Palpitation, Breathlessness, arrhythmia

1. Breathlessness
Palpitation
Arrhythmia
Dr. Doha Rasheedy
Lecturer of Geriatric Medicine
Department of Geriatric and Gerontology
Ain Shams University

2. Breathlessness

3. Breathlessness or shortness of breath
• Difficulty in breathing / uncomfortable awareness of
breathing.
• It can be caused by various mechanisms related to
different problems in the body.
• In one’s lifetime, one may experience rare episodes of
shortness of breath as part of high levels of activity like
exhaustive exertion, or during environmental
conditions such as high altitude or very warm or cold
temperatures. Other than these extreme conditions,
shortness of breath is commonly a sign of a medical
problem.

4. When Is Shortness of Breath a Sign of a Medical Problem?
If the shortness of breath is prolonged and persistent, it is likely to be related to a
medical condition. If it is sudden and severe in intensity, even if it is of short
duration, however, it may warrant medical evaluation.
The following are other clues of existence of a medical problem:
• Shortness of breath at rest
• Shortness of breath with activity or exercise
• Shortness of breath when lying down
• Shortness of breath on exposure to allergens or provoking agents
• Shortness of breath accompanied with:
• Chest pain or chest discomfort
• Discomfort or pain in 1 or both arms, pain radiating to jaw, or pain in the neck
• Swelling in ankles and feet
• Fluid weight gain or unintentional weight loss with loss of appetite
• Unusual fatigue
• Sweating
• Yellow, green, or rusty colored sputum or phlegm or blood in the sputum
• Fever
• Wheezing or whistle-like sounds with breathing
• Persistent, chronic cough
• Blue discoloration of lips or fingertips
• Fainting, dizzy spells, lightheadedness
• Club-shaped deformation of fingertips

5. Causes

8. Lung Problems
• Recent infections, such as bronchitis or pneumonia, or prolonged
(chronic) infections, such as tuberculosis or chronic bronchitis.
Shortness of breath may be accompanied by discolored phlegm and/or
fever.
• Asthma, chronic obstructive lung disease (COPD), and emphysema: The
airways are narrowed with increased resistance to exhaling air from the
lung, resulting in air entrapment in the lung. Shortness of breath may
be accompanied by wheezing. With asthma, there is usually an allergy
history, whereas with COPD or emphysema, there is usually a smoking
history.
• Lung cancer and other tumors: Shortness of breath is commonly
accompanied by unintentional appetite and weight loss. There is usually
a long history of heavy smoking.
• Scarring and damage of lung tissue by toxins (such as asbestosis) or by
systemic illnesses (such as rheumatoid arthritis). There is usually a
known history of these systemic illnesses or occupational exposures.

9. • Clot in the lung circulation (pulmonary embolus):
Breathlessness is usually sudden and associated with rapid
breathing and may be accompanied by chest pain. People
with blood clots in the legs or pelvis (deep vein thrombosis,
or DVT), debilitating medical conditions, immobility, or
inherited tendency of forming clots may be prone to this
condition.
• Diseases of the lung sac (pleura): If the pleura thickens,
becomes scarred, or gets filled with fluid or blood because of
infection (pleurisy), cancer, or toxins (asbestosis), or if it
becomes filled with air (called pneumothorax) because of
trauma, it will hinder expansion of the lung, resulting in
shortness of breath.
• Diseases of the diaphragm : The diaphragm is the muscle
that expands the lung. It may become paralyzed after chest
surgery.
• diseases of chest wall: Obesity and spine or chest wall
deformities also can produce difficulty in breathing.

10. Cardiac causes

11. Systemic Illness Problems
• Anemia, low red blood cell count: Because the red cells
carry oxygen, when their number is extremely low, the
oxygen demands of the body will not be met, resulting in
shortness of breath.
• Increased metabolic states such as high thyroid level,
severe systemic infection (sepsis), or fever: The increased
oxygen demands of the body will try to be met by breathing
heavily and rapidly.
• Kidney or chronic liver problems: Because of increased fluid
in the lungs and body and impaired oxygen exchange in the
lungs, patients may experience shortness of breath in the
advanced stages of both conditions.

12. Nervous System Problems
• Increased intracrainial tension: caused by trauma,
tumors, stroke, or bleeding. When the portion of
the brain that regulates respiration is affected,
these rare conditions may result in difficulty in
breathing. Other neurological symptoms usually
precede shortness of breath.
• Nerve and muscle disorders that affect the ability
to coordinate and expand the chest and that
affect movement of the diaphragm may produce
difficulty in breathing. Muscular dystrophies,
Guillain-Barre syndrome, ALS / Polio, myasthenia
gravis.

13. other
• Obesity
• Physical deconditioning
• Anxiety: Anxiety is sometimes accompanied
by heavy and rapid breathing
(hyperventilation). Shortness of breath usually
resolves once the anxiety episode ends.

