Oxygenation and Gas Exchange

Oxygenation

• Oxygenation is adding oxygen to any chemical or physical system.
• Three important processes involved in oxygenating the body are ventilation, transport, and perfusion.
• Ventilation is inhaling oxygen and exhaling carbon dioxide.
• Transport is hemoglobin's ability to carry oxygen from alveoli to cells and carbon dioxide from cells to alveoli.
• Perfusion is blood's ability to transport oxygenated hemoglobin to the cells and return carbon dioxide-laden cells to the alveoli.

Gas Exchange

• Gas exchange is the process by which oxygen is transported to cells and carbon dioxide is transported from the cells.
• It requires interaction among the neurologic, respiratory, and cardiovascular systems.

Neural Control of Respiration

• Neural control of respiration involves: generating "quiet breathing" with inspiration/expiration rhythm, regulating the magnitude of ventilation, and modifying respiratory activity.
• Respiratory activity can be modified voluntarily, like breath control for speech, or involuntarily, like coughing.

Respiratory Rhythm and Rate

• Unlike cardiac muscle, respiratory muscles are skeletal, contracting only when stimulated.
• Rhythmic breathing patterns are established in the brain, not the lungs or respiratory muscles.
• Neural signaling mechanisms help maintain breathing rate and adjust to changes in O2 and CO2 levels.
• Respiratory activity is subject to voluntary modification.
• Rhythmic quiet breathing occurs due to alternate contraction and relaxation of inspiratory muscles (mainly diaphragm and external intercostal).
• Respiratory centers that innervate these are located in the pons and medulla.

Medullar Control Centers

• The dorsal respiratory group contains inspiratory neurons and receives afferent signals from chemoreceptors, sending impulses to the diaphragm and intercostal muscles.
• The ventral respiratory group contains both inspiratory and expiratory neurons.
• The ventral respiratory group is inactive during quiet breathing and activated during increased ventilator effort.

Pons Control Centers

• These centers perform “fine-tuning” activity, modifying depth and rate set by the dorsal & ventral respiratory groups.
• The pneumotaxic center helps limit the duration of inspiration.
• The apneustic center acts as a balance by keeping inspiratory neurons active.

Magnitude of Ventilation

• Goal of respiratory activity is for consistent arterial blood PO2 and PCO2, regardless of O2 extracted from blood or CO2 added.
• Blood gas content is precisely regulated
• The maintenance of a normal range is achieved by varying the magnitude of ventilation
• Increased O2 extraction/CO2 removal causes increased ventilation, bringing in more fresh O2 and blowing off more CO2.

Increasing Ventilation

• Bodily requirements for gas exchange are communicated to the medullary respiratory center from several pathways.
• The two most obvious signals for increased ventilation are decreased arterial PO2 and increased arterial PCO2.
• Increased levels of H+ influence the level of activity.
• Arterial PO2 is monitored by peripheral chemoreceptors, while PCO2 is monitored by central chemoreceptors.

Peripheral Chemoreceptors

• Peripheral chemoreceptors are in the carotid and aortic bodies.
• Peripheral chemoreceptors respond to changes in chemical content of arterial blood
• Peripheral chemoreceptors differ from baroreceptors, which respond to changes in pressure, in the same areas.
• Peripheral chemoreceptors aren't sensitive to minor PO2 changes.
• Peripheral chemoreceptors play a minor role except as an emergency mechanism for dangerously low PO2 ( < 60 mm Hg).
• PCR respond to PO2, not total O2 content of blood (only dissolved O2 contributes to PO2 )
• If O2 -carrying Hgb is reduced, arterial O2 levels may fall to emergent levels without stimulation of PCR.

Central Chemoreceptors

• PCO2 is the most important regulator of the magnitude of ventilation at rest.
• The central chemoreceptors are located in the medulla, near the respiratory center.
• Central chemoreceptors do not monitor CO2 directly but are sensitive to changes in CO2-induced H+ concentration in the ECF of the brain.
• The blood-brain barrier is permeable to CO2
• Any increase in arterial PCO2 triggers receptors causing CO2 to combine with H2O, resulting in an increased H+ concentration.
• Increased H+ activates central chemoreceptors to stimulate increased ventilation.
• Excess CO2 is blown off, and levels of CO2 in the brain return to normal.

Exercise and Ventilation

• Alveolar ventilation may increase up to 20 times during strenuous exercise.
• The mechanisms of this increased ventilation are not well understood.
• Increased alveolar ventilation means PO2 does not decrease despite increased O2 use during exercise.
• It also means PCO2 does not increase (or may decrease) because extra CO2 is removed by increased ventilation.
• H+ concentration is constant because H+ generating CO2 is constant.
• In heavy exercise, some increase in H+ results from increased release of lactic acid (anaerobic metabolism) but is not enough to account for an increase in ventilation.

Mechanical Receptors

• Stretch receptors in the lungs respond to mechanical signals to prevent over-inflation, in addition to neural receptors that respond to the blood's chemical changes.
• Stretching with large tidal volumes activates and inhibits inspiratory neurons in the DRG.

Other factors

• Protective mechanisms, such as sneezing or coughing, govern respiratory mechanisms to expel irritant materials from respiratory passageways.
• Pollen in the nose sends a signal down the trigeminal nerve (CN5) to sneeze.
• Smoke in the lungs triggers a vagal nerve (CN10) response to cough.
• The respiratory center is reflexively inhibited during swallow when the airway is closed to prevent material entering the lungs.
• Hiccups occur with spastic contractions of the diaphragm, wherein rapid air intake is stopped by closure of the glottis; its underlying mechanism is unknown.

