Sinus node dysfunction refers to a number of conditions causing physiologically inappropriate atrial rates. Symptoms may be minimal or include weakness, effort intolerance, palpitations, and syncope. Diagnosis is by electrocardiography. Symptomatic patients require a pacemaker.

1. SA NODE
DYSRHYTHMIA
Mr.Jagdish Sambad
Assistant Professor
Balaji College of Nursing.

2. OUTLINES:
 Introduction about dysrhythmia.
 Introduction of SA node dysrhythmias.
 Various condition of sinus dysrhythmia.
 Causes, menifestations and management of each
condition.
 Medical management of each condition.
 Nursing management of condition.

3. DYSRHYTHMIA:
 A dysrhythmia is a disorder of heartbeat that
includes a disturbance of rate or rhythm or both.
 Dysrhythmias are derangements of heart’s
conduction system and not of heart structure. They
are identified by analyzing electrocardiogram
waveforms.
 Dysrhythmias are named as site of origin like if it is
from SA node then it is called sinusdysrhythmias.
 Possible alterations includes bradycardia,
tachycardia, flutter, fibrillation,premature beats and
heart blocks.

4. PROPERTIES OF CARDIAC MUSCLES:
 The cardiac muscle possesses physiologic
properties of excitability, automaticity, conductivity,
and contractility.
 Excitability: ability to be electrically stimulated
 Automaticity: ability to initiate an impulse
spontaneously and continuosly.
 Conductivity: ability to transmit an impulse along a
membrane in an orderly manner.
 Contractility: ability to respond mechanically to an
impulse.
 Disturbance in any of this lead to dysrhythmias.

5. PATHOPHYSIOLOGY:
 Significantly all dysrhythmias is their effect on
cardiac output and therefore cerebral and vascular
perfusion.
 Cardiac output is result of stroke volume times the
heart rate.
 During normal sinus rhythm, the atria contract to fill
and stretch ventricles called ATRIAL KICK,
increases amount of bllod in ventricles before
contracility, thereby increasing cardiac output by
30%.
 When impulse originates below SA node, or more
than one area fires in atria to originate a beat, the
atrial kick lost and cardiac output falls 30%.

6. CAUSES:
 Cardiac conditions:
 Accesory pathways
 Cardiomyopathy
 Conduction defects
 Heart failure
 Myocardial cell degenearation
 Valve disease.
 Other condition:
 Drugs
 Electrolytes imbalance
 Electrical shock
 Hypoxia, shock
 Metabolic conditions( thyroid problems)
 poisioning

7. CLINICAL MENIFESTATION:
 By flashcard

8. DIAGNOSTIC FINDINGS:
 Initial assessment includes a careful history
regarding onset, duration, symptoms and some
factors.
 A detailed past medical history including CVD.
 physical examination for auscultation of abnormal
heart sounds, rate, irregularity, murmur sounds.
 Electrocardiography
 Holter monitoring
 Event monitoring

9. NORMAL CONDUCTION PATHWAY:
 By chart.

10. NORMAL CONDUCTION PATHWAY:
Site of origin mechanism of conduction
Sinus node Bradycardia
Atria Tachycardia
AV node or junction Flutter
Ventricles Fibrillation
bundle of his Premature beats
parkinje fibers Heart blocks

11. AUTONOMIC NERVOUS SYSTEM
 The heart is under control of autonomic nervous
system, which consists of sympathetic and
parasympathetic.
 The word sympathetic is also referred to as
‘adrenrgic’, a word derived root from “adrenal”.
 Stimulation of sympathetic system lead to
accelerates heart rate, blood pressure and enhance
force of myocardial contraction.
 Conversely, parasympathetic slows down heart
rate, blood pressure and contraction.
 Manipulation of system forms the foundation for
much of medication therapy such as b-adrenregic
blockers.

12. NORMAL ECG-ELECTROCARDIOGRAM
 The electrical activity of heart can be viewed by
means of an ECG. Each phase of cardiac cycle is
reflected by specific waveforms that are captured
and recorded on a strip of ECG paper.
 The electrical activity is picked up by a set of leads
or electrodes placed as specific points on body.

13. ECG ANALYSIS:
 When analyzed accurately, the ECG offers important
information about electrical activity of the
myocardium.
 ECG waveforms are printed on graph paper. Time
and rate is measured on horizontal axis of graph,
and amplitude or voltage measured on the vertical
axis.
 The ECG waveforms represents the function of
heart’s conduction system, which abnormally
initiates and conducts the electrical activity.

