- Email: [email protected]
A Man in His 40s With Fever and Hypotension
CHEST
Postgraduate Education Corner ULTRASOUND CORNER
A Man in His 40s With Fever and Hypotension Samir Raza, MD; and Robert Arntfield, MD, FCCP
CHEST 2014; 145(6):e17–e19
in his 40s presented to the ED complaining A man of chills and rigors. He had undergone prostate
biopsy earlier that day. The patient denied cough, purulent sputum, shortness of breath, nausea, vomiting, or chest pain. He had a medical history of hypertension and hypercholesterolemia for which he took metoprolol and atorvastatin, respectively. Six months previous, he was found to have elevated prostate-specific antigen levels, which led to the biopsy. On presentation, the patient was flushed, diaphoretic, febrile (temperature, 39.4°C), tachycardic (heart rate, 119 beats/min), normotensive (BP, 141/78 mm Hg), and breathing comfortably on room air. Physical examination was otherwise unremarkable, showing a normal precordial examination; good breath sounds bilaterally without rales; a soft, nontender abdomen; and no signs of rash. Initial blood work was unremarkable. A portable chest radiograph showed no signs of pneumonia or heart failure (Fig 1). A working diagnosis of bacteremia as a complication of prostate biopsy was made. The patient received 2 L crystalloid infusion and a broad-spectrum antibiotic and was admitted to the urology service for ongoing management. The patient became increasingly unstable overnight. His heart rate increased to 140 beats/min and BP dropped to 92/49 mm Hg, and he required high-flow oxygen by nonrebreather mask to maintain an oxygen saturation . 92%. The emergency physician performed a focused, bedside ultrasound to evalManuscript received September 15, 2013; revision accepted February 3, 2014. Affiliations: From the Department of Internal Medicine (Dr Raza), McMaster University, Hamilton, ON; and Department of Critical Care and Emergency Medicine (Dr Arntfield), The University of Western Ontario, London, ON, Canada. Correspondence to: Samir Raza, MD, Department of Internal Medicine, McMaster University, 1280 Main St W, Hamilton, ON, L8S 4L8, Canada; e-mail: [email protected] © 2014 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.13-1865 journal.publications.chestnet.org
Figure 1. Chest radiograph on presentation to ED.
uate for a cause of the patient’s respiratory failure and shock (Video 1). An additional 2 L crystalloid was administered, but the patient became increasingly hypotensive. Arterial blood analysis revealed a lactate level of 8.3 mg/dL. Infusions of norepinephrine 0.15 mg/kg/min and vasopressin 2.4 units/h were initiated, and the patient was admitted to the ICU. Noninvasive ventilation was initiated to reduce his work of breathing. Shortly after admission, the ICU team performed a repeat pointof-care ultrasound study (Videos 2-6). Based on these videos and the patient’s clinical history and physical examination findings, what is the likely diagnosis?
CHEST / 145 / 6 / JUNE 2014
e17
Answer: Sepsis-induced cardiomyopathy with cardiogenic pulmonary edema
Discussion The initial bedside echocardiogram shows a hyperdynamic left ventricle (elevated ejection fraction) (Video 1), whereas Videos 2 through 4 show depressed left ventricular (LV) function (decreased ejection fraction). In the context of sepsis, this rapid decline in LV function from hyperdynamic to severe is likely sepsis-induced cardiomyopathy with cardiogenic pulmonary edema (Videos 5 and 6, showing bilateral B lines). This case illustrates the challenges of managing sepsis and highlights the need for serial patient assessments. In the time-sensitive critical care setting, obtaining clear multiple views during bedside echocardiogram often is difficult, as reflected by only a single highquality view obtained in the ED. Video 1 of the parasternal long-axis view demonstrates a hyperdynamic left ventricle as indicated by near-complete collapse or obliteration of the LV cavity. In more grave forms of sepsis, significant vasodilation and vasoplegia are present. In response to this decrease in systemic vascular resistance is reduced cardiac afterload and a corresponding increase in stroke volume and ejection fraction. Evidence indicates that a hyperdynamic left ventricle in the context of nontraumatic, undifferentiated hypotension is in itself highly specific for sepsis as the etiology of shock.1 Furthermore, visual or qualitative estimates of LV function (LVF) agree with quantitative measurements of LVF in patients presenting to the ED with hypotension.2 Importantly, novice cliniciansonographers have been shown to be accurate in providing estimates of LVF derived from point-of-care echocardiograms.3,4
