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EKG Interpretation & Basic
Dysrhythmias
Interpretation & Management
By: Katrina D. Allen RN, MSN, CCRN
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Where Is This Information
Found???
EKG
Workbook…….Ba
sic
Dysrhythmias…In
terpretation and
Management –
Chapters
1-10
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Chapter 1
Anatomy & Physiology of the Heart

Anatomy of the
Heart
 Electrical
Conduction
Systems of the
Heart
 Cardiac Cycle
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Where does my blood all go???
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Atrial & Ventricular Diastole &
Systole
 The
heart performs its pumping
action over and over in a rhythmic
sequence
 See page 4
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Polarization
 Electrical
charges ready for discharge
 K intracellular and Na extracellular
 See page 12 – myocardial cell
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Depolarization
 Discharge
of energy that accompanies
the transfer of electrical charges across
the cell membrane
 Na moves into cell and K moves out of
the cell
 Associated with the MECHANICAL
act of systole
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Repolarization
 Return
of electrical charges to original
state
 Associated with the MECHANICAL
act of diastole
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Conduction System
 SA node
 Intra-atrial
and
internodal
pathways to AV
node
 Bundle of His
 Left and right
bundle branches
 Purkinje fibers
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Inherent Rates (Automaticity)
 SA node = 80 to 100 beats/min
 AV node = 40 to 60 beats/min
 Ventricles (Purkinje fibers) = 15
to 40 beats/min
 Failsafe mechanism to ensure
some cardiac output
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CONDUCTION SYSTEM CELL
PROPERTIES
 CONDUCTIVITY
- ability to transmit
impulses from one cell to another
 EXCITABILITY - capability to respond
to a stimulus
 AUTOMATICITY - capacity to initiate
an impulse
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Properties of Cardiac Cells
 Automaticity
 Excitability
 Conductivity
 Contractility
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Phases of Cardiac Action
Potential
Fig. 36-1
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Nervous System Control of
the Heart
 Autonomic
nervous system
controls:
 Rate of impulse formation
 Speed of conduction
 Strength of contraction
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Parasympathetic Nervous System
 The
following maneuvers and bodily
functions stimulate the
parasympathetic nervous system:
 Pressure on the carotid
 Valsalva maneuver
 Straining to have BM
 Distention of the urinary bladder
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Nervous System Control of
the Heart
 Parasympathetic
nervous system:
Vagus nerve
 Decreases rate
 Slows impulse conduction
 Decreases force of contraction
 Sympathetic
nervous system
 Increases rate
 Increases force of contraction
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Parasympathetic Stimulation
 Decreased heart rate
 Decreased AV conduction
 Decreased irritability
 Mediated through vagus nerve
 See video
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Sympathetic Stimulation
 Increased heart rate
 Increased AV conduction
 Increased irritability
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Chapter 2
The Electrocardiogram
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Graph Paper
 Used
to
standardize
tracings
 Vertical lines =
time
 Horizontal lines
= voltage
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Squares
 Small
 Large
= .04 seconds / 0.1 mv
= .20 seconds / 0.5 mv
 10 large blocks = 2 seconds
 15 large blocks = 3 seconds
 Hash
marks used to designate
seconds at top of paper
 Varies from 1 to 3 second intervals
 Check system using
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Lead Placement
Fig. 36-2
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Lead Placement
Determines Configuration
 Impulses
toward
electrode = positive
deflection on EKG
 Impulses away from
electrode = negative
deflection on EKG
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12-Lead ECG
 12
recording leads
 Six leads measure electrical forces
in the frontal plane (leads I, II, III,
aVR, aVL, and aVF)
 Six leads (V1–V6) measure the
electrical forces in the horizontal
plane (precordial leads)
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Methods
 12-lead EKG
 Bedside
monitoring
 Holter
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12-Lead ECG
Fig. 36-3
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Dysrhythmias
 Abnormal
cardiac rhythms
are termed dysrhythmias
 Prompt assessment of
dysrhythmias and the
patient’s response to the
rhythm is critical
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Bedside Monitoring
 3-lead
versus 5-lead
 Electrode placement
 Choosing
which lead to monitor
 Choose leads to monitor for ischemia
 Newer monitors have the capacity for
monitoring more than one lead
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Monitoring Systems
 Hard
wire
 Cable connected from patient directly to
bedside monitor
 Rhythm viewed on bedside and central
station monitors
 Telemetry
 Cable connected to battery pack
 Signal transmitted to a central station for
viewing
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12-Lead EKG
 Limb
leads (I, II, III, AVR, AVL,
AVF)
 Precordial leads (V1 - V6)
 Additional right precordial leads
 Additional posterior leads
 See video on lead placement
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COMPONENTS OF THE EKG
P
WAVE
 P-R INTERVAL
 QRS
 S-T SEGMENT
 T WAVE
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Waves

