Heinz Michael Loick

High thoracic epidural anesthesia, but not clonidine, attenuates the perioperative stress response via sympatholysis and reduces the release of troponin T in patients undergoing coronary artery bypass grafting.

UNLABELLED In this prospective study, we evaluated whether high thoracic epidural anesthesia (TEA) or i.v. clonidine, in addition to general anesthesia, affects the cardiopulmonary bypass- and surgery-associated stress response and incidence of myocardial ischemia by their sympatholytic properties. Seventy patients scheduled for elective coronary artery bypass graft (CABG) received general anesthesia with sufentanil and propofol. TEA was randomly induced before general anesthesia and continued during the study period in 25 (anesthetized dermatomes C6-T10). Another 24 patients received i.v. clonidine as a bolus of 4 microg/kg before the induction of general anesthesia. Clonidine was then infused at a rate of 1 microg x kg(-1) x h(-1) during surgery and at 0.2-0.5 microg x kg(-1) x h(-1) postoperatively. The remaining 21 patients underwent general anesthesia as performed routinely (control). Hemodynamics, plasma epinephrine and norepinephrine, cortisol, the myocardial-specific contractile protein troponin T, and other cardiac enzymes were measured pre- and postoperatively. During the preoperative night and a follow-up of 48 h after surgery, five-lead electrocardiogram monitoring was used for ischemia detection. Both TEA and clonidine reduced the postoperative heart rate compared with the control group without jeopardizing cardiac output or perfusion pressure. Plasma epinephrine increased perioperatively in all groups but was significantly lower in the TEA group. Neither TEA nor clonidine affected the increase in plasma cortisol. The release of troponin T was attenuated by TEA. New ST elevations > or = 0.2 mV or new ST depression > or = 0.1 mV occurred in > 70% of the control patients but only in 40% of the clonidine group and in 50% of the TEA group. We conclude that TEA (but not i.v. clonidine) combined with general anesthesia for CABG demonstrates a beneficial effect on the perioperative stress response and postoperative myocardial ischemia. IMPLICATIONS Thoracic epidural anesthesia combined with general anesthesia attenuates the myocardial sympathetic response to cardiopulmonary bypass and cardiac surgery. This is associated with decreased myocardial ischemia as determined by less release of troponin T. These findings may have an impact on the anesthetic management for coronary artery bypass grafting.

Effects of Dopexamine on Creatinine Clearance, Systemic Inflammation, and Splanchnic Oxygenation in Patients Undergoing Coronary Artery Bypass Grafting

Impairment of splanchnic and peripheral tissue perfusion during cardiopulmonary bypass (CPB) may be responsible for endotoxin-mediated systemic inflammation and acute phase responses. We examined the effects of dopexamine on hemodynamic parameters, creatinine clearance, systemic and splanchnic oxygenation, gastric mucosal pH (pHi), and mixed and hepatic venous plasma levels of endotoxin, interleukin-6 (IL-6), serum amyloid A (SAA), and C-reactive protein (CRP) in 44 patients scheduled for coronary artery bypass grafting. Patients were randomized to receive continuous infusions of 0.5, 1.0, or 2 micro g [centered dot] kg-1 [centered dot] min-1 dopexamine (n = 10 per group) or placebo (n = 14) prior to surgery, intraoperatively, and postoperatively. Dopexamine infusion increased systemic oxygen delivery (P <or=to 0.01). Hepatic venous oxygen saturation did not change, and pHi decreased during and after CPB in all patients (P <or=to 0.01). Postoperative increases in IL-6 were smallest in patients who received 2.0 micro g [centered dot] kg-1 [centered dot] min-1 dopexamine (P <or=to 0.02). SAA and CRP increases during the postoperative period were less pronounced with dopexamine throughout the study. Creatinine clearance was elevated in all dopexamine groups (P <or=to 0.025). This elevation was higher with lower dopexamine doses (P <or=to 0.025). We conclude that dopexamine improves creatinine clearance and reduces systemic inflammation without affecting splanchnic oxygenation. (Anesth Analg 1997;84:950-7)

