Chapter - 036 Arrhythmias Class
Chapter - 036 Arrhythmias Class
Chapter - 036 Arrhythmias Class
Chapter 36
Properties of Cardiac
Cells
Automaticity
Excitability
Conductivity
Contractility
Conduction System of
the Heart
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
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Case Study
Describe the appropriate
location to apply the leads
for both the 5-lead cardiac
monitor as well as the 12lead ECG.
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Lead Placement
Lead Placement
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
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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
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
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
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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
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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
Second-Degree AV Block,
Type 2 (Mobitz II)
Second-Degree AV Block,
Type 2 (Mobitz II)
Premature Ventricular
Contractions
Premature Ventricular
Contractions
Premature Ventricular
Contractions
Treatment
Correct cause
Antidysrhythmics
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
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
Pulseless Electrical
Activity
Treatment
CPR followed by intubation and
IV epinephrine
Treatment is directed toward
correction of the underlying
cause
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
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
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Case Study
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Case Study
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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)
Decreases mortality
Preprocedure and
postprocedure care same as
pacemaker
Participation in an ICD
support group should be
Follow-up appointments
Incision care
Arm restrictions
Sexual activity
Driving
Avoid direct blows
Avoid large magnets, MRI
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
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
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Case Study
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Case Study
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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
Injury
ST-segment elevation occurs
Significant if >1 mm above the
isoelectric line
Infarction
Physiologic Q wave is the first
negative deflection following
the P wave
Small and narrow (<0.04 second
in duration)
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)