Pulmonary Physiology Flashcards
Define lung volumes and capacities.
• Tidal volume (TV) = Volume of gas inspired and passively expired with normal breathing
• Expiratory reserve volume (ERV) = Volume of gas that can be maximally exhaled from rest
• Residual volume (RV) = Volume of gas remaining in the lung after maximal exhalation
• Functional residual capacity (FRC) = ERV + RV
• Inspiratory reserve volume (IRV) = Volume of gas that can be maximally inhaled above a TV
• Inspiratory capacity (IC) = IRV + TV
• Vital capacity (VC) = IRV + TV + ERV
• Total lung capacity (TLC) = IRV + TV + ERV + RV
(Fig. 6.1).
Describe the mechanics of respiration.
The combination of surface tension of water within the alveoli and the intrinsic elastic properties of the lung create a force (Flung) favoring collapse, whereas the chest wall force (Fchest) favors expansion. These two forces directly oppose one another, creating a spring-like physiology, opposing any deviation in lung volume above or below FRC. For example, following a forced inhaled volume above FRC, the recoil force of the lung (Flung) is greater than the expansion force of the chest wall (Fchest), facilitating a passive return to FRC. Likewise, following a forced exhaled volume below FRC, Fchest is greater in magnitude than Flung, causing a passive return to FRC.
What is FRC? What factors affect it?
FRC results when the opposing forces of the expanding chest wall and the recoil forces of the lung are equal. In other words, lung volume is at FRC when Fchest + Flung = 0.
The average FRC for a 70-kg, 5’10” male in the supine position around 2.5 L.
FRC is increased by:
• Body size (increases with height)
• Age (increases slightly with age)
• Asthma and chronic obstructive pulmonary disease (COPD)
FRC is decreased by:
• Female sex (females have a 10% decrease in FRC compared with males)
• Muscle relaxation (anesthetic agents and neuromuscular blocking agents decrease diaphragmatic muscle tone
and other accessory muscles of respiration)
• Posture (FRC is greatest in standing >sitting >prone >lateral >supine)
• Decreased chest wall compliance (e.g., obesity, thoracic burns, kyphoscoliosis, abdominal compartment
syndrome, ascites, laparoscopy)
• Decreased lung compliance (e.g., interstitial lung disease, acute respiratory distress syndrome [ARDS])
How long will it take for an apneic patient to develop hypoxemia following induction of anesthesia?
In a healthy, 70-kg, 5’10 (body mass index [BMI] 22), male preoxygenated (or denitrogenated) to an end-tidal O2 =100%, it will take approximately 10 minutes. At rest (i.e., a metabolic equivalent of 1), the O2 consumption
(3.5 mL/kg/min) for a 70-kg adult male is approximately 250 mL/min. Following induction in the supine position, this patient’s lung volume will equal FRC, which is approximately 2.5 L. Assuming this lung volume contains 100% O2, it will take 2500 mL O2/(250 mL O2/min) = 10 minutes.
However, the earlier is under ideal conditions for a healthy, nonobese patient, assuming an FRC volume equal to 100% oxygen.
Realistically, preoxygenation would yield a more commonly obtained end-tidal O2 of approximately 80% (not 100%), which will decrease the effective volume of O2 in the FRC by 20%. Also muscle relaxation caused by either anesthetic agents or paralytics will reduce FRC by 20%. Therefore the effective FRC volume containing oxygen is 2500 mL O2 x 80% x 80% = 1600 mL O2, yielding 6.4 minutes before the onset of hypoxemia.
Further, given the high prevalence of obesity and its effects on reducing FRC (decreases outward Fchest) and increasing O2 consumption (increased body mass), the time to hypoxemia can be severely reduced in the general population. Assume the aforementioned patient is 30-kg overweight and now weighs 100 kg (BMI 32). Because obesity decreases FRC by approximately 30 mL/kg for each kg above normal body weight, his effective O2 volume in FRC, although apneic, will be (2500 mL – 900 mL) x 80% x 80% = 1024 mL O2 and his O2 consumption will
increase to 350 mL O2/min. Therefore time to hypoxemia will be 1024 mL O2 /(350 mL O2/min) = 2.9 minutes. This is a more realistic time to hypoxemia for a large percentage of patients who are obese (BMI 32) but otherwise healthy.
What is closing capacity and what factors affect it? What is the relationship between closing capacity and FRC?
Closing capacity (CC) is the lung volume at which small, noncartilaginous airways begin to close, resulting in atelectasis and subsequent hypoxemia. It is calculated by the following equation:
Closing capacity = Closing volume + RV
In a young, healthy patient, CC is approximately equal to RV. The clinical significance of this is that having a closing volume at RV effectively provides a large physiological oxygen reserve, that is, atelectasis will not occur at FRC. With age, CC increases. At approximately 45 years old, CC equals FRC when supine and at 65 years of age, equals FRC when standing. The end result is a greater likelihood of resting hypoxemia in older patients because of atelectasis.