Milrinone Modulates Endotoxemia, Systemic Inflammation, and Subsequent Acute Phase Response after Cardiopulmonary Bypass (CPB)

BACKGROUND Compromised splanchnic perfusion and the resulting intestinal mucosal injury leads to a decreased mucosal barrier function, which allows translocation of intestinal flora and endotoxemia. The authors evaluated the effects of milrinone on splanchnic oxygenation, systemic inflammation, and the subsequent acute-phase response in patients undergoing coronary artery bypass grafting. METHODS This open, placebo-controlled randomized clinical study enrolled 22 adult patients in two groups. Before induction of anesthesia, baseline values were obtained and patients were randomized to receive milrinone (30 microg/kg bolus administered progressively in 10 min, followed by a continuous infusion of 0.5 microg x kg(-1) x min(-1)) or saline. The following parameters were determined: hemodynamics; systemic oxygen delivery and uptake; arterial, mixed venous and hepatic venous oxygen saturation; intramucosal pH (pHi); and mixed and hepatic venous plasma concentrations of endotoxin, interleukin 6, serum amyloid A, and C-reactive protein. RESULTS Milrinone did not prevent gastrointestinal acidosis as measured by pHi, but its perioperative administration resulted in significantly higher pHi levels compared with control. Venous and hepatic venous endotoxin and the interleukin 6 concentration were reduced significantly in the milrinone group. Serum amyloid A values were attenuated in the milrinone group 24 h after surgery. No significant differences could be seen in routinely measured oxygen transport-derived variables. CONCLUSIONS Perioperative administration of low-dose milrinone may have antiinflammatory properties and may improve splanchnic perfusion in otherwise healthy patients undergoing routine coronary artery bypass grafting.

Cardiac Pacemaker Infection: Surgical Management With and Without Extracorporeal Circulation

BACKGROUND Pacemaker infections are rare, but serious complications of pacemaker therapy. The generator pocket, the pacing leads, or both may be involved. METHODS We report on 12 patients with infected pacemaker systems. Four patients suffered from localized generator pocket infections, 6 had infected leads, and 2 patients had both. Pacemaker systems were completely removed in all patients. When the infection was limited to the generator pocket, the pacemaker system was removed at the original implantation site. Extracorporeal circulation was employed for the explantation of infected pacing leads. RESULTS No complications occurred in patients with localized generator pocket infections. One patient with infected leads who was preoperatively already in a serious clinical condition died of septic shock in the early postoperative period; another patient died of pulmonary complications after tricuspid valve replacement 14 months after pacemaker explantation. No recurrent infections were observed. CONCLUSIONS Explantation of the complete pacemaker system has proved a reliable method to eradicate infection. Complications have been rare, except in patients in a critically ill state who undergo cardiopulmonary bypass.

Neonatal mechanical bridging to total orthotopic heart transplantation

BACKGROUND Until recently, newborns with medically intractable cardiac failure caused by congenital malformations were mostly doomed to death because of the severity of the disease, which precludes a palliative operation, or because of fatal deterioration before availability of a suitable donor heart. METHODS The recently developed paracorporeal pneumatically driven Medos HIA ventricular assist device offers a therapeutic option for these small infants because it is manufactured in various sizes and is even suitable for cardiac assistance in neonates with a body surface area less than 0.3 m2. RESULTS We report our initial experience with this device, which we used for univentricular bridging to total orthotopic cardiac transplantation in 3 infants. The device was inserted to support the left ventricle in two instances and to support the right heart in one. Successful bridging to transplantation was achieved in 2 infants for periods of 2 and 7 weeks. CONCLUSIONS Our experience demonstrates the feasibility of univentricular mechanical support followed by successful cardiac transplantation in infants and newborns.

Increased plasma concentrations of serum amyloid A: an indicator of the acute-phase response after cardiopulmonary bypass.

