Medical-Surgical Nursing | NCM 0112
MODULE 16
Nursing Care Management of Adult
Clients with Inflammatory Conditions of
the Heart and Dysrhythmias
Heart Inflammation
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Also known as Endocarditis, Myocarditis, Pericarditis
Inflammation is the body’s response to infection or injury. It can affect
many areas of the body and is a cause of many major diseases.
Horizontal lines = time/duration
1 sec = 5 large boxes
Inflammation in the heart causes damage and can lead to serious
health problems.
There are three main types of heart inflammation: endocarditis,
myocarditis, and pericarditis.
o Endocarditis is inflammation of the inner lining of the heart’s
chambers and valves.
o Myocarditis is inflammation of the heart muscle.
o Pericarditis is inflammation of the tissue that forms a sac
around the heart.
Many things cause heart inflammation. Common causes include viral
or bacterial infections and medical conditions that damage the
heart and cause inflammation.
The patient may have different signs and symptoms depending on the
type and severity of the heart inflammation that he has. The treatment
may depend on the type. The patient may be treated with medicine,
procedures, or possibly surgery to treat the condition and its
complications. Complications may include a dysrhythmia and heart
failure.
Nurses often struggle with identifying ECG rhythms, but rapidly
interpreting these rhythms is an essential skill that every nurse should
master.
Nurses who are trained to read ECGs can improve patient care
through the early identification of actual or potential complications
and the prompt referral of patients.
Vertical lines = amplitude/voltage ® could determine the
presence and degree of atrial and ventricular hypertrophy
(increase in cell size)
COMPONENTS OF AN ECG WAVEFORM
1 mm = 0.1mV
G.M.M.E. – MARILAG
Breakdown of an ECG
Medical-Surgical Nursing | NCM 0112
PR Interval (PRI)
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Time at which impulse travels from the SA node to the atria
and downward to the ventricles
= conduction delay in the AV node
Normally 0.12-0.20 seconds
Measured from beginning of P wave to the end of the R
segment
Measured from beginning of P wave and beginning of QRS
(P WAVE + PR SEGMENT)
hyPeRkalemia = prolonged PR interval
QRS Complex
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There is no distinctly visible wave that shows atrial
repolarization in the ECG, yet it occurs during ventricular
depolarization (QRS complex). Because the wave of atrial
repolarization is relatively small in amplitude (i.e., has low
voltage), it is masked by the much larger ventricular-generated
QRS complex.
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Ventricular depolarization
0.04 to 0.11 seconds
R wave = 25mm in V5, V6 = ventricles
Generally tall R waves are a sign of left ventricular hypertrophy
(R wave greater than 25mm in V5, V6 = precordial leads) note however that, in order to be confident about the diagnosis
of left ventricular hypertrophy, there should also be inversion
of the T wave in these leads
Tall wave is common in young, thin people and athletes
P Wave
Atrial depolarization
Approximately 0.11 seconds in length
<2.5 mm in height
ST Segment
• Time period between depolarization and repolarization of
ventricles
• Measured from end of QRS complex to beginning of T wave
• Normally isoelectric (baseline) = negative and positive
forces are equally balanced
Notched (w/ division) = 1 atrium is larger than the other
IF INCREASED: enlarged atria or forceful contraction of the atria
G.M.M.E. – MARILAG
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Medical-Surgical Nursing | NCM 0112
•
Elevation or depression of the ST segment indicates an
abnormality in the onset of recovery of the ventricular muscle
usually because of an injury
INTERPRETATION OF THE ECG
ST segment elevation (chair-like image) = MI
Long lead II is usually checked (from
RA to LL), the same with the heart
conduction
T Wave
