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 first question is whether the edema is localized or
generalized. If it is localized, the local phenomena that
may be responsible should be considered.
 If the edema is generalized, one should first determine
if there is serious hypoalbuminemia, e.g., serum
albumin <25 g/L. If so, the history, physical
examination, urinalysis, and other laboratory data will
help evaluate the question of cirrhosis, severe
malnutrition, or the nephrotic syndrome as the
underlying disorder
 If hypoalbuminemia is not present, it should be
determined if there is evidence of heart failure severe
enough to promote generalized edema
 Finally, it should be ascertained as to whether or not
the patient has an adequate urine output or if there is
significant oliguria or anuria.
 The principal goal in assessing patients with
palpitations is to determine whether the symptom is
caused by a life-threatening arrhythmia.
 Patients with preexisting coronary artery disease
(CAD) or risk factors for CAD are at greatest risk for
ventricular arrhythmias
 Palpitations are brought about by cardiac (43%),
psychiatric (31%),miscellaneous (10%), and unknown
(16%) causes, according to one large series.
 Syncope is a transient, self-limited loss of
consciousness due to acute global impairment of
cerebral blood flow.
 The onset is rapid, duration brief, and recovery
spontaneous and complete
 Other causes of transient loss of consciousness need to
be distinguished from syncope; these include seizures,
vertebrobasilar ischemia, hypoxemia, and
hypoglycemia.
 A syncopal prodrome (presyncope) is common,
although loss of consciousness may occur without any
warning symptoms.
 Typical presyncopal symptoms include dizziness,
lightheadedness or faintness, weakness, fatigue, and
visual and auditory disturbances
 The causes of syncope can be divided into three
general categories:
 (1) neurally mediated syncope (also called reflex or
vasovagal syncope),
 (2) orthostatic hypotension, and
 (3) cardiac syncope.
 The clinical features, underlying pathophysiologic
mechanisms, therapeutic interventions, and prognoses
differ markedly among these three causes.
 Vasovagal syncope
Provoked fear, pain, anxiety, intense emotion, sight of
blood, unpleasant sights and odors, orthostatic stress
 Situational reflex syncope: Cough syncope ,
Postmicturition syncope , Swallow syncope,
glossopharyngeal neuralgia , Carotid sinus sensitivity ,
Ocular pressure
 B. Orthostatic Hypotension
Primary autonomic failure due to idiopathic central
and peripheral neurodegenerative diseases
Secondary autonomic failure due to autonomic
peripheral neuropathies
 C. Cardiac Syncope
 Arrhythmias
 Cardiac structural disease
 Chest pain suggesting
coronary ischemia
 Features of congestive heart
failure
 Moderate or severe valvular
disease
 Moderate or severe
structural cardiac disease
 Electrocardiographic
features of ischemia
 History of ventricular
arrhythmias
 Prolonged QT interval (>500
ms)
 Repetitive sinoatrial block or
 Persistent sinus bradycardia
Bi- or trifascicular block or
intraventricular conduction
delay with QRS
 duration≥120 ms
 Atrial fibrillation
 Nonsustained ventricular
tachycardia
 Family history of sudden
death
 Preexcitation syndromes
 Brugada pattern on ECG
 Palpitations at time of
syncope
 Syncope at rest or during
 Typically cerebral blood flow ranges from 50 to 60
mL/min per 100 g brain tissue and remains relatively
constant over perfusion pressures ranging from 50 to
150 mmHg.
 Cessation of blood flow for 6–8 swill result in loss of
consciousness, while impairment of consciousness
ensues when blood flow decreases to 25 mL/min per
100 g brain tissue.
 A decrease in cardiac output and/or systemic vascular
resistance—the determinants of blood pressure—thus
underlies th patho physiology of syncope.
 Classification of Neurally Mediated Syncope Neurally
mediated syncope may be subdivided based on the
afferent pathway and provocative trigger.
 Differential Diagnosis
 Initial Evaluation: The initial evaluation should
include a detailed history, thorough questioning of
eyewitnesses, and a complete physical and neurologic
examination
 Blood pressure and heart rate should be measured in
the supine position and after 3 min of standing to
determine whether orthostatic hypotension is present
 An ECG should be performed & Cardiac Evaluation
 Laboratory Tests Baseline laboratory blood tests are
rarely helpful
 Autonomic Nervous System testing, including tilt-
table testing, can be performed in specialized centers
 Carotid sinus massage: in patients over age 50 years with
recurrent syncope of unknown etiology. This test should
only be carried out under continuous ECG and
bloodpressure monitoring and should be avoided in
patients with carotid bruits, plaques, or stenosis.
 Psychiatric Evaluation

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clinical presenting Edema, palp,sync.pptx

  • 1.
