Lung Ventilation and Respiration

• Lungs facilitate the body's oxygen supply and carbon dioxide removal via adequate ventilation. Ventilation is the movement of gas into and out of the lungs, distinct from respiration, which is oxygen use at the cellular level. Ventilation adapts to the body's needs; impairment increases breathing effort.

Mechanics of Ventilation

• Ventilation is a cyclic process involving inspiration and expiration. Tidal volume (VT) refers to the gas volume moved per phase, aiding carbon dioxide removal and replenishing oxygen. Respiratory muscles generate pressure gradient changes which facilitate gas flow in and out of the lungs. Lung and thorax compliance and resistance influence ventilation. The inspiratory load is minimal in healthy, resting lungs, and expiration is typically passive.

Pressure Differences During Breathing

• Gases move from high to low-pressure areas due to pressure gradients created by thoracic expansion/contraction and elastic properties of airways, alveoli, and the chest wall.
  • Transrespiratory pressure (PTR) exists between the pressure at the airway opening (PAO) and the body surface pressure (PBS): PTR = PAO – PBS.
  • Transairway pressure (PTAW) exists between the pressure at the airway opening and the pressure in the alveoli of the lungs: PTAW = PAO – PA.
  • Transalveolar pressure (PTA) exists between the pressure in a model alveolus and the pressure in the pleural space (Ppl): PTA = PA – Ppl.
  • Transpulmonary pressure difference (PTP) helps maintain alveolar inflation. In the pulmonary system, PTP = PAO – Ppl. Pressures must be measured under static (no flow) or dynamic (breathing) conditions to derive the pulmonary system's mechanical properties.
  • Transthoracic pressure difference (PTT) causes gas to flow into and out of the alveoli during breathing: PTT = PA – PBS. During spontaneous breathing, PA is subatmospheric at the start of inspiration, causing air to flow into the alveoli. The opposite occurs at the beginning of exhalation, with PA higher than PAO, causing air to flow out.

Inspiration and Expiration Explained

• Muscular effort expands the thorax, decreasing Ppl and positively changing expiratory PTP and PTA, inducing flow into the lungs. Inspiratory flow is proportional to the positive change in the transairway pressure difference. Ppl continues to decrease until the end of inspiration, with alveolar filling slowing as alveolar pressure approaches equilibrium with the atmosphere and inspiratory flow decreases to zero. Thoracic recoil causes Ppl to rise, decreasing the transpulmonary pressure difference (PTP) at the beginning of expiration. Flow is in the opposite (negative) direction. The driving force for expiratory flow is energy stored in the combined elastances of the lungs and chest wall. Pleural pressures are always negative (subatmospheric) during normal inspiration and exhalation.

Spontaneous versus Positive Pressure Breathing

• Both spontaneous breathing (SB) and positive pressure ventilation (PPV) accomplish inspiration by increasing PL, the pressure distending the lungs. PPV raises Ppl, compressing veins and impeding cardiac output, opposite to spontaneous breathing.

Inhalation

• Thoracic cavity expansion during inhalation increases lung volume, decreasing pleural pressure, and the lower number of collisions decreases the pressure exerted by the gas, which reduces PA below PB so air flows into the lungs until PA again equals PB at end inspiration, increasing the transpulmonary pressure gradient to maintain alveolar inflation. The higher the pressure gradient, the higher the flow.

Exhalation

• Lung recoil compresses the alveolar gas volume during exhalation as inspiratory muscles relax. Exhalation should normally be passive. Diaphragm relaxation decreases the thoracic cavity size, increasing pleural pressure, which is transmitted to the alveoli, increasing intra-alveolar pressure. This causes gas to flow from the higher intra-alveolar pressure to the lower atmospheric pressure.

