Arrhythmias: Hyperfunction

Cardiac Rhythm Disorders
By Laurie Dickson
Electrical System
 Each beat that is generated from the same pacemaker will
look identical
 Impulses from other cardiac cells are called ectopic (PVC,
 This electrical activity produces mechanical activity that is
seen as waveforms.
 The ECG is the electrical activity of the heart.
 Electrical precedes mechanical
 Without electricity, we have no pump!!
Action Potentials
 Na K pump
 Calcium channels
 Depolarization
 Repolarization
ECG waveforms are produced by the movement
of charged ions across the semipermeable membranes
of myocardial cells.
Normal Cardaic Cycle
Yellow is the isoelectric phase.
The purple is the "P"wave.
The purple and yellow split is the "PR" interval.
The red is the "Q" wave.
The light blue is the "R" wave.
The light green is the "S" wave.
The black is the "ST" segment.
The orange is the "T" wave.
Yellow again is isoelectric.
The dark blue is the "U" wave (seldom seen).
Characteristics of Cardiac Cells
 Cardiac cells are either contractile cells influencing the
pumping action or pacemaker cells influencing the electrical
activity of the heart
 Refractoriness- Refractory period
 Absolute/ Relative/ Full
Refractory Period
Pacemakers other than SA node
 A pacemaker from another site can lead to dysrhythmias and
may be discharged in a number of ways.
 Secondary pacemakers may originate from the AV node or His-
Purkinje system.
 Secondary pacemakers can originate when they discharge more
rapidly than the normal pacemaker of the SA node.
 Triggered beats (early or late) may come from an ectopic focus
(area outside the normal conduction pathway) in the atria, AV
node, or ventricles.
Conduction system
 SA node 60-100
 AV node 40-60
 Bundle of His
 Left and Right Bundle Branch
 Purkinge Fibers 20-40
Nervous System Control
of the Heart
 Parasympathetic nervous system: Vagus nerve
 Decreases rate
 Slows impulse conduction
 Decreases force of contraction
 Sympathetic nervous system
 Increases rate
 Increases force of contraction
Risk Factors for Arrhythmias
 Hypoxia
 Structural changes
 Electrolyte imbalances
 Central nervous system stimulation
 Medications
 Lifestyle behaviors
ECG waveforms
 P wave = Atrial depolarization (stimulation)
 QRS = Ventricular depolarization (stimulation)
 T wave = Ventricular repolarization (recovery)
 Atrial recovery wave hidden under QRS wave
 Stimulus causes atria to contract before ventricles
 Delay in spread of stimulus to ventricles allows time for
ventricles to fill and for atrial kick
ECG Monitoring
based on 12 lead ECG
 Each lead has positive, negative and ground electrode.
 Each lead looks at a different area of the heart.
 This can be diagnostic in the case of an MI
 ECG leads
Leads to monitor
 Best- lead II and MCL or V1 leads- lead II easy to see P
waves. MCL or V1 easy to see ventricular rhythms.
 If impulse goes toward positive electrode complex is
positively deflected or upright
 If impulse goes away from positive electrode complex is
negatively deflected or goes down form baseline
 ECG leads
 Lead II positive R arm
looking to LL neg
 3 lead placement:
 Depolarization wave
moving toward a positive
lead will be upright.
 Depolarization wave
moving toward a negative
lead will inverted.
 Depolarization wave
moving between negative
and positive leads will
have both upright and
inverted components.
 Lead II R arm looking to LL
 Five lead placement allows
viewing all leads within
limits of monitor
 Grass under clouds, smoke above
 V1 is 2nd ICS right of sternum
ECG graph paper
 Horizontal measures time
 Vertical measures voltage
 Helps us determine rate
 Width of complexes
 Duration of complexes
ECG graph paper
 Calculate rate
 Big block
 Little block
 Number of R waves in 6 sec times 10
 Calculate rhythm-reg or irreg
 Measure PR interval, <.20
 QRS interval .04-.12
 P to QRS relationship
Rate Calculation
1 lg box= .20
5 lg boxes =1 sec
30 lg boxes =6 secs
Therefore there are 300 lg boxes in 1 min.
