Definition

• Pneumonia is an inflammatory disease of the lungs.
• In pneumonia, some or all of the alveoli become filled with fluid and blood cells instead of air. (Fig. 43.5)
• This filling of the alveoli interferes with normal gas exchange.

Bacterial Pneumonia

• A common type is bacterial pneumonia, which is most often caused by pneumococci.

Development of the Disease

• The infection begins in the alveoli.
• The pulmonary (alveolar) membrane becomes inflamed.
• Because of inflammation, the membrane becomes highly porous (more permeable).
• As a result:
  • Fluid leaks from the blood into the alveoli.
  • Red blood cells leak into the alveoli.
  • White blood cells also enter the alveoli to fight the infection.
• Consequently, the infected alveoli gradually fill with fluid and inflammatory cells.
• The infection spreads from one alveolus to another through the movement of bacteria or viruses.
• As the disease progresses:
  • Large areas of the lung may become involved.
  • Sometimes an entire lobe or even a whole lung is affected.
• These affected regions become consolidated, meaning they are:
  • Filled with fluid.
  • Filled with inflammatory cells and cellular debris.
  • Unable to participate effectively in gas exchange.

Effect on Gas Exchange

• In pneumonia, the gas exchange function of the lungs gradually decreases as the disease progresses.

Early Stage

• In the early stage, only one lung or one part of a lung may be affected.
• In the diseased area:
  • Alveolar ventilation decreases because the alveoli are filled with fluid.
  • Blood flow continues normally through the pulmonary capillaries.

Major Pulmonary Abnormalities

1. Reduced Respiratory Membrane Surface Area

• Fluid-filled alveoli cannot participate effectively in gas exchange.
• Therefore, the total surface area available for diffusion decreases.
• This reduces the exchange of oxygen and carbon dioxide.

2. Decreased Ventilation–Perfusion (V̇A/Q̇) Ratio

• The affected alveoli receive little or no ventilation.
• However, blood continues to flow through their capillaries.
• This causes a decreased ventilation–perfusion (V̇A/Q̇) ratio.
• Because blood passes through poorly ventilated alveoli, it:
  • Receives less oxygen.
  • Removes less carbon dioxide.
• As a result:
  • Hypoxemia develops (low oxygen level in the blood).
  • Hypercapnia develops (high carbon dioxide level in the blood).

Oxygen Saturation in Pneumonia

• Fig. 43.6 illustrates the effect of a low V̇A/Q̇ ratio.
• Blood flowing through the normal (aerated) lung becomes approximately 97% saturated with oxygen.
• Blood flowing through the affected (unaerated) lung becomes only about 60% saturated with oxygen.
• When these two blood streams mix in the left side of the heart, the average arterial oxygen saturation falls to about 78%.
• This oxygen saturation is far below the normal level, resulting in significant hypoxemia.

KEY CONCEPT

• Pneumonia is inflammation of the lungs in which alveoli become filled with fluid and blood cells (Fig. 43.5).
• Bacterial pneumonia is most commonly caused by pneumococci.
• Inflammation increases alveolar membrane permeability, allowing fluid, red blood cells, and white blood cells to enter the alveoli.
• The infection spreads from alveolus to alveolus, and large lung areas may become consolidated with fluid and cellular debris.
• Pneumonia reduces gas exchange by decreasing the respiratory membrane surface area and lowering the ventilation–perfusion (V̇A/Q̇) ratio.
• These changes produce hypoxemia (low blood O₂) and hypercapnia (high blood CO₂).
• Blood from normal alveoli is about 97% oxygen saturated, whereas blood from fluid-filled alveoli is only about 60% saturated; after mixing, arterial oxygen saturation falls to about 78% (Fig. 43.6).

ATELECTASIS—COLLAPSE OF THE ALVEOLI

Definition

• Atelectasis means collapse of the alveoli.
• It may involve:
  • A small (localized) area of the lung, or
  • An entire lung.

Common Causes of Atelectasis

The two most common causes are:

1. Complete obstruction of an airway.
2. Lack of surfactant in the fluid lining the alveoli.

Airway Obstruction Causes Lung Collapse

Causes of Airway Obstruction

Airway obstruction usually occurs because of:

• Blockage of many small bronchi by mucus, or
• Blockage of a major bronchus by a large mucus plug or a solid object such as a tumor.

What Happens After Airway Obstruction?

• Air becomes trapped in the alveoli beyond the obstruction.
• This trapped air is gradually absorbed into the blood flowing through the pulmonary capillaries.
• Absorption usually occurs within minutes to hours.

If the Lung Is Pliable (Flexible)

• If the lung tissue is soft and flexible, the alveoli simply collapse after the trapped air is absorbed.
• This produces atelectasis.

