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Shock
CHEST
Postgraduate Education Corner CONTEMPORARY REVIEWS IN CRITICAL CARE MEDICINE
Shock Ultrasound to Guide Diagnosis and Therapy Gregory A. Schmidt, MD, FCCP; Seth Koenig, MD; and Paul H. Mayo, MD, FCCP
The availability of portable ultrasound devices is changing the approach to the diagnosis and management of shock by offering timely diagnosis and acting to guide therapy. Goal-directed echocardiography (GDE) can be performed well by noncardiologists and consists of a limited number of standard cardiac views: parasternal long axis, parasternal short axis, apical four chamber, subcostal long axis, and inferior vena cava long axis. GDE allows the intensivist to assess left and right ventricular pump function, pericardial effusion, septal dynamics, valvular morphology, major valve failure, and fluid fl responsiveness. Here, we review the questions involved in a systematic approach to the patient in shock, employing GDE: (1) Is there an imminently lifethreatening cause for the shock? (2) Is the shock state likely to be fluid fl responsive? (3) Is there evidence of pump failure? (4) Is there more than one cause for the shock state? (5) Is the cause of the shock state other than cardiac in origin? In contrast to formal echocardiography, GDE is qualitative, can be performed in a few minutes, is interpreted immediately, can be repeated as often as needed, and is always integrated with other elements of the intensivist’s assessment to arrive at an understanding of the basis for the shock and a rational treatment plan. An important part of using GDE is recognizing its limitations and judging when to proceed to a comprehensive echocardiography examination. Competence in GDE has become an essential skill for the practicing intensivist. CHEST 2012; 142((4):1042–1048 Abbreviations: GDE 5 goal-directed echocardiography; IVC 5 inferior vena cava; LV 5 left ventricular; LVOT 5 left ventricular outfl flow tract; PAOP 5 pulmonary artery occlusion pressure; PLR 5 passive leg raising; RAP 5 right atrial pressure; RV V 5 right ventricular; SV V 5 stroke volume; VTI 5 velocity-time integral
is common in the ICU and is associated with Shock substantial mortality rates. Prompt and accurate
diagnosis is a priority. The availability of portable ultrasound devices is changing the approach to the diagnosis and management of shock by offering timely diagnosis and acting to guide therapy. Critical care ultrasonography differs from standard ultrasonography as practiced by radiologists and cardiologists in that the intensivist personally performs and interprets the Manuscript received May 23, 2012; revision accepted June 11, 2012. Affiliations: fi From the University of Iowa Carver College of Medicine (Dr Schmidt), Iowa City, IA; and Hofstra North Shore School of Medicine (Drs Koenig and Mayo), Hempstead, NY. Correspondence to: Gregory A. Schmidt, MD, FCCP, University of Iowa Carver College of Medicine, 200 Hawkins Dr, C33-GH, Iowa City, IA, 52242; e-mail: [email protected] © 2012 American College of Chest Physicians. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details. DOI: 10.1378/chest.12-1297 1042
ultrasound examination at the bedside and immediately integrates the results into the overall clinical assessment and plan. The examination is goal directed and may be repeated as needed to track the evolution of the illness and the response to therapy. This avoids some common problems of standard ultrasonography: the lag between ordering and obtaining the study, the delay before the image is interpreted, the dissociation of the image interpreter from the clinical reality, the requirement for full study in all circumstances, and the resistance to repeating studies over a short period of time. Critical care ultrasonography requires that the intensivist have specifi fic training in image acquisition, image interpretation, and clinical applications. Two statements have defined fi the competence and training standards for critical care ultrasonography.1,2 Skill in general critical care ultrasonography includes basic or goal-directed echocardiography (GDE). Advanced Postgraduate Education Corner
critical care echocardiography requires a comprehensive knowledge of echocardiography similar to the knowledge a cardiologist possesses, in addition to competence in aspects of echocardiography that are not commonly used by cardiologists but are relevant to critical care medicine. For the purposes of this article, the emphasis will be on GDE, with limited discussion of advanced-level techniques for the assessment of fluid responsiveness. The statement on training in critical care ultrasonography makes the recommendation that all critical care training programs include training in general critical care ultrasonography, including GDE. GDE can be performed well by noncardiologists3-9 and consists of a limited number of standard cardiac views: parasternal long axis, parasternal short axis, apical four chamber, subcostal long axis, and inferior vena cava (IVC) long-axis (Video 1). These allow the intensivist to rapidly assess left and right ventricular (LV and RV, respectively) pump function, pericardial effusion, septal dynamics, valvular morphology, and fluid responsiveness. Color Doppler analysis for major fl valve failure is included in the goal-directed examination, as long as the examiner is cognizant of the pitfalls of the technique. GDE is qualitative and is designed to answer a limited number of questions. It may be repeated as often as required during the course of disease. It can be performed in a few minutes and is a key element in the initial and ongoing management of shock. Competence in GDE is easy to achieve and should be regarded a key skill for the frontline intensivist. It is always linked to other elements of overall patient assessment: history, physical examination, other imaging studies, and laboratory results. If necessary, the goal-directed examination may be followed by a comprehensive echocardiography examination. An important part of competence in goaldirected examination is knowing of when to request full echocardiography. GDE allows the intensivist to answer several important questions about the shock state: 1. Is there an imminently life-threatening cause for the shock? 2. Is the shock state likely to be fluid responsive? 3. Is there evidence of pump failure? If so, what is the pattern and what is the appropriate therapeutic response? 4. Is there more than one cause for the shock state, or are there findings that will complicate management of the hemodynamic failure? 5. Is the cause of the shock state other than cardiac in origin? Would ultrasonography of other organ systems be useful in rendering a diagnosis? We will consider these five questions in order. journal.publications.chestnet.org
Is There an Imminently Life-Threatening Cause for the Shock? GDE may make a diagnosis that requires immediate life-saving intervention. For example, severe pericardial tamponade (Video 2), acute cor pulmonale (Video 3), catastrophic valve failure (Video 4), and aortic dissection (Video 5) are diagnoses that are life threatening but are amenable to ultrasound imaging. Although it is unusual to find fi a process that requires emergency intervention, immediate GDE in all shock cases occasionally allows the intensivist to identify and treat a patient who would otherwise die while awaiting a delayed comprehensive echocardiogram. This is a strong argument in favor of early GDE to evaluate shock. Is the Shock State Likely to Be Fluid Responsive? A key decision in the management of shock is whether to give volume resuscitation, and, if so, how much to give. GDE allows the intensivist to identify whether volume infusion will increase cardiac output. Identification fi of fluid-responsive shock mandates volume infusion to improve hemodynamic function. Conversely, if the shock state is not apt to be fluid fl responsive, volume infusion may harm the patient.10 One of the highest priorities in the treatment of shock is fluid resuscitation, which may raise cardiac output and restore critical organ perfusion. Many patients fail to respond, and indiscriminant fluid fl infusion raises the risk of edema and other complications. Surveys of fluid therapy in septic patients in the ICU show that fl fluids are as likely to be useless as effective.11,12 GDE fl plays a key role in helping the intensivist distinguish those patients who will respond to fluids fl from those who will not. Static Predictors of Fluid Responsiveness Fluid responsiveness is defi fined as a clinically relevant increase in cardiac output (generally at least 15%) following an adequate volume challenge. Unless they are very low, static cardiovascular parameters, such as right atrial pressure (RAP) or pulmonary artery occlusion pressure (PAOP), are poor predictors of whether a patient will respond to a fluid fl bolus with a rising cardiac output.13-15 Static ultrasonographic measures are similarly defi ficient. For example, in a series of passively ventilated patients with septic shock, LV end-diastolic area was identical in fluid fl responders and nonresponders.16 Most other studies have also reported that LV end-diastolic area, as well as the ratio of pulsed Doppler transmitral flow fl in early diastole to the early diastolic mitral annular velocity, CHEST / 142 / 4 / OCTOBER 2012
