Name and state the drug classes used to treat idiopathic pulmonary hypertension [4]
Idiopathic pulmonary hypertension may be treated with:
Calcium channel blockers
Intravenous prostaglandins e.g., epoprostenol
Endothelin receptor antagonists e.g., macitentan
Phosphodiesterase-5 inhibitors e.g., sildenafil
Which inherited disorders increase the risk of PE? [5]
Factor V Leiden mutation:
- Normally used for blood clotting: helps enzyme reaction to form fibrin in blood clot
- Once the coagulation process is turned on in people with factor V Leiden, it turns off more slowly than in people with normal factor V
Antithrombin deficiency
- Normally anti-thrombin acts as the inhibitory component to thrombin formation
Prothrombin deficiency
Protein C & S deficiencies
Antiphospholiipid syndrome
Which type of hormone therapy increases the risk of PE? [1]
Hormone therapy with oestrogen (e.g., combined oral contraceptive pill or hormone replacement therapy)
Explain what is meant by the PERC rule
The pulmonary embolism rule-out criteria (PERC) are recommended by the NICE guidelines (2020) when the clinician estimates less than a 15% probability of a pulmonary embolism to decide whether further investigations for a PE are needed. If all the criteria are met, further investigations for a PE are not required.
What ABG results would indicate PE? [1]
Explain your answer [1]
TOM TIP: Patients with a pulmonary embolism often have respiratory alkalosis on an ABG.
Hypoxia causes a raised respiratory rate.
Breathing fast means they “blow off” extra CO2.
A low CO2 means the blood becomes alkalotic.
A V/Q scan is of limited use in patients with which co-morbidities? [3]
A V/Q scan is of limited use in patients with:
* significant underlying lung disease
* left ventricular failure
* congestive cardiac failure
Describe the treatment algorithm for patients who have PE confirmed and are haemodynamically unstable [4]
First line:
- heparin: 10,000 units intravenously as a loading dose initially, followed by 18 units/kg/hour intravenous infusion
PLUS: thrombolysis: (involves injecting a fibrinolytic (breaks down fibrin) medication that rapidly dissolves clot)
- Alteplase or
- Streptokinase or
- Urokinase
PLUS:
- anticoagulation with unfractionated heparin (UFH) for several hours after the end of thrombolysis before: switching to apixaban or rivaroxaban; low molecular weight heparin (LMWH) is an alternative if these are unsuitable - this is preferable
CONSIDER: vasoactive drug if SBP < 90 mmHG after thrombolysis
- noradrenaline or
- dobutamine
-
Describe the treatment algorithm for patients who have PE confirmed and are haemodynamically stable [4]
First line: anticoagulation:
- apixaban or
- rivaroxaban
instead of using low-molecular weight heparin (LMWH) until the diagnosis is confirmed, NICE now advocate using a DOAC once a diagnosis is suspected, with this continued if the diagnosis is confirmed
- if neither apixaban or rivaroxaban are suitable then either LMWH followed by dabigatran or edoxaban OR LMWH followed by a vitamin K antagonist (VKA, i.e. warfarin)
Stable, no renal impairment or co-morbidities: offer apixaban/rivaroxaban. If not-suitable, LWMH for 5 days then offer edoxaban/warfarin*
Describe the long term managment of PE for:
DOACs: most people
- apixaban
- rivaroxaban
- edoxaban
- dabigatran
Warfarin: for antiphospholipid syndrome patients
LMWH for pregnant people
Describe how massive PE causes hemodyanmic collapse [7]
Describe how PE can cause cardiogenic shock [2]
Cardiogenic shock
- Severe PE may lead to decreased cardiac output, causing systemic hypotension, impaired end-organ perfusion, and ultimately cardiogenic shock.
Which arrythmias can PE lead to [3]
Arrhythmias: PE can provoke supraventricular and ventricular arrhythmias, such as:
- atrial fibrillation
- ventricular tachycardia
- ventricular fibrillation
which can further compromise hemodynamics.
Describe three subacute complications of PE
Infarction and lung necrosis
- PE can cause ischemic injury to the lung parenchyma, leading to pulmonary infarction, haemorrhage, or lung necrosis.
Pleural effusion:
- Inflammatory processes triggered by PE may cause pleural effusion, which may be exudative or hemorrhagic.
Pneumothorax:
- Rarely, PE-induced lung infarction may lead to pneumothorax due to the rupture of a bulla or necrotic lung tissue
Describe a chronic complication of PE [1]
Chronic thromboembolic pulmonary hypertension (CTEPH):
What is the most appropriate next step in the investigation of suspected pulmonary embolism if D-dimer negative?
Stop anticoagulation and consider an alternative diagnosis
What is the most appropriate next step in the investigation of suspected pulmonary embolism if medium-high (> 15%) pre-test probability of PE? [1]
A 2-level PE Wells score should be performed:
Clinical probability simplified scores
PE likely - more than 4 points
PE unlikely - 4 points or less
What is the most appropriate next step in the investigation of suspected pulmonary embolism if CTPA negative? [1]
Consider the possibility of DVT and arrange proximal leg vein ultrasound if suspected
PE would cause change to axis deviation? [1]
Right axis deviation
State 4 invasive procedures used to treat PE if needed
Which of the following is used to treat chronic PEs unresolved after 3 months
Pulmonary thombro-endarterectomy (PTE)
Name a risk [1] and benefits [2] of using unfractionated heparin in treating PE [4]
Risks:
- Heparin induced thrombocytopenia (HIT)
Benefits:
- Rapid reversal possible
- More rapid anticoagulation
Describe the different bridging times for LMWH if using:
- Warfarin
- Dabigatran or edoxaban
- Rivaroxaban or apixaban
Warfarin:
- Start LMWH and initiate warfarin at same time then after 5-10 days change to just warfarin
Dabigatran or edoxaban
- 5 days of LMWH with both then switch to doac same day
Rivaroxaban or apixaban
- No bridge - only use them
a prolonged PR interval