14. WAVES, COMPLEXES AND INTERVALS:
 The ECG is composed of several waveforms,
including the P wave, the QRS complex, the T
wave, the ST segment, the PR interval, and
possibly a U wave.
 The P wave represents atrial muscle depolarization.
It normally 2.5 mm high or less and 0.11 second or
less in duration.
 PR interval= pause between atrial and ventricular
depolarization
 QRS =ventricular depolarization
 T wave= ventriculardepolarization

15. NORMAL SINUS RHYTHM

16. TYPES OF DYSRHYTHMIAS
 Sinus node dysrhythmia
 sinus bradycardia
 Sinus tachycardia
 Sinus arrhythmia
 Sinus axit block
 Ventricular dysrhythmias
 Premature ventricular contractions
 Ventricular tachycardia
 Ventricular fibrilation
 Supra ventricular tachycardia

17. SINUS BRADYCARDIA:

18. ETIOLOGY:
 Increased vagal stimulation
 Normal variation in althlets and healthy young
adults
 Medical condition ( anorexia nervosa,
atheroscelorosis, hypothermia, increased ICP,
hypoendocrine disease, MI)
 Medications( antihypertensive, beta blockers,
calcium channel blockers, digoxin)

19. SYMPTOMS
-Chest pressure and pain
-Hypotension
-Decreased level of consciousness
-Heart failure
-Dyspnea
-Dizziness
-Seizures
-syncope

20. TREATMENT:
 Management only if symptomatic aimed at
increasing heart rate .
 Medications:
 Atropine
 Supression of parasympathetic nervous system
 Stimulation of sympathetic nervous system

22. ETIOLOGY
 Diet-caffine
 Lifestyle-smoking/nicotine
 Medical conditions( anemia, haemorrhage, fever,
hypotension, pain, shock)
 Medications( central nervous system stimulants)
 Myocardial damage/ infraction
 Hypothyroidism
 Hypercalcemia
 Increased automacity of SA node
 Heart failure

23. SYMPTOMS:
 Chest pressure or pain
 Dysponea
 Fluttering in the chest
 Dizziness
 Syncope

24. MANAGEMENT:
 Medications such as beta blockers, calcium
channel blockers although rarely used to reduce
heart rate quickly
 Catheter ablation of the SA node if persistent sinus
tachycardia is seen and unresponsive to the other
treatments.
 Digoxin, anti-anxiety agents, adenosine agents are
used.
 Carotid massage
 Elimination of tobacco, alcohol, caffine, and other
stimulant is recommended.

25. MANAGEMENT ACCORDING AHA
( AMERICAN HEART ASSOCIATION)
 By leaflet.

26. SINUS ARRYTHMIA:
 sinus arrhythmia occurs when the sinus node creates an
impulse at irregular rhythm, the rate usually increases
with inspiration and decreases with expiration.
Nonrespiratory causes include heart disease and
valvular disease, but these are rare.
 Sinus arrhythmias has following characteristics:
 Ventricular and atrial rate: 60 to 100 in adult
 Ventricular and atrial rhythm: irregular
 QRS shape and duration: usually normal
 P wave: normal and consistent shape
 PR interval: consistent interval between o.12 to 0.20
seconds
 P:QRS=1:1

28. MANAGEMENT
 sinus arrhythmia usually not require any
intervention until blood pressure is affected,
particularly with orthostatic position changes.
 If dizziness, pre-syncope, or syncope occur, elastic
support stockings and/or sodium retaining drugs
are helpful.

29. SICK SINUS SYNDROME:
 Sick sinus syndrome is also known as syno-atrial
disease it can occur at any age but it is most
common in older age. The underlying pathology
involves fibrosis, degenerative changes, or
ischemia of the SA node. The condition is
characterized by variety of arrhythmias and may
present with following symptoms.
 Palpitation
 Dizzy spells
 Syncope
 Intermittent tachycardia
 Bradycardia
 Pauses with no atrial or ventricular-activity.

31. COMMON FEATURES OF SSS:
 Sinus bradycardia
 Sinus tachycardia
 Sinus arrest
 Paroxysmal atrial fibrillation
 Paroxysmal atrial tachycardia
 Atriovenricular block

32. MANAGEMENT:
 Often clients are found to have tachycardia and are
prescribed digitalis, propranolol, verapamil, or other
medications that slow the SA node impulse.
 The drugs can affect impulse conduction and can lead
to bradycardia recurrence of tachycardia.
 Treatment is two-fold including drugs to slow
automaticity and heart rate, along with insertion of a
permanent trans-venous pacemaker to prevent
symptomaticbradycardia.
 A permanent pacemaker may benefits in patient with
troublesome symptoms due to spontaneous
bradycardias or those with symptomatic bradycardias
induced by drugs required to prevent tachyrrthmias.
 Atrial pacing may prevent episodes of atrial fibrillation.
 Pacing improves symptoms but not prognosis, and is
not indicated in patients who are asymptomatic.

