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DYSRHYTHMIAS
Neelu Aryal
Lecturer
DEFINITION
• A normal sinus rhythm is the usual heart
rhythm that begins in the sinoatrial (SA) node,
is between 60 and 100 beats/min, and has
normal intervals and no aberrant or ectopic
beats.
• Dysrhythmias are disorders of the heart
rhythm.
• It is the disturbance in the electric cycle of the
heart.
• It is a disorder of the formation or conduction
(or both) of the electrical impulses within the
heart.
ETIOLOGY AND RISK FACTORS
• It results from the disturbances in three major
mechanisms:
1. Automaticity
2. Conduction
3. Reentry of impulses
1) DISTURBANCES IN AUTOMATICITY
RISK FACTORS
• Myocardial ischemia
• Decreased left ventricular function
• Valvular heart disease
• Electrolyte imbalance
• Hypoxia
• Digitalis toxicity
• Administration of atropine
2) DISTURBANCES IN CONDUCTION
RISK FACTORS
• Myocardial ischemia
• Valvular heart disease/ valvular surgery
• Inflammation of AV node
• Electrolyte imbalances
• Digitalis toxicity
• Beta blocking agents
• Myocardial infarction (especially inferior)
3) REENTRY OF IMPULSES
RISK FACTORS
• Myocardial ischemia
• Action of antidysrhythmic medications
• Myocardial fibrosis
• Bundle branch block
PATHOPHYSIOLOGY
• The significance of all dysrhythmias is their
effect on cardiac output and therefore
cerebral and vascular perfusion.
• CO=SV*HR
• During normal sinus rhythm
• The atria contract to fill and stretch the
ventricle with about 30% more blood.
• This process (atrial kick) increases the amount
of blood (SV) in the ventricles before
contractility
• This increases CO by 30%
NOTE: when the impulses originates below the
SA node or more than one area fires in the
atria to originate a beat (eg: atrial
fibrillation/atrial flutter)
Loss of atrial kick
CO falls (30%)
CLINICAL MANIFESTATIONS
The reduced CO leads to:
• Palpitations
• Dizziness
• Presyncope/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
DIAGNOSTIC ASSESSMENT
1) History: regarding onset, duration, associated
manifestations, aggravating factors and
relieving factors.
2) Past medical history including CVD risk
factors analysis.
3) Past health history and hospitalization
4) Surgical history, allergy, medications, dietary
habits, social habits (tobacco, alcohol) and
family history
5) Physical examination
• Auscultation of heart for abnormal heart
tones, slow or fast rate, irregularity, murmur
6) ECG
7) Holter monitors
• Continuously record cardiac rhythm for 24
hours
8) Event monitors
• For those clients who do not experience
dysrhythmia within 24 hours period of
recording, event monitors are available
9) Invasive Electrophysiologic Studies
• It involves the positioning of a multipolar
catheter electrode into the venous system,
placing the electrode at various sites along the
atria, ventricles, His bundles, bundle branches,
accessory pathways and other structures to
record electrical activity
TYPES OF DYSRHYTHMIAS
A) Rhythms originating in sinoatrial (SA) node
• Sinus bradycardia
• Sinus tachycardia
• Sinus arrest
B) Rhythm originating in Atria
• Atrial flutter
• Atrial fibrillation
• Paroxysmal supraventricular tachycardia
• Premature atrial contraction
C) Rhythm originating in the atrioventricular
junction
• Premature junctional complex
• Junctional escape rhythm
• Junctional tachycardia
D) Rhythm originating in ventricles
• Premature ventricular contraction
• Ventricular fibrillation
• Ventricular tachycardia
A) RHYTHMS ORIGINATING IN SINOATRIAL (SA)
NODE
1) SINUS BRADYCARDIA
• A heart rhythm is initiated in the sinoatrial
node at a rate of less than 60 beats per
minute
 TREATMENT
• Atropine (an anticholinergic drug)
• Pacemaker therapy
2) SINUS TACHYCARDIA
• A heart rhythm is initiated in the sinoatrial node
at a rate greater than 100 beats per minute
TREATMENT
• It is based on underlying causes
• Treating hypovolemia should resolve any
associated tachycardia.
