Surfactant, hb oxygen dissociation curve , functional residual volume, vital capacity, transport of gases, neural regulation of respiration From guyton only

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Here is the complete Guyton-based coverage of all six topics:

Respiratory Physiology — Guyton & Hall

1. SURFACTANT, SURFACE TENSION, AND COLLAPSE OF THE ALVEOLI

Principle of Surface Tension

Water molecules at the alveolar air-fluid interface have a strong mutual attraction, causing the surface to contract. This tends to force air out of the alveoli and collapse them — producing what is called the surface tension elastic force of the lung.

What Is Surfactant?

Surfactant is a surface-active agent that greatly reduces the surface tension of water lining the alveoli. It is secreted by type II alveolar epithelial cells, which constitute ~10% of the alveolar surface area. These cells contain lipid inclusions that are secreted as surfactant.

Surfactant is a complex mixture of:

Dipalmitoyl phosphatidylcholine (DPPC) — the most important phospholipid
Surfactant apoproteins
Calcium ions

DPPC does not dissolve uniformly in the alveolar fluid; part of its molecule remains on the surface, reducing surface tension to 5–30 dynes/cm (vs. 72 dynes/cm for pure water; 50 dynes/cm for alveolar fluid without surfactant).

Pressure Due to Surface Tension (LaPlace's Law)

Pressure = 2 × Surface tension / Radius of alveolus

For an average alveolus (radius ~100 µm) with normal surfactant → ~4 cm H₂O Without surfactant → ~18 cm H₂O (4.5× greater)

Key point: The smaller the alveolus, the greater the pressure from surface tension. Surfactant prevents small alveoli from collapsing into large ones — it stabilises all alveoli equally by reducing surface tension proportionally more in small alveoli (where surfactant molecules are more compressed and more effective).

2. FUNCTIONAL RESIDUAL CAPACITY (FRC)

Definition

FRC = Expiratory Reserve Volume (ERV) + Residual Volume (RV)

It is the volume of air remaining in the lungs at the end of normal quiet expiration — normally ~2300 mL.

Lung Volumes & Capacities (Summary)

Capacity	Components	Normal Value
Inspiratory Capacity (IC)	TV + IRV	~3500 mL
Functional Residual Capacity (FRC)	ERV + RV	~2300 mL
Vital Capacity (VC)	IRV + TV + ERV	~4600 mL
Total Lung Capacity (TLC)	VC + RV	~5800 mL

Key equations:

FRC = ERV + RV
TLC = IC + FRC

All values are ~20–30% less in women than men, and greater in athletic individuals.

Measurement of FRC — Helium Dilution Method

FRC cannot be measured directly by spirometry (residual volume cannot be expired). The helium dilution method is used:

A spirometer of known volume is filled with air + helium at known concentration
The subject expires normally, then begins breathing from the spirometer
Helium becomes diluted by the FRC gases

FRC = (C_He / C_fHe − 1) × V_spir

Where C_He = initial [He], C_fHe = final [He], V_spir = initial spirometer volume.

3. VITAL CAPACITY

Definition

VC = IRV + Tidal Volume + ERV

The maximum amount of air a person can expel after maximum inspiration — normally ~4600 mL.

Forced Expiratory Vital Capacity (FVC / FEV)

In clinical practice, the forced expiratory vital capacity (FVC) is measured — the person inspires maximally, then expires as forcefully and rapidly as possible into a spirometer.

FEV₁ (forced expiratory volume in 1 second): normally ~80% of the FVC
In obstructive disease (e.g., asthma, emphysema): FEV₁/FVC ratio is reduced
In restrictive disease: both FVC and FEV₁ fall, but ratio may be normal

4. TRANSPORT OF GASES

Transport of Oxygen (O₂)

97% of O₂ is transported bound to hemoglobin in RBCs. Only 3% is dissolved in plasma.

O₂-Hemoglobin Dissociation Curve

(Figure 41.8 — Guyton & Hall)

Key values:

Systemic arterial blood: PO₂ ~95 mmHg → saturation 97% → O₂ content ~19.4 mL/100 mL
Venous blood returning from tissues: PO₂ ~40 mmHg → saturation 75% → O₂ content ~14.4 mL/100 mL
O₂ delivered to tissues per 100 mL = 19.4 – 14.4 = ~5 mL/100 mL blood
Hemoglobin capacity: 15 g/dL × 1.34 mL/g = ~20 mL O₂/100 mL blood (oxygen-carrying capacity)

Shifts in the Dissociation Curve

Rightward shift (↓ affinity, ↑ O₂ release to tissues):

↑ CO₂
↓ pH (acidosis) — Bohr effect
↑ Temperature
↑ 2,3-BPG (biphosphoglycerate)

Leftward shift (↑ affinity, ↑ O₂ loading in lungs):

↓ CO₂, ↑ pH, ↓ temperature, ↓ BPG

Bohr Effect: In tissues, CO₂ and H⁺ shift the curve rightward → O₂ is released. In lungs, CO₂ leaves blood → curve shifts leftward → O₂ is loaded. This doubles O₂ delivery efficiency.

