How to Remove Blood Clots From Lungs

Lung blood clots, known medically as pulmonary embolisms, are treated through a spectrum of approaches ranging from blood-thinning medications that let the body dissolve the clot on its own, to clot-busting drugs, catheter-based procedures that physically break up or suction out the clot, and in the most severe cases, open-heart surgery. Which method your medical team chooses depends almost entirely on how dangerous the clot is right now, specifically whether it is straining your heart and threatening your blood pressure.

How Doctors Decide What Your Clot Needs

Not all pulmonary embolisms are equally dangerous, and the treatment path hinges on a rapid assessment of risk. Doctors classify acute pulmonary embolism into roughly three tiers. A low-risk clot means the heart is coping fine and blood pressure is stable. An intermediate-risk (sometimes called “submassive”) clot means imaging shows the right side of the heart is under strain, even though blood pressure is still holding. A high-risk or “massive” clot means the heart is failing to keep up, blood pressure is dropping, and the situation is immediately life-threatening.

This stratification drives every decision that follows. Researchers evaluating over 500 patients with acute pulmonary embolism found that right ventricular dysfunction on imaging was the most reliable marker for separating patients who needed aggressive intervention from those who could be managed with medication alone.¹ CT pulmonary angiography, the gold-standard imaging test for diagnosing a pulmonary embolism, can simultaneously show the size of the clot burden and whether the right ventricle is enlarged.² Both clot volume and visible right ventricular dysfunction on CT scans have been studied as ways to sort patients by risk.³

At many hospitals, a pulmonary embolism response team coordinates this assessment. These multidisciplinary groups, often including pulmonologists, cardiologists, interventional radiologists, and cardiac surgeons, meet rapidly to review imaging and lab results and decide on a treatment strategy together.⁴ The goal is to avoid both under-treating a dangerous clot and over-treating a manageable one.

Anticoagulation and the Body’s Own Clot-Dissolving System

For most pulmonary embolisms, the first-line treatment is anticoagulation, commonly called blood thinners. These drugs do not actively dissolve the clot. Instead, they prevent the clot from growing larger and stop new clots from forming, giving the body’s built-in clot-dissolving machinery time to do its work. Your body naturally produces plasminogen activators, enzymes that break down the fibrin mesh holding a clot together.⁵ In a low-risk pulmonary embolism, anticoagulation alone is usually enough because the clot is small enough that your body can clear it over days to weeks without further help.

The medications used include injectable heparins (often started in the hospital) and oral anticoagulants taken at home afterward, typically for at least three months. For many people, this is the entire treatment: stay on blood thinners, let the body do the rest, and monitor for complications. The clot does not vanish overnight. It shrinks gradually as fibrinolysis chews through it and the body remodels the remaining material.

Systemic Thrombolysis for Severe Clots

When a pulmonary embolism is massive, meaning blood pressure is crashing and the heart is in crisis, anticoagulation alone is too slow. Systemic thrombolysis delivers a powerful clot-dissolving drug, most commonly alteplase, through an intravenous line. The drug floods the entire bloodstream and rapidly activates plasminogen throughout the body, accelerating clot breakdown in the lungs.

The trade-off is bleeding risk. Because the drug works everywhere in the body, not just at the clot, it can trigger serious bleeding, including in the brain. The risk of major hemorrhage is significant enough that systemic thrombolysis is generally reserved for the sickest patients, those in hemodynamic collapse where the immediate threat of death from the clot outweighs the bleeding danger.⁶ People with recent surgery, active bleeding, or a history of hemorrhagic stroke are typically excluded from receiving it. For patients in the intermediate-risk category, the decision is harder and more controversial, which is partly why catheter-based alternatives have gained ground.

Catheter-Directed Thrombolysis

Catheter-directed thrombolysis tries to get the benefits of clot-dissolving drugs while reducing the bleeding risk. Instead of flooding the whole bloodstream, a doctor threads a thin catheter through a vein, typically starting from the groin or neck, and positions its tip directly inside or next to the clot in the pulmonary artery. The clot-busting drug is delivered locally, at a fraction of the dose used in systemic thrombolysis.

One widely studied system combines this local drug delivery with ultrasound energy. The ultrasound waves loosen the fibrin strands within the clot and increase its surface area, allowing the drug to penetrate more deeply and work more efficiently. This combination of low-power ultrasound and localized thrombolytic drug uses shorter infusion times and lower doses than systemic therapy, which should translate into fewer bleeding complications.⁷ In practice, treatment protocols have used roughly 11 to 12 mg of alteplase per catheter delivered over about 15 hours in some centers,⁸ while other protocols have explored even shorter five-hour infusions at 1 mg per hour per catheter.⁹ Compare that to a standard systemic dose of 100 mg, and the reduction is dramatic.