• In certain situations adenosine and beta-
adrenergic blockers used to decrease the heart
rate
3) SINUS ARREST
• Sinus node automaticity is decreased and impulse
are not formed when expected. This result in the
absence of P wave, the QRS complex and no
electrical activity for 3 seconds
TREATMENT
• Atropine, 0.5 to 1 mg IV, may increase the rate.
• Pacemaker therapy
B) RHYTHMS ORIGINATING IN ATRIA
1) ATRIAL FLUTTER
• It is single atrial ectopic focus firing at a rate
of 250 to 350 beats per minute resulting in a
ventricular response that is slower, usually a
multiple of the atrial rate
• P wave are replaced by flutter waves that
take on a “sawtooth appearance.”
TREATMENT
• Calcium channel blocker
• Beta adrenergic blockers
• Cardioversion
2) ATRIAL FIBRILLATION
• It is an abnormal rhythm originating from a
multiple ectopic focus in the atrium.
• It is the disorganized twitching of the atria at a
rate greater than 350 beats per minutes.
TREATMENT
• Calcium channel blocker (eg: diltiazem)
• Beta adrenergic blockers (eg: metoprolol)
• Digoxin
• Amiodarone
• cardioversion
3) PAROXYSMAL SUPRAVENTRICULAR
TACHYCARDIA
• It is a dysrhythmia originating in an ectopic
focus anywhere above the bifurcation of the
bundle of His.
TREATMENT
• Beta adrenergic blockers
C) RHYTHMS ORIGINATING IN THE
ATRIOVENTRICULAR JUNCTION
1) PREMATURE JUNCTIONAL COMPLEX
• It occurs when an ectopic beat originates
from a site in the atrioventricular junction
outside of the normal cardiac cycle.
 TREATMENT
• No treatment necessary
2) JUNCTIONAL ESCAPE RHYTHM
• It occurs when the atrial rate is slow, usually
less than 30 beats per minute, and the
atrioventricular node assumes responsibilty
for pacing the heart at a rate of 35 to 60 beats
per minute.
3) JUNCTIONAL TACHYCARDIA
• It occurs when the atrioventricular node
becomes irritable and “overrides” the sinus
impulses, becoming the primary pacemaker at
a rate of greater than 60 beats per minutes.
TREATMENT
• If a patient has symptoms with an escape
junctional rhythm atropine can be used.
• In accelerated junctional rhythm and junctional
tachycardia
Beta adrenergic blockers
Calcium channel blockers
Amiodarone are used for rate control
• Cardioversion should not be used
D) RHYTHMS ORIGINATING IN VENTRICLES
1) PREMATURE VENTRICULAR CONTRACTIONS
• It is an ectopic beat originating from a site in
the ventricles outside of the normal cardiac
cycle.
TREATMENT
• Beta adrenergic blockers
• Procainamide
• Amiodarone or lidocaine
2) VENTRICULAR FIBRILLATION
• If a premature ventricular contraction falls on
a T wave, it may precipitate ventricular
fibrillation.
TREATMENT
Immediate initiation of CPR and advanced
cardiac life support measures with the use of
the defibrillation and definite drug therapy
3) VENTRICULAR TACHYCARDIA
• It occurs when there are three or more
consecutive premature ventricular
contractions.
TREATMENT
• Hemodynamically stable ventricular
tachycardia (with pulse) : Amiodarone,
Lidocaine
• Hemodynamically unstable ventricular
tachycardia (with pulse): cardioversion
• Pulseless ventricular tachycardia: defibrillation
THANK YOU

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Dysrhythmias

  • 2. DEFINITION • A normal sinus rhythm is the usual heart rhythm that begins in the sinoatrial (SA) node, is between 60 and 100 beats/min, and has normal intervals and no aberrant or ectopic beats. • Dysrhythmias are disorders of the heart rhythm.
