Copia - Pulmonary hypertension completo

Gonzalez MD

START

HY:Pulmonary hypertension

Identify common signs and symptoms of vascular lung diseases. Explain the pathophysiological mechanisms underlying vascular lung diseases, including pulmonary hypertension and pulmonary embolism. Discuss diagnostic approaches, including imaging (e.g., CT angiography, echocardiography) and pulmonary function tests. Outline principles of management and treatment options, focusing on disease-specific therapies (e.g., vasodilators, anticoagulation) and supportive care. Discuss the prognosis and potential complications associated with vascular lung diseases, including right heart failure and thromboembolic events.

LEARNING OBJECTIVES (CANVAS):

ÍNDICE

Unlike the systemic circulation (where the smooth muscle cells in the media of the arterioles regulates resistance), pulmonary arterioles appear to have at most incomplete layers of smooth muscle in the media regulating poorly the vascular resistance ( Low resistance) Pulmonary circulation = Incomplete layers of smooth muscle= Low resistance/Low imput impedance "INPUT IMPEDANCE (the resistance of the circulation to flow)"

ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension.ESC Clinical Practice Guidelines 2022

Low pressure pulmonary circulation: Low Pulmonary Input impedance

ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension.ESC Clinical Practice Guidelines 2022

Circulation. Evaluation and Management of Pulmonary Hypertension: A Scientific Statement From the American Heart Association. 2023

Pulmonary vascular resistance is 1/20 of systemic vascular resistance, and mean pulmonary artery pressure may not be much higher than central venous pressure. Minimal RV contractile function is normally necessary to maintain cardiac output

Low pressure pulmonary circulation: Low Pulmonary Input impedance

ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension.ESC Clinical Practice Guidelines 2022

Circulation. Evaluation and Management of Pulmonary Hypertension: A Scientific Statement From the American Heart Association. 2023

IMPAIRED INPUT IMPEDANCE

ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension.ESC Clinical Practice Guidelines 2022

Circulation. Evaluation and Management of Pulmonary Hypertension: A Scientific Statement From the American Heart Association. 2023

IMPAIRED INPUT IMPEDANCE

Normal PAP levels are 8-20 mmHg ******

1. Pulmonary hypertension is a fatal disease that is defined hemodynamically as a mean pulmonary artery pressure ≥ 25 mmHg at rest.
2. A hallmark of PH is an increased pulmonary vascular resistance which leads to elevations in pulmonary artery pressure, resulting in compensatory right ventricular hypertrophy and, ultimately, heart failure.
3. Clinically, vascular changes initially present as nonspecific symptoms, including unexplained dyspnea on exertion, fatigue, chest pain, and syncope.
4. Pathogenic features include sustained vasoconstriction, vascular remodeling of the small arteries, in situ thrombosis, and increased vascular wall stiffness, resulting in increased vascular resistance.
5. Current therapies are limited to supportive care and targeting pulmonary vasoconstriction.

ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension.ESC Clinical Practice Guidelines 2022

Circulation. Evaluation and Management of Pulmonary Hypertension: A Scientific Statement From the American Heart Association. 2023

Pulmonary hypertension: Concept

ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension.ESC Clinical Practice Guidelines 2022

Right heart failure: the inability of the RV to generate adequate forward flow, can develop acutely in response to increases in pulmonary vascular resistance (such as mechanical obstruction of the pulmonary vasculature by pulmonary emboli, or from reactive vasoconstriction in response to hypoxemia).

Right heart failure (Pulmonary hypertension) and HEMODYNAMIC COLLAPSE

ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension.ESC Clinical Practice Guidelines 2022

1. Initially, the rise in pulmonary artery pressure is well tolerated, the RV pressure increases gradually due to elevated afterload
2. Central venous pressure begins to rise
3. The right ventricle overload results in reduced cardiac output and systemic hypotension
4. When the RV pressure reaches a threshold, systemic pressure drops abruptly, this reduces RV tissue perfusion pressure; once this drops below a critical value, RV free wall ischemia develops.
5. RV ischemia causes reduced contractile function, compromising the RV’s capacity to handle the elevated RV afterload, further reducing cardiac output, and causing hemodynamic collapse

MECHANISM:

Right heart failure (Pulmonary hypertension) and HEMODYNAMIC COLLAPSE

As afterload increases (pulmonary hypertension), RV end diastolic volume rises while ejection fraction falls.

