The problem of acute pulmonary embolism (PE) of the lungs is quite common and comes along with many different symptoms, which can make it difficult to diagnose. A thrombus that is formed at another place, breaks loose, and travels to the pulmonary artery or its branches is the cause of pulmonary embolism, which blocks the flow of blood further. Most of the time, this is due to DVT, where the clot is made in the deep veins, which are usually in the lower legs, as a complication.  

This clot can become released and float to the lungs, which can result in PE. The other causes of PE are like presence of air, far or tumor cells in the lungs and pulmonary blood circulation. The diseases can occur in emergency departments, intensive care units, and hospitals. Specialized PERTs (Pulmonary Embolism Response Teams) can help to treat the disease. The combination of PE (Pulmonary Embolism) and DVT (Deep Vein Thrombosis) is called VTE (Venous Thromboembolism). 

The incidences of PE vary from 39 to 115 per 100,000 person-years, and that for DVT, from 53 to 162 per 100,000 person-years. After coronary artery disease (CAD) and stroke, acute PE is the third most common cardiovascular disease. Generally, the incidences of PE are higher in men than women. 

PE has a high mortality rate. It is responsible for as many as 100,000 deaths annually in the United States. It is difficult to estimate the mortality rates for PE because sudden cardiac death is believed quite often to be caused by thromboembolic disorders like PE. However, case-fatality rates for PE have probably decreased in recent years due to improved diagnostic methods and early treatment. 

PE is a condition characterized by the breaking off of these clots and entering the circulation in the pulmonary region. It more often occurs in the lower lobes and includes bilateral lung involvement. Large emboli block the main pulmonary artery, resulting in saddle embolus, while the smaller ones block peripheral arteries, resulting in pulmonary infarction.  

Blockage in pulmonary vascular pathways may lead to inhibition of gas exchange in patients who have PE. This can lead to imbalance in ventilation to perfusion ratio. It may cause dead space ventilation and hypoxemia. It stimulates the release of serotonin. Inflammatory mediators can cause vasospasm in unaffected areas of the lungs and decrease the pulmonary flow.  

Pulmonary vascular resistance increases due to mechanical obstruction of the vascular bed with hypoxic vasoconstriction and thrombus. Increased PVR results in an increased afterload to right ventricle which is leading to right ventricular dilatation and flattening of the interventricular septum, hence decreasing left ventricular filling and, therefore, cardiac output. 

Severe PE represents the result of RV failure from acute pressure overload. Clinical symptoms and signs in patients with a high risk of early mortality are reflected by RV failure and hemodynamic instability. 

The vast majority of pulmonary emboli are derived from lower-extremity deep vein thromboses. Thus, risk factors for PE are similar to those for DVT. Virchow’s triad, comprising endothelial injury, venous stasis, and hypercoagulability, is a useful construct in the conceptualization of risk factors. 

Risk factors for PE can be divided into genetic and acquired causes. Among the genetic risk factors are thrombophilia, including hyperhomocysteinemia, deficiency of proteins C and S, factor V Leiden mutation, and prothrombin gene mutation. The acquired risk factors include conditions such as prolonged immobilization, for instance, bed rest longer than 3 days and long journeys of more than 4 hours by bus, air, train, or car and recent malignancy, orthopedic surgery, obesity, cigarette smoking, pregnancy, use of oral contraceptives and the presence of an indwelling venous catheter. 

Other factors that might influence VTE are: 

Major trauma 

Replacement of knee or hip 

Chemotherapy 

Oral contraceptive therapy 

Lower limb fracture 

HRT (hormone replacement therapy) 

Postpartum period 

Obesity 

Bed rest more than 3 days 

Central venous lines 

Thrombophilia 

Cancer 

Infections, specifically HIV, UTI, and pneumonia 

Prior venous thromboembolism 

Hospitalization for atrial fibrillation or heart failure 

Cancer increases the risk of formation of thrombus and PE. Brain cancer, lung cancer, pancreatic cancer, gastric cancer, and hematological malignancy are associated with the high risk of venous thromboembolism. Different infections can lead to formation of VTE. Myocardial infarction and CHF can also elevate the risk of PE.  

Hemodynamically unbalanced PE is known as high-risk or massive PE. It is hypotension which needs inotropes or vasopressors. It is a more severe form of PE. It causes RVF failure of the right ventricle, which can be life-threatening.  

Hemodynamically balanced PE has a range which can go from small embolisms, mild asymptomatic or symptomatic to mild hypotension. This can improve with treatment of fluids or those who have right ventricular dysfunction without severe hemodynamic instability. Both types must be diagnosed properly to assess the severity of disease.  

Pulmonary Embolism Severity Index (PESI) and sPESI are the prognosis tools of PE. PESI predicts the 30 days mortality risk for patients who are diagnosed with PE. Both PESI and sPESI detect low-risk patients for 30 days of mortality groups.  

PESI is divided into 5 risk classes as per the score: 

Class I: ≤ 65 points, 1 to 6% of the mortality risk in 30 days 

Class II: 66 to 85 points, 3.2 to 7.1 % risk 

Class III: 86 to 105 points, 10 to 24.5 % of risk 

Class IV: 106 to 125 points, 10 to 24.5 % of risk 

Class V: > 125 points, 10 to 24.5 % of risk 

Early diagnosis of PE is important because it has a high rate of morbidity and mortality. Acute PE with no specific signs and symptoms like dyspnea, pleuritic chest pain, cough, hemoptysis, presyncope, or syncope. Patients may also have arrhythmias, syncope, or hemodynamic collapse. Some patients who have large PE may have no symptoms or mild symptoms. The risk of PE must be assessed to determine the risk factor of patient for VTE. 