P-wave = atrial
depolarization
 normally indicates
firing of the
sinoatrial node

QRS = ventricular
depolarization
 Various
configurations

T wave =
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PR Interval
 Atrial
depolarization/ delay in AV
node
 Beginning of P-wave to beginning of
QRS complex
 .12 to .20 seconds
 Shorter interval = impulse from AV
junction
 Longer interval = 1st degree AV
block
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QRS Duration

Ventricular
depolarization
 0.06 to .10 seconds
 Various
configurations
 Wide: slowed
conduction
 Bundle branch
block (BBB)
 Ventricular rhythm
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Conduction System of Heart
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ST Segment
 Look for depression or elevation
 ST elevation: myocardial injury
 ST depression: reciprocal changes,
digoxin, ischemia
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QT Interval





Beginning of QRS
complex to end of T wave
.32 to .50 seconds
Varies with heart rate
Measures the total time
interval from the onset of
depolarization to the
completion of
repolarization
Prolonged QT interval
may develop into
polymorphic VT
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U wave
 Sometimes seen after T wave
 May indicate hypokalemia
 Hypokalemia impairs myocardial
conduction and prolongs ventricular
repolarization
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Artifact or Problem
 Is
this artifact or is there something
really wrong with this client???
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Determining heart rate

Regular
 Small blocks into
1500
 Large blocks into
300

Irregular = 6second strip
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Determine the Heart Rate
Method 1 – measure the distance in
seconds between the peaks of two
consecutive R waves and divide this
number into 60 to obtain the heart rate
 Method 2 – Count the large squares
between the two peaks of two consecutive
R waves and divide the number by 300
 Method 3 – Count the small squares
between the peaks of two consecutive R
waves and using a rate conversion table
convert the number of small squares into
the heart rate

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Quick EKG Rate Method

Memorize
“300-150-100”
 Then
“75-60-50”
 Possibly
“43-38-33”
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Assessment of Cardiac Rhythm
Fig. 36-5
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Assessment of Cardiac Rhythm
Fig. 36-6
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Assessment of Cardiac Rhythm
Fig. 36-9
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Normal Sinus Rhythm
 Sinus
node fires 60 to 100 bpm
 Follows normal conduction
pattern
Fig. 36-8
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Normal Sinus Rhythm

NSR or SR
 P, QRS, T
 Normal; intervals
 Rate 60 to 100
beats/min
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Normal Sinus Rhythm
 Sinus
node fires 60 to 100 bpm
 Follows normal conduction
pattern
Fig. 36-8
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Sinus Bradycardia

Sinus node fires <60 bpm
 Normal rhythm is aerobically trained
athletes and during sleep
Fig. 36-11 A
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Sinus Bradycardia
 Clinical
associations
 Occurs in response to
 Carotid sinus massage
 Hypothermia
 Increased vagal tone
 Administration of
parasympathomimetic drugs
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Sinus Bradycardia
 Clinical
associations
 Occurs in disease states
Hypothyroidism
 Increased intracranial pressure
 Obstructive jaundice
 Inferior wall MI

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Sinus Bradycardia

Clinical significance
 Dependent on symptoms
 Hypotension
 Pale, cool skin
 Weakness
 Angina
 Dizziness or syncope
 Confusion or disorientation
 Shortness of breath
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Sinus Bradycardia
 Treatment
 Atropine
 Pacemaker may be required
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Sinus Tachycardia

Discharge rate from the sinus node is
increased as a result of vagal inhibition
and is >100 bpm
Fig. 35-11 B
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Sinus Tachycardia
 Clinical
associations
 Associated with physiologic stressors
 Exercise
 Pain
 Hypovolemia
 Myocardial ischemia
 Heart failure (HF)
 Fever
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Sinus Tachycardia
 Clinical
significance
 Dizziness and hypotension due
to decreased CO
 Increased myocardial oxygen
consumption may lead to angina
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Sinus Tachycardia
 Treatment
 Determined by underlying cause
 -Adrenergic blockers to reduce
HR and myocardial oxygen
consumption
 Antipyretics to treat fever
 Analgesics to treat pain
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Premature Atrial Contraction
 Contraction
originating from
ectopic focus in atrium in
location other than SA node
 Travels across atria by abnormal
pathway, creating distorted P
wave
 May be stopped, delayed, or
conducted normally at the AV
node
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Premature Atrial Contraction
Fig. 36-12
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Premature Atrial Contraction
 Clinical
associations
 Can result from
 Emotional stress
 Use of caffeine, tobacco, alcohol
 Hypoxia
 Electrolyte imbalances
 COPD
 Valvular disease
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Premature Atrial Contraction
 Clinical
significance
 Isolated PACs are not significant in
those with healthy hearts
 In persons with heart disease, may
be warning of more serious
dysrhythmia
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Premature Atrial Contraction
 Treatment
 Depends on symptoms
 -Adrenergic blockers may be
used to decrease PACs
 Reduce or eliminate caffeine
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Paroxysmal Supraventricular
Tachycardia (PSVT)
 Originates
in ectopic focus
anywhere above bifurcation of
bundle of His
 Run of repeated premature beats
is initiated and is usually a PAC
 Paroxysmal refers to an abrupt
onset and termination
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Paroxysmal Supraventricular
Tachycardia (PSVT)
 Some
degree of AV block may be
present
 Can occur in presence of WolffParkinson-White (WPW)
syndrome
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Paroxysmal Supraventricular
Tachycardia (PSVT)
Fig. 36-13
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Paroxysmal Supraventricular
Tachycardia (PSVT)
 Clinical
associations
 In a normal heart