During severe pressure overload (Pulmonary hypertension), the interventricular septum shifts, increasing RV diastolic volume. At the same time, there is a reduction in LV end-diastolic volume and surface area, resulting in impaired LV pump function.

ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension.ESC Clinical Practice Guidelines 2022

Circulation. Evaluation and Management of Pulmonary Hypertension: A Scientific Statement From the American Heart Association. 2023

The right ventricle and pulmonary circulation (BASIC CONCEPTS)

ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension.ESC Clinical Practice Guidelines 2022

Sequence of events

Drugs and toxins (anorexigenic agents), amphetamines and cocaine), HIV infection, portal hypertension, connective tissue disorders (most commonly systemic sclerosis), congenital heart disease (Eisenmenger syndrome)

1. Pulmonary arterial hypertension associated with heritable forms and diseases that affect small pulmonary muscular arterioles :

2. Pulmonary VENOUS hypertension due to left-sided heart disease, including systolic and diastolic dysfunction and valvular disease
3. Pulmonary hypertension due to lung diseases and/or hypoxia, including COPD and interstitial lung disease
4. Chronic thromboembolic pulmonary hypertension (CTEPH)
5. Pulmonary hypertension with unclear or multifactorial mechanisms

The most current PH classifications were defined at the WHO Symposium:

Clinical Classification of Pulmonary Hypertension

ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension.ESC Clinical Practice Guidelines 2022

Hypoxic pulmonary hypertension, as one of the most common types, belongs to the third subtype HPH is commonly seen in chronic hypoxic lung diseases: COPD Obstructive sleep apnea syndrome Interstitial lung disease Chronic mountain sickness It is caused by hypoxia-induced endothelium injury, imbalance of vascular endothelial synthesis and secretion of vasodilators, leading to early pulmonary vasoconstriction and pulmonary vascular remodeling. Long-term oxygen therapy can only slightly reduce the pulmonary artery pressure of patients

Pulmonary hypertension caused by Hypoxia Pulmonary venous hypertension/group 3

ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension.ESC Clinical Practice Guidelines 2022

Circulation. Evaluation and Management of Pulmonary Hypertension: A Scientific Statement From the American Heart Association. 2023

Clinical signs on physical exam (right-sided heart failure & hypoperfusion):

1. Jugular venous distension
2. Hepatomegaly
3. Hepatojugular reflex
4. Mottled extremities
5. Cyanosis
6. Diminished peripheral pulses
7. Peripheral edema
8. Ascites

Cardiac auscultation: S3 and S4 sounds, pulmonic valve component (P2) of the second heart sound, systolic murmur indicating tricuspid regurgitation, diastolic murmur indicating pulmonary regurgitation, and a parasternal lift may be detectable.

Patients with PH typically present with symptoms indicating: Poor oxygen transport + impaired cardiac output: Unexplained dyspnea with exertion, fatigue, chest pain, syncope, hemoptysis, and Raynaud’s phenomenon (associated with connective tissue disease).

Pulmonary Hypertension: Signs & Symptoms

ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension.ESC Clinical Practice Guidelines 2022

Circulation. Evaluation and Management of Pulmonary Hypertension: A Scientific Statement From the American Heart Association. 2023

Pulmonary Hypertension: Systemic consequences

ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension.ESC Clinical Practice Guidelines 2022

Circulation. Evaluation and Management of Pulmonary Hypertension: A Scientific Statement From the American Heart Association. 2023

• Electrocardiography
• Pulmonary function testing
• Chest radiography
• Echocardiography
• Serologic testing
• Right heart catheterization

Therapies are limited to supportive care and targeting pulmonary vasoconstriction.

