Lecture 3 cardiac rhythms
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JB 9/10
CARDIACRhythms
ArrhythmiasDysrhythmias
Oh, my!
Lecture 3
NUR240
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Arrhythmia
ARRHYTHMIA – VARIATION IN NORMAL RHYTHM
DYSRHYTHMIA – ABNORMAL, DISTURBED RHYTHM
RESULTS FROM IMPULSE FORMATION DISTURBANCE OR CONDUCTION DISTURBANCE
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AXIOM
ALL RHYTHM INTERPERTATION MUST BE CORRELATED WITH SIGNS & SYMPTOMS AND PATIENT CONDITION…
“TREAT THE PATIENT,NOT THE MONITOR”
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Dysrhythmia
Impulse formation
(site of impulse origin)
SA Node
AV Node
Ventricle
Ectopic
Premature Beat
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Dysrhythmia
Altered conduction• Bradycardia / Tachycardia• Flutter / Fibrillation• Heart blocks
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Basic Rhythm Strip Interpretation
1. Determine the rate. Does the atrial rate equal the ventricular rate.
2. Is the rhythm regular/irregular?3. Find the P wave. Is there a P wave for every
QRS?4. Determine the PRI (Normal 0.12-0.20 sec)5. Find the QRS (Normal <0.12seconds)6. Any ectopic beats?7. Find the T wave.http:www.rnceus.comEKG strip identification and evaluation
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Determine heart rate
REGULAR RHYTHM – count boxes between 2 “R” waves and divide
into 300
5
300 / 5 = 60
1 small box = .04 second 30 large boxes = 6 seconds1 large box = .20 second 300 large boxes = 1 minute15 large boxes = 3 seconds 1 mm = 0.1 millivolt (mV)
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Determine heart rate
• Irregular rhythm – count R - R intervals on a 6 sec. strip and multiply by 10
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Normal Sinus Rhythm
• NORMAL SINUS RHYTHM IS PRODUCED BY THE SA NODE– P – WAVE FOLLOWS QRS COMPLEX IN A
PREDICTABLE RELATIONSHIP– ALL “P” WAVES LOOK ALIKE, ALL QRS
COMPLEXES ARE NARROW– R – R INTERVAL IS REGULAR– RATE: 60 – 100 bpm
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Normal Sinus Rhythm
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Normal Sinus Rhythm
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Sinus / Atrial dysrhythmia
• ORIGINATE FROM SA NODE OR ATRIA
(ABOVE VENTRICLES)
• CONDUCTION WITH VENTRICLE IS UNDISTURBED
• USUALLY BENIGN & SYMPTOMATIC
• RHYTHM MAY BE IRREGULAR
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Sinus / Atrial dysrhythmias
– SINUS TACHYCARDIA– SINUS BRADYCARDIA– ATRIAL FIBRILLATION– ATRIAL FLUTTER– Premature atrial contractions– Paroxysmal atrial tachycardia– Supraventricular Tachycardia
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Sinus Tachycardia
• VENTRICULAR RATE 100 bpmETIOLOGY:
– MAY REFLECT PHYSIOLOGIC
DEMAND FOR O2
– SYMPATHOMIMETIC DRUGS– FEVER
– PAIN
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Sinus Tachycardia
• CLINICAL SIGNS:– HR MYOCARDIAL DEMAND
FOR O2
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Treatment
– MAY RESOLVE WITH TREATMENT
OF UNDERLYING CAUSE
– DRUGS WITH RATE SLOWING
EFFECT: DIGOXIN, β-BLOCKERS
– CAROTID MASSAGE
– VAGAL MANEUVER
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Sinus Bradycardia
• VENTRICULAR RATE = 60
ETIOLOGY:
RESPONSE TO MYOCARDIAL ISCHEMIA
VAGAL STIMULATION
ELECTROLYTE IMBALANCE
DRUGS
I.C.P.
