- Email: [email protected]
Dynamic Left Ventricular Outflow Tract Obstruction During Liver Transplantation: The Role of Transesophageal Echocardiography
Dynamic Left Ventricular Outflow Tract Obstruction During Liver Transplantation: The Role of Transesophageal Echocardiography Stephen Aniskevich, MD, Timothy S. Shine, MD, Neil G. Feinglass, MD, and Wolf H. Stapelfeldt, MD
P
ATIENTS WITH advanced liver disease are prone to multiple hemodynamic abnormalities.1,2 This susceptibility can be attributed to several factors, including a hyperdynamic left ventricle and chronically lowered systemic vascular resistance (SVR). Surgical manipulation and blood loss during liver transplantation can further worsen this precarious hemodynamic balance. A case of refractory hypotension secondary to dynamic left ventricular outflow tract obstruction (DLVOTO) in a patient with a normal preoperative cardiac evaluation is presented. Intraoperative transesophageal echocardiography (TEE) played a vital role in the diagnosis and management of this disorder after standard pharmacologic therapies failed to improve the blood pressure. The authors believe that intraoperative TEE should be used whenever hemodynamic instability is refractory to standard therapy during liver transplantation. CASE REPORT
A 56-year-old white man (64 kg, 183 cm) presented for orthotopic liver transplantation (OLT) for end-stage liver disease secondary to sclerosing cholangitis complicated by cholangiocarcinoma. His past medical history was significant for renal cell carcinoma that had been in remission since a partial nephrectomy in 2000. He received a standard preoperative evaluation consisting of laboratory testing, echocardiogram, and chest X-ray, all of which were within acceptable limits. Additionally, he received a 2D dobutamine stress echocardiogram that revealed no evidence of ischemia at a maximum heart rate of 139 beats/min. Also noted was a mild degree of mitral regurgitation (MR) and concentric remodeling. No left ventricular outflow tract abnormalities were identified. His ejection fraction was 56%, increasing to 81% with stress. He underwent an uneventful rapid-sequence induction using propofol, succinylcholine, and fentanyl. Anesthesia was then maintained using isoflurane and intermittent fentanyl boluses. Neuromuscular blockade was achieved with cisatracurium. Routine intravenous access consisting of an 8.5F antecubital catheter, 2 radial arterial catheters, and a right internal jugular venous catheter were then obtained. A pulmonary artery catheter (PAC) was placed to monitor continuous cardiac output. His initial intraoperative course was unremarkable except for a brief hypotensive episode occurring with partial inferior vena cava clamping at the initiation of the anhepatic period. This resolved with intravenous fluids, a dopamine infusion, and several 10-g epinephrine boluses. Shortly thereafter, during initiation of graft recirculation, the patient’s blood pressure became very labile. He was administered intravascular volume resuscitation with blood products, and 5% albumin, and aggressive vasopressor support was initiated with intermittent epinephrine boluses and a vasopressin infusion, followed by a phenylephrine infusion. His hemodynamic instability did not improve despite escalating vasopressor dosages. Of note, the readings on the PAC were unchanged with respect to central venous pressure, pulmonary capillary wedge pressure, systolic pulmonary artery pressure, diastolic pulmonary artery pressure (PAD), and SVR in the period immediately preceding the hypotension. During the instability, however, his PAD became elevated, whereas other PAC measurements were near or at baseline (Fig 1). The decision was then made to insert a multiplane TEE probe to assess left ventricular function. Rapid evaluation revealed moderateto-severe DLVOTO with systolic anterior motion (SAM) of the mitral
valve associated with severe MR (Figs 2 and 3). Based on these findings, epinephrine was immediately discontinued and labetalol, 2.5 mg intravenously, was given. This resulted in a rapid reversal of the hemodynamic instability, allowing for the discontinuation of all vasoactive agents with the exception of phenylephrine. The remainder of the intraoperative course was unremarkable. The patient was observed in the ICU after surgery where he had an uneventful recovery. Postoperative echocardiography revealed a hyperdynamic left ventricle with no septal asymmetry and mild MR caused by a prolapsed posterior mitral leaflet. Ejection fraction was noted to be 75% to 80%. DISCUSSION
