Bedside Ultrasound for Assessing Patients in Shock · Key Words: shock, bedside ultrasound,...

Bedside Ultrasound for Assessing Patients in Shock

Cameron M. Bass, MD* and Amy E. Morris, MDw

Abstract: Patients in shock require rapid assessment and intervention,often before laboratory studies have returned or complete radiographicstudies can be obtained. In such situations, clinician-performed diag-nostic ultrasound provides a useful adjunct to the traditional clinicaltools of history and physical examination. This review describesmultiple easily acquired ultrasound examinations to be performed atthe bedside by the primary clinician to provide new windows into theunderlying etiology of a shock state.

Key Words: shock, bedside ultrasound, hypotension, lung ultrasound

(Clin Pulm Med 2016;23:120–135)

Since the 1743 translation of Henri Le Dran’s French thesison gunshot wounds, the word “shock” has been used to

describe the condition caused by hypotension with signs ofend-organ damage.1 The high mortality associated with shockhas led to significant efforts to understand the most effectiveway to evaluate the patient with hypoperfusion. In 1972, Weiland Shubin2 described shock as a pathophysiological response,and proposed a classification system that is still used today.Their system is focused on the physiology that deprives thetissues of oxygenation, therefore helping one to guide treat-ment. This divides the shock state into several familiar cate-gories: cardiogenic, distributive, obstructive, and hypovolemic.Although not all cases of shock fit neatly into 1 of these cat-egories, in most situations, it is useful to narrow the differentialdiagnosis.3

Many physical examination maneuvers have beendeveloped as indicators of systemic hypotension.4 Theseinclude the assessment of an altered mental status, orthostaticblood pressure, capillary refill time in the fingernails, sub-ungual perfusion measurements, and markers of end-organperfusion such as cold limbs, crackles on lung auscultation,and a narrow pulse pressure.5 Dr Weil described these physicalexamination findings as providing “windows” into the bodythrough which one could glimpse the overall perfusion.3

Unfortunately, these windows are cloudy. In fact, with a fewexceptions, these findings lack both sensitivity and specificityfor the causes of hypotension (Table 1).4,6

One of the strengths of using physical examinationmaneuvers is the examiner’s immediate awareness of theclinical situation. Whereas traditional radiographic techniquesmay provide clearer windows into the body, they are oftenremoved from the bedside. Formal ultrasounds and otherradiographic examinations are interpreted by a radiologist who

usually has not seen the patient, and knows little about thespecifics of a given case. Formal studies also often require thatinpatients be transported to the radiology department, whichcan delay needed care and carries inherent risk.7 Providersoften have to balance this risk with the potential benefit ofobtaining a definitive answer to a clinical question. In contrast,ultrasound examinations performed rapidly at the bedsideallow the clinician caring directly for the patient to answermany focused clinical questions more precisely than usingphysical examination alone, but without the risk of transport.Naturally, these examinations must be used with the knowl-edge of the limitations of their scope and accuracy; sometimesa complete examination with expert interpretation is needed totruly answer a clinical question. Throughout this review, wepoint out not just the utility, but also the limitations of point-of-care examinations in answering specific clinical questionspertaining to shock.

One easily recognized potential limitation in the use ofpoint-of-care ultrasound is the ability of the sonographer toobtain and interpret relevant images. Although specific rec-ommendations of professional societies vary, it is widely rec-ognized that clinicians must not only achieve cognitive andtechnical competence, they must maintain their skills withongoing practice.8–13 Bedside clinician-performed diagnosticstudies are also only as valuable as the history and physicalexamination findings that guide them. Ultrasound cannot takethe place of a good history and physical nor essential lab anddiagnostic studies. A careful, complete physical examination isan essential early step in evaluating any patient presenting withshock, as is an assessment of the acid-base status and anelectrocardiogram.

Once the initial history and physical has been performed,focused bedside ultrasound can be performed rapidly, targetedat specific clinical questions. Like the traditional physicalexamination, ultrasound examination is comprised of a numberof individual maneuvers, each of which has a specific diag-nostic performance. Also, like the physical examination, someare quite simple, whereas others require more training to beconsidered reliable. For example, whereas tachycardia is easyto detect, auscultating a summation gallop requires morepractice. Similarly, the ability to recognize B lines on lungultrasound has been shown to be an easily acquired and reli-able skill, whereas correct identification and characterizationof regional wall motion abnormalities is more difficult tomaster.14,15

Several groups have combined common ultrasoundtechniques to create protocols for the evaluation of patientspresenting with specific complaints, such as dyspnea orhypotension (Table 2).16–24 These protocols are attractivebecause they allow the performance characteristics of severalmaneuvers to be grouped, and provide a framework forteaching and evaluating results. A clinician trained in theCLUE protocol, for example, can easily communicate theresults of the examination to another so trained.25 Whereasthese are primarily diagnostic systems of inquiry, at least 1published protocol provides an example of utilizing serial

From the *Department of Internal Medicine; and wDivision of Pulmonaryand Critical Care Medicine, University of Washington, Seattle, WA.

Disclosure: The authors declare that they have no conflicts of interest.Address correspondence to: Cameron M. Bass, MD, Department of Internal

Medicine, University of Washington, 1959 NE Pacific Ave., Seattle,WA 98195. E-mail: [email protected].

Copyright r 2016 Wolters Kluwer Health, Inc. All rights reserved.ISSN: 1068-0640/16/2303-0120DOI: 10.1097/CPM.0000000000000151

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ultrasound examinations to guide therapy.26 It is important tonote, however, that no published protocol applicable to patientsin undifferentiated shock has been demonstrated to affectsignificant clinical outcomes. In addition, as with any proto-colized approach, the disadvantage of any 1 system is that it isdesigned to answer a particular set of questions, and no pro-tocol is perfectly matched to every clinical situation. Under-standing the performance of each component of a given pro-tocol for a specific question allows the clinician to tailor theultrasound examination in the same way that one would tailorthe physical examination.