14. Urgently Life Threatening causes
• Upper airway obstruction
– Foreign body
– Angioedema/anaphylaxis
• Tension pneumothorax
• Pulmonary embolism
• Neuromuscular weakness
– Myasthenia gravis
– Guillain-Barre

15. Evaluation for pulmonary causes
• PFTs: spirometry (screening/simple), lung
volumes, DLCO, O2 assessment; [assess for copd, asthma,
ILD]
• Exercise assessment (6MWT) [assess functional status of any
cardiopulm disease]
• Bronchoprovocation challenge [assess for asthma]
• Serial chest radiographs, CTA / HRCT chest [assess
for ILD, cancer, CHF, HP, other]
• Targeted Labs: cbc, chems, HPP, CVD, other [assess
for anemia, CVD, HP, sarcoid, vasculitis]
• Bronchoscopy [assess for any parenchymal lung disease that
produces infiltrates on CXR/CT]
• Surgical lung biopsy [assess for any parenchymal lung disease that
produces infiltrates on CXR/CT]

16. Evaluation for Cardiac causes
• ECG
• Echocardiography
• BNP
• Exercise testing
• Coronary angiography

17. ACUTE DYSPNEA MANAGEMENT

18. Immediate Actions (in 10 minutes)
• Supplemental oxygen
• Pulse oximetry with complete vital signs
• Decide need for endotracheal intubation
• IV access, labs, and ABG
• Portable chest x-ray
• ECG if concerned for cardiac etiology
• Brief history and focused physical exam
• Form initial differential, begin treatment

19. Rapid Physical Exam
• Vital signs
– RR, HR, BP, temp, O2 Sat
• Mental Status
– Alert, confused, lethargic
• Heart
– JVP, muffled heart sounds, S3, S4
• Lungs
– Rales, wheezing, diminished or absent BS, stridor
– Respiratory accessory muscle use
• Abdomen
– Hepatomegaly, ascites
• Skin
– Diaphoresis, cyanosis
• Extremities
– Edema
– Unilateral leg swelling
• Neurologic
– Focal neurologic deficits

20. Palpitation

21. Palpitation
• The subjective awareness of the heart beating
due to change in heart rate, rhythm, or force
of cardiac contraction.
• Palpitations can be symptomatic of life-
threatening cardiac arrhythmias. However,
most palpitations are benign

22. Etiology

23. Clinical manifestation
• Fluttering, Skipping, or Pounding sensation in
the chest.
• Associated with light headiness, dizziness,
dyspnea, presyncope or syncope.
• Possible etiology:

25. Examination
• Murmurs (valvular heart disease)
• Midsystolic click (Mitral valve prolapse)
• Elevated jugular venous pressure, rales (heart
failure)
• Thyroid enlargement or nodules

26. Work up
• A 12-lead ECG evaluation is appropriate in all patients who
complain of palpitations.(may not detect arrhythmia episode)
Serious finding include:
– previous myocardial infarction
– left or right ventricular hypertrophy
– atrial enlargement
– atrial ventricular block
– short PR interval and delta waves (Wolff-Parkinson-White syndrome),
– prolonged QT interval.
– finding of an isolated premature ventricular contraction or premature
atrial contraction warrants further monitoring or exercise testing.

27. • 24-hour ECG monitoring, ambulatory event
monitor, implantable loop recorder:
For assessment of infrequent palpitation

28. • ECG exercise testing is appropriate in patients
who have palpitations with physical exertion
and patients with suspected coronary artery
disease or myocardial ischemia.
•

29. • Echocardiography to evaluate structural
abnormalities and ventricular function.

30. Electrophysiological testing
• Failed documentation of arrhythmia by 24-
hour ECG monitoring, ambulatory event
monitor, implantable loop recorder

31. Blood tests
• may be appropriate in the following conditions:
– complete blood cell count for suspected anemia or
infection
– electrolytes for arrhythmia from suspected
electrolyte imbalance
– thyroid-stimulating hormone for suspected
hyperthyroidism or hypothyroidism.
– ABG: hypoxia:

33. Arrhythmia

34. Definition of Arrhythmia
• Any abnormality in the Origin, Rate, Rhythm,
Conduct velocity and sequence of heart
activation.

35. The electrical system of the heart

36. Mechanisms of cardiac arrhythmias
• Arrhythmic activity can be categorized as passive
(e.g., atrioventricular [AV] block) or active
• The mechanisms responsible for active cardiac
arrhythmias:
– Abnormal impulse formation:
• Automaticity (enhanced pacemaker, protected pacemaker
parasystole )
• triggered activity
– reentry (most common)

37. Automaticity
• Cells in the sinus node possess the fastest
intrinsic rates. Thus the SA node is the primary
pacemaker in the normal heart. When impulse
generation or conduction within or out of the
SA node is impaired, latent or subsidiary
pacemakers within the atria or ventricle are
capable of taking control of pacing the heart.
The intrinsically slower rates of these latent
pacemakers result in bradycardia.

38. Enhanced automaticity
• Heart cells other than those of the SA node depolarize
faster than SA node cells, and take control as the cardiac
pacemaker.
• Factors that enhance automaticity include: acute
cardiac ischemia, hypoxemia, hypokalemia,
hypomagnesemia, acid–base disturbances, high
sympathetic tone, or the use of sympathomimetic
agents.
• Examples: Ectopic atrial tachycardia or multifocal
tachycardia in patients with chronic lung disease OR
ventricular ectopy after MI

39. Protected automaticity (Parasystole)
• Latent pacemakers throughout the heart are generally reset by the
propagating wavefront initiated by the dominant pacemaker and are
therefore unable to activate the heart.
• An exception to this rule occurs when the pacemaking tissue is
protected from the impulse of sinus origin. A region of entrance block
arises when cells exhibiting automaticity are surrounded by ischemic,
infarcted, or otherwise compromised cardiac tissues that prevent the
propagating wave from invading the focus, but which permit the
spontaneous beat generated within the automatic focus to exit and
activate the rest of the myocardium.
• A pacemaker region exhibiting entrance block and exit conduction
defines a parasystolic focus.
• The ectopic activity generated by a parasystolic focus is characterized by
premature ventricular complexes.
• This rhythm is fairly rare. Although it is usually considered benign, any
premature ventricular activation can induce malignant ventricular
rhythms in the ischemic myocardium or in the presence of a suitable
myocardial substrate.

