Transcript Syncope & Dizziness Case Review

Amy Gutman MD ~ EMS Medical Director
[email protected] /
www.TEAEMS.com
“The only difference between syncope & sudden death is that in one
you wake up”. Engel GL. Ann Intern Med 1978

“Weak & Dizzy” is a common
complaint with both benign &
lethal causes
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Etiologies of dizziness & syncope
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Connection of cardiovascular &
neurovascular disorders

Assessment & management
strategies

No specific “dizziness” or
“syncope” protocols
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Protocol(s) used depends upon
cause & effect(s) of symptoms

A good history & physical exam
provides diagnosis in most patients

Not the patients to test how good
you are at obtaining refusals!
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82 yo WF presents with CC of “dizziness”. States intermittent,
but persistent & unpredictable moments of dizziness that “made
her head spin”. During the episodes, patient would nearly pass
out, c/o dizziness & lightheadedness with some “blurred” vision.
No CP, SOB, palpitations, seizure, loss of consciousness. No
trauma, recent illness or other complaints

Vitals & exam unremarkable by BLS crew. Patient initially did
not want to be transported to the hospital but was convinced to
get checked out. ALS crew called but unavailable

What is your differential diagnosis based upon this info?

History fairly unremarkable in otherwise healthy
patient who recently started OTC antihistamines
for sinus congestion
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Vitals stable but patient had at least 3 more
episodes on the way to the ED in which she would
lean back in stretcher & become extremely dizzy

In ED, placed on a hallway bed. During her triage,
while the RN had the patient on a monitor and
was checking her pulse he noted the following:
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Syncope (Greek: sunkoptein / to cut short)
 Sudden & self-limiting loss of consciousness with loss of postural
tone & a spontaneous recovery. A symptom, not a diagnosis
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Vertigo (Latin: vertere / to turn)
 Sensation of dizziness or abnormal motion resulting from a
disorder of the sense of balance
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Dizzy
 Having a whirling sensation with tendency to fall; bewildered or
confused; producing giddiness

50% with no specific causes

Significant cost & time to
diagnose & manage

Unpredictability leads to
negative impact on quality of life

Management specific to the
cause / suspected cause(s); varies
significantly in effectiveness


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Syncope, dizziness & vertigo are
generally symptoms rather than
diseases
Benign to fatal causes
Cardiac causes have highest
mortality rates
>500,000 new patients annually
 70,000 have recurrent, infrequent,
unexplained syncope
 3-6% ED visits annually
 2-10% hospital admissions
25%
Syncope Mortality

20%
15%
10%
5%
0%
Overall
Due to Cardiac Causes
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Traumatic sequellae

Fever, signs of illness

Focal neurological
symptoms
 Prodromal or post-episodic
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Palpitations / CP

SOB

Seizures

Nausea, Vomiting

Micturition

Loss of continence

>2 associated with 10-20%
incidence of death from
neurovascular or cardiovascular
causes within 1 year
 CAD, CHF, arrhythmia
 Chest pain
 Abnormal ECG
 Persistent orthostatic hypotension
 Age >45yrs
 Traumatic sequellae for any fall
Cause
Prevalence (Mean) %
Reflex-Mediated:
Vasovagal
18
Situational
5
Carotid Sinus
1
Orthostatic hypotension
8
Medications
3
Psychiatric
2
Neurological
10
Organic Heart Disease
4
Cardiac Arrhythmias
14
Unknown
34
Neurological
Orthostatic
11%
24%
• Vasovagal
Arrhythmia
•
Meds
•
Autonomic
Failure
14%
•
• Carotid Sinus
• Peripheral
vestibular
dysfunction
• Brainstem lesion
•
•
Presyncope
• Situational
•Cough
•Micturition
•
Non-CV
4%
12%
Brady
• Sick sinus
• AV block
• Aortic
Stenosis
*
Tachy
• VT
• SVT
• HOCM
Long QT
Unknown Cause = 34%
*DG Benditt, UM Cardiac Arrhythmia Center
Structural
• Pulmonary
HTN
• Psychogenic
• Metabolic
• Neurological
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Migraine

Hypoxia

Hyperventilation

Somatization / Psychiatric

Intoxication

Seizures

Hypoglycemia

Sleep disorders / OSA

Subclavian steal syndrome

Basilar artery migraine (syncope + headache)