For each category of shock, we can identify unifyingphysiological aspects that are reflected in ultrasound exami-nation findings. The underlying pathophysiology in hypo-volemic shock is one of underfilling during diastole. As aresult, findings will be apparent when we examine vascularregions that normally should be full, or perform maneuversthat should cause intravascular volume to move from one areato another. With cardiogenic shock, the underlying pathologyis one of impaired cardiac function. We can evaluate for vis-ually impaired myocardial function as well as signs of reducedforward blood flow with evidence of volume overload in areasthat drain into the heart. Obstructive shock is not a widely usedclinical term, but refers to states of impaired blood flow despiteadequate volume and intrinsic cardiac function. The mostcommon causes are tension pneumothorax, cardiac tamponade,or pulmonary artery thromboembolism, which have in com-mon an ultrasound finding of high filling pressures, in additionto diagnosis-specific abnormalities. Finally, distributive shockhas a number of causes: septic, anaphylactic, Addisonian, orneurogenic. This category is often a diagnosis of exclusionwhen it comes to ultrasound examination, although we willdiscuss some findings that suggest this etiology. In realpatients, these categories frequently overlap, and the point-of-care ultrasound user must be wary of the possibility that thismodality can actually hinder diagnosis if there is prematureclosure based on a single abnormal finding in a limitedexamination.

HYPOVOLEMIC SHOCKMany physical examination findings and maneuvers are

used to identify hypovolemia. However, few reach a high levelof clinical utility based on likelihood ratios.4,6 The absence ofaxillary sweat has been shown to correlate reliably with ahypovolemic state, as such patients have dry mucous mem-branes or an abnormal skin turgor. None of these are directassessments of intravascular depletion, but instead use super-ficial capillary beds as an imperfect window into the patient’soverall volume status.

One of the simplest assessments of larger vessel filling isthe measurement of the height of the internal jugular vein

TABLE 1. Likelihood Ratios (LRs) for Selected PhysicalExamination Maneuvers for Shock (McGee, Elsevier; 2012)4

Examination Maneuver + LR �LR

Dry axilla to predict hypovolemia 2.8 NSOrthostatic tachycardia to predict hypovolemia 1.7 0.8Dry mucus membranes to predict hypovolemia NS 0.3Elevated neck veins to detect low ejection fraction 7.9 NSCrackles on lung auscultation to detect

congestive heart failureNS NS

NS indicates not significant.

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Clinical Pulmonary Medicine � Volume 23, Number 3, May 2016 Bedside US for Assessing Patients in Shock

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distention to estimate the central venous pressure (CVP). Thisis a time-honored component of the cardiac physical exami-nation, but can be challenging due to facial hair or bodyhabitus. Ultrasound provides a more direct window to theintravascular space, as identification of the height of theinternal jugular fluid column by ultrasound correlates reliablywith CVP.27,28 The image is acquired either transversely orlongitudinally (Fig. 1). In the longitudinal view, the“paintbrush sign” shows the point of respiratory vein collapse,correlating with the jugular venous pressure (Fig. 2). Alter-natively, the vein can be visualized transversely, but thetransducer must be held very lightly against the skin so as tonot collapse the vein with external pressure.

It is important to recognize that this technique, performedwith or without ultrasound, estimates CVP as a static correlateof the right atrial pressure. However, using this information topredict volume responsiveness requires extrapolating the left-heart output from right-heart filling pressures. The accuracy ofsuch a prediction has been called into question in the criticalcare literature, and has fallen out of favor among many clini-cians.29–36 Ultrasound of the inferior vena cava (IVC) allows amore dynamic assessment of vascular filling pressures as theychange with the respiratory cycle, which has a higher pre-dictive value in very specific situations.

The IVC is often visualized easily, and in certain clinicalsituations can predict volume responsiveness reliably inhypotensive patients.37,38 The basic physiological principlebehind IVC assessment is that the respiratory cycle changes thepressure differential between the thoracic and the abdominalcompartments. During spontaneous inspiration, the intra-thoracic pressure becomes negative, essentially drawingvenous blood flow into the heart and decreasing the IVC dia-meter. The opposite is true in positive-pressure mechanicalventilation (Fig. 3). As the abdominal IVC is visualizeddirectly, each breath functions as a small autotransfusion

between the abdominal IVC and the right heart. In hypo-volemia, shifting the same amount of blood into or out of theIVC will cause a greater relative change in the diameter of thevessel (Table 3).

FIGURE 1. A transverse view of the right-sided cervical vascular of a mildly hypovolemic patient showing the carotid (C) and collapse ofthe internal jugular vein (IJ) during inspiration.

FIGURE 2. The internal jugular vein (IJ) in the longitudinal viewwith the left side of the screen cephalad on the patient. Thisallows the “paintbrush” to be visualized at the point representingthe jugular venous pressure.

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Given the average American adult habitus, to visualizethe IVC with ultrasound, one should use a transducer that canpenetrate 10 to 15 cm with good resolution. In most cases, aphased array, a curvilinear or microconvex transducer, isappropriate. One approach is to apply the transducer to thesubxyphoid region with the orientation marker toward thepatient’s head and the transducer perpendicular to the skin(Fig. 4). This process may require some pressure to movebowel gas out of the way. The transducer is then fanned ortranslocated (slid) laterally until the IVC is found in thelongitudinal view (Fig. 5). By tilting the transducer such that itis directed slightly cephalad, the IVC can be followed throughthe liver to where it empties into the right atrium (RA). Notethat some providers prefer to obtain a subcostal 4-chamberview of the heart, then adjust the transducer to find this view.Alternatively, a useful approach if bowel gas is too obstructiveis to place the transducer in the mid-axillary line roughly at thelevel of the xiphoid process, and fan through the liver until theIVC comes into view. Regardless of how the view is obtained,the IVC is observed through the respiratory cycle, and itsdiameter measured during inspiration and exhalation at a pointapproximately 2 to 3 cm from where it joins the RA.37 Thesemeasurements are performed most precisely using the M-modefunction if available (Fig. 6).

