NURSING

1. Thara Noel
Welcare college of Nursing
Mulanthuruthy

2. CONDUCTION SYSTEM OF
THE HEART
2

3. CONDUCTION SYSTEM OF HEART
– SA Node lies subepicardially on
the right atrium
– SA node is the “Pace maker”
– SA Node fibers fires at a rate 60-
100 beats
– SA node is innervated by A.N.S.
• Sympathetic ANS increases H.Rate
• Parasympathetic ANS reduces HR.
3

4. 4

5. CARDIAC MYOCYTE ACTION
POTENTIAL

7. • AUTOMATICITY (ability to initiate an
impulse spontaneously &
continuously)
• CONDUCTIVITY (ability to transmit
impulses)
• RHYTHMICITY (ability to maintain the
rhythm)
• EXCITABILITY (ability to electrically
stimulated)

8. 8
– SA Node fibers 60-100 beats /m
– A.V. Node fibers 40-60 beats /m
– His-Purkinge system 30-40
beats /m
– Ventricles < 30 beats /m

9. 9

10. 10

11. 11

17. Normal sinus rhythm originates in the Sino
atrial (SA) node and is characterized by
the following
Rate: 60 to 100 beats/minute
P waves: Precede each QRS complex
(atrial depolarization)
P-R interval: Interval between atrial and
ventricular depolarization
QRS complex: Ventricular depolarization
17

18. ARYTHMIA(DYSRHYTHMIA)
DEFINITION
Arrhythmias are deviations from normal
heartbeat pattern. They include
abnormalities of impulse formation,such
as heart rate,rhythm,or site of impulse
origin and conduction disturbances,
which disrupt the normal sequence of
atrial and ventricular activation.
18

19. •Physiolgical
•Pathological
•Others

20. ETIOLOGY
• Physiological – Exercise, exertion, emotion,
temperature, etc.
• Others- Metabolic disorders, electrolyte
imbalance, emotional crisis, acid-base
imbalance, sympathetic over
activity,hemodynamic abnormalties.
dehydration, thyrotoxicosis, anemia
20

21. ETIOLOGY
Pathological:
Valvular heart disease.
Ischemic heart disease.
Hypertensive heart diseases.
Congenital heart disease.
Cardiomyopathies.
Carditis.
RV dysplasia.
Drug related.
Pericarditis.
Pulmonary diseases
Anemia,Thyroid dysfunctions.

22. Dysrhythmias result three major
mechanisms:
Disturbance in automaticity
Disturbance in conduction
Reentry of impulses.

23. Automaticity is used here to describe the
normal processes of generating a heart rhythm.
The process of automatically initiating an
impulse can be altered if the normal
pacemaker cells are firing too rapidly or if an
impulse is generated by a cell that normally
does not initiate heartbeats, called an ectopic
pacemaker.

24. • Reentry of impulses occurs when cardiac tissue is
depolarized multiple times by the same impulse.
• Normally the impulse enters into the tissue,
excites the tissue (causing depolarization), and
leaves the tissue after the refractory period is over
(repolarization).
• Reentry of impulses creates problems because
some cells can prematurely depolarize again,
producing ectopic beats and rhythm disturbances.

25. MECHANISM OF REENTRY
• It occurs along one pathway with a constant conduction
velocity. Reentry of impulses occurs when two
pathways are present (a "slow" pathway and a "fast"
pathway).
• The two pathways are separated by an area of
unexcitable tissue. As the impulse enters both
pathways, the "fast" pathway exhibits a resistance that
will not allow the impulse to travel forward but the
impulse is able to travel down the slow pathway.
• When the impulse reaches the distal end of the slow
pathway, it travels backwards into the fast pathway,
causing the impulse to repeat itself.

28. PATHOPHYSIOLOGY

29. CLINICAL MANIFESTATION
Reduced cardiac output
leads to:-
 Palpitations
 Dizziness,Syncope
 Pallor,Diaphoresis
 Altered mentation
(restlessness and agitation
to lethargy and coma
 Shortness of breath
 Chest pain
 Orthopnea
 Paroxysmal nocturnal
dyspnea
 Hypotension
 Sluggish capillary refill
 Swelling of the
extremities
 Decreased urine output

30. Diagnostic Evaluation
 Echocardiogram: This ultrasound exam uses sound
waves to take moving pictures of the heart chambers
and valves.
 Electrocardiogram (EKG): EKG helps to measure the
electrical activity of the heart and can also help to
determine, if heart's part are enlarged, overworked or
damaged.

31. Diagnostic Evaluation
Event monitor: This EKG device records the
heart rate when a button is pressed. It can be
worn for weeks or until symptoms occur
Holter monitor: It continuously records the
heart's rhythms and is worn for 24 to 48 hours
during normal activity.

