pulmonary disorders
Pulmonary Embolism (PE)
Pathophysiology of Pulmonary Embolism
Once deep venous thrombosis develops, clots may dislodge and travel through the venous system and the right side of the heart to lodge in the pulmonary arteries, where they partially or completely occlude one or more vessels. The consequences depend on the size and number of emboli, the underlying condition of the lungs, how well the right ventricle (RV) is functioning, and the ability of the body’s intrinsic thrombolytic system to dissolve the clots. Death, when is does occur, is often due to right ventricular failure. Small emboli may have no acute physiologic effects and may begin to lyse immediately and resolve within hours or days. Larger emboli can cause a reflex increase in ventilation (tachypnea), hypoxemia due to ventilation/perfusion (V/Q) mismatch, low mixed venous oxygen content as a result of low cardiac output, Atelectasis due to alveolar hypocapnia and abnormalities in surfactant, and an increase in pulmonary vascular resistance caused by mechanical obstruction and vasoconstriction resulting in tachycardia and hypotension. Endogenous lysis reduces most emboli, even those of moderate size, and physiologic alterations decrease over hours or days. Some emboli resist lysis and may organize and persist and sometimes cause chronic thromboembolic pulmonary hypertension (CTEPH). Pulmonary emboli may be classified according to the physiologic effects as described by the European Society of Cardiology/American Heart Association ( Pathophysiology reference ) into the following: High risk (massive): Impaired right ventricular function causing hypotension, as defined by systolic blood pressure < 90 mm Hg or a drop in systolic blood pressure of ≥ 40 mm Hg from baseline for a period of 15 minutes Intermediate risk (submassive): Impaired right ventricular function without hypotension. This is evidenced by right ventricular enlargement and/or hypokinesis on imaging (eg, CT angiography, echocardiography) as well as by increases in circulating biomarkers (eg, troponin, brain natriuretic peptide). Note that the European Society of Cardiology defines intermediate-risk pulmonary embolism also as patients with a simplified pulmonary embolism severity index (sPESI) of > 0, thus including patients with other disorders or findings ( Pathophysiology reference ). Intermediate-risk pulmonary embolism can be further divided into intermediate high risk (the presence of right ventricular dysfunction by imaging Low risk: Absence of right ventricular impairment and absence of hypotension (and by European Society of Cardiology, sPESI score = 0) Saddle pulmonary embolismdescribes a pulmonary embolus that lodges in the bifurcation of the main pulmonary artery and into the right and left pulmonary arteries; saddle emboli are usually, but not always, intermediate risk or high risk. A saddle configuration does not dictate a specific therapeutic approach. Although saddle emboli are often large, causing near-complete or complete obstruction, they may also be a relatively thin, nonobstructive embolus. In 1 to 3% of cases, chronic residual obstruction leads to Pulmonary Hypertension (chronic thromboembolic pulmonary hypertension) that evolves over months to years and can result in chronic right heart failure. When a large embolus acutely occludes major pulmonary arteries or when many smaller emboli combine to occlude a significant proportion of the more distal vessels, RV pressure increases, which may lead to RV failure , shock, or sudden death. The risk of death depends on the degree and rate of rise of right-sided pressures and on the patient’s underlying cardiopulmonary status. Patients with preexisting cardiopulmonary disease are at higher risk of death, but young and/or otherwise healthy patients may survive a PE that occludes > 50% of the pulmonary bed. Pulmonary infarction (interruption of pulmonary artery blood flow leading to ischemia of lung tissue, sometimes represented by a pleural-based [peripherally located], often wedge-shaped pattern on chest x-ray [Hampton hump] or other imaging modalities) occurs in<10% of patients diagnosed with PE. This low rate has been attributed to the dual blood supply to the lung (ie, bronchial and pulmonary). Generally, pulmonary infarction is due to smaller emboli that become lodged in more distal pulmonary arteries and is nearly always completely reversible; pulmonary infarction is recognized early, often before necrosis occurs. 1.Konstantinides SV, Meyer G, Becattini C, et al: 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS).Eur Heart J2020;41(4):543-603. doi:10.1093/eurheartj/ehz405 