Interpreting IVC respiratory variation requires cautionand a great deal of knowledge about the clinical situation dueto multiple potential confounders (Table 4). For example,excessive respiratory effort can lead to markedly negative and/or positive intrathoracic pressure, leading to changes in the

IVC diameter that reflect these pressure swings more than theyreflect the intravascular volume.39 A meta-analysis of availabledata suggests that IVC diameter assessment was a reliablepredictor of volume responsiveness only in the specific pop-ulation of mechanically ventilated patients who are not makingspontaneous respiratory effort, not on lung protective ven-tilation with small tidal volumes, and whose IVC diametervaries by at least 12% (published studies range from 12% to33%).37,38,40 In spontaneously breathing patients, the data areeven less directive. A small (< 2.1 cm), very collapsible(>50%) IVC suggests low CVP or right atrial pressure.41

However, as discussed above, this has not been shown tocorrelate reliably with volume responsiveness.42 A large-dia-meter IVC with absent respiratory variation suggests highfilling pressures and a hemodynamic state unlikely to respondto fluid administration, assuming that no confounders arepresent (Table 4). Values in between these extremes providelittle guidance, and the clinician must rely on other assessmentmethods.

Other dynamic techniques have been proposed to assessvolume responsiveness, such as the end-expiratory occlusiontest or, more broadly applicable, a passive leg raise. Lifting anadult patient’s legs above the level of the heart provides anautotransfusion of approximately 300 mL of blood to theabdominal and the thoracic cavities, the results of which can beevaluated most reliably using a direct measurement of thecardiac output.43,44 This requires a transducer equipped withcontinuous-wave Doppler functionality to measure the outflowvelocity at the aortic valve to estimate the stroke volume.45

FIGURE 3. Mechanistic inferior vena cava (IVC) changes withrespiration.

TABLE 3. Anticipated Inferior Vena Cava (IVC) DiameterChanges With Respiration

Maneuver

Intrathoracic

Pressure

IVC

Diameter

Spontaneous inspiration k kForced exhalation m mMechanically ventilated

inspirationm m

Valsalva m m

FIGURE 4. The correct probe position for acquiring images of theinferior vena cava.

FIGURE 5. An ultrasound image of the inferior vena cava (IVC) inthe longitudinal view including the liver, the IVC, and the rightatrium (RA).




This requires a greater level of technical expertise and is verydependent on transducer positioning, and so should be usedonly by experienced practitioners with advanced training. Aswith IVC diameter measurement, several caveats apply toappropriate use, and neither method has been correlateddefinitively with changes in clinical outcomes.

Direct evaluation of the heart can be very useful in theevaluation of shock. Published recommendations from severalprofessional societies outline the information that can reason-ably be acquired from focused bedside echocardiographyperformed by providers other than cardiologists and echo-cardiographers.8,9,46 None of these findings are diagnostic ofhypovolemic shock, but some are suggestive of hypovolemia.In the absence of coexisting cardiac contractility impairment, ahypovolemic state will often result in a small, hyperdynamicleft ventricle (LV), which becomes almost completely effacedat end systole. This can be evaluated qualitatively in the par-asternal long axis (PLAX), the parasternal short access, or theapical 4-chamber (A4C) views. Visually, this is assessed by thechange in the area of the ventricle during systole (Fig. 7). Inaddition, in the PLAX view of a significantly hypovolemicpatient, the left atrium (LA) in diastole tends to be smaller thanthe aortic outflow tract (Fig. 8).47 As always, one must keep inmind potential confounders in interpreting these findings, suchas preexisting left atrial enlargement from mitral valve (MV)disease or an alternative reason for low left-sided filling suchas obstructive shock from a large pulmonary embolism (PE).

A lung ultrasound can be a useful indicator of the volumestatus. To acquire thoracic images, the International ConsensusConference on Lung Ultrasound recommends dividing each

lung into 4 geographic regions and acquiring images in eachzone (Fig. 9).48 This can be performed with a microconvex,phased array, or linear transducer, with the linear transducercreating the sharpest images in most patients. The examinerholds the transducer with the indicator oriented toward thepatient’s head to acquire a single frame showing a clear pleuralline between 2 rib shadows (Fig. 10). To interpret the resultingimages, providers must learn to differentiate between “A-line”and “B-line” artifact patterns (Fig. 11). Both are reverberationartifacts, but with very different implications. Because ultra-sound waves essentially do not penetrate through air, beamsemanating from the ultrasound transducer will pass through thesubcutaneous tissue of the thoracic wall to the pleura, and thenreflect back to the transducer. The machine interprets thisstrong reflected signal as a bright white line on the ultrasoundscreen. Some ultrasound waves will then reverberate from thetransducer to the pleura and back. Because the machine sentout only 1 signal, these reverberating waves are interpreted as asecond echogenic density that took twice as long to return andmust therefore be twice as deep, appearing as the first hori-zontal A line on the ultrasound screen. This cycle repeats itself,with each A line occurring on the screen at regular intervalsidentical to the distance from the skin to the pleura.

