Approach to Lightheadedness, Dizziness and Syncope Flashcards
Vertigo
False sense of motion or spinning
Presyncope
Prodromal symptom of fainting, but no loss of consciousness (i.e. tunnel vision)
Syncope
Transient loss of consciousness (TLOC)
Disequilibrium
Sense of imbalance primarily when walking
What can cause reflex syncope?
A brief loss of consciousness due to a neurologically induced drop in blood pressure (postural hypotension)
Tilt-table test should not be used in which patients?
What does it help with?
Patients w/ heart disease
Vasovagal syncope, orthostatic hypotension, etc.
The following account for what percentages of reported syncope?
Cardiac syncope
Reflex syncope
Orthostatic hypotension syncope
Cardiac syncope - 20%
Reflex syncope - 60-70% (aka neurally-mediated syncope)
Orthostatic hypotension syncope - 10-20%
Hypertrophic CM is characterized by…
How many people does it affect?
What is the pathphysiology?
LVH without a clear secondary cause
1/500, most common inheritable CM
Genetic mutations resulting myocyte hypertrophy and disarray which leads to LVH and LVOT obstruction (AD pattern)
The clinical symptoms of HCM depend on:
Most patients have…
SX include:
Major complication of HCM:
Severity of LVH and LVOT obstruction
No SX or mild SX
DOE, fatigue, CP, presyncope, syncope, palpitations
Sudden cardiac death (SCD)
On physical exam of HCM, what abnormal heart sound might be heard?
What kind of murmur does it cause?
What will increase the intensity of the murmur?
What will decrease the intensity?
S4
Systolic murmur
Increase: squatting, valsalva and standing
Decrease: sustained handgrip
Hoe is HCM diagnosed? (2)
Family Hx
Echo
-LV wall thickness > 15 mm
-LVOT obstruction with pressure gradient of > 30 mmHg
Treatment of HCM
If symptomatic give (3), why?
Avoid strenuous activity because it could worsen LVOT obstruction
ASX patients do not need additional treatment
BB or CCBs (Diltiazem, Veramapil - improve diastolic filling
Diuretics - use w/ caution as it decreases preload and can worsen LVOT obstruction
Implantable cardioverter-defibrilators (ICDs) - for patients with high risk for ventricular arrhythmias
What kind of syncope has the greatest risk of mortality?
Cardiac syncope
3 major types of Reflex Syncope (Neurally-mediated Syncope)
Carotid sinus hypersensitivity and syndrome
Situational syncope
Vasovagal syncope
Carotid sinus hypersensitivity and syndrome is seen most in:
What is Carotid sinus syndrome?
What is Carotid sinus hypersensitivity (CSS)?
What triggers these events?
Older males with atherosclerosis
CSS with symptoms (lightheadedness, syncope, presyncope, etc.)
Heart pause > 3 sec and systolic BP drop > 50 mmHg
Stimulation of carotid a. baroreceptor from mechanical forces (turning head, shaving, tight shirt, etc.)
What triggers Situational syncope?
Micturition Defecation Coughing Sneezing Laughing
What triggers Vasovagal syncope?
Is it common?
Prolonged sitting, standing, emotional stress, fear, pain, etc.
Most common type of reflex syncope. It is the common fainting.
What is the pathophysiology of reflex syncope?
A neurally-mediated reflex response leading to VD and/or bradycardia resulting in systemic hypotension and cerebral hypoperfusion causing TLOC.
4 parts of a diagnosis of reflex syncope
Hx/exam
ECG
Til-table test
Carotid sinus massage for carotid sinus syndrome
What advice should be given to patients with reflex syncope?
Reassure them that it is benign
Avoid triggers
Lay down supine with legs raised when SX onset
Avoid movements that trigger SX
What is the treatment of reflex syncope? (4)
Liberalize salt intake
Encourage fluid intake
Compression socks
Pacemaker for carotid sinus syndrome
RIsk factors for Orthostatic hypotension syncope:
What are the 4 types:
What is the pathophysiology?
Age, carotid stenosis, some meds.
Drug-induced, Autonomic failure, Postural tachycardia syndrome, Volume depletion
It is a normal physiologic response to change in position
Patients with Autonomic failure orthostatic hypotensions have what BPs when supine and upright?