40. REENTRY

41. Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Reentry Requires…
Electrical Impulse
Cardiac
Conduction
Tissue
1. 2 distinct pathways that come together at
beginning and end to form a loop.
2. A unidirectional block in one of those pathways.
3. Slow conduction in the unblocked pathway.

42. Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Premature Beat Impulse
Cardiac
Conduction
Tissue
1. An arrhythmia is triggered by a premature beat
2. The fast conducting pathway is blocked because of its
long refractory period so the beat can only go down the
slow conducting pathway
Repolarizing Tissue
(long refractory period)
Reentry Mechanism

43. 3. The wave of excitation from the premature beat
arrives at the distal end of the fast conducting
pathway, which has now recovered and therefore
travels retrogradely (backwards) up the fast pathway
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Cardiac
Conduction
Tissue
Reentry Mechanism

44. 4. On arriving at the top of the fast pathway it finds the
slow pathway has recovered and therefore the wave of
excitation ‘re-enters’ the pathway and continues in a
‘circular’ movement. This creates the re-entry circuit
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Cardiac
Conduction
Tissue
Reentry Mechanism

45. Atrial Reentry
• atrial tachycardia
• atrial fibrillation
• atrial flutter
Atrio-Ventricular
Reentry
• WPW
• SVT
Ventricular Re-entry
• ventricular tachycardia
AV Nodal Reentry
•SVT
Reentry Circuits
SA Node

46. Triggered activity
• abnormal fluxes of positive ions (usually
calcium) into cardiac cells.
• Two subclasses traditionally recognized: (1)
early, and (2) delayed. EADs interrupt or retard
repolarization during phase 2 and/or phase 3
of the cardiac action potential, whereas DADs
occur after full repolarization.
• If the after- depolarizations are of sufficient
amplitude, they can trigger the rapid sodium
channels and thus cause another action
potential to be generated.

47. • Delayed after-depolarizations arise during the resting
phase of the last beat and may be the cause of
digitalis-induced arrhythmias.
• Early after-depolarizations arise during the plateau
phase or the repolarization phase of the last beat and
may be the cause of torsades de pointes (ex.
Quinidine induced

48. Sinus Arrhythmia

49. Sinus tachycardia
• Sinus rate > 100 beats/min (100-180)
• Causes:
1. Some physical condition: exercise,
anxiety, exciting, alcohol, coffee
2. Some disease: fever, hyperthyroidism,
anemia, myocarditis
3. Some drugs: Atropine, Isoprenaline
• Needn’t therapy

50. Sinus Bradycardia
• Sinus rate < 60 beats/min
• Normal variant in many normal and older people
• Causes: Trained athletes, during sleep, drugs (ß-
blocker) , Hypothyriodism, CAD or SSS
• Symptoms:
1. Most patients have no symptoms.
2. Severe bradycardia may cause dizziness, fatigue,
palpitation, even syncope.
• Needn’t specific therapy, If the patient has severe
symptoms, planted an pacemaker may be needed.

51. Sinus Arrest or Sinus Standstill
• Sinus arrest or standstill is recognized by a
pause in the sinus rhythm.
• Causes: myocardial ischemia, hypoxia,
hyperkalemia, higher intracranial pressure,
sinus node degeneration and some drugs
(digitalis, ß-blocks).
• Symptoms: dizziness, amaurosis, syncope
• Therapy is same to SSS

52. • Sinus pause or arrest means failure of sinus node
discharge with lack of atrial activation of sinus origin.
This results in absence of P waves and periods of
ventricular asystole if lower pacemakers (junctional or
ventricular) do not initiate escape beats.
• The resulting pause in sinus activity should not be in
multiples of preceding sinus cycle length (P-P interval).
• Pauses longer than 3 sec need careful clinical
correlation with symptoms and warrant further
evaluation.

53. Sinoatrial exit block (SAB)
• SAB: Sinus pulse was blocked so it couldn’t active the
atrium.
• In SA exit block, the impulse is formed in the sinus
node but fails to conduct to the atria, unlike sinus
arrest. This particular arrhythmia is recognized on ECG
by pauses resulting from the absence of normal P
waves and the duration of the pause measuring an
exact multiple of the preceding P-P interval
• Causes: CAD, Myopathy, Myocarditis, digitalis toxicity
• Symptoms: dizziness, fatigue, syncope
• Therapy is same to SSS

54. Sinoatrial exit block (SAB)
• SA block can also be described in the same way as AV block. In first-
degree SA block, there is significant prolongation of the time for the
sinus impulse to exit into the atria (SA conduction time). This cannot be
identified clinically or electrocardiographically.
• Similar to AV block, second-degree SA block can be type I (Wenckebach)
or type II. In type I there is progressive prolongation of SA conduction,
manifested on surface ECG as progressive shortening of P-P interval,
prior to the pause created by loss of a P wave. In type II SA exit block,
the P-P intervals remain constant before the pause.
• Third-degree or complete SA block will manifest as absence of P waves,
with long pauses resulting in lower pacemaker escape rhythm; it is
impossible to diagnose with certainty without invasive sinus node
recordings..

