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Medicine 2 > Dizziness and Syncope > Flashcards

Dizziness and Syncope Flashcards

1
Q

differential diagnosis of dizziness

A
  • Vertigo (Central, Peripheral)
  • Disequilibrium
  • Presyncope/Syncope
  • Nonspecific dizziness (Psychiatric, Unknown/Other)
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2
Q

dizziness by etiology

A
  • 40% vestibular
  • 10% central brainstem
  • 15% psych
  • 25% other (Presyncope, Disequilibrium, Hypoglycemia, Hyperventilation, Head trauma/whiplash)
  • 10% unknown
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3
Q

evaluation of dizziness

A
  • History is most important (Sensation of movement, esp with head movement, Assoc sx including tinnitus, hearing loss, ataxia, fall, syncope, sweating, LOC, post-ictal state, Duration of symptoms, timing, risk factors)
  • PE to confirm suspected dx, eval for neuro deficits – a good physical exam will give you a diagnosis, you don’t usually need labs. If anything, may want a glucose level (Orthostatic changes, observe gait, nystagmus most helpful signs)
  • Labs/dx studies usually not needed (Should be tailored to suspected etiology)
  • Other PE that may be indicated/helpful: Weber/Rinne test if hearing loss; Dix-Hallpike or head thrust test if vertigo; etc
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4
Q

Dix-hallpike maneuver

A

-With the patient sitting, the neck is extended and turned to one side. The patient is then placed supine rapidly, so that the head hangs over the edge of the bed. The patient is kept in this position and observed for nystagmus for 30 seconds. In patients with benign paroxysmal positional vertigo, nystagmus usually appears with a latency of a few seconds and lasts less than 30 seconds. It has a typical trajectory, beating upward and torsionally, with the upper poles of the eyes beating toward the ground. After it stops and the patient sits up, the nystagmus will recur but in the opposite direction. Therefore, the patient is returned to upright and again observed for nystagmus for 30 seconds. If nystagmus is not provoked, the maneuver is repeated with the head turned to the other side. If nystagmus is provoked, the patient should have the maneuver repeated to the same (provoked) side; with each repetition, the intensity and duration of nystagmus will diminish.

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5
Q

vertigo

A
  • Main symptom of vestibular disease
  • Sensation or illusion of movement (like they are on a boat)
  • Usually acute in onset, aggravated by moving head
  • Nystagmus suggests vertigo as cause of dizziness
  • Associated symptoms help differentiate peripheral from central etiology
  • Neurologic signs suggest central brainstem etiology (Ataxia, incoordination, visual changes, vomiting, slurred speech, focal neurologic deficits, VISUAL CHANGES MEAN ITS NOT PERIPHERAL!!, If patients have enough vertigo to have vomiting, then its probably central)
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6
Q

Presyncope/syncope

A
  • Presyncope is defined as the symptoms preceding the event (lightheadedness, etc) that may or may not lead to collapse
  • Syncope is the transient loss of consciousness due to reduced cerebral blood flow associated with the absence of postural tone (collapse) and spontaneous, rapid and complete recovery
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7
Q

differential for impaired consciousness

A
  • Seizure
  • TIA
  • Anxiety
  • Hypoglycemia
  • Acute hemorrhage (Most commonly large acute GI bleed)
  • Medication / drug use
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8
Q

syncope

A
  • Most often benign and self-limited
  • Abrupt in onset, transient (seconds to minutes), rapid spontaneous recovery
  • Injuries associated with events in 35% of patients
  • Single or recurrent episodes may occur
  • Can be a premonitory sign of cardiac arrest
  • Common clinical problem (30% of people will have a syncopal event during their lifetime, >75% noneldery pts have single isolated event, 3-5% of all ED visits, 1% of all hospital admissions)
  • Incidence increases with age (Impaired ability to respond to physiologic stressors or changes)
  • Similar among men and women (Men more likely to have cardiac cause)
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9
Q

risk factors for syncope

A
  • Cardiovascular disease is the major risk factor
  • History of stroke or TIA
  • Low BMI (particularly young females) are at much higher risk of neurogenic and vasovagal syncope
  • Increased EtOH intake
  • Diabetes or elevated blood glucose levels or low blood glucose levels
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10
Q

pathophysiology of syncope

A
  • Depends on etiology… not enough blood to brain
  • Sudden impairment of brain metabolism brought on by hypotension with reduction of cerebral blood flow
  • Interference of venous return → decreased cardiac output → cerebral underperfusion
  • Defective vasomotor reflexes
  • Prevented by pressor reflexes that induce vasoconstriction, aortic/carotid reflexes that increase heart rate, and improved venous return by limbs via skeletal muscle constriction
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11
Q

causes of syncope

A
  • Neurocardiogenic (vasovagal) – 58%
  • Vascular tone or blood volume disruption (Orthostatic hypotension, carotid sinus hypersensitivity, situational)
  • Cerebrovascular disease – < 1%
  • Cardiovascular disease – 23% (Arrhythmias, conduction abnormalities, blood flow obstruction)
  • Unknown – 18%
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12
Q

