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

FIGURE 2-2 Ultrastructure of the respiratory membrane. (From Guyton AC, Hall JE: Textbook of medical physiology, ed 9, Philadelphia, 1996, Saunders, p 508.)

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

V_T × RR = _E (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 (_A) and physiologic dead space ventilation (_D):

_E = _D + _A

where = 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 (d_anat) and alveolar dead space ventilation (d_A).

(3) Ratio of dead space to tidal volume (V_D/V_T) 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:

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 co₂ 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 = ↑ _A

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

Normal Paco₂ = normal _A

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

↑ Paco₂ = ↓ _A

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:

(1) Structural architecture of the upper respiratory tract, which reduces deposited and inhaled materials

(2) Processing system, including respiratory tract fluid alteration and phagocytic activity

(3) Transport system, which removes material from the lung

(4) Humoral and cell-mediated immune responses, which may be the most important bronchopulmonary defense mechanisms

(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

1) Normal quiet breathing is accomplished almost entirely by this dome-shaped muscle, which divides the chest from the abdomen

2) Divided into two “leaves”—the right and left hemidiaphragms

3) Downward contraction increases the superior-inferior diameter of the chest and elevates the lower ribs

4) Innervation is from the C3 to C5 level through the phrenic nerve

5) Normally, accounts for 75% of tidal volume during quiet inspiration

6) Facilitates vomiting, coughing and sneezing, defecation, and parturition

b) External intercostal muscles

1) Increase the anterior-posterior (A-P) diameter of the thorax by elevating the ribs

2) A-P diameter is about 20% greater during inspiration than during expiration

3) Innervation is from T1 to T11

c) Accessory muscles in the neck: Scalene and sternocleidomastoid

1) Lift upward on the sternum and ribs and increase A-P diameter

2) Are not used in normal, quiet ventilation

(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:

a) Abdominals: Force abdominal contents upward to elevate the diaphragm

b) Internal intercostals: Decrease A-P diameter by contracting and pulling the ribs inward

(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)

TABLE 2-1

Example of Changes in Pressures Throughout the Ventilatory Cycle

(1) Air flows into the lungs when intrapulmonary air pressure falls below atmospheric pressure

(2) Air flows out of the lungs when intrapulmonary air pressure exceeds atmospheric pressure

(3) Intrapleural pressure is normally negative with respect to atmospheric pressure as a result of the elastic recoil of the lungs, which tend to pull away from the chest wall. This “negative” pressure prevents the collapse of the lungs.

(4) Increased effort (forced inspiration or expiration) may produce much greater changes in intrapulmonary and intrapleural pressures during inspiration and expiration

(1) For protection: Sternum, spine, ribs

(2) Pleura

a) Visceral layer next to the lungs; parietal layer next to the chest wall

b) Pleural fluid between layers: Allows smooth movement of the visceral layer over the parietal layer

c) Adherence: Pleural space is normally a potential space (vacuum); because of a constant negative pressure (less than atmospheric pressure by 4 to 8 mm Hg), any change in the volume of the thoracic cage is reflected by a similar change in the volume of the lungs

d) Nerve supply: Parietal pleura has fibers for pain transmission, but visceral pleura does not

(d) Resistances

(1) Elastic resistance (static properties)

a) Lung, if removed from the chest, collapses to a smaller volume because of lung elastic recoil. This tendency of the lungs to collapse is normally counteracted by the chest wall tendency to expand. Volume of air in the lungs depends on the equal and opposite balance of these forces.

b) Compliance (C_L) is an expression of the elastic properties of the lung and is the change in volume (ΔV) accomplished by a change in pressure (ΔP):

If compliance is high, the lung is more easily distended; if compliance is low, the lung is stiff and more difficult to distend

(2) Flow resistance (dynamic properties)

a) Airway resistance must be overcome to generate flow through the airways

b) Changes in airway caliber affect airway resistance. Examples are changes caused by bronchospasm or secretions.

c) Flow through the airway depends on pressure differences between the two ends of the tube as well as resistance. Driving pressure for flow in airways is the difference between atmospheric and alveolar pressures.

(e) Work of breathing

(1) To minimize the work required to maintain a given level of ventilation, the body automatically changes the respiratory pattern

(2) Work performed must be sufficient to overcome the elastic resistance and the flow resistance

(3) In diseased states, the workload increases

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.

FIGURE 2-3 Schematic diagram depicting the organization of the respiratory control system. The dashed lines show feedback loops affecting the respiratory generator. Pco₂, Partial pressure of carbon dioxide; Po₂, partial pressure of oxygen. (From Weinberger SE: Principles of pulmonary medicine, ed 2, Philadelphia, 1992, Saunders, p 206.)

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

(1) One group initiates respiration and regulates its rate

(2) One group controls the “switching off” of inspiration and thus the onset of expiration

(b) Input from other regions of the CNS

(1) Pons: Input is necessary for normal, coordinated breathing

(2) Cerebral cortex: Exerts a conscious or voluntary control over ventilation

(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)

a) Respond not directly to blood partial pressure of carbon dioxide (Pco₂) but, rather, to the pH of the extracellular fluid (ECF) surrounding the chemoreceptor

b) Feedback loop for CO₂ can be summarized as follows: Increased arterial Pco₂ → increased brain ECF Pco₂ → decreased brain ECF pH → decreased pH at chemoreceptor → stimulation of central chemoreceptor → stimulation of medullary respiratory center → increased ventilation → decreased arterial Pco₂

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

a) Sensitive to changes in the partial pressure of oxygen (Po₂),with hypoxemia stimulating chemoreceptor discharge

b) Minor role in sensing Pco₂

(d) Other receptors

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

a) As the lung inflates, receptor discharge increases

b) Contribute to the start of expiration

(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

a) Cause rapid shallow breathing in response to deformation from increased interstitial volume due to high pulmonary capillary pressures (such as in heart failure or inflammation)

b) Stimulation can also cause bradycardia, hypotension, and expiratory constriction of the glottis

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

a) Involved in the fine tuning of ventilation

b) Adjust the output of the respiratory muscles for the degree of muscular work required

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 (D_L). 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

(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.

TABLE 2-2

Driving Pressures

PaCO₂, Arterial partial pressure of carbon dioxide; PAO₂, alveolar partial pressure of oxygen; PCO₂, mixed venous partial pressure of carbon dioxide; PO₂, mixed venous partial pressure of oxygen.

(1) During the breathing of 100% O₂, the alveolar O₂ tension (PAo₂) becomes so large that the difference between PAo₂ and Po₂ (mixed venous O₂ tension) significantly increases, proportionately increasing the driving pressure

(2) Therefore, hypoxemia due solely to diffusion defects is usually improved by breathing 100% O₂

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 = (P_b − 47) × FIo₂

where

47 = vapor pressure of water at 37° C (in mm Hg)

PIo₂ = pressure of inspired O₂

0.8 = assumed respiratory quotient (ratio of CO₂ produced to O₂ consumed per unit time)

P_b = barometric pressure (sea level normal P_b is 760 mm Hg)

FIo₂ = fraction (percent) of inspired O₂

Therefore,

FIo₂ (P_b − 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:

(1) Mismatching of ventilation () to perfusion () (/ abnormalities)

(2) Shunting

(3) Diffusion abnormalities

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)

FIGURE 2-4 The oxyhemoglobin dissociation curve, relating percent hemoglobin saturation and arterial partial pressure of oxygen (Pao₂). The normal curve is depicted by the solid line; the curves shifted to the right or left (along with the conditions leading to them), by the dashed lines. 2,3-DPG, 2,3-Diphosphoglycerate; Pco₂, partial pressure of carbon dioxide; Temp, temperature. (From Weinberger SE: Principles of pulmonary medicine, ed 2, Philadelphia, 1992, Saunders, p 10.)

