Interpretation of arterial blood gas (ABG) levels can be difficult, especially if the nurse is under pressure to do it quickly and accurately. One method that can help ensure accuracy when analyzing ABG levels is to follow the same steps of interpretation each time. A specific method to be used each time that blood gas values must be interpreted is presented here (Box 19-1).

Oxygen Saturation

Oxygen saturation is a measure of the amount of oxygen bound to hemoglobin, compared with hemoglobin’s maximal capability for binding oxygen. It can be assessed as a component of the ABG (Sao₂) or can be measured noninvasively using a pulse oximeter (Spo₂).9,10 Oxygen saturation is reported as a percentage or as a decimal; normal values are greater than 95% when the patient is on room air. Normally, the saturation level cannot reach 100% (on room air) because of physiologic shunting.¹ However, when supplemental oxygen is administered, oxygen saturation may approach 100% so closely that it is reported as 100%.

Proper evaluation of the oxygen saturation level is vital. For example, an Sao₂ of 97% means that 97% of the available hemoglobin is bound with oxygen. The word available is essential to evaluating the Sao₂ level, because the hemoglobin level is not always within normal limits and oxygen can bind only with what is available. A 97% saturation level associated with 10 g/dL of hemoglobin does not deliver as much oxygen to the tissues as does a 97% saturation level associated with 15 g/dL of hemoglobin. Assessing only the Sao₂ level and finding it within normal limits does not ensure that the patient’s oxygenation status is normal. The hemoglobin level must also be evaluated before a decision on oxygenation status can be made.1,9,10

Oxygen Content

Oxygen content (Cao₂) is a measure of the total amount of oxygen carried in the blood, including the amount dissolved in plasma (measured by the Pao₂) and the amount bound to the hemoglobin molecule (measured by the Sao₂). Cao₂ is reported in milliliters of oxygen carried per 100 mL of blood. The normal value is 20 mL of oxygen per 100 mL of blood. To calculate the oxygen content, the Pao₂, the Sao₂, and the hemoglobin level are used (see Appendix B). A change in any one of these parameters will affect the Cao₂.¹

The value of assessing the Cao₂ is best illustrated by the examples in Table 19-3. The ABG parameters that are used most commonly to evaluate oxygenation status (Pao₂ and Sao₂) are both normal. Assessing only the Pao₂ and the Sao₂ would lead to the invalid conclusion that Patient B’s oxygenation status is normal. However, consideration of the hemoglobin level and the Cao₂ reveals that the oxygenation of Patient B’s blood is significantly abnormal.

Base Excess and Base Deficit

Base excess and base deficit reflect the nonrespiratory contribution to acid–base balance and are reported in milliequivalents per liter (mEq/L) above or below the normal range of −2 mEq/L to +2 mEq/L. A negative base level is reported as a base deficit, which correlates with metabolic acidosis, whereas a positive base level is reported as a base excess, which correlates with metabolic alkalosis.1,4,8

Classic Shunt Equation and Oxygen Tension Indices

The efficiency of oxygenation can be assessed by measuring the degree of intrapulmonary shunting that occurs in a patient at any one time, using the classic shunt equation and oxygen tension indices. Intrapulmonary shunting (QS/QT [the portion of cardiac output not exchanging with alveolar blood divided by the total cardiac output]) refers to venous blood that flows to the lungs without being oxygenated because of nonfunctioning alveoli.¹ Other names for this condition include shunt effect, low V/Q, wasted blood flow, and venous admixture.^1,11,12

Direct determination of intrapulmonary shunting requires the use of the classic shunt equation (see Appendix B), which is invasive and cumbersome. A shunt greater than 10% is considered abnormal and indicative of a shunt-producing disorder. A shunt greater than 30% is a serious and potentially life-threatening condition, which requires pulmonary intervention.^1,11,12

Often, intrapulmonary shunting is estimated by using the oxygen tension indices. One advantage to these methods is the ease of performance, although they have been found to be unreliable in critically ill patients.1,11 An estimate of intrapulmonary shunting can be determined by computing the difference between the alveolar and arterial oxygen concentrations. Normally, alveolar (a) and arterial (a) Po₂ values are approximately equal. When they are not, it indicates that venous blood is passing malfunctioning alveoli and returning unoxygenated to the left side of the heart.^1,11 The most common oxygen tension indices used to estimate intrapulmonary shunting are the Pao₂/Fio₂ ratio, the Pao₂/Pao₂ ratio, and the a-a gradient (P[a − a]o₂).