55. Sick Sinus Syndrome (SSS)
• SSS: The function of sinus node was degenerated. SSS
encompasses both disordered SA node automaticity
and SA conduction.
• Causes: CAD, SAN degeneration, myopathy, connective
tissue disease, metabolic disease, tumor, trauma and
congenital disease.
• With marked sinus bradycardia, sinus arrest, sinus exit
block or junctional escape rhythms
• Bradycardia-tachycardia syndrome: These patients
are at increased risk for thromboembolism, and the
issue of long-term anticoagulation should be
addressed to prevent strokes.

56. Sick Sinus Syndrome (SSS)
ECG Recognition:
1. Sinus bradycardia, ≤40 bpm;
2. Sinus arrest > 3s
3. Type II SAB
4. Nonsinus tachyarrhythmia ( SVT, AF or Af).

58. Sick Sinus Syndrome (SSS)
• Therapy:
1. Treat the etiology
2. Treat with drugs: anti-bradycardia agents,
the effect of drug therapy is not good.
3. Artificial cardiac pacing.

59. Tachyarrhythmias
• Supraventricular tachycardia
• Atrial fibrillation
• Atrial flutter
• Ventricular tachycardia
» Monomorphic
» Polymorphic (Torsades de pointe)
• Ventricular fibrillation

60. Premature contractions
• The term “premature contractions” are
used to describe non sinus beats.
• Common arrhythmia
• The morbidity rate is 3-5%

61. Atrial premature contractions (APCs)
• APCs arising from somewhere in either the left or
the right atrium.
• Causes: rheumatic heart disease, CAD,
hypertension, hyperthyroidism, hypokalemia
• Symptoms: many patients have no symptom, some
have palpitation, chest incomfortable.
• Therapy: Needn’t therapy in the patients without
heart disease. Can be treated with ß-blocker,
propafenone, verapamil.

62. Atrial tachycardia
• Classify by automatic atrial tachycardia (AAT);
intra-atrial reentrant atrial tachycardia (IART);
chaotic atrial tachycardia (CAT).
• Etiology: atrial enlargement, MI; chronic
obstructive pulmonary disease; drinking;
metabolic disturbance; digitalis toxicity;
electrolytic disturbance.

63. Atrial tachycardia
• May occur transient; intermittent; or persistent.
• Symptoms: palpitation; chest uncomfortable,
tachycardia may induce myopathy.

64. Intra-atrial reentry tachycardia (IART)
• ECG characters:
1. Atrial rate is around 130-150bpm;
2. P’ wave is different from sinus P wave;
3. P’-R interval ≥ 0.12”
4. Often appear type I or type II, 2:1 AV block;
5. EP study: atrial program pacing can induce and
terminate tachycardia

65. Automatic atrial tachycardia (AAT)
• ECG characters:
1. Atrial rate is around 100-200bpm;
2. P’ wave is different from sinus P wave;
3. P’-R interval≥ 0.12”
4. Often appear type I or type II, 2:1 AV block;
5. EP study: Atrial program pacing can’t induce
or terminate the tachycardia

67. Chaotic atrial tachycardia (CAT)
• Also termed “Multifocal atrial tachycardia”.
• Always occurs in COPD or CHF,
• Have a high in-hospital mortality ( 25-56%). Death
is caused by the severity of the underlying disease.
• ECG characters:
1. Atrial rate is around 100-130bpm;
2. The morphologies P’ wave are more than 3 types.
3. P’-P’, P’-R and R-R interval are different.
4. Will progress to af in half the cases
5. EP study: Atrial program pacing can’t induce or
terminate the tachycardia

69. MAT
• Automatic atrial rhythm from various
different foci
• Seen in hypoxia, COPD, atrial stretch and
local metabolic imbalance.
• Three or more types of p waves and a rate
> 100
• Digoxin worsens it, so treat with oxygen
and slow calcium channel blocker like
verapamil or diltiazem.

70. Therapy
• IRAT: RFCA, Ic and IV class anti-tachycardia
agents
• AAT: Digoxin, IV, II, Ia and III class anti-
tachycardia agents; RFCA
• CAT: treat the underlying disease, verapamil or
amiodarone.
• Associated with SSS: Implant pace-maker.

71. Atrial fibrillation
• Prevalence increases with increasing age of the
population: 0.5% in ages 50–59 years and 8.8% in ages
80–89 years.
A classification by Camm has divided AF into the following:
• Paroxysmal: characterized by self-terminating episodes
that generally last <7 days (most <24 hours),
• persistent AF generally lasts >7 days and often requires
electrical or pharmacologic cardioversion.
• Permanent: established AF. Cannot be terminated by
drugs or DC cardioversion. Patients need rate control
therapy plus consideration of anticoagulation. Ablation
can be successful

73. Common Causes
• Ischaemic heart disease
• Alcohol: chronic alcohol consumption
• Thyrotoxicosis
• Mitral valve disease: LA dilatation caused by
mitral stenosis and/or regurgitation
• Hypertension: accounts for about 50% cases
• Cardiac surgery: right atrial cannulation;
thoracotomy.
• Pyrexial illness, chest infection, etc.