Septic Cardiomyopathy The present patient showed decreased LVF in parasternal long-axis view (Video 2), parasternal shortaxis view (Video 3), and apical four-chamber view (Video 4). Several hours elapsed between Videos 1 and 2 through 4. During this time, the patient progressed from severe sepsis to septic shock, and vasopressors were initiated. This deterioration of LVF in the context of sepsis is termed septic cardiomyopathy (SCM). SCM is an acute reversible myocardial depression5,6 associated with normal or low LV filling pressures as opposed to cardiogenic shock. The mechanism of SCM, although not well understood, is believed to be cytokine mediated. Coronary hypoperfusion is not implicated in SCM. LV afterload can have a significant impact on cardiac output. As seen in Video 1, the ejection fraction is near 100% because afterload is very low from significant vasodilation. With fluid resuscitation and vasopressors, afterload will increase sharply and unmask the depressed myocardial function of SCM as seen in Videos 2 through 4.7 In sepsis, ejection fraction on its own is not a reliable indicator of myocardial contractility. With the increasing availability of bedside echocardiogram, SCM is being recognized earlier and more frequently. Studies have shown an 18% incidence of LV systolic dysfunction in septic shock when echocardiograms are performed within 6 h.8 Incidence increases to 60% when performed after 2 or 3 days.9 SCM is not selective for the left ventricle because right ventricular dysfunction is also common in SCM and was seen in nearly 30% of patients in one study.8 Assessing LVF In time-sensitive settings, such as undifferentiated shock, qualitative assessments of LVF are usually performed. As mentioned, the literature shows a high
Table 1—Qualitative and Quantitative Methods of Assessing LV Function Method Qualitative assessment Observe for symmetric endocardial wall motion, wall thickening, and change in LV cavity size Classify EF as normal (50%-70%), impaired (30%-50%), severely impaired (, 30%), or hyperdynamic (ⱖ 70%) Quantitative assessment Fractional shortening: the difference between the LV diastolic and systolic internal diameters using parasternal long-axis or parasternal short-axis views (normal, 25%-45%) Fractional area change: change in cross-sectional area between end systole and end diastole using parasternal short-axis view (normal, . 45%) Modified Simpson’s rule: typically, used in comprehensive, diagnostic echocardiography, the algorithm calculates EF by estimating systolic and diastolic volumes in two different planes perpendicular to each other. Tissue Doppler echocardiography: mitral annular descent velocity (normal range, 8-10 cm/s) EF 5 ejection fraction; LV 5 left ventricular. e18
Postgraduate Education Corner
degree of agreeability between qualitative and more formal quantitative assessments. Table 1 summarizes methods of determining LVF; this article focuses on qualitative methods. During qualitative assessment, a normal left ventricle should have symmetric endocardial wall motion and wall thickening. It is important to image the heart in at least two different planes to ensure accurate qualitative determination of systolic function. For example, in the parasternal short-axis view, a plane too close to the apex may result in a falsely normal or even hyperdynamic interpretation. In the parasternal longaxis view, a plane too near the lateral wall may again result in overestimation of systolic function. Multiple imaging planes minimize the chance of error in determining systolic function. Discussion Video 1 provides an introduction to qualitative LV assessment. Interstitial Syndrome Discussion Video 2 shows the present patient’s thoracic ultrasound with bilateral B lines consistent with interstitial syndrome. In a decompensating patient with sepsis, pulmonary edema, ARDS, or pneumonia should always be considered. B lines are produced by conditions with interlobular septal thickening, such as pulmonary edema, multifocal pneumonia, ARDS, interstitial lung disease and fibrosis, and metastatic disease. A recent CHEST Ultrasound Corner article has provided further elaboration on the diagnosis and significance of B lines.10 With judicious use of IV fluids and broad-spectrum antibiotics, the patient slowly improved and was weaned from vasopressors. Point-of-care echocardiogram was repeated 5 days postadmission and showed normal LVF. The patient was discharged home 7 days postadmission. Reverberations 1. LVF can be accurately determined by a novice clinician-sonographer using qualitative methods. 2. A hyperdynamic left ventricle in the context of medical hypotension is highly specific for sepsis.
journal.publications.chestnet.org
3. SCM results in reversible global LV dysfunction, and serial goal-directed echocardiograms can aid in its diagnosis and management. Acknowledgments Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article. Other contributions: CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met. The authors thank Ryan Smith, MD, and Drew Thompson, MD, for image acquisition. Additional information: To analyze this case with the videos, see the online article.
