Download Arrhythmia

NOTES: Dysrhythmias cmj
Module #3 Nursing Care of the Individual with
Cardiovascular Disorders: Cardiac Rhythm Disorders
Dysrhythmias
Etiology/Pathophysiology
Dysrhythmias; alterations in normal heart rate produced by various pacemaker
cells in the myocardium.
Dysrhythmias can occur as natural consequence of emotion, body demand
for oxygen, or sympathetic nervous system stimulation, athletic training,
aging
____________________________________________________
Physiology (Review only)
* Cardiac muscle: unique- can generate electrical impulse and
contraction independent of nervous system
I. Cardiac conduction system: network of specialized cells and
conduction pathways that initiate and spread electrical impulses
causing heart to beat
* Electrical stimulation of heart muscle always precedes
mechanical contraction (*electrical precedes mechanical)
*
Pacemaker cells of heart
1. Sinoatrial (SA) or sinus node: intrinsic rate 60–100
bpm; 1st pacemaker
2. Atrioventricular (AV) node: intrinsic rate 40–60 bpm;
2nd pacer…, controls # of impulses that reach ventricles;
#conduction fibers narrow through AV node; allow atrial
muscle to contract and deliver extra bolus of blood to
ventricles before they contract (atrial kick)
3. Purkinje fibers (or ventricle conduction system): intrinsic
rate 15 – 40 bpm; prompt mechanical contraction or
systole
RNSG 2432  41
II. Electrophysiologic properties of cardiac cells Text p. 839 +
1. Automaticity: pacemaker cells spontaneously initiate
electrical stimulation (*SA node pacemaker of heart; has
highest level of automaticity; stimulated by nervous system
through vagus nerve; sympathetic stimulation increases
rate of firing; parasympathetic decreases firing). *Under
variety of circumstances cardiac cells in any part of heart
(pacemaker cells or non-pacemaker) cells, can take on role
of a pacemaker and begin generating extraneous impulses,
called ectopics. *(Any cardiac muscle can generate an
electrical impulse and contraction independent of
nervous system!)
2. Excitability: ability of myocardial cells to respond to stimuli
generated by pacemaker cells (action potential)
3. Conductivity: ability to transmit impulse from cell to cell
4. Contractility: ability of myocardial fibers to shorten in
response to stimulus; “All or nothing” manner
III. Action Potential
1. *Electrical activity = waveforms on ECG strips due to ion
movement across cell membranes stimulating muscle
contraction
2. Stages
a. Resting State: polarized state
1) Positive and negative ions align on either side
of cell membrane
2) Relatively negative charge within cell and
positive charge extracellularly
3) Negative resting membrane potential
maintained at -90 millivolts (mV)
b. Depolarization *(important- consider how
medications affect heart rhythm and pumping
action)
1) Resting cell stimulated by charge
2) Na ions enter cell rapidly through fast
sodium channels
3) Calcium enter cells via slow calciumsodium channels
4) Membrane less permeable to K ions
5) Membrane potential changes to slightly
positive at +20 - +30 mV
Using this information how does a medication
such as verapamil work in controlling
dysrhythmia? What drug class? (text p. 854)
c. Threshold potential
1) As cell becomes more positive a point is
reached when action potential is generated
2) Causes chemical reaction of Ca within
cell
3) Actin and myosin filaments slide
together producing cardiac muscle
contraction
42  RNSG 2432
4) Once myocardium completely depolarized,
repolarization begins
d. Repolarization (protects heart muscle from spasm
& tetany)
1) Cell return to resting, polarized state
2) Fast sodium channels close abruptly
3) Cell regains negative charge (rapid
repolarization)
4) Muscle contraction prolongs as slow calciumsodium channels remain open (plateau phase)
5) Once closed, sodium-potassium pump
restores ion concentration and cell membrane
is polarized again
e. Refractory period
1) Myocardial cells resistive to stimulation;
dysrhythmias triggered during relative
refractory and supernormal periods*
a) Three periods
(1) Absolute refractory period: no
depolarization can occur
(2) Relative refractory period: greater
than normal stimulus required for
depolarization
(3) Supernormal period: mild stimulus
can cause depolarization
**Many cardiac dysrhythmias are
triggered during Relative and
Supernormal period!!
Refractory Period
*Ectopic stimulus
during refractory period
lead to dangerous
arrhythmia!!