HIGHLY TRAINED ATHLETE
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CLINICAL SIGNS
C.O. IF BODY CAN’T COMPENSATE
OR IMPROVED C.O. DUE TO DIASTOLIC FILLING TIME MAY LEAD TO ARRHYTHMIA
• TREATMENT – DEPENDS ON CAUSE:– ATROPINE– AVOID VALSALVA– HOLD RATE SLOWING DRUGS
I.E.: DIGOXIN, blockers
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Atrial Flutter• ATRIAL RATE = 250 – 400 IMPULSES/ MINUTE
– ETIOLOGY:• OCCURS /W HEART DISEASE• CAD• VALVE DISORDERS
– CLINICAL SIGNS• “SAW TOOTH” P-WAVES, CALLED F-WAVES• ATRIAL RATE = 250 – 400/ MIN• AV NODE BLOCKS SOME IMPULSES• INCOMPLETE EMPTYING OF ATRIA CAUSE RISK
FOR THROMBUS GIVE ANTICOAGULANTSGIVE ANTICOAGULANTS
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Atrial Flutter
• TREATMENT– TREAT UNDERLYING CAUSE IRRITABILITY, RAPID VENTRICULAR
RESPONSE– DIGOXIN SLOWS RATE BY ENHANCING
AV BLOCK– QUINIDINE SUPRESSES ATRIAL ECTOPIC
BEATS– AMIODARONE– CALCIUM CHANNEL & β-BLOCKERS– CONSIDER CARDIOVERSION
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Atrial Fibrillation
• CHAOTIC ELECTRICAL ACTIVITY IN ATRIA
• ATRIA QUIVER (>500 beats/minute) INSTEAD OF CONTRACTING AS A UNIT
• ETIOLOGY: ADVANCED AGEVALVE DISORDERS
CARDIOMYOPATHY
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Atrial Fibrillation
“F” FIBRILLATORY WAVES
ø P-WAVES, ø P-R INTERVALQRS normalVENTRICULAR RATE IS IRREGULARRAPID VENTRICULAR RESPONSE PULSE DEFICIT
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Atrial Fibrillation
TREATMENT1. Amiodarone-may cause liver, lung damage and
worsening of arrhythmias. Pt to report SOB, wheezing, jaundice, palpitations, lightheadedness
2. Pronestyl, Ca channel blockers, beta blockers, digoxin
3. Synchronized cardioversion if unstable4. Radio frequency catheter ablation5. Anticoagulation therapy
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Atrial Rhythms
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Synchronized Electrical Cardioversion
Oh O2 Saturation Monitoring
Say Suction Equipment
It IV Line
Isn’t Intubation equipment
So Sedation and possibly analgesics
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Cardioversion
Synchronized shock with the QRS complex
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JUNCTIONAL DYSRHYTHMIAS
• IMPULSE BEGINS IN AV NODE
• VENTRICULAR RATE IS EXTREMELY SLOW
• MONITOR FOR SYMPTOMS OF REDUCED CARDIAC OUTPUT AND HEMODYNAMIC INSTABILITY
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Paroxysmal Supraventricular Tachycardia
• ABRUPT ONSET OF HR
• ETIOLOGY: SNS STIMULATION
CARDIOMYOPATHY
• CLINICAL SIGNS:
ABRUPT ONSET/ CESSATION
S/S ARE RELATED TO C.O.
