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Interventions for Clients
with Dysrhythmias
Cardiac dysrhythmias are disturbances of
cardiac electrical impulse formation,
conduction, or both
Cardiac Conduction System
Sinoatrial node
– Electrical impulses at 60 to 100
Atrioventricular junctional area
 Bundle branch system
Electrocardiogram (ECG) - provides a graphic representation, or picture, of cardiac activity
A lead provides one view of the heart's electrical activity.
Multiple leads, or views, can be obtained. Electrode
placement is the same for male and female clients.
Lead systems are made up of a positive pole and a
negative pole. An imaginary line joining these two poles
is called the lead axis.
The direction of electrical current flow in the heart is the
cardiac axis.
The relationship between the cardiac axis and the lead
axis is responsible for the deflections seen on the ECG
ECG cables may be attached directly to a wall-mounted
monitor (a hard-wired system) if the client's activity is
restricted to bedrest and sitting in a chair, as in a critical
care unit.
For an ambulatory client, the ECG cable is attached to a
battery-operated transmitter (a telemetry system)
held in a pouch worn by the client.
The ECG is transmitted via antennae located in strategic
places, usually in the ceiling, to a remote monitor. This
device allows freedom of movement within a certain
radius without losing transmission of the ECG
Electrocardiographic Complexes,
Segments, and Intervals
P wave
PR segment
PR interval - it normally measures from 0.12 to 0.20
QRS complex
QRS duration - it normally measures from 0.04 to 0.10
ST segment - it is normally not elevated more than 1
mm or depressed more than 0.5 mm from the isoelectric
line. Its amplitude is measured at a point 1.5 to 2 mm
after the J-point
T wave
U wave
QT interval
Rhythm Analysis
Normal Rhythms
Normal sinus rhythm - is the rhythm
originating from the sinoatrial (SA) node
(dominant pacemaker) that meets the
following electrocardiographic (ECG)
– Rhythm: Atrial and ventricular rhythms regular
– Rate: Atrial and ventricular rates of 60 to 100
– P waves: Present, consistent configuration, one P
before each QRS complex
– PR interval: 0.12 to 0.20 second and constant
– QRS duration: 0.04 to 0.10 second and constant
Normal Rhythms
Sinus arrhythmia
 Sinus arrhythmia is a variant of NSR. It
results from changes in intrathoracic
pressure during breathing.
 In this context the term arrhythmia does
not denote an absence of rhythm, as the
term suggests.
 Instead, the heart rate increases slightly
during inspiration and decreases slightly
during exhalation
Tachydysrhythmias - are heart rates greater than 100
Bradydysrhythmias - are characterized by a heart rate
less than 60 beats/min
Premature complexes - are early complexes. They occur
when a cardiac cell or cell group, other than the
sinoatrial (SA) node, becomes irritable and fires an
impulse before the next sinus impulse is generated. This
abnormal focus is called an ectopic focus and may be
generated by atrial, junctional, or ventricular tissue
Repetitive rhythms - premature complexes may occur repetitively in
a rhythmic fashion
– bigeminy exists when normal complexes and premature complexes
occur alternately in a repetitive two-beat pattern, with a pause
occurring after each premature complex so that complexes occur in
– trigeminy is a repetitive three-beat pattern, usually occurring as two
sequential normal complexes followed by premature complex and a
pause, with the same pattern repeating itself in triplets.
– quadrigeminy - is a repetitive four-beat pattern, usually occurring as
three sequential normal complexes followed by a premature complex
and a pause, with the same pattern repeating itself in a four-beat
Escape complexes and rhythms - occur when the SA node fails to
discharge or is blocked or when a sinus impulse fails to depolarize
the ventricles because of an atrioventricular (AV) nodal block
Sinus tachycardia
When the rate of SA node discharge exceeds 100
Clinical manifestations - the client may be asymptomatic
except for the increased pulse rate. However, if the
rhythm is not well tolerated, he or she may become
symptomatic. The client is assessed for fatigue,
weakness, shortness of breath, orthopnea, neck vein
distention, decreased oxygen saturation, and decreased
blood pressure. The nurse also assesses for restlessness
and anxiety from decreased cerebral perfusion and for
decreased urine output from decreased renal perfusion.
The adult client may experience anginal pain. The
electrocardiographic (ECG) pattern may show T-wave
inversion or ST-segment elevation or depression in
response to myocardial ischemia
Sinus tachycardia (heart rate, 110 beats/min; PR interval, 0.12 second; QRS complex, 0.08 second)
Sinus tachycardia
The goal is to decrease the heart rate to normal levels by treating
the underlying cause.
