Factors Affecting Body Temperature

Table 2-2 lists several factors that affect body temperature. Knowing these factors can help the practitioner to better assess the significance of expected or normal variations in a patient’s body temperature.

Body Temperature Measurement

The measurement of body temperature establishes an essential baseline for clinical comparison as a disease progresses or as therapies are administered. To ensure the reliability of a temperature reading, the practitioner must (1) select the correct measuring equipment, (2) choose the most appropriate site, and (3) use the correct technique or procedure. The four most commonly used sites are the mouth, rectum, ear (tympanic), and axilla. Any of these sites is satisfactory when proper technique is used.

Additional measurement sites include the esophagus and pulmonary artery. Temperatures measured at these sites and in the rectum and at the tympanic membrane are considered core temperatures. The skin, typically that of the forehead or abdomen, may also be used for general temperature purposes. However, practitioners must remember that although skin temperature–sensitive strips or disposable paper thermometers may be satisfactory for general temperature measurements, the patient’s precise temperature should always be confirmed—when indicated—with a glass or tympanic thermometer.

Because body temperature is usually measured orally, the practitioner must be aware of certain external factors that can lead to false oral temperature measurements. For example, drinking hot or cold liquids can cause small changes in oral temperature measurements. The most significant temperature changes have been reported after a patient drinks ice water. Drinking ice water may lower the patient’s actual temperature by 0.2° to 1.6° F. Before taking an oral temperature, the practitioner should wait 15 minutes after a patient has ingested ice water. Oral temperature may increase in the patient receiving heated oxygen aerosol therapy and decrease in the patient receiving a cool mist aerosol. Table 2-3 lists the body temperature sites, their advantages and disadvantages, and the equipment used.

Hypertension

Hypertension is the condition in which an individual’s blood pressure is chronically above normal range. Whereas blood pressure normally increases with aging, hypertension is considered a dangerous disease and is associated with an increased risk of morbidity and mortality. According to the Joint National Committee on Detection, Evaluation, and Treatment of High Blood Pressure, the physician may make the diagnosis of hypertension in the adult when an average of two or more diastolic readings on at least two different visits is 90 mm Hg or higher or when the average of two or more systolic readings on at least two visits is consistently higher than 140 mm Hg.

An elevated blood pressure of unknown cause is called primary hypertension. An elevated blood pressure of a known cause is called secondary hypertension. Factors associated with hypertension include arterial disease, obesity, a high serum sodium level, pregnancy, obstructive sleep apnea, and a family history of high blood pressure. The incidence of hypertension is higher in men than in women and is twice as common in blacks as in whites. People with mild or moderate hypertension may be asymptomatic or may experience suboccipital headaches (especially on rising), tinnitus, light-headedness, easy fatigability, and cardiac palpitations. With sustained hypertension, arterial walls become thickened, inelastic, and resistant to blood flow. This process in turn causes the left ventricle to distend and hypertrophy. Hypertension may lead to congestive heart failure.

Hypotension

Hypotension is said to be present when the patient’s blood pressure falls below 90/60 mm Hg. It is an abnormal condition in which the blood pressure is not adequate for normal perfusion and oxygenation of vital organs. Hypotension is associated with peripheral vasodilation, decreased vascular resistance, hypovolemia, and left ventricular failure. Hypotension can also be caused by analgesics such as meperidine hydrochloride (Demerol) and morphine sulfate, severe burns, prolonged diarrhea, and vomiting. Signs and symptoms include pallor, skin mottling, clamminess, blurred vision, confusion, dizziness, syncope, chest pain, increased heart rate, and decreased urine output. Hypotension is life threatening.

Orthostatic hypotension, also called postural hypotension, occurs when blood pressure quickly drops as the individual rises to an upright position or stands. Orthostatic hypotension develops when the peripheral blood vessels—especially in central body organs and legs—are unable to constrict or respond appropriately to changes in body positions. Orthostatic hypotension is associated with decreased blood volume, anemia, dehydration, prolonged bed rest, and antihypertensive medications. The assessment of orthostatic hypotension is made by obtaining pulse and blood pressure readings when the patient is in the supine, sitting, and standing positions.

Decreased blood pressure during inspiration

During inspiration the asthmatic patient frequently relies on accessory muscles of inspiration. The accessory muscles help produce an extremely negative intrapleural pressure, which in turn enhances intrapulmonary gas flow. The increased negative intrapleural pressure, however, also causes blood vessels in the lungs to dilate, creating pooled blood. Consequently the volume of blood returning to the left ventricle decreases, causing a reduction in cardiac output and arterial blood pressure during inspiration.

Increased blood pressure during expiration

During expiration, the patient often activates the accessory muscles of expiration in an effort to overcome an increased airway resistance (R_aw). The increased power produced by these muscles generates a greater positive intrapleural pressure. Although increased positive intrapleural pressure helps offset R_aw, it also works to narrow or squeeze the blood vessels of the lung. This increased pressure on the pulmonary blood vessels enhances left ventricular filling and results in increased cardiac output and arterial blood pressure during expiration.

Imaginary Lines

Various imaginary vertical lines are used to locate abnormalities on chest examination (Figure 2-4). The midsternal line, which is located in the middle of the sternum, equally divides the anterior chest into left and right hemithoraces. The midclavicular lines, which start at the middle of either the right or left clavicle, run parallel to the sternum.

On the lateral portion of the chest, three imaginary vertical lines are used. The anterior axillary line originates at the anterior axillary fold and runs down along the anterolateral aspect of the chest, the midaxillary line divides the lateral chest into two equal halves, and the posterior axillary line runs parallel to the midaxillary line along the posterolateral wall of the thorax.

Posteriorly, the vertebral line (also called the midspinal line) runs along the spinous processes of the vertebrae. The midscapular line runs through the middle of either the right or the left scapula parallel to the vertebral line.