Dynamic left ventricular outflow tract obstruction in the absence of septal asymmetry has been well described in the literature3-11; however, the authors believe this is the first time DLVOTO has been described intraoperatively during an OLT in a patient with a normal preoperative stress echocardiogram. This patient presented to the operating room with a normal cardiac evaluation and developed hemodynamic instability during graft recirculation. DLVOTO induced during dobutamine cardiac stress testing has been described12,13; however, this patient had an uneventful stress test despite reaching a heart rate of 139 beats/min. During recirculation of the donor liver, he developed acute outflow tract obstruction. Although it is uncertain as to the exact etiology of the new outflow obstruction, several factors may have played a contributory role. First, the uptake of blood by the donor liver would have decreased preload, as evidenced by a decrease in the pulmonary artery diastolic pressure. Second, the release of cold blood from the cadaveric liver along with vasoactive substances (the reperfusion syndrome)14 may have stunned the peripheral circulation. This loss of preload, coupled with the sudden drop in SVR, may have been enough to allow for a “perfect storm” in which a patient with a predisposition for DLVOTO may actually develop the obstruction. DLVOTO is characterized by turbulence through the left ventricular outflow tract, hypercontractility of the left ventricle, SAM, and some degree of late mitral regurgitation.11 Patients undergoing OLT are at an elevated risk of developing DLVOTO because of their pre-existing hyperdynamic cardiac state and their chronically low SVR. During periods of relative hypovolemia, this hyperdynamic state is further worsened and DLVOTO may occur. The first clue to the development of DLVOTO may be a paradoxic decrease in the blood pressure after administration of positive inotropes.15 Another intraoper-
From the Department of Anesthesiology, Mayo Clinic, Jacksonville, FL. Address reprint requests to Stephen Aniskevich, MD, Department of Anesthesiology, Mayo Clinic, 4500 San Pablo Rd, Jacksonville, FL 32224. E-mail: [email protected] © 2007 Elsevier Inc. All rights reserved. 1053-0770/07/2104-0021$32.00/0 doi:10.1053/j.jvca.2006.07.024 Key words: liver transplantation, transesophageal echocardiography, dynamic left ventricular outflow tract obstruction, refractory hypotension, systolic anterior motion, mitral valve
Journal of Cardiothoracic and Vascular Anesthesia, Vol 21, No 4 (August), 2007: pp 577-580
577
578
ANISKEVICH ET AL
Fig 1. Intraoperative hemodynamics. The period of dynamic left ventricular outflow obstruction is defined by the rectangular box. (Color version of figure is available online.)
ative finding is the sudden occurrence of a systolic murmur of increasing intensity if an esophageal stethoscope is being monitored. At this institution, epinephrine is the first-line medication to treat severe hypotension during liver transplantation. In this case, the patient developed tachycardia with little improvement in blood pressure. SAM worsened because of the hypercontractile state, resulting in outflow obstruction and severe mitral regurgitation. The intraventricular geometry combined with the hyperdynamic state of advanced liver disease were predetermining factors for the development of DLVOTO. Because the vasoactive agents were increased, the DLVOTO worsened, as did the degree of MR, consistent with the pres-
ence of a rising V wave on the PAC tracing. This continued despite seemingly adequate fluid resuscitation as assessed by the elevated pulmonary diastolic pressures. It was not until proper evaluation with TEE revealed the pathology that the appropriate steps were taken to reverse the condition. Typically, treatment of DLVOTO consists of increasing left ventricular end-diastolic dimensions and decreasing the inotropic state of the heart. Several approaches can be used concurrently. End-diastolic dimension can be improved with aggressive intravascular volume loading to increase preload. Additionally, improving the SVR will splint open the outflow tract by decreasing the role of the Venturi effect. The drug of choice for this is
DLVOTO DURING LIVER TRANSPLANTATION
579
Fig 2. Transesophageal echocardiogram color Doppler. Note the severe mitral regurgitation and turbulence through the outflow tract indicative of dynamic left ventricular outflow obstruction.
phenylephrine because of its selectivity for ␣-adrenergic receptors. Phenylephrine may also cause a reflex bradycardia and allow for a longer time in diastole to allow for improved filling. -Adrenergic receptor blockers and calcium channel blockers have proven to be efficacious in the treatment of hypertrophic cardiomyopathy,16 and their efficacy is also valid in the management of DLVOTO without septal asymmetry. They act to improve the ob-
struction by decreasing both the chronotropic and inotropic state of the left ventricle. In this case, intravenous labetalol was given. Although this is a mixed ␣- and -adrenergic blocker, its beneficial effect in this patient can be explained by inhibition of the profound -adrenergic mediated splanchnic vasodilation that is common in end-stage liver disease17,18 in conjunction with its negative inotropic and chronotropic effects on the heart. Thus,
Fig 3. Two-dimensional transesophageal echocardiogram image showing the anterior leaflet of the mitral valve in the left ventricular outflow tract.