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are unable to distinguish between responders and nonresponders.17,18 The LV ejection time fails similarly in separating responders from nonresponders.19 RV end-diastolic volume has not been shown to be effective in identifying fluid responsiveness.20 The diameter of the IVC is readily measured in critical illness and has been proposed to estimate fluid fl responsiveness. The IVC is easily imaged in a subxiphoid, long-axis view either off the frozen image with caliper function or with M-mode imaging. The diameter is measured 2 to 3 cm below the right atrium or just caudad to the inlet of the hepatic veins.21 The diameter should be measured at end-expiration. The time-motion record simplifi fies identifying the respiratory cycle, and, as described in the “Dynamic Predictors of Fluid Responsiveness” section, the calculation of respiratory variation. The IVC diameter allows an estimation of RAP22 but, like RAP, IVC diameter is not an accurate predictor of fluid responsiveness. For example, Feissel and colleagues21 described only a weak correlation between fluid responsiveness and the minimal or maximal IVC diameter (r 5 0.58 and 0.44, respectively). Dynamic Predictors of Fluid Responsiveness In contrast to static measures, which capture a snapshot of the circulation, dynamic predictors rely on the quantitative response to some perturbation, often the effect of respiration. Ultrasound plays an important role because of its ability to both assess preload responsiveness dynamically and measure changes in cardiac output or stroke volume (SV). Using dynamic predictors in clinical practice and understanding their limitations requires knowledge of underlying physiologic principles. Cardiac function is described graphically as the relationship between ventricular preload and pump output as exemplified fi by the Starling cardiac function curve. Respiration alters the loading conditions of the heart, producing cyclic changes in systolic BP, pulse pressure, SV, and arterial flow velocity. During mechanical ventilation of a passive subject (pharmacologically paralyzed or suffi ficiently sedated to ablate any spontaneous respiratory activity), pleural and juxtacardiac pressures rise during inspiration, causing the RAP to rise, thereby impeding filling fi of the right side of the heart. Transient underfi filling of the right ventricle results in a fall in pulmonary artery flow, fl less filling of the left ventricle, and (several cardiac cycles after the positive pressure breath) reduced LV SV. The respiratory impact on RAP may be compounded by compression of the vena cavae (especially in hypovolemia); and, together, these explain most of the variation in SV related to respiration. The magnitude of these respirophasic changes in SV changes can be used to predict 1044
fluid responsiveness: Large respirophasic variations in SV indicate that the heart is functioning on the steep part of the Starling cardiac function curve and that fluids will boost perfusion; small variations indicate that the circulation is operating on the flat fl part of the cardiac function curve and fluids fl will be ineffective. This provides a framework for understanding how ultrasonography may detect fluid responsiveness. For example, a fluid-responsive circulation will show signifi ficant cyclic variation in vena caval volume and LV SV (or a surrogate). On the other hand, if the circulation is not fluid responsive (and, therefore, not varying much with respiratory perturbations), ultrasound will reveal only small respirophasic changes in the vena cavae or LV SV. Several additional respiration-related mechanisms affect SV, and these may be important in specific fi circumstances. For example, lung distention raises the pressure surrounding pulmonary capillaries, augmenting RV afterload. Generally, this has little consequence for the circulation, but during RV failure it may contribute greatly to respiratory variation. This is one circumstance in which patients are fluid fl nonresponsive despite signifi ficant respiratory variation in SV.23 Another mechanism by which respiration produces cyclic circulatory variation during passive inflafl tion is the inspiratory increase in pulmonary capillary pressure relative to pleural pressure. During passive infl flation, blood is squeezed out of the lung and into the left atrium (raising LV preload).24 This results in augmentation of blood flow fl into the left ventricle. If the left ventricle is fluid fl responsive, LV SV will be augmented during the inspiratory phase of the ventilator. Inspiration also reduces LV afterload both by boosting juxtacardiac pressure (thus, lowering transmural pressure during ejection) and hastening thoracic aortic emptying during diastole.25 Although these effects are real, patients with depressed LV function tend not to have increased SV variation overall because there is little depressive effect on filling of the right side of the heart when right-sided pressures are high and because changes in LV preload have little impact on the flat portion of the cardiac function curve. Thus, in contrast to patients with RV failure, those with LV failure are unlikely to show falsely positive dynamic predictors. Studies validating dynamic predictors have used a tidal volume of 8 to 10 mL/kg. Smaller tidal volumes have proportionately smaller circulatory effects and are probably too small to be diagnostically useful.26 Because this tidal volume is higher than many intensivists would accept for patients with acute lung injury, it is necessary to temporarily increase the tidal volume above 8 mL/kg to assess the likelihood of fluid fl responsiveness. Postgraduate Education Corner
Respiratory effort also invalidates most ultrasonographic fluid fl predictors because inspiration lowers pleural pressure, augmenting RV preload. Although spontaneous breathing also produces cyclic changes in IVC diameter, aortic Doppler flow, fl and other measures of SV variation, these have not been shown to accurately predict fluid fl responsiveness.20,27 Because both inspiratory and expiratory effort can be subtle in mechanically ventilated patients, care must be taken when using dynamic predictors to ensure that patients are truly passive. For patients who are actively i breathing, passive leg raising (PLR), combined with ultrasound assessment of response, provides excellent prediction of fluid responsiveness (see the “Passive Leg Raising” section). IVC Diameter Respiratory Variation During mechanical ventilation of the passive patient, inspiration raises RAP (and abdominal pressure much less so), tending to distend the IVC, whereas expiration lowers RAP, tending to collapse the IVC. Barbier and colleagues28 studied septic patients with acute respiratory failure in whom the tidal volume was sufficient to raise the pleural pressure by about 5 cm water. The IVC distensibility index was calculated as the difference in maximal and minimal diameters divided by the minimal diameter and converted to percentage, with a threshold of 18% discriminating responders and nonresponders (sensitivity and specificity both 90%). Feissel and colleagues21 calculated IVC variation as the difference in diameters divided by the mean of the diameters while patients were ventilated with tidal volumes of 8 to 10 mL/kg. A threshold IVC variation of 12% separated responders from nonresponders (positive and negative predictive values of 93% and 92%, respectively).21 The superior vena cava also varies with respiration, and its distensibility index may be an even better predictor of fluid responsiveness,29 but it requires transesophageal echocardiography and is beyond the scope of this review. Arterial Doppler Flow and Variation Doppler methods allow measurement of the aortic blood velocity and calculation of the velocity-time integral (VTI). SV can be measured as the product of the VTI and LV outfl flow tract (LVOT) cross-sectional area. Respiratory changes in peak aortic flow velocity are quite accurate in distinguishing fluid fl responders from nonresponders (threshold value, 12%; sensitivity, 100%; specificity, fi 89%).16 Although this study used transesophageal echocardiography, the LVOT VTI can be measured with transthoracic echocardiography as well. Similar methods can be applied to measure journal.publications.chestnet.org