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Ventricular repolarization
Normally upright and 1/3 of height of the QRS complex
Any condition that interferes with atrial repo may cause the T
wave to invert
HKTG = Potassium imbalances
­Potassium = ­T wave
Usually rounded
Flat or inverted: hypokalemia or myocardial ischemia
Tall peaked: hyperkalemia
Hyper-acute: MI
Artifacts
• Abnormal waves and spikes in an ECG that result from sources
other than the electrical activity of the heart
• Interfere and distort components
• Make evaluation difficult or impossible
*Check patient’s status ® check the machine (pads/wires
may not be properly connected/attached)
QT Interval
• Measured from beginning of QRS to end of T wave
• QT interval varies with heart rate, gender, and age
• Normally less than 0.40 seconds
U Wave
• Sometimes follows a T wave
• Appears to represent repolarization of the Purkinje fibers
• Usually in the same direction as T wave
Presence of U wave = hypUkalemia (hypokalemia)
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ALTERNATING CURRENT INTERFERENCE: Extrinsic electric
sources due to io improper grounding of the electrical
equipment
CHAOTIC TRACING: Poor contact with skin, dried electrode
paste or jelly = using water-based jelly
WANDERING BASELINE: due to anxiety, pain, restlessness,
heavy breathing = check patient’s status
G.M.M.E. – MARILAG
Prolonged QT interval = hypocalcemia
Chvostek’s sign & Trousseau’s sign
Medical-Surgical Nursing | NCM 0112
4. Measure PR Interval = N: 0.12-0.20 secs
5. Measure QRS Duration = N: 0.04-0.11 secs; 25mm in
height
6. Measure QT Interval = N: <0.40 secs
7. Examine ST Segment deviation = N: isoelectric (elevation
or depression means abnormality in the onset of recovery
of the ventricular muscle)
8. Examine T Wave = N: upright, 1/3 of the QRS complex,
rounded
2. Determine the heart rate
a. 6-Second Strip Method
i. Have a six second strip (30 large boxes), count
the QRS complexes (ventricular rhythm)
and multiple by 10.
ii. Have a six second strip (30 large boxes), count
the P waves (atrial rhythm) and multiple by
10.
NORMAL: atrial rate = ventricular rate
iii. For accuracy, timing should begin on the P
wave or QRS complex
b. (shortcut method) Count the number of small boxes
within an R-R interval and divide 1500 by that number or
count the number of large boxes between within an R-R
interval and divide 300 by the number. = for regular
rhythms only
c. The Box Method
i. Find a QRS complex that lands on a heavy line.
ii. Place the following values on succeeding
heavy lines.
(300-150-100-75-60-50-43-37-35-30)
iii. If the next QRS complex falls on a heavy line,
assign the appropriate rate for it.
3. Examine the P wave
a. P wave should precede every QRS
b. All P waves should appear the same
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Heart rate = YES
Rhythm/regularity = YES
Impulse conduction time intervals = YES
Abnormal conduction pathways = YES
Pumping action = NO
Cardiac output = NO
Blood pressure = NO
Cardiac muscle hypertrophy = YES
Which of the following is true regarding normal sinus rhythm?
a. It has an inherent heartbeat of 40-60 beats per minutes (60-100)
b. it is a result of electrical impulse initiated by the AV node (SA)
c. it is best characterized by the presence of ectopic beats (none)
d. P-R interval is 0.12-0.20 seconds
Normal Sinus Rhythm (NSR)
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Ventricular and atrial rate: 60-100 bpm (SA node firing
rate) = initiated by SA node (primary pacemaker)
Heart rhythm: regular
QRS shape and duration: usually normal but may be
regularly abnormal
P wave: normal and consistent shape (has normal
intervals with no aberrant or ectopic beats
P:QRS ratio: 1:1
G.M.M.E. – MARILAG
1. Determine the heart rhythm
5 large boxes = 1 sec strip (6 secs = 30 large boxes)
a. Regular or irregular?
b. Measure ventricular rhythm by measuring the interval
between R-to-R waves
c. Measure atrial rhythm by measuring the P-to-P waves.
d. If measurement is the same or varies less than 0.12
seconds, it is regular.
