Albert T. Cheung

ASE/SCA guidelines for performing a comprehensive intraoperative multiplane transesophageal echocardiography examination: recommendations of the American Society of Echocardiography Council for Intraoperative Echocardiography and the Society of Cardiovascular Anesthesiologists Task Force for Certification in Perioperative Transesophageal Echocardiography.

Since the introduction of transesophageal echocardiography (TEE) to the operating room in the early 1980s,1-4 its effectiveness as a clinical monitor to assist in the hemodynamic management of patients during general anesthesia and its reliability to make intraoperative diagnoses during cardiac operations has been well established.5-26 In recognition of the increasing clinical applications and use of intraoperative TEE, the American Society of Echocardiography (ASE) established the Council for Intraoperative Echocardiography in 1993 to address issues related to the use of echocardiography in the operating room. In June 1997, the Council board decided to create a set of guidelines for performing a comprehensive TEE examination composed of a set of anatomically directed cross-sectional views. The Society of Cardiovascular Anesthesiologists Task Force for Certification in Perioperative Transesophageal Echocardiography has endorsed these guidelines and standards of nomenclature for the various anatomically directed cross-sectional views of the comprehensive TEE examination. This document, therefore, is the collective result of an effort that represents the consensus view of both anesthesiologists and cardiologists who have extensive experience in intraoperative echocardiography. The writing group has several goals in mind in creating these guidelines. The first is to facilitate training in intraoperative TEE by providing a framework in which to develop the necessary knowledge and skills. The guidelines may also enhance quality improvement by providing a means to assess the technical quality and completeness of individual studies. More consistent acquisition and description of intraoperative echocardiographic data will facilitate communication between centers and provide a basis for multicenter investigations. In recognition of the increasing availability and advantages of digital image storage, the guidelines define a set of cross-sectional views and nomenclature that constitute a comprehensive intraoperative TEE examination that could be stored in a digital format. These guidelines will encourage industry to develop echocardiography systems that allow quick and easy acquisition, labeling, and storage of images in the operating room, as well as a simple mechanism for side-by-side comparison of views made at different times. ASE/SCA Guidelines for Performing a Comprehensive Intraoperative Multiplane Transesophageal Echocardiography Examination: Recommendations of the American Society of Echocardiography Council for Intraoperative Echocardiography and the Society of Cardiovascular Anesthesiologists Task Force for Certification in Perioperative Transesophageal Echocardiography

Echocardiographic and Hemodynamic Indexes of Left Ventricular Preload in Patients with Normal and Abnormal Ventricular Function

BackgroundTransesophageal echocardiography (TEE) is used to diagnose hypovolemia despite the lack of validation studies. The objective was to determine the effects of acute graded hypovolemia on TEE and conventional hemodynamic determinants of left ventricular (LV) preload in anesthetized patients with normal and abnormal LV function. MethodsDeterminants of LV preload derived from TEE and hemodynamic monitoring were measured serially in 35 anesthetized cardiac surgical patients without valvular heart disease. Patients were stratified into two groups: those with normal LV function (group 1, n = 17) and those with LV wall motion abnormalities (group 2, n = 13). Patients in groups 1 and 2 were subjected to graded hypovolemia produced by collecting 6 aliquots of blood, each equal to 2.5% of their estimated blood volume (EBV). A third group of patients (group 3, n = 5), not subjected to graded hypovolemia, were studied to test for time-dependent changes. ResultsGroup 2 had a significantly greater baseline (mean ± SD) pulmonary artery occlusion pressure (17 ± 6 vs. 11 ± 6 mmHg), LV end-diastolic area (23 ± 5 vs. 18 ± 4 cm2), LV enddiastolic wall stress (23 ± 10 vs. 14 ± 6 X 103 dyne · cm−2), and smaller fractional area change (35 ± 13 vs. 59 ± 7%). In groups 1 and 2, the LV end-diastolic area, pulmonary artery occlusion pressure, and LV end-diastolic wall stress decreased linearly in response to blood loss in the range of 0–15% of the EBV. No significant changes in the measured parameters occurred in group 3. A significant decrease in the central venous pressure, pulmonary artery occlusion pressure, and LV end-diastolic area was detected in response to a 2.5% EBV deficit (approximately 1.75 ml · kg−1) in groups 1 and 2. The mean change in LV end-diastolic area (0.3 cm2/1.0% EBV deficit) in response to equivalent EBV deficits was the same in groups 1 and 2. In contrast, the mean change in cardiac output and LV end-diastolic wall stress was less in group 2 despite a greater decrease in pulmonary artery occlusion pressure. Compared to group 1, a greater EBV deficit (7.5% to 12.5% vs. 2.5% to 5%) was required in group 2 to cause a significant decrease in the cardiac output, stroke volume, mixed venous oxygen saturation, and LV end-diastolic wall stress. ConclusionsTEE and hemodynamic determinants of LV preload detected changes in LV function caused by acute blood loss. Acute blood loss caused directional changes in LV end-diastolic area, pulmonary artery occlusion pressure, and LV end-diastolic wall stress even in patients with LV wall motion abnormalities. Changes in LV end-diastolic wall stress, derived from both TEE and hemodynamic measurements corresponded to changes in cardiac output, stroke volume, and mixed venous oxygen saturation that occurred during acute blood loss.

