Evaluation and Management of Syncope/media/files/heart and vascular/heartsymposiu… · Chest x ray...
Transcript of Evaluation and Management of Syncope/media/files/heart and vascular/heartsymposiu… · Chest x ray...
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Evaluation and Management of Syncope
Marilyn M. Cox, MD, FACC
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Definition of Syncope
A sudden and transient loss of consciousness associated with loss of
postural tone
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Syncope
• Accounts for 3% of all emergency room visits
• Accounts for 6% of a hospital’s medical
admissions
• Up to 20% of adults have one episode by age 75
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One year mortality rate in patients with syncope
• 20 to 30% with cardiac syncope • 5% for non cardiac syncope • 10 % for unexplained syncope
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Cardiac Syncope-mechanical/obstructive
Aortic stenosis Hypertrophic cardiomyopathy Pulmonary embolism Cardiac tamponade Aortic dissection Tetrology of Fallot Pulmonary hypertension Atrial myxoma
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Cardiac Syncope-arrhythmic
• AV block with bradycardia • Sinus node dysfunction with bradycardia • Supraventricular tachycardia • Ventricular tachycardia • Long QT syndrome
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Reflex Syncope
• Vasovagal • Neurocardiogenic or neurally mediated • Vasovagal (situational) • Micturiton • Deglutition • Defecation • Post-tussive • Post-prandial • Carotid sinus syncope
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Reflex Syncope
• Failure of sympathetic efferent vasoconstrictor traffic (and hypotension) occurs episodically and, frequently in response to trigger
• In chronic autonomic failure, sympathetic efferent activity is chronically impaired
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Diagnostic Evaluation-History • Premonitory symptoms • Supine or during sleep • During/ after exercise • Positional changes • Family history • Medication
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Diagnostic evaluation-Physical
• Orthostatic vital signs • Carotid sinus massage • Cardiac exam
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Definition of orthostatic hypotension
• After 2-5 minutes of quiet standing • At least a 20 mmHg fall in systolic
pressure • At least a 10 mmHg fall in diastolic
pressure Symptoms of cerebral hypoperfusion
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Orthostatic
• Dysautonomia • Volume depletion • Illness, bedrest • Drugs
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Carotid sinus massage
• Recommended in patients over age 40 years with syncope of unknown etiology
• EKG monitoring and continued blood pressure measurements during CSM is mandatory
• Duration of CSM is a minimum of 5 and a maximum of 10 sec
• Should be performed with the patient both supine and erect
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Definition of positive carotid sinus massage
• Symptoms are reproduced during or immediately after massage, in the presence of asystole longer than 3 sec and/or a fall in blood pressure of 50mmHg or more
• A positive response is diagnostic of the cause of syncope in the absence of any other competing diagnosis
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Cardiac exam • Mitral valve prolapse • Aortic stenosis • Left ventricular hypertrophy • Left ventricular outflow tract
obstruction
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Electrocardiogram findings
AV block Right or left bundle branch block Prior MI Pre-excitation Long QT interval
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Imaging studies Chest x ray –identify pneumonia, CHF, lung
mass, effusion or widened mediastinum CT of the head-low diagnostic yield in
syncope but may be helpful in patients with head trauma or new neurologic deficits
CT of chest and abdomen-indicated only in select cases ( aortic dissection, ruptured AAA, or pulmonary embolism
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Imaging studies -continued
Ventilation-perfusion scan- suspected PE Echocardiography- test of choice for
suspected mechanical cause of syncope
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EKG monitoring
-Holter monitor-use for patients with daily symptoms and/ or when looking for high grade AV block
-Event monitoring- use for patients monthly symptoms
-Implantable loop recorder- use when event recorder or EPS is unrevealing
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Other studies
Head up tilt test EEG – at discretion of neurologist if seizure
is considered likely Stress test-cardiac syncope suspected and
patient has risk factors for CAD
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Differentiating cardiac syncope versus neurocardiogenic syncope