e. For accuracy, timing should begin on the P wave or the
QRS complex and exactly at 30 large blocks later
= 6 second rhythm strip
INFORMATION OBTAINABLE FROM
ECG RHYTHM STRIP ANALYSIS
Medical-Surgical Nursing | NCM 0112
Dysrhythmias
also known as arrhythmias
Problem: abnormal heart rhythm
Priority nursing diagnosis: decreased cardiac output
® decreasing cerebral and vascular perfusion
SUMMARY OF ANTIDYSRHYTHMIC MEDICATIONS
Class
Na Channel
Blockers
IA
Action
Moderate depression of depolarization, prolongs
repolarization
Drugs
Treats and prevents atrial and ventricular
dysrhythmias
Quinidine
Procainamide
IB
Depolarization – electrical stimulation
Repolarization – electrical relaxation
Minimal depression of depolarization,
repolarization
IC
Treats ventricular dysrhythmias
Marked depression of depolarization, little effect on
repolarization
shortens
Treats atrial and ventricular dysrhythmias
Indirectly blocks calcium channel
II
Beta
blockers
III
K Channel
Blockers
IV
Ca Channel
Blockers
Blocks the ability of the catecholamines to cause
dysrhythmias
Treats atrial and ventricular dysrhythmias
(-) Inotropic – strength of cardiac contractility
(-) Dromotropic – conduction of cardiac impulses
(-) Chronotropic – heart rate (slows)
Prolongs repolarization
Treats and prevents atrial and ventricular
dysrhythmias especially in patients with
ventricular dysfunction
Slows SA node cells and AV node cell conduction by direct
blockage of L-type voltage gated calcium channel
Treats atrial dysrhythmias
Flecainide
Propafenone
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Acebutolol
Esmolol
Metoprolol
Propranolol
Atrial
Dysrhythmia
DISTURBANCES
IN CONDUCTION
Blockage on the
conduction
pathway
RE-ENTRY OF IMPULSE
Occurs when cardiac
tissue is depolarized
multiple times by the
same impulse
Normal electric
signal: SA ® AV
® His Purkinje
system ®
dies out
Propagating impulse
fails to die and
persists to re-excite
the heart after the
refractory period has
ended (usually
ventricular
dysrhythmias)
1. Sinus arrest
2. Sinus exit
All characteristics are the same as those of NSR, except the rate
>100/min
Usually ASYMPTOMATIC
Occurs when abnormal electrical signals interfere with
signals coming from SA node ® can prevent heart
from filling properly and reduces overall blood flow
out of the heart
Verapamil
Diltiazem
Felodipine
Nicardipine
CATEGORIES
aka. RHYTHMICITY
– ability of the
cardiac pacemaker
cells to initiate an
electric impulse
spontaneously &
repetitively
1. Sinus Tachycardia
2. Sinus Bradycardia
3. Sinus Dysrhythmia
4. Premature Atrial
Contractions
5. Atrial Flutter
6. Atrial Fibrillation
1. Premature Ventricular
Contractions
2. Ventricular Tachycardia
3. Torsade’s de Pointes
4. Ventricular Fibrillation
Amiodarone
Ibutilide
hyperkalemia = Class III (K Channel Blockers)
hypercalcemia = Class IV (Ca Channel Blockers)
Dysrhythmia
1. Supraventricular
Tachycardia
DISTURBANCES IN AUTOMATICITY
Sinus Tachycardia
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But, if it is already isolated case, such as knowledge regarding the
electrolyte imbalance, give specifics
Alteration in the
normal heart rate
produced by various
pacemaker
Ventricular
Dysrhythmia
Lidocaine
For an UNKNOWN ETIOLOGY of a dysrhythmia, the safest initial
management that’ll be given is a CLASS II (BETA-BLOCKERS)
DISTURBANCES IN
AUTOMATICITY
Atrioventricular
Junctional
Dysrhythmia
1. First Degree AV
Block
2. Second Degree
AV Block
3. Third Degree AV
Block
4. Bundle Branch
Block
1. Ventricular
Asystole
Paroxysmal Atrial
Tachycardia
Etiology:
o Increased SNS = increased heart rate / Decreased PNS
stimulation = decreased VAGAL stimulation
o Increased BMR = tachycardia, Stimulants = release of
epi/norepinephrine ® increasing HR, Compensatory
increased SNS = d/t hypovolemia, Hypercalcemia = Ca
is essential in automaticity and plays a vital role in
cardiac contraction ® increased cardiac contractility
Management:
o Bed Rest = to reduce metabolic demands
o Oxygen Therapy = to supply the myocardium with
oxygen adequately
o Determine the cause
(hypercalcemia = treat with Ca channel blocker meds)
o Vagal Maneuvers
Carotid sinus massage – firm pressure applies over
carotid sinus ® stimulate vagal response
Valsalva maneuver
— usually performed by a practitioner or
nurse specialist
G.M.M.E. – MARILAG
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1. Premature
Junctional
Contractions
2. Paroxysmal
Junctional
Tachycardia
Medical-Surgical Nursing | NCM 0112
o
o
Sinus Bradycardia
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All characteristics are the same as those of NSR, except the rate
<60/min
This may be normal for some individuals
= ATHLETES (have greater than normal stroke volume)
CO = SV x HR = Athletes: CO = ­SV x ¯HR (compensates)
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Premature Atrial Contraction (PAC)
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Etiology:
o Increased PNS / Decreased SNS stimulation.
