Hiển thị các bài đăng có nhãn Pulmonary. Hiển thị tất cả bài đăng

Thứ Tư, 3 tháng 8, 2011

Chapter 49 Arterial Blood Gases

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990.

Bookshelf ID: NBK371 PMID: 21250212

Chapter 49 Arterial Blood Gases

E. P. Trulock, III.

Definition

Arterial blood gases (ABGs) is a collective term applied to three separate measurements—pH, Pco₂, and Po₂—generally made together to evaluate acid–base status, ventilation, and arterial oxygenation. Oxygen (O₂) and carbon dioxide (CO₂) are the most important respiratory gases, and their partial pressures in arterial blood reflect the overall adequacy of gas exchange. Pao₂ is affected by age and altitude. Paco₂ by altitude. Therefore, Pao₂ must be individually calculated for each patient, and both determinations must be interpreted against local normal values. Hydrogen is not present in blood as a gas and, therefore, does not exert a partial pressure. However, pH, which measures hydrogen ion activity, is a conventional part of every arterial blood gas determination. The normal range for blood pH is 7.35 to 7.45.
Some calculated or derived variables may be reported with the ABGs. The bicarbonate concentration, which can be calculated from the pH and Pco₂, is the most useful of these. Others, such as base excess and base deficit, are not essential and may be confusing.

Technique

Accurate results for ABGs depend on collecting, handling, and analyzing the specimen properly. Clinically important errors may occur at any of these steps, but ABG measurements are particularly vulnerable to preanalytic errors. The most common problems include nonarterial samples, air bubbles in the sample, either inadequate or excessive anticoagulant in the sample, and delayed analysis of an un-cooled sample.
A proper blood sample for ABG analysis consists of a 2 to 3 ml arterial specimen collected anaerobically from a peripheral artery in a 3- or 5-ml plastic or glass, airtight syringe fitted with a small-bore needle. Any air bubbles inadvertently introduced during sampling must be promptly evacuated. Room air has a Po₂, of approximately 150 mm Hg (sea level) and a Pco₂ of essentially zero. Thus, air bubbles that mix and equilibrate with arterial blood will shift the Pao₂ toward 150 mm Hg and will lower the Paco₂.
Heparin must be added to the syringe as an anticoagulant. Because the pH of heparin is near 7.0, and the Po₂ and Pco₂ of the heparin solution are near room air values, excess heparin can alter all three ABG measurements. Very little heparin is actually needed in the sample to prevent clotting; 0.05 to 0.10 ml of a dilute solution (1000 units/ml) will anticoagulate 1 ml of blood without affecting its pH. Pco₂, or Po₂. After flushing the syringe with heparin, a sufficient amount usually remains in the dead space of the syringe and needle for anticoagulation without distortion of the ABG determination.
After collection, the specimen should be analyzed expeditiously. If a delay of more than 10 minutes is anticipated, the specimen must be immersed in an ice bath. Leukocytes and platelets continue to consume oxygen in the sample after it is drawn and can cause a significant fall in Pao₂ over time at room temperature, especially in the setting of leukocytosis or thrombocytosis. Cooling will prevent any clinically important effect for at least 1 hour by decreasing the metabolic activity of these cells.
ABGs are now routinely measured with an automated analyzer. The basic components of such a unit are three electrodes, one each for determining pH, Pco₂, and Po₂. The pH electrode measures the potential difference between a measuring electrode (which contains the sample in contact with a special glass membrane permeable only to H⁺ ions) and a reference electrode (which has a known, stable pH). From the voltage across these electrodes, the sample pH is calculated. The Pco₂ electrode (Severinghaus electrode) employs an adaptation of the pH measurement. Carbon dioxide from the blood sample equilibrates across a gas-permeable membrane with a bicarbonate solution in a reaction that generates H⁺ ions. The Pco₂ of the sample is determined indirectly by sensing the pH change in this solution. The Po₂ electrode (Clark electrode) determines Po₂ amperometrically. Oxygen from the blood sample diffuses across a semipermeable membrane and is reduced at the cathode of a polarographic electrode. This reaction produces a measurable current that is directly proportional to the sample Po₂.
Each electrode is calibrated at two reference points in the typical operational range. For the pH electrode, two buffer solutions (pH = 6.840 and 7.384) are the standards. For the Pco₂ and Po₂ electrodes, two references gases (usually 5% CO₂, 20% O₂, 75% N₂; and 10% CO₂, 90% N₂) are utilized. After calibration, the accuracy and reliability of measurements may be checked by analyzing commercially available quality-control samples with known values of pH, Pco₂ and Po₂ that span the range of common clinical values. Although these procedures generally ensure valid measurements, high Pao₂ values (>150 mm Hg) present a potential source of error. The Po₂ electrode is not linear and therefore may be inaccurate at values far beyond its calibration points (0 mm Hg and 140 mm Hg at sea level for the reference gases above). Consequently, the precision of Pao₂ values exceeding 150 mm Hg is uncertain unless the electrode has been recalibrated in an appropriate range, and this is not generally feasible in an automated analyzer.
The electrodes are maintained at 37°C in a thermostatically regulated waterbath; therefore, all ABG measurements are made at 37°C regardless of the patient's temperature. Nonetheless, pH, Paco₂, and Pao₂ are all temperature dependent because gas solubilities are a function of temperature. When body temperature is higher than 37°C, the reported Pao₂ and Paco₂ measured at 37°C will be lower than the actual values in the patient; the converse holds when body temperature is below 37°C. Both equations and nomograms have been developed to adjust the 37°C values to those corresponding to the patient's temperature. The equations, however, are too complex for easy calculation. The effect of varying temperature on a "normal" set of ABGs is illustrated in Table 49.1. Whether to correct ABG measurements (especially the Pao₂) to the patient's temperature or simply to report them at 37°C is a controversial issue, and laboratory practices vary in this area. It is relatively standard practice to report the pH and Paco₂ at 37°C without correction. There is no uniform practice regarding Pao₂, and the clinician must be familiar with local policy. As shown in Table 49.1, the effect of temperature changes on pH, Paco₂, and Pao₂ over the usual clinical range of 35° to 39°C is relatively small. The issue is clinically relevant primarily in hypothermia and hyperthermia.