74. Less Common Causes
• General anaesthesia
• Hypoxia: chronic pulmonary disease
• Pulmonary embolism
• After ASD closure
• Chest trauma
• Pregnancy
• Heart muscle disease: dilated cardiomyopathy ,
hypertrophic
• Obstructive sleep apnoea
• Provocation by pacing wire, catheter in either atrium
• Part of the rhythm spectrum of sinoatrial disease
• Malignant infiltration.

75. • If no cause is apparent and the heart is otherwise
normal clinically and on echocardiography, the
term ‘lone AF’ is used.

76. Treatment
1- Anticoagulation
Stroke Risk and Stratification for long term
anticoagulation CHADS2 Scoring System:
• A total score of 0–1 should be managed with soluble
aspirin. A score of 2 or more should be anticoagulated
with warfarin, but the hypertension must be well
controlled.

77. Rhythm control
• Cardioversion can be accomplished using either antiarrhythmic drugs
or the direct-current approach. In situations where urgent
cardioversion is needed, such as marked hypotension, the direct-
current approach is preferred.
The need for anticoagulation prior to cardioversion must be considered:
• There is general consensus that AF that has been present for <48 hours
can be cardioverted without prior anticoagulation, but there are no
randomized trial data to support this, and probable systemic emboli
can occur in this situation.
• Because often it is impossible to time accurately the onset of AF,
anticoagulation therapy is recommended for AF of uncertain duration.
• There are two basic strategies to deal with cardioversion: (1) oral
warfarin with a therapeutic INR (2–3) for 3 to 4 weeks before
cardioversion followed by continued warfarin thereafter or (2)
transesophageal echocardiography (TEE) and heparin immediately
before cardioversion followed by oral warfarin thereafter.
• Anticoagulation should be continued for 1 month after successful
cardioversion

78. DC Cardioversion
• Start with 200J shock (100 J if in atrial fl utter). If
failure to cardiovert: second shock, 300 J. If
failure: give disopyramide 100 mg i.v or flecainide
50–100 mg slowly over 5–10 min. Third shock
360 J with paddles in anteroposterior position.
• If still fails: consider treatment with amiodarone
for 1 month and a further attempt, or just accept
AF as definitive rhythm and treat with rate
control and long-term warfarin.
• Successful cardioversion: Disopyramide, ß
blockade or amiodarone helps maintain sinus
rhythm.

79. Pharmacological cardioversion
• This is most likely to succeed with recent-onset AF.
• Flecainide 2 mg/kg i.v. over 10 min is the drug of choice but should
be avoided in patients with poor LV function because it has a
negative inotropic effect.
• Disopyramide 50– 150 mg i.v. slowly over 5 min is an alternative.
• Fibrillatory waves may coarsen and the ventricular response
increase before sinus rhythm is achieved.
• Amiodarone given orally (200 mg three times daily up to 400 mg
three times daily for 1 week) may also result in version to sinus
rhythm. The dose is reduced after 1 week. Amiodarone is also very
useful given intravenously: 5 mg/kg over 4 h in 5% dextrose. The
maximum intravenous dose over 24 h in an adultis 1200 mg. An
immediate result should not be expected: it may take 24–48 h to
convert the patient back to sinus rhythm. The patient can be
converted to oral amiodarone when practical.

81. Rate control
• In permanent AF, drug therapy is used to control
the rate of ventricular response by increasing AV
node refractoriness.
• Control of the ventricular rate involves both
acute and chronic phases. In the acute phase,
intravenous diltiazem, metoprolol, esmolol, or
verapamil have all been demonstrated to
provide slowing of AV nodal conduction within 5
minutes; these drugs are indicated for patients
with severe symptoms related to a rapid
ventricular rate.

82. • Target rate: is 60 to 80 beats/min at rest and
between 90 and 115 beats/min during moderate
exercise.
• Digoxin may provide effective control of the
resting heart rate but is often ineffective during
exertion.
• β Adrenergic blockers or calcium channel
antagonists provide much better control of the
ventricular rate during exercise and should be
considered for most patients.
• Digoxin is most useful in the setting of impaired
systolic function, and can be used in combination
withβ blockers or calcium antagonists if these
agents do not provide adequate rate control.

83. Catheter ablation
• Recent approaches to catheter ablation of AF,
especially paroxysmal AF, have been to
eliminate triggering foci, primarily within the
pulmonary veins

84. Atrial Flutter
• There are several types of atrial flutter, all having rapid,
regular atrial rates, generally 240 to 340 beats/min,
because of a reentrant mechanism in the atria.
• Types:
– Typical, also called counterclockwise atrial flutter is
characterized by negative sawtooth flutter waves in ECG leads
II, III, and aVF
– reverse typical, also called atypical or clockwise atrial flutter
by positive flutter waves in ECG leads II, III, and aVF
• Both types use the sub-Eustachian or cavotricuspid
isthmus (i.e., the isthmus between the tricuspid annulus
on one side and the inferior vena cava–Eustachian ridge-
coronary sinus on the other) as a part of the reentrant
circuit
• Usually a 2:1 conduction pattern.

