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CPR II Exam #2 > Approach to Lightheadedness, Dizziness and Syncope > Flashcards

Approach to Lightheadedness, Dizziness and Syncope Flashcards

1
Q

Vertigo

A

False sense of motion or spinning

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2
Q

Presyncope

A

Prodromal symptom of fainting, but no loss of consciousness (i.e. tunnel vision)

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3
Q

Syncope

A

Transient loss of consciousness (TLOC)

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4
Q

Disequilibrium

A

Sense of imbalance primarily when walking

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5
Q

What can cause reflex syncope?

A

A brief loss of consciousness due to a neurologically induced drop in blood pressure (postural hypotension)

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6
Q

Tilt-table test should not be used in which patients?

What does it help with?

A

Patients w/ heart disease

Vasovagal syncope, orthostatic hypotension, etc.

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7
Q

The following account for what percentages of reported syncope?
Cardiac syncope
Reflex syncope
Orthostatic hypotension syncope

A

Cardiac syncope - 20%
Reflex syncope - 60-70% (aka neurally-mediated syncope)
Orthostatic hypotension syncope - 10-20%

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8
Q

Hypertrophic CM is characterized by…

How many people does it affect?

What is the pathphysiology?

A

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)

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9
Q

The clinical symptoms of HCM depend on:

Most patients have…

SX include:

Major complication of HCM:

A

Severity of LVH and LVOT obstruction

No SX or mild SX

DOE, fatigue, CP, presyncope, syncope, palpitations

Sudden cardiac death (SCD)

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10
Q

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?

A

S4

Systolic murmur

Increase: squatting, valsalva and standing
Decrease: sustained handgrip

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11
Q

Hoe is HCM diagnosed? (2)

A

Family Hx
Echo
-LV wall thickness > 15 mm
-LVOT obstruction with pressure gradient of > 30 mmHg

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12
Q

Treatment of HCM

If symptomatic give (3), why?

A

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

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13
Q

What kind of syncope has the greatest risk of mortality?

A

Cardiac syncope

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14
Q

3 major types of Reflex Syncope (Neurally-mediated Syncope)

A

Carotid sinus hypersensitivity and syndrome
Situational syncope
Vasovagal syncope

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15
Q

Carotid sinus hypersensitivity and syndrome is seen most in:

What is Carotid sinus syndrome?

What is Carotid sinus hypersensitivity (CSS)?

What triggers these events?

A

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.)

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16
Q

What triggers Situational syncope?

A 
Micturition
Defecation
Coughing
Sneezing
Laughing
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17
Q

What triggers Vasovagal syncope?

Is it common?

A

Prolonged sitting, standing, emotional stress, fear, pain, etc.

Most common type of reflex syncope. It is the common fainting.

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18
Q

What is the pathophysiology of reflex syncope?

A

A neurally-mediated reflex response leading to VD and/or bradycardia resulting in systemic hypotension and cerebral hypoperfusion causing TLOC.

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19
Q

4 parts of a diagnosis of reflex syncope

A

Hx/exam
ECG
Til-table test
Carotid sinus massage for carotid sinus syndrome

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20
Q

What advice should be given to patients with reflex syncope?

A

Reassure them that it is benign
Avoid triggers
Lay down supine with legs raised when SX onset
Avoid movements that trigger SX

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21
Q

What is the treatment of reflex syncope? (4)

A

Liberalize salt intake
Encourage fluid intake
Compression socks
Pacemaker for carotid sinus syndrome

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22
Q

RIsk factors for Orthostatic hypotension syncope:

What are the 4 types:

What is the pathophysiology?

A

Age, carotid stenosis, some meds.

Drug-induced, Autonomic failure, Postural tachycardia syndrome, Volume depletion

It is a normal physiologic response to change in position

23
Q

Patients with Autonomic failure orthostatic hypotensions have what BPs when supine and upright?