Basic Science

The hydrogen ion (H⁺) concentration determines the acid–base status of the blood. For convenience, the H⁺ concentration is customarily expressed as pH, defined as the negative logarithm (base 10) of the H⁺ concentration:

Note that H⁺ concentration and pH are inversely related; an increasing H⁺ concentration (increasing acidity) corresponds to a declining pH, and vice versa. The normal H⁺ concentration of 0.0004 mEq/L is equivalent to a pH of 7.40. The normal range of blood pH is 7.35 to 7.45.
The Pao₂ is the partial pressure of oxygen in arterial blood. The normal range for Pao₂ is affected by age and altitude. As a result of changes in overall matching of ventilation with perfusion, normal Pao₂ declines with advancing age. Regression equations have been published to estimate this decrease; however, there is some disparity in the results, probably attributable to heterogeneous study populations and nonuniform study conditions. Hence, these equations are only guidelines. For example, Sorbini et al. (1968) found the following prediction equation for supine subjects at sea level:

Based on this equation, the lower limit of normal for Pao₂ at age 70 would be approximately 70 mm Hg.
At elevations above sea level, the partial pressure of inspired oxygen falls with the barometric pressure, and the normal Pao₂ decreases concomitantly. For example, at 1500 m (barometric pressure 634 mm Hg), the predicted normal Pao₂ in a healthy, young subject is approximately 80 mm Hg; this contrasts with a value close to 95 mm Hg at sea level. Therefore, at locations substantially above sea level, local normal values that correct for altitude must be utilized in ABG interpretation.
The Paco₂ is the partial pressure of carbon dioxide in arterial blood. The normal range is 35 to 45 mm Hg and does not vary significantly with age. Nevertheless, normal Paco₂, tends to be lower at high altitudes because ventilation is stimulated, and local norms must be established.
Cellular metabolism and whole organ function are optimum over a relatively narrow range of pH. Hence, the acid–base status of the blood is closely regulated. Homeostasis is maintained by three mechanisms: (1) buffers that mitigate changes in pH, especially the carbonic acid/bicarbonate (H₂CO₃/HCO₃⁻) pair; (2) the lungs, which control Paco₂; and (3) the kidneys, which regulate plasma bicarbonate. The central relationship among these is the following reaction:

Dissolved CO₂ is hydrated in an equilibrium reaction to form the strong acid, H₂CO₃. The amount of dissolved CO₂ is directly proportional to the Paco₂, the proportionality constant (α) being the solubility coefficient of CO₂. Therefore, the lungs effectively regulate the H₂CO₃ concentration. Carbonic acid reversibly dissociates into H⁺ and HCO₃⁻. Metabolic acids are titrated primarily by HCO₃⁻, and the HCO₃⁻ concentration is ultimately under renal control.
The interdependence among these may be expressed as the classic Henderson-Hasselbalch equation for pH or rearranged into an equation for [H⁺].

Notice in both equations that pH, or H⁺ concentration, depends on the ratio of Paco₂ to HCO₃⁻, and not on the absolute value of either one alone.
Acidosis and alkalosis refer to pathophysiologic disturbances that tend to increase or decrease hydrogen ion concentration respectively. Primary disturbances in Paco₂ cause the respiratory acid–base disorders, whereas primary alterations in bicarbonate are responsible for the metabolic derangements. Each primary disturbance elicits a compensatory response, which is usually incomplete, but returns the pH toward normal. Thus, an acidosis or alkalosis does not necessarily result in an acidemia (pH < 7.35) or alkalemia (pH > 7.45). The simple acid–base disorders are illustrated in Table 49.2. Mixed acid–base disturbances are the result of two or more simple disorders occurring together. While these are more complex, their recognition and analysis are predicated on a thorough understanding of the primary disorders.
The primary purposes of respiration are to provide oxygen to the cells for aerobic metabolism and to excrete the carbon dioxide produced by this metabolic activity. This requires the integrated function of both the respiratory system for gas exchange between alveolar air and pulmonary capillary blood, and the cardiovascular system for gas transport to and from the metabolizing tissues. The respiratory system may be divided into two parts: the respiratory pump and the lung. The respiratory pump includes the thoracic cage and abdomen, the respiratory muscles, the respiratory control centers, and the neural interconnections. The major function of the respiratory pump is ventilation of the lung, whereas the primary role of the lung itself is gas transfer. Factors that influence gas exchange in the lung include (1) movement of gas into and out of the lung (ventilation); (2) blood flow through the lung (perfusion); (3) the regional distributions of ventilation and perfusion (ventilation–perfusion matching); and (4) diffusion across the alveolar–capillary membrane. The overall adequacy of gas exchange for oxygen and carbon dioxide is reflected by the Pao₂ and Paco₂.
Carbon dioxide, the major by-product of oxidative metabolism, is transported to the lung in venous blood and eliminated through alveolar ventilation. The Paco₂ is directly proportional to carbon dioxide excretion rate ( Image v.jpg

co₂) and inversely proportional to alveolar ventilation ( Image v.jpg

_A).