-Syncope surrounding activity -65% vs.18% -Family history of cardiac disease or sudden
cardiac death- 41% vs. 25% -Abnormal physical findings suggesting a cardiac
diagnosis- 29% vs. 0% -Abnormal EKG -76% vs. 0% Tretter et al Dec 2013
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Neurocardiogenic Syncope
• Triggering of a neural reflex which results in a usually self limited episode of systemic hypotension characterized by both bradycardia ( asystole or relative bradycardia) and peripheral vasodilatation
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Pathophysiological Mechanisms
• Venous pooling in lower limbs reduces ventricular volume and increases sympathetic activity
• Vigorous myocardial contraction stimulates ventricular mechanoreceptors
• Triggering of a inhibitory reflex which causes paradoxical sympathetic withdrawal and vagal overactivity
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Neurocardiogenic Syncope • Usually young patients who are otherwise
healthy • Prodrome of nausea, warmth, pallor,
lightheadedness and/or diaphoresis • Induced by prolonged standing,
venipuncture (experienced or witnessed), heat exposure, painful or noxious stimuli, fear of bodily injury or exertion
• Older patients may not have an identifiable cause
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Drugs that exacerbate Neurocardiogenic Syncope
• Alcohol • Diuretics • Ace inhibitors • Nitrates • Tricyclic antidepressants • Nifedipine • Prazosin
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Tilt test protocols
• Prolonged standing ( 30-60 min) without medication provocation
• Abbreviated standing (10-15 min) with isoproterenol challenge
• Abbreviated standing ( 10-15) with nitroglycerin challenge
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Responses to tilt testing
• Normal- no hypotension or bradycardia
• Mixed response- vasodepressor and cardioinhibitory (most common)
• Pure vasodepressor (elderly) • Pure cardioinhibitory (rare)
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Treatment of Neurocardiogenic Syncope
• Avoid predisposing factors-extreme heat, dehydration
• Remove underlying causes-drugs • Interrupt any part of the cascade of
events associated with the development of syncope with drug therapy or pacing
• Behavior modification-high salt , caffeine free diet
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Physical counterpressure -Leg crossing with simultaneous tensing of
leg, abdominal and buttock muscles -Handgrip –maximum grip on rubber ball or
similar object -Arm tensing –gripping one hand with the
other while abducting both
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Drugs to treat Neurocardiogenic Syncope
• Beta blockers-may have high placebo effect
• Midodrine • Fludrocortisone • Serotonin reuptake inhibitors
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Rationale for Beta Blockers
• Catecholamines are often elevated prior to a syncopal episode
• Beta-blockers can antagonize the neuroautonomic reflex in response to this increase
• Beta-blockers reduce myocardial contractility and can prevent or reduce the frequency of ventricular contractions that activate mechanoreceptors
• Beta 2 adrenergic blockers can prevent a reduction in systemic vascular resistance
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Midodrine
• Selective, peripherally acting alpha agonist
• Causes arteriolar constriction and decreased venous capacity
• Decreases plasma volume, redistributing plasma into the extra cellular space and thereby decreasing peripheral venous pooling
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Fludrocortisone
• Mineral corticoid used to treat orthostatic hypotension
• Causes sodium retention thereby maintaining vascular volume and venous return
• May prevent vigorous contraction caused by under filling of the ventricle that activates mechanoreceptors
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Selective serotonin reuptake inhibitors
• Elevated serotonin levels have been shown to reduce central nervous system sympathetic activity and cause hypotension and bradycardia
• Elevated serotonin levels may suppress the baroreceptor reflex
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Indications for pacing in Neurocardiogenic syncope- Class I
Carotid sinus hypersensitivity- syncope and greater than 3 seconds of asystole followed by minimal carotid sinus massage
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Indications for pacing in HCSS and NCS-Class IIa
• Recurrent syncope without clear, provocative events and a hypersensitive cardioinhibitory response
• Significantly symptomatic and recurrent NCS associated with bradycardia documented spontaneously or at the time of tilt table testing
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Class III-not indicated
