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A pulmonary embolism (PE) is a blood clot that travels to the lungs and blocks blood flow, usually having formed in a leg vein. It can cause sudden breathlessness, chest pain and a fast heart rate, and is a medical emergency needing prompt blood-thinning treatment. Most people recover well, but a small number develop a long-term form called chronic thromboembolic pulmonary hypertension (CTEPH), where old clots raise the pressure in the lungs. Rehabilitation and gradually rebuilding activity are part of recovery. This page explains clots in the lungs, both acute and chronic.
Pulmonary embolism (PE) is a common, time-critical cardiovascular emergency. A subset of survivors develops long-term sequelae — post-PE syndrome (10–30%) and chronic thromboembolic pulmonary hypertension (CTEPH, 3–4%) — both of which benefit from structured rehabilitation. The 2019 ESC Guideline on acute PE is the current international reference.
Definition
Pulmonary embolism is obstruction of the pulmonary arterial bed by a thrombus, almost always originating from deep vein thrombosis in the lower limbs or pelvis. CTEPH is the persistence of organised thromboembolic material in the pulmonary arteries causing pulmonary hypertension at least 3 months after acute PE despite adequate anticoagulation.
Pathophysiology
Acute PE causes mechanical obstruction and reflex vasoconstriction, increasing right ventricular afterload. The clinical impact depends on the size of the embolus and the pre-existing cardiopulmonary reserve. RV dysfunction is the principal mechanism of mortality in massive and submassive PE.
Co-morbidities and risk factors
Major transient risk factors: recent surgery, major trauma, immobilisation, hospitalisation, pregnancy and postpartum, hormone therapy. Persistent risk factors: active cancer, antiphospholipid syndrome, inflammatory bowel disease, heart failure, obesity, thrombophilia, prior VTE.
Prevalence
VTE affects approximately 1–2 per 1000 Australians annually, with rates increasing with age. PE accounts for around 10% of in-hospital deaths.
Symptoms
Symptoms — acute PE
Sudden-onset dyspnoea, pleuritic chest pain, cough (occasionally haemoptysis), pre-syncope or syncope, tachycardia, tachypnoea, hypoxaemia, hypotension in massive PE, and signs of DVT in the lower limb.
Symptoms — post-PE and CTEPH
Persistent dyspnoea, reduced exercise tolerance, fatigue, anxiety, and chest discomfort in the weeks and months after acute PE. Persistence beyond 3 months warrants formal assessment for CTEPH.
Diagnosis
Acute PE — diagnostic pathway
Clinical assessment with a validated probability score (Wells, Geneva, or YEARS) directs subsequent testing. Low probability with negative age-adjusted D-dimer rules out PE; intermediate or high probability requires CT pulmonary angiography (or V/Q scan in pregnancy or renal impairment). Bedside echocardiography is useful for haemodynamically unstable patients.1
Severity assessment
PE is stratified into high-risk (haemodynamic instability), intermediate-high risk (RV dysfunction plus positive troponin), intermediate-low risk (one or neither), and low risk. The simplified PESI score identifies patients suitable for early discharge or ambulatory management.
Investigations for underlying cause
Age-appropriate cancer screening; consideration of thrombophilia testing in younger patients with unprovoked PE, recurrent VTE, or strong family history; antiphospholipid antibody testing in selected cases (positivity influences anticoagulant choice).
Post-PE and CTEPH evaluation
Patients with persistent symptoms at 3 months post-PE should undergo a structured assessment including echocardiography, BNP/NT-proBNP, 6-minute walk test, V/Q scan (more sensitive than CT for CTEPH), and pulmonary function testing. Suspected CTEPH warrants referral to a designated PH centre for right heart catheterisation and treatment planning.
Management
Acute treatment
High-risk PE: systemic thrombolysis or, in selected patients, catheter-directed thrombolysis or surgical embolectomy at experienced centres.2,3,4
Intermediate- and low-risk PE: anticoagulation, usually with a direct oral anticoagulant (rivaroxaban or apixaban from day 1, or dabigatran/edoxaban after 5 days of parenteral anticoagulation). Low-risk PE may be managed as an outpatient.