85. Atrial Flutter

86. Management
Acute Treatment of Atrial Flutter
atrial flutter should be treated acutely to restore sinus rhythm, or at the very
least, to control the ventricular response rate as needed.
• Cardioversion: Transthoracic direct current (DC) cardioversion of atrial
flutter to sinus rhythm has a very high likelihood of success.
• Pharmacological cardioversion: Antiarrhythmic drug therapy to restore
sinus rhythm is primarily intravenous ibutilide, procainamide.
• Drug therapy may also be used to slow the ventricular response rate as
needed:
• Useful agents include β blockers, verapamil, diltiazem, and digitalis, alone
or in combination. It is often difficult to achieve sufficient AV nodal block
to slow adequately the ventricular response during atrial flutter, and 2:1
AV conduction frequently recurs.
• Rapid atrial pacing can also be used to restore sinus rhythm.

87. Long-Term Treatment of Atrial Flutter
Catheter Ablation Therapy: is highly successful, typically 90 percent or greater, to cure
atrial flutter.3 This coupled with the recognized difficulty in achieving adequate long-term
suppression with antiarrhythmic drug therapy make catheter ablation a first-line treatment
option for many patients.
• Because classical atrial flutter is usually preceded by a variable period of AF, successful
ablation of the atrial flutter reentrant circuit per se may not prevent either the new
appearance or the recurrence of AF.
Antiarrhythmic Drug Therapy
• Selection of an antiarrhythmic drug to treat atrial flutter mirrors that to treat AF. However,
this form of therapy is no longer the treatment of choice for long-term therapy in most
patients with atrial flutter, because catheter ablation to cure atrial flutter has superseded
it.
Anticoagulant Therapy
• In patients with atrial flutter, daily warfarin therapy to achieve an INR between 2 and 3
(target 2.5) is recommended using the same criteria as for AF. In addition, several studies
indicate that the incidence of stroke associated with atrial flutter approaches that of AF
Antitachycardia Pacemaker Therapy
• Although available and effective, little use has been made of implantation of an
antitachycardia pacemaker to treat (interrupt) atrial flutter. Antitachycardia pacing can be
used acutely in patients with atrial flutter who have an implanted pacemaker or
defibrillator with the capability of temporary rapid atrial pacing therapies.

88. Multifocal Atrial Tachycardia

89. VENTRICULAR ARRHYTHMIA

90. Ventricular Premature Contractions (VPCs)
• Etiology:
1. Occur in normal person
2. Myocarditis, CAD, valve heart disease,
hyperthyroidism, Drug toxicity (digoxin,
quinidine and anti-anxiety drug)
3. electrolyte disturbance, anxiety, drinking,
coffee

91. VPCs
• Manifestation:
1. palpitation
2. dizziness
3. syncope
4. loss of the second heart sound

92. PVCs
• Therapy: treat underlying disease, antiarrhythmia
• No structure heart disease:
1. Asymptom: no therapy
2. Symptom caused by PVCs: antianxiety agents, ß-
blocker and mexiletine to relief the symptom.
• With structure heart disease (CAD, HBP):
1. Treat the underlying diseas
2. ß-blocker, amiodarone
3. Class I especially should be avoided because of
proarrhytmia and lack of benefit of prophylaxis

93. Ventricular tachycardia
Non-sustained VT
• three or more ventricular premature beats at a rate of >100 beats/min
terminating in <30 s.
Sustained VT
• VT lasting >30 s, or requiring termination resulting form haemodynamic
compromise in <30 s.
VT may be monomorphic with a stable single QRS morphology, or
polymorphic with a changing multiform QRS morphology

95. Ventricular Flutter
• This is a term occasionally used to describe
monomorphic VT at a rate of approximately
300/min. No isoelectric interval between QRS
complexes.
Ventricular Fibrillation
• This is a rapid ventricular rate >300/min with
marked variability in QRS cycle length and QRS
amplitude.

97. Management of VT in a
Haemodynamically Stable Patient
• Establish intravenous access. Check blood for K , acid–
base balance and arterial blood gases and correct if
necessary.
• Start amiodarone 300 mg in 5% dextrose over 10 min
then aim to deliver a total of 1200 mg over 24 h.
• Assume hypomagnesaemia. Give 10 mmol magnesium
sulphate over 30 min.
• If VT persists, or haemodynamics deteriorates: for DC
shock. It is much safer to shock a patient early for VT
than to try several different antiarrhythmic drugs.

98. Management of VT in a
Haemodynamically Unstable Patient
• Establish intravenous access. Check blood for K, acid–base balance
and blood gases in all patients and correct if necessary (including
artifi cial ventilation
• Cardiac massage may help correct the arrhythmia.
• High-flow oxygen.
• DC synchronized shock 200 J. If fails: DC shock 360 J.
• Give amiodarone 300 mg i.v. in 20 ml 5% dextrose over 5–10 min. If
unavailable, give lidocaine 100–200 mg bolus followed by infusion.
• Assume hypomagnesaemia. Give 10 mmol magnesium sulphate
over 30 min
• If still in VT: further 360 J shock.
• Consider overdrive pacing.
• Consider alternative antiarrhythmic drug, e.g. intravenous
mexiletine.

99. Long-term Prophylaxis
• Once successfully cardioverted, prophylactic therapy is
started orally and ICD implantation is considered .
• The effect of the chosen drug is monitored with 24-
hour Holter). It is important to keep the serum K
between 4.5 and 5.5 mmol/l.
• If VT was secondary to MI or acute myocarditis, it is
probably wise to continue drug therapy for 3 months in
the first instance, and then repeat 24-hour monitoring
both on the drug and after its withdrawal. In some
cases more than one drug will be necessary and
indefinite oral therapy may be required.