580
ANISKEVICH ET AL
labetalol’s benefit in this case was most likely multifactorial. Additionally, the discontinuation of epinephrine allowed for the heart rate to decrease to a rate that promoted diastolic filling and relief of SAM. Disopyramidol has also been used in one case report.11 This is a type 1A antiarrhythmic that exerts its effect by improving diastolic function as well as a modest improvement in SVR. It has a slightly less negative inotropic effect when compared with propranolol. TEE played a crucial role in management of this patient. He presented with hemodynamic instability that despite escalating doses of medications and adequate volume resuscitation failed to improve. Upon diagnosing DLVOTO, appropriate measures were taken that led to clinical improvement. Transesophageal echocardiography has been used multiple times during OLT with benefit and with little evidence of detriment.19-22 Suriani et al,20 in a retrospective study, showed that TEE was beneficial and safe in the management of OLT patients intraoperatively. Their study included 23 patients with esophageal varices, and they reported no evi-
dence of variceal bleeding. These findings are supported by 2 earlier studies by Steltzer et al21 and de la Morena et al22 who reported increased sensitivity when comparing TEE with traditional monitors in the evaluation of cardiac function during OLT. It is the authors’ opinion that insertion of a TEE after graft recirculation is associated with an even lower risk of variceal rupture because of decompression of portosystemic shunts. In summary, DLVOTO should be considered in the differential diagnosis of refractory hemodynamic instability during OLT based on the predilection of these patients to this condition. Proper management is similar to that of hypertrophic cardiomyopathy and includes increasing preload and afterload, as well as decreasing the chronotropic and inotropic state of the left ventricle. TEE played an invaluable role in the diagnosis and management of refractory hemodynamic instability in this patient. Based on the evidence supporting its safety, the authors recommend routine use of TEE for management of refractory hypotension during OLT.
REFERENCES 1. Iwakiri Y, Groszmann RJ: The hyperdynamic circulation of chronic liver disease: From the patient to the molecule. Hepatology 43:121-131, 2006 (suppl) 2. Moller S, Henriksen JH: Cardiopulmonary complications in chronic liver disease. World J Gastroenterol 12:526-538, 2006 3. Brown JM, Murtha W, Fraser J, et al: Dynamic left ventricular outflow tract obstruction in critically ill patients. Crit Care Resusc 4:170-172, 2002 4. Turnage WS, Zeller FA, Divertie GD: Dynamic left ventricular outflow tract obstruction. Diagnosis by transesophageal echocardiography in a critically ill patient. Chest 104:1629-1632, 1993 5. Vaughn-Whitley K, Mooss A: Dynamic left ventricular outflow obstruction related to atrial fibrillation. Chest 102:1618-1619, 1992 6. Murtha W, Guenther C: Dynamic left ventricular outflow obstruction complicating bilateral lung transplantation. Anesth Analg 94:558559, 2002 7. Glas KE, Shanewise JS, Guyton RA: An unusual cause of left ventricular outflow tract obstruction after mitral valve repair. Anesth Analg 99:38-40, 2004 8. Zvara DA, Olympio MA, Frankland MJ, et al: Dynamic left ventricular outflow obstruction during lumbar laminectomy as an unexpected cause of intraoperative hypotension. J Neurosurg Anesthesiol 14:146-148, 2002 9. Armstrong WF, Marcovitz PA: Dynamic left ventricular outflow obstruction as a complication of acute myocardial infarction. Am Heart J 131:827-830, 1996 10. Haley JH, Sinak LJ, Tajik AJ, et al: Dynamic left ventricular outflow tract obstruction in acute coronary syndromes: An important cause of new systolic murmur and cardiogenic shock. Mayo Clinic Proc 74:901-906, 1996 11. Ashudagawa M, Ohara M, Koide Y: An intraoperative diagnosis of dynamic left ventricular outflow tract obstruction using transesophageal echocardiography leads to treatment with intravenous disopyramide. Anesth Analg 92:310-312, 2002
