Pacemaker Cells
Electrical cells
Spontaneously generate
electrical impulses
Conduct electrical
impulses
Marian Williams RN

CARDIAC CELLS
Current
Electrical charge

flow from one point

to another
Voltage
Energy

measurement
between positive
and negative points
Measured in
millivolts
Marian Williams RN

CARDIAC CELLS
Action Potential
Five Phase cycle

reflecting the
difference in
concentration of
electrolytes (Na+,
K+, Ca++, Cl-) which
are charged
particles across a
cell membrane
The imbalance of
these charged
particles make the
cells excitable
Marian Williams RN

Cardiac Cell Action

Potential

Phase 0
Depolarization

Rapid Na+ entry into

cell
Phase 1
Early depolarization
Ca++ slowly enters cell
Phase 2
Plateau-continuation of
repolarization
Slow entry of Sodium
and Calcium into cell

Cardiac Cell Action

Potential
Phase 3
Potassium is moved

out of the cell

Phase 4
Return to resting

membrane
potential

CARDIAC CELLS
At rest
K+ leaks out
Protein & phosphates

are negatively
charged, large and
remain inside cell
Polarized Cell
More negative inside

than outside

Membrane potential is

difference in electrical
charge (voltage)
across cell membrane
Marian Williams RN

CARDIAC CELLS
Current (flow of

energy) of
electrolytes from
one side of the cell
membrane to the
other requires
energy (ATP)
Expressed as volts
Measured as ECG

Marian Williams RN

CARDIAC CELLS
Depolarization
When interior of cell

becomes more
positive than negative
Na+ and Ca+ move
into cell and K+ and
Cl- move out
Electrical impulse
begins (usually) in SA
node through
electrical cells and
spreads through
myocardial cells
Marian Williams RN

CARDIAC CELLS
Repolarization
Inside of cell

restored to
negative charge
Returning to
resting stage
starts from
epicardium to
endocardium

Marian Williams RN

CARDIAC CELLS
Action Potential
Phase 0 rapid
depolarization
Na+ into cell rapidly
Ca++ into cell slowly
K+ slowly leaks out

Phase 1 early

rapid
repolarization
Na+ into cell slows
Cl- enters cell
K+ leaves

Marian Williams RN

Phase 2 Plateau
Ca++ slowly enters

cell
K+ still leaves

Phase 3 Final

rapid
repolarization
K+ out of cell quickly
Na+ & Ca++ stop

entering
VERY SENSITIVE TO
ELECTRICAL
STIMULATION

CARDIAC CELLS
Phase 4 Resting

membrane
potential
Na+ excess outside
K+ excess inside
Ready to discharge

Marian Williams RN

CARDIAC CELLS
Properties
1. Automaticity
1. Cardiac pacemaker
cells create an
electrical impulse
without being
stimulated from
another source
2. Excitability
1. Irritability
2. Ability of cardiac
muscle to respond to
an outside stimulus,
Chemical, Mechanical,
Electrical
Marian Williams RN

CARDIAC CELLS
3.Conductivity
Ability of cardiac

cell to receive an
electrical impulse
and conduct it to an
adjoining cardiac
cell

4.Contractility
Ability of myocardial

cells to shorten in
response to an
impulse
Marian Williams RN

CARDIAC CELLS
Refractory Periods
Period of recovery cell

needs after being

discharged before they
are able to respond to
a stimulus
Absolute
Refractory
Relative
Refractory
Supernormal
ERP Effective

refractory period
Marian Williams RN

CARDIAC CELLS
Absolute refractory
Cell will not respond

to further stimulation
Relative refractory
Vulnerable period
Some cardiac cells

have repolarized and

can be stimulated to
respond to a stronger
than normal stimulus

Marian Williams RN

CARDIAC CELLS
Supernormal

Period
A weaker than

normal stimulus
can cause
cardiac cells to
depolarize
during this
period
Marian Williams RN

CONDUCTION
SYSTEM
Sinoatrial Node

(SA)
Primary pacemaker
Intrinsic rate 60-

100/min
Located in Rt.
Atrium
Supplied by
sympathetic and
para-sympathetic
nerve fibers
Blood from RCA60% of people
Marian Williams RN

CONDUCTION
SYSTEM
Three internodal

pathways
Anterior tract
Bachmanns Bundle
Left atrium
Wenckebachs

Bundle
Thorels Pathway
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CONDUCTION
SYSTEM
Atrioventricular

Junction
Internodal

pathways merge
AV Node
Non-branching
portion of the
Bundle of His

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CONDUCTION
SYSTEM
AV Node
Supplied by RCA