The hemodynamic and adrenergic effects of perioperative dexmedetomidine infusion after vascular surgery.

UNLABELLED We tested dexmedetomidine, an alpha(2) agonist that decreases heart rate, blood pressure, and plasma norepinephrine concentration, for its ability to attenuate stress responses during emergence from anesthesia after major vascular operations. Patients scheduled for vascular surgery received either dexmedetomidine (n = 22) or placebo (n = 19) IV beginning 20 min before the induction of anesthesia and continuing until 48 h after the end of surgery. All patients received standardized anesthesia. Heart rate and arterial blood pressure were kept within predetermined limits by varying anesthetic level and using vasoactive medications. Heart rate, arterial blood pressure, and inhaled anesthetic concentration were monitored continuously; additional measurements included plasma and urine catecholamines. During emergence from anesthesia, heart rate was slower with dexmedetomidine (73 +/- 11 bpm) than placebo (83 +/- 20 bpm) (P = 0.006), and the percentage of time the heart rate was within the predetermined hemodynamic limits was more frequent with dexmedetomidine (P < 0.05). Plasma norepinephrine levels increased only in the placebo group and were significantly lower for the dexmedetomidine group during the immediate postoperative period (P = 0.0002). We conclude that dexmedetomidine attenuates increases in heart rate and plasma norepinephrine concentrations during emergence from anesthesia. IMPLICATIONS The alpha(2) agonist, dexmedetomidine, attenuates increases in heart rate and plasma norepinephrine concentrations during emergence from anesthesia in vascular surgery patients.

Deep hypothermic circulatory arrest: I. Effects of cooling on electroencephalogram and evoked potentials

BACKGROUND Deep hypothermia is an important cerebral protectant and is critical in procedures requiring circulatory arrest. The purpose of this study was to determine the factors that influence the neurophysiologic changes during cooling before circulatory arrest, in particular the occurrence of electrocerebral silence. METHODS In 109 patients undergoing hypothermic circulatory arrest with neurophysiologic monitoring, five electrophysiologic events were selected for detailed study. RESULTS The mean nasopharyngeal temperature when periodic complexes appeared in the electroencephalogram after cooling was 29.6 degrees C +/- 3 degrees C, electroencephalogram burst-suppression appeared at 24.4 degrees C +/- 4 degrees C, and electrocerebral silence appeared at 17.8 degrees C +/- 4 degrees C. The N20-P22 complex of the somatosensory evoked response disappeared at 21.4 degrees C +/- 4 degrees C, and the somatosensory evoked response N13 wave disappeared at 17.3 degrees C +/- 4 degrees C. The temperatures of these various events were not significantly affected by any patient-specific or surgical variables, although the time to cool to electrocerebral silence was prolonged by high hemoglobin concentrations, low arterial partial pressure of carbon dioxide, and by slow cooling rates. Only 60% of patients demonstrated electrocerebral silence by either a nasopharyngeal temperature of 18 degrees C or a cooling time of 30 minutes. CONCLUSIONS With the high degree of interpatient variability in these neurophysiologic measures, the only absolute predictors of electrocerebral silence were nasopharyngeal temperature below 12.5 degrees C and cooling longer than 50 minutes.

