Transcript Arrhythmias: Hyperfunction

Dysrhythmias
EKG DANCE-click here
EKG shows electrical activity of the heart.
Electrical precedes mechanical
(Without electricity…no pump!!)
Click here
How is the electricity generated?
By action potentials (click for animated visuals)
Na K pump (animation)
Calcium channels
Depolarization-contraction
RepolarizationThink about this when administering cardiac meds…antidysrhytmics
*ECG wave forms- Produced by movement of charged ions across the
semipermeable membranes of myocardial cells. Click here- YouTube- How Body Works-A Nerve
Impulse
Understanding cardiac
action potential & meds
Electrical system
Multimedia Tutorials
Each beat that is generated from 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
*Note pattern that occurs with atrial depolarization, repolarization; ventricular depolarization, re-polarization
Cardiac Cycle
Intrinsic rates
Yellow = isoelectric phase.
SA node 60-100
AV node 40-60
Bundle of His; Left and
Right Bundle Branch;
Purkinge Fibers 15-40
Purple= "P"wave.
Purple and yellow split = "PR" interval
Red = "Q" wave;
Light blue = “R" wave
Light green = "S" wave; Black = "ST" segment
Orange = "T" wave; Yellow again = isoelectric.
Dark blue ="U" wave (seldom seen)* risk for *hypokalemia, med effect,
hypercalcemia, .
How is rate controlled?
Nervous System Control of Heart
Parasympathetic nervous system:
when? Vagus nerve
Decreases rate
Slows impulse conduction
Decreases force of contraction
Sympathetic nervous system: when?
Increases rate
Increases force of contraction
Pacemakers other than *SA node
•Pacemaker from another site can lead to dysrhythmias
and may be discharged in a number of ways.
oSecondary pacemakers may originate from AV node
or His-Purkinje system.
oSecondary pacemakers can originate when they
discharge more rapidly than the normal pacemaker of
the SA node.
oTriggered beats (early or late) may come from
ectopic focus (area outside normal conduction
pathway) in atria, AV node, or ventricles.
EKG waveforms
 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
EKG graph paper
Horizontal measures time
Vertical measures voltage
Helps to determine rate
Width of complexes
Duration of complexes
EKG graph paper
Cardiac Monitoring- based on 12 lead EKG
Each lead has positive, negative and ground
electrode.
Each lead looks at different area of heart.
*Can be diagnostic as in 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
Leads to monitor EKG
Best- lead II and MCL or V1 leads- lead II easy to see P
waves. MCL or V1 easy to view 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
Five lead system- uses all leads shown: three lead system uses only
black, white and red leads. Two lead telemetry systems use black and red
leads- placement may change depending on what EKG lead (view) is
required. Black and white leads are placed on shoulder area; green and
red leads placed on lowest rib on both sides of torso, and brown lead
(ground) is placed at 4th intercostal space, just to right of sternum. (follow
guidelines of facility)
Key Characteristics of Cardiac Cells
Cardiac cells- either contractile cells
influencing pumping action or pacemaker
cells influencing electrical activity of heart
Automaticity
Excitability
Conductivity
Contractility
*Refractoriness
Relative
Absolute
Refractory Period
Myocardial cells resistive to stimulation; **dysrhythmias triggered
during relative refractory and absolute refractory periods
•Absolute refractory period: no depolarization can occur- from Q wave
until middle of T wave
•Relative refractory period: greater than normal stimulus needed for
depolarization (contraction); goes through 2nd half T wave
Risk Factors for Dysrhythmia
(Arrhythmia)
Hypoxia
Structural changes
Electrolyte imbalances
Central nervous system stimulation
Medications
Lifestyle behaviors
Assessment
 Calculate rate (know how to do this)
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.
Each small box represents 0.04 seconds on horizontal axis and 1 mm or 0.1 millivolt
on vertical axis. PR interval-measured from beginning of P wave to beginning of
QRS complex; QRS complex -measured from beginning of Q wave to end of S
wave; QT interval -measured from beginning of Q wave to end of T wave; and TP
interval- measured from end of T wave to beginning of next P wave.
Sinus Rhythm
 Normal P wave
 PR interval<.20
 QRS.04-.12
 T wave for every complex
 Rate is regular 60-100
 *Rate >100: Sinus Tachycardia
Causes-anxiety, hypoxia, shock, pain, caffeine, drugs
Treatment-eliminate cause
Sinus Tachycardia
Rhythm:
Rate:
P Waves:
PR Interval:
QRS Complex:
Regular
Fast (>/= 100 bpm)
“Normal” and upright, one for each QRS
“Normal” (0.12-0.20 seconds)
“Normal” (0.08-0.12 seconds)
•Due to an increase in rate of sinus node discharge.