It will rise if CO₂ production increases and is not balanced by an appropriate rise in alveolar ventilation, or if alveolar ventilation decreases at a given CO₂ production. Therefore, the Paco₂ is an index of the adequacy of alveolar ventilation in relation to carbon dioxide production.
Alveolar ventilation is that portion of the total minute ventilation ( Image v.jpg

_E) that participates effectively in gas exchange. The remainder of minute ventilation reaches only anatomic or physiologic dead space; it does not participate in gas exchange and is called dead space ventilation ( Image v.jpg

_D). Alveolar ventilation, then, is total minute ventilation minus dead space ventilation.

Alveolar ventilation may fall due to a decrease in minute ventilation with a normal dead space, or due to an increase in dead space ventilation without a compensatory increase in minute ventilation.
Oxygen is essential for aerobic metabolism. The transfer of oxygen from alveolar air to pulmonary capillary blood is affected by the partial pressure of oxygen in the alveoli, its diffusion across the alveolar–capillary membrane, and the matching of alveolar ventilation to capillary perfusion. There are five possible causes of a reduction in Pao₂: low inspired oxygen tension, alveolar hypoventilation, diffusion impairment, ventilation–perfusion mismatching, and right-to-left shunt. In addition, a low mixed venous oxygen tension will magnify the reduction in Pao₂ due to ventilation–perfusion mismatching and shunt.
The partial pressure of oxygen in the alveoli (P_Ao₂) may be determined from the ideal alveolar gas equation,

where P_B is barometric pressure, PH₂O the partial pressure of water vapor (47 mm Hg), F_Io₂ the fractional concentration of inspired oxygen, and R the respiratory exchange ratio (usually 0.80). The alveolar–arterial oxygen tension gradient, P(A-a)o₂, is the difference between calculated P_Ao₂ and measured Pao₂. The normal gradient increases with age, but is usually in the range of 5 to 20 mm Hg. If either alveolar hypoventilation or a low inspired oxygen tension is the cause of a decreased Pao₂, this gradient remains normal. In contrast, an abnormality in either diffusion or ventilation–perfusion matching will increase P(A-a)o₂. Diffusion, however, is rarely the cause of a low Pao₂ at rest.
Arterial oxygen content (Cao₂) is the sum of hemoglobin-bound oxygen and dissolved oxygen

where Hb is the hemoglobin concentration and Sao₂ the arterial O₂ saturation. The contribution of dissolved oxygen is very small, and the major impact of Pao₂ on oxygen content is through its effect on hemoglobin saturation (Figure 49.1). Above a Pao₂ of 60 mm Hg, the dissociation curve is relatively flat and Sao₂ increases very little even with a large increment in Pao₂. In contrast, below Pao₂ 60 mm Hg, the curve is steeper and Sao₂ decreases significantly with any decrement in Pao₂. Also, as illustrated in Figure 49.1, the position of the oxyhemoglobin dissociation curve may be shifted by factors that alter the configuration of the hemoglobin molecule and change its affinity for binding oxygen.
Oxygen delivery to the tissues is the product of cardiac output and arterial oxygen content. Oxygen delivery can be compromised by a reduction in any component (cardiac output, hemoglobin concentration, or Sao₂). However, a decrease in one component may be offset by an increase in another to maintain oxygen delivery.