The ECLIPSE trials: comparative studies of clevidipine to nitroglycerin, sodium nitroprusside, and nicardipine for acute hypertension treatment in cardiac surgery patients.

BACKGROUND: Acute hypertension during cardiac surgery can be difficult to manage and may adversely affect patient outcomes. Clevidipine is a novel, rapidly acting dihydropyridine L-type calcium channel blocker with an ultrashort half-life that decreases arterial blood pressure (BP). The Evaluation of CLevidipine In the Perioperative Treatment of Hypertension Assessing Safety Events trial (ECLIPSE) was performed to compare the safety and efficacy of clevidipine (CLV) with nitroglycerin (NTG), sodium nitroprusside (SNP), and nicardipine (NIC) in the treatment of perioperative acute hypertension in patients undergoing cardiac surgery. METHODS: We analyzed data from three prospective, randomized, open-label, parallel comparison studies of CLV to NTG or SNP perioperatively, or NIC postoperatively in patients undergoing cardiac surgery at 61 medical centers. Of the 1964 patients enrolled, 1512 met postrandomization inclusion criteria of requiring acute treatment of hypertension based on clinical criteria. The patients were randomized 1:1 for each of the three parallel comparator treatment groups. The primary outcome was the incidence of death, myocardial infarction, stroke or renal dysfunction at 30 days. Adequacy and precision of BP control was evaluated and is reported as a secondary outcome. RESULTS: There was no difference in the incidence of myocardial infarction, stroke or renal dysfunction for CLV-treated patients compared with the other treatment groups. There was no difference in mortality rates between the CLV, NTG or NIC groups. Mortality was significantly higher, though, for SNP-treated patients compared with CLV-treated patients (P = 0.04). CLV was more effective compared with NTG (P = 0.0006) or SNP (P = 0.003) in maintaining BP within the prespecified BP range. CLV was equivalent to NIC in keeping patients within a prespecified BP range; however, when BP range was narrowed, CLV was associated with fewer BP excursions beyond these BP limits compared with NIC. CONCLUSIONS: CLV is a safe and effective treatment for acute hypertension in patients undergoing cardiac surgery.

Hematocrit, volume expander, temperature, and shear rate effects on blood viscosity.

Our goal was to determine and predict the effects of temperature, shear rate, hematocrit, and different volume expanders on blood viscosity in conditions mimicking deep hypothermia for cardiac operations. Blood was obtained from six healthy adults. Dilutions were prepared to hematocrits of 35%, 30%, 22.5%, and 15% using plasma, 0.9% NaCl, 5% human albumin, and 6% hydroxyethyl starch. Viscosity was measured over a range of shear rates (4.5–450 s−1) and temperature (0°–37°C). A parametric expression for predicting blood viscosity based on the study variables was developed, and its agreement with measured values tested. Viscosity was higher at low shear rates and low temperatures, especially at temperatures less than 15°C (P < 0.016 for all conditions in comparison with 37°C). Decreasing hematocrit, especially to less than 22.5%, decreased viscosity. Hemodilution with albumin or 0.9% NaCl decreased blood viscosity more than hemodilution with plasma or 6% hydroxyethyl starch (P < 0.01 for all cases). The derived mathematical model for viscosity as a function of temperature, hematocrit, shear rate, and diluent predicted viscosity values that correlated well with the measured values in experimental samples (r2 > 0.92, P < 0.001). Implications A theoretical model for blood viscosity predicted independent effects of temperature, shear rate, and hemodilution on viscosity over a wide range of physiologic conditions, including thermal extremes of deep hypothermia in an experimental setting. Moderate hemodilution to a hematocrit of 22% decreased blood viscosity by 30%–50% at a blood temperature of 15°C, suggesting the potential to improve microcirculatory perfusion during deep hypothermia.