References 1. Jones AE, Craddock PA, Tayal VS, Kline JA. Diagnostic accuracy of left ventricular function for identifying sepsis among emergency department patients with nontraumatic symptomatic undifferentiated hypotension. Shock. 2005;24(6): 513-517. 2. Weekes AJ, Tassone HM, Babcock A, et al. Comparison of serial qualitative and quantitative assessments of caval index and left ventricular systolic function during early fluid resuscitation of hypotensive emergency department patients. Acad Emerg Med. 2011;18(9):912-921. 3. 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. 4. Moore CL, Rose GA, Tayal VS, Sullivan DM, Arrowood JA, Kline JA. Determination of left ventricular function by emergency physician echocardiography of hypotensive patients. Acad Emerg Med. 2002;9(3):186-193. 5. Parker MM, Shelhamer JH, Bacharach SL, et al. Profound but reversible myocardial depression in patients with septic shock. Ann Intern Med. 1984;100(4):483-490. 6. Natanson C, Danner RL, Elin RJ, et al. Role of endotoxemia in cardiovascular dysfunction and mortality. Escherichia coli and Staphylococcus aureus challenges in a canine model of human septic shock. J Clin Invest. 1989;83(1):243-251. 7. Robotham JL, Takata M, Berman M, Harasawa Y. Ejection fraction revisited. Anesthesiology. 1991;74(1):172-183. 8. Vieillard Baron A, Schmitt JM, Beauchet A, et al. Early preload adaptation in septic shock? A transesophageal echocardiographic study. Anesthesiology. 2001;94(3):400-406. 9. Vieillard-Baron A, Caille V, Charron C, Belliard G, Page B, Jardin F. Actual incidence of global left ventricular hypokinesia in adult septic shock. Crit Care Med. 2008;36(6):1701-1706. 10. Glen C, Acquah S, Kory P. Beyond belief. Chest. 2013; 143(3):e1-e4.
CHEST / 145 / 6 / JUNE 2014
e19
Postgraduate Education Corner ULTRASOUND CORNER
A Man in His 40s With Fever and Hypotension Samir Raza, MD; and Robert Arntfield, MD, FCCP
CHEST 2014; 145(6):e17–e19
in his 40s presented to the ED complaining A man of chills and rigors. He had undergone prostate
biopsy earlier that day. The patient denied cough, purulent sputum, shortness of breath, nausea, vomiting, or chest pain. He had a medical history of hypertension and hypercholesterolemia for which he took metoprolol and atorvastatin, respectively. Six months previous, he was found to have elevated prostate-specific antigen levels, which led to the biopsy. On presentation, the patient was flushed, diaphoretic, febrile (temperature, 39.4°C), tachycardic (heart rate, 119 beats/min), normotensive (BP, 141/78 mm Hg), and breathing comfortably on room air. Physical examination was otherwise unremarkable, showing a normal precordial examination; good breath sounds bilaterally without rales; a soft, nontender abdomen; and no signs of rash. Initial blood work was unremarkable. A portable chest radiograph showed no signs of pneumonia or heart failure (Fig 1). A working diagnosis of bacteremia as a complication of prostate biopsy was made. The patient received 2 L crystalloid infusion and a broad-spectrum antibiotic and was admitted to the urology service for ongoing management. The patient became increasingly unstable overnight. His heart rate increased to 140 beats/min and BP dropped to 92/49 mm Hg, and he required high-flow oxygen by nonrebreather mask to maintain an oxygen saturation . 92%. The emergency physician performed a focused, bedside ultrasound to evalManuscript received September 15, 2013; revision accepted February 3, 2014. Affiliations: From the Department of Internal Medicine (Dr Raza), McMaster University, Hamilton, ON; and Department of Critical Care and Emergency Medicine (Dr Arntfield), The University of Western Ontario, London, ON, Canada. Correspondence to: Samir Raza, MD, Department of Internal Medicine, McMaster University, 1280 Main St W, Hamilton, ON, L8S 4L8, Canada; e-mail: [email protected] © 2014 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.13-1865 journal.publications.chestnet.org
Figure 1. Chest radiograph on presentation to ED.
uate for a cause of the patient’s respiratory failure and shock (Video 1). An additional 2 L crystalloid was administered, but the patient became increasingly hypotensive. Arterial blood analysis revealed a lactate level of 8.3 mg/dL. Infusions of norepinephrine 0.15 mg/kg/min and vasopressin 2.4 units/h were initiated, and the patient was admitted to the ICU. Noninvasive ventilation was initiated to reduce his work of breathing. Shortly after admission, the ICU team performed a repeat pointof-care ultrasound study (Videos 2-6). Based on these videos and the patient’s clinical history and physical examination findings, what is the likely diagnosis?
