THE CONDUCTION
SYSTEM
Unit 10 O2 Perfusion Dysrhythmias
The Conduction System
•
Conduction system
•
•
Specialized electrical (pacemaker) cells
Arranged in a system of pathways
Unit 10 O2 Perfusion Dysrhythmias
The Conduction System
•
Primary pacemaker
•
Sinoatrial (SA) node
Unit 10 O2 Perfusion Dysrhythmias
•
The Conduction System
Atria
•
•
Impulse leaves SA node
Spreads from cell to cell across atrial muscle
Unit 10 O2 Perfusion Dysrhythmias
The Conduction System
• Internodal pathways
• Impulse is spread to AV
node via internodal
pathways
• Merge gradually with cells of
AV node
Unit 10 O2 Perfusion Dysrhythmias
The Conduction System
•
AV node
•
Located in floor of right atrium
•
•
Supplied by right coronary artery in most people
Delays conduction of impulse from atria to the ventricles
•
Allows time for atria to empty into ventricles
Unit 10 O2 Perfusion Dysrhythmias
The Conduction System
Unit 10 O2 Perfusion Dysrhythmias
The AV node and AV bundle
Unit 10 O2 Perfusion Dysrhythmias
The Conduction System
•
Bundle of His (AV bundle)
•
•
•
Connects AV node with bundle branches
Pacemaker cells have an intrinsic rate of 40 to 60 bpm
Conducts impulse to right and left bundle branches
Unit 10 O2 Perfusion Dysrhythmias
The Conduction System
• Right bundle branch
• Left bundle branch
• Divides into three fascicles
• Anterior fascicle
• Posterior fascicle
• Septal fascicle
Unit 10 O2 Perfusion Dysrhythmias
The Conduction System
• Purkinje fibers
• Receive impulse from
bundle branches
• Relay it to ventricular
myocardium
• Pacemaker cells have an
intrinsic rate of 20 to 40
bpm
Unit 10 O2 Perfusion Dysrhythmias
The Conduction System
Unit 10 O2 Perfusion Dysrhythmias
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
Unit 10 O2 Perfusion Dysrhythmias
Electrocardiogram Monitoring
•
Graphic tracing of electrical impulses produced in the heart
•
Waveforms of ECG represent the electrical activity produced by the movement of
charged ions across membranes of heart cells
Unit 10 O2 Perfusion Dysrhythmias
The ECG
•
Can provide information about:
The orientation of the heart in the chest
• Conduction disturbances
• The electrical effects of medications and electrolytes
• The mass of cardiac muscle
• The presence of ischemic damage
•
Unit 10 O2 Perfusion Dysrhythmias
The ECG
•
Does not provide information about the mechanical (contractile) condition of the
myocardium
•
Evaluated by assessment of pulse and blood pressure
Unit 10 O2 Perfusion Dysrhythmias
Unit 10 O2 Perfusion Dysrhythmias
Electrocardiogram Monitoring (2 of 2)
Fig. 31-4
Unit 10 O2 Perfusion Dysrhythmias
12-Lead ECG
Fig. 35-3
Unit 10 O2 Perfusion Dysrhythmias
Lead Placement
Fig. 35-4
Unit 10 O2 Perfusion Dysrhythmias
ECG Time and Voltage
Fig. 35-5
Unit 10 O2 Perfusion Dysrhythmias
Calculating HR
•
Count
•
•
Number of QRS complexes in 1 minute*
IF the rhythm is regular:
•
•
•
Number of QRS complexes 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
Unit 10 O2 Perfusion Dysrhythmias
Assessment of Cardiac Rhythm
Fig. 35-6
Unit 10 O2 Perfusion Dysrhythmias
Artifact
Fig. 35-8
Unit 10 O2 Perfusion Dysrhythmias
ECG Waveforms and Intervals Table 35-2
•
P Wave: 0.06-0.12 sec
•
PR Interval: 0.12-0.20 sec
•
Q Wave: <0.03 sec
•
QRS Interval: <0.12 sec
•
ST Segment: 0.12 sec
•
T wave: 0.16 sec
Unit 10 O2 Perfusion Dysrhythmias
Normal Sinus Rhythm
•
SA node fires 60 to100 beats/min
•
Follows normal conduction pattern
•
P wave is normal and precedes QRS
•
QRS has normal shape and duration
•
PR interval is normal
Unit 10 O2 Perfusion Dysrhythmias
Unit 10 O2 Perfusion Dysrhythmias
Sinus Bradycardia
•
SA nodes fires at less than 60 beats/min
•
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
Unit 10 O2 Perfusion Dysrhythmias
Sinus Bradycardia
Fig. 35-11A
Unit 10 O2 Perfusion Dysrhythmias
Sinus Bradycardia
•
Manifestations
Hypotension
• Pale, cool skin
• Weakness
• Angina
• Dizziness or syncope
• Confusion or disorientation
• Shortness of breath
•
• Treatment
•
•
•
•
Stop offending drugs
IV Atropine (Anticholinergic) blocks
sympathetic response
Pacemaker
Dopamine or epinephrine infusion
Unit 10 O2 Perfusion Dysrhythmias
Sinus Tachycardia
Fig. 35-11B
Unit 10 O2 Perfusion Dysrhythmias
Sinus Tachycardia (3 of 4)
• Manifestations
•
•
•
•
Dizziness
Dyspnea
Hypotension
Angina in patients with CAD
•
100-150 sinus tachy
•
150+ is V tachy
• Treatment
•
•
•
•
Guided by cause (e.g., treat pain)
Vagal maneuver
β-blockers, adenosine, or calcium
channel blockers
Synchronized cardioversion
Unit 10 O2 Perfusion Dysrhythmias
Premature Atrial Contraction
Fig. 35-12
Unit 10 O2 Perfusion Dysrhythmias
Premature Atrial Contraction
• Causes
•
•
•
•
•
•
•
•
Emotional stress
Physical fatigue
Caffeine
Tobacco
Alcohol
Hypoxia
Electrolyte imbalances
Disease states
• Manifestations
•
•
Palpitations
Heart “skips a beat”
• Treatment
•
•
•
Monitor for more serious dysrhythmias
Withhold sources of stimulation
β-blockers
Unit 10 O2 Perfusion Dysrhythmias
Paroxysmal Supraventricular Tachycardia
(PSVT)
Reentrant phenomenon: PAC triggers a run of repeated premature beats
Paroxysmal refers to an abrupt onset and ending
Associated with overexertion, stress, deep inspiration, stimulants, disease,
digitalis toxicity
Unit 10 O2 Perfusion Dysrhythmias
Paroxysmal Supraventricular Tachycardia
(PSVT)
• Manifestations
•
•
HR is 151 to 220 beats/min
HR greater than 180 leads to decreased
cardiac output and stroke volume
• Treatment
•
• Hypotension
• Palpitations
• Dyspnea
• Angina
•
•
•
•
Vagal stimulation (bear down like
going to poop) to get a baby to do it,
put ice on their face to vagal them
down)
IV adenosine
IV β-blockers
Calcium channel blockers
Synchronized cardioversion
Unit 10 O2 Perfusion Dysrhythmias
Atrial Flutter
Typically associated with disease
Symptoms result from high ventricular rate and loss of atrial “kick”
associated with atrial flutter decrease CO; can cause heart failure
Increases risk of stroke
Something wrong with AV node
Treatment
Pharmacologic agent- maybe beta blocker or calcium channel blocker
Electrical cardioversion
Radiofrequency ablation
Unit 10 O2 Perfusion Dysrhythmias
Atrial Fibrillation
Need anticoagulants
No adenosine here!
Paroxysmal or persistent
Need calcium channel blockers
Most common dysrhythmia
Xeralto therapeutic labs can’t
Prevalence increases with age
be measured for toxic levels
Usually occurs in patients with underlying heart disease
Can occur with other disease states
As with atrial flutter—causes a decrease in CO and an increased risk of stroke
The client with uncontrolled atrial fibrillation with a ventricular rate over 100 beats
per minute is at risk for low cardiac output caused by loss of atrial kick.
The nurse should assess the client for palpitations, chest pain or discomfort,
hypotension, pulse deficit, fatigue, weakness, dizziness, syncope, shortness of breath,
and distended neck veins.
Unit 10 O2 Perfusion Dysrhythmias
Atrial Fibrillation (4 of 4)
• Treatment
•
•
•
•
•
Drugs to control ventricular response, prevent stroke, and/or convert to sinus rhythm
(amiodarone most common)
Electrical cardioversion
Anticoagulation (Table 35-8)
Radiofrequency ablation
Maze procedure with cryoablation
Pt will complain of chest pain
Unit 10 O2 Perfusion Dysrhythmias
Junctional Dysrhythmias (1 of 3)
•
Dysrhythmias that start in the AV junction
•
SA node fails to fire, or impulse is blocked at the AV node
•
AV node becomes pacer—retrograde transmission of impulse to atria
•
Abnormal P wave; normal QRS
•
Associated with disease, certain drugs
•
Accelerated: 61-100 beats/min
•
Junctional tachycardia: 101-180 beats/min
Unit 10 O2 Perfusion Dysrhythmias
Junctional Dysrhythmias
Fig. 35-16
Unit 10 O2 Perfusion Dysrhythmias
First-Degree AV Block (1 of 2)
Prolonged PR interval
This one is 0.4seconds
Associated with increasing age, disease states, and certain drugs
Usually not serious
Patients asymptomatic
No treatment
Monitor for changes in heart rhythm
Unit 10 O2 Perfusion Dysrhythmias
Second-Degree AV Block,
Type 1 (Mobitz I, Wenckebach) (1 of 2)
Second-degree AV block, type I,
with progressive lengthening of
the PR interval until a QRS
complex is blocked.
Longer, longer, then DROP
Caused by drugs, CAD
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, observe closely
Unit 10 O2 Perfusion Dysrhythmias
Second-Degree AV Block,
Type 2 (Mobitz II) (1 of 2)
Associated with heart disease and drug toxicity
Often progressive and results in decreased CO
Treat with pacemaker
These drops are the same length P wave, still dropping the QRS
Unit 10 O2 Perfusion Dysrhythmias
Third-Degree AV Heart Block
(Complete Heart Block) (1 of 2)
Associated with severe heart disease, some systemic diseases, certain drugs
Usually results in decreased CO, ischemia, HF, and shock
Can lead to syncope
Treat with pacemaker
Drugs to increase heart rate if needed while awaiting pacing
Unit 10 O2 Perfusion Dysrhythmias
Premature Ventricular Contractions
(1 of 3)
PVCs are abnormal ectopic
beats (occurring in otherwise
normal sinus rhythm)
originating in the ventricles.
They are characterized by an
absence of P waves, wide and
bizarre QRS complexes, and a
compensatory pause that
follows the ectopy
Need to be able to tell if its
PVC
Trigeminy not need to know
Premature Ventricular Contractions
(2 of 3)
•
Associated with stimulants, electrolyte imbalances, hypoxia, heart disease
•
Not harmful with normal heart but may reduce CO, lead to angina and HF in
diseased heart
•
Assess the hemodynamic status
•
As an isolated occurrence, the PVC is not life-threatening.
•
Frequent PVCs may be precursors of more life-threatening rhythms,
such as ventricular tachycardia and ventricular fibrillation.
•
Lidocaine hydrochloride are used to treat frequent PVCs who are
symptomatic and has decreased CO
• Treatment
•
•
Correct cause
β-blockers, lidocaine, or amiodarone
Unit 10 O2 Perfusion Dysrhythmias
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/min
•
Atropine if patient symptomatic
•
Temporary pacing
•
Do not suppress rhythm
Unit 10 O2 Perfusion Dysrhythmias
Ventricular Tachycardia (1 of 5)
Rate 240
Ectopic foci take over as pacemaker
Monomorphic, polymorphic, sustained, and nonsustained
Considered life-threatening because of decreased CO and the possibility of development
to ventricular fibrillation
QRS tells about the VENTRICLE
We only have QRS here which makes it a problem with the ventricle
QRS IS WIDE COMPLEX TACHY
Shock the unstable patient with synchronized defibrillation= deliver shock on the R wave
Ventricular Tachycardia (3 of 5)
Torsades de Pointes
Associated with heart disease, long QT syndrome, electrolyte imbalances, drug toxicity,
CNS disorders
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
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
Ventricular Fibrillation (1 of 2)
Unit 10 O2 Perfusion Dysrhythmias
Ventricular Fibrillation (2 of 2)
• Associated with acute MI, ischemia, disease states,
cardiac procedures
• Unresponsive, pulseless, and apneic
• If not treated rapidly, death will result
• Treat with immediate CPR and ACLS
•
•
Defibrillation
Drug therapy (epinephrine, amiodarone)
Unit 10 O2 Perfusion Dysrhythmias
Asystole (1 of 2)
•
Total absence of ventricular electrical activity
•
No ventricular contraction
•
Patient unresponsive, pulseless, apneic
•
Must assess in more than one lead
Usually result of advanced cardiac disease, severe
conduction system problem, or end-stage HF
Treat with immediate CPR and ACLS measures
Epinephrine
Intubation
Poor prognosis
Unit 10 O2 Perfusion Dysrhythmias
Pulseless Electrical Activity (1 of 3)
•
Electrical activity can be observed on the ECG, but no mechanical activity of the
heart is evident, and the patient has no pulse
•
Prognosis is poor unless underlying cause quickly identified and treated
Unit 10 O2 Perfusion Dysrhythmias
Pulseless Electrical Activity (2 of 3)
Hs and Ts Mnemonic
• Hypovolemia
• Toxins
• Hypoxia
• Tamponade (cardiac)
• Hydrogen ion (acidosis)
• Thrombosis (MI and
• Hyper-/hypokalemia
pulmonary)
• Tension pneumothorax
• Trauma
• Hypoglycemia
• Hypothermia
Treatment
CPR followed by intubation and IV epinephrine
Treatment is directed toward the correction of the underlying cause
Hypothermia code will go longer bc the patient has to be warmed
PEA due to acidosis = give bicarb IV push
How to treat cardiac tampanade= needle drainage= thoracotomy
Sudden Cardiac Death (SCD)
• Death from a cardiac cause
• Most SCDs result from ventricular dysrhythmias
•
•
Ventricular tachycardia
Ventricular fibrillation
Unit 10 O2 Perfusion Dysrhythmias
Defibrillation (1 of 6)
• Treatment of choice for VF and pulseless VT
•
Most effective when completed within 2 minutes of dysrhythmia onset
•
Passage of electrical shock through the heart to depolarize myocardial cells
• Allows SA node to resume pacemaker role
Unit 10 O2 Perfusion Dysrhythmias
Defibrillation (2 of 6)
• Monophasic defibrillators deliver energy in one
direction will charge up to 300
• Biphasic defibrillators deliver energy in two
directions only go to 200 – less energy used
•
•
Use lower energies
Fewer post shock ECG dysrhythmias
Unit 10 O2 Perfusion Dysrhythmias
Defibrillation (3 of 6)
Fig. 35-22
Unit 10 O2 Perfusion Dysrhythmias
Defibrillation (4 of 6)
• Output is measured in joules or watts per second
• Recommended energy for initial shocks in
defibrillation
•
•
Biphasic: 120 to 200 J
Monophasic: 360 J
• Immediate CPR after first shock
Unit 10 O2 Perfusion Dysrhythmias
Defibrillation (5 of 6)
Fig. 35-23
Unit 10 O2 Perfusion Dysrhythmias
Defibrillation (6 of 6)
1.
Continue CPR until defibrillator is charged
2.
Turn on and select proper energy level
3.
Make sure sync button is turned off
4.
Apply gel pads
5.
Charge defibrillator
6.
Position paddles firmly on chest wall
7.
Ensure “All clear”!!!!!
8.
Deliver charge
Unit 10 O2 Perfusion Dysrhythmias
Synchronized Cardioversion (1 of 2)
•
Therapy of choice for ventricular or supraventricular tachydysrhythmias (VT with
a pulse)
•
Synchronized circuit delivers a shock on the R wave of the QRS complex of the
ECG
Unit 10 O2 Perfusion Dysrhythmias
Synchronized Cardioversion (2 of 2)
• Procedure similar to defibrillation except sync
button turned ON
• If patient stable, sedate prior
• Initial energy lower
•
•
50 to 100 J (biphasic)
100 J (monophasic)
• If patient becomes pulseless, turn sync button off
and defibrillate
Unit 10 O2 Perfusion Dysrhythmias
Implantable Cardioverter-Defibrillator
(ICD) (1 of 7)
• 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
• Decreases mortality
Unit 10 O2 Perfusion Dysrhythmias
Implantable Cardioverter-Defibrillator
(ICD) (2 of 7)
•
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 J or less to heart when
detects lethal dysrhythmia
Unit 10 O2 Perfusion Dysrhythmias
Implantable Cardioverter-Defibrillator
(ICD) (3 of 7)
Fig. 35-24
Unit 10 O2 Perfusion Dysrhythmias
Implantable Cardioverter-Defibrillator
(ICD) (4 of 7)
• Includes antitachycardia and antibradycardia
pacemakers
Overdrive pacing for tachycardias
• Backup pacing for bradycardias
•
• Pre-procedure and postprocedure care same as
pacemaker
• S-ICD
Unit 10 O2 Perfusion Dysrhythmias
Implantable Cardioverter-Defibrillator
(ICD) (5 of 7)
• 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
Unit 10 O2 Perfusion Dysrhythmias
Implantable Cardioverter-Defibrillator
(ICD) (6 of 7)
Patient and caregiver teaching
1.
Follow-up appointments
2.
Incision care
3.
Arm restrictions
4.
Sexual activity
5.
Driving
6.
