respiratory system - pt 2 1/2

Three ways CO₂ is transported in the blood

(1) Dissolved CO₂ in plasma. (2) Carbaminohemoglobin – CO₂ bound to the globin part of hemoglobin. (3) Bicarbonate (HCO₃⁻) – the major form; formed via CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻.

Role of carbonic anhydrase and the chloride shift

Carbonic anhydrase in RBCs converts CO₂ + H₂O into carbonic acid, which dissociates into H⁺ and HCO₃⁻. HCO₃⁻ exits the RBC in exchange for Cl⁻ (chloride shift), allowing large amounts of CO₂ to be carried as plasma bicarbonate.

Hypoxia

Insufficient O₂ at the tissue level; cells are not getting or using enough oxygen even if blood flow or PO₂ might seem okay.

Hyperoxia

Above-normal arterial PO₂ (greater than ~100 mmHg), usually from breathing high-O₂ gas mixtures. Increases dissolved O₂ but can be toxic at very high levels or long exposure.

Hypercapnia

Excess CO₂ in arterial blood (elevated PCO₂), typically due to hypoventilation. Often leads to respiratory acidosis (increased H⁺, decreased pH).

Hypocapnia

Below-normal arterial PCO₂, usually caused by hyperventilation, which blows off CO₂ faster than it is produced, often causing respiratory alkalosis (decreased H⁺, increased pH).

Effect of hypoventilation on alveolar PO₂ and PCO₂

Hypoventilation decreases alveolar PO₂ (less O₂ brought in and more is used) and increases alveolar PCO₂ (CO₂ not removed efficiently), leading over time to hypoxia and hypercapnia.

Effect of hyperventilation on alveolar PO₂ and PCO₂

Hyperventilation slightly increases or maintains alveolar PO₂ but significantly decreases alveolar PCO₂, causing hypocapnia and possible dizziness or tingling.

Alveolar PO₂ and PCO₂ during exercise

In healthy people, ventilation increases enough during exercise to match the higher O₂ use and CO₂ production, so alveolar and arterial PO₂ and PCO₂ usually stay close to normal.

Two major components of neural control of respiration

(1) Mechanisms that generate the basic rhythm of breathing (alternating inspiration and expiration). (2) Mechanisms that adjust the depth and rate of ventilation to match metabolic needs (rest vs exercise).

Medullary respiratory centers

The medulla contains the dorsal respiratory group (DRG, mainly inspiratory neurons), the ventral respiratory group (VRG, inspiratory and expiratory neurons used in forced breathing), and the pre-Bötzinger complex (pacemaker region that helps generate rhythmic breathing).

Pons respiratory centers – pneumotaxic and apneustic centers

The pneumotaxic center helps switch off inspiration and shapes a smooth rhythm. The apneustic center provides a tonic drive that promotes longer inspiration. Together they fine-tune the basic rhythm from the medulla.

Neural pathway from medulla to diaphragm

Inspiratory neurons (mainly in DRG) send action potentials down the phrenic nerve to the diaphragm. When they fire, the diaphragm contracts and inspiration occurs; when firing stops, the diaphragm relaxes and expiration follows.

Central chemoreceptors – location and stimulus

Central chemoreceptors are in the medulla and sense H⁺ concentration in cerebrospinal fluid. CO₂ from blood diffuses into CSF, is converted to H⁺ and HCO₃⁻, and increased H⁺ stimulates these receptors to increase ventilation.

Peripheral chemoreceptors – location and what they detect

Peripheral chemoreceptors are in the carotid and aortic bodies. They respond mainly to large falls in arterial PO₂, rises in PCO₂, and decreases in pH, sending signals to brainstem centers to adjust breathing.

Overall chemoreceptor control of ventilation

Central and peripheral chemoreceptors work together: increased CO₂ or H⁺ (and very low O₂) stimulates them, which increases respiratory drive; this raises ventilation, lowers PCO₂, and helps stabilize blood gas and pH levels.