Lightheadedness, Dizziness, and/or Syncope Flashcards

1
Q

pathophysiology of HCM

A

AR genetic mutations –> myocyte hypertrophy and disarray –> LVH and LV outflow tract obstruction

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2
Q

clinical manifestations HCM

A
  • Presyncope or syncope during or immediately following exercise
  • dyspnea on exertion
  • fatigue
  • chest pain
  • palpitations
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3
Q

complications HCM

A
  • sudden cardiac death
  • heart failure
  • mitral valve regurg
  • arrhythmias
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4
Q

how to diagnose HCM

A
  • S4 may be present
  • systolic murmur
  • *squatting increases intensity of all murmurs except MVP and HCM
  • *Valsalva and standing will increase intensity of HCM
  • *sustained hand grip decreases intensity of HCM
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5
Q

treatment for HCM

A
  • B-blockers
  • Dilitiazem
  • Verapamil
  • Diuretics
  • Implanted carioverter-difibrillators
  • Surgery if severe (myomectomy, mitral valve replacement)
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6
Q

what pts get carotid sinus hypersensitivity and syndrome

A

older males w/ atherosclerosis

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7
Q

what is carotid sinus hypersensitivity and syndrome

A

A type of reflex syncope triggered by stimulation of carotid artery baroreceptor from mechanical forces like turning head, shaving, tight shirt collars, etc

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8
Q

pathophysiology of carotid sinus hypersensitivity and syndrome

A

reflex response leads to vasodilation and/or bradycardia resulting in systemic hypotension and cerebral hypoperfusion causing transient LOC

Hypersensitivity (CSS): heart pause > 3 seconds and systolic BP drop > 50mmHG

Syndrome: CSS w/ sx of lightheadedness, presyncope, syncope, unexplained falls

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9
Q

sx of carotid sinus hypersensitivity and syndrome

A
  • lightheadedness
  • Feeling warm or cold
  • sweating
  • palpitations
  • nausea
  • abd discomfort
  • tunnel vision
  • decreased hearing
  • pallor
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10
Q

how to diagnose carotid sinus hypersensitivity and syndrome

A
  • ECG
  • tilt-table test
  • carotid sinus massage for syndrome
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11
Q

tx for carotid sinus hypersensitivity and syndrome

A
  • liberalize salt intake
  • encourage fluid intake
  • compression socks
  • abdominal binders
  • rarely fludrocortisone
  • For the syndrome, consider pacemaker
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12
Q

what triggers situational syncope

A

micturition, defecating, coughing, sneezing, swallowing, laughing, etc.

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13
Q

pathophysiology of situational syncope

A

reflex response leads to vasodilation and/or bradycardia resulting in systemic hypotension and cerebral hypoperfusion causing transient LOC

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14
Q

sx of situational syncope

A
  • lightheadedness
  • Feeling warm or cold
  • sweating
  • palpitations
  • nausea
  • abd discomfort
  • tunnel vision
  • decreased hearing
  • pallor
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15
Q

how to diagnose situational syncope

A
  • ECG

- tilt-table test

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16
Q

tx for situational syncope

A
  • liberalize salt intake
  • encourage fluid intake
  • compression socks
  • abdominal binders
  • rarely fludrocortisone
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17
Q

what triggers vasovagal response

A

prolonged sitting or standing, emotional stress or fear, pain or noxious stimuli, or heat

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18
Q

pathophysiology of vasovagal response

A

reflex response leads to vasodilation and/or bradycardia resulting in systemic hypotension and cerebral hypoperfusion causing transient LOC

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19
Q

sx vasovagal response

A
  • lightheadedness
  • Feeling warm or cold
  • sweating
  • palpitations
  • nausea
  • abd discomfort
  • tunnel vision
  • decreased hearing
  • pallor
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20
Q

how to diagnose vasovagal response

A
  • ECG

- Tilt-table test

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21
Q

tx vasovagal response

A
  • liberalize salt intake
  • encourage fluid intake
  • compression socks
  • abdominal binders
  • rarely fludrocortisone
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22
Q

risk factors for orthostatic hypotension syndrome

A
  • Old age
  • carotid stenosis
  • certain meds
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23
Q

pathophysiology orthostatic hypotension syndrome

A

Autonomic reflex failure or severe intravascular depletion –> significant BP drop w/ postural changes

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24
Q

4 types orthostatic hypotension syndrome

A

1) Drug-Induced
2) Autonomic Failure
3) Postural Tachycardia Syndrome
4) Volume Depletion

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25
Q

sx orthostatic hypotension syndrome

A

W/ Sudden Postural Changes:

  • generalized weakness
  • dizziness or lightheadedness
  • visual blurring

Autonomic Failure Pts:

  • supine hypertension
  • upright hypotension
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26
Q

how to diagnose orthostatic hypotension syndrome

A
  • orthostatic vital signs (>20 drop systolic, >10 drop diastolic within 5 mins)
  • CBC –> testing for anemia
  • BUN –> testing for dehydration
  • Glucose –> testing for hypoglycemia
  • ECG
  • Tilt-table test
27
Q

tx orthostatic hypotension syndrome

A
  • slowly change position from supine to upright
  • physical maneuvers to increase BP (leg crossing)
  • encourage fluid and salt intake
  • compression stockings
  • abd binders
    Pharm:
  • flurocortisone
  • Midodrine
  • caffeine
28
Q

what patients get postural tachycardia syndrome (POTS)

A

Seen in younger adults (14-45) females > males

29
Q

pathophysiology POTS

A

Likely multifactorial

- exaggerated increase in heart rate with position changes –> redistribution of blood –> reduced cerebral flow