B-line patterns occur when ultrasound beams encounterfluid-filled alveoli or an abnormal, thickened interstitium. Inthis situation, some ultrasound signals can penetrate past thepleura, and will reverberate over much smaller distances in thisabnormal lung, resulting in an infinite series of very smallhorizontal lines that appear collectively as the laser-like ver-tical B line. The term “B-line predominant” is used when threeor more B lines appear in a single frame.48 It is important tonote that the B-line artifact is a nonspecific pattern often calledthe “alveolar interstitial syndrome.” It may represent pulmo-nary edema, but may also be found in any process with poorlyaerated alveoli or interstitial thickening including fibrotic lungdisease and the acute respiratory distress syndrome (ARDS).These phenomena are described in detail in otherliterature.49,50

Several studies have demonstrated the ability to use A-line and B-line patterns to differentiate a normally aerated lung(A-line predominant) from pulmonary edema in a volume-overloaded state (diffuse B line predominance in the majorityof the fields).48,49,51,52 This is consistent with evidence that B-line patterns correlate with pathologic measurements ofextravascular lung water as well as with clinical changes in thevolume status.15,20,26,48,53–55 In contrast, normal lung ultra-sound findings suggest a well-aerated parenchyma, whichwould support a clinical impression of hypovolemic shock.However, because a B-line-predominant pattern is not inher-ently specific for pulmonary edema, interpreting lung ultra-sound images in the setting of shock requires an understandingof the pretest probability in the population being evaluated.

FIGURE 6. Visualization of the inferior vena cava in M-Mode,showing the changing diameter with time in a spontaneouslybreathing patient. The collapsibility ratio can be calculated asthe distance (A-B)/A.

TABLE 4. Conditions Causing Plethoric or Unchanging Inferior Vena Cava (IVC)

Congestive heart failure Left-heart volume overload leading to right heart volume overloadPulmonary embolism Right-heart pressure overloadPulmonary hypertension Right-heart pressure overloadCardiac tamponade Impaired right-atrial fillingRestrictive cardiomyopathy Impaired right-atrial fillingConstrictive pericarditis Impaired right-atrial fillingLow volume respiration Small pressure changes during respiratory cycleTricuspid regurgitation Volume overload of right atrium from the right ventricleTricuspid stenosis Impaired right-atrial emptyingIVC thrombus Impaired IVC drainage into heart




In the emergency department or in a patient with known heartfailure, diffuse B lines are very likely to represent a volumeoverload. However, in the intensive care unit, diffuse lungdisease such as ARDS could complicate the diagnostic inter-pretation. In short, whereas an A-line pattern supports adiagnosis of hypovolemic shock (or more accurately arguesagainst volume overload), a B-line-predominant pattern doesnot rule it out. As is always the case with point-of-care ultra-sound, providers must incorporate isolated examination find-ings into a comprehensive evaluation before reaching a clinicalconclusion.

If cardiovascular and lung ultrasound findings are sug-gestive of hypovolemic shock, further investigation at thebedside may help determine the cause. For example, whereashemorrhage from the gastrointestinal tract or penetratingtrauma is often clinically apparent, intra-abdominal or intra-thoracic bleeding may not be noticed on a physical examina-tion. Techniques such as diagnostic peritoneal lavage orcomputerized tomography (CT) are invasive or require thepatient to be transported from the care area. The extendedFocused Assessment with Sonography for Trauma (eFast) is awell-validated tool to identify internal bleeding in blunt trauma

FIGURE 7. Parasternal short access change in size and appearance during systole in a normal and abnormal heart, with the left ventriclecavity outlined for easier visibility.

FIGURE 8. The placement of the probe to acquire the parasternal long-axis view and the visualized anatomy, showing several struc-tures, including the right ventricle (RV), the left ventricle (LV), the left atrium (LA), the papillary muscle (P), the mitral valve (MV), theaorta (Ao), and the aortic valve (AV).




patients and one of the few published ultrasound protocolsdemonstrated to affect clinical outcomes.19,56 This examina-tion visualizes the areas of the abdomen where blood is mostlikely to accumulate, as well as the heart and the pleural spaceto identify pericardial effusion and hemothorax, respectively.

A transducer with sufficient penetration to visualizeabdominal organs is used, either curvilinear or phased array.With the indicator marker oriented toward the patient’s head,the examiner applies the transducer to the right and the leftcosto-diaphragmatic area to visualize the hepatorenal and thesplenorenal recesses. The bladder and its posterior potentialspace are then visualized through the suprapubic window byfanning inferiorly below the pubic symphysis (Fig. 12). Asubcostal view of the heart is used to evaluate for pericardialeffusion (see discussion of tamponade in obstructive shockbelow), and a view of the diaphragmatic recesses allows theidentification of hemothorax or other pleural effusion (Fig. 13).In the specific setting of the hypotensive trauma patient, theeFAST examination has excellent diagnostic performance

when compared with the CT scan for the discovery of blood onexploratory laparotomy, with sensitivity in 1 meta-analysisapproaching 100%.19 Although there are few large, high-quality trials to confirm the efficacy, this scan is becoming thestandard of care in most modern emergency rooms.57 Providersmust keep in mind that because it can be performed with suchease and speed, an initial negative scan in high-risk patientsmay need to be repeated to ensure that it was not performedbefore enough time elapsed for visible blood to accumulate.

CARDIOGENIC SHOCKPhysical findings of cardiogenic shock are primarily those

of impaired distal perfusion, in combination with abnormalheart and lung auscultation. Soft pulses and cold extremitiesargue for an impairment of pump function, and crackles in thelungs suggest increased fluid pressure from the LV. However,clinical confounders limit the specificity of these findings. Forexample, a patient with interstitial lung disease and hypo-volemic shock from an undiagnosed gastrointestinal bleedcould have similar findings. More specific findings such as adisplaced point of maximal impulse, which has excellent testperformance in the detection of chronically decreased LVfunction, are less reliable in the critically ill patient withshock.4

Focused cardiac ultrasound at the point of care providesa direct window into the cardiac function of the hypotensivepatient, more specific than physical examination findings andoften allowing an immediate diagnosis. Although the PLAXhas been used as a solo view for this purpose in several studies,the qualitative function of the LV can be evaluated from any ofthe 4 standard cardiac echo windows.8,9,16,25,46 Most patientswill not have clear acoustic windows for all 4 views, but it isdifficult to predict as to which will be the most useful inadvance.21 For this reason, it is best to attempt all 4 andinterpret the images with the clearest view of the LV function.