diagnosis of syncope

A
  • History, physical examination, simple laboratory tests, and EKG (Results of these guide further diagnostic evaluation and analysis)
  • European Society of Cardiology 2002 guidelines commonly used
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13
Q

history for pt with syncope

A
  • Presence of risk factors
  • Number of episodes
  • Associated symptoms
  • Prodrome
  • Position
  • Warning
  • Preceding events (Exertional, Eating / Swallowing)
  • Duration of symptoms
  • Recovery
  • Witness
  • Age
  • PMH
  • Injury
  • Meds / Drugs / EtOH
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14
Q

syncope vs seizure

A
  • Seizure is cause in 5-15% of apparent syncopal episodes
  • Seizures associated with postictal state, confusion, slow recovery, incontinence, injuries especially tongue biting, tonic-clonic movements
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15
Q

physical examination for syncope vs seizure

A
  • Orthostatic blood pressure (Supine for 5 minutes, then 2-3 minutes apart from supine to sitting to standing)
  • Disturbances in heart rhythm or breathing
  • Cardiac auscultatory findings
  • Physiologic maneuvers (Valsalva)
  • Abnormal neurologic findings
  • GI bleeding (stool guaiac)
  • Carotid sinus massage (check for bruits first)
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16
Q

initial diagnostic testing

A
  • Labs (Chem 7, CBC (H&H), Cardiac enzymes if MI suspected, Tox screens, UPT, other testing as H&P dictates)
  • EKG (Helpful in looking for arrhythmias, conduction abnormalities)
  • Abnormal EKG not proof of causality, especially if pt is asymptomatic at time of recording
17
Q

secondary diagnostic testing

A
  • Ambulatory monitoring x 24-48 hrs (Useful only if sx occur during monitoring)
  • Echocardiography (Structural abnormalities; may not be that helpful)
  • Neurologic testing – rarely useful
  • Exercise testing – in pts with cardiac disease
  • Upright tilt table testing – commonly used by Neurologists
  • Advanced cardiologic testing – rarely necessary
18
Q

neurocardiogenic (vasovagal)

A
  • Most common cause; 50% of all episodes
  • Mostly in young, otherwise healthy people
  • Frequently recurrent
  • Presyncope prodrome of diaphoresis, nausea, pallor, weak/fatigue, lightheaded
  • Initiated by offending stimuli (Hot environment, EtOH, fatigue, pain, hunger, prolonged standing, venipuncture, fear)
  • Excessive vagal tone or impaired reflex control of the peripheral circulation
  • Stimuli → increased peripheral sympathetic activity, venous pooling → cardiac/vagal reflexes inhibit sympathetic fibers, increase parasympathetic activity → vasodilation, bradycardia → hypotension, syncope
  • Resolves with recumbence, removal of noxious stimuli
  • Counseling patients to avoid predisposing situations, dehydration
  • Lie down if presyncopal symptoms occur
  • β-blockers may be helpful in some patients
  • Permanent pacing may be of benefit in rare cases
19
Q

orthostatic hypotension definition

A
  • Postural decrease in SBP ≥ 20mmHg
  • Decrease in DBP ≥ 10mmHg
  • Increase in HR ≥ 10 bpm
  • Symptoms reproduced on tilt testing
  • Normal vasoconstrictive response to upright posture is impaired
  • Upright position → loss of vasoconstrictive reflexes in LE vessels → fall in systolic BP → syncope
20
Q

orthostatic hypotention

A
  • Elderly, diabetics, other patients with autonomic neuropathy, patients with hypovolemia or acute blood loss, medications such as vasodilators, diuretics, adrenergic blocking agents
  • 30% of the elderly (Especially those with polypharmacy)
  • Often familial in otherwise healthy people
  • Autonomic nervous system insufficiency
  • Peripheral neuropathies
  • Decreased intravascular volume
  • Physical deconditioning (aging, etc)
  • Drug effects (Antidepressants, antihypertensives, opiates)
  • Alcohol consumption
  • Avoidance of volume depletion and medications that can contribute
  • Tensing the legs while standing; dorsiflexion of the feet before standing
  • Arising slowly in stages
  • Wearing compression stockings to minimize venous pooling
  • Various drug therapies
21
Q

Carotid sinus hypersensitivity

A
  • Activation of carotid sinus baroreceptors → branch of glossopharyngeal nerve → medulla → sympathetic fibers via vagus nerve → heart, vessels → AV block, vasodilation → hypotension, syncope
  • Less common cause of syncope
  • More common in men ≥ 50 years of age
  • Pressure on the carotid sinus leads to pause of 3 seconds or more
  • Treatment similar to that of neurocardiogenic syncope
  • Loosen clothing around the neck
  • Pacemakers are of benefit to rare patients with only cardioinhibitory responses without vasodepressor responses
22
Q