brachial artery peak flow velocity variation near the antecubital fossa, and this both correlates well with fl arterial pulse pressure variation30 and predicts fluid responsiveness.31 Passive Leg Raising Raising a patient’s legs reduces the unstressed volume of the circulation, effectively mimicking the effects of a reversible fluid bolus. The method involves making an initial measurement of cardiac output from the VTI of the LVOT in the semirecumbent position (45° head-of-bed elevation), then tilting the patient (without changing the angle between legs and trunk) so that the lower limbs are raised to 45°, and measuring r again the SV or a surrogate (threshold values for SV variation by transthoracic echocardiography 5 12.5%,17 SV variation using Flotrac [Edwards Lifesciences, fl variation 5 8%33). LLC] 5 16%,32 and aortic blood flow Measuring the change in femoral artery flow velocity with PLR provides an alternative to echocardiography for assessing the SV response.33 A major advantage of PLR-based predictions of fluid responsiveness is that actively breathing patients and those with arrhythmias can also be assessed. For example, in a group of 71 ventilated subjects, roughly one-half of whom had either spontaneous breathing or arrhythmias, PLR was 97% sensitive and 94% specific. fi 20 Several other studies have corroborated these findfi ings.20,32-35 All the aforementioned methods that involve measurement of blood flow velocity or VTI require competence in Doppler measurements and are, therefore, not performed as part of GDE. Recognizing Untoward Effects of Further Fluids The decision to infuse fluids fl should be paired with a plan to recognize its end points, the simplest of which is resolution of the shock. When shock persists, additional ultrasonographic findings may be useful. First, fl fluid responsiveness may be remeasured: if the circulation no longer varies much with passive respiration, additional fluids fl are not likely to be helpful and may be harmful. A common hazard of excessive volume infusion is pulmonary edema, so lung ultrasonography may be helpful in guiding volume infusion. The presence of A lines in the anterior lung zone predicts that the PAOP is below 18 mm with a high degree of certainty.36 This pattern allows the intensivist to proceed with volume infusion with safety regarding the risk of hydrostatic pulmonary edema, although it does not aid in determining whether the circulation is fluid responsive. The presence of extensive, profuse, anterior lung zone B lines, in combination with a smooth pleural line, is both sensitive and specifi fic for hydrostatic pulmonary edema and might CHEST / 142 / 4 / OCTOBER 2012
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contraindicate further volume resuscitation.377 The PAOP can be estimated by echocardiography,38 but this requires training in Doppler measurement and is not part of GDE. The presence of a high filling fi pressure would contraindicate further volume resuscitation for fear of producing hydrostatic pulmonary edema. The central venous pressure can be estimated by using ultrasound to visualize the collapse point of the internal jugular vein, although this has little usefulness in identifying fluid responsiveness.39 Practical Application of GDE for Determination of Fluid Responsiveness By definition, fi the intensivist with profi ficiency in GDE is not trained to perform Doppler-based measurements of cardiac function. Many measurements of preload sensitivity require knowledge of Doppler because they rely on measurement of blood flow fl velocity across the respiratory cycle or on straight leg raising. Realistically, the intensivist with proficiency fi in GDE alone is limited to the study of IVC dynamics. A limitation of this method is that the patient must be on ventilatory support, without any spontaneous respiratory effort. In this case, IVC variation is a well-validated method and should be the preferred method for determining fluid responsiveness. If the patient is breathing spontaneously or on a ventilator but making respiratory effort, the authors use the following pragmatic approach to identify fluid fl responsiveness in the patient in shock: 1. If the left ventricle is hyperdynamic with endsystolic effacement, there is a high probability of fluid responsiveness. 2. If the IVC is , 1 cm in diameter, there is a high probability of fluid responsiveness. 3. If the IVC is . 2.5 cm in diameter, there is a low probability of fluid responsiveness. 4. If the IVC is between 1 and 2.5 cm, there is an indeterminate probability of fluid fl responsiveness. Is There Evidence of Pump Failure? If So, What Is the Pattern and What Is the Appropriate Therapeutic Response? A major goal of early GDE is to define fi the underlying cause of shock. GDE allows the intensivist to quickly assess whether pump failure is the cause of the hemodynamic crisis. Pump failure may be subcategorized into LV, RV, or valvular causes, each of which may result in a different management strategy. Categorization of pump dysfunction allows the intensivist to develop a management plan. Occasionally, echocardiography results will lead to an immediate life-saving intervention, as discussed. More 1046
commonly, the results will not identify an immediately remediable cause for the shock, but they serve to guide evaluation and management. For example, the pattern of end-systolic effacement of the left ventricle with a virtual (collapsed) IVC mandates volume resuscitation (Video 6), and acute cor pulmonale pattern with massive RV dilation specifically fi contraindicates volume resuscitation and requires evaluation for the cause of RV failure (Video 7), whereas severe LV dysfunction cautions against major volume resuscitation and favors inotropic support rather than vasopressor use (Video 8). Sepsis is a common cause of shock in the ICU. Echocardiography may show normal LV function (Video 9). In this case, the focus should be on vasoconstrictor infusion rather than inotropes to counteract the vasoplegia of septic shock. Reversible LV dysfunction is commonly observed fl in septic shock.40 If this is associated with a low-flow state, a mixed inotrope-vasopressor may be indicated. In this case, it is important to do serial GDE to document the improvement in LV function that frequently occurs with remission of septic shock. Otherwise, the patient may be labeled inappropriately as having permanent LV dysfunction. The value of GDE is in guiding volume resuscitation and vasoactive drug infusion in logical fashion. Is There More Than One Cause for the Shock State, or Are There Findings That Will Complicate Management of Hemodynamic Failure? GDE may detect more than one cause for the shock state or may identify findings fi that complicate the management of the primary cause. This is especially problematic in patients with chronic, complex illness, especially in the elderly patient with shock. For example, septic shock may coexist with severe aortic stenosis, or a massive pulmonary embolism with acute cor pulmonale may be complicated by preexisting severe LV dysfunction. Sorting out what is a new abnormality from preexisting pump failure is challenging. GDE results must always be interpreted within the context of the overall clinical picture. Is the Cause of the Shock State Other Than Cardiac in Origin? Would Ultrasonography of Other Organ Systems Be Useful in Rendering a Diagnosis? Although GDE is the mainstay for the assessment of hemodynamic failure, general critical care ultrasonography is useful as a total body approach to the assessment of the patient with shock. Using the skill set defined fi in the Competence Statement, the intensivist is uniquely qualifi fied in other aspects of the Postgraduate Education Corner
ultrasound examination that are useful in identifying the source of the hemodynamic failure. With a wholebody ultrasound approach, thoracic, abdominal, and vascular ultrasonography are used to search for causes of shock. Lung ultrasonography is more sensitive than conventional chest radiography for detecting pneumothorax41 and may facilitate recognition of tension as the cause of shock. A generalized normal aeration pattern on lung ultrasonography in the patient with shock, in concert with a finding fi of DVT on vascular examination, is strongly associated with pulmonary embolism.42 Intensivists are able to diagnose DVT with an accuracy similar to that of conventional technicianperformed compression ultrasound d43; this skill is useful for the rapid assessment of shock where pulmonary embolism is within the differential. Identifying lung consolidation supports a diagnosis of septic shock, whereas various other fi findings (hydronephrosis, abdominal free fluid, fl biliary dilation) may point to an abdominal source. Screening abdominal ultrasonography may also reveal a bleeding abdominal aneurysm, dissection (Video 10), peritonitis, ischemic bowel, or abdominal free air. The intensivist may use GDE as a primary tool for assessment of shock but extends the ultrasound examination when clinically indicated.
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Acknowledgments Financial/nonfi financial disclosures: The authors have reported to CHEST T that no potential confl flicts of interest exist with any companies/organizations whose products or services may be discussed in this article. Additional information: The Videos can be found in the “Supplemental Materials” area of the online article.
References 1. Mayo PH, Beaulieu Y, Doelken P, et al. American College of Chest Physicians/La Société de Réanimation de Langue Française statement on competence in critical care ultrasonography. Chest. 2009;135(4):1050-1060. 2. Expert Round Table on Ultrasound in ICU. International expert statement on training standards for critical care ultrasonography. Intensive Care Med. 2011;37(7):1077-1083. 3. Mandavia DP, Hoffner RJ, Mahaney K, Henderson SO. Bedside echocardiography by emergency physicians. Ann Emerg Med. 2001;38(4):377-382. 4. Vignon P, Chastagner C, François B, et al. Diagnostic ability of hand-held echocardiography in ventilated critically ill patients. Crit Care. 2003;7(5):R84-R91. 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. Pediatrics. 2004;114(6): e667-e671. 6. Melamed R, Sprenkle MD, Ulstad VK, Herzog CA, Leatherman JW. Assessment of left ventricular function by intensivists using hand-held echocardiography. Chest. 2009; 135(6):1416-1420. 7. Manasia AR, Nagaraj HM, Kodali RB, et al. Feasibility and potential clinical utility of goal-directed transthoracic journal.publications.chestnet.org
17.
