U12C2 DVT And PE Flashcards
What are the types of PE?
- Mycotic- transfer of infective pathogens to the lungs from a distant source eg. IV injections
- Fat- enters circulation, can occur after long bone fractures and causes multi focal inflammation in lungs
- Air- commonly from cannulation
- Thrombotic- usually from the deep veins of the legs, but could be other sites e.g. iv lines. Paget Schroetter
What are the diagnotic tests for PE?
D-dimer- is the degradation product of crosslinked (by factor XIII) fibrin
Well’s score for DVT and PE
Doppler Ultrasound
V/Q matching- Air that reaches your lungs matched by the amount of blood flow in the capillaries in your lungs. Dead space is an area with ventilation but inadequate perfusion, in which oxygen can’t enter the bloodstream. Anatomically, there are areas in the respiratory tract with oxygen and no blood flow. Physiologic, when the alveoli has oxygen but not enough blood flow to carry this oxygen. Shunt occurs when there’s adequate blood flow or perfusion, but not enough ventilation.
- Echocardiography- assesses haemodynamic effects of emoticons burden
- CTPA-CT pulmonary angiography
How does D-dimer work?
What is the intrinsic and extrinsic pathway of coagulation?
What are the signs and symptoms of DVT?
- Oedema – DVT causes block in the affected vein, impeding venous return of blood from lower leg. This causes extravasation of fluid because of increased venous pressure, resulting in oedema.
- Distension/dilation of superficial veins – increased venous pressure in the deep veins of the leg results in distension of superficial veins as they become an alternative route for blood flow back to the heart, also the increased venous pressure of the affected deep vein also causes increased pressure in the superficial veins.
- Pain, fever, redness and swelling indicates acute inflammation
What are the signs and symptoms of PE?
- Poor perfusion of lung tissue due to emboli, results in poor gas exchange
- Reduced cross-sectional area of pulmonary arterial bed due to emboli causing blockage, this increases pressure in the pulmonary artery
As a result; - Reduced cardiac output due to pressure difference between the pulmonary artery (higher than normal pressure) and right ventricle
- Decreased stroke volume and cardiac output (hypotension)
- Right ventricle dilation to accommodate for increased blood volume since blood cannot enter the pulmonary artery as normal
- Haemoptysis – clot in blood vessel contains platelets that secrete enzymes causing vasoconstriction of pulmonary vascular system. Hypoxemia of lung tissue can cause pulmonary infarction, causing alveolar capillary membrane to rupture -> coughing up blood.
- Tachycardia – activated chemoreceptors in the aortic arch induces sympathetic response to increase perfusion of viable aveoli and
- Increased RR and depth – increase oxygen supply to (can cause respiratory alkalosis due to increased CO2 exhalation)
- Syncope – lack of blood supply to the brain
What are the clinical manifestations of DVT?
What is the pathophysiology of DVT to PE?
- Thrombosis is the pathological process by which a localized solid mass of blood constituents (a blood clot or thrombus ) forms within a blood vessel, mostly as a result of fibrin formation with a variable contribution from platelets and other cells.
- This differentiates it from physiological haemostasis, the process in which a fibrin-rich blood clot occurs outside the vessel-wall lining (or endothelium) as a result of injury. Thrombi form on, and are attached to, the vessel wall but fragments ( emboli ) may break off and occlude vessels downstream
What is virchows triad?
Endothelial injury
• Promotes Platelet adhesion and aggregation
• Causes the production of pro-coagulant factors
• In heart and arterial circulation
• Over ulcerated plaques in Atherosclerosis
• Endocardial injury in MI- mural thrombus
• Traumatic or inflammatory vascular injury - vasculitis
Abnormal flow of blood
• Prevents blood diluting activated clotting factors
• Causes include:
• Stasis (venous thrombosis) – allows platelets to encounter endothelium (due to loss of laminar
blood flow) and slows the washout of activated clotting factors
• Turbulence (arterial, near valves/cardiac thrombosis) – Physical trauma to endothelial cells or dysfunction and Countercurrents and local pockets of stasis
Hypercoagulable state
• Primary
• Leiden factor V mutation, Congenital deficiency of antithrombin III, protein C & S,
• Secondary: increased concentration of fibrinogen and
prothrombin
• Immobilization, MI, neoplasia, tissue damage (surgery, fracture, burns), cancer, prosthetic cardiac valves
• Heparin induced thrombocytopaenia syndrome
• Antiphospholid antibody syndrome
Arterial vs venous thrombus
What are the fates of a thrombus?
•Lysis: due to the potent thrombolytic activity of the blood.
•Propagation (increase in size): because the thrombus acts as a focus for further thrombosis.
•Organisation: the eventual invasion of connective tissue elements, which causes a thrombus to become firm and greyish white.
•Canalisation: by which new lumens lined by endothelial cells form in an organised thrombus.
•Embolisation: in which part or all of the thrombus becomes dislodged, travels through the circulation, and lodges in a blood vessel some distance from the site of thrombus formation.
What are the complications of a PE?
What are the risk factors for a DVT?
