Decision Making in Emergency Critical Care
SECTION 3 - Critical Care Ultrasonography
Principles of Critical Care Ultrasonography
Phillips Perera, Laleh Gharahbaghian, Thomas “Tom” Mailhot, Sarah R. Williams, and Diku P. Mandavia
Traditionally, clinicians have divided shock into four distinct categories. In each category, there are several subtypes (Table 6.1).
TABLE 6.1 Categories of Shock States
Rapidly determining the type of shock state in the critically ill patient and initiating the appropriate resuscitative measures can lower patient mortality.1,2 With the decreased reliance on invasive monitoring tools for shock assessment, focused bedside ultrasonography, or ultrasound (US), has evolved to become a key means for evaluation. As US allows for the rapid assessment of both the anatomy and physiology of the shock patient, multiple resuscitation protocols have been created.
The major resuscitation US protocols in critically ill medical and trauma patients include ACES,3 BEAT,4 BLEEP,5 Boyd ECHO,6 EGLS,7 Elmer/Noble Protocol,8 FALLS,9 FATE,10 FAST,11 extended FAST,12 FEEL resuscitation,13 FEER,14 FREE,15 POCUS (FAST and RELIABLE),16 RUSH-HIMAP,17 RUSH (pump/tank/pipes),18–20 Trinity,21 and UHP.22 These algorithms have many similar components but differ in the sequence of exam performance (Table 6.2).
TABLE 6.2 Ultrasound Resuscitation Protocols and Examination Components
Numbers indicate order of exam sequence for each protocol.
The RUSH protocol, named for Rapid Ultrasound in Shock, offers one easily remembered and comprehensive resuscitation protocol first to identify the shock state and then to monitor targeted therapy.
SOCIETY SUPPORT FOR FOCUSED ULTRASOUND IN CRITICALLY ILL PATIENTS
The use of focused US, including the individual components of the RUSH exam, has been supported by the major emergency medicine organizations. These organizations include the American College of Emergency Physicians (ACEP), the Society for Academic Emergency Medicine, and the Council of Emergency Medicine Residency Directors (CORD).23–26 Critical care societies have endorsed both training in and the clinical use of bedside US. US has become an increasingly important diagnostic modality for this specialty.27–30 In 2010, an important collaborative paper was published jointly between the American Society of Echocardiography (ASE) and ACEP that endorsed focused echocardiography (echo) for a defined set of emergent conditions.31 These exam indications and goals include the core exam components of the RUSH exam (Tables 6.3 to 6.5).
TABLE 6.3 ACEP/ASE Consensus Guidelines for Ultrasound Exam—Clinical Indications
TABLE 6.4 ACEP/ASE Consensus Guidelines for Core Ultrasound Exam—Clinical Goals
TABLE 6.5 ACEP/ASE Consensus Guidelines for Advanced Ultrasound Exam—Exam Goals
In addition, other components of the RUSH exam, including the FAST, lung, aorta, and deep venous thrombosis (DVT) US exams, are supported by ACEP as core applications for use by the emergency physician.23
PERFORMANCE OF THE RUSH EXAMINATION: BASIC CONCEPTS
Ultrasound Probe Selection
A phased array probe at 2 to 3 MHz is used for the cardiac and thoracic components of the exam. A curvilinear probe at 2 to 3 MHz can be used for the abdominal components (FAST and aorta). A linear array probe at 8 to 12 MHz is used for the more superficial vascular components (DVT, internal jugular (IJ) veins).
The heart moves rapidly in reference to other body structures. For this reason, selection of a high frame rate on the US machine settings will allow for optimal imaging. This is done by selecting the cardiac preset, which is preloaded on most current US machines. The abdominal preset is best for the FAST and aorta exams. The vascular or venous preset is best for the DVT and IJ vein exams.
The RUSH US exam utilizes modalities that can image both critical anatomy and physiology.32 This is done by first employing two-dimensional B-mode imaging. B-mode imaging projects the body as a continuum of color in the gray spectrum, termed echogenicity. Echogenicity results from the fact that the US probe first acts as a transducer that sends sound waves into the body. The sound waves then penetrate into the body, traveling a distance until they are bounced back to the probe. Different tissues will have varying resistance to the movement of sound. Higher-density (hyperechoic) structures will reflect an increasing amount of the sound back to the probe, resulting in a brighter appearance (i.e., a calcified heart valve, diaphragm). Fluid-filled structures (hypoechoic or anechoic) will allow for increased propagation of sound through the body, leading to a darker appearance (i.e., blood, body fluids) (Fig. 6.10).
M-mode or “motion” mode illustrates an “ice pick” image of movement across a defined anatomical axis in relation to time. This generates a gray-scale illustration of movement over time that can be used to easily document motion on a static image (Figs. 6.11 and 6.12).
Doppler US allows for the evaluation of motion within the body. The Doppler shift is defined as the movement of body structures relative to the position of the US probe. A positive Doppler shift results from structures (such as blood cells) moving toward the probe and a negative Doppler shift from movement away from the probe. The Doppler shift can be interpreted in several imaging modalities, two of which are discussed below.
This modality demonstrates directionality of flow both toward and away from the probe and is often used in echo and vascular applications. Movement toward the probe results in a shorter frequency of sound. It is traditionally represented as red on the US image. Movement away from the probe results in a longer frequency of sound and is typically represented as blue. The scale that displays the color-flow Doppler setting should be set high (>70 cm/s) for echo to best capture the fast flow of the blood traveling through the heart. A lower scale can be used for the evaluation of the aorta and other vascular applications (DVT, IJ veins).
Pulsed-wave Doppler allows for assessment of flow velocity in a waveform that identifies the specific speed of blood flow over time. This modality is often used in advanced echo to define the velocity of blood flow through cardiac valves.
Orientation of Indicator on Machine and Probe
Historically, there has been practice variation between different US exams with regard to the orientation of the indicator dot on the screen and the marker on the probe. The reason for this being that the first widespread applications used in emergency medicine practice, such as the FAST and OB/GYN exams, were oriented based on traditional radiology practice, with the US screen indicator dot oriented to the left. Emergency medicine-practiced echo was therefore configured similarly. This differs from traditional cardiology practice, where the indicator dot is oriented to the right on the US screen. Despite this difference, the standard practice has been to orient the US probe (at a 180-degree variance, depending on screen orientation), so that the cardiac images obtained with the screen indicator dot on either side display the heart in the same configuration. In this chapter, the probe orientation for all RUSH exam components, including the cardiac views, will be described with the screen indicator dot located to the left side. This convention avoids having to flip the screen marker dot between different exams.
THE RUSH EXAM: PROTOCOL COMPONENTS
The RUSH exam involves a 3-part bedside physiologic patient assessment, which is simplified as “the pump,” “the tank,” and “the pipes.”
RUSH STEP 1: THE PUMP
Clinicians caring for the patient in shock should begin with assessment of “the function of the pump,” which is a goal-directed echo exam looking specifically for:
1.The degree of left ventricular contractility
2.Detection of pericardial effusion and cardiac tamponade
3.The presence of right ventricular enlargement
In addition, other cardiac pathology may be detected on bedside echo. A confirmatory test should generally be ordered if more advanced pathology is seen on bedside US, in accordance with the joint ACEP/ASE guidelines. The information gained by this exam can also allow a better assessment of the need for an emergent cardiac procedure. If indicated, US can then allow more accurate guidance of both the pericardiocentesis procedure and placement of a transvenous pacemaker wire.
Performance of the Echocardiography Examination
There are three traditional windows used for performance of cardiac US. These are the parasternal (long- and short-axis views), subxiphoid, and apical views (Fig. 6.1).