Lung Borders and Fissures

Anteriorly, the apex of the lung extends about 2 to 4 cm above the medial third of the clavicle. Under normal conditions the lungs extend down to about the level of the sixth rib. Posteriorly, the superior portion of the lung extends to about the level of T-1 and down to about the level of T-10 (Figure 2-5).

The right lung is separated into the upper, middle, and lower lobes by the horizontal fissure and the oblique fissure. The horizontal fissure runs anteriorly from the fourth rib at the sternal border to the fifth rib at the midaxillary line. The horizontal fissure separates the right anterior upper lobe from the middle lobe. The oblique fissure runs laterally from the sixth or seventh rib and the midclavicular line to the fifth rib at the midaxillary line. From this point the oblique fissure continues to run around the chest posteriorly and upward to about the level of T-3. Anteriorly, the oblique fissure divides the lower lobe from the lower border of the middle lobe. Posteriorly, the oblique fissure separates the upper lobe from the lower lobe.

The left lung is separated into the upper and lower lobes by the oblique fissure. Anteriorly, the oblique fissure runs laterally from the sixth or seventh rib and the midclavicular line to the fifth rib at the midaxillary line. The fissure continues to run around the chest posteriorly and upward to about the level of T-3.

Common Clinical Manifestations Observed during Inspection

Box 2-4 lists common clinical manifestations observed during the inspection of the patient with a pathologic respiratory condition. For example, during a systematic visual inspection, the respiratory practitioner might note the patient’s ventilatory pattern. Is the patient using accessory muscles of inspiration? Is the patient engaging in pursed-lip breathing? Are substernal or intercostal retractions occurring during inspiration? Does the patient appear to be splinting or to have decreased chest expansion because of chest pain? Are the shape and configuration of the chest normal? Do the patient’s skin, lips, fingers, or toenails appear cyanotic? Does the patient have digital clubbing, pedal edema, or distended neck veins? Is the patient coughing? How strong is the patient’s cough? What are the characteristics of the patient’s sputum? A more in-depth discussion of common clinical manifestations observed during inspection can be found later in this chapter (see page 28).

Chest Excursion

The symmetry of chest expansion is evaluated by lightly placing each hand over the patient’s posterolateral chest so that the thumbs meet at the midline at about the T-8 to T-10 level. The patient is instructed to exhale slowly and completely and then to inhale deeply. As the patient is inhaling, the examiner evaluates the distance that each thumb moves from the midline. Normally, each thumb tip moves equally about 3 to 5 cm from the midline (Figure 2-7).

The examiner next faces the patient and lightly places each hand on the patient’s anterolateral chest so that the thumbs meet at the midline along the costal margins near the xiphoid process. The patient is again instructed to exhale slowly and completely and then to inhale deeply. As the patient is inhaling, the examiner observes the distance each thumb moves from the midline.

A number of pulmonary disorders can alter the patient’s chest excursion. For example, a bilaterally decreased chest expansion may be caused by both obstructive and restrictive lung disorders. An unequal chest expansion may be caused by alveolar consolidation (e.g., pneumonia), lobar atelectasis, pneumothorax, large pleural effusions, and chest trauma (e.g., fractured ribs).

Tactile and Vocal Fremitus

Vibrations that can be perceived by palpation over the chest are called tactile fremitus. This condition is commonly caused by gas flowing through thick secretions that are partially obstructing the large airways. Vibrations that can be perceived by palpation or auscultation over the chest during phonation are called vocal fremitus. Sounds produced by the vocal cords are transmitted down the tracheobronchial tree and through the lung parenchyma to the chest wall, where the examiner can feel the vibration. Vocal fremitus can often be elicited by having the patient repeat the phrase “ninety-nine” or “blue moon.” These are resonant phrases that produce strong vibrations. Normally, fremitus is most prominent between the scapulae and around the sternum, sites where the large bronchi are closest to the chest wall.

Tactile and vocal fremitus decrease when anything obstructs the transmission of vibration. Such conditions include chronic obstructive pulmonary disease, tumors or thickening of the pleural cavity, pleural effusion, pneumothorax, and a muscular or obese chest wall. Tactile and vocal fremitus increase in patients with alveolar consolidation, atelectasis, pulmonary edema, lung tumors, pulmonary fibrosis, and thin chest walls.

Crepitus (also called subcutaneous emphysema) is a coarse, crackling sensation that may be palpable over the skin surface. It occurs when air escapes from the thorax and enters the subcutaneous tissue. It may occur after a tracheostomy and mechanical ventilation, open thoracic injury, or thoracic surgery.

Abnormal Percussion Notes

A dull percussion note is heard when the chest is percussed over areas of pleural thickening, pleural effusion, atelectasis, and consolidation. When these conditions exist, the sounds produced by the examiner do not freely vibrate throughout the lungs. A dull percussion note is described as flat or soft, high in pitch, and short in duration, similar to the sound produced by knocking on a full barrel (Figure 2-11).

When the chest is percussed over areas of trapped gas, a hyperresonant note is heard. These sounds are described as very loud, low in pitch, and long in duration, similar to the sound produced by knocking on an empty barrel (Figure 2-12). A hyperresonant note is commonly elicited in the patient with chronic obstructive pulmonary disease or pneumothorax.

Diaphragmatic Excursion

The relative position and range of motion of the diaphragms also can be determined by percussion. Clinically, this evaluation is called the determination of diaphragmatic excursion. To assess the patient’s diaphragmatic excursion, the examiner first maps out the lower lung borders by percussing the posterior chest from the apex down and identifying the point at which the percussion note definitely changes from a resonant to flat sound. This procedure is performed at maximal inspiration and again at maximal expiration. Under normal conditions the diaphragmatic excursion should be equal bilaterally and should measure about 4 to 8 cm in the adult.