Pulmonary Hypertension: Diagnosis/Investigations

ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension.ESC Clinical Practice Guidelines 2022

Circulation. Evaluation and Management of Pulmonary Hypertension: A Scientific Statement From the American Heart Association. 2023

Findings: Enlargement of the central pulmonary arteries pruning of peripheral vessels (vascular pruning) Cardiomegaly (right atrial and ventricular enlargement, suggestive of advanced disease)

Pulmonary Hypertension: Chest XRAY

ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension.ESC Clinical Practice Guidelines 2022

Circulation. Evaluation and Management of Pulmonary Hypertension: A Scientific Statement From the American Heart Association. 2023

Characteristic Xray of a patient with PAH

ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension.ESC Clinical Practice Guidelines 2022

Circulation. Evaluation and Management of Pulmonary Hypertension: A Scientific Statement From the American Heart Association. 2023

Characteristic Xray of a patient with PAH

ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension.ESC Clinical Practice Guidelines 2022

Circulation. Evaluation and Management of Pulmonary Hypertension: A Scientific Statement From the American Heart Association. 2023

Characteristic Xray of a patient with PAH

ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension.ESC Clinical Practice Guidelines 2022

Circulation. Evaluation and Management of Pulmonary Hypertension: A Scientific Statement From the American Heart Association. 2023

Right heart catheterization: Is the gold-standard test for measurement of pulmonary artery pressure and diagnosis of pulmonary hypertension. Useful test in the selection of appropriate medical therapy for PH. pulmonary artery hypertension Increased mean PAP (mPAP >25 mmHg)

Pulmonary Hypertension: Investigations

ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension.ESC Clinical Practice Guidelines 2022

Image of increased measurements of tricuspid annulus diameter, right atrial area, ascending aortic diameter and main pulmonary arterial diameter in patients with pulmonary hypertension.

Pulmonary Hypertension: CT scan (right heart dilation)

ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension.ESC Clinical Practice Guidelines 2022

Circulation. Evaluation and Management of Pulmonary Hypertension: A Scientific Statement From the American Heart Association. 2023

PAH has no cure. Medical management is targeted towards alleviating symptoms and slowing disease progression. Pulmonary hypertension secondary to other diseases – treat the underlying cause.

Tratable traits in PHA

ESC/ERS Guidelines for the diagnosis and treatment of pulmonary hypertension.ESC Clinical Practice Guidelines 2022

Any questions? karla.belen@edu.uag.mx

Gonzalez MD

START

HY:Pulmonary embolism

LEARNING OBJECTIVES (CANVAS):

1. Describe the different types of pulmonary embolism (thrombotic, fat, air, and more).
2. Explain the Virchow's triad and how its components contribute to the development of pulmonary embolism.
3. Recognize the risk factors and predisposing conditions for pulmonary embolism.
4. Understand the pathophysiology of pulmonary embolism and its impact on the pulmonary vasculature.
5. Learn about the clinical manifestations of pulmonary embolism and the various diagnostic tools.

ÍNDICE

Etiology

Students´ Resources (EXAM FOCUS)

Clinical setting

Pathophysiology *******

Guidelines on Acute Pulmonary Embolism (Diagnosis and Management of) ESC Clinical Practice Guidelines

ESC Clinical Practice Guidelines 2022

For foundational understanding only, NOT INTENDED FOR EXAM PURPOSES

Etiology

Proffesors´ Resources:

Clinical setting

Pathophysiology

Virchow’s Triad is used to determine the contributing factors to venous thromboembolism: The three limbs of Virchow’s Triad (which lead to arterial thrombosis) are satisfied in the arterial processes of: Inflammation Endothelial dysfunction Atherosclerosis Turbulent blood flow Abnormal function of platelet and coagulation pathways Limb of Virchow’s triad: Hypercoagulable state Vascular damage Intravascular stasis of blood)

Virchow’s Triad and the Role of Thrombosis

Guidelines on Acute Pulmonary Embolism (Diagnosis and Management of) ESC Clinical Practice Guidelines

ESC Clinical Practice Guidelines 2022

• Reduced mobility: Increases length of contact of coagulation factors with endothelium. Examples: Long-haul air travel, hospitalization
• Polycythemia: Hyperviscosity, due to excessive overproduction of red blood cells, leads to stasis of blood in the veins.
• Endothelial injury: Stasis directly damages the endothelium as well as reduces the natural fibrinolysis.
• Congestive heart failure: Failure to pump blood forward results in venous stasis and elevated central venous pressure.

