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```CARDIAC
Rhythms
Arrhythmias
Dysrhythmias
Oh, my!
NUR240
Lecture 3
JB 9/10
Arrhythmia
ARRHYTHMIA – VARIATION IN
NORMAL RHYTHM
DYSRHYTHMIA – ABNORMAL,
DISTURBED RHYTHM
RESULTS FROM IMPULSE
FORMATION DISTURBANCE OR
CONDUCTION DISTURBANCE
AXIOM
ALL RHYTHM INTERPERTATION MUST
BE CORRELATED WITH SIGNS &
SYMPTOMS AND PATIENT
CONDITION…
“TREAT THE PATIENT,
NOT THE MONITOR”
Dysrhythmia
Impulse formation
(site of impulse origin)
SA Node
Ectopic
AV Node
Premature Beat
Ventricle
Dysrhythmia
Altered conduction
• Flutter / Fibrillation
• Heart blocks
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.com
EKG strip identification and evaluation
Determine heart rate
REGULAR RHYTHM – count boxes
between 2 “R” waves and divide
into 300
5
300 / 5 = 60
1 small box = .04 second
1 large box = .20 second
15 large boxes = 3 seconds
30 large boxes = 6 seconds
300 large boxes = 1 minute
1 mm = 0.1 millivolt (mV)
Determine heart rate
• Irregular rhythm – count R - R intervals
on a 6 sec. strip and multiply by 10
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
Normal Sinus Rhythm
Normal Sinus Rhythm
Sinus / Atrial dysrhythmia
• ORIGINATE FROM SA NODE OR ATRIA
(ABOVE VENTRICLES)
• CONDUCTION WITH VENTRICLE IS
UNDISTURBED
• USUALLY BENIGN & SYMPTOMATIC
• RHYTHM MAY BE IRREGULAR
Sinus / Atrial dysrhythmias
– SINUS TACHYCARDIA
– ATRIAL FIBRILLATION
– ATRIAL FLUTTER
– Premature atrial contractions
– Paroxysmal atrial tachycardia
– Supraventricular Tachycardia
Sinus Tachycardia
• VENTRICULAR RATE  100 bpm
ETIOLOGY:
– MAY REFLECT PHYSIOLOGIC
DEMAND FOR  O2
– SYMPATHOMIMETIC DRUGS
– FEVER
– PAIN
Sinus Tachycardia
• CLINICAL SIGNS:
–  HR   MYOCARDIAL DEMAND
FOR O2
Treatment
– MAY RESOLVE WITH TREATMENT
OF UNDERLYING CAUSE
– DRUGS WITH RATE SLOWING
EFFECT: DIGOXIN, β-BLOCKERS
– CAROTID MASSAGE
– VAGAL MANEUVER
• VENTRICULAR RATE =  60
ETIOLOGY:
RESPONSE TO MYOCARDIAL ISCHEMIA
VAGAL STIMULATION
ELECTROLYTE IMBALANCE
DRUGS
 I.C.P.
HIGHLY TRAINED ATHLETE
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
Atrial Flutter
• ATRIAL RATE = 250 – 400 IMPULSES/ MINUTE
– ETIOLOGY:
• OCCURS /W HEART DISEASE
• 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 ANTICOAGULANTS
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
Atrial Fibrillation
• CHAOTIC ELECTRICAL ACTIVITY IN
ATRIA
• ATRIA QUIVER (>500 beats/minute)
UNIT
• ETIOLOGY:
VALVE DISORDERS
CARDIOMYOPATHY
Atrial Fibrillation
“F” FIBRILLATORY WAVES
ø P-WAVES,
ø P-R INTERVAL
QRS normal
VENTRICULAR RATE IS IRREGULAR
RAPID VENTRICULAR RESPONSE 
PULSE DEFICIT
Atrial Fibrillation
TREATMENT
1. Amiodarone-may cause liver, lung damage and
worsening of arrhythmias. Pt to report SOB,
2. Pronestyl, Ca channel blockers, beta blockers,
digoxin
3. Synchronized cardioversion if unstable
5. Anticoagulation therapy
Atrial Rhythms
Synchronized Electrical
Cardioversion