When severe alveolar hyperinflation is present (e.g., severe emphysema, asthma), the diaphragm is low and flat in position and has minimal excursion. Lobar collapse of one lung may pull the diaphragm up on the affected side and reduce excursion. The diaphragms may be elevated and immobile in neuromuscular diseases that affect them.

Normal Breath Sounds

Three different normal breath sounds can be auscultated over the normal chest. They are called bronchial, bronchovesicular, and vesicular breath sounds.

Bronchovesicular breath sounds

Bronchovesicular breath sounds are auscultated directly over the mainstem bronchi. They are softer and lower in pitch than bronchial breath sounds and do not have a pause between the inspiratory and expiratory phase. These sounds are reduced in intensity and pitch as a result of the filtering of sound that occurs as gas moves between the large airways and alveoli.

Anteriorly, bronchovesicular breath sounds can be heard directly over the mainstem bronchi between the first and second ribs. Posteriorly, they are heard between the scapulae near the spinal column between the first and sixth ribs, especially on the right side (Figure 2-14, A).

Vesicular breath sounds

Vesicular breath sounds are the normal sounds of gas rustling or swishing through the small bronchioles and possibly the alveoli. Under normal conditions, vesicular breath sounds are auscultated over most of the lung field, both anteriorly and posteriorly (see Figure 2-14, B). Vesicular breath sounds are described as soft and low in pitch and are primarily heard during inspiration. As the gas molecules enter the alveoli, they are able to spread out over a large surface area and, as a result of this action, create less gas turbulence. As gas turbulence decreases, the breath sounds become softer and lower in pitch, similar to the sound of the wind in the trees. Vesicular breath sounds also are heard during the initial third of exhalation as gas leaves the alveoli and bronchioles and moves into the large airways (Figure 2-15).

Adventitious (Abnormal) Breath Sounds

Adventitious (abnormal) breath sounds are additional or different sounds that are not normally heard over a particular area of the thorax. Bronchial breath sounds heard over an area of the chest that normally demonstrates vesicular breath sounds are one example. Several different types of adventitious breath sounds exist, each indicating a particular pulmonary abnormality.

Bronchial breath sounds

If gas molecules are not permitted to dissipate throughout the parenchymal areas (because of alveolar consolidation or atelectasis, for example) the gas molecules have no opportunity to spread out over a larger surface area and therefore become less turbulent. Consequently, the sounds produced in this area are louder because the gas sounds are coming mainly from the tracheobronchial tree and not the lung parenchyma. These sounds are called bronchial breath sounds.

It is commonly believed that breath sounds in patients with alveolar consolidation should be diminished because the consolidation acts as a sound barrier. Although alveolar collapse or consolidation does act as a sound barrier and reduces bronchial breath sounds, the reduction is not as great as it would be if the gas molecules were allowed to dissipate throughout normal lung parenchyma. In addition, liquid and solid materials transmit sounds more readily than air-filled spaces and therefore may further contribute to the bronchial quality of the breath sound. Therefore when disease causes alveolar collapse or consolidation, harsher, bronchial-type sounds rather than the normal vesicular sounds are heard over the affected areas (Figure 2-16).

Diminished breath sounds

Breath sounds are diminished or distant in respiratory disorders that lead to alveolar hypoventilation, regardless of the cause. For example, patients with chronic obstructive pulmonary disease often have diminished breath sounds. These patients hypoventilate because of air trapping and increased functional residual capacity. In addition, when the functional residual capacity is increased, the gas that enters the enlarged alveoli during each breath spreads out over a greater-than-normal surface area, resulting in less gas turbulence and a softer sound (Figure 2-17). Heart sounds also may be diminished in patients with air trapping.

Diminished breath sounds also are found in respiratory disorders that cause hypoventilation by compressing the lung. Such disorders include flail chest, pleural effusion, and pneumothorax. Diminished breath sounds also are characteristic of neuromuscular diseases that cause hypoventilation. Such disorders include Guillain-Barré syndrome and myasthenia gravis.

Wheezing

Wheezing is the characteristic sound produced by airway obstruction. Found in all bronchospastic disorders, it is one of the cardinal findings in bronchial asthma. The sounds are high-pitched and whistling and generally last throughout the expiratory phase. The mechanism of a wheeze is similar to the vibrating reed of a woodwind instrument. The reed, which partially occludes the mouthpiece of the instrument, vibrates and produces a sound when air is forced through it (Figure 2-18). The softest, higher-pitched wheezes occur in the tightest airway obstruction.

Whispering pectoriloquy

Whispering pectoriloquy is the term used to describe the unusually clear transmission of the whispered voice of a patient as heard through the stethoscope. When the patient whispers “one, two, three,” the sounds produced by the vocal cords are transmitted not only toward the mouth and nose but throughout the lungs as well. As the whispered sounds travel down the tracheobronchial tree, they remain relatively unchanged, but as the sound disperses throughout the large surface area of the alveoli, it diminishes sharply. Consequently, when the examiner listens with a stethoscope over a normal lung while a patient whispers “one, two, three,” the sounds are diminished, distant, muffled, and unintelligible (Figure 2-19).

When a patient who has atelectasis or consolidated lung areas whispers “one, two, three,” the sounds produced are prevented from spreading out over a large alveolar surface area. Even though the consolidated area may act as a sound barrier and diminish the sounds somewhat, the reduction in sound is not as great as it would be if the sounds were allowed to dissipate throughout a normal lung. Consequently the whispered sounds are much louder and more intelligible over the affected lung areas (Figure 2-20).

Table 2-8 provides an overview of the common assessment abnormalities found during inspection, palpation, percussion, and auscultation.