85%-90% of
people
Left circumflex

artery in rest of
people

Delay in

conduction due to
smaller fivers
Marian Williams RN

CONDUCTION
SYSTEM
Bundle of His
Located in upper

portion of
interventricular
septum
Intrinsic rate 4060/min
Blood from LAD
and Posterior
Descending
Less vulnerable to

ischemia
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CONDUCTION
SYSTEM
Right & Left

Bundle Branches
RBB
Right Ventricle

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CONDUCTION
SYSTEM
LBB Left Bundle

Branch
Anterior Fasicle
o Anterior portion
left ventricle
Posterior Fascicle
Posterior

portions
of left ventricle

Septal Fasicle
Mid-spetum

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Marian Williams RN

CONDUCTION
SYSTEM
Spread from

interventricular
septum to
papillary muscles
Continue
downward to
apex of heartapprox 1/3 of way
Fibers then
continuous with
muscle cells of Rt
and Lt ventricles
Marian Williams RN

CONDUCTION
SYSTEM
Purkinje Fibers
Intrinsic

pacemaker rate
20-40/min
Impulse spreads
from
endocardium to
epicardium

Marian Williams RN

ECG
Records electrical

voltage of heart
cells
Orientation of heart
Conduction

disturbances
Electrical effects of
medications and
electrolytes
Cardiac muscle
mass
Ischemia / Infarction

Marian Williams RN

ECG
Leads
Tracing of

electrical activity
between 2
electrodes
Records the
Average current
flow at any
specific time in
any specific
portion of time
Marian Williams RN

ECG
Types of leads
Limb Lead (I, II, III)
Augmented

(magnified) Limb
Leads (aVR, aVL,
aVF)
Chest (Precordial)
Leads
(V1,V2,V3,V4,V5,V6)
Each lead has

Positive electrode
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ECG
Each lead sees

heart as
determined by 2
factors
1. Dominance of

left ventricle
2. Position of
Positive electrode
on body
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Marian Williams RN

ECG
Lead I
Negative

electrode
Right arm

Positive

electrode
Left arm

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ECG
Lead II
Negative

Electrode
Right Arm

Positive

Electrode
Left Leg

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ECG
Lead III
Negative Lead
Left Arm
Positive Lead
Left Leg

Marian Williams RN

ECG PAPER
Graph Paper
Small boxes
1mm wide; 1 mm
high
Horizontal axis
Time in seconds
1 mm box

represents 0.04
seconds
ECG paper speed is
25 mm/second
One large box is 5 (1
mm boxes or 0.04
sec)=.20 seconds
Marian Williams RN

Marian Williams RN

ECG PAPER
Vertical Axis
Voltage or amplitude
Measured in

millivolts
1mm box high is 0.1
mV
1 large box is (5 x
0.1=0.5 mV)
However, in practice
the vertical axis is
described in
millimeters.
Marian Williams RN

ECG PAPER
Waveforms
Movement from

baseline
Positive (upward)
Negative
(downward)
Isoelectric along

baseline
Biphasic - Both
upward and
downward
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Marian Williams RN

ECG
P Wave
First waveform
Impulse begins in

SA Node in Right
Atrium
Downslope of P
wave is stimulation
of left atrium
2.5 mm in height
(max)
O.11 sec. duration
(max)
Positive in Lead II
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Marian Williams RN

Marian Williams RN

Marian Williams RN

Marian Williams RN

Marian Williams RN

ECG
QRS Complex
Electrical impulse

through ventricules
Larger than P wave
due to larger
muscle mass of
ventricles
Follows P wave
Made up of a
Q wave
R wave
S wave

Marian Williams RN

ECG
Q wave
First negative

deflection following
P wave
Represents
depolarization of
the interventricular
septum activated
from left to right

Marian Williams RN

ECG
R wave
First upright

waveform
following the P
wave
Represents
depolarization of
ventricles

Marian Williams RN

ECG
S wave
Negative waveform

following the R
wave
Normal duration of

QRS
0.06 mm 0.10 mm

Not all QRS

Complexes have a
Q, R and S
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Marian Williams RN

Marian Williams RN

Marian Williams RN

Marian Williams RN

ECG
T wave
Represents

ventricular
repolarization
Absolute refractory
period present
during beginning of
T wave
Relative refractory
period at peak
Usually 0.5 mm or
more in height
Slightly rounded
Marian Williams RN

Marian Williams RN

Marian Williams RN

Marian Williams RN

Marian Williams RN

ECG
U wave
Small waveform
Follows T wave
Less than 1.5

mm in amplitude

Marian Williams RN

Marian Williams RN

ECG
J Point
Point where the
QRS complex and
ST-segment meet

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Marian Williams RN

Marian Williams RN

ECG
PR Interval
Measurement

where P wave
leaves baseline to
beginning of QRS
complex
Activation
AV Node
Bundle of His
Bundle Branches
Purkinje Fibers
Atrial repolarization

0.12 - .20 sec.

