Chapter 30: Critical Care Ultrasound

An intensivist assesses a patient's volume responsiveness to determine if a fluid bolus will increase a patient's stroke volume and cardiac output. Traditionally, static parameters of cardiac filling pressures, such as the central venous pressure (CVP) or the pulmonary artery occlusion pressure (PAOP), have been used as surrogates of a patient's volume status. Clinicians have also assessed volume status via echocardiographic parameters such as the left ventricular end-diastolic volume or estimated filling pressures. Most of these traditional parameters, however, poorly predict volume responsiveness because Frank-Starling forces, cardiopulmonary interactions, and changes in systolic, diastolic, intra-abdominal, and intrathoracic pressures influence the patient's response to volume loading.^{1, 2}

If a patient lies on the steep portion of the Frank-Starling curve, an increase in preload will increase the stroke volume (volume responsive). On the other hand, if the patient is on the flat portion of the Frank-Starling curve, an increase in preload will not increase stroke volume and indeed may reduce it (nonvolume responsive).

Volume assessment aided by dynamic parameters, in contrast to static measurements, recognizes the characteristic respirophasic changes that occur as a patient's intrathoracic pressure changes with positive-pressure ventilation (Figures 30-1 and 30-2). These changes are more dramatic in the hypovolemic patient and can be recognized via the arterial pressure waveform. During a positive-pressure breath with mechanical ventilation, right ventricular (RV) stroke volume drops for two main reasons. First, the RV has less preload owing to decreased venous return from an increased intrathoracic pressure. Second, there is a concomitant increase in afterload to the RV secondary to the pneumatic compression of the pulmonary capillaries. Simultaneously, during mechanical insufflation, the venous return to the left ventricle (LV) is increased as the pulmonary capillaries are compressed and blood is pushed to the left side of the heart. Therefore, LV stroke volume increases during mechanical inspiration. After two to three cardiac cycles (pulmonary transit time), the LV stroke volume falls as a consequence of the aforementioned reduction in RV stroke volume and cardiac output. The converse is true for the expiratory phase of mechanical ventilation. As a patient becomes increasingly hypovolemic, this relationship becomes exaggerated and is manifested as arterial line waveform variation from inspiration to expiration.

Dynamic parameters such as the arterial pulse pressure variation, systolic blood pressure variation, and stroke volume variation can be assessed via an arterial blood pressure tracing.

Measuring the inferior vena cava (IVC) variation is another dynamic measurement that is noninvasive and easy to perform.^{3, 4} The IVC returns 80% of the venous blood to the right atrium (RA). It briefly passes through the thoracic cavity before joining the inferior aspect of the right atrium. The vena cava is a collapsible vessel, and as such its diameter is dependent on the internal distending pressure and the external compressing pressure. The intrathoracic vena cava's diameter is determined by the right atrial pressure (RAP) minus the pleural pressure (P_pl). During mechanical ventilation, the greater the P_pl, the more likely the vena cava is to collapse. As the RAP rises, collapse becomes less likely. This relationship can be evaluated by assessing IVC respiratory diameter and respirophasic variation. The higher the change in IVC diameter, the more likely the patient will respond to fluid loading with an increase in stroke volume (SV) and carbon monoxide (CO). Typical cutoff values that differentiate between responders and nonresponders depend on the method used: 12% (using max IVC diameter − minimal IVC diameter/mean diameter) or 18% (using max IVC diameter − min IVC diameter/min IVC diameter) IVC respiratory variability during mechanical ventilation.^{3, 4}

Respiratory variation of the superior vena cava (SVC) may also predict fluid responsiveness. In a study of 66 septic mechanically ventilated patients, SVC variability of greater than 36% predicted fluid-responsive hemodynamics with a 100% sensitivity and a 90% specificity.⁵ However, this imaging is only readily obtainable with a transesophageal echocardiography (TEE) and therefore may have limited utility. IVC imaging has the advantage of being easily performed even by physicians untrained in echocardiography.⁶

The patient should be in a position that optimizes ultrasound windows. For evaluation of the IVC, the patient should be in a supine or semirecumbent position. The patient's legs may be bent to reduce tension on the abdominal wall. To produce a good ultrasound image there must be copious ultrasound gel between the skin surface and the ultrasound probe. This is important because air will limit the transmission of ultrasound waves, worsening image quality.

It is important to orient the probe properly. Each ultrasound probe has an index marker on one side, which at any time corresponds to the side of the screen marker (Figures 30-3 and 30-4) on the ultrasound machine. It is recommended that a consistent orientation be used.

