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The role of intraoperative transesophageal echocardiographic monitoring in a patient with hypertrophic cardiomyopathy undergoing laparoscopic surgery
Journal of Clinical Anesthesia (2016) 34, 124–127
Case report
The role of intraoperative transesophageal echocardiographic monitoring in a patient with hypertrophic cardiomyopathy undergoing laparoscopic surgery☆ Stephen H. Gregory MD, Michael A. Fierro MD ⁎ Department of Anesthesiology, Duke University Medical Center, DUMC 3094, Durham, NC, 27710, USA Received 22 January 2016; revised 29 February 2016; accepted 5 March 2016
Keywords: Cardiomyopathy; Hypertrophic; Anesthesia; Echocardiography; Transesophageal; Laparoscopy
Abstract Hypertrophic cardiomyopathy (HCM) presents a significant perioperative challenge. Anesthetic drugs, patient positioning, and surgical technique can provoke worsening left ventricular outflow tract obstruction and hemodynamic deterioration. In this case report, we present the perioperative management of a 70-year-old male with a history of HCM who underwent a robotic laparoscopic prostatectomy. Discussion focuses on the utilization of echocardiographic guidance in the care of patients with HCM undergoing noncardiac surgery, as well as the pathophysiology of laparoscopic insufflation and its effects on left ventricular outflow tract obstruction in HCM. Crown Copyright © 2016 Published by Elsevier Inc. All rights reserved.
1. Introduction Hypertrophic cardiomyopathy (HCM) is a somewhat common medical condition that serves as an important cause of morbidity and mortality, often resulting in sudden cardiac death in previously asymptomatic patients [1]. While the prevalence was initially estimated at approximately 1 in 500 individuals, more recent data suggests that the prevalence may be much higher [1,2]. Patients with HCM may manifest either malignant tachyarrhythmias or dynamic left ventricular outflow tract (LVOT) obstruction that can cause rapid clinical ☆ Disclosures: The authors have no disclosures related to the content of this case report. No funding was utilized for this report. ⁎ Corresponding author at: Duke University Hospital, DUMC 3094, Durham, NC, 27710. Tel.: +1 919 681 3551; fax: +1 919 681 8994. E-mail addresses: [email protected] (S.H. Gregory), Michael.fi[email protected] (M.A. Fierro).
http://dx.doi.org/10.1016/j.jclinane.2016.03.028 0952-8180/Crown Copyright © 2016 Published by Elsevier Inc. All rights reserved.
deterioration [3]. It can be an important cause of sudden intraoperative hemodynamic collapse, with a recent review of 364 rescue echocardiograms demonstrating LVOT obstruction as a cause of hemodynamic instability in 3.6% of patients who underwent an emergent perioperative echocardiogram [4]. Despite being a relatively common disease process, there exists little literature that describes the care of patients with HCM undergoing laparoscopic surgery [5,6]. In this case report, we describe a patient with a history of HCM with dynamic LVOT obstruction who underwent a robot-assisted laparoscopic prostatectomy for prostate cancer with positioning and insufflation guided by continuous transesophageal echocardiography (TEE) monitoring. The subsequent discussion focuses on the role of TEE in caring for patients with HCM undergoing noncardiac surgery, as well as the pathophysiology of laparoscopic insufflation and its application in patients with HCM. The patient gave written informed consent for the publication of this case report.
TEE for laparoscopic surgery in HCM
125 color flow Doppler. The abdomen was insufflated in 5 mmHg increments to a maximum of 15 mmHg with carbon dioxide gas. The patient had a sustained vagal response to insufflation with two episodes of bradycardia with a heart rate of 30 beats per minute that were treated with titrated 0.2 mg doses of atropine to correct the heart rate to his baseline rate of 50 to 60 beats per minute. A phenylephrine infusion was initiated and titrated to a mean arterial pressure of 70 to 90. The surgical procedure progressed uneventfully. The patient received two liters of crystalloid intraoperatively, and the estimated blood loss was 300 mL. At the conclusion of the surgical procedure, the LVOT was once again continuously interrogated during desufflation and return to the supine position without evidence of LVOT obstruction. The patient was successfully extubated in the operating room, transferred to the post-anesthesia care unit, and his recovery proceeded without incident.