32. Diagnostic Evaluation
Stress testing: Stress testing is conducted during
exercise. It is used along with an EKG, the test
can show changes to the heart's rate, rhythm or
electrical activity as well as blood pressure.
Tilt table test: This test helps to determine what's
causing fainting spells. It helps to measure the
difference in heart rate and blood pressure when
patient is standing up or lying down.

33. Diagnostic Evaluation
Invasive Electrophysiologic Studies
An electrophysiologic (EP) study involves the
positioning of a multipolar catheter electrode into
the system, placing the electrode at various sites
along the atria, ventricles, His bundle, bundle
branches, accessory pathways, and other
structures to record electrical activity. These areas
can also be stimulated through the catheter tip to
assess for function or rhythm disturbances.

35. TYPES OF DYSRHYTHMIAS
• Sino Atrial Node Dysrrythmias
• Atrial Dysrrhythmias
• Atrioventricular Junctional
Dysrhythmias
• Ventricular Dysrhythmias

36. SINO ATRIAL NODE
DYSRHYTHIAS
• Sinus Tachycardia
• Sinus Bradycardia
• Sick sinus syndrome
• Sinus exit block
• SAArrest

37. ATRIAL DYSRHYTHMAS
Premature Atrial contraction
Paroxysmal Atrial Tachycardia
Atrial Fibrillation
Atrial Flutter

38. AV JUNCTIONAL
DYSRYTHMIAS
Premature Junctional Contractions
First degree AV Block
Second Degree AV Blck
Third degree AV Block
Bundle branch Block

39. VENTRICULAR
DYSRHYTHMIAS
 Premture Venticular Contraction
 Ventricular Tachycardia
 Torsades de Pointes
 Ventricular Fibrillation
 Pre-Excitaton Syndromes
 Ventricular Asystole
 Pulseless Electrical activity
 Sudden Cardiac Death

40. Normal Sinus Rhythm
• Normal sinus rhythm occurs when the electrical impulse starts at a
regular rate and rhythm in the sinus node and travels through the
normal conduction pathway.
Normal sinus rhythm has the following characteristics:
• Ventricular and atrial rate: 60 to 100 in the adult
• Ventricular and atrial rhythm: Regular
• QRS shape and duration: Usually normal, but may be regularly
abnormal
• P wave: Normal and consistent shape; always in front of the QRS
• PR interval: Consistent interval between 0.12 and 0.20 seconds
40

41. 41

42. SINUS TACHYCARDIA
A condition in which the heart rate is 100-160/min
• Symptoms may occur with rapid heart rates including;
weakness, fatigue, dizziness, or palpitations.
• Sinus tachycardia is often temporary, occurring under
stresses from exercise, strong emotions, fever,
dehydration, thyrotoxicosis, anemia and heart failure.
42

43. SINUS TACHYCARDIA
 Rate: 101-160/min
 P wave: sinus
 QRS: normal
 Conduction: normal
 Rhythm: regular or slightly irregular
The clinical significance of this dysrhythmia depends on the underlying
cause. It may be normal.
Underlying causes include:
increased circulating catecholamines
CHF
hypoxia
Increased temperature
Stress
Response to pain
 Treatment includes identification of the underlying cause and
correction.
43

44. SINUS BRADYCARDIA
 Sinus bradycardia occurs when the sinus node
creates an impulse at a slower than normal rate.
 Causes
 Lower metabolic needs (eg, sleep, athletic
training, hypothyroidism)
 Vagal stimulation (eg, from vomiting, suctioning,
severe pain, extreme emotions)
 Medications (eg, calcium channel blockers,
amiodarone, beta-blockers)
 Idiopathic sinus node dysfunction
 Myocardial infarction (MI) 44

45. SINUS BRADYCARDIA
• Rate: 40-59 bpm
• P wave: sinus
• QRS: Normal (.06-.12)
• Conduction: P-R normal or slightly prolonged at slower rates
• Rhythm: regular or slightly irregular
• This rhythm is often seen as a normal variation in athletes,
during sleep, or in response to a vagal maneuver.
45

46. 46

47. 47
Treatment:
• Atropine, 0.5 mg (given rapidly as an intravenous (IV)
bolus every 3 to 5 minutes to a maximum total dose of
3 mg,) is the medication of choice in treating
symptomatic sinus bradycardia. It blocks vagal
stimulation, thus allowing a normal rate to occur.
• Catecholamines and emergency transcutaneous
pacing also are implemented.
• Temporary trans venous pacemaker

48. SICK SINUS SYNDROME
 Sick sinus syndrome, also known as sinus node
dysfunction, is a disorder of the sinoatrial node caused
by impaired pacemaker function and impulse
transmission producing abnormal rhythms.
 These include atrial bradyarrhythmias, atrial
tachyarrhythmias and, sometimes, bradycardia
alternating with tachycardia often referred to as tachy-
brady syndrome.
 These arrhythmias may result in palpitations and
decreased tissue perfusion and consequent fatigue,
lightheadedness, pre-syncope, and syncope.