•Common dysrhythmia due to many things as exercise, fever, caffeine, anxiety,
smoking, etc.
•Treatment : address underlying cause and/or determining if it is even a problem
(adenosine, beta blockers).
Clinical significance
Dizziness and hypotension due to decreased CO
Increased myocardial oxygen consumption may lead to angina
 Sinus Bradycardia- brady heart song
 Cause-vagal stimulation, athlete, drugs (Beta blockers; digoxin), head
injuries, MI
 Sinus node fires <60 bpm; Normal conduction; rhythm regular; P: QRS:
1:1; PR interval: 0:12 to .20 sec.; QRS complex: 0.04 to 0.12 sec
 Clinical significance- Dependent on symptoms
 Hypotension
 Pale, cool skin
 Weakness
 Angina
 Dizziness or syncope
 Confusion or disorientation
 Shortness of breath
 Treatment- if symptomatic, atropine or pacer
Name these rhythms & count rate!!
(What you just covered)
Sinus Dysrhythmias (Arrhythmia) (SA)
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
See pauses
May see ectopic beats (PAC’s PVC’s) do
not treat
Cause MI
Treatment
Atropine
Isuprel
Pacemaker
Atrial Dysrhythmias
Atria is the pacemaker
Atrial rate contributes 25-30% of cardiac
reserve
Serious in patients with MI- WHY?
Medications used to treat the atrial
dysrhythmias (if patient symptomatic)
Cardizem
Digoxin
Amiodarone
Tikosyn
Verapamil
? Atropine
Think-rate too slow, too fast??
Premature Atrial Contraction (PAC’s)
P wave abnormally shaped
PR interval shorter
QRS normal
Cause-age, MI, CHF, stimulants, dig,
electrolyte imbalance
Treatment- watch for SVT, depends upon cause
Supraventricular Tachycardia
(SVT)/PSVT (paroxysmal SVT)
 Rate- 150-250 (Very fast!)
 Atria is pacemaker (may not see p waves)
 Cause-SNS stimulation, MI, CHF,sepsis
 Treatment- adenosine, digoxin, cardizem or
verapamil (calcium channel blockers), inderal,
tikosyn, Vagal stimulation
Atrial Flutter
 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
Clinical significance
High ventricular rates (>100) and loss of the
atrial “kick” can decrease CO and precipitate
HF, angina
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 disease- CAD,
rheumatic, CHF, alcohol
 Complications- dec. CO and thrombi (stroke)
 Treatment- *convert if possible); digoxin, calcium
channel blockers, beta blockers, amiodorone, pronestyl,
cardioversion (TEE ck for thrombus) Coumadin- ck PT
and INR, ablation and Maze
 *Thrombus formation, pulse deficit, AR>RR
Atrial Fibrillation
Video here
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
*Thrombus formation, pulse deficit
Dysrhythmias- AV Node
AV Conduction Blocks
Junctional Rhythm
 AV node is pacemaker- slow rhythm (40-60) but
very regular impulse goes to atria from AV nodebackward)
 P wave patterns
Absent or hidden
Short < .0.12 or negative or RP interval
P wave precedes QRS inverted in II, III, and AVF
P wave hidden in QRS
P wave follows QRS
 QRS normal
 Often no treatment
.
First Degree AV Block
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
Second Degree AV Block
more P’s than QRS’s
 A. Mobitz I (Wenckebach) YouTube - Diagnosis
Wenckebach
PR progressively longer then drops QRS
Cause- MI, drug toxicity
Treatment- watch for type II and 3rd degree
 B. Mobitz II
More P’s but skips QRS in regular pattern 2:1,3:1, 4:1
Constant PR interval
Treatment-Pacemaker
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 disturbance
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
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, syncope
Treatment- atropine, pacemaker
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
(patient may present with history of fall)
Bundle Branch Blocks *not in text- understand
concept
 Left BBB
 Right BBB
 QRS.12 or greater
 Rabbit ears- RR’
 No change in rhythm
Normal bundle
conduction
Ventricular Arrythmias
Most serious
Easy to recognize
Premature Ventricular Contractions
(PVC’s)-ectopic
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, *abalation
No longer prophylactic
Premature Ventricular Contractions
Clinical significance
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 Contractions
Clinical significance
Represents ventricular irritability > VF .