(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

(1) Upper flat portion of the curve is the arterial association portion. Dissociation relationship in this range protects the body by enabling Hb to retain high saturation with O₂ despite large decreases (down to 60 mm Hg) in Pao₂.

(2) Lower steep portion of the curve is the venous dissociation portion. Dissociation relationship in this range protects the body by enabling the tissues to withdraw large amounts of O₂ with small decreases in Pao₂.

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

(1) When Po₂ is increased (as in pulmonary capillaries), O₂ binds readily with Hb

(2) When Po₂ is decreased (as in tissues), O₂ unloads from Hb

(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:

a) pH decrease (acidosis), the Bohr effect

b) Pco₂ increase

c) Increase in body temperature

d) Increased levels of 2,3-diphosphoglycerate (2,3-DPG)

(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:

a) pH increase (alkalosis), the Bohr effect

b) Pco₂ decrease

c) Temperature decrease

d) Decreased levels of 2,3-DPG

e) Carbon monoxide poisoning

(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

(a) P₅₀ = the partial pressure of O₂ at which the Hb is 50% saturated, standardized to a pH of 7.40

(b) Normal P₅₀ is about 26.6 mm Hg; varies with the disease process

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

(1) O₂ capacity is the maximal amount of O₂ the blood can carry. It is expressed in milliliters of O₂ per deciliter (100 ml) of blood (ml/dl) and is calculated by multiplying Hb in grams by 1.34.

(2) O₂ saturation is the percentage of Hb actually saturated with O₂ (Sao₂ or So₂) and is usually measured directly. It is equal to the O₂ content divided by the O₂ capacity multiplied by 100.

(3) O₂ content is the actual amount of O₂ the blood is carrying (oxyhemoglobin plus dissolved O₂)

O₂ content = (O₂ capacity × O₂ saturation) + (0.0031 × Pao₂)

(b) Systemic O₂ transport

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

(1) Normal cardiac output = approximately 5 to 6 L/min (range, 4 to 8 L/min)

(2) Normal arterial O₂ content = approximately 20 ml/dl

(3) Therefore, systemic O₂ transport averages about 1000 to 1200 ml/min

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 − Co₂) is the difference between arterial O₂ content (Cao₂) and mixed venous O₂ content (Co₂) and reflects the actual amount of O₂ extracted from the blood during its passage through the tissues

(a) Of the 1000 to 1200 ml of O₂ delivered per minute to tissues, cells typically use only about 250 to 300 ml (o₂ or O₂ consumption). If o₂ remains constant, changes in cardiac output can be related to changes in the Cao₂ − Co₂ gradient or difference. Mixed venous O₂ values are measured from the distal tip of pulmonary artery catheters.

(b) Normal Cao₂ − Co₂ is 4.5 to 6 ml/dl

(Hb × 1.34) (Sao₂ − So₂) + (Pao₂ − Po₂) (0.0031)

(c) Fall in Co₂ resulting in a rise in the Cao₂ − Co₂ gradient signifies decreased cardiac output and inadequate tissue perfusion if o₂ is constant

(d) These are average values; actual O₂ utilization is different for different tissues. The heart uses almost all the O₂ it receives.

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

(a) Physically dissolved (Paco₂), which accounts for 7% to 10% of CO₂ transported in the blood

(b) Chemically combined with Hb as carbaminohemoglobin. This reaction occurs rapidly, and reduced Hb can bind more CO₂ than oxyhemoglobin. Thus, unloading of O₂ facilitates loading of CO₂ (Haldane effect) and accounts for about 30% of CO₂ transport.

where CA = carbonic anhydrase

(1) Reaction accounts for 60% to 70% of CO₂ in the body

(2) Reaction is slow in plasma and fast in red blood cell owing to the CA enzyme

(3) When the concentration of these ions increases in red blood cells, HCO₃⁻ diffuses but H⁺ remains

(4) To maintain electrical neutrality, chloride diffuses from the plasma (the “chloride shift”)

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:

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

1) Mean pulmonary artery pressure: 10 to 15 mm Hg

2) Mean pulmonary venous pressure: 4 to 12 mm Hg

3) Mean pressure gradient: Approximately 10 mm Hg (considerably less than the systemic gradient)

4) Pressures are higher at the base of the lung than at the apex

5) Perfusion is better in the dependent areas of the lung

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

a) Transvascular fluid filtration in the lung (and all other organs) is described by the Starling equation. This means that fluid and solutes move due to increases or decreases in hydrostatic or osmotic filtration pressures or due to changes in the permeability of vessel walls to fluids or proteins.

b) Thus, excess fluid in the lung (pulmonary edema) can result from either a net increase in hydrostatic pressure forces (favoring filtration) or a decreased resistance to filtration

2) Metabolic transport

a) All cardiac output passes through the lung before reaching systemic circulation. Therefore, pulmonary circulation can influence the composition of the blood supplying all organs.

b) Several humoral substances are added, extracted, or metabolized in the lung. Examples are inactivation of vasoactive prostaglandins, conversion of angiotensin I to angiotensin II, and inactivation of bradykinin.

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

i. Pressure gradients allow for the diffusion of O₂ and CO₂ among systemic capillaries, interstitial fluid, and cells (Figures 2-5 and 2-6)

FIGURE 2-5 Diffusion of oxygen from a tissue capillary to the cells. Po₂, Partial pressure of oxygen. (From Guyton AC, Hall JE: Textbook of medical physiology, ed 9, Philadelphia, 1996, Saunders, p 514.)

FIGURE 2-6 Uptake of carbon dioxide by the blood in the capillaries. (Guyton AC, Hall JE: Textbook of medical physiology, ed 9, Philadelphia, 1996, Saunders, p 515.)

ii. Within the mitochondria of each individual cell, O₂ is consumed through aerobic metabolism. This process produces the energy bonds of adenosine triphosphate and the waste products of CO₂ and water.

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

i. Reduced ambient pressure (P_b) or reduced O₂ concentration of inspired air (FIo₂)

ii. If the lungs are normal, the A–a gradient will be normal

iii. Rarely a clinically important cause of arterial hypoxemia. Reduced P_B occurs at high altitudes in healthy humans and in enclosed spaces such as mine cave-ins where fresh air is not replenished; FIo₂ remains normal, however.

b. Alveolar hypoventilation (increased Paco₂)

i. Decrease in alveolar ventilation from disorders of the respiratory center, peripheral nerves that supply the muscles of respiration, the respiratory muscles of the chest wall, or the lungs; medications that diminish ventilation

ii. This causes an increase in Paco₂, which results in a fall in PAo₂ according to the alveolar air equation

iii. If the lungs are normal, the A–a gradient will be normal. Hypoxemia will improve with ventilation.

c. / mismatch

i. Most common cause of hypoxemia; A–a gradient increased

ii. Ideally, ventilation of each alveolus is accompanied by a comparable amount of perfusion, which yields a / ratio of 1.00. Usually, however, there is relatively more perfusion than ventilation, which yields a normal / ratio of 0.8. Normal amount of blood perfusing the alveoli () is 5 L/min, and normal amount of air ventilating the alveoli () is 4 L/min. Figure 2-7 presents in simplified form the possible relationships between ventilation and perfusion in the lung.