Table 2-8

Common Assessment Abnormalities

Finding	Description	Possible Etiology and Significance
Inspection
Pursed-lip breathing	Exhalation through mouth with lips pursed together to slow exhalation.	COPD, asthma. Suggests ↑ breathlessness. Strategy taught to slow expiration, ↓ dyspnea.
Tripod position; inability to lie flat	Leaning forward with arms and elbows supported on overbed table.	COPD, asthma in exacerbation, pulmonary edema. Indicates moderate to severe respiratory distress.
Accessory muscle use; intercostal retractions	Neck and shoulder muscles used to assist breathing. Muscles between ribs pull in during inspiration.	COPD, asthma in excerbation, secretion retention. Indicates severe respiratory distress, hypoxemia.
Splinting	Voluntary ↓ in tidal volume to ↓ pain on chest expansion.	Thoracic or abdominal incision. Chest trauma, pleurisy.
↑ AP diameter	AP chest diameter equal to lateral. Slope of ribs more horizontal (90 degrees) to spine.	COPD, asthma, cystic fibrosis. Lung hyperinflation. Advanced age.
Tachypnea	Rate >20 breaths/min; >25 breaths/min in elderly.	Fever, anxiety, hypoxemia, restrictive lung disease. Magnitude of ↑ above normal rate reflects increased work of breathing.
Kussmaul’s respirations	Regular, rapid, and deep respirations.	Metabolic acidosis; ↑ in rate aids body in ↑ CO2 excretion.
Cyanosis	Bluish color of skin best seen in earlobes, under the eyelids, or in nail beds.	↓ Oxygen transfer in lungs, ↓ cardiac output. Nonspecific, unreliable indicator.
Clubbing of fingers	↑ Depth, bulk, sponginess of distal digit of finger.	Chronic hypoxemia. Cystic fibrosis, lung cancer, bronchiectasis.
Peripheral edema	Pitting edema.	Congestive heart failure, cor pulmonale.
Distended neck veins	Jugular venous distention.	Cor pulmonale, flail chest, pneumothorax.
Cough	Productive or non-productive.	Bronchial airway and alveolar disease.
Sputum	See Table 2-11	COPD, asthma, cystic fibrosis.
Abdominal paradox	Inward (rather than normal outward) movement of abdomen during inspiration.	Inefficient and ineffective breathing pattern. Nonspecific indicator of severe respiratory distress.
Palpation
Tracheal deviation	Leftward or rightward movement of trachea from normal midline position.	Nonspecific indicator of change in position of mediastinal structures. Medical emergency if caused by tension pneumothorax.
Altered tactile fremitus	Increase or decrease in vibrations.	↑ In pneumonia, atelectasis; pulmonary edema; ↓ in pleural effusion, lung hyperinflation; absent in pneumothorax.
Altered chest movement	Unequal or equal but diminished movement of two sides of chest with inspiration.	Unequal movement caused by atelectasis, pneumothorax, pleural effusion, splinting; equal but diminished movement caused by barrel chest, restrictive disease, neuromuscular disease.
Percussion
Hyperresonance	Loud, lower-pitched sound over areas that normally produce a resonant sound.	Lung hyperinflation (COPD), lung collapse (pneumothorax), air trapping (asthma).
Dullness/Flatness	Medium-pitched sound over areas that normally produce a resonant sound.	↑ Density (pneumonia, large atelectasis), ↑ fluid pleural space (pleural effusion).
Auscultation
Fine crackles	Series of short, explosive, high-pitched sounds heard just before the end of inspiration; result of rapid equalization of gas pressure when collapsed alveoli or terminal bronchioles suddenly snap open; similar sound to that made by rolling hair between fingers just behind ear.	Interstitial fibrosis (asbestosis), interstitial edema (early pulmonary edema), alveolar filling (pneumonia), loss of lung volume (atelectasis), early phase of congestive heart failure.
Coarse crackles	Series of short, low-pitched sounds caused by air passing through airway intermittently occluded by mucus, unstable bronchial wall, or fold of mucosa; evident on inspiration and, at times, expiration; similar sound to blowing through straw under water; increase in bubbling quality with more fluid.	Congestive heart failure, pulmonary edema, pneumonia with severe congestion, COPD.
Rhonchi	Continuous rumbling, snoring, or rattling sounds from obstruction of large airways with secretions; most prominent on expiration; change often evident after coughing or suctioning.	COPD, cystic fibrosis, pneumonia, bronchiectasis.
Wheezes	Continuous high-pitched squeaking sound caused by rapid vibration of bronchial walls; first evident on expiration but possibly evident on inspiration as obstruction of airway increases; possibly audible without stethoscope.	Bronchospasm (caused by asthma), airway obstruction (caused by foreign body, tumor), COPD.
Stridor	Continuous musical sound of constant pitch; result of partial obstruction of larynx or trachea.	Croup, epiglottitis, vocal cord edema after extubation, foreign body.
Absent breath sounds	No sound evident over entire lung or area of lung.	Pleural effusion, mainstem bronchi obstruction, large atelectasis, pneumonectomy, lobectomy.
Pleural friction rub	Creaking or grating sound from roughened, inflamed surfaces of the pleura rubbing together; evident during inspiration, expiration, or both and no change with coughing; usually uncomfortable, especially on deep inspiration.	Pleurisy, pneumonia, pulmonary infarct.
Bronchophony, whispered pectoriloquy	Spoken or whispered syllable more distinct than normal on auscultation.	Pneumonia.
Egophony	Spoken “e” similar to “a” on auscultation because of altered transmission of voice sounds.	Pneumonia, pleural effusion.

Modified from Lewis S, Heitkemper MM, Dirksen SR: Medical-surgical nursing: Assessment and management of clinical problems, ed 7, vol. 1, St. Louis, 2007, Mosby.

