heart disease

1. ARRYTHMIA

2. Conduction system of the heart

3. MECHANISMS OF CARDIAC ARRYTHMIA
1. Alterations in Impulse Initiation: Automaticity
2. Afterdepolarizations and Triggered Automaticity
3. Abnormal Impulse Conduction: Reentry

4. AUTOMATICITY
 Spontaneous (phase 4) diastolic depolarization underlies the
property of automaticity (pacemaking)
 The rate of phase 4 depolarization and, therefore, the firing
rate of pacemaker cells are dynamically regulated
 Normal or enhanced automaticity of subsidiary latent
pacemakers produces escape rhythms in the setting of failure
of more dominant pacemakers

5. AUTOMATICITY

6. AFTERDEPOLARIZATIONS AND TRIGGERED
AUTOMATICITY

7. REENTERY
 Defined as a continuous repetitive propagation of an
excitatory wave traveling in a circular path, returning to its
site of origin to reactivate that site
 It is the electrophysiologic mechanism responsible for most of
the clinically important arrhythmias

8. REQUIREMENTS FOR THE DEVELOPMENT OF
REENTERANCE TACHYCARDIS
 The one event crucial to the development of a reentrant
tachycardia is the failure of a group of fibers to activate during
a depolarization wave
 Adjacent tissue or pathways must have different
electrophysiologic properties (conduction and refractoriness)
and be joined proximally and distally, forming a circuit
 Each involved pathway of the circuit must be capable of
conducting an impulse in an antegrade and retrograde
direction

9. REQUIREMENTS FOR THE DEVELOPMENT OF
REENTERANCE TACHYCARDIS
 Conduction velocity in the normal unblocked pathway must be
slow enough relative to the refractoriness of the blocked
pathway to allow recovery of the previously blocked pathway
 Retrograde conduction in this previously blocked pathway
must be slow enough to allow the normal pathway to recover,
and again be capable of being excited

10. Schematic diagram of reentry

11. THERAPY OF ARRYTHMIA
1. Antiarrythmic drugs
2. Catheter ablation
3. Pacemakers
4. External Defibirilators
5. ICDs (Intracardiac Defibrilators)

12. Antiarrhythmic Drug Therapy
 The interaction of antiarrhythmic drugs with cardiac tissues and the
resulting electrophysiologic changes are complex
o The structural similarity of target ion channels
o Regional differences in the levels of expression of channels and
transporters, which change with disease
o Time and voltage dependence of drug action
o The effect of these drugs on targets other than ion channels

13. The Vaughan-Williams classification of
antiarrhythmic action
 Class I: local anesthetic effect due to blockade of Na+ current
 Class II: interference with the action of catecholamines at the
adrenergic receptor
 Class III: delay of repolarization due to inhibition of K+ current
or activation of depolarizing current
 Class IV: interference with calcium conductance

14. The Vaughan-Williams classification of
antiarrhythmic action

15. CATHETER ABLATION

16. BRADYARRYTHMIAS

17. BRADYCARDIA
1. Failure of impulse initiation (SA node dysfunction)
2. Failure of impulse conduction (AV conduction block)

18. SA NODE DYSFUNCTION

19. ETIOLOGIES OF SA NODE DYSFUNCTION
EXTRENSIC INTERINSIC
 Autonomic dysfunction
 Drugs
 Hypothyrodism
 Sleep apnea
 Hypoxia
 Endotracheal suctioning
 Hypothermia
 Increased ICP
 Sick Sinus Syndrome (SSS)
 Coronary artery disease
 Inflammatory
 Senile amyloidosis
 Congenital heart disease
 Iatrogenic
 Chest trauma
 Familial and heriditary diseases

20. CLINICAL MANIFESTATIONS OF SA NODE DYSFUNCTION
 Asymptomatic
 Hypotension
 Syncope
 Presyncope
 Fatigue and weakness
 In many cases, symptoms associated with SA node dysfunction are the
result of concomitant cardiovascular disease
 A significant minority of patients with SSS will develop signs and
symptoms of heart failure that may be related to slow or fast heart rates
 One-third to one-half of patients with SA node dysfunction will develop
HF
 Up to one-quarter of patients with SA node disease will have concurrent
AV conduction disease or supraventricular tachycardia