To acquire parasternal cardiac views, the examiner placesthe transducer on the left parasternal chest wall at the second tothe fourth intercostal space. With the dot of the transducerangled toward the patient’s left shoulder, the level of para-sternal short access most useful for evaluating the LV functionis acquired when (by fanning and rotating the transducer asnecessary) a transverse cross-section of the heart is visible atthe level of the LV papillary muscles (Fig. 14). The PLAX isacquired by rotating the transducer 90 degrees so that the dot ispointed toward the patient’s right shoulder. To be adequate, theexaminer should see the MV, the LA, the LV, the aortic valve,and the right ventricular outflow tract (Fig. 8). Note that manyproviders choose to obtain the long-axis view first, and thenrotate to obtain the short-axis view. Regardless of the order inwhich they are acquired, it is important to ensure the anatomicstructures described above are all reasonably well seen toensure that the view of the ventricle is not foreshortened or offthe appropriate axis.

The A4C view is acquired by placing the transducer nearthe apex of the heart, often near the point of maximal impulse,and directing the orientation indicator toward the patient’s leftshoulder. The LV, the RV, the LA, the RA, the MV, and thetricuspid valve should all be seen simultaneously (Fig. 15).This view requires more depth from the machine settings andcan easily be foreshortened if the transducer is placed incor-rectly, and so is more difficult for the novice practitioner.

To obtain the subxyphoid view, the provider places thetransducer at the subxyphoid space as described above whileimaging the IVC. The indicator mark on the transducer is

FIGURE 9. The left thorax divided into the 4 zones described bythe international consensus statement. Horizontal lines are drawnat the parasternal line, the anterior axillary line, and the posterioraxillary line. Upper and lower divisions made by vertical linesbelow the fifth rib.

FIGURE 10. A view of the lung with a phased array probe. Ribsare highlighted with white ovals, and the rib shadows are high-lighted by dashed lines. The pleural stripe is highlighted by thedotted line.




FIGURE 11. A lung ultrasound showing (A) horizontal reflections of the pleura (thick arrow) that occur in a normally aerated lung andare called “A lines” (thin arrows) as well as (B) vertical artifacts descending from the pleura (thick arrow) to the bottom of the screen thatmove with respiration, which are called “B lines” (dashed arrows) and were seen in this case of pulmonary edema.

FIGURE 12. A FAST examination showing normal views of the RUQ (A), LUQ (B), and the suprapubic (C) recesses. The liver (L), thekidneys (K), the spleen (S), and the bladder (b) are visualized clearly with no pathologic fluid collections. LUQ indicates left upperquadrant; RUQ, right upper quadrant.

FIGURE 13. A view of a pleural effusion (A) with the indicator dot pointed cranially, and with cartoon labeling of the anatomy (B).




FIGURE 14. The placement of the probe to acquire the parasternal short axis, and the anatomy showing the right ventricle (RV), the leftventricle (LV), and the papillary muscles, which ensure that the image is acquired at an appropriate plane for EF evaluation.

FIGURE 15. The placement of the probe to acquire the apical 4-chamber view, and the anatomy showing the left ventricle (LV), theright ventricle (RV), the left atrium (LA), the right atrium (RA), the tricuspid valve (TV), and the mitral valve (MV).

FIGURE 16. To acquire the subcostal or the subxyphoid view, the phased array probe is held in the subxyphoid area with the indicatordot toward the patient’s right shoulder. The probe is flattened out against the patient’s stomach to obtain the ideal angle of the heart.The acquired anatomy is visible on the right, showing the left ventricle (LV), the right ventricle (RV), the mitral valve (MV), and thetricuspid valve (TV). LA indicates left atrium; RA, right atrium.




rotated to point toward the patient’s right shoulder or neck andthe transducer is tilted down so that it is nearly parallel to thefloor (Fig. 16). In this view, all of the same landmarks iden-tified in the A4C should be identified, but it is even moresusceptible to foreshortening when assessing left-ventricularfunction.

Interpreting bedside cardiac imaging can be performedquantitatively or qualitatively. Quantitative assessment is anadvanced skill and not pertinent to the focused cardiacultrasound examination. A qualitative approach has been dem-onstrated to be a rapidly learned and reliable method fordifferentiating normal function from moderately or severelydepressed LV function.58 In the hypotensive patient, that level ofdifferentiation is usually sufficient for identifying a primarycardiac cause of shock.

Additional information may augment the qualitativeassessment and bolster a diagnosis of impaired ventricularfunction causing cardiogenic shock. For example, E-point-septal-separation refers to the excursion of the anterior leafletof the MV toward the ventricular septum in the PLAX view:movement to within 1 cm of the septum suggests that theejection fraction is likely preserved.16,59 The gross valvularpathology or severe regurgitation may be appreciated on mostpoint-of-care ultrasound machines, but detailed interpretationof the valve function is best conducted with a full echo-cardiogram machine and several additional views. Similarly,experts can assess regional wall-motion abnormalities sug-gestive of acute myocardial ischemia, which may certainly berelevant in a case of cardiogenic shock, but requires advancedtraining.8