For example, if the client has angina, the nurse administers oxygen,
helps the client to rest, and administers nitroglycerin or morphine as
Diuretics and inotropic agents may be given for heart failure. The
nurse initiates intravascular volume replacement for hypovolemia,
administers antipyretics and antibiotics to the client with fever and
infection, or provides comfort measures and administers analgesics
or opioids to the client with noncardiac pain, as ordered.
The nurse collaborates with the respiratory therapist when indicated
to oxygenate and suction the client with hypoxemia from excessive
airway secretions.
Beta-adrenergic blocking agents may be prescribed for the client
with inappropriate sympathetic nervous system stimulation.
Emotional support and relevant teaching are important for the client
and family
Sinus Bradycardia
Rate of sinus node discharge < 60
 Clinical manifestations - the client may be
asymptomatic, except for the decreased
pulse rate. However, at times the rhythm
may not be well tolerated. The nurse
assesses the client for dizziness,
weakness, syncope, confusion,
hypotension, diaphoresis, shortness of
breath, ventricular ectopy, and anginal
Sinus bradycardia (heart rate, 52 beats/min; PR interval, 0.18 second; QRS complex, 0.08 second)
Sinus Bradycardia
If the client is symptomatic and the underlying cause
cannot be determined, the treatment of choice is
atropine administration, given as prescribed to increase
the heart rate to approximately 60 beats/min.
Oxygen should be applied. If the heart rate does not
increase sufficiently, the nurse may apply an external
pacemaker to increase the heart rate and notify the
However, if atropine administration succeeds in
achieving an adequate heart rate but the client remains
hypotensive, the nurse initiates intravascular volume
replacement, as ordered, rather than administering
another dose of atropine. Excessive atropine may induce
Premature Atrial Complexes
Ectopic focus of atrial tissue fires an impulse before the
next sinus impulse is due.
 Clinical manifestations - the client is usually
asymptomatic, except for possible heart palpitations,
because PACs usually have no hemodynamic
 Interventions - no intervention is usually needed except
to treat the cause, such as heart failure or valvular
disease. The nurse administers prescribed type
antidysrhythmics, such as quinidine and procainamide
(Pronestyl), or other drugs such as digitalis and
propranolol (Inderal, Apo-Propranolol). Measures to
reduce stress are also initiated, and the client is taught
to avoid substances known to increase atrial irritability
Normal sinus rhythm with a premature atrial complex (PAC) at arrow
Supraventricular Tachycardia
Rapid stimulation of atrial tissue
occurs at a rate of 100 to 280
beat/min with a mean of 170
beats/min in adults.
 Paroxysmal supraventricular
tachycardia rhythm is intermittent
and terminated suddenly with or
without intervention.
Sustained supraventricular tachycardia in a client with Wolff-Parkinson-White syndrome. Heart
rate is 200 beats/min
Supraventricular Tachycardia
Clinical manifestations - the clinical
manifestations depend on the duration of the
SVT and the rate of the ventricular response. In
clients with a sustained rapid ventricular
response, the nurse assesses for palpitations,
weakness, fatigue, shortness of breath,
nervousness, anxiety, hypotension, and
syncope. Hemodynamic deterioration may occur
in the client with cardiac disease, causing
angina, heart failure, and shock. With a
nonsustained or slower ventricular response, the
client may be asymptomatic except for transient
Supraventricular Tachycardia
If SVT occurs in a healthy person and terminates spontaneously, no
intervention is necessary other than eliminating identified causative
If it is recurrent, the client should be studied in the
electrophysiology laboratory. The preferred treatment for recurrent
SVT is radiofrequency catheter ablation. In sustained SVT with a
rapid ventricular response, the goals of treatment are to decrease
the ventricular response, convert the dysrhythmia to a sinus rhythm,
and treat the cause. Vagal stimulation (e.g., carotid massage) may
be successful, but often only transiently, and must be performed
only by a physician.
The nurse administers oxygen and prescribed antidysrhythmic
drugs, which slow the ventricular rate by increasing the AV block.