IV. Electrocardiography (see p. 842, fig 29-9 & 10) (ECG)
a. Graphic recording of electrical activity of heart
b. Electrodes-applied to body surface, detect magnitude and direction
of electrical current produced by heart
c. *Standard 12-lead ECG; simultaneous recording of 6 limb leads
and 6 precordial leads
1. Limb leads: bipolar leads (I, II, III); unipolar leads: aVR,
aVL. aVF
RNSG 2432  43
2. Precordial leads (chest leads): V1, V2, V3, V4, V5, V6
*Monitor lead II or MCL (main chest lead) also known as V1best view of each component of EKG.
FYI: Bipolar lead- 2 electrodes of opposite polarity; unipolarity lead
uses positive electrode and a negative reference point at center of
heart; electrical potential between 2 monitoring points is
graphically recorded as ECG waveform.
Leads of the 12-lead ECG
Bipolar limb leads
Pearson Education
Copyright 2004
Unipolar limb leads
Image Bank
Unipolar precordial leads
Medical-Surgical Nursing
Priscilla LeMone, Karen Burke
3. Waveforms reflect direction of electrical flow (what you see
on the EG strip)
a. Positive (upward) waveform is toward the 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
4. *ECG waveforms recorded on paper with marking
representative of time (*MUST know this!) See text p.
843, fig. 29-11 &12
a. Each small box = 0.04 seconds (sec)
b. One large box (5 small boxes) = 0.20 sec.
c. 5 large boxes measure 1 second
d. Vertically, each small box = 0.1 millivolt (mV)
44  RNSG 2432
5. *Cardiac cycle-depicted as series of waveforms
(electrical precedes mechanical!)
a. P wave: atrial depolarization and contraction= “p”
wave on EKG
b. PR interval
1) 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)
2) Normal 0.12 - 0.20 seconds
c. QRS Complex
1) Ventricular depolarization and
contraction
2) Transmission of impulse through ventricular
conduction system
3) Normal 0.06 – 0.10 seconds
d. ST segment
1) Beginning of ventricular repolarization
2) End of QRS complex to beginning of T wave
3) Should be isoelectric
4) *Remember significance of elevated ST
segment with MI!!
e. T wave
1) Ventricular repolarization
2) Smooth and round < 10 mm tall
3) Same direction as QRS complex
4) Abnormalities= myocardial injury or ischemia,
electrolyte imbalances
5) No defibrillation on “T” wave. Danger!
f. QT interval
1) Total time of ventricular depolarization and
repolarization
2) Beginning of QRS complex to end of T wave
3) Normal: 0.32 – 0.44 seconds
4) Prolonged QT: prolonged relative
refractory period; greater risk for
dysrhythmias
5) Shortened QT: due to medications or
electrolyte imbalance (often measure QT for
meds; becoming increasing important!)
g. U wave
RNSG 2432  45
1) Signify repolarization of terminal Purkinje
fibers;
2) Same direction as T wave
3) Seen with hypokalemia
___________________________________________________________
Dysrhythmia
Pathophysiology; *Primary significance-effect on cardiac output and
cerebral or vascular perfusion!
With dysrhythmias, loose “atrial kick”. What is significance? P. 839.
In normal sinus rhythm (NSR), atria fill and stretch ventricles with about 30%
more blood; “atrial kick” occurs; improves contractility of ventricles; increases
cardiac output.
Note: impulse start in AV node or ventricles, atrial and ventricular contraction not
coordinated; atrial kick is lost- cardiac output falls.
1. 2 major mechanisms for dysrhythmia development
a. Altered impulse formation (includes changes in rate and rhythm
and development of ectopic beats); result from change in
automaticity of heart cells
1) Tachydysrhythmias (rapid heart rates)
2) Bradydysrhythmia (slow heart rates)
3) Ectopic rhythms (impulses originate outside normal
conduction pathways)
4)*Re-entry phenomenon
a. Cause of tachydysrhythmias (PVC, VT caused by this
phenomenon)
b.Dysrhythmia propagates itself
*Example..ectopic beats triggers re-entry phenomenon;
impulse delayed in one area of heart; conducted normally
through rest of heart muscle. Muscle depolarized by
normally conducted impulse repolarized by time impulse
traveling through area of slow conduction reaches it, thus
initiating another cycle of depolarization.