18. 19. 20. 21. 22. 23.
24. 25. 26.
echocardiography performed by noncardiologist intensivists using a small hand-carried device (SonoHeart) in critically ill patients. J Cardiothorac Vasc Anesth. 2005;19(2):155-159. Vignon P, Dugard A, Abraham J, et al. Focused training for goal-oriented hand-held echocardiography performed by noncardiologist residents in the intensive care unit. Intensive Care Med. 2007;33(10):1795-1799. Vignon P, Mücke F, Bellec F, et al. Basic critical care echocardiography: validation of a curriculum dedicated to noncardiologist residents. Crit Care Med. 2011;39(4):636-642. Durairaj L, Schmidt GA. Fluid therapy in resuscitated sepsis: less is more. Chest. 2008;133(1):252-263. Marik PE, Baram M, Vahid B. Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares. Chest. 2008;134(1): 172-178. Michard F, Teboul JL. Predicting fl fluid responsiveness in ICU patients: a critical analysis of the evidence. Chestt. 2002;121(6): 2000-2008. Kumar A, Anel R, Bunnell E, et al. Pulmonary artery occlusion pressure and central venous pressure fail to predict ventricular filling volume, cardiac performance, or the response to volume infusion in normal subjects. Crit Care Med. 2004; 32(3):691-699. Tavernier B, Makhotine O, Lebuffe G, Dupont J, Scherpereel P. Systolic pressure variation as a guide to fluid therapy in patients with sepsis-induced hypotension. Anesthesiology. 1998;89(6): 1313-1321. Tousignant CP, Walsh F, Mazer CD. The use of transesophageal echocardiography for preload assessment in critically ill patients. Anesth Analg. 2000;90(2):351-355. Feissel M, Michard F, Mangin I, Ruyer O, Faller JP, Teboul JL. Respiratory changes in aortic blood velocity as an indicator of fluid responsiveness in ventilated patients with septic shock. fl Chest. 2001;119(3):867-873. Lamia B, Ochagavia A, Monnet X, Chemla D, Richard C, Teboul JL. Echocardiographic prediction of volume responsiveness in critically ill patients with spontaneously breathing activity. Intensive Care Med. 2007;33(7):1125-1132. Solus-Biguenet H, Fleyfel M, Tavernier B, et al. Non-invasive prediction of fluid responsiveness during major hepatic surgery. Br J Anaesth. 2006;97(6):808-816. Monnet X, Rienzo M, Osman D, et al. Esophageal Doppler monitoring predicts fluid responsiveness in critically ill ventilated patients. Intensive Care Med. 2005;31(9):1195-1201. Monnet X, Rienzo M, Osman D, et al. Passive leg raising predicts fluid responsiveness in the critically ill. Crit Care Med. d 2006;34(5):1402-1407. Feissel M, Michard F, Faller J-P, Teboul JL. The respiratory variation in inferior vena cava diameter as a guide to fluid fl therapy. Intensive Care Med. 2004;30(9):1834-1837. Brennan JM, Blair JE, Goonewardena S, et al. Reappraisal of the use of inferior vena cava for estimating right atrial pressure. J Am Soc Echocardiogrr. 2007;20(7):857-861. Vieillard-Baron A, Loubières Y, Schmitt JM, Page B, Dubourg O, Jardin F. Cyclic changes in right ventricular output impedance during mechanical ventilation. J Appl Physiol. 1999;87(5): 1644-1650. Brower R, Wise RA, Hassapoyannes C, Bromberger-Barnea B, Permutt S. Effect of lung inflation fl on lung blood volume and pulmonary venous flow fl . J Appl Physiol. 1985;58(3):954-963. Fessler HE, Brower RG, Wise RA, Permutt S. Mechanism of reduced LV afterload by systolic and diastolic positive pleural pressure. J Appl Physiol. 1988;65(3):1244-1250. De Backer D, Heenen S, Piagnerelli M, Koch M, Vincent JL. Pulse pressure variations to predict fluid fl responsiveness: infl fluence of tidal volume. Intensive Care Med. d 2005;31(4):517-523. CHEST / 142 / 4 / OCTOBER 2012
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27. Heenen S, De Backer D, Vincent JL. How can the response to volume expansion in patients with spontaneous respiratory movements be predicted? Crit Care. 2006;10(4):R102. 28. Barbier C, Loubières Y, Schmit C, et al. Respiratory changes in inferior vena cava diameter are helpful in predicting fluid fl responsiveness in ventilated septic patients. Intensive Care Med. 2004;30(9):1740-1746. 29. Vieillard-Baron A, Chergui K, Rabiller A, et al. Superior vena caval collapsibility as a gauge of volume status in ventilated septic patients. Intensive Care Med. 2004;30(9):1734-1739. 30. Brennan JM, Blair JEA, Hampole C, et al. Radial artery pulse pressure variation correlates with brachial artery peak velocity variation in ventilated subjects when measured by internal medicine residents using hand-carried ultrasound devices. Chest. 2007;131(5):1301-1307. 31. Monge García MI, Gil Cano A, Díaz Monrové JC. Brachial artery peak velocity variation to predict fluid responsiveness in mechanically ventilated patients. Crit Care. 2009;13(5): R142. 32. Lafanechère A, Pène F, Goulenok C, et al. Changes in aortic blood flow induced by passive leg raising predict fluid responsiveness in critically ill patients. Crit Care. 2006;10(5):R132. 33. Préau S, Saulnier F, Dewavrin F, Durocher A, Chagnon JL. Passive leg raising is predictive of fluid responsiveness in spontaneously breathing patients with severe sepsis or acute pancreatitis. Crit Care Med. 2010;38(3):819-825. 34. Biais M, Vidil L, Sarrabay P, Cottenceau V, Revel P, Sztarkk F. Changes in stroke volume induced by passive leg raising in spontaneously breathing patients: comparison between echocardiography and Vigileo/FloTrac device. Crit Care. 2009; 13(6):R195.
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35. Thiel SW, Kollef MH, Isakow W. Non-invasive stroke volume measurement and passive leg raising predict volume responsiveness in medical ICU patients: an observational cohort study. Crit Care. 2009;13(4):R111. 36. Lichtenstein DA, Mezière GA, Lagoueyte JF, Biderman P, Goldstein I, Gepner A. A-lines and B-lines: lung ultrasound as a bedside tool for predicting pulmonary artery occlusion pressure in the critically ill. Chest. 2009;136(4):1014-1020. 37. Copetti R, Soldati G, Copetti P. Chest sonography: a useful tool to differentiate acute cardiogenic pulmonary edema from acute respiratory distress syndrome. Cardiovasc Ultrasound. 2008;6:16. 38. Nagueh SF, Appleton CP, Gillebert TC, et al. Recommendations for the evaluation of left ventricular diastolic function by echocardiography. J Am Soc Echocardiogr. r 2009;22(2):107-133. 39. Deol GR, Collett N, Ashby A, Schmidt GA. Ultrasound accurately refl flects the jugular venous examination but underestimates central venous pressure. Chest. 2011;139(1):95-100. 40. Vieillard-Baron A. Septic cardiomyopathy. Ann Intensive Care. 2011;1(1):6. 41. Soldati G, Testa A, Sher S, Pignataro G, La Sala M, Silverii NG. Occult traumatic pneumothorax: diagnostic accuracy of lung ultrasonography in the emergency department. Chest. 2008; 133(1):204-211. 42. Lichtenstein DA, Mezière GA. Relevance of lung ultrasound in the diagnosis of acute respiratory failure: the BLUE protocol. Chest. 2008;134(1):117-125. 43. Kory PD, Pellecchia CM, Shiloh AL, Mayo PH, DiBello C, Koenig S. Accuracy of ultrasonography performed by critical care physicians for the diagnosis of DVT. Chest. 2011;139(3): 538-542.