Supine - HTN
Upright - hypotension
Dx of Orthostatic hypotension syncope includes: (4)
> 20 mmHg drop in systolic BP OR > 10 mmHg drop in diastolic BP within 5 min of standing
Labs - CBC for anemia, BUN/creatinine for dehydration, Glc for hypoglycemia
ECG
Tilt-table test
Treatment includes:
What meds can be used? (3)
D/C exacerbating meds, slowly change positions
Flurocortisone (MC R agonist), Midodrine (a1 agonist), Caffeine
Postural tachycardia syndrome (POTS) occurs most in:
Clinical manifestations:
Pathophysiology:
Young adults, 14-45 y/o F>M (est. 500k Americans)
Dizziness, LHness, weakness, blurred vision
Not well understood, but autonomic reflexes are relatively preserved, but there is an exagerrated increase in HR with position changes which lead to redistribution of blood which causes reduced cerebral blood flow
What findings must occur on the Tilt-table test to Dx POTS? (2)
Sustained HR increased > 30 beats/min or absolute HR > 120 beats/min within first 10 min of testing
NO hypotension throughout
Other than conservative care, what are the suggested pharmaceuticals for POTS? (3)
Flurocortisone (MC R agonist)
Midodrine (a1 agonist)
BBs
Inherited thrombophilia risks for PE (4)
Factor 5 Leiden mutation
Prothrombin mutation
Protein C or S deficiency
Anti-thrombin deficiency
6 major complications of PE
Sudden death RSHF Lung infarct Hypoxia Pulm HTN AFib
What can help determine pretest probability of PE?
Wells criteria
In patients with a low/intermediate risk of PE on Wells criteria, what will R/O a PE?
Normal D-dimer: <500 ng/ml
If there is a high risk on Wells criteria and an elevated D-dimer, what could be done for Dx?
CT angio
VQ scan
MR pulmonary angio
Pulmonary angio
Doppler US is used to assess:
DVT in LE
What happens in the heart as a result of a PE?
Right heart strain: increased RV size, worsened RV function, Tricuspid regurg, abnormal septal wall motion.
Treatment for PE includes:
DOACs
- Factor Xa inhibitors: Rivaroxaban (Xarelto), Apixaban (Eliquis) and Edoxaban (Savaysa)
- Direct thrombin inhibitors: Dabigatran (Pradaxa)
Warfarin
SubQ anticoagulants
-LMW heparin, Fondaparinux
IV anticoagulants
-Unfractioned heparin
What Tx for PE is preferred?
When is Warfarin preferred?
When is LMW heparin preferred?
DOACs, because of a lower bleed risk and no need to check INR
Preferred over LMWH
Preferred in patients with underlying malignancy or if they cannot take oral meds
Duration of Tx for PE is at minimum:
3 mo
Which patients should receive lifelong anticoagulation?
Cancer pts
IVC filters are recommended for..
Pts. whom anticoagulation is contraindicated
Thrombolytics are recommended for…
Hemodynamically unstable pts.
Embolectomy is recommended for…
Hemodynamically unstable pts. in which thrombolysis is contraindicated
2 requirements for forming concentrated urine
Hypertonic medullary interstitium (needed for water reabsorption)
High levels of ADH (increases water permeability in DCT and CD)
Serum Osm is approx:
What 2 systems regulate it?
282 mOsm/kg
Osmoreceptor-ADH system
Thirst mechanism
How long is the ADH half-life? Why?
15-20 min.
It is metabolized quickly by liver and kidney, which allows for rapid means to alter water excretion by the kidneys.
Most (approx 180 L) of fluid is filtered by the glomerulus. What is the remaining 18 L reabsorbed under the regulation of?
ADH
Where is ADH made?
Where is it secreted?
What are the triggers for its release? (2)
Hypothalamus: 5/6 from SON, 1/6 from PVN
Secreted into the posterior pituitary
- Increased serum Osm (detected by osmoreceptors in anterior hypothalamus).
- Decreases in BP or increases in BV (detected by baroreceptors and atrial stretch receptors)
What is the effect of ADH on CD? (Biochemistry wise)
Binds V2R and increases cAMP which upregulates AQP2 and urea transporters
This is why during dehydration, urea levels go up (BUN/creatinine 20:1)
DI definition:
DO from decreased ability to concentrate urine resulting in polyuria (>3 L/day), polydipsia and hypernatremia (high Na+ conc.)
Central DI vs Nephrogenic DI
Central DI: caused by decreased release of ADH. Tx with Vasopressin.
Nephrogenic DI: caused by lack of response to ADH. Associated with Lithium toxicity.
How is DI Dx?
24 hr urine collection to confirm polyuria
Urine Osm < 300 mOsm/kg
Water deprivation test
Water deprivation test results in Central and Nephrogenic DI:
Urinary Osm
Serum ADH
Change in urine Osm once given exogenous ADH
Central
Urinary Osm - <300 Osm
Serum ADH - undetectable
Change in urine Osm once given exogenous ADH - substantially increased
Nephrogenic
Urinary Osm - <300-500 Osm
Serum ADH - >5
Change in urine Osm once given exogenous ADH - no change
Tx for Central (1) vs. Nephrogenic DI (4)
Central
-vasopressin (ADH)
Nephrogenic
- decrease solute intake
- Thiazide diuretics
- NSAIDs
- Vasopressin