49. Treatment
For clients with sick sinus syndrome, treatment
is two-fold including:-
• Drugs to slow the automaticity and heart rate
• Insertion of a permanent trans- venous
pacemaker to prevent symptomatic
bradycardia.

50. SINUS EXIT BLOCK
 In SA exit block, sinus node depolarization is
normal, but it fails to conduct to surrounding
atrial tissues.
SA blocks are characterized by pauses of less than
or equal to two P–P intervals.
Treatment
• Atropine
• Sympathomimetic drugs (Epinephrine,Dopamin)
• Transvenous pacing

51. SAARREST
 Sinus pause or arrest is characterized by
temporary cessation of sinus node discharges.
 Electrocardiographically, there are no P
waves and associated QRS-T during sinus pause.
 This pause is sometimes followed by junctional
rhythm or idioventricular rhythm. Absence of this
may results in asystole.
• Sinus arrest is present if SA activity ceases for
longer than two P–P intervals.

52. Treatment
• Atropine
• Sympathomimetic (Epiephrine,
Dopamin)
• Transvenous pacing

54. SINO ATRIAL
ARRYTHMIAS

55. PREMATURE ATRIAL
CONTRACTION.
• A premature atrial contraction (PAC) is an early
beats arising from atrial ectopic focus ,interrupting
normal rhythm.
• The ectopic signal originates in the left or right
atrium and travels across the atria by an abnormal
pathway creating a distorted P wave.
• At the AV node it may be stopped delayed or 55

57. Treatment.
• Normally no treatment required.
• If symptoms persists:-
57

58. PAROXYSMAL ATRIAL
TACHYCARDIA
• Paroxysmal supraventricular tachycardia
(PSVT) or Paroxysmal atrial tachycardia
(PAT) is the sudden onset and sudden
termination of a rapid firing from an ectopic
atrial pacemaker.
• The atrial rate is 150 to 200 beats/min with
change in P-wave contour from the sinus P
wave

59. PAROXYSMAL ATRIAL
TACHYCARDIA (PSVT)
• P waves are difficult to detect
• QRS usually normal

60. Treatment.
• Treatment for PSVT includes:-
• Common vagal maneuvers .
• IV adenosine is the first drug of choice
• IV β-adrenergic blockers
• Calcium channel blockers
• If hemodynamically unstable - direct current (DC)
cardioversion 60

61. ATRIAL FLUTTER
• Dysrhythmia resulting from an ectopic pacemaker or the
site of rapid reentry circuit in the atria.
• Characterised by recurring regular “saw tooth-shaped”
flutter (F) waves that followed by a slower regular
ventricular response
• Originate from a single ectopic focus in the right atrium

62. 62

63. ATRIAL FLUTTER
• Atrial Rate is 250-300 beats/mnt
• Rhythm : Regularly irregular
• P:QRS – 2:1, 4:1, 6:1 and vary with PR
interval
• May leads to thrombus formation in the atria
from the stasis of blood.

64. Treatment:
• Calcium channel blockers and β-adrenergic blockers.
• Sodium channel blockers (procainamide , propafenon,flecainide)
• Potassium channel blockers ( amiodarone, ibutilide)
• Digitalis
• Electrical cardioversion may be used to convert the atrial flutter
to sinus rhythm in an emergency situation (i.e. the patient is
hemodynamically unstable)
• Radiofrequency catheter ablation
• Anticoagulation (heparin/LMWH,Coumadin/warfarin) 64

65. ATRIAL FIBRILLATION.
• Atrial fibrillation is characterized by a total
disorganization of atrial electrical activity due to
multiple ectopic foci resulting in rapid chaotic
depolarisation of atria without effective atrial
contraction.
• Because of quivering atria,pooling of blood ,
forming mural thrombus ,may leads to cerebral or
peripheral vascular emboli. 65

67. ATRIAL FIBRILLATION
• Rate : atrial rate usually between 350-600/bpm.
• P wave : not present; wavy baseline is seen
instead.
• QRS : normal
• Rhythm: irregularly irregular. (This is the
hallmark of this dysrhythmia).
67

69. Treatment
• Beta blockers
• Calcium channel blockers (Diltiazem,Verapamil)
• Digoxin
• Anticoagulants (heparin,warfarin)
• Achieve INR of 2-3
• Cardioversion
• Surgical management (Cox –Maze procedure-
Making series of incisions that encircle abnormal
foci,usually near the pulmonary vein)

70. JUNCTIONAL
DYSRHYTHMIAS

71. Junctional Dysrhythmias.
• Junctional dysrhythmias refers to dysrhythmias that
originate in the area of the AV node primarily
because the SA node has failed to fire or the signal
has been blocked.
• In this situation the AV node becomes the pacemaker
of the heart.
71

72. JUNCTIONAL
DYSRHYTHMIAS
• The impulse from the AV node usually moves
in a retrograde (backward) fashion that
produces an abnormal P wave, occurring just
before or after the QRS complex or that is
hidden in the QRS complex.
• The impulse usually moves normally through
the ventricles.