12. Roldan FJ, Vargas-Barron J, Espinola-Zavaleta N, et al: Severe dynamic obstruction of the left ventricular outflow tract induced by dobutamine. Echocardiography 17:37-40, 2000 13. Sorrentino MJ, Marcus RH, Lang RM: Left ventricular outflow obstruction as a cause of hypotension and symptoms during dobutamine stress echocardiography. Clin Cardiol 19:225-230, 1996 14. Aggarwal S, Kang Y, Freeman JA, et al: Postreperfusion syndrome: Cardiovascular collapse following hepatic reperfusion during liver transplantation. Transplant Proc 119:54-55, 1987 (suppl 3) 15. Madu EC, Brown R, Geraci SA: Dynamic left ventricular outflow tract obstruction in critically ill patients: Role of transesophageal echocardiography in therapeutic decision making. Cardiology 88:292-295, 1997 16. Maron BJ: Hypertrophic cardiomyopathy. JAMA 287:13081320, 2002 17. Bihari D, Westaby D, Gimson A, et al: Reductions in portal pressure by selective beta 2-adrenoceptor blockade in patients with cirrhosis and portal hypertension. Br J Clin Pharmacol 17:753-757, 1984 18. Braillon A, Lee SS, Valla D, et al: Comparative haemodynamic effects of betaxolol and propranolol in patients with cirrhosis. Scand J Gastroenterol 23:691-695, 1988 19. Harley ID, Jones EF, Liu G, et al: Orthotopic liver transplantation in two patients with hypertrophic obstructive cardiomyopathy. Br J Anaesth 77:675-677, 1996 20. Suriani RJ, Cutrone A, Feierman D, et al: Intraoperative transesophageal echocardiography during liver transplantation. J Cardiothorac Vasc Anesth 10:699-707, 1996 21. Steltzer H, Blazek G, Gabriel A, et al: Two-dimensional transesophageal echocardiography in early diagnosis and treatment of hemodynamic disturbances during liver transplantation. Transplant Proc 23:1957-1958, 1991 22. De la Morena G, Acosta F, Villegas M, et al: Transesophageal echocardiographic evaluation of left ventricular function during orthotopic liver transplantation. Transplant Proc 25:1832, 1993
P
ATIENTS WITH advanced liver disease are prone to multiple hemodynamic abnormalities.1,2 This susceptibility can be attributed to several factors, including a hyperdynamic left ventricle and chronically lowered systemic vascular resistance (SVR). Surgical manipulation and blood loss during liver transplantation can further worsen this precarious hemodynamic balance. A case of refractory hypotension secondary to dynamic left ventricular outflow tract obstruction (DLVOTO) in a patient with a normal preoperative cardiac evaluation is presented. Intraoperative transesophageal echocardiography (TEE) played a vital role in the diagnosis and management of this disorder after standard pharmacologic therapies failed to improve the blood pressure. The authors believe that intraoperative TEE should be used whenever hemodynamic instability is refractory to standard therapy during liver transplantation. CASE REPORT
A 56-year-old white man (64 kg, 183 cm) presented for orthotopic liver transplantation (OLT) for end-stage liver disease secondary to sclerosing cholangitis complicated by cholangiocarcinoma. His past medical history was significant for renal cell carcinoma that had been in remission since a partial nephrectomy in 2000. He received a standard preoperative evaluation consisting of laboratory testing, echocardiogram, and chest X-ray, all of which were within acceptable limits. Additionally, he received a 2D dobutamine stress echocardiogram that revealed no evidence of ischemia at a maximum heart rate of 139 beats/min. Also noted was a mild degree of mitral regurgitation (MR) and concentric remodeling. No left ventricular outflow tract abnormalities were identified. His ejection fraction was 56%, increasing to 81% with stress. He underwent an uneventful rapid-sequence induction using propofol, succinylcholine, and fentanyl. Anesthesia was then maintained using isoflurane and intermittent fentanyl boluses. Neuromuscular blockade was achieved with cisatracurium. Routine intravenous access consisting of an 8.5F antecubital catheter, 2 radial arterial catheters, and a right internal jugular venous catheter were then obtained. A pulmonary artery catheter (PAC) was placed to monitor continuous cardiac output. His initial intraoperative course was unremarkable except for a brief hypotensive episode occurring with partial inferior vena cava clamping at the initiation of the anhepatic period. This resolved with intravenous fluids, a dopamine infusion, and several 10-g epinephrine boluses. Shortly thereafter, during initiation of graft recirculation, the patient’s blood pressure became very labile. He was administered