Overexertion
Emotional stress
Stimulants
 Digitalis toxicity
 Rheumatic heart disease
 CAD
 Cor pulmonale
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Supraventricular Tachycardia
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Paroxysmal Supraventricular
Tachycardia (PSVT)
 Clinical
significance
 Prolonged episode and HR >180
bpm may precipitate ↓ CO
 Palpitations
 Hypotension
 Dyspnea
 Angina
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Paroxysmal Supraventricular
Tachycardia (PSVT)
 Treatment
 Vagal maneuvers: Valsalva, coughing
 IV adenosine
 If vagal maneuvers and/or drug
therapy is ineffective and/or patient
becomes hemodynamically unstable,
DC cardioversion should be used
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Paroxysmal Supraventricular
Tachycardia (PSVT)
 Treatment
 If PSVT recurs in patients with
WPW, they may ultimately be
treated with radiofrequency
catheter ablation of the accessory
pathway
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Atrial Flutter
 Atrial
tachydysrhythmia
identified by recurring, regular,
sawtooth-shaped flutter waves
 Originates from a single ectopic
focus
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Atrial Flutter
Fig. 36-14A
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Atrial Flutter
 Ectopic
foci in atria
 Classic “sawtooth” pattern
 Atrial rate fast and regular (250 to 350
beats/min)
 Ventricular rate slower
 Degree of conduction varies
may be 1:3, 1:4
 May need drugs or cardioversion
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Atrial Flutter
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Wolff-Parkinson-White Syndrome

Wolff-Parkinson-White (WPW) syndrome is
associated with a triad of ECG findings
 Short PR interval
 Wide QRS
 Delta wave
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Wolff-Parkinson-White Syndrome
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Wolff-Parkinson-White
Syndrome
 Is the patient stable or unstable?

Is the patient experiencing serious signs and
symptoms due to the tachycardia?

Is the patient’s cardiac function normal or impaired?

Attempt to identify the patient’s cardiac rhythm using
12-lead ECG, clinical information

Is Wolff-Parkinson-White syndrome (WPW) present?
 Young patient – Family History!
 HR > 300
 ECG: short PR interval, wide QRS, delta wave)
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Atrial Flutter
 Clinical
associations
 Usually occurs with








CAD
Hypertension
Mitral valve disorders
Pulmonary embolus
Chronic lung disease
Cardiomyopathy
Hyperthyroidism
Drugs: Digoxin, quinidine, epinephrine
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Atrial Flutter
 Clinical
significance
 High ventricular rates (>100) and
loss of the atrial “kick” can decrease
CO and precipitate HF, angina
 Risk for stroke due to risk of
thrombus formation in the atria
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Atrial Flutter
 Treatment
 Primary goal is to slow ventricular
response by increasing AV block

Drugs to slow HR: Calcium channel
blockers, -adrenergic blockers

Electrical cardioversion may be used
to convert the atrial flutter to sinus
rhythm emergently and electively
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Atrial Flutter
 Treatment
 Primary goal is to slow ventricular
response by increasing AV block
Antidysrhythmia drugs to convert
atrial flutter to sinus rhythm or to
maintain sinus rhythm (e.g.,
amiodarone, propafenone)
 Radiofrequency catheter ablation can
be curative therapy for atrial flutter