Clinical Significance

An ABG contains data relevant to three areas: acid–base status, ventilation, and arterial oxygenation. Clinical estimates of the presence or severity of abnormalities in these areas are often deceptive. Consequently, an ABG is useful when disturbances are apparent or suspected in any of the three parameters. A systematic approach to interpretation, in conjunction with appropriate clinical correlation, will help delineate problems in each of these areas and will guide the institution and adjustment of supportive therapy when necessary.
First, consider the acid–base status. The simple acid–base disorders are presented in Table 49.2. The differential diagnosis for each category is relatively limited and may be found in most medicine texts. Diagnosis is often aided by using other laboratory parameters, such as serum electrolytes, along with the ABG and clinical data. Treatment should be directed toward the underlying cause and will depend on the nature and severity of the disturbance. Prompt intervention is generally necessary at the extremes of acidemia (pH < 7.20) and alkalemia (pH > 7.60) because adverse effects on the cardiovascular and central nervous systems are common when pH exceeds these limits.
Next, the ventilatory status should be evaluated. While this is an extension of the acid–base analysis, it focuses attention on ventilatory function. Recall that the Paco₂ is an index of the adequacy of alveolar ventilation in relation to carbon dioxide production [Eq. (49.5)]. Normally a primary rise in Paco₂ will trigger an increase in ventilation and restore the Paco₂ if the respiratory pump is intact. Hence, when hypercapnia and respiratory acidosis are present, some degree of ventilatory failure has occurred. Common causes include central nervous system depression or disease, neuromuscular disorders, thoracic cage deformities, and obstructive lung disease. In addition, respiratory muscle fatigue due to increased work of breathing from any cause may culminate in ventilatory failure. If the respiratory acidemia is severe or progressive, mechanical support of ventilation may be necessary while other measures are directed at the underlying process.
Finally, arterial oxygenation should be assessed. A Pao₂ below the predicted lower limit of normal [Eq. (49.2)] or a widened P(A-a)o₂ indicates an abnormality in gas exchange that should be recognized, but may not always significantly impair arterial oxygenation. A Pao₂ of 60 mm Hg provides approximately 90% hemoglobin saturation if acid–base status and temperature are normal (Figure 49.1). However, below Pao₂ 60 mm Hg significant desaturation occurs as the Pao₂ falls, and arterial oxygen content [Eq. (49.8)] decreases proportionately. When oxygen delivery is compromised by a low arterial oxygen content (desaturation, anemia) or by an inadequate cardiac output, critical tissue hypoxia may occur. The most sensitive sites are the central nervous system and the heart, but oxygen deprivation is potentially harmful to all aerobic, metabolically active tissues. In most clinical circumstances a reasonable goal of therapy is to maintain the Pao₂ in the 60 to 80 mm Hg range. In some cases, slightly lower levels may be acceptable; however, there is generally little to be gained by increasing the Pao₂ substantially above this range. When needed, supplemental oxygen should be administered with these guidelines in mind. In addition, attention should be given to hemoglobin concentration and cardiac output to optimize oxygen delivery.

References

Andritsch RF, Muravchick S, Gold MI. Temperature correction of arterial blood gas parameters: a comparative review of methodology. Anesthesiology. 1981;55:311–16. [PubMed: 6791530]
Chillar RK, Belman MJ, Farbstein M. Explanation for apparent hypoxemia associated with extreme leukocytosis: leukocytic oxygen consumption. Blood. 1980;55:922–24. [PubMed: 7378581]
Fox MJ, Brody JS, Weintraub LR. et al. Leukocyte larceny: a cause of spurious hypoxemia. Am J Med. 1979;67:742–46. [PubMed: 292309]
Hess CE, Nichols AB, Hunt WB. et al. Pseudohypoxemia secondary to leukemia and thrombocytosis. N Engl J Med. 1979;301:361–63. [PubMed: 460325]
Kelman GR, Nunn JF. Nomograms for correction of blood PO₂, PCO₂, pH and base excess for time and temperature. J Appl Physiol. 1966;21:1484–90. [PubMed: 5923219]
Kryger MH, ed. Pathophysiology of respiration. New York: Wiley, 1981.
Mellemgaard K. The alveolar-arterial oxygen difference: its size and components in normal man. Acta Physiol Scand. 1966;67:10–20. [PubMed: 5963295]
Narins RG, Emmett M. Simple and mixed acid-base disorders: a practical approach. Medicine (Baltimore). 1980;59:161–87. [PubMed: 6774200]
Severinghaus JW. Blood gas calculator. J Appl Physiol. 1966;21:1108–16. [PubMed: 5912737]
Shapiro BA, Harrison RA, Walton JR. Clinical application of blood gases, 3d ed. Chicago: Year Book Medical Publishers, 1982.
Sorbini CA, Grassi V, Solinas E. et al. Arterial oxygen tension in relation to age in healthy subjects. Respiration. 1968;25:3–13. [PubMed: 5644025]

Figures

Figure 49.1

The oxyhemoglobin dissociation curve and variables that affect oxygen–hemoglobin affinity. 2-3 DPG = 2,3-diphosphoglycerate; CO = carbon monoxide. From Kryger MH, ed. Pathophysiology of respiration. New York: Wiley, 1981. Reprinted with permission.

Tables

Table 49.1Temperature-Corrected Values for a "Normal" ABG

Temperature (°C)	pH	Paco₂ (mm Hg)	Pao₂ (mm Hg)
20	7.65	19	27
30	7.50	30	51
35	7.43	37	70
37	7.40	40	80
39	7.37	44	91

: Source: Adapted and reproduced with permission from Shapiro BA, Harrison RA, Walton JR. Clinical application of blood gases. 3rd ed.

Table 49.2Simple Acid–Base Disorders

Disorder	Primary disturbance	Compensatory mechanism
Respiratory		Renal
Acidosis	↑ Paco₂	H⁺ excretion; HCO₃⁻ generation/retention
Alkalosis	↓ Paco₂	HCO₃⁻ excretion
Metabolic		Ventilatory
Acidosis	↓ HCO₃	Hyperventilation (↓ Paco₂)
Alkalosis	↑ HCO₃	Hypoventilation (↑ Paco₂)

Chapter 48 Chest Roentgenography for Pulmonary Evaluation

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990.

Bookshelf ID: NBK370 PMID: 21250211

Chapter 48 Chest Roentgenography for Pulmonary Evaluation

Michael Boyars.

Definition

X-rays are a form of electromagnetic radiation. They have a very short wavelength located just before the far ultraviolet band on the electromagnetic spectrum.