21. Electrocardiography of SA Node Disease
1. Sinus bradycardia: by definition sinus bradycardia is a rhythm driven by
the SA node with a rate of <60 beats/min; sinus bradycardia is very common
and typically benign. Resting heart rates of <60 beats/min are very common in
young healthy individuals and physically conditioned subjects. A sinus rate of
<40 beats/min in the awake state in the absence of physical conditioning is
generally considered abnormal
2. Sinus pause and sinus arrest: sinus pauses of up to 3 s are common in
the awake athlete, and pauses of this duration or longer may be observed in
asymptomatic elderly subjects
3. Sinus exit block
4. Tachycardia (in SSS)
5. Chronotropic incompitance

22. Diagnostic Testing
 Resting ECG
 Holter and event monitors
 Implantable ECG monitors (12 to 18 months)
 Exercise testing (failure to reach 85% of predicted maximal
heart rate at peak exercise, or failure to achieve a heart rate >
100 beats/min with exercise or a maximal heart rate with
exercise less than two standard deviations below that of an
age-matched control population)
 Autonomic nervous system
 Electrophysiologic testing

23. Therapy of Sinoatrial Node Dysfunction
 Since SA node dysfunction is not associated with increased
mortality, the aim of therapy is alleviation of symptoms
 Chronic pharmacologic therapy for sinus bradyarrhythmias has
limited value (atropin, theophylin and isoproterenol)
 Pace maker implantation

24. Summary of Guidelines for Pacemaker Implantation in
SA Node Dysfunction

25. ATRIOVENTRICULAR CONDUCTION DISEASE

26. Etiologies of Atrioventricular Block
 Autonomic dysfunction
 Metabolic/Endocrine disorders
 Drug-related
 Infectious
 Heritable/Congenital
 Inflammatory
 Infiltrative
 Neoplastic/Traumatic
 Degenerative
 Coronary Artery Disease

27. CLASSIFICATION AV BLOCK
 10 AV block
 20 AV block
• Mobitz type 1 or Wenckebach
• Mobitz type 2
• 30 AV block

28. FIRST DEGREE AV BLOCK
 Atrioventricular impulse transmission is delayed in first degree
AV block, resulting in a PR interval longer than 200 msec
(>210 msec at slow heart rates)
 The PR interval includes activation of the atrium, AV node, His
bundle, bundle branches and fascicles, and terminal Purkinje
fibers

29. SECOND DEGREE AV BLOCK
 Mobitz type 1: progressive PR interval prolongation preceded a
nonconducted P wave
 Mobitz type 2: the PR interval remained unchanged prior to
the P wave that suddenly failed to conduct to the ventricles

30. THIRD DEGREE AV BLOCK

31. Guideline Summary for Pacemaker Implantation
in Acquired AV Block

32. TACHYARRYTHMIAS

33. CLASSIFICATION OF TACHYARRYTHMIAS
SVT = supraventricular tachycardia; CSM = carotid sinus massage; AV = atrioventricular; AVNRT = AV nodal reentrant
tachycardia; AVRT = AV reciprocating tachycardia; AT = atrial tachycardia; SANRT = sinoatrial nodal reentry tachycardia; AP =
accessory pathway

34. Classification of narrow QRS complex tachycardias by
structures required for initiation and maintenance

35. PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA
 The term paroxysmal supraventricular tachycardia
(PSVT) is applied to intermittent SVTs other than
AF, atrial flutter, and MAT

36. CAUSES OF WIDE QRS COMPLEX TACHYCARDIA

37. SINUS TACHYCARDIA

38. CLASSIFICATION OF SINUS TACHYCARDIA
PHYSIOLOGIC INAPPROPRIATE
 Hyperthyroidism
 Fever
 Effective volume depletion
 Anxiety
 Pheochromocytoma
 Sepsis
 Anemia
 Hypotension and shock
 Pulmonary embolism
 Acute coronary ischemia and myocardial
infarction
 Heart failure
 Chronic pulmonary disease
 Hypoxia
 Exposure to stimulants (nicotine, caffeine)
or illicit drugs
 Inappropriate sinus tachycardia
(IST) is an unusual condition that
occurs in individuals without
apparent heart disease or other
cause for sinus tachycardia, such
as hyperthyroidism or fever
 Affected patients have an elevated
resting heart rate and/or an
exaggerated heart rate response
to exercise; many patients have
both