intravascular volume resuscitation with blood products, and 5% albumin, and aggressive vasopressor support was initiated with intermittent epinephrine boluses and a vasopressin infusion, followed by a phenylephrine infusion. His hemodynamic instability did not improve despite escalating vasopressor dosages. Of note, the readings on the PAC were unchanged with respect to central venous pressure, pulmonary capillary wedge pressure, systolic pulmonary artery pressure, diastolic pulmonary artery pressure (PAD), and SVR in the period immediately preceding the hypotension. During the instability, however, his PAD became elevated, whereas other PAC measurements were near or at baseline (Fig 1). The decision was then made to insert a multiplane TEE probe to assess left ventricular function. Rapid evaluation revealed moderateto-severe DLVOTO with systolic anterior motion (SAM) of the mitral
valve associated with severe MR (Figs 2 and 3). Based on these findings, epinephrine was immediately discontinued and labetalol, 2.5 mg intravenously, was given. This resulted in a rapid reversal of the hemodynamic instability, allowing for the discontinuation of all vasoactive agents with the exception of phenylephrine. The remainder of the intraoperative course was unremarkable. The patient was observed in the ICU after surgery where he had an uneventful recovery. Postoperative echocardiography revealed a hyperdynamic left ventricle with no septal asymmetry and mild MR caused by a prolapsed posterior mitral leaflet. Ejection fraction was noted to be 75% to 80%. DISCUSSION
Dynamic left ventricular outflow tract obstruction in the absence of septal asymmetry has been well described in the literature3-11; however, the authors believe this is the first time DLVOTO has been described intraoperatively during an OLT in a patient with a normal preoperative stress echocardiogram. This patient presented to the operating room with a normal cardiac evaluation and developed hemodynamic instability during graft recirculation. DLVOTO induced during dobutamine cardiac stress testing has been described12,13; however, this patient had an uneventful stress test despite reaching a heart rate of 139 beats/min. During recirculation of the donor liver, he developed acute outflow tract obstruction. Although it is uncertain as to the exact etiology of the new outflow obstruction, several factors may have played a contributory role. First, the uptake of blood by the donor liver would have decreased preload, as evidenced by a decrease in the pulmonary artery diastolic pressure. Second, the release of cold blood from the cadaveric liver along with vasoactive substances (the reperfusion syndrome)14 may have stunned the peripheral circulation. This loss of preload, coupled with the sudden drop in SVR, may have been enough to allow for a “perfect storm” in which a patient with a predisposition for DLVOTO may actually develop the obstruction. DLVOTO is characterized by turbulence through the left ventricular outflow tract, hypercontractility of the left ventricle, SAM, and some degree of late mitral regurgitation.11 Patients undergoing OLT are at an elevated risk of developing DLVOTO because of their pre-existing hyperdynamic cardiac state and their chronically low SVR. During periods of relative hypovolemia, this hyperdynamic state is further worsened and DLVOTO may occur. The first clue to the development of DLVOTO may be a paradoxic decrease in the blood pressure after administration of positive inotropes.15 Another intraoper-
From the Department of Anesthesiology, Mayo Clinic, Jacksonville, FL. Address reprint requests to Stephen Aniskevich, MD, Department of Anesthesiology, Mayo Clinic, 4500 San Pablo Rd, Jacksonville, FL 32224. E-mail: [email protected] © 2007 Elsevier Inc. All rights reserved. 1053-0770/07/2104-0021$32.00/0 doi:10.1053/j.jvca.2006.07.024 Key words: liver transplantation, transesophageal echocardiography, dynamic left ventricular outflow tract obstruction, refractory hypotension, systolic anterior motion, mitral valve
Journal of Cardiothoracic and Vascular Anesthesia, Vol 21, No 4 (August), 2007: pp 577-580
577
578
ANISKEVICH ET AL
Fig 1. Intraoperative hemodynamics. The period of dynamic left ventricular outflow obstruction is defined by the rectangular box. (Color version of figure is available online.)
