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CSI > PE > Flashcards

PE Flashcards

1
Q

where PEs come from

A

anything proximal to popliteal can embolize, below can propagate then embolize

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2
Q

PEs are often missed bc

A

symptoms may be vague, need high clinical suspicion
atypical symptoms of no symptoms at all
3rd leading cause of death in hospitalized pts.

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3
Q

risk of blood clot formation

A

Virchow’s triad

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4
Q

Virchow’s triad

A

hypercoagulability
stasis
venous injury

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5
Q

hypercoagulability risk factors

A 
Ca, pregnancy/high estrogen
Protein C or S def.
antiphospholipid syndrome
prothrombin 202010 gene mutation
antithrombin def.
pneumonia
anemia
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6
Q

stasis/acquired hyper coagulable states

A

bed-ridden, wheelchair bound, cast, recent travel, advanced age

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7
Q

venous injury

A

surgery, trauma, fx bones

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8
Q

clin. features are result of

A

cardiopulmonary stress secondary to PE

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9
Q

s/s PE

A

SOB*, CP (2nd), hypoxemia, tachypnea, tachycardia

may be intermittent

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10
Q

more clinical features PE

A 
Hemoptysis (TB also)
Fever (of "unknown origin")
Epigastric pain
Cardiac arrest (lack of hx, "throw thrombolytic at")
CP usually pleuritic (worse w/ breathing)
Syncope 
Unilateral leg pain
Anxiety
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11
Q

PE dx gold standard

A

pulmonary angiogram in cath lab

but use CT more often* less invasive?

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12
Q

PE EKG findings

A 
S1Q3T3
Sinus tachycardia*
RBBB
Non-specific ST changes*
Normal!!!*
Very non specific
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13
Q

PE ABG dx

A

hypoxemia

resp. alkalosis
v. non-specific
* not used much

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14
Q

WELLS criteria

A

see book

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15
Q

PE dx D-dimer

A

“blood clot” test
inaccurate after 72 hrs of sx if no more clot formation
-helpful if negative, but not v. specific (45%) but sens. (95-97%)

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16
Q

PE dx CXR

A

Very non specific
May be normal
Elevated hemidiaphragm

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17
Q

PE CXR: Westermark sign

A

sharp cutoff of pulmonary vasculature

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18
Q

PE CXR: Hamptons Hump

A

pleural based, wedge shaped consolidation with the base against the pleural surface

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19
Q

PE VQ scan

A

Ventilation/perfusion mismatch (where perfusing, where ventilating)
(Negative, low prob, high prob, indeterminate)
Used to be most widely used, now replaced by CT

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20
Q

PE CT chest

A

Spiral CT scan chest with IV contrast
Finds smaller non-obstructing and possibly more incidentalomas
(most widely used modality in US)
Quite sensitive and specific

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21
Q

PE tx

A

LMWH
Heparin (drip)
Thrombolytic tx
new oral agents

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22
Q

Thrombolytic therapy

A

streptokinase, urokinase, alteplase

-directly lyse clot

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23
Q

give thrombolytic therapy for

A

Echocardiogram with high RV pressure
Unstable pt (hypotensive, respiratory failure)
Very large bilateral PE (saddle embolism)

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24
Q

new oral agents

A

?? not tested on

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25
Q

what to do if pt can not be anticoagulated

A

recent surgery
dural puncture
hx of hemorrhagic/ischemic stroke

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26
Q

best PE tx

A

prevention

Heparin pre-op etc.

27
Q

Heparin

A

binds thrombin, blocks clotting cascade, allows lysis
dosed over to coumadin/lovanox (oral) (6 mos)
may be on tx temp. if temp. risk factor (pregnant)
-should be on long-term if constant risk factor (genetic predisp)
higher risk of hemorrhage

28
Q

if can not be anti coagulated, use

A

IVC filter: basket placed in IVC, catches clot
(removed w/in 2 yrs)
manual thombectomy (if large PE)

29
Q

PE risk pops

A

Ca pts: Hypercoaguable state, ports and long term IV sites and ports, and fatigue with decreased mobility

pregnancy-heparin or LMWH (does not cross placenta) NOT warfarin/coumadin (does cross placenta)

30
Q

what else can embolize

A

fat: trauma from long bone or pelvis fx

air, preg, iatrogenic, etc

31
Q

PE sleep related breathing disorders definition

A

-breathing cessation for at least 10 seconds

32
Q

hypopnea

A

dec. in pulse ox by 4%

33
Q

PE iatrogenic

A

tips of catheters, guide wires during procedures, talc (drug use), starch, cellulose from meds or IDA