2. Case description A 70-year-old male presented for elective robot-assisted laparoscopic prostatectomy for high-grade prostate cancer. The patient had a history notable for supraventricular tachycardia well controlled on metoprolol, hypertension, hyperlipidemia, obstructive sleep apnea, and HCM. A transthoracic echocardiogram performed 6 months preoperatively was remarkable for a resting LVOT gradient of 20 mmHg with a gradient of 130 mmHg during Valsalva. On preoperative assessment, he reported he was asymptomatic with greater than 4 metabolic equivalents of exercise tolerance. The patient was instructed to drink 500 mL of an over-thecounter carbohydrate drink 2 hours prior to arriving to the preoperative holding area. He received an additional liter of intravenous lactated Ringer’s solution prior to the induction of anesthesia. After the placement of a preinduction arterial line and external defibrillator pads, anesthesia was induced with fentanyl, lidocaine, propofol, and rocuronium. Phenylephrine was titrated in 100 mcg increments to maintain arterial afterload and keep the patient's mean arterial pressure within 10% of baseline. After intubation, a TEE probe was advanced into the esophagus atraumatically. In the supine position, the patient's ventricle was adequately filled, and asymmetric septal hypertrophy with trace systolic anterior motion (SAM) of the anterior mitral leaflet was identified (Figure 1). No hemodynamically significant flow obstruction was noted. He also demonstrated moderate mitral valve insufficiency, mild aortic valve insufficiency, and grade II diastolic dysfunction. The LVOT was continuously evaluated via a midesophageal long axis view with and without color flow Doppler during the incremental addition of steep Trendelenburg position and during laparoscopic insufflation. Assessment focused on evaluating for an increased gradient across the LVOT which would manifest as turbulence and aliasing on
3. Discussion Hypertrophic cardiomyopathy is a disease process characterized by asymmetric septal hypertrophy resulting from myocardial fiber disorganization that predisposes to obstruction of the LVOT by the mitral valve apparatus, most commonly the anterior mitral leaflet [7]. A decrease in left ventricular preload or systemic vascular resistance (SVR) or an increase in myocardial contractility or heart rate can precipitate worsening LVOT obstruction and result in hemodynamic deterioration [8]. Transesophageal echocardiography can play an important role in understanding the etiology of intraoperative hemodynamic instability and monitoring the patency of the LVOT. While only 1/3 of patients with HCM exhibit resting LVOT obstruction (gradient N 30 mmHg), an additional 1/3 (including our patient in this case) demonstrate LVOT obstruction
PML AML LA LVOT
SAM
RV LV Asymmetric septal hypertrophy
Figure 1 Two-dimensional midesophageal long axis view demonstrating SAM of the anterior mitral leaflet of the mitral valve and asymmetric septal hypertrophy during a baseline exam in the supine position. LA = left atrium; LV = left ventricle; AML = anterior mitral leaflet; PML = posterior mitral leaflet; RV = right ventricle; BPM = beats per minute.