Airway Resistance and Its Effect on the Ventilatory Pattern

R_aw is defined as the pressure difference between the mouth and the alveoli (transairway pressure) divided by the flow rate. Therefore the rate at which a certain volume of gas flows through the airways is a function of the pressure gradient and the resistance created by the airways to the flow of gas. Mathematically, R_aw is calculated as follows:

Raw=ΔP(cmH2O)V˙(L/sec)

For example, if a patient produces a flow rate of 6 L/sec during inspiration by generating a transairway pressure difference of 12 cm H₂O, R_aw would be 2 cm H₂O/L/sec:

Raw=ΔPV˙=12cmH2O6L/sec=2cmH2O/L/sec

Under normal conditions the R_aw in the tracheobronchial tree is about 1.0 to 2.0 cm H₂O/L/sec. However, in large airway obstructive pulmonary diseases (e.g., bronchitis, asthma), the R_aw may be extremely high. An increased R_aw has a profound effect on the patient’s ventilatory pattern.

When airway resistance increases significantly, the patient’s ventilatory rate usually decreases while the tidal volume simultaneously increases (see Figure 2-23). This type of breathing pattern is commonly seen in large airway obstructive lung diseases (e.g., chronic bronchitis, bronchiectasis, asthma, cystic fibrosis) during the advanced stages.

The ventilatory pattern adopted by the patient in either a restrictive or an obstructive lung disorder is thought to be based on minimum work requirements rather than gas exchange efficiency. In physics, work is defined as the force multiplied by the distance moved (work = force × distance). In respiratory physiology the change in pulmonary pressure (force) multiplied by the change in lung volume (distance) may be used to quantify the amount of work required to breathe (work = pressure × volume).

The patient’s usual adopted ventilatory pattern may not be seen in the clinical setting because of secondary heart or lung problems. For example, a patient with chronic bronchitis who has adopted a decreased ventilatory rate and an increased tidal volume because of the increased airway resistance associated with the disorder demonstrates an increased ventilatory rate and decreased tidal volume in response to a secondary pneumonia (a restrictive lung disorder superimposed on a chronic obstructive lung disorder).

Because the patient may adopt a ventilatory pattern based on the expenditure of energy rather than on the efficiency of ventilation, the examiner cannot assume that the ventilatory pattern acquired by the patient in response to a certain respiratory disorder is the most efficient one in terms of physiologic gas exchange.

Peripheral Chemoreceptors and Their Effect on the Ventilatory Pattern

The peripheral chemoreceptors (also called carotid and aortic bodies) are oxygen-sensitive cells that react to a reduction of oxygen in the arterial blood (Pao₂). The peripheral chemoreceptors are located at the bifurcation of the internal and external carotid arteries (Figure 2-24) and on the aortic arch (Figure 2-25). Although the peripheral chemoreceptors are stimulated whenever the Pao₂ is less than normal, they are generally most active when the Pao₂ falls below 60 mm Hg (Sao₂ of about 90%). Suppression of these chemoreceptors, however, is seen when the Pao₂ falls below 30 mm Hg.

When the peripheral chemoreceptors are activated, an afferent (sensory) signal is sent to the respiratory centers of the medulla by way of the glossopharyngeal nerve (cranial nerve IX) from the carotid bodies and by way of the vagus nerve (cranial nerve X) from the aortic bodies. Efferent (motor) signals are then sent to the respiratory muscles, which results in an increased rate of breathing.

In patients who have a chronically low Pao₂ and a high Paco₂ (e.g., during the advanced stages of emphysema), the peripheral chemoreceptors may be totally responsible for the control of ventilation because a chronically high CO₂ concentration in the cerebrospinal fluid (CSF) inactivates the hydrogen ion (H⁺) sensitivity of the central chemoreceptors.

Causes of hypoxemia

In respiratory disease, a decreased arterial oxygen level (hypoxemia) is the result of a decreased ventilation-perfusion ratio, pulmonary shunting, and venous admixture (see Chapter 5 for a broader discussion of hypoxemia).

Decreased ventilation-perfusion ratios

Ideally, each alveolus should receive the same ratio of ventilation and pulmonary capillary blood flow. In reality, however, this is not the case. Alveolar ventilation is normally about 4 L/min, and the pulmonary capillary blood flow is about 5 L/min, which makes the overall ratio of ventilation to blood flow 4 : 5, or 0.8. This relationship is referred to as the ventilation-perfusion () ratio (Figure 2-26).

In some disorders, such as pulmonary embolism, the lungs receive less blood flow in relation to ventilation. When this condition develops, the ratio increases. A larger portion of the alveolar ventilation therefore will not be physiologically effective and will be said to demonstrate “wasted” or dead-space ventilation (Figure 2-27).

In most lung disorders (e.g., asthma, emphysema, pulmonary edema, or pneumonia), the lungs receive less ventilation in relation to blood flow. When this condition develops, the ratio decreases. A larger portion of the pulmonary blood flow is not physiologically effective in terms of molecular gas exchange and is said to be “shunted” blood (see the following section on pulmonary shunting). Generally, when the ratio decreases, the Pao₂ decreases and the Paco₂ increases.

Pulmonary shunting

Pulmonary shunting is defined as that portion of the cardiac output that moves from the right side to the left side of the heart without being exposed to alveolar oxygen (Pao₂). Clinically, pulmonary shunting can be subdivided into absolute shunts and relative shunts.

Absolute shunts

Absolute shunts (also called true shunts) are divided into the following two major groups: anatomic shunts and capillary shunts.