- Cancer – coagulation system gets highly activated contributing to a hypercoagulable state
- Genetics - decreased protein C or protein S means increased tendency to clot. Leiden factor V mutation or abnormal prothrombin levels contribute to a hypercoagulable state
- 60 – with ↑ age, fibrinogen, factors VIII and IX ↑without proportional ↑ in anticoagulant factors. Also, with age, ↑ risk for comorbid conditions
- Overweight/obese –
- contributes to chronic inflammation which leads to production of inflammatory cytokines in the liver which will then stimulate vascular endothelium, platelets. Tissue factor is upregulated by TNF-a and IL6 and is an important initiator of coagulation
- impaired fibrinolysis. –Rate of fibrinolysis is highly regulated by plasminogen activator inhibitor-1 (PAI-1). PAI-1 in an irreversible inhibitor of plasminogen activators including tPA preventing conversion of plasminogen to plasmin preventing breakdown of clots. Expression of PAI-1 is markedly upregulated in obese patients
- Male – higher first occurrence and recurrence risk but no definitive reason for exactly why
- Medical illness e.g. acute infection or inflammatory disorders – driver of inflammation (same process as described in obesity)
- Smoking – toxic substances can cause endothelial injury or dysfunction
- Recent major surgery/trauma - endothelial injury which means blood clots more likely to form around surgery site. Usually followed by immobility if major surgery, which causes blood to slow which also makes it more likely to clot
- Significant immobility bedbound, unable to walk unaided or likely to spend a substantial portion of the day in bed or in a chair, prolonged travel – stasis of blood flow in venous system
- Significant trauma or direct trauma to a vein (for example intravenous catheter) – foreign object → blood more likely to clot, site of infection
- Hormone treatment (for example oestrogen-containing contraception or hormone replacement therapy) – increase in fibrinogen conc, factors II, VII, IX, X and XII and decreased antithrombin III. This is through gene transcription as they are steroid hormones
- Pregnancy and the postpartum period – oestrogen increases coagulability as it increases production of clotting factors in the liver leading to hypercoagulable state
- Dehydration – increases viscosity of blood, which slows circulation
What are the diagnostic tests for DVT and PE?
-Wells score: calculates the risk through a series of questions of DVT and PE
- ABG: levels often normal, but can show hypoxaemia, low Paco2 (secondary to hyperventilation) or acidosis.
- FBC:
- Low Hb – may be anemia is a risk factor for a clot occurring, but could also be that endothelial dysfunction causes anemia
- Raised neutrophils – inflammation is known to have pro-thrombotic effect, especially chromatin from neutrophils
- High platelet to lymphocyte ratio – thought to indicate elevated predisposition to a clot occurring
- Us&Es – DOAC are filtered by the body through the kidneys, so kidney function is tested to calculate the correct dose for the patient to minimize the risk of adverse effects
- Activated prothrombin time (aPTT)
- Using citrated blood assay
- Triggered by an activator (koalin) and partial thromboplastin (PS)
- Shows defects inFXII, FXI, FIX, FVIII, FX, FV, FII, FI – intrinsic
- Is used to measure a patient’s response to heparin therapy
- Prothrombin time (INR)
- Using citrated blood assay
- Triggered by thromboplastin (FIII and PS) and Ca2+
- Shows defects inFVII, FX, FV, FII, FI – extrinsic
- Is more reliable in an acute trauma setting and is used to monitor warfarin
-D-dimer: its main value is as a negative result to exclude thromboemboli in low-risk patients.
-ECG: often normal but tachycardia is the most common finding; right bundle branch block and right ventricular strain are indicative. The S 1 Q 3 T 3 pattern (deep S wave in I, Q waves in
III and inverted T waves in III) is ‘textbook’ but uncommon.
-** CXR:** usually normal but may show atelectasis or a small wedge shadow (Hampton hump).
- CTPA: the gold standard for diagnosing PE. It allows visualization of the pulmonary vasculature.
- V/Q scanning (isotope lung scanning): looking for a mismatch defect. This method requires a normal CXR.
- Lower limb compression venous ultrasound scan: to confirm deep vein thrombosis (DVT).
- Heart sounds:
S1 – produced as mitral and tricuspid valve closes in systole
S2 – produced by the closing of aortic and pulmonic valves in diastole
Pulmonic valve closes after aortic, this is because the pressure in the aorta is greater than that in the pulmonary artery
If the S2 is split, the second sound heard would be louder if there is a pulmonary issue
In PE:
Lound S2 – the pulmonic component would be louder due to the increased pulmonic pressure
May have systolic murmur due to right sided heart strain
Can have a third heart sound present if there is right sided heart failure
-Echocardiography: may show evidence of acute right ventricular dysfunction, especially in large haemodynamically significant PEs.
What are the classes of haemorrhage?
What is the pathophysiology of hypovolemic shock?
- vol)
- Dec venous return
- Dec preload
- Dec SV
- So dec CO (as CO = SV x HR)
- So dec Pa (as Pa = CO x TPR)
- Dec tissue perfusion - leads to tissue hypoxia = impaired cellular metabolism (lack of O2 to tissue)
- Organ dysfunction due to impaired aerobic metabolism – so anaerobic takes over (O2 demands not met) = lactic acid = metabolic acidosis (due to hyperlactatemia)
- Multiorgan failure
What are the signs and symptoms of a haemhorrage?
What is the gender recognition certificate?
What is the pathological process of pulmonary oedema?
Pulmonary oedema results from either the elevation of pulmonary hydrostatic pressure or the increased capillary permeability from various causes
