CARDIOVASCULAR SYSTEM:
PATHOPHYSIOLOGY:
GROUP 8
DYSRHYTHMIAS:
MEMBERS:
 Joshua Atandi
 Kelvin Subati
 Lilian Kyule
 Faith Mwende
 Ann Mwatha
 Juliet Ongachi
 Dennis Bomett
 Bramwel Kipkoskei
 Jawa Joseph
 Mercy Ngugi
 Faith Chebet
ANATOMY
 Blood Flow through heart :
Superior and Inferior Vena Cava – Right Atrium – Right
Ventricle – Pulmonary Artery – Lungs – Pulmonary
Vein – Left Atrium – Left Ventricle – Aorta – Body.
 Chambers of the heart:
Right and Left Atrium, Right and Left Ventricles.
The ventricles have a thicker myocardial layer and
constitutes much of the bulk of the heart.
Septal membranes separates the right and left sides
of the heart and prevents blood from crossing over.
 Conduction System – The heart has a conduction
system separate from any other system.
– The conduction system makes
up the PQRST complex we see on
paper.
– An arrhythmia is a disruption of
the conduction system.
 Understanding how the heart conducts
normally is essential in understanding and
identifying arrhythmias.
 Normal heart rhythms are generated by the
Sino atrial (SA) node and travels through
the heart’s conduction system causing the
atrial and ventricular myocardium to
contract and relax at a regular rate that is
appropriate to maintain circulations at
various levels of physical activity.
CONDUCTION SYSTEM
 SA Node
 Inter-nodal and inter-atrial pathways
 A-V Node
 Bundle of His
 Purkinje Fibers
SA Node
 The primary pacemaker of the heart.
 Each normal beat is initiated by the SA node. The
atria and ventricles then depolarize sequentially as
electrical depolarization passes through specialized
conducting tissues. The sinus node acts as a
pacemaker and its intrinsic rate is regulated by the
autonomic nervous system; vagal activity slows the
heart rate, and sympathetic activity accelerates it via
cardiac sympathetic nerves and circulating
catecholamines.
 Inherent rate of 60-100 beats per minute.
 Represents the P-wave in the QRS complex or atrial
depolarization (firing).
 If the sinus rate becomes unduly slow, a lower
centre may assume the role of pacemaker. This
is known as an escape rhythm and may arise in
the AV node (nodal rhythm) or the ventricles
(idioventricular rhythm).
AV Node
 Located in the septum of the heart.
 Receives impulse from inter-nodal pathways and
holds the signal before sending on to the Bundle
of His.
 Represents the PR segment of the QRS complex
AV Node
 Represents the PR segment of the cardiac cycle.
 Has an inherent rate of 40-60 beats per minute.
 Acts as a back up when the SA node fails.
 Where all junctional rhythms originate
QRS Complex
 Represents the ventricles depolarizing (firing)
collectively. (Bundle of His and Purkinje fibers).
 Origin of all ventricular rhythms.
 Has an inherent rate of 20-40 beats per minute
NORMAL
ELECTROCARDIOGRAM:
 Isoelectric line (baseline).
 P-wave – Atria firing.
 PR interval – Delay at AV.
 QRS – Ventricles firing.
 T-Wave – Ventricles repolarizing.
 ST segment
– Ventricle contracting.
– Should be at isoelectric line.
– Elevation or depression may be important.
• U wave
– Purkinje fiber repolarization.
 Normal:
– Heart rate = 60 – 100 bpm
– PR interval = 0.12 – 0.20 sec
– QRS interval <0.12
– SA Node discharge = 60 – 100 / min
– AV Node discharge = 40 – 60 min
– Ventricular Tissue discharge = 20 – 40 min
Cardiac cycle
 P wave = atrial depolarization
 PR interval = pause between atrial and ventricular
depolarization
 QRS = ventricular depolarization
 T wave = ventricular depolarization
DEFINATION
 Cardiac Arrhythmia is a condition in which the heart
beats with an irregular or abnormal rhythm.
 It is a disturbance of the heart rhythm.
 Dysrhythmias range in severity from occasional or
rapid beats to serious disturbances that impair the
pumping ability of the heart, contributing to heart
failure and death.
ABNORMAL RHYTHM
CAN BE OF TWO EXTREME FORMS
1. Bradycardia - Cardiac beats below 60 beats per
minute .
2. Tachycardia – Cardiac beat above 100 beats per
minute.
Mechanisms of Cardiac Arrhythmias
 Result from disorders of impulse formation,
conduction, or both.
 Dysrhythmias can be caused by either an
abnormal rate of impulse generation by the SA
node or other pacemaker or the abnormal
condition of impulses through the heart’s
conduction system, including the myocardial cells
themselves. The disturbances appear to disrupt
the normal sequence of atrial and ventricular
activation.
ETIOLOGY
 Coronary artery disease.
 Electrolyte imbalances in your blood (such as sodium or
potassium).Hyperkalemia/hypokalemia
 Changes in your heart muscle.
 Injury from a heart attack.
 Irregular heart rhythms can also occur in "normal,
healthy" hearts.
 Healing process after heart surgery.
Causes of arrhythmias
 Cardiac ischemia. Ischemic Heart Disease
 Chronic obstructive pulmonary disease(COPD).
 Thyroid disorders
 Excessive discharge or sensitivity to autonomic
transmitters
 Exposure to toxic substances. Drugs related.
 Unknown etiology
Disorders of impulse formation
 No signal from the pacemaker site.
 Development of an ectopic pacemaker:
◦ May arise from conduction cells (most are
capable of spontaneous activity).
