Three-view bedside ultrasound to differentiate acute decompensated heart failure from chronic obstructive pulmonary disease

Three-view bedside ultrasound to differentiate acute decompensated heart failure from chronic obstructive pulmonary disease

American Journal of Emergency Medicine 31 (2013) 759.e3–759.e5 Contents lists available at SciVerse ScienceDirect American Journal of Emergency Medi...

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American Journal of Emergency Medicine 31 (2013) 759.e3–759.e5

Contents lists available at SciVerse ScienceDirect

American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem

Case Report

Three-view bedside ultrasound to differentiate acute decompensated heart failure from chronic obstructive pulmonary disease☆,☆☆,★

Abstract Identifying the cause of acute dyspnea in the emergency department is often challenging, even for the most experienced provider. Distinguishing chronic obstructive pulmonary disease from acute decompensated heart failure in the acutely dyspneic patient who presents in respiratory distress is often difficult. Patients are often unable to give a detailed history when in extremis, yet primary management needs to be initiated before further testing can be completed. Bedside diagnostic ultrasound has emerged as a tool for emergency physicians to rapidly evaluate the cardiopulmonary status in patients presenting with undifferentiated shortness of breath [1-3]. A rapid 3-view sonographic evaluation of the heart, lungs, and inferior vena cava or “Triple Scan” may be a useful tool in identifying the cause of acute dyspnea and may aid the clinician in the initial management of the critically ill dyspneic patient. We present a case where a 3-view ultrasound examination, the “Triple Scan,” allowed for detection of new onset congestive heart failure and initiation of appropriate medical therapy without waiting for further standard diagnostic testing. A 54-year-old male smoker with history of chronic obstructive pulmonary disease (COPD) presented to the emergency department (ED) complaining of gradually progressive shortness of breath and productive cough for 2 weeks. The review of systems was notable for an absence of fever or chest pain but presence of worsening bilateral lower extremity swelling for 2 weeks. Six weeks earlier, he was diagnosed with a lower extremity deep venous thrombosis and began oral warfarin therapy. During that hospitalization, an intravenous computed tomography of the chest was negative for pulmonary embolism, and comprehensive echocardiography revealed a left ventricular (LV) ejection fraction of 50%. The vital signs were blood pressure of 142/98 mm Hg, pulse rate of 120 beats per minute, respirations of 24 breaths per minute, and SaO2 of 94% on room air. He was in moderate respiratory distress and able to speak in only 4- to 5-word sentences. There was no jugular venous distension. He had bilateral diffuse expiratory wheezes, and no murmurs or gallops were appreciated. Examination of the lower extremities revealed mild bilateral pitting edema to the knees. A portable anteroposterior chest radiograph was interpreted by the radiologist as flattened bilateral hemidiaphragms and bullous disease with no cardiomegaly, infiltrates, or signs of pulmonary edema (Fig. 1). ☆ This has not been submitted to another publication. ☆☆ There are no conflicts of interest. ★ There are no copyright restraints. 0735-6757/$ – see front matter © 2013 Elsevier Inc. All rights reserved.

After evaluation by a senior emergency medicine provider, the patient was treated in the ED with nebulized albuterol and ipratropium and oral prednisone. Approximately 15 minutes after initiation of β-2 agonist therapy, the patient's heart rate increased to 140 to 160 beats per minute, and an electrocardiogram demonstrated atrial flutter with variable atrioventricular block and low-voltage QRS. Because of the change in the patient's clinical status, a 3-view bedside ultrasound examination was performed. The cardiac examination revealed grossly diminished LV contractility without right ventricular (RV) enlargement or pericardial effusion (Fig. 2A). The lung examination revealed diffuse B-lines (lung rockets) in bilateral anterior lung fields (Fig. 2B). The inferior vena cava (IVC) examination revealed a plethoric vena cava with no collapse during the respiratory cycle (Fig. 3). A diagnosis of acute decompensated heart failure (ADHF) was made at the bedside, and β-2 agonist therapy was discontinued. Continuous positive airway pressure and intravenous furosemide were administered. The patient's cardiac rhythm returned to sinus tachycardia at 120 beats per minute, and subsequent brain natriuretic peptide level was 1805 pg/mL. An in-patient comprehensive echocardiography reported a LV ejection fraction of 10% to 15%, and computed tomography of the chest with intravenous contrast was again negative for pulmonary embolus. Emergency department studies have demonstrated the accuracy of bedside focused cardiac ultrasound in accurately estimating gross LV contractility, determining the presence or absence of pulmonary interstitial fluid on lung ultrasound, and estimating central venous pressures by assessing the change in diameter of the IVC during the respiratory cycle [1-5]. These rapid bedside point-of-care studies can provide reliable information in regard to the cardiopulmonary status of the acutely dyspneic patient. The physical examination, even with the addition of chest radiography, cannot reliably differentiate ADHF from COPD, two conditions with significantly different treatment strategies [6-8]. At our institution, we have adopted a focused point-of-care ultrasound protocol for patients with undifferentiated respiratory distress coined the “Triple Scan.” The examination consists of limited transthoracic echocardiography, sonographic evaluation of both the lungs/pleura, and assessment of IVC respirophasic collapsibility. Numerous studies have demonstrated that individually, each component of the examination can aid in the diagnosis of ADHF and when used in combination can better differentiate ADHF from other causes of respiratory distress [1,2,5,9,10]. Focused echocardiography is used to evaluate global LV function by gross visual estimation and determine the presence or absence of a pericardial effusion or right ventricular enlargement that could be suggestive of pulmonary hypertension or a large pulmonary embolism. Pulmonary ultrasound

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Case Report / American Journal of Emergency Medicine 31 (2013) 759.e3–759.e5

Fig. 3. Subxyphoid view of a large IVC without collapse during the respiratory cycle.