Dead Space Equation

The efficiency of ventilation can be measured using the clinical dead space (V_d/V_t) equation (see Appendix B). The formula measures the fraction of tidal volume not participating in gas exchange. A dead space value greater than 0.6 indicates a dead space-producing disorder and is considered abnormal. The major limitations to using this formula are that it requires the measurement of exhaled carbon dioxide to complete and that the work of breathing by patients must remain stable during the collection.^12,14

Sputum Studies

Careful analysis of sputum specimens is crucial for the rapid identification and treatment of pulmonary infections. The most difficult aspect of sputum examination is proper collection of the specimen. Collection of a good sputum sample requires a conscious, cooperative, and sufficiently hydrated patient.¹² When the patient has difficulty producing sputum, heated, nebulized saline may help to loosen secretions for expectoration.¹² Chest physiotherapy combined with nebulization improves the success rate. Collection of a sputum specimen is best done in the morning, because a greater volume of secretions is present as a result of nighttime pooling. Brushing the teeth and rinsing the oropharyngeal airway is recommended to reduce contamination before collecting a sample.^12,15

Many critically ill patients cannot cough effectively, and sputum collection by other means is required. These methods include tracheobronchial aspiration, transtracheal aspiration, and the use of a fiberoptic bronchoscopy with a protected brush catheter. Because each method has its own benefits and risks, the patient’s clinical condition determines the appropriate technique.¹²

Many critically ill patients have endotracheal or tracheostomy tubes already in place. Collecting sputum specimens from these patients requires special attention to technique (Box 19-4). Deep specimens are obtained to avoid collecting specimens that contain resident upper airway flora that may have migrated down the tube. Colonization of the lower airways with upper airway flora can occur within 48 hours of intubation.¹⁶

Box 19-4   Procedure for Collection of Tracheal or Endotracheal Sputum Specimen

1. Clear the endotracheal or tracheostomy tube of all local secretions, avoiding deep airway penetration.

2. Attach a sputum trap to a sterile suction catheter, and advance the catheter into the trachea while trying to avoid contact with the endotracheal tube or tracheostomy tube (Fig. 19-1).

3. After the catheter is fully advanced, apply suction until secretions return to the sputum trap. When enough secretions are collected, discontinue suctioning, and remove the catheter.

4. Do not apply suction while the catheter is being withdrawn, because this can contaminate the sample with sputum from the upper airway. Do not flush the catheter with sterile water, because this dilutes the sample.

5. If the catheter becomes plugged with secretions, place it in a sterile container, and send it to the laboratory. The specimen must be transported immediately or refrigerated if a delay is necessary.

After a sputum specimen is obtained, it is examined for volume, physical properties, mucopurulence, and color. Next, a microscopic examination is done to identify the source of the specimen. If a bacterial infection is suspected, a Gram stain is performed, followed by culture and sensitivity (C&S) assessments.12,15,16

Fiberoptic bronchoscopy is a relatively safe procedure done at the bedside, and it is most often used as a diagnostic and therapeutic tool (Fig. 19-2). Diagnostic indications include hemoptysis, infectious pneumonia, difficult intubation, pulmonary injury after chest trauma, acute burn inhalation injury, aspiration lung injuries, and acute upper airway obstruction. Therapeutic indications include the aspiration of foreign bodies, removal of obstructing secretions, atelectasis, difficult intubation, and resection of small, benign growths from the airway.^12,17,18

Before the bronchoscopy, a complete medical history is obtained, and a thorough examination, including a chest x-ray examination, is performed.12,17 Preprocedural evaluation of the patient includes clotting studies (prothrombin time [PT], partial thromboplastin time [PTT], and platelet count) and evaluation of the ABG levels.^12,17 Hypoxemic patients need supplemental oxygen during the procedure. The patient must have no oral intake for 6 to 8 hours before the bronchoscopy to reduce the risk of aspiration.^12,17

Although a topical anesthetic can be used alone, it is usually supplemented by an intravenous sedative or analgesic, or both. A benzodiazepine for sedative effects and a opioid analgesic are administered intravenously during the procedure.12,17,18 Preprocedural medications for a diagnostic bronchoscopy may include atropine and intramuscular codeine. Atropine lessens the vasovagal response and reduces the secretions, whereas codeine decreases the cough reflex. When bronchoscopy is performed therapeutically to remove secretions, the patient has decreased cough and gag reflexes, which may impair secretion clearance.^12,17,18 Maintenance of the airway is essential to prevent complications.