b. Altered conductivity (result from failure or delay of impulse
transmission)
1) Block in normal conduction pathway
2) Varying degrees of heart block at AV node
3) Bundle branch blocks (common in acute MI
Risk Factors for dysrhythmia (*understand this concept)
1. Hypoxia: heart needs oxygen
2. Structural changes: atherosclerosis, atrial fibrillation, changes after MR or
acute coronary syndrome
3. Electrolyte imbalance: Potassium most important, Ca, Mg, Na also for
cardiac cells
4. Central nervous system stimulation: caffeine, nicotine, cocaine, heroine
46  RNSG 2432
5. Medications: Digoxin (potentially dangerous-recall what occurs with dig
toxicity); beta blockers (drugs that end in “al” or “ol:” slow down
heart!; ”bedrest” for heart)
6. Lifestyle behaviors: stress, smoking, drugs, caffeine
Manifestations/Therapeutic Interventions/Collaborative Care
1. Reduced cardiac output: clinical manifestations-palpitations dizziness or
syncope, pallor, diaphoresis, altered mental status, hypotension, sluggish
capillary refill, swelling of extremities, diminished urine output (depends upon
degree of decreased cardiac output)
2. EKG Changes/Assessment (See text p. 844, Box 29-3) *Important
steps
Assessment

Calculate rate







Big block
Little block
Number of R waves in 6 sec times
10
Calculate rhythym-reg or irreg
Measure PR interval, <.20
QRS interval .06-.10
P to QRS relationship
a.*Determine rate: (see text p. 844)
1) Count # complexes in 6 second rhythm; top margin of ECG paper
marked at 3 second intervals; multiply by 10
2) Count # large boxes (Big block) between two consecutive
complexes; divide 300 by this number (the number of large boxes
in 1 minute)…memorize a sequence….see text
3) Count number small boxes (Little block) between two consecutive
complexes; divide 1500 by this number (the number of small
boxes in 1 minute) by this number…* most precise measurement
of heart rate! You must know how to calculate using each
method!
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.
RNSG 2432  47
b. Determine regularity/underlying rhythm; consistency with which P
waves or QRS complexes occur
c. Assess “P” wave; presence or absence and appearance; should be alike
in size and shape
d. Assess “P” wave to “ORS” relationship; should be 1 to 1
e. Determine interval durations (“PR”, QRS”, “QT” and evaluate (need to
measure intervals of PR, QRS, QT…know normals)
f. Identify abnormalities; presence or frequency of ectopic beats, shape
of complexes, etc. Note presence of ectopics (extra beats, deviations of ST
segments if above or below baseline, and abnormalities in waveform
shape and duration.
3. Classifications: according to site of impulse formation (See text p. 845-7,
Table 29-6) *Must identify the major arrhythmias! (NSR, sinus
bradycardia, atrial fibrillation, PVC, ventricular tachycardia,
ventricular fibrillation, first degree heart block, third degree/
complete heart block and asystole)
* Other common dysrhythmia FYI
***For EKG characteristics and treatment each rhythm; refer to text,
summary only below!
***Note-textbook-chart p. 845 and to top p,846 (atrial flutter) has typo’s
re QRS complex…should be .06 not .6
I. SUPRAVENTRICULAR rhythms (rhythm originates above ventricles; SA
node as pacemaker)
1. Normal Sinus Rhythm**
a. Normal conduction; normal P wave; P:QRS; 1:1; PR
interval: 0.12-.20 sec; ORS <.12 or 0.06-0.10 sec; QT
interval <.32-.40
b. Rhythm originates in SA node
c. Rate 60 – 100 bpm
d. No treatment
2. Sinus Tachycardia (SA node is pacemaker); see text
a. Normal conduction; rate greater than 100 bpm
b. Causes: sympathetic nervous system stimulation; blockage
of vagal activity; body response to condition or event that
requires increase in oxygen and/or nutrition; anxiety, pain,
caffeine, etc
c. Manifestations: palpitations; shortness of breath; dizziness
48  RNSG 2432
d. Treatment: eliminate cause such as caffeine, stimulates
sympathetic nervous system
3. Sinus Arrhythmia (SA node is pacemaker); see text
a. Sinus rhythm but irregular; speeds up with inspiration and
decreases with expiration; common in very young and very
old
b. Causes: “youth”, drugs especially morphine, post
myocardial infarction
c. Manifestations: P. QRS, T wave normal; no clinical signs (P
to p interval varies, but configuration is the same
d. Treatment: none required
4. Sinus bradycardia**
a. Normal conduction; rate less than 60 bpm; rhythm regular;
P: QRS: 1:1; PR interval: 0:12 to .20 sec.; QRS complex:
0.06 to 0.10 sec
b. Causes: increased vagal (parasympathetic) activity;
injury or ischemia to sinus node; normal (athletic heart
syndrome, asleep; inferior wall damage with acute MI;
increased intracranial pressure; medications such as betablockers and digoxin; hypothermia; acidosis
c. Manifestations
1) Asymptomatic (none)
2) Symptomatic: decreased level of consciousness,
syncope, hypotension
*d. Treatment: determine cause; treat if symptomatic (can
develop decreased CO); use *atropine to increase rate of
pacemaker!