RATE = 150 – 250 bpm
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PSVT
• TREAT UNDERLYING CAUSE– DRUGS: ADENOSINE, β-BLOCKERS,
DIGOXIN, MS, QUINIDINE
– CAROTID / VAGAL MANEUVERS– SYNCHRONIZED CARDIOVERSION IF
UNSTABLE
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Ventricular Arrhythmias
• ORIGINATES IN VENTRICLES
• PATIENT MAY BE SYMPTOMATIC, REQUIRES IMMEDIATE ATTENTION
– PVC, couplet, bigeminy, trigeminy
– V-TACH (ventricular tachycardia)
– V-Fib (Ventricular fibrillation)
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PREMATURE VENTRICULAR CONTRACTION(PVC)
– EARLY IRREGULAR VENTRICULAR BEATS
– QRS IS WIDE /BIZZARE– CAN BE CHRONIC ASYMPTOMATIC
ABNORMALITY OR WARNING OF SERIOUS DYSRHYTHMIA
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PREMATURE VENTRICULAR CONTRACTION(PVC)
• ETIOLOGY:
HYPOXIA
DIGOXIN TOXICITY
MECHANICAL STIMULATION
ELECTROLYTE (K) IMBALANCE
MI
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PVCs
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PREMATURE VENTRICULAR CONTRACTION(PVC)
• CLINICAL SIGNS:– DEPEND ON FREQUENCY– PVC SHORT DIASTOLIC FILLING TIME
C.O.– FREQUENT PVC – SENSATION OF
PALPATIONS, SKIPPED BEATS– BIGEMINY – PVC EVERY OTHER BEAT– TRIGEMINY – PVC EVERY 3RD BEAT
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PREMATURE VENTRICULAR CONTRACTION(PVC)
• TREATMENT:– TREAT IMPAIRED HEMODYNAMICS– ANTIARRHYTHMICS– OXYGEN– MONITOR FOR PVC LANDING ON
T-WAVE– OBSERVE FOR UNIFOCAL (VS) MULTIFOCAL
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Ventricular Arrhythmias
• VENTRICULAR TACHYCARDIA– 3 OR MORE PVC’s– QRS IS WIDE/ BIZARRE
EXTREMELY SERIOUS
MAY LEAD TO LETHAL RHYTHMS
• ETIOLOGY: SAME CAUSES AS PVC, ALSO CARDIOMYOPATHY, MYOCARDIAL
IRRITABILITY
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Ventricular Tachycardia
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Treatment
– VT /W PULSE - CARDIOVERT– MONITOR MORE CLOSELY– PREPARE FOR CARDIOVERSION
(O2, LIDOCAINE, TREAT CAUSE)
– VT W/O PULSE - DEFIBRILLATE
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VENTRICULAR FIBRILLATION
TOTAL UNORGANIZED MULTIFOCAL
RHYTHM, VENTRICLES QUIVER,
NO CARDIAC OUTPUT
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V-fib
• ETIOLOGY: SAME AS VT, PVCSURGICAL MANIPULATION OF HEARTFAILED CARDIOVERSION
• CLINICAL SIGNS:SAME AS CARDIAC ARRESTEKG SHOWS DISORGANIZED RHYTHM
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V-fib
• TREATMENT
IMMEDIATE DEFIBRILLATION X3
CPR
SURVIVAL IS < 10% FOR EVERY MINUTE THE PATIENT REMAINS IN V-fib
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SCREAM for Vfib and Pulseless VTach
1.Shock360J* monophasic, 1st and subsequent shocks.(Shock every 2 minutes if indicated)
2.CPR After shock, immediately begin chest compressions followed by respirations (30:2 ratio) for 2 minutes.
3.Rhythm check after 2 minutes of CPR (and after every 2 minutes of CPR thereafter) and shock again if indicated. Check pulse only if an organized or non-shockable rhythm is present.
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SCREAM
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CARDIAC ARREST• VENTRICULAR ASYSTOLE
80 – 90% DUE TO V-fib TOTAL ABSENCE OF ELECTRICAL AND
MECHANICAL ACTIVITY
• ETIOLOGYTRAUMAOVERDOSEMI
• CLINICAL SIGNS
– ASYSTOLE or V-fib– NO DEFINABLE WAVE FORMS– ABSENCE OF VITAL SIGNS
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Ventricular Asystole
Acronym Comments
T Transcutaneous Pacemaker
Only effective with early implementaion
E Epinephrine 1 mg IV q3-5 min
A Atropine 1 mg IV q3-5 min
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PEA- Pulseless Electrical Activity
• Asystole Algorithm
• P E A
• Problem search
• Epinephrine – 1mg IV/IO q3-5min
• Atropine- with a slow HR, I mg IV/IO q3-5min
• Consider termination of efforts if asystole persists despite appropriate interventions.
