The Pulmonary System

CHAPTER 2

The Pulmonary System

SYSTEMWIDE ELEMENTS

Physiologic Anatomy

1. Respiratory circuit

a. The pulmonary system exists for the purpose of gas exchange. Oxygen (O2) and carbon dioxide (CO2) are exchanged between the atmosphere and the alveoli, between the alveoli and pulmonary capillary blood, and between the systemic capillary blood and all body cells.

b. Atmospheric O2 is consumed by the body through cellular aerobic metabolism, which supplies the energy for life

c. CO2, a by-product of aerobic metabolism, is eliminated primarily through lung ventilation

d. The respiratory circuit includes all structures and processes involved in the transfer of O2 between room air and the individual cell, and the transfer of CO2 between the cell and room air

e. Cellular respiration cannot be directly measured but is estimated by the amount of CO2 produced (imageco2) and the amount of O2 consumed (imageo2). Ratio of these two values is called the respiratory quotient. Respiratory quotient is normally about 0.8 but changes according to the nutritional substrate being burned (i.e., protein, fats, or carbohydrates). Patients fully maintained on intravenous (IV) glucose alone will have a respiratory quotient approaching 1.0 as a result of the metabolic end product, CO2.

f. Exchange of O2 and CO2 at the alveolar-capillary level (external respiration) is called the respiratory exchange ratio (R). This is the ratio of the CO2 produced to the O2 taken up per minute. In homeostasis, the respiratory exchange ratio is the same as the respiratory quotient, 0.8.

g. Proper functioning of the respiratory circuit requires efficient interaction of the respiratory, circulatory, and neuromuscular systems

h. In addition to its primary function of O2 and CO2 exchange, the lung also carries out metabolic and endocrine functions as a source of hormones and a site of hormone metabolism. In addition, the lung is a target of hormonal actions by other endocrine organs.

2. Steps in the gas exchange process

a. Step 1—Ventilation: Volume change, or the process of moving air between the atmosphere and the alveoli and distributing air within the lungs to maintain appropriate concentrations of O2 and CO2 in the alveoli

i. Structural components involved in ventilation

(a) Lung

(b) Conducting airways: Entire area from the nose to the terminal bronchioles where gas flows, but is not exchanged, is called anatomic dead space (Vdanat). Amount is approximately 150 ml but varies with patient size and position. Airways are a series of rapidly branching tubes of ever-diminishing diameter that eventually terminate in the alveoli.

(1) Nose

(2) Pharynx: Posterior to nasal cavities and mouth

(3) Larynx: Complex structure consisting of incomplete rings of cartilage and numerous muscles and ligaments

a) Vocal cords: Speech function

b) Valve action by the epiglottis helps to prevent aspiration

c) Cough reflex: Cords close and intrathoracic pressure increases to permit coughing or Valsalva maneuver

d) Cricoid cartilage

(4) Trachea: Tubular structure consisting of 16 to 20 incomplete, or C-shaped, cartilaginous rings that stabilize the airway and prevent complete collapse with coughing

(5) Major bronchi and bronchioles

(6) Terminal bronchioles

(c) Gas exchange airways: Semipermeable membrane permits the movement of gases according to pressure gradients. These airways are not major contributors to airflow resistance but do contribute to the distensibility of the lung. The acinus (terminal respiratory unit) is composed of the respiratory bronchiole and its subdivisions (Figure 2-1).

(1) Respiratory bronchioles and alveolar ducts

(2) Alveoli and alveolar bud

a) Most important structures in gas exchange

b) Alveolar surface area is large and depends on body size. Total surface area is about 70 m2 in a normal adult. Thickness of the respiratory membrane is about 0.6 μm. This fulfills the need to distribute a large quantity of perfused blood into a very thin film to ensure near equalization of O2 and CO2.

c) Alveolar cells

d) Pulmonary surfactant

e) Alveolar-capillary membrane (alveolar epithelium, interstitial space, capillary endothelium)

f) Gas exchange pathway (Figure 2-2): Alveolar epithelium → alveolar basement membrane → interstitial space → capillary basement membrane → capillary endothelium → plasma → erythrocyte membrane → erythrocyte cytoplasm

ii. Alveolar ventilation (imageA): That part of total ventilation taking part in gas exchange and, therefore, the only part useful to the body

(a) Alveolar ventilation is one component of minute ventilation

(1) Minute ventilation (imageE): Amount of air exchanged in 1 minute. Equal to exhaled tidal volume (VT) multiplied by respiratory rate (RR or f). Normal resting minute ventilation in an adult is about 6 L/min:

VT × RR = imageE (500 ml × 12 = 6000 ml)

    Tidal volume is easily measured at the bedside by hand-held devices or a mechanical ventilator. Exhaled minute ventilation is a routinely measured parameter for patients on ventilators.