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Atrial Fibrillation
 Total
disorganization of atrial
electrical activity due to multiple
ectopic foci resulting in loss of
effective atrial contraction
 Most common dysrhythmia
 Prevalence increases with age
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Atrial Fibrillation
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Atrial Fibrillation
Fig. 36-14B
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Atrial Fibrillation
 Clinical
associations
 Usually occurs with
 Underlying heart disease, such as
rheumatic heart disease, CAD
 Cardiomyopathy
 HF
 Pericarditis
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Atrial Fibrillation
 Clinical
associations
 Often acutely caused by
 Thyrotoxicosis
 Alcohol intoxication
 Caffeine use
 Electrolyte disturbance
 Cardiac surgery
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Atrial Fibrillation
 Clinical
significance
 Can result in decrease in CO due to
ineffective atrial contractions (loss
of atrial kick) and rapid ventricular
response
 Thrombi may form in the atria as a
result of blood stasis
 Embolus may develop and travel to
the brain, causing a stroke
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Atrial Fibrillation
 Treatment
 Goals
 Decrease ventricular response
 Prevent embolic stroke
 Drugs for rate control: digoxin, adrenergic blockers, calcium
channel blockers
 Long-tern anticoagulation:
Coumadin
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Atrial Fibrillation
 Treatment
 For some patients, conversion to
sinus rhythm may be considered
 Antidysrhythmic drugs used for
conversion: Amiodarone,
propafenone
 DC cardioversion may be used to
convert atrial fibrillation to
normal sinus rhythm
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Atrial Fibrillation
 Treatment
 If patient has been in atrial
fibrillation for >48 hours,
anticoagulation therapy with
warfarin is recommended for
3 to 4 weeks before cardioversion
and for 4 to 6 weeks after
successful cardioversion
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Atrial Fibrillation
 Treatment
 Radiofrequency catheter ablation
 Maze procedure
 Modifications to the Maze
procedure
 Use of cold (cryoablation)
 Use of heat (high-intensity
ultrasound)
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Junctional Dysrhythmias
 Dysrhythmia
that originates in
area of AV node
 SA node has failed to fire or
impulse has been blocked at the
AV node
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Junctional Dysrhythmias
Fig. 36-15
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Junctional Dysrhythmias
 Clinical
associations
 CAD
 HF
 Cardiomyopathy
 Electrolyte imbalances
 Inferior MI
 Rheumatic heart disease
 Drugs: Digoxin, amphetamines,
caffeine, nicotine
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Junctional Dysrhythmia
 Clinical
significance
 Serves as safety mechanism
when SA node has not been
effective
 Escape rhythms should not be
suppressed
 If rhythms are rapid, may result
in reduction of CO and HF
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Junctional Dysrhythmias

Treatment
 If symptomatic, atropine
 Accelerated junctional rhythm and
junctional tachycardia caused by
digoxin toxicity, digoxin is held
 -Adrenergic blockers, calcium channel
blockers, and amiodarone used for rate
control for junctional tachycardia not
caused by digoxin toxicity
 DC cardioversion is contraindicated
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AV Blocks

CONSIDER
 Slowing of impulse
 Coronary artery
in the conduction
disease
system
 Myocardial
 May cause
infarction (e.g.,
bradycardia
inferior wall)
 Always assess for
 Infections
decreased cardiac
 Enhanced vagal
output and treat the
tone
cause
 Drug effects (e.g.,
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First-Degree AV Block
 Every
impulse is conducted to the
ventricles, but duration of AV
conduction is prolonged
Fig. 36-16A
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First Degree Block

Delayed conduction
from sinus node to
AV node
 Prolonged (> .20
seconds) PR
interval
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Sinus Bradycardia with
1st-degree AV Block
Long P-R Interval
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First-Degree AV Block
 Clinical
associations
 Usually occurs with






MI
CAD
Rheumatic fever
Hyperthyroidism
Vagal stimulation
Drugs: Digoxin, -adrenergic blockers,
calcium channel blockers, flecainide
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First-Degree AV Block
 Clinical
significance
 Usually asymptomatic
 May be a precursor to higher
degrees of AV block
 Treatment
 Check medications
 Continue to monitor
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Second-Degree AV Block,
Type 1 (Mobitz I, Wenckebach)

Gradual lengthening of the PR
interval, due to prolonged AV
conduction time
 Atrial impulse is nonconducted
and a QRS complex is blocked
(missing)
 Usually block occurs at AV node,
but can occur in His-Purkinje
system
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Second-Degree AV Block,
Type 1 (Mobitz I, Wenckebach)
Fig. 36-16B
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Second-Degree AV Block,
Type 1 (Mobitz I, Wenckebach)
 Clinical
associations
 Drugs: digoxin, -adrenergic
blockers
 May be associated with CAD and
other diseases that can slow AV
conduction
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Second-Degree AV Block,
Type 1 (Mobitz I, Wenckebach)
 Clinical
significance
 Usually a result of myocardial
ischemia or infarction
 Almost always transient and well
tolerated
 May be a warning signal of a more
serious AV conduction disturbance
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Second-Degree AV Block,
Type 1 (Mobitz I, Wenckebach)
 Treatment
 If symptomatic, atropine or a
temporary pacemaker
 If asymptomatic, monitor with a
transcutaneous pacemaker on
standby
 Symptomatic bradycardia is more
likely with one or more of the
following: hypotension, HF, shock
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Second-Degree AV Block,
Type 2 (Mobitz II)
P
wave is nonconducted
without progressive antecedent
PR lengthening
 Usually occurs when a block in
one of the bundle branches is
present
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Second-Degree AV Block,
Type 2 (Mobitz II)
Fig. 36-16C
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Second-Degree AV Block,
Type 2 (Mobitz II)
 Clinical
associations
 Rheumatic heart disease
 CAD
 Anterior MI
 Digitalis toxicity
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Second-Degree AV Block,
Type 2 (Mobitz II)
 Clinical
significance
 Often progresses to thirddegree AV block and is
associated with a poor
prognosis
 Reduced HR often results in
decreased CO with subsequent
hypotension and myocardial
ischemia
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Second-Degree AV Block,
Type 2 (Mobitz II)
 Treatment
 If symptomatic (e.g., hypotension,
angina) before permanent
pacemaker can be inserted,
temporary transvenous or
transcutaneous pacemaker
 Permanent pacemaker
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Third-Degree AV Heart Block
(Complete Heart Block)

