Pulmonary embolism LO's Flashcards
1
Q
Define embolus
A
- intravascular mass that is carried by the blood to a site distant from its point of origin
2
Q
Causes of embolus
A
FAT BAT
- fat: entry of fat cells into circulation eg fracture of long bone
- air: gases are introduced during surgery or sudden changes in atmospheric pressure , deep sea diving
- thrombus: deep vein thrombosis dislodges and enters circulation, pulmonary vessels are most common site of obstruction
- bacteria: masses of infected lesions enter blood eg vegetation on heart valves, blood clots containing bacteria
- amniotic fluid: entry of fetal cells and debris from amniotic fluid enter maternal circulation, rare but potentially life threatening
- tumor: solid tumor cells or fragments enter systemic circulation
3
Q
Genetic and environmental factors that predispose to thrombus
A
- endothelial damage
- hypercoagulability
- Alterations to blood flow (venous stasis)
4
Q
Endothelial damage and thrombus predisposition
A
- Inflammatory or traumatic vessel injuries can lead to activation of clotting factors through contact with exposed subendothelial collagen
- smoking, hypertension, surgery, catheter lines, trauma, IV drug user –> exposure of subendothelial tissue factor and collagen
5
Q
Hypercoagulability and thrombus predisposition
A
- increased platelet activation, thrombophilia, (eg factor V Leiden mutation) oral contraceptive use, pregnancy, protein S deficiency, protein C deficiency, antithrombin deficiency, underlying malignancy, cancer treatment, HRT, central obesity, heparin induced thrombocytopenia, nephrotic syndrome
6
Q
Alterations to blood flow (blood stasis) and thrombus predisposition
A
- immobilization: leg paralysis, stroke, bedrest, prolonged sitting during travel, immobilization of extremity after fracture –> increased length of contact of coagulation factors with coagulation
- ## CHF/MI: failure to pump blood forward results in venous stasis and increased central venous pressure
7
Q
Factor V leiden
A
- factor Va cofactor
- to regulate and protect against clot formation, activated protein C cleaves and inactivates Va
- Factor V leiden –> mutation at one of protein C cleavage sites –> renders Va resistant to inactivation
8
Q
Prothrombin G20210A variant
A
- mutation at 20210 nucleotide causing a substitute from guanine to adenine
- increased production of prothrombin –> increase in liklihood of causing a clot
9
Q
Heparin induced thrombocytopenia
A
- heparin dependent IgG antibodies bind to heparin/platelet factor 4 complexes to activate platelets and produce a hypercoagulable state
10
Q
Polycythemia
A
-an increase in the number of red blood cells in the body. The extra cells cause the blood to be thicker, and this, in turn, increases the risk of other health issues, such as blood clots
11
Q
Signs and symptoms of PE
A
- acute onset of symptoms often triggered by a specific event (physical strain)
- dyspnea and tachypnea
- sudden pleuritic chest pain
- cough and hemoptysis
- decreased breath sounds, dullness on percussion, split second heart sound audible in some cases
- Tachycardia, hypotension
- jugular venous distention
- low grade fever
- Features of DVT : unilaterally painful leg swelling
- Features of massive PE: syncope and obstructive shock with circulatory collapse ( due to saddle thrombus)
12
Q
Pathophysiology of PE
A
- thrombus formation (virchow’s triad) –> deep vein thrombosis in the legs or pelvis (most commonly iliac vein) –> embolization to pulmonary arteries via inferior vena cava –> partial or complete obstruction of pulmonary arteries
13
Q
Pathophysiologic response of the lung to arterial obstruction
A
- infarction and inflammation of the lungs and pleura –> pleuritic pain chest pain and hemoptysis
- surfactant dysfunction –> atelectasis–> decrease PaO2
- Triggers respiratory drive –> hyperventilation and tachypnea–> respiratory alkalosis with hypocapnia ( decreased PaCO2)
- Mechanical vessel obstruction –> ventilation perfusion mismatch –> arterial hypoxemia (decreased PaO2)
- Cardiac compromise: elevated pulmonary artery pressure (PAP) due to blockage –> right ventricular pressure overload –> forward failure with decreased cardiac output –> hypotension and tachycardia
- pulmonary vasoconstriction: thromboxane A2 prostaglandins, adenosine, thrombin and serotonin secreted by activated platelet and the thrombus–> pulmonary vasoconstriction and bronchospasm
14
Q
Principles of diagnosis of PE
A
- wells criteria to assess PE probability
- Low probability: PERC score performed–> negative PE ruled out–> positive D-dimer test–> <500ng/ml –> PE ruled out–> >500ng/ml –> CT pulmonary angiography (see high probability)
High probability: start anticoagulation –> CT pulmonary angiography –> negative –> stop anticoagulation–> positive PE confirmed–> inconclusive –> V/Q scan
15
Q
Changes in ABG in PE
A
- limited use in diagnosis of PE, may be normal
- hypoxemia –> decreased O2–> V/Q mismatch –> hyperventilate and tachypnea–> leads to lowered CO2 and respiratory alkalosis