FIGURE 2-7 The theoretical respiratory unit. A, Normal ventilation, normal perfusion. B, Normal ventilation, no perfusion. C, No ventilation, normal perfusion. D, No ventilation, no perfusion. (From Shapiro BA, Peruzzi WT, Templin R, et al: Clinical application of blood gases, ed 5, St Louis, 1994, Mosby, p 22.)

iii. When / is decreased (<0.8), a decrease of ventilation in relation to perfusion has occurred. This is similar to a right-to-left shunt because more deoxygenated blood is returning to the left side of the heart. Low / ratios and hypoxemia occur together, because good areas of the lung cannot be overventilated to compensate for the underventilated areas. (Hb cannot be saturated to more than 100%.) Atelectasis, pneumonia, and pulmonary edema are clinical examples of intrapulmonary shunt.

iv. When / is increased (>0.8), a decreased perfusion relative to ventilation exists, the equivalent of dead space or wasted ventilation. Examples of cases in which this occurs are pulmonary emboli and cardiogenic shock.

v. Hypoxemia that is thought to be due to / mismatch can be corrected by giving the patient a simple incremental FIo₂ test. For example, if the Pao₂ increases significantly in response to an FIo₂ change from 0.30 to 0.60, the primary problem is low /. If the Pao₂ does not increase significantly, a right-to-left shunt exists.

d. Shunting

i. Shunting occurs when a portion of venous blood does not participate in gas exchange. An anatomic shunt may occur (a portion of right ventricular blood does not pass through the pulmonary capillaries) or a portion of pulmonary capillary blood may pass by airless alveoli.

ii. Normal physiologic shunting amounts to 2% to 5% of cardiac output (this is bronchial and thebesian vein blood)

iii. Shunting occurs in arteriovenous malformations, adult respiratory distress syndrome (ARDS), atelectasis, pneumonia, pulmonary edema, pulmonary embolus, vascular lung tumors, and intracardiac right-to-left shunts

iv. Breathing at an increased FIo₂ level does not correct shunting because not all blood comes into contact with open alveoli and shunted blood passes directly from pulmonary veins to arterial blood (venous admixture). Lack of improvement of hypoxemia with O₂ therapy is a hallmark of shunting.

v. Usually, shunting does not result in elevated Paco₂, even though shunted blood is rich in CO₂. Brain chemoreceptors sense elevated Paco₂ and respond by increasing ventilation.

vi. Shunting is measured by comparing mixed venous O₂ (from the pulmonary artery catheter) to arterial O₂ (Cao₂ − Co₂). Amount of true shunt can be estimated by having the patient breathe 100% O₂ for 15 minutes, which eliminates the effects of abnormal / and diffusion defects. Normal shunt is 5 vol% (5 ml/dl).

e. Diffusion defects

i. Seen in patients with a thickened alveolar-capillary membrane, as in pulmonary fibrosis, which enlarges the distance between alveolar gas and the pulmonary capillaries

ii. May be overcome by diffusion because the rate of diffusion always depends on the pressure gradient

iii. Is rarely a cause of hypoxemia by itself at rest but may contribute to hypoxemia in patients with / mismatch and/or shunting caused by a disease state or in certain patients during exercise

4. Acid-base physiology and blood gases

a. Terminology

i. Acid: Donor of hydrogen ions (H⁺); substance with a pH below 7.0

ii. Acidemia: Condition in which the blood pH is below 7.35

iii. Acidosis: Process (metabolic or respiratory) that causes acidemia

iv. Base: Acceptor of H⁺ ions; any substance with a pH above 7.0

v. Alkalemia: Condition in which the blood pH is above 7.45

vi. Alkalosis: Process (metabolic or respiratory) that causes alkalemia

vii. pH: Negative logarithm of the H⁺ ion concentration

(a) Increase in [H⁺] = lower pH, more acidic

(b) Decrease in [H⁺] = higher pH, more alkaline

b. Buffering: Normal body mechanism that occurs rapidly in response to acid-base disturbances to prevent changes in [H⁺]

i. Bicarbonate (HCO₃⁻) buffer system

[H⁺] + HCO₃⁻ ←→ H₂CO₃ ←→ CO₂ + H₂O

This system is very important because HCO₃⁻ can be regulated by the kidneys and CO₂ can be regulated by the lungs

ii. Phosphate system

iii. Hb and other proteins

c. Henderson-Hasselbalch equation: Defines the relationship between pH, Pco₂, and bicarbonate. Arterial pH is determined by the logarithm of the ratio of bicarbonate concentration to arterial Pco₂. Bicarbonate is regulated primarily by the kidney and Pco₂ is regulated by alveolar ventilation:

where pK = a constant (6.1)

i. As long as the ratio of HCO₃⁻ to CO₂ is about 20:1, the pH of the blood will be normal. It is this ratio, rather than the absolute values of each, that determines blood pH.

ii. pH must be maintained within a narrow range of normal because the functioning of most enzymatic systems in the body depends on the H⁺ concentration (Figure 2-8)

FIGURE 2-8 The balance between bicarbonate (HCO₃⁻) (24) and dissolved carbon dioxide (CO₂) (1.2 of arterial partial pressure of CO₂ [Paco₂] = 40) is normally 20:1, and this is usually associated with a pH of about 7.40 and an H⁺ concentration of about 40 nmol/L. (From Cherniack RM, Cherniack L: Respiration in health and disease, ed 3, Philadelphia, 1983, Saunders, p 85.)

d. Normal adult blood gas values (at sea level): See Table 2-3. Note: Knowledge of blood gas values neither supersedes nor replaces sound clinical judgment.

TABLE 2-3

Normal Adult Blood Gas Values (at Sea Level)

	Arterial	Mixed Venous
pH	7.40 (7.35-7.45)	7.36 (7.31-7.41)
PO₂	80-100 mm Hg	35-40 mm Hg
SaO₂	≥95%	70%-75%
PCO₂	35-45 mm Hg	41-51 mm Hg
HCO₃⁻	22-26 mEq/L	22-26 mEq/L
Base excess	− 2 to +2	− 2 to +2

HCO₃⁻, Bicarbonate; PCO₂, partial pressure of carbon dioxide; PO₂, partial pressure of oxygen; SaO₂, arterial oxygen saturation.

e. Effect of altitude on blood gas values

i. Pao₂ and Sao₂ are lower at high altitudes because of a lower ambient O₂ tension

ii. Normal for 5280 feet (Denver) = Pao₂ of 65 to 75 mm Hg, Sao₂ of 94% to 95%

f. Respiratory parameter (Paco₂): If the primary disturbance is in the Paco₂, the patient is said to have a respiratory disturbance

i. Paco₂ is a reflection of alveolar ventilation

(a) If increased, hypoventilation is present

(b) If decreased, hyperventilation is present

(d) To assess relationships, measurements of both Paco₂ and minute ventilation are needed

ii. Respiratory acidosis (elevated Paco₂), caused by hypoventilation of any etiology (may be acute or chronic). Treatment generally consists of improving alveolar ventilation.

(a) Obstructive lung disease, sleep apnea, and other lung diseases resulting in inadequate excretion of CO₂

(b) Oversedation, head trauma, anesthesia, and drug overdose

(d) Pneumothorax, flail chest, or other types of chest wall trauma that interfere with breathing mechanics

(e) Inappropriate mechanical ventilator settings

iii. Respiratory alkalosis (low Paco₂) caused by hyperventilation of any etiology. Treatment consists of correcting the underlying cause.