FIGURE 6.1 RUSH step 1, standard windows for cardiac ultrasound.
The Parasternal Long-Axis View
This view can be performed with the patient in a supine position. Turning the patient into a left lateral decubitus position will often improve this view by moving the heart away from the sternum and closer to the chest wall. This displaces the lung from the path of the sound waves.
The probe should initially be positioned just lateral to the sternum at about the third intercostal space. The probe position can then be adjusted for optimal imaging by moving the probe up or down one additional intercostal space. The probe indicator should be oriented toward the patient's left elbow (Fig. 6.2).
FIGURE 6.2 Parasternal long axis, probe position.
Anatomic and Sonographic Correlation
The parasternal long-axis view will visualize three cardiac chambers and the aorta. The right atrium is not seen from this view. Optimally, the parasternal long-axis images have both the aortic and mitral valves in the same view. The aortic valve and aortic root can be visualized as the area known as the left ventricular outflow tract (Fig. 6.3).
FIGURE 6.3 Parasternal long axis, anatomy.
Parasternal Short-Axis View
This view is obtained by first identifying the heart in the parasternal long-axis view and then rotating the probe 90 degrees clockwise. The probe indicator dot is aligned toward the patient's right hip (Fig.6.4).
FIGURE 6.4 Parasternal long axis, probe position.
Anatomic and Sonographic Correlation
The short-axis view visualizes the left and right ventricles in cross section and is known as the ring, or doughnut view, of the heart (Fig. 6.5). The traditional view is of the left ventricle at the level of the mitral valve, which appears as a “fish mouth” opening and closing during the cardiac cycle. Visualizing the heart as a cylinder with the US beam cutting tangentially through different levels, one can look as far inferiorly as the apex of the left ventricle and superiorly to the level of the aortic valve.
FIGURE 6.5 Parasternal short axis, anatomy.
To best evaluate left ventricular contractility, the probe is moved inferiorly to the level of the papillary muscles, allowing confirmation of the assessment taken from the parasternal long-axis view. In addition, cardiologists routinely evaluate for segmental wall motion abnormalities on this view. If the probe is angled superiorly and medially from the above location, the aortic valve and right ventricular outflow tract will come into view. The aortic valve should appear as the “Mercedes-Benz sign” with a normal tricuspid configuration. A calcified bicuspid valve that may be prone to stenosis and pathology can be identified here.33
This view is performed with the patient supine. Bending the patient's knees will relax the abdominal muscles and can improve imaging.
Place the probe just inferior to the xiphoid tip of the sternum, with the indicator oriented toward the patient's right side (Fig. 6.6). Flattening and pushing down on the probe will aim the US beam up and under the sternum to best image the heart. If gas-filled stomach or intestine impedes imaging, one can move the probe to the patient's right while simultaneously aiming the probe toward the patient's left shoulder, to utilize more of the blood-filled liver as an acoustic window.
FIGURE 6.6 Subxiphoid view, probe position.
Anatomic and Sonographic Correlation
The liver, which will be seen anteriorly, will act as the acoustic window to the heart from the subxiphoid view, allowing all four cardiac chambers to be seen. Because of the superior ability to visualize the right side of the heart from the subxiphoid window, it is often employed when close assessment of these chambers is needed (Fig. 6.7).
FIGURE 6.7 Subxiphoid view, anatomy.
Roll the patient into the left lateral decubitus position to bring the heart closer to the lateral chest wall, and obtain optimal imaging from this view.
Palpate the point of maximal impulse on the lateral chest wall and place the transducer at this point. This is generally just below the nipple line in men and under the breast in women. For the apical view, the probe marker will be oriented toward the patient's right elbow (Fig. 6.8).
FIGURE 6.8 Apical view, probe position.
Anatomic and Sonographic Correlation
The apical window allows for detailed assessment of the sizes and movements of all four cardiac chambers in relation to one another (Fig. 6.9). The apical four-chamber view is the first traditional view from this window. The optimal views from this position have both the mitral and tricuspid valves in the image. From this position, the probe can then be angled more superiorly to obtain the apical 5-chamber view. The “5th chamber” will be the aortic valve and aortic outflow tract in the middle of the image.
FIGURE 6.9 Apical view, anatomy.
RUSH STEP 1A: ASSESSMENT OF CARDIAC CONTRACTILITY
A relatively high percentage of critical patients may have compromised cardiac function contributing to their shock state, which may be diagnosed with bedside echo.34 Published studies have demonstrated that emergency physicians with focused training can accurately evaluate left ventricular contractility.35
Qualitative Evaluation of Left Ventricular Contractility
Evaluating motion of the left ventricular walls by a visual estimation of the volume change from diastole to systole provides a qualitative assessment of contractility.34–36 A ventricle that has good contractility will have a large-volume change between the two cycles (Fig. 6.10), while a poorly contracting heart will have a small percentage change. The poorly contracting heart may also be dilated in size. Based on these assessments, a patient's contractility can be broadly categorized as being normal, mildly to moderately decreased, or severely decreased. A fourth category, known as hyperdynamic, can be seen in advanced hypovolemia or in distributive shock states. The heart will have small chambers and vigorous, hyperkinetic contractions with the endocardial walls almost touching during systole.
FIGURE 6.10 Left ventricle, good contractility.
Semiquantitative Means for Assessment of Contractility
M-mode can be used to graphically depict the movements of the left ventricular walls through the cardiac cycle. In the parasternal long-axis view, the M-mode cursor is placed across the left ventricle beyond the tips of the mitral valve leaflets at about the midventricle area. The resulting tracing allows a two-dimensional length-based measurement of the chamber diameters over time. Fractional shortening is calculated according to the following formula:
where ESD is the end-systolic diameter, measured at the smallest dimension between the ventricular walls, and EDD is the end-diastolic diameter, where the distance is greatest (Fig. 6.11).
FIGURE 6.11 M-mode, good contractility.
In general, fractional shortening above 35% to 40% correlates to a normal ejection fraction.37 Compared to the comprehensive volumetric assessment required for measuring ejection fraction, fractional shortening is a semiquantitative method for determining systolic function that is relatively fast and easy to perform.38
E-Point Septal Separation
Motion of the anterior leaflet of the mitral valve in the parasternal long-axis view can also be used to assess left ventricular contractility. In the early diastolic phase of a normal contractile cycle, the anterior mitral leaflet can be observed to fully open to a position close to the septal wall. This is with the caveat that mitral valve abnormalities (stenosis, regurgitation), aortic regurgitation, and extreme left ventricle hypertrophy are not present. Early diastolic opening of the mitral valve is represented on M-mode US as the E-point. The distance measured between the E-point, representing the position of the fully open mitral valve, and the septum is known as the E-point septal separation or EPSS.39 To measure the EPSS, the M-mode cursor is placed over the tip of the anterior mitral valve leaflet. In a normal contractile state, the EPSS will be <7 mm, as the mitral valve will almost approximate the septum during early diastolic filling.39–41 As left ventricular contractility decreases, diastolic flow through the valve will diminish. This results in decreased mitral valve opening to a position relatively farther from the septum and a corresponding increase in the EPSS (Fig. 6.12). Further research is ongoing to determine the accuracy of correlation between EPSS and fractional shortening.42
FIGURE 6.12 Mitral valve, E-point septal separation.