- No renal compensation as PE is acute and renal compensation takes 3 days to kick in
16
Q
Changes in ECG in PE
A
- may be normal
- arrhythmias: sinus tachycardia, bradycardia, atrial fibrilation
- new right bundle branch block
- right axis deviation due to strain on right side of heart
- S1Q3T3 pattern: S wave lead 1, Q wave lead 3, inverted T wave lead 3
17
Q
Right bundle branch block
A
slowing of electrical impulses to the heart’s right ventricle
18
Q
radiological investigations used to investigate pulmonary embolus
A
- CXR
- radionuclide imaging (V/Q scan)
- spiral CT angiography
- conventional (invasive) pulmonary angiography
19
Q
radiological investigations used to investigate pulmonary embolus
A
- CXR: used to rule out other causes eg pneumonia, pneumothorax
- radionuclide imaging (V/Q scan): alternative to CT pulmonary angiography eg renal insufficiency or contrast allergy, areas of V/Q mismatch detected
- spiral CT angiography/CT pulmonary angiography–> definitive and diagnostic test for PE–> IV line inserted –> contrast to view arteries
- conventional (invasive) pulmonary angiography: right heart catherization–> PA–> angiography with contrast
20
Q
treatment for pulmonary embolus
A
- PE with dynamic instability/massive pulmonary embolism –> yes –> thrombolytic eg tPA–> contraindication to thrombolytic–> consider embolectomy, thromectomy, iliac stenting, also if thrombolytics fail
- PE with dynamic instability/massive pulmonary embolism –> No–> anticoagulants –> contraindication to anticoagulants –> IVC filter, also if anticoagulants fail or recurrence
Other: IV fluids, pain medication (morphine or oxycodone), avoid analgesics, O2 therapy, ABG’s, ECG, FBC, BMP, troponin, BNP
21
Q
WELLS ‘s criteria
A
- probability of PE or DVT
- different criteria for each
- eg PE: previous PE, surgery or immobilization in last 4 weeks, malignancy, hemoptysis
22
Q
NSAID’s and anticoagulation/thrombolytics
A
- avoid taking NSAID’s as risk of hemorrhage due to gastric irritation and antiplatelet effect
- Gastric protection if necessary
- Morphine or oxycodone instead
23
Q
Risk factors PE
A
- obesity
- smoking
- pregnancy
- oral contraceptive pill or HRT
- Immobolization
- IV dug use
- > 60 years
- active cancer
- nephrotic syndrome
- Factor V leiden
- Promthrombin mutation
- Antithrombin III deficiency, protein C deficiency and protein S deficiency
24
Q
Risks of air travel and DVT
A
Air travel –> prolonged immobility –> risk factor DVT ( blood stasis)
-decreased activity in lower legs (MSK pump)–> decreased venous return –> increased stasis of blood
25
Hill's criteria of causation
- Strength
- Consistency
- Specificity
- Temporality
- Biological gradient
- Plausibility
- Coherence
- Experiment
- Analogy
26
Signs and symptoms DVT
- may be asymptomatic
- localized unilateral symptoms --> deep veins of legs, thighs or pelvis
- swelling, feeling of tightness or heaviness
- warmth, erythema and possibly livid discolouration
- progressive tenderness, dull pain --> worse when walking and improves with elevation
- Homans sign: calf pain on dorsal flexion of the foot
- Meyer sign: compression of calf causes pain
- Payr sign: pain when pressure is applied over the medial part of the sole of the foot
- distention of superficial veins
- distal pulses normal
- fever
- PE signs: dyspnea, chest pain, dizziness, weakness
27
Diagnosis of DVT
```
DVT probability (wells criteria)
- low--> D-dimer --> <500ng/ml--> DVT ruled out --> > 500ng/ml --> venous doppler ultrasound
```
-Intermediate/High: venous ultrasound doppler
Inconclusive U/S: consider venography, CT venography or MR venography
28
Investigations for DVT
- Venous doppler U/S
- D-dimer
- FBC's
- LFT's
- coagulation studies
- basic metabolic panel
29
V/Q scan
CXR should be obtained. Radioactive agents (e.g. TC-99m) are inhaled and administered intravenously. Their distribution in the alveoli and pulmonary arteries is registered via gamma cameras. Perfusion scintigraphy is usually performed first, followed by ventilation scintigraphy.
30
Pharmacology of warfarin
- blocks function of epoxide function enzyme which is responsible for reduction of vitamin k which acts as a clotting co-factor--> reduced synthesis of clotting factors
- side-effects: bleeding, teratogenic, skin necrosis (rare)
- metabolism: liver (CYP450 enzymes)
31
Protein S
- inhibits blood coagulation
32
Protein C
- provides control of blood coagulation by regulating the activities of factor VIIIa (FVIIIa) and factor Va (FVa), cofactors in the activation of factor X and prothrombin, respectively
33
Vitamin K is involved in which clotting factors
II, VII, IX, X, S, P
34
Direct thrombin inhibitors
- dagibatran, argatroban, lepirudin, bivalirudin
- bind to and inhibit thrombin (IIa) directly
- No fibrinogen--> fibrin etc
35
Direct factor Xa inhibitors
- apixaban, rivaroxaban, fondaparinux
- binds and inhibits factor Xa directly
- No fibrinogen--> fibrin ...
36
lifestyle advice that might be given to a patient with a genetic predisposition to clotting so as to avoid DVT/PE
-
37
Clotting cascade
see written notes
