A cardiac dysrhythmia (also called an arrhythmia) is an abnormal rhythm of your heartbeat. It can be slower or faster than a normal heart rate. It can also be irregular. It can be life-threatening if the heart cannot pump enough oxygen-rich blood to the heart itself or the rest of the body.

1. AV DYSRRYTHMIAS
PREPARED BY: SAMBAD JAGDISH
M.Sc.Nursing –MSN
Assistant Professor
Balaji College of Nursing

2. THE CONDUCTION
SYSTEM OF HEART
• Through 2-d Model

3. THE NORMAL SINUS
RYTHM
 Through Flash Card

5. CHARACTERISTICS OF
NORMAL SINUS RYTHM
CHARACTERISTICS OF SINUS RYTHM
P wave Regular, P-P intervals and R-R intervals may
vary as much as 3mm and still be considered
regular.
Rate 60-100 beats/min
P waves One P wave preceding each QRS complex
P-R interval 0.12-0.20 sec, consistent with each complex
QRS complex 0.04-0.10 sec, consistent with each complex
Q-T interval <0.40 seconds

6. • Dysrythmias are the disorders of heart rhythm.
dysrythmias are common in people with cardiac disorders
but also occur in people with normal hearts.
•Dysrythmias are often detected because of associated
manifestations of dizziness, palpitations, and syncope.
•These can cause reduced cardiac output, which can lead
to impaired cerebral perfusion.
•Most serious complication of a dysrythmia is sudden
death.
DYSRYTHMIA INTRODUCTION

7. DEFINITION
 Cardiac dysrythmia is a group of
conditions in which the electrical activity
of the heart is irregular or is faster or
slower than normal.
 An abnormal rhythm, especially a
disordered rhythm exhibited in a record of
electrical activity of the heart.

8. JUNCTIONAL RYTHM
 It describes an abnormal heart rhythm resulting from
impulses coming from a locus of tissue in the area of
the atrioventricular node.
CHARACTERISTICS:
 HEART RATE: 40-60 bpm
 RHYTHM: regular
 P WAVE: inverted, absent or after QRS.
 PR interval: <0.12 seconds
 QRS: <0.12 seconds

9. JUNCTIONAL RHYTHM
ECG

10. JUNCTIONAL RYTHM

11. JUNCTIONAL RYTHM

12. CAUSES
 Hypokalemia
 MI
 Cardiac surgery
 Digitalis toxicity
 Sinus node dysfunction
 Ablation for AV node reentrant tachycardia

13. MANAGEMENT
 Treatment to junctional rhythm is not necessary,
but treating underlying cause is essential.
 Discontinuation of offending medications that
slow sinus rate.
 Permanent pacemaker implantation
 For chronic symptomatic junctional rhythm
associated with sinus node dysfunction, ablation
of junctional focus may be considered with risk
of creating AV block.

14. VENTRICULAR
DYSRYTHMIAS
 Ventricular dysrythmias arise below the level of AV
junction and are caused by abnormality of
automaticity or conduction.
 Ventricular dysrythmias are more serious and life
threatening Than atrial or junctional arrythmias
because ventricular dysrythmias develop commonly
in association with intrinsic heart disease.
 They cause greater hemodynamic
compromise(hypotension, heart failure, shock).

15. DISTURBANCES IN
AUTOMATICITY
 Dysrythmias resulting from problems in
automaticity are characterized by ectopic
impulses, which result from either myocardial
irritability or the phenomenon of re-entry.
 Ventricular dysrythmias caused by problems
with automaticity are premature ventricular
contractions (PVCs), ventricular tachycardia
(VT), and Torsades de Pointes.

16. 1) PREMATURE
VENTRICULAR
CONTRACTIONS:
PVCs are the most common of all dysrythmias other
than those of the sinus node. They are usually caused by
the firing of an irritable pacemaker in the ventricles and
results from enhanced ventricular automaticity or re-
entry. The T wave is commonly large and in the
opposite direction of the QRS deflection.

17. CONTINUE…
PVC have the ventricular contractions have the
following characteristics:
Rate : 60 to 100 beats per minute.
P waves: will not be present because the impulses
originate in the ventricles.
QRS Complex: usually wide and bizarre. Usually
longer than 0.10 seconds in duration. May have the
same focus in the ventricle, or may have a wide
variety of configurations if occurring from multiple
foci in the ventricles.
Conduction: occasionally retrograde through the
junctional tissue and atria.
Rhythm: irregular when the premature beat occurs.

