Handout Version Syncope 2013

8/13/2019 Handout Version Syncope 2013

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Syncope eeping Passing Outfrom Passing OnCarmine DAmico, D.O.

Eric Milie, D.O.

Syncope

Overview Learning objectives

Introduction

Etiology

Diagnosis

Treatment

Prognosis

Summary


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Syncope

Learning objectives1. Define syncope.

2. Discuss the relative incidences of the variouscauses of syncope.

3. State theminimum diagnostic workup forevery patient with syncope.

4. Identify themost likely cause of syncope basedon clinical presentation.

5. Name the diagnostic test of choice for apatient suspected of having neurocardiogenicsyncope.

Syncope

Introduction

Definition:

Temporary loss of consciousness and

postural tone due to transient cerebral

hypoperfusion, followed by spontaneous

recovery.


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Syncope

Introduction (cont.)Syncope is only one of many conditions that cause

transient loss of consciousness (TLOC)

Transient Loss of ConsciousnessTransient Loss of Consciousness

Concussion TLOC mimics,without true loss

of consciousnesse.g., psychogenic

pseudo-syncope

drop attacks

cataplexy

Trauma-induced Not Trauma-induced Not True TLOC

Syncope

Seizures Intoxications

Metabolic disorders

Syncope


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Syncope Mimics:Syncope Mimics:

Real or seemingly real TLOC not due to cerebral hypoperfusion:

Acute Intoxication (e.g. alcohol)

Seizures

Sleep disorders

Somatization disorder

psychogenic pseudo-syncope

Trauma/concussion

Hypoglycemia

Hyperventilation

Syncope

Syncope

Introduction (cont.)

Incidence

Children and adolescents

15 to 20% will experience syncope before

adulthood

Adults

30 to 50%

Elderly

2 to 6% annual incidence


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Syncope

Introduction (cont.)Impact

3% of emergency room visits

1% of hospital admissions

Estimated annual cost (eval. and tx):

$2,400,000,000 *

*Benjamin C. Sun, MD, MPP, Jennifer A. Emond, MS, and Carlos A.

Camargo, Jr., MD, DrPH Direct medical costs of syncope-related

hospitalizations in the USA Am J Cardiol 2005;95:668-671

Syncope

Etiology

The specific cause of syncope can be

identified in approximately 75% of

patients.


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Syncope

Etiology (cont.) Cardiovascular

Cardiac

Vascular

Neurological / Cerebrovascular

Metabolic

Psychiatric Unexplained

Syncope

Etiology (cont.)

Neurological / Cerebrovascular (


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Syncope

Etiology (cont.) Neurological / Cerebrovascular (cont.)

Cerebral syncope (cont.)

Rare cause of syncope

Orthostatic cerebral vasoconstriction in the absence ofsystemic hypotension

Cerebrovascular dysautoregulation syndrome

Syncope

Etiology (cont.)

Metabolic (


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Syncope

Etiology (cont.) Psychiatric (estimated that up to 25%

of unexplained syncopal episodes may

be psychogenic)

Hysterical faint

Panic disorder

Anxiety disorder

Syncope

Etiology (cont.)

Cardiovascular (50 to 60%)

Cardiac

Electrical

Mechanical

Vascular

Reflex-mediated

Anatomical

Orthostatic


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Syncope

Etiology (cont.)In order to fully understand the

cardiovascular causes of syncope

Syncope

Plumbing 101

CO = SV x HRCO = cardiac output

SV = stroke volume

HR = heart rate

SV is determined by: Contractility

Preload

Afterload


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Syncope

Etiology (cont.) Cardiac

Electrical

Bradyarrhythmia

Sinus node dysfunction

AV nodal block

Artificial pacemaker malfunction

Tachyarrhythmia Supraventricular

Ventricular

Syncope

Etiology (cont.)

Cardiac (cont.)

Electrical (cont.)

In general, in normal individuals, heart rates

between 30 and 180 bpm donot result in

significant reduction in cerebral blood flow

(esp. in the supine position).


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Syncope

Etiology (cont.) Cardiac (cont.)

Electrical (cont.)

Circumstances in which extremes of heart

rate are poorly tolerated:

Severe LV systolic dysfunction

Significant LV diastolic dysfunction

Significant mitral stenosis (esp. AF with RVR) Significant coronary artery disease

Syncope

Etiology (cont.)

Cardiac (cont.)

