INTRODUCTION, ELECTRICAL CONDUCTION SYSTEM OF HEART, ATRIOVENTRICULAR (AV) BLOCK, ETIOLOGY/ RISK FACTORS, PATHOPHYSIOLOGY, CLINICAL MANIFESTATIONS, DIAGNOSTIC EVALUATION,, MANAGEMENT, COMPLICATION, NURSING MANAGEMENT, CONCLUSION

1. HEART BLOCK
SWATILEKHA DAS
(RN,MSN)

2. INTRODUCTION
Heart block is a disturbance of impulse conduction
that can be permanent or transient owing to
anatomical or functional impairment. It must be
distinguished from interference, a normal
phenomenon that is a disturbance of impulse
conduction caused by physiological refractoriness
due to in excitability from a preceding impulse.

3. ELECTRICAL CONDUCTION SYSTEM OF
HEART
The heart is able to create its own electrical impulses and
control the route the impulses take via a specialised
conduction pathway.
This pathway is made up of 5 elements:
1.The sino-atrial (SA) node
2.The atrio-ventricular (AV) node
3. The bundle of His
4.The left and right bundle branches
5. The Purkinje fibres

4. Conduction system of heart

5. The SA node is the natural pacemaker of the heart. The SA node releases
electrical stimuli at a regular rate, the rate is dictated by the needs of
the body. Each stimulus passes through the myocardial cells of the atria
creating a wave of contraction which spreads rapidly through both atria.
The electrical stimulus from the SA node eventually reaches the AV
node and is delayed briefly so that the contracting atria have enough
time to pump all the blood into the ventricles. Once the atria are empty
of blood the valves between the atria and ventricles close.
At this point the atria begin to refill and the electrical stimulus passes
through the AV node and Bundle of His into the Bundle branches and
Purkinje fibres. As the ventricles contract, the right ventricle pumps
blood to the lungs where carbon dioxide is released and oxygen is
absorbed, whilst the left ventricle pumps blood into the aorta from
where it passes into the coronary and arterial circulation.
At this point the ventricles are empty, the atria are full and the valves
between them are closed. The SA node is about to release another
electrical stimulus and the process is about to repeat itself.

6. The 3 stages of a single heart beat are:
Atrial depolarisation
Ventricular depolarisation
Atrial and ventricular repolarisation.
Normal sinus rhythm of heart

7. ATRIOVENTRICULAR (AV) BLOCK
1. First degree AV block
2. Second degree AV block
i. Mobitz type I or Wenkebach AV block
ii. Mobitz types II AV block
3. Third degree AV block

8. 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.
Clinical Associations- First-degree AV block is associated with MI, CAD,
rheumatic fever, hyperthyroidism, vagal stimulation, and drugs such as
digoxin, β-adrenergic blockers, calcium channel blockers, flecainide.
ECG Characteristics- In first-degree AV block, HR is normal and rhythm is
regular.
Clinical Significance- First-degree AV block is usually not serious but can be a
precursor of higher degrees of AV block. Patients with first AV degree block
are asymptomatic.
Treatment- There is no treatment for first-degree AV block, modification to
causative medications may be considered. Patients should continue to be
monitored for any new changes in heart rhythm.

9. 1st degree heart block

10. Second-degree AV block, Type I
Type I second-degree AV block (Mobitz I or Wenckebach heart block) includes a
gradual lengthening of the PR interval. It occurs because of a prolonged AV
conduction time until an atrial impulse is non-conducted and a QRS complex is
block (missing). Type I AV block most commonly occurs in the AV node, but it can
also occur in the His-Purkinje system.
Clinical Associations- Type I AV block may result from use of drugs such as digoxin
or β-adrenergic blockers. It may also be associated with CAD and other diseases
that can slow AV conduction.
ECG Characteristics- Atrial rate is normal, but ventricular rate may be slower as a
result of non-conducted or blocked QRS complexes.
Clinical Significances- Type I AV block is usually a result of myocardial ischemia or
infarction. It is almost transient and is usually well tolerated. However, in some
patients (e.g following MI) it may be a warning signal of a more serious AV
conduction disturbance.
Treatment- If the patient is symptomatic, atropine is used to increase HR, or a
temporary pacemaker may be needed, especially if the patient has experience an
MI. if the patient is asymptomatic, the rhythm should be closely observed with a
transcutaneous pacemaker on standby. Bradycardia is more likely to become
symptomatic when one or more of the following are present: (1) hypotension, (2)
HF, or (3) shock.

