Respiratory System: mechanics of breathing, neural control (lecture 14)

Mechanics of Breathing and Neural Control

• Chapter 22 focuses on the mechanics of breathing and neural control of the respiratory system.

Objectives

• Describe the roles of muscles in breathing.
• Identify brainstem centers that control breathing.
• Explain how pressure gradients influence breathing.
• Explain how pressure gradients are produced.
• Describe sources of respiratory resistance.
• Explain the significance of dead space to ventilation.

Pulmonary Ventilation

• Pulmonary ventilation involves the repetitive cycle of inspiration (inhaling) and expiration (exhaling).

• One complete breath (in and out) is termed a respiratory cycle.

• The only muscle in the lungs is smooth muscle in the walls of the bronchioles. This muscle adjusts the diameter of the airway and affects the speed of airflow; it does not create airflow.

  • Blood vessels

• The recruitment of muscles, including the diaphragm and intercostal muscles, help to expand and contract the chest cavity, which in turn changes the pressure inside the lungs and drives air in and out.

• Diaphragm

  • The diaphragm is the prime mover, responsible for producing about 2/3 of airflow.
  • Stimulation of the diaphragm pulls it down, increasing thoracic volume.
  • Relaxation of the diaphragm results in recoil, decreasing thoracic volume.

Other Muscles (non-diaphragm)

• Intercostals
  • The intercostals stiffen the thoracic cage during inhalation to prevent collapsing and pull ribs upwards, expanding the cavity.
  • Involved in transverse and anteroposterior dimension changes
    • transverse dimension: lateral expansion of the thoracic cavity, helping to create more space for the lungs to fill with air
    • anteroposterior dimension: forward and backward expansion of the thoracic cavity, allowing the lungs to expand further, facilitating a greater volume for air intake
  • Contribute about 1/3 of airflow.
  • Intercostals also assist with forced expiration by pushing ribs downward.
• Accessory Muscles
  • usually involved with forced breathing.
  • Erector Spinae arches the back.
  • Pectoralis major and minor lift the ribs.
    • erector spinae and pectoralis major/minor increases the volume of the chest cavity
    • Rectus abdominis and other abdominal muscles aid in breathing.

Normal Expiration

• Normal expansion is an energy-saving passive process achieved by:
  • Lung elasticity.: these structures recoil when the muscles relax
    • Bronchial tree
    • Rib attachments
    • Tendons of muscles
• Braking action - occurs during expiration.
  • the only muscular effort involved in normal expiration
  • Muscles gradually relax, preventing the lungs from recoiling too suddenly.
  • This makes a smooth transition from inspiration to expiration.

Abdominal Pressure

• Thoracic pressure can influence the abdomen.
• Diaphragm depression raises abdominal pressure to help expel contents of abdominal organs.
  • Examples: urination, defecation, childbirth, and vomiting.
• The Valsalva maneuver involves taking a deep breath, holding it, and contracting abdominal muscles to push the organ contents out.

Brain Respiratory Centers

1. Ventral Respiratory Group (VRG)

• The location of the VRG is in the medulla oblongata.
• VRG uses a reverberating circuit.
• Inspiratory (I) neurons stimulate the phrenic nerve and costal nerves, which contract the diaphragm and intercostal muscles
• Expiratory (E) neurons inhibit I neurons, leading to recoil.
• The I circuit issues signals to the spinal cord (SC) integration center to the phrenic nerve, which leads to the diaphragm and the intercostal nerves, which lead to external intercostal muscles. Contraction of these muscles enlarges the thoracic cage and causes inspiration.
• Eupnea: normal quiet breathing that operates at 12 breaths/min.

2. Dorsal Respiratory Group (DRG)

• Present and active during quiet breathing
• Located in the medulla oblongata.
• DRG activity modifies the basic respiratory rhythm set by the VRG.
• This is done by integration of sensory information from chemoreceptors (medulla oblongata, arteries), stretch receptors (airways), and brainstem centers for emotional pathways.
• DRG output affects the VRG, changing the respiratory rhythm to adapt to varying conditions.

3. Pontine Respiratory Group (PRG)

• Located on each side of the pons.
• PRG receives sensory input from the hypothalamus, limbic system, and cerebral cortex.
• PRG relays information and output to the VRG and DRG centers in the medulla oblongata.
• PRG regulates short/long and shallow/deep breaths and adapts to conditions like sleep, exercise, and emotions (breathing during crying, laughing, etc.)

Input to Respiratory Centers

Central Chemoreceptors

• Brainstem neurons that monitor CSF pH.

Peripheral Chemoreceptors

• Peripheral chemoreceptors are located in carotid arteries (via glossopharyngeal nerves) and aortic arteries (via vagus nerves).
• Peripheral chemoreceptors monitor oxygen and carbon dioxide levels and pH in the blood.
• Information is then sent into the DRG, triggering changes in rate and depth of breathing to enhance oxygen intake, expel more carbon dioxide from the body, or restore normal acid-base balance.