Two probes are commonly used in the intensive care unit (ICU). A linear array probe (Figure 30-5A) has a high resolution, with limited penetration (at most 9 cm). The second probe is a phased array probe (Figure 30-5B) with a small footprint that generates high frame rates to analyze moving organs like the heart and is also able to penetrate deeply into the tissue.

Since the IVC is located deep in the abdominal cavity, a phased array probe is used. After the application of ultrasound gel, place the probe to the left of the patient's midline in the epigastric area along the longitudinal plane and angled slightly cranially. From top to bottom, the image obtained will show a short axis cut through the left liver lobe that has a homogeneous texture and is hypoechoic (gray color). Below and directly adjacent to the hepatic parenchyma you will see a longitudinal cut through the IVC lumen, which is anechoic (black). Identification of the IVC is enhanced by visualizing the hepatic veins draining from the liver parenchyma into the IVC just underneath the diaphragm. The IVC should continue cranially through the diaphragm into the right atrium. The diaphragm image is a crescent-shaped hyperechoic (very white) line that moves with respiration. This image of the diaphragm is a landmark that separates the intra-abdominal from intrathoracic cavities. If the IVC is not visualized, tilt the probe to the right or left side of the patient until the images come into view. The IVC should be differentiated from the abdominal aorta, which lies in close proximity. The aorta is usually deeper and to the patient's left side. Additionally, it has a clear hyperechoic layer of connective tissue separating the posterior aspect of the liver and the anterior wall of the aorta, whereas the IVC is directly adjacent to the liver parenchyma (Figure 30-6). The venous wall of the IVC is thinner than the aortic wall. Pulsations may be visualized in the IVC or aorta.

Alternatively, the IVC can be visualized from a more lateral position with the ultrasound probe placed at the patient's right anterior axillary line, directing the ultrasound beam medially (with the index marker pointing to the head in the longitudinal axis) toward the patient's spine (Figure 30-7). The ultrasound beam will pass through the right hepatic lobe, imaging the IVC adjacent to the liver parenchyma.

Once the IVC is identified, respirophasic variations are assessed via time-motion mode, or M-mode. This mode analyzes real-time images as a function of time, along only one line (M-mode cursor), making dynamic events appear on static images. Typically, the picture consists of horizontal black (anechoic) or white (hyperechoic) bands. Once the cursor appears on the screen, you place it within 2 to 3 cm distal to the diaphragm, perpendicular to the vessel wall (Figure 30-8). Also, the hepatic vein–IVC junction may not cross the M-mode cursor during respirations since it would lead to a false-positive test result. The IVC will be shown as a continuous anechoic band that varies in size depending on the degree of collapsibility during the respiratory cycle (Figure 30-9). Observing the ventilator or patient's chest is necessary to determine inspiration and expiration. After the widest and narrowest point of the IVC diameter is measured using the caliper function, the collapsibility index is calculated as described above.

Assessment of IVC variation is most reliable when patients are intubated and synchronous with mechanical ventilation. The sensitivity and specificities for predicting fluid responsiveness are not as strong in spontaneously ventilating patients.

Visualization of the IVC may be limited in obese patients. Air limits ultrasound penetration, so tissue emphysema, bowel loops, and recent laparotomy will all effect image quality. Well-aerated lung tissue may also extend into the costophrenic angles and come to lie between the ultrasound probe and the liver and will intermittently obscure the picture. Finally, respiratory variations in the IVC have only been studied in patients without increased intra-abdominal pressures. One could safely assume that if the patient has abdominal hypertension or even compartment syndrome, the compliance of the IVC is limited and subsequent analysis of variation in diameter may not be accurate.

One technique that has repeatedly been shown to be useful is the passive leg raise test. This test is performed by elevating a patient's legs either manually or by tilting the bed cranially from a semir-ecumbent position and measuring a dynamic parameter before and after the test.⁷ When using this method, the patient is challenged with increased preload with the advantage of total reversibility by putting the legs down. If there is a significant improvement in the measured dynamic parameter with leg elevation, the patient likely is volume responsive. Investigators have used the pulse-pressure variation, the aortic flow variation via esophageal Doppler,⁸ or the velocity time integral (VTI) variation in the left ventricular outflow tract (LVOT) via the Apical 5 chamber view⁹ to determine fluid responsiveness.