73. ECG Characteristics:
• In junctional escape rhythm the HR is 40 to 60
beats/minute
• Accelerated junctional rhythm it is 61 to 100
beats/minute
• Junctional tachycardia it is 101 to 150 beats/minute.
• Rhythm is regular.
• The P wave is abnormal in shape and inverted or it
may be hidden in the QRS complex.
• The QRS complex is usually normal.
73

74. JUNCTIONAL RHYTHM

75. JUNCTIONAL RHYTHM

76. 76
Treatment.
• Treatment varies according to the type of junctional
dysrhythmia.
• Escape junctional rhythm atropine can be used.
• Accelerated junctional rhythm and junctional
tachycardia caused by digoxin toxicity the digoxin
is withheld.
• β-adrenergic blockers ,calcium channel blockers
and potassium chanel blockers are used for rate
control.

77. BUNDLE BRANCH BLOCK
• Bundle-branch block indicates that conduction is
impaired in one of the bundle branches (distal to
the bundle of His), and thus the ventricles do not
depolarize simultaneously.
• The abnormal conduction pathway through the
ventricles is causing a wide (greater than 0.20
second) or notched QRS complex.
• The defect may result from Myocardial
fibrosis,Chronic CAD,MI,Cardiomyopathy and
Pulmonary embolism
77

78. BUNDLE BRANCH BLOCK
These disturbances of conduction through the
ventricles result in either a right bundle-branch
block (RBBB)or a left bundle-branch block
(LBBB).
A 12-lead electro-cardiogram is needed to
distinguish left and right BBB.
In LBBB the QRS complex in V₁ is described as
rs
In RBBB the QRS complex in V₁ is described as
Rsr
Because of its association with left ventricular
disease, LBBB carries a worse prognosis.

79. BUNDLE BRANCH BLOCK
• Rate : variable
• P wave : normal if the underlying rhythm is sinus
• QRS: wide ; > 0.12 seconds, mid QRS notching
• Conduction : This block occurs in the right or left bundle branches or in
both. The ventricle that is supplied by the blocked bundle is depolarized
abnormally.
• Rhythm : regular or irregular depending on the underlying rhythm.
• Artificial pacing.
• Cardiac Resynchronisation therapy (CRT)
79

80. RIGHT BBB
80

81. BUNDLE BRANCH BLOCK
81

82. 82
FIRST-DEGREE AV BLOCK:
• First-degree AV block is a type of AV block in which
every impulse is conducted to the ventricles but the
duration of AV conduction is prolonged.
• After the impulse moves through the AV node it is
usually conducted normally through the ventricles.

83. 1st Degree AV Block
EKG Characteristics:
Prolongation of the PR interval, which is constant
All P waves are conducted
The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/
83

84. FIRST –DEGREE AV BLOCK
84

85. 85
Clinical Significance.
• First-degree AV block is usually not serious but can
be a precursor of higher degrees of AV block.
• Patients with first-degree AV block are
asymptomatic.
Treatment.
• There is no treatment for first-degree AV block.
• Modifications to causative medications may be
considered.
• Patients should continue to be monitored for any
new changes in heart rhythm.

86. SECOND-DEGREE AV BLOCK
TYPE I (MOBITS 1)
• Type I second-degree AV block (Mobitz I) includes a
gradual lengthening of the PR interval.
• It occurs because of a prolonged AV conduction time
until an atrial impulse is not conducted and a QRS
complex is blocked (missing).
• Type I AV block most commonly occurs in the AV node
but it can also occur in the His-Purkinje system. 86

87. SECOND DEGREE A-V BLOCK (MOBITZ
I )
• Rate: variable
• P wave: normal morphology with constant P-P interval
• QRS: normal
• Conduction: the P-R interval is progressively longer until one P wave
is blocked; the cycle begins again following the blocked P wave.
• Rhythm: irregular
87

88. SECOND-DEGREE AV BLOCK TYPE II
• Type II second-degree AV block is a more serious
type of block in which a certain number of impulses
from the SA node are not conducted to the
ventricles.
• This occurs in ratios of 2:1 3:1 and so on (i.e. two P
waves to one QRS complex three P waves to one
QRS complex). It may occur with varying ratios.
• Type II AV block almost always occurs in the His-
Purkinje system.
88

89. SECOND DEGREE A-V BLOCK
MOBITZ TYPE II
• Rate: variable
• P wave: normal with constant P-P intervals
• QRS: usually widened because this is usually associated with a
bundle branch block.
• Conduction: P-R interval may be normal or prolonged, but it is
constant until one P wave is not conducted to the ventricles.
• Rhythm: usually regular when AV conduction ratios are constant
89

90. 2nd Degree AV Block
Type 1 (Wenckebach)
EKG Characteristics: Progressive prolongation of the PR interval until a P
wave is not conducted.
As the PR interval prolongs, the RR interval actually
shortens
EKG Characteristics: Constant PR interval with intermittent failure to conduct
Type 2
90

91. Treatment of second degree block
 Administration of atropine or isoproterenol
(which speed the rate of impulse conduction)
 Insertion of a temporary or permanent
pacemaker
 With holding cardiac depressant drugs (e.g.,
digitalis, beta-blockers, certain calcium-
channel blockers).