In the severely compromised client, the nurse may assist the
physician in attempting atrial overdrive pacing or in delivering a
synchronized electrical shock (cardioversion) to reestablish an
organized rhythm and regain cardiac stability
Atrial Flutter
Rapid atrial depolarization occurring at a rate of 250 to
350 times per minute
Clinical manifestations - the clinical manifestations
depend on the rate of ventricular response. The nurse
assesses the client for palpitations, weakness, fatigue,
shortness of breath, nervousness, anxiety, syncope,
angina, and evidence of heart failure and shock. Carotid
sinus massage transiently decreases the ventricular rate
to facilitate rhythm interpretation but can be performed
only by the physician. The client with a normal
ventricular rate is usually asymptomatic
Atrial flutter (F) with 4:1 block. The atrial rate is 280 beats/min; the ventricular rate is 70 beats/min
Atrial flutter with 4:1 conduction, then an 11-beat run with 2:1 conduction
Atrial Flutter
The treatment goals are the same as those for supraventricular
tachycardia (SVT). The nurse administers oxygen and prescribed
drugs such as ibutilide (Covert), amiodarone (Cordarone), diltiazem
(Cardizem), and verapamil (Calan, Isoptin) to slow the rapid
ventricular response.
Quinidine or procainamide (Pronestyl) must not be administered
unless one of the above agents has slowed the ventricular response.
Both drugs slow the atrial rate and may increase AV conduction,
which could cause a 1:1 conduction with an increase in ventricular
rate and hemodynamic deterioration.
The nurse helps the physician to attempt rapid atrial overdrive
pacing or to achieve cardioversion if the client is hemodynamically
compromised. If he or she fails to respond to these therapies,
radiofrequency catheter ablation may be necessary
Atrial Fibrillation
Multiple, rapid impulses from many
atrial foci at a rate of 350 to 600
times per minute
Atrial Fibrillation
Clinical manifestations
The nurse assesses the client for the presence of a pulse deficit,
fatigue, weakness, shortness of breath, distended neck veins,
dizziness, decreased exercise tolerance, anxiety, syncope,
palpitations, chest discomfort or pain, and hypotension.
The client is also at risk for pulmonary embolism. The nurse should
assess for shortness of breath, chest pain, hemoptysis, and a feeling
of impending doom.
The client is at risk for systemic emboli, particularly an embolic
stroke. Changes in mentation, speech, sensory function, and motor
function are particularly noted.
The nurse also assesses pulses, urine output, back pain, and
complaints of gastrointestinal (GI) disturbances.
Any of these symptoms should be reported to the health care
provider immediately.
Atrial Fibrillation
 Treatment is the same as for atrial flutter. In
addition, the nurse may administer
anticoagulants, such as heparin, enoxaparin
(Lovenox), and sodium warfarin, as prescribed
by the physician for clients considered to be at
high risk for emboli.
 Before elective cardioversion, the nurse must
initiate anticoagulation therapy for 4 to 5 weeks
as prescribed to prevent a thromboembolic
event if the rhythm is successfully converted
Junctional Dysrhythmias
Atrioventricular cells generating
electrical impulses at a rate of 40 to
60 beats/min
 These rhythms are most commonly
transient, and clients usually remain
hemodynamically stable.
Idioventricular Rhythm
Also called ventricular escape rhythm: ventricular nodal cells pace
the ventricles. P waves are independent of the QRS complex (AV
Clinical manifestations - because idioventricular pacemakers are
unstable, unreliable, and slow, the client is hypotensive and in shock
or, most typically, is pulseless and therefore in cardiac arrest. The
nurse assesses the client's airway, breathing, circulation, level of
consciousness, and pupillary response
Interventions - usually, idioventricular rhythms require immediate
resuscitation measures, unless there is a do-not-resuscitate (DNR)
order. The nurse initiates cardiopulmonary resuscitation (CPR) and
summons assistance. The team may initiate advanced cardiac life
support (ACLS) measures, including epinephrine administration,
intravascular volume replacement, and other measures. The
physician may attempt pacemaker therapy or discontinue
resuscitation efforts
Idioventricular rhythm with a rate of 35 beats/min
Premature Ventricular
A result of increased irritability of
ventricular cells: early ventricular
complexes followed by a pause
Ventricular dysrhythmias. A, Normal sinus rhythm with unifocal premature ventricular complexes (PVCs). B,
Normal sinus rhythm with multifocal PVCs (one negative and the other positive). C, Normal sinus rhythm
with three consecutive PVCs (nonsustained ventricular tachycardia) and another unifocal PVC
Premature Ventricular
Clinical manifestations
The client may be asymptomatic or may experience palpitations or
chest discomfort caused by increased stroke volume of the normal
beat after the pause. Peripheral pulses may be diminished or absent
with the PVCs themselves because the decreased stroke volume of
the premature beats may decrease peripheral perfusion. Since other
rhythms also cause widened QRS complexes, it is essential that the
nurse assess whether the premature complexes perfuse. This is
done by palpating the carotid, brachial, or femoral arteries while
observing the monitor for widened complexes, or auscultating for
the apical heart sounds. With acute myocardial infarction, PVCs may
be considered warning dysrhythmias, possibly heralding the onset of
ventricular tachycardia (VT) or ventricular fibrillation (VF). For a
client with chest discomfort or pain, the nurse reports to the
physician whether PVCs increase in frequency, are multiform, are Ron-T phenomena, or occur in runs of VT
Premature Ventricular
If there is no underlying heart disease, PVCs are
not usually treated other than by eliminating any
contributing cause (e.g., caffeine, stress).