If the Lung Is Rigid

• If the lung is stiff because of fibrotic tissue, it cannot collapse easily.
• As the trapped air is absorbed:
  • Very negative pressure develops inside the alveoli.
  • This negative pressure pulls fluid from the pulmonary capillaries into the alveoli.
• Consequently, the alveoli become completely filled with edema fluid.
• When an entire lung collapses, this condition is called massive collapse of the lung.

Effects of Massive Atelectasis on Pulmonary Function

(Fig. 43.7 given above )

1. Collapse of Alveoli

• The collapsed lung tissue closes the alveoli, preventing ventilation.

2. Increased Pulmonary Vascular Resistance

• Lung collapse compresses and folds the pulmonary blood vessels.
• This increases resistance to blood flow through the affected lung.
• In addition:
  • Hypoxia in the collapsed alveoli causes pulmonary vasoconstriction.
• Therefore, pulmonary vascular resistance increases even further.

3. Blood Flow Is Redirected

• Because vascular resistance increases, much less blood flows through the collapsed lung.
• Most of the blood is redirected to the healthy, ventilated lung.
• This helps maintain better oxygenation.
• In the example shown in Fig. 43.7:
  • Five-sixths of the blood flows through the ventilated lung.
  • Only one-sixth flows through the collapsed (unventilated) lung.

4. Ventilation–Perfusion Relationship

• Although one lung receives no ventilation, most blood is diverted to the functioning lung.
• Therefore:
  • The overall ventilation–perfusion (V̇A/Q̇) ratio is only moderately reduced.
  • Arterial oxygen saturation decreases only slightly (mild O₂ desaturation) despite complete collapse of one lung.

KEY CONCEPT

• Atelectasis is the collapse of alveoli and may involve part of a lung or an entire lung.
• The two major causes are complete airway obstruction and lack of surfactant.
• Airway obstruction allows trapped air to be absorbed into the blood, leading to alveolar collapse within minutes to hours.
• If the lung is rigid and cannot collapse, negative alveolar pressure draws fluid into the alveoli, producing pulmonary edema.
• Massive atelectasis increases pulmonary vascular resistance because lung collapse compresses blood vessels and hypoxia causes pulmonary vasoconstriction (Fig. 43.7). (given above )
• Most blood is redirected to the normal lung (about five-sixths), while only one-sixth passes through the collapsed lung.
• As a result, the overall V̇A/Q̇ ratio is only moderately impaired, and arterial oxygen desaturation is usually mild despite complete collapse of one lung.

LACK OF SURFACTANT AS A CAUSE OF LUNG COLLAPSE

Normal Role of Surfactant

• Surfactant is secreted by special alveolar epithelial cells.
• It is released into the fluid lining the inner surface of the alveoli.
• Surfactant reduces the surface tension of alveolar fluid by 2–10 times.
• By lowering surface tension, surfactant helps keep the alveoli open during breathing.
• Therefore, surfactant plays a major role in preventing alveolar collapse.

Surfactant Deficiency

• In some conditions, the amount of surfactant produced by the alveoli is greatly reduced.
• One important example is hyaline membrane disease, also called respiratory distress syndrome (RDS).
• This condition commonly occurs in premature newborn infants.
• Because too little surfactant is present:
  • Surface tension of the alveolar fluid becomes several times higher than normal.
  • The alveoli have a strong tendency to collapse (atelectasis).
  • The alveoli may also fill with fluid.

Effects of Surfactant Deficiency

• Large portions of the lungs may collapse (atelectasis).
• As more alveoli collapse:
  • Ventilation decreases markedly.
  • Gas exchange becomes severely impaired.
  • The infant develops severe respiratory distress.
• Without treatment:
  • Many premature infants die from suffocation because large areas of the lungs become atelectatic.

Treatment

• Survival of premature infants has improved greatly with:
  • Surfactant replacement therapy.
  • Assisted mechanical ventilation.
  • Administration of corticosteroids before birth.
  • Other supportive treatments.
• Despite these advances, hyaline membrane disease remains an important cause of illness (morbidity) and death (mortality) in premature infants.
• The more premature the infant, the more severe the respiratory distress.

KEY CONCEPT

• Surfactant is produced by alveolar epithelial cells and lines the inner surface of the alveoli.
• It reduces alveolar surface tension by 2–10 fold, helping to prevent alveolar collapse.
• Surfactant deficiency occurs in hyaline membrane disease (respiratory distress syndrome), especially in premature newborns.
• Without adequate surfactant, surface tension increases, causing alveolar collapse (atelectasis) and fluid accumulation.
• Severe surfactant deficiency leads to respiratory distress, impaired gas exchange, and may cause death if untreated.
• Surfactant therapy, assisted ventilation, and antenatal corticosteroids have significantly improved survival, although the disease remains a major cause of morbidity and mortality in preterm infants.

Made by self learning Dr sheen