(2) Minute ventilation is composed of both alveolar ventilation (imageA) and physiologic dead space ventilation (imageD):

imageE = imageD + imageA

where image = volume of gas per unit of time

    Physiologic dead space ventilation is that volume of gas in the airways that does not participate in gas exchange. It is composed of both anatomic dead space ventilation (imagedanat) and alveolar dead space ventilation (imagedA).

(3) Ratio of dead space to tidal volume (VD/VT) is measured to determine how much of each breath is wasted (i.e., does not contribute to gas exchange). Normal values for spontaneously breathing patients range from 0.2 to 0.4 (20% to 40%).

(b) Alveolar ventilation cannot be measured directly; it is inversely related to arterial CO2 pressure (Paco2) in a steady state by the following formula:

image

where 0.863 = correction factor for differences in measurement units and conversion to STPD (standard temperature [0° C] and pressure [760 torr], dry)

(c) Since imageco2 remains the same in a steady state, measurement of the patient’s Paco2 reveals the status of the alveolar ventilation

(d) Paco2 is the only adequate indicator of effective matching of alveolar ventilation to metabolic demand. To assess ventilation, Paco2 must be measured.

(e) If Paco2 is low, alveolar ventilation is high; hyperventilation is present

↓ Paco2 = ↑ imageA

(f) If Paco2 is within normal limits, alveolar ventilation is adequate

Normal Paco2 = normal imageA

(g) If Paco2 is high, alveolar ventilation is low and hypoventilation is present

↑ Paco2 = ↓ imageA

iii. Defense mechanisms of the lung

(a) Although an internal organ, the lung is unique in that it has continuous contact with particulate and gaseous materials inhaled from the external environment. In the healthy lung, defense mechanisms successfully defend against these natural materials by the following means:

(b) Loss of normal defense mechanisms may be precipitated by disease, injury, surgery, insertion of an endotracheal tube, or smoking

(c) Upper respiratory tract warms and humidifies inspired air, absorbs selected inhaled gases, and filters out particulate matter. Soluble gases and particles larger than 10 μm are aerodynamically filtered out. Normally, no bacteria are present below the larynx.

(d) Inhaled and deposited particles reaching the alveoli are coated by surface fluids (surfactant and other lipoproteins) and are rapidly phagocytized by pulmonary alveolar macrophages

(e) Macrophages and particles are transported in mucus by bronchial cilia, which beat toward the glottis and move materials in a mucus-fluid layer, eventually to be expectorated or swallowed. This process is referred to as the mucociliary escalator. Pulmonary lymphatics also drain and transport some cells and particles from the lung.

(f) Antigens activate the humoral and cell-mediated immune systems, which add immunoglobulins to the surface fluid of the alveoli and activate alveolar macrophages

(g) Disruption of or injury to these defense mechanisms predisposes to acute or chronic pulmonary disease

iv. Lung mechanics

(a) Muscles of respiration: Act of breathing is accomplished through muscular actions that alter intrapleural and pulmonary pressures and thus change intrapulmonary volumes

(1) Muscles of inspiration: During inspiration, the chest cavity enlarges. This enlargement is an active process brought about by the contraction of the following:

a) Diaphragm: Major inspiratory muscle

b) External intercostal muscles

c) Accessory muscles in the neck: Scalene and sternocleidomastoid

(2) Muscles of expiration: During expiration, the chest cavity decreases in size. This is a passive act unless forced, and the driving force is derived from lung recoil. Muscles used when increased levels of ventilation are needed are the following:

(b) Pressures within the chest: Movement of air into the lungs requires a pressure difference between the airway opening and alveoli sufficient to overcome the resistance to airflow of the tracheobronchial tree (Table 2-1)

(c) Structural components of the thorax

(d) Resistances

(1) Elastic resistance (static properties)

(2) Flow resistance (dynamic properties)

(e) Work of breathing

v. Control of ventilation: Although the process of breathing is a normal rhythmic activity that occurs without conscious effort, it involves an intricate controlling mechanism within the central nervous system (CNS). Basic organization of the respiratory control system is outlined in Figure 2-3.