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-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:
>5 PVC’s a minute
Runs of PVC’s
Multi focal PVC’s
“R on T”
What is this?
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, dig
 Life- threatening, dec. CO, watch for V-fib
 Treatment- same as for PVC’s and defibrillate
for sustained (if not responsive)
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
Polymorphic Ventricular Tachycardia- Torsades de
Pointes” (“twisting around a point”)
Rhythm:
Rate:
P Waves:
PR Interval:
QRS Complexes:
Well…irregular…but…
100-250 bpm
Usually not seen (buried in QRS if they exist)
None
Wide, distorted, bizarre, and “rhythmic” – getting smaller, then
larger, then smaller, then…
AKA: “Torsades de Pointes” (“twisting around a point”)
Usually caused by hypo/hyperkalemia, HYPOMAGNESEMIA, TCA OD, and some
antidysrhythmic medications.
Treatment - includes treating cause(s), medications, and defibrillation or cardioversion.
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
Hypotension
Tissue ischemia
Thrombi- low dose heparin, or ASA
Heart failure
Shock
Death
Diagnostic Tests
 Telemetry- 5 lead (lead II and V1)
 12 lead EKG
 Holter or event monitoring
 Exercise stress test
 Electrophysiology studies- induce
arrhythmias under controlled
situation
EKG changes in an acute MI
Not linked…but watch EKG
changes in evolving MI
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
Goals-
Medications
 Classified by effect on action potential
 Class I- fast Na blocking agents-ventricular
Quinidine, Pronestyl, Norpace,Lidocaine, Rhythmol
 Class II- beta blockers (esmolol, inderal) SVT,
Atrial fibrillation, Atrial flutter
 Class III- K blocking (sotalol, amiodorone)both
atrial and ventricular
 Class IV- Calcium channel blockers (verapamil
cardiazem) SVT,Afib, atrial flutter
 Other- adenosine, dig, atropine, magnesium
(correct electrolytes)
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
Rest- dec. cardiac demands; careful monitoring!!
O2
IV access; Select appropriate therapy
Relieve fear and anxiety- valium
Invasive procedures Defibrillation
Emergency- start at 200 watt/sec, go to 400
Safety precautions
AED’s now
 Synchronized Cardioversion- vent tachycardia or
SVT or a- fib, flutter to convert
Usually planned
Get permit
Start at 50 watt/sec
Awake, give O2 and sedation
Have to synchronize with rhythm
cardioversion
Implanted Cardiac Defibrillator (AICD)
Senses rate and width of QRS
Goes off 3 times, then have to be reset
Some combined with pacemaker
Pacemaker
 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
 Review classifications- (Wikipedia)
Pacemaker resources
Pacemaker Problems:
•Failure to sense
•Failure to capture
Ablation
View video
Done in special cardiac procedures lab
Use a laser to burn abnormal pathway
EKG CHANGES ASSOCIATED WITH ACUTE CORONARY
SYNDROME
 12-lead ECG - primary diagnostic tool used to evaluate patients
presenting with ACS.
 Definitive ECG changes occur in response to ischemia, injury,
or infarction of myocardial cells; will be seen in leads that face the
area of involvement.
 Typical ECG changes seen in myocardial ischemia include STsegment depression and/or T wave inversion.
 Typical ECG change seen during myocardial injury is STsegment elevation.
 ST-segment elevation and a pathologic Q wave may be seen
on ECG with myocardial infarction.
3 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)
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-segmentelevation myocardial infarction
(STEMI) has occurred
ECG Changes Associated with
Acute Coronary Syndrome (ACS)
 Infarction/Necrosis
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 A
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc
ECG Changes Associated with
Acute Coronary Syndrome (ACS)
Fig. 36-29 B
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc
Syncope
Brief lapse in consciousness
CausesVasovagal
Cardiac dysrhythmias
Other- hypoglycemia, seizure, hypertrophic
cardiomyopathy
1-year mortality rate as high as 30% for
syncope from cardiovascular cause
QuizzesDiscussionQuestions
Casestudies
Practice!
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 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
 Cardiac rhythms are being observed for clients in the
CCU. Which client needs 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
 Cardiac rhythms are being observed for clients in the
CCU. Which client needs 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
 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
 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.