RNSG 2432  49
*How and why does atropine work to increase rate? What
are examples of drugs that lower rate and may lead to a
sinus bradycardia? (P. 854)
5. Sick Sinus Syndrome – SSS (sinus node dysfunction; conduction
problem; may experience multiple rhythm changes)
a. Dysfunction of sinus node often with aging; various
rhythm changes including: sinus bradycardia or
arrhythmias; sinus pauses or arrest; atrial
tachydysrhythmias, such as atrial fibrillation, flutter, or
tachycardia and bradycardia-tachycardia syndrome:
paroxysmal tachyrhythms followed by sinus pauses and/or
bradycardias
b. Causes: use of medications which slow heart (e.g. digitalis,
beta blockers)
c. Manifestations; intermittent fatigue; dizziness; lightheadedness; syncope
d. Treatment: determine cause; eliminate source; pacemaker
6. Sinus arrest (SA): see pauses, may see ectopic beats, premature
atrial contractions (PAC) or premature ventricular contractions
(PVC); cause MI; treatment by use of atropine, Isuprel and
pacemaker for definitive care.
Why is isuprel effective? (refer to list of cardiac
emergency drugs)
Supraventricular dysrhythmias (atrial arrythmias) Can be serious: atria
contributes 25-30% cardiac output (atrial kick); especially in patients with MI
already decreased cardiac reserve. (an ectopic pacemaker overrides the SA
node); may also develop as “escape rhythm” if SA node fails …are all
paroxysmal (occur in bursts with abrupt onset and end)
1. Premature Atrial Contractions (PAC)*** (see text for criteria)
a. Atrial is pacemaker; P:QRS: 1:1; ectopic atrial beat occurring
earlier than next expected sinus beat; P wave-abnormally
shaped, or P wave lost in QRS; PR interval shorter; QRS normal
(0.06 to 0.10); have a non-compensatory pause (early beat
affects P wave appearance)
50  RNSG 2432
b. Causes age, CHF, stimulants, digitalis, electrolyte imbalance;
anxiety, alcohol, nicotine, MI, heart failure, hypoxemia
c. Manifestations: usually asymptomatic and benign; monitor for
supraventricular tachycardia
d. Treatment: monitor for development of SVT; identify cause
2. Paroxysmal Supraventricular Tachycardia (PSVT) or SVT
a. Rate 150-250; atria is pacemaker, may not see P waves due
to rapid rate (ectopic foci above ventricles)
b. Causes: sudden onset and termination initiated by a “reentry” loop in or around AV node; precipitated by
sympathetic nervous system stimulation and stressors including
fever, sepsis, hyperthyroidism; heart diseases including CHD,
myocardial infarction, rheumatic heart disease, myocarditis or
acute pericarditis; Wolff-Parkinson-White syndrome
c. Manifestations: palpitations, “racing heart”, anxiety, dizziness,
dyspnea, anginal pain, extreme fatigue, diaphoresis, polyuria
d. *Treatment:
 Adenocard/ adenocin which stops heart, allows SA
node to take over (brief asystole); similar to medical
cardioversion; only given in ICU, ER (temporary)
 Vagal stimulation to return to sinus rhythm
 Digoxin, verapamil, inderal, quinidine, cardiazem,
tikosyn (know classification of each and why and how
they work!) Must treat, increases myocardial oxygen
demands! **Review meds here-see emergency cardiac med
list!
3. Atrial Flutter
a. 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; QRS complex: 0.06-0.10 sec.
RNSG 2432  51
b. Causes: Sympathetic nervous system stimulation:
anxiety, caffeine and alcohol intake, thyrotoxicosis, CHD,
pulmonary embolism, Wolff-Parkinson-White syndrome
(WPW), rheumatic heart disease and/or valvular disease
c. Manifestations: palpitations or fluttering sensations in chest or
throat; if rapid ventricular response: hypotension, cool, clammy
skin, decreased level of consciousness
d. Treatment:
 Synchronized cardioversion
 Meds to slow ventricular response such as beta
blocker or calcium channel blocker followed by
quinidine, procainamide, flecainide or amiodarone.
*Important think about why, how these meds work!
 Ablation to obliterate abnormal conduction pathways.