  • 3. • It is the disturbance in the electric cycle of the heart. • It is a disorder of the formation or conduction (or both) of the electrical impulses within the heart.
  • 4. ETIOLOGY AND RISK FACTORS • It results from the disturbances in three major mechanisms: 1. Automaticity 2. Conduction 3. Reentry of impulses
  • 5. 1) DISTURBANCES IN AUTOMATICITY RISK FACTORS • Myocardial ischemia • Decreased left ventricular function • Valvular heart disease • Electrolyte imbalance • Hypoxia • Digitalis toxicity • Administration of atropine
  • 6. 2) DISTURBANCES IN CONDUCTION RISK FACTORS • Myocardial ischemia • Valvular heart disease/ valvular surgery • Inflammation of AV node • Electrolyte imbalances • Digitalis toxicity • Beta blocking agents • Myocardial infarction (especially inferior)
  • 7. 3) REENTRY OF IMPULSES RISK FACTORS • Myocardial ischemia • Action of antidysrhythmic medications • Myocardial fibrosis • Bundle branch block
  • 8. PATHOPHYSIOLOGY • The significance of all dysrhythmias is their effect on cardiac output and therefore cerebral and vascular perfusion. • CO=SV*HR
  • 9. • During normal sinus rhythm • The atria contract to fill and stretch the ventricle with about 30% more blood. • This process (atrial kick) increases the amount of blood (SV) in the ventricles before contractility
  • 10. • This increases CO by 30% NOTE: when the impulses originates below the SA node or more than one area fires in the atria to originate a beat (eg: atrial fibrillation/atrial flutter)
  • 11. Loss of atrial kick CO falls (30%)
  • 12. CLINICAL MANIFESTATIONS The reduced CO leads to: • Palpitations • Dizziness • Presyncope/syncope • Pallor • Diaphoresis • Altered mentation (restlessness and agitation to lethargy and coma)
  • 13. • Shortness of breath • Chest pain • Orthopnea • Paroxysmal nocturnal dyspnea • Hypotension • Sluggish capillary refill • Swelling of the extremities • Decreased urine output
  • 14. DIAGNOSTIC ASSESSMENT 1) History: regarding onset, duration, associated manifestations, aggravating factors and relieving factors. 2) Past medical history including CVD risk factors analysis. 3) Past health history and hospitalization 4) Surgical history, allergy, medications, dietary habits, social habits (tobacco, alcohol) and family history
  • 15. 5) Physical examination • Auscultation of heart for abnormal heart tones, slow or fast rate, irregularity, murmur 6) ECG 7) Holter monitors • Continuously record cardiac rhythm for 24 hours
  • 16. 8) Event monitors • For those clients who do not experience dysrhythmia within 24 hours period of recording, event monitors are available
  • 17. 9) Invasive Electrophysiologic Studies • It involves the positioning of a multipolar catheter electrode into the venous system, placing the electrode at various sites along the atria, ventricles, His bundles, bundle branches, accessory pathways and other structures to record electrical activity
  • 18. TYPES OF DYSRHYTHMIAS A) Rhythms originating in sinoatrial (SA) node • Sinus bradycardia • Sinus tachycardia • Sinus arrest
  • 19. B) Rhythm originating in Atria • Atrial flutter • Atrial fibrillation • Paroxysmal supraventricular tachycardia • Premature atrial contraction
  • 20. C) Rhythm originating in the atrioventricular junction • Premature junctional complex • Junctional escape rhythm • Junctional tachycardia
  • 21. D) Rhythm originating in ventricles • Premature ventricular contraction • Ventricular fibrillation • Ventricular tachycardia
  • 22. A) RHYTHMS ORIGINATING IN SINOATRIAL (SA) NODE
  • 23. 1) SINUS BRADYCARDIA • A heart rhythm is initiated in the sinoatrial node at a rate of less than 60 beats per minute  TREATMENT • Atropine (an anticholinergic drug) • Pacemaker therapy
  • 24.
