Con: cardiac anesthesia and elitism: where does SIGMA end and ROA begin?
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Biomedical subjects
Publications and source records attributed to J H Tinker.
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The authors studied the redistribution of myocardial blood flow in a collateral-dependent (CD) zone as a function of coronary perfusion pressure (CPP) during isoflurane and halothane anesthesia. A swine model with CD myocardium distal to a chronically occluded left anterior descending coronary artery was developed and studied. Sixteen piglets were allowed to grow for 8-10 weeks after banding of the left anterior descending coronary artery. They were randomly anesthetized with either isoflurane (n = 8) or halothane (n = 8) as the sole anesthetic, which was used to regulate specific CPP. The resultant regional myocardial blood flows were measured using radiolabeled microspheres. Four randomly allocated CPPs, of 30, 40, 45, and 55 mmHg, were studied in each animal. Four additional collateralized animals were anesthetized with alpha-chloralose, and the same CPPs were obtained using an intravenous adenosine infusion (1-5 microM kg-1) to validate this model. There was a proportional decrease in heart rate and blood pressure in both the isoflurane and and the halothane group with CPP. Cardiac output was significantly decreased in the halothane group at 30 mmHg when compared to 55-mmHg CPP, but it was maintained in the isoflurane group. Systemic vascular resistance was significantly lower in the isoflurane group at 30 and 40 mmHg when compared to 55-mmHg CPP. Both the isoflurane and the halothane group showed a proportional and significant decrease in endo-, mid-, and epicardial blood flows at 30-mmHg CPP when compared to baseline. In both CD and normal perfusion zones, isoflurane consistently sustained a higher endocardial blood flow than halothane (5.7-41.1%).(ABSTRACT TRUNCATED AT 250 WORDS)
Cerebral blood flow (CBF) during human hypothermic cardiopulmonary bypass has been reported to decrease with time, suggesting that progressive cerebral vasoconstriction or embolic obstruction may occur. We tested the hypotheses: 1) that observed CBF reductions were due to continued undetected brain cooling and 2) that CBF during cardiopulmonary bypass would be stable after achievement of constant brain temperature. Anesthetized New Zealand White rabbits underwent cardiopulmonary bypass (membrane oxygenator, centrifugal pump, bifemoral arterial perfusion) and were assigned to one of three bypass management groups based on perfusate temperature and PaCO2 management: group 1 (37 degrees C, n = 8); group 2 (27 degrees C, pH-stat, n = 9); and group 3 (27 degrees C, alpha-stat, n = 8). Systemic hemodynamics, and cerebral cortical, esophageal, and arterial perfusate temperatures were recorded every 10 min for the first hour of bypass and again at 90 min. CBF and masseter blood flow (radiolabeled microspheres) were determined at 30, 60, and 90 min of bypass, while the cerebral metabolic rate for oxygen (CMRO2) was determined at 60 and 90 min. Groups were comparable with respect to mean arterial pressure, central venous pressure, hematocrit, and arterial oxygen content throughout bypass. Cortical temperature was stable in normothermic (group 1) animals, and there was no significant change in CBF between 30 and 90 min of bypass: 68 +/- 18 versus 73 +/- 20 ml.100 g-1.min-1 (mean +/- SD). In the hypothermic groups (2 and 3), cortical temperature equilibration (95% of the total change) required 41 +/- 6 min.(ABSTRACT TRUNCATED AT 250 WORDS)
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The efficacy, with respect to preventing i.v. catheter damage, of creating a skin entry site by first piercing the skin with a large gauge needle through which an over-the-needle teflon catheter is then placed was evaluated. In 50 adult volunteers two 22-gauge i.v. catheters and two 24-gauge catheters were placed through the forearm skin into the subcutaneous tissue. One catheter of each size was placed through an entry site created by piercing the skin with an 18-gauge disposable, stainless steel needle. One catheter of each size was inserted through nearby skin without creation of an entry site. Two to three weeks after insertion all catheters, along with 50 catheters of each size that had not been inserted, were examined under a microscope for evidence of damage. Intravenous catheter damage was more prevalent in the 24-gauge catheters than the 22-gauge catheters (P less than 0.05). No differences in frequency of damage were noted for either gauge catheter inserted through an entry site compared with those inserted without a prior skin puncture. Twenty-four-gauge catheters, but not 22-gauge catheters, placed into the subcutaneous tissue were damaged more frequently than were catheters that had never been inserted (control catheters). This study demonstrated that 24-gauge catheters are more likely to be damaged during insertion into the subcutaneous tissue than are 22-gauge catheters. We also demonstrated that creation of a skin entry site by piercing the epidermis with a needle of larger gauge than the catheter to be placed is not efficacious in preventing intravenous catheter damage during insertion.