4. Atrial Fibrillation*** Must knows (read text on this one!)
a. No P waves, “garbage baseline”; rate of atria 300-600;
too rapid to count; ventricular rate of 100-180 BPM in
untreated clients; multiple pacemaker initiate beats;
disorganized atrial activity without discrete atrial
contractions; irregular ventricular response; pulse deficit;
irregularly irregular
Atrial Fibrillation






Rate of atria 350-600
Ventricular response irregular
No P waves, “garbage baseline”
Cause-#1 arrhythmia in elderly,CHF
Treatment- same as SVT, start with digoxin
Thrombus formation, pulse deficit, AR>RR
b. Causes: associated with heart failure, rheumatic heart
disease, CHD, HPT, hyperthyroidism: #1 arrhythmia
elderly!
c. Manifestations (relate to ventricular response):
hypotension, shortness of breath, fatigue, angina, may
develop syncope, heart failure (loss of atrial* kick),
increased risk for *thromboemboli, high incidence of
stroke
d. Treatment:
 Prevent blood clots- antiplatelet drug,
anticoagulation; reduce risk of stroke***
52  RNSG 2432



Attempt to convert to sinus rhythm or at get to
controlled rate of>100 by synchronized
cardioversion
Medications to reduce ventricular response
rate; verapamil, propranolol, or digoxin, rate
may still be irregular, cardiac output improved)
Ablation therapy option to eradicate fibrillation,
requires cardiac mapping!
Junctional Dysrhythmias (junctional escape)
1. Rhythms that originate in AV nodal tissue; AV node is pacemaker; slow
rhythm of 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
2. Causes: drug toxicity, hyperkalemia, increased vagal tone, cardiac causes;
hypoxia, hypoxia, ischemia, electrolyte imbalances
3. Treatment: None usually, correct underlying problem; symptomatic require
atropine, or pacemaker
II. *VENTRICULAR DYSRHYTHMIAS (originate in ventricles; most serious!)
1. Dsruption of ventricular rhythm- serious impact cardiac output
and tissue perfusion!
2. 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
A. Premature Ventricular Contractions (PVCs)*** (see text p. 846)
1. ECG Characteristics: Occur before next expected beat; rate varies,
rhythm is irregular, PVC interrupt underlying rhythm; followed by a
compensatory pause; P: QRS: No P wave noted before PVC; PR
interval: absent with PVC; QRS complex: wide (>0.12 sec) and
bizarre in appearance; differs form normal QRS
RNSG 2432  53
Premature Ventricular
Contractions (PVC’s)







From ectopic focus
QRS wide and bizarre
No P waves
T opposite deflection of PVC
Cause- 90% with MI
Treatment- lidocaine,
pronestyl,amiodarone
No longer prophylactic
2. Due to either enhanced automaticity or a re-entry phenomenon
3. ECG Descriptors
1) Couplet or pair: 2 PVC’s in a row
2) Triplet or salvo: 3 PVC’s in a row
3) Bigeminy: PVC every other beat
4) Trigeminy: PVC every third beat
5) Unifocal PVC’s: arise from one site; all PVC’s look the same
6) Multifocal PVC’s: from different ectopic sites’ all PVC’ s look
different arise from different foci
4. Significance
1) None in persons without heart disease
2) Frequent, recurrent, multifocal PVC’s associated with increased risk
for lethal dysrhythmias
5. Causes: (multiple) anxiety or stress, tobacco, alcohol, caffeine use,
*hypoxia, *acidosis, *electrolyte imbalance, sympathomimetic drugs,
*coronary heart disease, *heart failure, *mechanical stimulation of
heart (insertion of cardiac catheter), *reperfusion after thrombolytic
therapy, *post MI (90% develop…greatest risk of death!)
6. Indicators of myocardial irritability and increased risk for lethal
dysrhythmias
1) PVC’s occurring within 4 hours of MI
2) Frequent (> 6 per minute)
3) Couplets or triplets
4) Multifocal PVC’s
**5) R on T phenomenon (PVC’s falling on T wave…time of repolarization lead to fatal ventricular fibrillation!)
54  RNSG 2432
7. Treatment:
 Medications: Lidocaine (IB), pronestyl (IA), amiodorone
(III), beta blockers, (must treat is greater than 5 PVC’s a
minute, runs of PVS, multifocal PVC or “R” falling on T wave
(know why these drugs work!) Amiodorone now first line
drug for treatment…then Lidocaine.
