PE, pulmonary hypertension & ventilation flashcards
23 high-yield MRCP Part 1 cards from the Intellect Medicos Respiratory Medicine course. Try to answer each question before you open it — then study them properly with spaced repetition, which brings each card back just before you would forget it.
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A patient with suspected PE has a 2-level PE Wells score of 6. What is the next step (NICE)?
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Immediate CTPA (or interim therapeutic anticoagulation if CTPA is delayed).
Why? A score > 4 means PE is likely, so go straight to imaging; a D-dimer cannot rule PE out in this group.
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A patient with suspected PE has a 2-level PE Wells score of 4 or less. What is the first investigation (NICE)?
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A quantitative D-dimer test (result within 4 hours).
Why? If negative, PE is unlikely and anticoagulation can be stopped; if positive, arrange CTPA.
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What is the most common ECG finding in pulmonary embolism?
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Sinus tachycardia.
Why? Other signs of right heart strain: right axis deviation, RBBB, and the classic but uncommon S1Q3T3 pattern.
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What is the first-line anticoagulant for confirmed PE or DVT in a patient without renal impairment, active cancer or antiphospholipid syndrome (NICE)?
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Apixaban or rivaroxaban.
Why? These DOACs need no LMWH lead-in. If unsuitable: LMWH then dabigatran/edoxaban, or LMWH plus a VKA.
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Which anticoagulant regimen is used for VTE in triple-positive antiphospholipid syndrome (NICE)?
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LMWH plus a VKA (warfarin) for at least 5 days or until the INR is ≥ 2.0 on 2 consecutive readings, then warfarin alone.
Why? DOACs are linked with more arterial thrombosis than warfarin in high-risk antiphospholipid syndrome.
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What is the first-choice anticoagulant for VTE in a patient with active cancer (NICE)?
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A DOAC (LMWH, or LMWH plus a VKA, if a DOAC is unsuitable).
Why? Treatment is for 3–6 months, then reviewed, taking account of tumour site, drug interactions and bleeding risk.
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Which anticoagulants are offered for VTE when creatinine clearance is BELOW 15 mL/min (NICE)?
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LMWH, UFH, or LMWH/UFH plus a VKA — DOACs are avoided.
Why? DOACs are renally cleared to varying degrees. With CrCl 15–50 mL/min, apixaban, rivaroxaban, edoxaban or dabigatran (if CrCl ≥ 30) can still be used.
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How long is anticoagulation given after a PROVOKED PE (e.g. after surgery), and what is the approach for an UNPROVOKED PE?
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Provoked: 3 months, then consider stopping if the trigger has gone. Unprovoked: at least 3 months, then consider continuing beyond 3 months after weighing bleeding risk.
Why? Unprovoked VTE has a higher recurrence risk once anticoagulation stops.
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What is the anticoagulant of choice for VTE in pregnancy, and for how long?
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LMWH, throughout the rest of pregnancy and for at least 6 weeks postpartum (minimum 3 months total).
Why? LMWH does not cross the placenta. DOACs are contraindicated, and warfarin is teratogenic (but safe when breastfeeding).
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A pregnant woman with suspected PE also has symptoms of DVT. What is the first investigation?
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Compression duplex ultrasound of the legs.
Why? If DVT is confirmed, treat as VTE and avoid chest radiation. Without leg symptoms, start with a chest X-ray, then V/Q or CTPA.
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What is the treatment for massive PE (PE with sustained hypotension)?
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Thrombolysis (e.g. IV alteplase), alongside a UFH infusion.
Why? Thrombolysis rapidly relieves right ventricular obstruction. If thrombolysis is contraindicated, consider surgical or catheter embolectomy.
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If thrombolysis is given for suspected PE during cardiac arrest, how long should CPR be continued?
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60–90 minutes.
Why? The thrombolytic needs time to work, so prolonged resuscitation is justified.
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Reversal agents: dabigatran is reversed by ______; apixaban and rivaroxaban are reversed by andexanet alfa.
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idarucizumab
Why? Idarucizumab is a monoclonal antibody fragment that binds dabigatran; andexanet alfa is a decoy factor Xa.
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Reversal agents: dabigatran is reversed by idarucizumab; apixaban and rivaroxaban are reversed by ______.
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andexanet alfa
Why? Idarucizumab is a monoclonal antibody fragment that binds dabigatran; andexanet alfa is a decoy factor Xa.
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How is pulmonary hypertension defined, and what is the gold-standard diagnostic test?
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Mean pulmonary artery pressure > 20 mmHg at rest, measured by right heart catheterisation.
Why? A pulmonary capillary wedge pressure ≤ 15 mmHg indicates pre-capillary PH (e.g. pulmonary arterial hypertension) rather than left heart disease.
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In pulmonary arterial hypertension, what treatment is used if acute vasoreactivity testing is POSITIVE?
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High-dose calcium-channel blocker (e.g. nifedipine, diltiazem).
Why? Only a minority of patients respond to vasoreactivity testing; those who do can be managed with CCBs.
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What is the mechanism of bosentan, and what must be monitored?
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Endothelin receptor antagonist; monitor liver function tests (hepatotoxic).
Why? PAH has too much endothelin and too little nitric oxide and prostacyclin. Bosentan is also teratogenic.
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Which drug class must NOT be co-prescribed with sildenafil in pulmonary hypertension?
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Nitrates (risk of severe hypotension).
Why? Sildenafil is a PDE-5 inhibitor that raises cGMP and causes vasodilation; nitrates also raise cGMP. Prostacyclin analogues (e.g. epoprostenol) are another PAH option.
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Which form of non-invasive ventilation is used for acute hypercapnic respiratory failure: CPAP or BiPAP?
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BiPAP (bilevel: IPAP and EPAP).
Why? The pressure difference supports ventilation and removes CO2. CPAP gives one constant pressure that improves oxygenation but does not ventilate.
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Name three contraindications to non-invasive ventilation.
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Any three of: cardiac or respiratory arrest, inability to protect the airway, GCS < 8, facial trauma or burns, fixed upper airway obstruction, uncontrolled vomiting.
Why? These patients need intubation or cannot tolerate a tight-fitting mask safely.
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What is the first-line investigation for suspected obstructive sleep apnoea, and the gold standard?
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First-line: home respiratory polygraphy (or oximetry if unavailable). Gold standard: polysomnography.
Why? The apnoea–hypopnoea index (AHI) grades severity: < 5 normal, 5–14 mild, 15–29 moderate, ≥ 30 severe.
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What is the mainstay of treatment for moderate to severe obstructive sleep apnoea?
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CPAP (with weight loss and other lifestyle measures).
Why? CPAP splints the upper airway open during sleep. A customised mandibular advancement splint is the NICE alternative for people who cannot tolerate or decline CPAP.
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How is obesity hypoventilation syndrome defined?
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BMI ≥ 30 kg/m² with daytime hypercapnia (awake PaCO2 ≥ 6.0 kPa) not explained by another cause.
Why? OSA alone gives a normal daytime PaCO2; OHS causes daytime hypercapnia and usually coexists with OSA.