Approach to syncope
-
Upload
gagan-velayudhan -
Category
Health & Medicine
-
view
106 -
download
5
description
Transcript of Approach to syncope
Approach to syncope
Dr. Gagan VSR – Cardiology
• Syncope (Greek:synkope) literally means a “cessation”, “cutting short” or “pause”
• Syncope is a transient loss of consciousness due to transient global cerebral hypoperfusion characterized by rapid onset, short duration, and spontaneous recovery.
• Cessation of blood flow leads to loss of conciousness within 10 minutes
• Important clinical problem• Disabling, may cause injuries• Upto 25% of victims of sudden cardiac death
in age 15 to 35 years presented initially with syncope/presyncope
• first episode of syncope between 10 and 30 years with a peak at 15 years of age
• Second peak ≥ 65
• Prognosis of syncope– Structural heart disease/arrhythmias – increased
risk of sudden cardiac death– Orthostatic hypotension – twofold increased risk
of mortality because of associated comorbidities– Neurally mediated syncope – excellent prognosis
Causes of real/apparent loss of conciousness
• Syncope• Neurologic
– Epilepsy– Vertebrobasilar TIA
• Metabolic syndromes/Coma– Hyperventilation with
hypocapnia– Hypoglycemia– Hypoxemia– Drug/alcohol intoxication– Coma
• Psychogenic syncope– Anxiety/panic disorders– Somatization disorders
• Syncope is characterized by– Loss of conciousness– Transient– Rapid– Short duration– And rapid recovery
Causes of Syncope
• Vascular• Cardiac• Syncope of Unknown origin
Vascular
• Anatomic– Vascular steal syndrome
(subclavian artery steal syndrome)
• Orthostatic– Autonomic insufficiency– Idiopathic– Volume depletion– Drug and alcohol
induced
• Reflex induced– Carotid sinus hypersensitivity– Neurally mediated syncope
(common faint,vasodepressor,neurocardiogenic,vasovagal)
– Glossopharyngeal syncope– Situational (acute
hemorrhage, cough, defecation, laugh, micturition, sneeze, laugh, swallow, postprandial)
Cardiac• Anatomic
– Obstructive cardiac valve disease
– Aortic dissection– Atrial myxoma– Pericardial disease,
tamponade– Hypertrophic obstructive
cardiomyopathy– Myocardial ischemia,
infarction – Pulmonary embolism– Pulmonary hypertension
• Arrhythmias• Bradyarrhythmias
– AV block,– Sinus node dysfunction, bradycardia
• Tachyarrhythmias– Supraventricular tachycardia
• Atrial fibrillation • Paroxysmal supraventricular tachycardia
(AVNRT, WPW) • Other
– Ventricular tachycardia • Structural heart disease• Inherited syndromes (ARVD, HCM,
Brugada syndrome, long-QT syndrome)• Drug-induced proarrhythmia
– Implanted pacemaker or ICD malfunction
Vascular causes
• Reflex mediated and orthostatic hypotension • Most common• One third of all syncopal episodes
VascularOrthostatic hypotension
• Standing causes 500 – 800 ml blood to displace into abdomen and lower extremities
• Decrease in cardiac output• Stimulation of aortic, carotid and cardiopulmonary
baroreceptors• Reflex increase in sympathetic outflow• Increase in heart rate, cardiac contractility and systemic
resistance• Any abnormality in this mechanism causes orthostatic
intolerance
• Syncope, presyncope, tremulousness, palpitation, fatigue, diaphoresis, blurred/tunnel vision
• Orthostatic hypotension defined as drop of 20/10 mm Hg within 3 minutes of standing
• Asymptomatic/symptomatic• Usually worse in morning, after food, after exercise• After food occurs due to redistribution in gut esp in
elderly• Upto 20 mm Hg drop in SBP after food can be seen in
elderly upto one third
• Initial orthostatic hypotension– Decrease of > 40 mm Hg immediately after
standing with rapid return to normal (<30 sec)• Delayed progressive orthostatic hypotension– Slow progressive decrease in SBP on standing
• Drugs most common cause of orthostatic hypotension, either by volume depletion or vasodilation
• Elderly are susceptible– Reduced baroreceptor sensitivity– Decreased cerebral blood flow– Renal sodium wasting– Impaired thirst mechanism
Orthostatic hypotensionneurogenic causes
• Primary and secondary autonomic failure• Primary autonomic failure