92. THRD –DEGREE HEART BLOCK
• Third-degree AV block is the complete
dissociation of the impulse between the atria and
ventricles.
• The atria are regularly paced by the SA node, but
because the message is completely blocked, the
ventricles are being regularly paced by a
ventricular ectopic pacemaker
• Third-degree heart block is sometimes called AV
dissociation or complete heart block because
upper and lower chambers of the heart are
working independently of each other.
92

93. THIRD DEGREE (COMPLETE) A-V
BLOCK
• Rate : atrial rate is usually normal; ventricular rate is usually
less than 70/bpm. The atrial rate is always faster than the
ventricular rate.
• P wave : normal with constant P-P intervals, but not "married"
to the QRS complexes.
• QRS : may be normal or widened depending on where the
escape pacemaker is located in the conduction system
• Conduction : atrial and ventricular activities are unrelated due
to the complete blocking of the atrial impulses to the
ventricles.
• Rhythm : irregular
• Complete block of the atrial impulses occurs at the A-V
junction, common bundle or bilateral bundle branches.
93

94. 94

95. 95

96. TREATMENT OF THIRD
DEGREE AV BLOCK
 Atropine
 Catecholamine infusions (dopamine or
epinephrine)
 Transcutaneous pacing
 Transvenous pacemaker
 If asystole develops, CPR is used until a
transvenous pacemaker can be inserted.
 Long-term management for irreversible causes
includes permanent pacemaker implantation.

97. VENTRICULAR
ARHYTHMIAS

98. PREMATURE VENTRICULAR
CONTRACTON
• premature ventricular contraction (PVC) is a
contraction coming from an ectopic focus in
the ventricles.
• It is the premature (early) occurrence of a QRS
complex.
• A PVC is wide and distorted in shape
compared with a QRS complex coming down
the normal conduction pathway

99. PREMATURE VENTRICULAR
CONTRACTION
• PVCs that arise from different foci appear
different in shape from each other and are called
multifocal PVCs.
• PVCs that have the same shape are called
unifocal PVCs.
• When every other beat is a PVC, the rhythm is
called ventricular bigeminy.
• When every third beat is a PVC, it is called
ventricular trigeminy.
• Two consecutive PVCs are called a couplet.

101. 101

104. COUPLET

105. 105
Treatment:
• Treatment is often based on the cause of the PVCs (e.g.
oxygen therapy for hypoxia and electrolyte replacement).
• Assessment of the patient's hemodynamic status is
important to determine if treatment with drug therapy is
indicated.
• Drugs that should be considered include :-
β-adrenergic blockers ,procainamide,Lidocaine (Sdium
channel blockers) and amiodarone (potassium channel
blockers)

106. VENTRICULAR
TACHYCARDIA
• Ventricular tachycardia (VT) occurs when there are
three or more consecutive PVCS.
• It occurs when an ectopic focus or foci fire repetitively
and the ventricle takes control as the pacemaker.
• R-on-T phenomenon occurs when a PVC falls on the T
wave of a preceding beat. This is especially dangerous
because the PVC is firing during the relative refrac
tory phase of ventricular repolarization. Excitability of
the heart cells increases during this time, and the risk
for the PVC to start VT or ventricular fibrillation (VF)
is great.

108. VENTRICULAR TACHYCARDIA:
• The diagnosis of ventricular tachycardia (VT) is
made when a run of three or more PVCs occurs.
• Different forms of ventricular tachycardia exist
depending on QRS configuration.
• Monomorphic VT - QRS complexes that are the
same in shape size and direction.
• Polymorphic VT occurs when the QRS complexes
gradually change back and forth from one shape size
and direction to another over a series of beats.
• Torsades de pointes (French “twisting of the
points”) is polymorphic VT associated with a
prolonged QT interval of the underlying rhythm
108

109. ECG Characteristics.
• Ventricular rate is 150 to 250 beats/minute.
• Rhythm may be regular or irregular.
• AV dissociation may be present with P waves
occurring independently of the QRS complex.
• The P wave is usually buried in the QRS complex
and the PR interval is not measurable.
• The QRS complex is distorted in appearance with a
duration exceeding 0.12 second and with the ST-T
wave in the opposite direction of the QRS complex.
• The R-R interval may be irregular or regular.
109