Ultrasound of the IVC can provide additional informationto support or refute a diagnosis of cardiogenic shock. Details ofdynamic IVC interpretation are described above; in cardiacfailure, the IVC is usually large, with little respiratory variationin the diameter, but the practitioner must remember that thisfinding is not specific for cardiogenic shock. A lung ultrasoundcan also provide supplemental data to assist in decision mak-ing. As discussed above, an abnormal B-line-predominantpattern would support a diagnosis of cardiogenic pulmonaryedema, whereas a normal A-line pattern suggests well-aeratedlungs, arguing against this diagnosis. Recall the caveat that Blines are not specific for pulmonary edema, cardiogenic, or

otherwise; hence, this finding should be considered supportive,but not diagnostic, of a cardiac cause of shock.60,61

OBSTRUCTIVE SHOCKThe term “obstructive shock” is not often used in modern

clinical parlance. It is a useful concept in ultrasound, however,because it groups together mechanical etiologies of hypotension inwhich the cardiac output is low despite adequate LV function andvolume status. Indeed, the causes of obstructive shock are asso-ciated with high filling pressures illustrated by a plethoric IVCwith minimal respiratory variation. Flow from the right heartthrough the lungs may be physically obstructed as in PE, or car-diac filling may be pressure-limited as in tension pneumothorax orcardiac tamponade. History and physical examination often pro-vide clues to all these diagnoses, but classically described findingssuch as pulsus paradoxus in tamponade or tracheal deviation inpneumothorax may be difficult to detect, or may not occur untillate in the course when the patient is in extremis. The use ofultrasound allows the examiner to follow a careful physicalexamination with direct evaluation of the heart and lungs, in manycases leading to early definitive diagnosis, without the need forfurther confirmatory testing that may delay the immediate actionsneeded to address these life-threatening pathologies.

Tension PneumothoraxPneumothorax may be suspected, particularly in the right

clinical setting, after thoracic auscultation and percussion.After blunt trauma, the presence of decreased breath soundsperforms well as an indicator for pneumothorax, but in thecritically ill medicine patient, decreased breath sounds are notspecific for this diagnosis.62 Most other maneuvers have asimilar low interobserver reliability, especially in early pneu-mothorax.63 Using ultrasound, the pneumothorax can bedefinitively ruled out by the presence of normal artifact pat-terns (lung sliding) or strongly suggested by the presence ofabnormal findings (the “lung point”).64 Discovering thesefindings early, before a chest radiograph or CT scan can beperformed, may mean identifying a simple pneumothoraxbefore it progresses to a tension pneumothorax.

First, the examiner acquires the previously describedview of the lungs, and focuses on the bright pleural line to

FIGURE 17. M-mode imaging in the pneumothorax (A). Called the “stratosphere” sign, there is no movement deep to the pleural line,and so the pattern is unchanged with depth. This contrasts with M mode of the normal lung (B). Called the “sandy beach” sign,movement of the lung with respiration creates haziness deep to the pleural line.




confirm that it glistens or shimmers with respiration. Thisartifact, termed “lung sliding” or “gliding,” is created by thenormal interface between the parietal and the visceral layers ofthe pleura as they slide against each other with respiration. Itdisappears when that interface is disrupted by air, fluid, orfusion of the pleural layers. Alternatively, one can use M modeimaging of the lung space to identify the “stratosphere” or“sandy beach” signs, when looking at a line drawn through thepleura (Fig. 17). The presence of lung sliding (or a sandy beach

sign on M mode) rules out pneumothorax effectively in thevisualized area, and performs better in excluding this diagnosisthan a supine chest radiograph, using CT as a gold standard.65

However, the converse is not true: the absence of lung slidingdoes not confirm a pneumothorax, because other abnormalitieswill abolish this normal finding (Table 5). In contrast, a “lungpoint” is defined as a single view of the pleura in which onecan see both a normal sliding appearance and a fixed areawithout sliding. This is a very specific finding for the presence

TABLE 5. Conditions Associated With Absent Lung Sliding

Condition Mechanism

Pneumothorax Separation of the visceral and the parietal pleuraNo respiration Lack of pleural sliding, usually a cardiac pulse is still visible as a slight shimmerPleurodesis Sclerosis of the pleural interfaceAcute respiratory distress syndrome Inflammation interfering with the pleural interfacePneumonia Inflammation interfering with the pleural interfacePulmonary embolism Infarction of the pleural interfacePleural Effusion Separation of the visceral and the parietal pleuraHistory of empyema Sclerosis of the pleural interfacePleural plaques/malignancy Impaired movement of the visceral on the parietal pleura

FIGURE 18. Compression ultrasound of the femoral veins. A and B, The femoral artery and vein in a patient without a deep-veinthrombus (DVT). C and D, A patient with a DVT. To create images on the right, pressure is applied until the artery starts to deform.




of pneumothorax as it identifies its border, at the point wherethe pleural layers come back into contact.20,64

Massive PEIn suspected PE, some physical examination findings

such as a new RV heave, or new unilateral calf pain andswelling, have likelihood ratios in the 2 to 2.4 range to suggestthe diagnosis.4 However, other classically described findingssuch as a loud P2, new gallop, pleural friction rub, and clearlungs on auscultation are not statistically reliable.4 In ahypotensive patient in whom massive PE is the suspectedcause of obstructive shock, the ultrasound examination mayidentify additional abnormalities that are highly suggestive ofthis diagnosis. Because definitive testing requires moving thepatient to the CT scanner or the angiography suite, which maybe impossible in a truly unstable patient, these ultrasoundfindings provide the clinician with crucial additional infor-mation and have become a part of several diagnostic andtreatment algorithms.66 Primary components of the ultrasoundexamination in this setting are the heart and lower-extremitydeep veins. There are potentially subtle findings on lungultrasound that may correlate with PE, but there is as yet aninsufficient body of evidence to recommend the inclusion ofthose techniques as definitive.