RUSH STEP 1B: DIAGNOSIS OF PERICARDIAL EFFUSION AND CARDIAC TAMPONADE
Published studies have documented that pericardial effusions may be found relatively commonly in critical patients presenting with acute shortness of breath, respiratory failure, shock, and cardiac arrest.43,44 Fortunately, the literature also indicates that emergency physicians with focused echo training can accurately identify effusions.45 Pericardial effusions may result in hemodynamic instability as the pressure in the pericardial sac acutely increases, resulting in reduced cardiac filling.46 Acute pericardial effusions (as small as 50 cc) may result in tamponade. This pathology may quickly compromise the trauma patient. Conversely, in chronic conditions, the pericardium may slowly stretch to accommodate large effusions over time without tamponade.47
Sonographic Appearance of Pericardial Effusions
Pericardial effusions are generally recognized by a dark, or anechoic, appearance. However, inflammatory or infectious conditions may result in effusions with a brighter, or more echogenic, appearance. In addition, traumatic pericardial effusions will take on a more echogenic appearance over time as blood clots.
Grading Scale for the Size of Pericardial Effusions
One scale for describing the size of the effusion is shown below (Table 6.6).48
TABLE 6.6 Grading Scale for Pericardial Effusions
Specific Echocardiographic Windows for Evaluating Pericardial Effusions
Parasternal Long-Axis View
Size and Location of Effusions
Smaller effusions will first layer posteriorly behind the heart. As effusions grow in size, they will surround the heart in a circumferential manner, moving into the anterior pericardial space.47 Most effusions are free flowing in the pericardial sac. However, occasionally loculated effusions may occur. These typically occur in postoperative cardiac surgery patients and in inflammatory conditions.49
Differentiation of Pleural from Pericardial Fluid
The critical landmarks for detection of a pericardial effusion are the descending aorta and the posterior pericardial reflection. The descending aorta will appear as a circle directly behind the left atrium, posterior to the mitral valve (Fig. 6.13). The posterior pericardial reflection will be identified as a hyperechoic structure immediately anterior to the descending aorta. First, select the appropriate depth of the US image, so that the descending aorta and pericardial reflection are adequately visualized posteriorly on the screen. Pericardial effusions will be located anterior to the descending aorta and above the posterior pericardial reflection (Fig. 6.13). In contrast, pleural effusions will be located posterior to the descending aorta and below the posterior pericardial reflection (Fig. 6.14). To further confirm the presence of a left pleural effusion, the probe can be moved to a lateral position on the chest wall as for the FAST views and aimed above the diaphragm to visualize the lower thoracic cavity (Fig. 6.17).
FIGURE 6.13 Pericardial fluid.
FIGURE 6.14 Pleural fluid.
Pericardial Fat Pad
A pericardial, or epicardial, fat pad may at times be confused with a pericardial effusion. The typical location for this structure is in the area just deep to the near-field pericardial reflection and anterior to the heart. The fat pad often has a classic appearance, with an interspersed speckling of bright, or hyperechoic, regions. From the parasternal views, an isolated anterior “echo-dense” structure is more suggestive of a fat pad and not of an effusion. For an effusion to be visualized anteriorly on the parasternal views, a circumferential effusion would usually be present (with the exception of the presence of a rarer loculated pericardial effusion). From the subxiphoid view, the fat pad would be seen closer to the probe, located just beneath the near-field pericardial reflection and anterior to the heart.
Size and Location of Effusions
Because the subxiphoid window is taken from a position inferior to the heart, small effusions will typically first layer out with gravity along the near-field pericardial reflection. This is especially noted in cases where the patient has been in an upright position. Larger effusions will spread to surround the heart circumferentially.
Differentiation of Pericardial Effusion from Ascites
Ascites may be confused with a pericardial effusion. To help differentiate between the two, ascites will be seen nearer to the probe, anterior to the near-field pericardial reflection, outside the pericardial sac, and surrounding the liver within the abdominal cavity. In contrast, a pericardial effusion is located posterior to the near-field pericardium, adjacent to the heart, and within the pericardial sac.
Echocardiographic Diagnosis of Cardiac Tamponade
As pericardial effusions accumulate, the pressure in the pericardial sac rises and will first compromise the lower pressure circuit of the right heart. This is best recognized sonographically as an inability of these chambers to fully expand during the relaxation phase of the cardiac cycle. Cardiac tamponade is thus classically defined on US as diastolic collapse of either the right atrium or the right ventricle. While both right heart chambers should be evaluated, diastolic collapse of the right ventricle is a more specific finding. This is because as tamponade progresses, the right atrium may take on an appearance of a “furiously contracting chamber” with hyperdynamic contractions. This can at times make differentiation of atrial systolic contraction from diastolic collapse more difficult.
Diastolic collapse of the right ventricle in tamponade is best understood as a spectrum of US findings, from a subtle serpentine deflection of the wall to complete chamber compression (Fig. 6.15).50 One important pitfall to this general diagnostic strategy is seen in the patient with pulmonary hypertension, where diastolic collapse of the right heart may occur late in the disease process.
FIGURE 6.15 Cardiac tamponade, right ventricular collapse. PE, pericardial effusion.
Advanced Strategies in the Identification of Tamponade
There are several more advanced strategies used to document diastolic compression of the right heart in tamponade.51 The first is to attach an EKG monitoring lead to the US machine to allow for simultaneous display of both the US and electrical phases. Systole will be identified immediately following the QRS, and diastole will follow later in the electrical cycle, just prior to the next P–QRS complex. Slowing the video down and scrolling through the echo with simultaneous attention to both the EKG phase and the US will allow discrimination of systolic from diastolic movements of the right atrium and ventricle. In tamponade, right atrial diastolic collapse may be noted first, occurring directly after atrial systole and early after the QRS complex. Right ventricular diastolic collapse will be noted later as tamponade progresses. This will be seen on EKG later in the electrical cycle and just before the following P–QRS complex.
Evaluation of the inferior vena cava (IVC) may also be performed to confirm tamponade physiology. A dilated, or plethoric, IVC without respiratory collapse implies tamponade.52 A more advanced exam using Doppler US allows for one of the most sensitive tests to evaluate for tamponade. From the apical 4-chamber view, color-flow Doppler can first be used to identify the flow of blood through the tricuspid and mitral valves. Pulsed-wave Doppler is then used to identify the augmented respiratory variation in the flow velocities across these valves, which is noted in tamponade. In inspiration, an increase in blood flow through the tricuspid valve and a decrease in flow through the mitral valve will be seen. Flow variations >25% across the tricuspid valve and >15% across the mitral valve are considered abnormal.53
Ultrasound Guidance of Pericardiocentesis
In cases of cardiac tamponade and shock, an emergent pericardiocentesis is generally indicated. Emergency physicians have classically been taught the subxiphoid approach for pericardiocentesis. However, a large review from the Mayo Clinic included 1,127 pericardiocentesis procedures and found that the optimal position for placement of the needle was the apical position in 80% of patients.54 The subxiphoid approach was only chosen in 20% of these procedures, due to the interposition of the liver. US allows for accurate guidance of the pericardiocentesis needle and guidewire into the pericardial sac. In addition, agitated saline can be used as a form of US contrast to confirm proper needle placement in the pericardial space.55,56
RUSH STEP 1C: ECHOCARDIOGRAPHY IN PULMONARY EMBOLUS AND EVALUATION FOR RIGHT VENTRICULAR ENLARGEMENT
While a CT scan is typically thought of as the current diagnostic standard for pulmonary embolism, focused echo can identify one of the more serious complications of this disease, right ventricular strain. This finding correlates with a poorer prognosis and the need for more immediate treatment.57,58 Right ventricular enlargement on focused echo may also suggest this pathology in the undifferentiated patient presenting in shock, potentially leading to more timely diagnosis and treatment.
