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The cardiothoracic surgery intensive care unit (CTICU) has evolved as a separate entity from the general surgical intensive care unit as management for cardiac surgery patients has become streamlined and algorithm driven. Critical care is best managed when the service is designed for a homogeneous population with a circumscribed set of medical and surgical issues. The repetition involved with the subspecialty care allows health care providers such as primary care nurses, nurse practitioners, physician assistants, and other ancillary services to become appropriately focused on issues pertinent to this population. The goals of the CTICU include the attainment of rapid and safe recovery from surgery and anesthesia despite decreasing resources, increasing patient age and comorbidity, and increasing complexity of the operative procedure. The coordinated and systematic approach to the postoperative cardiac surgery patient under the direction of a staff physician offers the most effective opportunity to achieve these expectations at this time. The traditional model of staffing by a physician with responsibilities that conflict temporally with the immediacy often needed for the postoperative care of cardiac patients may expose patients to unnecessary risks. A responsible physician should be available in the CTICU, especially during the immediate postoperative period when physical assessment and direct hands-on involvement are essential. In an era when the operative team (ie, cardiac surgeon and cardiac anesthesiologist) must return to the surgical suite soon after the patient arrives in the intensive care unit, the presence of a physician dedicated to postoperative medical and surgical management becomes mandatory. According to the Joint Commission on Accreditation of Healthcare Organizations, "Each special care unit is properly directed and staffed according to the nature of the special patient care needs anticipated and scope of services provided." The assignment of staff is designed to match experience with patient acuity.

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UNLABELLED: The objective of this study was to evaluate the efficacy of nicardipine, a dihydropyridine calcium channel antagonist, administered as an IV bolus dose to acutely decrease arterial pressure in anesthetized cardiac surgical patients. We performed a double-blind, randomized, self-controlled, dose-ranging study in 40 adult cardiac surgical patients to determine the pharmacokinetics and pharmacodynamics of nicardipine 0.25 mg, 0.50 mg, 1.00 mg, and 2.00 mg administered as an IV bolus. Transesophageal echocardiography was used to assess left ventricular preload, afterload, and global systolic function. Plasma nicardipine concentration was measured using high-performance liquid chromatography. Nicardipine selectively decreased arterial pressure in a dose-dependent manner with a maximum response within 100 s and recovery to half the maximum response within 3-7 min without associated changes in heart rate. The decreases in arterial pressure were associated with only small decreases in left ventricular end-systolic wall stress and small increases in global left ventricular systolic function without changes in left ventricular end-diastolic cavity area or cardiac output. The time course for nicardipine bolus was consistent with a two-compartment pharmacokinetic model with rapid redistribution from a small central compartment. IMPLICATIONS: Nicardipine was effective for selectively decreasing arterial blood pressure acutely, but had no effects on ventricular preload or cardiac output. The absence of dose-dependent changes in cardiac output, left ventricular systolic performance, and left ventricular afterload despite significant decreases in arterial pressure suggested that nicardipine had a small negative inotropic action.

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A novel simple method of extraction, separation, identification and quantification of nicardipine in human plasma samples was completely studied. The human plasma samples were initially purified by solid-phase extraction (SPE) using a C18 cartridge. The extracted samples were separated and nicardipine present in the samples was quantified by high-performance liquid chromatography (HPLC) on a reversed-phase C18 column employing a mobile phase consisting of 60% (v/v) acetonitrile in 0.02 M NaH2PO4 with pH of 6.3 and a variable wavelength UV detector set at 254 nm. The recovery of nicardipine from plasma samples using selective SPE was 91+/-6.0% and had less interfering compounds in the HPLC analysis compared to the use of liquid-liquid (L/L) extraction. In the HPLC analysis, examining the effect of pH values of the mobile phase on the capacity factor (k') of nicardipine revealed a method for selecting a critical k' value of nicardipine to eliminate interfering peaks near the peak specific to the analyte. This method for quantification of nicardipine in human plasma samples was suitable for studying the pharmacokinetic profile of nicardipine administered as an intravenous bolus to cardiac surgical patients.

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A 58-year-old man with fever and chest wall tenderness was seen 8 weeks after aortic valve replacement. His initial postoperative course had been complicated by mediastinitis, requiring antibiotics and surgical debridement. A transthoracic echocardiogram did not reveal the culprit lesion. Pseudoaneurysm of the ascending aorta was suspected, based on computerized tomographic and magnetic resonance images of the chest. Intraoperative transesophageal echocardiography confirmed the diagnosis of pseudoaneurysm and was a key component in the patient's operative management.

