IM Syncope

Syncope

• Etiology:
  • sudden and brief loss of consciousness associated with loss of postural tone, from which recovery is spontaneous
  • pathophysiology of all forms of syncope consists of a sudden decrease in or brief cessation of cerebral blood flow
• Presentation:
  • Lightheadedness
    
  • Visual blurring
    
  • Visual spots
    
  • Diaphoresis
    
  • Heaviness in LE
    
  • Postural sway
    
  • Nausea
    
  • Vomiting
    
  • Pallor or ashen gray face
    
  • Sense of “feeling bad”
  • Loss of consciousness precipitated by pain, exercise, micturition, defecation, or stressful events
  • Sweating or nausea before or during the episode
• Distinguishing syncope from other symptoms:
  • Dizziness, presyncope, and vertigo
    • Do not result in loss of consciousness or postural tone
      
    • Vertigo is associated with a sense of motion
  • Use of cardioversion to regain consciousness
    • is by definition cardiac arrest, not syncope
• Distinguishing Syncope From Seizure – Symptoms suggesting seizure:
  • Aura prior to event
    
  • Rhythmic movements, e.g. clonic or myoclonic jerks, suggests seizure, (but syncope can cause movements)
    
  • Disorientation after the event, headaches, slow to return to consciousness, and unconsciousness lasting more than five minutes suggest a seizure
• Types:
  • – Neurogenic Syncope (neurocardiogenic) – Most Common
    
    • Vasovagal (vasodepressor)
      
    • Carotid sinus hypersensitivity (syndrome)
      
    • Glossopharyngeal neuralgia
      
    • Situational syncope (post-mictural, post-tussive, post-defecation)
  • – Cardiogenic Syncope
    
    • Organic heart disease
      
    • Arrhythmia
  • – Orthostatic disease (postural hypotension)
    
    • Medication side effect
      
    • Volume depletion
      
    • Endocrinologic (hypoglycemia, DM, Addison’s)
      
    • Amyloidosis
      
    • POTS (postural orthostatic tachycardia syndrome)
  • – Neurologic Disease (central, spinal peripheral)
    
  • – Psychiatric
• DDX (SNOWPAMED):
  • Seizure, grand mal / Convulsive syncope
  • Neurogenic
    
  • Orthostatic (volume vs. dysautonomia)
    
  • VasoVagal
  • Psych/PE
  • Arrhythmia/Aortic stenosis
  • Mechanical
  • Electrolytes
    
  • Drugs
• Physical Exam:
  • 1. Search for FND = neurogenic mass vs. other
    
  • 2. Context (prodrome? seizure-like? Exertional?)
    
• Physical Exam to check for: 
  • – VS: State (or WNL or WNL except…) (no orthostatic changes)
  • – General: Patient is in no acute distress
  • – HEENT: Inspect head, mouth, carotid auscultation and palpation, thyroid exam
    • – NC/AT, PERRLA, EOMI without nystagmus, no papilledema, no cerumen, TMs normal, mouth and oropharynx normal
  • – Neck Exam: Carotid auscultation
    • – Supple, No carotid bruits, 2+ carotid pulses with good upstroke bilaterally, thyroid normal
  • – Chest Exam: Auscultation
    • – Clear breath sounds bilaterally
  • – Heart Exam: Palpation, Auscultation (orthostatic vital signs)
    • – Apical impulse not displaced, RRR, S1, S2 wnl, No murmurs, rubs, or gallops heard
  • – Extremities: Palpated peripheral Pulses Symmetric, brachial, radial, and dorsalis pedis pulses bilaterally
  • – Neuro Exam: Cranial nerves (including fundoscopic exam), Motor exam, DTRs, cerebellar, Romberg sign, gait, sensory exam
    • – CN 2-12 intact grossly; Motor: Strength 5/5 in all muscle groups; Sensation: Intact to pinprick and soft touch; DTRs, symmetric 2+ in upper and lower extremities, (-) babinski bilaterally; Cerebellar: (-) Romberg, finger to nose normal; Gait: Normal
• Work-up:
  • – CBC with diff
    