110. VENTRICULAR
TACHYCARDIA

112. Treatment of VT
1. Treat underlying disease
2. Cardioversion : Hemodynamic unstable VT
(hypotension, shock, angina, CHF) or
hemodynamic stable but drug was no effect
3. Pharmacological therapy: ß-blockers, lidocain or
amiodarone
4. Implantable cardioverter defibrillator or surgical
therapy
112

113. TORSADE DE POINTES:
• Torsades de pointes (TdP or simply torsade(s))
translated as "twisting of the spikes"), is a
specific type of abnormal heart rhythm that can
potentially lead to sudden cardiac death.
• It is a polymorphic ventricular tachycardia that
exhibits distinct characteristics on the
electrocardiogram (ECG).
113

114. TORSADES DE POINTES
114

115. Treatment:
• Withdrawal of the offending agent
• Infusion of magnesium sulfate
• Antiarrhythmic drugs
• Temporary pacemaker as needed
• Because of the polymorphic nature of torsades de
pointes, synchronized cardioversion may not be
possible, and the patient may require an unsynchronized
shock (or defibrillation).
115

116. PRE-EXCITATION
SYNDROME:
Pre-excitation syndrome is a
condition in which the
ventricles of the heart
become depolarized too
early, which leads to their
partial premature
contraction
116

118. PRE-EXCITATION
SYNDROME

119. Pathophysiology
the ventricles are depolarized (excited) before normal conduction system.
However, there is no such delay in the abnormal pathway, so the electrical stimulus
passes to the ventricle by this tract faster than via normal atrioventricular/bundle of
His system,
Physiologically, the normal electrical depolarization wave is delayed at the
atrioventricular node to allow the atria to contract before the ventricles.
In all pre-excitation syndromes, at least one more conductive pathway is present.
Normally, the atria and the ventricles are electrically isolated, and electrical contact
between them exists only at the "atrioventricular node".
119

120. VENTRICULAR FIBRILLATION.
• Ventricular fibrillation is a severe derangement
of the heart rhythm characterized on ECG by
irregular undulations of varying shapes and
amplitude.
• This represents the firing of multiple ectopic foci
in the ventricle.
• Mechanically the ventricle is simply “quivering,”
and no effective contraction and consequently no
CO occurs.
120

121. Clinical Associations:
• Acute MI
• Myocardial ischemia
• CAD
• Cardiomyopathy
• It may occur during cardiac pacing or cardiac
catheterization procedures as a result of catheter
stimulation of the ventricle.
• It may also occur with coronary reperfusion after
fibrinolytic therapy.
• Other clinical associations are accidental electric
shock ,hyperkalemia ,hypoxemia. acidosis and drug
toxicity. 121

122. ECG Characteristics
• HR is not measurable. Rhythm is irregular
• Rate is usually above 300 beats/mnt
• The P wave is not visible and the PR
interval and the QRS interval are not
measurable
122

123. VENTRICULAR
FIBRILLATION

124. VENTRICULAR
FIBRILLATION

125. Clinical Significance
 VF results in an unresponsive, pulse- less, and
apneic state. If it is not rapidly treated, the
patient will not recover.
 Treatment consists of immediate initiation of
CPR and advanced cardiovascular life support
(ACLS) with the use of defibrillation and
definitive drug therapy (e.g. epinephrine,
vasopressin).
 There should be no delay in starting chest
compressions and using a defibrillator once
available.

126. Treatment:
 Immediate initiation of CPR and advanced
cardiac life support (ACLS) measures
 Defibrillation
 Drug therapy
126

127. ASYSTOLE
• Asystole represents the total absence of ventricular electrical
activity.
• Occasionally P waves can be seen
• No ventricular contraction occurs because depolarization does
not occur.
• Patients are unresponsive pulseless and apneic.
• This is a lethal dysrhythmia that requires immediate treatment.
• Ventricular fibrillation may leads to asystole
• The prognosis of a patient with asystole is extremely poor.
127

128. ASYSTOLE
128

129. Treatment:
CPR with initiation of IV therapy with
epinephrine and atropine
129

130. PULSELESS ELECTRICAL
ACTIVITY.
• Pulseless electrical activity (PEA) describes a
situation in which electrical activity can be
observed on the ECG but there is no mechanical
activity of the ventricles and the patient has no
pulse.
• Prognosis is poor unless the underlying cause can
130

131. 131
CAUSES PEA
• Hypovolemia
• Hypoxia
• Metabolic acidosis
• Hyperkalemia or hypokalemia
• Hypothermia
• Drug overdose, cardiac tamponade
• MI
• Tension pneumothorax
• Pulmonary embolus.

