Dysrhythmias
EKG DANCE-click here
Dysrhythmias
Abnormal cardiac rhythms are termed
dysrhythmias.
Prompt assessment of dysrhythmias and
patient’s response to the rhythm is critical.
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2
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 hereYouTube- How Body Works-A Nerve Impulse
Understanding cardiac
action potential & meds
Cardiac action potential of a fast-response Purkinje fiber.
Arrows indicate the approximate time and direction of movement
of each ion influencing membrane potential. Ca++ movement out
of the cell is not well defined but is thought to occur during phase
4
Key Characteristics of Cardiac Cells
Multimedia Tutorials
*Great site
 Cardiac cells- either contractile cells influencing pumping action or
pacemaker cells influencing electrical activity of heart
 Automaticity
 Excitability
 Conductivity
 Contractility
 *Refractoriness
Relative
Absolute
 Each beat generated from same pacemaker - look identical.
 Impulses from other cardiac cells = “ectopic” (PVC, PAC)
 Electrical activity produces mechanical activity= waveforms
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
Conduction System of the Heart
Fig. 32-4. A, Conduction system of the heart. AV, Atrioventricular; SA, sinoatrial. B, The normal
electrocardiogram (ECG) pattern. The P wave represents depolarization of the atria. The QRS
complex indicates depolarization of the ventricles. The T wave represents repolarization of the
ventricles. The U wave, if present, may represent repolarization of the Purkinje fibers or it may
be associated with hypokalemia. The PR, QRS, and QT intervals reflect the length of time it takes
for the impulse to travel from one area of the heart to another.
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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, .
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
Pacemakers other than *SA node
•Pacemaker from another site > lead to dysrhythmias;
may be discharged in number of ways.
oSecondary pacemakers- may originate from AV node
or His-Purkinje system.
oSecondary pacemakers can originate when they
discharge more rapidly than normal pacemaker of SA
node.
oTriggered beats (early or late) may come from
ectopic focus (area outside normal conduction
pathway) in atria, AV node, or ventricles.
How is rate controlled?
Nervous System Control of Heart
Parasympathetic nervous system: when?
Vagus nerve
Dec. rate
Slows impulse conduction
Dec. force of contraction
Sympathetic nervous system: when?
Inc. rate
Inc. force of contraction
EKG graph paper
Horizontal measures time
Vertical measures voltage
Helps to determine
rate
Width of complexes
Duration of
complexes
Graphic tracing of electrical impulses produced by heart;
waveforms of ECG represent activity of charged ions across
membranes of myocardial cells.
Each small square box on the
graph paper is equal to:
1.
2.
3.
4.
0.06 sec.
0.08 sec.
0.04 sec.
0.20 sec.
If you didn’t know, look at
previous slide- 0.04
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)
Lead Placement
Fig. 36-4. A, Lead placement for MCL, using a three-lead system. B, Lead placement for V1 or V6 using a
five-lead system. C, Typical electrocardiogram tracing in lead MCL1. C, Chest; LA, left arm; LL, left leg;
MCL, modified chest lead; RA, right arm; RL, right leg.
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18
Risk Factors for Dysrhythmia (Arrhythmia)






Hypoxia
Structural changes
Electrolyte imbalances
Central nervous system stimulation
Medications
Lifestyle behaviors
Who is/are at Greatest Risk for Dysrhythmia? Patient(s) with
1. COPD
2. MI
MI; valvular disease (best two answers3. Valvular disease
have high risk for hypoxia (MI) and structural
4. Colon resection
chg with valvular)
Evaluation of Dysrhythmias
Holter monitoring
Event recorder monitoring
Exercise treadmill testing
Signal-averaged ECG
Electrophysiologic study
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Calculate rate (*know
how to do this)
Count
Big block
Little block
Number of R waves in 6
sec times 10
 Calculate rhythm-reg or
irreg
 Measure PR interval,
<0.20
 QRS interval .04- 0.12
 P to QRS relationship
 *Recognize artifact
1. Number of QRS complexes in 1 minute
R-R intervals in 6 seconds; multiply by 10
2. Number of small squares between one R-R
interval; divide this number into 1500
3. Number of large squares between one R-R
interval; divide this number into 300
Rate Calculation
1 lg box= .20
5 lg boxes =1 sec
*Therefore 300 lg boxes in 1 min.
