Pulmonary Embolism: Symptoms, Types, Causes and Treatment

Pulmonary embolism (PE) is a life-threatening condition that occurs when a blockage—most often a blood clot—obstructs the arteries in the lungs. Its subtle, variable symptoms and complex causes make it both a diagnostic and therapeutic challenge. Early recognition and prompt treatment are crucial, as PE remains a leading cause of cardiovascular death worldwide. In this article, we explore the symptoms, types, causes, and treatment of pulmonary embolism with a focus on evidence-based insights and practical details for patients and clinicians alike.

Symptoms of Pulmonary Embolism

Pulmonary embolism can strike suddenly and with a variety of symptoms, often mimicking other more common medical conditions. Many patients are caught off-guard by the abruptness and severity of symptoms, making both awareness and clinical suspicion vital for early diagnosis.

Symptom	Frequency	Feature	Source(s)
Dyspnea	60–81%	Sudden onset, most frequent	1, 2
Chest Pain	39–56%	Sharp, pleuritic, or vague	1, 3
Syncope	22–26%	Fainting or near-fainting	1
Hemoptysis	5–7%	Coughing up blood	1, 2
Cough	>60%	Often non-specific	2
Tachypnea	>60%	Rapid breathing	2
Fatigue	Variable	Especially in chronic/PPES	4, 12
Lightheadedness	Variable	Especially in post-PE syndrome	4

Table 1: Key Symptoms of Pulmonary Embolism

The Most Common Symptoms

Sudden onset dyspnea (shortness of breath) is by far the most frequent symptom of PE, reported in 60–81% of cases. It often appears suddenly and without warning, sometimes during rest or minor exertion. Chest pain, usually sharp and pleuritic (worsened by breathing in), occurs in up to half of patients. Syncope (fainting) and hemoptysis (coughing up blood) are less common but highly suggestive, particularly when unexplained by other conditions 1, 2, 3.

Symptom Clusters and Overlaps

PE symptoms often overlap with those of other respiratory or cardiac conditions. Patients may experience a combination of symptoms, such as cough and dyspnea or chest pain and tachypnea (rapid breathing). Cluster analyses reveal that some patients present with nearly identical symptom profiles, complicating diagnosis 2.

Chronic and Post-PE Symptoms

After the acute phase, some patients develop post-pulmonary embolism syndrome (PPES), characterized by persistent chest pain, dyspnea, fatigue, and lightheadedness lasting more than three months. While most recover fully, a significant minority experience ongoing symptoms that can impact quality of life 4, 12. Chronic symptoms may also signal complications such as chronic thromboembolic pulmonary hypertension.

Less Frequent and Atypical Presentations

• Isolated signs of deep vein thrombosis (DVT) (e.g., leg swelling or pain) occur in a small minority (about 3%).
• Rarely, PE may be asymptomatic or present only with subtle signs, especially in elderly or critically ill patients 1, 6.
• Shock, arrhythmia, or sudden death may occur in severe cases, particularly with large or multiple emboli 5, 20.

Types of Pulmonary Embolism

Pulmonary embolism is not a one-size-fits-all diagnosis. There are several types, each with unique causes, clinical impacts, and treatment considerations. Understanding these distinctions is essential for accurate risk assessment and management.

Type	Main Feature	Common Cause(s)	Source(s)
Thrombotic PE	Blood clot in lung arteries	DVT, hypercoagulability	7, 10, 11
Nonthrombotic PE	Emboli other than blood clots	Fat, air, tumor, amniotic	7, 15
Acute PE	Sudden onset, severe symptoms	Large clot, sudden block	3, 8, 14
Chronic PE	Long-standing, persistent symptoms	Unresolved clots	12, 13
Massive PE	Hemodynamic instability/shock	Large/central embolus	9, 20
Submassive PE	RV dysfunction, stable BP	Segmental/lobar emboli	9, 18
Low-risk PE	Stable, no RV dysfunction	Smaller clots	8, 18

Table 2: Types of Pulmonary Embolism

Thrombotic vs. Nonthrombotic PE

• Thrombotic PE is by far the most common, resulting from blood clots (usually from deep veins of the legs or pelvis) that travel to and block the pulmonary arteries 7, 10, 11.
• Nonthrombotic PE involves emboli made of substances other than blood clots—such as fat (following fractures), air (from intravenous lines), amniotic fluid (during childbirth), tumor fragments, or foreign material. These are rare but can be catastrophic and are often harder to diagnose 7, 15.

