Transcript Arrhythmias: Hyperfunction

Arrhythmias:
By Nancy Jenkins
The EKG is the electrical activity
of the heart.
Electrical precedes mechanical
(Without electricity, we have no
pump!!)
How is the electricity generated?
action potentials excellent resource (view on
own)
By action potentials- Na, K and Ca
very important for this
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Na K pump
Calcium channels
Depolarization
Repolarization
YouTube - How the Body Works : A Nerve Impulse
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ECG waveforms are produced by the movement
of charged ions across the semipermeable membranes
of myocardial cells.
Na K pump
Animation: How the Sodium Potassium Pump Works
Electrical system
Multimedia Tutorials
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.
Cardiac Cycle
EKG waveforms
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P wave associated with atrial depolarization
(stimulation)
QRS complex associated with ventricular
depolarization (stimulation)
T wave associated with 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
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 15-40
How is the rate controlled?
Nervous System Control of the Heart
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Parasympathetic nervous system:when?
Vagus nerve
Decreases rate
 Slows impulse conduction
 Decreases force of contraction
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Sympathetic nervous system: when?
Increases rate
 Increases force of contraction
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Pacemakers other than SA node
A pacemaker from another site can lead to dysrhythmias and
may be discharged in a number of ways.
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Secondary pacemakers may originate from the AV node
or His-Purkinje system.
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Secondary pacemakers can originate when they discharge
more rapidly than the normal pacemaker of the SA node.
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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 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 negative R arm looking to LL positive
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
Refractoriness
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Relative
absolute
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 .06-.10
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
PR interval<.20
QRS.06-.10
T wave for every complex
Rate is regular 60-100
Rate >100: Sinus Tachycardia
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Causes-anxiety, hypoxia, shock, pain, caffeine, drugs
Treatment-eliminate cause
Sinus Tachycardia
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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
Treatment- if symptomatic, atropine or pacer
Sinus Bradycardia
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Clinical significance
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Dependent on symptoms
 Hypotension
 Pale, cool skin
 Weakness
 Angina
 Dizziness or syncope
 Confusion or disorientation
 Shortness of breath
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
Isuprel
Pacemaker
Atrial Arrythmias
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Atria is the pacemaker
Atrial rate contributes 25-30% of cardiac
reserve
Serious in patients with MI- WHY?
Medications used to treat the
atrial rhythms
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Cardizem
Digoxin
Amiodarone
Tikosyn
Verapamil
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 150-300, regular, p often hidden
Atria is pacemaker (may not see p waves)
Cause-SNS stimulation, MI, CHF,sepsis
Treatment- vagal stimulation, * adenosine,
digoxin, verapamil, inderal,
cardizem,tikosyn, or cardioversion
Paroxysmal Supraventricular
Tachycardia (PSVT)
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Clinical significance
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Prolonged episode and HR >180 bpm may
precipitate ↓ CO
 Palpitations
 Hypotension
 Dyspnea
 Angina
Atrial Flutter
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Rate of atria is 250-300, vent rate varies
Regular rhythm
P waves saw tooth, ratio 2:1, 3:1, 4:1
Flutter waves- No PR interval
Cause-diseased heart, dig
Treatment- cardioversion, calcium channel
blockers and beta blockers, amiodorone,
ablation coumadin
3:1 flutter
Atrial Flutter
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Clinical significance
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High ventricular rates (>100) and loss of
the atrial “kick” can decrease CO and
precipitate HF, angina
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Risk for stroke due to risk of thrombus
formation in the atria
Atrial Fibrillation-most common
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Rate of atria 350-600- (disorganized rhythm)
Ventricular response irregular
No P waves, “garbage baseline”
Cause-#1 arrhythmia in elderly, heart diseaseCAD, rheumatic, CHF, alcohol
Complications- dec. CO and thrombi (stroke)
Treatment- start with digoxin, ca channel
blockers, beta blockers, amiodorone, pronestyl,
cardioversion (TEE to see if clots before)
Coumadin- check PT and INR, ablation and Maze
Thrombus formation, pulse deficit, AR>RR
QuickTime™ and a
YUV420 codec decompressor
are needed to see this picture.