126 only with provocation [9]. Echocardiographic assessment should focus on systolic and diastolic function, as well as ascertaining the degree of SAM and LVOT obstruction at rest and with provocation [7]. Abnormal motion of the mitral valve should prompt a comprehensive assessment of the mitral valve apparatus, as patients with HCM are predisposed to anatomic abnormalities of this structure [7]. Intraoperative hemodynamic instability should prompt echocardiographic reassessment to assist in guiding therapy. Intraoperative hemodynamic instability must be treated aggressively and appropriately to prevent total cardiovascular collapse. Anesthetic management should focus on the maintenance of adequate ventricular preload, normal or slightly increased SVR, and avoiding medications that may precipitate an increase in either myocardial contractility, heart rate, or both [3]. Hypotension should be treated with phenylephrine or vasopressin, which increase SVR without any associated inotropic or chronotropic effects [8,10]. This should be coupled with volume resuscitation to promote adequate preload and minimize LVOT obstruction. Beta adrenergic blockade may be beneficial to minimize increases in heart rate in response to surgical stimulation, conferring both increased diastolic filling time and improved diastolic relaxation [10]. Conversely, drugs that promote inotropy and/or chronotropy, including epinephrine, dopamine, dobutamine, and isoproterenol, may worsen LVOT obstruction and are typically avoided [10]. Maintenance of sinus rhythm is crucial, as atrial kick is often necessary to overcome diastolic dysfunction and ensure adequate left-ventricular filling [8]. Caring for a patient with HCM undergoing laparoscopic surgery necessitates an understanding of the pathophysiology of laparoscopic insufflation and its potential effects on the LVOT gradient. Joris et al. initially characterized these changes, where they demonstrated that laparoscopic insufflation causes a significant increase in the mean arterial pressure, systemic vascular resistance (SVR), and pulmonary vascular resistance, while at the same time decreasing the cardiac index [11]. This is beneficial in HCM, as it decreases the gradient across the LVOT, but at the same time an increase in SVR may result in elevated end-systolic ventricular wall stress and increased myocardial oxygen demand, especially in obese patients [12]. Of note, it appears that the hemodynamic effects of laparoscopic insufflation are not immediately reversed, with evidence suggesting these hemodynamic perturbations may persist for over an hour following desufflation [13]. Careful postoperative monitoring is critical, as decompensation in patients with preexisting myocardial dysfunction may occur up to 3 hours postoperatively [13]. In addition to increasing ventricular afterload, laparoscopic insufflation also appears to augment ventricular preload. Another study by Rist et al evaluated the effect of patient positioning and abdominal insufflation on both right and left ventricular preload [14]. Abdominal insufflation up to 15 mmHg was associated with an increase in the right and left ventricular end-diastolic and end-systolic volumes. Trendelenberg position did not appear to further augment preload, but
S.H. Gregory, M.A. Fierro the transition to the reverse Trendelenberg position caused a significant decrease in end-diastolic and end-systolic volume, though the calculated volumes were still greater than the baseline measurement in the supine position without insufflation [14]. Thus, the evidence suggests that laparoscopic pathophysiology should produce favorable hemodynamic conditions for patients with HCM, especially in the Trendelenberg position.
4. Conclusion This case report demonstrates the utility of continuous TEE monitoring in the care of patients with HCM undergoing noncardiac surgery. Monitoring of the LVOT for evidence of worsening outflow tract obstruction is helpful in patients undergoing procedures in which acute changes in left ventricular preload and afterload are anticipated. Similarly, this case demonstrates that the increase in preload and SVR afforded by laparoscopic insufflation, especially in the Trendelenberg position, produces a hemodynamic profile that is favorable in minimizing LVOT obstruction and promoting intraoperative hemodynamic stability in patients with HCM.