Anatomic shunts

An anatomic shunt exists when blood flows from the right side of the heart to the left side without coming in contact with an alveolus for gas exchange (Figure 2-28, B). In the healthy individual, the normal anatomic shunt is about 3% of the cardiac output. This normal shunting is caused by nonoxygenated blood completely bypassing the alveoli and entering (1) the pulmonary vascular system by means of the bronchial venous drainage, and (2) the left atrium by way of the thebesian veins. Common causes of anatomic shunts include the following:

• Congenital heart diseases

• Intrapulmonary fistulas

• Pulmonary vascular tumors

Capillary shunts

A capillary shunt is commonly caused by (1) alveolar collapse or atelectasis, (2) alveolar fluid accumulation, or (3) alveolar consolidation or pneumonia (see Figure 2-28, C).

The sum of the anatomic shunt and capillary shunt is called the absolute, or true, shunt. Patients with absolute shunting respond poorly to oxygen therapy. This is because alveolar oxygen does not come in contact with the shunted blood. As a result, absolute shunting is refractory to oxygen therapy. In short, the reduced arterial oxygen level caused by absolute shunting cannot be easily treated by increasing the concentration of oxygen for these two major reasons: (1) because of the alveolar pathology associated with an absolute shunt, the alveoli are unable to accommodate any form of ventilation, and (2) the blood that bypasses the normal, functional alveoli is unable to carry more oxygen once it has become fully saturated—except for a very small amount that dissolves in the plasma (Po₂ × 0.003 = dissolved O₂).

Relative shunts

When pulmonary capillary perfusion is in excess of alveolar ventilation, a relative shunt, or shuntlike effect, is said to be present (see Figure 2-28, D). Common causes of a relative shunt include (1) hypoventilation, (2) decreased ratios (e.g., emphysema, chronic bronchitis, asthmatic episode, excessive airway secretions), and (3) increased alveolar-capillary membrane thickness disorders (e.g., pulmonary edema, acute respiratory distress syndrome, pneumoconiosis, chronic interstitial lung disease).

Even though the alveolus may be ventilated in the presence of an alveolar-capillary defect, the blood passing by the alveolus does not have enough time to equilibrate with the alveolar oxygen tension. If the diffusion defect is severe enough to completely block gas exchange across the alveolar-capillary membrane, the shunt is called an absolute or true shunt (see earlier discussion). A relative shunt may also develop after the administration of drugs that cause an increase in cardiac output or the dilation of the pulmonary blood vessels. Unlike an absolute shunt, which is refractory to oxygen therapy, conditions that cause a relative shunt (shuntlike effect) are readily corrected by oxygen therapy.

Table 2-9 illustrates the type of pulmonary shunting associated with common diseases.

Table 2-9

Type of Pulmonary Shunting Associated with Common Respiratory Diseases

Respiratory Diseases	Capillary Shunt	Relative or Shuntlike Effect
Chronic bronchitis		X
Emphysema		X
Asthma		X
Croup/epiglottitis		X
Bronchiectasis*	X	X
Cystic fibrosis*	X	X
Pneumoconiosis*	X	X
Pneumonia	X
Lung abscess	X
Pulmonary edema	X
Near-drowning	X
Adult respiratory distress syndrome	X
Chronic interstitial lung disease	X
Flail chest	X
Pneumothorax	X
Pleural diseases	X
Kyphoscoliosis	X
Tuberculosis	X
Fungal diseases	X
Idiopathic (infant) respiratory distress syndrome	X
Smoke inhalation	X

^*Relative or shuntlike effect is most common.

Venous admixture

The result of pulmonary shunting is venous admixture, which is the mixing of shunted nonreoxygenated blood with reoxygenated blood distal to the alveoli (i.e., downstream in the pulmonary circulatory system; Figure 2-29). When venous admixture occurs, the shunted nonreoxygenated blood gains oxygen molecules while the reoxygenated blood loses oxygen molecules. The result is a blood mixture that has (1) higher Po₂ and Cao₂ values than the nonreoxygenated blood and (2) lower Po₂ and Cao₂ values than the reoxygenated blood—in other words, a blood mixture with Pao₂ and Cao₂ values somewhere between the original values of the reoxygenated and nonreoxygenated blood. Clinically, this mixed blood is sampled downstream (e.g., from the radial artery) to assess the patient’s arterial blood gases.

The peripheral chemoreceptors are frequently stimulated in respiratory disease because they respond to hypoxemia caused by decreased ratios, pulmonary shunting, and venous admixture. The decreased arterial oxygen tension then stimulates the peripheral chemoreceptors to send a signal to the medulla to increase ventilation (Figure 2-30).

Central Chemoreceptors and Their Effect on the Ventilatory Pattern

Although the mechanism is not fully understood, it is now believed that two special respiratory centers in the medulla, the dorsal respiratory group (DRG) and the ventral respiratory group (VRG), are responsible for coordinating respiration (Figure 2-31). Both the DRG and VRG are stimulated by an increased concentration of H⁺ in the CSF. The H⁺ concentration of the CSF is monitored by the central chemoreceptors, which are located bilaterally and ventrally in the substance of the medulla. A portion of the central chemoreceptor region is actually in direct contact with the CSF. The central chemoreceptors transmit signals to the respiratory neurons by the following mechanism:

1. When the CO₂ level increases in the blood (e.g., during periods of hypoventilation), CO₂ molecules readily diffuse across the blood-brain barrier and enter the CSF. The blood-brain barrier is a semipermeable membrane that separates circulating blood from the CSF. The blood-brain barrier is relatively impermeable to ions such as H⁺ and HCO₃⁻ but is very permeable to CO₂.

2. After CO₂ crosses the blood-brain barrier and enters the CSF, it forms carbonic acid:

CO2+H2O⇔H2CO3−⇔H++HCO3−

3. Because the CSF has an inefficient buffering system, the H⁺ produced from the previous reaction rapidly increases and causes the pH of the CSF to decrease.

4. The central chemoreceptors react to the liberated H⁺ by sending signals to the respiratory components of the medulla, which in turn increases the ventilatory rate.

