1/19
Looks like no tags are added yet.
Acute Pulmonary Embolism (PE)
PP: blocks center of vascular lumenâvessel distention
or
occludes a vesselâvessel distention
RF: 2nd m/c sudden death
3rd m/c hospitalized pts death
1/1000 people
DVT (60-80%)
E: virchowâs triad
venous stasisâaccumulation of platelets+thrombin in veins
endothelial/venous wall injury
-catheter
-PICC lines
-HTN/smoking
-atherosclerosis
hypercoagulability
-factor v leiden mutation
-antithrombin 3 deficiency
-m/câantiphospholipid sx
-malignancy
-hormone replacement
-OCPs
CM: asx (50+%)
or
abrupt onset
pleuritic chest pain
dyspnea
unexplained breathlessness
tachycardia
tachypnea
hypoxemia
cough
hemoptysis
PE: jugular venous distention (JVD)
deep vein thrombosis (DVT)
hypotension
fever
crackles
rare:
wheezing
s3
s4
cyanosis
DX: clinical+PE findings+vitals
CTAâstrong suspicion
SpO2ânormal
CBCâleukocytosis
CMP
BMP
PT
PTT
troponinâelevated
BNPâelevated
ABG
d-dimer
EKG
CXR
wellâs score
PERC rule
venous doppler
CTA
pulmonary angiography
v/q scan
echo
P: poor cardiac reserve/large vasoconstriction (massive emboli)âpulmonary HTN+RHF
small embolusâdissolved by fibrinolytic systemâlung fxn returns to normal
Chronic Pulmonary Embolism (PE)
PP: blocks arteryâreduces artery diameter over 50+%ârecanalization in thrombus+arterial web
RF: 2nd m/c sudden death
3rd m/c hospitalized pts death
1/1000 change
DVT (60-80%)
E: virchowâs triad
venous stasisâaccumulation of platelets+thrombin in veins
endothelial/venous wall injury
-catheter
-PICC lines
-HTN/smoking
-atherosclerosis
hypercoagulability
-factor v leiden mutation
-antithrombin 3 deficiency
-m/câantiphospholipid sx
-malignancy
-hormone replacement
-OCPs
CM: asx (50+%)
or
abrupt onset
pleuritic chest pain
dyspnea
unexplained breathlessness
tachycardia
tachypnea
hypoxemia
cough
hemoptysis
PE: jugular venous distention (JVD)
deep vein thrombosis (DVT)
hypotension
fever
crackles
rare:
wheezing
s3
s4
cyanosis
DX: clinical+PE findings+vitals
CTAâstrong suspicion
SpO2ânormal
CBCâleukocytosis
CMP
BMP
PT
PTT
troponinâelevated
BNPâelevated
ABG
d-dimer
EKG
CXR
wellâs score
PERC rule
venous doppler
CTA
pulmonary angiography
v/q scan
echo
P: poor cardiac reserve/large vasoconstriction (massive emboli)âpulmonary HTN+RHF
small embolusâdissolved by fibrinolytic systemâlung fxn returns to normal
Pulmonary Embolism PP (General)
emboliâobstruction of pulmonary blood flowâincreased physiologic dead spaceâimpaired gas exchangeâincreased pulmonary resistance+loss of alveolar surfactantâatelectasis (collapsed lung)+shrinking of lung tissue+scarring of lung tissue
Embolus Causes
m/câthrombus
air
IV infusion
central venous catheters
diving
amniotic fluid entering maternal circulation+pulmonary arteries post-delivery
fat moves to BM post-fracture
foreign bodies
parasites
infxn
tumor cells
DVT Embolism
thrombus that forms in femoral vein
below calf/UEârare
50-60%âdevelop PE
-50%+embolic eventsâasx
-50%+DVTâasx
Provoked vs Unprovoked PE
provoked
RF/E that directly caused PE
-virchowâs triad
unprovoked
PE occurred idiopathically (no RF/E)
-need hypercoagulable dx
-ask FHx+ROS/PEâr/o malignancy
-need cancer screening
increased blood clot RF
PE EKG Findings
70% ptsâabnormal
m/c dx patternâS1Q3T3 pattern
other abnormalities:
sinus tachycardia+non-specific ST+T wave changes (40%)