Postgraduate Education Corner
Postgraduate Education Corner CONTEMPORARY REVIEWS IN CRITICAL CARE MEDICINE
Shock Ultrasound to Guide Diagnosis and Therapy Gregory A. Schmidt, MD, FCCP; Seth Koenig, MD; and Paul H. Mayo, MD, FCCP
The availability of portable ultrasound devices is changing the approach to the diagnosis and management of shock by offering timely diagnosis and acting to guide therapy. Goal-directed echocardiography (GDE) can be performed well by noncardiologists and consists of a limited number of standard cardiac views: parasternal long axis, parasternal short axis, apical four chamber, subcostal long axis, and inferior vena cava long axis. GDE allows the intensivist to assess left and right ventricular pump function, pericardial effusion, septal dynamics, valvular morphology, major valve failure, and fluid fl responsiveness. Here, we review the questions involved in a systematic approach to the patient in shock, employing GDE: (1) Is there an imminently lifethreatening cause for the shock? (2) Is the shock state likely to be fluid fl responsive? (3) Is there evidence of pump failure? (4) Is there more than one cause for the shock state? (5) Is the cause of the shock state other than cardiac in origin? In contrast to formal echocardiography, GDE is qualitative, can be performed in a few minutes, is interpreted immediately, can be repeated as often as needed, and is always integrated with other elements of the intensivist’s assessment to arrive at an understanding of the basis for the shock and a rational treatment plan. An important part of using GDE is recognizing its limitations and judging when to proceed to a comprehensive echocardiography examination. Competence in GDE has become an essential skill for the practicing intensivist. CHEST 2012; 142((4):1042–1048 Abbreviations: GDE 5 goal-directed echocardiography; IVC 5 inferior vena cava; LV 5 left ventricular; LVOT 5 left ventricular outfl flow tract; PAOP 5 pulmonary artery occlusion pressure; PLR 5 passive leg raising; RAP 5 right atrial pressure; RV V 5 right ventricular; SV V 5 stroke volume; VTI 5 velocity-time integral
is common in the ICU and is associated with Shock substantial mortality rates. Prompt and accurate
diagnosis is a priority. The availability of portable ultrasound devices is changing the approach to the diagnosis and management of shock by offering timely diagnosis and acting to guide therapy. Critical care ultrasonography differs from standard ultrasonography as practiced by radiologists and cardiologists in that the intensivist personally performs and interprets the Manuscript received May 23, 2012; revision accepted June 11, 2012. Affiliations: fi From the University of Iowa Carver College of Medicine (Dr Schmidt), Iowa City, IA; and Hofstra North Shore School of Medicine (Drs Koenig and Mayo), Hempstead, NY. Correspondence to: Gregory A. Schmidt, MD, FCCP, University of Iowa Carver College of Medicine, 200 Hawkins Dr, C33-GH, Iowa City, IA, 52242; e-mail: [email protected] © 2012 American College of Chest Physicians. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details. DOI: 10.1378/chest.12-1297 1042
ultrasound examination at the bedside and immediately integrates the results into the overall clinical assessment and plan. The examination is goal directed and may be repeated as needed to track the evolution of the illness and the response to therapy. This avoids some common problems of standard ultrasonography: the lag between ordering and obtaining the study, the delay before the image is interpreted, the dissociation of the image interpreter from the clinical reality, the requirement for full study in all circumstances, and the resistance to repeating studies over a short period of time. Critical care ultrasonography requires that the intensivist have specifi fic training in image acquisition, image interpretation, and clinical applications. Two statements have defined fi the competence and training standards for critical care ultrasonography.1,2 Skill in general critical care ultrasonography includes basic or goal-directed echocardiography (GDE). Advanced Postgraduate Education Corner
critical care echocardiography requires a comprehensive knowledge of echocardiography similar to the knowledge a cardiologist possesses, in addition to competence in aspects of echocardiography that are not commonly used by cardiologists but are relevant to critical care medicine. For the purposes of this article, the emphasis will be on GDE, with limited discussion of advanced-level techniques for the assessment of fluid responsiveness. The statement on training in critical care ultrasonography makes the recommendation that all critical care training programs include training in general critical care ultrasonography, including GDE. GDE can be performed well by noncardiologists3-9 and consists of a limited number of standard cardiac views: parasternal long axis, parasternal short axis, apical four chamber, subcostal long axis, and inferior vena cava (IVC) long-axis (Video 1). These allow the intensivist to rapidly assess left and right ventricular (LV and RV, respectively) pump function, pericardial effusion, septal dynamics, valvular morphology, and fluid responsiveness. Color Doppler analysis for major fl valve failure is included in the goal-directed examination, as long as the examiner is cognizant of the pitfalls of the technique. GDE is qualitative and is designed to answer a limited number of questions. It may be repeated as often as required during the course of disease. It can be performed in a few minutes and is a key element in the initial and ongoing management of shock. Competence in GDE is easy to achieve and should be regarded a key skill for the frontline intensivist. It is always linked to other elements of overall patient assessment: history, physical examination, other imaging studies, and laboratory results. If necessary, the goal-directed examination may be followed by a comprehensive echocardiography examination. An important part of competence in goaldirected examination is knowing of when to request full echocardiography. GDE allows the intensivist to answer several important questions about the shock state: 1. Is there an imminently life-threatening cause for the shock? 2. Is the shock state likely to be fluid responsive? 3. Is there evidence of pump failure? If so, what is the pattern and what is the appropriate therapeutic response? 4. Is there more than one cause for the shock state, or are there findings that will complicate management of the hemodynamic failure? 5. Is the cause of the shock state other than cardiac in origin? Would ultrasonography of other organ systems be useful in rendering a diagnosis? We will consider these five questions in order. journal.publications.chestnet.org
Is There an Imminently Life-Threatening Cause for the Shock? GDE may make a diagnosis that requires immediate life-saving intervention. For example, severe pericardial tamponade (Video 2), acute cor pulmonale (Video 3), catastrophic valve failure (Video 4), and aortic dissection (Video 5) are diagnoses that are life threatening but are amenable to ultrasound imaging. Although it is unusual to find fi a process that requires emergency intervention, immediate GDE in all shock cases occasionally allows the intensivist to identify and treat a patient who would otherwise die while awaiting a delayed comprehensive echocardiogram. This is a strong argument in favor of early GDE to evaluate shock. Is the Shock State Likely to Be Fluid Responsive? A key decision in the management of shock is whether to give volume resuscitation, and, if so, how much to give. GDE allows the intensivist to identify whether volume infusion will increase cardiac output. Identification fi of fluid-responsive shock mandates volume infusion to improve hemodynamic function. Conversely, if the shock state is not apt to be fluid fl responsive, volume infusion may harm the patient.10 One of the highest priorities in the treatment of shock is fluid resuscitation, which may raise cardiac output and restore critical organ perfusion. Many patients fail to respond, and indiscriminant fluid fl infusion raises the risk of edema and other complications. Surveys of fluid therapy in septic patients in the ICU show that fl fluids are as likely to be useless as effective.11,12 GDE fl plays a key role in helping the intensivist distinguish those patients who will respond to fluids fl from those who will not. Static Predictors of Fluid Responsiveness Fluid responsiveness is defi fined as a clinically relevant increase in cardiac output (generally at least 15%) following an adequate volume challenge. Unless they are very low, static cardiovascular parameters, such as right atrial pressure (RAP) or pulmonary artery occlusion pressure (PAOP), are poor predictors of whether a patient will respond to a fluid fl bolus with a rising cardiac output.13-15 Static ultrasonographic measures are similarly defi ficient. For example, in a series of passively ventilated patients with septic shock, LV end-diastolic area was identical in fluid fl responders and nonresponders.16 Most other studies have also reported that LV end-diastolic area, as well as the ratio of pulsed Doppler transmitral flow fl in early diastole to the early diastolic mitral annular velocity, CHEST / 142 / 4 / OCTOBER 2012