Sinus Rhythm
 Normal P wave- 0.06-0.12 sec
 PR interval – 0.12-0.20
 QRS- 0.04-0.12
 T wave for every complex- 0.16
 Rate is regular 60-100
Sinus Tachycardia
Rate >100: Sinus Tachycardia
 Causes-anxiety, hypoxia, shock, pain, caffeine, drugs
 Treatment-eliminate cause
Clinical significance
 Dizziness and hypotension due to decreased CO
 Increased myocardial oxygen consumption may lead
to angina
brady heart song
 Rate<60: Sinus Bradycardia- relative-symptomatic, absolute-
 Cause-vagal stimulation, athlete, drugs (Blockers and digoxin),
head injuries, MI
 Watch for syncope
Sinus Bradycardia
 Clinical significance-Dependent on symptoms
 Hypotension , Weakness
 Pale, cool skin
 Angina, Shortness of breath
 Dizziness or syncope
 Confusion or disorientation
Treatment- if symptomatic,
o atropine or pace maker
Sinus Arrhythmia (SA)
 Rate 60-100
 Irregular rhythm- increases with inspiration, decreases with
 P, QRS,T wave normal
 Cause- children, drugs(MS04), MI
 Treatment- none
Sinus Arrest
 See pauses
 May see ectopic beats(PAC’s PVC’s) do not treat
 Cause MI
 Treatment
 atropine
 Pacemaker
Medications used to treat
atrial rhythms
 diltiazem (Cardizem)
 digoxin (Lanoxin)
 amiodarone (Cordarone)
 dofetilide (Tikosyn)
 verapamil (Calan, Calan SR, Covera-HS, Isoptin SR,
Verelan, Verelan PM, Isoptin, Isoptin I.V.)
Premature Atrial Contraction (PAC’s)ectopic
 P wave abnormally shaped
 PR interval shorter
 QRS normal
 Cause-age, MI, CHF, stimulants, dig, electrolyte
 Treatment- remove stimulants and watch for SVT
Paroxysmal Supraventricular
Tachycardia (PSVT)
 Rate is 100-300, regular, p often hidden
 Ectopic foci in atrium above bundle of HIS
 Cause-SNS stimulation, MI, CHF,sepsis
Paroxysmal Supraventricular
Tachycardia (PSVT)
 Clinical significance -Prolonged episode and HR >180
bpm may precipitate ↓ CO
 Palpitations, Hypotension, Dyspnea, Angina
 Treatment Vagal stimulation *
 adenosine, B blockers, Calcium channel blockers,
digoxin, amiodarone.
 Cardioversion
Atrial Flutter
 Rate of atria is 250-300, vent rate varies
 Regular rhythm
 P waves saw tooth, one ectopi focus
 AV block in ratio 2:1, 3:1, 4:1
 Flutter waves- No PR interval
 Cause-diseased heart, drugs (digoxin)
3:1 flutter
Atrial Flutter
 Clinical significance
 High ventricular rates (>100) + loss of the atrial “kick” can
decrease CO, precipitate HF, angina
 Risk for stroke due to risk of thrombus formation in the
 Treatment Calcium channel blockers, Beta blockers
 amiodarone, Cardioversion
 Ablation
 warfarin (Coumadin)
Atrial Fibrillation-most common
 Rate of atria 350-600- (disorganized rhythm)
 Ventricular response irregular
 No P waves, “garbage baseline”
 PR cannot measure
 QRS- normal
 Cause-#1 arrhythmia in elderly, heart disease- CAD,
rheumatic, CHF, alcohol
Atrial Fibrillation
 Clinical significance
 Can result in decrease in CO due to ineffective atrial contractions
(loss of atrial kick) and rapid ventricular response
 Thrombi may form in the atria as a result of blood stasis, travel to
the brain, causing a stroke
 Complications- dec. CO and thrombi
 stroke risk increases x5
Atrial Fibrillation-most common
 Treatment digoxin, Ca channel
blockers, Beta blockers
 amiodorone, procainamaide
 Cardioversion – warfarin +
 Ablation, Maze
Arrhythmias of AV Node
AV Conduction Blocks
First Degree AV Block
 Transmission through AV node delayed
 PR interval >.20
 QRS normal and regular
 Cause- digoxin toxicity, MI, CAD, vagal, and blocker drugs
First-Degree AV Block
 Clinical significance
 Usually asymptomatic
 May be a precursor to higher degrees of AV block
 Treatment
 Check medications
 Continue to monitor
Second Degree AV Block
more P’s than QRS’s