Prior reports suggest cerebral blood flow (CBF) responses to changing bypass (systemic) flow rates may differ between alpha-stat and pH-stat management. To compare the effect of blood gas management upon CBF responses to changing systemic flow and pressure, 15 New Zealand White rabbits, anesthetized with fentanyl and diazepam, underwent nonpulsatile cardiopulmonary bypass at 25 degrees C. One group of animals (n = 8) was randomized to alpha-stat blood gas management that maintained arterial carbon dioxide tension (PaCO2) approximately 40 mmHg when measured at 37 degrees C. A second group (n = 7) was managed with pH-stat technique, maintaining PaCO2 approximately 40 mmHg when corrected to the animal's actual temperature. Bypass was initiated at a flow rate of 100 ml.kg-1.min-1 and, after approximately 20 min, control hemodynamic and CBF measurements (radioactive microspheres) were made. Thereafter, bypass flow rate was changed in random order at 15-min intervals to 50, 70, and 100 ml.kg-1.min-1. CBF and hemodynamic measurements were repeated at the end of each period of altered bypass flow. Groups differed significantly with respect to both pHa and PaCO2. There were no significant differences between groups with respect to bypass flow rate, mean arterial pressure (MAP), central venous pressure, temperature, hematocrit, arterial oxygen tension (PaCO2), or bypass duration at any measurement point. MAP decreased significantly, from approximately 80 to approximately 65 mmHg with decreasing bypass flow (P = 0.0001). Over the entire range of bypass flows, CBF decreased with decreasing bypass flow (P = 0.001), and the degree of change was equivalent among regions and between groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Differences in cerebral blood flow (CBF) between alpha-stat and pH-stat management depend on preserved responsiveness of the cerebral vasculature to changes in arterial carbon dioxide tension (PaCO2). We tested the hypothesis that hypothermia-induced reductions in CBF would decrease the CBF response to changing PaCO2 (delta CBF/delta PaCO2). Anesthetized New Zealand white rabbits were randomly assigned to one of three temperature groups--group 1 (37 degrees C, n = 9); group 2 (31 degrees C, n = 10); or group 3 (25 degrees C, n = 10)--and were cooled using cardiopulmonary bypass. After esophageal temperature equilibration (approximately 40 min), oxygenator gas flows were serially varied to achieve PaCO2 values of 20, 40, and 60 mm Hg (temperature-corrected). All animals were studied at all three PaCO2 levels in random order. At each level of PaCO2, CBF and masseter blood flow were determined using radiolabeled microspheres. There were no significant differences between groups with respect to mean arterial pressure (approximately 80 mmHg), central venous pressure (approximately 4 mmHg), or hematocrit (approximately 22%). Prior normothermic studies have found delta CBF/delta PaCO2 to be proportional to CBF. Nevertheless, in this study, with hypothermia-induced reductions in CBF, delta CBF/delta PaCO2 was not significantly different between temperature groups. Thus, hypothermia either increased the sensitivity of the cerebral vasculature to carbon dioxide and/or increased the effective level of cerebrospinal fluid respiratory acidosis produced by each increment of temperature-corrected PaCO2.(ABSTRACT TRUNCATED AT 250 WORDS)
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To study the effect of oncotic pressure on brain water content during cardiopulmonary bypass (CPB), 14 anesthetized New Zealand White rabbits underwent 60 min of nonpulsatile CPB at normothermia. Animals were grouped according to the composition of the circuit priming fluid. Group 1 animals (n = 7) received a priming fluid (6.5% hydroxyethyl starch in 0.72 N NaCl; 323 +/- 13 mOsm/kg [mean +/- SD]) that maintained normal colloid oncotic pressure (COP) during CPB (19.0 +/- 1.5 mmHg). Group 2 animals (n = 7) received a priming fluid (0.9 N NaCl; 324 +/- 23 mOsm/kg) that led to a hypooncotic state (COP = 6.2 +/- 1.2 mmHg). Blood chemistries and hemodynamics were recorded every 15 min during CPB. Animals were given additional priming fluid and sodium bicarbonate during CPB to maintain a circuit flow of 85 ml.kg-1.min-1 and arterial pH greater than 7.35. There were no significant differences between groups 1 and 2 with respect to temperature, central venous pressure, mean arterial pressure, PaO2, PaCO2, plasma sodium concentration, or osmolality at any time during CPB, although osmolality increased in both groups. After 60 min of bypass, animals were killed and organ water contents were determined by wet/dry weight ratios. A separate group of nine similarly prepared and anesthetized animals that did not undergo cannulation or CPB also underwent measurement of plasma chemistries and tissue water contents and served as nonbypass controls (group 3). Brain and kidney water contents were unaffected by oncotic pressure, whereas duodenum and skeletal muscle had significantly greater water content (P = 0.003 and P = 0.008, respectively) after hypooncotic CPB.(ABSTRACT TRUNCATED AT 250 WORDS)