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are unable to distinguish between responders and nonresponders.17,18 The LV ejection time fails similarly in separating responders from nonresponders.19 RV end-diastolic volume has not been shown to be effective in identifying fluid responsiveness.20 The diameter of the IVC is readily measured in critical illness and has been proposed to estimate fluid fl responsiveness. The IVC is easily imaged in a subxiphoid, long-axis view either off the frozen image with caliper function or with M-mode imaging. The diameter is measured 2 to 3 cm below the right atrium or just caudad to the inlet of the hepatic veins.21 The diameter should be measured at end-expiration. The time-motion record simplifi fies identifying the respiratory cycle, and, as described in the “Dynamic Predictors of Fluid Responsiveness” section, the calculation of respiratory variation. The IVC diameter allows an estimation of RAP22 but, like RAP, IVC diameter is not an accurate predictor of fluid responsiveness. For example, Feissel and colleagues21 described only a weak correlation between fluid responsiveness and the minimal or maximal IVC diameter (r 5 0.58 and 0.44, respectively). Dynamic Predictors of Fluid Responsiveness In contrast to static measures, which capture a snapshot of the circulation, dynamic predictors rely on the quantitative response to some perturbation, often the effect of respiration. Ultrasound plays an important role because of its ability to both assess preload responsiveness dynamically and measure changes in cardiac output or stroke volume (SV). Using dynamic predictors in clinical practice and understanding their limitations requires knowledge of underlying physiologic principles. Cardiac function is described graphically as the relationship between ventricular preload and pump output as exemplified fi by the Starling cardiac function curve. Respiration alters the loading conditions of the heart, producing cyclic changes in systolic BP, pulse pressure, SV, and arterial flow velocity. During mechanical ventilation of a passive subject (pharmacologically paralyzed or suffi ficiently sedated to ablate any spontaneous respiratory activity), pleural and juxtacardiac pressures rise during inspiration, causing the RAP to rise, thereby impeding filling fi of the right side of the heart. Transient underfi filling of the right ventricle results in a fall in pulmonary artery flow, fl less filling of the left ventricle, and (several cardiac cycles after the positive pressure breath) reduced LV SV. The respiratory impact on RAP may be compounded by compression of the vena cavae (especially in hypovolemia); and, together, these explain most of the variation in SV related to respiration. The magnitude of these respirophasic changes in SV changes can be used to predict 1044
fluid responsiveness: Large respirophasic variations in SV indicate that the heart is functioning on the steep part of the Starling cardiac function curve and that fluids will boost perfusion; small variations indicate that the circulation is operating on the flat fl part of the cardiac function curve and fluids fl will be ineffective. This provides a framework for understanding how ultrasonography may detect fluid responsiveness. For example, a fluid-responsive circulation will show signifi ficant cyclic variation in vena caval volume and LV SV (or a surrogate). On the other hand, if the circulation is not fluid responsive (and, therefore, not varying much with respiratory perturbations), ultrasound will reveal only small respirophasic changes in the vena cavae or LV SV. Several additional respiration-related mechanisms affect SV, and these may be important in specific fi circumstances. For example, lung distention raises the pressure surrounding pulmonary capillaries, augmenting RV afterload. Generally, this has little consequence for the circulation, but during RV failure it may contribute greatly to respiratory variation. This is one circumstance in which patients are fluid fl nonresponsive despite signifi ficant respiratory variation in SV.23 Another mechanism by which respiration produces cyclic circulatory variation during passive inflafl tion is the inspiratory increase in pulmonary capillary pressure relative to pleural pressure. During passive infl flation, blood is squeezed out of the lung and into the left atrium (raising LV preload).24 This results in augmentation of blood flow fl into the left ventricle. If the left ventricle is fluid fl responsive, LV SV will be augmented during the inspiratory phase of the ventilator. Inspiration also reduces LV afterload both by boosting juxtacardiac pressure (thus, lowering transmural pressure during ejection) and hastening thoracic aortic emptying during diastole.25 Although these effects are real, patients with depressed LV function tend not to have increased SV variation overall because there is little depressive effect on filling of the right side of the heart when right-sided pressures are high and because changes in LV preload have little impact on the flat portion of the cardiac function curve. Thus, in contrast to patients with RV failure, those with LV failure are unlikely to show falsely positive dynamic predictors. Studies validating dynamic predictors have used a tidal volume of 8 to 10 mL/kg. Smaller tidal volumes have proportionately smaller circulatory effects and are probably too small to be diagnostically useful.26 Because this tidal volume is higher than many intensivists would accept for patients with acute lung injury, it is necessary to temporarily increase the tidal volume above 8 mL/kg to assess the likelihood of fluid fl responsiveness. Postgraduate Education Corner
Respiratory effort also invalidates most ultrasonographic fluid fl predictors because inspiration lowers pleural pressure, augmenting RV preload. Although spontaneous breathing also produces cyclic changes in IVC diameter, aortic Doppler flow, fl and other measures of SV variation, these have not been shown to accurately predict fluid fl responsiveness.20,27 Because both inspiratory and expiratory effort can be subtle in mechanically ventilated patients, care must be taken when using dynamic predictors to ensure that patients are truly passive. For patients who are actively i breathing, passive leg raising (PLR), combined with ultrasound assessment of response, provides excellent prediction of fluid responsiveness (see the “Passive Leg Raising” section). IVC Diameter Respiratory Variation During mechanical ventilation of the passive patient, inspiration raises RAP (and abdominal pressure much less so), tending to distend the IVC, whereas expiration lowers RAP, tending to collapse the IVC. Barbier and colleagues28 studied septic patients with acute respiratory failure in whom the tidal volume was sufficient to raise the pleural pressure by about 5 cm water. The IVC distensibility index was calculated as the difference in maximal and minimal diameters divided by the minimal diameter and converted to percentage, with a threshold of 18% discriminating responders and nonresponders (sensitivity and specificity both 90%). Feissel and colleagues21 calculated IVC variation as the difference in diameters divided by the mean of the diameters while patients were ventilated with tidal volumes of 8 to 10 mL/kg. A threshold IVC variation of 12% separated responders from nonresponders (positive and negative predictive values of 93% and 92%, respectively).21 The superior vena cava also varies with respiration, and its distensibility index may be an even better predictor of fluid responsiveness,29 but it requires transesophageal echocardiography and is beyond the scope of this review. Arterial Doppler Flow and Variation Doppler methods allow measurement of the aortic blood velocity and calculation of the velocity-time integral (VTI). SV can be measured as the product of the VTI and LV outfl flow tract (LVOT) cross-sectional area. Respiratory changes in peak aortic flow velocity are quite accurate in distinguishing fluid fl responders from nonresponders (threshold value, 12%; sensitivity, 100%; specificity, fi 89%).16 Although this study used transesophageal echocardiography, the LVOT VTI can be measured with transthoracic echocardiography as well. Similar methods can be applied to measure journal.publications.chestnet.org