Yes, ever since Lichtenstein published his first paper on using chest ultrasonography to rule out a pneumothorax in 1995,¹⁰ its popularity has been steadily rising as it has established itself as a possible alternative to computed tomography (CT). Chest ultrasonography can be quickly performed at the bedside, providing real-time results while avoiding time delays, ionizing radiation, and potentially risky patient transportation. It has been used to diagnose pulmonary edema, lung consolidations, large pleural effusions, and pneumothoraces. Furthermore, an easy-to-use algorithm for the systematic approach to the evaluation of the patient with acute respiratory distress or failure using ultrasound findings has been published.¹¹

The patient should be in the supine or semirecumbent position. Two different probes may be used: the phased array probe or the longitudinal probe. The phased array probe has a small footprint, which makes imaging between the ribs straightforward. This probe can identify deeper structures in the chest, making it useful to determine the extent of a large pleural effusion or lung consolidation (Figure 30-10A). Some intensivists suggest that the linear array probe is sufficient. It better visualizes, with higher resolution, proximal structures such as the pleura, intercostal arteries, and the periphery of the lung (Figure 30-10B). It has great utility for procedural superficial needle placement.

It is advisable to start with the phased array probe since more structures can be visualized at once. First, the diaphragm should be identified to clearly determine the extent of the intrathoracic space. Second, the chest and lung should be scanned sequentially along longitudinal lines (from cranial to caudal) with the probe held perpendicularly to the chest wall. Each hemithorax should be divided into six scanning zones (Figure 30-11). The three large areas from the lateral edge of the sternum to the anterior axillary line, the anterior axillary line to the posterior axillary line, and from the posterior axillary line to the spine should be divided into superior and inferior regions. These regions make up the six scanning zones. The ultrasonographer examines the anterior chest wall to identify signs of a pneumothorax or pulmonary edema, then examines the lateral chest wall for pleural effusions and consolidations, which tend to develop in the dependent areas.¹² The posterior scan zone may be accessed by rolling the patient slightly and orienting the probe anteriorly. Other approaches have been described; however, all used the delineated chest wall sections for orientation.¹³

When scanning the lung or abdomen, the diaphragm should initially be identified in order to differentiate the thorax from the abdomen. Next, the ribs should be identified. They are superficial and produce a clean black acoustic shadow. A hyperechoic "sliding line" moving synchronously with respiration can be seen between the ribs about 0.5 cm deeper than the proximal rib surface (Figure 30-12). This line is called the pleural line, and the sliding movement is produced by the parietal and visceral pleurae sliding against each other during respiration. Using the time-motion mode (M-mode), the "seashore sign"¹⁰ can be appreciated (Figure 30-13). Underneath the pleural line, motionless horizontal hyperechoic lines, called A-lines, appear repeatedly in fixed intervals and are generated by subpleural air (Figure 30-12). A-lines are a reverberation artifact created by the soft tissue–air interface at the pleura and are normal. A normal chest ultrasound is defined by the presence of lung sliding and A-lines and referred to as an A-profile.¹¹

Occasionally, vertically oriented B-lines will be seen. They tend to be seen in the dependent lung zones and are usually nonpathologic. B-lines (also know as "comet tails" or "lung rockets") are ultrasound artifacts caused by the reflection of ultrasound beams within thickened interlobular septa just under the pleura and are seen as hyperechoic vertical lines arising at the pleural line.¹⁴ These lines span the entirety of the ultrasound image without fading, are well defined, efface A-lines, and move with the visceral pleura. They may be part of a normal lung picture if they occur occasionally, mostly representing, for example, a lung fissure. Their significance changes as they become more numerous; typically more than three in one window or when they appear in nondependent lung zones (Figure 30-14).

Pleural effusions and alveolar consolidations are easily detected by chest ultrasonography (Figure 30-15). Interstitial pulmonary edema, pneumothoraces, and pulmonary emboli can also be imaged but require more expertise.

Pleural effusions are present in up to 60% of medical ICU patients and 40% are present upon admission.¹⁵ Effusions appear as an anechoic layer of fluid separating the two pleural membranes. The fluid collection is typically dependent, resting upon the diaphragm. You can often differentiate between a transudative or exudative effusion. A transudate is totally anechoic and is clearly defined with sharp borders, whereas an exudate, parapneumonic effusion, or empyema is hypoechoic, with much less differentiation.

When lung becomes consolidated it generates an echotexture very similar to liver tissue. This pattern is called hepatization. Since the alveoli are filled with fluid and not air, A-lines will not be generated.¹¹ Most lung consolidations will have some degree of pleural effusion surrounding them. Often, small hyperechoic spots that are accentuated during inspiration can be appreciated. These spots are air bronchograms (Figure 30-16).¹²

Once the lung is injured and the pathology extends to the periphery, the ultrasound image will have an increasing number of B-lines. When B-lines are separated by 7 mm, they correlate with thickened interlobular septa, and when 3 mm apart or almost confluent, they tend to represent alveolar flooding or ground-glass opacities (Figure 30-17).¹⁶ Depending on the type and the extent of the pathologic process, the B-lines may be localized or disseminated.

