electrocardiogram power point, basic ecg interp

ekg

1. Marian Williams RN BN CEN CCRN CFRN
CTRN
BASIC ECG INTERPRETATION
Marian Williams RN

2. Heart Anatomy
Layers
Pericardium
Myocardium
Endocardium
Four Chambers
Atria
Left
Right
Ventricles
Left
Right
Marian Williams RN

3. Marian Williams RN

4. Heart Valves
Atrioventricular
Bicuspid
Tricuspid
Semi-lunar
Pulmonic
Aortic
Marian Williams RN

5. Marian Williams RN

6. Major Vessels
Superior Vena Cava
Inferior Vena Cava
Coronary Sinus
Aorta
Pulmonary Vein
Pulmonary Artery
Marian Williams RN

7. Heart Blood Flow
Marian Williams RN

8. Cardiac Cycle
Atrial Systole
Atrial Kick
Atrial Diastole
Ventricular Systole
Ventricular Diastole
Marian Williams RN

9. Marian Williams RN

12. 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
Marian Williams RN

13. Marian Williams RN

14. 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

15. Coronary Arteries
Circumflex
Left Atrium
Lateral –Left Ventricle
Inferior–Left Ventricle
(15%)
Posterior-Left Ventricle
SA Node (40%)
AV Node (10%-15%)
Marian Williams RN

17. Cardiac Muscle
Syncytium
Network of cells –
Electrical impulses
Atrial
Ventricular
Sarcolemma
Membrane enclosing
cardiac cell
Marian Williams RN

18. 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

19. Cardiac Muscle
Sarcomeres
Made of thick and thin
filaments
Thin
Troponin
Thick
Myosin
Contraction
Thin/thick filaments
slide over each other
Marian Williams RN

20. Cardiac Muscle
Marian Williams RN

21. ION Concentrations
Extracellular
Sodium and
Chloride
Intracellular
Potassium and
Calcium

22. Cardiac Muscle
Channels
Openings (pores) in
cell membrane
Sodium –Na+
Potassium –K+
Calcium –Ca++
Magnesium –Mg++
Marian Williams RN

23. 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

24. Autonomic Nervous
System
Parasympathetic
SA Node
AtrialMuscle
AV Node
VagusNerve
Acetycholineis
released and binds to
parasympathetic
receptors
Slows SA node rate
Slows AV Conduction
Decreases atrial
contraction strength
Marian Williams RN

25. Autonomic Nervous
System
Sympathetic
Electrical system
Atrium
Ventricles
Norepinephrine
release
Increased force of
contraction
Increased heart rate
Increased BP
Marian Williams RN

26. 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
Dopaminergic
Receptors
Coronary arteries
Renal Blood Vessels
Mesenteric Blood
Vessels
Visceral Blood
Vessels
Marian Williams RN

27. CARDIAC OUTPUT
Stroke Volume x
Heart Rate = CO (4-8
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

28. CARDIAC OUTPUT
Decrease in Force of
Contraction
Severe hypoxia
Decreased pH
Elevated carbon
dioxide
Medications –
Calcium channel
blockers, Beta
Blockers
Marian Williams RN

29. BLOOD PRESSURE
Definition
Force exerted by
circulating blood on
artery walls
Equals: Cardiac
output x’s peripheral
vascular resistance
CO x PVR
Marian Williams RN

30. 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

31. Marian Williams RN

32. STROKE VOLUME
Afterload influenced
by:
Arterial BP
Ability of arteries to
stretch
Arterial resistance
Marian Williams RN

33. STROKE VOLUME
Frank Starling’s 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

34. 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

35. 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

36. 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

37. 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

38. Cardiac Cell Action
Potential
Phase 3
Potassium is moved
out of the cell
Phase 4
Return to resting
membrane potential

40. 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

41. 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

42. 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

43. CARDIAC CELLS
Repolarization
Inside of cell
restored to negative
charge
Returning to resting
stage starts from
epicardium to
endocardium
Marian Williams RN

44. 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
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
Marian Williams RN

45. CARDIAC CELLS
Phase 4 –Resting
membrane potential
Na+ excess outside
K+ excess inside
Ready to discharge
Marian Williams RN

46. 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, ElectricalMarian Williams RN

47. 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

48. 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

49. CARDIAC CELLS
Absolute refractory
Cell will not respond
to further stimulation
Relative refractory
Vulnerable period
Some cardiac cells
have repolarized and
canbe stimulated to
respond to a stronger
than normal stimulus
Marian Williams RN