 May use ablation
B. Ventricular Tachycardia (VT, V Tach) ***(See text p. 846)
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. Result of re-entry phenomenon
Ventricular Tachycardia (VT)





Ventricular rate 100-250, regular
No P waves
QRS>.12
Cause- electrolyte imbalance, MI
Treatment- same as for PVC’s and
defibrillate for sustained
RNSG 2432  55
3. Cause: electrolyte imbalance, MI, dig toxicity, mechanical irritability,
dysfunctional “pacemaker”; MI most common factor
4. Manifestations, if sustained VT:
1) Severe hypotension
2) Weak or non-palpable pulse
3) Loss of consciousness
4) *If allowed to continue, deteriorate into ventricular
fibrillation
5. Treatment: same as for PVCs
 Immediate defibrillation if unconscious for sustained VT
 IV amiodarone, lidocaine, procainamide
 Surgical ablation and/or antitachycardia pacing with implanted
cardioverter/defibrillator (ICD) for repeated episodes;
antiarhytmic drugs; medical emergency!
 Need to know/recognize this one; drugs/treatment.
C. Ventricular Fibrillation (VF, V fib)*** (See text p. 846)
1. Extremely rapid, chaotic rhythm in which ventricles quiver and do
not contract; *cardiac arrest and death will result within 4
minutes if rhythm not terminated; 400-1000 beats per minute…too
rapid to count!
2. Garbage baseline; no P waves, no QRS’S, NO cardiac output!
3. Causes: severe myocardial ischemia or infarction, precipitated by PVC
or V Tach, digitalis toxicity, reperfusion therapy, antidysrhythmic
drugs, hypo and hyperkalemia, hypothermia, metabolic acidosis,
mechanical stimulation, electric shock
4. Manifestations
1) Absence of palpable or audible pulse
2) Loss of consciousness
3) No treatment= breathing stops and death!
5. Treatment:
 CODE situation: ACLS, CPR, IMMEDIATE defibrillate
(cannot cardiovert…no rhythm to cardiovert!)
56  RNSG 2432
D. Asystole/Ventricular Standstill**
1. No electrical conduction/ no ventricular activity; CARDIAC arrest, death
2. No rate; typically no “p” wave, or even if one, no ventricular response; no
QRS, no conduction; no rhythm
3. Asystole occurs most commonly follows termination of atrial, AV
junctional or ventricular tachycardias; usually insignificant in those
cases (adenosine used to terminate these abnormal rhythms)
 Asystole of longer duration in the presence of acute MI and CAD is
frequently fatal.
4. Interventions:



ACLS/ CPR,
artificial pacing, and
atropine
III. Atrioventricular (AV) Conduction Blocks: Delayed or block transmission of
sinus impulse through AV node due to tissue injury or disease, increased vagal
tone, drug effects
A. First degree AV block***
1. Slowed transmission through AV node; PR interval is > 0.20 sec
(prolonged, a block); SA node is pacemaker but is blocked, QRS
normal, P wave normal; rate: 60-100 BPM; rate regular
RNSG 2432  57
2. Cause: ischemia of AV node, dig toxicity, MI, any of blocker meds
3. Manifestation: No symptoms
4. Treatment:
 If on digitalis or beta blockers, hold meds
 Evaluate for further blockage; usually no treatment
B. Second-degree AV block (See text p. 847)***
(Mobitz type I, Wenckeback phenomenon)
1. Failure to conduct one or more impulses from atria to ventricles;
usually transient (repeated pattern of increasing AV conduction delays
until impulse fails to conduct to ventricles.
2. “Long, longer, longest, drop, then you have a Wenkeback!”; PR
progressively longer until drops QRS; PR interval variable
3. Cause: acute MI or drug intoxication, ischemia, same as 1st degree;
rarely progresses
4. Manifestation: pulse feel irregular, then skip a beat…usually no
symptoms
5. Treatment: Monitor for progression
3. (Type 2 AV block (Mobitz type II) (See text p. 847)
1. Characterized by intermittent failure of AV node to conduct impulse;
frequently associated with acute anterior MI and high mortality rate
2. More P’s but skips QRS in regular pattern 2:1; 3:1, 4:1
58  RNSG 2432
3. Constant PR interval
4. Manifestations: More symptomatic than type I due to slowed rate
5. Treatment
 Pacemaker
 Atropine, Isuprel (know why)
4. Third-degree AV block (complete heart block)*** (See text p. 847)
1. Atrial impulses blocked at AV node; fail to reach ventricles;
atria and ventricles beat independently; rhythm from junctional
fibers (rate 40 –60 BPM) or ventricular (<30 BPM); No PR
interval; wide QRS; *Separate rates atria and ventricles
2. Causes: Inferior or anteroseptal MI, congenital, active, or degenerative
cardiac disease, drug effects, electrolyte imbalances, CHF
3. Manifestations: fatigue, SOB, fainting; if untreated -go into VT and
V fib; decreased cardiac output!
4. Treatment:
 Pacemaker
 atropine, Isuprel (Know “why these drugs are effective)
IV.