Although FRC is dependent on position and only slightly correlated with aging, CC is independent of position and increases with aging. CC is thought to be an independent pathological process responsible for decreased pulmonary reserve and hypoxemia in the elderly patient.
Discuss the factors that affect resistance to gas flow. How is laminar versus turbulent flow different?
Resistance to gas flow through a tube can be separated into two components: (1) physical properties of the tube (e.g., length and radius), and (2) physical properties of the gas flowing through the tube (e.g., laminar vs. turbulent flow). At low flow rates, flow is laminar and the relationship between flow and pressure is linear as shown by the Hagen-Poiseuille equation:
Δ P = 8 l μ x Q
πr4
Notice how the pressure gradient (ΔP) increases linearly with increasing flow (Q_) with a slope governed by resistance, R = 8lμ/πr4.
Resistance (R) increases with tube length and gas viscosity (μ), while resistance decreases as radius (r) increases by the fourth power. At high flow rates (e.g., bronchospasm, asthma, and COPD), gas velocity significantly increases, resulting in turbulent flow, and the relationship between flow and pressure becomes nonlinear, where√ΔP∝Q_ implying a much higher pressure will be necessary for a given flow(Q_) relative to laminar flow, where ΔP∝Q_. During turbulent flow, resistance is proportional to the density(ρ) of the gas and inversely proportional to the radius of the tube (r) to the fifth power: R ∝ ρ/r5.
Give an example of how gas flow resistance applies to clinical practice.
Patients who are intubated must exchange gas through a smaller diameter than their normal airway. Recall, resistance is inversely proportional to radius to the fourth power for laminar flow. Because of the smaller radius of the endotracheal tube, resistance will increase, requiring increased work of breathing if unassisted by the ventilator. This increased work of breathing can be reduced by assisting the patient with a synchronized ventilator mode, such as pressure support. Pressure support allows the patient to trigger the ventilator, which can provide positive pressure to “overcome” the resistance of the endotracheal tube and decrease the work of breathing on inspiration. However, the work of breathing will still be increased on expiration as the ventilator only assists on inspiration. Other examples that pertain to increased airway resistance include bronchospasm, secretions, postextubation stridor, and a kinked endotracheal tube.
What determines laminar versus turbulent flow? What are the clinical implications of this?
Laminar flow is more efficient than turbulent flow for gas exchange, as turbulent flow will require a larger pressure gradient to obtain the same amount of flow. Reynolds number (Re) is a dimensionless number that can be used to predict if flow will be turbulent or laminar. A lower Re is associated with laminar flow, and a higher Re is associated with turbulent flow. Re can be calculated by the following equation: Re 1⁄4 2rvρ/η, where r is tube radius,
v is gas velocity, ρ is gas density, and η is gas viscosity. Notice how increasing gas velocity increases Re, leading to more turbulent flow and decreasing gas density lowers Re, leading to more laminar flow.
Discuss clinical interventions that may mitigate turbulent flow.
Increased airway resistance (e.g., bronchospasm) can lead to turbulent flow because of an increased inspiratory flow or gas velocity (see equation for Reynolds number). One method to treat problems related to turbulent flow is to lower the gas density. This can be accomplished with the addition of helium. When helium and oxygen are combined, the result is a gas composition called heliox, which has a similar viscosity as air, but importantly, has a much lower density. This accomplishes the following: (1) decreases Reynolds number, allowing for less turbulent and more laminar flow, and (2) decreases turbulent flow resistance. Recall that resistance during turbulent flow
is R ∝ ρ/r5 (where ρ is gas density). A common mixture is 70% helium and 30% oxygen. Applications where heliox may prove helpful include postextubation stridor and status asthmaticus.
What is compliance? How is it calculated?
Compliance is a measurement that reflects the amount of volume the pulmonary system can store for a given pressure. The overall compliance of the pulmonary system is determined by the lung, chest wall, and state of the patient’s respiratory cycle (inhalation or exhalation). Pulmonary compliance (C) can be calculated by measuring the change in volume for a given change in pressure:
C = ΔV/ΔP
Two factors that affect the compliance of the lung itself are: (1) water tension, (2) amount of functional lung connective tissue, such as elastin and collagen. A patient may exhibit decreased compliance from the lung itself (e.g., pulmonary fibrosis) or from decreased outward chest wall force (Fchest) and/or increased abdominal pressure (e.g., obesity, ascites, pregnancy).
Describe how pulmonary compliance changes with inspiration and expiration.
