This document discusses palpitations, syncope, and dysrhythmias. It defines palpitations as an awareness of one's heartbeat and notes that a clear history is important for evaluation. Syncope is defined as a transient loss of consciousness due to decreased cerebral blood flow. It has multiple potential causes including neural, cardiac, neurological, and unknown factors. Dysrhythmias refer to abnormalities in cardiac rhythm that range from benign to life-threatening. Evaluation involves obtaining a thorough history, physical exam, and ECG to determine the cause and appropriate treatment. Common dysrhythmias discussed include bradycardias, atrioventricular conduction disturbances, sinus node dysfunction, atrial arrhythmias like atrial fibrill

1. Palpitations Syncope
Dysrrhythmias
Hippocrates
“Those who suffer from recurrent
Fainting die suddenly”

3. Palpitations and Syncope
Symptoms
Cardiovascular origin
May be related to Cardiac rhythm
abnormalities
Multiple causes
Assessment priority-those at risk
Treatment –Reassurance to
Intervention

4. Palpitations
“Awareness of
ones heart beat”
History important!!!!
Physical exam
Investigations
(Aim)-Correlate
symptoms with
cardiac rhythm

5. History
A clear description of the palpitation
is helpful
-Onset
-Duration of symptom
-Heart rate estimate
-Regularity of rhythm
-Trigger factors

6. Palpitations
Common
Causative
Factors
Sinus Tachycardia
Gradual onset
Anxiety and panic
Premature
Ectopic
beats
Tachydysrythmias

7. Physical Findings and Investigations
Physical Findings
Normal or Abnormal
Investigations
Electrocardiogram
Ambulatory Monitoring

8. Treatment
Reassurance-Sinus Tachycardia and
ectopic beats
Treatment of specific arrhythmias

9. Syncope
Transient loss of consciousness and
postural tone with spontaneous
recovery ( Due to decrease cerebral
blood flow)
Do not confuse with a seizure
disorder
Common 6% hospital admissions and
1-2% emergency admissions
Can occur at any age - Elderly

10. Causes
Any cause of decrease cerebral flow
particularly to the area of brain know
as the *Reticular Activating System*
Classification of causes – Prognosis
(cardiac causes mortality 18 to 33%)
“Those who suffer from recurrent
fainting die suddenly’’

11. Causes
Neurally Mediated
Cardiac
Neurological or psychiatric
Syncope of unknown origin*

12. Neurally Mediated
Disorders of Autonomic control –
orthostatic intolerance - syncope
Reflex syncope – due to an increased sensitivity of
normal reflex responses or autonomic dysfunction
where abnormal neurovascular control results in
orthostatic hypotension

13. Neurally Mediated
Reflex Mediated
Vasovagal or neurocardiogenic syncope
Carotid sinus hypersensitivity
Situational(micturation, defaecation,cough ,swallow)
Autonomic dysfunction
Pure autonomic failure atrophy(Parkinsonism,cerebellar
Multiple system)
Postural orthostatic tachycardia syndrome
Secondary autonomic failure
Vasovagal commonest cause

14. Vasovagal Syncope
Commonest cause
Affect all age groups
Hypersensitivity of the Autonomic System to any
Stimuli
Postural

15. Pathophysiology
Upright position venous pooling
Decrease CO decrease VR
Increase symp A Activation Mechanoreceptors
Withdrawal of symp and activation of
Parasymp
Vasodilatation bradycardia
Decrease cerebral flow

16. Carotid Sinus Hypersensitivity
Abnormal sensitivity of a normal
reflex
Carotid sinus massage result in
sympathetic withdrawal and
parasympathetic activation
Bradycardia prominent feature

17. Situational reflex-mediated syncope
Autonomic dysfunction
Orthostatic hypotension
Upright posture BP decrease
20mmhg systolic or decrease to 90mmhg
More common in the elderly
Do not forget drugs that may ppt syncope

18. Cardiac syncope
Rhythm Disturbances
Bradycardia
Atrioventricular block
Sinus node dysfunction
Tachycardia
Ventricular Arrhythmia
Supraventricular arrhythmia
Structural cardiac disease
Aortic stenosis
Hypertrophic cardiomyopathy

19. Neurogenic or Psychiatric
Neurological
Migraine
Vertebrobasilar disease
Subclavian steal
Psychiatric
Anxiety
Depression
Hyperventilation(Psychogenic syncope)

20. How does one evaluate a patient with
syncope ?
History Important++++
Eye witness description if possible
Physical examination
(Neurological Exam)
Logical approach to investigations

21. History
Description of syncopal episode
Provocative factors
Preceding symptoms
Recovery period
Family history
Associated injury