Marian Williams RN

Marian Williams RN

Marian Williams RN

ECG
QT interval
Begins at

isoelectric line from

end of S wave to
the beginning of
the T wave - 0.44
sec.
Represents total
ventricular activity
Measured from
beginning of QRS
complex to end of T
wave
Marian Williams RN

Marian Williams RN

Marian Williams RN

ECG
Artifact
Distortion of

electrical activity
Noncardiac in
origin
Caused by
Loose electrodes
Broken cables/wires
Muscle tremor
Patient movement
60 cycle

interference
Chest compressions
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Marian Williams RN

Marian Williams RN

Marian Williams RN

ECG
Analysis
Rate
Six Second Method
Two

3 second
markers
Count complexes
and multiply x
10

Marian Williams RN

Marian Williams RN

Marian Williams RN

Marian Williams RN

ECG
Analysis
Regularity
Atrial Rate
Measure

distance
between P waves
Ventricular Rate
Measure distance
between R-R
intervals
0.04 mm off is
considered regular

Marian Williams RN

Marian Williams RN

Marian Williams RN

Marian Williams RN

ECG
Analysis
Measure P wave

length
Measure PR Interval
Measure QRS wave

duration
Measure QT interval

Marian Williams RN

Marian Williams RN

Marian Williams RN

Marian Williams RN

ECG
Analysis
ST segment
Elevated?
Depressed?
T wave
Normal height
Upright?

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Marian Williams RN

Marian Williams RN

ECG
Normal Sinus

Rhythm
Electrical activity

activity starts in SA
node
AV Junction
Bundle Branches
Ventricles
Depolarization of atria

and ventricles

Rate: 60-100

/Regular
PR interval / QRS
duration normal
Marian Williams RN

Marian Williams RN

Marian Williams RN

Marian Williams RN

Marian Williams RN

ECG
Sinus Bradycardia
Sinus Node fires at a rate slower than normal
Conduction occurs through atria, AV junction,

Bundle Branches and Ventricles

Depolarization of atria and ventricles occurs
In adults rate is slower than 60 / minute
Rate is regular
Why?
Athletes;

Vagal Stimulation
Medications Cardiac disease

Treatment: TCP; Atropine 0.5 mg IVP if symptomatic

(maybe); Epinephrine or Dopamine 2-10 mcg/kg/min
infusion
Marian Williams RN

ECG
Sinus Bradycardia
Causes
Hs and Ts
Hypoxia
Toxins
Hypovolemia Tamponade, cardiac
Hydrogen Ion (acidosis)
Tension Pneumothorax
Hypo-Hyperkalemia
Thrombosis (coronary or
pulmonary)
Hypoglycemia

hypovolemia)
Hypothermia

Marian Williams RN

Trauma (Increased ICP;

Marian Williams RN

Marian Williams RN

Marian Williams RN

ECG
Sinus Tachycardia
SA node fires faster than 100-180/minute
Normal pathway of conduction and

depolarization
Regular rate
Why?
Coronary artery disease
Hypoxia
Fever

Treatment:
Treat Cause
Beta-Blockers

Marian Williams RN

Fear; anger; exercise;

Marian Williams RN

Marian Williams RN

Marian Williams RN

ECG
Sinus Arrhythmia
The SA node fires Irregularly / Rate 60-

100/min.
Normal pathway of electrical conduction and
depolarization
PR and QRS durations are normal
Why?
Respiratory- Increases with inspiration; decreases

with expiration
Often in children;
Inferior Wall MI;
ICP;
Medications:
Digoxin; Morphine

Treatment: Often None

Marian Williams RN

Increased

Marian Williams RN

Marian Williams RN

Marian Williams RN

ECG
Sinus Arrest
SA node fails to initiate electrical impulse for

one or more beats

May see no beats on monitor or other
pacemaker cells in the heart may take over
Rate: Variable ;
Rhythm: Irregular
Why?
Hypoxia;

Coronary artery disease; Hyperkalemia

Beta-Blockers; CA channel blockers; Increased
vagal tone

Treatment
Pacemaker;

Marian Williams RN

Atropine; Epinephrine or Dopamine

Marian Williams RN

Marian Williams RN

Marian Williams RN

ECG
Premature Atrial Complexes
An electrical cell within the atria fires before

the SA node fires

Rate: Usually closer to 100;
Irregular
rhythm
P wave usually looks abnormal and complex
occurs before it should
Why?
Emotional stress; CHF; Acute coronary syndromes
Stimulants;
Digitalis Toxicity; etc.

