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Pulmonary Embolism

Definition and pathophysiology
Pulmonary embolism is a potentially life threatening emergency which refers to the obstruction of the pulmonary arteries (one of the vessels that leads out of the heart into the lungs) or one of its branches by thrombi most commonly. Thrombi are platelet groupings that pathologically grow within the vasculature anywhere in the body and can eventually break off lodging into smaller vessels elsewhere. In the coronary vessels of the heart, thrombi can lead to occlusion and cause heart attacks, but in the vasculature of the lung, thrombi can lodge leading to pulmonary embolism. There are a number of causes for thrombus formation, but the basic idea revolves around Virchow’s triad of vessel lining injury, blood not moving, or conditions where the blood clots inside of a vessel too easily.

You may have heard in the past that if you’re on a long transcontinental flight you should get up and walk around, stretching your legs. The reason is to help prevent the formation of these thrombi, by sitting in one place for too long you’re keeping your blood in stasis, fulfilling one part of Virchow’s triad, giving the system the opportunity to form intra-vessel clots.

Thrombi love forming in the deep vessels of the lower extremities, if for whatever reason they break off and lodge into the small vessels of the lung, the clot will impede flow of blood to the lungs, preventing oxygenation of the blood and thus oxygen delivery to the rest of the vital organs. It’s important to keep in mind that not all pulmonary embolisms are deadly. Some small ones can pass and be completely gobbled up by our immune system. The large ones however, can potentially cut off circulation and result in hemodynamic instability very, very quickly and so, prevention is key.

Risk factors
-Recent surgical procedure, especially orthopedic surgery
-Cancer (hypercoagulable)
-Acquired Thrombophilia (Lupus Anticoagulant, Nephrotic Syndrome, Oral Contraceptive usage)
-Inherited Thrombophilia (ie Factor V Leiden Mutation)
-Pregnancy

Symptoms/signs
-Sudden onset of difficulty breathing
-Unilateral thigh or calf swelling
-Chest pain during inhalation
-Coughing up of blood
-Increased Respiratory Rate
-Increased Heart Rate
-Lungs are clear to auscultation
-Hypotensive
-Increased Jugular Venous Distention

Cardiac manifestations/Consequences

When a clot lodges in the pulmonary arterial circuit, pulmonary vascular resistance increases which can lead to right ventricular (RV) dysfunction. Increase in right pulmonary artery pressure brings about increased right ventricular wall tension, which ultimately leads to impaired right ventricular dilatation, ischemia, and impairment. It can also lead to left ventricular (LV) filling impairment and thus reduced cardiac output and systemic hypoperfusion.
Its important to clinically evaluate such patients in order to attain early diagnosis. The most common complaint is dyspnea (82%) and the most common physical exam finding is tachypnea (62%) (Goldhaber, Visani and De Rosa, 1999). Other indicators of RV dysfunction on exam include right sided S3, accentuated P2, systemic arterial hypotension, tricuspid regurgitation murmur, elevated JVP and parasternal lift.
An electrocardiogram may also be useful in determining the severity of the PE. An anterior ischemic pattern of negative T waves in leads V1-V4 is a common finding in a massive PE, and has been shown to correlate with the severity of the PE. Other patterns include S1Q3T3, a new or incomplete right bundle branch block, a pulmonary P wave (Stein, Dalen, McIntyre 1975). Moreover, an EKG scoring system has been shown to correlate with severity of pulmonary hypertension and defect on V/Q scanning due to PE.
While echocardiogram are not shown to be useful in assessing the severity of acute
PE, it is useful in identifying severe RV dysfunction, including RV/LV end diastolic diameter >1 in the apical 4 chamber view, RV end diastolic diameter >30mm and the paradoxical RV septal motion. Another common echocardiogram finding with RV dysfunction associated with PE is the McConnel sign, which is where this is akinesia of the RV free wall but normal motion at the apex.
Troponin levels have been shown to be elevated in 30 to 40% of patients with PE, which may be due to the development of microinfarctions from abrupt increase in PA pressure and the elevation of a RB wall tension (Sohne, ten Wolde, Buller 2004). Troponins have been shown to be a risk factor for poor outcomes in acute PE and elevation of troponin T are correlated to serious complications including hypotension/shock, CPR and intubation.
RV dysfunction due to PE predicts increased PE related mortality if normatensive and hypotensive subjects are grouped together (Nijkeuter et al.). However, the ability of RV dysfunction to predict PE in purely normatensive patients is still inconclusive (Sanchez et al.).

Diagnosis
General Tests Performed for Diagnosis
-Arterial Blood Gas
-Chest X-Ray
-Electrocardiogram

Specific Tests Performed for Diagnosis:
-Spiral CT Scan
-Ventilation Perfusion Scan
-Pulmonary Angiogram
-Duplex Ultrasound
-D-Dimer (only diagnostic in low risk patients)

Treatment

Resuscitation (stabilize)
-Respiratory
Give oxygen
Consider intubation and mechanical ventilation if there is severe hypoxemia (low oxygen in the blood)
-Hemodynamics (get hypotension under control)
Give intravenous (IV) fluid, usually normal saline (no more than 500-1000 mL in one period)
If no improvement, give medication (norepinephrine, dopamine, epinephrine, dobutamine with norepinephrine)
-Anticoagulation
Heparin, if appropriate

After resuscitation (treatment after stabilized)
-Anticoagulation (if not already started)
-Inferior vena cava filter (mesh that allows blood to pass through but stops clots from traveling into the heart and lungs)
Used in people who have failed anticoagulant therapy or developed complications from it
Also used for those who have a high bleeding risk
-Thrombolytic therapy for severe cases
-Embolectomy (removal of emboli surgically or using catheters)
Appropriate in severe cases who have failed thrombolytics or cannot use thrombolytics

References:

Daniel KR, Courtney DM, Kline JA. Assessment of Cardiac Stress From Massive Pulmonary Embolism With 12-Lead ECG. Chest 2001;120;474 – 481.

Iles S, Le Heron CJ, Davies G, et al. ECG Score Predicts Those With the Greatest Percentage of Perfusion Defects Due to Acute Pulmonary Thromboembolic Disease. Chest 2004; 125;1651 – 1656.

Lualdi J, Goldhaber S. Right Ventricular Dysfunction After Acute Pulmonary Embolism: Pathophysiologic Factors, Detection, and Therapeutic Implications. American Heart Journal 1995;130;1276-1282

Nijkeuter M, Söhne M, Tick LW, et al. The natural course of hemodynamically stable pulmonary embolism: Clinical outcome and risk factors in a large prospective cohort study. Chest 2007; 131:517.

Ouellette, D. (2014, September 2). Pulmonary Embolism . Retrieved October 27, 2014, from http://emedicine.medscape.com/article/300901-overview

Sanchez O, Trinquart L, Colombet I, et al. Prognostic value of right ventricular dysfunction in patients with haemodynamically stable pulmonary embolism: a systematic review. Eur Heart J 2008; 29:1569.

Sohne M, ten Wolde M, Buller H. Biomarkers in Pulmonary Embolism. Current Opinion in Cardiology 2004;19;558-562.

Stein PD, Dalen JE, McIntyre KM, et al. The Electrocardiogram in Acute Pulmonary Embolism. Prog Cardiovasc Dis 1975;17;247-257.

Tapson, V.F. (2014, March 25). Treatment of acute pulmonary embolism. UpToDate. Retrieved from http://www.uptodate.com/contents/treatment-of-acute-pulmonary-embolism

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