100. Regimens of choice are one or more of
these drugs:
• Disopyramide 100 mg three or four times daily
• Mexiletine 200 mg three times daily
• Amiodarone 200 mg three times daily for 1 week then
reducing
• Propafenone 150–300 mg three times daily
• ß-Blocking agent flecainide 100–200 mg twice daily.
Drugs of second choice may be added or tried separately:
• Procainamide 375 mg 4-hourly
• Quinidine durules, two twice daily
• Phenytoin 100 mg three times daily to 200 mg twice daily.
The best combinations (e.g. disopyramide or mexiletine and
amiodarone).

101. Ventricular flutter and fibrillation
1. Cardio-Pulmonary Resuscitate (CPR)
2. ICD

102. Long QT Syndromes
• A long QT interval may be congenital (inherited gene defects) or
acquired (drug or electrolyte effects), resulting from abnormalities
of the ion channels controlling the duration of repolarization.
• long QT interval may predispose to VT often of the polymorphic
torsades de pointes type.
Acquired Long QT Interval
• This is most commonly drug-induced or secondary to
hypocalcaemia or hypomagnesaemia. It may occur in anorexia
nervosa. Prolongation of the QT interval is part of the therapeutic
benefit of drugs such as amiodarone and sotalol, and the finding
of a long QT interval is not necessarily an indication to stop the
drug unless the QT interval is >500 ms.

103. Management of Torsades de Pointes
• Torsades respond poorly to conventional drugs and may be made
worse by class Ia agents, e.g. lidocaine, or class III agents. The
probable culprit drug is stopped.
Consider the following:
• Pacing: temporary or permanent. Atrial pacing at 90–110/min
shortens the QT interval, helping to prevent torsades.
• Magnesium sulphate infusion (even if magnesium level is normal):
1–2 g i.v. over 2–3 min (equivalent to 2–4 ml 50% magnesium
sulphate). Then infuse at 2–8 mg/min.
• Isoprenaline infusion 2–10 µg/min, intravenous magnesium (even
if magnesium level is normal) or overdrive atrial pacing to rates of
90–110/min.
• Potassium replacement to get K to 4.5–5.0 mmol/l.

105. SUPRAVENTRICULAR TACHYCARDIA

106. • paroxysmal supraventricular tachycardia (PSVT) refers to
a clinical syndrome characterized by a rapid, regular
tachycardia with abrupt onset and termination.
• Approximately two-thirds of cases of PSVT result from
AV nodal reentrant tachycardia (AVNRT). Orthodromic
AV reentrant tachycardia (AVRT), which involves an
accessory pathway, is the second most common cause of
PSVT, accounting for approximately one-third of cases.
• The heart rate may be 140–240 beats/min (usually 160–
220 beats/min) and is regular (despite exercise or
change in position) The P wave usually differs in contour
from sinus beats and is often buried in the QRS complex.

107. Treatment
Mechanical Measures:
• increase in vagal tone and include the Valsalva
maneuver
• Carotid sinus massage is often performed by
physicians but should be avoided if the patient
has carotid bruits or a history of transient
cerebral ischemic attacks

108. Drug Therapy
• Adenosine: a 6 mg bolus is administered. If no response is observed
after 1–2 minutes, a second 12 mg bolus should be given, followed by
a third if necessary.
• Intravenous verapamil may be given as a 2.5 mg bolus, followed by
additional doses of 2.5–5 mg every 1–3 minutes up to a total of 20 mg
if BP and rhythm are stable. If the rhythm recurs, further doses can be
given. Oral verapamil, 80–120 mg every 4–6 hours, can be used as well
in stable patients who are tolerating the rhythm without difficulty, but
avoid it if there is any concern that the arrhythmia may be ventricular
in origin.
• Intravenous diltiazem (0.25 mg/kg over 2 minutes, followed by a
second bolus of 0.35 mg/kg if necessary and then an infusion of 5–15
mg/h) may cause less hypotension and myocardial depression.
• Esmolol, a short-acting -blocker, may also be effective; the initial dose
is 500 mcg/kg intravenously over 1 minute followed by an infusion of
25–200 mcg/min. Metoprolol is also effective and can be given in 5 mg
boluses every 5 minutes and repeated up to two times

109. Cardioversion
• If the patient is hemodynamically unstable or if
adenosine and verapamil are contraindicated or
ineffective, synchronized electrical cardioversion
(beginning at 100 J) is almost universally
successful. If digitalis toxicity is present or
strongly suspected, as in the case of paroxysmal
tachycardia with block, electrical cardioversion
should be avoided

110. Catheter Ablation
• Because of concerns about the safety and the
intolerability of antiarrhythmic medications,
radiofrequency ablation is the preferred
approach to patients with recurrent
symptomatic reentrant supraventricular
tachycardia, whether it is due to dual
pathways within the AV node or to accessory
pathways.

111. Atrioventricular Block
• AV block is a delay or failure in transmission of
the cardiac impulse from atrium to ventricle.
• Etiology:
Atherosclerotic heart disease; myocarditis;
rheumatic fever; cardiomyopathy; drug toxicity;
electrolyte disturbance, collagen disease, lev’s
disease.