Vertebrobasilar insufficiency (syncope + vascular disease)
History & Physical Exam Including ECG
ENT Evaluation
•
Sinus CT
•
Otolith evaluation
•
Hearing exam
Neurological Testing
•
Head CT / MRI / MRA
•
Carotid Doppler
•
EEG
Metabolic
•
Cardiovascular
•
Ambulatory
•
Tilt Table
•
Echocardiogram
•
EPS
•
Angiogram
•
Stress Testing
Psychological Evaluation
Laboratory

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SSX:

Onset & Duration



Provocation or Palliation
+/- & what is the reaction
Medications:





Allergies:


Associated symptoms
Sequelae
Include OTCs & topicals
PMH:

Cardiovascular, neurovascular
diseases, migraine, prior similar
episodes

Last Oral Intake:

Events
Position
Medications
Temperature

Quality

Region & Radiation
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Severity


Loss of consciousness
Time

Time of day, duration of event
History & physical exam leads to cause identification in nearly half of patients
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Sudden death
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Deafness

Arrhythmias

Congenital heart disease

Heart attack or CVA at
young age
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Seizures
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Metabolic disorders

Serial vitals

Focus on cardiac &
neurologic exams
 Stroke scale
 Glucose
 Monitor / ECG

If syncope + fall, presume a
spinal injury present until
proven otherwise
Vasovagal
Episodes after pain, fear, excitation, exertion; standing w/ locked
knees “i.e. “at attention”
Situational
Micturition, cough, swallowing
Neuralgic or
Migranous
Facial Pain or headache
Carotid Sinus
Head rotation or pressure on carotid sinus
TIA / CVA
Focal neurological symptoms that persist (CVA) or resolve within 172 hours (TIA); positive stroke scale
Subclavian
Steal
Post exercise
Seizure
Seizure activity, LOC >5 mins with post-ictal period
Murmur
Presence of heart murmur on exam or echocardiogram
Arrhythmia
Intermittent or persistent irregularity of rhythm or regularity
Psychogenic
Anxiety, hyperventilating, personal gain
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Vertebral-Basilar Stroke
 Diplopia, dysarthria, dysphagia,
weakness, numbness
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Meniere’s
 Aural fullness, deafness, tinnitus
 Brainstem evoked audiometry
95% sensitive for detecting
acoustic neuromas
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Multiple Sclerosis
 Vertigo preceded by other
neurologic dysfunction
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Psychiatric disorders
 Depression 25%
 Anxiety or panic disorder 25%
 Somatization
 Alcohol / drug abuse
 Personality disorder
 Hyperventilation
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Syncope & presyncope
overlap
 CAD, CHF, PE, dysrhythmias
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Multisensory disorder
 Peripheral neuropathy
 Visual impairment
 Musculoskeletal disorder interfering with
gait
 Vestibular disorder
 Cervical spondylosis

Symptoms worsened with
antidepressants & anticholinergics

May occur while sitting, driving or
position change
PERIPHERAL VERTIGO
CAUSES

Vestibular neuronitis
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Labyrinthitis
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Meniere’s syndrome
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Head trauma

Drug-induced
CENTRAL VERTIGO CAUSES

Cerebellar infarction or
hemorrhage
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Lateral medullary infarction
(Wallenberg’s syndrome)
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Brainstem infarction or
hemorrhage
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Multiple sclerosis
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Vertebrobasilar insufficiency
 Aminoglycosides, phenytoin,
phenobarbital, carbamazepine,
salicylates, quinine
Central vertigo associated with poor outcomes while peripheral vertigo is often
“benign”. Can have overlap in symptoms, therefore difficult to differentiate
CENTRAL ORIGIN
PERIPHERAL ORIGIN
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Vertical, horizontal or rotary
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Horizontal, torsional
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May change direction with
gaze
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Does not change direction with
gaze change
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Not diminished by fixation
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Diminished by fixation
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May fatigue (if elicited by head
movement)

Does not significantly worsen
with head movement
CEREBELLAR INFARCTION

Nystagmus + dizziness
Horner’s
Syndrome:
LATERAL
MEDULLARY
INFARCTION:
WALLENBERG SYNDROME
Ptosis, Miosis, Anhidrosis