Atrial Fibrillation
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
 Embolus may develop and travel to the
brain, causing a stroke
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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-dig toxicity, MI, CAD vagal, and
blocker drugs
Treatment- none but watch for further
blockage
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
Treatment- watch for type II and 3rd degree
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
Treatment-Pacemaker
Occurs in HIS bundle with bundle branch block
Second-Degree AV Block,
Type 1 (Mobitz I, Wenckebach)
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Clinical significance
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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
Second-Degree AV Block,
Type 2 (Mobitz II)
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Clinical significance
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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
3rd Degree AV Block
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Atria and ventricles beat independently
Atrial rate- 60-100
Slow ventricular rate 20-40
No PR interval
Wide or normal QRS (depends on where block is)
Cause- severe heart disease, blockers elderly, MI
Complications- dec. CO, ischemia, HF, shock,
and syncope
Treatment- atropine, pacemaker
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 (patient may present with
history of fall)
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
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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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QRS wide and bizarre
No P waves
T opposite deflection of PVC
Cause- 90% with MI, stimulants, dig,
electrolyte imbalance
Treatment- O2, lidocaine,
pronestyl,amiodarone
No longer prophylactic
Premature Ventricular Contractions
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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 Contraction
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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
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, dig
Life- threatening, dec. CO, watch for V-fib
Treatment- same as for PVC’s and defibrillate for
sustained
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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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
Complications of Arrhythmias
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Hypotension
Tissue ischemia
Thrombi- low dose heparin, or ASA
Heart failure
Shock
Death
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
Medications
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Classified by effect on action potential
Class I- fast Na blocking agents-ventricular
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Quinidine, Pronestyl, Norpace,Lidocaine, Rhythmol
Class II-beta blockers (esmolol, atenolol, inderal)
SVT,Afib,flutter
Class III- K blocking (amiodorone, tikosyn,
sotalol)both atrial and ventricular
Class IV- Ca, channel blockers (verapamil
cardiazem)SVT,Afib,flutter
Other- adenosine, dig, atropine, covert,
magnesium
Antiarrhythmics
Remembering that of all anti-arrhythmics "some block
potassium channels" can help you:
Class I "Some" = S = Sodium
Class II "Block" = B =Beta blockers
Class III "Potassium" = Potassium channel blockers
Class IV "Channels" = C =Calcium channel blockers
Comfort Measures
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Rest
O2
Relieve fear and anxiety- valium
Invasive procedures
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Defibrillation
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Emergency- start at 200 watt/sec, go to 400
Safety precautions
AED’s 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 back up pacing
Implantable CardioverterDefibrillator (ICD)
Fig. 36-22
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
http://www.vmth.ucdavis.edu/cardio/cases/case14/pacemaker.htm
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
Review classificationshttp://en.wikipedia.org/wiki/Artificial_pacemaker
Pacemakers
Fig. 36-27
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
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
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http://www.aboutatrialfibrillation.com/treated.html # cardioversion
EKG CHANGES ASSOCIATED WITH ACUTE
CORONARY SYNDROME
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The 12-lead ECG is the primary diagnostic tool used to
evaluate patients presenting with ACS.
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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.
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Typical ECG changes seen in myocardial ischemia include
ST-segment depression and/or T wave inversion.
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The typical ECG change seen during myocardial injury is
ST-segment elevation.
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An ST-segment elevation and a pathologic Q wave may be
seen on the ECG with myocardial infarction.
3 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)
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Injury/Infarction
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ST segment elevation is significant if
>1 mm above the isoelectric line
 If
treatment is prompt and effective,
may avoid infarction
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If serum cardiac markers are
present, an ST-segment-elevation
myocardial infarction (STEMI) has
occurred
ECG Changes Associated with Acute
Coronary Syndrome (ACS)
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Infarction/Necrosis
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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 A
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
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.
Syncope
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Brief lapse in consciousness
CausesVasovagal
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Cardiac dysrhythmias
Other- hypoglycemia, seizure, hypertrophic
cardiomyopathy
1-year mortality rate as high as 30% for
syncope from cardiovascular cause
QuizzesDiscussionQuestions
Casestudies
Video acting out rhythms
YouTube - cardiac arrhythmias
Practice-
Rhythm Practice
ACLS
Prioritization Question
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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
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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.
Prioritization question
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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.