  • – Electrolytes
    
  • – Glucose
    
  • – Urine Toxicology (Urine Tox)
    
  • – EEG
    
  • – MRI
    
  • – CT
    
  • – Lumbar Puncture (LP)
    
  • – ECG and Orthostatics

Neurogenic Syncope (neurocardiogenic)

• Etiology:
  • reflex-mediated effects or direct effects by higher brain centers on the medullary center leading to changes in vascular tone and heart rate.
    
  • Activation of receptors in wall of bladder, esophagus, heart, respiratory tract, and carotid sinus lead to reflex vagal efferent activity and sympathetic withdrawal.
  • Net effect is a vicious cycle of “inappropriate peripheral vasodilatation” and “relative bradycardia” –> progressive hypotension and syncope (reversible by a supine posture or elevation of legs)
• Types:
  
  • Vasovagal (vasodepressor)
    
  • Carotid sinus hypersensitivity (syndrome)
    
  • Glossopharyngeal neuralgia
    
  • Situational syncope (post-mictural, post-tussive, post-defecation)
    • -Post-micturition Syncope
      
    • -Post-defecation Syncope
      
    • -Post-tussive Syncope
• Presentation:
  • fainting spell
• Episodes occur after:
  • – sudden unexpected:
    
    • pain
      
    • fear
      
    • unpleasant sight, sound, or smell
      
  • – after prolonged standing at attention, during heat exhaustion, or in closed overheated environments
• Exacerbating factors of Carotid Sinus Hypersensitivity:
  • -tumors
    -shaving
    -tight collars or neckties

Vasovagal Syncope

• Presentation:
  • – Syncope is often heralded by nausea, sweating, tachycardia, pallor, and feeling “faint” (same mechanism as posmicturation syncope)
  • – Emotional, Stressful situation/Pain ( may be due to excessive vagal tone with resulting hypotension)
    
  • – Quick recovery in minutes
    
  • – No seizure activity
• Physical Exam: 
  • – Normal vital signs (when recovered)

Cardiogenic Syncope

• Types of Cardiogenic Syncope:
  • Decreases in LV outflow:
    • – Aortic stenosis
      
    • – Aortic insufficiency
      
    • – Hypertrophic obstructive cardiomyopathy
      
    • – Mitral stenosis
      
    • – Left atrial myxoma
      
    • – Ball-valve thrombus
  • Obstruction to pulmonary flow:
    • – Pulmonic stenosis
      
    • – Primary pulmonary hypertension
      
    • – Pulmonary emboli
  • Dysrhythmias (Stokes-Adams attack) Bradys:
    • AV block (2nd or 3rd degree)
      
    • Sinus bradycardia, sinoatrial block, transient sinus arrest, sick sinus syndrome
  • Dysrhythmias (Stokes-Adams attack) Tachys:
    • Episodic ventricular tachycardia +/- associated bradyarrhythmias
      
    • SVT without AV block
  • LOC associated with these are often referred to as syncope but they are not genuine syncopal episodes:
    • Myocardial: massive MI with pump failure
      
    • Pericardial: cardiac tamponade
      
    • Aortic dissection

Aortic Stenosis

• Presentation:
  • – Commonly exertional or postecertional and occur w/o warning
  • – Shortness of breath
    
  • – Anginal chest discomfort
    
  • – Family history of AS
  • – Age 60 and up
    
• Physical Exam/Vital Signs:
  
  • – Narrow pulse pressure
    
  • – Displaced PMI

Cardiac Arrhythmia

• Causes:
  • – Cardiac syncope typically occurs w/o warning, although a history of palpitations may indicate the presence of underlying arrhythmias
  • – MI/Stroke = Increased risk for developing ventricular tachycardia
  • – Beta-blockers can contribute to bradyarrhythmia
• Presentation:
  • – Palpitations
  • – Chest discomfort
  • – Shortness of breath
  • – Medication history
• Physical Exam/Vital Signs
  • – Abnormal heart rate
  • – Irregular heartbear
• DDX:
  • – Cardiac Arrhythmia (causing syncope)*
    
