PE Flashcards
where PEs come from
anything proximal to popliteal can embolize, below can propagate then embolize
PEs are often missed bc
symptoms may be vague, need high clinical suspicion
atypical symptoms of no symptoms at all
3rd leading cause of death in hospitalized pts.
risk of blood clot formation
Virchow’s triad
Virchow’s triad
hypercoagulability
stasis
venous injury
hypercoagulability risk factors
Ca, pregnancy/high estrogen Protein C or S def. antiphospholipid syndrome prothrombin 202010 gene mutation antithrombin def. pneumonia anemia
stasis/acquired hyper coagulable states
bed-ridden, wheelchair bound, cast, recent travel, advanced age
venous injury
surgery, trauma, fx bones
clin. features are result of
cardiopulmonary stress secondary to PE
s/s PE
SOB*, CP (2nd), hypoxemia, tachypnea, tachycardia
may be intermittent
more clinical features PE
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
PE dx gold standard
pulmonary angiogram in cath lab
but use CT more often* less invasive?
PE EKG findings
S1Q3T3 Sinus tachycardia* RBBB Non-specific ST changes* Normal!!!* Very non specific
PE ABG dx
hypoxemia
resp. alkalosis
v. non-specific
* not used much
WELLS criteria
see book
PE dx D-dimer
“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%)
PE dx CXR
Very non specific
May be normal
Elevated hemidiaphragm
PE CXR: Westermark sign
sharp cutoff of pulmonary vasculature
PE CXR: Hamptons Hump
pleural based, wedge shaped consolidation with the base against the pleural surface
PE VQ scan
Ventilation/perfusion mismatch (where perfusing, where ventilating)
(Negative, low prob, high prob, indeterminate)
Used to be most widely used, now replaced by CT
PE CT chest
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
PE tx
LMWH
Heparin (drip)
Thrombolytic tx
new oral agents
Thrombolytic therapy
streptokinase, urokinase, alteplase
-directly lyse clot
give thrombolytic therapy for
Echocardiogram with high RV pressure
Unstable pt (hypotensive, respiratory failure)
Very large bilateral PE (saddle embolism)
new oral agents
?? not tested on
what to do if pt can not be anticoagulated
recent surgery
dural puncture
hx of hemorrhagic/ischemic stroke
best PE tx
prevention
Heparin pre-op etc.
Heparin
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
if can not be anti coagulated, use
IVC filter: basket placed in IVC, catches clot
(removed w/in 2 yrs)
manual thombectomy (if large PE)
PE risk pops
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)
what else can embolize
fat: trauma from long bone or pelvis fx
air, preg, iatrogenic, etc
PE sleep related breathing disorders definition
-breathing cessation for at least 10 seconds
hypopnea
dec. in pulse ox by 4%
PE iatrogenic
tips of catheters, guide wires during procedures, talc (drug use), starch, cellulose from meds or IDA
PE amniotic fluid
dyspnea leads to cyanosis, hypotension and eventually DIC
PE: air
central line placement, barotrauma (diving), or AV defect w/ air bolus
sources of apnea
Central-effort is absent
Obstructive-effort persists but no airflow occurs
Mixed-absent effort comes before obstruction
sleep related breathing disorders are associated with
arrhythmias
OSA (obesity rel. sleep apnea) common clinical findings
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?
OSA dx
sleep study
OSA tx
Lifestyle modifications:
Weight loss, avoid alcohol and sedative meds
Nasal CPAP
Uvulopalatopharyngoplasty (UPPP) and other anatomic corrections
tracheostomy
nasal CPAP
full mask, portable, tolerated well
acute resp. failure definition
Abnormality of oxygenation or ventilation (elimination of CO2) leading to possible multisystem organ failure
PO2 less than 60mm Hg, PCO2 over 50mm Hg
ARF findings
dyspnea, hypoxia, (alt ment stat) AMS, ha
UPPP
remove part of tonsilar pillars and uvula
definitive OSA tx
tracheostomy
ARF tx
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
resp support: non-ventilatory
Nasal cannula (1-3L/min) (now up to 6L/min-high flow) Venturi mask 24-40% FIO2
resp. support: ventilatory
Noninvasive positive pressure-full face mask or nasal
(Bipap>Cpap)
Tracheal intubation
Mechanical ventilation
when use vent. support (CPAP, BIPAP)
ES COPD, DNR, bridge before intubation, CHF
indications for tracheal intubation
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
what would obstruct an airway
acute epiglottitis status asthmaticus trauma burns foreign bodies mucous
now what after intubated
mechanical ventilation
bag em
controlled mechanical ventilation (CMV) or assist control (AC)
Gives breath when triggered and otherwise scheduled
Full tidal volume breaths
(will push to tidal volume when breathing)
Synchronized intermittent mandatory ventilation (SIMV)
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
complications with mech. ventilation
Displacement of ETT, barotrauma (inc. pressures–>pneumothorax; more likely on CMV), acute respiratory acidosis from over ventilation, hypotension, pneumonia, strictures (lungs, trachea), etc
why hypotension
???
ARDS def
Acute hypoxemic respiratory failure following a systemic or localized injury/insult without heart failure
Typically occurs within one week of event
ARDS clinical findings
Rapid onset
Dyspnea with profound hypoxemia
Diffuse patchy bilateral infiltrates on imaging
what prevents ARDS
nothing
ARDS risks
see table
ARDS tx
ID and tx cause
supportive care
improve/correct hypoxemia
for correcting hypoxemia (ARDS)
Intubation with high PEEP(positive end expiratory pressures) (small volumes)
Occasional prone positioning
Avoid O2 toxicity
this is not considered tx for PE
aspirin
