Alveolar Ventilation and Lung Mechanics

Alveolar Ventilation and Lung Mechanics

Core Concepts

  • Lung Volumes and Capacities

  • Alveolar Ventilation and Dead Space

  • Alveolar Ventilation and Alveolar O2 and CO2 Levels

  • Regional Distribution of Alveolar Ventilation

  • Closing Capacity and Volume

What is Alveolar Ventilation?

  • The exchange of oxygen and carbon dioxide between the alveoli and the external environment.

  • Further defined as the volume of fresh air entering the alveoli per minute.

  • How is this different from minute ventilation? Alveolar ventilation specifically refers to the air reaching the alveoli for gas exchange, whereas minute ventilation is the total volume of air moved in or out of the lungs per minute, including dead space.

  • How do we calculate minute ventilation? Minute ventilation (\dot{V_E}) is typically calculated as Tidal Volume (VT) multiplied by Respiratory Rate (RR). This includes both alveolar ventilation and dead space ventilation.

Lung Volumes & Capacities

Lung Volumes (Four Standard)

  • Tidal Volume (VT)

    • Volume of air entering or leaving the nose or mouth per breath.

    • Approximately 500 ext{ ml} in a 70 ext{ kg} adult during normal quiet breathing.

    • Mean tidal volume is 7 ext{ ml/kg} (range: 6-8 ext{ ml/kg}).

    • Pulmonary volumes and capacities are 20-25\% less in females than males.

  • Expiratory Reserve Volume (ERV)

    • Volume of gas expelled from the lungs during a maximal forced expiration that starts at the end of a normal tidal expiration.

    • Approximately 23 ext{ ml/kg} or 1.5 ext{ L} in a healthy 70 ext{ kg} adult.

    • May change due to positioning and obesity.

  • Inspiratory Reserve Volume (IRV)

    • Volume of gas that is inspired into the lungs during a maximal forced inspiration that starts at the end of a normal tidal inspiration.

    • Determined by:

      • Strength of contraction of the inspiratory muscles.

      • The inward elastic recoil of the lung and chest wall.

      • The starting point (Functional Residual Capacity + Tidal Volume, or ext{FRC} + ext{Vt}).

    • Approximately 35-39 ext{ ml/kg} or 2.5 ext{ L} in a 70 ext{ kg} adult.

  • Residual Volume (RV)

    • The volume of gas remaining in the lungs after a maximal forced expiration.

    • Determined by:

      • The force generated by the muscles of expiration.

      • The inward recoil forces of the lungs.

      • The outward recoil of the chest wall.

      • Dynamic compression.

    • Approximately 1.5 ext{ L} in a 70 ext{ kg} adult.

    • Prevents the lungs from collapsing.

Lung Capacities (Derived from two or more standard lung volumes)

  • Functional Residual Capacity (FRC)

    • Volume of gas remaining in the lungs at the end of a normal tidal expiration.

    • Equal to: ext{RV} + ext{ERV}, or ext{TLC} - ext{IC}.

    • Represents the balance point between the inward elastic recoil of the lungs and the outward elastic recoil of the chest wall.

    • Approximately 46 ext{ ml/kg} or 3 ext{ L} in a 70 ext{ kg} adult.

  • Inspiratory Capacity (IC)

    • Volume of air that is inhaled into the lungs during a maximal inspiratory effort that begins at the end of a normal tidal expiration.

    • Equal to: ext{VT} + ext{IRV}, or ext{TLC} - ext{FRC}.

    • Approximately 43-45 ext{ ml/kg} or 3 ext{ L} in a 70 ext{ kg} adult.

  • Vital Capacity (VC)

    • Volume of air expelled from the lungs during a maximal forced expiration starting after a maximal forced inspiration.

    • Equal to: ext{TLC} - ext{RV}, or ext{VT} + ext{IRV} + ext{ERV}.

    • Determined by factors that determine the TLC and RV.

    • Approximately 60-70 ext{ ml/kg} or 4.5 ext{ L} in a 70 ext{ kg} adult.

  • Total Lung Capacity (TLC)

    • Volume of air in the lungs at maximal inspiratory effort.

    • Determined by the strength of contraction of inspiratory muscles and the inward elastic recoil of the lungs and chest wall.