Oh
O2 Saturation Monitoring
Say
Suction Equipment
It
IV Line
Isn’t
Intubation equipment
So
Sedation and possibly analgesics
Cardioversion
Synchronized shock with the QRS complex
JUNCTIONAL DYSRHYTHMIAS
• IMPULSE BEGINS IN AV NODE
• VENTRICULAR RATE IS EXTREMELY
SLOW
• MONITOR FOR SYMPTOMS OF
REDUCED CARDIAC OUTPUT AND
HEMODYNAMIC INSTABILITY
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
PSVT
• TREAT UNDERLYING CAUSE
DIGOXIN, MS, QUINIDINE
– CAROTID / VAGAL MANEUVERS
– SYNCHRONIZED CARDIOVERSION IF
UNSTABLE
Ventricular Arrhythmias
• ORIGINATES IN VENTRICLES
• PATIENT MAY BE SYMPTOMATIC,
REQUIRES IMMEDIATE ATTENTION
– PVC, couplet, bigeminy, trigeminy
– V-TACH (ventricular tachycardia)
– V-Fib (Ventricular fibrillation)
PREMATURE VENTRICULAR CONTRACTION
(PVC)
– EARLY IRREGULAR VENTRICULAR
BEATS
– QRS IS WIDE /BIZZARE
– CAN BE CHRONIC ASYMPTOMATIC
ABNORMALITY OR WARNING OF
SERIOUS DYSRHYTHMIA
PREMATURE VENTRICULAR CONTRACTION
(PVC)
• ETIOLOGY:
HYPOXIA
DIGOXIN TOXICITY
MECHANICAL STIMULATION
ELECTROLYTE (K) IMBALANCE
MI
PVCs
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
PREMATURE VENTRICULAR CONTRACTION
(PVC)
• TREATMENT:
– TREAT IMPAIRED HEMODYNAMICS
– ANTIARRHYTHMICS
– OXYGEN
– MONITOR FOR PVC LANDING ON
T-WAVE
– OBSERVE FOR UNIFOCAL (VS) MULTIFOCAL
Ventricular Arrhythmias
• VENTRICULAR TACHYCARDIA
– 3 OR MORE PVC’s
– QRS IS WIDE/ BIZARRE
EXTREMELY SERIOUS
• ETIOLOGY: SAME CAUSES AS PVC, ALSO
CARDIOMYOPATHY, MYOCARDIAL
IRRITABILITY
Ventricular Tachycardia
Treatment
– VT /W PULSE - CARDIOVERT
– MONITOR MORE CLOSELY
– PREPARE FOR CARDIOVERSION
(O2, LIDOCAINE, TREAT CAUSE)
– VT W/O PULSE - DEFIBRILLATE
VENTRICULAR FIBRILLATION
TOTAL UNORGANIZED MULTIFOCAL
RHYTHM, VENTRICLES QUIVER,
NO CARDIAC OUTPUT
V-fib
• ETIOLOGY:
SAME AS VT, PVC
SURGICAL MANIPULATION OF HEART
FAILED CARDIOVERSION
• CLINICAL SIGNS:
SAME AS CARDIAC ARREST
EKG SHOWS DISORGANIZED
RHYTHM
V-fib
• TREATMENT
IMMEDIATE DEFIBRILLATION X3
CPR
SURVIVAL IS < 10% FOR EVERY
MINUTE THE PATIENT REMAINS IN
V-fib
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.
SCREAM
CARDIAC ARREST
• VENTRICULAR ASYSTOLE
 80 – 90% DUE TO V-fib
 TOTAL ABSENCE OF ELECTRICAL AND
MECHANICAL ACTIVITY
• ETIOLOGY
TRAUMA
OVERDOSE
MI
• CLINICAL SIGNS
– ASYSTOLE or V-fib
– NO DEFINABLE WAVE FORMS
– ABSENCE OF VITAL SIGNS
Ventricular Asystole
Acronym
T
Transcutaneous
Pacemaker
Only effective with early
implementaion
E
Epinephrine
1 mg IV q3-5 min
A
Atropine
1 mg IV q3-5 min
PEA- Pulseless Electrical
Activity
•
•
•
•
•
•
Asystole Algorithm
PEA
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.
CARDIAC ARREST
Review ACLS Guidelines 2005
TREATMENT: IMMEDIATE CPR
CONTROL
B. BREATHING/ POSITIVE PRESSURE
VENTILATION
C. CIRCULATION/ CPR, START IV
D. DEFIBRILLATE (V-fib, V-tach ONLY)
E. DRUGS-Antidysrhythmic tx
CARDIAC ARREST
•
•
•
•
•
•
EPINEPHRINE 1:10,000 IV PUSH
REPEAT Q 5 MIN.