Catheter-directed thrombolysis has become a preferred option for many intermediate-high-risk patients, where the heart is straining but the patient is not yet in full cardiovascular collapse. It threads the needle between doing nothing beyond anticoagulation and unleashing a full systemic dose of clot-busting drugs.

Mechanical Thrombectomy

Rather than dissolving the clot chemically, mechanical thrombectomy physically removes it. A catheter equipped with a suction device is guided into the pulmonary arteries, positioned at the clot, and used to aspirate or extract the thrombus. The appeal is obvious: no clot-dissolving drugs at all, which means the bleeding risk associated with thrombolytics is taken off the table entirely.

Devices designed for this purpose have become increasingly sophisticated. The FlowTriever system, for example, uses large-bore aspiration combined with mechanical disruption to pull clot material out of the lungs.¹⁰ In a study of high-risk pulmonary embolism patients, the composite rate of major adverse events within the hospital stay was reached in about 17% of patients treated with this mechanical approach, compared to roughly 64% in a comparison group treated primarily with systemic thrombolysis or anticoagulation alone. In-hospital mortality was under 2% in the thrombectomy group versus nearly 30% in the comparison group.¹¹ Those numbers are striking, though it is worth noting that comparison groups in device studies are not always perfectly matched to the treatment arm.

A recent randomized trial provided stronger evidence. In patients with intermediate-high-risk pulmonary embolism, mechanical thrombectomy produced a greater reduction in heart strain at 48 hours compared to anticoagulation alone, and early normalization of vital signs was more frequent. The rate of major adverse events within seven days was similar between the two groups, suggesting the procedure did not add significant safety risk.¹² A meta-analysis of available studies found that mechanical thrombectomy was associated with markedly lower 30-day mortality compared to anticoagulation alone in intermediate-risk patients, though there was no significant difference in hospital length of stay.¹³

When catheter-directed thrombolysis fails or is not appropriate, mechanical suction thrombectomy can serve as a rescue option.¹⁴ The two catheter-based approaches are sometimes complementary rather than competing.

Open Surgical Embolectomy

Surgical pulmonary embolectomy is the most invasive option: open-heart surgery performed on cardiopulmonary bypass to directly extract clots from the pulmonary arteries. A surgeon opens the chest, places the patient on a heart-lung machine, opens the pulmonary arteries, and manually removes the clot material. It sounds dramatic because it is, but in the right circumstances it is lifesaving.

Surgery is typically reserved for patients whose hemodynamics have collapsed and who either cannot receive thrombolytics (because of contraindications like recent surgery or active bleeding), have failed thrombolytic therapy, or have failed catheter-based interventions.¹⁵ It is also the approach of choice when a clot is physically trapped in transit across the heart, such as lodged in a patent foramen ovale, where catheter-based retrieval would be too risky.¹⁶ Recent surgical series have reported in-hospital mortality below 10%, which is remarkable given that these patients are, by definition, the sickest of the sick.¹⁵

ECMO as a Bridge When the Heart Cannot Keep Up

Some patients arrive in cardiac arrest or near-arrest from a massive pulmonary embolism, too unstable for any procedure to begin immediately. Veno-arterial extracorporeal membrane oxygenation, commonly called VA-ECMO, can buy time. This machine takes blood out of the body, oxygenates it, and pumps it back in, essentially doing the work the heart and lungs cannot. It reduces the crushing load on the right ventricle and restores oxygen delivery to organs.¹⁷

ECMO is not a treatment for the clot itself. It is a support system that stabilizes the patient long enough for a definitive clot-removing procedure, whether that is catheter-directed therapy, mechanical thrombectomy, or surgery. It can also be used as a standalone therapy in some cases, keeping the patient alive while anticoagulation and the body’s own fibrinolysis slowly clear the clot.¹⁸ VA-ECMO can even rescue patients who have already gone into cardiac arrest from a pulmonary embolism.¹⁹ Outcomes are better when ECMO is started before cardiac arrest occurs, which underscores why early risk assessment matters so much.¹⁸

Inferior Vena Cava Filters

IVC filters are small metal devices placed inside the inferior vena cava, the large vein that carries blood from the lower body back to the heart. They work like a cage, catching blood clots traveling up from the legs before they reach the lungs. Filters do not remove a clot already in the pulmonary arteries. Their role is purely preventive: stopping the next clot from arriving.

They are most commonly considered for patients who cannot take anticoagulants, either because of active bleeding or a very high bleeding risk. Usage has increased over the years, and newer retrievable designs can be removed once the patient is able to start blood thinners. However, filters come with their own complications, including the risk of the filter itself migrating, tilting, or becoming a site where new clots form.²⁰ Timely retrieval is important, as leaving a filter in place longer than necessary increases the chance of problems.

