Dysrhythmias

Chapter 36

Copyright 2014 by Mosby, an

imprint of Elsevier Inc.

Properties of Cardiac
Cells

Automaticity
Excitability
Conductivity
Contractility

Conduction System of
the Heart

Nervous System Control

of Heart
Autonomic nervous system
controls
Parasympathetic nervous system
Decreases rate of SA node
Slows impulse conduction of AV node

Sympathetic nervous system

Increases rate of SA node
Increases impulse conduction of AV node
Increases cardiac contractility

Dysrhythmias
Disorder of impulse formation,
conduction of impulses, or both
SA node normal pacemaker of
heart (60100 beats/minute)
Secondary pacemakers
AV node (4060 beats/minute)
His-Purkinje fibers (2040
beats/minute)

Electrocardiogram
Monitoring
Graphic tracing of electrical
impulses produced by heart
Waveforms of ECG represent
activity of charged ions
across membranes of
myocardial cells

Electrocardiogram
Monitoring

12-Lead ECG

Case Study
iStockphoto/Thinkstock

S.D. is a 45-year-old woman who

comes to the ED complaining of
sudden onset of palpitations and
shortness of breath.
Standard protocol requires you to
obtain a 12-lead ECG and attach
S.D. to the cardiac monitor for
continuous monitoring.

Case Study
Describe the appropriate
location to apply the leads
for both the 5-lead cardiac
monitor as well as the 12lead ECG.

iStockphoto/Thinkstock

Lead Placement

Lead Placement

ECG Time and Voltage

Calculating HR
Count
Number of QRS complexes in 1 minute
R-R intervals in 6 seconds, and
multiply by 10
Number of small squares between one
R-R interval, and divide this number
into 1500
Number of large squares between one
R-R interval, and divide this number
into 300

Assessment of Cardiac
Rhythm

Patient Preparation
Clip excessive hair on chest
wall
Rub skin with dry gauze
May need to use alcohol for
oily skin
Apply electrode pad

Artifact

Telemetry Monitoring
Observation of HR and
rhythm at a distant site
Two types
Centralized monitoring system
Advanced alarm system alerts
when it detects dysrhythmias,
ischemia, or infarction

Assessment of Cardiac
Rhythm
Interpret the rhythm AND
evaluate the clinical status of
the patient
Is the patient
hemodynamically stable?
Determine cause of
dysrhythmia
Treat the patient, not the
monitor!

Case Study
iStockphoto/Thinkstock

The UAP obtains the 12-lead

ECG recording for S.D. while
you print out a rhythm strip
from the cardiac monitor.
Describe the method you
would use to assess S.D.s
rhythm strip.

Assessment of Cardiac
Rhythm
1.
2.
3.
4.
5.
6.
7.
8.

P wave
Atrial rate and rhythm
P-R interval
Ventricular rate and rhythm
QRS complex
ST segment
Q-T interval
T wave

Normal Sinus Rhythm

Sinus node fires 60100
beats/minute
Follows normal conduction
pattern

Sinus Bradycardia

Sinus Bradycardia
Normal rhythm in aerobically
trained athletes and during
sleep
Can occur in response to
parasympathetic nerve
stimulation and certain drugs
Also associated with some
disease states

Sinus Bradycardia
Manifestations

Hypotension
Pale, cool skin
Weakness
Angina
Dizziness or syncope
Confusion or disorientation
Shortness of breath

Sinus Bradycardia
Treatment
Atropine
Pacemaker
Stop offending drugs

Audience Response Question

A patients cardiac rhythm is sinus
bradycardia with a heart rate of 34
beats/minute. If the bradycardia is
symptomatic, the nurse would expect the
patient to exhibit
a. Palpitations.
b. Hypertension.
c. Warm, flushed skin.
d. Shortness of breath.