The definitive diagnosis of a pneumothorax using ultrasound is not easy. The real value of chest ultrasonography in this instance is in its negative predictive value to rule out a pneumothorax.¹⁰ The absence of lung sliding alone carries a low positive predictive value because many things such as acute respiratory distress syndrome (ARDS), atelectasis, pleural adhesions, phrenic palsy, or mainstem or esophageal intubation may cause this.

The only sign that confirms and quantifies a pneumothorax is a "lung point."¹⁷ It is characterized by a normal lung pattern (A-profile: lung sliding in the presence of A-lines) alternating with the A'-profile (absent lung sliding in the presence of A-lines) during the respiratory cycle within the same acoustic window. The M-mode facilitates the detection of the lung point. The image shows the regular seashore sign intermittently replaced by the "stratosphere sign"; that is, continuous straight lines throughout the entire M-mode picture (Figure 30-18). By marking the lung point in all intercostal spaces on the patient's chest wall, the extent of the partial pneumothorax may be assessed.

The presence or absence of pleural artifacts, lung sliding, and an alveolar consolidation or pleural effusion can be combined to create certain profiles that indicate different pathologic conditions. The A-profile is characterized by A-lines with lung sliding; the A'-profile is similar but without lung sliding. The B-profile is characterized by B-lines (more than three per view between two ribs) and lung sliding; the B'-profile is the same without lung sliding. The A/B-profile shows mostly A-lines on one side of the chest and mostly B-lines on the other half. The C-profile is consistent with anterior lung consolidation.¹¹

Lung ultrasound may clarify equivocal chest radiographs that are limited by artifacts such as rotation and differences in penetration. In addition, chest ultrasonography may reduce the number of chest radiographs and CT scans performed and radiation exposure to critically ill patients.¹⁸

In the setting of acute dyspnea, an algorithm such as the bedside-lung-ultrasound-in-emergency (BLUE) protocol can guide diagnosis.¹¹ This three-step algorithm is quick and can be performed at the bedside.

First, the anterior chest is examined for lung sliding. The presence of lung sliding excludes a pneumothorax with a specificity of 100%. Second, anterior B-lines are assessed. The B-profile (see above) suggests pulmonary edema, and in the majority of cases, edema will be cardiogenic in origin (95% specificity). If an A/B-, C-, or B′-profile is noted, pneumonia is more likely. The sensitivity of a pneumonia diagnosis, however, only reaches 89% if all profiles are found together, which is unlikely. Thus, pneumonia is difficult to diagnose with ultrasound. If normal patterns are observed with chest ultrasonography, pulmonary thromboembolism should be ruled out. If there is no evidence of deep venous thrombosis with a normal profile, assessment for the presence of a posterior consolidation with or without some pleural effusion should be undertaken (posterolateral alveolar/pleural syndrome [PLAPS]). In cases in which PLAPS is present, pneumonia may be responsible for the acute respiratory distress. If PLAPS is absent, chronic obstructive pulmonary disease (COPD) or asthma should be considered (Figure 30-19).

Lung ultrasonography can assess focal or disseminated disease in patients with ARDS/acute lung injury (ALI) and, therefore, help titrate positive end-expiratory pressure (PEEP) to avoid hyperinflation of the normal lung parenchyma.¹⁹ The changes of lung aeration scores based on ultrasound findings correlate with changes found on chest CT scans after interventions like pleural drainage or antimicrobial therapy for ventilator-associated pneumonia.²⁰

Diagnosis should integrate the patient's clinical picture with ultrasound findings. Generating a narrow differential diagnosis prior to ultrasonography scanning may prevent unnecessary treatment. For example, most healthy human beings will show signs of volume responsiveness but are in perfect homeostasis and will not need treatment or intervention. However, in the setting of an oliguric or hypotensive patient, these signs suggest a need for volume loading. In our patient, we found scattered B-lines in all segments of his chest. His transthoracic echocardiogram (TTE) showed a hyperdynamic heart with no signs of fluid responsiveness. A subsequent CT scan of his chest showed a picture consistent with early ARDS/ALI, possibly secondary to his intra-abdominal sepsis.

Chest ultrasonography requires training and acquisition of specific skills to have a clinical impact. It has been shown that the learning curve is steep and quick (under 6 weeks) for proficiency in diagnosing simple pathologies like pleural effusions, alveolar consolidations, and alveolar interstitial syndrome.²¹ Presumably, it may take longer to diagnose a pneumothorax.

Lung ultrasonography is limited by the fact that lesions or pathologies surrounded by normally aerated parenchyma will not be seen, since air is considered impermeable to ultrasound waves. Obese patients or those with thick chest walls, subcutaneous emphysema, and thoracic wound dressings may have suboptimal images.