50. CARDIAC CELLS
Supernormal
Period
A weaker than
normal stimulus can
cause cardiac cells
to depolarize during
this period
Marian Williams RN

51. 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 RCA-
60% of people
Marian Williams RN

52. CONDUCTION
SYSTEM
Three internodal
pathways
Anterior tract
Bachmann’s Bundle
Left atrium
Wenckebach’s
Bundle
Thorel’s Pathway
Marian Williams RN

53. CONDUCTION
SYSTEM
Atrioventricular
Junction
Internodal pathways
merge
AV Node
Non-branching
portion of the
Bundle of His
Marian Williams RN

54. 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

55. CONDUCTION
SYSTEM
Bundle of His
Located in upper
portion of
interventricular
septum
Intrinsic rate 40-
60/min
Blood from LAD and
Posterior
Descending
Less vulnerable to
ischemia
Marian Williams RN

56. CONDUCTION
SYSTEM
Right & Left Bundle
Branches
RBB
Right Ventricle
Marian Williams RN

57. CONDUCTION
SYSTEM
LBB –Left Bundle
Branch
Anterior Fasicle
oAnterior portion
left ventricle
Posterior Fascicle
Posterior portions
of left ventricle
Septal Fasicle
Mid-spetum
Marian Williams RN

58. Marian Williams RN

59. CONDUCTION
SYSTEM
Spread from
interventricular
septum to papillary
muscles
Continue downward
to apex of heart-
approx 1/3 of way
Fibers then
continuous with
muscle cells of Rt
and Lt ventricles
Marian Williams RN

60. CONDUCTION
SYSTEM
Purkinje Fibers
Intrinsic pacemaker
rate 20-40/min
Impulse spreads
from endocardium
to epicardium
Marian Williams RN

61. 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

62. 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

63. 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
Marian Williams RN

64. ECG
Each lead ‘sees’ heart
as determined by 2
factors
1. Dominance of left
ventricle
2. Position of Positive
electrode on body
Marian Williams RN

65. Marian Williams RN

66. ECG
Lead I
Negative electrode
Right arm
Positive electrode
Left arm
Marian Williams RN

67. ECG
Lead II
Negative Electrode
Right Arm
Positive Electrode
Left Leg
Marian Williams RN

68. ECG
Lead III
Negative Lead
Left Arm
Positive Lead
Left Leg
Marian Williams RN

69. 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

70. Marian Williams RN

71. 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

72. ECG PAPER
Waveforms
Movement from
baseline
Positive (upward)
Negative
(downward)
Isoelectric –along
baseline
Biphasic -Both
upward and
downward
Marian Williams RN

73. Marian Williams RN

74. 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
Marian Williams RN

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80. 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

81. ECG
Q wave
First negative
deflection following P
wave
Represents
depolarization of the
interventricular
septum activated from
left to right
Marian Williams RN

82. ECG
R wave
First upright
waveform following
the P wave
Represents
depolarization of
ventricles
Marian Williams RN

83. 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
Marian Williams RN

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88. 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 roundedMarian Williams RN

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93. ECG
U wave
Small waveform
Follows T wave
Less than 1.5 mm in
amplitude
Marian Williams RN

94. Marian Williams RN

95. ECG
J Point
Point where the QRS
complex and ST-
segment meet
Marian Williams RN

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98. 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

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101. 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

102. Marian Williams RN

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104. 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
Marian Williams RN

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108. ECG
Analysis
Rate
Six Second Method
Two –3 second
markers
Count complexes
and multiply x 10
Marian Williams RN

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112. ECG
Analysis
Regularity
AtrialRate
Measure distance
between P waves
VentricularRate
Measure distance
between R-R
intervals
0.04 mm ‘off’ is
considered regular
Marian Williams RN

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116. ECG
Analysis
Measure P wave
length
Measure PR Interval
Measure QRS wave
duration
Measure QT interval
Marian Williams RN

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120. ECG
Analysis
ST segment
Elevated?
Depressed?
T wave
Normal height
Upright?
Marian Williams RN

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123. 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

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128. 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
infusionMarian Williams RN

129. ECG
Sinus Bradycardia
Causes
H’s and T’s
Hypoxia Toxins
Hypovolemia Tamponade, cardiac
Hydrogen Ion (acidosis) Tension Pneumothorax
Hypo-Hyperkalemia Thrombosis (coronary or
pulmonary)
Hypoglycemia Trauma (Increased ICP;
hypovolemia)
Hypothermia
Marian Williams RN