Pulmonary Embolism During Pregnancy

Pregnancy raises the risk of blood clots, and treating a pulmonary embolism in a pregnant patient adds layers of complexity. The standard treatment is anticoagulation with low-molecular-weight heparin, which does not cross the placenta and is considered safe for the fetus. Treatment is continued for at least three months total and until at least six weeks after delivery.²¹

For life-threatening massive PE during pregnancy, thrombolysis has been used with high maternal and fetal survival rates, despite the theoretical risks. Guidelines suggest it in truly desperate situations. However, in the peripartum period, when the risk of hemorrhage is at its peak, non-drug-based treatments like catheter-directed therapy or mechanical thrombectomy may be preferred as a first option when available.²² The evidence base for these decisions is thin, mostly drawn from case reports and small series rather than randomized trials, so treatment is highly individualized.

Children and Pulmonary Embolism

Pulmonary embolism in children is rare, but it does happen, particularly in kids with central venous catheters, congenital heart disease, or inherited clotting disorders. The challenge is that almost all treatment protocols have been borrowed from adult medicine. Evidence-based guidelines specifically designed for pediatric patients are lacking, and current practices rely heavily on extrapolation from adult data. Treatment options include thrombolysis and anticoagulation with heparins or oral vitamin K antagonists, while newer direct oral anticoagulants have been studied in clinical trials for this age group.²³ The general approach follows the same logic as in adults: anticoagulation for most cases, with escalation to thrombolysis or interventional procedures in severe situations, adjusted for the child’s size and developmental stage.

When Clots Do Not Fully Resolve

Most pulmonary embolisms are treated, the clot dissolves over weeks to months, and the patient recovers. But in a small fraction of people, the clot does not fully clear. Instead, it organizes into scar-like tissue that permanently narrows or blocks pulmonary arteries. Over time, this raises blood pressure in the lungs and strains the right side of the heart, a condition called chronic thromboembolic pulmonary hypertension, or CTEPH.²⁴ A large registry study found that roughly 2.3% of pulmonary embolism patients were diagnosed with CTEPH within three years.²⁵

CTEPH is treatable, and the treatment depends on where in the pulmonary arteries the obstruction sits. For clots in the main, lobar, or segmental vessels, the treatment of choice is pulmonary endarterectomy, a surgical procedure performed under deep hypothermia and circulatory arrest. The surgeon peels the organized clot material away from the artery walls. In expert centers performing more than 50 of these operations per year, the procedure is potentially curative, with three-year survival above 80%.²⁶

For patients whose disease is too far downstream in smaller vessels for surgery, or who have residual high pressure after endarterectomy, balloon pulmonary angioplasty offers an alternative. A balloon catheter is threaded into the narrowed pulmonary arteries and inflated to widen them. European guidelines now give this procedure a top-tier recommendation for inoperable CTEPH.²⁷ After more than three decades of refinement, its long-term outcomes are now considered comparable to surgical endarterectomy in the patient populations where it is used.²⁸

Why Symptoms Can Linger Even After the Clot Is Gone

Even when the acute clot resolves and CTEPH is not present, a sizable number of people do not feel fully recovered. Post-pulmonary embolism syndrome, sometimes called PPES, encompasses lingering breathlessness, reduced exercise tolerance, and a measurable drop in quality of life that persists well beyond the acute event.²⁹ In a nationwide study, over half of people who had survived a pulmonary embolism reported shortness of breath on exertion, compared to about 17% of a matched control population that had never had one.³⁰

The causes are not entirely understood. Some of it may be residual damage to the pulmonary vascular bed even without frank CTEPH. Some of it may involve deconditioning during and after the acute illness, compounded by fear of exertion. Structured exercise programs are being studied as both a treatment and preventive measure for PPES, though this is still a relatively young area of research.²⁹ If you have been treated for a pulmonary embolism and still feel short of breath months later, it is worth raising this with your doctor rather than assuming it will pass on its own. Further evaluation can distinguish between normal slow recovery, deconditioning, CTEPH, and other causes.

How Diagnosis Can Be Tricky

One of the most frustrating aspects of pulmonary embolism is that its symptoms overlap with many other conditions. Sudden shortness of breath, chest pain, a racing heart, coughing, and lightheadedness can all point to cardiac, respiratory, or anxiety-related problems. This overlap leads to a high rate of initial misdiagnosis, especially when patients present to clinics focused on heart disease where PE is not top of mind.³¹

CT pulmonary angiography remains the standard test. It is fast, widely available, and highly accurate at showing both the presence of clots and their downstream effects on the heart.³² For patients who cannot receive the iodine-based contrast dye needed for CT, or for pregnant patients where minimizing radiation is preferred, a ventilation-perfusion scan is an alternative that looks for mismatches in airflow and blood flow within the lungs.³² Getting the right imaging quickly is what sets the entire treatment cascade into motion, which is why any acute onset of unexplained breathlessness or chest pain warrants urgent medical evaluation rather than a wait-and-see approach.