5. The increased ventilatory rate causes the Paco₂ and subsequently the Pco₂ in the CSF to decrease. Therefore the CO₂ level in the blood regulates ventilation by its indirect effect on the pH of the CSF (Figure 2-32).

Pulmonary Reflexes and Their Effect on the Ventilatory Pattern

Several reflexes may be activated in certain respiratory diseases and influence the patient’s ventilatory rate.

Pain, Anxiety, and Fever

An increased respiratory rate may result from the chest pain or fear and anxiety associated with the patient’s inability to breathe. Chest pain and fear occur in a number of cardiopulmonary pathologies, such as pleurisy, rib fractures, pulmonary hypertension, and angina. An increased respiratory rate also may be caused by fever. Fever is commonly associated with infectious lung disorders such as pneumonia, lung abscess, tuberculosis, and fungal disease.

Scalenes

The anterior, medial, and posterior scalene muscles are separate muscles that function as a unit. They originate on the transverse processes of the second to sixth cervical vertebrae and insert into the first and second ribs (Figure 2-33). These muscles normally elevate the first and second ribs and flex the neck. When they are used as accessory muscles of inspiration, their primary role is to elevate the first and second ribs.

Sternocleidomastoids

The sternocleidomastoid muscles are located on each side of the neck (Figure 2-34), where they rotate and support the head. They originate from the sternum and clavicle and insert into the mastoid process and occipital bone of the skull.

Normally, the sternocleidomastoid pulls from its sternoclavicular origin, rotates the head to the opposite side, and turns it upward. When the sternocleidomastoid muscle functions as an accessory muscle of inspiration, the head and neck are fixed by other muscles, and the sternocleidomastoid pulls from its insertion on the skull and elevates the sternum. This action increases the anteroposterior diameter of the chest.

Pectoralis Major Muscles

The pectoralis major muscles are powerful, fan-shaped muscles that originate from the clavicle and sternum and insert into the upper part of the humerus. The primary function of the pectoralis muscles is to pull the upper part of the arm to the body in a hugging motion (Figure 2-35).

When operating as an accessory muscle of inspiration, the pectoralis pulls from the humeral insertion and elevates the chest, resulting in an increased anteroposterior diameter. Patients with chronic obstructive pulmonary disease usually secure their arms to something stationary and use the pectoralis major muscles to increase the anteroposterior diameter of the chest (Figure 2-36). This braced position is called the emphysematous habitus.

Trapezius

The trapezius is a large, flat, triangular muscle that is situated superficially in the upper part of the back and the back of the neck. The muscle originates from the occipital bone, the ligamentum nuchae, the spinous processes of the seventh cervical vertebra, and all the thoracic vertebrae. It inserts into the spine of the scapula, the acromion process, and the lateral third of the clavicle (Figure 2-37). The trapezius muscle rotates the scapula, raises the shoulders, and abducts and flexes the arm. Its action is typified in shrugging the shoulders (Figure 2-38). When used as an accessory muscle of inspiration, the trapezius helps elevate the thoracic cage.

Rectus Abdominis

A pair of rectus abdominis muscles extends the entire length of the abdomen. Each muscle forms a vertical mass about 4 inches wide, separated by the linea alba. It arises from the iliac crest and pubic symphysis and inserts into the xiphoid process and the fifth, sixth, and seventh ribs. When activated, the muscle assists in compressing the abdominal contents, which in turn push the diaphragm into the thoracic cage (Figure 2-39).

External Obliques

The broad, thin, external oblique muscle is on the anterolateral side of the abdomen. The muscle is the longest and most superficial of all the anterolateral muscles of the abdomen. It arises by eight digitations from the lower eight ribs and the abdominal aponeurosis. It inserts in the iliac crest and into the linea alba. The muscle assists in compressing the abdominal contents. This action also pushes the diaphragm into the thoracic cage during exhalation (see Figure 2-39).

Internal Obliques

The internal oblique muscle is in the lateral and ventral part of the abdominal wall directly under the external oblique muscle. It is smaller and thinner than the external oblique. It arises from the inguinal ligament, the iliac crest, and the lower portion of the lumbar aponeurosis. It inserts into the last four ribs and the linea alba. The muscle assists in compressing the abdominal contents and pushing the diaphragm into the thoracic cage (see Figure 2-39).

Transversus Abdominis

The transversus abdominis muscle is found immediately under each internal oblique muscle. It arises from the inguinal ligament, the iliac crest, the thoracolumbar fascia, and the lower six ribs. It inserts into the linea alba. When activated, it constricts the abdominal contents (see Figure 2-39).

When all four pairs of accessory muscles of exhalation contract, the abdominal pressure increases and drives the diaphragm into the thoracic cage. As the diaphragm moves into the thoracic cage during exhalation, the intrapleural pressure increases and enhances expiratory gas flow (Figure 2-40).

Pursed-Lip Breathing

Pursed-lip breathing occurs in patients during the advanced stages of obstructive pulmonary disease. It is a relatively simple technique that many patients learn without formal instruction. During pursed-lip breathing the patient exhales through lips that are held in a position similar to that used for whistling, kissing, or blowing through a flute. The positive pressure created by retarding the airflow through pursed lips provides the airways with some stability and an increased ability to resist surrounding intrapleural pressures. This action offsets early airway collapse and air trapping during exhalation. In addition, pursed-lip breathing has been shown to slow the patient’s ventilatory rate and generate a ventilatory pattern that is more effective in gas mixing (Figure 2-41).