Technique

The standard x-ray examination of the chest consists of a frontal (PA) and lateral view. The frontal view is called a PA view because the patient stands with the anterior chest on the cassette and the back to the x-ray beam. The x-rays first hit the posterior and then the anterior chest before hitting the cassette; thus the name PA. The cassette is 6 feet from the x-ray tube. The lateral film is taken the same way except the patient is standing with his or her side perpendicular to the x-ray cassette. Unless otherwise specified, a left lateral is taken. An AP film of the chest is the usual technique when patients are too ill to leave the bedside. It is usually taken with the cassette behind the patient and the x-ray beam 40 (rather than 72) inches from the cassette, thus magnifying all structures.
An apical lordotic technique is used to evaluate the apices of the lungs. The x-ray beam is angled in a slightly upward projection, causing anterior thoracic structures to be projected above the posterior thoracic structures. The clavicle and first several sets of ribs are projected above the apices of the lung, allowing a good view of this area. It is particularly useful in evaluating the upper lobes for evidence of tuberculous disease. The lateral decubitus technique is one in which the patient is placed lying on the cassette with either the left or right side dependent. It is most frequently used for evaluating the presence of free-moving pleural fluid. The usual technique is to have the patient lie on the side with the fluid and look for a radiodense fluid line along the dependent side. With small amounts of pleural fluid, it is helpful to have the patient lie with the normal side dependent and see if the diaphragmatic angle on the involved side becomes sharp, thus indicating the presence of a small, free-moving effusion.
The closer an intrathoracic structure is to the cassette, the sharper and more accurate will be its image on the cassette. This is because as x-rays strike structures, they travel in a slightly divergent rather than totally parallel manner. Therefore, the further the distance between an object and the cassette, the greater the amount of magnification and the lesser the sharpness that object's image is represented on the cassette. Hence, the cardiac silhouette appears larger and less sharp on an AP than a PA film. Similarly, a right-sided process is better defined in the right and not the left lateral position.
When a chest x-ray is taken with optimal technique, the intervertebral spaces should be barely visible through the cardiac silhouette. If the intervertebral spaces are not apparent, then the film is relatively light. This means that an existing infiltrate may seem more prominent, or it may appear that an infiltrate is present when in fact there is just normal vasculature. In other words, a light film is more likely to be overread. When one can very clearly see the intervertebral space and outline the vertebral bodies, then the x-ray is somewhat overpenetrated. This tends to make an infiltrate appear less prominent, or sometimes even cause the infiltrate not to be appreciated on the film. In other words, a dark film is more likely to be underread. The above guidelines for over- and underpenetration should be kept in mind when comparing the progression or resolution of a process on serial films.

Basic Science

In 1895 Wilhelm von Roentgen described x-rays and ushered medical science into a new era of technology. By 1896, physicians in the United States were already putting Roentgen's discovery to clinical use. Today the chest x-ray is the most frequently requested radiologic examination, accounting for one-quarter to one-third of all x-ray procedures. We have indeed come a long way since that November day in Wurzburg when Roentgen made his first observations of these magical rays that could pass through objects opaque to light and cause a visible fluorescence.
X-rays are produced by bombarding a tungsten filament with an electron beam. While x-rays and visible light are both forms of electromagnetic radiation, they have different physical properties. These different properties make the x-ray medically useful. Specifically, many substances opaque to light can be penetrated by x-rays. As the x-ray traverses the thoracic cavity, it hits the structures in its path; in doing so, part of its energy is dissipated. The thicker and denser the structure, the greater the amount of energy dissipated. Once it has traversed the thoracic cavity, the x-ray strikes the film; metallic silver is precipitated photochemically within the gelatinous emulsion on the film.
In clinical practice the x-ray film is put in a cassette that contains a fluorescent coating in front and in back. This coating is activated by the x-rays that cause it to emit light rays that reinforce the photochemical effect. If the x-rays traverse the thorax without going through much tissue, they will strike the cassette with a relatively large amount of energy, and when the cassette is developed, this area will be black. Conversely, an x-ray that has passed through a very dense and thick thoracic structure will have a much lower energy when it hits the cassette and will look white. Structures of intermediate density and thickness will give intermediate or gray appearances. These varying shades of black, white, and gray provide contrast on the x-ray film. A film taken with suboptimal x-ray voltage (i.e., a white or underpenetrated film) results in an x-ray where the intrathoracic structures have hazy borders and are difficult to differentiate from adjacent structures. Conversely, a film taken with too much voltage (i.e., an overpenetrated or black x-ray) will result in a radiograph that has relatively little contrast, making differentiation of intrathoracic structures difficult.