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OBJECTIVES: The objectives of this study were to determine if monitoring of intraoperative somatosensory evoked potentials could be used to detect stroke during cardiac operations and to establish indicators of cerebral ischemia based on changes in these potentials. METHODS: Twenty-five patients undergoing cardiac operations underwent preoperative and postoperative neurologic examinations as well as intraoperative recording of somatosensory evoked potentials. Detailed analysis of the waveforms of these potentials was performed. RESULTS: Two of the 25 patients had intraoperative strokes. These patients and only these patients had changes in their somatosensory evoked potentials during the operation suggesting cerebral ischemia. The unilateral disappearance of the cortical somatosensory evoked potential waves correlated significantly with the clinical outcome of stroke (p < 0.004). Ischemic changes were detected in real time and were related to the removal of the aortic crossclamp in one patient and to the initiation of cardiopulmonary bypass in the other. CONCLUSIONS: Somatosensory evoked potentials can detect intraoperative stroke during cardiac operations. Acute, unilateral decreases in amplitude of the cortical potential are more useful than changes in latency in detecting intraoperative stroke.

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OBJECTIVE: To determine the incidence, predictors, and cost of atrial fibrillation and flutter (AFIB) following coronary artery bypass graft (CABG) surgery. DESIGN: Prospective observational study (MultiCenter Study of Perioperative Ischemia). SETTING: Twenty-four university-affiliated hospitals in the United States from 1991 to 1993. SUBJECTS: A total of 2417 patients undergoing CABG with or without concurrent valvular surgery selected using a systematic sampling interval. MEASUREMENTS: Detailed preoperative, intraoperative, and postoperative data collected on standardized reporting forms. RESULTS: The overall incidence of postoperative AFIB was 27 percent. Independent predictors of postoperative AFIB included advanced age (odds ratio [OR], 1.24 per 5-year increase; 95 percent confidence interval [CI], 1.18-1.31); male sex (OR, 1.41; 95 percent CI, 1.09-1.81); a history of AFIB (OR, 2.28; 95 percent CI, 1.74-3.00); a history of congestive heart failure (OR, 1.31; 95 percent CI, 1.04-1.64); and a precardiopulmonary bypass heart rate of more than 100 beats per minute (OR, 1.59; 95 percent CI, 1.00-2.55). Surgical practices such as pulmonary vein venting (OR, 1.44; 95 percent CI, 1.13-1.83); bicaval venous cannulation (OR, 1.40; 95 percent CI, 1.04-1.89); postoperative atrial pacing (OR, 1.27; 95 percent CI, 1.00-1.62); and longer cross-clamp times (OR, 1.06 per 15 minutes; 95 percent CI, 1.00-1.11) also were identified as independent predictors of postoperative AFIB. Patients with postoperative AFIB remained an average of 13 hours longer in the intensive care unit and 2.0 days longer in the ward when compared with patients without AFIB. CONCLUSION: Postoperative AFIB is common after CABG surgery and has a significant effect on both intensive care unit and overall hospital length of stay. In addition to expected demographic factors, certain surgical practices increase the risk of postoperative AFIB. Randomized controlled trials are necessary to determine if modification of these surgical practices, especially in patients at high risk, would decrease the incidence of postoperative AFIB.

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Surgery for valvular heart disease corrects systolic or diastolic dysfunction of the mitral, aortic, or tricuspid valves. The intraoperative echocardiographic assessment of the native heart valve is aimed at defining the pathology of valve disease, determining the mechanism of valve dysfunction, and quantitating the degree (grade) of valvular stenosis or insufficiency.

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BACKGROUND: Measuring the effects of intraaortic balloon counterpulsation (IABP) in single cardiac beats may permit an improved understanding of the physiologic mechanisms by which IABP improves the circulation. The objective of the study was to use trans- esophageal echocardiography in combination with hemodynamic measurements to test the hypothesis that IABP improves global left ventricular systolic function selectively in the IABP-augmented cardiac beats by acutely decreasing left ventricular afterload. METHODS: Twenty-seven studies in which the IABP-to-R wave trigger ratio was serially changed from 1:1, 1:2, 1:4, 0:1 (IABP off) and back to 1:1 were performed in 20 anesthetized cardiac surgical patients during IABP support. Left ventricular short-axis end-diastolic cross-sectional area, end-systolic area, mean end-systolic wall thickness, and ejection time were measured by transesophageal echocardiography at the midpapillary muscle level. Aortic pressure was measured simultaneously from the central lumen of the intraaortic balloon catheter. These measurements were used to calculate the fractional area change, end-systolic meridional wall stress, and heart rate-corrected velocity of circumferential fiber shortening. The echocardiographic and hemodynamic parameters of left ventricular preload, afterload, and systolic function immediately after balloon deflation (IABP-augmented cardiac beats) were compared to the parameters measured during nonaugmented cardiac beats to determine the beat-to-beat effects of IABP on left ventricular function. RESULTS: IABP-augmented cardiac beats had a decreased systolic arterial pressure and end-systolic meridional wall stress and increased diastolic blood pressure, fractional area change, and velocity of circumferential fiber shortening compared to nonaugmented cardiac beats. IABP did not cause significant beat-to-beat changes in heart rate, pulmonary artery diastolic pressure, or central venous pressure. The improvement in left ventricular systolic function associated with IABP-augmented cardiac beats correlated with the decrease in end-systolic meridional wall stress for that cardiac beat. CONCLUSIONS: Beat-to-beat echocardiographic and hemodynamic measurements performed in anesthetized cardiac surgical patients during IABP support demonstrated improved left ventricular systolic function and decreased left ventricular systolic wall stress in the cardiac beats immediately after balloon deflation. The relationship between left ventricular systolic function and left ventricular systolic wall stress during IABP support suggests that afterload reduction was an important mechanism by which IABP instantaneously improved circulatory function in anesthetized cardiac surgical patients.