  • – Severe aortic stenosis
    
  • – Syncope (other causes)
    
  • – Seizure
    
  • – Pulmonary embolism
• Work-up:
  • – ECG
    
  • – Holter monitoring
    
  • – CBC with diff, Electrolytes, Glucose
    
  • – Echocardiography
    
  • – CT—head

Convulsive Syncope

• Presentation:
  • – Seizure-like activity often occurs after syncope and is due to global cerebral hypoperfusion
    
  • – There is no EEG correlate and seizure w/u is not required

Hypertrophic Cardiomyopathy

• Presentations:
  • – Commonly exertional or postecertional and occur w/o warning
    
  • – Palpitations
    
  • – Dizziness
    
  • – Shortness of breath
    
  • – Younger athlete
    
  • – Family history
    
  • – Occurs with exercise
• Physical Exam:
  
  • – Heart Murmur

Orthostatic (Postural) Hypotension

• Etiology:
  • Defined as low blood pressure induced upon standing upright
    
  • Criteria: an increase in HR of 30 bpm, a decrease in systolic BP of >20 mm Hg, or diastolic BP > 10 mm Hg, after standing for at least 2 minutes (30-20-10 rule)
• Causes:
  
  • – Volume depletion (e.g. acute illness, dehydration, GI bleeding, Addison’s disease)
  • – Alcohol ingestion
    
  • – Medications that alter the vascular tone and HR
  • – Endocrinologic
    
  • – Amyloidosis
    
  • – Postural orthostatic tachycardia syndrome
• Presentation:
  
  • – Tachycardia
    
  • – Hypotension when standing
    
  • – Advanced age

Medications Causing Syncope / Drug-Induced Orthostatic Hypotension 

• Causes:
  • Vasodilators
    
  • Psychoactive Drugs
    
  • Diuretics
    
  • Drugs associated w/ Torsades de pointes
    
  • Others
• Medications Causing Syncope – Vasodilators:
  • -Nitrates
    
  • -ACE inhibitors
    
  • – CCBs
    
  • -Hydralazine
    
  • -Alpha-adrenergic blockers
• Medications Causing Syncope – Psychoactive Drugs:
  • -Phenothiazines
    
  • -Tricyclic Antidepressants
    
  • -Barbiturates
    
  • -Narcotics
• Medications Causing Syncope (Drugs associated w/ Torsades de pointes):
  • -Quinidine
    
  • -Procainamide
    
  • -Amiodarone
    
  • -Sotalol
• Medications Causing Syncope – Others:
  • -Digitalis
    
  • -Insulin
    
  • -Marijuana
    
  • -Ethanol
    
  • -Cocaine
• Presentation:
  • – Anti-hypertensive meds, diuretics, etc. can cause orthostatic hypotension and syncope
    
  • – However, lightheadedness and syncope in this condition is usually postural (i.e., occurs when getting up from a lying or seated position), and this patient’s orthostatic vital signs were normal
• DDX:
  • – Drug-induced orthostatic hypotension (causing
    syncope)
    
  • – Cardiac arrhythmia
    
  • – Syncope (vasovagal, other causes)
    
  • – Stroke
    
  • – MI
    
  • – Pulmonary embolism
• Work-up:
  • – Orthostatic Vital Signs
    
  • – CBC with diff, Electrolytes
    
  • – CT—head
    
  • – ECG
    
  • – V/Q Scan
    
  • – CTA—Chest with IV contrast

Postural Orthostatic Tachycardia Syndrome (POTS)

