RNSG 2432 ONLINE NOTES
Module 3: Cardiac Rhythm Disorders
Carolyn Morse Jacobs, RN, MSN, ONC
Etiology/Pathophysiology of Cardiac Rhythm Disorders
1. Normal conduction system of the heart as it relates to dysrhythmia (Lewis p.
741-742 & 842-843; Fig 32-5 & 32-6) * Know normal conduction of heart
beat- SA, AV, Bundle of His etc - how each component is represented on EKG
Network specialized cells and conduction pathways that initiate and spread
electrical impulses causing heart to beat
a. *Cardiac muscle: unique- generate electrical impulse and contraction
independent of nervous system
b. Cardiac muscle: unique- generate electrical impulse and contraction
independent of nervous system
c. Abnormal cardiac rhythms= dysrhythmias
2. Properties of cardiac cells (Table 36-1 p. 843)
a. Automaticity
1) spontaneous; *SA node highest level automaticity
2) stimulated by nervous system via vagus nerve
3) sympathetic increases rate of firing; parasympathetic decreases
rate
4) *cardiac cells in any part of heart (pacemaker cells or nonpacemaker) cells can take on role of a pacemaker- begin
generating extraneous impulses, called ectopics. *(Any
cardiac muscle can generate an electrical impulse and
contraction independent of nervous system!)
b. Excitability- ability of myocardial cells to respond to stimuli generated
by pacemaker cells (action potential)-be electrically stimulated
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c. Conductivity- ability to transmit impulse from cell to cell, orderly
manner
d. Contractility-ability of myocardial fibers to shorten in response to
stimulus; mechanical
e. Refractory (absolute & relative) P. 846-847
3. Cardiac Action Potential (Fig 36-1 p. 843) *See 3 Lead EKG video BB
a. Measured in millivolts (mV), vertical axis EKG paper, time (sec),
horizontal axis
b. *Electrical activity = waveforms on ECG strips due to ion movement
across cell membranes stimulating muscle contraction
c. Phases
1) Resting state-polarized state
a) Positive and negative ions align on either side of cell
membrane; Na high, K low; relatively negative charge
within cell; positive charge extracellularly
b) Negative resting membrane potential
2) Contraction- depolarization *(important- consider how meds
work to affect heart rhythm and pumping action)
a) Resting cell stimulated by charge
(1) Na ions enter cell through fast sodium channels
(2) Calcium enter cells via slow calcium-sodium
channels
(3) Membrane less permeable to K ions
(4) Membrane potential change to slightly positive
at +20 - +30 mV
(5) Dysrhythmic meds as Verapamil (Calan,
Isoptin) control dysrhythmia What drug class;
how? (text p. 856)
3) Threshold potential
a) Cell more positive-point reached when action potential
generated
b) Cause chemical reaction of Ca within cell
(1) Actin and myosin filaments slide togetherproduce cardiac muscle contraction
(2) Once myocardium completely depolarized,
repolarization begin
4) Repolarization (protect heart muscle from spasm, tetany)
a) Cell return to resting, polarized state
b) Fast sodium channels close abruptly
c) Cell regains negative charge (rapid repolarization)
d) Muscle contraction prolonged-slow calcium-sodium
channels remain open (plateau phase)
e) Once closed, sodium-potassium pump restore ion
concentration - cell membrane polarized again
5) Refractory period (Tab 36.3 p. 847)
a) Myocardial cells resistive to stimulation; **dysrhythmias
triggered during relative refractory and absolute
refractory periods
(1) Absolute refractory period: no depolarization
can occur- from Q wave until middle of T wave
(2) Relative refractory period: greater than normal
stimulus needed for depolarization
(contraction); goes through 2nd half T wave
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Refractory Period
Ectopic stimuli occurring during
refractory period (even by
cardioversion) allow re-entry
impulses-cause premature beats,
abnormal conduction p, 847
4. Nervous System Control
a. Autonomic
1) Rate of impulse formation
2) Speed of conduction
3) Strength of contraction
b. Parasympathetic nervous system: **Vagus nerve
1) Decreases rate
2) Slows impulse conduction
3) Decreases force of contraction
c. Sympathetic nervous system
1) Increases rate
2) Increases force of contraction
5. Etiology of Dysrhythmia
a. Causes vary; treatment based upon causative factors
b. Cardiac cells either contractile cells influencing pumping action or
pacemaker cells influencing electrical activity of heart
c. Factors that trigger
1) Hypoxia
2) Structural changes (atherosclerosis, atrial fibrillation, changes
after MI etc)
3) Electrolyte imbalances (especially altered
*potassium,*calcium,*magnesium, sodium levels)
4) CNS stimulation as caffeine, nicotine, cocaine;
5) Lifestyles behaviors
6) Medications (*digoxin, recall therapeutic levels), beta blockersend in “lol”, drugs that slow down or drugs that speed-up heart
rate.
d. Identify, evaluate, treat dysrhythmia-determined by client response
6. Significance of dysrhythmiasa. Dec. cardiac output and cerebral/vascular perfusion
b. Normal Sinus Rhythm- (NSR), atria fill, stretch ventricles with about
30% more blood; “atrial kick” occurs; improves contractility of
ventricles; increases cardiac output. ie- if impulse start in AV node or
ventricles, atrial and ventricular contraction not coordinated; “atrial
kick” is lost- cardiac output falls.