20. CAUSES OF PVC
 Myocardial hypoxia
 Hypokalemia
 Hypocalcemia
 Acidosis
 Alcohol
 Caffeine
 Hypermetabolic states
 Intracardiac catheters
Nicotine
Coronary artery
disease
Heart failure
Toxic agents (eg.
Digitalis, tricyclic
antidepressants)
Exercise

21. MANAGEMENT OF PVC
 lidocaine or any of the other class I, II, III
antidysrythmics can be given to treat PVC.
Intravenous magnesium can also be useful.
 The treatment with beta blockers helps to suppress
PVCs alongwith restoring myocardial blood flow.
 In ischemia, PVCs can progress to VT or
ventricular fibrillation quickly, so prompt attention
and treatment is needed.

22. MANAGEMENT OF PVC
 Suppress irritable foci
 Management of dangerous PVC involves the
administration of antidysrythmic agents that have
myocardial depressant actions.
 Improve myocardial oxygenation
 Oxygen administration is vital to all patient at
risk of ventricular dysrythmias such as those
with chest pain or hypoxemia or during cardiac
arrest.

23. 2) VENTRICULAR
TACHYCARDIA
 Ventricular tachycardia is a life threatening
dysrythmia that occurs when an irritable ectopic
focus in the ventricles takes over as the pacemaker. It
occurs in the presence of significant cardiac disease,
such as in clients with CAD, cardiomyopathy, mitral
valve prolapse, heart failure, acute MI with hypoxia
and acidosis, and digitalis toxicity.
 Ventricular tachycardia is characterized by a rapidly
occurring series of PVCs (three or more) with no
normal beats in between. VT can be polymorphic or
monomorphic.

24. Accelerated ventricular rhythm and ventricular
tachycardia have the following characteristics:
 Rate: 150-200 beats per minute
 P waves: usually buried in the QRS complex, if seen they do not
fall necessarily in the normal pattern with the QRS. The
ventricular contractions are dissociated from the atrial
contractions.
 QRS complex: have the same configurations as those of a PVC-
wide and bizarre, with T waves in the opposite direction
 Conduction: originates in the ventricle, with possible retrograde
conduction to the junctional tissue and atria.
 Rhythm: usually regular, but irregular ventricular tachycardia is
also seen.

25. VENTRICULAR
TACHYCARDIA
(monomorphic)

26. VT (polymorphic)

27. MANAGEMENT OF
VENTRICULAR
TACHYCARDIA
Antidysrythmics
Cardioversion may be required for conversion to
sinus rhythm.
When the client is in VT and unconscious ,
defibrillation is indicated.
 Precordial thump or thumpversion.
Implantation of an automatic internal
cardiodefibrillator by an electrophysiologist.

28. 3) TORSADES DE
POINTES
 It is a form of VT in which the QRS complexes appear
to be constantly changing or twisting around an
isoeletric line. Delayed repolarization of the ventricle
is revealed as a prolonged Q-T interval and a broad flat
T wave in the preceding sinus rhythm. The rhythm is
regular or irregular with a ventricular rate of 150-250
beats/min. the QRS complex is wide and bizarre. It
occurs as a result of drug toxicity or imbalances
(hpokalemia, hypomagnesemia), which can lengthen
the Q-T interval. Clinical manifestations begin with
palpitations and syncope. This rhythm often precedes
ventricular fibrillation and sudden death.

29. TORSADES SE POINTES

32. MANAGEMENTOF
TORSADES DE POINTES:
 Torsades de pointes is treated only if the Q-T
interval is prolonged. Intravenous magnesium is
the initial treatment of choice, along with
intravenous potassium if indicated, followed by
temporary ventricular or atrial pacing.
Discontinuation of offending agents is also
crucial.

33. REENTRY OF IMPULSES
 Two rhythms occur in the ventricles as a
result of the re-entry phenomenon:
ventricular fibrillation and pre-exitation
syndromes. The usual pathway through the
ventricles is not used and the wave of
depolarization must spread from cell to
cell. As a result the complex is wide and
prolonged

34. 1)VENTRICULAR
FIBRILLATION:
 It is a life threatening dysrythmia characterized by extremely
rapid, erratic impulse formation and conduction. Ventricular
fibrillation leads to inadequate myocardial contractions. The
heart consequently immediately loses its ability to function as a
pump. As the initial re-entry pattern of excitation breaks up into
smaller wavelets, the level of disorganization increases. Sudden
loss of cardiac output with subsequent tissue hypoperfusion
creates global tissue ischemia, brain and myocardium are most
susceptible. VF is the primary cause of sudden cardiac death
(SCD). This lethal dysrythmia usually results from severe
myocardial damage (such as MI), hypothermia, R on T
phenomenon, hypoxia, contact with high voltage
electricity,electrolyte imbalance, antidysrythmic drug side effect,
or toxicity from quinidine, procainamide or digitalis .

35. CONTINUE….
 Ventricular fibrillation has the following characteristics:
 P waves: not seen
 QRS complex: rapid, irregular undulation without any specific
pattern (multifocal). The ventricles have only a quivering
motion.
 Conduction: foci are located in the ventricles, but so many foci
are firing at one time that there is no organized conduction, no
ventricular contractions occur.
 Rhythm: extremely irregular and uncoordinated, without
specific pattern.
 Immediate treatment is defibrillation.