(a) Nervousness and anxiety

(b) Hypoxemia, interstitial lung disease

(c) Excessive ventilation with mechanical ventilator, as a response to metabolic acidosis (diabetic ketoacidosis) or from respiratory stimulant drugs, such as salicylates, theophylline, catecholamines

(d) Pregnancy

(e) Pulmonary embolus, pulmonary edema

(f) Bacteremia (sepsis), liver disease, or fever

(g) CNS disturbances, such as brainstem tumors and infections

g. Nonrespiratory (renal) parameters (HCO₃⁻): If the primary disturbance is in the bicarbonate level, the patient has a metabolic disturbance

i. Concentration influenced by metabolic processes

(a) When HCO₃⁻ is elevated, metabolic alkalosis results

(1) Loss of nonvolatile acid

(2) Gain of HCO₃⁻

(b) When HCO₃⁻ is decreased, metabolic acidosis results

(1) H⁺ is added in excess of the capacity of the kidney to excrete it

(2) HCO₃⁻ is lost at a rate exceeding the capacity of the kidney to regenerate it

ii. Causes of metabolic alkalosis (elevated HCO₃⁻)

(a) Chloride depletion (vomiting, prolonged nasogastric suctioning, diuretic therapy)

(b) Cushing’s syndrome, hyperaldosteronism, potassium deficiency, renal artery stenosis, licorice ingestion

(c) Exogenous administration of alkali (massive blood transfusions containing citrate, bicarbonate administration, ingestion of antacids)

iii. Causes of metabolic acidosis (decreased HCO₃⁻)

(a) Increase in unmeasurable anions (acids that accumulate in certain diseases and poisonings); high anion gap

(1) Diabetic ketoacidosis, starvation

(2) Drugs: Salicylates, ethylene glycol, methanol alcohol, paraldehyde

(3) Lactic acidosis resulting from tissue hypoperfusion and subsequent anaerobic metabolism (shock, sepsis)

(4) Renal failure, uremia

(5) Easy mnemonic is MULEPAK—methanol, uremia, lactic acidosis, ethylene glycol, paraldehyde, aspirin (salicylates), and ketoacidosis

(b) No increase in unmeasurable anions, normal anion gap

(1) Diarrhea, ureterosigmoidostomy (long or obstructed ileal conduit)

(2) Drainage of pancreatic juices

(3) Rapid IV infusion of non–bicarbonate-containing solutions causing a dilutional acidosis

(4) Certain drugs, renal tubular acidosis

(5) Hyperalimentation (causes hyperchloremic acidosis)

h. Compensation for acid-base abnormalities: Physiologic response to minimize pH changes by maintaining a normal bicarbonate to Pco₂ ratio

i. pH returned to near normal by changing component that is not primarily affected

ii. Respiratory disturbances result in kidney compensation, which may take several days to become maximal

(a) Compensation for respiratory acidosis

(1) Kidneys excrete more acid

(2) Kidneys increase HCO₃⁻ reabsorption

(3) Compensation is slow (days)

(b) Compensation for respiratory alkalosis

(1) Kidneys excrete HCO₃⁻

(2) Compensation is slow (days)

iii. Metabolic disturbances result in pulmonary compensation, which begins rapidly but takes a variable amount of time to reach maximal levels

(a) Compensation for metabolic acidosis

(1) Hyperventilation to decrease Paco₂

(2) Compensation is rapid (begins in 1 to 2 hours and reaches maximum in 12 to 24 hours)

(b) Compensation for metabolic alkalosis

(1) Hypoventilation (limited by the degree of the rise in Paco₂)

(2) Compensation is rapid (minutes to hours)

iv. Body does not overcompensate. Therefore, the acidity or alkalinity of the pH identifies the primary abnormality if there is only one. Abnormalities may be multiple; each is not a discrete entity. Mixed acid-base disturbances often occur.

i. Correction of acid-base abnormalities: Caused by a physiologic or therapeutic response

i. pH returned to normal by altering the component primarily affected; blood gas values are returned to normal

ii. Correction for respiratory acidosis: Increased ventilation, treatment of cause

iii. Correction for respiratory alkalosis: Decreased ventilation, treatment of cause

iv. Correction for metabolic acidosis

(a) Treatment of underlying cause

(b) Administration of bicarbonate intravenously or orally (given only under specific circumstances)

v. Correction for metabolic alkalosis

(a) Treatment of underlying cause

(b) Direct reduction by isotonic hydrochloric acid solution (cautious IV administration required) via a central line at a rate no higher than 0.2 mEq/kg/hr)

(c) Arginine monohydrochloride or ammonium chloride used rarely; acetazolamide (carbonic anhydrase inhibitor–diuretic) used in certain situations

j. Arterial blood gas (ABG) analysis

i. Purpose

(a) Shows end result of what occurs in the lung

(b) Confirms the presence of respiratory failure and indicates acid-base status

ii. Main components: Pao₂, Paco₂, pH, base excess, HCO₃⁻, Sao₂, O₂ content, Hb. Both FIo₂ and body temperature must be measured for proper interpretation. It is also essential to know whether HCO₃⁻ and SaO₂ are directly measured or are calculated.

k. Guidelines for interpretation of ABG levels and acid-base balance

i. Examine pH first (Table 2-4)

TABLE 2-4

Analysis of the Acid-Base Balance of an Arterial Blood Gas

pH and PaCO₂ go in opposite directions; pH and HCO₃⁻ go in the same direction.

HCO₃⁻, Bicarbonate; PaCO₂, arterial partial pressure of carbon dioxide.

(a) If pH is reduced (<7.35), the patient is acidemic

(1) If Paco₂ is elevated, the patient has respiratory acidosis

(2) If HCO₃⁻ is reduced, the patient has metabolic acidosis

(3) If Paco₂ is elevated and HCO₃⁻ is reduced, the patient has combined respiratory and metabolic acidosis

(b) If pH is elevated (>7.45), the patient is alkalemic

(1) If Paco₂ is decreased, the patient has respiratory alkalosis

(2) If HCO₃⁻ is elevated, the patient has metabolic alkalosis

(3) If Paco₂ is decreased and HCO₃⁻ is elevated, the patient has combined metabolic and respiratory alkalosis

(c) Expected change in pH for changes in Paco₂: Commonly used rule is that the pH rises or falls 0.08 (or 0.1) in the appropriate direction for each change of 10 mm in the Paco₂

(d) If the pH is normal (7.35 to 7.45), alkalosis or acidosis may still be present as a mixed disorder (Box 2-1)

BOX 2-1 ARTERIAL BLOOD GAS ANALYSIS: ACID-BASE EXAMPLE

pH: Normal, but on acidic side

Paco₂: Elevated—acidotic

HCO₃⁻: Elevated—alkalotic

Primary disorder is respiratory acidosis (pH is on the acidic side and Paco₂ is elevated). Secondary disorder is metabolic alkalosis (HCO₃⁻ is elevated) as compensation.

INTERPRETATION

Compensated respiratory acidosis (e.g., patient with stable chronic obstructive pulmonary disease).

ii. Assess the hypoxemic state and tissue oxygenation state (Box 2-2)

BOX 2-2 ARTERIAL BLOOD GAS ANALYSIS: OXYGENATION EXAMPLE

On 2 L/min O₂ by nasal cannula, at sea level

ANALYSIS

pH: Normal, not in lactic acidosis from hypoxia

Pao₂: Low but adequate

Sao₂: Low but adequate

Cao₂: Within normal limits

Hb: Elevated

Hct: Elevated

INTERPRETATION

Adequate oxygenation on 2 L/min O₂. Hb/Hct elevated as compensatory mechanism to increase O₂-carrying capacity and compensate for underlying lung disease (chronic obstructive pulmonary disease) producing hypoxemia.

Cao₂, Arterial oxygen concentration; Hb, hemoglobin level; Hct, hematocrit; HCO₃⁻, Bicarbonate; Paco₂, arterial partial pressure of carbon dioxide; Pao₂, arterial partial pressure of oxygen; Sao₂, arterial oxygen saturation.

(a) Arterial oxygenation is considered compromised when Hb saturation is less than 88% (Pao₂ is <60 mm Hg). If the Pao₂ is below 55 mm Hg, hypoxemia is present.