(a) Respiratory generator: Located in the medulla and composed of two groups of neurons

(b) Input from other regions of the CNS

(c) Chemoreceptors: Contribute to a feedback loop that adjusts respiratory center output if blood gas levels are not maintained within the normal range

(1) Central chemoreceptors: Located near the ventrolateral surface of the medulla (but are separate from the medullary respiratory center)

(2) Peripheral chemoreceptors: Located in the carotid body and aortic body

(d) Other receptors

(1) Stretch receptors in the bronchial wall respond to changes in lung inflation (Hering-Breuer reflex)

(2) Irritant receptors in the lining of the airways respond to noxious stimuli, such as irritating dust and chemicals

(3) “J” (juxtacapillary) receptors in the alveolar interstitial space

(4) Receptors in the chest wall (in the intercostal muscles)

b. Step 2—Diffusion: Process by which alveolar air gases are moved across the alveolar-capillary membrane to the pulmonary capillary bed and vice versa. Diffusion occurs down a concentration gradient from a higher to a lower concentration. No active metabolic work is required for the diffusion of gases to occur. Work of breathing is accomplished by the respiratory muscles and the heart, which produce a gradient across the alveolar-capillary membrane.

i. Ability of the lung to transfer gases is called the diffusing capacity of the lung (DL). Diffusing capacity measures the amount of gas (O2, CO2, carbon monoxide) diffusing between the alveoli and pulmonary capillary blood per minute per millimeter Hg mean gas pressure difference.

ii. CO2 is 20 times more diffusible across the alveolar-capillary membrane than O2. If the membrane is damaged, its decreased capacity for transporting O2 into the blood is usually more of a problem than its decreased capacity for transporting CO2 out of the body. Thus, the diffusing capacity of the lungs for O2 is of primary importance.

iii. Diffusion is determined by several variables:

(a) Surface area available for gas exchange

(b) Integrity of the alveolar-capillary membrane

(c) Amount of hemoglobin (Hb) in the blood

(d) Diffusion coefficient of gas as well as contact time

(e) Driving pressure: Difference between alveolar gas tensions and pulmonary capillary gas tensions (Table 2-2). This is the force that causes gases to diffuse across membranes.

iv. A–a gradient (PAo2 − Pao2) is the alveolar to arterial O2 pressure difference (i.e., the difference in the partial pressure of O2 in the alveolar gas spaces [PAo2] and the pressure in the systemic arterial blood [Pao2]). This gradient is always a positive number.

(a) Normal gradient in young adults is less than 10 mm Hg (on room air) but increases with age and may be as high as 20 mm Hg in people over age 60 years

(b) A–a gradient provides an index of how efficient the lung is in equilibrating pulmonary capillary O2 with alveolar O2. It indicates whether gas transfer is normal.

(c) Large A–a gradient generally indicates that the lung is the site of dysfunction (except with cardiac right-to-left shunting)

(d) Formula for calculation (on room air)

A–a gradient = PAo2 − Pao2

PAo2 = PIo2 − (Paco2 ÷ 0.8)

PIo2 = (Pb − 47) × FIo2

where

Therefore,

FIo2 (Pb − 47) − (Paco2 ÷ 0.8) − Pao2 = A–a gradient

Example of calculation:

0.21 (760 − 47) − (40 ÷ 0.8) − 90 = 10

(e) Normally, A–a gradient increases with age and increased FIo2

(f) Pathologic conditions that increase the A–a gradient (difference) include the following:

c. Step 3—Transport of gases in the circulation

i. Approximately 97% of O2 is transported in chemical combination with Hb in the erythrocyte and 3% is carried dissolved in the plasma. Pao2 is a measurement of the O2 tension in the plasma and is a reflection of the driving pressure that causes O2 to dissolve in the plasma and combine with Hb. Thus, O2 content is related to Pao2.

ii. Oxyhemoglobin dissociation curve (Figure 2-4)

(a) Relationship between O2 saturation (and content) and Pao2 is expressed in an S-shaped curve that has great physiologic significance. It describes the ability of Hb to bind O2 at normal Pao2 levels and release it at lower Po2 levels.

(b) Relationship between the content and pressure of O2 in the blood is not linear

(c) Hb O2 binding is sensitive to O2 tension. The binding is reversible; the affinity of Hb for O2 changes as Po2 changes.