Acute, Chronic, and Post-PE Syndrome

• Acute PE refers to a sudden, new blockage and typically causes abrupt symptoms such as severe dyspnea, chest pain, and sometimes cardiovascular collapse 3, 8, 14.
• Chronic PE develops when emboli are not fully resolved, leading to persistent symptoms and, in some cases, chronic thromboembolic pulmonary hypertension (CTEPH) 12, 13.
• Post-PE syndrome encompasses chronic symptoms and decreased functional capacity after a PE event, regardless of clot resolution 12.

Risk Stratification: Massive, Submassive, and Low-Risk PE

• Massive PE: Characterized by hemodynamic instability (e.g., shock, hypotension), right ventricular failure, and high mortality risk. Immediate, aggressive management is essential 9, 20.
• Submassive PE: Patients are hemodynamically stable but have evidence of right ventricular dysfunction or myocardial injury. These cases require careful monitoring and may benefit from advanced therapies 9, 18.
• Low-risk PE: Stable patients with no signs of right heart strain. These individuals often respond well to standard anticoagulation and may be treated as outpatients 8, 18.

Causes of Pulmonary Embolism

Understanding the causes of PE is crucial for prevention, early detection, and tailored management. While most cases are due to blood clots, a complex interplay of risk factors and underlying conditions pave the way for emboli to form and travel to the lungs.

Cause	Mechanism	Key Risk Factors	Source(s)
Deep vein thrombosis	Clot formation in leg veins	Surgery, immobility	10, 11, 13
Hypercoagulability	Increased clotting tendency	Cancer, genetics, OCP	10, 14, 13
Vascular injury	Endothelial damage	Trauma, surgery	10, 14
Nonthrombotic sources	Embolization of non-blood material	Fat, amniotic fluid	7, 15
Chronic conditions	Ongoing risk or recurrence	Heart failure, cancer	11, 14

Table 3: Main Causes and Risk Factors for Pulmonary Embolism

The Virchow’s Triad

The pathogenesis of PE is best explained by Virchow’s triad:

1. Venous stasis: Reduced blood flow (e.g., prolonged immobility, surgery, long travel).
2. Hypercoagulability: Increased tendency to clot, due to inherited (e.g., Factor V Leiden) or acquired (e.g., cancer, pregnancy, oral contraceptives) factors.
3. Endothelial injury: Damage to the blood vessel wall, often from trauma or surgical procedures 10, 14.

Deep Vein Thrombosis (DVT): The Most Common Source

• Most PEs originate from thrombi in the deep veins of the legs or pelvis. These clots can dislodge, travel through the bloodstream, and lodge in the pulmonary arteries 10, 13.
• Risk factors include:
  • Recent surgery or trauma
  • Prolonged bed rest or immobility
  • Active malignancy
  • Previous DVT/PE history
  • Pregnancy and postpartum period
  • Use of estrogen-containing medications

Nonthrombotic Emboli

• Fat embolism: Common after long bone fractures.
• Air embolism: Can occur during intravenous procedures or trauma.
• Amniotic fluid embolism: Rare, but potentially fatal complication of childbirth.
• Tumor embolism: Fragments of cancerous tissue entering the circulation.
• Foreign material: Rarely, substances like cement, silicone, or catheter fragments may embolize 7, 15.

Chronic and Recurrent PE

Patients with persistent risk factors—such as cancer, chronic heart failure, or certain genetic conditions—are at ongoing risk for recurrent PE, which underscores the importance of long-term management and surveillance 11, 14.

