Pulmonary EmbolismPulmonary Embolism
Yuan Zhiming Department of Emergency Medicine
The General Hospital
Tianjin Medical University
Contents
● General Considerations
● Etiology
● Pathophysiology
● Symptoms
● Diagnosis
● Treatment
● Prevention
Key TermsKey Terms
General considerations
Prevalence & Incidence
● Emboli
● Thrombosis
● Deep vein thrombosis
● Pulmonary embolism
Key TermsKey Terms
•Emboli
Clots or other substances that travel through the blood stream and get stuck in a blood vessel, blocking circulation.
• Thrombosis
The development of a blood clot inside a blood vessel.
•Deep vein thrombosis
The development of a blood clot in the calf's deep vein. This frequently leads to pulmonary embolism if untreated.
•Pulmonary embolism
The occlusion of one or more vessels in the pulmonary arterial tree by matter from a source extrinsic to the lung. The process is almost invariably acuate but may on occasion be chronic.
How dose pulmonary embolism occur ?
Prevalence & Incidence
● The term 'prevalence' of pulmonary embolism usually refers to the estimated population of people who are managing pulmonary embolism at any given time.
● The term 'incidence’ of pulmonary embolism refers to the annual diagnosis rate, or the number of new cases of pulmonary embolism diagnosed each year.
Incidence (annual): approximately 650,000 cases in the USA
Incidence Rate: approx 1 in 418 or 0.24% in USA
EtiologyEtiology
Pulmonary embolism is caused by emboli that travel through the blood stream to the lungs and block a pulmonary artery. When this occurs, circulation and oxygenation of blood is compromised. The emboli are usually formed from blood clots but are occasionally comprised of air, fat, amniotic fluid, tumor tissue, or particulate matter from intravenous injection, etc.
Common risk factors for pulmonary embolism:
oral contraceptives;the early postpartum period; surgery; DVT; hypercoagulable states; right heart failure;fractures of the pelvic and lower extremities
etc.
congestive heart failure;leukemia; polycythemia; sickle cell anemia; dysproteinemias; massive obesity; immobility; cancer; pregnancy;
any cause of venous stasis
such as: ① venous valvular insufficiency
② right-side HF
③ the postoperative period
④ prolonged bed rest
Risk factors for pulmonary thromboembolism include:
Pathophysiology
Increased pulmonary vascular resistance due to vascular obstruction, neurohumoral agents, or pulmonary artery baroreceptors.
Alveolar hyperventilation due to reflex stimulation of irritant receptors.
Pulmonary embolism can have the following pathophysiological effects:
Decreased pulmonary compliance due to lung edema, lung hemorrhage,and loss of surfactant.
Impaired gas exchange due to increased alveolar dead space from vascular obstruction and hypoxemia, V/Q mismatch.
Increased airway resistance due to broncho- constriction.
Pulmonary embolismAnatomicalobstruction
Neurohumoraleffects
PA pressure RV afterload
RV wall tension
RV O2 demand
RV dilation/dysfunction RV ischemia
RV output
LV preload
LV output
Interventricularseptal shift to LV
Systemic perfusion
hypotension
Coronary perfusion
RV O2 supply
SymptomsSymptoms
Each individual may experience symptoms differently, which depend on the size and number of emboli.
● chest pain
● labored breathing, dyspnea, cyanosis
● cough
● syncope
● anxiety
● a rapid pulse.
● a low fever
● hypotension, shock
● fluid build-up in the lungs
DiagnosisDiagnosis
The diagnosis of pulmonary embolism should be based on the patient's history, physical exam, and diagnostic tests.
● Symptoms & Signs
● Plasma D-dimer levels
● ECG
● Arterial Blood Gas
● Chest Radiograph
● Ventilation/Perfusion Lung Scanning
● Pulmonary Angiography
Plasma D-dimer levelsPlasma D-dimer levels
● Low specificity (40-43%) High sensitivity (92-100%)
● Plasma D-dimer levels <500ug/L by ELISA may exclude PE
● S1-Q3-T3
● RBBB (right bundle branch block)
● right axis deviation
● ischemia
● prominent P waves
● tachycardia
● atrial arrhythmia
●Ⅰ0 AVB(atrioventricular block)
ECGECG
S1-Q3-T3
Arterial Blood GasArterial Blood Gas
● hypoxemia ( Po2 )
●respiratory alkalosis ( Pco2 )
● increased A-a(Alveoli-artery) gradient
● can be normal
● pulmonary infiltrate
● pleural effusion
● elevated hemidiaphragm
● atelectasis
● Hampton’s hump ( a pleural-based, wedge-shaped infiltrate )
Chest RadiographChest Radiograph
Posteroanterior chest film of patient with pulmonaryembolism showing "Hampton's hump" in right lower lung field, a homogeneous, wedge-shaped density in the peripheral field, convex to the hilum.