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The purpose of this study was to determine the extent to which localized hypothermia of a monitored extremity alters the assessment of recovery from vecuronium-induced neuromuscular blockade. Bilateral integrated evoked electromyographic (IEMG) responses were measured in the ulner distribution of 14 anaesthetized patients who had differing upper extremity temperatures as measured at the adductor pollicis to determine whether localized hypothermia alters the clinical assessment of spontaneous recovery from vecuronium-induced neuromuscular blockade. All patients received general anaesthesia with thiopentone, N2O/O2 and opioid; 11/14 patients received isoflurane for blood pressure control. Bilateral adductor pollicis, oesophageal and ambient temperatures, and IEMG evoked response (t1) expressed as percent unparalyzed control were recorded during the anaesthetic. The difference in evoked response between the warmer and the colder upper extremity was calculated at 25%, 50% and 75% spontaneous recovery from neuromuscular blockade in the warm extremity. Differences in temperature between extremities ranged from 0.2-11 degrees C. The difference in IEMG-evoked response between extremities was proportional to the difference in temperature, and there was a direct correlation (r = 0.78) between IEMG response and extremity temperature; IEMG response was absent when extremity temperature was less than 25 degrees C. We concluded that localized hypothermia in the monitored extremity decreases the IEMG-evoked response to vecuronium neuromuscular blockade; the greater the temperature decrease, the less the evoked response.(ABSTRACT TRUNCATED AT 250 WORDS)

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BACKGROUND: Transesophageal 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. METHODS: Determinants 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. RESULTS: Group 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 end-diastolic wall stress (23 +/- 10 vs. 14 +/- 6 x 10(3) 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. CONCLUSIONS: TEE 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.

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A large animal model of ischemic mitral regurgitation (MR) that resembles the multiple presentations of the human disease was developed in sheep. In 76 sheep hearts, the anatomy of the coronary arterial circulation was determined by observation and polymer casts. Two variations, types A and B, which differed by the vessel that supplied the left ventricular apex, were found. In all hearts, the circumflex coronary artery has three marginal branches and terminates in the posterior descending coronary artery. The amount and location of left ventricular (LV) mass supplied by each marginal circumflex branch was determined by dye injection and planimetry. In type A hearts, ligation of the first and second marginal branches infarcts 23% +/- 3.0% of the LV mass, does not infarct either papillary muscle, significantly (p < 0.001) increases LV cavity size 48% at the high papillary muscle level by 8 weeks, and does not cause MR. Ligation of the second and third marginal branches infarcts 21.4% +/- 4.0% of the LV mass, includes the posterior papillary muscle, significantly increases (p < 0.001) LV cavity size 75%, and causes severe MR by 8 weeks. Ligation of the second and third marginal branches and the posterior descending coronary artery infarcts 35% to 40% of the LV mass, increases LV cavity size 39% within 1 hour, and causes massive MR. After moderate (21% to 23%) LV infarction, development of ischemic MR requires both LV dilatation and posterior papillary muscle infarction; neither condition alone produces MR. Large posterior wall infarctions (35% to 40%) that include the posterior papillary muscle produce immediate, severe MR.(ABSTRACT TRUNCATED AT 250 WORDS)

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Transesophageal echocardiography permits measurement of the pulmonary artery diameter (two-dimensional echocardiography) and pulmonary artery blood flow velocity (pulsed-wave Doppler). These measurements considered with the heart rate allow for the determination of pulmonary artery blood flow, which is equivalent to cardiac output. This study compared the precision of transesophageal Doppler-derived cardiac output (DdCO) with the precision of thermodilution cardiac output (TdCO) and examined the agreement between DdCO and TdCO in 33 cardiac surgical patients. The proximal pulmonary artery diameter was measured in triplicate during systole and end expiration, and the local blood flow velocity was recorded on video tape. The instantaneous pulmonary artery blood flow velocity (centimeters per second) for three random cardiac beats was integrated with respect to time. DdCO was calculated as the product of the flow velocity integral (centimeters per beat), heart rate (beats per min), and the mean cross-sectional area (centimeters squared) of the main pulmonary artery. At the same time that the velocity recordings were made, three serial determinations of TdCO were made by an independent observer. Pulmonary blood flow could be measured in 25 of the 33 patients. The anatomical relationship among the esophagus, the left main stem bronchus, and the pulmonary artery did not allow adequate imaging of the pulmonary artery in 8 (24%) of the patients. A total of 45 sets of triplicate measurements were made. The range of cardiac outputs encountered was 1.7-6.6 l.min-1 by TdCO and 1.5-6.9 l.min-1 by DdCO. The 95% confidence limits for the difference between the two methods (agreement) was 0.030 +/- 0.987 l.min-1.(ABSTRACT TRUNCATED AT 250 WORDS)

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