39. SYMPTOMS OF SINUS TACHYCARDIA
 Sinus tachycardia is often asymptomatic, although the patient
may complain of a rapid heart beat
 Underlying cardiac disease
Decrease the cardiac output by shortening ventricular filling
time
 Exacerbate coexisting myocardial and/or valvular heart disease
 Increase myocardial oxygen consumption
 Reduce coronary blood flow

40. TREATMENT OF SINUS TACHYCARDIA
 Treatment of physiologic sinus tachycardia is directed at the
underlying condition causing the tachycardia response.
Uncommonly, beta blockers are used to minimize the
tachycardia response if it is determined to be potentially
harmful, as may occur in a patient with ischemic heart disease
and rate-related anginal symptoms.
 Pharmacotherapy with beta blockers or catheter ablation can
be used for symptomatic patients with IST

41. ATRIAL FIBRILLATION

42. GENERAL REMARKS ABOUT AF
 AF is the most common sustained arrhythmia
 Atrial fibrillation (AF) is characterized by rapid and irregular
atrial fibrillatory waves at a rate of 350 to 600
impulses/minute and, in the presence of normal
atrioventricular (AV) nodal conduction, by an irregularly
irregular ventricular response of 90 up to 140 to 170
beats/min, but it may be higher in some patients

43. EPIDEMIOLOGY OF AF

44. EPIDEMIOLOGY OF AF

45. CLASSIFICATION OF AF
 Paroxysmal (i.e., self-terminating) — AF is classified as paroxysmal if
episodes terminate spontaneously in less than seven days, usually less than
24 hours.
 Persistent AF — AF is classified as persistent if it fails to self-terminate
within seven days. Episodes may eventually terminate spontaneously, or
they can be terminated by cardioversion. A patient who has had an
episode of persistent AF can have later episodes of AF that classify as
paroxysmal (i.e., self-terminating in less than seven days).
 Permanent AF — Permanent AF is considered to be present if the
arrhythmia lasts for more than one year and cardioversion either has not
been attempted or has failed.
 "Lone" AF — "Lone" AF describes paroxysmal, persistent, or permanent
AF in individuals without structural heart disease

46. ETIOLOGIES OF AF
 Valvular heart disease
 Hypertensive heart disease
 Coronary heart disease
 Heart failure (10-30%)
 HCMP (10-28%)
 Congenital heart disease
 Other types of
cardiopulmonary disease
 Obesity
 Hyperthyrodism
 Surgery
 Inflammation and infection
 Autonomic dysfunction
 Other supraventricular
tachyarrhythmias
 Diet
 Medications
 Genetics

47. VALVULAR HEART DISEASE AND AF
 MS,MR, and TR — 70 percent
 MS and MR — 52 percent
 Isolated MS — 29 percent
 Isolated MR — 16 percent
 Isolated AS-1%

48. CLINICAL MANIFESTATIONS OF AF
 Asymptomatic
 Symptoms of underlying disease
 Symptoms directly related to AF(mechanisms)
• The loss of atrial contractility
• The inappropriate fast ventricular response
• The loss of atrial appendage contractility and emptying leading to the risk of clot
formation and subsequent thromboembolic events

49. ECG FINDINGS OF AF

50. GENERAL TREATMENT ISSUES
 Rate control
 Rhythm control
 Rate Vs Rhythm control
 Prevention of systemic embolization
 Nonpharmacologic therapy

51. FACTORS TO BE CONSIDERED UPON DECIDING A
TREATMENT PLAN FOR AF
 Is the patient hemodynamically stable
 Is left ventricular function normal or impaired?
 Does the patient have WPW?
 Is the duration of AF less than or more than 48 hours?
 Is anticoagulation indicated?
 Can the patient undergo electrical cardioversion safely?
 Is the ventricular rate too high?