Fig. 1. Anteroposterior chest radiograph initially interpreted by radiology as flattened bilateral hemidiaphragms and bullous disease with no cardiomegaly, infiltrates, or signs of pulmonary edema.

of the anterior chest identifies the presence of diffuse anterior B-lines, which are artifacts arising from the pleura representing alveolar interstitial syndrome. Alveolar interstitial syndrome most often signifies either cardiogenic or noncardiogenic pulmonary edema but can also occur with pulmonary fibrosis [2,10]. Previous studies have shown that bilateral B-lines are 97% to 100% sensitive for pulmonary edema [2,11]. The absence of sonographic B-lines essentially rules out ADHF despite a low LV ejection fraction [12]. Evaluation of the IVC size and collapsibility is used to predict right-sided cardiac pressures and/ or CVP. A large or plethoric IVC that does not collapse during inspiration is consistent with ADHF but can also with pulmonary hypertension, tricuspid regurgitation, pulmonary embolism, and cardiac tamponade [3,9]. In contrast, a flat IVC or one that collapses more than 50% during the respiratory cycle strongly suggests a low central venous pressure and would be inconsistent with an episode of ADHF [3,9,10]. In our case, the Triple Scan accurately and rapidly identified the etiology of acute dyspnea without testing delay, allowing for appropriate medical therapies that improved our patient's cardiopulmonary status. The patient's normal recent comprehensive echocardiography and history of COPD allowed the initial clinicians to assume

a noncardiogenic etiology of his acute dyspnea. Chest radiograph, considered a more objective classic test, did not demonstrate cardiomegaly or pulmonary edema. After clinical deterioration with β-agonist therapy, ultrasound evaluation with the Triple Scan clearly demonstrated ADHF. A decreased ejection fraction from the parasternal views of the LV, bilateral B-lines in the anterior chest wall, and a plethoric IVC indicated acute decompensated congestive heart failure and facilitated appropriate therapy and further diagnostic testing. The Triple Scan may be an ideal adjunct to the clinical examination in patients who present to the ED with an unclear cause of acute respiratory distress. Daniel Mantuani MD Department of Emergency Medicine Alameda County Medical Center, Highland General Hospital Oakland, CA 94602, USA E-mail address: [email protected] Arun Nagdev MD Emergency Ultrasound, Alameda County Medical Center Highland General Hospital, Oakland, CA 94602, USA UCSF School of Medicine http://dx.doi.org/10.1016/j.ajem.2012.11.028

Fig. 2. A, Bedside echocardiography parasternal long view showing poor LV contractility. RV, right ventricle; AO, aortic outflow tract; LA, left atrium. B, Lung ultrasound of anterior lung fields demonstrating multiple B-line artifacts suggesting cardiogenic pulmonary edema. Asterisks indicate B-line artifacts arising from pleural line.

Case Report / American Journal of Emergency Medicine 31 (2013) 759.e3–759.e5

References [1] Randazzo MR, Snoey ER, Levitt MA, Binder K. Accuracy of emergency physician assessment of left ventricular ejection fraction and central venous pressure using echocardiography. Acad Emerg Med 2003;10(9):973-7. [2] Lichtenstein DA, Mezière GA. Relevance of lung ultrasound in the diagnosis of acute respiratory failure: the BLUE protocol. Chest 2008;134(1):117-25. [3] Nagdev AD, Merchant RC, Tirado-Gonzalez A, Sisson CA, Murphy MC. Emergency department bedside ultrasonographic measurement of the caval index for noninvasive determination of low central venous pressure. Ann Emerg Med 2010;55(3):290-5. [4] Moore CI, Rose GA, Tayal VS, et al. Determination of left ventricular function by emergency physician echocardiography of hypotensive patients. Acad Emerg Med 2002;9(3):186-93. [5] Liteplo AS, Marill KA, Villen T, Miller RM, Murray AF, Croft PE, et al. Emergency thoracic ultrasound in the differentiation of the etiology of shortness of breath (ETUDES): sonographic B-lines and N-terminal pro-brain-type natriuretic peptide in diagnosing congestive heart failure. Acad Emerg Med 2009;16(3): 201-10.

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[6] Wang CS, FitzGerald JM, Schulzer M, Mak E, Ayas NT. Does this dyspneic patient in the emergency department have congestive heart failure? JAMA 2005;294(15):1944-56. [7] Collins SP, Lindsell CJ, Storrow AB, et al. Prevalence of negative chest radiography results in the emergency patient with decompensated heart failure. Ann Emerg Med 2006;47(1):13-8. [8] Singer AJ, Emerman C, Char DM, et al. Bronchodilator therapy in acute decompensated heart failure patients without a history of chronic obstructive pulmonary disease. Ann Emerg Med 2008;51(1):25-34. [9] Blehar DJ, Dickman E, Gaspari R. Identification of congestive heart failure via respiratory variation of inferior vena cava diameter. Am J Emerg Med 2009;27(1): 71-5. [10] Mantuani D, Nagdev A, Stone M. Three-view bedside ultrasound for the differentiation of acute respiratory distress syndrome from cardiogenic pulmonary edema. Am J Emerg Med 2012;30(7):1324-8. [11] Lichtenstein DA, Meziere G. A lung ultrasound sign allowing bedside distinction between pulmonary edema and COPD: the comet-tail artifact. Intensive Care Med 1998;24(12):1331-4. [12] Lichtenstein DA. Ultrasound in the management of thoracic disease. Crit Care Med 2007;35(5):S250-61.