How the state of the respiratory cycle can impact lung compliance can be demonstrated as follows: at the end of exhalation, certain areas of the lung will favor atelectasis (i.e., zone 3 dependent regions) compared with others (i.e., zone 1 nondependent regions). Assume a patient takes a large breath from RV to TLC. At the start of inhalation, pulmonary compliance is low, because the atelectatic regions of the lung contain alveoli that are collapsed and water filled, thereby creating a less energetically favorable state (i.e., requiring more energy to inflate). After these alveoli are recruited, compliance increases until the lung is maximally inflated, at which point lung and chest wall compliance begin to decrease, impairing further inhalation. Here, the elastic recoil forces of the lung itself increase, and the chest wall, which normally favors lung expansion, reaches its maximum limit.
On exhalation, the pulmonary compliance for a given volume or pressure is higher than it is on inhalation. At the beginning of inhalation, atelectatic alveoli are recruited from closed to open, which initially decreases lung compliance (think of blowing up a deflated balloon); however, at the end of inhalation, these formerly atelectatic alveoli are now opened, favoring a higher overall compliance for a given volume or pressure during exhalation (it is easier to keep a balloon inflated once inflated). This concept is known as hysteresis, where the current state of a system
(i.e., pulmonary compliance) is dependent upon its past state (i.e., inhalation or exhalation).
What is surface tension? How does it affect pulmonary mechanics?
Surface tension occurs whenever you have an interface between two mediums (e.g., liquid and gas), where one consists of polar molecules (i.e., water) and the other of nonpolar molecules (i.e., oxygen and nitrogen). To minimize the interface between water (a polar molecule) with air (nonpolar molecules), water will preferentially form the shape of a closed sphere. This shape will yield the largest volume to surface area ratio possible. The large volume of the sphere will facilitate maximum hydrogen bonding between water molecules, while minimizing the exposed surface area (i.e., the interface that is exposed to nonpolar molecules, which cannot undergo hydrogen bonding with oxygen and nitrogen).
In a patent alveolus, water forms a coat on the surface (analogous to a bubble) with a surface tension that wants to collapse this bubble into sphere of water (resulting in atelectasis). Surface tension, resulting from hydrogen bonding, is the primary underlying force contributing to lung recoil and the promotion of atelectasis. However other factors, such as alveolar interdependence between walls of shared alveoli, prevent collapse. Further, the structure of alveoli is not spherical but rather more polygonal in shape. Taken together, alveolar interdependence, their polygonal shape, and probably other factors prevent the formation of perfectly spherical, collapsed alveoli, despite the natural tendency of water to do so.
To summarize, alveoli are coated by a layer of water, which creates an alveolar wall surface tension at the liquid-gas interface. This force plays an important role in understanding atelectasis and pulmonary compliance.
Discuss Laplace’s law. How does it apply to pulmonary physiology?
Laplace’s law describes the relationship of pressure across an interface (ΔP), wall-surface tension (T), and the radius (R) of a sphere. It can be used to model the physical properties of an alveolus. ΔP = 2T/R
The Laplace equation states that as the diameter (or radius) of an alveolus decreases, the pressure inside that alveolus will increase, assuming surface tension is constant. This implies that the pressure inside smaller alveoli is greater relative to larger alveoli, causing gas to preferentially flow from small to large alveoli. This would cause small alveoli to get smaller and smaller until atelectasis occurs, although the large alveoli would get larger and larger leading to volutrauma. Note, this phenomenon only occurs if the alveolar surface tension remains constant (i.e., patients who are deficient in pulmonary surfactant). As will be explained, surfactant plays an important role in stabilizing alveoli and preventing this problem from occurring.
What is surfactant?
Pulmonary surfactant is a phospholipid substance that contains both polar and nonpolar regions at opposite ends. It is produced in the lung by type II alveolar cells and coats the water already present in the alveoli. This coating forms an interface in the alveoli between the water (polar regions of surfactant) and air (nonpolar regions of surfactant) that reduces surface tension, thereby enabling alveoli to remain open at smaller lung volumes. Because water surface tension is responsible for approximately two-thirds of the recoil force of the
lung, pulmonary surfactant plays an important role in preventing atelectasis and increasing pulmonary compliance.
What role does surfactant play in pulmonary physiology?
Surfactant plays an important role in stabilizing alveoli.
When an alveolus becomes smaller (e.g., during exhalation), the concentration of surfactant increases, thereby decreasing water surface tension. Conversely, when the alveolus becomes larger, the concentration of surfactant decreases, causing water surface tension to increase.
Note how surface tension and alveolar radius are intrinsically linked; surface tension increases as radius increases and decreases as radius decreases. Thus this relationship helps minimize any differences in ΔP between smaller and larger alveoli (Laplace’s law).
Surfactant also plays a role in elastic recoil. As previously discussed, the concentration of surfactant is a function of alveolar size. Thus surfactant enables the lung to exhibit elastic properties similar to a rubber band, where its recoil force increases as the rubber band is stretched. This property allows the lung to exhibit a higher compliance at low TVs, while also facilitating exhalation at larger TVs.
Because surface tension plays such a large role in contributing to the lung’s elastic recoil forces, disorders associated with surfactant deficiency are readily apparent.
