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A Patient With Acute COPD Exacerbation and Shock
CHEST
Postgraduate Education Corner ULTRASOUND CORNER
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A Patient With Acute COPD Exacerbation and Shock Tathagat Narula, MD; Dileep Raman, MBBS; Jonathan Wiesen, MD; Chirag Choudhary, MBBS; Anita J. Reddy, MD, FCCP; and Ajit Moghekar, MBBS
CHEST 2013; 144(6):e1–e3
elderly man with a history of COPD on home A noxygen presented to the ED with shortness of
breath of 2 days’ duration. On physical examination, the patient had jugular venous distension and distant breath sounds without rales bilaterally. Laboratory evaluation was significant for leukocytosis (29,000 WBC/mL, 94% neutrophils), acute renal failure (BUN, 87 mg/dL and creatinine, 2.36 mg/dL), and a troponin T level of 0.44 ng/mL. ECG revealed an incomplete right bundle branch block and no significant ST segment or T-wave changes. Chest radiograph revealed hyperinflated lung fields with bibasilar atelectasis without a focal opacity. Arterial blood gas analysis results were significant for combined hypoxemic and hypercapnic respiratory failure. Bilevel positive airway pressure ventilation was initiated, and the patient subsequently became hypotensive and was endotracheally intubated. The patient remained hypotensive with systolic BP in the 70 to 80 mm Hg range despite aggressive resuscitation with IV fluids. In the ED, a femoral central venous catheter (CVC) was placed, and a norepinephrine drip was initiated. The patient was then admitted to the medical ICU with
a diagnosis of acute respiratory failure due to acute exacerbation of COPD and shock. On arrival to the ICU, an assessment of mechanical ventilatory graphics for assessment of intrinsic positive end-expiratory pressure (PEEPi) revealed significant PEEPi; however, with adjustments to the ventilator modes and resolution of PEEPi, the need for vasopressors decreased but persisted. To evaluate the shock further, the intensivist should perform a bedside echocardiogram (ECHO) (Video 1). Based on the interpretation of these videos, what would be the next step in the patient’s care?
Manuscript received June 18, 2013; revision accepted August 1, 2013. Affiliations: From the Respiratory Institute, Cleveland Clinic, Cleveland, OH. Correspondence to: Ajit Moghekar, MBBS, Pulmonary, Allergy and Critical Care, Cleveland Clinic, 9500 Euclid Ave G62, Cleveland, OH 44195; e-mail: [email protected] © 2013 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.13-1412 journal.publications.chestnet.org
CHEST / 144 / 6 / DECEMBER 2013
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Next steps: Measures to identify causes of right ventricular (RV) dilatation and RV systolic failure should be pursued A subsequent bedside lower extremity ultrasound did not reveal any evidence of thrombus. A careful assessment of all the possible sources from where air could be getting entrained into the venous circulation was warranted. All of the patient’s IV accesses, including the femoral CVC and two peripheral lines, were carefully examined to exclude any breach in integrity. The bubbles only disappeared once infusions were stopped through the central line. The femoral CVC was, therefore, identified as the source of air entry into the venous system. After the CVC was capped, the patient’s hemodynamics continued to improve, and he was successfully weaned off vasopressors. A follow-up ECHO 20 min later did not show any more bubbles (see Discussion Video, Clip 8). A nasopharyngeal swab was positive for influenza A, and the patient was treated with oseltamivir. The patient was successfully extubated the following day and was discharged 3 days later without any further complications. Discussion Initial ECHO revealed a dilated right ventricle and moderately to severely reduced RV systolic function. This was based on visual assessment of the systolic movement of the base of the RV free wall in the apical four-chamber view. Visual assessment of RV systolic function is more difficult than assessing the left ventricular systolic function and several quantitative measurements can be used. There was also evidence of hypertrophy of the RV free wall as measured in the subcostal view at the level of the tip of the anterior tricuspid leaflet indicating an acute on chronic