Normal Radiographic Anatomy

Before examining a chest x-ray for signs of disease, acquaint yourself with the normal anatomy. The right lung is divided into an upper, a middle, and a lower lobe; the left lung is divided into an upper and lower lobe. The lingula, anatomically part of the left upper lobe, is the analog of the right middle lobe. The lobes are separated from each other by septa. Visceral pleura from the surfaces of adjacent lobes form the interlobar septa. The space between is called the interlobar fissure, although the terms septum and fissure are used synonymously. The septa have an average thickness of about 0.2 mm (see Figures 48.1 and 48.2).
The major (or oblique) fissure of each lung separates the lower lobes from the middle and upper lobes on the right, and from the upper lobe on the left. The major fissure can usually be seen on the lateral view where it normally runs from about the level of the fifth thoracic vertebra or fifth rib interspace, crossing inferiorly and anteriorly parallel to the sixth rib to reach the diaphragm a few centimeters behind the anterior costophrenic angle. The oblique fissure presents a smooth, concave surface as it courses around the lung. Anterior or posterior deviation of this fissure often represents loss of volume in the lung segment toward which the fissure is deviated. The minor (or horizontal) fissure can be seen in 50 to 60% of PA and lateral chest x-rays. On the PA view its normal position is between the second and fourth anterior ribs, presenting a slightly convex but horizontal appearance. When there is loss of volume, the minor fissure will be drawn out of its normal horizontal position; it is pulled up with upper lobe volume loss and down and posteriorly with lower lobe volume loss.
Assessment of pulmonary vasculature can be a difficult and confusing task. Pulmonary arterial segments converge toward the hila and meet in the right and left main pulmonary arteries. The left pulmonary artery is slightly higher than the right 97% of the time. This means that the right hilum is never normally higher than the left. If the right hilum is higher than the left, then something is either pulling (or pushing) the right hilum up or something is pulling (or pushing) the left hilum down. The hila are best appreciated on the lateral projection (see Figure 48.3). In the lateral view, the right and left upper lobe bronchi can be seen as two circular radiolucent areas with the right above the left. The right pulmonary artery can be seen projecting anteriorly above the upper lobe bronchi; the left pulmonary artery projects posteriorly. The inferior vena cava can also frequently be seen on the lateral view, coursing up from the left hemidiaphragm to join the posterior cardiac silhouette. On the PA projection the superior vena cava can sometimes be seen coursing superiorly from the hila.
The right hemidiaphragm is normally slightly higher than the left in about 90% of cases. The diaphragm normally has a smooth and convex contour that tapers to give a sharp costophrenic angle. With a good inspiratory effort, the level of the diaphragm should be near the level of the ninth posterior rib.
The trachea is normally midline on the PA or AP film. The tracheal air shadow is readily visible on the normal PA film, and under normal circumstances the spinous processes of the vertebral bodies will be located in the center of the tracheal lucency. If the tracheal air column is deviated, you must determine if this is secondary to pathologic change or rotation of the patient. On a well-centered PA chest film the ends of both clavicles will be equidistant from the spinous processes of the vertebral bodies. Therefore, when you notice deviation of the tracheal air column, check if the spinous processes of the vertebral bodies maintain these relationships with the clavicles. If this is the case, then there is true tracheal deviation; if not, then the patient is rotated toward the clavicle farthest from the spinous processes.

Radiographic Interpretation

The chest x-ray is a two-dimensional, static, black-and-white representation of a three-dimensional, dynamic living structure. Our job is to take these two-dimensional, black-and-white images and reconstruct what is going on inside the patient's chest. Most people accomplish this by "pattern reading." This involves learning the radiologic patterns of various pathologic entities. For example, one sees a blunted costophrenic angle, and one instantly comes up with the diagnosis of pleural effusion. Or one sees a fluffy, mottled density in the right lower lobe and comes up with the diagnosis of pneumonia. While this method can lead to the correct diagnosis a good percentage of the time, someone faced with a difficult x-ray, or who sees something with which he is not familiar, will be at a total loss. This is very similar to programming a computer to recognize patterns and then giving it a pattern it has never seen before. It will not be able to come up with the diagnosis.
The optimal way to read x-rays is to learn certain radiographic principles and then apply these principles in a logical and consistent manner to reading x-rays. If you do this, you should almost always be able to come up with the diagnosis, even if you have never seen it before. Air, water or tissue, and bone are three basic radiologic densities. Air density, as represented by the lung parenchyma, is black on the x-ray. Bone density is white on the x-ray. Water or tissue density is gray on the x-ray. We must keep in mind that the thickness of a structure also affects its projected density on the x-ray film. Even though the heart is less dense than bone, it is projected whiter on the chest x-ray because it is significantly thicker than the ribs or vertebral bodies. We can see the borders between the various intrathoracic structures because of this difference in contrast.
Dr. Benjamin Felson (Felson and Felson, 1950) described the now-famous silhouette sign: "An intrathoracic lesion touching a border of the heart, aorta, or diaphragm will obliterate that border on the roentgenogram. An intrathoracic lesion not anatomically contiguous with the border of one of these structures will not obliterate that border. We have applied the term silhouette sign to indicate the loss of the silhouette of any of these borders by adjacent disease" (p. 364). By using the silhouette sign, one is able to locate a pathologic process on a single x-ray view. For example, a right middle lobe infiltrate will obliterate the right heart border as outlined by the silhouette sign, whereas a right lower lobe infiltrate will not. This is because both the right middle lobe and the right heart border are anterior and adjacent structures, and when there is water density in both structures, the borders between the two become obliterated. Thus, on a PA view of the chest, we can locate any structure in the superioinferior dimension as well as the mediolateral dimension, and the silhouette sign allows us to locate it in the posterioanterior dimension. This can be corroborated by looking at the lateral film.
By using a systematic approach to the reading of the chest x-ray, one can usually easily define the pathology. Define an abnormality on chest x-ray by asking a series of questions. First, is it an intraparenchymal or extraparenchymal process? One can see 360 degrees around an intraparenchymal process because it is surrounded by aerated lung, thus providing contrast. By definition an extraparenchymal process has one border either on the mediastinum, diaphragm, or pleural surface, and so one can see only about 180 degrees around it. In addition, intraparenchymal processes are usually projected on the PA or AP film as greater in their mediolateral dimension than their superioinferior dimensions. Therefore, the second hallmark of an intraparenchymal process is that it is usually wider than it is long. Conversely, an extraparenchymal process that is either in the pleural, mediastinal, or soft tissue space tends to be longer than it is wide. Next, ask whether the process is a mass or an infiltrate. This differentiation is easily made. A mass has a homogeneously white density; an infiltrate has a mottled, black-and-white density. The exception to this rule is a consolidation, which is a special form of infiltrative process in which all the alveolar spaces in the involved bronchopulmonary segments are involved, thus giving a homogeneously white appearance. If the process is a mass and one can see all the way around it, then it is a parenchymal mass. If it is a mass and one cannot see all the way around, it is either a hilar, mediastinal, pleural, or soft tissue process, depending on its location.
If it is an infiltrative process, then ask if it is alveolar or interstitial. The hallmark of an alveolar filling process is the presence of air bronchograms. The air bronchogram is another term coined by Dr. Felson (1973). He states that "parenchymal consolidation may result in the visualization of these bronchi (normally invisible) since the air within their lumens will stand out in contrast to the surrounding opaque lung" (p. 60). Finding air bronchograms in an area of infiltration is not as easy as it sounds and is frequently the cause of disagreement among radiologist and clinician alike. An easy way to detect the presence of an alveolar infiltrate is to use the fact that it tends to obliterate the borders of the normal blood vessels in that area. This is because of the silhouette sign described above. The alveolar filling process causes a water density around blood vessels, and so the borders of these vessels are not visualized as sharply. Unlike an alveolar infiltrate, an interstitial infiltrate tends to accentuate the vascular markings in the area of infiltration. Because alveolar and interstitial infiltrates have opposite effects on the visibility of pulmonary vasculature, this is of great help in differentiation. Although the above rules will not always hold true, they will aid the beginner and inexperienced clinician in making sense of the chest x-ray.