Treatment of Pulmonary Embolism

Treatment of PE is determined by the severity of the event, the patient’s overall risk profile, and the underlying cause. The mainstay of therapy is anticoagulation, but advanced interventions may be necessary in severe or life-threatening cases.

Treatment	Indication	Key Features	Source(s)
Anticoagulation	All confirmed PE (unless contraindicated)	Prevents new clots, aids dissolution	8, 11, 16
Thrombolysis	Massive or high-risk PE	Dissolves clot quickly, major bleed risk	9, 19, 20
Catheter-based therapies	Selected high/intermediate-risk PE	Local clot removal or lysis	17, 18, 20
Surgical embolectomy	Failed thrombolysis or contraindications	Surgical clot removal	18, 20
Supportive care	All cases	Oxygen, fluids, hemodynamic support	20, 8
Extended therapy	Persistent or unprovoked PE	Continued anticoagulation	8, 19

Table 4: Main Treatment Modalities for Pulmonary Embolism

Anticoagulation: The Foundation

• First-line therapy for almost all patients with PE is anticoagulation, which prevents further clot formation and allows the body to break down existing clots.
• Options include low molecular weight heparin, direct oral anticoagulants (DOACs), and vitamin K antagonists.
• Duration depends on the cause: typically 3 months for provoked PE, longer for unprovoked or persistent risk factors, and indefinite in cases of ongoing risk (e.g., active cancer) 8, 11, 19.

Thrombolytic Therapy

• Reserved for massive PE causing hemodynamic instability (shock, hypotension), as it rapidly dissolves clots but carries a significant bleeding risk.
• Systemic thrombolysis is not routinely used in stable or low-risk cases due to this risk 9, 19, 20.

Catheter-Directed and Surgical Interventions

• Catheter-directed thrombolysis or embolectomy offers targeted therapy for patients with contraindications to thrombolysis or those in whom systemic treatment fails. These techniques minimize bleeding risks compared to systemic thrombolysis 17, 18, 20.
• Surgical embolectomy is a last resort for patients who cannot receive thrombolytics or fail other interventions 18, 20.

Supportive and Adjunctive Therapies

• Supplemental oxygen for hypoxemia
• Fluids or vasopressors for hypotension
• Mechanical ventilation in severe cases
• Extracorporeal membrane oxygenation (ECMO) may be used in refractory shock or cardiac arrest due to PE 20.

Special Considerations

• Risk stratification is crucial; not all patients require aggressive therapy.
• Outpatient management is increasingly feasible for stable, low-risk patients, especially with the advent of DOACs 8, 19.
• Prevention: Prophylactic anticoagulation is indicated for high-risk hospitalized patients to reduce PE incidence 11.

Management of Chronic and Post-PE Syndrome

• Long-term follow-up for symptoms
• Screening and treatment for chronic thromboembolic pulmonary hypertension when indicated 12, 19.

Conclusion

Pulmonary embolism is a complex, multifaceted condition requiring vigilance, rapid diagnosis, and individualized management. Its variable symptoms, diverse causes, and evolving treatment landscape demand a nuanced, patient-centered approach.

Key points:

• PE often presents with sudden dyspnea, chest pain, cough, and sometimes syncope or hemoptysis.
• Major types include thrombotic (most common), nonthrombotic, acute, chronic, massive, submassive, and low-risk PE.
• Causes center on DVT, hypercoagulability, vascular injury, and less commonly, nonthrombotic sources like fat or air.
• Anticoagulation is the mainstay of treatment; advanced therapies (thrombolysis, catheter-based, or surgery) are reserved for severe or high-risk cases.
• Risk stratification, preventive measures, and long-term follow-up are vital for optimal outcomes.

By understanding the spectrum of pulmonary embolism—from its subtle symptoms to its most extreme presentations—patients and clinicians can work together toward timely diagnosis and lifesaving care.