5.1 Pulmonary embolism

Question 1

Virchow’s triad

Answer 1

-haemodynamic changes/stasis
-hypercoagulability
-endothelial injury

Question 2

risk factors for each category of virchows triad

Answer 2

-haemodynamic changes/stasis
-long haul flight
-prolonged immobility
-hypercoagulability
-contraceptives/HRT
-smoking
-cancer (pancreatic,colon)
-thrombophilia
-endothelial injury
-injury/trauma

Question 3

explain how acute R heart strain can be caused by PE

Answer 3

1. LV can’t fully expand so output drops, BP drops
2. inotropes (NA/adrenaline) released to raise BP via vasoconstriction, but also vasoconstrictor pulmonary circulation X
3. also RV wall thins, damaged so wont conduct electrical impulses properly so can lead to arrhythmias
4. also possible PFO opens as RV pressure>LV, so deoxy blood can’t deliver enough O2 to tissues, or clot could pass through systemic circumstances = stroke

Question 4

PE on CXR

Answer 4

-wedge/ Hampton hump
-maybe nothing visible

Question 5

clinical signs of PE

Answer 5

-RR>16
-crackles
-HR>100
-murmur if severe
-DVT signs
-cyanosis
-sweating
-low grade fever <39

Question 6

ECG appearance of PE

Answer 6

-sinus tachy *****
-deep S wave lead 1
-pathological Q wave lead 3
-inverted T wave lead 3 (RV strain)

-RBBB
-non specific ST changes

Question 7

positive predictive value or D dimers

Answer 7

poor
could be raised in pregnancy, surgery, heart disease, trauma

Question 8

first line imaging for PE suspicion

Answer 8

CXR

Question 9

when would CTPA be contraindicated?

Answer 9

-pregnancy
-poor renal function
-allergy to dye

Question 10

what’s involved in a CTPA?

Answer 10

radio opaque dy should fill all pulmonary arteries, dark areas i.e. polo mint view = clot

Question 11

first treatment for PE

Answer 11

oxygen

Question 12

do we thrombolyse PE?

Answer 12

not unless its a massive one

Question 13

thrombolysing treatments

Answer 13

streptokinase
tPA

Question 14

danger of anticoagulants

Answer 14

heparin induced thrombocytopenia

Question 15

how does HIT occur?

Answer 15

1. antibodies to heparin form nd bind heparin-platelet complexes
2. platelets activated and clump, thrombi form and propagate
3. spread throughout body = stroke, MI, ishaemia

Question 16

longer term treatment of PE

Answer 16

-anticoagulants for low risk patients
-if severe:
haemodynamic support
respiratory support
thrombolysis

Question 17

what constitutes a severe PE?

Answer 17

massive submissive PE
-affects CO so that systolic BP <90
-evidence of heart damage e.g. RV strain, even if systolic BP>90

Question 18

how long would patients be on oral anticoagulants for after discharge?

Answer 18

3 months if identifiable and preventable risk factor
indefinitely if no identifiable risk, or cancer

Question 19

who can’t you prescribe anticoagulants to?

Answer 19

-oesophagael varices
-previous haemorrhage stroke
-severe thrombocytopenia

Question 20

how would you treat someone with recurrent PE despite anticoagulation?

Answer 20

vena cava filter, prevents progression to PE

Question 21

prevention techniques for each category of virchows triad

Answer 21

-haemodynamic changes/stasis
-AES stockings
-mobilisation
-intermittent pneumatic compression
-hypercoagulability
-anticoagulants
-endothelial injury
-falls prevention
-avoud necessary invasive procedures

Question 22

most common cause of pulmonary infarction

Answer 22

PE

Question 23

explain how PE causes pulmonary infarction

Answer 23

occlusion of distal pulmonary artery, -bronchial arteries are recruited as new primary source of perfusion for pulmonary capillaries
-higher blood pressure of bronchial arteries increases capillary blood flow
-erythrocytes extravasate (alveolar haemorrhage)
-tissues necroses and infarct