Form of AV dissociation in which
no impulses from the atria are
conducted to the ventricles
 Atria are stimulated and contract
independently of the ventricles
 Ventricular rhythm is an escape
rhythm
 Ectopic pacemaker may be above
or below the bifurcation of the
bundle of His
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Third-Degree AV Heart Block
(Complete Heart Block)
Fig. 36-16 D
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Third-Degree AV Heart Block
(Complete Heart Block)
 Clinical
associations
 Severe heart disease: CAD, MI,
myocarditis, cardiomyopathy
 Systemic diseases: Amyloidosis,
scleroderma
 Drugs: Digoxin, -adrenergic
blockers, calcium channel blockers
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Third-Degree AV Heart Block
(Complete Heart Block)
 Clinical
significance
 Decreased CO with
subsequent ischemia, HF, and
shock
 Syncope may result from
severe bradycardia or even
periods of asystole
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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
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Premature Ventricular
Contractions
 Contraction
originating in
ectopic focus of the ventricles
 Premature occurrence of a wide
and distorted QRS complex
 Multifocal, unifocal, ventricular
bigeminy, ventricular trigeminy,
couples, triplets, R on T
phenomena
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Premature Ventricular
Contractions
Fig. 36-17
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Premature Ventricular
Contractions

Clinical associations
 Stimulants: Caffeine, alcohol, nicotine,
aminophylline, epinephrine, isoproterenol
 Digoxin
 Electrolyte imbalances
 Hypoxia
 Fever
 Disease states: MI, mitral valve prolapse,
HF, CAD
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Premature Ventricular
Contractions

Clinical significance
 In normal heart, usually benign
 In heart disease, PVCs may decrease CO
and precipitate angina and HF
 Patient’s response to PVCs must be
monitored
 PVCs often do not generate a sufficient
ventricular contraction to result in a
peripheral pulse
 Apical-radial pulse rate should be
assessed to determine if pulse deficit
exists
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Premature Ventricular
Contractions
 Clinical
significance
 Represents ventricular irritability
 May occur
 After lysis of a coronary artery
clot with thrombolytic therapy in
acute MI—reperfusion
dysrhythmias
 Following plaque reduction after
percutaneous coronary
intervention
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Premature Ventricular
Contractions
 Treatment
 Based on cause of PVCs
 Oxygen therapy for hypoxia
 Electrolyte replacement
 Drugs: -Adrenergic blockers,
procainamide, amiodarone,
lidocaine
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Ventricular Tachycardia
 Run
of three or more PVCs
 Monomorphic, polymorphic,
sustained, and nonsustained
 Considered life-threatening
because of decreased CO and the
possibility of deterioration
ventricular fibrillation
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Ventricular Tachycardia
Fig. 36-18A
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Ventricular Tachycardia
Fig. 36-18B
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Ventricular Tachycardia
 Clinical
associations
 MI
 CAD
 Electrolyte imbalances
 Cardiomyopathy
 Mitral valve prolapse
 Long QT syndrome
 Digitalis toxicity
 Central nervous system disorders
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Ventricular Tachycardia
 Clinical
significance
 VT can be stable (patient has a pulse)
or unstable (patient is pulseless)
 Sustained VT: Severe decrease
in CO
–Hypotension
–Pulmonary edema
–Decreased cerebral blood flow
–Cardiopulmonary arrest
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Ventricular Tachycardia
 Clinical
significance
 Treatment for VT must be rapid
 May recur if prophylactic
treatment is not initiated
 Ventricular fibrillation may
develop
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Ventricular Tachycardia

Treatment
 Precipitating causes must be identified
and treated (e.g., hypoxia)
 Monomorphic VT
 Hemodynamically stable
(e.g., + pulse) + preserved LV
function: IV procainamide, sotalol,
amiodarone, or lidocaine
 Hemodynamically unstable or poor
LV function: IV amiodarone or
lidocaine followed by cardioversion
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Ventricular Tachycardia
 Treatment
 Polymorphic VT with a normal
baseline QT interval: Adrenergic blockers, lidocaine,
amiodarone, procainamide, or
sotalol
 Cardioversion is used if drug
therapy is ineffective
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Ventricular Tachycardia

