Pulmonary Function Flashcards

The Alveoli

• Alveoli are small, balloon-like structures at the end of terminal bronchioles and alveolar ducts.
• Alveolar septa, which are extremely thin layers of tissue, form the walls between neighboring alveoli.
• Each alveolus contains an alveolar space.
• Clusters of alveoli open into alveolar sacs, creating the appearance of tiny bunches of grapes.
• A few alveoli directly open into terminal bronchioles.
• Pores of Kohn, which are holes in the walls of some alveoli, allow communication between adjoining alveoli or alveolar sacs.
• Alveoli serve as the functional units of the lungs and are the primary sites for gaseous exchange
• Inspired gases enter the blood in the pulmonary circulation from the alveolar space, while expired gases leave the pulmonary circulation to enter the alveolar space.
• The gas-blood barrier (or alveolar-capillary barrier) enables rapid gaseous exchange.
• Each alveolus is lined with a thin layer of tissue fluid, essential for gas diffusion, as gases must dissolve in liquid to enter or leave a cell.

Diffusion of Gases Between Gas Phase in Alveoli and Dissolved Phase in Pulmonary Blood

• The partial pressure of each gas in the alveolar respiratory gas mixture forces molecules of that gas into solution in the blood of the alveolar capillaries.
• Gas molecules already dissolved in the blood bounce randomly and some escape back into the alveoli.
• The rate at which they escape is directly proportional to their partial pressure in the blood.

Diffusing Capacity of the Respiratory Membrane

• Defined as the volume of a gas that diffuses through the membrane each minute for a partial pressure difference of 1 mm Hg.

Diffusion of Oxygen from the Alveoli to the Pulmonary Capillary Blood

• Demonstrates diffusion of O_2 between alveolar air and pulmonary blood.
• P{O2} in the alveolus averages 104 mm Hg.
• P{O2} of venous blood entering the pulmonary capillary at its arterial end averages 40 mm Hg.
• The initial pressure difference that causes O_2 to diffuse into the pulmonary capillary is 104 - 40 = 64 mm Hg.
• Blood P{O2} rises rapidly and reaches almost 104 mm Hg by the time the blood has moved one-third of the distance through the capillary.
• The diffusing capacity for CO2 has never been measured because CO2 diffuses through the respiratory membrane so rapidly that the average P{CO2} in the pulmonary blood is not very different from the P{CO2} in the alveoli—the average difference is less than 1 mm Hg.

Diffusion of CO_2 From Peripheral Tissue Cells into Capillaries and From Pulmonary Capillaries into Alveoli

• P{CO2} of the blood entering the pulmonary capillaries at the arterial end: 45 mm Hg.
• P{CO2} of the alveolar air: 40 mm Hg.
• A 5 mm Hg pressure difference causes all the required CO_2 diffusion out of the pulmonary capillaries into the alveoli.
• The P{CO2} of the pulmonary capillary blood falls to almost exactly equal the alveolar P{CO2} of 40 mm Hg before it has passed more than about one-third of the distance through the capillaries.

The Gas–Blood Barrier

• The gas-blood barrier facilitates rapid and efficient gaseous exchange.
• Gases such as oxygen have to diffuse across the gas–blood barrier to reach the blood; carbon dioxide travels in the opposite direction.
• The gas–blood barrier is only 0.5 µm wide and consists of:
  • Alveolar epithelium (type I and type II alveolar cells)
  • Fused membrane of the alveolar epithelial cells and capillary endothelium
  • Vascular epithelium of the pulmonary capillaries (the capillary endothelial cells).
• Gases pass through the plasma, red blood cell wall, and cytoplasm to reach hemoglobin.
• The total surface area of the gas–blood barrier is estimated to be 70–100 {m^2} in the adult man.
• Gaseous exchange occurs via diffusion, driven by gas pressure gradients.
• Alveolar capillaries are thin-walled and lined with capillary endothelial cells.
• Each capillary endothelial cell has a thickness of only 0.1 µm, except in its nuclear region.
• Neutrophils can move between endothelial cells by extravasation.

Factors Involved in the Regulation of Ventilation

• Many factors regulate ventilation, including the rate and depth of breathing.
• The basic rhythm of breathing is established by inspiratory and expiratory respiratory centers in the medulla.
  • The inspiratory center initiates inspiration.
  • During normal, quiet breathing (eupnea), the average respiratory rate (RR) is 12-14 cycles/minute.
  • The inspiratory center always produces active inspiration.
• The expiratory center limits and inhibits the inspiratory center, producing passive expiration.

Respiratory Center

• The dorsal respiratory group generates inspiratory action potentials and sets the basic rhythm of respiration.
• This group is located in the dorsal portion of the medulla and receives input from peripheral chemoreceptors via the vagus and glossopharyngeal nerves.
• The pneumotaxic center, located dorsally in the superior portion of the pons, helps control the rate and pattern of breathing.
• It transmits inhibitory signals to the dorsal respiratory group, limiting inspiration and increasing the respiratory rate.
• The ventral respiratory group, located in the ventrolateral part of the medulla, can cause either expiration or inspiration.
• The ventral respiratory group is inactive during normal quiet breathing but stimulates the abdominal expiratory muscles when higher levels of respiration are required.

Overview of Ventilatory Control

• The strongest stimulant to ventilation is a rise in P{aCO2}, which increases {[H^+]} in cerebrospinal fluid.

Factors That Shift the Oxygen-Hemoglobin Dissociation

• Several factors can displace the dissociation curve.
• When blood becomes slightly acidic (pH decreases from 7.4 to 7.2), the O_2-hemoglobin dissociation curve shifts about 15% to the right.
• An increase in pH from 7.4 to 7.6 shifts the curve a similar amount to the left.
• Shift to right:
  • Increased hydrogen ions
  • Increased CO_2
  • Increased temperature
  • Increased BPG

Respiratory Acidosis

• Characterized by a failure of ventilation and an accumulation of carbon dioxide.
• The primary disturbance of elevated arterial P{CO2} is the decreased ratio of arterial bicarbonate to arterial P{CO2}, which leads to a lowering of the pH.
• Alveolar hypoventilation features respiratory acidosis and hypercapnia.
• To compensate, the kidneys excrete more acid (hydrogen and ammonium) and reabsorb more base (bicarbonate).
• Symptoms:
  • Drowsiness, dizziness, disorientation
  • Muscle weakness, hyperreflexia
• Causes:
  • Respiratory depression (anesthesia, overdose, ICP)
  • Airway obstruction
  • Alveolar capillary diffusion (pneumonia, COPD, ARDS, PE)
• Hypoventilation can lead to hypoxia.
• Other signs:
  • Rapid, shallow respirations
  • Decreased BP
  • Pale to cyanotic skin/mucosa
  • Headache
  • Hyperkalemia
  • Dysrhythmias
• Lab values:
  • pH decreased (<7.35)
  • P{CO2} increased (>48mmHg)