◦ Usually under control of SA node if it
slows down too much conduction cells could
become dominant.
◦ Often a result of other injury (ischemia,
hypoxia).
Disorders of impulse conduction
 Development of oscillatory afterdepolariztions: ◦ Can
initiate spontaneous activity in nonpacemaker tissue.
◦ May be result of drugs (digitalis,
norepinephrine) used to treat other cardiopathologies.
 May result in:
◦ Bradycardia:
1. SA node : Slowed / Absent.
 Causes -Decreased Sympathetic Signals: reduced
automaticity (e.g. sinus bradycardia)
-Increased Parasympathetic Signals
-SA node Damage
2. Blockage of Conduction from SA node:
 AV node Blockage
 Causes -Ischemia
-Fibrosis
-Viral Infection
RESULTS in HEART ATTACK
 LEFT BUNDLE BRUNCH BLOCK (LBBB)
 No Impulse conduction through Bundle Brunch.
 Action Potential transferred through Right Ventricle
to Left Ventricle.
 RESULTS in Wide QRS complex
◦ Tachycardia:
1. Increased Pacemaker Activity (SA Node)-Sinus
Tachycardia. There is increased automaticity-the tachycardia
is produced by repeated spontaneous depolarization of an
ectopic focus, often in response to catecholamines.
 Causes -Increased Sympathetic Signals.
-Decreased Parasympathetic Signals.
-SA node Dysfunction.
Example : Sick Sinus Syndrome.
2. Re-entry Tachycardias:
Tachycardia is initiated by an ectopic beat and sustained by
a re-entry circuit. Most tachyarrhythmias are due to re-entry.
These include:
 Atrial Fibrillation:
- loss of the normal organized propagation of electrical
activity .
- atria fibrillate, they no longer contract in a mechanically
useful way.
- a degree of stasis to blood flow and predisposing to clot
(thrombus) formation within the chambers.
 Ventricular Fibrillation:
- Uncoordinated contraction of the Cardiac Muscle.
- Quiver rather than contract properly.
Commonly identified arrhythmia in Cardiac Arrest patients.
As a consequence, Sudden Cardiac Death.
 Wolf Parkinson White Syndrome (WPW):
-WPW is caused by the presence of an abnormal
accessory electrical conduction pathway btn the atria and
the ventricles.
-Electrical Signals through abnormal pathway stimulate the
ventricles to contract prematurely.
Its a unique type of supraventricular tachycardia
referred to as an “atrioventricular reciprocating
tachycardia.”
3. Delayed Repolarization:
 Causes include: - Ischemia.
-Drugs related (Potassium Blockers).
- Electrolyte Imbalance.
 Its effects include:-Long QT interval
-R on T Phenomenon.
-Premature Ventricular Beat.
-Ventricular Fibrillation.
PATHOPHYSIOLOGY
Inadequate acceleration of sinus rate
Failure of sinus impulse formation
Abrupt sinus prolonged pause MI, HT, Coronary spasm
SA node dysfunction Aortic & mitral valve stenosis
AV conduction block Degeneration or damage of
the conduction system
Atrial dysfunction
Ventricular dysfunction
CARDIAC
ARRYTHMIA
Arrhythmia Presentation
(SYMPTOMS)
 Palpitations.
 Dizziness.
 Chest Pain.
 Dyspnea.
 Anxiety and confusion(reduced blood perfusion)
 Fainting.
 Sudden cardiac death
 Swelling
 Shortness of Breath
 Exercise Intolerance
 Can trigger heart failure or even sudden death.
SINUS NODE ARRHYTHMIAS
Sinus Tachycardia:
 Rapid heart rate.
 Rate is greater than 100 beats per minute (Usually
between 100-160 ).
 Is a normal response during fever and exercise and
in situations that incite sympathetic stimulation.
CAUSES:
-Cardiac conditions i.e heart failure
-Hyperthyroidsm
- Medications such as epinephrine.
- Myocardial infarction
- Other causes are Anemia, Respiratory distress,
pulmonary embolism, sepsis.
Sinus Bradycardia:
 Slow heart rate, Regular rhythm
 Rate less than 60 beats per minute
 SA node firing slower than normal
 P wave precedes QRS
Indications include poor prognosis.
Pathophysiology:
It’s a normal response to a reduced demand for blood
flow.
 Vagal stimulation increases
 Sympathetic stimulation decreases.
 Decreased movement of impulse from S.A node.
 Automacity of S.A node diminishes.
 Decrease in conduction to the A.V node causes
reduced heart failure.
 CAUSES:
- Non-cardiac disorders
- Conditions producing excess vagal stimulation or
decreased sympathetic stimulation
- Cardiac diseases
- Certain drugs
MANIFESTATIONS:
- Hypotension - Altered mental status
- Cool, clammy skin - Dizziness
- Blurred vision -Crackles, dyspnea
- Chest pain -Syncope
Sinus Arrest: Sinus Pause
(Stop of sinus rhythm, New rhythm starts).
 Failure of SA Node to discharge and results in an
irregular pulse. Sinus node doesn’t fire.
 An escape rhythm develops. Another pace maker takes
over.
CAUSES: -Disease of S.A Node
- Digitalis toxicity
-Myocardial infarction.
- Excessive vagal tone.
-Hyperkalemia
Sick Sinus Syndrome:
 Sick sinus syndrome describes dysfunction of the intrinsic
pacemaker of the heart, the Sino atrial node.
 As a result, the heart rhythm becomes abnormal
characterized by:
 Sinus bradycardia -- slow heart rates
 Tachycardias -- fast heart rates.
