Focus on
Dysrhythmias
(Relates to Chapter 36,
“Nursing Management: Dysrhythmias,”
in the textbook)
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Dysrhythmias
 Abnormal
cardiac rhythms are
termed dysrhythmias
 May cause disturbances in rate,
rhythm or both
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Normal Electrical Conduction

The impulse that stimulates and paces the cardiac
muscle normally originates in the sinoatrial (SA)
node of the heart, located in the right atrium

Impulse travels quickly from the SA node, down to
the atrioventricular (AV node) - this causes atrial
contraction (“atrial kick)

Impulse then travels quickly through the bundle of
His, to the right and left bundle branches and the
Purkinje fibers, located in the ventricles - this causes
ventricular contraction
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Cardiac Conduction
QuickTime™ and a
decompressor
are needed to see this picture.
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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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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Lead Placement
Fig. 36-2
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12-Lead ECG
Fig. 36-3
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Assessment of Cardiac Rhythm
Fig. 36-9
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Assessment of Cardiac Rhythm
Fig. 36-6
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Interpreting ECGs


Determining heart rate
1 minute strip contains 300 large boxes, 1500 small
boxes
 1. 1500/# small boxes between R waves
 2. 300 / #large boxes between R waves
 3. A less accurate way: count the # of R waves
The heart’s normal pacemaker is the SA node (rate 60100
 If the SA node fails, the AV node kicks in (rate 40-60
 If the AV node fails, the ventricles take over (rate 2040)
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Interpreting ECGs

P wave
 Represents depolarization of the atria

QRS complex





Represents ventricular depolarization
Q is the first negative deflection after the P wave
R is the first positive deflection after the P wave
S is the negative deflection after the R wave
<.12 sec in duration
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Interpreting ECGs
 T wave
 Ventricular repolarization
 Same direction as QRS
U
wave
 ?repolarization of Purkinje fibers
 Not usually present
 May be seen in hypokalemia, HTN, heart
disease
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Analysis of Rhythm Strips


1. Determine the ventricular rate
2. Determine the rhythm
 Is the R-R interval regular?

3. Identify P waves
 Is there a P for every QRS?
 Is it upright?

4. Determine the PR interval duration
 Is it consistent?

5. Determine the QRS duration
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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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Evaluation of Dysrhythmias
 Holter monitoring
 Event
recorder monitoring
 Exercise treadmill testing
 Signal-averaged ECG
 Electrophysiologic study
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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
 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)
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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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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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
 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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QuickTime™ and a
YUV420 codec decompressor
are needed to see this picture.
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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 surgical 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
 Treatment
 If symptomatic, atropine
 -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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Heart Block
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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
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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
 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)
 With a pulse
 Chemical cardioversion with
amiodarone, lidocaine
 Electrical cardoversion
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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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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
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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Prodysrhythmia State
 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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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
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)
 ICD
sensing system monitors the
HR and rhythm and identifies
VT or VF
 Approximately 25 seconds after
detecting VT or VF, ICD delivers
shock
 If first shock is unsuccessful, ICD
recycles and delivers successive
shocks
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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

Initially indicated for symptomatic
bradydysrhythmias
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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
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
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
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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ECG Changes Associated with Acu
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
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
ECG Changes Associated with Acute
Coronary Syndrome (ACS)
Fig. 36-29 B
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.