Pulmonary Embolism (cont.)
Benjamin Wedro, MD, FACEP, FAAEM
Dr. Ben Wedro practices emergency medicine at Gundersen Clinic, a regional trauma center in La Crosse, Wisconsin. His background includes undergraduate and medical studies at the University of Alberta, a Family Practice internship at Queen's University in Kingston, Ontario and residency training in Emergency Medicine at the University of Oklahoma Health Sciences Center.
George Schiffman, MD, FCCP
Dr. Schiffman received his B.S. degree with High Honors in biology from Hobart College in 1976. He then moved to Chicago where he studied biochemistry at the University of Illinois, Chicago Circle. He attended Rush Medical College where he received his M.D. degree in 1982 and was elected to the Alpha Omega Alpha Medical Honor Society. He completed his Internal Medicine internship and residency at the University of California, Irvine.
Melissa Conrad Stöppler, MD
Melissa Conrad Stöppler, MD, is a U.S. board-certified Anatomic Pathologist with subspecialty training in the fields of Experimental and Molecular Pathology. Dr. Stöppler's educational background includes a BA with Highest Distinction from the University of Virginia and an MD from the University of North Carolina. She completed residency training in Anatomic Pathology at Georgetown University followed by subspecialty fellowship training in molecular diagnostics and experimental pathology.
In this Article
- Pulmonary embolism facts
- What is a pulmonary embolism?
- What are the causes and risk factors for pulmonary embolism?
- What are the signs and symptoms of pulmonary embolism?
- How is pulmonary embolism diagnosed?
- Basic testing (CBC, electrolytes, BUN, creatinine blood test, chest X-ray, EKG)
- Pulmonary angiogram
- d-Dimer blood test
- CT Scan
- Ventilation-perfusion scans
- Venous Doppler study
- Echocardiography (EKG, ECG)
- What is the treatment for pulmonary embolism?
- Thrombolytic therapy
- What is the prognosis for pulmonary embolism?
- Can pulmonary embolism be prevented?
What are the causes and risk factors for pulmonary embolism?
Pulmonary embolus is the end result of a deep vein thrombosis or blood clot elsewhere in the body. Most commonly, the DVT begins in the leg, but they also can occur in veins within the abdominal cavity or in the arms.
The risk factors for a pulmonary embolism are the same as the risk factors for deep vein thrombosis. These are referred to as Virchow's triad and include:
- prolonged immobilization or alterations in normal blood flow (stasis)
- increased clotting potential of the blood (hypercoagulability)
- damage to the walls of the veins.
Examples of these include the following:
- Extended travel (sitting in a car, airplane, train, etc.)
- Hospitalization or prolonged bed rest
Increased blood clotting potential
- Medications: birth control pills, estrogen
- Genetic predisposition most commonly, Factor V Leiden deficiency, MHFTHR mutation, Protein C or Protein S deficiencies or anitithrobin III deficiency
- Polycythemia (increased number of red blood cells, the opposite of anemia)
- Pregnancy, including 6-8 weeks after delivery
Damage to vessel wall
- Prior deep venous thrombosis
- Trauma to the lower leg with or without surgery or casting
What are the signs and symptoms of pulmonary embolism?
A pulmonary embolus may present with the sudden onset of chest pain and shortness of breath. The pain is classically sharp and worsens when taking a deep breath, often called pleuritic pain or pleurisy. There may be cough that produces bloody sputum.
The patient may have stable vital signs (blood pressure, heart rate, respiratory rate, and oxygen saturation) but frequently presents with an elevated heart rate. If the blood clot is large enough, it can block blood from leaving the right side of the heart thus preventing blood from entering the lungs. There is then no blood entering the left side of the heart to pump to the rest of the body. This can result in circulatory collapse (shock) and death.
Often referred to as saddle embolus (named such as it sits in the division between the left and right pulmonary artery like a saddle). Depending on the amount of blood clot (clot burden or clot load), oxygen saturation can be variably affected as can the blood pressure and heart rate. Classic signs are such that the heart rate and respiratory rate are elevated as the body tries to compensate for less oxygen transfer capabilities in the lung. Increases in breathing and heart rate circulate the blood around the body more quickly, so that whatever oxygen is available is distributed best as possible.
Oxygen saturation may be decreased (red blood cells that do not have oxygen molecules attached to them). Oxygen saturation in a healthy individual approaches 100% at sea level.
The patient may be cyanotic (a blue tinged discoloration of the skin caused by red blood cells without oxygen), lightheaded, and weak.
In some cases, pulmonary embolus will present with sudden death, where the patient collapses, stops breathing, and their heart stops beating (cardiac arrest).
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