Duration of anticoagulation
Provoked PE with a transient risk factor: at least 3 months. Unprovoked PE: anticoagulation for ≥3 months with subsequent decision based on bleeding risk, patient preference, and risk-of-recurrence scoring; extended anticoagulation (often at reduced dose) is increasingly used. Cancer-associated VTE: extended therapy with DOAC or LMWH while cancer is active.
CTEPH management
Lifelong anticoagulation. Pulmonary endarterectomy is the treatment of choice for operable disease. Balloon pulmonary angioplasty and medical therapy (riociguat) are used for inoperable or residual disease.5,6
Post-PE rehabilitation
Structured exercise rehabilitation in the months after acute PE improves exercise capacity, dyspnoea, and quality of life in patients with post-PE syndrome. Programmes follow pulmonary rehabilitation principles, with attention to anxiety and post-traumatic stress that are common after this acute illness.7,8
Medications
Anticoagulants
Direct oral anticoagulants (apixaban, rivaroxaban, dabigatran, edoxaban) are first-line for most patients. Low-molecular-weight heparin and warfarin retain a role in specific populations (pregnancy, severe renal impairment, antiphospholipid syndrome, active cancer). Reduced-dose apixaban or rivaroxaban is used for extended therapy.
Reversal and bleeding management
Idarucizumab reverses dabigatran; andexanet alfa is available in some centres for factor Xa inhibitor reversal. Prothrombin complex concentrate is widely used where specific reversal agents are unavailable.
Multi-system manifestations
Post-PE syndrome
A clinical entity defined by persistent dyspnoea, reduced exercise capacity, and impaired quality of life after acute PE in the absence of CTEPH. Affects 10–30% of PE survivors and is responsive to structured exercise rehabilitation.9,10
Anxiety, post-traumatic stress, and fear of recurrence
Acute PE is a frightening experience often associated with intensive care admission, prolonged anticoagulation, and lasting health anxiety. Routine screening and access to psychological support are appropriate.
Bleeding
The principal risk of long-term anticoagulation. Bleeding-risk assessment (HAS-BLED in AF, VTE-BLEED in VTE) and patient education on bleeding management are essential.
Recurrent VTE
Recurrence is most common in the first year after the index event. Persistent risk factors require ongoing risk-benefit reassessment of anticoagulation duration.
Warning signs
Living with PE and CTEPH
Exercise after acute PE
Most patients with low-risk PE can resume normal activity within days of starting anticoagulation. Structured exercise rehabilitation from 4–8 weeks post-PE improves recovery and reduces post-PE syndrome.
Travel
Long-haul travel within 6–8 weeks of acute PE is generally discouraged unless essential. Patients on anticoagulation can travel safely with appropriate precautions (compression stockings, hydration, mobilisation, medication adherence).
Lifestyle and risk-factor modification
Weight management, smoking cessation, treatment of obstructive sleep apnoea, and review of contributory medications (combined hormonal contraception, hormone replacement therapy) reduce recurrence risk.
Prognosis
Most patients with low- and intermediate-risk PE recover fully with appropriate anticoagulation. CTEPH is potentially curable with pulmonary endarterectomy in eligible patients; untreated CTEPH carries poor long-term survival.
Role of the physiotherapist
Once anticoagulation is established and the patient is stable, the physiotherapist supports safe early mobilisation and a graded return to activity, and delivers exercise rehabilitation for the deconditioning and persistent breathlessness that often follow a PE (including in CTEPH). They teach breathing and pacing techniques and provide reassurance and education during recovery.
Part 1 · References
- Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society. Eur Heart J 2020;41(4):543–603.
- EINSTEIN–PE Investigators. Oral rivaroxaban for the treatment of symptomatic pulmonary embolism. N Engl J Med 2012;366(14):1287–1297.
- Meyer G, Vicaut E, Danays T, et al. Fibrinolysis for patients with intermediate-risk pulmonary embolism (PEITHO). N Engl J Med 2014;370(15):1402–1411.