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Anesthesiologist-reviewers examined 1,175 anesthetic-related closed malpractice claims from 17 professional liability insurance companies. The claims were filed between 1974 and 1988. The reviewers were asked to determine if the negative outcome was preventable by proper use of additional monitoring devices available at the time of the review even if not available at the time the incident occurred, and if so, which devices could have been preventative. In 1,097 cases sufficient information was available to make a judgment regarding preventability of the morbidity or mortality by application of additional monitoring devices. It was determined that 31.5% of the negative outcomes could have been prevented by application of additional monitors. Using the insurance industry's scale of 0 (no injury) to 9 (death), the median severity of injury for incidents deemed preventable was 9 compared with 5 for those deemed not preventable (P less than 0.01, scale detailed in text). The severity of injury scores were the same for preventable mishaps occurring during regional or general anesthesia, suggesting that additional monitoring devices may be equally efficacious in preventing serious negative outcomes during either regional or general anesthesia. The judgements or settlements of the incidents judged preventable by additional monitoring were 11 times more costly (P less than 0.01) than those mishaps not judged preventable. The monitors determined by the reviewers to be most useful in mishap prevention were pulse oximetry plus capnometry. Applied together, these two technologies were considered potentially preventative in 93% of the preventable mishaps.(ABSTRACT TRUNCATED AT 250 WORDS)
The aim of this study was to determine the effect of choice of invasive monitoring on cost, morbidity, and mortality in cardiac surgery. Two hundred and twenty-six adults undergoing elective cardiac surgery were initially assigned at random to receive either a central venous pressure monitoring catheter (group I), a conventional pulmonary artery (PA) catheter (group II), or a mixed venous oxygen saturation (SvO2) measuring PA catheter (group III). If the attending anesthesiologist believed that the patient initially randomized to group I should have a PA catheter, that patient was then reassigned to receive either a conventional PA catheter (group IV) or SvO2 measuring PA catheter (group V). The total costs were defined as the total amount billed to the patient for the catheter used; the professional cost of its insertion; and the determinations of cardiac output, arterial blood gas tensions, hemoglobin level, and hematocrit. Mean total monitoring and laboratory costs in Group I ($591 +/- 67) were statistically significantly (P less than 0.05) less than costs in Group II ($856 +/- 231). Further, mean monitoring and laboratory costs in Group II were statistically significantly (P less than 0.05) less than those in Group III ($1128 +/- 759). Patients in group IV incurred mean total costs of $986 +/- 578, while those in group V had mean total costs of $1126 +/- 382 (NS). There were no significant differences between any of the groups with respect to length of stay in the intensive care unit, morbidity, or mortality.(ABSTRACT TRUNCATED AT 250 WORDS)
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During the years 1974 and 1975 at our institution, 587 patients who had suffered previous myocardial infarctions underwent anesthesia and surgery. Thirty-six (6.1%) had a reinfarction and 25 (69%) died. Patients operated on within three months of the previous infarction had a 27% reinfarction rate. This decreased to 11% if the infarct had occurred three to six months previously and stabilized at 4% to 5% if the interval was more than six months. Risk factors associated with significantly increased reinfarction rates included preoperative hypertension, intraoperative hypotensive episodes, and noncardiac thoracic or upper abdominal operations of more than three hours' duration. Time under anesthesia was strikingly correlated with reinfarction rates in the entire group. Postoperative intensive care unit admission did not significantly affect the reinfarction rate, nor did diabetes, angina, patient age or sex, or site of the previous myocardial infarction.
Between 1962 and 1975, a total of 159 patients with previously implanted man-made cardiac valve prostheses underwent 180 subsequent noncardiac operations at Mayo Clinic. All of these patients were receiving anticoagulants. The overall incidence of their documentable thromboembolic complications was approximately 10%. None of the postoperative complications occurred while the patient was in hospital, with the earliest such complication seen two years later. Patients receiving anticoagulants on a long-term basis did, however, have a 13% incidence of various difficulties with hemostasis during and following the later operations. We conclude that there is minimal risk to patients with cardiac valve prostheses who are receiving anticoagulants when the drug regimen is stopped for one to three days preoperatively and one to seven days postoperatively.