With acute myocardial ischemia or infarction, the
nurse treats significant PVCs by administering
oxygen and lidocaine as prescribed.
The nurse may administer other drugs as ordered,
including procainamide (Pronestyl), bretylium
(Bretylol, Bretylate), magnesium sulfate,
propranolol (Inderal, Apo-Propranolol), quinidine,
and mexiletine (Mexitil).
Potassium is administered as ordered for
replacement therapy if hypokalemia is the cause
Ventricular Tachycardia
Also called V tach: repetitive firing of an irritable
ventricular ectopic focus, usually at a rate of 140
to 180 beats/min
Clinical manifestations
Slower rates are better tolerated. Clients may be
hemodynamically compromised if the cardiac
output decreases because of the shortened
ventricular filling time and loss of the atrial kick.
In some clients, VT causes cardiac arrest. The
nurse assesses the client's airway, breathing,
circulation, level of consciousness, and pupillary
Ventricular dysrhythmias. Sustained ventricular tachycardia at a rate of 166 beats/min
Ventricular Tachycardia
For the stable client with sustained VT, the nurse administers oxygen and
confirms the rhythm via a 12-lead electrocardiogram (ECG). Amiodarone,
procainamide, or magnesium sulfate may be given.
The physician may prescribe an oral antidysrhythmic agent, such as
procainamide (Procan SR), mexiletine (Mexitil), or sotalol (Betapace,
For the client with unstable VT, the nurse assists the physician in
attempting emergency cardioversion followed by oxygen and
antidysrhythmic therapy. The nurse may instruct the client to perform
cough cardiopulmonary resuscitation (CPR) if prescribed, telling him or her
to inhale deeply and cough hard every 1 to 3 seconds. The physician may
attempt rapid atrial or ventricular overdrive pacing if the VT is related to a
significant bradydysrhythmia.
A precordial thump is sometimes successful in terminating VT, at least
transiently. The physician or the nurse may administer a precordial thump
to a client with unstable VT only if a defibrillator and pacemaker are
immediately available.
Ventricular Tachycardia
With pulseless VT, the physician or nurse or other health care provider must
immediately defibrillate the client or initiate CPR and defibrillate as soon as
possible. A precordial thump may be administered initially, although it is
frequently not successful in terminating VT. If the client remains pulseless,
the nurse or other health care provider must resume CPR and full
resuscitative measures following defibrillation. This includes airway
management and administration of oxygen, epinephrine, and
antidysrhythmic therapy with amiodarone, magnesium sulfate, and
 If the rhythm has been successfully converted, attention is given to treating
reversible causes of VT, such as myocardial ischemia, hypokalemia, and
hypomagnesemia. The nurse ensures that oxygen therapy and
antidysrhythmic agent administration are continued, and the client is closely
monitored for premature ventricular complexes (PVCs) and the recurrence
of VT.
 Some forms of VT may require surgical intervention, such as coronary
artery bypass graft (CABG) surgery, implantation of a
cardioverter/defibrillator, aneurysmectomy, encircling endocardial
ventriculotomy, cryosurgery, or endocardial resection
Ventricular Fibrillation
Also called V fib: a result of electrical chaos in the
Clinical manifestations
On initiation of VF, the client becomes faint,
immediately loses consciousness, and becomes
pulseless and apneic. There is no blood pressure,
and heart sounds are absent. Respiratory and
metabolic acidosis develop. Seizures may occur.