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133. ECG
Sinus Tachycardia
SA node fires faster than 100-180/minute
Normal pathway of conduction and
depolarization
Regular rate
Why?
Coronary artery disease Fear; anger;
exercise;
Hypoxia Fever
Treatment:
Treat Cause
Beta-Blockers
Marian Williams RN

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137. 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; Increased ICP;
Medications: Digoxin; Morphine
Treatment: Often None
Marian Williams RN

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141. 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; Atropine; Epinephrine or Dopamine
Marian Williams RN

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145. 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

146. ECG
Marian Williams RN

147. ECG
Marian Williams RN

148. ECG
Marian Williams RN

149. 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

150. ECG

Marian Williams RN

151. ECG

Marian Williams RN

152. ECG

Marian Williams RN

153. ECG

Marian Williams RN

154. 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-HypoxiaPulmonary embolism
MI Chronic Lung diseasePneumonia etc.
S & S: SOB; Weakness; Dizziness; Fatigue; Chest
discomfort
Treatment: Ca Channel Blocker; Beta Blockers;
Amiodarone; Cardioversion –anticoagulants;
Corvert
Marian Williams RN

155. ECG

Marian Williams RN

156. ECG

Marian Williams RN

157. ECG

Marian Williams RN

158. 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)
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159. ECG
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160. ECG
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161. ECG
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162. ECG
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163. ECG
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164. ECG
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165. 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
oInferior MIIncreased Vagal Tone
Treatment?Usually None
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166. ECG
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167. ECG
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168. ECG
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169. ECG
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170. 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
oAtropine
oPacing
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171. ECG
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172. ECG
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173. ECG
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174. ECG
Second Degree AV Block –Mobitz Type II
Why
Ischemia LCA –Anterior MI
Organic heart disease
Important:
Ventricular Rate
QRS duration
How many dropped QRS’s in relation to P waves?
What is the ratio?
Treatment
Atropine
Pacing
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175. ECG
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176. ECG
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177. ECG
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178. 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; Anterior MI
Serious
Treatment
Atropine 0.5 mg IV
Epinephrine 2-10 mcg/kg or Dopamine 2-10 mcg/kg/min
Pacing
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179. ECG
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180. ECG
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181. ECG
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182. ECG
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183. ECG
Ventricular Rhythms
Are the heart’s 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
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184. 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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185. ECG
May be from Different sites (Foci) and are called
Multifocal PVC’s
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186. ECG
May occur every other beat –Ventricular
Bigeminy
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187. ECG
May occur every third beat –Ventricular
Trigeminy
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188. ECG
R on T PVC
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189. ECG
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190. ECG
Couplets(2 PVC’s in a row); Triplets (3 PVC’s in
a row)
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191. ECG
Couplets also known as ‘Salvos’.
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192. ECG
Run of PVC’s
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193. ECG
Ventricular Tachycardia
Defined as Three or more PVC’s 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)
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194. ECG
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195. ECG
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196. ECG
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197. 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
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198. ECG
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199. ECG
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200. ECG
Ventricular Fibrillation
Chaotic rhythm of the ventricles
Lethal if not treated
Causes: MI; Electrolyte Imbalance; Drug OD’s;
Trauma
Heart Failure; Vagal Stimulation; Increased SNS
Electrocutions etc.
Treatment: Defibrillation and CPR; AICD
Defibrillation: 360 Joules (monophasic defibrillators)
150 Joules (biphasic defibrillators)
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201. ECG
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202. ECG
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203. 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 1
st
or 2
nd
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)
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204. ECG
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205. ECG
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206. ECG
Pulseless Electrical Activity –PEA
Rhythm on monitor but no corresponding pulse
Why? Look for Cause!
H’s and T’s
Hypoxia Toxins
Hypovolemia Tamponade, cardiac
Hydrogen Ion (acidosis) Tension
Pneumothorax
Hypo-Hyperkalemia Thrombosis (coronary
or
Hypoglycemia
pulmonary)
Hypothermia Trauma (Increased
ICP,
hypovolemia)

207. 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 1
st
or 2
nd
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

208. ECG
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209. ECG
Asystole
No electrical activity on monitor
No pulse
Why? Look for Cause!
H’s and T’s
Hypoxia Toxins
Hypovolemia Tamponade, cardiac
Hydrogen Ion (acidosis) Tension
Pneumothorax
Hypo-Hyperkalemia Thrombosis (coronary
or
Hypoglycemia
pulmonary)
Hypothermia Trauma (Increased
ICP,
hypovolemia)
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210. 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 1
st
or 2
nd
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
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211. ECG
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