Sinus Tachycardia

Sinus Tachycardia
Caused by vagal inhibition or
sympathetic stimulation
Associated with physiologic
and psychologic stressors
Drugs can increase rate

Sinus Tachycardia
Manifestations

Dizziness
Dyspnea
Hypotension
Angina in patients with CAD

Sinus Tachycardia
Treatment
Guided by cause (e.g., treat
pain)
Vagal maneuver
-adrenergic blockers

Premature Atrial
Contraction

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

Premature Atrial
Contraction
Causes

Stress
Fatigue
Caffeine
Tobacco
Alcohol
Hypoxia
Electrolyte imbalance
Disease states

Premature Atrial
Contraction
Manifestations
Palpitations
Heart skips a beat

Treatment
Monitor for more serious
dysrhythmias
Withhold sources of
stimulation
-adrenergic blockers

Paroxysmal Supraventricular
Tachycardia (PSVT)

Paroxysmal Supraventricular
Tachycardia (PSVT)
Reentrant phenomenon: PAC
triggers a run of repeated
premature beats
Paroxysmal refers to an abrupt
onset and termination
Associated with overexertion,
stress, deep inspiration,
stimulants, disease, digitalis
toxicity

Paroxysmal Supraventricular
Tachycardia (PSVT)
Manifestations
HR is 150220 beats/minute (add
for clarification)
HR > 180 leads to decreased
cardiac output and stroke volume
Hypotension
Dyspnea
Angina

Paroxysmal Supraventricular
Tachycardia (PSVT)

Treatment

Vagal stimulation
IV adenosine
IV -adrenergic blockers
Calcium channel blockers
Amiodarone
DC cardioversion

Atrial Flutter

Atrial Flutter
Typically associated with
disease
Symptoms result from high
ventricular rate and loss of
atrial kick decreased CO
heart failure
Increases risk of stroke

Atrial Flutter
Treatment
Pharmacologic agent
Electrical cardioversion
Radiofrequency ablation

Case Study
iStockphoto/Thinkstock

S.D.s ECG reveals atrial

fibrillation with a rapid
ventricular response
(HR = 168).
Describe what S.D.s rhythm
would look like.
What might be the cause of
this dysrhythmia for S.D.?

Atrial Fibrillation

Atrial Fibrillation
Paroxysmal or persistent
Most common dysrhythmia
Prevalence increases with
age
Usually occurs in patients
with underlying heart
disease
Can also occur with other
disease states

Case Study
iStockphoto/Thinkstock

S.D.s blood pressure is 94/58

with HR of 168.
What treatment might you
expect the health care
provider to initially order for
S.D.s atrial fibrillation?

Atrial Fibrillation
As with atrial flutter causes
a decrease in CO and an
increased risk of stroke

Atrial Fibrillation
Treatment
Drugs to control ventricular rate
and/or convert to sinus rhythm
(amiodarone and ibutilide most
common)
Electrical cardioversion
Anticoagulation
Radiofrequency ablation
Maze procedure with cryoablation

Junctional Dysrhythmias
Dysrhythmias that originate in area
of AV node
SA node has failed to fire, or impulse
has been blocked at the AV node
AV node becomes pacerretrograde
transmission of impulse to atria
Abnormal P wave; normal QRS
Associated with disease, certain
drugs

Junctional Dysrhythmias

Junctional Dysrhythmia
Serves as safety mechanismdo
not suppress
If rhythms are rapid, may result
in reduction of CO
Treat if patient is symptomatic
Atropine for escape rhythm
Correct cause
Drugs to reduce rate if tachycardia

First-Degree AV Block

First-Degree AV Block
Associated with disease
states and certain drugs
Typically not serious
Patients asymptomatic
No treatment
Monitor for changes in heart
rhythm

Second-Degree AV Block,
Type 1 (Mobitz I, Wenckebach)

Second-Degree AV Block,
Type 1 (Mobitz I, Wenckebach)
May result from drugs or CAD
Typically associated with ischemia
Usually transient and well
tolerated
Treat if symptomatic
Atropine
Pacemaker

If asymptomatic, monitor closely

Second-Degree AV Block,
Type 2 (Mobitz II)

Second-Degree AV Block,
Type 2 (Mobitz II)

Associated with heart

disease and drug toxicity
Often progressive and results
in decreased CO
Treat with pacemaker

Third-Degree AV Heart Block

(Complete Heart Block)

Third-Degree AV Heart Block

(Complete Heart Block)