Complications of the procedure may be related to the procedure itself, the anesthetic, or an ancillary procedure. Minor complications include laryngospasm, bronchospasm, epistaxis, fever, vomiting, altered pulmonary mechanics, and hemodynamic instability. Major complications include anaphylaxis, infection, hypotension, cardiac dysrhythmias, pneumothorax, hemorrhage, respiratory failure, hypoxemia, and cardiopulmonary arrest.12,17,18

Thoracentesis

Thoracentesis is a simple, usually uncomplicated procedure done at the bedside for the removal of fluid or air from the pleural space (Fig. 19-3). It is used most often as a diagnostic measure; it may also be performed therapeutically for the drainage of a pleural effusion or empyema.^19,20 No absolute contraindications to thoracentesis exist, although there are some risks that may contraindicate the procedure in all but emergency situations. These risk factors include unstable hemodynamics, coagulation defects, mechanical ventilation, the presence of an intraaortic balloon pump, and patients who are uncooperative. In most clinical situations, diagnostic thoracentesis can be delayed until these risk factors are eliminated.¹⁹

The patient is placed in a sitting position with legs over the side of the bed and with hands and arms supported on a padded overbed table. If the patient’s condition precludes sitting, the side-lying position with the back flush with the edge of the bed and the affected side down can be used.19,20,21 The patient is cautioned not to move or cough during the procedure.²¹ During the thoracentesis, the site of the needle insertion is usually determined by previous chest x-ray examination, computed tomography (CT) scan, or chest percussion. A local anesthetic is used to minimize the patient’s discomfort during insertion of the thoracentesis needle.⁹

Complications associated with thoracentesis include pain, pneumothorax, and re-expansion pulmonary edema. Pneumothorax can occur as a result of introduction of air into the pleural space, puncture of the lung, or rupture of the visceral pleura.19,20,21 Re-expansion pulmonary edema can occur when a large amount of effusion fluid (approximately 1000 to 1500 mL) is removed from the pleural space. Removal of the fluid increases the negative intrapleural pressure, which can lead to edema when the lung does not reexpand to fill the space. The patient experiences severe coughing and shortness of breath. The onset of these symptoms is an indication to discontinue the thoracentesis.²¹

Chest Radiography

Chest radiography is an important diagnostic procedure for any critically ill patient. Chest x-ray examinations aid in the diagnosis of various disorders and complications and assist in the evaluation of treatment.²⁷

When interpreting a chest radiograph, a systematic method is used for viewing it (Box 19-6). Areas of the radiographic film that are assessed include bones, mediastinum, diaphragm, pleural space, and lung tissue. Fig. 19-4 provides an example of a normal chest radiograph.

Box 19-6   Steps for Interpretation of a Chest Radiograph

Step 1

Look at the different densities (black, gray, and white), and answer this question: What is air, fluid, tissue, and bone?

Step 2

Look at the shape or form of each density, and answer this question: What normal anatomic structure is this?

Step 3

Look at the right and left sides, and answer this question: Are the findings the same on both sides, or are there physiologic and pathophysiologic differences?

Step 4

Look at all the structures (bones, mediastinum, diaphragm, pleural space, and lung tissue), and answer this question: Are any abnormalities present?

Step 5

Look for all tubes, wires, and lines, and answer this question: Are the tubes, wires, and lines in the proper place?

Bones

The clavicles, ribs, thoracic and cervical spine, and scapulas are assessed. The clavicles should be symmetric, and the ribs should be an equal distance apart. Intervertebral disk spaces should be evident, indicating an adequately exposed inspiratory film.²⁷ The thoracic and cervical spine should be straight, without signs of curvature. The scapulas usually appear as areas of added density in the upper lung fields. There should be no evidence of fractures, calcification and lesions (increased density), or demineralization (decreased density).^27,28

Mediastinum

The structures assessed in the mediastinal area are the aortic knob and the trachea. The trachea should be positioned in the midline, with a slight deviation to the right as it approaches the carina.²⁷ Shifting of the mediastinal structures can occur with atelectasis and removal of all or a portion of a lung (toward the area of involvement), pneumothorax (away from the area of involvement), pleural effusion, and tumors.^27,28