RV failure. This echo also demonstrated a continuous stream of hyperechoic freely mobile structures that were consistent with air bubbles. Once the PEEPi was corrected and embolic load due to air bubbles abolished, his hemodynamics improved. A repeat ECHO the following day after extubation demonstrated decreased RV size and improved RV systolic function (See Discussion Video, Clip 9). The initiation of positive pressure ventilation can have significant hemodynamic consequences due to its effects on preload and afterload. Due to increased intrathoracic pressures, venous return is reduced and this decreases RV preload. Positive pressure ventilation may also increase RV afterload secondary to elevation of transpulmonary pressure. Both these phenomena may be exaggerated due to effects of PEEPi.1 Physiologic strain from hypoxic vasoconstriction and coronary hypoperfusion places the RV at further e2
risk for failure.2,3 As a consequence of ventricular interdependence, RV impairment can have deleterious effects on the left ventricular function by causing a decrease in cardiac output.4 A leftward shift of the interventricular septum noted during systole and diastole is seen in Video 1, Clips 4 and 5. This is indicative of volume and pressure overload in the right ventricle. Venous air embolism is a rare but well-documented complication of central venous catheterization.5 Although generally benign, severe complications have been reported with air emboli as small as 20 mL.6 Air emboli can be prevented with Trendelenburg positioning, adequate volume resuscitation, minimization of air introduction, and improvement of the catheter seal during the insertion of the CVC. Symptoms of air embolism include tachycardia, dyspnea, and chest pain. Significant events can lead to hypoxemia, respiratory distress, and cardiovascular collapse. Catheters which have an air leak leading to air emboli should be removed immediately. Treatment is supportive, and a theoretical advantage to left lateral decubitus positioning has been traditionally recommended. Based on the temporal profile of the hemodynamic improvement, we believe that the hypotension in this case was primarily being driven by airway obstruction causing dynamic hyperinflation with resultant PEEPi. The air emboli exacerbated the hemodynamic insult by increasing the afterload on the right ventricle.5 This case depicts the interaction between positive end-expiratory pressure delivered or generated during mechanical ventilation and RV function. It also highlights the utility of point-of-care bedside ultrasound in diagnosing unsuspected etiologies for hemodynamic compromise in the critical care setting. Reverberations 1. In patients with acute respiratory failure who are mechanically ventilated, bedside ECHO is helpful to understand the dynamic effects of positive pressure ventilation on RV function. 2. Hemodynamic compromise in this setting can be mirrored on bedside ECHO that can guide management decisions. 3. Use of point-of-care bedside ultrasound can be serendipitous. 4. Unsuspected etiologies of shock, as noted with air emboli in this case, can have significant implications in patient care. 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. Postgraduate Education Corner
Other contributions: CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met. Additional information: To analyze this case with the videos, see the online article.
References 1. Jardin F, Vieillard-Baron A. Right ventricular function and positive pressure ventilation in clinical practice: from hemodynamic subsets to respirator settings. Intensive Care Med. 2003;29(9):1426-1434.
journal.publications.chestnet.org
2. Feihl F, Broccard AF. Interactions between respiration and systemic hemodynamics. Part II: practical implications in critical care. Intensive Care Med. 2009;35(2):198-205. 3. Smeding L, Lust E, Plötz FB, Groeneveld AB. Clinical implications of heart-lung interactions. Neth J Med. 2010;68(2):56-61. 4. Luecke T, Pelosi P. Clinical review: positive end-expiratory pressure and cardiac output. Crit Care. 2005;9(6):607-621. 5. Mirski MA, Lele AV, Fitzsimmons L, Toung TJ. Diagnosis and treatment of vascular air embolism. Anesthesiology. 2007; 106(1):164-177. 6. Toung TJ, Rossberg MI, Hutchins GM. Volume of air in a lethal venous air embolism. Anesthesiology. 2001;94(2):360-361.