Associated with severe heart

disease, some systemic
diseases, certain drugs
Usually results in decreased
CO
Can lead to syncope, HF,
shock
Treat with pacemaker
Drugs to increase heart rate

Premature Ventricular
Contractions

Premature Ventricular
Contractions

Associated with stimulants,

electrolyte imbalances,
hypoxia, heart disease
Not harmful with normal heart
but CO reduction, angina, and
HF in diseased heart
Assess apical-radial pulse
deficit

Premature Ventricular
Contractions

Treatment
Correct cause
Antidysrhythmics

Audience Response Question

A patient has a diagnosis of acute myocardial
infarction, and his cardiac rhythm is sinus
bradycardia with 6 to 8 premature
ventricular contractions (PVCs) per minute.
The pattern that the nurse recognizes as the
most characteristic of PVCs is
a.
b.
c.
d.

An irregular rhythm.
An inverted T wave.
A wide, distorted QRS complex.
An increasingly long P-R interval.

Ventricular Tachycardia

Ventricular Tachycardia
Ectopic foci take over as
pacemaker
Monomorphic, polymorphic,
sustained, and nonsustained
Considered life-threatening
because of decreased CO and
the possibility of
deterioration to ventricular
fibrillation

Ventricular Tachycardia
Torsades de Pointes

Ventricular Tachycardia
Associated with heart disease,
electrolyte imbalances, drugs, CNS
disorder
Can be stable (patient has a pulse) or
unstable (pulseless)
Sustained VT causes severe decrease
in CO
Hypotension, pulmonary edema,
decreased cerebral blood flow,
cardiopulmonary arrest

Ventricular Tachycardia
Precipitating causes must be
identified and treated (e.g.,
hypoxia)
VT with pulse (stable) treated
with antidysrhythmics or
cardioversion
Pulseless VT treated with CPR
and rapid defibrillation

Accelerated Idioventricular
Rhythm (AIVR)
Develops when the intrinsic
pacemaker rate (SA node or AV
node) becomes less than that of
ventricular ectopic pacemaker
Rate is between 40 and 100
beats/minute
Atropine if patient symptomatic
Temporary pacing
Do not suppress rhythm

Ventricular Fibrillation

Ventricular Fibrillation
Associated with MI, ischemia,
disease states, procedures
Unresponsive, pulseless, and
apneic
If not treated rapidly, death
will result
Treat with immediate CPR
and ACLS
Defibrillation

Audience Response Question

A patient in the coronary care unit develops
ventricular fibrillation. The first action the
nurse should take is to
a.
b.
c.
d.

Perform defibrillation.
Initiate cardiopulmonary resuscitation.
Prepare for synchronized cardioversion.
Administer IV antidysrhythmic drugs per
protocol.

Asystole
Represents total absence of
ventricular electrical activity
No ventricular contraction
Patient unresponsive,
pulseless, apneic
Must assess in more than
one lead

Asystole
Usually result of advanced
cardiac disease, severe
conduction disturbance, or endstage HF
Treat with immediate CPR and
ACLS measures
Epinephrine and/or vasopressin
Intubation

Poor prognosis

Pulseless Electrical
Activity
Electrical activity can be
observed on the ECG, but no
mechanical activity of the
ventricles is evident, and the
patient has no pulse
Prognosis is poor unless
underlying cause quickly
identified and treated

Pulseless Electrical
Activity

Hs and Ts
Pneumonic
Hypovolemia

Hypoxia
Hydrogen ion
(acidosis)
Hyper-/hypokale
mia
Hypoglycemia
Hypothermia

Toxins
Tamponade
(cardiac)
Thrombosis (MI
and pulmonary)
Tension
pneumothorax
Trauma

Copyright 2014 by Mosby, an imprint of

Pulseless Electrical
Activity
Treatment
CPR followed by intubation and
IV epinephrine
Treatment is directed toward
correction of the underlying
cause

Sudden Cardiac Death

(SCD)
Death from a cardiac cause
Majority of SCDs result from
ventricular dysrhythmias
Ventricular tachycardia
Ventricular fibrillation