 Bradycardia-tachycardia -- alternating slow and fast heart
rhythms
A person with sick sinus syndrome may
have heart rhythms that are too fast, too
slow, punctuated by long pauses or an
alternating combination of all of these
CAUSES:
Total or subtotal dysfunction of the S.A node.
Areas of nodal atrial discontinuity.
Inflammatory or degenerative changes of nerves and
ganglia surrounding the nodes.
Pathologic changes in the heart wall.
Electrical signals move too slowly through the sinus
node, causing an abnormally slow heart rate.
 Sick sinus syndrome usually occurs in people older
than 50, in whom the cause is often a nonspecific,
scar-like degeneration of the heart's conduction
system like amyloidosis, sarcoidosis, Chagas
disease and cardiomyopathies.
 In children, a common cause of sick sinus syndrome
is heart surgery, especially on the upper chambers.
 Coronary artery disease, high blood pressure, and
aortic and mitral valve diseases may be associated
with sick sinus syndrome.
It manifests as:
-dizziness
-syncope
-slower than normal pulse; bradycardia
- Lighteadnness.
- Fatigue.
- Fainting.
- Dyspnea.
- Trouble sleeping .
- Confusion.
- Palpitations
Premature Atrial Contraction (PAC)
:
 These are contractions in atria conduction pathway
and occurs before the next expected S.A node
impulse.
 CAUSES: Stress, tobacco, caffeine.
 They have been associated with:
-a flutter in your chest
-shortness of breath
-dyspnea.
-dizziness.
-Myocardial infarction
-Digitalis toxicity, Low serum Potassium.
Paraxymal Supraventricular
Tachycardia:
 These arrhythmias originate above the bifurcation of
Bundle of His and have a sudden onset and
termination.
 Heart beats ranges 140-240
 Manifests as hypoxia, rapid heart beat.
 CAUSES: -Heavy nodal reentry
-Wolf Parkinson White Syndrome (WPW):
-Intraartrial or Sinus node reentry.
ATRIAL FLUTTER:
 Rapid atrial ectopic tachycardia with a range that
ranges between 240-450 beats per minute.
 The heart beats fast, but in a regular pattern
CLASSIFICATION OF ATRIAL FLUTTER:
Type I:Typical Atrial Flutter (Common, or Type I Atrial
Flutter)
 Involves the Idioventricular Rhythm & tricuspid isthmus in
the reentry circuit.
 A result of reentry rhythm in the right atrium that can be
entrained and interrupted with atrial pacing techniques.
 Atrial rate normally 300 beats/minute.(240-340).
Type II: Atypical Atrial flutter
(Uncommon, or Type II Atrial Flutter):
Include atrial macro-reentry caused by
surgical scars, idiopathic fibrosis in areas
of the atrium.
Often associated with higher atrial rates
and rhythm instability.
ATRIAL FIBRILLATION:
ATRIAL FIBRILLATION:
 These are chaotic impulses propagating in different
directions and causing disorganized atrial
depolarization without effective atrial contraction.
 Occurs when atrial cells cannot repolarize in time for
the next stimulus.
 The ventricular rate is rapid and the rhythm is
irregular .
 Atrial rate 400-600 beats per minute.
 CAUSES:
 Pulmonary embolus, pulmonary disease, post-
operative, pericarditis.
 Ischemic heart disease, idiopathic.
 Rheumatic valvular disease. (specifically mitral
stenosis or mitral regurgitation).
 Anemia
 Alcohol, advanced age, autonomic tone (vagally
mediated atrial fibrillation).
 Thyroid disease (hyperthyroidism).
 Elevated blood pressure (hypertension).
 Sleep apnea, sepsis, surgery (Breathing disorder
while sleep.)
 Common signs and symptoms of atrial fibrillation:
 Irregular pulse
 Palpitations or racing irregular heart-beats
 Shortness of breath
 Feeling overtired or lacking energy
 Dizziness or confusion
 Light-headedness or fainting
 Feelings of fear or anxiousness
 Chest discomfort or chest pain
RISK FACTORS OF ATRIAL
FIBRILLATION
 Atrial Fibrillation is typical of elderly age, but there
are other conditions that can favor its insurgence,
like co- morbidities and risk factors.
Co-morbidities:
 Valvular heart disease
 Hypertensive heart disease
 Ischemic heart disease
 Cardiomyopathies
 Heart failure
COMPLICATIONS OF ATRIAL
FIBRILLATION
 Stroke
the chaotic rhythm may cause blood to pool in your
heart's upper chambers (atria) and form clots. If a
blood clot forms, it could dislodge from your heart
and travel to your brain. There it might block blood
flow, causing a stroke.
 Heart failure
Atrial fibrillation, especially if not controlled, may
weaken the heart and lead to heart failure — a
condition in which your heart can't circulate
enough blood to meet your body's needs.
Premature Ventricular Contraction
(PVC)
 Caused by ventricular ectopic pacemaker. Electrical
irritability.
 Factors influencing electrical irritability ;
-Ischemia - Electrolyte imbalances
- Drug intoxication
 After occurrence, the ventricles are unable to
repolarize sufficiently to respond to the next impulse
arising from the S.A Node.
 The compensatory pause occurs when ventricles
waits to reestablish its previous rhythms.
 Diastolic volume is insufficient for blood ejection into
the arteriole system.
 Premature Ventricular Contraction (PVC)
- The ectopic beat is not preceded by a p-wave.
Irregular rhythm due to ectopic beat.
QRS is wide and may be bizarre in appearance.
Caused by a irritable focus within the ventricle which
fires prematurely .
