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)
I have tried to summarize experimental work in human and animal models. This work is complex and difficult to interpret. Clinicians should not take isolated experimental studies and jump to conclusions about clinical use of anaesthetics. Experimenters should not arrive at sweeping conclusions based on a particular experimental study performed under some or other carefully or not so carefully controlled conditions. Editorialists, such as Becker in a recent issue of Anesthesiology, should not conclude that an anaesthetic is "dangerous," based on these kinds of studies. It is especially invalid to use the term "dangerous" unless the author is willing to present us with a viable, experimentally proven, safer alternative. To tell us that isoflurane is "dangerous" implies that we should switch to some unspecified other agent. What conclusions can be arrived at based on these studies? (1) It is possible to produce coronary steal, in dogs, at constant coronary flow, with isoflurane at 41 mmHg perfusion pressure. The comparison between halothane and isoflurane is suspect because is was performed at two markedly different coronary perfusion pressures. (2) Myocardial ischaemia can be induced in humans with coronary artery disease when hypotension and tachycardia is permitted during isoflurane anaesthesia. During these conditions, relative preservation of coronary blood flow greater than that which would be expected because of measured or calculated demand has been interpreted as meaning that the mechanism was that of coronary steal. I am not convinced that this mechanism needs to be invoked here, but we can conclude from these studies that if hypotension and tachycardia are allowed to occur in patients with coronary artery disease, ischaemia is possible.(ABSTRACT TRUNCATED AT 250 WORDS)
To assess the dose-response effects of isoflurane and halothane anesthesia on hemodynamics and coronary artery reactivity, the authors studied myocardial hyperemic responses following brief single artery flow arrests in 21 open chest, isocapnic swine in which arterial blood pressures and cardiac outputs were recorded. A specially designed Doppler probe was used to measure the peak and time course of coronary blood flow velocity in the left anterior descending coronary artery (LAD) after 15-s LAD occlusions. The ratio of peak velocity of blood flow to resting velocity (coronary reserve), relative repayment of flow debt, and duration of hyperemic responses were studied. Surgery was performed at MAC end-tidal concentrations ([Et]isoflurane = 1.45%. [Et]halothane = 1.25%) of isoflurane (n = 7) or halothane (n = 7), and recordings were made after 15-min steady state [Et]agent at 0.5, 1, 1.25, 1.5, 1.75, 2 MAC, and further 0.5 MAC increments until the demise of each animal. To compare coronary reactivity at similar coronary pressures, an aortic snare was used to elevate arterial pressures in a third group of halothane anesthesized pigs (n = 7) to those in the previously studied isoflurane group at each MAC level. There were three major differences between halothane and isoflurane. First, cardiac depression (reduction in arterial pressure, cardiac output, and stroke volume) was less with isoflurane compared with halothane anesthesia. Second, with halothane anesthesia, there was a marked decrease in coronary reactivity independent of coronary perfusion pressures with marked, dose-dependent reductions in both coronary reserve and relative flow repayment. During isoflurane anesthesia, coronary reactivity and coronary reserve was well preserved within physiologic limits up to 1.75 MAC [Et]. Third, halothane anesthesized pigs died in cardiac collapse at much lower agent concentrations than with isoflurane (no animals survived 1.75 MAC halothane, whereas all animals survived 2.5 MAC isoflurane). Therefore, pigs anesthesized with isoflurane had greater coronary reserve, better preserved cardiac function, and greater tolerance to increasing agent concentration than pigs anesthesized with halothane.
A greater proportion of blood replacement needs are being met by packed red cell concentrates rather than whole blood in situations of major blood loss. Twelve patients, who required major blood replacement during elective surgery, were studied to determine the changes in coagulation when packed red cells were used to replace major blood loss. In addition, the coagulation abnormalities present at the time an observer noted excessive bleeding were determined. Prior to blood product replacement and after the estimated loss of each 0.3 blood volume, coagulation tests were obtained including prothrombin time (PT), partial thromboplastin time (aPTT), platelet count, thrombin time (TT), fibrinogen levels, and assays of coagulation Factors V, VIII, and IX. Coagulation tests were repeated when clinical hemostasis was judged inadequate by the anesthesiologist and attending surgeon. Significant decreases in platelet count, fibrinogen levels, and Factor V, VIII, and IX levels occurred as increasing blood volumes were replaced. Increases in PT and aPTT above control occurred in nine of the 12 patients prior to replacement of 1 blood volume; none of the nine patients had increased clinical bleeding. In four of seven patients who had blood replacement of greater than 1 blood volume, increased clinical bleeding was noted by the observer. Platelet counts were less than 100,000/mm3 in each of these four patients, and a platelet concentrate obtained by pheresis of a single donor was administered. In two of the four patients platelet counts increased, but clinical bleeding did not resolve.(ABSTRACT TRUNCATED AT 250 WORDS)
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