o Valsalva, Drugs (Digitalis, Class II, Class IV Antidysrhythmic
agents), Inferior MI = problem with conduction,
presence of abnormality in the lower chambers of
heart, Decreased BMR, Hyperkalemia = HyperK reduces
myocardial excitability, with depression of both
pacemaking and conducting tissues
Drugs:
BB/Class II – negative dromo & chrono effect
CCB/Class IV – slow HR
Digitalis – lengthens PR interval
Management:
o Determine the cause
o Oxygen = to supply myocardium with adequate O2
o Atropine = prevents vagal effects on SA and AV nodes
® enhancing conduction on AV node and increasing
HR (WOF tachycardia)
o Dopamine
Dobutamine
Isoproterenol
ADRENERGIC AGONISTS/SYMPATHOMIMETIC DRUGS –
mimic the effects of transmitter substances of the SNS
® increasing HR
PACEMAKER – Provides electrical stimulation and maintains
the heart rate when the client’s intrinsic pacemaker fails to
provide a perfusion rhythm
o Transcutaneous pacing – temporary noninvasive; delivered through the skin
o Permanent pacemaker: pulse generator is
internal and surgically implanted in a subcutaneous
pocket under the clavicle or abdominal wall
*when the intrinsic pacemaker fails to
produce a perfusion rhythm ® will initiate
the electrical signal
ECG reveals a premature P wave (abnormal) that differs in
morphology from the sinus P wave P wave = atrial
depolarization; sinus P wave = initiated by SA node
(normal)
Early beats arising from ectopic atrial foci interrupting the
normal rhythm = does not originate from the pacemaker
(SA node)
irritable cell in the atria causes EXTRA HEARTBEAT
Etiology:
o VHD, CAD, HF = abnormalities in the heart
o Stress, Fatigue, Smoking = releases the stress hormones:
epi/norepinephrine, catecholamines
Management:
o No treatment if the client remains ASYMPTOMATIC
o May lead to ATRIAL FIBRILLATION ® WOF for signs
o Avoid stimulants that could further cause of
epi/norepinephrine
o Digitalis/Class II/ Class IV = PACs are often seen with
SINUS TACHYCARDIA
Atrial flutter
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Arises from a single irritable focus in the atria
Atrial rhythm: regular
Ventricular rhythm: usually regular but may be irregular
because of a change in the AV conduction
ATRIAL RHYTHM: P-P interval
VENTRICULAR RHYTHM: R-R interval
Atrial rate (250-400) > ventricular rate (75-150)
G.M.M.E. – MARILAG
o
ü Record an ECG strip before, during and after
the procedure to observe the change in
rhythm (procedure can slow the HR)
ü Have a defibrillator and resuscitative
equipment available (emergency)
Cardiac glycosides (Digoxin, Digitoxin)
(+) Inotropic – strength of cardiac contractility
(-) Dromotropic – conduction of cardiac impulses
(-) Chronotropic – heart rate
Antidysrhythmic agents (rarely used; to decrease HR
quickly)
o Class II (to slow HR)
o Class IV (hypercalcemia)
Eliminate stimulants = etiology (epinephrine,
norepinephrine)
Medical-Surgical Nursing | NCM 0112
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The AV node cannot conduct all the atrial impulses that
bombard it, therefore ventricular rate is always slower than the
atrial rate
P wave: saw-toothed pattern (referred to as F waves;
bigger)
P:QRS ratio: 2:1; 3:1; 4:1
Can also be reentry of impulses; impulses travel in circular
course in atria
N: SA node ® AV node ® His purkinje system
What happens: SA node ® AV node ® His purkinje
system ® SA node (or d/t irritable focus firing
electrical impulse)
Etiology:
o CAD, MVD, Pericarditis
Management:
o Cardioversion – direct current cardioversion 25-100 J
o Classes IA, II, III, IV
o Ibutilide (IV) or Amiodarone (III) short-acting
antidysrhythmic, 60-90% converts A. flutter to NSR
Atrial Fibrillation
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Atrial and ventricular rhythm: irregular
Atrial rate (300-600) > ventricular rate (120-200) in
untreated Afib
Erratic or no identifiable P wave: small, irregular baseline
undulations that vary in shape and size called smaller f waves
No effective pumping of blood into the ventricles, only
quivers ® blood pooling in the atria ® can lead to
stroke or other heart-related complications
P:QRS ratio: Many:1
Etiology:
o CAD, MVD, Pericarditis
– Mechanical and electrical disorganization of the atria without