33. DISTURBANCE IN CONDUCTION PATHWAY:
 Sino-atrial node-conduction disturbances:
 under certain circumstances, the impulse from the SA
node is either (1) not generated in SA node or (2) not
conducted from SA node.
 CAUSES:
 Condition that increase vagal tone
 Coronary artery-disease
 MI
 Digitalis and calcium channel blockers
 Tissue hypoxia
 Hypertensive disease
 Scarring of intra-atrial pathways
 Electrolyte disturbances

34. SA ARREST:
 During SA arrest , neither the atria nor the
ventricles are stimulated , resulting in a pause in
the rhythm.
 An entire PQRST complex will be missing for one
or more cycles.
 After the pause of sinus arrest, a new pacemaker
focus assumes the pacing responsibility.
 The new pacemaker paces the heart at its inherent
rate, which is usually slower than the original SA
node rate.
 The new pacemaker is often another atrial focus,
but the AV junction or ventricles can also assume
pacing responsibility.

36. MANAGEMENT:
 intervention may include administration of vagolytic
agent ( atropine) or a sympthomematics
 ( isoproterenol) agent to increase the rate of SA
node firing.
 -if pharmacological measures fail, a permanent
transcutenous pacemaker may also be warrented
depending on the underlying cause of
dysrhythmias.

37. SINUS EXIT BLOCK:
 During sinus exit block , a conduction delay occurs
between the sinus node and the atrial muscles. Unlike
the rhythm in SA arrest , the rhythm of SA node
discharge in sinus exit block, remains constant and
uninterrupted.
 The ECG characteristically displays a normal sinus
rhythm interrupted intermittently by pauses. This creates
pattern of pauses that , when measured it comprises
multiplies of underlying p-p interval.
 Sinus arrest differs from SA exit block in that the SA
node at times does not fire at all.
 The result is the occurrence of pauses that are longer
and not a multiply of the underlying p-p interval.
 These pauses are also frequently terminated by escape
ectopic beats.
 Sinus arrest often is associated with a more serious
prognosis.

39. CONT...
 SYMPTOMS:
 Lightheadness
 Dizziness
 Presyncope or syncope
 MANAGEMENT:
 Intervention is not necessary unless the client
becomes symptomatic and exihibits menifestations
of decreased cardiac out-put.
 Management is similar to SA arrest and it based on
symptoms or alterations in vital signs.

40. MEDICAL MANAGEMENT:
 The goal of medical management is to stop dysrhythmia
immediately and to restore normal sinus rhythm. Remember,
because there is inadequate perfusion or no perfusion of
blood during dysrhthmias, CPR ( CARDIO-PULMONARY
RESUSCITATION) with advanced cardiac life support
measures are performed.
 Finally, the cause of dysrhythmias is identified and treated.
 Life-threating dysrhythmias can often be effectively controlled
by DEFIBRILLATION. The most crucial element for survival
after cardiac arrest is time interval from collapse to care,
especially DEFIBRILLATION.
 With passing minute, the chances of survival decline as much
as 10 % electrical intervention can (1) abruptly stop the
heart’s erractic electrical discharge (2) restore the flow of
electrical current where there is none.

41. INTERVENTIONAL MANAGEMENT:
 Ablating conduction pathways: a variety of
procedures can be used to treat dysrhythmias when
medications are not successful in bringing about
conversion of abnormal rhythm to a normal rhythm.
 Intervention include (1) chemical and mechanical
ablation and (2) radiofrequency ablation of the
abnormal pathway. These procedures involve risk
to normal conduction tissue, and a pacemaker may
be needed either temporarily and permanent.

42. SURGICAL MANAGEMENT
 Clients with persistent heart rhythm problems may
benefit from implanted devices to control their
rhythm to control abnormal impulses or generate an
impulse.
 Controlling impulses:
 Automatic implantable cardioverter defibrilator (
ICD)
 Restoring impulse generation
 pacemakers

44. CONT…
 ELECTROPHYSIOLOGIC STUDIES: ( EPSs)
 It allows the clinician to induce troubling dysrhythmias
controlled environment for the purpose of determining
appropriate treatment .
 Catheters containing electrodes in the distal position are
placed within heart .
 stimulation of these electrode- containing catheter induces
dysrhythmias. Once a dysrhythmia is induced, different
medications are administered to determine which is the most
effective in suppressing dysrhytmia.
 CARDIAC CONDUCTION SURGERY:
 any tachycardia that does not respond to any anti-tachycardia
pacing may be treated by methods others than medications
and pacemakers.
 such methods include endocardial isolation, endocardial
resection, cryoablation, electrical ablation, radiofrequency
ablation. An implantable cardioverter defibrillation may be
used in conjunction with these surgical intervention.