Within minutes, the pupils become fixed and
dilated, and the skin becomes cold and mottled.
Death ensues without prompt restoration of an
organized rhythm and cardiac output
Ventricular Fibrillation
The goals of treatment are to terminate VF promptly and convert it
to an organized rhythm. The physician or the ACLS nurse or other
health care provider must immediately defibrillate the client to
accomplish this goal. This is the management priority, and the ACLS
algorithm for VF must be followed. If a defibrillator is not readily
available, a precordial thump may be delivered. CPR must be
continued until the defibrillator arrives.
If the VF does not terminate after three rapid successive shocks of
increasing energy, the nurse and resuscitation team resume CPR
and provide airway management. They also administer oxygen and
antidysrhythmic therapy with epinephrine, amiodarone,
procainamide (Pronestyl), lidocaine, and magnesium sulfate, along
with attempting defibrillation frequently.
If VF is successfully converted to an organized rhythm, the nurse
continues supportive therapy and assists the physician in treating
potential causes of VF and preventing its recurrence.
Ventricular Asystole
Also called ventricular standstill: complete
absence of any ventricular rhythm
 Clinical manifestations
 Clients are in full cardiac arrest with loss
of consciousness and absence of pulse,
respirations, and blood pressure.
Ventricular asystole is often unresponsive
to resuscitation measures and fatal
Ventricular asystole with one idioventricular complex
Ventricular Asystole
The goal of treatment is to restore cardiac electrical activity.
The nurse or other health care provider initiates CPR immediately
and summons assistance.
Another ECG lead is assessed to ensure that the rhythm is asystole
and not fine VF, which warrants immediate defibrillation. When in
doubt, the client should be defibrillated.
The nurse and resuscitation team manage the airway and
administer oxygen, epinephrine, and atropine.
The nurse assists the physician with the initiation of noninvasive
pacing or invasive transvenous or epicardial pacing, although
pacemaker therapy is generally not effective.
An isoproterenol infusion may also be tried.
The prognosis for clients with asystole is poor
Atrioventricular Blocks
Atrioventricular blocks are
differentiated by their PR interval.
– First-degree atrioventricular block
– Second-degree atrioventricular block
– Third-degree atrioventricular block
Atrioventricular Block
PR interval greater than 0.20 second
Clinical manifestations
First-degree AV block has no hemodynamic consequences and
produces no symptoms. Any symptoms are the result of the
underlying rhythm (e.g., sinus bradycardia). First-degree AV block
may be insignificant and transient or may progress to more severe
AV blocks
In the stable client, no treatment is needed. If the PR interval is
particularly long or is getting progressively longer, the nurse must
notify the physician. If the first-degree AV block is due to drug
therapy, the nurse must withhold the offending drug and notify the
physician. When first-degree AV block is associated with
symptomatic bradycardia, oxygen and atropine are administered as
prescribed to accelerate AV conduction
Normal sinus rhythm with first-degree AV block (PR interval, 0.36 second)
Atrioventricular Block
Progressive prolongation of the PR interval, followed by
a dropped beat and a pause; each group has one more P
wave than QRS complexes
Clinical manifestations
The client is usually asymptomatic if the frequency of
dropped beats and the overall ventricular rate do not
decrease the cardiac output. If the ventricular rate is too
slow, decreasing the cardiac output, the client will have
symptoms of a symptomatic bradydysrhythmia. This
rhythm is usually transient and terminates spontaneously
Second-degree AV block type I (Wenckebach AV) with an irregular rhythm, grouped beating, and
progressive prolongation of the PR interval until a P wave is completely blocked and not followed by a
QRS complex
Atrioventricular Block
 No intervention is required in the stable client,
because this rhythm rarely progresses to a more
severe block. In the symptomatic client, the
nurse administers oxygen and atropine as
prescribed. If atropine is not successful in
speeding AV nodal conduction time and
increasing the heart rate, the nurse initiates
pacemaker therapy as ordered and notifies the
Second-Degree Heart Block
Type II
Mobitz type II block is an infranodal
block occurring below the bundle of
 Constant block in one of the bundle
branches results in a wide QRS
complex and dropped beats.
Second-degree AV block type II (Mobitz II) with 2:1 conduction, a constant PR interval, and wide QRS complex
Second-Degree Heart Block
Type II
Clinical manifestations
Symptoms depend on the frequency of dropped beats and the
overall ventricular rate. If the cardiac output is inadequate, the
client presents with a symptomatic bradydysrhythmia.