 Classified as unifocal, or multifocal PVC’s :
 Unifocal-originating from same area of the ventricle;
distinguished by same morphology.
 Multifocal-originating from different areas of the
ventricle; distinguished by different morphology.
Ventricular Tachycardia:
 A cardiac rhythm originating distal to the
bifurcation of the Bundle of His, in the specialized
conduction system in ventricular muscle.
 Ventricular rate is about 70-250 beats per minute.
 Onset can be sudden or insidious..
 Usually exhibited by
Etiology
 Acute MI
 After chronic infarction
 Ischemic heart disease
 Dilated cardiomyopathy
 Hypertrophic cardiomyopathy
 Electrolyte abnormalities
 Idiopathic
 Specific etiology-- genetic
Ventricular Flutter
 Heart rate: 300 bpm
 Rhythm: Regular and uniform
 Mechanism: Reentry
 Recognition: – No isoelectric interval
– No visible T wave
– Degenerates to ventricular fibrillation
 • Treatment: Cardioversion
Ventricular Fibrillation
 Heart rate: Chaotic, random and asynchronous
 Rhythm: Irregular
 Mechanism: Multiple wavelets of reentry
 Recognition: – No discrete QRS complexes
 Treatment: – Defibrillation
DISORDERS OF
ATRIOVENTRICULAR
CONDUCTION:
 Conduction defects of the A.V Node are most
commonly associated with fibrosis or scar tissue in
the fibres of the conduction system.
 Conduction defects may also result from medications
including digoxin, beta-adrenergic blocking agents,
Calcium channel blocking agents, etc.
 Heart Block refers to the abnormalities of impulse
conduction. It may be normal, physiologic (i.e. vagal
tone), or pathologic.
 It may occur in AV nodal fibers or in the AV bundle
(i.e. Bundle of His), which is continuous with the
Purkinje conduction system that supplies the
ventricles.
FIRST-DEGREE AV BLOCK:
 Prolonged PR interval (> 0.20s)
 Delays AV conduction, but all atrial impulses are
conducted to the ventricles.
 This condition usually produces a regular atrial
and ventricular rhythm.
 The prolonged PR interval results from
conduction delays in the AV Node, the His-
Purkinje system, or both.
 May be the result of a disease in AV Node, such
as ischemia or infarction, or of infections such as
rheumatic fever or myocarditis.
SECOND DEGREE AV BLOCK
 Intermittent failure of conduction of one or more
impulses from the atria to the ventricles.
 The non conducted P wave can appear
intermittently or frequently.
 Conducted P waves relate to QRS waves with
recurring PR intervals
 Association of P waves with QRS complex is not
random.
 Can be either: type I ; Characterized by
progressive lengthening of the PR interval until
the impulse is blocked and the sequence begins
again. Mostly in people with inferior wall
 In Type II AV Block; an intermittent block of atrial
impulses occurs with a constant PR interval.
 It frequently accompanies anterior wall myocardial
infarction and is mostly associated with other types
of organic heart disease and anything causing heart
block.
THIRD DEGREE AV BLOCK:
 Also complete AV Block.
 Result from an interruption of at the level of the
AV Node, in the Bundle of His or in the Purkinje
System.
 Third degree block at the AV node usually are
congenital whereas the blocks in the purkinje
system usually are acquired.
 Normal QRS complexes.
 Rate ranges from 40-60 complexes per minute.
 Complete heart block causes a decrease in
cardiac output with possible periods of syncope
(fainting).
 Other symptoms include: dizziness, fatigue,
exercise intolerance, or episodes of acute heart
failure.
 Most patients with complete heart block require a
permanent cardiac pacemaker.
JUNCTIONAL RHYTHMS:
Premature junctional contraction
 A premature junctional contraction (PJC) is an
early beat that originates in the AV junction.
 As a result of increased automaticity within
junctional cells
 Rhythm: Premature ectopic beat causes slight
irregularity.
 Rate: Overall HR depends on rate of underlying
rhythm.
 P waves: P wave may be inverted, come after
the QRS complex, or be lost in the QRS complex.
 Appears secondary to depression of the SA node
 Occurs when the SA node is firing at a rate lower
than that of the inherent rate of the AV node
 Or if the electrical impulse of the SA node fails to
reach the AV node
Causes:
 Disease of the SA node
 Acute MI
 Drug Effects (digitalis, quinidine, BB’s, or CCB’s)
 May also occur with Complete Heart Block
Junctional Rhythm:
 P waves: Consistently either inverted before QRS,
hidden in QRS complex, or inverted & after the QRS
complex
 QRS: Narrow (< 0.12 sec)
 Causes of Accelerated junctional rhythm include:
 Enhanced automaticity secondary to digitalis toxicity,
 Damage to the AV node, secondary to acute inferior
wall, MI,
 heart failure,
 acute rheumatic fever,
 myocarditis, valvular heart disease and
 cardiac surgery (especially valve surgery)
Junctional Tachycardia
 Causes:
-Enhanced automaticity secondary to digitalis
toxicity
-Damage to the AV node secondary to acute
inferior wall MI, heart failure, acute rheumatic fever,
myocarditis, valvular heart disease, and cardiac
surgery (especially valve surgery)
 P waves: Consistently either inverted before
QRS, hidden in QRS complex, or inverted & after
the QRS complex
 QRS: Narrow
Read and make notes also on:
 Inherited types of Arrhythmias:
-Congenital long QT syndrome.