Echocardiography Literature for Pulmonary Embolus
Studies have previously evaluated the use of echo for the diagnosis of pulmonary embolus, specifically looking for the presence of right ventricular enlargement due to acute cardiac strain. The documented sensitivity of this test in all patients with pulmonary embolus is only moderate. Therefore, echo cannot be used to rule out a pulmonary embolus, especially in those patients who are hemodynamically stable. However, identification of right ventricular enlargement can be of increased diagnostic utility in cases of hypotension with suspected thromboembolic disease, where it will have a higher specificity and positive predictive value.59–64
The traditional treatment of patients with a pulmonary embolus has been with anticoagulation. However, more recent guidelines recommend the combined use of anticoagulants and fibrinolytics in cases of severe pulmonary embolism.65–68 This is defined as the presence of acute right heart strain and clinical signs and symptoms of hypotension, severe shortness of breath, or altered mental status.
Echocardiographic Findings of Hemodynamically Significant Pulmonary Embolism
The relative sizes of the left and right ventricles can be evaluated from this window. A normal ratio of the right to the left ventricle is defined as 0.6:1 with a greater than 1:1 ratio indicating right ventricular dilatation.69,70 A higher relative ratio, combined with deflection of the interventricular septum from right to left, indicates the right ventricular strain that may be seen in a severe pulmonary embolus. In acute right ventricular strain, the chamber wall will typically be thin, due to the lack of time for compensatory hypertrophy. Conversely, in cases of chronic pulmonary strain seen in conditions of long-standing pulmonary artery hypertension, the right ventricle will compensate with hypertrophy. This will result in a thicker wall, typically measuring >5 mm.48,71 These findings can allow the clinician to further differentiate the US findings of acute from chronic right heart enlargement. On the parasternal short-axis view, the interventricular septum may be seen to bow from right to left with high right-side pressures. This can result in a finding known as the left ventricular “D-shaped cup,” or “D-sign,” as the septum is pushed down and away from the right ventricle (Fig. 6.16).72
FIGURE 6.16 Parasternal views, RV strain.
Subxiphoid and Apical Views
The subxiphoid view may also be used in the assessment of right ventricular strain: however, one must take care to aim the probe to capture the widest chamber size, avoiding underestimation of dimensions by imaging the right ventricle off-axis. The apical window is another excellent view for visualization of both right ventricular enlargement and septal bowing. In addition to findings of right ventricular strain, occasionally clot may be visualized within the heart.73
RUSH STEP 1 - OTHER USES: THE PATIENT WITH HEART BLOCK AS CAUSE FOR SHOCK: ULTRASOUND GUIDANCE OF TRANSVENOUS PACEMAKER PLACEMENT
In cases of cardiogenic shock due to pump failure from bradycardia, immediate transvenous pacemaker placement may be indicated in cases unresponsive to medications. US guidance of transvenous pacemaker placement can be performed from either the subxiphoid or apical window. The pacing wire should be observed to pass from the right atrium through the tricuspid valve and into the right ventricle. Optimally, the wire can be observed to float up against the electrically active right ventricular septum and mechanical capture then confirmed with US.
RUSH STEP 2: THE TANK
The second part of the RUSH protocol focuses on the determination of the effective intravascular volume status, referred to as “the tank” (Fig. 6.17). This information, in conjunction with evaluation of cardiac status, provides a key guide to fluid management in the critical patient. The evaluation of “the tank” is composed of three components: (1) “Tank Fullness”, (2) “Tank Leakiness”, and (3) “Tank Compromise.”
FIGURE 6.17 RUSH step 2, evaluation of the “tank.”
1) “Fullness of the Tank”: Inferior Vena Cava and Internal Jugular (IJ) Veins
Following evaluation of the heart and quantification of contractility, assessment of the central venous pressure (CVP) or “fullness of the tank” should be performed. The IVC will typically be the primary structure evaluated to give this information (Fig. 6.17, position A). However, if the IVC cannot be seen well in a given patient, evaluation of the IJ veins can provide an alternate means for volume assessment.
Ultrasound Evaluation of the Inferior Vena Cava
The IVC is best evaluated with patient in the supine position.
From the subxiphoid window, there are several variant views that are utilized in the imaging of the IVC. First, identify the right atrium in the four-chamber subxiphoid view and angle the probe inferiorly toward the spine to visualize the IVC as it joins this chamber. The IVC can then be followed inferiorly as it runs from the right atrium through the liver to the confluence with the three hepatic veins. Next, rotate the probe from the subxiphoid four-chamber view to the subxiphoid two-chamber view, by orienting the probe with the indicator oriented superiorly toward the ceiling. This allows for imaging of the right ventricle above the left ventricle, with the aorta typically seen in a long-axis orientation inferior to the heart. Moving the probe toward the patient's right side will then bring the IVC into view.
Anatomic and Sonographic Correlation
Current recommendations for the measurement of the IVC are at the point just inferior to the confluence with the hepatic veins. This is approximately 2 cm from the junction of the right atrium and the IVC.74 Examining the IVC first as a circular structure in a short-axis plane is recommended. This can avoid slicing the US beam to the side of IVC and resulting in a falsely low measurement, in a pitfall known as the cylinder tangent effect. The probe can then be rotated to image the IVC in a longitudinal plane. This will allow confirmation of the accuracy of vessel measurements.
Differentiation of IVC from Aorta
The aorta and the IVC may be confused with one another. The aorta can be identified as a thicker-walled and pulsatile structure, with more prominent branch vessels and a location to the patient's left side. In contrast, the IVC has thinner walls, is often compressible with the probe, can be seen to move through the liver, and is located to the patient's right side. While the IVC may have pulsations due to its proximity to the aorta, Doppler US will allow differentiation of arterial pulsations from the phasic movement of IVC blood with respirations.
Ultrasound Evaluation of the IVC for Volume Status
A noninvasive estimation of the patient's intravascular volume can be determined by examining both the relative size and the respiratory dynamics of the IVC. The assessment of the IVC should follow the determination of cardiac contractility, allowing the clinician to evaluate both parameters together to more accurately gauge the volume status. As the patient breathes, the IVC will have a normal pattern of inspiratory collapse. This respiratory variation can be further accentuated by having the patient sniff, or inspire forcefully. M-mode US, positioned in both the short- and long-axis planes of the IVC, can graphically document these dynamic respiratory changes in vessel size. Previous studies have demonstrated a positive correlation between the size and respiratory change of the IVC taken simultaneously with the patient's measured CVP, in an examination termed sonospirometry (Figs. 6.18 and 6.19).75–83 Changes in the size and respiratory variation of the IVC and/or IJ veins can then be followed over time as fluid is given to the patient in shock, to assess for a therapeutic response. Clinical decisions to continue fluid loading, or to start vasopressor agents, can be assisted through knowledge of the “fullness of the tank.”
FIGURE 6.18 IVC evaluation, low CVP.
FIGURE 6.19 IVC evaluation, high CVP.
Newer published guidelines by the ASE support this general use of the evaluation of IVC size and respiratory change in assessment of CVP, but suggest more specific ranges for the pressure measurements (Table 6.7).84
TABLE 6.7 IVC Correlation to CVP, ASE Guidelines
In intubated patients, the respiratory dynamics of the IVC will be reversed. In these patients, the IVC becomes less compliant and more distended in both respiratory phases. However, important physiologic data can still be obtained in these patients, as fluid responsiveness has been correlated with an increase in IVC diameter over time.85 This highlights the importance of serial examinations of the IVC in the shock patient to better assess response to therapy. In the nonintubated patient, the size and percentage respiratory collapse of the IVC can be used to assess for changes in CVP with fluid loading. In the intubated patient, the absolute size of the IVC may be a better indicator of CVP and successful fluid loading will be seen as a progressively larger IVC noted on serial US exams.