(b) If the patient is receiving supplemental O₂ therapy, Pao₂ values must be interpreted in relation to the FIo₂ delivered. One way involves examination of the two as a ratio (Pao₂/FIo₂). Normal Pao₂/FIo₂ ratio is 286 to 350, although levels as low as 200 may be clinically acceptable. Another way to assess oxygenation is to use the following formula to calculate the A–a arterial Po₂ gradient (PAo₂ − Pao₂):

PAo₂ = [FIo₂ (P_b − 47) − Paco₂]/R

where

47 = vapor pressure of water at 37° C (in mm Hg)

R = respiratory quotient, the ratio of CO₂ production to O₂ consumption (co₂/o₂); assumed to be 0.8

Normal PAo₂ − Pao₂ difference is less than 10 to 15 mm Hg. Although it provides an estimate of oxygenation, the gradient does not take into account the normal increasing gradient as a function of increasing FIo₂ levels. The higher the FIo₂, the larger the increase in the A–a gradient can be without changing the level of intrapulmonary shunt or oxygenation. (Note: Primarily used for patients on a ventilator when the FIo₂ is known. FIO₂ is unknown [and its value therefore unreliable] with other O₂ delivery methods, but it can be estimated.)

(d) Assessment of cardiac output and O₂ transport determines tissue oxygenation. Po₂ and So₂ may be useful guides in evaluating the adequacy of overall tissue oxygenation.

(e) Effectiveness of O₂ transport may be judged clinically by examining the patient carefully for mental status, skin color, urine output, and heart rate. Tests that measure end-organ function are also important clinical assessment tools.

Patient Assessment

1. Nursing history: Nursing history follows the sequence and length of the standard history-taking process and is modified as needed for acutely ill patients

a. Patient health history: Patient’s interpretation of his or her signs and symptoms and the emotional response to them play a significant role in the development or exacerbation of symptoms, especially as related to dyspnea

i. Common symptoms

(a) Dyspnea: Subjective feeling of shortness of breath or breathlessness; considered the sixth vital sign in pulmonary patients, in whom it may be more significant than pain

(1) Difficult to quantify objectively

a) Count the average number of words the patient is able to speak between breaths, or whether the patient can speak in full sentences

b) Ask the patient to rate breathing comfort on a visual analogue or dyspnea scale from 1 to 10

(2) Emotional problems may cause an increased awareness of respirations and complaints of inability to get enough air, despite normal blood gas values

(3) Dyspnea caused by increased work of breathing accompanies both obstructive and restrictive lung diseases as well as the dysfunction of nerves, respiratory muscles, or thoracic cage

(4) Question the patient regarding exercise tolerance; some dyspnea is normal with exercise but is abnormal if exercise tolerance is decreased

(5) Assess whether the patient’s dyspnea is acute or chronic, and whether it has recently increased or decreased

(6) Determine all circumstances under which dyspnea occurs (walking, stair climbing, eating) and how long the patient has experienced dyspnea with those activities

(7) Assess orthopnea or dyspnea when the patient is lying flat; ask how many pillows the patient generally uses for sleep and whether for comfort or shortness of breath

(8) Assess for paroxysmal nocturnal dyspnea by asking whether dyspnea ever awakens the patient from sleep

(9) Determine whether dyspnea is accompanied by other symptoms, such as cough, wheezing, or chest pain

(10) In some patients, it is difficult to differentiate cardiac from pulmonary dyspnea

(b) Cough: Normal when it occurs as a lung defense mechanism

(1) Determine whether cough is acute and self-limiting or chronic (lasting more than 6 weeks) and persistent

(2) Note any change in character and frequency

(3) Determine what the timing is (both daily and seasonal) and whether the cough is accompanied by sputum production, hemoptysis, wheezing, chest pain, blackouts or falls, or dyspnea

(4) Most common etiologic mechanisms

a) Inhaled irritants or airway diseases (asthma, bronchitis)

b) Aspiration or lung diseases (pneumonia, lung abscess, tumor)

c) Left ventricular failure (pulmonary edema)

d) Side effect of medications (some angiotensin-converting enzyme inhibitors)

(1) Quantify amount by asking how many teaspoons, cups, or shot glasses of sputum are coughed up daily

(2) Determine aggravating and alleviating factors

(3) Assess the character of the sputum (color, odor, consistency)

(4) Determine whether current sputum characteristics (quantity and quality) are changed from usual

(d) Hemoptysis: Expectoration of blood from the lungs or airways

(1) Determine whether the material coughed up is grossly bloody, blood streaked, or blood tinged (pinkish)

(2) Try to differentiate from hematemesis. Product of hemoptysis is often frothy, alkaline, and accompanied by sputum; product of hematemesis is nonfrothy, acidic, and dark red or brown, with food particles.

(3) Determine the approximate amount of blood produced in hemoptysis using a reasonable measurement guideline, such as the number of teaspoons or shot glasses per day. Assess whether all expectorated specimens contain blood or whether this is an isolated event.

(4) Blood may originate from the nasopharynx, airways, or lung parenchyma; blood from these sites remains red because of the contact with atmospheric O₂

(5) Etiologic mechanisms of hemoptysis fall into three categories by location: Airways, pulmonary parenchyma, and vasculature

a) Airways disease: Most common; bronchitis, bronchiectasis, and bronchogenic carcinoma

b) Parenchymal causes: Often infectious—tuberculosis (TB), lung abscess, pneumonia

c) Cardiovascular disease: Mitral stenosis, pulmonary embolism, pulmonary edema

d) Autoimmune disorders: Wegener’s granulomatosis, Goodpasture’s syndrome

(6) Suspect neoplasm if hemoptysis occurs in a patient without prior respiratory symptoms

(e) Chest pain: As a reflection of the respiratory system, does not originate in the lung, because the lung is free of sensory nerve fibers

(1) Chest wall pain: Arises from the parietal pleura, intercostal muscles, ribs, or overlying skin

a) Well localized

b) Often exacerbated by deep inspiration

(2) Diaphragm pain: Often caused by an inflammatory process; pain often referred to the ipsilateral shoulder

(3) Mediastinal pain: Caused by a mass or air under the mediastinum (pneumomediastinum); pain is substernal and dull

ii. Miscellaneous symptoms of respiratory disease: Postnasal drip, sinus pain, epistaxis, hoarseness, general fatigue, weight loss, fever, sleep disturbances, night sweats, anxiety, nervousness, anorexia

iii. Past medical history

(a) Question the patient regarding the presence of any allergy to either medications (herbal, over the counter) or food. Obtain a description of the type and severity of the reaction.

(b) Determine past instances of the present illness, with treatment and outcome. Assess for previous episodes of TB, exposure to TB, or positive TB skin test result. Assess for childhood lung diseases or infections such as asthma, pneumonia, and whooping cough. Record the treatment given (if any) and the length of time the patient followed the medication regimen.

(c) Identify past surgeries or hospitalizations: Dates, diagnosis, and complications; previous use of O₂ or mechanical ventilation

(d) Question about previous chest radiographs: Dates, reasons, findings

(e) Determine whether any pulmonary function tests were performed previously and the results if known

b. Family history (extremely important)

i. Assess for similar illness or signs and symptoms in the patient’s parents, siblings, and grandparents

ii. Determine the current state of health or cause of death for parents, siblings, and grandparents

iii. Find out if there is a family history of diseases such as asthma, cystic fibrosis, bronchiectasis, and α₁-antitrypsin deficiency (emphysema)

iv. Determine whether a family member ever had TB with consequent exposure of the patient

c. Social history and habits

i. Personal status: Assess education, socioeconomic class, marital status, general life satisfaction, interests

ii. Health habits

(a) Smoking

(1) Determine whether the patient is a current or past smoker of cigarettes, cigars, or pipe

a) Calculate pack-year history:

No. of packs/day × No. of years smoked = pack-years

b) Determine whether the patient has tried to quit and, if so, what methods were used and whether the effort was successful. If the patient is a former smoker, determine the time since the last cigarette; otherwise, determine the desire for information on smoking cessation resources and readiness to quit.