-Brugada Syndrome
-Catecholaminergic Polymorphic Ventricular
Tachycardia
REFERENCES:
Huether, S.E. & McCance, K. L. (2000),
Understanding Pathophysiology,
Second Edition. :St. Louis: Mosby,
(PACKAGE). Pages 666-671.
www.dysrhythmias.slideshare./com
BScN,
Atandi, JOSHUA

PRESENTING GROUP 8.pptx

  • 1.
  • 2.
  • 3.
    MEMBERS:  Joshua Atandi Kelvin Subati  Lilian Kyule  Faith Mwende  Ann Mwatha  Juliet Ongachi  Dennis Bomett  Bramwel Kipkoskei  Jawa Joseph  Mercy Ngugi  Faith Chebet
  • 4.
    ANATOMY  Blood Flowthrough heart : Superior and Inferior Vena Cava – Right Atrium – Right Ventricle – Pulmonary Artery – Lungs – Pulmonary Vein – Left Atrium – Left Ventricle – Aorta – Body.  Chambers of the heart: Right and Left Atrium, Right and Left Ventricles. The ventricles have a thicker myocardial layer and constitutes much of the bulk of the heart. Septal membranes separates the right and left sides of the heart and prevents blood from crossing over.
  • 5.
     Conduction System– The heart has a conduction system separate from any other system. – The conduction system makes up the PQRST complex we see on paper. – An arrhythmia is a disruption of the conduction system.
  • 6.
     Understanding howthe heart conducts normally is essential in understanding and identifying arrhythmias.  Normal heart rhythms are generated by the Sino atrial (SA) node and travels through the heart’s conduction system causing the atrial and ventricular myocardium to contract and relax at a regular rate that is appropriate to maintain circulations at various levels of physical activity.
  • 7.
    CONDUCTION SYSTEM  SANode  Inter-nodal and inter-atrial pathways  A-V Node  Bundle of His  Purkinje Fibers
  • 8.
    SA Node  Theprimary pacemaker of the heart.  Each normal beat is initiated by the SA node. The atria and ventricles then depolarize sequentially as electrical depolarization passes through specialized conducting tissues. The sinus node acts as a pacemaker and its intrinsic rate is regulated by the autonomic nervous system; vagal activity slows the heart rate, and sympathetic activity accelerates it via cardiac sympathetic nerves and circulating catecholamines.  Inherent rate of 60-100 beats per minute.  Represents the P-wave in the QRS complex or atrial depolarization (firing).
  • 9.
     If thesinus rate becomes unduly slow, a lower centre may assume the role of pacemaker. This is known as an escape rhythm and may arise in the AV node (nodal rhythm) or the ventricles (idioventricular rhythm).
  • 10.
    AV Node  Locatedin the septum of the heart.  Receives impulse from inter-nodal pathways and holds the signal before sending on to the Bundle of His.  Represents the PR segment of the QRS complex
  • 11.
    AV Node  Representsthe PR segment of the cardiac cycle.  Has an inherent rate of 40-60 beats per minute.  Acts as a back up when the SA node fails.  Where all junctional rhythms originate
  • 12.
    QRS Complex  Representsthe ventricles depolarizing (firing) collectively. (Bundle of His and Purkinje fibers).  Origin of all ventricular rhythms.  Has an inherent rate of 20-40 beats per minute
  • 13.
    NORMAL ELECTROCARDIOGRAM:  Isoelectric line(baseline).  P-wave – Atria firing.  PR interval – Delay at AV.  QRS – Ventricles firing.  T-Wave – Ventricles repolarizing.
  • 14.
     ST segment –Ventricle contracting. – Should be at isoelectric line. – Elevation or depression may be important. • U wave – Purkinje fiber repolarization.
  • 15.
     Normal: – Heartrate = 60 – 100 bpm – PR interval = 0.12 – 0.20 sec – QRS interval <0.12 – SA Node discharge = 60 – 100 / min – AV Node discharge = 40 – 60 min – Ventricular Tissue discharge = 20 – 40 min
  • 16.
    Cardiac cycle  Pwave = atrial depolarization  PR interval = pause between atrial and ventricular depolarization  QRS = ventricular depolarization  T wave = ventricular depolarization
  • 18.
    DEFINATION  Cardiac Arrhythmiais a condition in which the heart beats with an irregular or abnormal rhythm.  It is a disturbance of the heart rhythm.  Dysrhythmias range in severity from occasional or rapid beats to serious disturbances that impair the pumping ability of the heart, contributing to heart failure and death.
  • 19.
    ABNORMAL RHYTHM CAN BEOF TWO EXTREME FORMS 1. Bradycardia - Cardiac beats below 60 beats per minute . 2. Tachycardia – Cardiac beat above 100 beats per minute.
  • 20.
    Mechanisms of CardiacArrhythmias  Result from disorders of impulse formation, conduction, or both.  Dysrhythmias can be caused by either an abnormal rate of impulse generation by the SA node or other pacemaker or the abnormal condition of impulses through the heart’s conduction system, including the myocardial cells themselves. The disturbances appear to disrupt the normal sequence of atrial and ventricular activation.
  • 21.
    ETIOLOGY  Coronary arterydisease.  Electrolyte imbalances in your blood (such as sodium or potassium).Hyperkalemia/hypokalemia  Changes in your heart muscle.  Injury from a heart attack.  Irregular heart rhythms can also occur in "normal, healthy" hearts.  Healing process after heart surgery.
  • 22.
    Causes of arrhythmias Cardiac ischemia. Ischemic Heart Disease  Chronic obstructive pulmonary disease(COPD).  Thyroid disorders  Excessive discharge or sensitivity to autonomic transmitters  Exposure to toxic substances. Drugs related.  Unknown etiology
  • 23.