CHEST / 144 / 6 / DECEMBER 2013
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Postgraduate Education Corner ULTRASOUND CORNER
Scan here for article
A Patient With Acute COPD Exacerbation and Shock Tathagat Narula, MD; Dileep Raman, MBBS; Jonathan Wiesen, MD; Chirag Choudhary, MBBS; Anita J. Reddy, MD, FCCP; and Ajit Moghekar, MBBS
CHEST 2013; 144(6):e1–e3
elderly man with a history of COPD on home A noxygen presented to the ED with shortness of
breath of 2 days’ duration. On physical examination, the patient had jugular venous distension and distant breath sounds without rales bilaterally. Laboratory evaluation was significant for leukocytosis (29,000 WBC/mL, 94% neutrophils), acute renal failure (BUN, 87 mg/dL and creatinine, 2.36 mg/dL), and a troponin T level of 0.44 ng/mL. ECG revealed an incomplete right bundle branch block and no significant ST segment or T-wave changes. Chest radiograph revealed hyperinflated lung fields with bibasilar atelectasis without a focal opacity. Arterial blood gas analysis results were significant for combined hypoxemic and hypercapnic respiratory failure. Bilevel positive airway pressure ventilation was initiated, and the patient subsequently became hypotensive and was endotracheally intubated. The patient remained hypotensive with systolic BP in the 70 to 80 mm Hg range despite aggressive resuscitation with IV fluids. In the ED, a femoral central venous catheter (CVC) was placed, and a norepinephrine drip was initiated. The patient was then admitted to the medical ICU with
a diagnosis of acute respiratory failure due to acute exacerbation of COPD and shock. On arrival to the ICU, an assessment of mechanical ventilatory graphics for assessment of intrinsic positive end-expiratory pressure (PEEPi) revealed significant PEEPi; however, with adjustments to the ventilator modes and resolution of PEEPi, the need for vasopressors decreased but persisted. To evaluate the shock further, the intensivist should perform a bedside echocardiogram (ECHO) (Video 1). Based on the interpretation of these videos, what would be the next step in the patient’s care?
Manuscript received June 18, 2013; revision accepted August 1, 2013. Affiliations: From the Respiratory Institute, Cleveland Clinic, Cleveland, OH. Correspondence to: Ajit Moghekar, MBBS, Pulmonary, Allergy and Critical Care, Cleveland Clinic, 9500 Euclid Ave G62, Cleveland, OH 44195; e-mail: [email protected] © 2013 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.13-1412 journal.publications.chestnet.org
CHEST / 144 / 6 / DECEMBER 2013
e1
Next steps: Measures to identify causes of right ventricular (RV) dilatation and RV systolic failure should be pursued A subsequent bedside lower extremity ultrasound did not reveal any evidence of thrombus. A careful assessment of all the possible sources from where air could be getting entrained into the venous circulation was warranted. All of the patient’s IV accesses, including the femoral CVC and two peripheral lines, were carefully examined to exclude any breach in integrity. The bubbles only disappeared once infusions were stopped through the central line. The femoral CVC was, therefore, identified as the source of air entry into the venous system. After the CVC was capped, the patient’s hemodynamics continued to improve, and he was successfully weaned off vasopressors. A follow-up ECHO 20 min later did not show any more bubbles (see Discussion Video, Clip 8). A nasopharyngeal swab was positive for influenza A, and the patient was treated with oseltamivir. The patient was successfully extubated the following day and was discharged 3 days later without any further complications. Discussion Initial ECHO revealed a dilated right ventricle and moderately to severely reduced RV systolic function. This was based on visual assessment of the systolic movement of the base of the RV free wall in the apical four-chamber view. Visual assessment of RV systolic function is more difficult than assessing the left ventricular systolic function and several quantitative measurements can be used. There was also evidence of hypertrophy of the RV free wall as measured in the subcostal view at the level of the tip of the anterior tricuspid leaflet indicating an acute on chronic RV failure. This echo also demonstrated a continuous stream of hyperechoic freely mobile