References [1] Maron BJ, Gardin JM, Flack JM, Gidding SS, Kurosaki TT, Bild DE. Prevalence of hypertrophic cardiomyopathy in a general population of young adults. Echocardiographic analysis of 4111 subjects in the CARDIA study. coronary artery risk development in (young) adults. Circulation 1995;92(4):785-9. [2] Semsarian C, Ingles J, Maron MS, Maron BJ. New perspectives on the prevalence of hypertrophic cardiomyopathy. J Am Coll Cardiol 2015; 65(12):1249-54. [3] Gajewski M, Hillel Z. Anesthesia management of patients with hypertrophic obstructive cardiomyopathy. Prog Cardiovasc Dis 2012; 54:503-11. [4] Markin NW, Gmelch BS, Griffee MJ, Holmberg TJ, Morgan DE, Zimmerman JM. A review of 364 perioperative rescue echocardiograms: findings of an anesthesiologist-staffed perioperative echocardiography service. J Cardiothorac Vasc Anesth 2015;29(1):82-8. [5] Popescu WM, Perrino AC. Critical cardiac decompensation during laparoscopic surgery. J Am Soc Echocardiogr 2006;19(8):1074.e5-6. [6] Fujimoto H, Kamiya Y, Ohki H, Goto T. Anesthetic management of a patient with HOCM even after PTSMA. Masui 2008;57(10):1276-9. [7] Patil PV, Wiegers SE. Echocardiography for hypertrophic cardiomyopathy. Prog Cardiovasc Dis 2014;15:91-9. [8] Hensley N, Dietrich J, Nyhan D, Mitter N, Yee M, Brady M. Hypertrophic cardiomyopathy: a review. Anesth Analg 2015;120(3):554-69. [9] Gersh BJ, Maron BJ, Bonow RO, Dearani JA, Fifer MA, Link MS, et al. 2011 ACCF/AHA guideline for the diagnosis and treatment of hypertrophic cardiomyopathy: A report of the American college of cardiology foundation/American heart association task force on practice guidelines. Circulation 2011;124:e783-831. [10] Varma PK, Raman SP, Neema PK. Hypertrophic cardiomyopathy part II - anesthetic and surgical considerations. Ann Card Anaesth 2014;17: 211-21. [11] Joris JL, Noirot DP, Legrand MJ, Jacquet NJ, Lamy ML. Hemodynamic changes during laparoscopic cholecystectomy. Anesth Analg 1993;76: 1067-71.
TEE for laparoscopic surgery in HCM [12] Prior DL, Sprung J, Thomas JD, Whalley DG, Bourke DL. Echocardiographic and hemodynamic evaluation of cardiovascular performance during laparoscopy of morbidly obese patients. Obes Surg 2003;13: 761-7. [13] Portera CA, Compton RP, Walters DN, Browder IW. Benefits of pulmonary artery catheter and transesophageal echocardiographic monitoring
127 in laparoscopic cholecystectomy patients with cardiac disease. Am J Surg 1995;169:202-7. [14] Rist M, Hemmerling TH, Rauh R, Siebzehnrubl E, Jacobi KE. Influence of pneumoperitoneum and patient positioning on preload and splanchnic blood volume in laparoscopic surgery of the lower abdomen. J Clin Anesth 2001;13:244-9.
Case report
The role of intraoperative transesophageal echocardiographic monitoring in a patient with hypertrophic cardiomyopathy undergoing laparoscopic surgery☆ Stephen H. Gregory MD, Michael A. Fierro MD ⁎ Department of Anesthesiology, Duke University Medical Center, DUMC 3094, Durham, NC, 27710, USA Received 22 January 2016; revised 29 February 2016; accepted 5 March 2016
Keywords: Cardiomyopathy; Hypertrophic; Anesthesia; Echocardiography; Transesophageal; Laparoscopy
Abstract Hypertrophic cardiomyopathy (HCM) presents a significant perioperative challenge. Anesthetic drugs, patient positioning, and surgical technique can provoke worsening left ventricular outflow tract obstruction and hemodynamic deterioration. In this case report, we present the perioperative management of a 70-year-old male with a history of HCM who underwent a robotic laparoscopic prostatectomy. Discussion focuses on the utilization of echocardiographic guidance in the care of patients with HCM undergoing noncardiac surgery, as well as the pathophysiology of laparoscopic insufflation and its effects on left ventricular outflow tract obstruction in HCM. Crown Copyright © 2016 Published by Elsevier Inc. All rights reserved.
1. Introduction Hypertrophic cardiomyopathy (HCM) is a somewhat common medical condition that serves as an important cause of morbidity and mortality, often resulting in sudden cardiac death in previously asymptomatic patients [1]. While the prevalence was initially estimated at approximately 1 in 500 individuals, more recent data suggests that the prevalence may be much higher [1,2]. Patients with HCM may manifest either malignant tachyarrhythmias or dynamic left ventricular outflow tract (LVOT) obstruction that can cause rapid clinical ☆ Disclosures: The authors have no disclosures related to the content of this case report. No funding was utilized for this report. ⁎ Corresponding author at: Duke University Hospital, DUMC 3094, Durham, NC, 27710. Tel.: +1 919 681 3551; fax: +1 919 681 8994. E-mail addresses: [email protected] (S.H. Gregory), Michael.fi[email protected] (M.A. Fierro).