 A. Mobitz I (Wenckebach)
 PR progressively longer then drops QRS
 Cause- MI, drug toxicity
 B. MobitzII
 More P’s but skips QRS in regular pattern 2:1,3:1, 4:1(QRS
usually greater than .12-BBB)
 Constant PR interval- can be normal or prolonged
 Occurs in HIS bundle with bundle branch block
Second-Degree AV Block,
Type 1 (Mobitz I, Wenckebach)
 Clinical significance
 Usually a result of myocardial ischemia or infarction
 Almost always transient and well tolerated
 May be a warning signal of a more serious AV conduction
Treatment- watch for type II and 3rd degree
If symptomatic- atropine, pacer
Diagnosis Wenckebach
Second-Degree AV Block,
Type 2 (Mobitz II)
 Clinical significance
 Often progresses to third-degree AV block and is associated
with a poor prognosis
 Reduced HR often results in decreased CO with subsequent
hypotension and myocardial ischemia
 Treatment pacemaker
3rd Degree AV Block
 Atria and ventricles beat independently
 Atrial rate- 60-100
 Slow ventricular rate 20-40
 P normal
 No PR interval- no relationship with QRS
 Wide or normal QRS (depends on where block is)
 Cause- severe heart disease, blockers, elderly, MI
 Complications- dec. CO, ischemia, HF, shock, and
Third-Degree AV Heart Block
(Complete Heart Block)
 Clinical significance
 Decreased CO with subsequent ischemia, HF, and shock
 Syncope may result from severe bradycardia or even periods
of asystole
 Treatment- atropine, pacemaker
Bundle Branch Blocks
Left BBB
Right BBB
QRS.12 or greater
Rabbit ears- RR’
No change in rhythm
Right Bundle Branch Block
Junctional Rhythm
 AV node is pacemaker- slow rhythm (40-60) but very regular
impulse goes to atria from AV node- backward
 P wave patterns
 Absent
 P wave precedes QRS inverted in II, III, and AVF
 P wave hidden in QRS
 P wave follows QRS
Junctional Rhythm
 PR interval
 Absent or hidden
 Short <.12
 Negative or RP interval
 QRS normal
 No treatment
Ventricular Arrythmias
Most serious
Easy to recognize
Premature Ventricular Contractions
 No P waves
 QRS wide and bizarre
 T opposite deflection of PVC
 Cause- 90% with MI, stimulants, digoxin, electrolyte
Premature Ventricular Contractions
 Clinical significance
 In normal heart, usually benign
 In heart disease, PVCs may decrease CO and precipitate angina and
 Patient’s response to PVCs must be monitored
 PVCs often do not generate a sufficient ventricular
contraction to result in a peripheral pulse
 Apical-radial pulse rate should be assessed to determine
if pulse deficit exists
Premature Ventricular Contractions
 Clinical significance
 Represents ventricular irritability
 May occur:
 After lysis of a coronary artery clot with thrombolytic
therapy in acute MI—reperfusion dysrhythmias
 Following plaque reduction after percutaneous
coronary intervention
PVC’s multi-focal
Multifocal- from more than one foci
Bigeminy- every other beat is a PVC
trigeminy- every third beat is a PVC
Couplet- 2 PVC’s in a row
Treat if:
>5 PVC’s a minute
Runs of PVC’s
Multi focal PVC’s
R on T
 Treatment- based on cause
 O2, lidocaine,
Ventricular Tachycardia (VT)
 Ventricular rate 150-250, regular or irregular
 No P waves
 QRS>.12
 Can be stable- pulse or unstable –no pulse
 Cause- electrolyte imbalance, MI, CAD, digoxin
 Life- threatening, decreased CO, watch for V-fib
Ventricular Tachycardia
 Clinical significance
 VT can be stable (patient has a pulse) or unstable (patient is pulseless)
 Sustained VT: Severe decrease in CO
 Hypotension
 Pulmonary edema
 Decreased cerebral blood flow
 Cardiopulmonary arrest
Ventricular Tachycardia
 Clinical significance
 Treatment for VT must be rapid
 May recur if prophylactic treatment is not initiated
