From the Research
Yes, pulmonary embolism (PE) can cause supraventricular tachycardia (SVT). When a blood clot lodges in the pulmonary arteries, it creates increased pressure in the right side of the heart, which can trigger abnormal electrical activity in the atria. This hemodynamic stress often leads to rapid heart rhythms, including SVT, as the heart attempts to compensate for decreased cardiac output and oxygen delivery. SVT in PE patients typically presents as sinus tachycardia, but other forms like atrial fibrillation or atrial flutter may occur.
Pathophysiology of PE-induced SVT
The pathophysiology of PE-induced SVT is complex and involves multiple factors, including:
- Increased pressure in the right side of the heart
- Abnormal electrical activity in the atria
- Decreased cardiac output and oxygen delivery
- Hemodynamic stress and compensatory mechanisms
According to a study published in the Journal of the American Medical Association (JAMA) in 2022 1, PE is characterized by occlusion of blood flow in a pulmonary artery, typically due to a thrombus that travels from a vein in a lower limb. The incidence of PE is approximately 60 to 120 per 100 000 people per year, and approximately 60 000 to 100 000 patients die from PE each year in the US.
Clinical Presentation and Diagnosis
If a patient presents with unexplained SVT, especially with risk factors like immobility, recent surgery, or symptoms like shortness of breath and chest pain, PE should be considered in the differential diagnosis. Prompt diagnosis and treatment of the underlying PE with anticoagulation therapy is essential to resolve the arrhythmia and prevent further complications. A study published in the Internal Medicine Journal in 2019 2 highlights the importance of clinical prediction scores, such as the Wells score, in clinical decision-making and decreasing unnecessary radiological investigations.
Treatment and Management
The treatment and management of PE-induced SVT involve anticoagulation therapy, which is the foundation of PE management. Haemodynamically unstable patients require thrombolysis unless absolutely contraindicated, while stable patients with right ventricular dysfunction or ischaemia should be aggressively anti-coagulated. A study published in the Methodist DeBakey Cardiovascular Journal in 2024 3 reviews the primary and longer-term considerations for anticoagulation management in patients with PE and highlights special patient populations and risk factor considerations. Direct oral anticoagulants, such as apixaban, edoxaban, rivaroxaban, or dabigatran, are noninferior for treating PE and have a lower rate of bleeding compared to heparin combined with a vitamin K antagonist 1.