Neurotransmitters

• Two neurotransmitters communicate within the autonomic nervous system: acetylcholine and norepinephrine.
• Acetylcholine is secreted by cholinergic nerve fibers.
• Norepinephrine is secreted by adrenergic nerve fibers.
• Acetylcholine generally has parasympathetic effects.
• Norepinephrine generally has a sympathetic effect.
• Acetylcholine has some sympathetic effect, including increased sweat.

Adrenergic effects

• Increased heart rate and force of contraction
• Vasoconstriction
• Bronchodilation
• Decreased gastric secretion and motility
• Inhibition of insulin/stimulation of glucagon

Cholinergic effects

• Decreased heart rate and force of contraction
• Bronchoconstriction
• Increased gastric secretion and motility
• Stimulates pancreatic secretion

Response to Innervation in Ventilation

• Signals from the respiratory center innervate the phrenic nerve.
• The phrenic nerve stimulates the diaphragm to contract.
• When the diaphragm contracts it moves down, making the thoracic cavity larger.
• The external intercostal muscles contract to raise the ribs.
• This increases the circumference of the thoracic cavity.

Boyle’s Law

• When the volume of a container increases, pressure decreases; when volume decreases, pressure increases.

Ventilation and Pressure

• With the increased volume of the thoracic cavity, there is a corresponding decrease in pressure.
• Air moves from the area of higher pressure (the atmosphere) to an area of lower pressure (the lungs).
• Exhalation occurs when the phrenic nerve stimulus stops, and the diaphragm relaxes and moves up in the chest.
• As volume decreases, intrapulmonary pressure increases; therefore, air flows from the lungs to the lower atmosphere.
• Elastic fibers in the lungs recoil.

Forced Expiration

• Contraction of abdominal wall muscles, especially the oblique and transversus, increases intra-abdominal pressure, forcing the diaphragm superiorly.
• Depressing the rib cage decreases thoracic volume with help from internal intercostals and the latissimus dorsi.

Lung volume and capacity

• The amount of air that can be moved into and out of the lungs
• Compliance: the ability of lung tissue to expand
• Ventilation/Perfusion Match
• Resistance to airflow

Lung Volumes

• Tidal Volume: Air that moves in or out of the lungs during a normal breath.
• Inspiratory Reserve Volume: Additional air that is forcefully inhaled following a normal inhalation.
• Expiratory Reserve Volume: Additional air that is forcefully exhaled following a normal exhalation.
• Residual Volume: Air remaining in the lungs even after a forceful exhalation.
• Vital Capacity: Air that is forcefully exhaled after the deepest inhalation possible.
• Total Lung Capacity: the total amount of air the lungs can hold.

Residual Volume

• It helps keep the alveoli from collapsing at the end of expiration.
• Having too low alveolar pressures can lead to alveolar collapse (atelectasis).
• Trapped air in the lungs increases residual volume, leading to decreased tidal volumes, and being an obstruction to inhalation.
• High Residual Volume eventually diminishes the inspiratory reserve volume.

Compliance

• Compliance is the ease with which the chest wall, lungs, and alveoli can be distended during inflation.
• When the alveoli fill with air during inspiration, they fill and expand to take in adequate tidal volumes.
• Surface tension is the tendency for liquid molecules to adhere to one another at the liquid-air interface.
• Surfactant is a detergent-like compound that reduces surface tension by reducing the affinity of water molecules for each other at the air-liquid interface; easier for lungs to inflate.
• Surfactant decreases surface tension in the lungs by up to 50%.
• Without surfactant, all of the alveoli in our lungs would collapse as we could not generate enough inspiratory force to expand them.

Alveolar Compliance

• Low compliance means increased work of breathing
• High compliance means decreased work of breathing
• Person who is very compliant gives in easily, non-compliant will give you resistance.

Decreasing Alveolar Compliance

• Pulmonary Edema means fluid build-up outside can resist alveolar expansion.
• Edema can cause fluid seepage into the alveolus, diluting surfactant.
• Pulmonary Fibrosis or Scarring occurs with inflammation.
• Collagen accumulates in the lung interstitium.
• Collagen doesn't stretch making it hard to expand the alveoli.
• Reduced surfactant, such as prematurity, or injury to type II cells.

Increasing Alveolar Compliance

• Increased surfactant theoretically results in increased compliance, not caused by disease or physiological alteration.
• Emphysema is the main disease becoming pathogenic by increasing compliance.

Ventilation and Perfusion

• Ventilation (V) is the volume of air from the environment that is flowing in and out of the lungs per minute (L/min).
• Perfusion (Q) is the flow of blood through the lungs per unit volume of lung tissue.
• The body works hard to ensure the best match between ventilation and perfusion.
• V/Q ratio conceptualizes the match between ventilation and perfusion in the lungs.
• Normal V-Q ratio is 0.8-0.9, perfusion is slightly higher than ventilation.
• The V-Q ratio is close to 1, so often approximated.

V/Q Mismatch

• This is when ventilation or perfusion changes.
• Two scenarios are: decreased alveolar ventilation or decreased pulmonary capillaries' perfusion.
• Body compensates to bring the V-Q ratio back to normal.
• Poor ventilation leads to "shunting" of blood away from the no gas exchange area.
• Lack of blood flow to an area of the lungs leads to “dead space.”

Inadequate Ventilation: Shunt

• Alveolar perfusion is normal, but ventilation is reduced.
• The V/Q ratio is low.
• Airway obstruction or physical defect allows unoxygenated blood to bypass functional alveoli.

Inadequate Perfusion: Alveolar Dead Space

• Normal ventilation, but with reduced alveolar perfusion.
• The V/Q ratio is high.
• It results from perfusion defects, such as pulmonary embolism, or a disorder that decreases cardiac output.