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CARDIAC ARRESTReview ACLS Guidelines 2005TREATMENT: IMMEDIATE CPR
A. AIRWAY/ ADVANCED AIRWAY CONTROL
B. BREATHING/ POSITIVE PRESSURE VENTILATION
C. CIRCULATION/ CPR, START IV
D. DEFIBRILLATE (V-fib, V-tach ONLY)
E. DRUGS-Antidysrhythmic tx
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CARDIAC ARREST
• EPINEPHRINE 1:10,000 IV PUSH
REPEAT Q 5 MIN.
• AMIODORONE:
• ATROPINE:
• VASOPRESSIN:
• CONSIDER ANTIARRHYTHMICS
• USE ACLS ALGORITHMS
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CARDIAC ARREST
• TREATMENT: POST CARDIAC ARREST
MONITOR -
CARDIAC STATUS
RESPIRATORY STATUS
TREAT UNDERLYING CAUSE
EMOTIONAL SUPPORT
SAFE ENVIRONMENT
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DEFBRILLATION (vs) CARDIOVERSION
• DEFIBRILLATIONASYNCHRONOUS ELECTRICAL DISCHARGE THAT CAUSES DEPOLARIZATION OF ALL MYOCARDIAL CELLS AT ONCE. THIS ALLOWS (HOPEFULLY) THE SA NODE TO RESTORE ITS PACEMAKER FUNCTION AND DICTATE A REGULAR SINUS RHYTHM.
USED FOR PULSELESS V-tach AND V-fibVOLTAGE: 200 – 360 joules (“stacked shock”)
or AED
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CARDIOVERSION (aka) SYNCHRONIZED CONVERSION
ELECTRICAL IMPULSE IS DISCHARGED DURING QRS (VENTRICULAR DEPOLARIZATION)
USUALLY TIMED /W CARDIAC MONITOR TO PREVENT SHOCK ONT-WAVE
USED FOR RAPID A-fib, V-tach /W PULSE AND PERSISTENT PAT / PSVT
VOLTAGE: 50 – 100 joules
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EQUIPMENT REVIEW
• DEFIBRILLATORSELECT ENERGY LEVEL, THEN CHARGE
• PADDLESUSE 25 POUNDS OF PRESSURE WHEN APPLIED TO CHEST, Placed 2nd RICS and 5th LAAS
• CONDUCTING AGENTGEL OR PAD WHICH ESTABLISHES SKIN CONTACT, REDUCES SKIN BURNS
• JOULESMEASUREMENT OF ELECTRICAL ENERGY
• DISCHARGESNO ONE SHOULD COME IN CONTACT WITH PATIENT OR BED DURING DISCHARGE
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HEART BLOCK
• DEPRESSED CONDUCTION OF IMPULSE FROM ATRIA TO VENTRICLES
• AV NODE BECOMES DEFECTIVE AND IMPULSES (P-WAVES) ARE BLOCKED FROM BEING TRANSMITTED TO VENTRICLES
FIRST DEGREE
SECOND DEGREE
TYPE I
TYPE II
THIRD DEGREE
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1° HEART BLOCK
• PR INTERVAL > 0.20 SECONDS• CAUSES: MAY BE NORMAL VARIANT
INFERIOR WALL MIDRUGS: DIGOXIN
VERAPAMIL• TREATMENT:
MONITOROBSERVE FOR SYMPTOMS
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FIRST DEGREE HEART BLOCK
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2° HEART BLOCK
• ONE OR MORE P-WAVES ARE NOT CONDUCTED THROUGH THE VENTRICLE
• HEART RATE - VENTRICULAR RATE SLOW TO NORMAL
ATRIAL RATE MAY BE 2 – 4 X’s
FASTER THAN VENTRICULAR
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2° HEART BLOCKCAUSES: ORGANIC HEART DISEASE
MI, Dig toxicity, B and Ca Channel Blockers
DIGOXIN TOXICITYSYMPTOMS • Tx:
Monitor HR Atropine Temporary pacemaker
Avoid meds that decrease conductivity2 TYPES OF 2° HEART BLOCK
MOBITZ TYPE I- Wenkeback