Tachycardia and tachypnea are other nonspecific signs that are physical examination findings in patients with possible PE. PE represents 8% of cases of cardiac arrest of unknown causes, probably due to acute RVF (failure of right ventricle). In patients with PE, sudden onset of bradycardia or new broad complex tachycardia should immediately raise the concern for strain on right ventricle and impending shock in the clinician’s mind. This entity should also be entertained in the differential diagnosis of any hypotensive patient with distension of jugular vein, after acute MI (myocardial infarction), tension pneumothorax, or pericardial tamponade has been excluded.

General assessment: 

Patients may have distress or anxiety because of difficulty in breathing or chest pain. They also have signs of hypoxia or shock-like cyanosis or pallor.  

Vital signs: 

Tachypnea is a condition in which respiratory rate is increased. It is common in severe acute myocardial infarction. Tachycardia may also be present. Hypotension, especially in massive PE cases, indicates significant hemodynamic compromise. 

Inspection: 

Elevated jugular veins may indicate strain in the right heart or failure, especially when combined with hypotension, while a bluish discoloration of the lips, face, or extremities may indicate severe hypoxemia. 

Palpation: 

Tenderness on palpation may indicate PE, but it is not specific, and more relevant findings may include signs of right ventricular strain or heart failure. 

Auscultation: 

The classic electrocardiographic pattern of acute PE is the S1Q3T3 pattern, which includes prominent S waves in lead I, Q waves in lead III, and an inverted T wave in lead III.  

Auscultation shows a loud P2 which indicates an increased pulmonary artery pressure. New murmurs specifically those of tricuspid regurgitation indicates the overload at right ventricular. Crackles can be present in the lung sounds from pulmonary infarction or edema. 

• Cardiogenic shock  
• Pulmonary hypertension because of chronic thromboembolism 
• Failure of right heart 
• Recurrent thromboembolism 

Clots are managed by stopping their growth and preventing further development. Pulmonologists or Cardiologists can treat severe complications with the use of thrombolytics, anticoagulants, vena cava filters, and catheterization. Anticoagulants like warfarin, heparin, or NOACs stop the formation of new clots. Clot-dissolving medications can be administrated in life-threatening cases. Catheterization procedure is used to remove the clots in arteries of lungs in emergency cases. Patients who cannot take blood thinner medications have to place a filter in the major vein.  

Pulmonary Medicine

Anticoagulants are used to treat acute PE. Unfractionated heparin or LMWH (low molecular weight heparin) is frequently used, for it has a lower risk of major heparin-induced thrombocytopenia and bleeding compared to other agents. UFH is specifically indicated in patients with hemodynamic imbalances or with kidney impairment. The novel vitamin K antagonists and oral anticoagulants can also be used. 

Treatment regimens for suspected PE vary depending on the type of PE and clinician’s judgment of degree of suspicion, as quantified by the revised Wells or Geneva score categorized patients as high, intermediate, or low suspicion. In highly suspicious patients, anticoagulation is initiated before imaging. In patients with low clinical suspicion, imaging can be delayed up to 24 hours with initiation of anticoagulation after the imaging. 

In patients who might have high suspicion for a pulmonary embolism, diagnostic tests such as computed tomography pulmonary angiography, bedside transthoracic echocardiography, or portable perfusion scanning should be done immediately. Thrombolysis is generally the primary mode of reperfusion in high-risk PE patients. Following improvement, patients with high-risk PE may be transitioned to use oral anticoagulation from parenteral anticoagulants. 

Pulmonary Medicine

Thrombolysis is used to treat PE. It reduces the resistance in pulmonary artery and pressure as compared to UFH alone. It is generally preferred when treatment could be started within 48 hours of onset of symptoms. Use of thrombolytics significantly decreases the mortality rate and recurrence of PE. 

Absolute contraindications are previous hemorrhage, ischemic stroke, active bleeding, known malignant neoplasm, recent surgery, cerebrovascular disease, and suspected aortic dissection, significant trauma. 

Pulmonary Medicine

Surgical embolectomy: 

Surgical embolectomy should be done in patients with hemodynamically unstable PE in whom thrombolysis, either systemic or catheter-directed, is either contraindicated or has been shown to be ineffective. There are trials showing no evidence of a difference in mortality between thrombolysis and surgical embolectomy, but an excess risk of stroke and the need for reintervention have been linked with the thrombolysis group. 

Catheterization: 

This is a technique where the catheter is introduced into the pulmonary arteries is done to perform any of the following methods of suction embolectomy, ultrasound-assisted thrombolysis, thrombus aspiration, rotational embolectomy, or a combination of mechanical fragmentation with thrombolysis that is catheter-directed.  

This procedure has a success rate of 87%. The catheter-aided embolectomy has inherent risks, and pulmonary artery perforation can lead to severe complications like massive hemoptysis or cardiac tamponade. 

Vena cava filters: 

Filters are designed to obstruct the path of emboli from going through to the pulmonary circulation. They are used in patients suffering from VTE and who cannot use anticoagulants or in those who develop recurrent VTE regardless of being on anticoagulant therapy. Currently, retrievable filters are preferred because they can be easily removed once the contraindication to anticoagulation resolves and anticoagulant therapy continues. 

Pulmonary Medicine

Acute PE is a life-threatening disease. It requires a management plan. It starts with initial assessment and stabilization which can include clinical evaluation and monitoring the vital signs of a patient. Diagnostic tests like laboratory tests, imaging, ultrasound, and clinical evaluation can diagnose the disease. The treatment includes anticoagulation treatment, thrombolysis, and surgical or catheter-based procedures. 

Patient education, like awareness about the disease, treatment plan, and possible complications and support, is important. Patients must be assessed on a regular basis and treatment is adjusted as per the need.