Diaphragm

The diaphragm should be clearly visible, with sharp costophrenic angles seen where the chest wall and the tapered edges of the diaphragm meet.27,28 The level of the diaphragm (on deep inspiration) should appear at the 10th or 11th rib,^27,28 with the right side 1 to 2 cm higher than the left side.²⁷ A gastric air bubble may be found under the left side of the diaphragm.^27,28 An elevated diaphragm may be seen in pregnancy, obesity, conditions that cause air or fluid to accumulate in the peritoneal space, and intestinal obstruction.²⁷ An elevated hemidiaphragm is associated with several conditions, including phrenic nerve injury, previous chest surgery, subphrenic abscess, trauma, stroke, tumor, pneumonia, and radiation therapy.²⁷ Flattening of the diaphragm can be a sign of increased air in the lungs, as occurs with chronic COPD or a pleural effusion.^27,28 Obliteration or “blunting” of the costophrenic angle can occur with pleural effusion, atelectasis, or pneumothorax.^27,28

Pleural Space

Identification of the pleural space on a chest radiograph is an abnormal finding. The pleural space is not visible unless air (pneumothorax) or fluid (pleural effusion) enters it. As fluid accumulates in the pleural space, it surrounds the lung and eventually compresses it. With a pleural effusion, blunting of the costophrenic angle may be evident first, with flattening of the diaphragm and obscuring of the heart borders occurring as the effusion grows.²⁸ With a pneumothorax, the pleural edges become evident as the examiner looks through and between the images of the ribs on the film. A thin line appears just parallel to the chest wall, indicating where the lung markings have pulled away from the chest wall.^27,28 The collapsed lung manifests as an area of increased density separated by an area of radiolucency (blackness).

Lung Tissue

The lung tissue is viewed for any areas of increased density or increased radiolucency that may indicate an abnormality. Increased density can be the result of accumulation of fluid in the lungs (e.g., water, pus, blood, edema fluid) or collapse of lung tissue (e.g., with atelectasis or pneumothorax). Increased radiolucency is caused by increased air in the lungs, as may occur with COPD.27,28 In some patients, a fine line may be present on the right side at about the level of the sixth rib in the midlung field. This is a normal finding and represents the horizontal fissure, which separates the right upper lobe from the right middle lobe.^27,28

Tubes, Wires, and Lines

The chest radiograph is assessed for proper placement of all tubes, wires, and lines. When properly positioned, an endotracheal tube is 2 to 3 cm above the carina, and a nasogastric tube runs the length of the esophagus, with the tip in the stomach.²⁷ The origin of a central venous catheter is observed as a thin, continuous, radiopaque line at the level of the jaw, progressing toward the superior vena cava in an internal jugular approach, whereas a subclavian approach originates in the clavicular area. A pulmonary artery catheter is viewed running through the right atrium and right ventricle into the pulmonary artery.^27,28 Additional items that may be present include temporary or permanent pacing wires, a permanent pacing generator, an implantable cardioverter defibrillator (ICD), a peripherally inserted central catheter (PICC), chest tubes (pleural or mediastinal), electrocardiographic (ECG) electrodes, and surgical markers and clips.^27,28

Capnography is the measurement of exhaled carbon dioxide (CO₂) gas; it is also known as end-tidal CO₂ monitoring. Normally, alveolar and arterial CO₂ concentrations are equal in the presence of normal V/Q relationships. In a patient who is hemodynamically stable, the end-tidal CO₂ (Petco₂) can be used to estimate the Paco₂, with the Petco₂ levels 1 to 5 mm Hg less than Paco₂ levels. The practitioner must determine first that a normal V/Q relationship exists before correlation of the Petco₂ and the Paco₂ can be assumed.12–29 Causes of increased Petco₂ include situations in which CO₂ production is increased, such as hyperthermia, sepsis, and seizures, or in which alveolar ventilation is decreased, such as respiratory depression. Causes of decreased Petco₂ include situations in which CO₂ production is decreased, such as hypothermia, cardiac arrest, and pulmonary embolism, or in which alveolar ventilation is increased, such as hyperventilation.^12,29

In the critical care area, continuous capnography is used for assessment and monitoring of the patient’s ventilatory status in a variety of situations, including weaning from mechanical ventilation and undergoing procedural sedation. Assessment of changes in physiologic dead space can be carried out with end-tidal CO₂ monitoring, based on the degree of difference between the Paco₂ and the Petco₂. As the severity of pulmonary impairment increases, so does the disparity between the Paco₂ and the Petco₂, as indicated by an increased gradient. A gradient of greater than 5 mm Hg can be seen with underperfused alveolar-capillary units (dead space-producing situations) and nonperfused alveolar-capillary units (alveolar dead space). Increased dead space ventilation is a result of decreased pulmonary blood flow or cardiac output and lung disease. This leads to an abnormality in the transfer of CO₂ from the blood to the lung. The result is a Petco₂ level that is lower than the Paco₂ because of the mixing of carbon dioxide between perfused and nonperfused units. The end result is an increased or widened Paco₂/Petco₂ gradient.12,29