11. 2nd degree Mobitz I heart block

12. Second-Degree AV Block, Type II
In type II second-degree AV block (Mobitz II heart block), a P wave is non-conducted without
progressive antecedent PR lengthening. This almost always occurs when a block in one of the
bundle branches is present. On conducted beats, the PR is constant. 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.
Clinical Associations- Type II AV block is associated with rheumatic heart disease, CAD, anterior
MI, and digitalis toxicity.
ECG Characteristics- Atrial rate is usually normal. Ventricular rate depends on the intrinsic rate
and the degree of AV block. Atrial rhythm is regular, but ventricular rhythm may be irregular.
Clinical Significance- Type II AV block often progresses to third-degree AV block and is associated
with a poor prognosis. The reduced HR often results in decreased CO with subsequent
hypotension and myocardial ischemia. Type II Av block is an indication for therapy with a
permanent pacemaker.
Treatment- Temporary treatment before the insertion of a permanent pacemaker may be necessary
if the patient becomes symptomatic (e.g, hypotension, angina), and involves the use of a
temporary transvenous or transcutaneous pacemaker.

13. 2nd degree Mobitz II heart block

14. Third-Degree AV Block
Third-degree Av block, or complete heart block, constitutes one form of AV dissociation in which
no impulses from the atria are conducted to the ventricles. The atria are stimulated and
contract independently of the ventricles. The ventricular rhythm is an escape rhythm, and the
ectopic pacemaker may be above or below the bifurcation of the bundle of His.
Clinical Assiciations- Third-degree AV block is associated with severe heart disease, including
CAD, MI, myocarditis, cardiomyopathy, and some system diseases such as amyloidosis and
progressive systemic selerosis (acleroderma). Some medications can also cause third-degree
AV block, such as digoxin, β-adrenergic blockers, and calcium channel blockers.
ECG Characteristics- The atrial rate is usually a sinus rate of 60 to 100 beats/minute. The
ventricular rate depends on the site of the block. If it is in the AV node, the rate is 40 to 60
betas/minute, and if it is in the His-Purkinje system, it is 20 to 40 beats/minute. Atrial and
ventricular rhythms are regular but unrelated to each other.
Clinical Significance- Third-degree AV block almost always results in reduced CO with
subsequent ischemia, HF, and shock. Syncope from third-degree AV block may result from
severe bradycardia or even periods of asystole.
Treatment- For symptomatic patients, a transcutaneous pacemaker is used until a temporary
transvenous pacemaker can be inserted. The use of drugs such as atropine, epinephrine,
isoproterenol, and dopamine is a temporary measure to increase measure HR and Support
blood pressure (BP) until temporary pacing is initiated. Patients will need a permanent
pacemaker as soon as possible.

15. 3rd degree heart block

16. ETIOLOGY/ RISK FACTORS
Severe heart disease
CAD
MI
Myocarditis
Cardiomyopathy
System diseases such as amyloidosis
and progressive systemic selerosis
(acleroderma)
Medications such as digoxin, β-
adrenergic blockers, and calcium channel
blockers.

17. PATHOPHYSIOLOGY
No arterial impulse conducted
through the AV node into the
ventricles
Independent atrial and ventricular
complexes
Atrial rate greater than
ventricular rate

18. CLINICAL MANIFESTATIONS
Reduced CO with
subsequent ischemia
Heart failure
Shock
Syncope
Severe bradycardia or
even periods of asystole.

19. DIAGNOSTIC EVALUATION
1. ECG (electrocardiogram)
2. Holter monitoring
3. Echocardiogram
4. Electrophysiology test
5. Tilt-table test

20. MANAGEMENT
1. A transcutaneous pacemaker is used until a temporary
transvenous pacemaker can be inserted.
2. The use of drugs such as atropine, epinephrine,
isoproterenol, and dopamine is a temporary measure to
increase measure HR and Support blood pressure (BP)
until temporary pacing is initiated.
3. Patients will need a permanent pacemaker as soon as
possible.