AMIODORONE:
ATROPINE:
VASOPRESSIN:
CONSIDER ANTIARRHYTHMICS
USE ACLS ALGORITHMS
CARDIAC ARREST
•
TREATMENT: POST CARDIAC ARREST
MONITOR CARDIAC STATUS
RESPIRATORY STATUS
TREAT UNDERLYING CAUSE
EMOTIONAL SUPPORT
SAFE ENVIRONMENT
DEFBRILLATION (vs)
CARDIOVERSION
• DEFIBRILLATION
ASYNCHRONOUS 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-fib
VOLTAGE: 200 – 360 joules (“stacked shock”)
or AED
CARDIOVERSION (aka)
SYNCHRONIZED CONVERSION
ELECTRICAL IMPULSE IS DISCHARGED
DURING QRS (VENTRICULAR
DEPOLARIZATION)
USUALLY TIMED /W CARDIAC MONITOR TO
PREVENT SHOCK ON
T-WAVE
USED FOR RAPID A-fib, V-tach /W PULSE AND
PERSISTENT PAT / PSVT
VOLTAGE: 50 – 100 joules
EQUIPMENT REVIEW
• DEFIBRILLATOR
SELECT ENERGY LEVEL, THEN CHARGE
USE 25 POUNDS OF PRESSURE WHEN APPLIED TO
CHEST, Placed 2nd RICS and 5th LAAS
• CONDUCTING AGENT
GEL OR PAD WHICH ESTABLISHES SKIN CONTACT,
REDUCES SKIN BURNS
• JOULES
MEASUREMENT OF ELECTRICAL ENERGY
• DISCHARGES
NO ONE SHOULD COME IN CONTACT WITH PATIENT
OR BED DURING DISCHARGE
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
1° HEART BLOCK
• PR INTERVAL > 0.20 SECONDS
• CAUSES: MAY BE NORMAL VARIANT
INFERIOR WALL MI
DRUGS: DIGOXIN
VERAPAMIL
• TREATMENT:
MONITOR
OBSERVE FOR SYMPTOMS
FIRST DEGREE HEART BLOCK
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
2° HEART BLOCK
CAUSES:
ORGANIC HEART DISEASE
MI, Dig toxicity, B and Ca Channel
Blockers
DIGOXIN TOXICITY
SYMPTOMS
• Tx:
Monitor HR
Atropine
Temporary pacemaker
Avoid meds that decrease conductivity
2 TYPES OF 2° HEART BLOCK
MOBITZ TYPE I- Wenkeback
MOBITZ TYPE II
Second Degree Heart Block
Mobitz I
• PRI becomes progressively longer until
drops QRS
Second Degree Heart Block
Mobitz Type II
• PRI constant and regular, but in a 2:1 , 3:1
pattern
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
3° HEART BLOCK
(COMPLETE HEART BLOCK)
• CAUSES
ORGANIC HEART DISEASE
MI
DRUGS
ELECTROLYTE IMBALANCE
EXCESS VAGAL TONE
• SIGNS & SYMPTOMS
EXTREME DIZZINESS
HYPOTENSION
SYNCOPE
S/S OF  C.O.
ALTERED MENTAL STATUS
NSR vs 3RD Degree Block
3° HEART BLOCK
(COMPLETE HEART BLOCK)
• TREATMENT
PACEMAKER
TEMPORARY
OR
PERMANENT
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 PIECES
PULSE GENERATOR IMPLANTED IN CHEST
WALL UNDER R CLAVICLE
PACEMAKER ELECTRODES IMPLANTED IN
MYOCARDIAL TISSUE
Paced Rhythm
• Pacemaker spike
PACEMAKER
• TEMPORARY
PACEMAKER
– USED IN
EMERGENCY
SITUATION
– FIXED
(COMPETITIVE)
PACEMAKER SENDS
STIMULUS TO
VENTRICLE AT A
FIXED RATE,
REGARDLESS OF
VENTRICULAR
ACTIVITY
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
PATIENT TEACHING
•
•
•
•
•
•
•
•
Carry PM ID card
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
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
References
• http://www.rnceus.com/ekg/ekgsecond2.ht
ml
• ACLS Guidelines 2005
• www.EMS-ED.net
• http://www.doctorshangout.com/forum/topi
cs/acls-algorithms-1
```
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