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Interpretation of Cardiac Rhythms
1. ECG- Graphic recording electrical activity of heart
2. 12-Lead ECG (Fig 36 2&3 p. 844) *Standard 12-lead ECG; simultaneous
recording of 6 limb leads and 6 precordial leads (views of electrical
conduction)
a. Six leads measure electrical forces in frontal plane (Limb leads:
bipolar leads I, II, III, and unipolar leads or augmented limb leads:
aVR, aVL and aVF)
b. Six leads (V1 V2V3V4V5V6) measure electrical forces in horizontal
plane
3. Lead Placement- 3 lead/5 lead (Fig 36.4 p. 845) & access link -Theoretical
Basis for EKG & 3 Lead EKG videos-Introduction
a. Each lead has positive, negative and ground electrode
b. Each lead looks at a different area of heart.
c. Can be diagnostic –recall MI (ie ST elevation)
d. Best- lead II and MCL (modified chest lead) or V1 leads- lead II easy
to see P waves. MCL or V1 easy to see ventricular rhythms. view each
component of EKG. Lead II- use with 3 Lead system (ref 3 Lead EKG
video)
e. If impulse goes toward positive electrode-complex positively deflected
or upright
f. If impulse goes away from positive electrode-complex negatively
deflected or goes down form baseline
Assess link-Theoretical Basis for EKG & 3 Lead EKG videos- Introduction *(Videos
located with Module 3 in Blackboard; quiz items also in Blackboard) *ask if difficulty
in locating
EKG Standard Leads (from Theoretical Basis for EKC)
These leads- usually designated as I, II and III.
1. Bipolar (i.e., detect a change in electric potential between two points) and
detect an electrical potential change in frontal plane.
Lead I- between right arm and left arm electrodes,- left arm being positive.
Lead II is between right arm and left leg electrodes, left
leg being positive.
Lead III is between left arm and left leg electrodes, left
leg again being positive.
A diagrammatic representation of these three leadstermed Einthoven's triangle (shown in blue below), after
Dutch doctor who first described the relationship. Central
source of electrical potential in triangle is heart.
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EKG Augmented Limb Leads
1. Same three leads that form standard leads also form
the three unipolar leads- known as augmented leads: aVR
(right arm), aVL (left arm) and aVF (left leg); also record
change in electric potential in frontal plane.
2. Unipolar leads- measure electric potential at one point
with respect to a null point (one which doesn't register any
significant variation in electric potential during contraction
of heart).
3. Null point- obtained for each lead by adding potential
from the other two leads. For example, in lead aVR,
electric potential of right arm is compared to a null point
which is obtained by adding together the potential of lead
aVL and lead aVF.
EKG Precordial Leads
1. Six unipolar leads, each in different position on chest
2. Record electric potential changes in heart in a cross sectional plane
3. Each lead records electrical variations that occur directly under electrode.
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Assessment of Cardiac Rhythm
1. *Assess client first- what response to dysrhythmia (connected to monitor?)
2. EKG strip recognition: waveforms- reflect direction of electrical flow (what
seen on EKG strip)
a. Positive (upward) waveform is toward positive electrode
b. Negative (downward) waveform is away from positive electrode
c. Biphasic (both positive and negative) waveform shows perpendicular
to positive pole
d. Isoelectric line (straight line) absence of electrical activity
3. Identify components EKG (*electrical precedes mechanical) *(Tab 36-2-p.
847)
*Refer to p. 847 Table 36-2- Values may vary slightly with different sources-use
text book for test purposes
a. P wave: atrial depolarization and contraction= “p” , upright (0.060.12)
b. PR interval-time for sinus impulse to travel from SA node to AV node
and into bundle branches (beginning of P wave to beginning of QRS
complex) (0.12 - 0.20 seconds
c. QRS Complex-ventricular depolarization and contraction; transmission
of impulse through ventricular conduction system *(0.04 – 0.12)
seconds
d. ST segment-beginning of ventricular repolarization; end of QRS
complex to beginning of T wave; isoelectric; *Recall significance of
elevated ST segment with MI (0.12)
e. T wave- ventricular repolarization; smooth and round, < 10 mm tall;
same direction as QRS complex; abnormalities due to myocardial
injury or ischemia, electrolyte imbalances. *Danger area if “shock” on
T wave!
f. QT interval- total time ventricular depolarization and repolarization;
beginning of QRS complex to end of T wave; prolonged QT: prolonged
relative refractory period = greater risk for dysrhythmias; shortened
QT: due to medications or electrolyte imbalance; *measure QT interval
prior to admin. some meds (0.34 – 0.43 seconds)
g. U wave- repolarization of terminal Purkinje fibers; same direction as T
wave; seen with hypokalemia (contact healthcare provider!)
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4. Calculate rate *Know how to do this! (p. 843-836; fig. 36.5-36.9)
a. ECG waveforms recorded on paper- marking representative of time
(know this)
b. Each small box = 0.04 seconds (sec); one large box (5 small boxes) =
0.20 sec.; 5 large boxes measure 1 second; Vertically, each small box
= 0.1 millivolt (mV)
c. Method #1 -Count # complexes in 6 second strip; paper marked at 3
second intervals; multiply by 10 (Fig 36.6 p. 845)-easy, use if rhythm
regular; count only “complete” complex
d. Method #2- Count # large boxes (Big block) between two
consecutive complexes (R-R); divide 300 by this number= number of
large boxes 1 minute
e. Method #3- Count# number small boxes (Little block) between two
consecutive complexes (R-R); divide 1500 by this number (number
small boxes in 1 minute) by this number…* most precise
measurement
5. Normal Sinus Rhythm- sinus node fires 60-100 bpm; follows normal
conduction pattern
a. Normal P wave
b. PR interval<.20
c. QRS.06-.12
d. T wave for every complex
e. Rate is regular 60-100
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Evaluation of Dysrhythmias- *p. 848, 753 Tab 32-7 for description, care
1.
2.