 Ventricular fibrillation may develop
 Treatment- same as for PVC’s and defibrillate for sustained
VT- Torsades de Pointes
French for twisting of the points
Ventricular Fibrillation
 Garbage baseline-quivering
 No P’s
No QRS’s
 Cause-MI, CAD, CMP, shock, K+, hypoxia, acidosis, and
 Treatment- code situation, ACLS, CPR, **defibrillate
Diagnostic Tests
 Telemetry- 5 lead( lead II and V1)
 12 lead EKG
 Holter monitor- pt. keeps a diary
 Event monitoring- pt. records only when having the event
 Exercise stress test
 Electrophysiology studies- induce arrhythmias under
controlled situation
Nursing Assessment
 Apical rate and rhythm
 Apical/radial deficit
 Blood pressure
 Skin
 Urine output
 Signs of decreased
cardiac output
Nursing Diagnoses
 Decreased cardiac output
 Decreased tissue perfusion
 Activity intolerance
 Anxiety and Fear
 Knowledge deficit
 Maintain stable signs of effective cardiac output and
tissue perfusion
 Achieve a realistic program of activity that balances
physical activity with energy conserving activities
 Report decreased anxiety and increased sense of selfcontrol
 Describe risk factors, the disease process, and treatment
 Classified by effect on action potential
 Class I- fast Na blocking agents-ventricular
 quinidine, procainamide, lidocaine,
 disopyramide phosphate (Norpace), propafenone (Rhythmol)
 Class II- beta blockers
 SVT,Afib,flutter
 esmolol, atenolol (Tenormin), propranolol(Inderal)
 Class III- K blocking
 both atrial and ventricular
 amiodarone, dofetilide, sotalol
 Class IV- Ca, channel blockers
 SVT,Afib,flutter
 verapamil, diltiazem
 Other adenosine, digoxin, atropine, magnesium
 Remembering that of all anti-arrhythmics
 "some block potassium channels" can help you:
 Class I "Some" = Sodium
 Class II "Block" = Beta blockers
 Class III "Potassium" = Potassium channel blockers
 Class IV "Channels" = Calcium channel blockers
Comfort Measures
 Rest
 O2
 Relieve fear and anxiety diazapam (Valium)
Invasive procedures
 Defibrillation
 Emergency- start at 200 watt/sec, go to 400
 Safety precautions
 Synchronized Cardioversion- for vent. or SVT
 Can be planned- if stable
 Get permit
 Start at 50 watt/sec
 Awake, give O2 and sedation
 Have to synchronize with rhythm
 cardioversion
Journal of Patient Needing Heart Transplant
My journey started July 13th 2008. Went to doctor thinking I
had bronchitis. 2 days later went in because I got awoken
during the night not being able to breath. Dr thought I had
gone into pneumonia, gave chest xray,18th go back tells me I
have congestive heart failure, starts me on water pills and
something else has me scheduled for an echo on Monday, wait
2 days calls and wants me to come in on Friday and wants a
cardiologist to see me and the echo, go in tells me to go to a
hospital north of us saying they have a room ready and will
schedule a cath and the cardiologist can reveiw the echo. get
up there doc reviews echo, while nurses are hooking me up
with IVs, Dr comes in and says may have major heart damage
but will wait until cath on Monday. Monday comes have cath a
surgeon comes in with cardiologist telling us I have over half
my heart damaged may need transplant, cardiologist says
they would rather transport me to a major hospital that can
handle transplant surgery if something goes wrong with
bypass. EF is 15%. go to Indianapolis by ambulance,
I am in total shock by this point not being able to even
comprehend what is going on 2 weeks from going from
bronchitis or so I thought to maybe having heart transplant.
My wife god bless her is having her own stress out of her
mind over this. get to Indy Tues and Wed nuclear test, Friday
high risk bypass surgery.