Evaluation of the Internal Jugular Vein
The IJ veins may be evaluated as an alternative means of volume assessment. This is helpful in the patient in whom a gas-filled stomach or intestine prohibits imaging of the IVC. The patient should be positioned with the head of the bed elevated to 30 degrees. A high-frequency linear array probe is recommended for this exam. For volume assessment, one should examine both the relative fullness and the height of the vessel column in the neck. Both short- and long-axis views of the vein can be utilized (Figs. 6.20 and 6.21). The US measurement for jugular venous distention has been performed by identifying the absolute vertical height of the column of blood in the IJ vein at end expiration as measured above the sternal angle. To this measurement is added 5 cm, which is the distance from the right atrium to the sternal notch.
FIGURE 6.20 Internal jugular vein, low CVP. CA, carotid artery.
FIGURE 6.21 Internal jugular vein, high CVP.
Jugular venous distention measured >8 cm has been predictive of elevated CVP.86,87 The change in the column height, both with respiratory dynamics and with the Valsalva maneuver, can also be evaluated to help assess right atrial pressure. One study looked at the percentage change in the cross-sectional area of the vein during Valsalva and found a decreased measurement to be present with elevated right atrial pressure, suggesting a more plethoric and less compliant vein.86–88 Another study looked at the maximal IJ vein diameters (IJV max diam) in both expiration and inspiration to measure a collapsibility index.89
This was defined as follows:
A collapsibility index >39% correlated best with hypovolemia, with a sensitivity of 87.5% and specificity of 100%.
2) “Leakiness of the Tank”: FAST and Thoracic Ultrasound
Once a patient's intravascular volume status has been determined, the next step is to assess for “leakiness of the tank.” This refers to hemodynamic compromise due to a loss of fluid from the core vascular circuit. This assessment is initiated with the Extended Focused Assessment with Sonography for Trauma exam.11,12 The traditional FAST exam will identify fluid collections in the abdominal and pelvic cavities (Fig. 6.17, positions B, C, D). The extended FAST exam includes evaluation of the thoracic cavity for fluid and for pneumothorax (PTX).
A thoracic fluid collection, either a pleural effusion or hemothorax depending on the clinical scenario, can be identified by aiming the probe above the diaphragm from the standard right and left upper quadrant views (Fig. 6.22). Traumatic conditions resulting in hemothorax or hemoperitoneum cause hypovolemic shock due to a “hole in the tank.” This in combination with a hyperdynamic heart and flat IVC correlates with hypovolemic shock. In a female patient of childbearing age presenting in shock, this may reflect a ruptured ectopic pregnancy, resulting in physiology effectively similar to a traumatic condition. Conversely, medical conditions causing pleural effusions and ascites often occur due to “tank overload.” This occurs when there is failure of the heart, kidneys, or liver. Finally, lung US can identify pulmonary edema, a sign often indicative of both “tank overload” and “tank leakiness,” with fluid accumulation in the lung parenchyma.90–92 This exam is performed by placing the phased array probe over the thorax to look for US B-lines, or “lung rockets” (Fig. 6.23). Optimally, the clinician should inspect both anterior (Fig. 6.17, position E) and lateral areas of the thorax to increase exam sensitivity, as edema in the supine patient may be increasingly prominent in the more dependent lateral areas.93
FIGURE 6.22 Pleural effusion.
FIGURE 6.23 Ultrasound B-lines, lung rockets.
3) “Compromise of the Tank”: Tension Pneumothorax
The third component of the assessment of the tank is to look for “tank compromise.” A tension PTX may result in hypotension by severely limiting venous return to the heart within the superior and inferior venae cavae. A high-frequency linear array probe is optimal for use in the PTX exam. The probe should first be placed on the anterior chest at about the second intercostal space in the midclavicular line, as air from a PTX will first collect in this location in the supine patient (Fig. 6.24). Normal lung will appear to slide horizontally back and forth as the patient breathes. Vertical small “comet-tail artifacts” will also be noted to extend a short distance posteriorly off the pleura. These findings result from the US appearance of the normally apposed pleural line, made up of the combined inner visceral pleura of the lung and the outer parietal pleural layer of the thoracic cavity (Fig. 6.25).
FIGURE 6.24 Probe position, pneumothorax exam.
FIGURE 6.25 Normal lung on US.
In a PTX, air will collect within the thoracic cavity and will split the normally touching parietal and visceral layers. On US, a single line that represents the solitary parietal pleura will be seen, as the visceral pleura will be obscured by air. This single line will not slide back and forth with respirations, and vertical comet tails will not be seen.94–97
In an incomplete PTX, a portion of the lung may still be inflated and will touch up against the outer parietal pleura. The lead point, or transition point, is the area where the lung in an incomplete PTX makes contact with the outer pleural layer. This may be seen on US as an area where lung sliding is seen on one side of the image, while no sliding is seen on the other. The transition point of lung sliding may be observed to move across the US field as the patient breathes. To find the transition point, the probe is moved progressively more laterally on the chest wall from the midclavicular line toward the midaxillary line.
M-mode US can confirm the B-mode US findings of a PTX. Normal lung sliding gives the appearance of “waves on the beach” or “the seashore sign.” In PTX, the loss of lung sliding will result in the “stratosphere” or “the bar-code” signs.
An emergent needle decompression can then be performed rapidly in patient in shock where a PTX is identified on US, especially in cases where there may be a delay in obtaining a chest radiograph.
RUSH STEP 3: THE PIPES
The third and final step in the RUSH exam is to examine “the pipes,” or the major arterial and venous structures (Fig. 6.26).
FIGURE 6.26 RUSH step 3, evaluation of the “pipes.”
The first part of this exam is to assess the arterial side of the circulatory system. Vascular catastrophes, such as a ruptured abdominal aortic aneurysm (AAA) or an aortic dissection, are life-threatening causes of hypotension that may be accurately diagnosed with bedside US.98
AAA may be diagnosed by detection of an aorta larger than 3 cm in diameter. As most AAAs rupture into the retroperitoneal space, it may not be possible to visualize the actual area of aortic rupture. This is because the retroperitoneal area can be difficult to image with US. However, in the patient presenting in shock where AAA is diagnosed and rupture is clinically suspected, emergency surgical consultation and expedited therapy should be pursued. In the chest, dilation of the aortic root to a size >3.8 cm may be seen with a proximal, or Stanford class A, thoracic aortic dissection. This is measured just distal to the aortic valve.99 An intimal flap may at times be seen here, confirming dissection.100,101
The evaluation of the major venous structures would then be indicated if right ventricular enlargement is identified on echo and a thromboembolic etiology for shock is suspected. In this scenario, imaging of the veins of the lower extremities for a DVT would be indicated. The limited leg compression DVT examination can be performed rapidly by evaluation of a targeted portion of the proximal femoral and popliteal veins, where the majority of thrombi are located.102,103
For this exam, compression of the femoral vein is performed first, beginning superiorly at a level just below the inguinal ligament. The common femoral vein and artery should first be identified. Doppler flow can be used to differentiate arterial from venous structures. The vein should be located medially to the artery and fully compressible with probe pressure. Serial compressions of the vein in a short-axis, or side-to-side, orientation can then be performed every centimeter, moving the probe inferiorly past the confluence of the saphenous vein down to the bifurcation of the vein into the femoral vein of the thigh and the deep femoral vein. The femoral vein of the thigh (formerly the superficial femoral vein) then continues down the leg to become the popliteal vein behind the knee. From a posterior position behind the knee, the vein will generally be seen above or closer to the probe, in relation to the popliteal artery. The popliteal vein should be evaluated with serial compressions from high in the popliteal fossa down inferiorly to the level of trifurcation into the three calf veins. Failure to fully compress the femoral or popliteal vein with direct probe pressure is pathognomonic of thrombosis.