52. RATE CONTROL OF AF

53. RATE CONTROL (TARGET HEART RATE)
 Rest heart rate <=80 beats/min
 24-hour Holter average <=100 beats/min and no heart rate >110
percent of the age-predicted maximum
 Heart rate <=110 beats/min in six minute walk

54. RHYTHM CONTROL
 Synchronized external DC cardioversion (75-95%)
 patients with AF of more than 48 hours duration, of unknown
duration, or of less than 48 hours duration in the presence of mitral
stenosis or a history of thromboembolism may have atrial thrombi
that can embolize. In such patients, cardioversion should be delayed
until the patient has been anticoagulated at appropriate levels (INR
2.0 to 3.0) for three to four weeks or shorter term anticoagulation if
screening transesophageal echocardiography has excluded atrial and
atrial appendage thrombi
 pharmacologic cardioversion(30-60%)

55. INDICATIONS FOR URGENT CARDIOVERSION
 Active ischemia
 Significant hypotension, to which poor LV systolic function,
diastolic dysfunction, or associated mitral or aortic valve
disease may contribute
 Severe manifestations of HF
 The presence of a preexcitation syndrome, which may lead to
an extremely rapid ventricular rate

56. PHARMACOLOGIC THERAPY TO MAINTAIN
SINUS RHYTHM

57. RATE Vs RHYTHM CONTROL

58. INDICATIONS FOR RHYTHM CONTROL
 Persistent symptoms (palpitations, dyspnea, lightheadedness,
angina, presyncope, and heart failure) despite adequate rate
control.
 An inability to attain adequate rate control
 Patient preference

59. NONPHARMACOLOGIC APPROACHS
 Rhythm control — There are several alternative methods to
maintain NSR in patients who are refractory to conventional
therapy, including surgery, radiofrequency catheter ablation, and
pacemakers
 Rate control — Radiofrequency AV nodal-His bundle ablation with
permanent pacemaker placement or AV nodal conduction
modification are nonpharmacologic therapies for achieving rate
control in patients who do not respond to pharmacologic therapy
 LAA occlusion or ligation — Since the vast majority to thrombi in
nonvalvular AF arise within or involve the left atrial appendage
(LAA), the LAA is occluded at the time of surgery in patients who
undergo cardiac surgery for other reasons. Percutaneous approaches
have also been evaluated

60. PREVENTION OF SYSTEMIC EMBOLIZATION

61. RISK OF EMBOLIZATION (PAROXYSMAL Vs CHRONIC AF)
The stroke risk appears to be equivalent in
paroxysmal and chronic AF

62. ≥2 requires anticoagulation

65. ATRIAL FLUTTER

66. CLASSIFICATION OF ATRIAL FLUTTER
 Type I or typical atrial flutter is a macroreentrant arrhythmia, in which a
depolarizing stimulus (such as a single atrial ectopic beat) excites an area of the
atrium and then travels sufficiently slowly in a pathway that is sufficiently long
that there is an "excitable gap," that is, an area behind the wave of depolarization
that has recovered its excitability and can be reactivated, thereby forming a
circuit. The slowly conducting reentrant circuit is located in the low right atrial
isthmus. The isthmus is a path between the orifice of inferior vena cava and the
annulus of the tricuspid valve.The reenterant circute may be clockwise or counterclock
wise. The flutter rate 240 to 340 beats/min.
 Type II or true atypical atrial flutter seems to lack an excitable gap, is not isthmus-
dependent, and cannot be entrained. It is thought that these characteristics result from an
intraatrial reentrant circuit that is very short in contrast to the long isthmus in type I atrial
flutter.The flutter rate is 340 to 440 beats/min.

