Transcript Arrhythmias: Hyperfunction

Arrhythmias
By Laurie Dickson
With thanks to Nancy Jenkins
The EKG is the electrical activity
of the heart.
Electrical precedes mechanical
(Without electricity, we have no
pump!!)
By action potentials
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Na K pump
Calcium channels
Depolarization
Repolarization
YouTube - Action Potenital
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ECG waveforms are produced by the movement
of charged ions across the semipermeable membranes
of myocardial cells.
Animation: How the Sodium
Potassium Pump Works
Electrical System
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Each beat that is generated from the same
pacemaker will look identical
Impulses from other cardiac cells are called
ectopic (PVC, PAC)
This electrical activity produces
mechanical activity that is seen as
waveforms.
Nervous System Control of
the Heart

Parasympathetic nervous system:
Vagus nerve
Decreases rate
 Slows impulse conduction
 Decreases force of contraction
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Sympathetic nervous system
Increases rate
 Increases force of contraction
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Cardiac 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).
.
Conduction system
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SA node 60-100
AV node 40-60
Bundle of His
Left and Right Bundle Branch
Purkinge Fibers 20-40
Pacemakers other than SA node
A pacemaker from another site can lead to dysrhythmias and
may be discharged in a number of ways.
o
Secondary pacemakers may originate from the AV node
or His-Purkinje system.
o
Secondary pacemakers can originate when they discharge
more rapidly than the normal pacemaker of the SA node.
o
Triggered beats (early or late) may come from an ectopic
focus (area outside the normal conduction pathway) in the atria,
AV node, or ventricles.
EKG waveforms
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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
EKG graph paper
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Horizontal measures time
Vertical measures voltage
Helps us determine rate
Width of complexes
Duration of complexes
EKG graph paper
Monitoring leads- based on 12
lead EKG
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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
RNCEU’s
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.
*Five lead placement allows viewing all leads within limits of monitor
(Grass under clouds, smoke above fire)
V1 is 2nd ICS right of sternum
Lead II R arm looking to LL positive
Leads to monitor in
EKG leads
Best- lead II and MCL or V1 leads- lead II easy to see
Pwaves. 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
Cardiac cells are either
contractile cells influencing the
pumping action or pacemaker
cells influencing the electrical
activity of the heart
4 Characteristics of Cardiac Cells
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Automaticity
Excitability
Conductivity
Contractility
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Refractoriness- Refractory period
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Absolute/ Relative/ Full
Refractory Period
Risk Factors for Arrhythmias
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Hypoxia
Structural changes
Electrolyte imbalances
Central nervous system stimulation
Medications
Lifestyle behaviors
Assessment
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Calculate rate
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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
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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
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Causes-anxiety, hypoxia, shock, pain,
caffeine, drugs
Treatment-eliminate cause
Clinical significance
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Dizziness and hypotension due to decreased
CO
Increased myocardial oxygen consumption
may lead to angina
brady heart song
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Rate<60: Sinus Bradycardia- relativesymptomatic, absolute-normal
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Cause-vagal stimulation, athlete, drugs
(Blockers and digoxin), head injuries, MI
Watch for syncope
Sinus Bradycardia
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Clinical significance-Dependent on symptoms
Hypotension , Weakness
 Pale, cool skin
 Angina, Shortness of breath
 Dizziness or syncope
 Confusion or disorientation
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Treatment- if symptomatic,
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atropine or pace maker
Sinus Arrhythmia (SA)
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Rate 60-100
Irregular rhythm- increases with
inspiration, decreases with expiration
P, QRS,T wave normal
Cause- children, drugs(MS04), MI
Treatment- none
Sinus Arrest
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See pauses
May see ectopic beats(PAC’s PVC’s) do
not treat
Cause MI
Treatment
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atropine
Pacemaker
Medications used to treat the
atrial rhythms
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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
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P wave abnormally shaped
PR interval shorter
QRS normal
Cause-age, MI, CHF, stimulants, dig, electrolyte
imbalance
Treatment- remove stimulants and watch for SVT
Paroxysmal Supraventricular
Tachycardia (PSVT)
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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)
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Clinical significance -Prolonged episode
and HR >180 bpm may precipitate ↓ CO
 Palpitations,
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Hypotension, Dyspnea,
Angina
Treatment Vagal stimulation *
 adenosine, B blockers, Calcium channel
blockers, digoxin, amiodarone.