3.
4.
5.
6.
Holter monitor-wear while ambulatory- 24-48 hrs during daily activity
12 Lead EKG (Fig 36.3 p. 845)
Event monitor
Exercise treadmill testing
Averaged signaled ECG (SAECG)
Electrophysiologic study-*Use electrode catheters guided by fluroscopy into
heart via femoral or brachial vein: electrical stimulation induces dysrhythmias
similar to patient clinical diagnosis.
a. Invasive procedure-electrode catheters introduced into heart
b. Timing and sequence of electrical activity noted during normal and
abnormal rhythms
c. May involve treatment of dysrhythmia by overdrive pacing or
performing ablative therapy to destroy ectopic site
d. Possible complications: ventricular fibrillation, cardiac perforation,
venous thrombosis
7. *Require systematic approach to evaluate dysrhythmia (p. 848 Tab. 36-5)
*need to know “normal”
a. Assess “P” wave; presence or absence and appearance; should be
alike in size and shape
b. Evaluate atrial rhythm-regular, irregular?
c. Calculate atrial rate
d. Measure PR interval-normal, abnormal?
e. Evaluate ventricular rhythm- regular, irregular?
f. Measure duration QRS-normal, abnormal?
g. Assess ST segment
h. Measure QT interval duration-prolonged, shortened? Note T wave,
upright or inverted.
i. Consider- what is dominant rhythm?’ How significant? What
treatment?
j. Identify abnormalities; presence or frequency of ectopic beats, shape
of complexes,
**Suggest-when reading/reviewing the following dysrhythmia; highlight
characteristics of each including:
1. Regularity
2. Rate
3. Presence/character of “P” wave
4. PR interval (measurement)
5. Ratio of P wave to QRS
6. QRS measurement/characteristics
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Major Dysrhythmias (Table 36.7 p. 849) *Key reference
Sinus Rhythms - (electrical stimulus originates at SA nodes
1. Sinus Bradycardia
a. Characteristics: Sinus node fires <60 bpm; Normal conduction; rate
less than 60 bpm; rhythm regular; P: QRS: 1:1; PR interval: 0:12 to
.20 sec.; QRS complex: 0.04 to 0.12 sec
b. Clinical Associations/significance: normal in aerobically trained athletes
and during sleep; inc. vagal (parasympathetic) activity; injury or
ischemia to sinus node; inferior wall damage with acute MI; increased
intracranial pressure; medications such as beta-blockers and digoxin;
hypothermia; acidosis; response to carotid sinus massage
c. *Treatment: determine cause; treat if symptomatic, can lead to
decreased CO; use *atropine to increase rate or use pacemaker
2. Sinus Tachycardia
a. Description: normal conduction; except rate greater than 100 bpm
b. Clinical associations/causes: sympathetic nervous system stimulation;
blockage vagal activity; body response to physiological stressors:
anxiety, pain, caffeine, hypovolemia, MI, heart failure, fever, etc
c. Clinical Manifestations: palpitations; shortness of breath; dizziness,
lead to inc. myocardial oxygen consumption may lead to angina
d. Treatment: eliminate cause as caffeine, adm drugs to reduce heart
rate as -Adrenergic blockers and myocardial oxygen consumption,
antipyretics to treat fever, analgesics to treat pain. Note-Adenosine
(Adenocard) IV &/or bata blockers may be indicated. (see p. 850!!)
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3. Sinus Arrhythmia
a. Description: normal conduction, however irregular rhythm- rate 60100, increases with inspiration, decreases with expiration; P, QRS,T
wave normal
b. Clinical association/causes- normal in children, drug effect as (MS04),
MI
c. Treatment- none
Supraventricular dysrhythmias (atrial arrythmias) Can be serious: atria
contributes 25-30% cardiac output (atrial kick); especially in patients with MIalready decreased cardiac reserve. *ectopic pacemaker overrides the SA node; may
develop as “escape rhythm” if SA node fails- “paroxysmal” (occur in bursts- abrupt
onset and end) *Pacemaker- no longer SA node-atria becomes pacemaker.
Frequently used meds to treat atrial dysrhymias- *diltiazem (Cardizem)
calcium channel blocker (Class IV), digoxin (Lanoxin) inhibits sodium-potassium
ATPase, dec. AV conduction speed), amiodarone (Cardarone) Class III potassium
channel blocker), dofetilide (Tikosin) potassium channel blocker), verapamil *Calan)
calcium channel blockers * Know these
4. Premature Atrial Contraction
a. Description: atria is pacemaker; P:QRS: 1:1; ectopic atrial beat
occurs earlier than next expected sinus beat; P wave-abnormally
shaped, or P wave lost in QRS; PR interval shorter; QRS normal (0.06
to 0.12); have a non-compensatory pause (early beat affects P wave
appearance)
b. Clinical associations-due to emotional stress, caffeine, tobacco,
alcohol, hypoxia, electrolyte imbalances, COPD, valvular disease
c. Clinical significance- Isolated PACs -not significant if healthy heartsheart disease may required trt.