30 lg boxes =6 secs
Each small box = 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.
If there are 10 small squares between 2
QRS waves, the rate would be:
1.
2.
3.
4.
75
100
150
100
*Rate 150; 1500 / 10 = 150
Normal Sinus Rhythm
 Follows normal conduction pattern
 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 Bradycardia- brady heart song
 Normal in sleep; aerobically trained athlete
 Clinical assoc.: Response to carotid sinus massage; hypothermia; inc
vagal tone; adm. parasympathomimetic drugs (Beta blockers; digoxin),
head injuries (inc ICP), inferior MI, hypothyroidism
 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; shortness of breath
 Confusion or disorientation
 Shortness of breath
 Treatment- if symptomatic, atropine or pacer
Sinus BradycardiaTreatment- if symptomatic, atropine or pacer
Patients with bradycardia are likely to
display which of these symptoms:
1.
2.
3.
4.
Heart rate less than 60
Dizziness
Hypertension
Confusion
1.
2.
3.
4.
Heart rate less than 60
Dizziness
Hypertension (all except)
Confusion
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 inc. in rate of sinus node discharge (vagal inhibition).
•Common dysrhythmia; many causes as exercise, fever, caffeine, anxiety, smoking, heart
failure, hypovolemia, etc.
•Treatment : address underlying cause and/or determine if it is even a problem (Medsadenosine?, beta adrenergic blockers (dec. heart rate & myocardial oxygen
consumption)*, antipyretics for fever); analgesic for pain
Clinical significance
Dizziness and hypotension due to decreased CO
Inc. myocardial oxygen consumption may lead to angina
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 (Morphine sulphate), MI
 Treatment- none
Sinus Arrest
•See pauses
•May see ectopic beats (PAC’s PVC’s)*don’t treat
•Due to MI
•Treatment
Atropine
Isoproterenol (Isuprel)
Pacemaker
Isoproterenol-synthetic sympathomimetic amine
Atrial Dysrhythmias
 Atria is pacemaker
 Atrial rate contributes 25-30% of cardiac reserve
 Serious in patients with MI- WHY?
Medications - to treat atrial dysrhythmias (if patient symptomatic)
•Diltiazem (Cardizem) (Identify class)
•Amiodarone (Cordarone) (Identify class)
•Dofetilide (Tikosyn) (Identify class)
Verapamil (Calan) (Identify class)
Metoprololol (Lopressor) Identify class
Digoxin (Lanoxin)
Atropine
Think-rate too slow, too fast?? Ref to Tab. 36-9-next slide
Premature Atrial Contraction (PAC’s)
P wave abnormally shaped-contraction originates
from ectopic focus in atrium other than SA Node
 PR interval shorter-travels abnormal pathway (distorted
“P” waves)
QRS normal
 Cause-age, MI, CHF, stimulants, dig, electrolyte
imbalance; valvular disease; hypoxia
Treatment- remove stimulants; watch for SVT, depends upon
cause; isolated not significant; B-adrenergic blockers
Supraventricular Tachycardia
(SVT)/PSVT (paroxysmal SVT)
 Rate- 150-250 (Very fast!)