Surgical Management of Descending Thoracic Aortic Disease: Open and Endovascular Approaches A Scientific Statement From the American Heart Association

Recent years have witnessed the emergence of novel technologies that enable less invasive endovascular treatment of descending thoracic aortic disease (TAD). This has occurred against a backdrop of improved identification of various disease processes and better results with open surgical repair. The natural history of the specific acute aortic syndromes that affect the descending thoracic aorta has also been described with more clarity and has become more commonly recognized. This is in part secondary to the widespread availability and application of advanced imaging technologies that permit precise diagnoses. As data are accumulating, these pathological processes involving the descending thoracic aorta are no longer thought of as simply variants of one another but as distinct entities with well-defined clinical behavior. As the technology for endovascular repair continues to mature and its utilization increases, there is a need for a careful assessment of the current state of medical management, traditional open therapy, and evolving endovascular treatment of distinct thoracic aortic pathologies. The purpose of this scientific statement is to present a contemporary review of the various pathological processes that affect the descending thoracic aorta: Aneurysms, dissections, intramural hematomas (IMHs), penetrating atherosclerotic ulcers (PAUs), and aortic transections. These disorders will be considered in detail, with an exploration of the natural history, available treatment options, and controversies regarding management. Current intervention criteria will be reviewed with respect to both open surgical repair and endovascular treatment. Our goal is to provide the healthcare professional with a better understanding of the pathophysiology of the various disease processes that involve the descending thoracic aorta and to review current outcomes and technical pitfalls associated with these therapies to facilitate strong, evidence-based decision making in the care of these patients. Treatment of descending TAD involves complex, exigent decision making in an era of evolving technology. Survival data for nonoperative …

Interventions for reversing delayed-onset postoperative paraplegia after thoracic aortic reconstruction

BACKGROUND Delayed postoperative paraplegia is a recognized complication of thoracic (TAA) or thoracoabdominal aortic aneurysm (TAAA) repair. The purpose of this study was to evaluate the effectiveness of interventions to treat delayed-onset paraplegia. METHODS Between January 1, 2000 and August 31, 2001, 99 patients underwent surgical repair of TAA, Crawford type I, II, or III TAAA. Standard intraoperative management included distal aortic perfusion and cerebrospinal fluid (CSF) drainage unless contraindicated. Therapeutic interventions to treat delayed paraplegia included lumbar CSF drainage and vasopressor therapy. RESULTS Three of the 99 patients had paraplegia upon awakening. Delayed-onset paraplegia occurred in 8 patients, 2 of whom had recurrent episodes. In those 8 patients, the initial episode occurred at a median of 21.6 hours (range 6.4 to 110.0 hours) after surgery and the second episode averaged 176 hours after surgery. At the onset of paraplegia, the average mean arterial pressure was 74 mm Hg and CSF pressure was 14 mm Hg. Three of the 8 patients had a functioning CSF catheter at the onset and the other 5 patients had catheters subsequently placed. Therapeutic interventions increased blood pressure to a mean arterial pressure of 95 mm Hg and decreased CSF pressure to 10 mm Hg. Five of the 8 patients with delayed-onset paraplegia made a full neurologic recovery and 3 had partial recovery. CONCLUSIONS Patients with delayed-onset paraplegia had an increased chance of recovery as compared with those patients in whom paraplegia was diagnosed upon emergence from anesthesia. Acute interventions directed to increase spinal cord perfusion by increasing systemic blood pressure and decreasing CSF pressure were effective for the reversal of delayed onset of paraplegia after TAA or TAAA repair, resulting in an overall 3% incidence of permanent paraplegia and 3% incidence of residual paraparesis.