situational syncope

A
  • Cough, micturition, deglutition, defecation
  • Micturition occurs in 5% of cases, M>F (Abrupt change in position combined with strong vagal stimulus)
  • Abnormal autonomic control (Straining-type maneuver contributes to decreased BP by decreasing venous return, Increased ICP 2˚ to increased intrathoracic pressure which decreases cerebral blood flow)
23
Q

cardiogenic syncope

A
  • Arrhythmias and conduction abnormalities (Sinus bradycardia, AV block, Sustained ventricular tachycardia, Supraventricular tachycardia)
  • Blood flow obstruction (organic heart dz) (Aortic stenosis, Hypertrophic cardiomyopathy)
  • Higher rates of sudden cardiac death
  • Cardiac syncope occurs from a sudden decrease in cardiac output (Stroke volume and ventricular filling time help maintain cardiac output)
  • Usually exertional or postexertional
24
Q

arrhythmias

A
  • Most common cardiac cause of syncope (14% of syncope cases)
  • Syncope occurs without warning, especially bradyarrhythmias
  • Tachyarrhythmias may cause palpitations (Less well tolerated that bradycardias)
  • May suffer injury with the event
25
Q

sinus bradycardia

A
  • Intrinsic sinus node disease (sick sinus syndrome), drugs (β-blockers), or autonomic imbalance
  • Abnormal impulse generation or conduction through the AV node
  • HR is too low to maintain cardiac output
  • Abrupt onset, usually asymptomatic, may recur often
  • Permanent pacemaker is usual treatment
26
Q

atrioventricular (AV) block

A
  • Second or third degree AV block are usually the forms that cause syncope
  • Generally benign, not progressive (Type II second degree block is often progressive and warrants permanent pacemaker)
  • Permanent pacemaker implantation is indicated for most of these patients
27
Q

ventricular tachycardia

A
  • Most commonly due to underlying structural heart disease, particularly CAD (Atrial flutter, atrial fibrillation, Bypass AV node conduction)
  • Preceded by palpitations or lightheadedness; may be abrupt onset
  • Treatment includes antiarrhythmic drugs, ICD, radiofrequency ablation
28
Q

supraventricular tachycardia

A
  • Rarely associated with syncope
  • Probably neurally mediated (neurocardiogenic) response rather than direct result of the tachycardia
  • Organized SVT causes syncope more often than disorganized rhythm disturbances
  • Treatment includes antiarrhythmic drugs, radiofrequency ablation
29
Q

blood flow obstruction

A
  • arrhythmias are more common than blood flow obstruction)
  • Obstuction to blood flow due to cardiovascular abnormalities can lead to syncope
  • Aortic stenosis, hypertrophic cardiomyopathy most common
  • Less common include pulmonic stenosis, PE, pulmonary HTN, atrial myxoma
30
Q

aortic stenosis

A
  • Angina, CHF, dyspnea; rarely present with syncope; often associated with exertion
  • Laterally displaced, sustained apical impulse, palpable S4
  • Harsh, crescendo-decrescendo murmur best at RSB, radiates to the neck
  • EKG: LVH, LBBB common
  • Echo: etiology of stenosis, degree of obstruction
  • Cardiac cath may be needed for pts with severe stenosis and/or presence of CAD
  • High mortality if untreated
  • Treatment is usually surgical correction by aortic valve replacement
31
Q

hypertrophic cardiomyopathy

A
  • Up to 30% of patients who have dynamic outflow obstruction
  • LVH and hyperdynamic systolic function
  • Obstruction worsens with postural changes, hypovolemia, or drugs
  • Familial and sporadic; fairly common
  • DOE, chest pain, syncope on exertion
  • Harsh, crescendo-decrescendo systolic murmur best at LSB, intensified with maneuvers that decrease LV volume
  • S4 at apex, may be palpable; maybe S3
  • EKG: high QRS voltage, Q’s infero-lateral
  • Echo: LVH, LV function, mitral leaflets
  • Treatment is with β-blockers or calcium channel blockers
  • Surgical treatments may be required if pharmocotherapy is ineffective
  • Major concern is occurrence of sudden cardiac death – can occur at any time, even in asymptomatic patients – leading cause of death in these patients
32
Q

prognosis of syncope

A
  • Directly related to the underlying etiology, not the symptoms
  • Overall mortality in CV group after 5 yrs of FU approaches 50% (30% incidence of death in the first year, 2˚ to CV disease, not syncope)
  • Most patients have a low recurrence rate and excellent long-term survival
33
Q

San Francisco Syncope Rule to predict patients with serious outcomes

A
  • History of CHF
  • Hct < 30%
  • Abnormal EKG
  • Systolic BP < 90 mmHg
  • Complaint of shortness of breath
  • These patients presenting with syncope are more likely to have a serious cardiac outcome such as acute MI
  • The more items on this list that they have, the more likely that they are to have an adverse outcome
34
Q

resumption of driving

A
  • Due to temporary factors (Advised not to drive for at least 1 month)
  • Cardiogenic factors (such as symptomatic ventricular tachycardia) (Advised not to drive for at least 6 months)
  • Longer restrictions are warranted in patients if spontaneous arrhythmias persist despite treatment

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