Clinical Significance

Now that you have mastered some basic radiologic principles of interpretation, let us put them to clinical use. With the exception of pulmonary edema, alveolar infiltrates tend to be localized, whereas interstitial infiltrates tend to be diffuse. Certain other characteristics of an infiltrate may be helpful in the differential diagnosis. Location of an infiltrate is of prime importance. Tuberculosis is far more common in the upper lobes than in any other lobes. In addition, the tubercle bacillus favors the superior or posterior segments and will rarely be seen in the anterior segment alone. The superior segment of the lower lobes and the posterior segment of the upper lobes are the most frequently involved segments with aspiration pneumonia. Pneumocystis carinii pneumonia is the most frequently seen as a diffuse interstitial infiltrate.
The character of the infiltrate is also important. A consolidative infiltrate is most commonly seen with a bacterial pneumonia. The presence of multiple lucent areas within a pneumonic infiltrate suggest a necrotizing process. One would think of tuberculosis, proteus, and pseudomonas, as well as anaerobic pulmonary infections. An alveolar infiltrate in an area of severe emphysema can simulate a necrotizing process because the dilated alveolar spaces of the emphysematous process can simulate cavities.
When evaluating a pulmonary mass, the most important thing to try to exclude is a neoplastic process. The presence of dense central calcification is one of the most reliable signs that a mass is not malignant. A calcified mass most frequently represents an old healed and clinically inactive inflammatory process. If there is no calcium present, one must rely on previous chest x-rays to see how long the mass has been there and if it is growing in size. As a general rule, if a mass is seen on an older film and is unchanged in size for 4 to 5 years, it is most likely a benign process, and invasive investigation of the mass is not mandatory. If old films show that the mass was smaller previously and is now growing, or that it was not present previously, then invasive investigation is mandatory. A mass on a chest x-ray of a cigarette smoker should be considered cancer until proven otherwise. The same is true for a pulmonary mass with a pleural effusion or mediastinal node in a smoker.
Cavitation within a mass most frequently represents either a necrotizing infectious process or a cavitating neoplastic lesion. When a carcinoma cavitates, the walls of the mass are thick and irregular; when an inflammatory process cavitates, the walls are thinner and more regular.
One of the more difficult things to determine is whether a hilar mass represents a large pulmonary artery or an enlarged mediastinal node. On the PA or AP projection, if you can clearly see vessels going into and joining the mass, it is more likely to be a vascular structure. One can also perform fluoroscopy on the patient and have him or her perform a Valsalva maneuver. If the structure compresses with a Valsalva maneuver, it is more likely to be venous. Similarly, if one appreciates pulsations of the structure, it is more likely to be arterial. Nevertheless, one must be careful that these are not transmitted pulsations from a vascular structure underneath the mass. The lateral view is by far the more helpful view in evaluating the hilar area. The large pulmonary arteries can be appreciated on the lateral view as a large vascular shadow, as described previously. Tumorous enlargement of the hila area can be appreciated much earlier and with greater ease on the lateral.
Volume loss of the pulmonary parenchyma is caused by one of three pathophysiologic processes: obstruction, compression, or contraction. Obstruction of a lobar or segmental bronchus will result in a resorption of the air distal to the obstruction with loss of volume of the involved segments. This is seen most commonly with an endobronchial carcinoma; however, extrabronchial masses can cause bronchial obstruction by extrinsic compression. Compression of the parenchyma occurs with a pleural effusion or pneumothorax. Contraction or scarring of the lung occurs as a sequela of a previous inflammatory process such as tuberculosis. With compression there may be obvious signs of pleural effusion or pneumothorax. With contraction there will be the interstitial infiltrate from the fibrous scarring. Volume loss from endobronchial obstruction has several direct and indirect radiologic signs.
Dr. Felson has thoroughly described the radiologic signs of obstructive volume loss (see Table 48.1). Displacement of the fissures is the most reliable sign of volume loss. The fissure is displaced toward the affected segment. For example, with upper lobe collapse the major fissure is pulled superiorly and anteriorly toward the collapsed upper lobe; in lower lobe collapse the major fissure is pulled inferiorly and posteriorly toward the collapsed lower lobe. An increase in radiodensity in the affected segment occurs because, as the segment loses volume, the tissues in that segment come closer together and hence are more dense. The final direct sign of volume loss is vascular or bronchial crowding in the effected segment. This occurs for the same reason as the increase in radiodensity.
