Pulmonary Embolism Notes

Pulmonary Embolism

Anatomy of the Lungs and Circulation

• Refer to Slides CFB for details.

Role of Peripheral and Central Chemoreceptors

Peripheral Chemoreceptors

• Located in the carotid (CN9) and aortic bodies (CN10).
• Detect changes in:
  • Decrease in $PO_2$
  • Increase in $PCO_2$
  • Decrease in blood pH
• Upon detection, stimulate the inspiratory center (dorsal medullary center) to:
  • Increase ventilation
  • Increase gas exchange

Central Chemoreceptors

• Located in the medulla oblongata.
• Primarily detect an increase in $PCO_2$ and $H^+$.
• $H^+$ cannot cross the blood-brain barrier directly.
• When $CO_2$ increases in the blood:
  • It diffuses across the blood-brain barrier.
  • Converts into $H<em>2CO</em>3$, which hydrolyzes into $H^+$ and $HCO_3^-$.
• Chemoreceptors detect $H^+$ and send signals to the inspiratory center to:
  • Increase ventilation
  • Decrease $CO_2$ levels in the blood and CSF

Causes of Pulmonary Embolism (PE) and Mechanisms

Embolism: Transport of abnormal material via the bloodstream impacting blood vessels.

Risk Factors and Mechanisms

• Pregnancy
  • Growing fetus compresses veins, slowing blood flow.
  • Increased attachment of platelets and clotting factors to vascular endothelial cells.
  • Activation of the coagulation cascade.
  • May also involve a naturally hypercoagulable state mediated by increased clotting factors and fibrinogen.
• Inactivity in the Skeletal Muscle Pump
  • Slowed blood flow increases platelet and clotting factor attachment to blood vessels.
  • Activation of the coagulation cascade.
• Surgery
  • Damage to vascular endothelial cells exposes tissue factor and collagen.
  • Activation of platelets and clotting factors, leading to platelet aggregation and coagulation cascade.
• Inherited Antithrombin III Deficiency
  • Increased risk of clot formation.
  • Antithrombin III works by attaching to thrombin and clotting factors 7, 9, 10, 11, and 12.
• Oral Contraceptives and Hormone Replacement Therapy
  • Increase clotting factor production.
  • Decrease Protein C and Antithrombin III levels, promoting clot formation.
• Non-Main Causes
  • Fat embolism
  • Air embolism
  • Thrombus
  • Amniotic fluid embolism

Thrombosis

• Formation of a solid mass from blood constituents while moving through the vascular system.
• Related to Virchow's Triad
  • Stasis and Turbulent Flow:
    • Slow blood flow due to turbulence or skeletal muscle pump inactivity.
    • Platelets and clotting factors contact endothelium resulting in prolonged interaction leading to clotting factor adhesion and activation of clotting cascade.
  • Hypercoagulation:
    • Altered amount of clotting factors that increase primary or secondary hemostasis.
    • Can be due to genetics, surgery, or medications.
  • Damage to Endothelial Cell Lining: of a blood vessel.

Definition of Pulmonary Embolism

• Blockage of an artery in the pulmonary circulation by blood clots or thrombus.
  • 95% of PE cases are secondary to Deep Vein Thrombosis (DVT).
  • DVT involves thrombus formation in the legs or pelvis.
    • Fragmented emboli travel through the veins to the inferior vena cava and then to the pulmonary arteries.
• Emboli Location:
  • Occluding: in the main pulmonary artery
  • Straddle (Saddle): at the pulmonary artery bifurcation
  • Obstructing: in pulmonary arterioles
• Obstruction can be partial or complete.

Hemodynamic Changes Following PE

Impact on Pressure

• Increased right ventricular afterload.
  • Increased right ventricular pressure.
    • Increased right atrial pressure.
      • Increased central venous pressure.

Impact on Volume

• Pulmonary hypertension.
  • Increased right ventricular volume.
    • Increased stretch and dilation.
      • Stretch of the tricuspid valve.
        • Regurgitation during systole.
          • Increased right atrial blood volume and jugular venous pressure (JVP).

Impact on Blood Flow

• Obstruction of blood flow.
  • Decreased blood return to the left side of the heart.
    • Decreased end-diastolic volume (EDV).
      • Decreased stroke volume (SV) and cardiac output.
        • Decreased blood pressure (BP).

Clinical Features of PE

• Depend on the size of the embolus.
  • Small Embolus
    • Impacts distal/terminal arteries and arterioles.
    • Unlikely to cause significant signs or symptoms.
  • Large Embolus
    • Major arterial obstruction.
      • Acute pulmonary hypertension.
        • Right-sided heart failure.
    • If the embolus breaks up (due to blood force) and impacts terminal arteries near the pleural membrane, it can cause:
      • Pleural effusion and pleuritic chest pain.

Clinical Manifestations

• Collapse
• Pleuritic chest pain
• Acute breathlessness
• Pleural effusion
• Raised JVP
• Heave and crackles on auscultation
• Low BP
• Pulmonary hypertension
• Right ventricular failure
• Coughing blood

Changes in Arterial Blood Gases

• Low Oxygen
  • Due to obstruction by the clot.
  • Ventilation-perfusion mismatch.
• Low Oxygen
  • Due to pulmonary edema and fluid around alveoli, compromising gas exchange.
  • Ventilation-perfusion mismatch.
• Changes in $CO_2$ Levels
  • Initially, hypercapnia (increased $CO_2$).
  • Becomes hypocapnia (decreased $CO_2$) due to chemoreceptor activation, which increases ventilation.
• Low Sats (Low Blood $O_2$)

Pathogenesis of Pulmonary Edema

Exudate

• Divided into intravascular and extravascular components.
  • Intravascular
    • Embolus impact causes vascular endothelial injury.
      • Leads to inflammation.
        • Increased cytokines.
          • Increased vascular permeability.
            • Inflammatory cells and mediators leak out of blood vessels into the tissue, causing edema.
  • Extravascular
    • Embolus impact obstructs blood flow.
      • Ischemia of tissues and bronchioles distal to the obstruction.
        • Inflammation of lung tissues and bronchioles.
          • Increased cytokine production and recruitment of other inflammatory cells, leading to edema.

Transudate

• Embolus impact.
  • Obstruction of blood flow causes pulmonary hypertension.
    • Increased hydrostatic pressure in capillaries behind the obstruction.
      • Leakage of plasma into lung tissue, resulting in edema.
    • If pressure is excessively high, capillaries may rupture.
      • Leaking blood into the tissues, causing edema.