http://dx.doi.org/10.1016/j.jclinane.2016.03.028 0952-8180/Crown Copyright © 2016 Published by Elsevier Inc. All rights reserved.
deterioration [3]. It can be an important cause of sudden intraoperative hemodynamic collapse, with a recent review of 364 rescue echocardiograms demonstrating LVOT obstruction as a cause of hemodynamic instability in 3.6% of patients who underwent an emergent perioperative echocardiogram [4]. Despite being a relatively common disease process, there exists little literature that describes the care of patients with HCM undergoing laparoscopic surgery [5,6]. In this case report, we describe a patient with a history of HCM with dynamic LVOT obstruction who underwent a robot-assisted laparoscopic prostatectomy for prostate cancer with positioning and insufflation guided by continuous transesophageal echocardiography (TEE) monitoring. The subsequent discussion focuses on the role of TEE in caring for patients with HCM undergoing noncardiac surgery, as well as the pathophysiology of laparoscopic insufflation and its application in patients with HCM. The patient gave written informed consent for the publication of this case report.
TEE for laparoscopic surgery in HCM
125 color flow Doppler. The abdomen was insufflated in 5 mmHg increments to a maximum of 15 mmHg with carbon dioxide gas. The patient had a sustained vagal response to insufflation with two episodes of bradycardia with a heart rate of 30 beats per minute that were treated with titrated 0.2 mg doses of atropine to correct the heart rate to his baseline rate of 50 to 60 beats per minute. A phenylephrine infusion was initiated and titrated to a mean arterial pressure of 70 to 90. The surgical procedure progressed uneventfully. The patient received two liters of crystalloid intraoperatively, and the estimated blood loss was 300 mL. At the conclusion of the surgical procedure, the LVOT was once again continuously interrogated during desufflation and return to the supine position without evidence of LVOT obstruction. The patient was successfully extubated in the operating room, transferred to the post-anesthesia care unit, and his recovery proceeded without incident.
2. Case description A 70-year-old male presented for elective robot-assisted laparoscopic prostatectomy for high-grade prostate cancer. The patient had a history notable for supraventricular tachycardia well controlled on metoprolol, hypertension, hyperlipidemia, obstructive sleep apnea, and HCM. A transthoracic echocardiogram performed 6 months preoperatively was remarkable for a resting LVOT gradient of 20 mmHg with a gradient of 130 mmHg during Valsalva. On preoperative assessment, he reported he was asymptomatic with greater than 4 metabolic equivalents of exercise tolerance. The patient was instructed to drink 500 mL of an over-thecounter carbohydrate drink 2 hours prior to arriving to the preoperative holding area. He received an additional liter of intravenous lactated Ringer’s solution prior to the induction of anesthesia. After the placement of a preinduction arterial line and external defibrillator pads, anesthesia was induced with fentanyl, lidocaine, propofol, and rocuronium. Phenylephrine was titrated in 100 mcg increments to maintain arterial afterload and keep the patient's mean arterial pressure within 10% of baseline. After intubation, a TEE probe was advanced into the esophagus atraumatically. In the supine position, the patient's ventricle was adequately filled, and asymmetric septal hypertrophy with trace systolic anterior motion (SAM) of the anterior mitral leaflet was identified (Figure 1). No hemodynamically significant flow obstruction was noted. He also demonstrated moderate mitral valve insufficiency, mild aortic valve insufficiency, and grade II diastolic dysfunction. The LVOT was continuously evaluated via a midesophageal long axis view with and without color flow Doppler during the incremental addition of steep Trendelenburg position and during laparoscopic insufflation. Assessment focused on evaluating for an increased gradient across the LVOT which would manifest as turbulence and aliasing on
3. Discussion Hypertrophic cardiomyopathy is a disease process characterized by asymmetric septal hypertrophy resulting from myocardial fiber disorganization that predisposes to obstruction of the LVOT by the mitral valve apparatus, most commonly the anterior mitral leaflet [7]. A decrease in left ventricular preload or systemic vascular resistance (SVR) or an increase in myocardial contractility or heart rate can precipitate worsening LVOT obstruction and result in hemodynamic deterioration [8]. Transesophageal echocardiography can play an important role in understanding the etiology of intraoperative hemodynamic instability and monitoring the patency of the LVOT. While only 1/3 of patients with HCM exhibit resting LVOT obstruction (gradient N 30 mmHg), an additional 1/3 (including our patient in this case) demonstrate LVOT obstruction
PML AML LA LVOT
SAM
RV LV Asymmetric septal hypertrophy
Figure 1 Two-dimensional midesophageal long axis view demonstrating SAM of the anterior mitral leaflet of the mitral valve and asymmetric septal hypertrophy during a baseline exam in the supine position. LA = left atrium; LV = left ventricle; AML = anterior mitral leaflet; PML = posterior mitral leaflet; RV = right ventricle; BPM = beats per minute.