Treatment
 Polymorphic VT with a prolonged
baseline QT interval: IV
magnesium, isoproterenol,
phenytoin, lidocaine, or
antitachycardia pacing


Drugs that prolong the QT interval
should be discontinued
If the rhythm is not converted,
cardioversion may be needed
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Ventricular Tachycardia
 Treatment
 VT without a pulse is a lifethreatening situation
 Cardiopulmonary
resuscitation (CPR) and
rapid defibrillation
–Epinephrine if
defibrillation is
unsuccessful
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Accelerated Idioventricular
Rhythm (AIVR)
 AIVR
can develop when the
intrinsic pacemaker rate
(SA node or AV node) becomes
less than that of a ventricular
ectopic pacemaker
 Rate is between 40 and 100
bpm
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Accelerated Idioventricular
Rhythm (AIVR)
 Clinical
associations
 Acute MI
 Reperfusion of myocardium
after thrombolytic therapy or
angioplasty
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Accelerated Idioventricular
Rhythm (AIVR)
 Clinical
significance
 Can be escape mechanism
 Can be seen with digitalis toxicity
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Accelerated Idioventricular
Rhythm (AIVR)
 Treatment
 In the setting of acute MI, rhythm
is usually self-limiting and well
tolerated
 If patient becomes symptomatic
(e.g., hypotension, angina), atropine
can be considered
Temporary pacing may be required
 Drugs that suppress ventricular
rhythms (e.g., lidocaine) should not
be used

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Ventricular Fibrillation
 Severe
derangement of the
heart rhythm characterized
on ECG by irregular
undulations of varying
contour and amplitude
 No effective contraction or
CO occurs
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Ventricular Fibrillation
Fig. 36-19
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Ventricular Fibrillation

Clinical associations
 Acute MI, CAD, cardiomyopathy
 VF may occur during cardiac pacing
or cardiac catheterization
 VF may occur with coronary
reperfusion after fibrinolytic therapy
 Accidental electrical shock
 Hyperkalemia
 Hypoxia
 Acidosis
 Drug toxicity
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Ventricular Fibrillation
 Clinical
significance
 Unresponsive, pulseless, and
apneic state
 If not treated rapidly, death
will result
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Ventricular Fibrillation
 Treatment
 Immediate initiation of CPR
and advanced cardiac life
support (ACLS) measures with
the use of defibrillation and
definitive drug therapy
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Asystole
 Represents
total absence of
ventricular electrical activity
 No ventricular contraction
(CO) occurs because
depolarization does not occur
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Asystole
 Clinical
associations
 Advanced cardiac disease
 Severe cardiac conduction
system disturbance
 End-stage HF
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Asystole
 Clinical
significance
 Unresponsive, pulseless, and
apneic state
 Prognosis for asystole is
extremely poor
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Asystole
 Treatment
 CPR with initiation of ACLS
measures (e.g., intubation,
transcutaneous pacing, and IV
therapy with epinephrine and
atropine)
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Pulseless Electrical Activity
 Electrical
activity can be
observed on the ECG, but
there is no mechanical activity
of the ventricles and the
patient has no pulse
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Pulseless Electrical Activity
 Clinical
associations
 Drug overdose
 Hypovolemia
 Cardiac
 Hypoxia
tamponade
 Metabolic acidosis MI
 Hyperkalemia or  Tension
pneumothorax
hypokalemia
 Pulmonary
 Hypothermia
embolus
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Pulseless Electrical Activity
 Treatment
 CPR followed by intubation and
IV epinephrine
 Atropine is used if the ventricular
rate is slow
 Treatment is directed toward
correction of the underlying cause
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Sudden Cardiac Death (SCD)
 Death
from a cardiac cause
 Majority of SCDs result from
ventricular dysrhythmias
 Ventricular tachycardia
 Ventricular fibrillation
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Prodysrhythmia
 Clinical
significance
 Antidysrhythmic drugs may
cause life-threatening
dysrhythmias
 Risk increases in presence of
 Severe LV dysfunction
 Digoxin and class IA, IC, and
III antidysrhythmia drugs
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Prodysrhythmia
 Treatment
 First several days of drug
therapy are the vulnerable period
for developing prodysrhythmias
 Many oral antidysrhythmia drug
regimens are initiated in a
monitored hospital setting
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Defibrillation
 Most
effective method of
terminating VF and pulseless
VT
 Passage of DC electrical shock
through the heart to depolarize
the cells of the myocardium to
allow the SA node to resume
the role of pacemaker
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Defibrillation
 Deliver
energy using a
monophasic or biphasic
waveform
 Monophasic defibrillators deliver
energy in one direction
 Biphasic defibrillators deliver
energy in two directions
 Deliver successful shocks at
lower energies and with fewer
postshock ECG abnormalities
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Defibrillation
Fig. 36-20 A and B
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Defibrillation