22. Clinical Findings

23. Investigations
Electrocardiogram*
Ambulatory Monitoring*
Tilt Testing
Electrophysiological Testing
(Specialized Tests)
Other – Echocardiography*

24. Electrocardiography
Mandatory in ALL patients
May offer clues to cause
(Underlying structural heart disease
arrhythmia, Inherited disorders)
ECG recording coupled with certain
maneuvers

25. Ambulatory Monitoring
Holter Monitoring - 24 or 48hr ECG
recording- Limitations(Intermittent)
Event recorders – Limitations
(Patient Activation)

26. Tilt Testing
Very useful in confirming diagnosis in
vasovagal syncope
Availability of the necessary hardware

27. Electrophysiological Testing
Highly specialized
Restricted to a specific category of
patients

28. Other
Echocardiography- Clinical clues

29. Treatment
Depends on the cause*
Vasovagal syncope
Reassurance
Avoid provocative factors
Carotid sinus Hypersensitivity
(Pacing)

30. Dysrhythmia
Abnormality of cardiac rhythm
Range - benign to malignant
(Extrasystoles to ventricular fibrillation
and asystole)

31. Dysrhythmias (Cont)
Symptoms – Varied.
Brady episodes may present with
syncope, presyncope and even
sudden death – other –fatigue,
memory impairment and dyspnoea.
Tachy episodes may present with
angina, palpitations , syncope and
sudden death

32. Dysrhythmia (cont)
Role of the following in the
assessment – Important
HISTORY*****
ECG************* Must be of good
quality

33. Bradycardias
Ventricular rate less than
60/min(Physiological and
Pathological)

34. Bradycardia
Results from
: reduction in the rate of normal
sinus rhythm
:
Disturbances of Atrioventrcular
conduction

35. Pathological causes
Degeneration of the sinus node , AV
node or conduction system.
Extrinsic factors – vagal stimulation
drugs,myocardial infarction
ischaemia,infitration,hypothyroidism,
hypothermia, jaundice and raised
intracranial pressure

36. A-V Conduction Disturbances
First degree – prolongation of the PR
interval.Delayed conduction from A to V.
Second degree – Intermittent of
failure in conduction from the atria to
ventricle.2 types.Type I - Progressive
prolongation of PR interval followed
by a non conducted P wave.Type II –
Normal PR internal with sudden
failure of Conduction.

37. A-V conduction disturbance (cont)
Third degree A-V block – Complete
Complete dissociation of atrial and
ventricular activity(Atria and ventricle
beating at different rates)
There is an escape rhythm(His
bundle 50/min, Purkinje – 20 to
30/min)
Varying degrees of A-v block

38. A-V Conduction disturbances
Causes
Which ones need treatment
Treatment Strategies
Role of pacing in Prognosis

39. Sinus Node Dysfunction
(Sino atrial node disease)
Inappropriate
Sinus
bradycardia
Sinus
pauses
Prone
To
Tachy
Treatment : Symptoms

40. TACHYCARDIAS
TACYARRHYTHMIAS

41. Tachycardias
Origins :Atria: Ventricle:AV junction
Mechanisms
QRS morphology and duration
Role of antiarrhythmic therapy in Rx

42. Atrial Arrhythmias
Atrial Fibrillation
Sinus Tachycardia
Atrial Flutter
Atrial Tachycardias
Junctional tachycardias
other

43. Atrial Fibrillation
Common
Mechanism – re-entry
Prevalence increases with age(5%)
Multiple causes (“Lone”A F )
Increased risk of stroke
Classification :Paroxysmal,Persistent,
Permanent
Treatment strategies linked to duration and
clinical presentation

44. Atrial Fibrillation
Clinical features (underlying cause
and those related to AF)
ECG – Recent onset AF - Rapid
irregular “f” waves at a rate of 350 to
600. Irregular ventricular response
rate due to variable
conduction.Chronic atrial fibrillation –
Absence of atrial waves with an
irregular R- R interval

45. Treatment
Onset and duration
Presence of organic disease/ppt
factors
Haemodynamic Status
Anticoagulation
Antiarrhythmics
Other

46. Atrial Flutter
Re- entry RA
Saw tooth pattern on ECG – Flutter
waves(300/min)
Termination cardioversion ( medical
or Chemical)
Progression to atrial fibrillation

47. Ventricular Tachyarrhythmias
Ventricular tachycardia
Ventricula fibrillation

49. Ventricular Tachycardia
Sustained or nonsustained
( Duration)
Monomorphic or polymorphic(Related
to constant or change of the QRS
morphology)
Multiple causes – Myocardial
infarction,CMO,HCM,ARVD,
Treatment Strategies( ECV,Drugs)
LQTS-Torsades*