34
Q

PE amniotic fluid

A

dyspnea leads to cyanosis, hypotension and eventually DIC

35
Q

PE: air

A

central line placement, barotrauma (diving), or AV defect w/ air bolus

36
Q

sources of apnea

A

Central-effort is absent
Obstructive-effort persists but no airflow occurs
Mixed-absent effort comes before obstruction

37
Q

sleep related breathing disorders are associated with

A

arrhythmias

38
Q

OSA (obesity rel. sleep apnea) common clinical findings

A

obese middle aged man
HTN, cor pulmonale
Daytime somnolence, work problems, FALLS ASLEEP DURING EXAM OR HPI!!
Impaired thinking or concentration, depression
Weight gain, excessive soft tissue in oral cavity, large tonsils, narrowed airway or large tongue.
Impotence
Loud cycles of snoring
Apnea
Disturbed, restless sleeping
Erythrocytosis-why?

39
Q

OSA dx

A

sleep study

40
Q

OSA tx

A

Lifestyle modifications:
Weight loss, avoid alcohol and sedative meds
Nasal CPAP
Uvulopalatopharyngoplasty (UPPP) and other anatomic corrections
tracheostomy

41
Q

nasal CPAP

A

full mask, portable, tolerated well

42
Q

acute resp. failure definition

A

Abnormality of oxygenation or ventilation (elimination of CO2) leading to possible multisystem organ failure
PO2 less than 60mm Hg, PCO2 over 50mm Hg

43
Q

ARF findings

A

dyspnea, hypoxia, (alt ment stat) AMS, ha

44
Q

UPPP

A

remove part of tonsilar pillars and uvula

45
Q

definitive OSA tx

A

tracheostomy

46
Q

ARF tx

A

tx underlying cause: i.e. pneumonia secretions (pulm. toilet)

resp. supportive care to improve gas exchange w/ goal over 90% pulse ox
gen. supportive care

47
Q

resp support: non-ventilatory

A 
Nasal cannula (1-3L/min) (now up to 6L/min-high flow)
Venturi mask 24-40% FIO2
48
Q

resp. support: ventilatory

A

Noninvasive positive pressure-full face mask or nasal
(Bipap>Cpap)
Tracheal intubation
Mechanical ventilation

49
Q

when use vent. support (CPAP, BIPAP)

A

ES COPD, DNR, bridge before intubation, CHF

50
Q

indications for tracheal intubation

A

Hypoxemia despite attempt to correct
Upper airway obstruction Impaired airway protection
Severe respiratory acidosis
MS changes
Respiratory fatigue or maintained increased work of breathing
Apnea

51
Q

what would obstruct an airway

A 
acute epiglottitis
status asthmaticus
trauma
burns
foreign bodies 
mucous
52
Q

now what after intubated

A

mechanical ventilation

bag em

53
Q

controlled mechanical ventilation (CMV) or assist control (AC)

A

Gives breath when triggered and otherwise scheduled
Full tidal volume breaths
(will push to tidal volume when breathing)

54
Q

Synchronized intermittent mandatory ventilation (SIMV)

A

Pt triggered breaths are not supported with tidal volume

can breath naturally outside of that, will pull in whatever you’ll pull in-does not supplement

55
Q

complications with mech. ventilation

A

Displacement of ETT, barotrauma (inc. pressures–>pneumothorax; more likely on CMV), acute respiratory acidosis from over ventilation, hypotension, pneumonia, strictures (lungs, trachea), etc

56
Q

why hypotension

A

???

57
Q

ARDS def

A

Acute hypoxemic respiratory failure following a systemic or localized injury/insult without heart failure
Typically occurs within one week of event

58
Q

ARDS clinical findings

A

Rapid onset
Dyspnea with profound hypoxemia
Diffuse patchy bilateral infiltrates on imaging

59
Q

what prevents ARDS

A

nothing

60
Q

ARDS risks

A

see table

61
Q

ARDS tx

A

ID and tx cause
supportive care
improve/correct hypoxemia

62
Q

for correcting hypoxemia (ARDS)

A

Intubation with high PEEP(positive end expiratory pressures) (small volumes)
Occasional prone positioning
Avoid O2 toxicity

63
Q

this is not considered tx for PE

A

aspirin

CSI (75 decks)

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