OBJECTIVES To assess the expression of mixed and hepatic venous serum amyloid A (SAA) concentrations and its relationship to plasma concentrations of C-reactive protein, interleukin-6 (IL-6), and endotoxin during and after cardiopulmonary bypass (CPB). DESIGN Prospective, consecutive sample with repeated measurements. SETTING Surgical intensive care unit (ICU) in a university hospital. PATIENTS Twenty patients who underwent elective coronary bypass grafting. INTERVENTIONS A radial artery catheter, pulmonary artery catheter, and right hepatic vein catheter were inserted. Blood samples were collected to determine the different mediators, lactate concentrations, and oxygen saturations. MEASUREMENTS AND MAIN RESULTS After induction of anesthesia, baseline values were obtained and the following parameters were determined 20 mins after onset of CPB, 20 mins after termination of CPB, at admission to the ICU, and 6, 8, 12, and 24 hrs later: hemodynamics, body core temperature, hepatic venous oxygen saturation, and mixed and hepatic venous lactate, endotoxin, interleukin (IL)-6, C-reactive protein (CRP), and SAA concentrations. Endotoxin and IL-6 plasma concentrations increased during CPB, peaked 6 hrs after admission to the ICU (endotoxin: 23.1 +/- 6.2 pg/mL; IL-6: 646 +/- 104 pg/mL), and decreased thereafter; SAA and CRP concentrations began to increase after 6 and 8 hrs, respectively, with the highest concentrations reached 24 hrs postoperatively (CRP: 14 +/- 3.6 mg/L; SAA: 668 +/- 114 micrograms/mL). Lactate concentrations began to increase 20 mins after CPB, and continued to increase until 12 hrs postoperatively. There were no significant differences between mixed and hepatic venous values of endotoxin, IL-6, CRP, SAA, and lactate (p < .05). Body core temperature, which was < 37.5 degrees C before surgery for all patients, increased 6 hrs after admission to the ICU and peaked 12 hrs postoperatively (38.3 +/- 1.1 degrees C). Hepatic venous oxygen saturation did not change. Correlations were obtained between IL-6 values and heart rate (r2 = .20; p < .005), and endotoxin concentrations and systemic vascular resistance (r2 = .18; p < .001). Body core temperature correlated significantly closer with SAA (r2 = .52; p < .0001) values than with IL-6 (r2 = .27; p < .0001) or CRP (r2 = .16; p < .001) values (p < .05). CONCLUSIONS SAA is an additional and sensitive marker of the acute-phase response following CPB; the increase in SAA concentrations parallels the temporary increase in body core temperature and is preceded by endotoxemia and IL-6 secretion.

Combining nonpharmacologic therapies for advanced heart failure: the münster experience with the assist device–defibrillator combination

Implantable cardioverter defibrillators (ICDs) and ventricular assist devices (VADs) have been used as a bridge to cardiac transplantation. In selected patients, the combined implantation may be required. This study was motivated by a case of a 33-year-old female patient with giant cell myocarditis who died of ventricular tachyarrhythmias after having been placed on a VAD with which she had been treated on an out-of-hospital basis for a prolonged period of time. A subsequent retrospective analysis of our data showed that, of 73 patients who had to be bridged mechanically (54 Novacor, 12 TCI Heartmate, 4 Thoratec, 3 Medos) in our institution between 1993 and 1998, 10 patients had undergone defibrillator implantation either before (n = 8) or after (n = 2) implantation of a VAD. The cases are presented, and the feasibility of the combination therapy discussed.