Ventricular Conduction Blocks
(Bundle Branch Block) (not in textno test questions…understand principle!)
a. Sinus node fires; goes to AV node and down to bundle branch where it
is blocked, jumps across then comes back to other side; unusual shape
to QRS (conduction through right or left bundle branches of ventricle
impaired)
b. Prolonged QRS complex; can have left BBB, right BBB; QRS is .12 or
greater with rabbit ears appearance; widened QRS
RNSG 2432  59
c. Causes: previous injury
d. Treatment: none monitor
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Collaborative Care for Dysrhythmias
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!
ECG rhythm analysis process
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
I.
Diagnostic Tests
A. 12 lead Electrocardiogram
1. Identification of rhythm
2. Information about underlying disease processes
(Access slide online to see effect of ECG changes with MI)
EKG changes in an acute MI
60  RNSG 2432
3. Monitor effects of treatment
B. Cardiac monitoring
1. Continuous cardiac monitoring
2. Hospital use 5 lead (lead II and V1 for best viewing of heart
function)
3. Ambulatory or Holter monitoring
1. Identification of intermittent dysrhythmias
2. Monitor effects of treatments
3. Client records symptoms and events in a journal
4. Exercise stress testing
C. Electrophysiology Studies (understand principles)
*Use electrode catheters guided by fluroscopy into heart via femoral or
brachial vein: electrical stimulation induces dysrhythmias similar to
patient clinical diagnosis.
1.
2.
3.
4.
Diagnostic procedures used to identify dysrhythmias and cause of
Evaluation of treatment effectiveness
Invasive procedure-electrode catheters introduced into heart
Timing and sequence of electrical activity noted during normal and
abnormal rhythms
5. May involve treatment of dysrhythmia by overdrive pacing or
performing ablative therapy to destroy ectopic site
6. Nursing care is similar to that for coronary angiogram
7. Possible complications
1. Ventricular fibrillation
2. Cardiac perforation
3. Venous thrombosis
II.
Medications (understand how meds work & why; refer to med sheet)
1. Goal: suppression of dysrhythmia and rhythm stabilization and effective
cardiac output (See text P. 854 Medication Administration;
antidysrhythmic drugs & 818-819)
2. Can produce dysrhythmic effects: may worsen existing dysrhythmias or
precipitate new ones
3. Classifications- (see handout) by effects of cardiac action potential
a. Class I: fast sodium channel blockers; subclasses are A, B, C;
prolongs action potential to decrease automaticity and slow rate of
impulse conduction ; treat supraventricular and ventricular
tachycardia (Quinidine, Procainamide, Norpace, Xylocaine,
Tocainide, Phenytoin, Rythmol)
RNSG 2432  61
b. Class II: beta-blockers; also reduce heart rate; treat
supraventricular tachycardia and slow ventricular response to atrial
fibrillation (Esmolol, Propranolol)
1. Decrease SA node automaticity
2. AV conduction velocity
3. Myocardial contractility
c. Class III: block potassium channels; primarily for treatment of
ventricular tachycardias and ventricular fibrillation; amiodarone
also for supraventricular tachycardia) (Solatol, Amiodarone)
1. Delay repolarization
2. Prolong relative refractory period
d. Class IV: calcium channel blockers (decrease automaticity and AV
conduction; treatment of supraventricular tachycardia (verapamil,
diltiazem)
e. Not classified
1. Adenosine, Digoxin: reduce SA node automaticity, slow AV
conduction
2. Drugs affecting autonomic nervous system
a. Epinephrine (increase heart rate)
b. Atropine (increase heart rate) by blocking vagal
response
c. Magnesium for ventricular tachycardia
Invasive Procedures
III. Countershock
1. Interrupts cardiac rhythms that compromise cardiac output and client’s
well being
2. Delivery of direct current depolarizes all cells simultaneously
3. Types of countershock
a. Synchronized cardioversion
1. Direct electrical current synchronized with client’s heart
rhythm
2. Avoids shock during vulnerable period of repolarization
3. Elective procedure-treat supraventricular tachycardia, atrial
fibrillation or flutter, hemodynamically stable v. tachy
4. Clients in atrial fibrillation; need anticoagulation for
several weeks before cardioversion to decrease risk
for thromboembolism post cardioversion
62  RNSG 2432
b. Defibrillation
1. Emergency delivery of direct current without regard to
cardiac cycle (ventricular fibrillation)
2. Performed immediately when rhythm is recognized
3. Performed externally or internally (surgery, open chest);
also automatic external defibrillators
Note where the paddles are placed! Read text on this!