Prodysrhythmia
Life-threatening
dysrhythmias caused by
antidysrhythmia drugs
Severe LV dysfunction
increases risk
Digoxin and class IA, IC, and
III antidysrhythmia drugs
Most susceptible first few
days of drug therapy

Defibrillation
Treatment of choice for VF and
pulseless VT
Most effective when completed within
2 minutes of dysrhythmia onset
Passage of DC electrical shock
through the heart to depolarize cells
of myocardium
Allows SA node to resume pacemaker
role

Defibrillation
Monophasic defibrillators
deliver energy in one
direction
Biphasic defibrillators deliver
energy in two directions
Use lower energies
Fewer postshock ECG
abnormalities

Defibrillation

Defibrillation
Output is measured in joules
or watts per second
Recommended energy for
initial shocks in defibrillation
Biphasic: 120 to 200 joules
Monophasic: 360 joules

Immediate CPR after first

shock

Defibrillation

Defibrillation
1. Start CPR while obtaining and
setting up defibrillator
2. Turn on and select energy
3. Make sure sync button is turned off
4. Apply gel pads
5. Charge
6. Position paddles firmly on chest
7. Ensure All clear!!!!!
8. Deliver charge

Case Study
iStockphoto/Thinkstock

S.D. was admitted to the

telemetry unit and an IV
amiodarone drip was started.
The purpose of the drug was
to convert her atrial
fibrillation to normal sinus
rhythm.

Case Study
iStockphoto/Thinkstock

Although her heart rate has

decreased to 108
beats/minute, she remains in
atrial fibrillation 24 hours later.
A cardiologist was consulted
and electrical cardioversion is
planned.

Case Study
iStockphoto/Thinkstock

What would you teach S.D.

about the scheduled
procedure?
What are three differences
between defibrillation and
cardioversion?

Synchronized
Cardioversion
Choice of therapy for
ventricular ( VT with a pulse)
or supraventricular
tachydysrhythmias
Synchronized circuit delivers
a countershock on the R wave
of the QRS complex of the
ECG

Synchronized
Cardioversion
Procedure similar to defibrillation
except sync button turned ON
If patient stable, sedate prior
Initial energy lower
7075 joules (biphasic)
100 joules (monophasic)

If patient becomes pulseless, turn

sync button off and defibrillate

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

Decreases mortality

Implantable CardioverterDefibrillator (ICD)

Consists of a lead system

placed via subclavian vein to
the endocardium
Battery-powered pulse
generator is implanted
subcutaneously
Sensing system monitors HR
and rhythm delivering 25
joules or less to heart when

Implantable CardioverterDefibrillator (ICD)

Implantable CardioverterDefibrillator (ICD)

Includes antitachycardia and

antibradycardia pacemakers
Overdrive pacing for
tachycardias
Backup pacing for bradycardias

Preprocedure and
postprocedure care same as
pacemaker

Implantable CardioverterDefibrillator (ICD)

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

Implantable CardioverterDefibrillator (ICD)

Patient and Caregiver Teaching

1.
2.
3.
4.
5.
6.
7.

Follow-up appointments
Incision care
Arm restrictions
Sexual activity
Driving
Avoid direct blows
Avoid large magnets, MRI

Implantable CardioverterDefibrillator (ICD)

Patient and Caregiver Teaching

8. Air travel
9. Avoid antitheft devices
10.What to do if ICD fires
11.Medic Alert ID
12.ICD identification card
13.Caregivers to learn CPR

Pacemakers
Used to pace the heart when
the normal conduction
pathway is damaged
Pacing circuit consists of
Programmable pulse generator
(power source)
One or more conducting
(pacing) leads to myocardium

Pacemaker Spike

Pacemakers
Pace atrium and/or one or both of
ventricles
Most pace on demand, firing only
when HR drops below preset rate
Sensing device inhibits pacemaker
when HR adequate
Pacing device triggers when no QRS
complexes within set time frame

Pacemakers
Antitachycardia pacing:
delivery of a stimulus to the
ventricle to terminate
tachydysrhythmias
Overdrive pacing: pacing the
atrium at rates of 200500
impulses/minute to terminate
atrial tachycardias