• Hyperactive cardioinhibitory response to CSM in the absence of symptoms or in the presence of vague symptoms (dizziness)
• Recurrent syncope, lightheadedness, or dizziness in the absence of a hyperactive cardioinhibitory response
• Situational syncope in which avoidance behavior is effective
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Summary
• Treatment depends of the frequency and severity of symptoms as well as the patient’s occupation
• Sometimes patient education and behavior modification are sufficient for treatment
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CASE STUDY
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Case study
- 55 year old woman with recurrent syncope and hypertension
- Positive tilt test 2002 initially controlled on beta blocker therapy
- Beta blocker was chosen because she was also hypertensive
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Case study -Patient remained asymptomatic until 2012 -Had syncope while talking on the phone, noted fast heart beat before she fainted , also had some chest pain
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Work -up Lexiscan nuclear –negative for ischemia Echo- normal EF, stage III-VI diastolic dysfunction, prolapse on anterior leaflet of the mitral valve, mild mitral regurgitation
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EP work up Repeat tilt test –normal on current therapy EP study –normal conduction intervals, normal sinus node and AV nodal function, no inducible arrhythmias or high grade AV block
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Loop recorder implanted Subcutaneously implanted between 3rd and 4th intercostal space Programmed to detect asystole greater than 3 seconds, bradycardia <35 BPM, tachycardia> 150 BPM
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Implantable loop recorder
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Reveal XT size compared to Reveal LinQ
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AV Block is evident on recording
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Dysautonomia
• Disorder of autonomic nervous system • Failure of sympathetic or parasympathetic components
of the ANS • Can be local, as in reflex sympathetic dystrophy or
generalized as in pure autonomic failure • Can be acute and reversible as in Guillan-Barre
syndrome or chronic and progressive • Diabetes and alcoholism can include it • Can occur as a primary condition or in association with
degenerative neurological disease such as Parkinson’s disease
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Hallmarks of dysautonomia • Sympathetic failure -Impotence ( in men), orthostatic
hypotension
• Excessive sympathetic activity- hypertension or rapid heart rate
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Treatment of dysautonomia
• No cure
• Secondary forms may improve with treatment of underlying disease
• Primary dysautonomia treatment includes measures to combat orthostatic hypotension including frequent small meals, elevate head of bed, high salt diet, fludrocortisone and midodrine
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Guillain Barre Syndrome
• Acute inflammatory Demyelinating Polyneuropathy
• Acute autoimmune Polyneuropathy
• Acute idiopathic polyneuritis
• Idiopathic polyneuritis
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Guillain Barre and variants
• Antibodies in the blood affect the autoimmune system
• Risk factors include GI or respiratory viral infection
• Ages 15-35 and 50-75
• Surgery
• Vaccination
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Guillain Barre and variants
• Weakness or tingling in legs spreading to upper body
• Restricted muscle use
• Paralysis/Difficulty breathing
• High or low blood pressure
• Abnormal heart rate
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Chronic Inflammatory Demyelinating Polyneuropathy • Rare disorder
• Inflammation of nerve roots and peripheral nerves and
destruction of myelin sheaths
• Symptoms of weakness, paralysis and /or impairment of motor function especially of limbs
• Sensory disturbances
• May affect only the autonomic nervous system
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Chronic Inflammatory Demyelinating Polyneuropathy
• In contrast to Guillain Barre patients with CIPD cannot
identify a preceding viral or infectious illness
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Treatment of Guillain Barre and variants
• Plasmapheresis
• Immunoglobulin therapy
• Not benign treatment
• Refer to neurologist for definitive diagnosis
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Summary
• The history is the most important tool in the diagnosis of syncope
• Structural heart disease must be ruled out since the mortality is highest in cardiac syncope
• Neurocardiogenic syncope is the most common cause of syncope in otherwise healthy people