    Disorders of impulseformation  No signal from the pacemaker site.  Development of an ectopic pacemaker: ◦ May arise from conduction cells (most are capable of spontaneous activity). ◦ Usually under control of SA node if it slows down too much conduction cells could become dominant. ◦ Often a result of other injury (ischemia, hypoxia).
  • 24.
    Disorders of impulseconduction  Development of oscillatory afterdepolariztions: ◦ Can initiate spontaneous activity in nonpacemaker tissue. ◦ May be result of drugs (digitalis, norepinephrine) used to treat other cardiopathologies.
  • 25.
     May resultin: ◦ Bradycardia: 1. SA node : Slowed / Absent.  Causes -Decreased Sympathetic Signals: reduced automaticity (e.g. sinus bradycardia) -Increased Parasympathetic Signals -SA node Damage 2. Blockage of Conduction from SA node:  AV node Blockage  Causes -Ischemia -Fibrosis -Viral Infection RESULTS in HEART ATTACK
  • 26.
     LEFT BUNDLEBRUNCH BLOCK (LBBB)  No Impulse conduction through Bundle Brunch.  Action Potential transferred through Right Ventricle to Left Ventricle.  RESULTS in Wide QRS complex
  • 27.
    ◦ Tachycardia: 1. IncreasedPacemaker Activity (SA Node)-Sinus Tachycardia. There is increased automaticity-the tachycardia is produced by repeated spontaneous depolarization of an ectopic focus, often in response to catecholamines.  Causes -Increased Sympathetic Signals. -Decreased Parasympathetic Signals. -SA node Dysfunction. Example : Sick Sinus Syndrome. 2. Re-entry Tachycardias: Tachycardia is initiated by an ectopic beat and sustained by a re-entry circuit. Most tachyarrhythmias are due to re-entry. These include:
  • 28.
     Atrial Fibrillation: -loss of the normal organized propagation of electrical activity . - atria fibrillate, they no longer contract in a mechanically useful way. - a degree of stasis to blood flow and predisposing to clot (thrombus) formation within the chambers.  Ventricular Fibrillation: - Uncoordinated contraction of the Cardiac Muscle. - Quiver rather than contract properly. Commonly identified arrhythmia in Cardiac Arrest patients. As a consequence, Sudden Cardiac Death.
  • 29.
     Wolf ParkinsonWhite Syndrome (WPW): -WPW is caused by the presence of an abnormal accessory electrical conduction pathway btn the atria and the ventricles. -Electrical Signals through abnormal pathway stimulate the ventricles to contract prematurely. Its a unique type of supraventricular tachycardia referred to as an “atrioventricular reciprocating tachycardia.”
  • 31.
    3. Delayed Repolarization: Causes include: - Ischemia. -Drugs related (Potassium Blockers). - Electrolyte Imbalance.  Its effects include:-Long QT interval -R on T Phenomenon. -Premature Ventricular Beat. -Ventricular Fibrillation.
  • 32.
    PATHOPHYSIOLOGY Inadequate acceleration ofsinus rate Failure of sinus impulse formation Abrupt sinus prolonged pause MI, HT, Coronary spasm SA node dysfunction Aortic & mitral valve stenosis AV conduction block Degeneration or damage of the conduction system Atrial dysfunction Ventricular dysfunction CARDIAC ARRYTHMIA
  • 33.
    Arrhythmia Presentation (SYMPTOMS)  Palpitations. Dizziness.  Chest Pain.  Dyspnea.  Anxiety and confusion(reduced blood perfusion)  Fainting.  Sudden cardiac death  Swelling  Shortness of Breath  Exercise Intolerance  Can trigger heart failure or even sudden death.
  • 34.
  • 35.
    Sinus Tachycardia:  Rapidheart rate.  Rate is greater than 100 beats per minute (Usually between 100-160 ).  Is a normal response during fever and exercise and in situations that incite sympathetic stimulation. CAUSES: -Cardiac conditions i.e heart failure -Hyperthyroidsm
  • 36.
    - Medications suchas epinephrine. - Myocardial infarction - Other causes are Anemia, Respiratory distress, pulmonary embolism, sepsis. Sinus Bradycardia:  Slow heart rate, Regular rhythm  Rate less than 60 beats per minute  SA node firing slower than normal  P wave precedes QRS Indications include poor prognosis.
  • 37.
    Pathophysiology: It’s a normalresponse to a reduced demand for blood flow.  Vagal stimulation increases  Sympathetic stimulation decreases.  Decreased movement of impulse from S.A node.  Automacity of S.A node diminishes.  Decrease in conduction to the A.V node causes reduced heart failure.
  • 38.
     CAUSES: - Non-cardiacdisorders - Conditions producing excess vagal stimulation or decreased sympathetic stimulation - Cardiac diseases - Certain drugs MANIFESTATIONS: - Hypotension - Altered mental status - Cool, clammy skin - Dizziness - Blurred vision -Crackles, dyspnea - Chest pain -Syncope
  • 39.
    Sinus Arrest: SinusPause (Stop of sinus rhythm, New rhythm starts).  Failure of SA Node to discharge and results in an irregular pulse. Sinus node doesn’t fire.  An escape rhythm develops. Another pace maker takes over. CAUSES: -Disease of S.A Node - Digitalis toxicity -Myocardial infarction. - Excessive vagal tone. -Hyperkalemia
  • 41.