Pacemaker

Pacemakers
Cardiac resynchronization
therapy (CRT)
Resynchronizes the cardiac
cycle by pacing both ventricles
Biventricular pacing
Used to treat patients with
heart failure
Can be combined with ICD for
maximum therapy

Temporary Pacemakers
Power source outside the
body
Transvenous
Epicardial
Transcutaneous

Temporary Transvenous
Pacemaker

Epicardial Pacing
Leads placed on epicardium
during heart surgery
Passed through chest wall
and attached to external
power source as needed

Transcutaneous Pacing
For emergent pacing needs
Noninvasive
Bridge until transvenous
pacer can be inserted
Use lowest current that will
capture
Patient may need
analgesia/sedation

Transcutaneous Pacing

Fig 10-9. Anterioposterior placement of adhesive electrode pads for defibrillation or transcutaneous pacing.
From: Sole et al. Introduction to Critical Care Nursing, 5th Edition. W.B. Saunders

Temporary Pacemaker

Pacemakers
ECG monitoring for
malfunction
Failure to sense
Causes inappropriate firing

Failure to capture
Lack of pacing when needed
leads to bradycardia or asystole

Pacemakers
Monitor for other
complications

Infection
Hematoma formation
Pneumothorax
Atrial or ventricular septum
perforation
Lead misplacement

Pacemakers
Postprocedure care
OOB once stable
Limit arm and shoulder activity
Monitor insertion site for
bleeding and infection
Patient teaching important

Pacemakers
Patient and Caregiver Teaching
Follow-up
appointments for
pacemaker
function checks
Incision care
Arm restrictions
Avoid direct blows
Avoid high-output
generator

No MRIs unless
pacer approved
Microwaves OK
Avoid antitheft
devices
Air travel
Monitor pulse
Pacemaker ID card
Medic Alert ID

Copyright 2014 by Mosby, an imprint of

Radiofrequency Catheter
Ablation Therapy
Electrode-tipped ablation catheter
burns accessory pathways or
ectopic sites in the atria, AV node,
and ventricles
Nonpharmacologic treatment of
choice for several atrial
dysrhythmias
Postcare similar to cardiac
catheterization

Case Study
iStockphoto/Thinkstock

S.D.s electrical cardioversion

was successful.
S.D.s sinus rhythm has
remained stable for 24 hours
and she is ready to go home.

Case Study
iStockphoto/Thinkstock

As you enter her room to

provide discharge teaching,
she tells you she is
experiencing some chest
heaviness and tightness
right under her breast bone.

Case Study
iStockphoto/Thinkstock

You ask the UAP to obtain a

12-lead ECG while you notify
S.D.s health care provider.
What specific ECG change will
you be looking for to
determine if S.D.s chest pain
is related to cardiac ischemia?
Injury? Infarction?

ECG Changes Associated With

Acute Coronary Syndrome (ACS)

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
Changes reverse when
adequate blood flow is
restored to myocardium

Changes Associated With

Myocardial Ischemia

ECG Changes Associated With

Acute Coronary Syndrome (ACS)

Injury
ST-segment elevation occurs
Significant if >1 mm above the
isoelectric line

If treatment is prompt and

effective, may avoid or limit
infarction
Absence of serum cardiac
markers confirms no infarction

Changes Associated With

Injury

ECG Changes Associated With

Acute Coronary Syndrome (ACS)

Infarction
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

Changes Associated With

Infarction

ECG Finding With

Anterolateral Wall MI

Syncope
Brief lapse in consciousness
accompanied by a loss in
postural tone (fainting)
Noncardiovascular causes

Stress
Hypoglycemia
Dehydration
Stroke
Seizure

Syncope
Cardiovascular causes
Cardioneurogenic or vasovagal
syncope
Carotid sinus sensitivity

Dysrhythmias (tachycardias,
bradycardias)
Prosthetic valve malfunction
Pulmonary emboli
HF

Syncope
Diagnostic studies

Echocardiography
Stress test
EPS
Head-up, tilt test
To assess for cardioneurogenic syncope
Abnormal response to position change
causes paradoxic vasodilation and
bradycardia (vasovagal response)