67. ECG FINDINGS OF ATRIAL FLUTTER

68. ETIOLOGY, CLINICAL MANIFESTATION AND MANAGEMENT
 Etiology, clinical manifestations and management: similar to AF
 In all patients, an effort should be made to control the ventricular rate
pharmacologically or restore sinus rhythm. Rate control with calcium antagonists
(diltiazem or verapamil), beta blockers, and/or digoxin may be difficult. Even
higher grade AV slowing, such as a 4:1 AV response, may only be transient and is
easily overcome with activity or emotional stress. Owing to the typically faster
ventricular rate, AFL tends to be poorly tolerated in comparison to AF

69. WOLFF-PARKINSON-WHITE (WPW) SYNDROME

70. ORTHODROMIC TACHYCARDIA IN WPW SYNDROME

71. ANTIDROMIC TACHYCARDIA IN WPW SYNDROME

72. THERAPY OF WPW SYNDROME
 Asymptomatic patients does not need therapy
 Symptomatic patients
 Ablation (catheter/surgical): best option
 DC cardioversion
 Pharmacologic (for patients who are not candidates for ablation)

73. PHARMACOTHERAPY FOR WPW SYNDROME

74. PHARMACOTHERAPY FOR WPW SYNDROME

75. VENTRICULAR TACHYCARDIA

76. CLASSIFICATION
1. Duration
 Nonsustained VT: three or more consecutive ventricular beats at
a rate of greater than 100 beats/min with a duration of less than
30 seconds.There is, however, great variability in the literature in
the definition of this arrhythmia. Some definitions allow a rate of
120 beats/min or 140 beats/min
 Sustained: hemodynamically unstable VT that requires
termination before 30 s or VT that is terminated by therapy from
an implantable defibrillator is also typically classified as sustained

77. CLASSIFICATION
2. Morphology
Monomorphic: a uniform QRS complex morphology during VT
Polymorphic: beat to beat change in QRS complex morphology
Ventricular flutter: appears as a sine wave on the ECG and has
a rate of >250 beats/min
Ventricular Fibrilation

78. CLASSIFICATION
3. Hemodynamic stability
Stable
Unstable

79. ETIOLOGY
 Structural heart disease (IHD,DCMP,HCMP...)
 Drugs
 Electrolyte imbalance
 Anemia
 Hypoxia
 Idiopathic

80. CLINICAL MANIFESTATIONS
 Ventricular rate
 Presence and extent of underlying heart disease
 Function of the left ventricle
 Presence of atrioventricular (AV) asynchrony
 Location of the myocardial focus; this is associated with a
particular, often abnormal, sequence pattern of left ventricular
activation

81. DIFERENTIATING VT FROM SVT WITH ABERRANT
CONDUCTIONS
 History: presence of underlying heart disease
 Physical examination: features of undelying heart disease and
evidence for AV dissociation
 Maneuvers (carotid sinus pressure and pharmacologic interventions)
 Baseline ECG: preexcitation and LBBB/RBBB
 ECG during the attack

82. ECG Clues Supporting the Diagnosis of Ventricular Tachycardia

83. FUSION AND CAPTURE (DRESSLER)BEATS

84. DIFERENTIATING VT FROM SVT WITH ABERRANT
CONDUCTIONS(BASED ON QRS MORPHOLOGY)

85. MANAGEMENT OF HEMODYNAMICALLY UNSTABLE PATIENTS

86. MANAGEMENT OF HEMODYNAMICALLY STABLE PATIENTS
 Urgent or elective cardioversion is usually appropriate.
Following appropriate conscious sedation, an initial
synchronized shock of 100 to 200 joules (monophasic) or 50 to
100 joules (biphasic) is administered. Repeated shocks at
higher energies may be performed as necessary.
 Class I and III antiarrhythmic drugs are generally reserved for
refractory or recurrent arrhythmias.
 Any associated conditions should be treated, including cardiac
ischemia, heart failure, electrolyte abnormalities, or drug
toxicities

87. PREVENTION OF RECURRENCE
 Identify and treat reversible causes
 ICDs
 Antiarrythmic drugs
 Catheter ablation

88. DOSAGE, PRIMARY INDICATIONS AND SIDE EFFECTS OF
COMMONLY USED ANTIARRYTHMIC DRUGS

89. Commonly Used Antiarrhythmic Agents—Intravenous Dose
Range/Primary Indication

90. Commonly Used Antiarrhythmic Agents—Chronic Oral
Dosing/Primary Indications

91. Common Nonarrhythmic Toxicity of Most Frequently Used
Antiarrhythmic Agents

92. Proarrhythmic Manifestations of Most Frequently Used
Antiarrhythmic Agents