CHEST / 145 / 6 / JUNE 2014
e17
Answer: Sepsis-induced cardiomyopathy with cardiogenic pulmonary edema
Discussion The initial bedside echocardiogram shows a hyperdynamic left ventricle (elevated ejection fraction) (Video 1), whereas Videos 2 through 4 show depressed left ventricular (LV) function (decreased ejection fraction). In the context of sepsis, this rapid decline in LV function from hyperdynamic to severe is likely sepsis-induced cardiomyopathy with cardiogenic pulmonary edema (Videos 5 and 6, showing bilateral B lines). This case illustrates the challenges of managing sepsis and highlights the need for serial patient assessments. In the time-sensitive critical care setting, obtaining clear multiple views during bedside echocardiogram often is difficult, as reflected by only a single highquality view obtained in the ED. Video 1 of the parasternal long-axis view demonstrates a hyperdynamic left ventricle as indicated by near-complete collapse or obliteration of the LV cavity. In more grave forms of sepsis, significant vasodilation and vasoplegia are present. In response to this decrease in systemic vascular resistance is reduced cardiac afterload and a corresponding increase in stroke volume and ejection fraction. Evidence indicates that a hyperdynamic left ventricle in the context of nontraumatic, undifferentiated hypotension is in itself highly specific for sepsis as the etiology of shock.1 Furthermore, visual or qualitative estimates of LV function (LVF) agree with quantitative measurements of LVF in patients presenting to the ED with hypotension.2 Importantly, novice cliniciansonographers have been shown to be accurate in providing estimates of LVF derived from point-of-care echocardiograms.3,4
Septic Cardiomyopathy The present patient showed decreased LVF in parasternal long-axis view (Video 2), parasternal shortaxis view (Video 3), and apical four-chamber view (Video 4). Several hours elapsed between Videos 1 and 2 through 4. During this time, the patient progressed from severe sepsis to septic shock, and vasopressors were initiated. This deterioration of LVF in the context of sepsis is termed septic cardiomyopathy (SCM). SCM is an acute reversible myocardial depression5,6 associated with normal or low LV filling pressures as opposed to cardiogenic shock. The mechanism of SCM, although not well understood, is believed to be cytokine mediated. Coronary hypoperfusion is not implicated in SCM. LV afterload can have a significant impact on cardiac output. As seen in Video 1, the ejection fraction is near 100% because afterload is very low from significant vasodilation. With fluid resuscitation and vasopressors, afterload will increase sharply and unmask the depressed myocardial function of SCM as seen in Videos 2 through 4.7 In sepsis, ejection fraction on its own is not a reliable indicator of myocardial contractility. With the increasing availability of bedside echocardiogram, SCM is being recognized earlier and more frequently. Studies have shown an 18% incidence of LV systolic dysfunction in septic shock when echocardiograms are performed within 6 h.8 Incidence increases to 60% when performed after 2 or 3 days.9 SCM is not selective for the left ventricle because right ventricular dysfunction is also common in SCM and was seen in nearly 30% of patients in one study.8 Assessing LVF In time-sensitive settings, such as undifferentiated shock, qualitative assessments of LVF are usually performed. As mentioned, the literature shows a high
Table 1—Qualitative and Quantitative Methods of Assessing LV Function Method Qualitative assessment Observe for symmetric endocardial wall motion, wall thickening, and change in LV cavity size Classify EF as normal (50%-70%), impaired (30%-50%), severely impaired (, 30%), or hyperdynamic (ⱖ 70%) Quantitative assessment Fractional shortening: the difference between the LV diastolic and systolic internal diameters using parasternal long-axis or parasternal short-axis views (normal, 25%-45%) Fractional area change: change in cross-sectional area between end systole and end diastole using parasternal short-axis view (normal, . 45%) Modified Simpson’s rule: typically, used in comprehensive, diagnostic echocardiography, the algorithm calculates EF by estimating systolic and diastolic volumes in two different planes perpendicular to each other. Tissue Doppler echocardiography: mitral annular descent velocity (normal range, 8-10 cm/s) EF 5 ejection fraction; LV 5 left ventricular. e18