 Originates in ectopic focus above bifurcation of
bundle of His- atria=pacemaker (may not see p
waves); *Paroxysmal = abrupt onset and termination
 Cause-SNS stimulation, MI, CHF,sepsis
SVT/Paroxysmal Supraventricular Tachycardia
(PSVT)
 Clinical significance
Prolonged episode and HR >180 bpm may
precipitate ↓ CO
Palpitations
Hypotension
Dyspnea
Angina
•Treatment•Meds: adenosine, digoxin, diltiazem (Cardizem) or
verapamil (calcium channel blockers), propranolol
(inderal), dofetilide (Tikosyn)
•Vagal stimulation
This YouTube site explains
supraventriventricular tachycardias plus
atrial flutter and atrial fibrillation- Click here
to locate additional videos
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-*Originate from single ectopic
focus; No PR interval
 Cause-diseased heart (mitral valve), PE, chronic lung;
hyperthyroidism, drugs as dig, quinidine, epinephrine
3:1 flutter
Video Atrial flutter
Atrial Flutter
Clinical significance
High ventricular rates (>100) and loss of the atrial
“kick” can dec. CO and precipitate HF, angina
Risk for stroke due to risk of thrombus formation in
atria
 Treatment- *Goal slow ventricular resopnse
Cardioversion
Calcium channel blockers and beta blockers,
amiodorone (What classes?)
 Ablation
, warfarin (Coumadin)
Atrial Fibrillation-**most common
 Rate of atria 350-600- (total disorganized rhythm);
*multiple ectopic foci > loss effective atrial contraction
 Ventricular response irregular
 No P waves, “garbage baseline”
 Cause-#1 arrhythmia in elderly, heart disease- CAD,
rheumatic heart disease, HF, cardiomyopathy, caffeine,
alcohol, etc.
 Complications- dec. CO due to loss atrial kick and rapid
ventricular response; thrombi (stroke) from blood stasis
 Treatment-Goal dec. ventricular rate; pvt stroke; *convert if
possible);
 Meds: digoxin, calcium channel blockers, beta adrenergic blockers,
amiodorone, cardioversion (TEE ck for thrombus) warfarin - ck PT and INR,
 *ablation, Maze procedure (involves open heart) or Mini Maze
(modified)
Atrial Fibrillation
Rsult in dec. in CO due to ineffective atrial
contractions (loss of atrial kick) and rapid
ventricular response
Thrombi may form in atria as a result of blood
stasis
Embolus may develop and travel to the brain,
causing a stroke
*Thrombus formation, pulse deficit
Click to view You Tube video on
Abalation for Atrial fibrillation!
Dysrhythmias- AV Node
AV Conduction Blocks
Junctional Rhythm
Dysrhythmia that originates in area of AV node
 AV node is pacemaker- slow rhythm (40-60) but
regular impulse goes to atria from AV nodebackward); SA node failed to fire or impulse
delayed or blocked at AV node
 P wave patterns
Absent or hidden; Short < .0.12 or negative or PR
interval; P wave precedes QRS inverted in II, III, and
AVF or P wave hidden in QRS or P wave follows QRS
 QRS normal
 Often no treatment
.
Junctional Dysrhythmias
Junctional Dysrhythmia
 Clinical significance
Serves as safety mechanism when SA node has not been
effective
Escape rhythms should not be suppressed.
If rhythms rapid >result in reduction of CO and HF
 Treatment
If symptomatic, atropine
Accelerated junctional rhythm and junctional tachycardia
caused by digoxin toxicity; digoxin is held
-Adrenergic blockers, calcium channel blockers, and
amiodarone for rate control for junctional tachycardia not
caused by digoxin toxicity
DC cardioversion is contraindicated
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First Degree AV Block
Transmission through AV node delayed
PR interval >0.20
QRS normal and regular
Cause-dig toxicity, MI, CAD, vagal
stimulation; hyperthyroidism, betaadrenergic drugs; calcium channel
blockers, flecainaide drugs
Treatment- none but watch for further
blockage
First-Degree AV Block
Clinical significance
Usually asymptomatic
May be a precursor to higher degrees of AV
block
Treatment
Check medications.
Continue to monitor.
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Inc., an affiliate of Elsevier Inc.
46
Characteristics of 1st degree block
include ?