Mechanical

Aortic stenosis

Hypertrophic cardiomyopathy

Mitral stenosis

Myxoma / ball-valve thrombus

Prosthetic valve malfunction

Pulmonic stenosis

Tetralogy of Fallot


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Syncope

Etiology (cont.) Vascular (cont.)

Reflex-mediated

Trigger- varies with each specific type of

reflex-mediated syncope

Response (efferent) limb- essentially the same

for all types of reflex-mediated syncope:

Increased vagal tone Withdrawal of sympathetic tone

Syncope

Etiology (cont.)

Vascular (cont.)

Reflex-mediated (cont.)

Neurocardiogenic (a.k.a.: vasodepressor,

vasovagal, neurally mediated, common faint)

Carotid sinus hypersensitivity

Situational

Glossopharyngeal neuralgia


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Syncope



Neurocardiogenic syncope

Potential triggers:

Prolonged standing

Warm environment

Pain

Sight of blood Emotional distress


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Syncope

Etiology (cont.)

Vascular (cont.)


Carotid sinus hypersensitivity

Potential triggers:

Anything that stimulates the carotid sinus baroreceptors

3 types of abnormal responses: Cardioinhibitory

Vasodepressor

Mixed


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Syncope


Carotid sinus hypersensitivity (cont.)

Cardioinhibitory

> 3 second pause

Vasodepressor

> 50 mmHg fall in systolic BP in the absence ofbradycardia

Mixed

> 3 second pauseand > 50 mmHg fall in systolic BP


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Syncope



Situational syncope

Cough (tussive)

Micturition

Defecation

Valsalva

Deglutition

Syncope

Etiology (cont.)

Vascular (cont.)


Glossopharyngeal neuralgia

Syncope preceded by pain in oropharynx, tonsillarfossa, or tongue

Trigger: activation of afferent impulses in CN IX


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Syncope


Anatomical

Subclavian steal syndrome

Due to significant stenosis in the subclavian arteryproximal to the takeoff of the vertebral artery, useof the ipsilateral arm may result in reversal of bloodflow from the vertebral artery to the subclavian

artery (blood isstolen from the vertebral artery). So, why isnt this phenomenon called vertebralsteal

syndrome?


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Syncope


Orthostatic hypotension

Definition: > 20 mmHg drop in systolic BP or

> 10 mmHg drop in diastolic BP within 3

minutes of standing

Responsible for up to 30% of syncopal

episodes in the elderly

Syncope

Etiology (cont.)

Vascular (cont.)

Orthostatic hypotension (cont.)

Multiple causes:

Volume depletion (incl. drugs)

Vasodilatation (incl. drugs)

Neurogenic Primary autonomic failure

Secondary autonomic failure

Postprandial


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Diagnosis History and physical examination are usually

the most important clues

leading to the diagnosis.

A 12-lead electrocardiogram (EKG) should

be performed on every patient who presentswith syncope.

Further diagnostic testing should be tailored

to the suspected etiology.

Syncope

Diagnostic Evaluation of Syncope

Syncope


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Diagnosis (cont.)A 14-year-old girl experiences a

blackout when her boyfriend breaks up

with her. Physical examination, including

orthostatic blood pressures, is normal.

Syncope

Diagnosis (cont.)

A 12-lead EKG is performed. Lead II

from this EKG is shown below.

Do you notice anything unusual?

Syncope


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Diagnosis (cont.)A 55-year-old man with 11 previous

episodes of syncope over 7 years

remained undiagnosed following tilt

testing, ambulatory cardiac monitoring

with an external loop recorder, and

electrophysiological testing.

Syncope

Diagnosis (cont.)

7 months later, he experienced another

syncopal episode

Syncope


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TreatmentTherapy must be tailored to the specific

cause:

Avoidance

Correction

Interrupt reflex limbs (modulate the ANS)

Pacemaker and / or ICD implantation

Syncope

Treatment (cont.)

Recommendations for driving

Consider:

Potential for recurrence

Presence and duration of warning symptoms

Does syncope only occur while standing?

Frequency and capacity in which the patient

drives

Applicable state laws

Syncope


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Syncope

PrognosisUnderlying etiology determines prognosis

Cardiac syncope carries the worst prognosis:

Recurrent, unexplained syncope in individuals withstructural heart disease is associated with a 2-yearmortality of 40%.

Syncope

Summary

History and physical examination are usually

the most important clues leading to thediagnosis.

Always perform an EKG.

Further diagnostic testing should be tailoredto the suspected etiology.

Therapy should be directed at the specificcause whenever possible.

Handout Version Syncope 2013

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