Syncope - Harrisons 27

Front 1

Definition of syncope

Back 1

Syncope is a transient, self-limited loss of consciousness due to acuteglobal impairment of cerebral blood flow.

3 important things that are necessary to define something as syncope:

1. Rapid onset

2. Brief duration

2. Spontaneous and complete recovery

Front 2

Presyncope

Back 2

A syncopial prodrome, that can sometimes appear before loss of consciousness (but not always).

Typical symptoms include dizziness, lightheadedness or faintness, weakness, fatigue, and visual and auditory disturbances.

Front 3

Categories of causes of syncope

Back 3

1. Neurally mediated syncope (AKA reflex syncope, or vaso-vagal syncope)

2. Orthostatic hypotension

3. Cardiac syncope

Front 4

Neurally mediated syncope

Back 4

A heterogeneous group offunctional disorders that are characterized by a transient change inthe reflexes responsible for maintaining cardiovascular homeostasis.

Episodic vasodilation (or loss of vasoconstrictor tone) and bradycardiaoccur in varying combinations, resulting in temporary failure of bloodpressure control.

Front 5

Orthostatic hypotension

Back 5

Due to autonomic failure, the reflexes responsible for maintaining cardiovascular homeostasis arechronically impaired.

Definition of orthostatic hypotension:

a reduction in systolic BP of at least 20 mmHg or diastolic BP of at least10 mmHg, within 3 min of standing.

In many cases there is no compensatory increase in heart rate, despite hypotension.

Front 6

Cardiac syncope

Back 6

Due to arrhythmias orstructural cardiac diseases that cause a decrease in cardiac output.

Front 7

Incidence of syncope

Back 7

The peak incidencein the young occurs between ages 10 and 30 years, with a median peakaround 15 years.

Neurally mediated syncope is the etiology in the vastmajority of these cases.

In elderly adults, there is a sharp rise in theincidence of syncope after 70 years.

Neurally mediated is the most common cause, follow by cardiac syncope.

Both cardiac syncope and orthostatic hypotension are more common in hospitalized patients.

Orthostatic hypotension becomes more common with age (but even among the elderly is still the least common cause of the 3 categories).

Front 8

Prognosis of syncope

Back 8

The prognosis after a single syncopal event, for all age groups, is generally benign.

Syncope that is of noncardiac and unexplained origin in the young has an excellent prognosis, with no effect on life expectancy.

Cardiac syncope is associated with an increased risk of sudden cardiac death and mortality from other causes.

Mortality rate is increased in individuals with orthostatic syncope, but it is related to age and the associated comorbid conditions.

Front 9

High-risk features indicating hospitalization or intensive evaluation of syncope

Back 9

* 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 sinus pauses

* Persistent sinus bradycardia

* Bi- or trifascicular block or intraventricular conduction delay with QRSduration≥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 exercise

Front 10

"Reflex syncope"... what's this reflex everyone's talking about?

(Standing up? I too like to live dangerously)

(In short, physiology)

Back 10

Upright posture is a risky, complicated business.

Most syncopial episodes occur from a standing position.

Standing results in pooling of 500-1000 mL blood in the lower extremities and splanchnic circulation --> decrese in venous return to the heart and reduction in ventricular filling --> diminished cardiac output and blood pressure.

These hemodynamic changes provoke a compensatory reflex response, initiated by the baroreceptors in the carotid sinus and aortic arch --> increased sympathetic outflow and decreased vagal nerve activity --> increase in peripheral resistance, venous return, and cardiac output --> the fall in blood pressure is limited.

When this response fails there is cerebral hypoperfusion.

If it happens:

* chronically --> orthostatic hypotension

* transiently --> neurally mediated syncope

Front 11

Blood flow to the brain

Back 11

Typically cerebral blood flow ranges from 50 to 60 mL/min per100 g brain tissue, and remains relatively constant over perfusion pressuresranging from 50 to 150 mmHg.

Cessation of blood flow for 6–8 swill result in loss of consciousness, while impairment of consciousnessensues when blood flow decreases to 25 mL/min per 100 g braintissue.

A fall in systemic systolic blood pressureto ~50 mmHg or lower will result in syncope.

Front 12

EEG patterns in syncope

Back 12

1. "slow-fast-slow" pattern - in which normal background activity is replaced with high-amplitude slow delta waves.

This is followed by sudden flattening of the EEG - a cessation or attenuation of cortical activity - followed by the return ofslow waves, and then normal activity.

2. "slow pattern" - characterized by increasing and decreasing slow wave activityonly.

The EEG flattening that occurs in the slow-flat-slow pattern is amarker of more severe cerebral hypoperfusion.

No seizure discharges are detected.