In the asymptomatic client, the nurse may assist the physician in
initiating prophylactic pacing to avert the threat of sudden thirddegree AV block. If slow ventricular rates are present, the nurse
administers oxygen and atropine as prescribed. Atropine is usually
ineffective because it does not reverse the infranodal block. An
isoproterenol (Isuprel) infusion may be administered with caution
but may be dangerous in adults with ischemic heart disease.
Noninvasive (external) or invasive pacing is preferred. A permanent
pacemaker may be required with recurrent Mobitz type II block
Third-Degree Heart Block
Heart block is complete.
 None of the sinus impulses conducts
to the ventricles.
Third-degree AV block (complete heart block) with regular atrial and ventricular rhythms, inconstant PR
intervals (AV dissociation), and a junctional escape focus (normal QRS complexes) pacing the
ventricles at a rate of 44 beats/min
Third-Degree Heart Block
Clinical manifestations
Depend on the overall ventricular rate and cardiac
output. Transient third-degree heart block may be well
tolerated, particularly when the block is in the AV node.
If the block is infranodal, it may have serious
hemodynamic consequences. If cerebral perfusion is
inadequate, clients may be confused and lightheaded or
may experience episodes of syncope with or without
seizures (Stokes-Adams attacks). Inadequate cardiac
output may cause myocardial ischemia or infarction,
heart failure, or hypotension. Third-degree heart block
may predispose to cardiac arrest, causing VT, VF, or
asystole. Therefore it is regarded as a dangerous rhythm
Third-Degree Heart Block
Third-degree AV block with a junctional escape pacemaker is often
transient and well tolerated. If the client is symptomatic, the nurse
administers oxygen and atropine as prescribed.
Clients with third-degree heart block with a ventricular escape
pacemaker are frequently symptomatic. The nurse administers
oxygen and assists the physician in initiating pacing to avert the
threat of cardiac arrest. Atropine is usually not successful in
infranodal blocks with wide QRS complexes. Cautious use of
isoproterenol (Isuprel) infusions may be necessary as a temporary
measure while awaiting pacemaker therapy but is dangerous in
clients with acute myocardial infarction.
Implantation of a permanent pacemaker may be required for clients
with recurrent third-degree infranodal block
Bundle Branch Blocks
Conduction delay or block within one of the two main bundle
branches below the bifurcation of the bundle of His
Clinical manifestations
There are no clinical manifestations specifically related to bundle
branch block. The nurse must notify the physician when a new
bundle branch block develops, especially in the client with an acute
myocardial infarction. The conduction disorder may deteriorate to a
more significant block requiring pacemaker therapy
No interventions are specifically related to bundle branch block. The
client is assessed during alterations in heart rate for symptoms of
hemodynamic compromise, which are reported to the physician. The
nurse ensures that the client is resting and has adequate ventilation
and oxygenation
Normal sinus rhythm with bundle branch block (wide QRS complexes measuring 0.12 second)
Decreased Cardiac Output and
Ineffective Tissue Perfusion
Interventions include:
– Cardiac care
– Nonsurgical management
– Drug therapy
 Vaughn-Williams classification
 Other antidysrhythmic drugs
 Emergency cardiac drugs
Nonsurgical Management
Vagal maneuvers
 Carotid sinus massage
 Valsalva maneuvers
Temporary Pacing
Modes of pacing
– Synchronous pacing
– Asynchronous pacing
Noninvasive temporary pacing
 Invasive Temporary Pacing
Cardiopulmonary resuscitation
 Advanced cardiac life support
 Cardioversion: synchronized
countershock that may be used for
emergent hemodynamically unstable
ventricular or supraventricular
tachydysrhythmias or electively for
stable tachydysrhythmias resistant to
medical therapies
Asynchronous countershock
depolarizes a critical mass of
myocardium simultaneously to stop
the re-entry circuit and allow the
sinus node to regain control of the
 Maintain a patent airway.
 Administer oxygen.
Defibrillation (Continued)
Assess vital signs and level of
 Administer antidysrhythmic drugs.
 Monitor for dysrhythmias .
 Assess for burns, emotional support,
Other Therapies
Automatic external defibrillation
 Radiofrequency catheter ablation
 Surgical procedures:
– Permanent pacemaker
– Coronary artery bypass grafting
– Aneurysmectomy
– Insertion of implantable
– Open-chest cardiac massage
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