– Pure autonomic failure (Bradbury Eggleston syndrome)– Multiple System Atrophy (Shy Drager syndrome)– Parkinson diseases with autonomic failure
• Postural orthostatic tachycardia syndrome (POTS)– Milder form of chronic autonomic failure– Orthostatic intolerance char by symptoms– Increase of heart rate 28 beats/min– Absence of change in blood pressure within 5 minutes of
standing or upright tilt
Reflex mediated syncope
• Cardiovascular responses become inappropriate in response to a trigger that results in vasodilation with/without bradycardia and drop in BP and global cerebral hypoperfusion
• Trigger – afferent limb• Response – efferent limb• Efferent common – increased vagal tone and
withdrawal of peripheral sympathetic tone• Bradycardia, vasodilatation, hypotension,
presyncope/syncope
• Vasodepressor type response– Hypotension due to peripheral vasodilation
predominates• Cardioinhibitory response– Bradycardia/asystole predominates
• Mixed– Both vasodilation and bradycardia
• Micturition syncope– Mechanoreceptors in bladder– Elderly at night– Vasodilation following bladder emptying– Drugs – α adrenergic blockers for BOO
• Defecation syncope– Gut wall tension receptos
• Swallowing syncope– Afferents from upper GIT
Evaluation of syncope
• History and physical examination most important components of evaluation
• Cause can be identified in >25% of patients• Confirmation of syncope– Complete loss of conciousness?– Rapid onset, short duration and transient?– Recovery spontaneous, complete and without
sequelae?– Loss of postural tone?
• Past history of cardiac disease, diabetes• Family history of cardiac disease, syncope or sudden
cardiac death• Medications that can cause syncope• Quantify the number and chronicity of prior syncopal and
presyncopal episodes• Identify precipitating factors body position and activity
prior to syncope• Type and duration of prodromal and recovery symptoms• Witness accounts also important
Physical examination• Identify structural heart disease• Level of hydration• Neurological disease – dysautonomia or cerebrovascular
accident• Orthostatic vital signs
– BP and heart rate to be measured in supine and standing position after 3 mins
– Early orthostatic hypotension – 20/10 mm Hg drop in BP within 3 minutes of standing
– POTS – increase in 28 beats/min or more within 5 mins of standing with symptoms of orthostatic hypotension
• Carotid sinus massage– To identify carotid sinus hypersensitivity in patients more than 40 years
of age– To avoid in patients with history of TIA, CVA within 3 months, carotid
bruit unless significant stenosis ruled out by doppler– Apply gentle pressure over carotid bifurcation ie just below angle of
jaw– Pressure applied for 5 to 10 sec in both supine and upright position– Carotid sinus hypersensitivity defined as sinus pause more than 3
seconds in duration or fall in SBP of 50 mm Hg or more– Response can be cardioinhibitory (asystole) or vasodepressive (fall in
SBP)– Complications are neurologic
Tests Tilt-Table testing
• 20 min horizontal pre tilt stabilization phase• Upright tilt testing at angle between 60 to 80 degrees for
30 to 45 minutes• Sensitivity can be increased with decreased specificity by
– Longer tilt duration– Steeper tilt angles– Provocative agents like isoprenaline and Nitroglycerine– Isoprenaline – 1 – 3 μg/min to increase heart rate 25%– Nitroglycerine 300 to 400 μg spray sublingually after 20 min
unmedicated phase in upright position
• Positive response implies susceptibility to neurally mediated syncope
• Indication – confirmation of neurogenic syncope when initial evaluation is insufficient to confirm same
• Not recommended when diagnosis can be confirmed otherwise• Reflex hypotension or bradycardia without syncope is less specific
for neurally mediated syncope• In patients with structural heart disease other causes to be ruled
out before confirming neurally mediated syncope• Psychogenic pseudosyncope - loss of conciousness with no change
in vital signs• No value in assessing treatment of neurally mediated syncope