A

Supine - HTN

Upright - hypotension

24
Q

Dx of Orthostatic hypotension syncope includes: (4)

A

> 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

25
Q

Treatment includes:

What meds can be used? (3)

A

D/C exacerbating meds, slowly change positions

Flurocortisone (MC R agonist), Midodrine (a1 agonist), Caffeine

26
Q

Postural tachycardia syndrome (POTS) occurs most in:

Clinical manifestations:

Pathophysiology:

A

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

27
Q

What findings must occur on the Tilt-table test to Dx POTS? (2)

A

Sustained HR increased > 30 beats/min or absolute HR > 120 beats/min within first 10 min of testing

NO hypotension throughout

28
Q

Other than conservative care, what are the suggested pharmaceuticals for POTS? (3)

A

Flurocortisone (MC R agonist)
Midodrine (a1 agonist)
BBs

29
Q

Inherited thrombophilia risks for PE (4)

A

Factor 5 Leiden mutation
Prothrombin mutation
Protein C or S deficiency
Anti-thrombin deficiency

30
Q

6 major complications of PE

A 
Sudden death
RSHF
Lung infarct
Hypoxia
Pulm HTN
AFib
31
Q

What can help determine pretest probability of PE?

A

Wells criteria

32
Q

In patients with a low/intermediate risk of PE on Wells criteria, what will R/O a PE?

A

Normal D-dimer: <500 ng/ml

33
Q

If there is a high risk on Wells criteria and an elevated D-dimer, what could be done for Dx?

A

CT angio
VQ scan
MR pulmonary angio
Pulmonary angio

34
Q

Doppler US is used to assess:

A

DVT in LE

35
Q

What happens in the heart as a result of a PE?

A

Right heart strain: increased RV size, worsened RV function, Tricuspid regurg, abnormal septal wall motion.

36
Q

Treatment for PE includes:

A

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

37
Q

What Tx for PE is preferred?

When is Warfarin preferred?

When is LMW heparin preferred?

A

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

38
Q

Duration of Tx for PE is at minimum:

A

3 mo

39
Q

Which patients should receive lifelong anticoagulation?

A

Cancer pts

40
Q

IVC filters are recommended for..

A

Pts. whom anticoagulation is contraindicated

41
Q

Thrombolytics are recommended for…

A

Hemodynamically unstable pts.

42
Q

Embolectomy is recommended for…

A

Hemodynamically unstable pts. in which thrombolysis is contraindicated

43
Q

2 requirements for forming concentrated urine

A

Hypertonic medullary interstitium (needed for water reabsorption)
High levels of ADH (increases water permeability in DCT and CD)

44
Q

Serum Osm is approx:

What 2 systems regulate it?

A

282 mOsm/kg

Osmoreceptor-ADH system
Thirst mechanism

45
Q

How long is the ADH half-life? Why?

A

15-20 min.

It is metabolized quickly by liver and kidney, which allows for rapid means to alter water excretion by the kidneys.

46
Q

Most (approx 180 L) of fluid is filtered by the glomerulus. What is the remaining 18 L reabsorbed under the regulation of?

A

ADH

47
Q

Where is ADH made?

Where is it secreted?

What are the triggers for its release? (2)

A

Hypothalamus: 5/6 from SON, 1/6 from PVN

Secreted into the posterior pituitary

  1. Increased serum Osm (detected by osmoreceptors in anterior hypothalamus).
  2. Decreases in BP or increases in BV (detected by baroreceptors and atrial stretch receptors)
48
Q

What is the effect of ADH on CD? (Biochemistry wise)

A

Binds V2R and increases cAMP which upregulates AQP2 and urea transporters

This is why during dehydration, urea levels go up (BUN/creatinine 20:1)

49
Q

DI definition:

A

DO from decreased ability to concentrate urine resulting in polyuria (>3 L/day), polydipsia and hypernatremia (high Na+ conc.)

50
Q

Central DI vs Nephrogenic DI

A

Central DI: caused by decreased release of ADH. Tx with Vasopressin.

Nephrogenic DI: caused by lack of response to ADH. Associated with Lithium toxicity.

51
Q

How is DI Dx?

A

24 hr urine collection to confirm polyuria
Urine Osm < 300 mOsm/kg
Water deprivation test

52
Q

Water deprivation test results in Central and Nephrogenic DI:

Urinary Osm
Serum ADH
Change in urine Osm once given exogenous ADH

A

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

53
Q

Tx for Central (1) vs. Nephrogenic DI (4)

A

Central
-vasopressin (ADH)

Nephrogenic

  • decrease solute intake
  • Thiazide diuretics
  • NSAIDs
  • Vasopressin

CPR II Exam #2 (20 decks)

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