126 only with provocation [9]. Echocardiographic assessment should focus on systolic and diastolic function, as well as ascertaining the degree of SAM and LVOT obstruction at rest and with provocation [7]. Abnormal motion of the mitral valve should prompt a comprehensive assessment of the mitral valve apparatus, as patients with HCM are predisposed to anatomic abnormalities of this structure [7]. Intraoperative hemodynamic instability should prompt echocardiographic reassessment to assist in guiding therapy. Intraoperative hemodynamic instability must be treated aggressively and appropriately to prevent total cardiovascular collapse. Anesthetic management should focus on the maintenance of adequate ventricular preload, normal or slightly increased SVR, and avoiding medications that may precipitate an increase in either myocardial contractility, heart rate, or both [3]. Hypotension should be treated with phenylephrine or vasopressin, which increase SVR without any associated inotropic or chronotropic effects [8,10]. This should be coupled with volume resuscitation to promote adequate preload and minimize LVOT obstruction. Beta adrenergic blockade may be beneficial to minimize increases in heart rate in response to surgical stimulation, conferring both increased diastolic filling time and improved diastolic relaxation [10]. Conversely, drugs that promote inotropy and/or chronotropy, including epinephrine, dopamine, dobutamine, and isoproterenol, may worsen LVOT obstruction and are typically avoided [10]. Maintenance of sinus rhythm is crucial, as atrial kick is often necessary to overcome diastolic dysfunction and ensure adequate left-ventricular filling [8]. Caring for a patient with HCM undergoing laparoscopic surgery necessitates an understanding of the pathophysiology of laparoscopic insufflation and its potential effects on the LVOT gradient. Joris et al. initially characterized these changes, where they demonstrated that laparoscopic insufflation causes a significant increase in the mean arterial pressure, systemic vascular resistance (SVR), and pulmonary vascular resistance, while at the same time decreasing the cardiac index [11]. This is beneficial in HCM, as it decreases the gradient across the LVOT, but at the same time an increase in SVR may result in elevated end-systolic ventricular wall stress and increased myocardial oxygen demand, especially in obese patients [12]. Of note, it appears that the hemodynamic effects of laparoscopic insufflation are not immediately reversed, with evidence suggesting these hemodynamic perturbations may persist for over an hour following desufflation [13]. Careful postoperative monitoring is critical, as decompensation in patients with preexisting myocardial dysfunction may occur up to 3 hours postoperatively [13]. In addition to increasing ventricular afterload, laparoscopic insufflation also appears to augment ventricular preload. Another study by Rist et al evaluated the effect of patient positioning and abdominal insufflation on both right and left ventricular preload [14]. Abdominal insufflation up to 15 mmHg was associated with an increase in the right and left ventricular end-diastolic and end-systolic volumes. Trendelenberg position did not appear to further augment preload, but
S.H. Gregory, M.A. Fierro the transition to the reverse Trendelenberg position caused a significant decrease in end-diastolic and end-systolic volume, though the calculated volumes were still greater than the baseline measurement in the supine position without insufflation [14]. Thus, the evidence suggests that laparoscopic pathophysiology should produce favorable hemodynamic conditions for patients with HCM, especially in the Trendelenberg position.