1. Regular rhythm
2. Long PR interval
3. More P’s than
QRS’s
4. Rate less than
100
1.
2.
3.
4.
Regular rhythm
Long PR interval
More P’s than
QRS’s
Rate less than 100
Second Degree AV Block
more P’s than QRS’s
 A. Mobitz I (Wenckebach) YouTube - Diagnosis
Wenckebach
PR progressively longer then drops QRS due to prolonged
AV conduction; atrial impulse non-conducted and a QRS
complex is blocked
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/associations
Usually result of myocardial ischemia or infarction
Almost always transient; well tolerated
May be a warning signal of more serious AV
conduction disturbance
Drugs: Digoxin, -adrenergic blockers
Associated with CAD and other diseases that can
slow AV conduction
Second-Degree AV Block,
Type 2 (Mobitz II)
Clinical significance
Often progresses to third-degree AV block ;
associated with poor prognosis
Reduced HR often results in dec. CO with
subsequent hypotension and myocardial
ischemia
Second-Degree AV Block,
Type 2 (Mobitz II)
Fig. 36-16. Heart block. C, Second-degree AV block, type II, with constant PR intervals and
variable blocked QRS complexes.
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Second-Degree AV Block,
Type 2 (Mobitz II)
 Clinical associations
Rheumatic heart disease
CAD
Anterior MI
Digitalis toxicity
 Treatment
If symptomatic (e.g., hypotension, angina) before
permanent pacemaker can be inserted, temporary
transvenous or transcutaneous pacemaker
Permanent pacemaker
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Mobitz type 1 or Wenchebach has
a constant PR interval.
1. True
2. False
Answer: False-Mobitz I (Wenckebach)PR progressively longer then drops QRS
3rd Degree AV Block
 Atria and ventricles beat independently (ventricular
rhythm is “escape” rhythm
 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, systemic diseases; meds
as digoxin, beta-adrenergic blockers, calcium channels
blockers
 Complications- dec. CO, ischemia, HF, shock,
bradycardia, syncope, possible asystole
Third-Degree AV Heart Block
(Complete Heart Block)
Fig. 36-16. D, Third-degree AV block. Note that there is no relationship between P waves and QRS
complexes.
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Third-Degree AV Heart Block
(Complete Heart Block)
Treatment
If symptomatic, transcutaneous pacemaker until
a temporary transvenous pacemaker can be
inserted
Drugs (e.g., atropine, epinephrine): Temporary
measure to increase HR and support BP until
temporary pacing is initiated
Permanent pacemaker as soon as possible
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Bundle Branch Blocks *not in text- & no test items but to
understand concept





Left BBB
Right BBB
QRS.12 or greater
Rabbit ears- RR’
No change in rhythm
Normal bundle
conduction
Right Bundle Branch Block
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, procainamide
(Pronestyl), *amiodarone, *abalation
No longer prophylactic
Premature Ventricular Contractions
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
Fig. 36-17. Various forms of premature ventricular
contractions (PVCs). Note: Recorded from lead II.
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61
Premature Ventricular Contractions
Clinical significance
In normal heart, usually benign
In heart disease, PVCs may dec. 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- assess to
determine if pulse deficit exists
Premature Ventricular Contractions
Clinical significance
**Ventricular irritability > Ventricular
Fibrillation .
May occur
After lysis of coronary artery clot with
thrombolytic therapy in acute MI—
reperfusion dysrhythmias
Following plaque reduction after
percutaneous coronary intervention
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
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Ventricular Tachycardia
Clinical significance
VT can be stable (patient has a pulse) or
unstable (patient is pulseless)
Sustained VT: Severe dec. 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 Tachycardia
 Treatment
 Precipitating causes must be identified and treated (e.g.,
hypoxia).