45. CONT…
 Endocardial ablation: it involves making an incision
into the endocardium separating area where
dysrhythmias originates from surrounding endocardium.
 Endocardial resection: the origin of dysrhythmia is
identified and that area of endocardium is peeled away.
 Cryoablation: it involves placing a special probe,
cooled temperature of -60ċ on endocardium at site of
dysrhythmia’s origin of 2 minutes. The area becomes a
small scar and origin of dysrhythmia is eliminated.
 Electrical Ablation: a catheter is placed over origin and
1 to 4 shocks of 100 to 300 joules are administered
through catheter directly to endocardium and
surrounding tissue.
 Radiofrequency ablation: placing catheter and high
frequency sound waves are passed through catheter,
destroying dysrrhythmic tissue with less trauma to
surrounding tissue.

46. NURSING PROCESS:
 Assessment:
 History collection
 Physical examination
 Complaints of symptoms
 Lab investigations
 Psychological assessment

47. NURSING DIAGNOSIS:
 Decreased cardiac output related to electrical conduction
disturbances, decreased myocardial contractility as manifested by
bradycardia or tachycardia.
 Impaired tissue perfusion related to inadequate blood circulation
as manifested by decreased capillary refill time.
 Ineffective breathing pattern related to decreased lung expansion
as manifested by dyspnea.
 Anxiety related to fear of complications as manifested by different
questioning by patient and family members.
 Knowledge deficit related to complexity of treatment, and self care
management as manifested by different questioning by patient.
 Self care deficit related to weakness and fatigue as manifested by
decreased ability to daily activity.
 Increased risk of hypoxia and respiratory failure.
 Increased risk of hypovolemia related to haemorrhage and
impaired cardiac function.
 Risk of developing life threatening condition.

48. NURSING INTERVENTION:
 Monitoring and managing dysrhythmia:
 The nurse regularly evaluates patient’s blood pressure, pulse rate and
rhythm, rate and depth of respirations, and breathe sounds to determine the
dysrhythmia’s hemodynamic effect.
 The nurse also asks patient about episodes of lightheadness, dizziness, or
faintaing, as part of ongoing assessment. If a patient with a dysrhythmia is
hospitalized , the nurse may obtain 12 lead ECG , continuously monitor
patient, and analyze rhythm strips to track dysrhythmia.
 Control occurrence of effect of dysrhythmia, or both is often chieved with
antiarrhythmic medications.
 The nurse assess and observes for the benefits of and adverse effect of each
medication. The nurse in collaboration with physician, also manages
medication administration carefully so that a constant serum level of
medication is maintained.
 The nurse may also conduct a 6 minute walk test as prescribed, which is
used to identify pateint’s rate in response to exercise. The patient is asked to
walk for 6 minutes covering as much as possible.
 At the end the nurse records the distance covered and the pre-exercise heart
rate as well as patient’s response. The nurse for assesses for factors that
contribute to the dysrhythmia. The nurse also monitors for ECG and QT
interval, increased heart rate that increase risk of dysrhythmic event.

49.  Ineffective perfusion:
 Assess for signs of decreased signs of decreased tissue
perfusion. Particular clusters of signs and symptoms
occur with differing causes. Evaluation provides a
baseline for future comparison.
 Assess for probable contributing factors related to
temporarily impaired arterial blood flow. Some examples
include compartment syndrome, embolism, positioning ,
thrombus. Early detection of source facilities quick,
effective management.
 Review laboratory data like ABGs, BUN, creatinine,
prothombin time or partial thromboplastin time. Blood
coagulating studies used to conclude clotting factors
stay within therapeutic level.
 Check respirations and absence of work or breathing.
Cardiac pump malfunction and/or ischemic pain may
result in respiratory distress.
 Check rapid changes in shifts of mental status.
Electrolytes / acid –base variations and systemic emboli
influence cerebral perfusion. In addition, it is directly
related to cardiac output.

