Physiology of the Respiratory System: Structured Study Notes

Topic 6B – Physiology of the Respiratory System

6.3 Intrapulmonary, Intrapleural, and Transpleural Pressures

The movement of air in and out of the lungs (pulmonary ventilation) is driven by pressure differences between the atmosphere, alveoli, and pleural cavity.

• Atmospheric Pressure: Pressure exerted by air around the body (typically 760 mm Hg at sea level).

• Intrapulmonary Pressure: Pressure within the alveoli; rises and falls with breathing but always equalizes with atmospheric pressure.

• Intrapleural Pressure: Pressure within the pleural cavity; typically about 4 mm Hg less than intrapulmonary pressure, due to lung recoil, surface tension of alveolar fluid, and chest wall elasticity. This negative pressure prevents lung collapse.

• Transpleural (Transpulmonary) Pressure: The difference between intrapulmonary and intrapleural pressures. $P_{tp} = P_{pul} - P_{ip}$

Example: If intrapulmonary pressure is 760 mm Hg and intrapleural pressure is 756 mm Hg, then transpulmonary pressure is 4 mm Hg.

6.4 Roles of the Diaphragm & Accessory Muscles During Inspiration and Expiration

Breathing involves changes in thoracic cavity volume, primarily through the action of the diaphragm and intercostal muscles.

• Diaphragm: Contracts to increase thoracic cavity height, lowering pressure and drawing air in.

• Intercostal Muscles: Contract to lift the rib cage and pull the sternum forward, increasing thoracic diameter.

• Boyle’s Law: $P_1 V_1 = P_2 V_2$ (Pressure and volume are inversely related in a closed system).

• Quiet Inspiration: Diaphragm and intercostals contract, increasing lung volume by ~0.5 L and dropping intrapulmonary pressure by ~1 mm Hg.

• Quiet Expiration: Passive process relying on elastic recoil of lungs.

• Forced Inspiration/Expiration: Accessory muscles (neck, chest, abdominal wall) further increase or decrease thoracic volume for deep or forceful breathing.

6.5 Factors Influencing Pulmonary Ventilation

Pulmonary ventilation is affected by resistance, alveolar surface tension, and lung compliance.

6.5.1 Resistance

• Gas Flow: Determined by pressure gradient and resistance ($\text{Flow} = \frac{\Delta P}{R}$).

• Airway Diameter: Resistance is lowest in large airways and highest in medium-sized bronchi.

• Neural Influences: Parasympathetic stimulation constricts bronchioles; sympathetic stimulation dilates them.

• Pathological Factors: Mucus, inflammation, and tumors increase resistance.

6.5.2 Alveolar Surface Tension

• Surface Tension: Molecules at a gas/liquid boundary are attracted to each other, creating tension at the liquid surface.

• Surfactant: A detergent-like lipoprotein produced by type II alveolar cells reduces surface tension, preventing alveolar collapse.

• Clinical Note: Infant respiratory distress syndrome (IRDS) results from insufficient surfactant production.

6.5.3 Lung Compliance

• Definition: The ease with which lungs can be distended.

• Formula: $C_L = \frac{\Delta V_L}{\Delta P}$

• Determinants: Distensibility of lung tissue and alveolar surface tension.

• Factors Reducing Compliance: Fibrosis, increased surface tension, and reduced chest wall flexibility.

6.6 Measurement and Significance of Lung Volumes and Capacities

Lung volumes and capacities are measured to assess respiratory health and function.

Respiratory Volumes

• Tidal Volume (TV): ~500 ml; air moved during quiet breathing.

• Inspiratory Reserve Volume (IRV): ~3100 ml; air forcibly inspired after tidal inspiration.

• Expiratory Reserve Volume (ERV): ~1200 ml; air forcibly expired after tidal expiration.

• Residual Volume (RV): ~1200 ml; air remaining after forceful expiration.

Respiratory Capacities

• Inspiratory Capacity (IC): TV + IRV (~3600 ml).

• Functional Residual Capacity (FRC): ERV + RV (~2400 ml).

• Vital Capacity (VC): TV + IRV + ERV (~4800 ml).

• Total Lung Capacity (TLC): TV + IRV + ERV + RV (~6000 ml).

6.7 Dead Space and Alveolar Ventilation

Dead space refers to air that does not participate in gas exchange.

• Anatomic Dead Space: ~150 ml; air in conducting airways.

• Alveolar Dead Space: Air in non-functional alveoli.

• Total Dead Space: Anatomic + alveolar dead space.

• Alveolar Ventilation Rate (AVR): Measures effective ventilation. $\text{AVR} = \text{frequency (breaths/min)} \times (\text{TV} - \text{dead space})$

• Clinical Note: Increasing tidal volume is more effective for increasing AVR than increasing respiratory rate.

Table: Effects of Breathing Rate and Depth on Alveolar Ventilation

Breathing Pattern	Dead Space (ml)	Tidal Volume (ml)	Respiratory Rate	Minute Ventilation (ml/min)	Alveolar Ventilation (ml/min)	% Effective Ventilation
Normal rate and depth	150	500	12	6000	4200	70%
Slow, deep breathing	150	1000	6	6000	5100	85%
Rapid, shallow breathing	150	250	24	6000	2400	40%

6.8 Non-Respiratory Air Movements

Several reflexes and voluntary actions produce air movements not related to gas exchange.

• Hiccups: Spasms of the diaphragm; irritation of the phrenic nerve.