BPG Effect: In chronic hypoxia, ↑ BPG shifts curve rightward → O₂ released at up to 10 mmHg higher tissue PO₂ → important adaptation to hypoxia.

During exercise: CO₂, H⁺, and temperature all rise in muscle capillaries → massive rightward shift → O₂ released even when 70% has already been removed.

Transport of CO₂

CO₂ is transported by 3 mechanisms:

Mechanism	% of Total
As bicarbonate ion (HCO₃⁻) in plasma	~70%
As carbaminohemoglobin (CO₂Hb)	~23%
Dissolved in plasma	~7%

Bicarbonate Transport (Chloride Shift)

In tissue capillaries:

CO₂ enters RBCs → carbonic anhydrase (5000× faster) catalyses: CO₂ + H₂O → H₂CO₃
H₂CO₃ → H⁺ + HCO₃⁻
H⁺ is buffered by hemoglobin
HCO₃⁻ diffuses out into plasma
Cl⁻ enters RBC to maintain electrical neutrality → Chloride Shift (Hamburger shift)

This is reversed in the lungs.

Haldane Effect

When O₂ binds hemoglobin in the lungs (oxygenation), CO₂ is displaced from hemoglobin and released into alveoli. This doubles the amount of CO₂ released in the lungs — complementing the Bohr effect.

Respiratory Exchange Ratio (R)

Normal: R = 0.825 (mixed diet)
Carbohydrates only: R = 1.00
Fats only: R = 0.70

5. NEURAL REGULATION OF RESPIRATION

(Figure 42.1 — Guyton & Hall)

The Respiratory Center

Located bilaterally in the medulla oblongata and pons, divided into three groups:

1. Dorsal Respiratory Group (DRG) — Medulla

Located in the nucleus tractus solitarius (NTS)
Primarily responsible for inspiration and the basic rhythm of respiration
Receives sensory input from peripheral chemoreceptors, baroreceptors, and lung receptors via vagus and glossopharyngeal nerves
Generates the inspiratory ramp signal: starts weakly, builds steadily over ~2 seconds, then cuts off abruptly → elastic recoil produces expiration

Pre-Bötzinger Complex: A small region in the rostral ventral respiratory group with spontaneously firing pacemaker neurons. Critical for generating the basic rhythm — its removal eliminates respiratory rhythm generation.

2. Ventral Respiratory Group (VRG) — Medulla

Contains both inspiratory and expiratory neurons
Quiescent during normal quiet breathing
Activated during forced breathing (exercise) when extra respiratory effort is needed
Expiratory neurons actively contract abdominal and internal intercostal muscles during forced expiration

3. Pneumotaxic Center — Upper Pons

Located in the nucleus parabrachialis
Inhibits inspiration — limits the duration of the inspiratory ramp signal
When strong: shortens inspiration → ↑ respiratory rate
When weak: allows prolonged inspiration → slower rate but deeper breaths
Works together with the apneustic center (lower pons): apneustic center tries to sustain inspiration; pneumotaxic center cuts it off

Chemical Control of Respiration

CO₂ and H⁺ — Direct Central Control

The chemosensitive area (retrotrapezoid nucleus), lying 0.2 mm beneath the ventral medullary surface, is highly sensitive to:

H⁺ ions — direct stimulation (but H⁺ crosses blood-brain barrier poorly)
CO₂ — crosses BBB freely → reacts with water → forms H⁺ → stimulates chemosensitive neurons

CO₂ is the primary driver of respiration. A small rise in PCO₂ (35–75 mmHg range) causes a massive increase in ventilation. pH changes in the normal range (7.3–7.5) have <10% the effect of CO₂.

Important: The stimulatory effect of chronic CO₂ elevation attenuates over 1–2 days as kidneys raise plasma HCO₃⁻, which diffuses into CSF and buffers H⁺ → reduced drive (basis of CO₂ retention in COPD).

O₂ — Peripheral Chemoreceptors

O₂ has virtually no direct effect on the central respiratory center. It acts via peripheral chemoreceptors:

Carotid bodies (at bifurcation of common carotid arteries) — afferents via Hering nerve → glossopharyngeal nerve → DRG
Aortic bodies (along aortic arch) — afferents via vagus → DRG
Chemoreceptor cells = glomus cells (O₂-sensitive; respond through K⁺ channel inhibition)
Strongly stimulated when PO₂ falls below 60 mm Hg (on the steep part of the Hb dissociation curve)

Regulation During Exercise

At the onset of exercise:

Ventilation increases almost immediately — before any blood gas changes
This is due to collateral nerve impulses from the motor cortex to the respiratory center (neurogenic drive)
CO₂ and H⁺ serve as fine-tuning mechanisms to match ventilation precisely to metabolic demands
The neurogenic signal shifts the entire ventilatory response curve upward, maintaining arterial PCO₂ at ~40 mmHg even during heavy exercise

All content sourced from: Guyton and Hall Textbook of Medical Physiology (Guyton & Hall, 9780443111013), Chapters 38, 41, 42

Haemoglobin oxygen dissociation curve from guyton

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