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d. Treatment-depends on symptoms: -Adrenergic blockers to dec. PACs,
reduce or eliminate caffeine (See p. 856 Tab 36-8)
5. Supraventricular Tachycardia (SVT)/Paroxysmal Supraventricular
Tachycardia (PSVT)- Why important? >decreases cardiac output
a. Description: originates in ectopic focus –anywhere above bifurcation of
bundle of His-Rate 150-250; atria is pacemaker, may not see P waves
due to rapid rate (ectopic foci above ventricles); Run of repeated
premature beats= usually PACs
b. Description cont-paroxysmal- abrupt onset and termination; some
degree of AV block may be present; occur in presence of WolffParkinson-White (WPW) syndrome
c. Clinical Associations- initiated by a “re-entry” loop in or around AV
node; precipitated by sympathetic nervous system stimulation and
stressors including fever, sepsis, hyperthyroidism; heart diseases
including CHD, digitalis toxicity, myocardial infarction, rheumatic
heart disease, myocarditis or acute pericarditis; cor pulmonale, WolffParkinson-White syndrome (WPW)
d. Clinical Significance: palpitations, “racing heart”, anxiety, dizziness,
dyspnea, anginal pain, extreme fatigue, diaphoresis, prolonged heart
rate above 180 lead to decreased CO
e. Treatment:
2) *Vagal stimulation: Valsalva, coughing; IV adenosine
(how does it work?)
3) If vagal maneuvers and/or drug therapy ineffective and/or
patient hemodynamically unstable, DC cardioversion needed
4) *Adenocin (Adenocard)IV stops heart,- allows SA node to
reset (brief asystole); similar to electrical cardioversion; short
term use only; give only in ICU, ER, monitored situations.
(temporary); also digoxin, verapamil, inderal, cardiazem
tikosyn to prevent recurrance
5) *PSVT recurs in Wolff-Parkinson-White syndrome, may need
radiofrequency catheter ablation of accessory pathway
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6. Atrial Flutter
a. Description: originates in atria from single ectopic focus; rapid,
regular atrial rhythm due to intra-atrial re-entry mechanism; atrial
rate 240-300, ventricular rate depends upon degree of AV block,
usually < 150 BPM; P waves “saw- toothed”, ratio 2:1, 3:1, 4-1;
flutter waves; PR interval not measured
b. Clinical associations: CAD, hypertension, mitral valve disorders,
pulmonary embolus, chronic lung disease, cardiomyopathy,
hyperthyroidism, valvular diseases, WPW; due to sympathetic nervous
stimulation
c. Clinical Significance:
1) High ventricular rates (>100) and loss of the atrial “kick” decrease CO & precipitate HF, angina
2) Risk for stroke -risk of thrombus formation in the atria *not
as bad as with atrial fibrillation*
d. Treatment: Primary goal- slow ventricular response by increasing
AV block
1) Meds to slow ventricular response as -adrenergic
blockers or calcium channel blocker followed by quinidine,
procainamide, flecainide or amiodarone. *Think about why,
how these meds work!
2) Synchronized cardioversion - convert the atrial flutter to
sinus rhythm emergently and electively; maintain rhythm
with antidysrhymic meds
3) Ablation to obliterate abnormal conduction pathways
7. *Atrial Fibrillation
a. Total disorganization atrial electrical activity due to multiple ectopic
foci lead to loss of effective atrial contraction; no P waves, “garbage
baseline”; atrial rate 300-600; too rapid to count; ventricular rate
100-180 BPM if untreated;*disorganized atrial activity without
discrete atrial contractions; irregular ventricular response; pulse
deficit; irregularly irregular
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b. Clinical associations: underlying heart disease, rheumatic heart
disease heart disease, CAD, HTN cardiomyopathy, thyrotoxicosis,
caffeine use, HF, percarditis, #1 arrhythmia in elderly
c. Clinical Significance: lead to decrease in CO due to ineffective
atrial contractions (loss of atrial kick and rapid ventricular response
(RVR);
1) *Thrombi form in atria due to blood stasis
2) *Embolus develop and travel to brain cause *stroke
d. Treatment: Goals-decrease ventricular response; prevent emboli
1) *Prevent blood clots- antiplatelet, anticoagulation; reduce
risk of stroke*
2) Convert to sinus rhythm or get to controlled rate
of<100 by synchronized cardioversion; antidysrhythmic
drugs as amiodarone, propafenone (Rhymol-Class 1-C sodium
channel blocker to slow conduction velocity, inhibit
automacity)
3) *If patient in atrial fibrillation for >48 hours, anticoagulation
therapy with warfarin recommended for 3 to 4 weeks before
cardioversion and 4 to 6 weeks after successful cardioversiondue to high risk for emboli post procedure!!
4) Meds to reduce ventricular response rate; digoxin, adrenergic blockers, calcium channel blockers, rate may still
be irregular- CO better
5) Radiofrequency catheter ablation to eradicate fibrillationmost recent, even for chronic a-fib
6) Maze procedure/modifications to Maze procedure (coldcryoablation); heat (high intensity ultrasound) *Maze procedure
-surgical treatment for atrial fibrillation….surgeon use small incisions,
radio waves, freezing, or microwave or ultrasound energy to create
scar tissue- scar tissue, which does not conduct electrical activity,
blocks the abnormal electrical signals causing the arrhythmia. The
scar tissue directs electric signals through a controlled path, or
maze, to ventricles.
8. Junctional Dysrhythmias
a. Description: *AV node- pacemaker; SA node failed to fire or impulse
blocked at AV node; rate- 40-60 BPM, can have junctional tachycardia
or 60-140 BPM; P wave patterns vary, may be absent or precede QRS
inverted in II, III and AVF, or hidden in QRS or follow QRS); PR
interval is absent or hidden <.10; QRS normal at 0.06-0.10 sec
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b. Clinical Associations/causes: drug toxicity (Digoxin, amphetamines,
caffeine, nicotine), hyperkalemia, increased vagal tone, cardiac
causes; hypoxia, hypoxia, ischemia, inferior MI, electrolyte imbalances
c. Clinical Significance
1) Serve as safety mechanism when SA node has not been
effective
2) Escape rhythms should not be suppressed
3) If rhythms rapid, may result in reduction of CO and HF
d. Treatment (often none required)
1) If symptomatic (slow rate)- atropine
2) Accelerated junctional rhythm and junctional tachycardia
caused by digoxin toxicity-, hold digoxin
3) -Adrenergic blockers, calcium channel blockers, amiodaronefor control of junctional tachycardia not caused by digoxin
toxicity
4) No DC cardioversion
Atrioventricular (AV) Conduction Blocks: Delayed or blocked transmission of
sinus impulse through AV node due to tissue injury or disease, increased vagal tone,
drug effects
9. First-Degree AV Block
a. Description- *Every impulse conducted to ventricles- duration
AV conduction prolonged; transmission through AV node delayed.