(2) Ascertain whether the patient has smoked marijuana or another inhaled recreational drug (e.g., crack cocaine). If so, attempt to quantify the amount and frequency of drug use.

(3) Determine whether the patient chews tobacco. If so, quantify the type chewed and the amount per day.

(b) Drinking habits: Determine the frequency and amount consumed, and the type of alcoholic and caffeine-containing beverages

(c) Eating habits: Assess the quality of meals (adequacy or excess) and determine whether any respiratory symptoms occur with eating (i.e., meal-induced dyspnea or cough)

(d) Sexual history: Question about sexual activity and orientation

iii. Home conditions: Assess economic conditions, housing quality, presence of any pets and their health, presence of allergens

iv. Occupational history: Assess past and present work conditions

(a) Determine whether the patient was exposed to heat and cold, industrial toxins, or pollutants during work or military duty

(b) Assess the duration of exposure and the use of protective devices

d. Medication history (prescription and over-the-counter medications or home remedies)

i. Determine current and recent medications, dosage, and the reason for prescribing

ii. Assess whether the patient is using any inhaled medications

(a) Identify the device used: Metered-dose inhaler (MDI), nebulizer, or other delivery device (e.g., Spinhaler, HandiHaler)

(b) Assess the frequency of use—on an as-needed basis or on a regular schedule

(c) If possible, have the patient demonstrate the technique for inhaling medication. Many patients use an incorrect technique when inhaling their medications, which results in reduced deposition of the drug in the lung and reduced efficacy. Patients should exhale completely, inhale the drug slowly and deeply, and then hold the breath for 10 seconds if possible.

(d) Preferred delivery methods: Powder delivery devices (nonaerosol), MDI with spacer, nebulizer, MDI with open mouth, MDI with closed mouth (least amount of medication delivered)

2. Nursing examination of patient

a. Physical examination data

i. Inspection

(a) Ensure that the patient is stripped to the waist and, if possible, seated

(1) Warm room and good lighting should be available

(2) Nurse must have a thorough knowledge of anatomic landmarks and lines (Figure 2-9)

FIGURE 2-9 Landmarks of the chest. A, Anterior chest wall. B, Posterior chest wall. C, Lateral chest wall. (Courtesy American Association of Critical-Care Nurses, Aliso Viejo, Calif.)

a) Manubrium, body, and xiphoid process of the sternum, right and left sternal borders

b) Angle of Louis, point of maximal impulse, suprasternal notch

c) Interspaces, ribs, costal margins, costal angle, and spinous processes

d) Pulmonary lobes and areas of contact with the chest wall (Figure 2-10)

FIGURE 2-10 Topographic position of lung fissures. A, Anterior chest. B, Posterior chest. C, and D, Lateral chest. (From Ahrens TS: Pulmonary data acquisition. In Kinney MR, Packa DR, Dunbar SB, editors: AACN’s clinical reference for critical care nursing, ed 3, St Louis, 1993, Mosby, p 690.)

e) Lines: Midclavicular, midsternal, anterior-axillary, midaxillary, posterior-axillary, vertebral, and midscapular

(b) Observe general condition and musculoskeletal development

(1) State of nutrition, debilitation, evidence of chronic disease

(2) Pectus carinatum: Sternum protrudes instead of being lower than the adjacent hemithoraces

(3) Pectus excavatum: Sternum is abnormally depressed between the anterior hemithoraces

(4) Kyphosis: Exaggerated A-P curvature of the spine

(5) Scoliosis: Lateral curvature of the spine, causing widened intercostal spaces on the convex side and crowding of the ribs on the concave side; when accompanied by kyphosis, it is called kyphoscoliosis. If severe, it can result in restrictive lung disease.

(c) Observe the A-P diameter of the thorax; normal A-P diameter is approximately one third the transverse diameter. In patients with obstructive lung disease, the A-P diameter may be as great as or greater than the transverse diameter (“barrel chest”).

(d) Observe the general slope of the ribs

(1) Ribs are normally at a 45-degree angle in relation to the spine

(2) In patients with emphysema, the ribs may be nearly horizontal

(e) Observe for asymmetry

(1) One side may be larger because of tension pneumothorax or pleural effusion

(2) One side may be smaller because of atelectasis or unilateral fibrosis

(3) If asymmetry is present, the abnormal side will move less than the normal side

(f) Look for retraction or bulging of the interspaces

(1) Retraction of the interspaces, which can be observed during inspiration, indicates more negative intrapleural pressure due to obstruction of the inflow of air or increased work of breathing

(2) Bulging of the interspaces may result from a large pleural effusion or pneumothorax, often seen during a forced expiration in patients with asthma or emphysema

(g) Observe the ventilatory pattern

(1) Assess the level of dyspnea and the work of breathing

a) Position in which the patient can breathe most comfortably. Patients with chronic obstructive pulmonary disease (COPD) often assume a forward-leaning position, resting the arms on the knees or a bedside table.

b) Use of accessory muscles of breathing

c) Use of pursed-lip breathing

d) Flaring of the ala nasi during inspiration, a common sign of air hunger, especially in ventilated patients

e) Paradoxical movement of the diaphragm

(2) Assess for inspiratory stridor—low-pitched or crowing inspiratory sounds that occur when the trachea or major bronchi are obstructed for one of the following reasons:

a) Tumor (intrinsic or extrinsic), foreign body

b) Severe laryngotracheitis or crushing injury

c) Goiter, scar, or granulation tissue

(3) Observe for expiratory stridor—low-pitched crowing sound heard on expiration. Causes include foreign body or intrathoracic, tracheal, or main-stem tumor.

(4) Observe for unusual movements with breathing; on inspiration, the chest and abdomen should expand or rise together. Paradoxical breathing occurs with respiratory muscle fatigue: On inspiration, the chest rises and the abdomen is drawn in because the fatigued diaphragm does not descend on inspiration as it should. Instead, the diaphragm is drawn upward by the negative intrathoracic pressure during inspiration.

(5) Observe and assess the ventilatory pattern

a) Eupnea: Normal, quiet respirations

b) Bradypnea: Abnormally slow rate of ventilation

c) Tachypnea: Rapid rate of ventilation

d) Hyperpnea: Increase in the depth and, perhaps, in the rate of ventilation. Overall result is increased tidal volume and minute ventilation.

e) Apnea: Complete or intermittent cessation of ventilation

f) Biot’s breathing: Two to three short breaths alternating with long, irregular periods of apnea

g) Cheyne-Stokes respiration: Periods of increasing ventilation, followed by progressively more shallow ventilations until apnea occurs; pattern typically repeats itself. Sometimes occurs in normal persons when asleep, and usually indicates CNS disease, heart failure, or sleep apnea.

(6) Splinting of respirations—act of resisting full inspiration in one or both lungs as a result of pain

(7) Flail chest—inward movement of a portion of the chest on inspiration, usually associated with trauma to the chest; from fracture of the rib cage in two or more sections

(h) Other observations

(1) General state of restlessness, pain, altered mental status, fright, or acute distress. Earliest signs of hypoxemia often include a change in mental status and restlessness.

(2) If O₂ is being administered, record the amount (flow in liters per minute), type of device (liquid, compressed gas), method of delivery (nasal cannula, Oxymizer, mask)

(3) Inspect the extremities

a) Clubbing of the fingers is a late sign of a chronic pulmonary or cardiac disease

b) Cigarette stains on the fingers suggest a current smoking habit

c) Lower-extremity edema indicates possible right-sided heart failure from chronic pulmonary disease and hypoxemia-induced pulmonary hypertension

(4) Observe for cyanosis

a) Fundamental mechanism of cyanosis is an increase in the amount of reduced (deoxygenated) Hb in the vessels of the skin caused by one of the following:

1) Decrease in the O₂ saturation of the capillary blood

2) Increase in the amount of venous blood in the skin as a result of the dilation of venules and capillaries

b) Visible cyanosis requires the presence of at least 5 g of reduced Hb per deciliter of blood

1) This is an absolute, not a relative, value. It is not the percentage of deoxygenated Hb that causes cyanosis but the amount of deoxygenated Hb without regard to the amount of oxyhemoglobin. Presence or absence of cyanosis may be an unreliable clinical sign.