    • Sum of all 4 lung volumes ( ext{VT} + ext{ERV} + ext{IRV} + ext{RV}).

    • About 6 ext{ L} in a 70 ext{ kg} adult.

Measurement of Lung Volumes

  • Spirometry:

    • Can measure: VT, IRV, ERV, IC, VC, FEV1, FVC, FEV1/FVC.

    • Cannot measure: RV, FRC, TLC (because these volumes involve gas that cannot be fully inspired or expired).

  • Other methods for RV, FRC, TLC: Nitrogen-washout, helium dilution, and body plethysmography.

Importance of Functional Residual Capacity (FRC)

  • Gas Exchange Site: It is the lung volume in which gas exchange takes place.

  • Buffer Function: Acts as a buffer against extreme changes in O2 and CO2 concentrations with each breath.

    • Maintains relatively constant alveolar and arterial gas tensions.

    • Fluctuations of alveolar and arterial gas tensions occur with each tidal breath as fresh gas mixes with alveolar air, and FRC mitigates these.

  • In Infants: Physiologic PEEP (positive end-expiratory pressure) created by laryngeal braking preserves normal FRC.

    • Laryngeal braking: Involves constriction of the larynx following inspiration, resulting in a prolonged expiratory duration and enhanced gas exchange in the lungs.

  • Clinical Relevance: FRC decreases when intubated.

Factors Affecting FRC

Positional Changes in FRC

  • Standing to Supine: Transitioning from standing to a supine position decreases FRC.

    • This is due to gravitational forces no longer pulling the abdominal contents down, allowing the diaphragm to shift cephalad.

  • Anesthetic Implications: Patients are often in the supine position during anesthesia, which impacts gas exchange by reducing FRC.

Cephalad Shift of Diaphragm and FRC

  • Other events during anesthesia and surgery result in a reduction in FRC as the diaphragm is shifted upwards, including:

    • Anesthesia: With induction of anesthesia in the supine position, abdominal contents exert cephalad pressure on the diaphragm. At end-expiration, the dorsal portion of the diaphragm is more cephalad and the ventral portion is more caudal than when awake. The thoracic spine is more lordotic, and the rib cage moves inward, all secondary to loss of motor tone.

    • Paralysis.

    • Surgical positioning: e.g., steep Trendelenburg.

    • Surgical manipulation of abdominal contents.

  • Note: MAC (Minimal Alveolar Concentration) is mentioned in connection to anesthesia but not defined in the transcript.

Pathophysiologic Alterations of FRC

  • Restrictive Disease (e.g., Pulmonary fibrosis, ARDS)

    • Reduced lung compliance.

    • Increased elastic recoil.

    • A nearly proportional decrease in all lung volumes, including FRC.

  • Obstructive Disease (e.g., COPD)

    • Increased resistance to airflow.

    • Decreased elastic recoil.

    • RV, FRC, and TLC may be greatly increased due to air trapping.

    • Reduction in VC and ERV.

Lung Volume Changes After Surgery

  • Vital Capacity (VC) is often reduced after surgery.

Effects of Aging on Lung Volumes

  • Decreased chest wall compliance (due to calcified costochondral joints) leads to a decreased VC.

  • Decreased lung elasticity and alveolar wall tissue destruction leads to an increase in pulmonary compliance, resulting in an increase in residual volume (RV) and FRC.

  • The resting midposition of the diaphragm shifts away from the thoracic cavity.

  • The RV:TLC ratio changes (increases with age):

    • 15-34 years old: <0.2

    • 35-49 years old: =0.25

    • Approaches 0.35 to 0.40 in older individuals.

Alveolar Ventilation & Dead Space

  • Dead space refers to the percentage of air that enters the respiratory passages yet does not participate in gaseous exchange with the blood.

  • Three types of dead space:

    1. Anatomic Dead Space

    2. Alveolar Dead Space

    3. Physiologic Dead Space

Anatomic Dead Space

  • The volume of air entering and leaving the nose or mouth per minute is referred to as the minute volume. This minute volume is not equal to the volume of air entering and leaving the alveoli per minute because of anatomic dead space.

  • Definition: The last part of each inspiration remains in the conducting airways and does not reach the alveoli.

  • Components: Consists of generations 0-16 of the airways, as well as from the nose/mouth to the trachea.