PUTTING RUSH INTO ACTION
The RUSH protocol—pump, tank, and pipes—was created as an easily remembered physiologic roadmap for use in the resuscitation of the critical patient. The RUSH protocol was designed to be performed expediently by specifically choosing those exam components most applicable to the patient's clinical context. While the entire protocol is extensive and incorporates multiple US elements, the clinician should generally begin with evaluation of the heart, IVC, and/or the IJ veins. The RUSH exam should then be tailored based on clinical suspicion, as many patients may be assessed with an abbreviated exam. Incorporation of other components, such as the lung, FAST, aorta, and DVT exams, can be determined as the clinical picture dictates. Table 6.8 demonstrates how using the RUSH exam at the bedside can assist in the diagnosis of the type of shock in the critically ill patient.
TABLE 6.8 Using the RUSH Protocol to Diagnose the Type of Shock
Response to therapy can also be evaluated by repeating the RUSH exam in the hypotensive patient. Specifically as mentioned above, the clinician can monitor the function of the heart and the size and respiratory variation of the IVC and IJ veins over time to assess for the response to fluid loading or for the need to initiate vasopressor agents in the patient in shock.
Focused bedside US has evolved to become a key assessment tool in the evaluation of the critically ill patient in shock. Clinical information that once necessitated invasive measures, such as placement of a central line or a Swan-Ganz catheter, can now be measured by US assessment. The RUSH exam represents one of a series of resuscitation US algorithms for use in the critically ill patient. The physiologic basis for the protocol, simplified to “the pump, tank, and pipes,” allows for an easily remembered and rapidly performed protocol for shock assessment. While the RUSH protocol provides an extensive roadmap for shock evaluation, the exam should be adapted to best match the clinical presentation and not all elements may need to be performed in any given patient. Emergency physicians and critical care physicians caring for the sickest of patients should consider integrating US techniques, including the RUSH protocol, into their care.
Funding Sources: All authors disclose no funding sources.
Conflicts of Interest: Phillips Perera is an educational consultant for SonoSite Ultrasound. Diku Mandavia is the Chief Medical Officer for SonoSite Ultrasound, Bothell, WA. All other authors disclose no conflicts of interest.
CI, confidence interval.
1.Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med. 2001;345(19):1368–1377.
2.Sebat F, Musthafa AA, Johnson D, et al. Effect of a rapid response system for patients in shock on time to treatment and mortality during 5 years. Crit Care Med. 2007;35(11):2568–2575.
3.Atkinson PRT, McAuley DJ, Kendall RJ, et al. Abdominal and cardiac evaluation with sonography in shock (ACES): an approach by emergency physicians for use of ultrasound in patients with undifferentiated hypotension. Emerg Med J. 2009;26:87–91.
4.Gunst M, Gaemmaghami V, Sperry J. Accuracy of cardiac function and volume status estimates using the bedside echocardiographic assessment in trauma/critical care (BEAT). J Trauma. 2008;65:509–516.
5.Pershad J, Myers S, Plouman C, et al. Bedside limited echocardiography by the emergency physician is accurate during evaluation of the critically ill patient (BLEEP). Pediatrics. 2004;114:e667–e671.
6.Boyd JH, Walley KR. The role of echocardiography in hemodynamic monitoring. Curr Opin Crit Care. 2009;15:239–243.
7.Lanctot YF, Valois M, Bealieu Y. EGLS: echo guided life support. An algorithmic approach to undifferentiated shock. Crit Ultrasound J. 2011;3:123–129.
8.Elmer J, Noble VA. An evidence based approach for integrating bedside ultrasound into routine practice in the assessment of undifferentiated shock. ICU Director. 2010;1(3):163–174.
9.Lichtenstein DA, Karakitsos D. Integrating ultrasound in the hemodynamic evaluation of acute circulatory failure (FALLS-the fluid administration limited by lung sonography protocol). J Crit Care. 2012;27:533el–533el9.
10.Jensen MB, Sloth E, Larsen M, et al. Transthoracic echocardiography for cardiopulmonary monitoring in intensive care (FATE). Eur J Anaesthesiol. 2004;21:700–707.
11.Rozycki G, Oschner MG, Schmidt JA, et al. A prospective use of surgeon's performed ultrasound as the primary adjunct modality for injured patient assessment. J Trauma. 1995;39:879–885.
12.Kirkpatrick AW, Sirois M, Laupland KB, et al. Hand-held sonography for detecting post-traumatic pneumothoraces: the extended focused assessment of sonography for trauma (E-FAST). J Trauma. 2004;57:288–295.
13.Breitkreutz R, Price S, Steiger HV, et al. Focused echocardiographic examination in life support and peri-resuscitation of emergency patients (FEEL-Resus): a prospective trial. Resuscitation. 2010;81:1527–1533.
14.Breitkreutz R, Walcher F, Seeger F. Focused echocardiographic evaluation in resuscitation management (FEER): concept of an advanced life support-conformed algorithm. Crit Care Med. 2007;35(5):S150–S161.
15.Ferrada P, Murthi S, Anand RJ, et al. Transthoracic focused rapid echocardiography examination: real-time evaluation of fluid status in critically ill trauma patients (FREE). J Trauma. 2010;70(1):56–64.
16.Liteplo A, Noble V, Atkinson P. My patient has no blood pressure: point of care ultrasound in the hypotensive patient-FAST and RELIABLE. Ultrasound. 2012;20:64–68.
17.Weingart SD, Duque D, Nelson B. Rapid Ultrasound for Shock and Hypotension (RUSH-HIMAPP). EMedHome.com article; April, 2009.
18.Perera P, Mailhot T, Riley D, et al. The RUSH exam: Rapid Ultrasound in SHock in the evaluation of the critically ill. Emerg Med Clin North Am. 2010;28:29–56.
19.Perera P, Mailhot T, Riley D, et al. The RUSH exam: Rapid Ultrasound in SHock in the evaluation of the critically ill (2012 update). Ultrasound Clin. 2012;7(2):255–278.
20.Seif D, Perera P, Mailhot T, et al. Bedside ultrasound in resuscitation and the Rapid Ultrasound in SHock protocol. Crit Care Res Pract. 2012;2012:Article ID 503254.
21.Bahner DP. Trinity, a hypotensive ultrasound protocol. J Diagn Med Sonography. 2002;18:193–198.
22.Rose JS, Bair AE, Mandavia DP. The UHP ultrasound protocol: a novel ultrasound approach to the empiric evaluation of the undifferentiated hypotensive patient. Am J Emerg Med. 2001;19:299–302.
23.American College of Emergency Physicians. Emergency ultrasound guidelines. Ann Emerg Med. 2009;53:550–570.
24.Akhtar S, Theodoro D, Gaspari R, et al. Resident training in emergency ultrasound: consensus recommendations from the 2008 council of emergency medicine residency directors conference. Acad Emerg Med. 2009;16:S32–S36.
25.Society for Academic Emergency Medicine. Ultrasound Position Statement. Available at: http//www.saem.org. Accessed January 20, 2013.