1) QRS normal, P wave normal; rate: 60-100 BPM; slowed
transmission through AV node; PR interval is > 0.20
b. Clinical Associations: MI, CAD, Rheumatic fever, hyperthyroidism,
vagal stimulation, drugs as Digoxin, -adrenergic blockers, calcium
channel blockers, flecainide (like propafenone-Rythmol class 1C)
*Why these drugs implicated??
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c. Clinical Significance
1) Usually asymptomatic
2) May be precursor to higher degrees of AV block
d. Treatment
1) Check medications * If on digitalis or beta blockers, hold
meds
2) Continue to monitor
10. Second-Degree AV Block, Type 1 (Mobitz I, Wenckebach)
a. Description: *Gradual lengthening PR interval, due to prolonged
AV conduction time…“Long, longer, longest, drop, then you
have a Wenkeback!”; PR progressively longer until drops QRS; PR
interval variable
1) Atrial impulse nonconducted; QRS complex blocked (missing)
2) Block usually at AV node, but can occur in His-Purkinje
system
b. Clinical Associations/causes: CAD, disease that slow AV conduction,
acute MI or drugs as digoxin, -adrenergic blockers, intoxication,
ischemia, rarely progresses
c. Clinical Significance; Usually result of myocardial ischemia or
infarction; usually well tolerated; warning sign of more serious AV
conduction disturbancel
d. Treatment-depend upon symptoms
1) Symptomatic, atropine or a temporary pacemaker
2) Asymptomatic, monitor with transcutaneous pacemaker on
standby
3) Symptomatic bradycardia -likely with one or more of the
following: hypotension, HF, shock
11. Second-Degree AV Block, Type 2 (Mobitz II)
a. Description
1) P wave nonconducted without progressive antecedent
PR lengthening. Usually occurs when block in one of bundle
branches present
2) Intermittent failure of AV node to conduct impulse; more P’s
but skips QRS in regular pattern 2:1; 3:1, 4:1
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b. Clinical Associations; Rheumatic heart disease, CAD, Anterior MI,
Digitalis toxicity
c. Clinical Significance; *Progress to third-degree AV block;
associated with a poor prognosis; reduced HR result in dec. CO with
hypotension and myocardial ischemia
d. Treatment: If symptomatic (e.g., hypotension, angina) before
permanent pacemaker, use temporary transvenous or transcutaneous
pacemaker; May try atropine (likely not to be effective) , Isuprel
(why these drugs? ); long term-*Permanent pacemaker
12. *Third-Degree AV Heart Block (Complete Heart Block)
a. Description: Form of AV dissociation- *no impulses from atria
conducted to ventricles; atria stimulated, contract independently of
ventricles
1) Ventricular rhythm- “escape” rhythm
2) Ectopic pacemaker -above or below bifurcation of bundle of
His
3) Atria and ventricles beat independently (separate rates for
each); rhythm from junctional fibers (rate 40 –60 BPM) or
ventricular (<30 BPM); No PR interval; wide QRS
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b. Clinical Associations: Severe heart disease: CAD, MI, myocarditis,
cardiomyopathy; Systemic diseases: Amyloidosis, scleroderma; Drugs:
Digoxin, -adrenergic blockers, calcium channel blockers
c. Clinical Significance: fatigue, SOB, fainting; Syncope from severe
bradycardia or even periods of asystole; if untreated -decreased
cardiac output and shock
d. Treatment:
1) *Transcutaneous pacemaker until a permanent
pacemaker
2) Drugs (e.g., atropine, epinephrine): Temporary -increase HR
and support BP until temporary pacing is initiated then
permanent
3) Permanent pacemaker required
*VENTRICULAR DYSRHYTHMIAS (originate in ventricles; most serious!)Disruption of ventricular rhythm- serious impact cardiac output and tissue
perfusion. ECG Characteristics of ventricular rhythms: Wide and bizarre QRS
complex (> 0.12 sec). Increased amplitude of QRS complex. No relationship to
P wave; abnormal ST segment, T wave deflected in opposite direction from QRS
complex
13. *Premature Ventricular Contractions (*need to recognize)
a. Description: *Contraction originating in ectopic focus of
ventricles. Premature occurrence of a wide and distorted, wide
bizarre QRS complex (>0.12 sec)
1) Multifocal, unifocal, ventricular bigeminy, ventricular
trigeminy, couples, triplets, R on T phenomena (danger zone,
refractory period)
Couplet or pair: 2 PVC’s in a row
Triplet or salvo: 3 PVC’s in a row
Bigeminy: PVC every other beat
Trigeminy: PVC every third beat
Unifocal PVC’s: arise from one site; all PVC’s look same
Multifocal PVC’s: from different ectopic sites’ all PVC’ s
look different arise from different foci
2) Rate varies, rhythm irregular, PVC interrupt underlying
rhythm; followed by compensatory pause; No P wave before
PVC; no PR interval
3) Due to enhanced automaticity or a re-entry phenomenon
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b. Clinical Associations: Stimulants: Caffeine, alcohol, nicotine,
aminophylline, epinephrine, isoproterenol, Digoxin, electrolyte
imbalances, hypoxia, fever, disease states: MI, mitral valve prolapse,
HF, CAD
c. Clinical Significance: normal heart, usually benign
1) Heart disease, PVCs may decrease CO & precipitate angina
and HF; must monitor patient response to PVCs
2) PVCs often do not generate sufficient ventricular contraction
to result in peripheral pulse
3) Apical-radial pulse rate –assess to determine pulse deficits
4) Represents ventricular irritability
5) May occur after lysis of coronary artery clot with thrombolytic
therapy in acute MI—reperfusion dysrhythmias and after
plaque reduction with percutaneous coronary intervention
6) *post MI (90% develop PVC…represent ventricular irritabilitylead to lethal dysrhythmias (VT, VFib greatest risk of
death!) * **(R on T) phenomenon (PVC’s falling on T
wave….lead to fatal ventricular fibrillation!