Flail Chest

• During inhalation, the transpulmonary and transthoracic pressure gradients cause the lung to sink in a patient with flail chest, decreasing the amount of inspiratory volume. During exhalation, the pressure gradients cause the broken ribs to bulge outward. Some air from the unaffected lung moves into the affected lung rather than being exhaled. Positive pressure ventilation eliminates the negative intrapleural pressures changes during inspiration, stopping the adverse effects of transpulmonary and transthoracic pressure gradients.

Forces Opposing Lung Inflation

• Lungs tend to recoil inward, and the chest wall tends to move outwards; these forces maintain the lungs at their resting volume (FRC). Opposition to lung inflation includes:
  • Elastic forces from tissues of the lungs, thorax, and abdomen, and surface tension in the alveoli.
  • Frictional forces from gas flow through natural and artificial airways, and tissues moved during breathing

Elastic Opposition to Ventilation

• Elastic and collagen fibers resist lung stretch. Greater pressure application causes greater stretch until the elastic limit is reached. Deflation is passive recoil that requires less force to maintain the same volume.

Surface Tension Forces

• Hysteresis is partly caused by surface tension, which opposes lung inflation. Lung recoil occurs due to tissue elasticity and surface tension. Pulmonary surfactant, produced by alveolar type II pneumocytes, reduces lung surface tension and prevents collapse.

Hooke's Law

• Elastance is the natural ability of matter to respond directly to force and return to it’s original shape. Inflation stretches tissue. The elastic properties of the lungs and chest wall oppose inflation so to increase the volume, pressure must be applied: change in pressure per change in volume. Volume varies directly with pressure until the elastic limit is reached; exceeding this point can cause rupture.

Lung Compliance

• Compliance measures the lung's distensibility. Increased compliance is caused by loss of elastic fibers (like in emphysema). Decreased compliance may be caused by pulmonary fibrosis which affects the connective tissue making them stiff so they are unable to take in more volume. Hyperinflation describes an abnormally increased lung volume.

Relationship Between Chest Wall and Lung

• Lungs and chest wall recoil in opposite directions. Compliance in both is ~0.2 L/cm H2O. Each oppose other, resulting in system compliance of ~0.1 L/cm H2O. FRC is established at resting lung level where tendency of chest wall to expand equals that of lungs to collapse. This occurs at ~40% TLC.

Frictional Resistance to Ventilation

• Airway resistance (~80% of of the frictional to ventilation). Gas flow causes frictional resistance, which explains using heliox. Airway radius has an exponential effect (r4) on resistance, which is highest at the nose (50% of total). Laminar flow requires less driving pressure than turbulent flow.

Airway Resistance Reducing

• Reducing the radius of a tube by half requires a 16-fold increase in pressure to maintain a constant flow. Smaller endotracheal tubes increase work of breathing due to reduced radius.

Factors Affecting Distribution of Ventilation

• Due to varying transpulmonary pressure gradients, alveoli at the apices have larger resting volumes and expand less during inspiration than alveoli at the bases. Therefore an upright patient's lung base receives approximately four times as much ventilation.

V/Q Ratio

• When ventilation is altered, so is the V/Q Ratio, or the relationship between the two
• Without ventilation there is no oxygenation
• When the V/Q Ratio Is Low alveolar oxygen pressure (P A O2) increases and alveolar carbon dioxide pressure (P A C O2) decreases

Determinants of Alveolar Gas Tensions

• PACO2 varies directly with the body’s production of carbon dioxide (CO2) and inversely with alveolar ventilation (VA).
• Under normal conditions it is maintained at approximately 35 to 45 mm Hg.
• The PACO2 will increase above normal if carbon dioxide production increases while alveolar ventilation remains constant.
• An increase in dead space (gas not participating in gas exchange), can also lead to an increased PACO2
• PACO2 decreases if CO2 production decreases or alveolar ventilation increases

Alveolar air equation

• Alveolar oxygen tension (PAO2)
• In lungs the air is diluted by water vapor and CO2
• Gas fully saturated with water vapor at BTPS is 47 mmHg
• Moving into the alveoli our PO2 is less because it contains water vapor and CO2
• Healthy PCO2 is 40 mmHg (range is 35-45)
• Since the sum of all gases must equal PB (Duh Dalton) the PO2 falls by 40 mmHg when it enters the alveoli
• O2 diffuses out of the alveoli faster than CO2 diffuses into it