Output is measured in joules or
watts per second
 Recommended energy for initial
shocks in defibrillation
 Biphasic defibrillators: First and
successive shocks: 150 to 200 joules
 Monophasic defibrillators: Initial
shock at 360 joules

After the initial shock, chest
compressions (CPR) should be
started
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Defibrillation
Fig. 36-21
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Synchronized Cardioversion

Choice of therapy for
hemodynamically unstable
ventricular or supraventricular
tachydysrhythmias
 Synchronized circuit delivers a
countershock on the R wave of
the QRS complex of the ECG
 Synchronizer switch must be
turned
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Implantable CardioverterDefibrillator (ICD)
 Appropriate
for patients who
 Have survived SCD
 Have spontaneous sustained VT
 Have syncope with inducible
ventricular tachycardia/fibrillation
during EPS
 Are at high risk for future lifethreatening dysrhythmias
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Implantable CardioverterDefibrillator (ICD)

Consists of a lead system placed via
subclavian vein to the endocardium
 Battery-powered pulse generator is
implanted subcutaneously
 ICD sensing system monitors the HR
and rhythm and identifies VT or VF
 Approximately 25 seconds after
detecting VT or VF, ICD delivers <25
joules
 If first shock is unsuccessful, ICD
recycles and delivers successive shocks
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Implantable CardioverterDefibrillator (ICD)
 ICDs
are equipped with
antitachycardia and
antibradycardia pacemakers
 Initiates overdrive pacing of
supraventricular and ventricular
tachycardias
 Provides backup pacing for
bradydysrhythmias that may occur
after defibrillation discharges
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Implantable CardioverterDefibrillator (ICD)
Fig. 36-22
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Implantable CardioverterDefibrillator (ICD)

Education is extremely important
 Variety of emotions are possible
 Fear of body image change
 Fear of recurrent dysrhythmias
 Expectation of pain with ICD
discharge
 Anxiety about going home
 Participation in an ICD support
group should be encouraged
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Pacemakers

Used to pace the heart when the normal
conduction pathway is damaged or diseased
 Pacing circuit consists of a power source,
one or more conducting (pacing) leads,
and the myocardium
 Electrical signal (stimulus) travels from
the pacemaker, through the leads, to the
wall of the myocardium
 Myocardium is “captured” and stimulated
to contract
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Pacemakers
Fig. 36-23
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Pacemakers
 Electronic
device used to initiate heart
rhythm
 Temporary versus permanent
 Method of pacing
 Transcutaneous-emergency
 Transvenous
 Epicardial
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Types of Pacemakers

Atrial
 Ventricular
 Dual chamber
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Single Chamber Pacemakers
Atrial Demand Pacemakers (AAI) – A
pacemaker that senses spontaneously
occurring P waves and paces the atrial
when they do not appear
 Ventricular Demand Pacemaker (VVI) A
pacemaker that senses spontaneously
occurring QRS complexes and paces the
ventricles when they do not appear.
 See page 183

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Dual Chambered Pacemakers
 Atrial
synchronous ventricular
pacemaker (VDD)- synchronized
with the P wave
 AV sequential pacemaker (DVI)- a
pacemaker that senses
spontaneously occurring QRS
complexes and paces both the Atria
and Ventricles
 Optimal sequential pacemaker
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Pacemaker Terms
 Output;
milliamperes (mA)
 amount of electrical energy needed to
stimulate depolarization
 Sensitivity
 ability of pacer to recognize body’s
intrinsic electrical activity
 Spike
 electrical artifact noting electrical
stimulation by pacer
 Capture
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Complications
 Failure
to pace
 pacer fails to initiate an electrical impulse
 Failure
to capture
 pacer spike fires but no depolarization
 Failure
to sense
 pacer does not sense patient’s own
rhythm & initiates electrical impulse
LINE - What is patient’s
apical heart rate???
 BOTTOM
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Failure To Pace
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Failure To Capture
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Failure To Sense
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Pacemaker Spikes





The electrical discharge from a cardiac
pacemaker produces a narrow, often biphasic
spike.
A pacemaker lead positioned in the atria
produces a pacemaker spike followed by a
small often flattened P wave
A pacemaker lead positioned in the ventricles
produces a pacemaker spike followed by a wide
and bizarre QRS complex
A pacemaker spike not followed by a P wave or
QRS complex indicates the pacemaker is
discharging but not capturing.
See strips on page 182
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Pacemakers