Of the indirect signs of obstructive volume loss, hila displacement is the most reliable. The hilum is displaced upward with upper lobe volume loss and downward with lower lobe volume loss. Elevation of the hemidiaphragm is more pronounced with lower lobe volume loss than with upper lobe volume loss. Shift of the hilum and mediastinal structures toward the side of major volume loss is frequent. When there is major volume loss in one lobe, the adjacent lobe will frequently overdistend to take up the vacated space of the collapsed lobe. This results in overdistention of a normal segment, giving a more radiolucent appearance. This is known as compensatory emphysema. Armed with the above principles and a knowledge of bronchial and lobar anatomy, one can adequately evaluate a lobar or segmental collapse.
A pneumothorax is air loculated between the visceral and parietal pleura. The air is either introduced from the outside (as with chest trauma) or from the inside (as with a bronchopleural fistula). The hallmark of a pneumothorax is an area on the chest x-ray that has no pulmonary vasculature. One always feels more secure in making this diagnosis when one can actually visualize the lung parenchyma medial to the area of pneumothorax; however, this is not always the case. Sometimes it is necessary to "hot light" the film. This involves putting the film up to a strong light source, such as a 100-watt bulb, to look for the edge of the lung. With the increased light behind the x-ray, you can sometimes see the lung edge that was not appreciated on the view box. With small amounts of pneumothorax, there is no appreciable shift of the lung or mediastinal structures. With larger amounts of pneumothorax, the lung and mediastinum are pushed toward the contralateral chest as the volume and pressure within the pneumothorax increases. This results in deviation of the trachea and mediastinal structures, as well as compression of the contralateral lung with extreme degrees of pneumothorax. This is a critical situation known as tension pneumothorax. Immediate therapeutic measures must be taken to decompress the affected side at this point. One condition that causes confusion with pneumothorax is extensive bullous disease of the lung. Bulla and cysts of the lung are large, air-containing sacks within the lungs. They are the end results of various pathophysiologic processes. Sometimes these bulla or cysts can reach huge proportions and can simulate a pneumothorax. Because these bulla and cysts contain air, you will not see any pulmonary vasculature within them; however, if you look carefully, you can appreciate the walls of these bulla and cysts on the radiograph. There are none with pneumothorax. At times this can be a difficult differentiation.

References

Felson B, Felson H. Localization of intrathoracic lesions by means of the postero-anterior roentgenogram: the silhouette sign. Radiology. 1950;55:363–74. [PubMed: 14781343]
Felson B. The lobes and interlobar pleura: fundamental roentgen considerations. Am J Med Sci. 1955;230:572–84. [PubMed: 13268436]
Felson, B. Chest roentgenology. Philadelphia: W. B. Saunders, 1973.
Felson B. Radiologic evaluation of pleural disease. J Respir Dis. 1982;3087:41–47.
Proto A, Tocino I. Radiographic manifestations of lobar collapse. Semin Roentgenol. 1980;15:117–73. [PubMed: 7394541]
Squire L. Fundamentals of roentgenology. Cambridge: Harvard University Press, 1966.

Figures

Figure 48.1

(1) Minor fissure. (2) Right pulmonary artery. (3) Left pulmonary artery. (4) Inferior vena cava.

Figure 48.2

(1) Minor fissure. (2) Right major fissure. (3) Left major fissure. (4) Inferior vena cava.

Figure 48.3

(1) Right upper lobe bronchial orifice. (2) Left upper lobe bronchial orifice. (3) Right pulmonary artery. (4) Left pulmonary artery.

Tables

Table 48.1Roentgenographic Signs of Loss of Lung Volume

Direct signs

Displaced septa

Increased radiodensity in affected lobe

Crowding of vascular and bronchial markings

Indirect signs

Unilateral hemidiaphragm elevation

Deviation of the trachea

Shift of the heart and mediastinum

Hilar displacement

Chapter 48 Chest Roentgenography for Pulmonary Evaluation

NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990.

Bookshelf ID: NBK370 PMID: 21250211

Chapter 48 Chest Roentgenography for Pulmonary Evaluation

Michael Boyars.

Definition

X-rays are a form of electromagnetic radiation. They have a very short wavelength located just before the far ultraviolet band on the electromagnetic spectrum.

Technique