Avoid direct blows
7.
Avoid large magnets, MRI
Unit 10 O2 Perfusion Dysrhythmias
Implantable Cardioverter-Defibrillator
(ICD) (7 of 7)
Patient and caregiver teaching
8.
Air travel not restricted
9.
Avoid antitheft devices
10.
What to do if ICD fires
11.
Medic Alert ID
12.
ICD identification card
13.
Caregivers to learn CPR
Unit 10 O2 Perfusion Dysrhythmias
Pacemakers (1 of 5)
• Used to pace the heart when the normal conduction
pathway is damaged
• Pacing circuit consists of
•
•
Power source *battery-powered pulse generator)
Programmable circuitry
Unit 10 O2 Perfusion Dysrhythmias
Pacemaker Spike
Fig. 35-25
Unit 10 O2 Perfusion Dysrhythmias
Pacemakers (2 of 5)
• 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
Unit 10 O2 Perfusion Dysrhythmias
Pacemakers (3 of 5)
•
Antitachycardia pacing: delivery of a stimulus to the ventricle to end
tachydysrhythmias
•
Overdrive pacing: pacing the atrium at rates of 200 to 500 impulses/min to try to
stop atrial tachycardias
Unit 10 O2 Perfusion Dysrhythmias
Pacemakers (4 of 5)
Fig. 35-26
Unit 10 O2 Perfusion Dysrhythmias
Pacemakers (5 of 5)
• Cardiac resynchronization therapy (CRT)
•
Resynchronizes the heart cycle by pacing both ventricles
• Biventricular pacing
•
•
Used to treat patients with heart failure
Can be combined with ICD for maximum therapy
Unit 10 O2 Perfusion Dysrhythmias
Temporary Pacemakers (1 of 2)
• Power source outside the body
•
•
•
Transvenous
Epicardial
Transcutaneous
Unit 10 O2 Perfusion Dysrhythmias
Epicardial Pacing
•
Leads placed on epicardium during heart surgery
•
Passed through chest wall and attached to external power source
•
Leads placed prophylactically to treat dysrhythmias postoperatively
Unit 10 O2 Perfusion Dysrhythmias
Transcutaneous Pacing (1 of 2)
•
For emergency pacing needs
•
Noninvasive
•
Bridge until transvenous pacer can be inserted
•
Use lowest current that will “capture”
•
Patient may need analgesia/sedation
Unit 10 O2 Perfusion Dysrhythmias
Transcutaneous Pacing (2 of 2)
Fig. 35-29
Unit 10 O2 Perfusion Dysrhythmias
Temporary Pacemaker (2 of 2)
Fig. 35-30
Unit 10 O2 Perfusion Dysrhythmias
Pacemakers (6 of 9)
• ECG monitoring for malfunction
• Failure to sense
•
Causes inappropriate firing
• Failure to capture
•
Lack of pacing when needed leads to bradycardia or asystole
• Failure to pace
•
Pacemaker does not initiate electrical stimulus when it should fire
Unit 10 O2 Perfusion Dysrhythmias
Pacemakers (7 of 9)
• Monitor for other complications
•
•
•
•
•
Infection
Hematoma formation
Pneumothorax
Atrial or ventricular septum perforation
Lead misplacement
Unit 10 O2 Perfusion Dysrhythmias
Pacemakers (8 of 9)
• Postprocedure care
•
•
•
•
OOB once stable
Limit arm and shoulder activity
Observe insertion site for bleeding and infection
Patient teaching important
Unit 10 O2 Perfusion Dysrhythmias
Pacemakers (9 of 9)
• 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
• Travel not restricted
• Monitor pulse
• Pacemaker ID card
• Medic Alert ID
•
Unit 10 O2 Perfusion Dysrhythmias
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
Unit 10 O2 Perfusion Dysrhythmias
Syncope (1 of 3)
• Brief lapse in consciousness accompanied by a loss
in postural tone (fainting)
• Noncardiovascular causes
•
•
•
•
•
Stress
Hypoglycemia
Dehydration
Stroke
Seizure
Unit 10 O2 Perfusion Dysrhythmias
Syncope (2 of 3)
• Cardiovascular causes
•
Cardioneurogenic or “vasovagal” syncope
• Carotid sinus sensitivity
•
•
•
•
Dysrhythmias (tachycardias, bradycardias)
Prosthetic valve malfunction
Pulmonary emboli
HF
Unit 10 O2 Perfusion Dysrhythmias
Syncope (3 of 3)
• 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)
Unit 10 O2 Perfusion Dysrhythmias