Transcript ECG Interpretation - American Heart Classes

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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Heart Valves
 Atrioventricular
 Bicuspid
 Tricuspid
 Semi-lunar
 Pulmonic
 Aortic
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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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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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Coronary Arteries
 Left Coronary Artery
 Left Anterior
Descending
 Anterior – Left Ventricle
 Right Bundle Branch
 Part – Lateral Left Ventricle
 Most Interventricular Septum
 Left Bundle Branch
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Coronary Arteries
 Circumflex
 Left Atrium
 Lateral – Left Ventricle
 Inferior–Left Ventricle (15%)
 Posterior-Left Ventricle
 SA Node (40%)
 AV Node (10%-15%)
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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
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Cardiac Muscle
 Sarcomeres
 Made of thick and thin
filaments
 Thin
 Troponin
 Thick
 Myosin
 Contraction
 Thin/thick filaments slide
over each other
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Cardiac Muscle
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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++
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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)
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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





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Autonomic Nervous System
 Sympathetic
 Electrical system
 Atrium
 Ventricles
 Norepinephrine
release
 Increased force of
contraction
 Increased heart rate
 Increased BP
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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
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 Dopaminergic
Receptors


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
Coronary arteries
Renal Blood Vessels
Mesenteric Blood Vessels
Visceral Blood Vessels
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
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CARDIAC OUTPUT
 Decrease in Force of
Contraction
 Severe hypoxia
 Decreased pH
 Elevated carbon dioxide
 Medications – Calcium
channel blockers, Beta
Blockers
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BLOOD PRESSURE
 Definition
 Force exerted by
circulating blood on artery
walls
 Equals: Cardiac output x’s
peripheral vascular
resistance
 CO x PVR
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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
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STROKE VOLUME
 Afterload influenced by:
 Arterial BP
 Ability of arteries to
stretch
 Arterial resistance
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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)
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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
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CARDIAC CELLS
 Current
 Electrical charge flow from
one point to another
 Voltage
 Energy measurement
between positive and
negative points
 Measured in millivolts
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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
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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
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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
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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
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CARDIAC CELLS
 Repolarization
 Inside of cell restored
to negative charge
 Returning to resting
stage starts from
epicardium to
endocardium
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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
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 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
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CARDIAC CELLS
 Properties
Automaticity
1.
1.
Cardiac pacemaker cells
create an electrical impulse
without being stimulated
from another source
Excitability
2.
1.
2.
Irritability
Ability of cardiac muscle to
respond to an outside
stimulus, Chemical,
Mechanical, Electrical
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CARDIAC CELLS
3.Conductivity
 Ability of cardiac cell to
receive an electrical
impulse and conduct it to
an adjoining cardiac cell
4.Contractility