132. 132

133. TREATMENT
• Treatment begins with CPR followed by
intubation
• IV therapy with epinephrine.
• Atropine is also used if the ventricular rate is
slow.
• Treatment is directed toward correction of the
underlying cause. 133

134. SUDDEN CARDIAC DEATH:
• The term sudden cardiac death (SCD) refers to
death from a cardiac cause. Within a short
period of time(1 hour after the onset of
symptoms) in a person with known or
unknown cardiac disease.
• The majority of SCDs result from ventricular
dysrhythmias specifically ventricular
134

135. MANAGEMENT OF
ARHYTMIAS
• Pharmacological Intervention
• Electronic interventions
• Non –electronic interventions
• Surgical Management

138. ANTIARHYTHMC DRUGS
(MECHANISM OF ACTION )
• Class I: Sodium Channel Blockers (decrease
conduction velocity in the atria, ventricles, and His-
Purkinje system)
• Class II: β-Adrenergic Blockers (decrease automaticity
of the SA node, decrease conduction velocity in AV
node)
• Class III: Potassium Channel Blockers (delay repoClass
IV: Calcium Channel Blockers (decrease automaticity
of SA node, delay AV node conduction)
• Class IV: Calcium Channel Blockers (decrease
automaticity of SA node, delay AV node conduction)

139. ELECTRONIC INTERVENTIONS
Pacemaker Insertion
Cardioversion
Defibrillation
Automatic impantable cardioverter
Defibrillator

140. NON-ELECTRONIC
INTERVENTIONS
Carotid sinus massage
Radiofrequency ablation

141. SURGICAL MANAGEMENT
• Radiofrequency Catheter Ablation
• Maze Procedures
• Sub endocardial resection

142. PACEMAKERS
The artificial cardiac pacemaker is an electronic
device used to pace the heart when the normal
conduction pathway is damaged or diseased.
The basic pacing circuit consists of a power
source (battery-powered pulse generator) one or
more conducting leads (pacing leads) and the
myocardium.
The electrical signal (stimulus) travels from the
pacemaker through the leads to the wall of the
myocardium.
 The myocardium is “captured” and stimulated
to contract.
142

143. Pacemaker is an electronic device
used to pace the heart when the normal
conduction pathway is damaged or diseased.
Component of pacing system:
• Pulse Generator
• Pacing Lead
• Healthy Myocardium

144. FUNCTION OF PACEMAKER
Pacing function
 Sensing function
Capture function

145. PACING FUNCTION:
It is the ability of the pacemaker
to stimulate either the atrium, Ventricle, or
Depolarization and
both chambers in sequence and initiate
cardiac
electrical
contraction.
• Atrial pacing
• Ventricular pacing
• Atrio-ventricular
pacing.

146. SENSING FUNCTION:
Cardiac pacemaker have the
ability to see intrinsic cardiac Activity
when it occurs.
CAPTURE FUNCTION:
The ability to generate a response
from the heart [contraction] after
electrical stimulation is referred as
capture.

147. TYPES OF PACEMAKER
• Permanent pacemaker
• Temporary pacemaker
 Transvenous pacing
 Epicardial pacing
 Transcutaneous pacing

148. Permanent pacemaker
It is implanted totally with in the body. The
power source is implanted subcutaneously
usually over the pectoral muscle on the
patients non dominant side. The pacing leads
are threaded transvenously to the chamber to
be paced.

149. Indications
• AcquiredA
V block
• Second and third degree block
• Cardiomyopathy
• BBB
• SANode dysfunction
• Tachydysrhythmias

150. TYPES OF PERMANENT
PACEMAKER

151. 151

152. DUAL CHAMBER
PACEMAKER

153. BIVENTRICULAR PACE
MAKER

154. Pace maker modes
• Fixed rate: fire constantly at a preset rate with
out regard to the electrical activity of the
patient’s heart
• Demand: it detects the hearts electrical
activity. Fires only when the electrical activity
of heart drops below the pre set rate.

155. Temporary pacemaker
It has the power source outside the body
Types:
Transvenous pacemaker
Leads are threaded transvenously to the chambers
and attached to the power source
Epicardial pacing
The pacing leads are attached to the epicardium
during heart surgery
Transcutaneous pacemaker
Noninvasive, power source is attached to large
electrodes placed over the anterior and posterior chest

156. Trans venous pacing Epicardial pacing
Transcutaneous pacing

157. Nursing care
• Continuous ECG monitoring of heart rate & Rhythm.
• Monitor vital signs for every 15 minutes.
• Monitor urine output.
• Observe for the presence of dysarrhythmia.
• Avoid injury .
• Post insertion chest x-ray.
• Monitor signs &symptoms of haemothorax &
pneumothorax.
• Evaluate continuously for evidence of bleeding.

158. • Monitor for evidence of lead migration.
• Auscultate for pericardial friction rub.
• Provide an electrically safe environment.
• Prevent infection.
• Relieve anxiety.