Initially indicated for symptomatic
bradydysrhythmias
 Antitachycardia and overdrive pacing
 Antitachycardia pacing: Delivery of
a stimulus to the ventricle to
terminate tachydysrhythmias
 Overdrive pacing: Pacing the atrium
at rates of 200 to 500 impulses per
minute to terminate atrial
tachycardias
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Pacemakers
 Temporary
pacemaker: Power
source outside the body
 Transvenous
 Epicardial
 Transcutaneous
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Pacemakers
Fig. 36-25
Fig. 36-26
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Pacemakers
Fig. 36-27
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Pacemakers
 Permanent
pacemaker: Implanted
totally within the body
 Cardiac resynchronization therapy
(CRT): Pacing technique that
resynchronizes the cardiac cycle by
pacing both ventricles
 Combined CRT with an ICD for
maximum therapy
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Pacemakers
Fig. 36-24 A
Fig. 36-24 B
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Pacemakers

Pacemaker malfunction
 Failure to sense: Failure to recognize
spontaneous atrial or ventricular
activity and pacemaker fires
inappropriately
 Lead damage, battery failure,
dislodgement of the electrode
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Pacemakers

Pacemaker malfunction
 Failure to capture: Electrical charge
to myocardium is insufficient to
produce atrial or ventricular
contraction
 Lead damage, battery failure,
dislodgement of the electrode,
fibrosis at the electrode tip
 Patient education
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Catheter Ablation Therapy

Electrode-tipped ablation catheter
“burns” accessory pathways or
ectopic sites in the atria, AV node,
and ventricles
 Nonpharmacologic treatment for
 AV nodal reentrant tachycardia
 Reentrant tachycardia related
to accessory bypass tracts
 Control of ventricular response
of certain tachydysrhythmias
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Catheter Ablation Therapy
 Complete
ablation of the AV
node or bundle of His may be
performed in some cases of
uncontrolled ventricular
response in atrial fibrillation or
flutter unresponsive to medical
therapy
 Permanent pacemaker required
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ECG Changes Associated with
Acute Coronary Syndrome (ACS)

Definitive ECG changes occur in
response to ischemia, injury, or
infarction of myocardial cells
 Changes seen in the leads that face the
area of involvement
 Reciprocal (opposite) ECG changes
often seen in the leads facing opposite
the area involved
 Pattern of ECG changes will provide
information on the coronary artery
involved in ACS
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ECG Changes Associated with
Acute Coronary Syndrome (ACS)
 Ischemia
 ST segment depression and/or
T wave inversion
 ST segment depression is
significant if it is at least 1 mm
(one small box) below the
isoelectric line
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ECG Changes Associated with
Acute Coronary Syndrome (ACS)
 Ischemia
 Changes occur in response to the
electrical disturbance in
myocardial cells due to
inadequate supply of oxygen
 Once treated (adequate blood flow
is restored), ECG changes resolve
and ECG returns to baseline
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ECG Changes Associated with
Acute Coronary Syndrome (ACS)
Fig. 36-29 A
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ECG Changes Associated with
Acute Coronary Syndrome (ACS)

Injury/Infarction
 ST segment elevation is significant if
>1 mm above the isoelectric line

If treatment is prompt and effective,
may avoid infarction
– If serum cardiac markers are
present, an ST-segment-elevation
myocardial infarction (STEMI)
has occurred
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ECG Changes Associated with
Acute Coronary Syndrome (ACS)

Injury/Infarction
 Note: physiologic Q wave is the first
negative deflection following the P
wave

Small and narrow (<0.04 second in
duration)
 Pathologic Q wave is deep and >0.03
second in duration
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ECG Changes Associated with
Acute Coronary Syndrome (ACS)

Injury/Infarction
 Pathologic Q wave indicates that at
least half the thickness of the heart wall
is involved
 Referred to as a Q wave MI
 Pathologic Q wave may be present
indefinitely
 T wave inversion related to infarction
occurs within hours and may persist for
months
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ECG Changes Associated with
Acute Coronary Syndrome (ACS)
Fig. 36-29 B
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ECG Changes Associated with
Acute Coronary Syndrome (ACS)
Fig. 36-29 C
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ECG Changes Associated with
Acute Coronary Syndrome (ACS)
Fig. 36-30
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Syncope

Brief lapse in consciousness
accompanied by a loss in postural
tone (fainting)
 Cardiovascular causes
 Neurocardiogenic syncope or
“vasovagal” syncope (e.g., carotid
sinus sensitivity)
 Primary cardiac dysrhythmias
(e.g., tachycardias, bradycardias)
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Syncope

Noncardiovascular causes
 Hypoglycemia
 Hysteria
 Unwitnessed seizure
 Vertebrobasilar transient
ischemic attack
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Syncope

Diagnostic studies






Echocardiography
EPS
Head-upright tilt table testing
Holter monitor
Subcutaneously implanted loop
recording device
1-year mortality rate as high as 30%
for syncope from cardiovascular
cause
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Let’s Review Drugs
See ACLS Handout for Drug
Information
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