Stasis refers to a state of slow or stagnant blood flow, which can occur in areas of vessel narrowing, blockages, or inactivity. Turbulent flow can occur at sites where blood vessels branch or bend sharply. Both stasis + turbulent flow = disruption of the balance of blood constituents and promote the accumulation of platelets and clotting factors, facilitating thrombus formation. Causes:

Virchow’s Triad: Stasis

Guidelines on Acute Pulmonary Embolism (Diagnosis and Management of) ESC Clinical Practice Guidelines

ESC Clinical Practice Guidelines 2022

Hypercoagulable State Ocurrs due to igh expression levels of proinflammatory cytokines including: Interleukins IL-1β IL-1 receptor antagonist IL-7 IL-8 IL-9 IL-10 Basic fibroblast growth factor Granulocyte colony stimulating factor Granulocyte macrophage stimulating factor Interferon gamma Platelet derived growth factor, Tumor necrosis factor alpha Vascular endothelial growth factor. These pro-inflammatory plasma cytokines direct cytotoxicity and this proinflammatory state increases hypercoagulability by increasing expression of serum coagulation factors including: Tissue factor Von Willebrand factor Factor VIII, Activation of platelets, leading to thrombin generation and fibrin clot formation.

Virchow’s Triad and the Role of Thrombosis

Guidelines on Acute Pulmonary Embolism (Diagnosis and Management of) ESC Clinical Practice Guidelines

ESC Clinical Practice Guidelines 2022

1. Pulmonary embolism is when a blood clot (thrombus) becomes lodged in an artery in the lung and blocks blood flow to the lung.
2. Pulmonary embolism usually arises from a thrombus that originates in the deep venous system of the lower extremities
3. It rarely also originates in the pelvic, renal, upper extremity veins, or the right heart chambers
4. After traveling to the lung, large thrombi can lodge at the bifurcation of the main pulmonary artery or the lobar branches and cause hemodynamic compromise.

An embolus is any intravascular material that migrates from its original location to occlude a distal vessel. Although the embolus can be a blood clot (thrombus), fat, air, amniotic fluid, or tumour.

Pulmonary embolism

Guidelines on Acute Pulmonary Embolism (Diagnosis and Management of) ESC Clinical Practice Guidelines

ESC Clinical Practice Guidelines 2022

1. HIV infection (The risk of developing a pulmonary embolism or DVT is increased 40% in these individuals).
2. Venous stasis: may occur due to polycythemia and dehydration, immobility, raised venous pressure in cardiac failure, or compression of a vein by a tumor.
3. Factor V Leiden mutation. Primary or acquired deficiencies in protein C, protein S, and antithrombin III
4. Immobilization
5. Prolonged bed rest or immobilization of a limb in a cast.
6. Trauma: Leg amputations and hip, pelvic, and spinal surgery
7. Fractures of the femur and tibia are associated with the highest risk of fracture-related pulmonary embolism, followed by pelvic, spinal, and other fractures.
8. Pregnancy. Oral contraceptives. Estrogen replacement
9. Solid tumors, leukemias, and lymphomas. The neoplasms most commonly associated with pulmonary embolism, in descending order of frequency, are pancreatic carcinoma; bronchogenic carcinoma; and carcinomas of the genitourinary tract, colon, stomach, and breast.
10. Acute medical illness: AIDS (lupus anticoagulant) Behçet disease, Congestive heart failure, Myocardial infarction, Polycythemia Systemic lupus erythematosus Ulcerative colitis

Risk factors

Guidelines on Acute Pulmonary Embolism (Diagnosis and Management of) ESC Clinical Practice Guidelines

ESC Clinical Practice Guidelines 2022

Additional risk factors:

• Drug abuse (intravenous [IV] drugs)
• Hemolytic anemias

• Hyperlipidemias
• Thrombocytosis
• Varicose veins
• Inflammatory bowel disease
• Sleep-disordered breathing
• Travel of 4 hours or more in the past month
• Surgery within the last 3 months
• Smoking
• Central venous instrumentation within the past 3 months
• Stroke
• Paresis, or paralysis
• Prior pulmonary embolism
• Heart failure
• Chronic obstructive pulmonary disease