Nystagmus + dizziness
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Nausea & vomiting
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Nausea & vomiting
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Ataxia & ipsilateral
asynergia
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Ataxia & ipsilateral
asynergia
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No focal weakness or motor
abnormality
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Hoarseness
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Horner’s syndrome
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Ipsilateral facial analgesia;
contralateral body analgesia

No focal weakness or
motor abnormality
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Often spontaneous

Acute dizziness after neck trauma /
manipulation
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Presents with posterior circulatory
infarction symptoms
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MRA may reveal double-lumen, but full
angiography has higher yield

Neurally mediated reflex mechanism with
cardioinhibitory (bradycardia) &
vasodepressor (hypotension) components
 Vasovagal syncope (VVS)
 Carotid sinus syndrome (CSS)
 Situational syncope

Loss of the normal balance between sympathetic & parasympathetic
nervous system

Triggered by stretch & mechanoreceptors (carotid sinus, bladder,
esophagus, respiratory tract)

Peripheral venous pooling causes sudden decreased venous return
 Pallor, nausea, sweating, palpitations common
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Rare except in elderly
 “Falls after losing balance”
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Sensory nerves in carotid sinus walls
respond to stimulation increasing
afferent signals to brain stem
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Reflexive increase in efferent vagal
activity & decreased sympathetic tone
results in bradycardia & vasodilation
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Different syndrome than carotid sinus
hypersensitivity, similar management
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Drug-induced
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Primary autonomic failure
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Deconditioning, parkinsonism
Secondary autonomic failure

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Often from diuretics, vasodilators
Diabetes +/- neuropathy,
amyloidoisis
Alcohol
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Orthostatic intolerance +/neuropathy
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Decline of >20mmHg SBP or 10mmHg
DBP from supine to standing
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Elderly vulnerable due to decreased
baroreceptor sensitivity, decreased
cerebral blood flow, increased renal
sodium wasting, decreased thirst
response with aging

Peripheral sympathetic tone impairment
due to diabetic neuropathy, anti-HTN
medication

Non-contrast CT helps r/o
acute hemorrhage (but not
100% accurate)

MRI more sensitive than CT for
hypoxic injury or cerebellar &
brain-stem infarctions
 PET scan may improve diagnostic
accuracy
 CT angiography or MRA useful
within 24 hours

Carotids often included in
evaluation
Not 1st line testing
Differentiates syncope from seizures
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Evaluates NMS predisposition
 Specificity of negative test 90%
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Nystagmus & vertigo with peripheral
lesions when diseased side turned
downward
 Peripheral nystagmus may fatigue with repeated
maneuvers

Central lesions not significantly changed
with position change

Symptoms of peripheral nystagmus
dramatically worsened with head
movement & tends to fatigue with
repeated maneuvers
PERIPHERAL VERTIGO
CENTRAL VERTIGO
Time before onset of
nystagmus
2-20 secs
0 secs
Duration of nystagmus
<1 min
>1 min
Fatiguability
Yes with repetitiion
Non-fatiguiing
Direction of nystagmus
Upbeat & torsional
May change direction
Intensity of vertigo
severe
Minimal to moderate
• Potential consequence is carotid occlusion / clot resulting in stroke
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LOC often w/o prodrome
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Significant injury risk

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Structural heart disease is most important
risk factor for predicting risk of death from
syncope or dizziness
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Acute MI / Ischemia
Hypertrophic cardiomyopathy
Aortic dissection
Pericarditis
Pericardial tamponade
Pulmonary embolus
Pulmonary HTN
Aortic stenosis
Atrial myxoma
Bradyarrhythmias
Tachyarrhythmias

Normal or abnormal?

Normal “now” does not equal
normal “always”

Fast or slow?
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Pauses?
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Pacemaker?
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Holter
 24-48 hours
 symptoms w/ arrhythmia (5%) v.
symptoms without arrhythmia (17%)
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External Loop Event Recorder
 Weeks to months
 Limited value in sudden LOC

Loop Recorder
 Months
 Implantable type more convenient
 Provided diagnosis in 55% of pts with
unexplained syncope compared to
conventional methods
From the files of DG Benditt, UM Cardiac Arrhythmia Center