Postgraduate Education Corner
degree of agreeability between qualitative and more formal quantitative assessments. Table 1 summarizes methods of determining LVF; this article focuses on qualitative methods. During qualitative assessment, a normal left ventricle should have symmetric endocardial wall motion and wall thickening. It is important to image the heart in at least two different planes to ensure accurate qualitative determination of systolic function. For example, in the parasternal short-axis view, a plane too close to the apex may result in a falsely normal or even hyperdynamic interpretation. In the parasternal longaxis view, a plane too near the lateral wall may again result in overestimation of systolic function. Multiple imaging planes minimize the chance of error in determining systolic function. Discussion Video 1 provides an introduction to qualitative LV assessment. Interstitial Syndrome Discussion Video 2 shows the present patient’s thoracic ultrasound with bilateral B lines consistent with interstitial syndrome. In a decompensating patient with sepsis, pulmonary edema, ARDS, or pneumonia should always be considered. B lines are produced by conditions with interlobular septal thickening, such as pulmonary edema, multifocal pneumonia, ARDS, interstitial lung disease and fibrosis, and metastatic disease. A recent CHEST Ultrasound Corner article has provided further elaboration on the diagnosis and significance of B lines.10 With judicious use of IV fluids and broad-spectrum antibiotics, the patient slowly improved and was weaned from vasopressors. Point-of-care echocardiogram was repeated 5 days postadmission and showed normal LVF. The patient was discharged home 7 days postadmission. Reverberations 1. LVF can be accurately determined by a novice clinician-sonographer using qualitative methods. 2. A hyperdynamic left ventricle in the context of medical hypotension is highly specific for sepsis.
journal.publications.chestnet.org
3. SCM results in reversible global LV dysfunction, and serial goal-directed echocardiograms can aid in its diagnosis and management. Acknowledgments Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article. Other contributions: CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met. The authors thank Ryan Smith, MD, and Drew Thompson, MD, for image acquisition. Additional information: To analyze this case with the videos, see the online article.
References 1. Jones AE, Craddock PA, Tayal VS, Kline JA. Diagnostic accuracy of left ventricular function for identifying sepsis among emergency department patients with nontraumatic symptomatic undifferentiated hypotension. Shock. 2005;24(6): 513-517. 2. Weekes AJ, Tassone HM, Babcock A, et al. Comparison of serial qualitative and quantitative assessments of caval index and left ventricular systolic function during early fluid resuscitation of hypotensive emergency department patients. Acad Emerg Med. 2011;18(9):912-921. 3. 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. 4. Moore CL, Rose GA, Tayal VS, Sullivan DM, Arrowood JA, Kline JA. Determination of left ventricular function by emergency physician echocardiography of hypotensive patients. Acad Emerg Med. 2002;9(3):186-193. 5. Parker MM, Shelhamer JH, Bacharach SL, et al. Profound but reversible myocardial depression in patients with septic shock. Ann Intern Med. 1984;100(4):483-490. 6. Natanson C, Danner RL, Elin RJ, et al. Role of endotoxemia in cardiovascular dysfunction and mortality. Escherichia coli and Staphylococcus aureus challenges in a canine model of human septic shock. J Clin Invest. 1989;83(1):243-251. 7. Robotham JL, Takata M, Berman M, Harasawa Y. Ejection fraction revisited. Anesthesiology. 1991;74(1):172-183. 8. Vieillard Baron A, Schmitt JM, Beauchet A, et al. Early preload adaptation in septic shock? A transesophageal echocardiographic study. Anesthesiology. 2001;94(3):400-406. 9. Vieillard-Baron A, Caille V, Charron C, Belliard G, Page B, Jardin F. Actual incidence of global left ventricular hypokinesia in adult septic shock. Crit Care Med. 2008;36(6):1701-1706. 10. Glen C, Acquah S, Kory P. Beyond belief. Chest. 2013; 143(3):e1-e4.
CHEST / 145 / 6 / JUNE 2014
e19