- Aissaoui N, Martins E, Mouly S, Weber S, Meune C. A meta-analysis of bed rest versus early ambulation in the management of pulmonary embolism, deep vein thrombosis, or both. Int J Cardiol 2009;137(1):37–41.
- Delcroix M, Torbicki A, Gopalan D, et al. ERS statement on chronic thromboembolic pulmonary hypertension. Eur Respir J 2021;57(6):2002828.
- Ghofrani HA, D'Armini AM, Grimminger F, et al. Riociguat for the treatment of chronic thromboembolic pulmonary hypertension (CHEST-1). N Engl J Med 2013;369(4):319–329.
- Rolving N, Brocki BC, Andreasen J. Effect of a physiotherapist-guided home-based exercise intervention on physical capacity and patient-reported outcomes among patients with acute pulmonary embolism: a randomized clinical trial. JAMA Netw Open 2020;3(2):e200064.
- Nopp S, Klok FA, Moik F, et al. Outpatient pulmonary rehabilitation in patients with persisting symptoms after pulmonary embolism. J Clin Med 2020;9(6):1811.
- Klok FA, van der Hulle T, den Exter PL, Lankeit M, Huisman MV, Konstantinides S. The post-PE syndrome: a new concept for chronic complications of pulmonary embolism. Blood Rev 2014;28(6):221–226.
- Sista AK, Miller LE, Kahn SR, Kline JA. Persistent right ventricular dysfunction, functional capacity limitation, exercise intolerance, and quality of life impairment following pulmonary embolism: systematic review with meta-analysis. Vasc Med 2017;22(1):37–43.
References are numbered in citation order (Vancouver/BMJ style) and were current at the time of writing. Guidelines are living documents — verify against the latest version before clinical use.
Supervised exercise, breathing technique and self-management education are the mainstay of cardiorespiratory physiotherapy for this condition.
Clinical evidence
Part 1 covers the same condition without the technical detail. What follows is the evidence base behind it, written for clinicians — the literature, the reasoning and the gaps.
For clinicians: this summary supports clinical reasoning and is not a protocol. Check current guidelines and local policy before applying it, and read it alongside the key references and guidelines directory.
Framing. Acute pulmonary embolism is risk-stratified rather than uniformly admitted: haemodynamic status, right-ventricular function, troponin and validated scores (PESI, simplified PESI, Hestia) determine whether a patient needs reperfusion, admission or early discharge on a direct oral anticoagulant.1 Two facts matter most to physiotherapy — early mobilisation is safe once anticoagulated, and a substantial minority of survivors are left with persistent breathlessness and reduced exercise capacity that rehabilitation can address.2,3
Acute management
- Direct oral anticoagulants are first-line for most patients, with non-inferior efficacy and less major bleeding than warfarin-based therapy.1,4
- Systemic thrombolysis in intermediate-risk PE reduced haemodynamic decompensation but increased major bleeding and stroke in PEITHO, so it is reserved for haemodynamic instability or deterioration.5
- Selected low-risk patients are managed as outpatients, which means physiotherapists increasingly meet them in the community within days of diagnosis.1
- Early ambulation is safe: meta-analysis of early mobilisation versus bed rest in venous thromboembolism found no increase in new or recurrent PE, and bed rest confers no protection.2
After the acute event
- Post-PE syndrome is common: persistent breathlessness, reduced exercise capacity and impaired quality of life affect a substantial proportion at six to twelve months, frequently without residual obstruction.3,6
- Physiotherapist-guided home-based exercise improved physical capacity and patient-reported outcomes after acute PE in a randomised trial — direct evidence for rehabilitation in this group.7
- Outpatient pulmonary rehabilitation improved exercise capacity and symptoms in patients with persisting symptoms after PE, and is safe on anticoagulation.8
- Chronic thromboembolic pulmonary hypertension develops in a small percentage and is potentially curable by pulmonary endarterectomy, with balloon pulmonary angioplasty and riociguat for inoperable disease — so unexplained persistent breathlessness must be investigated, not rehabilitated.9,10
Physiotherapy implications
- Confirm anticoagulation is established and the patient is haemodynamically stable before mobilising, then mobilise progressively rather than resting them.1,2
- Watch for right-ventricular strain in the early days: exertional hypotension, syncope, disproportionate tachycardia or marked desaturation is a reason to stop and escalate, not to push through.