 Monomorphic VT
 Hemodynamically stable (e.g., + pulse) + preserved LV
function: IV procainamide, sotalol, amiodarone, or lidocaine
 Hemodynamically unstable or poor LV function: IV
amiodarone or lidocaine followed by cardioversion
 Polymorphic VT with a normal baseline QT interval: adrenergic blockers, lidocaine, amiodarone, procainamide, or
sotalol; cardioversion used if drug therapy is ineffective.
 Polymorphic VT with a prolonged baseline QT interval: IV
magnesium, isoproterenol, phenytoin, lidocaine, or
antitachycardia pacing; Drugs that prolong QT interval should be
discontinued if rhythm is not converted, cardioversion may be
needed.
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2007 by Mosby,
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Ventricular Tachycardia
Treatment
VT without a pulse is a life-threatening situation.
Cardiopulmonary resuscitation (CPR)
and rapid defibrillation
• Epinephrine if defibrillation is
unsuccessful
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Ventricular Fibrillation





Garbage baseline-quivering
No P’s
No QRS’s
No CO
Cause-MI, CAD, CMP, shock, altered K+, hypoxia,
acidosis, and drugs
 Treatment- code situation, ACLS, CPR, **defibrillate
*cannot cardiovert…no rhythm to cardiovert

Asystole
Clinical significance
Unresponsive, pulseless, and apneic state
Prognosis for asystole is extremely poor.
Treatment
CPR with initiation of ACLS measures (e.g.,
intubation, transcutaneous pacing, IV therapy
with epinephrine and atropine)
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Pulseless Electrical Activity (PEA)
Electrical activity can be observed on
ECG, but no mechanical activity of
ventricles is evident; patient has no pulse.
Treatment
CPR > intubation > IV epinephrine
Atropine if ventricular rate is slow.
Treatment directed toward correction of
underlying cause.
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Sudden Cardiac Death (SCD)
Death from a cardiac cause
Majority of SCDs result from ventricular
dysrhythmias.
Ventricular tachycardia
Ventricular fibrillation
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Complications Dysrhythmias






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 >
Ablation to correct underlying problem .
Nursing Assessment






Apical rate and rhythm
Apical/radial deficit
Blood pressure
Skin
Urine output
Signs of dec.
cardiac output
Nursing Diagnoses
•Dec. cardiac output
•Dec. tissue perfusion
•Activity intolerance
•Anxiety and Fear
•Knowledge deficit
Goals/Outcomes??
Interventions
Medications
Pacemaker (Types)
Mapping
Ablation
Maze & modified Maze
CPR
Cardioversion
Defibrillation
Medications- review *Know your meds
 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,
diltiazem(cardiazem) for SVT, Afib, atrial flutter
 Other- adenosine, dig, atropine, magnesium
(correct electrolytes)
Antiarrhythmics
Remember-phrase “Some Block Potassium Channels”
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- Diazepam (valium)
 Defibrillation
 Most effective method of terminating VF and pulseless VT
 Passage of DC electrical shock through heart to depolarize cells of
myocardium to allow SA node to resume the role of pacemaker
 Output is measured in joules or watts per second.
 Recommended energy for initial shocks in defibrillation
 Biphasic defibrillators: First and successive shocks: 150 to 200 joules
 Monophasic defibrillators: Initial shock at 360 joules
 Safety precautions**
 After initial shock, chest compressions (CPR) should be started
 AED’s
Fig. 36-20. Paddle placement and current flow in
monophasic
defibrillation (A) and biphasic defibrillation (B).
Fig. 36-21. LifePak contains monitor, defibrillator,
& transcutaneous
pacemaker.
Synchronized Cardioversion Choice of therapy for hemodynamically unstable ventricular or
supraventricular tachydysrhythmias
 Synchronized circuit delivers countershock on R wave of QRS
complex of ECG.
 Synchronizer switch must be turned ON.
 Use for Ventricular Tachycardia, 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
http://www.dearnurses.net/
cardioversion
To defibrillate a rhythm, it
needs to be synchronized to
the QRS? True or False?
False! No QRS to
synchronize with!!