right ventricular hypertrophy (RVH)
right axis deviation
right bundle branch block (RBBB)
PE CXR Findings
m/cânormal
other findingsâengorged pulmonary vasculature:
westermarkâs sign
blood vessel collapsesâhyperlucency
pallaâs sign
enlarged right descending pulmonary artery
hamptonâs hump
small PEâwedge-shaped opacity
-edge of the lung
-untxdâpleuritic cor pulmonale
E: hemorrhage
pulmonary infarct
Wells Score
estimates probability of PE
guide for further dx screenings

PERC Rule
low probability of PE (wells score u2)
determines if d-dimer is neededâavoids unnecessary testing
all 8 filledâno test
all 8 not filledâd-dimer

D-Dimer
I: low-moderate pretest probability of PE
negative+LOW probabilityâr/o PE
negative+HIGH probabilityâno r/o PE
high probability ptsâlow negative predictive value
high sensitivity+LOW SPECIFICITY (canât confirm dx)
CT Angiography (CTA)
gold standard+1st line dxâin high-suspicion pts
IV contrastânephrotoxic
CI: anaphylactic contrast dye allergy
hemodynamic instability
AMI
decompensated CHF
renal impairment
V/Q Scan
CTA not useable/CI to CTA
results equivocal+non-diagnostic
Venous Doppler (Ultrasound)
I: detecting proximal DVT
equivocal for PE V/Q scanâperform
distal/recurrent thrombi+asx ptsâless accurate
results:
positiveâPE dx
negativeârepeat dx x days 1-3+days 7-10ânegativeâlow chance of VTE
Pulmonary Angiography
most accurate
invasive
embolectomy can be done with dx
I: uncertain PE dx
catheter-directed thrombolysis
planned embolectomy
positiveâPE dx
negativeâr/o PE
Echocardiogram
m/cânormal
I: RV dysfxn
RV strain
pulmonary artery pressure
right chamber emboli
mcconnelâs sign
middle section of RV free wall doesnât moveâright side of heart strain
PE Thrombolytic vs Anticoagulant Mx Tx
thrombolytic
I: hypotension+no high bleeding RF
massive PE+high hypotension RF
high hypotension/hypoxemia death RF
MX: altepase
streptokinase
urokinase
CI: active internal bleeding+stroke x past 2 months
uncontrolled HTN+surgery x past 6 weeks
C: increased major hemorrhagic complications RFs
no difference x 1 week+1 month post-dx compared to heparin/warfarin
P: 24 hrsâresolution of emboli
anticoagulant
I: not txâsecondary prophx
MX:
DOACs
rivaroxaban
apixaban
dabigatran
warfarin âbridgeâ
heparinâPO warfarin x 6 months
takes ~5-7 days for tx effect
C: doesnât break down clotsâbody does that over time
hemorrhage
heparin induced thrombocytopenia (HIT)
PE Duration of Tx
optimal durationâpt specific
considerations
age
RFs
-inherited
-reversible
consequences of hemorrhage
pt functional status
provoked RFs
trauma/surgeryâtx x 3-6 months
proximal leg embolismâtx x 6 months
unprovoked PE episodeâtx x extended/indefinite
PE NP Tx
embolectomy
I: massive PE
thombolytic CI
unstable post-thrombolytic tx
bad prognosis
C: high mortality rateâlast resort tx
IVC filter
I: anticoagulation CI
recurrent VTE despite OAC
massive PE+high recurrent+fatal embolism RF
ROA: reduce short-term PE incidence
C: 2x increase recurrent DVT RF x first 2 years of insertions
P: clinically safeâadd OAC
once stableâremove
PE Prognosis
untxdâ30% mortality rate
RV dysfxnâ10% mortality rate
recurrent VTEâ3% mortality rate (rare)
mortality m/câprogressive RHF
1%âchronic thromboembolic pulmonary HTN develops
dx+txâfavorable
perfusion defectsâresolve in most