2) In anemia, cyanosis may be difficult to detect because the absolute amount of Hb is too low. Conversely, patients with polycythemia may be cyanotic at higher levels of arterial O₂ saturation than those with normal Hb levels.

c) Discoloration suggestive of cyanosis may occur in patients with abnormal blood or skin pigments (methemoglobinemia, sulfhemoglobin, argyria)

d) Factors influencing cyanosis include the rate of blood flow, perfusion, skin thickness and color, the amount of Hb, cardiac output, and the perception of the examiner

e) Central versus peripheral cyanosis

1) Central cyanosis implies arterial O₂ desaturation or an abnormal Hb derivative. Both mucous membranes and skin are affected.

2) Peripheral cyanosis without central cyanosis may result from the slowing of perfusion to the tissues (cold exposure, shock, decreased cardiac output). O₂ saturation may be normal.

f) In carbon monoxide poisoning, O₂ saturation may be dangerously low without obvious cyanosis because carboxyhemoglobin causes the skin to turn a cherry red

(i) Assess for neck vein distention, neck masses, and enlarged nodes

(j) Look for superior vena caval syndrome: Distention of the neck veins and edema of the neck, eyelids, and hands; often seen with lung cancer

(k) In elderly patients, examination shows flattening of the ribs and diaphragm, decreased chest expansion, use of accessory muscles, marked bony prominences, loss of subcutaneous tissue, pronounced dorsal curve of the thoracic spine, increased A-P diameter relative to lateral diameter, dyspnea on exertion, dry mucous membranes, decreased ability to clear mucus, and hyperresonance from increased distensibility of the lung

ii. Palpation

(a) Palpate the thoracic muscles and skeleton, feeling for any of the following: Pulsations, palpable fremitus, tenderness, bulges, or depressions in the chest wall

(b) Expansion of the chest wall

(1) Examiner’s hands should be placed over the lower lateral aspect of the chest, with the thumbs along the costal margin anteriorly or meeting posteriorly in the midline

(2) Movement of the hands is noted on inspiration and expiration. Asymmetry of movement is always abnormal. Reduced chest wall movement is often seen in patients with barrel chest and emphysema.

(1) Deviations of the trachea toward the defect are seen in atelectasis, unilateral pulmonary fibrosis, pneumonectomy, hemidiaphragm paralysis, and the inspiratory phase of flail chest

(2) Deviation of the trachea to the side opposite the lesion is seen with neck tumors, thyroid enlargement, tension pneumothorax, pleural effusion, mediastinal mass, and the expiratory phase of flail chest

(d) Point of maximal impulse: Deviates with mediastinal shift

(e) Palpation of ribs and chest for tenderness, pain, or air in subcutaneous tissue (crepitus)

(f) Vocal fremitus, palpable vibration of the chest wall, produced by phonation

(1) Patient should be instructed to say the word ninety-nine loud enough so that the fremitus can be felt with uniform intensity. Some soft-spoken women may need to falsely lower their voice so that the fremitus can be felt. Examiner should place the hands on the patient’s chest wall.

(2) Diminished fremitus is seen in any condition that interferes with the transference of vibrations through the chest

a) Pleural effusion or thickening, pleural tumors

b) Pneumothorax with lung collapse or emphysema

c) Obstruction of the bronchus (sputum plugs or tumors)

(3) Increased fremitus results from any condition that increases the transmission of vibrations through the chest, such as the following:

a) Pneumonia, consolidation

b) Atelectasis (with open bronchus)

c) Pulmonary infarction or pulmonary fibrosis

d) Secretions with a patent airway

(g) Pleural friction fremitus

(1) Occurs when inflamed pleural surfaces rub together during ventilation, producing a “grating” sensation that coincides with the respiratory excursion

(2) May be palpable during both phases of ventilation but sometimes is felt only during inspiration

(h) Rhonchal fremitus

(1) Produced by the passage of air through thick exudate, secretions, or an area of stenosis in the trachea or major bronchi

(2) Unlike friction fremitus, rhonchal fremitus can be relieved by coughing, suctioning, or clearing the secretions from the tracheobronchial tree

(i) Subcutaneous emphysema: Indicates a leak of air under the skin due to a communication with the airway, mediastinum, or pneumothorax

(1) May be palpated over the area

(2) On auscultation, may be mistaken for crackles (rales)

iii. Percussion: Tapping or thumping of parts of the body to produce sound. Nature of the sound produced depends on the density of the structures immediately under the area percussed.

(a) Sound vibrations produced by percussion probably do not penetrate more than about 4 to 5 cm below the surface; therefore, solid masses deep in the chest cannot be outlined with percussion. In addition, because a lesion must be several centimeters in diameter to be detectable by percussion, only large abnormalities can be located.

(b) Procedure: Accomplished by striking the dorsal distal third finger of one hand, which is held against the thorax, with the distal tip of the flexed middle finger of the other hand

(1) Striking finger must strike only the stationary finger instantaneously and then be immediately withdrawn

(2) All movement is executed at the wrist

(3) Examiner must be sensitive to the sounds that are received from the chest wall

(4) One side of the chest is compared with the other side

(5) Percussion of the posterior chest: Patient inclines the head forward and rests the forearms on the thighs to move the scapulae laterally

(6) Percussion begins at the apices and continues downward to the bases, alternating side to side

(1) Resonance: Sound heard normally over the lungs

(2) Hyperresonance: Sound heard over the lungs in normal children, in the apices of the lungs relative to the base in an upright adult, and throughout the lung fields in adults with emphysema or pneumothorax

a) Lower in pitch than normal resonance

b) Relatively intense and easy to hear

c) Indicates increased air (less dense)

(3) Tympany: Produced by air in an enclosed chamber; does not occur in the normal chest except below the dome of the left hemidiaphragm, where it is produced by air in the underlying stomach or bowel

a) Relatively musical sound

b) Usually higher-pitched than normal resonance; the higher the tension within the viscus, the higher the pitch

(4) Dullness: Sound that is heard with lung consolidation, atelectasis, masses, pleural effusion, or hemothorax

a) Short, not sustained

b) Soft, not loud; similar to a dull thud

c) Indicates that more dense material (fluid or solid) is in the underlying thorax

d) Normally heard over the liver and heart

(d) Percussion for diaphragmatic excursion: Range of motion of the diaphragm may be estimated with percussion

(1) Instruct the patient to take a deep breath and hold it

(2) Determine the lower level of resonance-to-dullness change (the level of the diaphragm) by percussing downward until a definite change is heard in the percussion note. Mark the spot with a felt-tipped marker.

(3) After instructing the patient to exhale and hold the breath, repeat the procedure

(4) Distance between the levels at which the tone change occurs is the diaphragmatic excursion

a) Normal diaphragmatic excursion is about 3 to 4 cm; partial descent or hemidescent of the diaphragm may be due to paralysis of the diaphragm or hemidiaphragm. Suspect nerve injury in postoperative patients with these signs following thoracic surgery.

b) Diaphragm is normally higher on the right than the left

c) Diaphragm is elevated in conditions that increase intraabdominal pressure (pregnancy, ascites) and conditions that decrease thoracic volume (atelectasis)

d) Diaphragm is fixed and lower than normal in emphysema

e) It is difficult to differentiate between an elevated diaphragm and a thoracic disease that causes dullness to percussion (e.g., pleural effusion). Paralysis of one or both hemidiaphragms may be present.

iv. Auscultation: Listening to sounds produced within the body

(a) Basic points

(1) Examiner should always compare one lung to the other by moving the stethoscope back and forth across the chest starting at the top of the thorax and moving downward

(2) Listening to the anterior chest will cover the upper and middle lobes; listening to the back covers the bases (see Figure 2-10)

(3) Patient should be asked to breathe through the mouth a little more deeply than usual. This minimizes turbulent flow sounds produced in the nose and throat.

