Regulation & Transport of the Respiratory System

Control of Breathing

1. Regulation centers in brain stem. Neurons in medulla oblongata

2. Local chemical controls

Goal is to optimize gas exchange

• Match rate of air and blood flow in lungs

• Link rate and depth of breathing to body’s requirements for O2 uptake and CO2 release

Rhythmical Breathing

Diaphragm and intercostal muscles are skeletal muscles. Will contract with motor neuron stimulation.

Inspiration

Initiated by a burst of APs in spinal motor nerves to inspiratory muscles. APs cease and muscles relax and then expiration occurs. During quiet breathing, there is little muscle contraction/relaxation during expiration

Regulation of Breathing

Basic rhythm of breathing is produced by neurons in the medulla. Medullary respiratory center: Two groups of neurons

1. DRG: dorsal respiratory group

2. VRG: ventral respiratory group

• Centers in pons lead to smooth respiratory movements by modulating medulla signals

• DRG primarily fire during inspiration

• VRG adds to rate and depth of breathing by stimulating forceful exhalation and adding signals to stimulate inhalation

• Surface receptors of medulla monitor CO2 levels in CSF and send signals to interneurons in medulla

• Receptors in carotid and aortic bodies monitor blood pH and O2 in arterial blood and send signals to medulla

DRG

Primarily fires during Inspiration and stimulates the diaphragm

They have input to the spinal motor neurons (phrenic and intercostal nerves) that activate muscles involved with inspiration. Phrenic nerves innervate the diaphragm

VRG

Is active during both inspiration and expiration. Adds to rate and depth of breath and stimulated forceful exhalation and adds to inhalation (exercise). Pacemaker cells and other neurons in upper VRG (Pre-Botzinger complex) comprise respiratory rhythm generator.

Blood Gas Control

Medulla detects changes in CO2 levels:

Detects through peripheral chemoreceptors in carotid and aortic bodies

Also through central chemoreceptors in medulla.

Medullary control centers and pons adjust rate and depth of breathing to compensate for any changes in blood gases

Major Stimuli for Central and Peripheral Chemoreceptors

Peripheral Chemoreceptors:

• Decreased PO2 (hypoxia)

• Increased [H+] (metabolic acidosis)

• Increased PCO2 (respiratory acidosis)

Central Chemoreceptors:

• Increased PCO2 leading to lower pH. CO2 + H2O → H2CO3 → HCO3- + H+

Local Controls

Keeps lung ventilation and perfusion rates consistent.

• If air flow becomes less than capillary blood flow, then O2 levels drop → smooth muscles in lung arterioles contract and reduce blood flow so there is more time for blood to pick up O2.

Gas Transport

Causes by differences in partial pressure.

Dalton’s Law: A gases partial pressure is independent of other gases in the mixture.

• Sum of partial pressures is the total pressure

O2 Transport:

• Partial pressure O2 higher in alveolar air than in capillary blood so O2 diffuses from air to blood

O2 and CO2 Levels

In cells of body tissue: O2 to CO2 40 to 46

At start of veins in body tissue 40 to 46

In pulmonary arteries 40 to 46

Dry inhaled air 160 to 0.3

in alveolar sacs 100 to 40

Moist exhaled air 120 to 27

Pulmonary veins 100 to 40

Start of capillaries in body tissue 100 to 40

Partial Pressure at Sea Level

120mmHg PO2 expired because the air breathed out is only 15.7% O2. 15.7% of 760 is about 120. PCO2 is 27mmHg since it’s only 3.6%.

Air flow is two-way through bronchi and trachea. Fresh air mixed with used air since be don’t expel all the air in our lungs

Air coming in includes some air from dead space. Not all fresh

Hemoglobin

O2 transport. O2 entering the blood combines with hemoglobin in erythrocytes

1 hemoglobin molecule can hold up to 4 O2 molecules so large quantities of O2 can be in the blood

PO2 in blood → % Saturation of Hb

Hb + O2 → HbO2

Lungs have high PO2 so reaction goes right

Binding of O2 to Hb enhanced by cooperativity

In tissues, HbO2 → Hb + O2

PO2 of tissues lower than that in blood and affinity of Hb for O2 is decreased by increased CO2, lower pH, and increased temperatures

Conditions

In alveoli:

• PO2 ~100mmHg and pH is 7.4 so most hemoglobin molecules are 100% saturated with O2.

• Binding of O2 and Hb increases fast and then plateaus starting at the right of the O2-Hb dissociation curve, Hb is 100% saturated at PO2 100mmHg, but only needs PO2 70mmHg to be 100% saturated. Some breathing space

• Drops to 90% by 60mmHg

At Venous:

• Venous PO2 is 40mmHg. Lower affinity for O2 by Hb. 20% unsaturated. Still 80% saturated meaning there is a reserve. More oxygen available than is used by tissue.

Active Tissue:

• Take up oxygen and creates gradient that favors more oxygen release from Hb

• Increases CO2 binding since Hb can bind to CO2

• Drops in pH can result from more CO2 or active muscles producing lactic acid. 7.2

• Contracting muscles generate heat which can lower O2 affinity

CO2 Transfer: Body Tissues

CO2 produced in active tissues diffuse from cells to interstitial fluid and to blood plasma.

PCO2 higher in tissues than blood.

• 10% dissolved in plasma

• 70% converted into H+ and HCO3-

• H+ Combine with hemoglobin or proteins

• 20% combines with hemoglobin

CO2 Transfer: Lungs

PCO2 in lungs is higher in blood than air

• Reactions that pack CO2 are reversed

• CO2 released from blood into alveolar air