  • Estimation (not measured clinically):

    • 1 ext{ ml} of dead space per pound of ideal body weight (IBW).

    • 2.2 ext{ ml} of dead space per kg of ideal body weight (IBW).

    • Ideal Body Weight (The Devine Formula):

      • Male: 50 ext{ kilograms} + (2.3 ext{ kilograms} imes ( ext{height (in)} - 60))

      • Female: 45.5 ext{ kilograms} + (2.3 ext{ kilograms} imes ( ext{height (in)} - 60))

Mathematical Calculation of Alveolar Ventilation & Anatomic Dead Space

  • The volume of gas reaching the alveoli and therefore participating in alveolar ventilation is equal to the volume of gas inspired minus the volume of the anatomic dead space.

  • Alveolar ventilation per breath (VA):
    V    A = VT - VD

  • Alveolar ventilation per minute ( ext{V} with a dot above, indicating per minute): ext{ } ormalsize egin{mi mathvariant='normal'> ext{ ext{ } ormalfont } ight) imes ext{RR}VA = (VT - V_D) imes ext{RR}

    • Example: With a VT of 500 ext{ ml}, a VD (anatomic dead space) of 150 ext{ ml}, and a Respiratory Rate (RR) of 12/ ext{min}.
      ext{ }
      ormalsize egin{mi mathvariant='normal'> ext{ ext{ }
      ormalfont }
      ight) imes ext{RR}V_A = (500 ext{ ml} - 150 ext{ ml}) imes 12/ ext{min} = 350 ext{ ml} imes 12/ ext{min} = 4200 rac{ ext{ml}}{ ext{min}}

Alveolar Dead Space

  • Definition: When alveoli are ventilated, but not perfused, no gas exchange occurs due to physiologic reasons (as opposed to anatomic obstruction). Alveolar dead space is the volume of gas that enters unperfused alveoli per breath.

  • Prevalence: Little to none in a healthy individual.

  • Presence in disease states: May be present in low cardiac output states, pulmonary emboli, high levels of PEEP.

  • Measurement: Alveolar dead space cannot be directly measured. Instead, it is estimated using the concept of physiologic dead space.

Physiologic Dead Space: The Bohr Equation

  • Definition: Physiologic dead space is the total dead space of the respiratory system, encompassing both anatomic dead space and alveolar dead space.
    ext{Physiologic Dead Space} = ext{Anatomic Dead Space} + ext{Alveolar Dead Space}

  • The Bohr Equation (for calculating physiologic dead space): V{DCO2} = VT imes rac{(P{aCO2} - P{ECO2})}{P{aCO_2}}

    • V{DCO2}: Physiological dead space.

    • V_T: Tidal Volume.

    • P{aCO2}: Arterial CO2 partial pressure (assumed to be equal to ideal alveolar P{CO2}).

    • P{ECO2}: Mixed expired CO2 partial pressure.

  • Assumptions of the Bohr Equation:

    • Little CO2 in inspired air (0.04\%).

    • Therefore, CO2 in expired gas must come solely from alveoli that are both ventilated and perfused.

  • Steps for calculation: After the physiologic dead space is calculated from the Bohr equation, the estimated anatomic dead space can be subtracted to find the alveolar dead space.
    ext{Alveolar Dead Space} = ext{Physiologic Dead Space} - ext{Anatomic Dead Space}

  • In young, healthy individuals, alveolar dead space is not present, therefore, physiologic dead space is equal to anatomic dead space.

  • Mixed expired CO2 partial pressure (P{ECO2}): Measured with a CO2 meter.

Mixed Expired PCO2 vs. End-tidal PCO2

  • Mixed Expired PCO2 (P{ECO2}):

    • The partial pressure of CO2 in the expired gas during a tidal expiration.

    • It is much lower in PCO2 compared to alveolar PCO2 because the CO2-free gas from anatomical dead space dilutes it.

  • End-tidal PCO2 (P{ETCO2}):

    • The partial pressure of CO2 at the end of expiration during tidal breathing.

    • Assumed to be more representative of alveolar PCO2.

    • However, it is typically lower than 'ideal' alveolar PCO2 because the almost CO2-free gas from alveolar dead space dilutes and lowers the end-tidal PCO2.

