Lung Circulation: Pulmonary and Bronchial (LEC#7)

• Lungs are perfused by two circulations: the pulmonary circulation and the bronchial circulation.

Pulmonary Circulation

• Pulmonary arteries deliver systemic venous blood from the heart to the lungs for oxygenation.
• Pulmonary arteries branch profusely and feed into pulmonary capillary networks.
• Pulmonary veins carry oxygenated blood from the respiratory zones back to the heart.
• The pulmonary circulation is a low-pressure, high-volume system.
• Lung capillary endothelium contains enzymes to act on substances in blood.
• Angiotensin-converting enzyme activates blood pressure hormone in the lungs.

Bronchial Circulation

• Bronchial arteries provide oxygenated blood to the lungs and lung tissue.
• Bronchial arteries arise from the aorta and enter the lungs at the hilum.
• It is part of systemic circulation, and is a high pressure, low volume system.
• Bronchial arteries supply all lung tissue except the alveoli.
• Bronchial veins anastomose with pulmonary veins.
• Pulmonary veins carry most venous blood back to the heart.

Respiratory Physiology

• Pulmonary ventilation consists of two phases: inspiration and expiration.
• Inspiration is when gases flow into the lungs.
• Expiration is when gases exit the lungs.

Pressure Relationships in the Thoracic Cavity

• Atmospheric pressure (Patm) is the pressure exerted by the air surrounding the body
• 760 mm Hg at sea level = 1 atmosphere
• Respiratory pressures are described relative to atmospheric pressure, e.g., a respiratory pressure of -5 mmHg means the pressure is lower than Patm by 5 mm Hg.

Intrapulmonary Pressure

• Intrapulmonary pressure (Ppul) is the pressure in the alveoli.
• It is also called intra-alveolar pressure
• It fluctuates with breathing.
• It always eventually equalizes with atmospheric pressure (Patm).

Intrapleural Pressure

• Intrapleural pressure (Pip) is pressure in the pleural cavity.
• Intrapleural pressure fluctuates with breathing
• It is always a negative pressure (<Patm and <Ppul).
• Pip is usually 4 mm Hg less than Ppul.
• Fluid level must be kept at a minimum to keep lungs inflated.
• Excess fluid is pumped out by the lymphatic system to maintain appropriate functioning.
• Positive Pip pressure causes the lung to collapse.

Additional Notes on Intrapleural pressure (Pip)

• Its pressure is created by two opposing elastic forces: a collapsing force and an expanding force.
• Two inward forces promote lung collapse.
• Lungs' natural tendency to recoil because of elasticity, causing the lungs to try to assume the smallest size.
• Surface tension of alveolar fluid: surface tension pulls on alveoli to try to reduce alveolar size.
• One outward force promotes lung expansion.
• The elasticity of the chest wall pulls the thorax outward.
• The negative Pip is affected by these opposing forces but is maintained by a strong adhesive force between the parietal and visceral pleurae.
• The chest wall pulls outward into the intrapleural space due to forces created by recoil and surface tension.
• The lungs pull inward, tending to separate the visceral and parietal pleurae.
• A negative intrapleural pressure is created that opposes the separation and outward recoil forces of the chest wall and inward recoil forces of the lungs.
• Fluid accumulation in the pleural cavity causes positive Pip.

Pulmonary Ventilation

• It consists of inspiration and expiration.
• It is a mechanical process that depends on volume changes in the thoracic cavity.
• Volume changes lead to pressure changes and are facilitated by muscles.
• Pressure changes lead to the flow of gases to equalize pressure.
• It is determined by Boyle's law.

Boyle's Law

• Boyle's law describes the relationship between pressure and volume of a gas.
• Gases always fill the container they are in.
• If the amount of gas is the same and the container size is reduced, pressure will increase.
• Pressure (P) varies inversely with volume (V) and can be expressed mathematically as P1V1 = P2V2.

Intrapulmonary Pressure

• It is dependent on Boyle's Law.

Clinical Imbalance: Atelectasis

• Atelectasis: lung collapse due to plugged bronchioles, which cause collapse of alveoli, or pneumothorax which introduces air in the pleural cavity.
• Pneumothorax can occur from a wound in the parietal pleura, or rupture of the visceral pleura.
• It is treated by removing air with chest tubes.
• The lungs reinflate when the pleurae heal.
• It is not a pathology, but a condition that describes an incomplete expansion of the lung, or collapse of a previously inflated lung.
• It can occur as a consequence of several respiratory pathologies.

3 main types of atelectasis found in adults:

• Resorption occurs due to incomplete airway obstruction.
• Compression occurs due to the accumulation of transudate, exudate, blood, or air (pneumothorax) in the pleural cavity.
• Contraction is caused by fibrosis that prevents the lungs from fully expanding (attenuated compliance).

Pulmonary Ventilation (At the start of a breath)

• Pressures inside and outside the thorax are identical, so there's no air movement.
• The expanding thoracic cavity expands the lungs.
• Parietal pleura is attached to the thoracic wall, and the visceral pleura is attached to the lungs.
• Pleural fluid forms a slick but tight bond between the two layers
• If injury allows air into the pleural cavity, the bond is broken, the lung collapses (atelectasis).

Pulmonary Ventilation (During exhalation)

• Thoracic cavity decreases in volume.
• Decreased volume causes increased pressure (Poutside < Pinside).
• Air is forced out from an area of high pressure to low pressure.