Risk factors, outcomes, and clinical manifestations of spinal cord ischemia following thoracic endovascular aortic repair

OBJECTIVE The purpose of this study was to assess the incidence, risk factors, and clinical manifestations of spinal cord ischemia (SCI) after thoracic endovascular aortic repair (TEVAR). METHODS A retrospective review of a prospectively collected database was performed for all patients undergoing TEVAR at a single academic institution between July 2002 and June 2010. Preoperative demographics, procedure-related variables, and clinical details related to SCI were examined. Logistic regression analysis was performed to identify risk factors for the development of SCI. RESULTS Of the 424 patients who underwent TEVAR during the study period, 12 patients (2.8%) developed SCI. Mean age of this cohort with SCI was 69.6 years (range, 44-84 years), and 7 were women. One-half of these patients had prior open or endovascular aortic repair. Indication for surgery was either degenerative aneurysm (n = 8) or dissection (n = 4). Six TEVARs were performed electively, with the remaining done either urgently or emergently due to contained rupture (n = 2), dissection with malperfusion (n = 2), or severe back pain (n = 2). All 12 patients underwent extent C endovascular coverage. Multivariate regression analysis demonstrated chronic renal insufficiency to be independently associated with SCI (odds ratio [OR], 4.39; 95% confidence interval [CI], 1.2-16.6; P = .029). Onset of SCI occurred at a median of 10.6 hours (range, 0-229 hours) postprocedure and was delayed in 83% (n = 10) of patients. Clinical manifestations of SCI included lower extremity paraparesis in 9 patients and paraplegia in 3 patients. At SCI onset, average mean arterial pressure (MAP) and lumbar cerebrospinal fluid (CSF) pressure was 77 mm Hg and 10 mm Hg, respectively. Therapeutic interventions increased blood pressure to a significantly higher average MAP of 99 mm Hg (P = .001) and decreased lumbar CSF pressure to a mean of 7 mm Hg (P = .30) at the time of neurologic recovery. Thirty-day mortality was 8% (1 of 12 patients). The single patient who expired, never recovered any lower extremity neurologic function. All patients surviving to discharge experienced either complete (n = 9) or incomplete (n = 2) neurologic recovery. At mean follow-up of 49 months, 7 of 9 patients currently alive continued to exhibit complete, sustained neurologic recovery. CONCLUSION Spinal cord ischemia after TEVAR is an uncommon, but important complication. Preoperative renal insufficiency was identified as a risk factor for the development of SCI. Early detection and treatment of SCI with blood pressure augmentation alone or in combination with CSF drainage was effective in most patients, with the majority achieving complete, long-term neurologic recovery.

Deep hypothermic circulatory arrest: II. Changes in electroencephalogram and evoked potentials during rewarming.

BACKGROUND Electrophysiologic studies during rewarming after deep hypothermic circulatory arrest probe the state of the brain during this critical period and may provide insight into the neurological effects of circulatory arrest and the neurologic outcome. METHODS Electroencephalogram (EEG) and evoked potentials were monitored during rewarming in 109 patients undergoing aortic surgery with hypothermic circulatory arrest. RESULTS The sequence of neurophysiologic events during rewarming did not mirror the events during cooling. The evoked potentials recovered first followed by EEG burst-suppression and then continuous EEG. The time to recovery of the evoked potentials N20-P22 complex was significantly correlated with the time of circulatory arrest even in patients without postoperative neurologic deficits (r = 0.37, (p = 0.002). The nasopharyngeal temperatures at which continuous EEG activity and the N20-P22 complex returned were strongly correlated (r = 0.44, p = 0.0002; r = 0.41, p = 0.00003) with postoperative neurologic impairment. Specifically, the relative risk for postoperative neurologic impairment increased by a factor of 1.56 (95% CI 1.1 to 2.2) for every degree increase in temperature at which the EEG first became continuous. CONCLUSIONS No trend toward shortened recovery times or improved neurologic outcome was noted with lower temperatures at circulatory arrest, indicating that the process of cooling to electrocerebral silence produced a relatively uniform degree of cerebral protection, independent of the actual nasopharyngeal temperature.