Pulmonary Embolism and Pulmonary Hypertension Flashcards
What is meant by a pulmonary embolism?
blockage of a pulmonary artery by:
- a blood clot
- fat
- tumour
- air
What is meant by a pulmonary infarction?
Blood flow and oxygen to the lung tissues is compromised
=> Lung tissue may die
How are DVTs classified?
Proximal (Ileo-femoral)
Distal (Polpiteal)
Which type of DVT is most likely to embolise?
Proximal (ileo-femoral)
Distal DVTs are most likely to lead to chronic venous insufficiency and venous leg ulcers. TRUE/FALSE?
FALSE!
- Its actually proximal leg ulcers which cause these
How do DVTs usually present?
- Whole leg or calf involved (depending on site)
- Swollen
- hot
- red
- tender
What are the potential differential diagnoses for a DVT?
Differential:
- Popliteal synovial rupture (Baker’s cyst)
- Superficial thrombophlebitis
- Calf cellulitis
What Investigation is first line for DVT?
Ultrasound Doppler leg scan
Other than a Doppler US, what scan can be completed if you suspect a DVT?
CT scan of:
- Ileo-femoral veins
- IVC
- pelvis
The DVT which predisposes a patient to a PE may be “silent” i.e. asymptomatic. TRUE/FALSE?
TRUE
=> first symptom they get may be that of a PE
Clinical presentation of a PE depends on its size. Describe the difference in presentation of varying sizes of PE.
Large:
- shock (low BP)
- central cyanosis
- sudden death
Medium
- pleuritic pain
- haemoptysis
- breathless
Small recurrent PEs
- progressive dyspnoea
- pulmonary hypertension
- right heart failure
There are many Risk Factors for developing a DVT or PE. Name some of these
These usually come under Virchow’s Triad:
- Stasis
- Hypercoagulable state
- Turbulent Blood flow/ Endothelial damage
Thrombophilia (hypercoag.) Contraceptive pill/HRT Pregnancy Pelvic obstruction Trauma Surgery Immobility e.g. bed rest, long haul flights Malignancy Obesity Pulmonary hypertension Vasculitis
How are DVTs prevented in those who are at risk?
- Early post-op mobilisation (prevent immobility)
- TED compression stockings
- Calf muscle exercises
- LMWH perioperatively (Fragmin)
- DOAC medications
Describe the findings on Arterial Blood Gases of a patients suffering from a PE?
ABGs: LOW PaO2 LOW SaO2 => (Type 1 resp failure) [PaCO2 can be normal or low]
Describe how a CXR of a PE can appear?
- Normal early on before infarction
- Basal atelectasis (collapse)
- consolidation
= Pleural effusion
What scoring systems can be used to predict if a patient has had a PE?
Wells Score (>4 = PE likely, >6 = HIGH RISK)
Revised Geneva Score (>10 = HIGH RISK)
How can you investigate a patient with a suspected PE?
- Assess risk using the Pulmonary Embolism Severity Index (PESI)
- ECG
- D-dimers usually raised
- Troponin +/- BNP
- Isotope V/Q Scan
- CT Pulmonary Angiogram (CTPA)
- Leg/pelvic US for DVT check
- ECHO
What are the advantages of a V/Q scan?
- Sensitive for small peripheral emboli
- Perfusion defect shows BEFORE infarction
- Perfusion+Ventilation matched defect after infarction
What is the stereotypical ECG pattern of a patient with a PE?
Acute Right heart strain pattern => S1Q3T3
- Prominent S wave in lead I
- Q wave and inverted T wave in lead III
- sinus tachycardia
- T wave inversion in leads V1 - V3
- Right Bundle Branch Block
- low amplitude deflections
Why would you consider doing a CTPA in the context of a PE?
- to image pulmonary artery filling defect
- to pick up larger clots in proximal vessels
Why would an ECHO be completed when investigating a PE?
- measure pulmonary artery pressure
- measure RV size
- If RV is acutely dilated this is in keeping with acute PE
What underlying cause for a PE should be considered if there are no obvious causes? How would you investigate for these?
- Consider cancer
Check: CXR, PSA, CA125, Pelvic US or CT Abdo/pelvis - Autoantibodies (e.g. Antiphospholipid syndrome)
Check: Anti-nuclear, Anti-Cardiolipin - Thrombophilia screen
Check: Anti-thrombin-III deficiency, Protein C or S deficiency, Factor V Leiden
What investigation modality should be used for a suspected PE in a VERY unwell patient?
CTPA
If a patient is admitted with a suspected low risk PE, and no previous respiratory disease (CXR NORMAL) what investigation should be done first?
Either - V/Q or CTPA
If a patient with a suspected PE is pregnant, what investigation should be done first?
1st - US of legs
OR perfusion only scan (Q scan)
=> Avoid radiation to breast tissue where possible.
If VERY unwell = CTPA (accept risk of radiation)
Where should patients with a PE be managed based upon their risk?
Low risk = ambulatory care pathway -> home Mid Risk = ward/ HDU if req'd High risk (inc. cardiovascular compromise) = HDU (They may require thrombolysis)
How is a DVT or PE usually treated?
Therapeutic dose of S/C LMWH
=> Dalteparin/Fragmin
- give tx empirically if pt is high risk and you are awaiting test results
- withhold tx for low risk pts until test results come back
How is LMWH given and how long do patients continue on this for?
- LMWH –once daily injection
- no monitoring required
- Start warfarin simultaneously
- After 3-5 days stop heparin when INR>2
What other type of drug can be used instead of LMWH and warfarin?
DOACs
Direct Factor Xa inhibitors
- Rivaroxaban
- Apixaban
What are the INR targets for patients who have remained on warfarin?