Implantable Cardioverter-Defibrillator (ICD)
 Appropriate for patients who have
 survived SCD
 spontaneous sustained VT
syncope with inducible ventricular
tachycardia/fibrillation during EPS
at high risk for future life-threatening dysrhythmias
 Consists of lead system placed via subclavian vein to endocardium
 Battery-powered pulse generator is implanted subcutaneously.
 Equipped with antitachycardia and antibradycardia pacemakers.
 Initiate overdrive pacing of supraventricular and ventricular
tachycardias; Provide backup pacing for bradydysrhythmias that may
occur after defibrillation discharges
Copyright © 2011, 2007 by Mosby,
Inc., an affiliate of Elsevier Inc.

88
Implanted Cardiac Defibrillator (ICD)
 Senses rate and width of QRS
 Goes off 3 times, then have to be reset
 Some combined with pacemaker
 If fires- seek medical attention!
 Teaching critical!
Pacemaker
 Used to pace heart when normal conduction pathway
damaged or diseased
Pacing circuit consists of a power source, one or more
conducting (pacing) leads, and myocardium.
 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
View Pacemaker insertion
Transcutaneousemergency
Temporary Transvenous Pacemaker
Fig. 36-26. Temporary transvenous pacemaker catheter insertion. A single lead is positioned in
the right ventricle through either the basilic or jugular vein.
Copyright © 2011, 2007 by Mosby,
Inc., an affiliate of Elsevier Inc.
92
Pacemaker Spike
Fig. 36-23. Ventricular capture (depolarization) secondary to signal (pacemaker spike) from
pacemaker lead in the right ventricle.
Copyright © 2011, 2007 by Mosby,
Inc., an affiliate of Elsevier Inc.
93
Pacemakers
 Antibradycardia pacing
 Antitachycardia pacing: Delivery of a stimulus to the ventricle to
terminate tachydysrhythmias
 Overdrive pacing: Pacing the atrium at rates of 200 to 500 impulses
per minute to terminate atrial tachycardias
 Permanent pacemaker: Implanted totally within the body
 Cardiac resynchronization therapy (CRT): Pacing technique that
resynchronizes cardiac cycle by pacing both ventricles
 Pacemaker Problems (next slide)
 Teaching critical (text table 36-11)
Copyright © 2011, 2007 by Mosby,
Inc., an affiliate of Elsevier Inc.
94
Pacemaker Problems:
•Failure to sense
•Failure to capture
Radiofrequency Catheter Ablation Therapy
 Electrode-tipped ablation catheter “burns” accessory
pathways or ectopic sites in atria, AV node, and ventricles.
Nonpharmacologic treatment for
AV nodal reentrant tachycardia
Reentrant tachycardia related to accessory bypass
tracts
Control of ventricular response of certain
tachydysrhythmias
 Done in special cardiac procedures lab
 Use a laser to burn abnormal pathway
View video
96
EKG changes in an acute MI
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; seen in leads that face 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)> STEMI
 Ischemia
 ST segment depression and/or T wave inversion
 ST segment depression- significant if at least 1 mm (one small box)
below isoelectric line
 Injury/Infarction
 ST segment elevation is significant if >1 mm above isoelectric line
 If treatment is prompt & effective, may avoid infarction
• If serum cardiac markers present, an ST-segment-elevation
myocardial infarction (STEMI) has occurred
 Infarction/Necrosis
 Note: physiologic Q wave is first negative deflection following P wave
 Small and narrow (<0.04 second in duration)
 *Pathologic Q wave- deep and >0.03 second in duration
ECG Changes Associated with Acute
Coronary Syndrome (ACS)
Typical EKG changes associated with an MI
include:
1.
2.
3.
4.
Long PR interval
Q waves
ST segment elevation
T wave inversion
1.
2.
3.
4.
Long PR interval
Q waves
(Pathological)
ST segment
elevation
T wave inversion
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
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 questions
 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.