brachial artery peak flow velocity variation near the antecubital fossa, and this both correlates well with fl arterial pulse pressure variation30 and predicts fluid responsiveness.31 Passive Leg Raising Raising a patient’s legs reduces the unstressed volume of the circulation, effectively mimicking the effects of a reversible fluid bolus. The method involves making an initial measurement of cardiac output from the VTI of the LVOT in the semirecumbent position (45° head-of-bed elevation), then tilting the patient (without changing the angle between legs and trunk) so that the lower limbs are raised to 45°, and measuring r again the SV or a surrogate (threshold values for SV variation by transthoracic echocardiography 5 12.5%,17 SV variation using Flotrac [Edwards Lifesciences, fl variation 5 8%33). LLC] 5 16%,32 and aortic blood flow Measuring the change in femoral artery flow velocity with PLR provides an alternative to echocardiography for assessing the SV response.33 A major advantage of PLR-based predictions of fluid responsiveness is that actively breathing patients and those with arrhythmias can also be assessed. For example, in a group of 71 ventilated subjects, roughly one-half of whom had either spontaneous breathing or arrhythmias, PLR was 97% sensitive and 94% specific. fi 20 Several other studies have corroborated these findfi ings.20,32-35 All the aforementioned methods that involve measurement of blood flow velocity or VTI require competence in Doppler measurements and are, therefore, not performed as part of GDE. Recognizing Untoward Effects of Further Fluids The decision to infuse fluids fl should be paired with a plan to recognize its end points, the simplest of which is resolution of the shock. When shock persists, additional ultrasonographic findings may be useful. First, fl fluid responsiveness may be remeasured: if the circulation no longer varies much with passive respiration, additional fluids fl are not likely to be helpful and may be harmful. A common hazard of excessive volume infusion is pulmonary edema, so lung ultrasonography may be helpful in guiding volume infusion. The presence of A lines in the anterior lung zone predicts that the PAOP is below 18 mm with a high degree of certainty.36 This pattern allows the intensivist to proceed with volume infusion with safety regarding the risk of hydrostatic pulmonary edema, although it does not aid in determining whether the circulation is fluid responsive. The presence of extensive, profuse, anterior lung zone B lines, in combination with a smooth pleural line, is both sensitive and specifi fic for hydrostatic pulmonary edema and might CHEST / 142 / 4 / OCTOBER 2012
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contraindicate further volume resuscitation.377 The PAOP can be estimated by echocardiography,38 but this requires training in Doppler measurement and is not part of GDE. The presence of a high filling fi pressure would contraindicate further volume resuscitation for fear of producing hydrostatic pulmonary edema. The central venous pressure can be estimated by using ultrasound to visualize the collapse point of the internal jugular vein, although this has little usefulness in identifying fluid responsiveness.39 Practical Application of GDE for Determination of Fluid Responsiveness By definition, fi the intensivist with profi ficiency in GDE is not trained to perform Doppler-based measurements of cardiac function. Many measurements of preload sensitivity require knowledge of Doppler because they rely on measurement of blood flow fl velocity across the respiratory cycle or on straight leg raising. Realistically, the intensivist with proficiency fi in GDE alone is limited to the study of IVC dynamics. A limitation of this method is that the patient must be on ventilatory support, without any spontaneous respiratory effort. In this case, IVC variation is a well-validated method and should be the preferred method for determining fluid responsiveness. If the patient is breathing spontaneously or on a ventilator but making respiratory effort, the authors use the following pragmatic approach to identify fluid fl responsiveness in the patient in shock: 1. If the left ventricle is hyperdynamic with endsystolic effacement, there is a high probability of fluid responsiveness. 2. If the IVC is , 1 cm in diameter, there is a high probability of fluid responsiveness. 3. If the IVC is . 2.5 cm in diameter, there is a low probability of fluid responsiveness. 4. If the IVC is between 1 and 2.5 cm, there is an indeterminate probability of fluid fl responsiveness. Is There Evidence of Pump Failure? If So, What Is the Pattern and What Is the Appropriate Therapeutic Response? A major goal of early GDE is to define fi the underlying cause of shock. GDE allows the intensivist to quickly assess whether pump failure is the cause of the hemodynamic crisis. Pump failure may be subcategorized into LV, RV, or valvular causes, each of which may result in a different management strategy. Categorization of pump dysfunction allows the intensivist to develop a management plan. Occasionally, echocardiography results will lead to an immediate life-saving intervention, as discussed. More 1046
commonly, the results will not identify an immediately remediable cause for the shock, but they serve to guide evaluation and management. For example, the pattern of end-systolic effacement of the left ventricle with a virtual (collapsed) IVC mandates volume resuscitation (Video 6), and acute cor pulmonale pattern with massive RV dilation specifically fi contraindicates volume resuscitation and requires evaluation for the cause of RV failure (Video 7), whereas severe LV dysfunction cautions against major volume resuscitation and favors inotropic support rather than vasopressor use (Video 8). Sepsis is a common cause of shock in the ICU. Echocardiography may show normal LV function (Video 9). In this case, the focus should be on vasoconstrictor infusion rather than inotropes to counteract the vasoplegia of septic shock. Reversible LV dysfunction is commonly observed fl in septic shock.40 If this is associated with a low-flow state, a mixed inotrope-vasopressor may be indicated. In this case, it is important to do serial GDE to document the improvement in LV function that frequently occurs with remission of septic shock. Otherwise, the patient may be labeled inappropriately as having permanent LV dysfunction. The value of GDE is in guiding volume resuscitation and vasoactive drug infusion in logical fashion. Is There More Than One Cause for the Shock State, or Are There Findings That Will Complicate Management of Hemodynamic Failure? GDE may detect more than one cause for the shock state or may identify findings fi that complicate the management of the primary cause. This is especially problematic in patients with chronic, complex illness, especially in the elderly patient with shock. For example, septic shock may coexist with severe aortic stenosis, or a massive pulmonary embolism with acute cor pulmonale may be complicated by preexisting severe LV dysfunction. Sorting out what is a new abnormality from preexisting pump failure is challenging. GDE results must always be interpreted within the context of the overall clinical picture. Is the Cause of the Shock State Other Than Cardiac in Origin? Would Ultrasonography of Other Organ Systems Be Useful in Rendering a Diagnosis? Although GDE is the mainstay for the assessment of hemodynamic failure, general critical care ultrasonography is useful as a total body approach to the assessment of the patient with shock. Using the skill set defined fi in the Competence Statement, the intensivist is uniquely qualifi fied in other aspects of the Postgraduate Education Corner
ultrasound examination that are useful in identifying the source of the hemodynamic failure. With a wholebody ultrasound approach, thoracic, abdominal, and vascular ultrasonography are used to search for causes of shock. Lung ultrasonography is more sensitive than conventional chest radiography for detecting pneumothorax41 and may facilitate recognition of tension as the cause of shock. A generalized normal aeration pattern on lung ultrasonography in the patient with shock, in concert with a finding fi of DVT on vascular examination, is strongly associated with pulmonary embolism.42 Intensivists are able to diagnose DVT with an accuracy similar to that of conventional technicianperformed compression ultrasound d43; this skill is useful for the rapid assessment of shock where pulmonary embolism is within the differential. Identifying lung consolidation supports a diagnosis of septic shock, whereas various other fi findings (hydronephrosis, abdominal free fluid, fl biliary dilation) may point to an abdominal source. Screening abdominal ultrasonography may also reveal a bleeding abdominal aneurysm, dissection (Video 10), peritonitis, ischemic bowel, or abdominal free air. The intensivist may use GDE as a primary tool for assessment of shock but extends the ultrasound examination when clinically indicated.
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Acknowledgments Financial/nonfi financial disclosures: The authors have reported to CHEST T that no potential confl flicts of interest exist with any companies/organizations whose products or services may be discussed in this article. Additional information: The Videos can be found in the “Supplemental Materials” area of the online article.
References 1. Mayo PH, Beaulieu Y, Doelken P, et al. American College of Chest Physicians/La Société de Réanimation de Langue Française statement on competence in critical care ultrasonography. Chest. 2009;135(4):1050-1060. 2. Expert Round Table on Ultrasound in ICU. International expert statement on training standards for critical care ultrasonography. Intensive Care Med. 2011;37(7):1077-1083. 3. Mandavia DP, Hoffner RJ, Mahaney K, Henderson SO. Bedside echocardiography by emergency physicians. Ann Emerg Med. 2001;38(4):377-382. 4. Vignon P, Chastagner C, François B, et al. Diagnostic ability of hand-held echocardiography in ventilated critically ill patients. Crit Care. 2003;7(5):R84-R91. 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. Pediatrics. 2004;114(6): e667-e671. 6. Melamed R, Sprenkle MD, Ulstad VK, Herzog CA, Leatherman JW. Assessment of left ventricular function by intensivists using hand-held echocardiography. Chest. 2009; 135(6):1416-1420. 7. Manasia AR, Nagaraj HM, Kodali RB, et al. Feasibility and potential clinical utility of goal-directed transthoracic journal.publications.chestnet.org
17.