26.Jang TB, Coates WC, Jiu YT. The competency based mandate for emergency bedside sonography and a tale of two residency programs. J Ultrasound Med. 2012;31:515–521.
27.Neri L, Storti E, Lichtenstein D. Toward an ultrasound curriculum for critical care. Crit Care Med. 2007;35(5 suppl):S290–S304.
28.Bealieu Y. Specific skill set and goals of focused echocardiography for critical care physicians. Crit Care Med. 2007;35:S144–S149.
29.Mayo PH, Beaulieu Y, Doelken P, et al. American College of Chest Physicians/La Societe de Reanimation de Langue Francaise statement on competence in critical care ultrasonography. Chest. 2009;135:1050–1060.
30.International expert statement on training standards for critical care ultrasonography. Intensive Care Med. 2011;37(7):1077–1083.
31.Labovitz AJ, Noble VE, Bierig M, et al. Focused cardiac ultrasound in the emergent setting: a consensus statement of the American Society of Echocardiography and the American College of Emergency Physicians. J Am Soc Echocardiogr. 2010;23:1225–1230.
32.Weekes AJ, Quirke DP. Emergency echocardiography. Emerg Med Clin North Am. 2011;29:759–787.
33.Chen RS, Bivens MJ, Grossman SA. Diagnosis and management of valvular heart disease in emergency medicine. Emerg Med Clin Nort Am. 2011;29:801–810.
34.Jones AE, Craddock PA, Tayal VS, et al. Diagnostic accuracy of identification of left ventricular function among emergency department patients with nontraumatic symptomatic undifferentiated hypotension. Shock. 2005;24:513–517.
35.Moore CL, Rose GA, Tayal VS, et al. Determination of left ventricular function by emergency physician echocardiography of hypotensive patients. Acad Emerg Med. 2002;9:186–193.
36.Joseph M, Disney P. Transthoracic echocardiography to identify or exclude cardiac cause of shock. Chest. 2004;126:1592–1597.
37.Lang RM, Bierig M, Devereux RB, et al. Recommendations for chamber quantification. Eur J Echocardiogr. 2006;7(2):79–108.
38.Weekes AJ, Tassone HM, Babcock A, et al. Comparison of serial qualitative and quantitative assessments of caval index and left ventricular systolic function during early fluid resuscitation of hypotensive emergency department patients. Acad Emerg Med. 2011;18:912–921.
39.Secko MA, Lazar JM, Salciccioli, L, et al. Can junior emergency physicians use E-point septal separation to accurately estimate left ventricular function in acutely dyspneic patients? Acad Emerg Med. 2011;18:1223–1226.
40.Ahmadpour H, Shah AA, Allen JW. Mitral E point septal separation: a reliable index of left ventricular performance in coronary artery disease. Am Heart J. 1983;106(1):21–28.
41.Silverstein JR, Laffely NH, Rifkin RD. Quantitative estimation of left ventricular ejection fraction from mitral valve E-point to septal separation and comparison to magnetic resonance imaging. Am J Cardiol. 2006;97(1):137–140.
42.Weekes AJ, Reddy A, Lewis MR, et al. E-point septal separation compared to fractional shortening measurements of systolic function in emergency department patients. J Ultrasound Med. 2012;31:1891–1897.
43.Blaivas M. Incidence of pericardial effusion in patients presenting to the emergency department with unexplained dyspnea. Acad Emerg Med. 2001;8(12):1143–1146.
44.Tayal VS, Kline JA. Emergency echocardiography to determine pericardial effusions in patients with PEA and near PEA states. Resuscitation. 2003;59:315–318.
45.Mandavia DP, Hoffner RJ, Mahaney K, et al. Bedside echocardiography by emergency physicians. Ann Emerg Med. 2001;38:377–382.
46.Grecu L. Cardiac tamponade. Int Anesthesiol Clin. 2012;50(2):59–77.
47.Shabetai R. Pericardial effusions: haemodynamic spectrum. Heart. 2004;90:255–256.
48.Ma OJ, Mateer JR, Blaivas M. Emergency Ultrasound. New York: McGraw Hill Publishers; 2008.
49.Russo AM, O'Connor WH, Waxman HL. Atypical presentations and echocardiographic findings in patients with cardiac tamponade occurring early and late after cardiac surgery. Chest. 1993;104:71–78.
50.Trojanos CA, Porembka DT. Assessment of left ventricular function and hemodynamics with transesophageal echocardiography. Crit Care Clin. 1996;12:253–272.
51.Goodman A, Perera P, Mailhot T, et al. The role of bedside ultrasound in the diagnosis of pericardial effusions and cardiac tamponade. J Emerg Trauma Shock. 2012;5:72–75.
52.Nabazivadeh SA, Meskshar A. Ultrasonic diagnosis of cardiac tamponade in trauma patients using the collapsibility index of the inferior vena cava. Acad Radiol. 2007;14:505–506.
53.Armstrong WF, Ryan T. Feigenbaum's Echocardiography. 7th ed. Philadelphia, PA: Lippincott, Williams and Wilkins; 2010.
54.Tsang T, Enriquez-Sarano M, Freeman WK. Consecutive 1127 therapeutic echocardiographically guided pericardiocenteses: clinical profile, practice patterns and outcomes spanning 21 years. Mayo Clin Proc. 2002;77:429–436.
55.Salazar M, Mohar D, Bhardwaj R, et al. Use of contrast echocardiography to detect displacement of the needle during pericardiocentesis. Echocardiography. 2012;29:E60–E61.
56.Ainsworth CD, Salehian O. Echo-guided pericardiocentesis: let the bubbles show the way. Circulation. 2011;123:e210–e211.
57.Gifroni S, Olivotto I, Cecchini P, et al. Short term clinical outcome of patients with acute pulmonary embolism, normal blood pressure and echocardiographic right ventricular dysfunction. Circulation. 2000;101:2817–2822.
58.Becattini C, Agnelli G. Acute pulmonary embolism: risk stratification in the emergency department. Intern Emerg Med. 2007;2:119–129.
59.Nazeyrollas D, Metz D, Jolly D, et al. Use of transthoracic Doppler echocardiography combined with clinical and electrographic data to predict acute pulmonary embolism. Eur Heart J. 1996;17:779–786.
60.Jardin F, Duborg O, Bourdarias JP. Echocardiographic pattern of acute cor pulmonale. Chest. 1997;111:209–217.
61.Jardin F, Dubourg O, Gueret P, et al. Quantitative two dimensional echocardiography in massive pulmonary embolism: emphasis on ventricular interdependence and leftward septal displacement. J Am Coll Cardiol. 1987;10:1201–1206.
62.Rudoni R, Jackson R. Use of two-dimensional echocardiography for the diagnosis of pulmonary embolus. J Emerg Med. 1998;16:5–8.
63.Jackson RE, Rudoni RR, Hauser AM, et al. Prospective evaluation of two-dimensional transthoracic echocardiography in emergency department patients with suspected pulmonary embolism. Acad Emerg Med. 2000;7:994–998.
64.Miniati M, Monti S, Pratali L, et al. Value of transthoracic echocardiography in the diagnosis of pulmonary embolism: results of a prospective study in unselected patients. Am J Med. 2001;110(7):528–535.
65.Stein J. Opinions regarding the diagnosis and management of venous thromboembolic disease. ACCP Consensus Committee on pulmonary embolism. Chest. 1996;109:233–237.
66.Konstantinides S, Geibel A, Heusel G, et al. Heparin plus alteplase compared with heparin alone in patients with submassive pulmonary embolus. N Engl J Med. 2002;347:1143–1150.