    Sick Sinus Syndrome: Sick sinus syndrome describes dysfunction of the intrinsic pacemaker of the heart, the Sino atrial node.  As a result, the heart rhythm becomes abnormal characterized by:  Sinus bradycardia -- slow heart rates  Tachycardias -- fast heart rates.  Bradycardia-tachycardia -- alternating slow and fast heart rhythms A person with sick sinus syndrome may have heart rhythms that are too fast, too slow, punctuated by long pauses or an alternating combination of all of these
  • 42.
    CAUSES: Total or subtotaldysfunction of the S.A node. Areas of nodal atrial discontinuity. Inflammatory or degenerative changes of nerves and ganglia surrounding the nodes. Pathologic changes in the heart wall. Electrical signals move too slowly through the sinus node, causing an abnormally slow heart rate.
  • 43.
     Sick sinussyndrome usually occurs in people older than 50, in whom the cause is often a nonspecific, scar-like degeneration of the heart's conduction system like amyloidosis, sarcoidosis, Chagas disease and cardiomyopathies.  In children, a common cause of sick sinus syndrome is heart surgery, especially on the upper chambers.  Coronary artery disease, high blood pressure, and aortic and mitral valve diseases may be associated with sick sinus syndrome.
  • 44.
    It manifests as: -dizziness -syncope -slowerthan normal pulse; bradycardia - Lighteadnness. - Fatigue. - Fainting. - Dyspnea. - Trouble sleeping . - Confusion. - Palpitations
  • 46.
    Premature Atrial Contraction(PAC) :  These are contractions in atria conduction pathway and occurs before the next expected S.A node impulse.  CAUSES: Stress, tobacco, caffeine.  They have been associated with: -a flutter in your chest -shortness of breath -dyspnea. -dizziness. -Myocardial infarction -Digitalis toxicity, Low serum Potassium.
  • 47.
    Paraxymal Supraventricular Tachycardia:  Thesearrhythmias originate above the bifurcation of Bundle of His and have a sudden onset and termination.  Heart beats ranges 140-240  Manifests as hypoxia, rapid heart beat.  CAUSES: -Heavy nodal reentry -Wolf Parkinson White Syndrome (WPW): -Intraartrial or Sinus node reentry.
  • 48.
    ATRIAL FLUTTER:  Rapidatrial ectopic tachycardia with a range that ranges between 240-450 beats per minute.  The heart beats fast, but in a regular pattern CLASSIFICATION OF ATRIAL FLUTTER: Type I:Typical Atrial Flutter (Common, or Type I Atrial Flutter)  Involves the Idioventricular Rhythm & tricuspid isthmus in the reentry circuit.  A result of reentry rhythm in the right atrium that can be entrained and interrupted with atrial pacing techniques.  Atrial rate normally 300 beats/minute.(240-340).
  • 49.
    Type II: AtypicalAtrial flutter (Uncommon, or Type II Atrial Flutter): Include atrial macro-reentry caused by surgical scars, idiopathic fibrosis in areas of the atrium. Often associated with higher atrial rates and rhythm instability.
  • 50.
  • 51.
    ATRIAL FIBRILLATION:  Theseare chaotic impulses propagating in different directions and causing disorganized atrial depolarization without effective atrial contraction.  Occurs when atrial cells cannot repolarize in time for the next stimulus.  The ventricular rate is rapid and the rhythm is irregular .  Atrial rate 400-600 beats per minute.
  • 52.
     CAUSES:  Pulmonaryembolus, pulmonary disease, post- operative, pericarditis.  Ischemic heart disease, idiopathic.  Rheumatic valvular disease. (specifically mitral stenosis or mitral regurgitation).  Anemia  Alcohol, advanced age, autonomic tone (vagally mediated atrial fibrillation).  Thyroid disease (hyperthyroidism).  Elevated blood pressure (hypertension).  Sleep apnea, sepsis, surgery (Breathing disorder while sleep.)
  • 53.
     Common signsand symptoms of atrial fibrillation:  Irregular pulse  Palpitations or racing irregular heart-beats  Shortness of breath  Feeling overtired or lacking energy  Dizziness or confusion  Light-headedness or fainting  Feelings of fear or anxiousness  Chest discomfort or chest pain
  • 54.
    RISK FACTORS OFATRIAL FIBRILLATION  Atrial Fibrillation is typical of elderly age, but there are other conditions that can favor its insurgence, like co- morbidities and risk factors. Co-morbidities:  Valvular heart disease  Hypertensive heart disease  Ischemic heart disease  Cardiomyopathies  Heart failure
  • 55.
    COMPLICATIONS OF ATRIAL FIBRILLATION Stroke the chaotic rhythm may cause blood to pool in your heart's upper chambers (atria) and form clots. If a blood clot forms, it could dislodge from your heart and travel to your brain. There it might block blood flow, causing a stroke.  Heart failure Atrial fibrillation, especially if not controlled, may weaken the heart and lead to heart failure — a condition in which your heart can't circulate enough blood to meet your body's needs.
  • 57.
    Premature Ventricular Contraction (PVC) Caused by ventricular ectopic pacemaker. Electrical irritability.  Factors influencing electrical irritability ; -Ischemia - Electrolyte imbalances - Drug intoxication  After occurrence, the ventricles are unable to repolarize sufficiently to respond to the next impulse arising from the S.A Node.  The compensatory pause occurs when ventricles waits to reestablish its previous rhythms.  Diastolic volume is insufficient for blood ejection into the arteriole system.
  • 58.
     Premature VentricularContraction (PVC) - The ectopic beat is not preceded by a p-wave. Irregular rhythm due to ectopic beat. QRS is wide and may be bizarre in appearance. Caused by a irritable focus within the ventricle which fires prematurely .  Classified as unifocal, or multifocal PVC’s :  Unifocal-originating from same area of the ventricle; distinguished by same morphology.  Multifocal-originating from different areas of the ventricle; distinguished by different morphology.