MOBITZ TYPE II
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Second Degree Heart BlockMobitz I
• PRI becomes progressively longer until drops QRS
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Second Degree Heart BlockMobitz Type II
• PRI constant and regular, but in a 2:1 , 3:1 pattern
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3° HEART BLOCK(COMPLETE HEART BLOCK)
• ATRIAL IMPULSES & VENTRICULAR RESPONSE ARE IN TOTAL DISASSOCIATION
• P-WAVES ARE SEEN & ARE IRREGULAR• QRS COMPLEX ARE SEEN & ARE IRREGULAR
(ESCAPE RHYTHM)• NO CORRELATION BETWEEN P-WAVES & QRS
(RATE IS SLOW) – independent rhythms
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3° HEART BLOCK(COMPLETE HEART BLOCK)• CAUSES
ORGANIC HEART DISEASEMIDRUGSELECTROLYTE IMBALANCEEXCESS VAGAL TONE
• SIGNS & SYMPTOMS EXTREME DIZZINESS HYPOTENSION SYNCOPE S/S OF C.O. ALTERED MENTAL STATUS
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NSR vs 3RD Degree Block
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3° HEART BLOCK(COMPLETE HEART BLOCK)
• TREATMENT
PACEMAKER
TEMPORARY
OR
PERMANENT
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PACEMAKER
• Indications: Speed up a slow HR or Slow down a rapid HR
• ELECTRICAL DEVICE THAT DELIVERS CONTROLLED ELECTRICAL STIMULUS THROUGH ELECTRODES PLACED IN CONTACT WITH HEART MUSCLE
• 2 PIECESPULSE GENERATOR IMPLANTED IN CHEST WALL UNDER R CLAVICLEPACEMAKER ELECTRODES IMPLANTED IN MYOCARDIAL TISSUE
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Paced Rhythm
• Pacemaker spike
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PACEMAKER
• TEMPORARY PACEMAKER– USED IN
EMERGENCY SITUATION
– FIXED (COMPETITIVE) PACEMAKER SENDS STIMULUS TO VENTRICLE AT A FIXED RATE, REGARDLESS OF VENTRICULAR ACTIVITY
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Types of Pacemakers
Use a 5 letter code system, first 3 used more often:
1. Chamber being paced: A, V, D
2. Chamber being sensed: A, V, D, O
3. Type of response by the PM to the sensing: I, T, D, O
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PATIENT TEACHING
• Carry PM ID card• MEDI ALERT BRACELET• Avoid swimming, golf and weight lifting• AVOID MRI• Check PM q3-6 mos.• PACEMAKER SURVEILANCE• Monitor pulse rates• Don’t hold cell phones over generators
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AUTOMATIC IMPLANTABLE CARDIOVERSION DEFIBRILLATOR
(AICD)• PROVIDES INTERNAL SHOCKS WHEN SERIOUS
ARRHYTHMIA IS DETECTED (V-tach OR V-fib)• Has a pulse generator and a sensor that monitors
the heart• If pt has dysrhythmia it delivers a shock which the
pt will feel
• USEFUL WHEN ARRHYTHMIA IS UNRESPONSIVE TO MEDS OR SURGICAL ABLATION OR IRRITABLE MYOCARDIAL TISSUE
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References
• http://www.rnceus.com/ekg/ekgsecond2.html
• ACLS Guidelines 2005
• www.EMS-ED.net
• http://www.doctorshangout.com/forum/topics/acls-algorithms-1