  • 2.
  • 3.
  • 4.
  • 5.
  • 6.  first question is whether the edema is localized or generalized. If it is localized, the local phenomena that may be responsible should be considered.  If the edema is generalized, one should first determine if there is serious hypoalbuminemia, e.g., serum albumin <25 g/L. If so, the history, physical examination, urinalysis, and other laboratory data will help evaluate the question of cirrhosis, severe malnutrition, or the nephrotic syndrome as the underlying disorder
  • 7.  If hypoalbuminemia is not present, it should be determined if there is evidence of heart failure severe enough to promote generalized edema  Finally, it should be ascertained as to whether or not the patient has an adequate urine output or if there is significant oliguria or anuria.
  • 8.
  • 9.  The principal goal in assessing patients with palpitations is to determine whether the symptom is caused by a life-threatening arrhythmia.  Patients with preexisting coronary artery disease (CAD) or risk factors for CAD are at greatest risk for ventricular arrhythmias  Palpitations are brought about by cardiac (43%), psychiatric (31%),miscellaneous (10%), and unknown (16%) causes, according to one large series.
  • 10.
  • 11.  Syncope is a transient, self-limited loss of consciousness due to acute global impairment of cerebral blood flow.  The onset is rapid, duration brief, and recovery spontaneous and complete  Other causes of transient loss of consciousness need to be distinguished from syncope; these include seizures, vertebrobasilar ischemia, hypoxemia, and hypoglycemia.
  • 12.  A syncopal prodrome (presyncope) is common, although loss of consciousness may occur without any warning symptoms.  Typical presyncopal symptoms include dizziness, lightheadedness or faintness, weakness, fatigue, and visual and auditory disturbances
  • 13.  The causes of syncope can be divided into three general categories:  (1) neurally mediated syncope (also called reflex or vasovagal syncope),  (2) orthostatic hypotension, and  (3) cardiac syncope.  The clinical features, underlying pathophysiologic mechanisms, therapeutic interventions, and prognoses differ markedly among these three causes.
  • 14.  Vasovagal syncope Provoked fear, pain, anxiety, intense emotion, sight of blood, unpleasant sights and odors, orthostatic stress  Situational reflex syncope: Cough syncope , Postmicturition syncope , Swallow syncope, glossopharyngeal neuralgia , Carotid sinus sensitivity , Ocular pressure
  • 15.
  • 16.  B. Orthostatic Hypotension Primary autonomic failure due to idiopathic central and peripheral neurodegenerative diseases Secondary autonomic failure due to autonomic peripheral neuropathies  C. Cardiac Syncope  Arrhythmias  Cardiac structural disease
  • 17.  Chest pain suggesting coronary ischemia  Features of congestive heart failure  Moderate or severe valvular disease  Moderate or severe structural cardiac disease  Electrocardiographic features of ischemia  History of ventricular arrhythmias  Prolonged QT interval (>500 ms)  Repetitive sinoatrial block or  Persistent sinus bradycardia Bi- or trifascicular block or intraventricular conduction delay with QRS  duration≥120 ms  Atrial fibrillation  Nonsustained ventricular tachycardia  Family history of sudden death  Preexcitation syndromes  Brugada pattern on ECG  Palpitations at time of syncope  Syncope at rest or during
  • 18.  Typically cerebral blood flow ranges from 50 to 60 mL/min per 100 g brain tissue and remains relatively constant over perfusion pressures ranging from 50 to 150 mmHg.  Cessation of blood flow for 6–8 swill result in loss of consciousness, while impairment of consciousness ensues when blood flow decreases to 25 mL/min per 100 g brain tissue.
  • 19.  A decrease in cardiac output and/or systemic vascular resistance—the determinants of blood pressure—thus underlies th patho physiology of syncope.  Classification of Neurally Mediated Syncope Neurally mediated syncope may be subdivided based on the afferent pathway and provocative trigger.
  • 20.  Differential Diagnosis  Initial Evaluation: The initial evaluation should include a detailed history, thorough questioning of eyewitnesses, and a complete physical and neurologic examination  Blood pressure and heart rate should be measured in the supine position and after 3 min of standing to determine whether orthostatic hypotension is present
  • 21.  An ECG should be performed & Cardiac Evaluation  Laboratory Tests Baseline laboratory blood tests are rarely helpful  Autonomic Nervous System testing, including tilt- table testing, can be performed in specialized centers  Carotid sinus massage: in patients over age 50 years with recurrent syncope of unknown etiology. This test should only be carried out under continuous ECG and bloodpressure monitoring and should be avoided in patients with carotid bruits, plaques, or stenosis.  Psychiatric Evaluation