Substernal and Intercostal Retractions

Substernal and intercostal retractions may be seen in patients with severe restrictive lung disorders such as pneumonia or adult respiratory distress syndrome. In an effort to overcome the low lung compliance, the patient must generate a greater-than-normal negative intrapleural pressure during inspiration. This greater negative intrapleural pressure causes the tissues between the ribs and the substernal area to retract during inspiration (Figure 2-42). Because the thorax of the newborn is quite flexible (as a result of the large amount of cartilage found in the skeletal structure), substernal and intercostal retractions are seen in infants with idiopathic respiratory distress syndrome (IRDS).

Pleuritic Chest Pain

Pleuritic chest pain is usually described as a sudden, sharp, or stabbing pain. The pain generally intensifies during deep inspiration and coughing and diminishes during breath holding or splinting. The origin of the pain may be the chest wall, muscles, ribs, parietal pleura, diaphragm, mediastinal structures, or intercostal nerves. Because the visceral pleura, which covers the lungs, does not have any sensory nerve supply, pain originating in the parietal region signifies extension of inflammation from the lungs to the contiguous parietal pleura lining the inner surface of the chest wall. This condition is known as pleurisy (Figure 2-43). When a patient with pleurisy inhales, the lung expands, irritating the inflamed parietal pleura and causing pain.

Because of the nature of the pleuritic pain, the patient usually prefers to lie on the affected side to allow greater expansion of the uninvolved lung and help splint the chest. Pleuritic chest pain is a characteristic feature of the following respiratory diseases:

Nonpleuritic Chest Pain

Nonpleuritic chest pain is usually described as a constant pain that is located centrally. The pain also may radiate. Nonpleuritic chest pain is associated with the following disorders:

Altered Skin Color

A general observation of the patient’s skin color should be routinely performed. For example, does the patient’s skin color appear normal—pink, tan, brown, or black? Is the skin cold or clammy? Does the skin appear ashen or pallid? This appearance could be caused by anemia or acute blood loss. Do the patient’s eyes, face, trunk, and arms have a yellow, jaundiced appearance (caused by increased bilirubin in the blood and tissue)? Is there redness of the skin, or erythema (often caused by capillary congestion, inflammation, or infection)? Does the patient appear cyanotic?

Cyanosis

Cyanosis is common in severe respiratory disorders. Cyanosis is the term used to describe the blue-gray or purplish discoloration of the mucous membranes, fingertips, and toes whenever the blood in these areas contains at least 5 g/dL of reduced hemoglobin. When the normal 14 to 15 g/dL of hemoglobin is fully saturated, the Pao₂ is about 97 to 100 mm Hg, and there is about 20 vol% of oxygen in the blood. In a cyanotic patient with one third (5 g/dL) of the hemoglobin reduced, the Pao₂ is about 30 mm Hg and there is 13 vol% of oxygen in the blood (Figure 2-45).

The detection and interpretation of cyanosis are difficult, and wide individual variations occur among observers. The recognition of cyanosis depends on the acuity of the observer, the light conditions in the examining room, and the pigmentation of the patient. Cyanosis of the nail beds also is influenced by temperature because vasoconstriction induced by cold may slow circulation to the point at which the blood becomes hypoxic (bluish) in the surface capillaries even though the arterial blood in the major vessels is not lacking in oxygen.

Central cyanosis, as observed on the mucous membranes of the lips and mouth, is almost always a sign of hypoxemia and therefore has a definite diagnostic value.

In the patient with polycythemia, cyanosis may be present at a Pao₂ well above 30 mm Hg because the amount of reduced hemoglobin is often greater than 5 g/dL in these patients, even when their total oxygen content is within normal limits. In respiratory disease, cyanosis is the result of (1) a decreased ratio, (2) pulmonary shunting, (3) venous admixture, and (4) hypoxemia.

Digital Clubbing

Digital clubbing is sometimes noticed in patients with chronic respiratory disorders. Clubbing is characterized by a bulbous swelling of the terminal phalanges of the fingers and toes. The contour of the nail becomes rounded both longitudinally and transversely, which results in an increase in the angle between the surface of the nail and the terminal phalanx (Figure 2-46).

The specific cause of clubbing is unknown. It is a normal hereditary finding in some families without any known history of cardiopulmonary disease. It is believed that the following factors may be causative: (1) circulating vasodilators, such as bradykinin and the prostaglandins, that are released from normal tissues but are not degraded by the lungs because of intrapulmonary shunting; (2) chronic infection; (3) unspecified toxins; (4) capillary stasis from increased venous backpressure; (5) arterial hypoxemia; and (6) local hypoxia. Successful treatment of the underlying disease may result in resolution of the clubbing and return of the digits to normal.

Peripheral Edema

Bilateral, dependent, pitting edema is commonly seen in patients with congestive heart failure, cor pulmonale, and hepatic cirrhosis. To assess the presence and severity of pitting edema, the health-care practitioner places a finger or fingers over the tibia or medial malleolus (2 to 4 inches above the foot), firmly depresses the skin for 5 seconds, and then releases. Normally, this procedure leaves no indentation, although a pit may be seen if the person has been standing all day or is pregnant. If pitting is present, it is graded on the following subjective scale: 1+ (mild, slight depression) to 4+ (severe, deep depression) (Figure 2-47).

Distended Neck Veins

In patients with cor pulmonale, severe flail chest, pneumothorax, or pleural effusion, the major veins of the chest that return blood to the right side of the heart may be compressed. When this happens, venous return decreases and central venous pressure (CVP) increases. This condition is manifested by distended neck veins (also called jugular venous distention; Figure 2-48). The reduced venous return also may cause the patient’s cardiac output and systemic blood pressure to decrease. In severe cases the veins over the entire upper anterior thorax may be dilated.

Nonproductive Cough

Common causes of a nonproductive cough include (1) irritation of the airway, (2) inflammation of the airways, (3) mucous accumulation, (4) tumors, and (5) irritation of the pleura.

Productive Cough

When the cough is productive, the respiratory practitioner should assess the following: