Pulmonary Embolism
16/8/10
PY Mind Maps
OH
Data Interpretation - Venkatesh
Sinclair, D (2007) “ICU management of Pulmonary Embolism” Anaesthesia and Intensive Care
8:12 pages 534-536
British Thoracic Society Standards of Care Committee Pulmonary Embolism Development
Group (2003) “The British Thoracic Society Guidelines for the management of acute
pulmonary embolism” Thorax, 58:470-484
Agnelli, G et al (2010) “Acute Pulmonary Embolism” New England Journal of Medicine,
363(3):266-74, Jul 15.
- effects are proportional to the time frame and degree of obstruction
- increased PVR -> RVF -> obstructive shock
- increased alveolar dead space -> V/Q mismatch -> pulmonary vasoconstriction to optimize
gas exchange
- pulmonary infarction
CLINICAL FEATURES
- subclinical -> massive
History
-
SOB
pleuritic chest pain
apprehension
cough
haemotypsis
leg pain
collapse = massive PE
- acute cardiovascular collapse
Examination
-
pale, mottled skin
tachypnoea
tachycardia
signs of DVT
hypotension
altered LOC
elevated JVP
parasternal heave
loud P2
central cyanosis
Jeremy Fernando (2011)
Risk factors
Major (relative risk 5-20) - SLOMMM
Surgery – major abdominal/pelvic, hip/knee replacements, post ICU
Lower limb problems - #, varicose veins
Obstetrics – late pregnancy, C/S, puerperium
Malignancy – abdominal/pelvic, advanced/metastatic
Mobility – hospitalization, institutional care
Miscellaneous – previous VTE
Minor (relative risk 2-4) - COM
Cardiovascular – congenital heart disease, CHF, HT, superficial venous thrombosis, CVL
Oestrogens – OCP, HRT
Miscellaneous – COPD, neurological disability, occult malignancy, thrombotic disorder, long
distance travel, obesity, other (IBD, nephrotic syndrome, dialysis, myeloproliferative
disorders, paroxysmal nocturnal haemoglobinuria, Bechet’s diseas)
Thrombophillia’s
-
Factor V Leiden mutation
Prothombin gene mutation
Hyperhomocysteinaemia
Antiphospholipid antibody syndrome
Deficiency of antithrombin III, protein C or protein S
High concentrations of factor VIII or XI
Increased lipoprotein (a)
-> test in those < 50years with recurrent or a strong FHx
INVESTIGATIONS
- goal = confirm diagnosis + assess severity
- normal compliance and peak pressures on ventilator
- increased PACO2 -> ETCO2 to gradient
- hypoxaemia
- ECG:
->
->
->
->
->
->
->
->
->
mostly normal
sinus tachycardia
SI, QIII, TIII
non specific ST changes or TWI in anterior leads (right heart strain),
right axis deviation
s wave (I and aVL) > 1.5mm
Q wave in III and aVF
p pulmonale
RBBB
- CXR: rules out other pathology, focal oligaemia, wedge density (pulmonary infarction)
- ABG: reduced PaO2 in keeping with size of PE, metabolic acidosis with circulatory collapse,
respiratory alkalosis
- D-Dimer: reassuring if negative to exclude PE, use in conjunction with clinical probability
Jeremy Fernando (2011)
- TNT: elevation is associated with adverse outcome even in normotensive patients, also
associated with haemodynamic instability in patients with non-massive PE
- BNP and NT-terminal BNP: if low correlates well with uneventful course
- CTPA: as good as pulmonary angiography (gold standard), can calculate RV/LV ratio (>0.9)
= severe
- ECHO: RV dialation, paradoxical septal motion towards the LV, TR, RVF, PHT or PA
thrombus on TOE,
- US: leg veins (not as accurate as initially thought -> have low threshold to re-scan)
- V/Q scan: only really used now when CT is contraindicated, (normal scan, low, intermediate
and high probability with various criteria)
- MRI – high rate of technical difficulty and insufficient sensitivity (PIOPED III study)
MANAGEMENT
Grade severity of PE
MASSIVE – haemodynamically unstable -> thrombolyse/embolectomy
SUB-MASSIVE – haemodynamically stable with evidence of RV dysfunction -> strongly
consider thrombolysis/embolectomy but need to balance risk of bleeding
MILD – haemodynamically stable with normal RV function -> anticoagulation
Management Goals
(1) prevent further embolism
(2) removal of emboli (massive or sub-massive)
(3) haemodynamic support (massive)
Jeremy Fernando (2011)
Resuscitate
A – may need intubation if in cardiovascular collapse or cardiac arrest
B – high flow O2 as a pulmonary vasodilator, ventilation to optimize V/Q mismatch,
hyperventilation to clear CO2
C – invasive monitoring, fluid management to optimize right ventricular function, inotropic
support, cautious fluid boluses, use milrinone, noradrenaline or adrenaline (rather than alpha
agonists)
Electrolyte + Acid-base
- proportional to the degree of shock
- may have a metabolic acidosis from hyperlactataemia from circulatory compromise
Antidotes
THROMBOLYSIS
- not used in small or sub-massive (although this is contentious – doesn’t reduce mortality
but does reduce deterioration)
Jeremy Fernando (2011)
- can be used up to 14 days after symptoms begin
- PE resolve more quickly than with heparin alone
- as successful as embolectomy in massive PE (earlier the better)
- indicated in patients with RV compromise + haemodynamically unstable
- rTPA 1.5mg/kg is maximum dose (as good through peripheral IV or CVL)
- 50mg bolus of alteplase IV
- contraindications: absolute - bleeding, recent stroke, HI, current GI bleeding, relative –
PUD, surgery within 7 day, prolonged CPR
- follow straight away with heparin
- if bleeds -> FFP and anti-fibrinolytics
ANTICOAGULATION
-
use UFH as first dose, in massive PE and where reversal may be required
start immediately when there is a suspicion (prior to imaging)
LMWH as good as heparin
give straight after thrombolysis
then needs warfarin (INR 2-3)
SURGICAL
- embolectomy (massive PE and unresponsive to thrombolysis or is contraindicated)
- right heart catheterisation with clot destruction
- IVC filter (high risk of further embolic or recurrent PE despite adequate anticoagulation,
contraindications to anticoagulation, extensive DVT, massive PE)
OTHER THERAPIES
- ECMO – its place in PE is unknown
- IABP – has been used with vasoactive medications
- NO – has been used with some effect
Underlying cause
- prophylaxis
- modify risk factors
- diagnose thrombophillias
Jeremy Fernando (2011)