Risk factors

Guidelines on Acute Pulmonary Embolism (Diagnosis and Management of) ESC Clinical Practice Guidelines

ESC Clinical Practice Guidelines 2022

Eight subtypes are identified: Fat embolism: characterized by the release of fat into the systemic circulation, often after fracture of a long bone. Fat embolism syndrome is a rare clinical consequence of FE characterized by respiratory distress, mental status changes, and a petechial rash. Amniotic fluid embolism: The embolism of amniotic fluid, which is a mixture of maternal extracellular fluid and fetal urine, squamous cells, lanugo hairs, vernix caseosa, mucin, and sometimes meconium, leads to an idiosyncratic response. The severity of symptoms of this so-called “anaphylactoid syndrome of pregnancy” is related to the host reaction to the antigenic components of the AF. AFE is the only NTPE that is associated with left-sided heart failure. Tumor embolism: characterized by the occlusion of pulmonary vessels by tumor cells Gstational trophoblastic disease: tumor arises from fetal, not maternal, tissue. Septic emboli: reach the lung from many sources, including thrombophlebitis and infected heart valves, catheters, and pacemaker wires. Cystic hydatid disease (echinococcosis): a parasitic infection caused by larval or cyst stage of the tapeworm Echinococcus granulosus affecting the liver (75%) and lungs (15%). Vesicles or cysts that mechanically obstruct bloodflow cause embolism. Particulate/foreign material embolism: embolic particles may reach lung after injection of foreign materials. Iatrogenic emboli: cement, gas, iodinated oil, glue, metallic mercury, radiotracer, silicone, hyaluronic acid, radioactive seeds, and ventriculoperitoneal shunts. Foreign bodies: bullets, talc, cotton. Gas embolism (venous of arterial): mainly air embolism, although other gases, such as carbon dioxide, nitrous oxide, helium, and nitrogen.

It is characterized as embolization to the pulmonary circulation of different cell types (adipocytes, haematopoietic, amniotic, trophoblastic or tumor), bacteria, fungi, foreign material or gas.

Non-thrombotic pulmonary embolism

Guidelines on Acute Pulmonary Embolism (Diagnosis and Management of) ESC Clinical Practice Guidelines

ESC Clinical Practice Guidelines 2022

Non-thrombotic pulmonary embolism

Guidelines on Acute Pulmonary Embolism (Diagnosis and Management of) ESC Clinical Practice Guidelines

ESC Clinical Practice Guidelines 2022

PE is defined by a process of venous thrombi dislodging from their origin and travelling as emboli through the vena cava and right side of the heart to the pulmonary arteries After travelling to the pulmonary arteries, thrombi may either break down and lodge into the peripheral pulmonary arteries or, if very large, remain at the main pulmonary artery bifurcation, which then gives rise to a ‘saddle embolism’; this latter event may cause severe haemodynamic compromise, collapse and severe dyspnoea. If the thrombi travel further to smaller arteries and end arteries, the latter may cause pulmonary infarction, which causes loss of aveoli function, loss of surfactant, severe pain that typically increases on respiration, respiratory failure and shoch states.

Pathophysiology of pulmonary embolism

Guidelines on Acute Pulmonary Embolism (Diagnosis and Management of) ESC Clinical Practice Guidelines

ESC Clinical Practice Guidelines 2022

1. The increase in RV afterload in acute PE is due to mechanical obstruction of the pulmonary vasculature by emboli and, by obstruction-associated vasoconstriction triggered by vasoactive mediators released by endothelial cells and platelets (among others thromboxane A2 and serotonin)
2. The resulting sudden increase in pulmonary artery pressure leads to an increase in RV dilatation, which is reflected by increases in serum N-terminal pro-brain-type natriuretic peptide (NT-proBNP) and troponin levels in acute PE

Pathophysiology of pulmonary embolism & RV failure

Guidelines on Acute Pulmonary Embolism (Diagnosis and Management of) ESC Clinical Practice Guidelines

ESC Clinical Practice Guidelines 2022

The symptoms of acute PE include:Acute chest pain Shortness of breath Palpitations Syncope Haemoptysis DVT symptoms such as leg swelling, pain and redness. Clinical signs comprise: Tachycardia (ECG: S1, Q3 T3) Tachypnoea Elevated jugular pressure Signs of shock with cyanosis and hypotension. PE shares symptoms and signs with other conditions, including acute coronary syndrome, dissection of the thoracic aorta, pneumothorax and pneumonia.