- Refer for rehabilitation where symptoms persist beyond a few weeks — supervised or structured home-based programmes both have evidence, and these patients are commonly discharged with no follow-up at all.7,8
- Screen for CTEPH before attributing persistent breathlessness to deconditioning: progressive exertional dyspnoea, disproportionate desaturation or right-heart signs at three to six months warrant echocardiography and specialist referral.9
- Manage anticoagulation risk: avoid contact and high-fall-risk activity on treatment-dose therapy, assess falls risk in older patients, and report unusual bruising or bleeding.
- Address the fear. Many patients are frightened of exertion after a PE and require explicit permission, graded exposure and an explanation of why activity is safe.
- Prevent the next one: early mobilisation, hydration and adherence to inpatient thromboprophylaxis protocols in surgical and immobilised patients.1
Clinical reasoning
- Sudden breathlessness with pleuritic pain, tachycardia, syncope or haemoptysis — particularly after immobility, surgery, travel or a limb thrombosis — is a PE until excluded. Withhold treatment and escalate.
- Distinguish deconditioning (gradual, improves with training) from CTEPH (progressive, disproportionate desaturation, right-heart signs) — the second gets worse with a training programme.9
- An unprovoked event changes long-term anticoagulation and warrants specialist review for thrombophilia or occult malignancy.1
- Persistent symptoms after a normal follow-up scan are not imaginary — post-PE syndrome is a recognised entity that responds to rehabilitation.3,6
Evidence gaps
- Optimal timing, intensity and setting of rehabilitation after PE are not established, and trials are few and small.7,8
- No validated tool predicts who will develop post-PE syndrome.6
- Safe exercise thresholds in the presence of residual right-ventricular dysfunction are undefined.
- Whether early rehabilitation reduces the incidence of post-PE functional limitation has not been tested.
References for the clinical evidence summary
- Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society. Eur Heart J 2020;41(4):543–603.
- Aissaoui N, Martins E, Mouly S, Weber S, Meune C. A meta-analysis of bed rest versus early ambulation in the management of pulmonary embolism, deep vein thrombosis, or both. Int J Cardiol 2009;137(1):37–41.
- Klok FA, van der Hulle T, den Exter PL, Lankeit M, Huisman MV, Konstantinides S. The post-PE syndrome: a new concept for chronic complications of pulmonary embolism. Blood Rev 2014;28(6):221–226.
- EINSTEIN–PE Investigators. Oral rivaroxaban for the treatment of symptomatic pulmonary embolism. N Engl J Med 2012;366(14):1287–1297.
- Meyer G, Vicaut E, Danays T, et al. Fibrinolysis for patients with intermediate-risk pulmonary embolism (PEITHO). N Engl J Med 2014;370(15):1402–1411.
- Sista AK, Miller LE, Kahn SR, Kline JA. Persistent right ventricular dysfunction, functional capacity limitation, exercise intolerance, and quality of life impairment following pulmonary embolism: systematic review with meta-analysis. Vasc Med 2017;22(1):37–43.
- Rolving N, Brocki BC, Andreasen J. Effect of a physiotherapist-guided home-based exercise intervention on physical capacity and patient-reported outcomes among patients with acute pulmonary embolism: a randomized clinical trial. JAMA Netw Open 2020;3(2):e200064.
- Nopp S, Klok FA, Moik F, et al. Outpatient pulmonary rehabilitation in patients with persisting symptoms after pulmonary embolism. J Clin Med 2020;9(6):1811.
- Delcroix M, Torbicki A, Gopalan D, et al. ERS statement on chronic thromboembolic pulmonary hypertension. Eur Respir J 2021;57(6):2002828.
- Ghofrani HA, D'Armini AM, Grimminger F, et al. Riociguat for the treatment of chronic thromboembolic pulmonary hypertension (CHEST-1). N Engl J Med 2013;369(4):319–329.
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