Pathophysiology

Voicethread 1. Pulmonary Embolism Normal Physiology and Pathophysiology
 
Note. Adapted from Pulmonary Embolism: The Route to Recovery, by Nature Video, 2018 
(https://www.youtube.com/watch?v=8UnPPZlnfbk).

NORMAL PHYSIOLOGY    

     For gas exchange to occur, our respiratory and circulatory systems work together. The protein molecule in red blood cells, hemoglobin, circulates in the bloodstream carrying oxygen to the tissues and carbon dioxide to the lungs to be removed. Three systematic mechanisms occur for this to happen: 

  1. Ventilation, the movement of air into and out of the lungs. 

  2. Diffusion, the movement of gases between air spaces in the lungs and the bloodstream.

  3. Perfusion, the movement of blood into and out of the capillary beds of the lungs and into the body organs and tissues (Brashers, chap. 35, para. 1). 

   Besides oxygen exchange, the pulmonary system has an extensive vasculature of arteries, capillaries, and veins that delivers nutrients to the lungs, acts as a blood reservoir for the left ventricle, and helps with filtration to remove clots, air and other particles from the circulation.

Figure 1

The Pulmonary Circulation

Note. From Pathophysiology: The Biologic Basis for Disease in Adults and Children, by McCance, K., & Huether, S., 2019, St. Louis, Missouri: Elsevier.

     After blood without oxygen (venous blood) passes through the right chambers of the heart, it passes to the pulmonary arteries and into the lungs branching out from each main bronchus and with the bronchi at every division. Each bronchus and bronchiole have an accompanying artery. The artery divides at the end of the bronchiole to form a network of capillaries around the alveoli sacs. The shared alveolar and capillary walls compose a very thin alveolocapillary membrane. The blood cell diffuses through the membrane carbon dioxide and receives oxygen. The oxygen-rich blood (arterial blood) then travels to the pulmonary veins and into the left chambers of the heart to pump blood to the rest of the body (Brashers, Pulmonary and Bronchial Circulation section). 

Figure 2

Gas exchange GIF

Note. From Oxygen Transport Presentation, 2014, (https://makeagif.com/gif/oxygen-transport-presentation-d6LzaX).

PATHOPHYSIOLOGY

If there is an occlusion or partial occlusion of the pulmonary artery or its branches, it will cause a pulmonary embolism. 

Common cause: 

An embolized clot from deep vein thrombosis (DVT) involving the lower leg.

Less common causes: 

  • Tissue fragments
  • Lipids
  • Foreign body
  • Air bubble
  • Amniotic fluid

Risk Factors 

Factors that promote venous thrombosis is known as the triad of Virchow. 

  • Venous stasis (immobilization, heart failure, obesity, prolonged leg dependency, age)
  • Hypercoagulability (inherited coagulation disorders, malignancy, hormone replacement, oral contraceptives, pregnancy, smoking)
  • Endothelial injury (trauma, infection, caustic intravenous infusions) 

Genetic risks include: factor V Leiden mutation, antithrombin II deficiency, protein S deficiency, activated protein C deficiency, and prothrombin 20210. 

Pulmonary emboli can result in any of the following: 

  1. Embolus with infarction: causes the death of a portion of the lung tissue.
  2. Embolus without infarction: doesn’t cause permanent lung injury since perfusion of the affected segment is maintained. 
  3. Massive occlusion: blocks a major portion of the pulmonary circulation. 
  4. Multiple pulmonary emboli: numerous emboli that may be chronic or recurring.

Pathogenesis: 

     When the conditions arise to form a thrombus, it can become dislodged and a piece can break off, known as an embolus.  When the embolus is navigating the circulatory system, it can obstruct the pulmonary circulation. The body sends a signal to release neurohormonal substances and inflammatory mediators, which cause vasoconstriction. Increased pulmonary hypertension occurs. The absent blood flow to the affected lung segment causes ventilation-perfusion mismatch and a decrease in surfactant production by the alveoli that help them expand during inspiration. This results in atelectasis and further worsens hypoxia. If the embolus is large enough, infarction of the lung tissue, dysrhythmias, decreased cardiac output, shock, and death are possible. (Brashers & Huether, 2019, Pulmonary Vascular Disease). 

Figure 3

How a Pulmonary Embolism Occurs

Note. From Pulmonary Embolism, by Ben-Barak, I., 2018, (https://healthand.com/us/topic/general-report/pulmonary-embolism).

Manifestations: 

  • DVT (s/s: calf pain, tenderness, calf asymmetry, mottled or cyanotic skin, may also be asymptomatic) 
  • Pleuritic chest pain
  • Cough
  • Dyspnea
  • Tachypnea
  • Tachycardia
  • Unexplained anxiety
  • Occasional syncope or hemoptysis
  • With large emboli; pleural friction rub, pleural effusion, fever, leukocytosis

Evaluation: 

Diagnosis can be made based on a patient’s symptoms, medical history and a series of tests and scans.  Clinical Decision Rules, such as the Well’s Score, can guide diagnostics of suspected acute venous thromboembolism.

  • In the first 24 hours, chest x-rays and pulmonary function tests are not definitive for a pulmonary embolism.
  • Oximetry and arterial blood gas typically show hypoxemia.
  • Echocardiography may show right ventricle strain.
  • Serum D-dimer levels will test positive for thrombus degradation by-products; fibrinogen and fibrin.
  • Ventilation-perfusion scan (V/Q) scan assesses the flow of air in and out of the lungs, while the perfusion scan assesses the blood flow within the lungs. (Ben-Barak, 2018)
  • Further evaluation may be conducted with CT arteriography, magnetic resonance arteriography, or in rare cases, a pulmonary angiogram. (Brashers & Huether, 2019, Pulmonary Vascular Disease).