Resp V Flashcards
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]
Stable, no renal impairment or co-morbidities: offer apixaban/rivaroxaban. If not-suitable, LWMH for 5 days then offer edoxaban/warfarin*
First line: anticoagulation:
- apixaban or
- rivaroxaban
OR
- UFH / LMWH / Fondaparinux lead AND warfarin
- Target INR 2-3 then stop heparin
Describe the long term managment of PE for:
- most people [4]
- patients suffering from antiphospholipid syndrome [1]
- pregnant people [1]
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):
- CTEPH is a rare but serious complication characterized by unresolved thrombotic occlusions in the pulmonary arterial system, turning into fibrotic tissue leading to increased pulmonary vascular resistance, pulmonary hypertension, and eventually right heart failure.
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
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
Hepatotoxicity
Optic neuritis
Gout
Type IV
Describe the diagnostic pathway for PEs