effective atrial contraction
– Impulses have chaotic, random pathways in atria (Ectopic foci
in atria) ® quivers (d/t ineffective pumping)
Complications:
o Angina d/t ineffective pumping of the atria ® impaired
cardiac output = decreased oxygenation of the cardiac
muscle tissues (chest pain)
o Heart Failure d/t ineffective pumping of the atria
o Shock = ¯ circulating blood volume
o Embolism = blood pooling/stasis in the atria ®
clot/thrombus ® embolus ® pulmonary embolism ® cerebral blood vessel (CVA)
Management:
o Initial tx goal is to reduce thromboembolism; and convert
rhythm to sinus rhythm
o Oxygen = to provide adequate O2 to myocardium
o Classes I, II, IV (Class II – most effective tx in promoting
adequate rate control)
o Digoxin = positive inotropic, negative dromo & chrono
effect
o Anticoagulants
o Low molecular weight heparin
o Warfarin
o Aspirin – antiplatelet
o Cardioversion
DISTURBANCES IN CONDUCTIVITY
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Usual causes of conduction problems: Ischemia, injury or
infarct
Myocardial cells cannot conduct impulse properly
Heart block occurs when the conduction signal passes weakly
from the atria to the ventricles, or completely fails to transmit
First degree AV block
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ECG reveals a regular rhythm, P wave followed by a QRS
complex but with prolonged P-R interval
(N: 0.12-20 secs)
Atria impulses are conducted through the AV node into the
ventricles at a rate slower than normal
G.M.M.E. – MARILAG
•
Medical-Surgical Nursing | NCM 0112
Etiology:
o Right atrial enlargement or atrial septal defect
PR = atrial depolarization and conduction delay at AV
node
If there is problem in RA ® problem in conduction of
impulses since SA node is located in RA
Atrial septum = AV node location
o Idiopathic Degenerative Diseases of the Conduction system
(progressive deterioration)
o Digitalis = lengthens PR interval
Management:
o Observe patient condition and monitor ECG changes for
progression to other types of disturbances in
conductivity
o Discontinue digitalis therapy
Second degree AV block
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Some initial impulses fall to conduct to the ventricles
Some impulses are conducted and others are blocked
Resulting in intermittently dropped QRS complex
*Expect that there will be missing QRS complexes in a
rhythm strip
A. Mobitz Type I
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Wenckebach phenomenon
PR Interval becomes longer with each succeeding QRS
complex until there is a P wave not followed by a QRS (with
warning) = there’s dropping of QRS complexes
Abnormally long refractory period at the AV node
Etiology:
o Ischemia, Digitalis toxicity, Anterior wall MI
Management:
o Close ECG monitoring
o Withhold cardiac depressants (Beta-blockers, Ca
channel blockers, digitalis)
o Atropine – blocks vagal effects on SA and AV nodes ®
enhancing conduction on the AV node and increasing
HR (WOF bradycardia)
o Isoproterenol – cardiac stimulant = speeds the rate of
impulse conduction
o Pacemaker – can be temporary or permanent = fires
electrical signals when the intrinsic pacemaker fails
to transmit one
Third degree AV block (AV dissociation)
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Complete Heart Block – the atria and the ventricles work
independently of each other, most severe
The atria are regularly paced by the SA node
The ventricles are regularly paced by a ventricular ectopic
pacemaker
ECG shows a regular P-P interval, regular R-R interval, normal
appearing P wave, absence of a consistent P-R interval
*works independently (atria & ventricles)
P-P interval normal and constant
QRS complexes normal, rate constant but below normal, 2055/min
Etiology:
o Similar to first-degree AV block except that this is caused by a
block in the AV node = located in the atrial septum (RA)
Management:
o Not required as long as the ventricular rate is adequate for
perfusion
o Assessed for progression to a higher degree of block
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ECG shows normal P waves that are followed by normal QRS
complex at regular intervals until a QRS complex is dropped
(no warning) = sudden drop of QRS complexes