Wide, weird & slow
 Sinus brady
 Symptomatic 1st degree HB
 3rd degree HB

Cause often correctible with
medication adjustment

Indication for atrial
pacemaker implantation
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Ventricular pacing indicated in
atrial fibrillation with slow
ventricular response
Bradycardia 36%
NSR 58%
Tachycardia 6%
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Ventricles depolarizing on their
own because of no atrial
conduction
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Rate between 20-40
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Rate of 60-120 (all PVCs) often
called “Slow VT”
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Diagnostic clue: no p waves or
flipped p waves in all leads
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Wide, weird & fast or narrow &
regular
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Regular or irregular, intermittent or
persistent
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Cause often structural, ischemic &
pathologic – not easily corrected
with a simple medication change

Surgery (if related to stenosis or
CAD) +/- ventricular pacing often
indicated

Risk of sudden cardiac death

AKA:
 Ventricular extrasystole,
premature beat, ectopic beat,
premature depolarization

Occasional monomorphic
PVCs common in normal
hearts but also seen in the
setting of heart disease

Polymorphic VT never normal
 Ischemia, metabolic or
structural disorders

QT widens to point when a PVC occurs early in the cardiac cycle
falling on the apex of preceding T wave leading to VT or torsades

Antiarrhythmics

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Psychoactive Agents

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Erythromycin, Pentamidine, Fluconazole
Antihistamines


Phenothiazines, Amitriptyline, Imipramine, Ziprasidone
Antibiotics


Class IA & III: Quinidine, Procainamide, Sotalol, Amiodarone
Terfenadine, Astemizole
Others

Cisapride, Droperidol
VENTRICULAR TACHYCARDIA

Abnormal tissues in ventricles
generating rapid & irregular rhythm

>3 PVCs in a row; can be sustained or
unsustained

Rhythm: Regular

Rate: 150-250bpm

QRS Duration: Prolonged >120ms

P Wave: Not seen, often dissociated
VENTRICULAR FIBRILLATION

Disorganized electrical signals cause
ventricles to quiver ineffectively

Rhythm: Irregular

Rate: >250, disorganized

QRS Duration: Unrecognizable

P Wave: Not seen

Patient emergently trans-thoracially
paced in ED while receiving fluid boluses &
amiodarone

Went to OR for permanent dual-chamber
(atrial & ventricular) pacemaker

Patient’s antihistamines discontinued
(unclear if contributed to symptoms)

Discharged home a few days later with no
permanent sequellae

Ventricular > atrial > dual
chamber

Most pacemakers are
“demand” type

EKG shows a “spike”
when pacer fires

Beware the patient with a
pacemaker, syncope /
dizziness with no pacer
spikes on EKG!

Recognize symptoms & avoid provocation
 Avoid alcohol, lack of sleep, environmental
stressors
 Adequate hydration & food intake
 Avoid drugs that lead to hypotension
 Avoid activities that precipitate syncope

Preventing LOC or Injury
 Supine position upon onset of prodrome
 Avoid driving or other activities that could
lead to injury

Cardiovascular / neurovascular
interventions
 Routine follow-up
 Take prescribed medications as prescribed!
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Dubin’s Guide to EKGs.
Images: Wikipedia, Google, Bing searches.
www.UpToDate.com. “Dizziness”, “Syncope”,
“Ventricular Tachyarrythmias”. 2013.
D. Okorn MD. “Approach to Dizziness”. Swedish
Family Medicine. Dec 2009
G. Bergey MD. “Acute Dizziness & Vertigo:
Diagnosis, Assessment and Management”. 2001
M. Lehmann MD. “Tacchyarrythmias”. 2010
E. Veiga, M.D, 2008
WN Kapoor. Syncope. NEJM 2000; 343: 1856-62
Freeman, R. “Neurogenic Orthostatic
Hypotension” NEJM 2008; 358: 615-624
Soteriades, et al. Incidence and Diagnosis of
Syncope. NEJM 2002; 347:878-885
Grubb, B. Neurocardiogenic Syncope. NEJM
2005; 1004-1010
DG Benditt. “Syncope - A Diagnostic & Treatment
Strategy”. Royal Brompton Hospital, London, UK
Kapoor W, Med. 1990;69:160-175
JJ Blanc, et al. Eur Heart J, 2002; 23: 815-820
WN Kapoor. “Evaluation and outcome of patients
with syncope”. Medicine 1990;69:160-175

History & exam important in
providing or eliminating a diagnosis

Most causes benign & self-limited
but almost impossible to make a
prehospital diagnosis

Serious causes suspected by
abnormal CV or neuro exam

Recognize stroke syndromes that
may present with dizziness as a
prominent feature