  • 25. 2) SINUS TACHYCARDIA • A heart rhythm is initiated in the sinoatrial node at a rate greater than 100 beats per minute TREATMENT • It is based on underlying causes • Treating hypovolemia should resolve any associated tachycardia. • In certain situations adenosine and beta- adrenergic blockers used to decrease the heart rate
  • 26.
  • 27. 3) SINUS ARREST • Sinus node automaticity is decreased and impulse are not formed when expected. This result in the absence of P wave, the QRS complex and no electrical activity for 3 seconds TREATMENT • Atropine, 0.5 to 1 mg IV, may increase the rate. • Pacemaker therapy
  • 28.
  • 30. 1) ATRIAL FLUTTER • It is single atrial ectopic focus firing at a rate of 250 to 350 beats per minute resulting in a ventricular response that is slower, usually a multiple of the atrial rate • P wave are replaced by flutter waves that take on a “sawtooth appearance.”
  • 31.
  • 32. TREATMENT • Calcium channel blocker • Beta adrenergic blockers • Cardioversion
  • 33. 2) ATRIAL FIBRILLATION • It is an abnormal rhythm originating from a multiple ectopic focus in the atrium. • It is the disorganized twitching of the atria at a rate greater than 350 beats per minutes.
  • 34.
  • 35. TREATMENT • Calcium channel blocker (eg: diltiazem) • Beta adrenergic blockers (eg: metoprolol) • Digoxin • Amiodarone • cardioversion
  • 36. 3) PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA • It is a dysrhythmia originating in an ectopic focus anywhere above the bifurcation of the bundle of His.
  • 37.
  • 39. C) RHYTHMS ORIGINATING IN THE ATRIOVENTRICULAR JUNCTION
  • 40. 1) PREMATURE JUNCTIONAL COMPLEX • It occurs when an ectopic beat originates from a site in the atrioventricular junction outside of the normal cardiac cycle.  TREATMENT • No treatment necessary
  • 41.
  • 42. 2) JUNCTIONAL ESCAPE RHYTHM • It occurs when the atrial rate is slow, usually less than 30 beats per minute, and the atrioventricular node assumes responsibilty for pacing the heart at a rate of 35 to 60 beats per minute.
  • 43.
  • 44. 3) JUNCTIONAL TACHYCARDIA • It occurs when the atrioventricular node becomes irritable and “overrides” the sinus impulses, becoming the primary pacemaker at a rate of greater than 60 beats per minutes.
  • 45.
  • 46. TREATMENT • If a patient has symptoms with an escape junctional rhythm atropine can be used. • In accelerated junctional rhythm and junctional tachycardia Beta adrenergic blockers Calcium channel blockers Amiodarone are used for rate control • Cardioversion should not be used
  • 47. D) RHYTHMS ORIGINATING IN VENTRICLES
  • 48. 1) PREMATURE VENTRICULAR CONTRACTIONS • It is an ectopic beat originating from a site in the ventricles outside of the normal cardiac cycle.
  • 49.
  • 50. TREATMENT • Beta adrenergic blockers • Procainamide • Amiodarone or lidocaine
  • 51. 2) VENTRICULAR FIBRILLATION • If a premature ventricular contraction falls on a T wave, it may precipitate ventricular fibrillation. TREATMENT Immediate initiation of CPR and advanced cardiac life support measures with the use of the defibrillation and definite drug therapy
  • 52.
  • 53. 3) VENTRICULAR TACHYCARDIA • It occurs when there are three or more consecutive premature ventricular contractions.
  • 54. TREATMENT • Hemodynamically stable ventricular tachycardia (with pulse) : Amiodarone, Lidocaine • Hemodynamically unstable ventricular tachycardia (with pulse): cardioversion • Pulseless ventricular tachycardia: defibrillation