Physical Factors Influencing Pulmonary Resistance

Airway Resistance:

• Friction is the major nonelastic source of resistance to gas flow and occurs in airways.
• Flow (F) is equal to the pressure differential divided by resistance (R): F = ΔP / R
• The pressure gradient between the atmosphere and alveoli is only 2 mm Hg or less during normal quiet breathing.
• A 2 mm Hg difference is sufficient to move 500 ml of air.
• Airway resistance is greatest in the bronchioles.
• Gas flow changes inversely with resistance.
• Resistance in the respiratory tree is usually insignificant, due to large airway diameters in the first part of the conducting zone.
• Progressive branching of airways (getting smaller) also increases total cross-sectional area.
• Resistance usually occurs in medium-sized bronchi.
• In terminal bronchioles, resistance is negligible because diffusion drives gas movement.

Alveolar Surface Tension:

• Surface tension is the attraction of liquid molecules to one another at a gas-liquid interface.
• It draws liquid molecules closer together and reduces contact with dissimilar gas molecules.
• Surface tension resists any force that tends to increase the surface area of a liquid.
• Water, which has very high surface tension, coats alveolar walls in a thin film and tends to cause alveoli to shrink to the smallest size (i.e., collapse).
• Surfactant reduces surface tension.
• A surfactant is the body's detergent-like lipid and protein complex that helps to reduce surface tension of alveolar fluid.
• It prevents alveolar collapse.
• A surfactant is produced by type II alveolar cells.

Lung Compliance

• Lung compliance is the measure of change in lung volume that occurs with a given change in transpulmonary pressure.
• Measure of how much lung stretches and is normally high because lungs are distensible, and there is surfactant, which decreases alveolar surface tension.
• Higher lung compliance means it is easier to expand the lungs.
• The formula for lung compliance is written mathematically as: CL = ΔV / Δ(Ppul - Pip), with Cl equal to compliance, ΔV₁ equal to the change in lung volume, and D(Ppul-Pip) equal to the change in transpulmonary pressure.
• Compliance can be diminished by: nonelastic scar tissue (fibrosis), reduced production of surfactant, and decreased flexibility of the thoracic cage.

Respiration

• External respiration: pulmonary gas exchange between alveoli and pulmonary capillaries
• Internal respiration: capillary gas exchange between blood capillaries and body tissues

External Respiration

• External respiration (pulmonary gas exchange) involves the exchange of O2 and CO2 across respiratory membranes.
• Exchange is influenced by: partial pressure gradients, and gas solubilities, thickness and surface area of respiratory membrane, and ventilation-perfusion coupling
• View the videos for additional understanding of the pleural space and pleural effusions.

Partial pressure gradients and gas solubilities in external respiration

• A steep partial pressure gradient for O2 exists between blood and lungs.
• Venous blood Po₂ = 40 mm Hg
• Alveolar Po₂ = 104 mm Hg
• Drives oxygen flow into blood
• Equilibrium is reached across the respiratory membrane in ~0.25 seconds, but it takes red blood cells ~0.75 seconds to travel from start to end of the pulmonary capillary.
• The partial pressure gradient for CO2 is less steep.
• Venous blood Pco₂ = 45 mm Hg
• Alveolar Pco₂ = 40 mm Hg
• Though the gradient is not as steep, CO2 still diffuses in equal amounts with oxygen. CO2 is 20x more soluble in plasma and alveolar fluid than oxygen.

Thickness of respiratory membrane in external respiration

• In addition to a steep partial pressure gradient, the respiratory membrane contributes to efficient gas exchange.
• Respiratory membranes are very thin, between 0.5 to 1 µm thick.
• The large total surface area of the alveoli is 40x the surface area of the skin.

Local PO2 and PCO2 levels on perfusion:

• Changes in PO2 in alveoli cause changes in diameters of arterioles.
• Where alveolar O2 is high, arterioles dilate to increase blood flow to those alveoli.
• Where alveolar O2 is low, arterioles constrict, directing blood to alveoli where oxygen is high, so that blood can pick up more oxygen
• This mechanism is opposite than seen in the systemic arterioles that dilate when oxygen is low and constrict when oxygen is high.
• Changes in PCO2 in alveoli cause changes in diameters of bronchioles.
• Where alveolar CO2 is high, bronchioles dilate, and this allows the elimination of CO2 more rapidly.
• Where alveolar CO2 is low, bronchioles constrict.

Balancing Ventilation and Perfusion

• Changing diameters of local arterioles and bronchioles synchronizes ventilation-perfusion.
• Ventilation-perfusion is never balanced for all alveoli because:
• Regional variations may be present, due to the effect of gravity on blood and air flow through lungs.
• Occasionally, alveolar ducts plugged with mucus create unventilated areas in the lungs.
• Ventilation and Q/Q are controlled by autoregulatory mechanisms that sense PO2 and PCO2
• V stands for Ventilation
• Q stands for the Perfusion rate

Distributions of Pulmonary Blood Flow

• Blood flow in the lungs is distributed differently because of the effect of gravity and creates three zones in the lungs
• Zone 1 is at the apex
• Zone 2 is midway
• Zone 3 is above the base
• Blood enters the hilum via the pulmonary artery and exerts an average pulmonary arterial pressure
• Arteries in Zone 1 are about 12 cm above hilum - gravity reduces pulmonary arterial pressure
• Arteries in Zone 3 are about 12 cm below the hilum - gravity increases pulmonary arterial pressure

Innervation of the lungs

• Lungs are innervated by parasympathetic and sympathetic motor fibers, as well as visceral sensory fibers.
• Nerves enter through the pulmonary plexus on the lung root (hilum) then run along bronchial tubes and blood vessels
• Parasympathetic motor fibers cause bronchoconstriction of airways and mucous production
• Autonomic excitatory cholinergic nerves secrete acetylcholine into bronchial smooth muscle cells and submucosal glands
• Sympathetic motor fibers regulate bronchodilation of airways
• Inhibitory nonadrenergic and noncholinergic nerves cause airway bronchodilation