 Cardioversion
Atrial Flutter
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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
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Clinical significance
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High ventricular rates (>100) + loss of the atrial
“kick” can decrease CO, precipitate HF, angina
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Risk for stroke due to risk of thrombus formation
in the atria
Treatment
Calcium channel blockers, Beta blockers
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amiodarone, Cardioversion
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Ablation
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warfarin (Coumadin)
Atrial Fibrillation-most common
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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 diseaseCAD, rheumatic, CHF, alcohol
Atrial Fibrillation
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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
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Complications- dec. CO and thrombi
(stroke risk increases x5)
Atrial Fibrillation-most common
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Treatment
digoxin, Ca channel blockers, Beta blockers
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amiodorone, procainamaide (Pronestyl)
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Cardioversion – warfarin + TEE
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Ablation, Maze
QuickTime™ and a
YUV420 codec decompressor
are needed to see this picture.
Atrial Fibrillation
Arrhythmias of AV Node
AV Conduction Blocks
First Degree AV Block
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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
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Clinical significance
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Usually asymptomatic
May be a precursor to higher degrees of
AV block
Treatment
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Check medications
Continue to monitor
Second Degree AV Block
more P’s than QRS’s
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A. Mobitz I (Wenckebach) YouTube - Diagnosis
Wenckebach
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PR progressively longer then drops QRS
Cause- MI, drug toxicity
B. MobitzII
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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)
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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 disturbance
Treatment- watch for type II and 3rd degree
If symptomatic- atropine, pacer
Second-Degree AV Block,
Type 2 (Mobitz II)
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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
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Atria and ventricles beat independently
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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 syncope
Third-Degree AV Heart Block
(Complete Heart Block)
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Clinical significance
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Decreased CO with subsequent
ischemia, HF, and shock
Syncope may result from severe
bradycardia or even periods of
asystole
Treatment- atropine, pacemaker
3rd Degree
Bundle Branch Blocks
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Left BBB
Right BBB
QRS.12 or greater
Rabbit ears- RR’
No change in rhythm
Right Bundle Branch Block
Junctional Rhythm
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AV node is pacemaker- slow rhythm (40-60) but
very regular impulse goes to atria from AV nodebackward
P wave patterns
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Absent
P wave precedes QRS inverted in II, III, and AVF
P wave hidden in QRS
P wave follows QRS
.
Cont.
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PR interval
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Absent or hidden
Short <.12
Negative or RP interval
QRS normal
No treatment
Ventricular Arrythmias
Most serious
Easy to recognize
Premature Ventricular
Contractions (PVC’s)-ectopic
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No P waves
QRS wide and bizarre
T opposite deflection of PVC
Cause- 90% with MI, stimulants, digoxin,
electrolyte imbalance
Premature Ventricular Contraction
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Clinical significance
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In normal heart, usually benign
In heart disease, PVCs may decrease CO
and precipitate angina and HF
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 Contractio
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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
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PVC’s-unifocal
PVC’s multi-focal
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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:
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>5 PVC’s a minute
Runs of PVC’s
Multi focal PVC’s
R on T
Treatment- based on cause
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O2, lidocaine, procainamide, amiodarone
Ventricular Tachycardia (VT)
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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
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Clinical significance
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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
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Clinical significance
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Treatment for VT must be rapid
May recur if prophylactic treatment is
not initiated
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Ventricular fibrillation may develop
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Treatment- same as for PVC’s and
defibrillate for sustained