ative finding is the sudden occurrence of a systolic murmur of increasing intensity if an esophageal stethoscope is being monitored. At this institution, epinephrine is the first-line medication to treat severe hypotension during liver transplantation. In this case, the patient developed tachycardia with little improvement in blood pressure. SAM worsened because of the hypercontractile state, resulting in outflow obstruction and severe mitral regurgitation. The intraventricular geometry combined with the hyperdynamic state of advanced liver disease were predetermining factors for the development of DLVOTO. Because the vasoactive agents were increased, the DLVOTO worsened, as did the degree of MR, consistent with the pres-
ence of a rising V wave on the PAC tracing. This continued despite seemingly adequate fluid resuscitation as assessed by the elevated pulmonary diastolic pressures. It was not until proper evaluation with TEE revealed the pathology that the appropriate steps were taken to reverse the condition. Typically, treatment of DLVOTO consists of increasing left ventricular end-diastolic dimensions and decreasing the inotropic state of the heart. Several approaches can be used concurrently. End-diastolic dimension can be improved with aggressive intravascular volume loading to increase preload. Additionally, improving the SVR will splint open the outflow tract by decreasing the role of the Venturi effect. The drug of choice for this is
DLVOTO DURING LIVER TRANSPLANTATION
579
Fig 2. Transesophageal echocardiogram color Doppler. Note the severe mitral regurgitation and turbulence through the outflow tract indicative of dynamic left ventricular outflow obstruction.
phenylephrine because of its selectivity for ␣-adrenergic receptors. Phenylephrine may also cause a reflex bradycardia and allow for a longer time in diastole to allow for improved filling. -Adrenergic receptor blockers and calcium channel blockers have proven to be efficacious in the treatment of hypertrophic cardiomyopathy,16 and their efficacy is also valid in the management of DLVOTO without septal asymmetry. They act to improve the ob-
struction by decreasing both the chronotropic and inotropic state of the left ventricle. In this case, intravenous labetalol was given. Although this is a mixed ␣- and -adrenergic blocker, its beneficial effect in this patient can be explained by inhibition of the profound -adrenergic mediated splanchnic vasodilation that is common in end-stage liver disease17,18 in conjunction with its negative inotropic and chronotropic effects on the heart. Thus,
Fig 3. Two-dimensional transesophageal echocardiogram image showing the anterior leaflet of the mitral valve in the left ventricular outflow tract.
580
ANISKEVICH ET AL
labetalol’s benefit in this case was most likely multifactorial. Additionally, the discontinuation of epinephrine allowed for the heart rate to decrease to a rate that promoted diastolic filling and relief of SAM. Disopyramidol has also been used in one case report.11 This is a type 1A antiarrhythmic that exerts its effect by improving diastolic function as well as a modest improvement in SVR. It has a slightly less negative inotropic effect when compared with propranolol. TEE played a crucial role in management of this patient. He presented with hemodynamic instability that despite escalating doses of medications and adequate volume resuscitation failed to improve. Upon diagnosing DLVOTO, appropriate measures were taken that led to clinical improvement. Transesophageal echocardiography has been used multiple times during OLT with benefit and with little evidence of detriment.19-22 Suriani et al,20 in a retrospective study, showed that TEE was beneficial and safe in the management of OLT patients intraoperatively. Their study included 23 patients with esophageal varices, and they reported no evi-
dence of variceal bleeding. These findings are supported by 2 earlier studies by Steltzer et al21 and de la Morena et al22 who reported increased sensitivity when comparing TEE with traditional monitors in the evaluation of cardiac function during OLT. It is the authors’ opinion that insertion of a TEE after graft recirculation is associated with an even lower risk of variceal rupture because of decompression of portosystemic shunts. In summary, DLVOTO should be considered in the differential diagnosis of refractory hemodynamic instability during OLT based on the predilection of these patients to this condition. Proper management is similar to that of hypertrophic cardiomyopathy and includes increasing preload and afterload, as well as decreasing the chronotropic and inotropic state of the left ventricle. TEE played an invaluable role in the diagnosis and management of refractory hemodynamic instability in this patient. Based on the evidence supporting its safety, the authors recommend routine use of TEE for management of refractory hypotension during OLT.