• Etiology:
  • Symptoms come when standing up from a reclining position, and might be relieved by sitting or lying back down.
  • The majority of POTS patients are women ages 13-50 years old
  • POTS may develop as an aftermath of significant illness, pregnancy, trauma, or mononucleosis or as a complication of an autoimmune disease such as celiac disease or Sjogren’s.
• Types:
  • Neuropathic POTS:
    • – Peripheral denervation (loss of nerve supply) leads to poor blood vessel muscles, especially in the legs and core body
  • Hyperadrenergic POTS:
    • – Overactivity of the SNS
  • Hypovolemic POTS:
    • – Reduced blood volume can lead to POTS. Low blood volume can cause similar symptoms that might overlap with neuropathic and hyperadrenergic POTS

Neurologic Diseases causing syncope

• Causes:
  • Basilar Artery Migraine
    
  • Autoimmune autonomic ganglionopathy
    
  • Parkinson disease
    
  • multiple system atrophy
    
  • pure autonomic failure
    
  • Cerebrovascular Disease
    
  • seizures

Cerebrovascular Disease

• Etiology:
  • – <5% of all TIA’s and strokes are associated with syncope
    
  • – Very rare manifestation carotid artery disease
    
  • – Almost always associated with neurologic symptoms

Seizure

• Etiology:
  • (not truly syncope by strict definition, HOWEVER, syncope can result in seizure secondarily)
  • – <2% of all syncope
    
  • – Drop attacks due to temporal lobe SZ
• Presentation:
  • – falling and losing consciousness
  • – rhythmic movements of the limbs, tongue biting and lost control of the bladder. subsequently confused 
  • – Seizures usually occur unpredictably in a manner unrelated to posture or exertion
  • – May stem from a variety of causes, including metabolic factors, trauma, vascular factors, and brain tumors
  • – Tonic-clonic seizures are often accompanied by tongue biting, incontinence, and prolonged confusion or drowsiness postictally
• Seizure Types:
  • Partial Seizures (Produced by a small area of the brain)
    1. Simple (awareness is retained)
       1. Simple Motor = Jerking, muscle rigidity, spasms, head-turning
       2. Simple Sensory = Unusual sensations affecting either the vision, hearing, smell taste, or touch
       3. Simple Psychological = Memory or emotional disturbances
    2. Complex (Impairment of awareness) = Automatisms such as lip smacking, chewing, fidgeting, walking and other repetitive, involuntary but coordinated movements
    3. Partial seizure with secondary generalization = Symptoms that are initially associated with a preservation of consciousness that then evolves into a loss of consciousness and convulsions.
  • Generalized Seizures (Produced by the entire brain) – 6 Types
    1. “Grand Mal” or Generalized tonic-clonic = Unconsciousness, convulsions, muscle rigidity
    2. Absence = Brief loss of consciousness
    3. Myoclonic = Sporadic (isolated), jerking movements
    4. Clonic = Repetitive, jerking movements
    5. Tonic = Muscle stiffness, rigidity
    6. Atonic = Loss of muscle tone
• DDX:
  • – Seizure, grand mal (now called complex tonic-clonic seizure)
  • – Convulsive syncope
    
  • – Substance abuse/overdose
    
  • – Malingering
    
  • – Hypoglycemia
• Work-up:
  • – CBC with diff, Electrolytes, Glucose
    
  • – Urine Toxicology
    
  • – EEG
    
  • – MRI—brain
    
  • – CT—head
    
  • – LP—CSF analysis
    
  • – ECG

Cataplexy

• Etiology:
  • is not syncope
    
  • a sudden and transient episode of muscle weakness accompanied by full conscious awareness, typically triggered by emotions such as laughing, crying, or terror.

Psychiatric Disorders

• Types:
  • Generalized anxiety disorder*
    
  • Panic disorder*
    
  • Major depression*
    
  • Alcohol and substance abuse
    
  • Hysteria
    
  • Conversion disorders
    
  • *predispose to a neurally-mediated reaction