Focus on
Dysrhythmias
(Relates to Chapter 36,
“Nursing Management: Dysrhythmias,”
in the textbook)
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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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Properties of Cardiac Cells
Automaticity – certain cardiac cells can
discharge spontaneously
Excitability – property of myocardial tissue
that allows it to be depolarized by a stimulus
Conductivity – ability to transmit an impulse
along a membrane in an orderly manner
Contractility – ability to respond
mechanically to an impulse
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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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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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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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Tips for applying electrodes
Make sure skin is thoroughly dry.
Clip chest hair.
Remove any excess skin oil with alcohol.
Apply tincture of benzoin if keeping electrodes is difficult.
Connect each lead wire to a disc before applying it to the chest.
Make sure the center of the electrode disc is moist.
Avoid applying electrodes over these areas:
Bony areas skin folds
Scar tissue breast tissue
Muscle mass (significant) heart apex
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Assessment of Cardiac Rhythm
Fig. 36-5
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EKG Paper
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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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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 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 Wolff-
Parkinson-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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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
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 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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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 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 third-degree
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 life-
threatening 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 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
Electricalactivity 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
Hypovolemia Drug overdose
Hypoxia Cardiac
tamponade
Metabolic acidosis MI
Hyperkalemia or Tension
hypokalemia pneumothorax
Hypothermia Pulmonary
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 Cardioverter-
Defibrillator (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 life-
threatening dysrhythmias
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Implantable Cardioverter-
Defibrillator (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 Cardioverter-
Defibrillator (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 Cardioverter-
Defibrillator (ICD)
Fig. 36-22
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Implantable Cardioverter-
Defibrillator (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
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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Pacer spikes
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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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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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―How will I know what to do?‖ you ask
Treat the patient, not the rhythm - is a good place to start
Anticipate the problem
Know your drugs
Know CPR
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