d. Treatment- based upon cause
1) Oxygen therapy for hypoxia
2) Electrolyte replacement
3) Drugs: Class II;-Adrenergic blockers (as metaprolol); Class
IA/IB-sodium channel blocker - Lidocaine, procainamide;
phenytoin (Dilantin)- 1st line for ventricular; Class III
potassium Channel Blocker- amiodarone)-1st line for
18  RNSG 2432
ventricular *Must treat if greater than 5 PVC a minute, runs of
PVC, multifocal PVCs – See p. 856 Tab 36-8 Antidysrhythmic
meds
4) Ablation
14. Ventricular Tachycardia (VT, VTach)
a. Description: Run of three or more PVCs; monomorphic,
polymorphic, sustained, and non-sustained; life-threatening due to
decreased CO; **deteriorate to ventricular fibrillation
1) rapid ventricular rhythm of 3 or more PVC’s; Rate > 100-250
with regular rhythm; no P wave, QRS >.12; wide and bizarre;
may occur in short bursts, runs or > 30 seconds.
2) due to re-entry phenomenon
b. Clinical Associations/causes: electrolyte imbalance, cardiomyopathy,
mitral valve prolapse, long QT syndrome, digitalis toxicity, MI, dig
toxicity, mechanical irritability, dysfunctional “pacemaker”; MI most
common factor
c. Clinical Significance- VT – “stable” (patient has pulse) or
“unstable” (patient pulseless)
1) Sustained VT: severe decrease CO, severe hypotension,
weak or non- palpable pulse, loss of consciousness,
pulmonary edema, decreased cerebral blood flow, ventricular
fibrillation, cardiac arrest.
2) Treatment must be rapid, will recur
d. Treatment
1) Precipitating causes -identify and treat (e.g., hypoxia)
2) Monomorphic VT and
(a) Hemodynamically stable (e.g., + pulse) + preserved LV
(left ventricular) function: give IV procainamide,
sotalol, amiodarone, or lidocaine
(b) Hemodynamically unstable or poor LV function: give IV
amiodarone or lidocaine followed by cardioversion
3) Polymorphic VT with a normal baseline QT interval: Adrenergic blockers, lidocaine, amiodarone, procainamide, or
sotalol; cardioversion used if drug therapy ineffective
4) Polymorphic VT with a prolonged baseline QT interval: IV
magnesium, isoproterenol, phenytoin, lidocaine, or
RNSG 2432  19
antitachycardia pacing: stop drugs that prolong the QT
interval; cardioversion if rhythm does not convert. (Torsades
de pointes, p. 855 36-18)
5) *VT without pulse-life-threatening situation (nonresponsive)
a) Cardiopulmonary resuscitation (CPR) and rapid
defibrillation
b) Epinephrine if defibrillation unsuccessful
15.
Ventricular Fibrillation- (VFib) Severe derangement of heart rhythm;
ECG shows irregular undulations of varying contour and amplitude- no
effective contraction or CO occurs
a. Description: extremely rapid, chaotic rhythm - ventricles quiver, do
not contract; *cardiac arrest and death result within 4 minutes if
rhythm not terminated; 400-1000 beats per minute…too rapid to
count!
1) Garbage baseline; no P waves, no QRS’S, NO cardiac
output!
b. Clinical Associations: Acute MI, CAD, cardiomyopathy, may occur
during cardiac pacing or cardiac catheterization, with coronary
reperfusion after fibrinolytic therapy, accidental electrical shock,
hyperkalemia, hypoxia, acidosis, drug toxicity
c. Clinical Significance: unresponsive, pulseless, apneic state,
untreated=death
d. Treatment:
1) CODE situation- Immediate initiation of CPR and advanced
cardiac life support (ACLS) measures with immediate use of
defibrillation and definitive drug therapy
*cannot cardiovert…no rhythm to cardiovert
16.
Asystole- total absence of ventricular electrical activity, no ventricular
contraction (CO) occurs- no depolarization
20  RNSG 2432
a. Description: No electrical conduction/ no ventricular activity; CARDIAC
arrest, death; no rate; no “p” wave, or even if “p” wave, no ventricular
response; no QRS, no conduction; no rhythm
b. Clinical association: most commonly after termination of atrial, AV
junctional or ventricular tachycardias; usually insignificant in those
cases (*adenosine was used to stop these abnormal rhythms)
1) aysystole of longer duration in presence of acute MI and CAD
frequently fatal
2) advanced cardiac disease, severe cardiac conduction system
disturbance
3) end-stage HF
c. Clinical significance: unresponsive, pulseless, and apneic state
1) prognosis for asystole- extremely poor
d. Treatment
1) *CPR with initiation of ACLS measures (e.g., intubation,
transcutaneous pacing, and IV therapy with
epinephrine and atropine)
17.