Front 13

Causes of syncope - neurally mediated

Back 13

Vasovagal syncope

# Provoked fear, pain, anxiety, intense emotion, sight of blood, unpleasantsights and odors, orthostatic stress

Situational reflex syncope

# Pulmonary

Cough syncope, wind instrument player’s syncope, weightlifter’ssyncope, “mess trick” and “fainting lark,” sneeze syncope, airwayinstrumentation

# Urogenital

Postmicturition syncope, urogenital tract instrumentation, prostaticmassage

# Gastrointestinal

Swallow syncope, glossopharyngeal neuralgia, esophageal stimulation,gastrointestinal tract instrumentation, rectal examination, defecationsyncope

# Cardiac

Bezold-Jarisch reflex, cardiac outflow obstruction

# Carotid sinus

Carotid sinus sensitivity, carotid sinus massage

# Ocular

Ocular pressure, ocular examination, ocular surgery

Front 14

Causes of syncope - orthostatic hypotension

Back 14

Primary autonomic failure due to idiopathic central and peripheral neurodegenerativediseases—the “synucleinopathies”

# Lewy body diseases

* Parkinson's disease

* Lewy body dementia

* Pure autonomic failure

# Multiple system atrophy (Shy-Drager syndrome)

Secondary autonomic failure due to autonomic peripheral neuropathies

# Diabetes

# Hereditary amyloidosis (familial amyloid polyneuropathy)

# Primary amyloidosis (AL amyloidosis; immunoglobulin light chain associated)

# Hereditary sensory and autonomic neuropathies (HSAN) (especially typeIII—familial dysautonomia)

# Idiopathic immune-mediated autonomic neuropathy

# Autoimmune autonomic ganglionopathy

# Sjögren’s syndrome

# Paraneoplastic autonomic neuropathy

# HIV neuropathy

Postprandial hypotension

Iatrogenic (drug-induced: alpha blockers, nitrates and other vasodilators, tricyclic agents and phenothiazines.)

Volume depletion

Front 15

Causes of syncope - cardiac syncope

Back 15

Arrhythmias

# Sinus node dysfunction

# Atrioventricular dysfunction

# Supraventricular tachycardias

# Ventricular tachycardias

# Inherited channelopathies

Cardiac structural disease

# Valvular disease

# Myocardial ischemia

# Obstructive and other cardiomyopathies

# Atrial myxoma

# Pericardial effusions and tamponade

Front 16

Pathophysiology of neurally mediated syncope

Back 16

In order to elicit neutrally mediated syncope, a functioning autonomic nervous systemis necessary.

There is a sudden, transient change in autonomic efferent activitywith increased parasympathetic outflow, plus sympathoinhibition(the vasodepressor response), resulting in bradycardia, vasodilation,and/or reduced vasoconstrictor tone.

The resulting fall in systemicblood pressure can then reduce cerebral blood flow to below thecompensatory limits of autoregulation.

Multiple triggers of the afferent limb of the reflex arc can resultin neutrally mediated syncope.

In some situations, these can be clearly defined, but often the trigger is less easily recognized and the cause is multifactorial.

Hyperventilationleading to hypocarbia and cerebral vasoconstriction,and raised intrathoracicpressure that impairs venous return to theheart, play a central role in many of thesituational reflex syncopes.

Front 17

Symptoms of neurally mediated syncope

Back 17

Symptoms of orthostatic intolerance: dizziness, lightheadedness, fatigue.

Premonitory features of autonomic activation (sometimes present): diaphoresis, pallor, palpitations, nausea, hyperventilation, yawning.

During the syncopal event (may occur): proximal and distal myoclonus, eyes open and deviating upwards, dilated pupils, urinary incontinence.

Very rare, and might indicate a different diagnosis: fecal incontinence, and postictal confusion.

Front 18

Treatment for neurally mediated syncope

Back 18

Reassurance, avoidance of provocative stimuli, and plasma volumeexpansion with fluid and salt.

And may the force be with you.

(Not "may the odds ever be in your favour" because it's usually benign, and noone's going to die. Everyone can just relax.)

Front 19

Symptoms of orthostatic hypotension

Back 19

Common symtpoms: lightheadedness, dizziness, and presyncope (near-faintness) occuring in response to sudden postural change.

Symptoms may be absent or nonspecific, such as generalized weakness, fatigue, cognitive slowing, leg buckling, or headache.

Visual blurring, neck pain, and orthostatic dyspnea or angina may occur.

Symtpoms may be exacerbated by exertion, prolonged standing, increased ambient temperature, ormeals.

Syncope is usually preceded by warning symptoms, but mayoccur suddenly, suggesting the possibility of a seizure or cardiac cause.

Front 20

Treatment for orthostatic hypotension

Back 20

The first step is to remove reversible causes - usually vasoactive medications.

Next, nonpharmacologic interventions:

* Patient education regarding staged moves from supine to upright

* Warnings about the hypotensive effects of large meals

* Instructions about theisometric counterpressure maneuvers that increase intravascularpressure

* Raising the head of the bed to reducesupine hypertension

* Expanding intravascular volume by increasing dietary fluid and salt.

Pharmacologic intervension:

* Fludrocortisone acetate

* Vasoactive agents like midodrine

More medications even our tutor didn't recognize.

Front 21

Treatment for cardiac syncope

Back 21

Surprisingly, treatment for the underlying heart disease (be it arrhythmia or a structural disease or both).

Front 22

Differential diagnosis - syncope vs. seizure

Back 22

Myoclonic and other movements may occur in syncope (so it doesn't help).

Urinary incontinence can occur in syncope, but fecal incontinence is very rare - and could indicate seizure.

Loss of consciousness associated with a seizure usually lasts >5 min, and is associated with prolonged postictal drowsiness and disorientation.

In contrast, reorientation occurs almostimmediately after a syncopal event.

Seizures, unlike syncope, are rarelyprovoked by emotions or pain.

Front 23

Two other conditions that it's important to rule out in the DDx (other than seizure)

Back 23

1. Hypoglycemia

2. Cataplexy