Ventilation Lung Scanning is normal, and perfusion Lung Scanning can show poor flow of blood in areas beyond blocked arteries.
Ventilation/Perfusion Lung ScanningVentilation/Perfusion Lung Scanning
Normal ventilation, perfusion Lung Scanning show poor flow of blood.
The most reliable test for diagnosing pulmonary embolism (“gold standard”)
Pulmonary AngiographyPulmonary Angiography
Right pulmonary arteriogram showedmultiple filling defects clustered mainly around the hilum (arrow)
Pulmonary angiogram with digital subtraction demonstrates a large, acuteembolus in the right lower lobar pulmonary artery (arrowhead).
TreatmentTreatment
Bed rest Haemodynamic and respiratory support Anticoagulation Therapy Thrombolytic Therapy IVC Filter Surgical Therapy
Haemodynamic and respiratory supportHaemodynamic and respiratory support
● Fluid loading
● Dobutamine and dopamine
● Vasopressive drugs
● Oxygen therapy
Anticoagulation TherapyAnticoagulation Therapy
● Patients with PE should be treated with intravenous heparin, with an adjusted activated partial thromboplastin time (aPTT) between 1.5 to 2.5 control
● Low-molecular-weight heparin may be used in patients with symptomatic non-massive PE.
●Oral anticoagulant treatment should he initiated during the first 3 days with an overlap with heparin treatments for at least 4 to 5 days. Heparins could be discontinued when the international normalized ratio ( INR ) has been therapeutic (range 2.0 to 3.0) for 2 consecutive days.
● Patients with a first episode of PE should be treated for at least 3 months if they have a reversible risk factor and for at least 6 months if they have idiopathic venous thromboembolism.
● Oral anticoagulants should be continued for a longer period, possibly indefinitely, in patients with recurrent venous thromboembolism, or continuing risk factors such as cancer.
Thrombolytic TherapyThrombolytic Therapy
● Thrombolytic regimens for PE: Recombinant tissue plasminogen activator (rtPA), Streptokinase, Urokinase
● Thrombolytic therapy is indicated in patients with massive pulmonary embolism, as shown by shock and/or hypotension
● Thrombolytic therapy in patients with sub-massive pulmonary embolism(right ventricular hypokinesia) is controversial
●Contraindications: (1) active internal bleeding; (2) recent acute cerebrovascular event(2-3mo); (3) recent cerebrovascular procedure (2-3 mo)
Left, A large embolus in the right pulmonary artery (arrow). Right, After a 2-hour infusion of rt-PA through a peripheral vein, there is pronounced resolution, with only a small amount of residual thrombus in segmental branches.
Venous filtersVenous filters
● Inferior vena cava (IVC) filters are indicated to prevent pulmonary embolism in patients with either absolute anticoagulation contraindications or patients who suffer from recurrent venous thromboembolism despite adequate anticoagulant treatment.
● Inferior vena cava filters are probably indicated after surgical embolectomy
Inferior vena caval filters. Most filters are placed percutaneouslv via the right femoral vein. Bird's Nest Filter
Surgical embolectomy
It might be considered in circumstances including (1) severe hemodynamic instability (2) almost certain clinical diagnosis of massive pul
monary embolus (3) contraindication to thrombolytic therapy (4) close proximity to the operating room with byp
ass capability
PrognosisPrognosis
About 10% of patients with pulmonary embolism die suddenly within the first hour of onset of the condition. The outcome for all other patients is generally good; only 3% of patients who are properly diagnosed and treated die. In cases of undiagnosed pulmonary embolism, about 30% of patients die.
PreventionPrevention
Pulmonary embolism risk can be reduced in certain patients through judicious use of antithrombotic drugs such as heparin, venous interruption, gradient elastic stockings and/or intermittent pneumatic compression of the legs.
Emphases
Definition of pulmonary embolism
Clinical presentation & diagnosis of PE
The treatment of PE