Lightheadedness, Dizziness, and/or Syncope Flashcards
pathophysiology of HCM
AR genetic mutations –> myocyte hypertrophy and disarray –> LVH and LV outflow tract obstruction
clinical manifestations HCM
- Presyncope or syncope during or immediately following exercise
- dyspnea on exertion
- fatigue
- chest pain
- palpitations
complications HCM
- sudden cardiac death
- heart failure
- mitral valve regurg
- arrhythmias
how to diagnose HCM
- 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
treatment for HCM
- B-blockers
- Dilitiazem
- Verapamil
- Diuretics
- Implanted carioverter-difibrillators
- Surgery if severe (myomectomy, mitral valve replacement)
what pts get carotid sinus hypersensitivity and syndrome
older males w/ atherosclerosis
what is carotid sinus hypersensitivity and syndrome
A type of reflex syncope triggered by stimulation of carotid artery baroreceptor from mechanical forces like turning head, shaving, tight shirt collars, etc
pathophysiology of carotid sinus hypersensitivity and syndrome
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
sx of carotid sinus hypersensitivity and syndrome
- lightheadedness
- Feeling warm or cold
- sweating
- palpitations
- nausea
- abd discomfort
- tunnel vision
- decreased hearing
- pallor
how to diagnose carotid sinus hypersensitivity and syndrome
- ECG
- tilt-table test
- carotid sinus massage for syndrome
tx for carotid sinus hypersensitivity and syndrome
- liberalize salt intake
- encourage fluid intake
- compression socks
- abdominal binders
- rarely fludrocortisone
- For the syndrome, consider pacemaker
what triggers situational syncope
micturition, defecating, coughing, sneezing, swallowing, laughing, etc.
pathophysiology of situational syncope
reflex response leads to vasodilation and/or bradycardia resulting in systemic hypotension and cerebral hypoperfusion causing transient LOC
sx of situational syncope
- lightheadedness
- Feeling warm or cold
- sweating
- palpitations
- nausea
- abd discomfort
- tunnel vision
- decreased hearing
- pallor
how to diagnose situational syncope
- ECG
- tilt-table test
tx for situational syncope
- liberalize salt intake
- encourage fluid intake
- compression socks
- abdominal binders
- rarely fludrocortisone
what triggers vasovagal response
prolonged sitting or standing, emotional stress or fear, pain or noxious stimuli, or heat
pathophysiology of vasovagal response
reflex response leads to vasodilation and/or bradycardia resulting in systemic hypotension and cerebral hypoperfusion causing transient LOC
sx vasovagal response
- lightheadedness
- Feeling warm or cold
- sweating
- palpitations
- nausea
- abd discomfort
- tunnel vision
- decreased hearing
- pallor
how to diagnose vasovagal response
- ECG
- Tilt-table test
tx vasovagal response
- liberalize salt intake
- encourage fluid intake
- compression socks
- abdominal binders
- rarely fludrocortisone
risk factors for orthostatic hypotension syndrome
- Old age
- carotid stenosis
- certain meds
pathophysiology orthostatic hypotension syndrome
Autonomic reflex failure or severe intravascular depletion –> significant BP drop w/ postural changes
4 types orthostatic hypotension syndrome
1) Drug-Induced
2) Autonomic Failure
3) Postural Tachycardia Syndrome
4) Volume Depletion
sx orthostatic hypotension syndrome
W/ Sudden Postural Changes:
- generalized weakness
- dizziness or lightheadedness
- visual blurring
Autonomic Failure Pts:
- supine hypertension
- upright hypotension
how to diagnose orthostatic hypotension syndrome
- 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
tx orthostatic hypotension syndrome
- 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
what patients get postural tachycardia syndrome (POTS)
Seen in younger adults (14-45) females > males
pathophysiology POTS
Likely multifactorial
- exaggerated increase in heart rate with position changes –> redistribution of blood –> reduced cerebral flow
sx POTS
- dizziness
- lightheadedness
- weakness
- blurred vision
- fatigue upon standing
- NO hypotension