30
Q

sx POTS

A
  • dizziness
  • lightheadedness
  • weakness
  • blurred vision
  • fatigue upon standing
  • NO hypotension
31
Q

how to diagnose POTS

A
  • Tilt-table test (sustained HR increase > 30 beats/min, or absolute HR of >120 beats/min within first 10 mins of test)
32
Q

tx POTS

A
  • compression stockings
  • abd binder
  • high salt diet and fluid intake
  • exercise
    Pharm:
  • Flurocortisone
  • Midodrine
  • B-blockers
33
Q

4 genetic causes PE

A
  • Factor 5 mutation
  • Prothrombin mutation
  • Protein C or S mutation
  • Anti-thrombin deficiency
34
Q

6 acquired causes PE

A
  • malignancy
  • surgery (orthopedic)
  • trauma
  • oral contraceptives
  • immobilization
  • antiphospholipid Ab syndrome
35
Q

sx PE

A

Can be asymptomatic

  • dyspnea
  • pleuritic CP
  • cough
  • sx of DVT

Less commonly:

  • hemoptysis
  • presyncope or syncope
  • wheezing
36
Q

complications PE

A
  • sudden death
  • RHF
  • lung infarction
  • hypoxia
  • pulmonary HTN
  • a fib
37
Q

how to diagnose PE

A
  • Wells Criteria
  • D-dimer
  • Doppler/US
  • Echocardiogram

Pts w/ high risk of PE and elevated D-Dimer:

  • CTPA
  • V/Q scan
  • MR pulmonary angiography
  • pulmonary angiography
38
Q

non-pharm tx of PE

A
  • Minimum of 3 months all pts
  • Minimum 3 months + reassessment of bleeding (unprovoked pts)
  • CA pts need lifelong anti-coags
  • IVC filter if pt cannot have anti-coags
  • thombolytics for hemodynamically unstable pts
  • embolectomy for hemodynamically unstable pts who can’t have thrombolytics
39
Q

DOAC tx of PE

A
Direct Oral Anti-coags (DOACs):
**Preferred Agents**
- Rivaroxaban
- Apixaban
- Edoxaban
(not pts w/ liver or renal failure)
40
Q

direct thrombin inhibitor for tx of PE

A

dabigatran

41
Q

subcutaneous anti-coags for tx of PE

A

LMWH and fondaparinux

42
Q

IV-anti-coag tx for PE

A

unfractionated heparin

43
Q

pathophysiology of central DI

A
  • decreased release of ADH
  • idiopathic (most common)
  • hereditary (AR and AD)
  • tumors
  • infiltrative dz
  • neurosurgery
  • trauma
  • meningitis/encephalitis
44
Q

pathophysiology of nephrogenic DI

A
  • decreased response to ADH
  • hereditary (rare – V2R and AQP-2 mutations)
  • lithium toxicity
  • hypercalcemia
  • hypokalemia
  • seen in renal dz
45
Q

sx DI

A
  • polyuria
  • nocturia
  • polydipsia
  • hypernatremia
  • orthostasis
46
Q

3 tests to diagnose DI

A

24 hour urine volume collection –> confirms polyuria

Urine osmolality < 300 mOsm/kg –> primary polydipsia, central or nephrogenic DI

Water deprivation test –> central or nephrogenic

47
Q

central DI results of water deprivation test

A

no vasopressin after dehydration, when given vasopressin –> greatly increases urine osmolality

48
Q

nephrogenic DI results of water deprivation test

A

high vasopressin after dehydration, when given vasopressin –> little or no increase in osmolality

49
Q

tx for central DI

A

vasopressin

50
Q

tx for nephrogenic DI

A
  • decreased solute intake
  • thiazide diuretic (increases prox. Tube Na+ and H2O reabsorption)
  • NSAIDs (decreases medullary prostaglandin production which antagonize ADH)
  • vasopressin
51
Q

tx for hypernatremia related to DI

A

Replace free water deficit

52
Q

define presyncope

A

near fainting

  • no LOC
  • tunnel vision
53
Q

pts with lightheadedness, dizziness, and/or syncope, PLUS rhythmic limb jerking, post-ictal confusion, tongue biting, head turning

A

indicative of seizure

54
Q

pts with lightheadedness, dizziness, and/or syncope, PLUS weakness, slurred speech, difficulty swallowing

A

stroke or TIA

55
Q

function of holter monitor

A

continuous ambulatory ECG worn 24-72 hours, pts can press button and mark ECG when having sx

56
Q

function of event (loop) monitor

A

ambulatory ECG that loops its recording tape, pt triggers device to record when having sx, worn for weeks-months

57
Q

function of implantable loop recorder

A

ambulatory ECG that can record up to 3 years

58
Q

function of echocardiogram

A

evaluate for structural dz, HF, valvular abnormalities, cardiac effusions, atrial myxomas

59
Q

3 types of syncope

A

cardiac (20%)
reflex (60-70%)
orthostatic hypotension (10-20%)

60
Q

causes of cardiac syncope

A
  • aortic stenosis
  • HCM
  • cardiac tamponade
  • cardiac mass or tumor
61
Q

types of primary autonomic failure that would cause orthostatic hypotension syncope

A

MS, Shy-Drager syndrome, Parkinson, Wernicke encephalopathy

62
Q

types of secondary autonomic failure that would cause orthostatic hypotension syncope

A

amyloidosis, chronic inflammatory demyelinating polyneuropathy, CT dz, DM, lewy body dementia, old age, spinal cord injury

63
Q

half life and function of ADH

A

short half-life, 15-20 mins

  • decreases serum osmolality when it’s too high
  • increases blood pressure when it’s too low
64
Q

effects of ADH on collecting duct

A

ADH binds to V2R receptors on basolateral membrane –> increases cAMP –> insertion of AQP-2 and urea transporters