structures that were consistent with air bubbles. Once the PEEPi was corrected and embolic load due to air bubbles abolished, his hemodynamics improved. A repeat ECHO the following day after extubation demonstrated decreased RV size and improved RV systolic function (See Discussion Video, Clip 9). The initiation of positive pressure ventilation can have significant hemodynamic consequences due to its effects on preload and afterload. Due to increased intrathoracic pressures, venous return is reduced and this decreases RV preload. Positive pressure ventilation may also increase RV afterload secondary to elevation of transpulmonary pressure. Both these phenomena may be exaggerated due to effects of PEEPi.1 Physiologic strain from hypoxic vasoconstriction and coronary hypoperfusion places the RV at further e2
risk for failure.2,3 As a consequence of ventricular interdependence, RV impairment can have deleterious effects on the left ventricular function by causing a decrease in cardiac output.4 A leftward shift of the interventricular septum noted during systole and diastole is seen in Video 1, Clips 4 and 5. This is indicative of volume and pressure overload in the right ventricle. Venous air embolism is a rare but well-documented complication of central venous catheterization.5 Although generally benign, severe complications have been reported with air emboli as small as 20 mL.6 Air emboli can be prevented with Trendelenburg positioning, adequate volume resuscitation, minimization of air introduction, and improvement of the catheter seal during the insertion of the CVC. Symptoms of air embolism include tachycardia, dyspnea, and chest pain. Significant events can lead to hypoxemia, respiratory distress, and cardiovascular collapse. Catheters which have an air leak leading to air emboli should be removed immediately. Treatment is supportive, and a theoretical advantage to left lateral decubitus positioning has been traditionally recommended. Based on the temporal profile of the hemodynamic improvement, we believe that the hypotension in this case was primarily being driven by airway obstruction causing dynamic hyperinflation with resultant PEEPi. The air emboli exacerbated the hemodynamic insult by increasing the afterload on the right ventricle.5 This case depicts the interaction between positive end-expiratory pressure delivered or generated during mechanical ventilation and RV function. It also highlights the utility of point-of-care bedside ultrasound in diagnosing unsuspected etiologies for hemodynamic compromise in the critical care setting. Reverberations 1. In patients with acute respiratory failure who are mechanically ventilated, bedside ECHO is helpful to understand the dynamic effects of positive pressure ventilation on RV function. 2. Hemodynamic compromise in this setting can be mirrored on bedside ECHO that can guide management decisions. 3. Use of point-of-care bedside ultrasound can be serendipitous. 4. Unsuspected etiologies of shock, as noted with air emboli in this case, can have significant implications in patient care. 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. Postgraduate Education Corner
Other contributions: CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met. Additional information: To analyze this case with the videos, see the online article.
References 1. Jardin F, Vieillard-Baron A. Right ventricular function and positive pressure ventilation in clinical practice: from hemodynamic subsets to respirator settings. Intensive Care Med. 2003;29(9):1426-1434.
journal.publications.chestnet.org
2. Feihl F, Broccard AF. Interactions between respiration and systemic hemodynamics. Part II: practical implications in critical care. Intensive Care Med. 2009;35(2):198-205. 3. Smeding L, Lust E, Plötz FB, Groeneveld AB. Clinical implications of heart-lung interactions. Neth J Med. 2010;68(2):56-61. 4. Luecke T, Pelosi P. Clinical review: positive end-expiratory pressure and cardiac output. Crit Care. 2005;9(6):607-621. 5. Mirski MA, Lele AV, Fitzsimmons L, Toung TJ. Diagnosis and treatment of vascular air embolism. Anesthesiology. 2007; 106(1):164-177. 6. Toung TJ, Rossberg MI, Hutchins GM. Volume of air in a lethal venous air embolism. Anesthesiology. 2001;94(2):360-361.
CHEST / 144 / 6 / DECEMBER 2013
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