Pulmonary embolism

Pulmonary embolism. It is a relatively common cardiovascular emergency. Diagnosis is difficult and can be overlooked because it does not have a specific clinical presentation. However, early diagnosis is essential, since immediate treatment is highly effective.

Summary

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  • 1 Definition
  • 2 Pathophysiology
  • 3 Predisposing factors
  • 4 Respiratory impact
  • 5 Hemodynamic impact
  • 6 Clinical assessment
  • 7 Diagnosis
  • 8 Differential diagnosis
  • 9 Sources
  • 10 External links

Definition

Clinical picture characterized by obstruction of blood circulation in the pulmonary arteries by an embolus from somewhere in the venous system.

The plungers are caused by detachment of a thrombus that obstructs all or part of light of blood vessels. The thrombi are caused by the deposit of some components of the blood on the walls, generally injured, the blood vessels.

Pathophysiology

90% of PE originate in the venous system of the lower extremities. Other possible origins are the inferior vena cava, the right heart chambers, the deep pelvic venous system, the renal veins, and the axillary veins.

Distal thrombi of the lower extremities (calves) are an infrequent cause of clinically significant embolism and rarely produce fatal PE. However, without treatment, 20-25% of these thrombi progress to the iliofemoral system, which is the most frequent source of emboli in patients with PE.

The spectrum of pulmonary embolism ranges from clinically insignificant embolism to massive embolism with sudden cardiac death , depending on the size of the embolus and the cardiorespiratory reserve of the patient.

The pulmonary circulation has great capacity to recruit vessels that are poorly perfused in response to stimuli such as exercise. This pulmonary vascular recruitment allows most patients with PE to remain hemodynamically stable. However, when massive embolism occurs, this recruitment cannot long compensate for the large loss of pulmonary vascularization. Therefore, there is a sudden increase in pulmonary vascular resistance that can cause pulmonary hypertension (PHT), dysfunction of the right ventricle and decreased cardiac output (GC).

When this happens, hypotension, tachypnea, tachycardia and increased jugular venous pressure occur . In patients with underlying lung disease, even small emboli, can cause severe PH and acute RV failure due to limited pulmonary vascular recruitment capacity.

In the lungs, the consequences of PE include increased alveolar dead space, bronchoconstriction, hyperventilation, atelectasis, pulmonary infarction, and hypoxia.

Predisposing factors

  • Coagulation disorders and fibrinolysis: neoplasms, use of contraceptives, nephritic syndrome.
  • Platelet disorders: paroxysmal nocturnal hemoglobinuria , hyperlipidemia, Diabetes mellitus .
  • Vascular disorders: venous ecstasy ( Obesity , postoperative, orthopedic surgery, prolonged immobilizations and multiple injuries, especially spinal injuries).
  • Vasculitis and chronic occlusive arterial disease.
  • Thrombotic purple.
  • Bone fractures.
  • Advanced age.
  • Deep venous approaches.
  • Pregnancy and puerperium.
  • Long trips.
  • Previous venous thromboembolism.

Respiratory impact

The main consequences of obstruction of the pulmonary vessels are:

  • Increased alveolar dead space that results in an alteration of the gas exchange due to an alteration in the ventilation-perfusion ratio.
  • Hyperventilation creating a temporary state of hypocapnia and respiratory alkalosis.

Later a state of mixed acidosis is established as a result of respiratory failure.

  • Decreased surfactant due to lack of blood supply.
  • Pulmonary insufficiency.

Hemodynamic impact

The embolus in the pulmonary circulation produces a vascular obstruction that results in:

  • Decreased pulmonary vascular area.
  • Serotonin release.
  • Increased lung resistance.
  • Increased afterload of the right ventricle.
  • Decreased cardiac output.
  • Cardiogenic shock .
  • Pulmonary constriction and pulmonary hypertension that increases venous pressure causing engorgement of the neck veins, Hepatomegaly , cerebral congestion, and myocardial dysfunction.

It also reduces cardiac output, along with hypoxemia that is already occurring, this effect causes an ischemia of almost all organs that leads to confusion, disorientation, Angina , Arrhythmias , Hypotension , oliguria and shock.

Clinical assessment

  • The most frequent symptoms and signs are: chest pain, dyspnea, anxiety, cough, hemoptysis, sweating, syncope , tachypnea, crackles on auscultation and / or decrease or absence of vesicular murmur, tachycardia, fever, phlebitis and edema.
  • We must look for the existence of deep vein thrombosis.
  • Find out the risk factors and etiology.
  • Control of vital signs: blood pressure, heart rate, respiratory rate, temperature, O2 saturation.
  • Chest rayoxy: the following findings can be found: atelectasis , parenchymal condensations, pleural effusion, hemidaphragm elevation, increase in the caliber of the pulmonary artery, cardiomegaly and pulmonary edema, in many cases the result is negative.
  • Electrocardiogram: non-specific ST and T wave abnormalities, right bundle branch block, hypertrophy of the right ventricle, deviation of the axis to the right. Large, pointy P waves (overload of the right atrium) that translates into increased pressure in the right ventricle.
  • Echocardiography: Signs of overload of the right ventricle, signs of pulmonary hypertension may appear, and thrombi may be seen.
  • Other diagnostic techniques: lung scintigraphy, pulmonary arteriography, computed axial tomography, nuclear magnetic resonance, among others.
  • Lab tests:

-Complete blood count: moderate leukocytosis with deviation to the left. -Increase of fibrinogen degradation products. -Increased plasma D-dimer. -Increased LDH. – Arterial blood gas analysis: hypoxemia with hypocapnia and respiratory alkalosis (30% of cases, PO2 is normal). Increased alveolar-arterial O2 difference

Diagnosis

The first thing is to have a clinical suspicion, based on a compatible clinical picture, the presence of known risk factors and basic complementary tests. The first step is to calculate the pretest probability, this calculation will be done with explicit criteria that are available in different protocols, the best known is presented below.

Wells Points Protocol

  • Signs and symptoms of DVT 3
  • PET more likely than an alternative diagnosis 3
  • Immobilization> 3 days or surgery <3 weeks 1,5
  • Cardiac> 100 bpm 1.5
  • History of DVT or PET 1.5
  • Hemoptysis 1
  • Neoplastic 1
  1. Low clinical probability <2 points. PE probability of 10%, occurs in 40% to 49% of patients.
  2. Moderate clinical probability 2-6 points. PE probability of 20% to 40%, occurs in 50%
  3. High clinical probability> 6 points. PE probability of 65%, occurs in 6% to 7%
  4. Low clinical probability with a negative D-dimer result: it allows to exclude PE with a very high degree of reliability (negative predictive value: 99%).
  5. Intermediate or high clinical probability or the D-dimer is positive, a helical CT or scintigraphy is performed and the procedure will be as indicated by the algorithm.

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