Treatment
Reduce stress; Reduce stimulants; Treat CHF; Beta-

blockers
Marian Williams RN

ECG

Marian Williams RN

ECG

Marian Williams RN

ECG

Marian Williams RN

ECG
Supraventricular Tachycardiac (SVT)
Fast rhythms generated Above the Ventricles
Paroxysmal SVT (starts or ends suddenly)
Rate usually 130-250
Why?
Stimulants; Infection; Electrolyte

Imbalance
MI

Altered atrial pathway (WPW)-Kent

S & S
Lightheadedness;
Palpitations;
SOB; Anxiety;
Weakness
Dizziness;
Chest Discomfort;
Shock
Treatment
Vagal maneuvers;
Adenosine 6 mg fast IVP; Repeat
with 12 mg Adenosine;
Cardioversion
Marian Williams RN

ECG

Marian Williams RN

ECG

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ECG

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ECG

Marian Williams RN

ECG
Atrial Flutter
Irritable focus within the atrium typically fires at a rate

of about 300 bpm

Waveforms resemble teeth of a saw
AV node cannot conduct faster than about 180
beats/minute
Atrial vs ventricular rate expressed as a ratio
Why:
Re-entry- Hypoxia
Pulmonary embolism
MIChronic Lung diseasePneumonia etc.

S & S: SOB; Weakness; Dizziness; Fatigue; Chest

discomfort
Treatment: Ca Channel Blocker; Beta Blockers;
Amiodarone; Cardioversion anticoagulants; Corvert
Marian Williams RN

ECG

Marian Williams RN

ECG

Marian Williams RN

ECG

Marian Williams RN

ECG
Atrial Fibrillation
Irritable sites in atria fire at a rate of 400-

600/minute
Muscles of atria quiver rather than contract
(fibrillate)
No P waves only an undulating line
Only a few electrical impulses get through to the
ventricles may be a lot of impulses or a few
A lot of impulses (ventricular rate high- then
called atrial fibrillation with rapid ventricular
response)
A few impulses (ventricular rate slow then
called atrial fibrillation with slow ventricular
response)
Marian Williams RN

ECG

Marian Williams RN

ECG

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ECG

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ECG

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ECG

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ECG

Marian Williams RN

ECG
AV Block
Delay or interruption in impulse conduction
Classified accordi8ng to degree of block and/or
to site of block
First Degree Block
Impulses from SA node to the ventricles is
DELAYED but not blocked
Why? Ischemia
Medications Hyperkalemia
o Inferior MI

Treatment?
Marian Williams RN

Increased Vagal Tone

Usually None

ECG

Marian Williams RN

ECG

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ECG

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ECG

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ECG
Second Degree Block Type I -

Wenckebach
Lengthening of the PR interval and then QRS wave is

dropped
Why? Usually RCA occlusion (90% of population)
Ischemia
Increase

in parasympathetic tome
Medications

Treatment
If

slow ventricular rate

o Atropine
o Pacing

Marian Williams RN

ECG

Marian Williams RN

ECG

Marian Williams RN

ECG

Marian Williams RN

ECG
Second Degree AV Block Mobitz Type II
Why
Ischemia LCA Anterior MI
Organic heart disease

Important:
Ventricular Rate
QRS duration
How many dropped QRSs in relation to P waves?
What

Treatment
Atropine
Pacing
Marian Williams RN

is the ratio?

ECG

Marian Williams RN

ECG

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ECG

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ECG
Third Degree AV Block (Complete Block)
No P waves are conducted to the ventricles
The atrial pacemakers and ventricle pacemakers
are firing independently
Why?
Inferior MI;
Serious

Anterior MI

Treatment
Atropine 0.5 mg IV
Epinephrine 2-10 mcg/kg or Dopamine 2-10

mcg/kg/min
Pacing
Marian Williams RN

ECG

Marian Williams RN

ECG

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ECG

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ECG

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ECG
Ventricular Rhythms
Are the hearts least efficient pacemakers
Generate impulses at 20-40/min
Assume pacemaking if:
SA nodes fail, very slow (below 20-40) or are

blocked
Ventricles site(s) is irritable
Irritable due to ischemia
Depolarization route is abnormal and longer,
therefore QRS looks different and is wider.
T wave is opposite in direction to QRS

Marian Williams RN

ECG
Premature Ventricular Contractions
May be from One Site and all look the same
Called Unifocal (from one focus or foci)

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ECG
May be from Different sites (Foci) and are

called Multifocal PVCs

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ECG
May occur every other beat Ventricular

Bigeminy

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ECG
May occur every third beat Ventricular

Trigeminy

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ECG
R on T PVC

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ECG

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ECG
Couplets (2 PVCs in a row); Triplets (3

PVCs in a row)

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ECG
Couplets also known as Salvos.