• Yawn: Deep inspiration ventilating all alveoli.

• Cough: Protective reflex; blast of air to clear lower respiratory tract.

• Sneeze: Protective reflex; air forced through nasal cavity to clear upper respiratory tract.

6.9 Dalton’s Law and Composition of Atmospheric & Alveolar Air

Dalton’s Law states that the total pressure exerted by a mixture of gases is the sum of the pressures exerted by each gas independently.

• Equation: $P_{total} = P_1 + P_2 + P_3 + \ldots$

• Atmospheric Air: Mostly nitrogen (N2), oxygen (O2), carbon dioxide (CO2), and water vapor (H2O).

• Alveolar Air: Contains more CO2 and H2O, less O2 than atmospheric air due to gas exchange and humidification.

Gas	% in Atmosphere	PP (mm Hg)	% in Alveoli	PP (mm Hg)
N2	78.6	597	74.9	569
O2	20.9	159	13.7	104
CO2	0.04	0.3	5.2	40
H2O	0.46	3.7	6.2	47

6.11 Factors Influencing Gas Exchange at the Lungs (External Respiration)

Gas exchange in the lungs depends on partial pressure gradients, gas solubility, membrane structure, and ventilation-perfusion coupling.

• Partial Pressure Gradients: O2 has a steep gradient (104 mm Hg in alveoli vs. 40 mm Hg in blood); CO2 gradient is less steep but CO2 is more soluble.

• Structural Characteristics: Thin respiratory membrane (0.5–1 μm) and large surface area (~140 m2).

• Ventilation-Perfusion Coupling: Local regulation matches air flow to blood flow; arterioles and bronchioles adjust diameter based on PO2 and PCO2.

6.12 Partial Pressure Gradients at the Tissues (Internal Respiration)

Internal respiration involves diffusion of gases between blood and tissues, driven by partial pressure gradients.

• In Tissues: PO2 < 40 mm Hg, PCO2 > 45 mm Hg.

• In Systemic Arteries: PO2 = 104 mm Hg, PCO2 = 40 mm Hg.

• Diffusion: O2 moves into tissues; CO2 moves into blood.

6.13 Transport of Oxygen in the Blood

Oxygen is transported in blood primarily bound to hemoglobin within red blood cells, and to a lesser extent dissolved in plasma.

• Oxyhemoglobin: $\text{HbO}_2$

• Reduced Hemoglobin: $\text{HHb}$

• Equation: $\text{HHb} + O_2 \rightleftharpoons \text{HbO}_2 + H^+$

• Hemoglobin Structure: Four polypeptide chains, each with an iron-containing heme group.

• Affinity for O2: Depends on PO2, temperature, pH, PCO2, and BPG.

6.14 Oxygen-Hemoglobin Dissociation Curve

The relationship between PO2 and hemoglobin saturation is sigmoidal, reflecting cooperative binding.

• Steep Slope: At PO2 10–50 mm Hg, small changes in PO2 cause large changes in saturation.

• Plateau: At PO2 70–100 mm Hg, hemoglobin is nearly fully saturated.

• Venous Reserve: Only about 25% of O2 is released to tissues during one pass; the rest is available for increased demand.

6.15 Factors Affecting Hemoglobin Saturation

• Bohr Effect: Increased CO2 and H+ weaken the Hb-O2 bond, promoting O2 release in tissues.

• Temperature: Higher temperature promotes O2 unloading.

• BPG: Produced by RBCs during glycolysis, decreases Hb affinity for O2.

6.16 Transport of Carbon Dioxide in the Blood

• Dissolved in Plasma: ~7–10% of CO2.

• Bound to Hemoglobin: ~20–30% as carbaminohemoglobin (CO2 binds to amino acids, not heme).

• Bicarbonate Ion: ~60–70% converted to HCO3- in RBCs via carbonic anhydrase. $\text{CO}_2 + \text{H}_2\text{O} \rightleftharpoons \text{H}_2\text{CO}_3 \rightleftharpoons \text{HCO}_3^- + \text{H}^+$

• Haldane Effect: Deoxygenated hemoglobin binds CO2 more readily.

6.17 Control of Respiration

Respiratory rate and depth are regulated by neural and chemical mechanisms.

• Medullary Respiratory Centers: Ventral and dorsal respiratory groups coordinate rhythm and integration.

• Chemoreceptors: Central (medulla) and peripheral (carotid and aortic bodies) detect changes in CO2, O2, and pH.

• CO2: Most potent regulator; increased CO2 (hypercapnia) stimulates increased ventilation.

• O2: Significant only when PO2 drops below 60 mm Hg.

• Hering-Breuer Reflex: Stretch receptors prevent over-inflation of lungs.

• Higher Brain Centers: Voluntary control (cortex), emotional responses (hypothalamus).

6.21 Respiration During Intense Exercise

Exercise increases O2 consumption and CO2 production, leading to increased respiratory rate and depth (hyperpnea).

• Hyperpnea: Increased ventilation in response to metabolic demand, not triggered by changes in PO2 or PCO2 initially.

• Mechanisms: Neural input from motor cortex, proprioceptors, and chemical changes in blood.

• Venous Blood: PO2 and PCO2 remain relatively constant due to efficient gas exchange.

Additional info: These notes are based on college-level Anatomy & Physiology content, specifically covering the physiology of the respiratory system as outlined in standard textbooks.