(4) Diaphragm of the stethoscope is more sensitive to higher-pitched tones and is thus best for hearing most lung sounds

(5) Stethoscope earpieces should fit snugly to exclude extraneous sounds but should not be so tight that they are uncomfortable

(6) Stethoscope tubing should be no longer than 20 inches. Optimal length is 12 to 14 inches.

(7) Place the stethoscope firmly on the chest to exclude extraneous sounds and eliminate sounds that result from light contact with the skin or air. Confusing sounds may be produced by moving the stethoscope on the skin or hair, breathing on the tubing, sliding the fingers on the tubing or chest piece, or listening through clothing.

(b) Normal breath sounds vary according to the site of auscultation

(1) Vesicular (always normal)

a) Soft sounds heard over the anterior, lateral, and posterior chest

b) Heard primarily during inspiration

(2) Bronchial (may be normal or abnormal, depending on the location of the sounds)

a) Heard normally over the trachea

b) High-pitched, harsh sound with long and loud expirations

c) When heard over the lung fields, the sound is abnormal and suggests consolidation

(3) Bronchovesicular (normal or abnormal, depending on the location)

a) Heard over large bronchi (near the sternum, between the scapulae, over the right upper lobe apex)

b) Abnormal when heard over the lung fields; signifies consolidation

(1) Absent or diminished sounds caused by decreased airflow (airway obstruction, COPD, muscle weakness, splinting) or increased insulation blocking the transmission of sounds to the stethoscope (obesity, pleural disease or fluid, pneumothorax)

(2) Bronchial sounds heard over the lung fields suggest consolidation or increased density of lung tissue (e.g., atelectasis, pulmonary infarction, pneumonia, large tumors with no airway obstruction)

(d) Adventitious sounds: Abnormal sounds that are superimposed on underlying breath sounds

(1) Evaluate whether position and coughing affect the sounds

(2) Terminology

a) Crackles (rales): Signify the opening of collapsed alveoli and small airways

1) Described as fine or coarse

2) Heard as small pops or crackles; the sound of fine crackles can be mimicked by rubbing together a few pieces of hair near one’s ear. Sound of coarse crackles can be mimicked by pulling open Velcro material.

3) Fine crackles occurring late in inspiration imply conditions that cause restrictive ventilatory defect

4) Fine crackles heard early in inspiration are often atelectatic, due to small airway closure

5) Coarse early inspiratory crackles are associated with bronchitis or pneumonia

b) Wheeze: Indicates an obstruction to airflow or air passing through narrowed airways

1) Continuous high-pitched sound with musical quality; also called “sibilant” wheeze

2) Commonly heard during expiration but may be heard during inspiration

3) Causes: Asthma, bronchitis, foreign body, tumor, pulmonary edema, pulmonary emboli, poorly mobilized secretions

c) Gurgles (rhonchi): Result from the passage of air through secretions in the large airways

1) Low-pitched, continuous sounds

2) May have a snoring quality when very large airways are involved (“sonorous” wheezes)

3) Tend to improve or disappear after coughing

d) Pleural friction rub: Indicates inflammation and loss of pleural fluid

1) Grating, harsh sound in inspiration and expiration; disappears with breath holding. Sound can be mimicked by cupping a hand over one’s ear and rubbing the fingers of the other hand over the cupped hand.

2) Heard with pleural infections, infarction, pulmonary emboli, fractured ribs. Located in the area of most intense chest wall pain.

e) Mediastinal crunch: Indicates air in the pericardium, mediastinum, or both. Heard synchronously with systole; often associated with pericardial friction rubs.

f) Pericardial friction rub

1) Occurs at atrial and ventricular systole with or without a diastolic component

2) Sounds persist with breath holding; heard most clearly at the left lower sternal border

(e) Voice sounds: Spoken words are modified by disease in a manner similar to breath sounds, which results in the increased or decreased conduction of sound

(1) Increased conduction occurs when normal lung tissue is replaced with denser, more solid tissue; it is associated with bronchial breathing

a) Bronchophony: Spoken word (e.g., ninety-nine) is heard distinctly but normal sound is muffled

b) Egophony: E sound changes to A; sound has the quality of sheep bleating

c) Whispered pectoriloquy: Whispered sounds are heard with clarity, as if the patient were speaking into the diaphragm of the stethoscope, but normal sound is muffled

(2) Decreased conduction of sound occurs in the presence of obstructed bronchi, pneumothorax, or large collections of fluid or tissue between the lung and the chest wall

a) Decreased ability to hear voice sounds

b) Accompanied by decreased fremitus

b. Monitoring data

i. Pulse oximetry

(a) Noninvasive estimate of arterial O₂ saturation (Spo₂) using an infrared light source placed at the finger or other acceptable extremity, forehead, or earlobe

(b) Uses two principles for measurement

(1) Spectrophotometry measures the infrared light absorption of Hb (to distinguish saturated from reduced Hb)

(2) Photoplethysmography uses light to measure the arterial pressure waveforms generated by the pulse (pulse rate and strength) in the capillaries of the tissue at the measurement site

(c) Pulse oximeters are generally accurate in the Spo₂ range of 70% to 100% but are inaccurate in states of low blood flow (decreased perfusion due to hypovolemia, hypotension, or vasoconstriction)

(d) Spo₂ reading is adversely affected by the following:

(1) Motion of the extremity (false pulse rate and waveform artifact)

(2) Light dilution (interferes with the probe’s ability to detect the correct light wavelength)

(3) Abnormal Hb (device cannot distinguish between oxyhemoglobin and carboxyhemoglobin and thus overestimates saturation); methemoglobin may interfere with light absorption

(4) IV dyes, some fingernail polish colors (e.g., metallic, dark colors such as black), or abnormal skin pigmentation (interfere with light absorption)

(5) Anemia (Hb level below 5 g/dl may result in insufficient signal to process readings)

(e) Useful for identifying the trend of changes in Pao₂ or acute desaturation episodes, especially when weaning from a ventilator

(f) Extreme caution must be exercised not to overrely on a normal Spo₂ level to indicate normal oxygenation in all cases. Numerous clinical situations (e.g., COPD) may cause erroneous readings. If in doubt, get an ABG.

ii. So₂ monitoring

(a) Mixed venous oxygen saturation (So₂) is monitored in the pulmonary artery, at the distal end of a flow-directed thermodilution pulmonary artery catheter

(b) Catheter holds an optical module that contains a light-emitting source, a photodetector, and a microprocessor to analyze reflected light

(c) Reflectance spectrophotometry is used to differentiate oxygenated blood from deoxygenated blood through light wavelengths in the red and infrared spectra

(d) Continuous So₂ monitoring allows for assessment of global oxygenation. It can detect cardiopulmonary instability and changes prior to changes in other hemodynamic parameters (Table 2-5). Some specific indications include the following:

TABLE 2-5

Factors Associated with Fluctuations in Mixed Venous Oxygen Saturation (So₂

From Jesurum J: SO₂ monitoring. In Chulay M, Gawlinski A, editors: Hemodynamic monitoring protocols for practice, Aliso Viejo, Calif, 1998, American Association of Critical-Care Nurses. Used with permission.