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ECG
Run of PVCs

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ECG
Ventricular Tachycardia
Defined as Three or more PVCs occurring in a row at a
rate > 100/min
Wide QRS
No P waves
No T waves
Why?
Ischemia;

Infarction; Congenital
Usually lethal

S & S: Weakness, Dizziness, Shock, Chest Pain;

Syncope
Treatment: Lidocaine or Amiodarone; Cardioversion
if pulse; Defibrillation if no pulse (see Ventricular
Fibrillation)
Marian Williams RN

ECG

Marian Williams RN

ECG

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ECG

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ECG
Torsades de Pointes (Twisting of the

Points)
Ventricular Tachycardia in which the QRS changes

in shape, amplitude and width

Causes:
Hypomagnesium;

Hypokalemia; Quinidine therapy

S & S:
Altered mental status; shock; Chest pain; SOB;

Hypotension
Treatment:
Magnesium Sulfate 2 Grams diluted in 20 cc D 5W

and given IV

Marian Williams RN

ECG

Marian Williams RN

ECG

Marian Williams RN

ECG
Ventricular Fibrillation
Chaotic rhythm of the ventricles
Lethal if not treated
Causes: MI; Electrolyte Imbalance; Drug ODs;
Trauma
Heart Failure; Vagal Stimulation; Increased SNS
Electrocutions etc.
Treatment: Defibrillation and

CPR; AICD

Defibrillation: 360 Joules (monophasic

defibrillators)
150 Joules (biphasic defibrillators)
Marian Williams RN

ECG

Marian Williams RN

ECG

Marian Williams RN

ECG
CPR 5 cycles (interrupt if defibrillator is there)
Defibrillate
Continue CPR for 5 cycles (2 minutes)
Epinephrine 1 mg of 1:10,000 IVP OR Vasopressin 40

Units IV for 1st or 2nd dose of Epinephrine.

Repeated every 3-5 minutes

CHECK PT/Monitor

CPR
Shock
CPR

Amiodarone 300 mg IV or Lidocaine 1 mg/kg

IV

CHECK PT/Monitor
Consider Magnesium Sulfate (Torsades)
Marian Williams RN

ECG

Marian Williams RN

ECG

Marian Williams RN

ECG
Pulseless Electrical Activity PEA
Rhythm on monitor but no corresponding pulse
Why?
Look for Cause!
Hs and Ts
Hypoxia
Toxins
Hypovolemia Tamponade, cardiac
Hydrogen Ion (acidosis)
Tension
Pneumothorax
Hypo-Hyperkalemia
Thrombosis (coronary or
Hypoglycemia
pulmonary)
Hypothermia
Trauma
(Increased ICP,
hypovolemia)

ECG
Pulseless Electrical Activity PEA
What do we do?
CPR for 5 cycles
Epinephrine 1 mg of 1:10,000 IVP OR may give

Vasopressin 40 Units IV for 1st or 2nd dose of

Epinephrine
Give Epinephrine 1 mg of 1:10,000 IVP every 3-5
minutes
If Rate is below 60/min. on monitor may give Atropine 1
mg IV up to 3 doses
Always give a bolus of Normal Saline (1000 cc)
Continue CPR

Always check rhythm in 2 leads

Check Patient

ECG

Marian Williams RN

ECG
Asystole
No electrical activity on monitor
No pulse
Why?
Look for Cause!
Hs and Ts
Hypoxia
Toxins
Hypovolemia Tamponade, cardiac
Hydrogen Ion (acidosis)
Tension
Pneumothorax
Hypo-Hyperkalemia Thrombosis (coronary or
Hypoglycemia
pulmonary)
Hypothermia
Trauma
(Increased ICP,
hypovolemia)
Marian Williams RN

ECG
What do we do?
CPR for 5 cycles
Epinephrine 1 mg of 1:10,000 IVP OR may give
Vasopressin 40 Units IV for 1st or 2nd dose of
Epinephrine
Give Epinephrine 1 mg of 1:10,000 IVP every 3-5
minutes
If Rate is below 60/min. on monitor may give
Atropine 1 mg IV up to 3 doses
Always give a bolus of Normal Saline (1000 cc)
Continue CPR
Always check rhythm in 2 leads

Check Patient
Marian Williams RN

ECG

Marian Williams RN