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Ability of myocardial
cells to shorten in
response to an impulse
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
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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
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CARDIAC CELLS
 Supernormal Period
 A weaker than normal
stimulus can cause
cardiac cells to
depolarize during this
period
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CONDUCTION SYSTEM
 Sinoatrial Node (SA)
 Primary pacemaker
 Intrinsic rate 60-
100/min
 Located in Rt. Atrium
 Supplied by
sympathetic and parasympathetic nerve
fibers
 Blood from RCA-60%
of people
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CONDUCTION SYSTEM
 Three internodal
pathways
 Anterior tract
 Bachmann’s Bundle
 Left atrium
 Wenckebach’s Bundle
 Thorel’s 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
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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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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
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CONDUCTION SYSTEM
 Purkinje Fibers
 Intrinsic pacemaker
rate 20-40/min
 Impulse spreads from
endocardium to
epicardium
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ECG
 Records electrical
voltage of heart cells
 Orientation of heart
 Conduction
disturbances
 Electrical effects of
medications and
electrolytes
 Cardiac muscle mass
 Ischemia / Infarction
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ECG
 Leads
 Tracing of electrical
activity between 2
electrodes
 Records the Average
current flow at any
specific time in any
specific portion of
time
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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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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
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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
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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.
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ECG PAPER
 Waveforms
 Movement from
baseline
 Positive (upward)
 Negative (downward)
 Isoelectric –along
baseline
 Biphasic - Both
upward and
downward
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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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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
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ECG
 Q wave
 First negative deflection
following P wave
 Represents depolarization
of the interventricular
septum activated from left
to right
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ECG
 R wave
 First upright waveform
following the P wave
 Represents
depolarization of
ventricles
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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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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
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ECG
 U wave
 Small waveform
 Follows T wave
 Less than 1.5 mm in
amplitude
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ECG
 J Point
 Point where the QRS
complex and ST-segment
meet
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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.
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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
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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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ECG
 Analysis
 Rate
 Six Second Method
 Two – 3 second
markers
 Count complexes and
multiply x 10
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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
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ECG
 Analysis
 Measure P wave length
 Measure PR Interval
 Measure QRS wave
duration
 Measure QT interval
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ECG
 Analysis
 ST segment
 Elevated?
 Depressed?
 T wave
 Normal height
 Upright?
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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
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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;
 Medications
Vagal Stimulation
Cardiac disease
 Treatment: TCP; Atropine 0.5 mg IVP if symptomatic (maybe);
Epinephrine or Dopamine 2-10 mcg/kg/min infusion
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ECG
 Sinus Bradycardia
 Causes
 H’s and T’s
 Hypoxia
 Hypovolemia
 Hydrogen Ion (acidosis)
 Hypo-Hyperkalemia
 Hypoglycemia
 Hypothermia
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Toxins
Tamponade, cardiac
Tension Pneumothorax
Thrombosis (coronary or
pulmonary)
Trauma (Increased ICP; hypovolemia)
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ECG
 Sinus Tachycardia
 SA node fires faster than 100-180/minute
 Normal pathway of conduction and depolarization
 Regular rate
 Why?
 Coronary artery disease
 Hypoxia
 Treatment:
 Treat Cause
 Beta-Blockers
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Fear; anger; exercise;
Fever
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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
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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;
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Atropine; Epinephrine or Dopamine
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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
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ECG
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ECG
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ECG
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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
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ECG
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ECG
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ECG
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ECG
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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
MI
Chronic Lung disease
Pneumonia etc.
 S & S: SOB; Weakness; Dizziness; Fatigue; Chest discomfort
 Treatment: Ca Channel Blocker; Beta Blockers; Amiodarone;
Cardioversion – anticoagulants; Corvert
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ECG
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ECG
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ECG
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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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ECG
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ECG
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ECG
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ECG
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ECG
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ECG
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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?
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Increased Vagal Tone
Usually None
ECG
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ECG
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Marian Williams RN
ECG
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Marian Williams RN
ECG
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Marian Williams RN
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)
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Ischemia
Increase in parasympathetic tome
Medications
 Treatment
 If slow ventricular rate
o Atropine
o Pacing
Marian Williams RN
ECG
Marian Williams RN
ECG
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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 QRS’s in relation to P waves?
 What is the ratio?
 Treatment
 Atropine
 Pacing
Marian Williams RN
ECG
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Marian Williams RN
ECG
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Marian Williams RN
ECG
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Marian Williams RN
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
Marian Williams RN
ECG
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Marian Williams RN
ECG
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Marian Williams RN
ECG
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Marian Williams RN
ECG
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Marian Williams RN
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
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Marian Williams RN
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
ECG
 Premature Ventricular Contractions
 May be from One Site and all look the same
 Called Unifocal (from one focus or foci)
Marian Williams RN
ECG
 May be from Different sites (Foci) and are called Multifocal
PVC’s
Marian Williams RN
ECG
 May occur every other beat – Ventricular Bigeminy
Marian Williams RN
ECG
 May occur every third beat – Ventricular Trigeminy
Marian Williams RN
ECG
 R on T PVC
Marian Williams RN
ECG
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Marian Williams RN
ECG
 Couplets (2 PVC’s in a row); Triplets (3 PVC’s in a row)
Marian Williams RN
ECG
 Couplets also known as ‘Salvos’.
Marian Williams RN
ECG
 Run of PVC’s
Marian Williams RN
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)
Marian Williams RN
ECG
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Marian Williams RN
ECG
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Marian Williams RN
ECG
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Marian Williams RN
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 D5W 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 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)
Marian Williams RN
ECG
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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!
 H’s and T’s
 Hypoxia
 Hypovolemia
 Hydrogen Ion (acidosis)
 Hypo-Hyperkalemia
 Hypoglycemia
 Hypothermia
Toxins
Tamponade, cardiac
Tension Pneumothorax
Thrombosis (coronary or
pulmonary)
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
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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
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No electrical activity on monitor
No pulse
Why? Look for Cause!
H’s and T’s
 Hypoxia
 Hypovolemia
 Hydrogen Ion (acidosis)
 Hypo-Hyperkalemia
 Hypoglycemia
 Hypothermia
Marian Williams RN
Toxins
Tamponade, cardiac
Tension Pneumothorax
Thrombosis (coronary or
pulmonary)
Trauma (Increased ICP,
hypovolemia)
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