112. AV Block
 AV block is divided into three categories:
1. First-degree AV block
2. Second-degree AV block: further
subdivided into type I and type II
3. Third-degree AV block: complete block

113. First Degree AV Block
• Delay at the AV node results in prolonged PR
interval
• PR interval>0.2 sec.
• Leave it alone

114. Second Degree AV Block Type 1
(Wenckebach)
• Increasing delay at AV node until a p wave is not
conducted.
• Often comes post inferior MI with AV node ischemia
• Gradual prolongation of the PR interval before a skipped
QRS. QRS are normal!
• No pacing as long as no bradycardia.

115. Second Degree AV Block Type 2
• Diseased bundle of HIS with BBB.
• Sudden loss of a QRS wave because p wave was
not transmitted beyond AV node. QRS are
abnormal!
• May be precursor to complete heart block and
needs pacing.

116. Third Degree AV Block
• Complete heart block where atria and ventricles
beat independently AND atria beat faster than
ventricles.
• Must treat with pacemaker.

117. AV Block
• Treatment:
1. I or II degree AV block needn’t
antibradycardia agent therapy
2. II degree II type and III degree AV block
need antibradycardia agent therapy
3. Implant Pace Maker

118. Intraventricular Conduction
Abnormalities
• There are multiple types of IVCA:
Block of one fascicle
• right bundle branch block (RBBB),
• left anterior fascicular block (LAFB),
• left posterior fascicular block (LPFB)
Bifascicular blocks,
• left bundle branch block (LBBB),
• The combination of RBBB and LAFB, or RBBB and
LPFB,
trifascicular block denotes a block in all three fascicles.

119. Right bundle branch block
ECG findings include:
• (1) widened QRS complex (O0.12 seconds),
• (2) deep, wide S wave in left-sided leads (I, V5, and V6), and
• (3) secondary R wave in right precordial leads (rsr-, rSR-, or rsR-
).

121. Left anterior fascicular block
• The ECG findings of LAFB include a QRS complex
generally<0.12 seconds, a leftward axis shift (usually -45 to -
90 ), rS pattern in the inferior leads (II, III, and aVF), and qR
pattern in leads I and aVL.

122. Left posterior fascicular block
Electrocardiographic findings in LPFB include:
1. a rightward axis shift,
2. an rS pattern in leads I and aVL,
3. and a qR pattern in lead III and often in lead aVF.
4. The QRS complex duration is usually normal

123. Bifascicular block
• is the combination of an RBBB and an LAFB, or an RBBB plus an LPFB.
• In addition, because the left bundle branch is composed of an anterior
and a posterior fascicle, LBBB can be thought of as bifascicular block.
• Bifascicular blocks are of particular importance in the setting of an
acute MI, because their presence may suggest impending complete
heart block.
• The most common type of bifascicular block is the combination of an
RBBB and an LAFB

124. RBBB and an LAFB
• The ECG is characterized by features of an RBBB (QRS duration
• O0.12 seconds, rsR# or qR in leads V1 and V2, wide or deep S
waves in leads I and V6), in addition to a leftward QRS axis and
the findings of LAFB (see earlier discussion) in the limb leads.

125. RBBB and an LPFB
• will demonstrate findings of an RBBB, plus
a right axis deviation and the other findings
of LPFB

126. LBBB
ECG criteria for LBBB include a QRS duration O0.12 seconds, a broad
monomorphic R wave in leads I, V5, and V6, a wide S wave following an
initial small (or absent) R wave in the right precordial leads, and absence
septal Q waves in leads I, V5, and V6 (Fig. 6). The term incomplete
LBBB is used to describe these findings in patients who have a QRS complex
duration !0.12 seconds (usually 0.10–0.11 seconds) Left bundle branch
block ECG findings include (1) widened QRS complex (O0.12 seconds),
2) QS or rS complex in lead V1, (3) late intrinsicoid deflection and monophasic R
wave in lead V6, and (4) no Q wave in lead V6 [5].

127. Classification of Anti-arrhythmics
Cla ss Action Exa mples Side Ef fects
1A Fa st sodium chan nel blocker va ries
depola riza tion a nd a ction potential
dura tion
Q uinidine,
proca ina mide,
disop yra mide
Cla ss: na usea , vomiting
Q uinidine: h emolytic
a nemia, thrombo cytope nia ,
tinnitus
Procaina mide: lupus
1B Lido ca ine,
Mex iletine
Lido ca ine: dizziness,
confusion, seizures, coma
Mex iletine: tremor, a taxia,
ras h
1C Fleca inide,
Prop afen one
Fleca inide: pro-a rrhythmia ,
na usea , dizzy ness
2 beta-b lockers SA nod e & AV node
conduction
Prop ra nolol,
metop rolol
Cla ss: CHF, b ronchospa sm,
bra dyca rdia , hypo tension
3 Prolong a ction poten tia l by blocking
K+ c ha nnels
Amioda rone,
sota lol
Amioda rone: hepa titis,
pulmona ry fibro sis, thyroid
disorde rs, periphe ra l
neu ro pa thy
So talol: bronchospa sm
4 calcium cha nnel blockers AV node
conduction
Vera pa mil,
dilitia zem
Cla ss:A V block,
hypotension, bra dycar dia,
constipa tion

128. THANK YOU