50.  Effective breathing pattern:
 Monitor patient closely for increasing respiratory distress
as indicated by tachycardia, dyspnea, cynosis, and
anxiety.
 Inspect trachea for deviation that may cause by
mediastinal shift.
 Check arterial blood gas result for hypoxemia low blood
oxygen and hypercapnia, high blood carbon diaoxide.
 After chest tube has been inserted, protect tube and
monitor function.
 Position patient for comfort in a fowler’s or semi-fowler’s
position.
 Avoid side-lying position until the affected lung has
reexpanded, because this position could foster
mediastinal shift,
 Administer oxygen as ordered.
 Support and encourage patient to do deep breathing
and coughing exercise.

51.  Minimizing anxiety:
 when patient experiences episodes of
dysrhythmias, the nurse stays with the patient and
provides assurance of safety and security while
maintaining a calm and reassuring attitude. This
assists in reducing anxiety and fosters a trusting
relationship’s with the patient.
 The nurse seeks patient’s view of events and
discusses emotional response to dysrhythmia,
encouraging verbalization of feelings and fears,
providing supportive and assisting patient
emphases and assisting patient torecognize
feelings of anxiety, fear, anger or sadness.
 The nurse emphasizes successes with the patient
to promote a sense of self-management.

52.  Improve knowledge about treatment:
 Render physical comfort for the patient. Based on maslow’s
theory, physiological needs must be addressed before the
patient education. Ensuring physical comfort allows patient to
concerntrate on what is being discussed or demonstrated.
 Grant a calm and peaceful environment without interruption. A
calm environment allows patient to concerntrate and focus
more completely.
 Provide an atmosphere of respect, openness, trust and
collaboration. Conveying respect is especially important when
providing education to patients with different values and
beliefs about health and illness.
 Include patient in creating teaching plan, beginning with
establishing objectives and goals for learning . it allows
learner to know what will be discussed and expected during
session. Adults tend to focus on here and now, problem
centered education.
 Explore reactions and feelings about changes. Assessment
assists nurse in understanding how learner may respond to
information and possibly how successful patient may
expected changes.

53.  Establish efficient fluid volume to prevent
hypovolemia:
 Oral fluid replacement is indicated for mild fluid deficit and is a cost-effective
method for replacement treatment. Being creative in selecting fluid sources can
facilitate fluid replacement. Oral hydrating solutions can be considered as
needed.
 Dehydrated patients may be weak and unable to meet prescribed intake
independently. Most elderly patients may have reduced sense of thirst and may
require continuing reminders to drink.
 Emphasize importance of oral hygiene. Fluid deficit can cause a dry, sticky
mouth, attention to mouth care promotes interest in drinking and reduces
discomfort of dry mucous membrane. Drop situations where patient can
experience overheating to prevent or treat hypovolemic complications.
 Fluids are necessary to maintain hydration status, determination of the type and
amount of fluid to be replaced and infusion rates will vary depending on clinical
status, blood transfusions may be required to correct fluid loss from active
gastro-intestinal bleeding.
 A central venous line allows fluids to be infused centrally and for monitoring of
CVP and fluid status. An arterial line allows for continuous monitoring BP. Fluid
losses from diarrhoea should be concomitantly treated with antidiarrheal
medications, as prescribed antipyretics can decrease fever and fluid losses from
diaphoresis,
 Patient needs to understand value of drinking extrafluid during bouts of
diarrhoea, fever and other conditions causing fluid deficits.
 An accurate measures of fluid intake and output is an important indicators
patient’s fluid status.

54.  Self care management:
 establish short term goals with patient, helping patient with
setting realistic goal will reduce frustration. Guideline patient in
accepting needed amount of dependence. Patient may require
help in determining safe limits of trying to be independence
versus asking for assistance when necessary.
 Present positive reinforcement for all activities attempted. Note
partial achievements, external resources of positive
reinforcement may promote ongoing efforts, patient often have
difficulty seeing progress.
 Render supervision for each activity until patient exhibits skill
effectively and is secured in independent care , re-evaluate
regularly to be certain that patient is keeping skill level and
remains safe in environment.
 Implement measures to promote independence, but intervene
when patient can not function. An appropriate level of assistive
care can prevent injury from activities without causing frustration
nurses can be key in helping patients accept both temporary and
permanent dependence.
 Boost maximum independence. The goal of rehabilitation is one
of achieving highest level of independence possible. Apply
regular routines, and allows adequate time for patient to
complete task. An edstablished routine becomes rote and
requires less effort. This helps patient in organize and carry out
self care skills.

55. POTENTIAL COMPLICATION:
 Cardiac failure
 Heart failure
 Thromboembolic event, especially with atrial
fibrillation

56. SUMMARY

57. THANK
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