- 0-3.0 (2.5) After 1st event
- 0 or more for recurrent events
- 5 if recurrent DVT/PE whilst on warfarin
Warfarin interacts with many other substances. TRUE/FALSE?
TRUE
- alcohol, antibiotics, grapefruit
- Anti-platelets/ drugs which increase bleeding tendency
e. g. Aspirin, NSAIDs, Clopidogrel
=> CHECK BNF
When would thrombolysis be used to treat a PE?
- life-threatening massive /sub-massive PE
- low BP (sustained sys <90 mmHg for 15mins)
- severe hypoxaemia
- imminent or actual cardiorespiratory arrest
What drug is used in thrombolysis?
tissue plasminogen activator (tPA) - tenecteplase
Give some examples of the relative and ABSOLUTE contraindications to thrombolysis.
Relative:
- Pregnancy/post partum
- anticoagulants
- TIA <6 months ago
- advanced liver disease
- active peptic ulcer disease
Absolute:
- haemorrhagic stroke
- ischaemic stroke <6 months
- cerebral neoplasm or trauma
- recent major trauma/surgery
- known bleeding disorder
- aortic dissection
How long should treatment be continued for after having a PE?
Unprovoked 1st PE 6 months
Provoked PE / temporary risk factor 3 months
Unprovoked low-risk distal DVT 3 months
High risk proximal DVT 6 months
Recurrent DVT/PE Life-long
IVDUs and patients with active cancer should be put on which type of anticoagulant?
LMWH (Fragmin)
- SHOULD NOT be given warfarin
If a young male has a life threatening PE at first presentation and has a high risk of recurrence, how long should he continue his treatment for?
- consider life long treatment after 1st event
Patients on anticoagulation have a risk of bleeding/ being over-anticoagulated. How is this treated?
- If bleeding STOP anticoagulant
- reverse effect with antidote
- LMWH and warfarin have long T1/2 => takes a while to leave system
- Consider prothrombin complex concentrate or fresh frozen plasma
- Reverse warfarin with vitamin K (esp. if liver disease)
- Reverse LMWH with protamine
The effect of DOACs cannot be reversed. TRUE/FALSE?
TRUE
- no antidote
What is a normal pulmonary artery pressure and what does this rise to in Pulmonary Hypertension?
Normal mean pulmonary arterial pressure (mPAP)
= 12-20 mmHg
Pulmonary HT mPAP >25 mmHg
How can the pulmonary artery pressure be measured?
- Measured with right heart catheter (invasive)
- Systolic pulmonary arterial pressure can be estimated with ECHO doppler
What are the two main types of Pulmonary Hypertension?
Pulmonary VENOUS HT
Pulmonary ARTERIAL HT
Pulmonary VENOUS HT is caused by what?
- left-sided heart disease
=> Left Ventricular Systolic Dysfunction
- ischaemic
- Mitral Regurgitation / Stenosis
- Cardiomyopathy
Pulmonary ARTERIAL HT is caused by what?
- this is considered PRIMARY pulmonary HT
- Hypoxic – COPD, Pulmonary fibrosis
- Multiple PEs
- Vasculitis
- Drugs
- HIV
- Cardiac Left to right shunt – ASD, VSD
What is cor pulmonale?
- Right-sided heart disease
- secondary to lung disease
- Fluid retention due to hypoxia +/- right heart failure
- Can complicate COPD, fibrotic lung disease, chronic PE etc
What are the clinical signs of Pulmonary Hypertension and Right sided heart failure?
- Central cyanosis
- Dependent oedema (oedema in lower body due to gravity)
- Raised JVP
- Right ventricular heave at left parasternal edge
- Murmur of tricuspid regurgitation
- Enlarged liver (pulsatile)
How can pulmonary hypertension be investigated?
- ECG - Right bundle branch block
- CXR – cardiomegaly
- Sats and ABGs
- Pulmonary function with DLCO (diffusion capacity)
- ECHO
- Right ventricular systolic pressure (RVSP)
- Measure RV and LV dimensions and function
- Measure mPAP
- D dimers
- VQ scan
- CTPA
How is Primary Pulmonary ARTERIAL HT treated?
- prophylactic anticoag. (warfarin)
- O2 if hypoxic
- Pulmonary Vasodilators
=> Ca2+ channel blockers (oral nifedipine,diltiazem)
=> Endothelin antagonist (e.g. Bosentan)
=> PDE5-inhibitor (e.g. Oral Sildenafil)
=> Prostanoids (IV Epoprostenol or Inhaled Iloprost)
=> Soluble Guanylate Cyclase stimulator (Riociguat)
OR Lung Transplant
What is Chronic Thromboembolic Pulmonary Hypertension (CTEPH)?
Pulmonary Hypertension caused by an accumulation of small PEs
How is CTEPH treated?
Riociguat – pulmonary arterial vasodilator
Pulmonary endarterectomy (removing blood clots from lungs) - curative (2% operative mortality)
Describe how the pulmonary circulation supplies the lung
Dual supply
=> Pulmonary arteries
=> Bronchial arteries
The Pulmonary artery receives the entire cardiac output TRUE/FALSE?
TRUE
The pulmonary circulation is a low pressure system. What does this mean?
- Thin walled vessels
- Low incidence of atherosclerosis
Describe the pathological morphology of Pulmonary Hypertension
- Medial hypertrophy of arteries
- Intimal thickening (fibrosis)
- Atheroma
- RV hypertrophy
What sign on CXR indicates Right sided heart failure?
Cardiomegaly
=> heart takes up more than 1/3 of CXR