(d) Increase in the rate of O2 utilization by tissues causes an automatic increase in the rate of O2 release from Hb

(e) Shifts of the oxyhemoglobin curve

(1) Shifts to the right: More O2 is unloaded for a given Po2, which thus increases O2 delivery to the tissues. These shifts are caused by the following:

(2) Shifts to the left: O2 is not dissociated from Hb until tissue and capillary O2 are very low, which thus decreases O2 delivery to the tissues. These shifts are caused by the following:

(3) 2,3-DPG is an intermediate metabolite of glucose that facilitates the dissociation of O2 from Hb at the tissues. Decreased levels of 2,3-DPG impair O2 release to the tissues. This may occur with massive transfusions of 2,3-DPG–depleted blood and anything that decreases phosphate levels.

iii. Ability of Hb to release O2 to the tissues is commonly assessed by evaluating the P50

iv. Each gram of normal Hb can maximally combine with 1.34 ml of O2 when fully saturated (values of 1.36 or 1.39 are sometimes used)

v. Amount of O2 transported per minute in the circulation is a factor of both the arterial O2 concentration (Cao2) and cardiac output. This amount reflects how much O2 is delivered to tissues per minute and is dependent on the interaction of the circulatory system (delivery of arterial blood), erythropoietic system (Hb in red blood cells), and respiratory system (gas exchange) according to the following equations:

(a) O2 content (Cao2) is calculated from O2 saturation, O2 capacity, and dissolved O2

(b) Systemic O2 transport

ml/min = arterial O2 content (ml/dl) × cardiac output (L/min) × 10 (conversion factor)

vi. Focusing only on the O2 tension of the blood is unwise because an underestimation of the severity of hypoxemia may result. O2 content and transport are more reliable parameters because they take into account the Hb concentration and cardiac output.

vii. Arterial–mixed venous differences in O2 content (Cao2 − Cimageo2) is the difference between arterial O2 content (Cao2) and mixed venous O2 content (Cimageo2) and reflects the actual amount of O2 extracted from the blood during its passage through the tissues

viii. CO2 transport: CO2 is carried in the blood in three forms, as follows:

ix. Pulmonary circulation (pulmonary artery, arterioles, capillary network, venules, and veins)

(a) Pulmonary vessels are peculiarly suited to maintaining a delicate balance of flow and pressure distribution that optimizes gas exchange. They are richly innervated by the sympathetic branch of the autonomic nervous system.

(b) In contrast to the systemic circulation, the pulmonary circulation is a low-resistance system. Pulmonary arteries have far thinner walls than systemic arteries do, and vessels distend to allow for increases in volume from systemic circulation. Intrapulmonary blood volume increases or decreases of approximately 50% occur with changes in the relationship between intrathoracic and extrathoracic pressure.

(c) Pulmonary arteries accompany the bronchi within the lung and give rise to a rich capillary network within the alveolar walls. Pulmonary veins are not contiguous with the bronchial tree.

(d) Primary function of the pulmonary circulation is to act as a transport system

(1) Transport of blood through the lung

    a) Flow resistance through vessels (R) is defined by Ohm’s law:

image

where

        ΔP = the pressure difference between the two ends of the vessel (upstream and downstream pressures)

F = flow

Driving pressure for flow in the pulmonary circulation is the difference between the inflow pressure in the pulmonary artery and the outflow pressure in the left atrium

    b) In the lung, measurement of flow resistance is pulmonary vascular resistance (PVR)

PVR = [mean pulmonary artery pressure − mean left atrial (or pulmonary wedge) pressure] ÷ cardiac output

    c) About 12% of the total blood volume of the body is in the pulmonary circulation at any given time

    d) Normal pressures in the pulmonary vasculature

    e) Unique characteristic of the pulmonary arterial bed is that it constricts in response to hypoxia. Diffuse alveolar hypoxia causes generalized vasoconstriction, which results in pulmonary hypertension. Localized hypoxia causes localized vasoconstriction that does not increase pulmonary hypertension. This localized vasoconstriction directs blood away from poorly ventilated alveoli and thus improves overall gas exchange.

    f) Chronic pulmonary hypertension (increased PVR) can result in right ventricular hypertrophy (cor pulmonale)

        1) Transvascular transport of fluids and solutes

        2) Metabolic transport

d. Step 4—Diffusion between the systemic capillary bed and body tissue cells

3. Hypoxemia: Hypoxemia is a state in which the O2 pressure or saturation of O2 in arterial blood, or both, is lower than normal. Hypoxemia is generally defined as Pao2 less than 55 mm Hg or Sao2 below 88% at sea level in an adult breathing room air. Disorders that lead to hypoxemia do so through one or more of the following processes.

a. Low inspired O2 tension

b. Alveolar hypoventilation (increased Paco2)

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Oct 29, 2016 | Posted by in NURSING | Comments Off on The Pulmonary System

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