159. Patient education
• Check pulse daily.
• Avoid weight lifting.[>20 lb]
• Avoid shower.
• Avoid lifting hand over shoulder level.
• Wear loose-fitting clothing.
• Avoid trauma to the area.
• Come for regular check up.

160. • Avoid close exposure to magnetic force,
radiation, metal detector etc
• Carry all time pacemaker identity card
• All electronic equipments should be grounded
and repaired

161. 161

162. DUAL CHAMBER PACING

163. CARDIOVERSION:
• Synchronized cardioversion is the therapy of
choice for the patient with hemodynamically
unstable ventricular or supraventricular
tachydysrhythmias.
• A synchronized circuit in the defibrillator is used
to deliver a counter shock that is programmed to
occur on the R wave of the QRS complex of the
ECG.
• The synchronizer switch must be turned on when
cardioversion is planned.
163

165. PRINCIPLES OF
CARDIOVERSION

166. INDICATIONS

167. IMPLANTABLE CARDIOVERTER-
DEFIBRILLATOR:
The implantable cardioverter-defibrillator (ICD) is
an important technology for patients who :-
 have spontaneous sustained VT
have syncope with inducible ventricular
tachycardia/fibrillation
are at high risk for future life-threatening
dysrhythmias (e.g. have cardiomyopathy).
167

168. Implantable cardioverter
defibrillator

169. DEFIBRILLATION
• Defibrillation is the most effective method of
terminating ventricular fibrillation and pulseless
VT.
• It is most effective when the myocardial cells are
not anoxic or acidotic making rapid defibrillation
critical to a successful patient outcome.
• Defibrillation is accomplished by the passage of a
DC electric shock through the heart that is
sufficient to depolarize the cells of the
myocardium.
169

170. DEFIBRILLATION:
• Defibrillators deliver energy using a monophasic
or biphasic waveform.
• The output of a defibrillator is measured in joules
or watts per second.
• The recommended energy for initial shocks in
defibrillation depends on the type of defibrillator
(150-360 Joules).
• Biphasic defibrillators deliver the first and any
successive shocks using 150 to 200 joules.
• After the initial shock CPR should be started
immediately beginning with chest compressions.
170

173. PADDLE PLACEMENT

175. RADIOFREQUENCY CATHETER ABLATION
THERAPY:
• Catheter ablation (RFA) is a procedure that uses
radiofrequency energy to destroy a small area of heart tissue
that is causing rapid and irregular heartbeats. Destroying this
tissue helps restore your heart’s regular rhythm. Catheter
ablation destroys the abnormal tissue without damaging the
rest of the heart.
• During the procedure, a thin catheter is inserted into the
heart to target areas that are causing the arrhythmia. Heat from
electrodes at the end of the catheter destroys these tissues,175

176. 176

177. RADIO FREQUENCY CATHETER
ABLATION

178. CAROTID SINUS MASSAGE
• The carotid sinus, also known as the carotid bulb, is a
neurovascular structure that appears as a dilation at the
bifurcation of the common carotid artery, and the beginning of
the internal carotid artery.
• A CSM is usually first performed on the right side of a
patient's neck. Press firmly on the patient's carotid sinus
massage point. Using a circular motion, rub and massage the
carotid sinus for a period of 5–10 seconds.
• There are baroreceptors in the carotid sinuses stimulate the
vagus nerve, causing inhibition of the sinus node and AV node
of the heart,there by reduce HR and BP,

181. SURGICAL MANGEMENT
• Maze Procedures
• The maze procedure is a technique used to
treat AF. It involves making
(cryoablation/scalpel/radiofrequency energy))
many small cuts within the wall of the upper
chambers. Scar tissue forms, blocking the
signals that cause heart rhythm problems.
• Mini-maze needs only 1 or 2 small cuts in the
chest.

182. Sub endocardial Resection
• In some cases of VT, certain problems
within the heart muscle might be the
cause. Taking out the scar tissue under
the lining of the heart may keep an
arrhythmia from starting.

183. NURSING DIAGNOSIS
• Acute pain related to tachycardia can be
caused by insufficient oxygenated blood to the
heart due to rapid heart contraction.
• Impaired gas exchange related to disrupted
blood flow and compromised gas exchange
from rapid heart rate, incomplete filling of
heart chambers, and decreased supply of
oxygenated blood

184. NURSING DIAGNOSIS
• Decresed cardiac output related to Impaired
cardiac muscle contraction secondary to
dysrhythmias as evidenced by
tachycardia,hypotensiondecreased EF.
• Ineffective tissue perfusion related t decreased
cardiac output as evidenced by
dyspnoea,syncope,palpitation

185. NURSING DIAGNOSIS
• Activity intolerance related to imbalanced
oxygen supply and demand
• Knowledge deficit
• Anxiety
• Risk for ineffective cerebral tissue perfusion
• Risk for unstable blood pressure
• Risk for decreased cardiac tissue perfusion.