Stretch Receptors

• Stretch receptors are located in smooth muscle of the visceral pleura and the bronchi & bronchioles.
  • Stretch receptors respond to inflation of the lungs.
  • Signals are sent via vagus nerves to the DRG.
• The inflation reflex is triggered by excessive inflation. In this situation, the I neurons are inhibited and stop inhalation
  • This protective somatic reflex strongly inhibits the I neurons, stopping inspiration and is important during vigorous exercise or taking deep breaths
  • Inflation Reflex in Infants
    • In infants, Inflation reflex may be a normal mechanism of transition from inspiration to expiration, but after infancy it is activated only by extreme stretching of the lungs

Irritant Receptors

• Irritant receptors are nerve endings located among epithelial cells.
• They respond to smoke, dust, pollen, fumes, cold, and mucus levels.
• The signals are sent via the vagus nerve signal to the DRG.
  • The DRG signals respiratory and bronchial muscles.
    • This results in reflexes like bronchoconstriction, shallower breathing, breath-holding (apnea), or coughing.

Voluntary Control

• Voluntary control originates in the cerebral motor cortex, which sends signals via the corticospinal tract to spinal cord (SC) integration centers, bypassing brainstem centers.
• It is impossible to hold one's breath until death. Holding your breath raises the CO2 level of the blood until the brainstem overrides you by forcing the body to breathe.

What Determines Airflow?

• Pressure and resistance.

Pressure, Airflow

• Atmospheric pressure is the weight of the air above us, while intrapulmonary pressure is the pressure within the lungs.

• Boyle's Law drives inspiration.

  • Pressure of gas is inversely proportional to volume.

• Air flows down concentration (pressure) gradient

• During inhalation:

  • Intrapulmonary pressure is less than atmospheric pressure, allowing air to flow into the lungs.

• e.g. Inspiration

  • Ribs and pleura expand outward, which causes pressure to decrease within the alveoli (Boyle's Law).
  • Air flows from high to low (pressure gradient) into alveoli

• If the lungs contain a quantity of gas and lung volume increases, their internal pressure falls.

• Conversely, if lung volume decreases, intrapulmonary pressure rises

Pneumothorax

• The presence of air in the pleural cavity.
• This happens because the thoracic wall is punctured.
• Inspiration sucks air through the puncture wound, which causes pleurae to separate.
  • Negative interpulmonary pressure can't be established, so the lung collapses.

Resistance to Airflow

• Resistance to airflow is affected by:
  • Diameter of bronchioles: dilation or constriction.
  • Pulmonary Compliance: How easily the lungs expand.

Bronchiole Diameter

• Bronchiole diamater is reduced (bronchoconstriction) or expanded (bronchodilation) and can be controlled by hormones like epinephrine & norepinephrine, which stimulates bronchodilation, or histamine, acetylcholine, cold temperature, & irritants, which stimulates bronchoconstriction.
• Many people have suffocated from extreme bronchoconstriction brought on by anaphylactic shock or asthma

Pulmonary Compliance

• High compliance (flexibility) causes decreased resistance and vice versa.
• Diseases such as tuberculosis and black lung disease cause scar tissue, which stiffens the lungs and reduces this compliance.

Surface Tension

• The thin water layer on the respiratory membrane creates potential for maintaining ventilation.

Water Attraction

• Water is attracted to other water molecules by hydrogen bonds, creating surface tension.
• Without surfactant, water attraction can cause walls of small airways (bronchioles and alveolar ducts) to collapse

Surfactant

• Surfactant is a solution to this problem that reduces surface tension.(examples: soap and detergent)
  • It does this by disrupting H-bonds.
• Deep breathing spreads surfactant in smaller airways.
  • Patients recovering from surgery are encouraged to breath deeply even in order to promote this spreading and prevent the lungs from collapsing.

Alveolar Ventilation

• Alveolar ventilation involves the actual movement of air into and out of alveoli.
• Key Features:
  • Anatomic Dead Space: Conducting zone where no gas exchange occurs (About 150 ml of inhaled air.)
  • Physiological Dead Space: Total dead space (includes pathological dead space)
  • Alveolar Ventilation Rate (AVR): Rate at which air moves in and out of the alveoli
    • Resistance: high at terminal bronchioles.
    • How does gas move into and out of the alveoli?
      • oxygen completes its journey to the alveoli, and carbon dioxide leaves them by simple diffusion
  • Residual volume
    • the lungs never completely empty during expiration
      • the leftover air is called residual volume
    • it cannot be exhaled even with maximum effort
    • It gets mixed with fresh incoming air and takes 18 average breaths to replace all the pulmonary air.
    • result if you could exhale it?
      • decreased gas exchange
      • potentially collapsed lungs
      • increase the workload of breathing
        • causing respiratory distress