  • 59.
    Ventricular Tachycardia:  Acardiac rhythm originating distal to the bifurcation of the Bundle of His, in the specialized conduction system in ventricular muscle.  Ventricular rate is about 70-250 beats per minute.  Onset can be sudden or insidious..  Usually exhibited by
  • 60.
    Etiology  Acute MI After chronic infarction  Ischemic heart disease  Dilated cardiomyopathy  Hypertrophic cardiomyopathy  Electrolyte abnormalities  Idiopathic  Specific etiology-- genetic
  • 64.
    Ventricular Flutter  Heartrate: 300 bpm  Rhythm: Regular and uniform  Mechanism: Reentry  Recognition: – No isoelectric interval – No visible T wave – Degenerates to ventricular fibrillation  • Treatment: Cardioversion
  • 65.
    Ventricular Fibrillation  Heartrate: Chaotic, random and asynchronous  Rhythm: Irregular  Mechanism: Multiple wavelets of reentry  Recognition: – No discrete QRS complexes  Treatment: – Defibrillation
  • 66.
  • 67.
     Conduction defectsof the A.V Node are most commonly associated with fibrosis or scar tissue in the fibres of the conduction system.  Conduction defects may also result from medications including digoxin, beta-adrenergic blocking agents, Calcium channel blocking agents, etc.  Heart Block refers to the abnormalities of impulse conduction. It may be normal, physiologic (i.e. vagal tone), or pathologic.  It may occur in AV nodal fibers or in the AV bundle (i.e. Bundle of His), which is continuous with the Purkinje conduction system that supplies the ventricles.
  • 68.
    FIRST-DEGREE AV BLOCK: Prolonged PR interval (> 0.20s)  Delays AV conduction, but all atrial impulses are conducted to the ventricles.  This condition usually produces a regular atrial and ventricular rhythm.  The prolonged PR interval results from conduction delays in the AV Node, the His- Purkinje system, or both.  May be the result of a disease in AV Node, such as ischemia or infarction, or of infections such as rheumatic fever or myocarditis.
  • 69.
    SECOND DEGREE AVBLOCK  Intermittent failure of conduction of one or more impulses from the atria to the ventricles.  The non conducted P wave can appear intermittently or frequently.  Conducted P waves relate to QRS waves with recurring PR intervals  Association of P waves with QRS complex is not random.  Can be either: type I ; Characterized by progressive lengthening of the PR interval until the impulse is blocked and the sequence begins again. Mostly in people with inferior wall
  • 70.
     In TypeII AV Block; an intermittent block of atrial impulses occurs with a constant PR interval.  It frequently accompanies anterior wall myocardial infarction and is mostly associated with other types of organic heart disease and anything causing heart block.
  • 71.
    THIRD DEGREE AVBLOCK:  Also complete AV Block.  Result from an interruption of at the level of the AV Node, in the Bundle of His or in the Purkinje System.  Third degree block at the AV node usually are congenital whereas the blocks in the purkinje system usually are acquired.  Normal QRS complexes.  Rate ranges from 40-60 complexes per minute.
  • 72.
     Complete heartblock causes a decrease in cardiac output with possible periods of syncope (fainting).  Other symptoms include: dizziness, fatigue, exercise intolerance, or episodes of acute heart failure.  Most patients with complete heart block require a permanent cardiac pacemaker.
  • 73.
  • 74.
    Premature junctional contraction A premature junctional contraction (PJC) is an early beat that originates in the AV junction.  As a result of increased automaticity within junctional cells  Rhythm: Premature ectopic beat causes slight irregularity.  Rate: Overall HR depends on rate of underlying rhythm.  P waves: P wave may be inverted, come after the QRS complex, or be lost in the QRS complex.
  • 75.
     Appears secondaryto depression of the SA node  Occurs when the SA node is firing at a rate lower than that of the inherent rate of the AV node  Or if the electrical impulse of the SA node fails to reach the AV node Causes:  Disease of the SA node  Acute MI  Drug Effects (digitalis, quinidine, BB’s, or CCB’s)  May also occur with Complete Heart Block
  • 76.
    Junctional Rhythm:  Pwaves: Consistently either inverted before QRS, hidden in QRS complex, or inverted & after the QRS complex  QRS: Narrow (< 0.12 sec)  Causes of Accelerated junctional rhythm include:  Enhanced automaticity secondary to digitalis toxicity,  Damage to the AV node, secondary to acute inferior wall, MI,  heart failure,  acute rheumatic fever,  myocarditis, valvular heart disease and  cardiac surgery (especially valve surgery)
  • 77.
    Junctional Tachycardia  Causes: -Enhancedautomaticity secondary to digitalis toxicity -Damage to the AV node secondary to acute inferior wall MI, heart failure, acute rheumatic fever, myocarditis, valvular heart disease, and cardiac surgery (especially valve surgery)  P waves: Consistently either inverted before QRS, hidden in QRS complex, or inverted & after the QRS complex  QRS: Narrow
  • 78.
    Read and makenotes also on:  Inherited types of Arrhythmias: -Congenital long QT syndrome. -Brugada Syndrome -Catecholaminergic Polymorphic Ventricular Tachycardia
  • 79.
    REFERENCES: Huether, S.E. &McCance, K. L. (2000), Understanding Pathophysiology, Second Edition. :St. Louis: Mosby, (PACKAGE). Pages 666-671. www.dysrhythmias.slideshare./com
  • 80.