22. COMPLICATION
1. Arrhythmia (irregular heart beat)
2. Bradycardia (low heart rate)
3. Cardiac arrest

23. Nursing
Diagnosis
Goals Implementation Expected
outcome
Impaired
physical
mobility
related to
activity
restriction
To prevent
complicati
ons of
immobility
o Assess patient’s general
condition.
o Implement therapies to prevent
complications of immobility.
o Instruct on range of motion
exercise, isometric exercises of
the lower extremities, deep
breathing exercises, and
shifting weight from side to side.
o Apply antiembolism stockings
and pressure-relieving pads and
appliances to bed.
o Assist patient with repositioning
and daily care activity
Patient will
participate in
therapies.
NURSING MANAGEMENT

24. Nursing
Diagnosis
Goals Implementation Expected
outcome
Anxiety
related to
cardiac
disorder and
the impending
temporary
pacemaker
insertion as
evidenced by
verbalisation
To relieve
anxiety
o Assess patient’s anxiety level.
o Teach about the dysrhythmia and its
cause and treatment, the temporary
pacemaker insertion procedure, the
local anesthesia and analgesia
used, places the patient will go after
the procedure, ways the patient will
feel the temporary lead in place, and
restriction of the affected extremity.
o Assess patient’s ability and
willingness to participate in
relaxation sessions before and
during the pacemaker insertion.
o Use guided imagery to ‘walk’ patient
through the procedure.
o Assess patient’s level of anxiety
after session.
o Take feedback from the patient.
Patient will
verbalize an
understanding
of the disease
and
management.
Patient will
participate in
relaxation
sessions.

25. Nursing
Diagnosis
Goals Implementation Expected
outcome
High risk for
fluid volume
deficit
related to
bleeding due
to the
transvenous,
epicardial, or
transthoracic
lead
insertion
To
maintain
fluid
balance
o Monitor insertion site for signs
and symptoms of hematoma
formation or decreased arterial
perfusion.
o Apply manual pressure to
insertion site
o Assess arterial pulses distal to
insertion site
o Monitor for signs and symptoms
of intrapericardial bleeding,
including decreasing blood
pressure, rising venous
pressure, pulus paradoxus, and
distal heart sounds.
o Monitor for signs and symptoms
of hemothorax, including a fall in
blood pressure, diaphoresis, or
pallor, rise in respiratory rate and
effort, and chest discomfort.
Patient will
not develop
bleeding/hem
atoma or
hemothroax

26. Nursing
Diagnosis
Goals Implementation Expected
outcome
High risk for
decrease
cardiac
output
related to
bradydysrhy
thmias and a
delay in the
insertion of
the
temporary
pacing
system
To prevent
signs and
symptoms
of
decreased
cardiac
output,
and
maintain
hemodyna
mical
stability
o Monitor for signs and symptoms
of decreases cardiac output
such as systolic blood pressure
less than 90 mm Hg, change in
level of consciousness,
abnormal arterial blood gas
levels, and urinary output less
than 30 ml/hr
o Initiate therapy to maintain or
achieves hemodynamic stability.
o For bradydysrhythmias
administer atropine and
isoproterenol and assess for
ventricular irritability.
o For tachydysrhythmia administer
digitalis, perfrom synchronized
cardioversion, and administer
lidocaine.
Patient will
be
hemodynami
cally stable.

27. Nursing
Diagnosis
Goals Implementation Expected
outcome
High risk for
infection
related to
precutaneou
s placement
To prevent
infection
o Assess patient’s vital signs and
record.
o Initiate appropriate infection
control measures and monitor for
signs and symptoms of infection.
o Apply antibacterial ointment and
sterile dressing to insertion site.
o Change sterile dressing daily
o Assess for pain, redness,
swelling, or purulent drainage.
o Culture drainage tip of lead on
removal.
Patient will
not develop
infection

28. Nursing
Diagnosis
Goals Implementation Expected
outcome
High risk for
microshock
related to the
presence of
the
temporary
pacing lead
To prevent
atrial or
ventricular
tachydysrh
ythmia
o Prevent microshock by
maintaining electrical safety
o Insulate all exposed parts of the
lead
o Wear rubber gloves when
handling pacemaker terminals or
the lead and when changing
batteries
o Use nonelectric beds
o Avoid applying 2 different line-
powered electrical devices to the
patient at one time
o Disconnect pacemaker from the
lead during defibrillation
o Instruct patient to avoid contact
with all other electrical
equipment
Patient will
not develop
atrial or
ventricular
tachydysrhyt
hmia.

29. CONCLUSION
In left bundle branch block (LBBB), the heart's two ventricles are
being stimulated by the cardiac electrical impulse in sequence instead
of simultaneously. Specifically, the left ventricle in a person with LBBB
is stimulated to contract only after the right ventricle is stimulated. This
loss of normal coordination between the two ventricles decreases the
efficiency of the heart beat, so that the heart has to do more work to
achieve its normal pumping capacity. This can be managed by drugs
and artificial pacemakers.