G.M.M.E. – MARILAG
B. Mobitz Type II
Medical-Surgical Nursing | NCM 0112
Etiology:
o Anterior wall MI, Cardiac surgery, Myocarditis, Drug toxicity
(Beta-blockers, Ca-channel blockers, Digitalis),
Cardiomyopathy
Complications:
o Heart Failure – ineffective pumping of the chambers of
the heart (AV dissociation)
o Asystole – may happen if an ectopic focus in the
ventricles does not initiate a heartbeat/impulse
BECAUSE IN 3RD DEG AV BLOCK:
atria = paced by the SA node
ventricles = paced by the ECTOPIC FOCUS
® No pumping ® No CO
Premature Ventricular Contraction (PVC)
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ECG reveals a premature QRS complex with a bizarre
morphology with T wave polarity opposite to the
normal QRS complex *most concern: fall on a T wave
*initiated by an irritable focus in the ventricle
An impulse that starts in a ventricle (should start from the
SA node at RA) and is conducted through the ventricles
before the next normal sinus impulse
Time interval between normal R peaks is a multiple of R-R
interval
Management:
o Atropine – blocks vagal effects on SA and AV nodes ®
enhancing conduction on the AV node and increasing
HR (WOF bradycardia)
o Dopamine – improve perfusion to other organs
= ­ cardiac output
o Epinephrine – restores cardiac rhythm when there is
asystole
o Pacemaker = if natural pacemaker fails to initiate an
impulse, an artificial pacemaker can be placed
(temporary or permanent) to initiate an impulse
o If Asystole: CPR ® Pacemaker when revived
Types:
1.
2.
3.
4.
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NORMALLY: Impulse is initiated by the SA node (natural
pacemaker) ® AV node ® His Purkinje system ®
propagating impulse will die
RE-ENTRY OF IMPULSES: propagating impulse fails to die
and persists to re-excite the heart after refractory period has
ended
Etiology and Risk Factors:
o Enhanced automaticity or reentry phenomenon
o CAD, Heart Failure, Hypocalcemia, Hypokalemia, Caffeine,
Nicotine, TCA, Hypermetabolic states
*increased irritability of the ventricles
Management:
o No Treatment if isolated / asymptomatic
o Determine the cause
o Evaluate electrolytes – particularly K levels (K has a role
in normal depolarization & repolarization)
o Oxygen Therapy – adequate O2 to myocardium
o Class I, Class II and Class III Antidysrhythmic Agents
G.M.M.E. – MARILAG
RE-ENTRY OF IMPULSES
Bigeminy – PVC every other beat
Trigeminy – PVC every third beat
Quadrigeminy – PVC every fourth beat
R on T phenomenon – if there would be an extra beat in
ventricular relaxation ® a vulnerable period that may
precipitate V fib = fatal dysrhythmia
R = PVC
T = ventricular relaxation
Medical-Surgical Nursing | NCM 0112
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ECG shows absent P waves, absent P-R interval wide and
bizarre QRS complex ventricular rate between 100 to 200
Characterized by 3 or more PVCs
Life-threatening dysrhythmia
Ventricular Fibrillation
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Etiology:
o Significant Cardiac Diseases
o CAD, AMI with hypoxia and acidosis,
Cardiomyopathy, MVP, HF
o REPETITIVE firing of an irritable ectopic focus
Complications:
o Cerebral and Myocardial ischemia – problem in the
pumping of ventricles
o Ventricular Fibrillation
Management:
STABLE CLIENT WITH VTachs
o Oxygen therapy – adequate O2 to myocardium
o Antidysrhythmic (Class I and Class III)
Na channel blockers & K channel blockers
o Magnesium Sulfate *Intracoronary administration of
MgS04 ® suppress sinoatrial automaticity and
ventricular contraction
UNSTABLE CLIENT WITH VTachs
o Same
o Cardioversion = synchronized cardioversion
o Cough CPR – instruct and coach the patient to cough
forcefully every one to three seconds during the initial seconds
of a sudden arrhythmia
*Vigorous rhythmic coughing could produce arterial
pulses and can convert V. tach to sinus rhythm
PULSELESS VTachs
o Defibrillation
o CPR
ECG shows fibrillatory wave patterns with no identifiable P
waves, QRS complex T waves
Characterized by extremely rapid, erratic impulse
formation and conduction always that causes ineffective
quivering of the ventricles
Characterized by an absence of audible heartbeat, a
palpable pulse and respirations