36. VENTRICULAR
FIBRILLATION ECG

38. MANAGEMENT OF
VENTRICULAR
FIBRILLATION
 When VF appears, the clinician must immediately
initiate CPR until the defibrillator is engaged.
Defibrillation along with CPR is the treatment for
VF. Medications such as lidocaine, magnesium
sulphate, sodium bicarbonate can be used depending
on clients cardiac rhythm and electrolyte and acid
base balance.

39. 2) PRE-EXCITATION
SYNDROMES:
 Preexcitation of ventricles is caused by a
structural defect with the heart. The ventricles
are depolarized earlier than normal because
conduction has not been slowed by the AV
node. It describes the presence of an additional
accessory pathway which bypasses the normal
conduction route. Most common is the wolff
parkinson syndrome (WPW), in which the
accessory pathway is called the bundle of kent.

40. Three basic ECG abnormalities are seen as a result
of the pre-exictation syndromes:
 1) P-R interval less than 120 miliseconds during sinus
rhythm
 2) a QRS complex duration exceeding 120 milliseconds
with a slurred, slowly rising QRS complex (delta
wave)with the remainder of the QRS complex being
normal
 3) secondary ST segment and T wave changes that are
usually directed in the opposite direction of the delta
wave and QRS complex vectors.

41. WPW SYNDROME ECG

42. MANAGEMENT:
 Clients do not require intervention unless
tachydysrythmias occur persistently. Physician
may elect to use vagotonic manoeuvres,
cardioversion, adenosine, propanolol and
amiodarone can affect both the AV node and
the accessory pathway. Electrophysiologic
evaluation is recommended for appropriate
drug therapy and possible accessory pathway
radiofrequency ablation.

43. DISTURBANCES IN CONDUCTION
1) VENTRICULAR ASYSTOLE
 Ventricular asystole or cardiac standstill represents
the total absence of ventricular electrical activity.
Client has no palpable pulse and a rhythm is absent
if client is monitored. In a conscious patient this
causes dizziness, loss of consciousness within
seconds, seizures and apnea. If not treated it causes
death.
 It can occur as a primary event or may follow VF or
PEA, can occur in complete heart block in whom
there is no escape pacemaker.

44. VENTRICULAR ASYSTOLE
ECG

46. CAUSES:
 Hypoxia
 Hyperkalemia and hypokalemia
 Pre-existing acidosis
 Drug overdose
 Hypothermia

47.  The treatment of choice consists of CPR,
epinephrine, atropine, trancutaneous
pacing and correction of cause.
MANAGEMENT

48. 2) PULSELESS
ELECTRICALACTVITY
(PEA)
 PEA represents the presence of electrical
activity in the heart, as seen on monitor
however a pulse cannot be detected by
palpation of any artery. Thus the ventricles fail
to produce an effective contraction despite
continued electrical activity.

49. PEA ECG

50. Causes
 End stage cardiac disease
 Cardiac tamponade
 Massive pulmonary embolism
 Tension pneumothorax
 Severe hypovolemia
 Prolonged cardiac resuscitation
 Exsanguination
 Acute malfunction of a prosthetic valve

51. MANAGEMENT
 Rapid searching for cause is imperative. Until the
cause is located, CPR is initiated in conjunction with
advanced cardiac life support measures

52. 3) SUDDEN
CARDIAC DEATH
 It is defined as death resulting from an
abrupt loss of heart function (cardiac
arrest). The victim may or may not have
known the heart disease. The time and
mode of death are unexpected, and death
occurs within minutes after manifestations
appear.

53. MANAGEMENT
 Sudden cardiac arrest requires immediate
action for survival. Immediate
cardiopulmonary resuscitation is critical to
treating sudden cardiac arrest. By
maintaining a flow of oxygen rich blood to
the body’s vital organs, CPR can provide a
vital link until more advanced emergency
care is available.

54. NURSING MANAGEMENT
 Assessment: causes of dysrrythmia,
contributing factors, and dysrythmias effect
on the heart’s ability to pump an adequate
blood volume.
 Detailed health history of the patient,
medications taken by the patient, signs and
symptoms, laboratory investigations, physical
assessment.

55. NURSING DIAGNOSIS
 Through leaflet

57. ASSIGNMENT
 Write a detailed nursing care plan on AV nodal and
ventricular dysrythmia.
 Submission date: 20/02/2018
 REFERENCES:
1. Black Joyce M., Hawks Jane Hokanson.
Medical surgical nursing.
2. Brunner and Suddharth’s, “Textbook Of
Medical Surgical Nursing.
3. Chintamani lewi’s. Medical surgical nursing.