On echocardiography, a number of published studies haveattempted to clarify the performance of various indicators ofPE.66–68 Although the evidence is mixed, the main finding ofan increased RV-to-LV diameter ratio (normally <1) is moreaccurately a sign of volume overload of the RV and so ispresent under multiple other clinical conditions. This results ina relatively poor test performance in a generalized population,but a reasonable performance in patients with an elevatedpretest probability.68,69 In addition, the oft-referenced“McConnell sign” (akinesia of the mid free wall of the RVwith preserved apical function) has been proposed as an indi-cator of pulmonary embolus, but studies assessing the diag-nostic performance show poor sensitivity and specificity inmost clinical scenarios.70Altogether, a large, poorly contractileright heart together with the expected finding of IVC plethorais consistent with a diagnosis of PE in the right clinical cir-cumstance, but should not be relied upon in isolation.

Ultrasound assessment of the lower extremity deep veinsfor signs of thrombosis is another well-established modalitythat can support a clinical suspicion of thromboembolic dis-ease. The highest performance is achieved using a “duplex”modality combining B-mode and Doppler imaging of the entireleg, but compression-only ultrasound has a sensitivity and aspecificity of 95% and 96%, respectively, for detecting a deep-vein thrombus (DVT) in the emergency department.71 Using ahigh-frequency transducer, the examiner locates the commonfemoral vein and artery in the cross-section at the inguinalcrease. Pressure is applied until the femoral artery starts todeform. If the vein completely collapses with this amount ofpressure, then the study is negative (thrombus is not present)(Fig. 18). If the vein is not collapsed, the study is consideredpositive, even if no echogenic material is seen in the vessel.The procedure is then repeated at the popliteal fossa, assessingthe popliteal vein. In the intensive care unit, where there is ahigher pretest probability of DVT, the sensitivity of thisexamination is improved when a third point is added at theconfluence of the deep and the superficial femoral veins.72

Many clinicians simply repeat the compression every 1 to 2 cmas they sweep between these 2 inguinal points, and perform asimilar sweep at the popliteal fossa (Fig. 19).

Like the cardiac examination, drawing conclusions aboutthe presence or the absence of PE from an isolated lowerextremity DVT screening examination would be problematic,as historically a substantial portion of patients with PE do nothave DVT at the time of PE diagnosis, and conversely not allpatients with DVT develop emboli to the lungs. Several studieshave used the presence of a DVT or right heart strain onultrasound as sufficient evidence for a PE, which is not wellsupported by the available evidence.20,73 However, in theabsence of any other explanation for hypotension, suggestiveechocardiographic findings, IVC plethora, and DVT screeningcan be useful diagnostic adjuncts to supplement the clinicalhistory when definitive diagnosis by CT is not possible.

Cardiac TamponadeCardiac tamponade is a clinical situation in which bedside

ultrasound can rapidly make a critical diagnosis and changemanagement. In contrast to the classically nonspecific physical

FIGURE 19. The anatomy of the popliteal fossa in the transverse view showing the popliteal artery and its two paired veins collapsingnormally with pressure, making deep-vein thrombus much less likely.




examination findings of PE, the presence of elevated neckveins, tachycardia, diminished heart tones, and pulsus para-doxus >12 mm Hg are strongly suggestive of tamponade.4

However, whereas these may be difficult to detect, particularlyin obese patients, pericardial fluid is usually detected quicklyand easily by ultrasound from several different cardiac win-dows. In 1 study, point-of-care ultrasound practitioners in theemergency room were able to demonstrate pericardial effusionwith a sensitivity of 96% and a specificity of 98%.74 Techni-ques for acquiring the 4 standard point-of-care views of theheart are described above, and all are useful for evaluating apericardial effusion, but the subxyphoid view often providesthe clearest image (Fig. 20). Determining whether a fluidcollection is a pleural or a pericardial effusion can be a sourceof error, but the relative position of the aorta can help: peri-cardial effusions will be visualized between the heart and thedescending aorta, and pleural effusions deep to the aorta(Fig. 21).

Given the ease with which the pericardial fluid may beidentified on ultrasound, it is crucial for the point-of-care

sonographer to recall that even large effusions do not neces-sarily cause tamponade physiology, and confirming the latterby ultrasound is more complex than simply identifying fluid inthe pericardial space. Some findings are suggestive of impairedvenous filling, such as RA or RV collapse in diastole, but noneare perfectly sensitive or specific.75 Like other causes ofobstructive shock, cardiac tamponade is typically associatedwith an enlarged IVC without respiratory variation. It is themost sensitive (97%), although the least specific (40%),echocardiographic sign of cardiac tamponade, as any cause ofpulmonary hypertension is a potential confounder.76 Certainly,the finding of a large effusion in a hypotensive patient shouldprompt rapid cardiology consultation, and in emergent casessuch as cardiac arrest without alternative explanation, drainagemay be a life-saving intervention. Point-of-care practitionersshould also be aware that localized or complex pericardialeffusions are more challenging to identify and may be missedby focused ultrasound examinations. In bloody effusions suchas postcardiac or thoracic surgery, tamponade can occur withsmaller, loculated effusions. Expert cardiology consultation isrecommended to rule out tamponade in these patients.

DISTRIBUTIVE SHOCKPhysical examination can suggest distributive shock,

particularly when a patient has warm extremities, comparedwith the peripheral vasoconstriction encountered in the causesdescribed up to this point. From an ultrasound standpoint, thereare no direct sonographic findings that definitively pointtoward a distributive cause of shock. Essentially, once car-diogenic and obstructive shock have been ruled out or deemedless likely, the differential narrows to either hypovolemic ordistributive shock. Focused cardiac ultrasound will be similarin either case, often with a small LA and a hyperdynamic LV.However, one must be mindful of the possibility of impairedmyocardial contractility in the setting of sepsis, which cancomplicate the interpretation of focused cardiac ultrasoundexaminations. In addition, later in the patient’s course aftervolume resuscitation, findings of pulmonary edema maydevelop. Although this makes the interpretation less straight-forward, it highlights the fact that ultrasound is an easilyrepeatable examination that allows for dynamic assessment

FIGURE 20. The subcostal 4-chamber view showing a largepericardial effusion in a patient with cardiac tamponade. Usingthe liver (L) as an acoustic window allows a clear view of theeffusion.