Ineffective pumping of ventricles ® Primary cause of
SCD (sudden cardiac death)
Etiology:
o Severe myocardial
(vulnerable period)
o Untreated VTach
damage,
R-on-T
Phenomenon
Management:
o Vfib is rapidly fatal if not successfully terminated within 3-5
minutes
o CPR = no palpable pulse
o Defibrillation up to 3x as needed
o Epinephrine, vasopressin or both – administered after the
2nd rhythm check
o Antidysrhythmic medications
Class I (lidocaine)
Class III (amiodarone)
– administered after the 3rd rhythm check
o Magnesium sulfate *Intracoronary administration of
MgS04 ® suppress sinoatrial automaticity and
ventricular contraction
G.M.M.E. – MARILAG
Ventricular Tachycardia
Medical-Surgical Nursing | NCM 0112
Ventricular Asystole
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State of cardiac standstill
V.Fib ® SCD
Problem with the conduction of impulses ® asystole
NR during defibrillation and cardioversion:
o Stop the oxygen – to avoid hazard of fire
o Be sure that no one is touching the bed or the client when
delivering the shock
“1 I’m clear, 2 You’re clear, 3 All clear”
Position of Paddles:
o 1st paddle on 3rd ICS, right of sternum
o 2nd paddle on 5th ICS, left MAL
(sternum)
Etiology and Risk Factors:
Primary
o Sinus node block-arrest
o Complete Heart Block
NURSING MANAGEMENT: (GENERAL)
Signs and Symptoms:
No ventricular depolarization ® no cardiac output:
o Fainting
o Loss of consciousness – d/t ¯ cerebral perfusion
o Seizure episode – hypoxia ® seizure (hyperexcitable
neural network)
o Apnea – cessation of breathing
o Death – eventually occurs in all dying patients
Medical Management:
o CPR = no respiration
o Epinephrine
o Vasopressin = after 2nd rhythm check
o Transcutaneous pacing = for electrical impulse to be
initiated by pacer
DEFIBRILLATION
CARDIOVERSION
Unsynchronized mode
No markers
Emergency
Patient in cardiac arrest
Patient has no pulse (pulseless VT or
VFib)
No need to premedicate (sedative)
The electrical voltage required is
usually greater than what is required
in cardioversion ® may cause
more myocardial damage
Synchronized mode – timed
Markers with R wave
Patient not arrested
Patient has pulse (atrial flutter, atrial
fib, SVT)
Premedicate as needed
Elective – Anticoagulation for a few
weeks before cardioversion =
thromboembolism
Check for digitalis toxicity because it
may predispose client to ventricular
dysrhythmias during cardioversion
Significance of all dysrhythmias: their effect on cardiac output
® cerebral & vascular perfusion
Decreased Cardiac Output
Change in the LOC, Chest Discomfort, Hypotension, Shortness of breath,
Respiratory Distress, Pulmonary Congestion, Crackles, Rapid, slow or
weak pulse, Dizziness, Syncope, Fatigue, Restlessness
o Assess VS
o Monitor I&O
o Restrict fluid as ordered
o Elevate the head of the bed
o Provide physical, emotional and mental rest
o Administer prescribed medications to reduce cardiac
workload
Activity Intolerance r/t ineffective cardiac contraction/ imbalance
between O2 supply and demand
o Monitor VS before, during and after exercise
o Encourage adequate rest
o Encourage self-care
o Increase activity levels gradually
o Assist with ADL as needed
o Formulate a schedule with alternating rest and activities
Anxiety related to fear of the unknown
Deficient knowledge about dysrhythmia and its treatment
AV BLOCK FAMILY STORY
P wave = wife; QRS complex = husband; Pacer = counselor
§ The wife (P wave) waits at home for the husband (QRS). The
husband (QRS) comes home on time every night. = NSR
§ The wife (P wave) is waiting at home. The husband (QRS) comes
home late every night, but he always comes home and it’s at
the same time every night. = FIRST-DEGREE AV BLOCK
§ The wife (P wave) is waiting at home. The husband (QRS) comes
home later and later every night until one night he doesn’t
come at all. = MOBITZ 1
§ The wife (P wave) is no longer waiting at home. She and her
husband (QRS) are now both on separate schedules and have
no relationship and they are no longer talking. Each spouse
has a regular, individual schedule.e = THIRD-DEGREE AV
BLOCK
G.M.M.E. – MARILAG
Secondary
o Severe Hypoxia
o Pre-existing acidosis
*outside of the heart’s electrical system that result in failure to
generate depolarization