EKG changes related to Acute Coronary Syndrome CS (p. 861 Fig
36.28, 29, 30 and Tab. 36.13) *Review previous notes n MI
a. ECG changes in response to ischemia, injury, or infarction of
myocardial cells
b. Changes in leads that face area of involvement
c. Reciprocal (opposite) ECG changes often seen in leads facing opposite
area involved
d. Pattern of ECG changes- information on coronary artery involved in
ACS
RNSG 2432  21
e. ST segment elevation is significant if >1 mm above isoelectric line
1) If treatment prompt, effective, may avoid infarction
2) If serum cardiac markers present, have ST-segment-elevation
MI (STEMI)
f. Physiologic Q wave - first negative deflection following P wave, small
and narrow (<0.04 second in duration); pathologic Q wave is deep and
>0.03 second in duration
g. Pathologic Q wave -at least half thickness of heart wall involved (Q
wave MI), May be present indefinitely
h. T wave inversion related to infarction-occurs within hours; may persist
for months
22  RNSG 2432
Pulseless Electrical Activity -Electrical activity can be observed on the ECG, but
there is no mechanical activity of the ventricles and the patient has no pulse;
Treatment- CPR followed by intubation and IV epinephrine; Atropine is used if the
ventricular rate is slow; directed toward correction of the underlying cause
Sudden Cardiac Death (SCD)- Death from a cardiac cause; majority of SCDs due
to ventricular dysrhythmias (ventricular tachycardia, ventricular fibrillation)
Prodysrhythmia - Antidysrhythmic drugs may cause life-threatening dysrhythmias
esp. Digoxin and class IA, IC, and III antidysrhythmia drugs; first several days of
drug therapy most vulnerable period for developing prodysrhythmias. *ideally be
monitored in hospital.
Collaborative Care for Dysrhythmias
1. Focus
a.
b.
c.
d.
Recognition and identification of dysrhythmia
Evaluating the effects, especially lethality
Treatment of underlying causes
Nursing assessment: apical rate and rhythm; apical/radial deficit;
blood pressure; skin, urine output, signs of decreased cardiac output!
e. Intervention in dysrhythmia
1) Antidysrhythmia drugs
2) Defibrillation
a) Cardioversion
b) Implantable cardioverter-defibrillator
c) Pacemaker
d) Radio-frequency catheter ablation therapy
2. ECG rhythm analysis process (as covered)
a. Rate determination
b. Regularity determination
c. P wave assessment
d. Assessment of P to QRS relationship
e. Determination of intervals
1) PR interval
2) QRS complex duration
3) QT interval
f. Identification of abnormalities
3. Diagnostic Tests (as covered-see also (p. 753-755 Tab 32-7)
a. 12 lead Electrocardiogram
1) Identification of rhythm
2) Information about underlying disease processes
3) Monitor effects of treatment
b. Cardiac Studies (review all)
1) Continuous cardiac monitoring
2) Ambulatory ECG monitoring (Holter monitoring or
Transtelephonic event recorder)
3) Exercise Treadmill test
RNSG 2432  23
4) Echocardiocgram /Stress echocardiogram/Pharmacologic ECHO
(what drug?)
5) Transesophageal Echocardiogram (TEE)
6) Nuclear Cardiology including pharmacological nuclear imaging
(what drug) MUGA, PET
7) MRA, MRI
8) Cardiac Catheterization etc
Interventions/Therapy for Dysrhythmia
1. Defibrillation
Emergency delivery of direct current without regard to cardiac cycle
(ventricular fibrillation); performed immediately when rhythm
recognized-performed externally or internally (surgery, open chest); also
automatic external Defibrillators. **Note where paddles are placed! P, 857
fig 36-29-Read text
a. Defibrillation *non-responsive, pulseless client
1) Most effective method -terminate VF and pulseless VT
2) Passage of DC electrical shock through heart to depolarize cells
of myocardium to allow SA node to resume role of pacemaker
3) Deliver energy using a monophasic or biphasic waveform
(Monophasic –Deliver energy –one direction; biphasic –deliver
energy – two directions successful shocks at lower energies,
fewer postshock ECG abnormalities)
4) Output- measured in joules/watts per second
b. Recommended energy for initial shocks
1) Biphasic –First and successive shocks: 150 to 200 joules
2) Monophasic-Initial at 360 joules
3) After initial shock, chest compressions (CPR)
2. Synchronized Cardioversion
Direct electrical current synchronized with heart rhythm; avoid shock during
vulnerable period of repolarization (R on T)
Elective procedure-treat SVT, a-fib, flutter, hemodynamically stable
VT
*Clients in afib-; need anticoagulation several weeks before
cardioversion, dec. risk for thromboembolism post cardioversion
24  RNSG 2432
1) Choice of therapy for hemodynamically unstable ventricular or
supraventricular tachydysrhythmias
2) Synchronized circuit -delivers countershock on R wave of QRS
complex of ECG
3) Synchronizer switch must be turned on!