Alveolar Ventilation and Alveolar Oxygen and Carbon Dioxide Levels

Partial Pressure and Respiratory Gases

  • Dalton’s Law: In a mixture of gases, the pressure exerted by each individual gas is independent of pressures of other gases in the mixture. The total pressure of the mixture is the sum of the partial pressures of each gas.

  • An individual gas’s partial pressure is equal to its fractional concentration times the total pressure of all the gases in the mixture:
    P{gas} = F{gas} imes P_{total}

  • 1 ext{ torr} = 1 ext{ mmHg}.

Impact of Humidification on Partial Pressures

  • Inspired air is warmed and humidified by water vapor in the respiratory passages.

  • The partial pressure of water vapor at body temperature is 47 ext{ mm Hg}.

  • This water vapor must be accounted for when calculating partial pressures of other gases.

  • If dry gas were in a closed container, humidification would increase total pressure (e.g., 760 ext{ mmHg} + 47 ext{ mmHg} = 807 ext{ mmHg}).

  • However, the body is not a closed container, and inspired gas, plus the water vapor, expands. This expansion results in the original 1 ext{ L} of gas at 760 ext{ mmHg} being diluted by the added water vapor.

  • Therefore, the partial pressure of inspired oxygen (P{IO2}) is equal to the fractional concentration of inspired oxygen (F{IO2}) times the barometric pressure (PB) minus the water vapor pressure (P{H2O}): P{IO2} = F{IO2} imes (PB - P{H2O})

  • The same principle holds for the partial pressures of other gases like nitrogen and carbon dioxide in inspired air.

  • Expired air is a mixture of approximately 350 ext{ mL} of alveolar air and 150 ext{ mL} of air from anatomical dead space.

Alveolar Gas Composition

  • Approximately 2.5 ext{ to } 3 ext{ L} of gas is already present in the lungs at the FRC.

  • About 350 ext{ ml} of gas enters and leaves the alveoli per breath.

  • 300 ext{ ml/min} of O2 continuously diffuses from alveoli into the pulmonary capillary blood and is being replaced by alveolar ventilation.

  • 250 ext{ ml/min} of CO2 is diffusing from mixed venous blood into alveoli per minute and is removed by alveolar ventilation.

  • Therefore, the partial pressures of oxygen and carbon dioxide in the alveolar air are determined by:

    • Alveolar ventilation.

    • Pulmonary capillary perfusion.

    • Oxygen consumption.

    • Carbon dioxide production.

  • Alveolar PO2: Increases by 2-4 ext{ mm Hg} per inspiration and slowly decreases until the next inspiration.

  • Alveolar PCO2: Decreases by 2-4 ext{ mm Hg} with each inspiration and increases until the next inspiration.

Alveolar Ventilation and CO2

  • The concentration of carbon dioxide in the alveolar gas is dependent upon the alveolar ventilation and the rate of bodily carbon dioxide production.

  • The volume of carbon dioxide expired per unit of time ( ext{V} ormalsize egin{mi mathvariant='normal'> ext{ ext{ } ormalfont } ight) imes ext{RR}E{CO2}) is equal to the alveolar ventilation ( ext{V} ormalsize egin{mi mathvariant='normal'> ext{ ext{ } ormalfont } ight) imes ext{RR}A) times the alveolar fractional concentration of CO2 (F{ACO2}). ext{V} ormalsize egin{mi mathvariant='normal'> ext{ ext{ } ormalfont } ight) imes ext{RR}E{CO2} = ext{V} ormalsize egin{mi mathvariant='normal'> ext{ ext{ } ormalfont } ight) imes ext{RR}A imes F{ACO2}

    • No carbon dioxide comes from the dead space.

  • The fractional concentration of CO2 in the alveoli is directly proportional to body CO2 production ( ext{V}
    ormalsize egin{mi mathvariant='normal'> ext{ ext{ }
    ormalfont }
    ight) imes ext{RR}CO_2}) and inversely proportional to alveolar ventilation ( ext{V}
    ormalsize egin{mi mathvariant='normal'> ext{ ext{ }
    ormalfont }
    ight) imes ext{RR}A).

  • Alveolar PCO2 is in equilibrium with arterial PCO2.