how to diagnose POTS
- Tilt-table test (sustained HR increase > 30 beats/min, or absolute HR of >120 beats/min within first 10 mins of test)
tx POTS
- compression stockings
- abd binder
- high salt diet and fluid intake
- exercise
Pharm: - Flurocortisone
- Midodrine
- B-blockers
4 genetic causes PE
- Factor 5 mutation
- Prothrombin mutation
- Protein C or S mutation
- Anti-thrombin deficiency
6 acquired causes PE
- malignancy
- surgery (orthopedic)
- trauma
- oral contraceptives
- immobilization
- antiphospholipid Ab syndrome
sx PE
Can be asymptomatic
- dyspnea
- pleuritic CP
- cough
- sx of DVT
Less commonly:
- hemoptysis
- presyncope or syncope
- wheezing
complications PE
- sudden death
- RHF
- lung infarction
- hypoxia
- pulmonary HTN
- a fib
how to diagnose PE
- 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
non-pharm tx of PE
- 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
DOAC tx of PE
Direct Oral Anti-coags (DOACs): **Preferred Agents** - Rivaroxaban - Apixaban - Edoxaban (not pts w/ liver or renal failure)
direct thrombin inhibitor for tx of PE
dabigatran
subcutaneous anti-coags for tx of PE
LMWH and fondaparinux
IV-anti-coag tx for PE
unfractionated heparin
pathophysiology of central DI
- decreased release of ADH
- idiopathic (most common)
- hereditary (AR and AD)
- tumors
- infiltrative dz
- neurosurgery
- trauma
- meningitis/encephalitis
pathophysiology of nephrogenic DI
- decreased response to ADH
- hereditary (rare – V2R and AQP-2 mutations)
- lithium toxicity
- hypercalcemia
- hypokalemia
- seen in renal dz
sx DI
- polyuria
- nocturia
- polydipsia
- hypernatremia
- orthostasis
3 tests to diagnose DI
24 hour urine volume collection –> confirms polyuria
Urine osmolality < 300 mOsm/kg –> primary polydipsia, central or nephrogenic DI
Water deprivation test –> central or nephrogenic
central DI results of water deprivation test
no vasopressin after dehydration, when given vasopressin –> greatly increases urine osmolality
nephrogenic DI results of water deprivation test
high vasopressin after dehydration, when given vasopressin –> little or no increase in osmolality
tx for central DI
vasopressin
tx for nephrogenic DI
- decreased solute intake
- thiazide diuretic (increases prox. Tube Na+ and H2O reabsorption)
- NSAIDs (decreases medullary prostaglandin production which antagonize ADH)
- vasopressin
tx for hypernatremia related to DI
Replace free water deficit
define presyncope
near fainting
- no LOC
- tunnel vision
pts with lightheadedness, dizziness, and/or syncope, PLUS rhythmic limb jerking, post-ictal confusion, tongue biting, head turning
indicative of seizure
pts with lightheadedness, dizziness, and/or syncope, PLUS weakness, slurred speech, difficulty swallowing
stroke or TIA
function of holter monitor
continuous ambulatory ECG worn 24-72 hours, pts can press button and mark ECG when having sx
function of event (loop) monitor
ambulatory ECG that loops its recording tape, pt triggers device to record when having sx, worn for weeks-months
function of implantable loop recorder
ambulatory ECG that can record up to 3 years
function of echocardiogram
evaluate for structural dz, HF, valvular abnormalities, cardiac effusions, atrial myxomas
3 types of syncope
cardiac (20%)
reflex (60-70%)
orthostatic hypotension (10-20%)
causes of cardiac syncope
- aortic stenosis
- HCM
- cardiac tamponade
- cardiac mass or tumor
types of primary autonomic failure that would cause orthostatic hypotension syncope
MS, Shy-Drager syndrome, Parkinson, Wernicke encephalopathy
types of secondary autonomic failure that would cause orthostatic hypotension syncope
amyloidosis, chronic inflammatory demyelinating polyneuropathy, CT dz, DM, lewy body dementia, old age, spinal cord injury
half life and function of ADH
short half-life, 15-20 mins
- decreases serum osmolality when it’s too high
- increases blood pressure when it’s too low
effects of ADH on collecting duct
ADH binds to V2R receptors on basolateral membrane –> increases cAMP –> insertion of AQP-2 and urea transporters