3. Implantable Cardioverter- Defibrillator (ICD) *Who is a candidate for
one? - read p. 857
Pulse generator implanted surgically into client with lead electrodes for
rhythm detection and current delivery; senses rate and width of QRS,
combined pacemaker; senses life-threatening rhythm changes; delivers
automatic electric shock to convert dysrhythmia
1. Provides pacing on demand
2. Stores ECG records of rhythms
3. Can be reprogrammed at bedside when
necessary
4. Needs to be surgically replaced every 5
years
a. For clients who survived SCD (Sudden cardiac death)
b. Have spontaneous sustained VT, syncope with VT, Vfib during EPS
c. At high risk for future life-threatening dysrhythmias;*If fires, contact
health care provider, or 911!
d. Consists of lead system placed via subclavian vein to endocardium
e. Battery-powered pulse generator implanted subcutaneously
f. ICD sensing system- monitors HR and rhythm, identifies VT or
VF
g. Approx. 25 sec. after detecting VT or VF, ICD delivers <25 joules; if
first shock unsuccessful, ICD recycles and delivers successive shocks
h. Equipped with antitachycardia and antibradycardia pacemakers
i. Initiates overdrive pacing of SVT and VT
j. Provides backup pacing for bradydysrhythmias
k. Education critical; fear, body image alteration, anxiety, support group
(*See Tab 36-8 p. 858)
RNSG 2432  25
4. Pacemakers (Indications - Tab 36-10 p. 859)
*Pulse generator- provides electrical stimulus to heart when heart fails
to generate or conduct own at a rate for adequate cardiac output
a. Used to pace heart when normal conduction pathway damaged or
diseased;
1) Pacing circuit consists of power source, one or more conducting
(pacing) leads and myocardium
2) Electrical signal (stimulus) travels from pacemaker, through
leads to wall of myocardium; myocardium “captured” stimulated to contract
3) Initially for symptomatic bradydysrhythmias; now
antitachycardia and overdrive pacing (antitachycardia
pacing=delivery of stimulus to ventricle to terminate
tachydysrhythmias); (overdrive pacing: pacing atrium at rates
of 200 to 500 impulses per minute to terminate atrial
tachycardias)
b. Types
1) Temporary pacemaker: Power source outside the body
a) Transvenous
b) Epicardial
c) Transcutaneous (Fig 36-27 p. 860)
Transcutaneous pacing
2) Permanent pacemaker: implanted totally within body: Singlechamber pacing (atria or ventricles stimulated) or dualchamber pacing (both are stimulated)
26  RNSG 2432
Click for more pacemaker information
3) Pacemakers (see Fig 36-24 p. 859)
a) Modes: aynchronous-preset time without fail or
synchronous or demand-when heart rate goes below set
rate
b) Sense activity in and pace ventricles only
c) *Most now sense activity in and pace both atria and
ventricles (atrio-ventricular sequential pacing stimulates
in sequence that imitates normal sequence of atrial
contraction followed by ventricular contraction)
4) Cardiac resynchronization therapy (CRT): Pacing technique
a) Resynchronizes- cardiac cycle by pacing both ventricles
b) Combined CRT with an ICD for maximum therapy
c) *Important for heart failure management
5) ECG characteristics (Fig 36.3-p, 858)
a) Pacing detected by presence of pacing artifact*sharp spike occur before P wave in atrial pacing or
before QRS complex in ventricular pacing
b) Capture noted by contraction of chamber following the
spike (seen as P wave in atrial pacing or QRS complex in
ventricular pacing)
6) Teaching (See Tab 36-12 p. 861) *Read carefully
a) Pre-op; teach, explain procedure; place electrodes away
from potential incision site; teach ROM exercises for affected
site- help prevent shoulder stiffness.
RNSG 2432  27
b) Post –op-c hest x-ray; minimize movement of affected
arm during initial post-op period-decrease risk of
dislodging pacer; monitor pacer with ECG; report failure to
pace, etc; assess for dysrhythmia, takes 2-3 days for
“seating”; document; date of pacer insertion, model etc.
a) Home Care: how it works, how placed, battery
replacement, how to take and record pulse, incision site
care, activity restrictions, ID card, don’t hold certain
electrical devices near it…sets off security devices…
b) Maintaining safety; Preventing infection and
complications
5. Catheter Ablation Therapy (Click here for video)
Electrode-tipped ablation catheter “burns” accessory pathways or ectopic
sites in atria, AV node, and/or ventricles
a. Nonpharmacologic treatment for AV nodal reentrant tachycardia,
re-entrant tachycardia related to accessory bypass tracts; control of
ventricular response of certain tachydysrhythmias
b. Complete ablation of AV node or bundle of His- may be done in some
cases of uncontrolled ventricular response in atrial fibrillation or flutter
unresponsive to medical therapy
1) Involves location/destruction (burn ectopic pathway) of
ectopic foci in heart2) Diagnosed in electrophysiology lab/performed in cardiac
cath lab
3) Cardiac mapping: identification of sites where impulse
initiated in atria or ventricles-use internal or external catheters
4) Ablation: destroy ectopic focus withradiofrequency energy with
catheters; *anticoagulant therapy may be started afterward to
decrease risk of clot forming at ablation site
6. Other measures to stop dysrhythmias
*For SVT
a. *Vagal maneuvers- client “bears down”: forced exhalation against a
closed glottis to slow heart rate
b. Carotid sinus massage, continuous monitoring- by physician only
c. Medications such as adenosine, calcium channel blockers
d. *See antidysrhtymic meds (know) Tab 36.8 p. 856 and Tab. 34-12 p.
800 and p. 798-801 and list of meds as included.
Nursing Care
1. Decrease risk for CHF/Dec. CO, which is major risk for dysrhythmias
28  RNSG 2432
2. Reduce sympathetic nervous system stimulants like caffeine
Nursing Diagnoses
1. *Decreased Cardiac Output
a. Always assess the client before treating the dysrhythmia
b. Monitor vital signs, ECG, and oxygen saturation frequently during
antidysrhythmic drug infusions
c. Nurses caring for clients with dysrhythmias- need to be competent in
CPR and ACLS
2. Ineffective Tissue Perfusion
3. Anxiety and fear
4. Knowledge deficit
RNSG 2432  29