18. 19. 20. 21. 22. 23.
24. 25. 26.
echocardiography performed by noncardiologist intensivists using a small hand-carried device (SonoHeart) in critically ill patients. J Cardiothorac Vasc Anesth. 2005;19(2):155-159. Vignon P, Dugard A, Abraham J, et al. Focused training for goal-oriented hand-held echocardiography performed by noncardiologist residents in the intensive care unit. Intensive Care Med. 2007;33(10):1795-1799. Vignon P, Mücke F, Bellec F, et al. Basic critical care echocardiography: validation of a curriculum dedicated to noncardiologist residents. Crit Care Med. 2011;39(4):636-642. Durairaj L, Schmidt GA. Fluid therapy in resuscitated sepsis: less is more. Chest. 2008;133(1):252-263. Marik PE, Baram M, Vahid B. Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares. Chest. 2008;134(1): 172-178. Michard F, Teboul JL. Predicting fl fluid responsiveness in ICU patients: a critical analysis of the evidence. Chestt. 2002;121(6): 2000-2008. Kumar A, Anel R, Bunnell E, et al. Pulmonary artery occlusion pressure and central venous pressure fail to predict ventricular filling volume, cardiac performance, or the response to volume infusion in normal subjects. Crit Care Med. 2004; 32(3):691-699. Tavernier B, Makhotine O, Lebuffe G, Dupont J, Scherpereel P. Systolic pressure variation as a guide to fluid therapy in patients with sepsis-induced hypotension. Anesthesiology. 1998;89(6): 1313-1321. Tousignant CP, Walsh F, Mazer CD. The use of transesophageal echocardiography for preload assessment in critically ill patients. Anesth Analg. 2000;90(2):351-355. Feissel M, Michard F, Mangin I, Ruyer O, Faller JP, Teboul JL. Respiratory changes in aortic blood velocity as an indicator of fluid responsiveness in ventilated patients with septic shock. fl Chest. 2001;119(3):867-873. Lamia B, Ochagavia A, Monnet X, Chemla D, Richard C, Teboul JL. Echocardiographic prediction of volume responsiveness in critically ill patients with spontaneously breathing activity. Intensive Care Med. 2007;33(7):1125-1132. Solus-Biguenet H, Fleyfel M, Tavernier B, et al. Non-invasive prediction of fluid responsiveness during major hepatic surgery. Br J Anaesth. 2006;97(6):808-816. Monnet X, Rienzo M, Osman D, et al. Esophageal Doppler monitoring predicts fluid responsiveness in critically ill ventilated patients. Intensive Care Med. 2005;31(9):1195-1201. Monnet X, Rienzo M, Osman D, et al. Passive leg raising predicts fluid responsiveness in the critically ill. Crit Care Med. d 2006;34(5):1402-1407. Feissel M, Michard F, Faller J-P, Teboul JL. The respiratory variation in inferior vena cava diameter as a guide to fluid fl therapy. Intensive Care Med. 2004;30(9):1834-1837. Brennan JM, Blair JE, Goonewardena S, et al. Reappraisal of the use of inferior vena cava for estimating right atrial pressure. J Am Soc Echocardiogrr. 2007;20(7):857-861. Vieillard-Baron A, Loubières Y, Schmitt JM, Page B, Dubourg O, Jardin F. Cyclic changes in right ventricular output impedance during mechanical ventilation. J Appl Physiol. 1999;87(5): 1644-1650. Brower R, Wise RA, Hassapoyannes C, Bromberger-Barnea B, Permutt S. Effect of lung inflation fl on lung blood volume and pulmonary venous flow fl . J Appl Physiol. 1985;58(3):954-963. Fessler HE, Brower RG, Wise RA, Permutt S. Mechanism of reduced LV afterload by systolic and diastolic positive pleural pressure. J Appl Physiol. 1988;65(3):1244-1250. De Backer D, Heenen S, Piagnerelli M, Koch M, Vincent JL. Pulse pressure variations to predict fluid fl responsiveness: infl fluence of tidal volume. Intensive Care Med. d 2005;31(4):517-523. CHEST / 142 / 4 / OCTOBER 2012
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27. Heenen S, De Backer D, Vincent JL. How can the response to volume expansion in patients with spontaneous respiratory movements be predicted? Crit Care. 2006;10(4):R102. 28. Barbier C, Loubières Y, Schmit C, et al. Respiratory changes in inferior vena cava diameter are helpful in predicting fluid fl responsiveness in ventilated septic patients. Intensive Care Med. 2004;30(9):1740-1746. 29. Vieillard-Baron A, Chergui K, Rabiller A, et al. Superior vena caval collapsibility as a gauge of volume status in ventilated septic patients. Intensive Care Med. 2004;30(9):1734-1739. 30. Brennan JM, Blair JEA, Hampole C, et al. Radial artery pulse pressure variation correlates with brachial artery peak velocity variation in ventilated subjects when measured by internal medicine residents using hand-carried ultrasound devices. Chest. 2007;131(5):1301-1307. 31. Monge García MI, Gil Cano A, Díaz Monrové JC. Brachial artery peak velocity variation to predict fluid responsiveness in mechanically ventilated patients. Crit Care. 2009;13(5): R142. 32. Lafanechère A, Pène F, Goulenok C, et al. Changes in aortic blood flow induced by passive leg raising predict fluid responsiveness in critically ill patients. Crit Care. 2006;10(5):R132. 33. Préau S, Saulnier F, Dewavrin F, Durocher A, Chagnon JL. Passive leg raising is predictive of fluid responsiveness in spontaneously breathing patients with severe sepsis or acute pancreatitis. Crit Care Med. 2010;38(3):819-825. 34. Biais M, Vidil L, Sarrabay P, Cottenceau V, Revel P, Sztarkk F. Changes in stroke volume induced by passive leg raising in spontaneously breathing patients: comparison between echocardiography and Vigileo/FloTrac device. Crit Care. 2009; 13(6):R195.
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35. Thiel SW, Kollef MH, Isakow W. Non-invasive stroke volume measurement and passive leg raising predict volume responsiveness in medical ICU patients: an observational cohort study. Crit Care. 2009;13(4):R111. 36. Lichtenstein DA, Mezière GA, Lagoueyte JF, Biderman P, Goldstein I, Gepner A. A-lines and B-lines: lung ultrasound as a bedside tool for predicting pulmonary artery occlusion pressure in the critically ill. Chest. 2009;136(4):1014-1020. 37. Copetti R, Soldati G, Copetti P. Chest sonography: a useful tool to differentiate acute cardiogenic pulmonary edema from acute respiratory distress syndrome. Cardiovasc Ultrasound. 2008;6:16. 38. Nagueh SF, Appleton CP, Gillebert TC, et al. Recommendations for the evaluation of left ventricular diastolic function by echocardiography. J Am Soc Echocardiogr. r 2009;22(2):107-133. 39. Deol GR, Collett N, Ashby A, Schmidt GA. Ultrasound accurately refl flects the jugular venous examination but underestimates central venous pressure. Chest. 2011;139(1):95-100. 40. Vieillard-Baron A. Septic cardiomyopathy. Ann Intensive Care. 2011;1(1):6. 41. Soldati G, Testa A, Sher S, Pignataro G, La Sala M, Silverii NG. Occult traumatic pneumothorax: diagnostic accuracy of lung ultrasonography in the emergency department. Chest. 2008; 133(1):204-211. 42. Lichtenstein DA, Mezière GA. Relevance of lung ultrasound in the diagnosis of acute respiratory failure: the BLUE protocol. Chest. 2008;134(1):117-125. 43. Kory PD, Pellecchia CM, Shiloh AL, Mayo PH, DiBello C, Koenig S. Accuracy of ultrasonography performed by critical care physicians for the diagnosis of DVT. Chest. 2011;139(3): 538-542.
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