  • If alveolar ventilation is doubled and CO2 production is unchanged, then the alveolar and arterial PCO2 are reduced by one-half.

Alveolar Ventilation and O2

  • As alveolar ventilation increases, so will Alveolar PO2 (P{AO2}).

  • However, doubling ventilation cannot double the normal P{AO2} of 104 ext{ mmHg} because inspired PO2 (P{IO2}) is 149 ext{ mmHg}.

  • Alveolar Air Equation (to calculate P{AO2}): P{AO2} = P{IO2} - rac{P{ACO2}}{R} + ext{F}

    • P{IO2}: Partial pressure of inspired oxygen.

    • P{ACO2}: Alveolar partial pressure of carbon dioxide (often approximated by arterial P{aCO2}).

    • R: Respiratory exchange ratio.

    • F: A small correction factor that is usually ignored.

  • Respiratory Exchange Ratio (R): Equal to carbon dioxide production / oxygen consumption ( ext{V} ormalsize egin{mi mathvariant='normal'> ext{ ext{ } ormalfont } ight) imes ext{RR}CO2} / ext{V} ormalsize egin{mi mathvariant='normal'> ext{ ext{ } ormalfont } ight) imes ext{RR}O2).

    • R for carbohydrates is 1.00.

    • R for fat is an average of 0.7.

    • R for protein averages 0.82.

    • R for the average American diet is 0.8 (e.g., 200 ext{ ml/min CO}2 produced / 250 ext{ ml/min O}2 consumed).

  • The partial pressures of oxygen are determined by alveolar ventilation, pulmonary capillary perfusion, oxygen consumption, and carbon dioxide production.

Alveolar-Arterial O2 Gradient (A-a gradient)

  • A measure of the difference between the alveolar concentration (A) of oxygen and the arterial (a) concentration of oxygen.
    A-a ext{ gradient} = P{AO2} - P{aO2}

Regional Distribution of Alveolar Ventilation

  • In healthy adults in the standing or seated position, lower lung regions receive more ventilation per unit volume than the upper regions due to the effects of gravity.

  • This gravity-dependent ventilation relationship is maintained in the supine, lateral, and prone positions.

  • Mechanism: Regional differences in intrapleural pressure caused by gravity and the mechanical interaction of the lung and chest wall.

    • Intrapleural pressure: Increases by about +0.2 ext{ to } +0.5 ext{ cm H}_2O per centimeter of vertical displacement down the lung.

    • Therefore, intrapleural pressure is more negative in upper (non-dependent) regions of the lung than it is in lower (dependent) regions of the lung.

    • Transpulmonary pressure: Because intrapleural pressure is greater (less negative) in the non-dependent regions, this means transpulmonary pressure (P{alveolar} - P{intrapleural}) is also greater in the non-dependent regions of the lung than it is in dependent regions.

    • Alveolar Volume/Compliance: Nondependent regions of the lung are subjected to greater distending pressures, and these alveoli have a greater “baseline” volume (already stretched).

      • Non-dependent alveoli start with a greater initial volume at FRC and are less compliant because they are already stretched.

      • The result is that changes in transpulmonary pressure lead to greater volume change in dependent alveoli as compared to non-dependent alveoli.

      • Conclusion: Dependent alveoli are better ventilated.

  • Seated, upright, at FRC:

    • Most of the alveolar air is located in the upper regions of the lung.

    • Therefore, most of the ERV is located in the upper regions.

    • The majority of the IRV and IC is located in the lower regions.

Closing Capacity and Volume

  • Closing Capacity (CC): The lung volume at which airway closure begins during a forced expiration.

  • Closing Volume (CV): The volume of air exhaled from the time the first airways close until the subject reaches RV and can exhale no more.

  • Clinical Significance: If closing capacity encroaches on FRC, airway closure may occur during normal expiration, which decreases ventilation to areas distal to the closure.

COPD and Closing Volume & Capacity

  • COPD potentially results in:

    • Higher closing capacity.

    • Lower closing volume (relative to increased lung volumes).

  • Compensatory mechanism: Patients with COPD often engage in pursed lip breathing.

    • This creates low levels of PEEP (1-5 ext{ cm H}_2O).

    • This PEEP helps to splint the airways open, preventing premature collapse.

    • This compensatory mechanism is eliminated with endotracheal intubation.