67.Kucher N, Goldhaber SZ. Management of massive pulmonary embolism. Circulation. 2005;112:e28–e32.
68.Jaff MR, McMurtry S, Archer S, et al. Management of massive and submassive pulmonary embolism, iliofemoral deep venous thrombosis and chronic thromboembolic pulmonary embolism: a scientific statement from the American Heart Association. Circulation.2011;123:1788–1830.
69.Vieillard-Baron A, Page B, Augarde R, et al. Acute cor pulmonale in massive pulmonary embolism: incidence, echocardiographic pattern, clinical implications and recovery rate. Intensive Care Med. 2001;27(9):1481–1486.
70.Mookadam F, Jiamsripong P, Goel R, et al. Critical appraisal on the utility of echocardiography in the management of acute pulmonary embolism. Cardiol Rev. 2010;18(1):29–37.
71.Cosby KS, Kendall JL. Practical Guide to Emergency Ultrasound. Philadelphia, PA: Lippincott Williams and Wilkins; 2006.
72.Riley D, Hultgren A, Merino D, et al. Emergency department bedside echocardiographic diagnosis of massive pulmonary embolism with direct visualization of thrombus in the pulmonary artery. Crit Ultrasound J. 2011;3(3):155–160.
73.Madan A, Schwartz C. Echocardiographic visualization of acute pulmonary embolus and thrombolysis in the ED. Am J Emerg Med. 2004;22:294–300.
74.Wallace DJ, Allison M, Stone MB. Inferior vena cava percentage collapse during respiration is affected by the sampling location: an ultrasound study in healthy volunteers. Acad Emerg Med. 2010;17(1):96–99.
75.Kircher BJ, Himelman RB, Schiller NB. Noninvasive estimation of right atrial pressure from the inspiratory collapse of the inferior vena cava. Am J Cardiol. 1990;66(4):493–496.
76.Simonson JS, Schiller NB. Sonospirometry: a new method for noninvasive estimation of mean right atrial pressure based on two-dimensional echographic measurements of the inferior vena cava during measured inspiration. J Am Coll Cardiol. 1988;11(3):557–564.
77.Randazzo MR, Snoey ER, Levitt, MA, et al. Accuracy of emergency physician assessment of left ventricular ejection fraction and central venous pressure using echocardiography. Acad Emerg Med. 2003;10(9):973–977.
78.Jardin F, Vieillard-Baron A. Ultrasonographic examination of the venae cavae. Intensive Care Med. 2006;32(2):203–206.
79.Marik PA. Techniques for assessment of intravascular volume in critically ill patients. J Intensive Care Med. 2009;24(5):329–337.
80.Blehar DJ, Dickman E, Gaspari R. Identification of congestive heart failure via respiratory variation of inferior vena cava diameter. Am J Emerg Med. 2009;27(1):71–75.
81.Nagdev AD, Merchant RC, Tirado-Gonzalez A, et al. Emergency department bedside ultrasonographic measurement of the caval index for noninvasive determination of low central venous pressure. Ann Emerg Med. 2010;55(3):290–295.
82.Schefold JC, Storm C, Bercker S, et al. Inferior vena cava diameter correlates with invasive hemodynamic measures in mechanically ventilated intensive care unit patients with sepsis. J Emerg Med. 2010;38(5):652–637.
83.Seif D, Mailhot T, Perera P, et al. Caval sonography in shock: a noninvasive method for evaluating intravascular volume in critically ill patients. J Ultrasound Med. 2012;31:1885–1890.
84.Rudski LG, Lai WW, Afilalo J, et al. Guidelines for the echocardiographic assessment of the right heart in adults: a report from the American society of echocardiography. J Am Soc Echocardiogr. 2010;23(7):685–713.
85.Barbier C, Loubieres Y, Schmit C, et al. Respiratory changes in the inferior vena cava diameter are helpful in predicting fluid responsiveness in ventilated septic patients. Intensive Care Med. 2004;30(9):1740–1746.
86.Simon MA, Kliner DE, Girod JP, et al. Jugular venous distention on ultrasound: sensitivity and specificity for heart failure in patients with dyspnea. Am Heart J. 2010;159:421–427.
87.Jang T, Aubin C, Naunheim R, et al. Ultrasonography of the internal jugular vein in patients with dyspnea without jugular venous distention on physical examination. Ann Emerg Med. 2004;44(2):160–168.
88.Jang T, Aubin C, Naunheim R, et al. Jugular venous distention on ultrasound: sensitivity and specificity for heart failure in patients with dyspnea. Ann Emerg Med. 2011;29:1198–1202.
89.Killu K, Coba V, Huang Y, et al. Internal jugular vein collapsibility index associated with hypovolemia in intensive care unit patients. Crit Ultrasound J. 2010;1:13–17.
90.Volpicelli G, Caramello V, Cardinale L, et al. Bedside ultrasound of the lung for the monitoring of acute decompensated heart failure. Am J Emerg Med. 2008;26:585–591.
91.Soldati G, Copetti R, Sher S. Sonographic interstitial syndrome: the sound of lung water. J Ultrasound Med. 2009;28:163–174.
92.Liteplo AS, Marrill KA, Villen T, et al. Emergency thoracic ultrasound in the differentiation of the etiology of shortness of breath (ETUDES): sonographic B-lines and N-terminal pro-brain-type natriuretic peptide in diagnosing heart failure. Acad Emerg Med.2009;16:201–210.
93.Volpicelli G, Noble VE, Liteplo A, et al. Decreased sensitivity of lung ultrasound limited to the anterior chest in emergency department diagnosis of cardiogenic pulmonary edema: a retrospective analysis. Crit Ultrasound J. 2010;2:47–52.
94.Lichtenstein DA, Menu Y. A bedside ultrasound sign ruling out pneumothorax in the critically ill. Lung sliding. Chest. 1995;108:1345–1348.
95.Lichtenstein D, Meziere G, Biderman P, et al. The comet-tail artifact: an ultrasound sign ruling out pneumothorax. Intensive Care Med. 1999;25:383–388.
96.Lichtenstein DA, Meziere GA. Relevance of lung ultrasound in the diagnosis of acute respiratory failure: the BLUE protocol. Chest. 2008;134:117–125.
97.Manson W, Hafez NM. The rapid assessment of dyspnea with ultrasound: RADIUS. Ultrasound Clin. 2011;6:261–276.
98.Rubano E, Mehta N, Caputo W, et al. Systematic review: emergency department bedside ultrasonography for diagnosing suspected abdominal aortic aneurysm. Acad Emerg Med. 2013;20:128–138.
99.Taylor RA, Oliva I, Van Tonder R, et al. Point of care focused cardiac ultrasound for the assessment of thoracic aortic dimensions, dilation and aneurysmal disease. Acad Emerg Med. 2012;19:244–247.
100.Fojtik, JP, Costantino TG, Dean AJ. The diagnosis of aortic dissection by emergency medicine ultrasound. J Emerg Med. 2007;32:191–196.
101.Budhram G, Reardon R. Diagnosis of ascending aortic dissection using emergency department bedside echocardiogram. Acad Emerg Med. 2008;15(6):584.
102.Bernardi E, Camporese G, Buller H, et al. Serial 2 point ultrasonography plus d-dimer vs. whole leg color ceded Doppler ultrasonography for diagnosing suspected symptomatic deep vein thrombosis. JAMA. 2008;300:1653–1659.
103.Farahmand S, Farnia M, Shahriaran S, et al. The accuracy of limited B-mode compression technique in diagnosing deep venous thrombosis in lower extremities. Am J Emerg Med. 2011;29(6):687–690.