4. Conclusion This case report demonstrates the utility of continuous TEE monitoring in the care of patients with HCM undergoing noncardiac surgery. Monitoring of the LVOT for evidence of worsening outflow tract obstruction is helpful in patients undergoing procedures in which acute changes in left ventricular preload and afterload are anticipated. Similarly, this case demonstrates that the increase in preload and SVR afforded by laparoscopic insufflation, especially in the Trendelenberg position, produces a hemodynamic profile that is favorable in minimizing LVOT obstruction and promoting intraoperative hemodynamic stability in patients with HCM.
References [1] Maron BJ, Gardin JM, Flack JM, Gidding SS, Kurosaki TT, Bild DE. Prevalence of hypertrophic cardiomyopathy in a general population of young adults. Echocardiographic analysis of 4111 subjects in the CARDIA study. coronary artery risk development in (young) adults. Circulation 1995;92(4):785-9. [2] Semsarian C, Ingles J, Maron MS, Maron BJ. New perspectives on the prevalence of hypertrophic cardiomyopathy. J Am Coll Cardiol 2015; 65(12):1249-54. [3] Gajewski M, Hillel Z. Anesthesia management of patients with hypertrophic obstructive cardiomyopathy. Prog Cardiovasc Dis 2012; 54:503-11. [4] Markin NW, Gmelch BS, Griffee MJ, Holmberg TJ, Morgan DE, Zimmerman JM. A review of 364 perioperative rescue echocardiograms: findings of an anesthesiologist-staffed perioperative echocardiography service. J Cardiothorac Vasc Anesth 2015;29(1):82-8. [5] Popescu WM, Perrino AC. Critical cardiac decompensation during laparoscopic surgery. J Am Soc Echocardiogr 2006;19(8):1074.e5-6. [6] Fujimoto H, Kamiya Y, Ohki H, Goto T. Anesthetic management of a patient with HOCM even after PTSMA. Masui 2008;57(10):1276-9. [7] Patil PV, Wiegers SE. Echocardiography for hypertrophic cardiomyopathy. Prog Cardiovasc Dis 2014;15:91-9. [8] Hensley N, Dietrich J, Nyhan D, Mitter N, Yee M, Brady M. Hypertrophic cardiomyopathy: a review. Anesth Analg 2015;120(3):554-69. [9] Gersh BJ, Maron BJ, Bonow RO, Dearani JA, Fifer MA, Link MS, et al. 2011 ACCF/AHA guideline for the diagnosis and treatment of hypertrophic cardiomyopathy: A report of the American college of cardiology foundation/American heart association task force on practice guidelines. Circulation 2011;124:e783-831. [10] Varma PK, Raman SP, Neema PK. Hypertrophic cardiomyopathy part II - anesthetic and surgical considerations. Ann Card Anaesth 2014;17: 211-21. [11] Joris JL, Noirot DP, Legrand MJ, Jacquet NJ, Lamy ML. Hemodynamic changes during laparoscopic cholecystectomy. Anesth Analg 1993;76: 1067-71.
TEE for laparoscopic surgery in HCM [12] Prior DL, Sprung J, Thomas JD, Whalley DG, Bourke DL. Echocardiographic and hemodynamic evaluation of cardiovascular performance during laparoscopy of morbidly obese patients. Obes Surg 2003;13: 761-7. [13] Portera CA, Compton RP, Walters DN, Browder IW. Benefits of pulmonary artery catheter and transesophageal echocardiographic monitoring
127 in laparoscopic cholecystectomy patients with cardiac disease. Am J Surg 1995;169:202-7. [14] Rist M, Hemmerling TH, Rauh R, Siebzehnrubl E, Jacobi KE. Influence of pneumoperitoneum and patient positioning on preload and splanchnic blood volume in laparoscopic surgery of the lower abdomen. J Clin Anesth 2001;13:244-9.