Mechanisms of Diffusion

• Diffusion occurs along pressure gradients
• Barriers to diffusion
  • A/C membrane has three main barriers
    • Alveolar epithelium
    • Interstitial space and its structures
    • Capillary endothelium
    • RBC membrane
      • Fick’s law: The greater the surface area, diffusion constant, and pressure gradient, the more diffusion will occur

Mechanism of gas diffusion

• Given that the area of and distance across the alveolar-capillary membrane are relatively constant in healthy people, diffusion in the normal lung mainly depends on gas pressure gradients.

Mechanisms of Diffusion

• Pulmonary diffusion gradients
• Diffusion occurs along pressure gradients
• Time limits to diffusion:
  • Pulmonary blood is normally exposed to alveolar gas for 0.75 second, during exercise may fall 0.25 second
  • Normally equilibration occurs in 0.25 second
  • With diffusion limitation or blood exposure time of less than 0.25 seconds, there may be inadequate time for equilibration

Shunting

• Ventilation & Perfusion is not perfect in the normal lungs
• PaO2 is normally 5-10 mmHg less than PAO2 because of shunts
  • Anatomical (right to left shunts)
    • Bronchial venous drainage
    • Thebesian venous drainage

PAO2 – PaO2 or P(A-a)O2 or A-a gradient

• Measures the difference between Alveolar and arterial PO2
• Indicates the efficiency of gas exchange
• Estimates the degree of hypoxemia and shunting
• 5-10 mmHg on 21% = normal
• 25-65 mmHg on 100% FIO2 = normal
• 66-300 mmHg = V/Q mismatch
• >300 mmHg = shunt
• PAO2 –PaO2: If increased then there is an abnormal O2 exchange
• A small difference between alveolar and arterial O2 is due to small number of veins carrying deoxygenaged blood that bypasses the lungs and empties into arterial circulation
• Thebesian vessels of the left ventricular myocardium drain directly into the left ventricle
• Some bronchial veins and mediastinal veins drain into pulmonary veins and decreases arterial PaO2

Normal Variations From Ideal Gas Exchange

• If ventilation and blood flow are mismatched, impairment of both O2 and CO2 transfer occurs
• If ventilation exceeds perfusion the V/Q is greater than 1
• If perfusion exceed ventilation the V/Q is less than 1

Normal Variations From Ideal Gas Exchange

• Ventilation with zero blood flow = alveolar dead space (increases PO2 and lowers alveolar PCO2)
• Lower alveolar PO2 increases PaCO2; perfusion but no ventilation
• In an upright person the V/Q at the top of the lung is increased which means increase ventilation relative to little blood flow in pulmonary circulation because of gravity

Oxygen Transport

Transported in two forms: dissolved and bound

• Physically dissolved in plasma
  • Gaseous oxygen enters blood and dissolves.
  • Henry’s law allows calculation of amount dissolved
  • Dissolved O2 (ml/dl) = PO2  0.003
• Chemically bound to hemoglobin (Hb) – Majority is carried here
  • Each gram of Hb can bind 1.34 ml of oxygen
  • [Hb g]  1.34 ml O2 provides capacity
  • 70 times more O2 transported bound than dissolved

Oxygen Transport

• Hemoglobin saturation
  • Saturation is % of Hb that is carrying oxygen compared to total Hb
  • SaO2 = [HbO2/total Hb]  100
  • Normal SaO2 is 95% to 100%
  • HbO2 dissociation curve
    • Relationship between PaO2 and SaO2 is S-shaped
    • Flat portion occurs with SaO2 >90%
    • Facilitates O2 loading at lungs even with low PaO2
    • Steep portion (SaO2<90%) facilitates O2 unloading to tissues with low PO2