Now its 6 weeks after surgery have had another echo EF
went up a whopping 5% now getting defibbed Tuesday, today
is Sunday and again my mind is wondering into the worst
scenarios, it is getting harder and harder to grasp this stuff.
hopefully sites like this will help, letting blow off steam, and
ICD Implanted defibrillator Device
Senses rate and width of QRS
 Goes off 3 times, then have to be reset
 Combined with pacemaker- overdrive pacing or backup pacing
 Indications for ICD
 Survived SCD
 Spontaneous sustained V Tach
 Syncope with V Tach/V Fib
 High risk for life threatening dysrhythmia
ICD teaching
 Avoid lifting arm on ICD side above shoulder until approved
by PCP
Avoid driving until cleared by PCP
Avoid large magnets and strong electromagnetic fields (no
If the ICD fire, call health care provider
If ICD fires and they do not feel well, call EMS
If ICD fires more than once, call EMS
Caregivers should know CPR
 ICD resources
 Used to pace the heart when the normal
conduction system is damaged
 Permanent battery under skin
 Temporary battery outside body
 Types
 Transvenous
 Epicardial- bypass surgery
 Transcutaneous- emergency
 Modes
 Asynchronous- at preset time without fail
 Synchronous or demand- when HR goes below set rate
 Classifications
Indications for pacemaker
 AV block
 A-Fib with slow ventricular response
 Bundle Branch Block
 Cardiomyopathy
 Heart failure
 SA node dysfunction
 Tachydysrhythmias (V Tach)
 Teaching Similar to ICD
 Daily Pulse
Pacemaker Problems:
Failure to sense
Failure to capture
 Done in special cardiac procedures lab
 Use a laser to burn abnormal pathway
 radiofrequency ablation
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
ECG Changes Associated with Acute
Coronary Syndrome (ACS)
Fig. 36-29 A
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
ECG Changes Associated with Acute
Coronary Syndrome (ACS)
 Injury/Infarction
 ST segment elevation is significant if >1 mm above the
isoelectric line
 If treatment is prompt and effective, may avoid infarction
 If serum cardiac markers are present, an ST-segment-elevation
myocardial infarction (STEMI) has occurred
ECG Changes Associated with Acute
Coronary Syndrome (ACS)
 Injury/Infarction
 Note: 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
EKG changes in an acute MI
ECG Changes Associated with Acute
Coronary Syndrome (ACS)
Fig. 36-29 B
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
ECG Changes Associated with Acute
Coronary Syndrome (ACS)
Fig. 36-30
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
ECG changes with ACS
 The 12-lead ECG is the primary diagnostic tool used to evaluate
patients presenting with ACS.
 There are definitive ECG changes that occur in response to
ischemia, injury, or infarction of myocardial cells and will be seen
in the leads that face the area of involvement.
 Typical ECG changes seen in myocardial ischemia include STsegment depression and/or T wave inversion.
 The typical ECG change seen during myocardial injury is STsegment elevation.
 An ST-segment elevation and a pathologic Q wave may be seen on
the ECG with myocardial infarction
 Brief lapse in consciousness accompanied by a loss of tone
 Causes
 Cardiovascular
 Vasovagal, Cardiac dysrhythmias, hypertrophic
cardiomyopathy , PE
 Noncardiovascular
 hypoglycemia, seizure, hysteria, TIA
 Diagnostic studies
 Echocardiography
 Head-upright tilt table testing
 Holter monitor
 Subcutaneously implanted loop recording device
 1-year mortality rate as high as 30% for syncope from
cardiovascular cause
Complications of Arrhythmias
 Hypotension
 Tissue ischemia
 Thrombi- low dose heparin, or ASA
 Heart failure
 Shock
 Death
Prioritization Question
A client with atrial fibrillation is ambulating in the hall on
the coronary step-down unit and suddenly tells you, “I
feel really dizzy.” which action should you take first?
 A. Help the client sit down.
 B. Check the client’s apical pulse
 C. Take the client’s blood pressure
 D. Have the client breathe deeply
Prioritization question
A diagnosis of ventricular fibrillation is identified for an
unresponsive 50 year old client who has just arrived in
the ED. Which action should be taken first?
 A. Defibrillate at 200 joules
 B. Begin CPR
 C. Administer epinephrine 1 mg IV
 D.Intubate and manually ventilate.
Prioritization question
Cardiac rhythms are being observed for clients in the CCU. Which
client will need immediate intervention? A client:
 A. admitted with heart failure who has atrial fibrillation with a
rate of 88 while at rest.
 B. with a newly implanted demand ventricular pacemaker, who
has occasional periods of sinus rhythm, rate 90-100.
 C. who has just arrived on the unit with an acute MI and has sinus
rhythm, rate 76, with frequent PVC’s.
 D. who recently started taking atenolol (Tenormin)) and has a
first-degree heart block rate 58.
Video Acting Out Rhythms
 mad german doctor dances to heart rhythms
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