The noninvasive measurement of Petco₂ enables assessment of the adequacy of cardiopulmonary resuscitation and endotracheal tube placement. Decreased pulmonary blood flow is associated with lower Petco₂ values, reflected clinically by decreased cardiac output, as in the case of cardiopulmonary resuscitation.12,29 During endotracheal intubation, a low Petco₂ reading indicates that the tube is positioned in the stomach, because the amount of carbon dioxide in the esophagus is expected to be low.^12,29

There are three forms of capnography: mainstream, side-stream, and proximal diverting. All forms can be used in intubated patients, but side-stream and microstream capnography can also be used in nonintubated patients, broadening the application of end-tidal CO₂ monitoring. Mainstream capnography measures the CO₂ level directly by a sensor in the exhalation port of the ventilator tubing. During exhalation, gas passes over the sensor, and the information is transferred by an electrical cable to the display unit. The display unit produces a waveform, called a capnogram (Fig. 19-5), and a numeric recording (Petco₂). Disadvantages to this form of capnography include the weight of the sensor on the ventilator tubing and possible obstruction of the sensor by secretions and condensation. In side-stream capnography, the CO₂ gas is continuously aspirated through a side port in the ventilator tubing or nasal cannula and is measured and analyzed by a side unit. Disadvantages to this form of capnography include obstruction of the sampling tube with secretions and slow response time. Proximal diverting capnography is a newer and improved version of side-stream capnography that transports gas a short distance from the airway to a site where the sensor is located thereby reducing the bulkiness at the airway.

Capnography and partial pressure of end-tidal carbon dioxide (Petco₂) analysis have many diverse applications in the critical care area, but the practitioner must never assume the Petco₂ values reflect arterial values of the partial pressure of carbon dioxide (Paco₂) without waveform analysis. Any change in the waveform can indicate a change in the patient’s pulmonary status and warrants further evaluation. Loss of the waveform may signal loss of effective respirations.12,29

Pulse Oximetry

Pulse oximetry is a noninvasive method for monitoring oxygen saturation (Spo₂). It is indicated in any situation in which the patient’s oxygenation status requires continuous observation. It consists of a microprocessor and a probe that attaches to the patient’s forehead, finger, ear, toe, or nose. The probe consists of two light-emitting diodes and a photodetector (Fig. 19-6). The diodes transmit red and infrared light wavelengths through the pulsating arterial vascular bed to the photodetector on the other side. The percentage of oxygen saturation is determined by the difference in absorbance of the red and infrared light caused by the difference in color between oxygen-bound (bright red) and oxygen-unbound (dark red) hemoglobin. The photodetector converts the light signals into an electric signal that is sent to the microprocessor, which converts it to a digital reading. The pulse oximeter is considered very accurate; readings vary less than 4% to 5% at a saturation level greater than 70%. However, several physiologic and technical factors limit the monitoring system.^9,12

Physiologic Limitations

Physiologic limitations of pulse oximetry include elevated levels of abnormal hemoglobins, presence of vascular dyes, and poor tissue perfusion. The pulse oximeter cannot differentiate between normal and abnormal hemoglobin. Elevated levels of abnormal hemoglobin falsely elevate the Spo₂. Vascular dyes such as methylene blue, indigo carmine, indocyanine green, and fluorescein interfere with pulse oximetry and can lead to falsely low readings. Poor tissue perfusion to the area with the probe leads to loss of pulsatile flow and signal failure.9,12 In the critically ill patient, pulse oximetry is reliable only for monitoring the patient’s oxygenation status. It is not a reliable method for monitoring the patient’s ventilatory status. The ability of a pulse oximeter to detect hypoventilation is accurate only when the patient is breathing room air.⁹ Because most critically ill patients require some form of oxygen therapy, pulse oximetry is not a reliable method of detecting hypercapnia and should not be used for this purpose.

Technical Limitations

Technical limitations of pulse oximetry include bright lights, excessive motion, and incorrect placement of the probe. Bright lights may interfere with the photodetector and cause inaccurate results. The probe must be covered to limit optical interference. Excessive motion can mimic arterial pulsations and can lead to false readings. Incorrect placement of the probe can lead to inaccurate results, because part of the light can reach the photodetector without having passed through blood (optical shunting).9,12 Interventions to limit these problems include using the proper probe in the appropriate spot (e.g., not using a finger probe on the ear), applying the probe according to the directions, and ensuring that the area being monitored has adequate perfusion.^9,24