REFERENCES 1. Iwakiri Y, Groszmann RJ: The hyperdynamic circulation of chronic liver disease: From the patient to the molecule. Hepatology 43:121-131, 2006 (suppl) 2. Moller S, Henriksen JH: Cardiopulmonary complications in chronic liver disease. World J Gastroenterol 12:526-538, 2006 3. Brown JM, Murtha W, Fraser J, et al: Dynamic left ventricular outflow tract obstruction in critically ill patients. Crit Care Resusc 4:170-172, 2002 4. Turnage WS, Zeller FA, Divertie GD: Dynamic left ventricular outflow tract obstruction. Diagnosis by transesophageal echocardiography in a critically ill patient. Chest 104:1629-1632, 1993 5. Vaughn-Whitley K, Mooss A: Dynamic left ventricular outflow obstruction related to atrial fibrillation. Chest 102:1618-1619, 1992 6. Murtha W, Guenther C: Dynamic left ventricular outflow obstruction complicating bilateral lung transplantation. Anesth Analg 94:558559, 2002 7. Glas KE, Shanewise JS, Guyton RA: An unusual cause of left ventricular outflow tract obstruction after mitral valve repair. Anesth Analg 99:38-40, 2004 8. Zvara DA, Olympio MA, Frankland MJ, et al: Dynamic left ventricular outflow obstruction during lumbar laminectomy as an unexpected cause of intraoperative hypotension. J Neurosurg Anesthesiol 14:146-148, 2002 9. Armstrong WF, Marcovitz PA: Dynamic left ventricular outflow obstruction as a complication of acute myocardial infarction. Am Heart J 131:827-830, 1996 10. Haley JH, Sinak LJ, Tajik AJ, et al: Dynamic left ventricular outflow tract obstruction in acute coronary syndromes: An important cause of new systolic murmur and cardiogenic shock. Mayo Clinic Proc 74:901-906, 1996 11. Ashudagawa M, Ohara M, Koide Y: An intraoperative diagnosis of dynamic left ventricular outflow tract obstruction using transesophageal echocardiography leads to treatment with intravenous disopyramide. Anesth Analg 92:310-312, 2002
12. Roldan FJ, Vargas-Barron J, Espinola-Zavaleta N, et al: Severe dynamic obstruction of the left ventricular outflow tract induced by dobutamine. Echocardiography 17:37-40, 2000 13. Sorrentino MJ, Marcus RH, Lang RM: Left ventricular outflow obstruction as a cause of hypotension and symptoms during dobutamine stress echocardiography. Clin Cardiol 19:225-230, 1996 14. Aggarwal S, Kang Y, Freeman JA, et al: Postreperfusion syndrome: Cardiovascular collapse following hepatic reperfusion during liver transplantation. Transplant Proc 119:54-55, 1987 (suppl 3) 15. Madu EC, Brown R, Geraci SA: Dynamic left ventricular outflow tract obstruction in critically ill patients: Role of transesophageal echocardiography in therapeutic decision making. Cardiology 88:292-295, 1997 16. Maron BJ: Hypertrophic cardiomyopathy. JAMA 287:13081320, 2002 17. Bihari D, Westaby D, Gimson A, et al: Reductions in portal pressure by selective beta 2-adrenoceptor blockade in patients with cirrhosis and portal hypertension. Br J Clin Pharmacol 17:753-757, 1984 18. Braillon A, Lee SS, Valla D, et al: Comparative haemodynamic effects of betaxolol and propranolol in patients with cirrhosis. Scand J Gastroenterol 23:691-695, 1988 19. Harley ID, Jones EF, Liu G, et al: Orthotopic liver transplantation in two patients with hypertrophic obstructive cardiomyopathy. Br J Anaesth 77:675-677, 1996 20. Suriani RJ, Cutrone A, Feierman D, et al: Intraoperative transesophageal echocardiography during liver transplantation. J Cardiothorac Vasc Anesth 10:699-707, 1996 21. Steltzer H, Blazek G, Gabriel A, et al: Two-dimensional transesophageal echocardiography in early diagnosis and treatment of hemodynamic disturbances during liver transplantation. Transplant Proc 23:1957-1958, 1991 22. De la Morena G, Acosta F, Villegas M, et al: Transesophageal echocardiographic evaluation of left ventricular function during orthotopic liver transplantation. Transplant Proc 25:1832, 1993