FIGURE 21. Differentiating between a pleural effusion and a pericardial effusion is most reliably accomplished by finding thedescending aorta. Pleural effusions will be located deep or posterior to the aorta, whereas pericardial effusions are found between theheart and the aorta.




over time, to guide both diagnosis and management. Onerecent nonrandomized trial suggested that the use of serialfocused cardiac ultrasound to guide fluid and vasoactive agentadministration reduced mortality in a cohort of patients withlargely sepsis-induced vasopressor-dependent shock.77 Otherpractitioners have proposed using serial lung ultrasound todetermine the point at which a patient begins to developpulmonary edema in the course of volume resuscitation, whena B-line pattern appears. At that point, further intravascularvolume may be excessive, and vasopressors should be con-sidered for blood pressure support.26 Although intriguing,these strategies have not yet been tested in a controlled trial.

In addition to elucidating the type of shock, when dis-tributive shock is suspected, ultrasound should not replace acareful physical examination, but can assist in identifyingpotential sources of sepsis. In the lung, for example, variousimaging profiles are described in the literature including var-iations of the A and the B patterns described above, con-solidation (sometimes called a “C” profile, or hepatization),pleural effusion, or “fractal” pattern.20,48,49,78 These findings

may help differentiate simple hypovolemia (which should havea normal A profile globally) from pneumonia or otherpulmonary sources of inflammation or infection causing dis-tributive shock. A mixed A/B profile describes a localized orunilateral area of B lines suggestive of an isolated alveolar orinterstitial process (Fig. 22). C, fractal, or hepatization profilesare usually seen at the base or the posterior lung and suggestconsolidation (Fig. 23).

Ultrasound may also identify potential sources of distrib-utive shock outside the lung parenchyma. Pleural effusions andascites are readily appreciated with focused examinations, whichcan then be used to guide the appropriate diagnostic procedure.Identification of abscess underlying an area of cellulitis can bemore challenging, particularly for smaller fluid collections, but isa well-described bedside diagnostic procedure.79 Evaluation ofthe gallbladder and bile ducts for signs of infection is a moredifficult technical skill, and so is not a part of most protocolsused by point-of-care practitioners without advanced training.

POTENTIAL PITFALLS AND REAL-WORLDPERFORMANCE

The body of evidence supporting the use of bedside ultra-sound in evaluating a patient with shock is growing, but there is asparsity of high-quality prospective trials comparing the use of thesetechniques with nonultrasound-based standard of care. This is due inpart to the very nature of point-of-care ultrasound, in that it must beinterpreted within the context of a patient’s entire presentation,including history, physical examination, and other data. Combinedwith the fact that ultrasound training and competence is not yetstandardized within critical care, this leads to significant hetero-geneity in the way ultrasound examinations are applied and inter-preted within individual cases. We have described some limitationsof specific examination types within this article, and we can gleansome insights into these challenges through published studies usingprotocolized bedside ultrasound examinations.16–18,22–24,78 Forexample, up to 20% of critically ill patients have insufficient win-dows for the beginning practitioner to acquire high-quality cardiacwindows.25 In addition to operator-dependent factors, the patientpopulation can impact the utility of ultrasound findings: whereas Blines on lung ultrasonography have excellent test performance fordiagnosing pulmonary edema in the emergency room, they may notbe as specific in a trauma or transplant center where there is a higherincidence of underlying parenchymal disease or ARDS.18,52,80

Without careful clinical context, point-of-care ultrasound can createconceptual fallacies and bias, which may cause the patient harm.30

FIGURE 22. When the A profile is present on one side of theanterior chest, but the B profile is present on the other, as seenabove, it is suggestive of a unilateral infiltrative process, such aspneumonia.

FIGURE 23. Two other findings consistent with the PosteroLateral Alveolar Syndrome (PLAPS). A, A densely consolidated lung, whichhas an echogenicity similar to that of the liver, a finding known as “hepatization.” There is also a small parapneumonic effusion (E). B,The “shred” or the “fractal sign” of horizontal artifacts appearing at multiple depths simultaneously (white arrows). This is from anotherpatient with a basilar pneumonia.




At the same time, to fully weigh the utility of this modality in termsof significant patient outcomes, we anticipate more prospective,randomized, protocolized trials like those referenced above.

CONCLUSIONSPatients with shock require rapid assessment and intervention,

often before laboratory studies have returned or complete radio-graphic studies can be obtained. The latter may not be feasible at allin unstable patients who cannot be transported safely to a radiologydepartment for a definitive study. In such situations, clinician-per-formed diagnostic ultrasound provides a useful adjunct to the tra-ditional clinical tools of history and physical examination. Most ofthe examinations described in this review are easily learned, andwith practice can be performed rapidly to provide the clinician withnew windows into the underlying etiology of a shock state. Inter-preting these findings in real time, with knowledge of the utility andlimitations of ultrasound to answer specific clinical questions,empowers the practitioner to make more accurate and timely clin-ical assessments in critically ill patients with shock.

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Bedside Ultrasound for Assessing Patients in Shock · Key Words: shock, bedside ultrasound,...

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Transcript of Bedside Ultrasound for Assessing Patients in Shock · Key Words: shock, bedside ultrasound,...