Effects of enflurane and isoflurane on splanchnic oxygenation in humans

STUDY OBJECTIVES To determine the effects of enflurane and isoflurane on hepatic venous oxygen saturation (ShvO2) and splanchnic oxygen (O2) extraction. To measure hemodynamic parameters and ShvO2, mixed venous, and arterial lactate concentrations during enflurane and isoflurane anesthesia. DESIGN Randomized, prospective study. SETTING University hospital. PATIENTS 20 ASA physical status I, II, and III adults, who underwent major abdominal surgery requiring mechanical ventilation a few hours postoperatively. INTERVENTIONS After placement of catheters in the pulmonary artery, radial artery, peripheral and right hepatic vein, one hour postoperatively either enflurane or isoflurane was applied at different minimum alveolar concentration (MAC) of 0.5, 1.0, and 1.5 in a randomized order. MEASUREMENTS AND MAIN RESULTS Before and 10 minutes after administration of each desired end-expiratory anesthetic concentration, the following parameters were determined: hemodynamic parameters, arterial (SaO2), mixed venous (SvO2), and hepatic venous oxygen saturations, systemic and splanchnic O2 extraction, arterial, mixed venous, and hepatic venous lactate concentrations. Cardiac output (CO) and mean arterial pressure (MAP) decreased in a dose dependent manner. SaO2, SvO2, and systemic O2 extraction remained unchanged with enflurane and isoflurane anesthesia. In the enflurane group, but not in the isoflurane group, ShvO2 decreased with increasing inhalational concentrations. This decrease in ShvO2 reflected an increase in splanchnic O2 extraction with enflurane; in contrast to isoflurane. CONCLUSIONS Enflurane causes a decrease in ShvO2, which indicates an impairment of splanchnic perfusion corresponding to the reduction in CO and MAP in a dose-dependent manner. Isoflurane maintains splanchnic perfusion in contrast to enflurane.

Phlegmasia cerulea dolens, cerebral venous thrombosis, and fatal pulmonary embolism due to heparin-induced thrombocytopenic thrombosis syndrome.

H eparin-induced thrombocytopenia (HIT) is a common complication of anticoagulant therapy with heparin (1). The early-onset mild type I is caused by hyperaggregation of platelets induced by heparin, resulting in increased peripheral platelet sequestration. It usually resolves spontaneously, even with continued heparin administration. The immunemediated HIT type II or “white clot syndrome” has a delayed onset of 4-14 days after starting heparin administration (except after previous exposure to the drug) (1). The clinical course is characterized by thromboembolic complications responsible for the high mortality rate of 30% (1). The etiology of the disease is an Immunoglobin G antibody specific for complexes of heparin or heparin-like molecules and platelet factor 4. Immuncomplexes formed by this antibody, platelet factor 4-heparin complexes, and Fc receptors of platelets induce a strong platelet aggregation, which results in white clots. Immune-mediated endothelial cell injury by the antibody reacting with heparin-like molecules on the endothelial cell surface may increase the risk of thrombosis and disseminated intravascular coagulation (2). We present a case of HIT type II with thrombosis of the left upper extremity, resulting in phlegmasia cerulea dolens, cerebral venous thrombosis, and fatal pulmonary embolism.

Thoracoscopic interruption of patent ductus arteriosus compromises cardiopulmonary function in newborn pigs.

Interruption of patent ductus arteriosus (PDA) using video-assisted thoracoscopic surgery (VATS) has recently been introduced into clinical practice. To study cardiovascular and pulmonary function during VATS, we treated 16 newborn pigs (weight 1421 +/- 44 g) with PDA with conventional surgical interruption (CSI; n = 7) or interruption via VATS (n = 9). Measurements of hemodynamics and gas exchange were performed before, during, and after surgery. Systemic perfusion was calculated using Ficks equation. Stress hormones (ACTH, epinephrine, and norepinephrine) were determined before and after surgery. The duration of the surgical procedure was 41 +/- 8 min for CSI and 49 +/- 9 min for VATS (mean +/- SEM). With VATS, PaO2 decreased during and after surgery (P < 0.05), whereas alveolar-arterial PO2 difference (PA-aO2) and PaCO2 were increased (P < 0.05). Compared with CSI after surgery, PaO2 with VATS was decreased (130 +/- 10 vs 171 +/- 12 mm Hg; P < 0.05). Systemic perfusion was lower during VATS (76.7% of baseline) than during CSI (107% of baseline; P < 0.05). Heart rate, mean arterial pressure, and right ventricular end-diastolic pressure remained unchanged with both treatments. Stress hormones were comparable between groups. We conclude that systemic perfusion and oxygenation were impaired during VATS compared with CSI. Therefore, VATS may be contraindicated in pediatric patients with minor cardiopulmonary reserve. Implications: We studied the cardiopulmonary effects of endoscopic interruption of the patent ductus arteriosus in an animal model of newborn pigs. Gas exchange and systemic perfusion were impaired compared with conventional interruption of the patent ductus arteriosus after thoracotomy. (Anesth Analg 1998;87:1037-40)