Invasive procedures

Defibrillation



Synchronized Cardioversion





IV.
Emergency- start at 200 watt/sec, go to
400
Safety precautions
Usually planned
Get permit
Start at 50 watt/sec
Awake, give O2 and sedation
Have to synchronize with rhythm
Pacemaker Therapy (see p. 860; Nursing Care of the Client with Permanent
Pacemaker) (read in text about follow-up nursing care.
1. Pulse generator provides electrical stimulus to heart when heart
fails to generate or conduct own at a rate for adequate cardiac
output
2. Conditions that can be treated with pacemaker
a. Third-degree AV block
b. Bradydysrhythmias
c. Tachydysrhythmias
3. Types
a. Temporary
1. External pulse generator attached to lead threaded
into right ventricle
2. Pacer wires implanted during surgery or as external
conductive pads for emergency pacing
b. Permanent
1. Pulse generator placed surgically in subcutaneous
pocket (often subclavian space); leads placed
RNSG 2432  63
a. Directly onto heart (epicardial with a
thoracotomy)
b. Transvenously into heart (endocardial)
2. Local anesthesia used with transvenous insertion
c. Single-chamber pacing (atria or ventricles are stimulated)
or dual-chamber pacing (both are stimulated)
Click online for more pacemaker information
d. Most commonly pacemakers
1. Modes: aynchronous-preset time without fail or
synchronous or demand-when heart rate goes below
set rate
2. Sense activity in and pace ventricles only
3. Sense activity in and pace both atria and ventricles
(atrioventricular sequential pacing stimulates in
sequence that imitates normal sequence of atrial
contraction followed by ventricular contraction)
e. ECG characteristics (need to recognize!)
1. Pacing detected by presence of pacing artifact which
is a sharp spike occurring before P wave in atrial
pacing or before QRS complex in ventricular pacing
2. Capture noted by contraction of chamber
following the spike (seen as P wave in atrial
pacing or QRS complex in ventricular pacing)
f.
64  RNSG 2432
Nursing Care
1. Pre-op; teach, explain procedure; place electrodes
away from potential incision site; teach ROM
exercises for affected site tol help prevent shoulder
stiffness.
2. Chest x-ray; minimize movement of affected arm
during initial post-op period to decrease risk of
dislodging pacer; assist with gentle ROM at least 3x
a day; after 24 hours; monitor pacer with ECG;
report failure to pace, improper sensing, intrinsic
rate, runaway pacer, hiccups, assess for dysrhythms,
takes 2-3 days for seating; document date of pacer
insertion, provide model etc.
3. Home Care: how it works, how placed, battery
replacement, last 6-12 years, 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…
4. Maintaining safety; Preventing infection and
complications
V.
Implantable Cardioverter-Defibrillator (ICD)
1. Pulse generator implanted surgically into client with lead electrodes
for rhythm detection and current delivery; senses rate and width of
QRS, some combined with pacemaker
2. ICD senses life-threatening rhythm changes and delivers automatic
electric shock to convert dysrhythmia
3. ICD
a. Provides pacing on demand
b. Stores ECG records of rhythms
c. May be reprogrammed at bedside when necessary
d. Needs to be surgically replaced every 5 years


 Implanted Cardiac Defibrillator (ICD)
 Senses rate and width of QRS
 Goes off 3 times, then have to be reset
 Some combined with pacemaker
4. Use of ICD indicated for clients with
a. Sudden death survivors
b. Recurrent ventricular tachycardia
RNSG 2432  65
c. Significant risk factors for sudden death
VI.
Cardiac Mapping and Catheter Ablation Click here for more information on
ablation.
1. Involves location and destruction (burn ectopic pathway) of ectopic
foci in heart2. Diagnosed in electrophysiology lab and performed in cardiac
catheterization laboratory
3. Cardiac mapping: identification of sites where impulse initiated in
atria or ventricles with use of internal or external catheters
4. Ablation: destruction of ectopic focus using radiofrequency energy
with catheters; anticoagulant therapy may be started afterward to
decrease risk of clot forming at ablation site
Other measures to stop dysrhythmias
*For SVT
1. Vagal maneuvers in which client “bears down”: a forced
exhalation against a closed glottis to slow heart rate
2. Carotid sinus massage with continuous monitoring done by
physician only
3. Medications such as adenosine, calcium channel blockers
____________________________________________________________
Nursing Care
1. Decrease risk for CHD, which is major risk for dysrhythmias
2. Reduce sympathetic nervous system stimulants like caffeine
Nursing Diagnoses (refer to text)
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
66  RNSG 2432