VT- Torsades de Pointes
French for twisting of the points
Ventricular Fibrillation
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Garbage baseline-quivering
No P’s
No QRS’s
No CO
Cause-MI, CAD, CMP, shock, K+,
hypoxia, acidosis, and drugs
Treatment- code situation, ACLS, CPR,
**defibrillate
Diagnostic Tests
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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
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Apical rate and rhythm
Apical/radial deficit
Blood pressure
Skin
Urine output
Signs of decreased
cardiac output
Nursing Diagnoses
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Decreased cardiac output
Decreased tissue perfusion
Activity intolerance
Anxiety and Fear
Knowledge deficit
Goals
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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
self-control
Describe risk factors, the disease process, and
treatment regimen
Medications
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Classified by effect on action potential
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Class I- fast Na blocking agents-ventricular
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quinidine, procainamide, lidocaine,
disopyramide phosphate (Norpace), propafenone
(Rhythmol)
Class II- beta blockers
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SVT,Afib,flutter
esmolol, atenolol (Tenormin), propranolol(Inderal)
Medications
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Class III- K blocking
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Class IV- Ca, channel blockers
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both atrial and ventricular
amiodarone, dofetilide, sotalol
SVT,Afib,flutter
verapamil, diltiazem
Other
adenosine, digoxin, atropine, magnesium
Antiarrhythmics
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
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Rest
O2
Relieve fear and anxiety
diazapam (Valium)
Invasive procedures
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Defibrillation
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Emergency- start at 200 watt/sec, go to 400
Safety precautions AED safety
AED’s now AED now!
Synchronized Cardioversion- for vent. or SVT
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Can be planned- if stable
Get permit
Start at 50 watt/sec
Awake, give O2 and sedation
Have to synchronize with rhythm
cardioversion
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Implanted Cardiac Defibrillator (ICD)
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Senses rate and width of QRS
Goes off 3 times, then have to be reset
Combined with pacemaker- overdrive pacing
or backup pacing
ICD resources
Implantable CardioverterDefibrillator (ICD)
Fig. 36-22
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
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 pnemonia, 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
cardioligist 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
shedule a cath and the cardiolgist can reveiew the ecko. get
up there doc reviews ecko, 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 cardiolisgist telling us i have over half
my heart damaged may need transplant, cardioligist 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
broncitis or so i thought to maybe haveing heart transplant.
My wife god bless her is haveing 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 ecko ef went
up a woping 5% now getting defibed tuesday, today is
sunday and again my mind is wondering into the worst
scenorios, it is gettting harder and harder to grasp this stuff.
hopefully sites like this will help, letting blow off steam, and
learning.
dave
Pacemaker
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Permanent- battery under skin
Temporary- battery outside
body
Types
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Modes
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Transvenous
Epicardial- bypass surgery
Transcutaneous- emergency
Asynchronous- at preset time
without fail
Synchronous or demand- when
HR goes below set rate
Classifications
pacemaker
classification
Pacemaker Problems:
Failure to sense
Failure to capture
Ablation
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Done in special cardiac procedures lab
Use a laser to burn abnormal pathway
radiofrequency ablation
ECG Changes Associated with Acute
Coronary Syndrome (ACS)
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Ischemia
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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
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ST segment elevation is significant if
>1 mm above the isoelectric line
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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
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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.
EKG CHANGES ASSOCIATED WITH ACUTE
CORONARY SYNDROME

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
ST-segment depression and/or T wave inversion.

The typical ECG change seen during myocardial injury is
ST-segment elevation.

An ST-segment elevation and a pathologic Q wave may be
seen on the ECG with myocardial infarction.
Syncope


Brief lapse in consciousness accompanied
by a loss of tone (fainting)
Causes

Cardiovascular


Vasovagal, Cardiac dysrhythmias, hypertrophic
cardiomyopathy , PE
Noncardiovascular

hypoglycemia, seizure, hysteria, TIA
Syncope

Diagnostic studies

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Echocardiography
EPS
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
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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


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mad german doctor dances to heart
rhythms
Practicehttp://www.skillstat.com/Flash/ECG_Sim_
2004.html
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