Signs and symptoms

Guidelines on Acute Pulmonary Embolism (Diagnosis and Management of) ESC Clinical Practice Guidelines

ESC Clinical Practice Guidelines 2022

Signs and symptoms: Deep Venous Thrombosis

Guidelines on Acute Pulmonary Embolism (Diagnosis and Management of) ESC Clinical Practice Guidelines

ESC Clinical Practice Guidelines 2022

Hypercoagulation workup should be performed if no obvious cause for embolic disease is apparent. This may include: Antithrombin III deficiency Protein C or protein S deficiency, Lupus anticoagulant, Homocystinuria. D-Dimer Follow-Up on Low-to-Moderate Pretest Probability:

• D-Dimer, is measured by ELISA which has a sensitivity of 0.95 and negative likelihood ratio of 0.13. Negative results on a high-sensitivity D-dimer test in a patient with a low pretest probability of embolism indicate a low likelihood of venous thromboembolism and reliably exclude pulmonary embolism.

• It is of questionable value in patients who are older than 80 years, who are hospitalized, who have cancer, or who are pregnant, because nonspecific elevation of D-dimer concentrations is common in such patients.

Approach considerations

Guidelines on Acute Pulmonary Embolism (Diagnosis and Management of) ESC Clinical Practice Guidelines

ESC Clinical Practice Guidelines 2022

Arterty cutoff image **

Brain Natriuretic Peptide higher BNP levels are expected. BNP testing had a sensitivity and specificity of only 60% and 62% Venography is the criterion standard for diagnosing DVT. Angiography Pulmonary angiography is the historical criterion standard for the diagnosis of pulmonary embolism. Positive results consist of a filling defect or sharp cutoff of the affected artery.

Arterial blood gas determinations characteristically reveal hypoxemia, hypocapnia, and respiratory alkalosis Serum troponin levels can be elevated in up to 50% of patients with a moderate to large pulmonary embolism, presumptively due to acute right ventricular myocardial stretch.

Approach considerations

Guidelines on Acute Pulmonary Embolism (Diagnosis and Management of) ESC Clinical Practice Guidelines

ESC Clinical Practice Guidelines 2022

Clinical risk assessment scales

Guidelines on Acute Pulmonary Embolism (Diagnosis and Management of) ESC Clinical Practice Guidelines

ESC Clinical Practice Guidelines 2022

Imaging: Chest XRAY--- Pulmonary circulation cutoff

Guidelines on Acute Pulmonary Embolism (Diagnosis and Management of) ESC Clinical Practice Guidelines

ESC Clinical Practice Guidelines 2022

Imaging: Chest XRAY--- Hampton Hump

Guidelines on Acute Pulmonary Embolism (Diagnosis and Management of) ESC Clinical Practice Guidelines

ESC Clinical Practice Guidelines 2022

Imaging: Chest XRAY--- Westermark sign

Guidelines on Acute Pulmonary Embolism (Diagnosis and Management of) ESC Clinical Practice Guidelines

ESC Clinical Practice Guidelines 2022

Imaging: Chest XRAY--- Local oligemia/Westermark sign

Guidelines on Acute Pulmonary Embolism (Diagnosis and Management of) ESC Clinical Practice Guidelines

ESC Clinical Practice Guidelines 2022

CT scan demonstrates a pulmonary embolus that results in an eccentrically positioned partial filling defect, which is surrounded by contrast material and forms acute angles with the arterial wall

Guidelines on Acute Pulmonary Embolism (Diagnosis and Management of) ESC Clinical Practice Guidelines

ESC Clinical Practice Guidelines 2022

Approachment and treatment (Summary)

Guidelines on Acute Pulmonary Embolism (Diagnosis and Management of) ESC Clinical Practice Guidelines

ESC Clinical Practice Guidelines 2022

Any questions??? karla.belen@edu.uag.mx