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Biomedical subjects

J H Tinker

Publications and source records attributed to J H Tinker.

At least 37 records · Page 2Linked to original sources
PubMed1991

Cerebral blood flow response to PaCO2 during hypothermic cardiopulmonary bypass in rabbits.

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)

Animals↗
PubMed1990

Differential effect of oncotic pressure on cerebral and extracerebral water content during cardiopulmonary bypass in rabbits.

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)

Animals↗
PubMed1989

Role of monitoring devices in prevention of anesthetic mishaps: a closed claims analysis.

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)

Anesthesia↗
PubMed1989

A cost/benefit analysis of randomized invasive monitoring for patients undergoing cardiac surgery.

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)

Blood Gas Analysis↗
PubMed1988

Anaesthesia for the patient with cardiac disease.

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)

Anesthesia↗
PubMed1988

Comparative coronary vascular reactivity and hemodynamics during halothane and isoflurane anesthesia in swine.

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.

Anesthesia, Inhalation↗
PubMed1988

Coagulation changes during packed red cell replacement of major blood loss.

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)

Blood Coagulation↗
PubMed1987

Halothane relaxes previously constricted isolated porcine coronary artery segments more than isoflurane.

Coronary vasodilation by halothane and isoflurane were compared using in vitro tension recording. Porcine left anterior descending coronary arterial segments (1.5-2.0 mm o.d.) were constricted with either K+ (30 mM) or prostanoid U44069 (6 X 10(-7) M) in the absence of other drugs or anesthetics. Following stabilization of constriction, arteries were exposed to halothane or isoflurane at 0.5, 1.0, 1.5, 2.0, and 3.0% concentrations. K+ (30 mM) induced constriction was reduced by halothane at 1.5, 2.0, and 3.0% and U44069 (6 X 10(-7) M) induced constriction was reduced at 0.5, 1.0, 1.5, 2.0, and 3.0%. K+ (30 mM) induced constriction was reduced by isoflurane only at 3.0% and U44069 (6 X 10(-7) M) induced constriction was reduced by isoflurane only at 2.0 and 3.0%. U44069 induced constriction was more susceptible than K+ induced constriction to relaxation by halothane or isoflurane. Halothane was more potent than isoflurane as a direct relaxant of porcine epicardial left anterior descending arterial segments previously constricted with K+ (30 mM) or U44069 (6 X 10(-7) M).

Animals↗
PubMed1987

Isoflurane has a greater margin of safety than halothane in swine with and without major surgery or critical coronary stenosis.

The fatal/anesthetic ratio (FAR) in 44 swine weighing 32.6 +/- 0.7 kg (SEM) was determined. Fatal anesthetic concentration (the numerator for FAR) was defined as the end-tidal concentration at which the pig lived at least 10 min, during experiments that involved step increments in anesthetic concentrations. Previously reported MAC was used as the "anesthetic" concentration (denominator) to determine FAR. Halothane was compared to isoflurane and the question of whether major surgery might reduce FAR was investigated. The major surgery groups included one open chest group with each volatile anesthetic studied during coronary reserve measurements, and two groups that had LAD critical coronary stenoses. Thus volatile agents were compared with vs without major surgery, and with vs without a critical coronary stenosis. The FAR for isoflurane was approximately double that of halothane. Further, addition of major surgery did not produce significant deterioration in FAR with isoflurane. In contrast, with halothane there was a significant (approximately 20%) decrease in FAR, despite values already only half that seen with isoflurane, when major surgery was added. Presence of a critical coronary stenosis was not associated with a worsened FAR for isoflurane or halothane. It was concluded that the fatal/anesthetic ratio for isoflurane in pigs is 1.9 times greater than that for halothane. Addition of major surgery did not affect FAR when isoflurane was the anesthetic but did when halothane was used. Critical coronary stenosis did not worsen FAR. Because these results are nearly identical with those reported previously in small mammals, the doubled safety margin seen with isoflurane may have clinical relevance.

Animals↗
PubMed1984

Verapamil worsens rate of development and hemodynamic effects of acute hyperkalemia in halothane-anesthetized dogs: effects of calcium therapy.

The hemodynamic effects of verapamil pretreatment versus no pretreatment were evaluated in five acutely hyperkalemic dogs. Using ECG evidence for severe hyperkalemia, the halothane-anesthetized dogs were rendered acutely hyperkalemic to similar plasma levels of K+ (K+ = 8.2 +/- 0.8 mEq/l verapamil plus hyperkalemia, K+ = 9.4 +/- 0.2 mEq/l hyperkalemic controls). The verapamil-hyperkalemic group had significantly lower cardiac indexes (CI) (CI = 1.3 +/- 0.5 1 X min-1 X m-2 verapamil plus hyperkalemia vs. CI = 3.0 +/- 0.2 1 X min-1 X m-2 hyperkalemic controls) and lower mean arterial pressures (MAP = 60 +/- 13 mmHg verapamil plus hyperkalemia vs. MAP = 96 +/- 7 mmHg hyperkalemic controls). Calcium therapy for hyperkalemia that returned CI to control levels in hyperkalemic controls only partially reversed the severe hemodynamic depression and did not improve the AV block seen during hyperkalemia in the presence of the calcium entry blocker verapamil. Surprisingly, the total mEq of KCl infused at the same rate into verapamil-pretreated dogs to result in similar high serum potassium levels was only one-third that required in dogs not pretreated with verapamil (1.6 +/- 0.3 mEq/kg KCl in verapamil-hyperkalemia group vs. 5.0 +/- 0.7 mEq/kg KCl in hyperkalemic controls).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1984

Influence of propranolol plasma levels on hemodynamics during coronary artery bypass surgery.

Hemodynamic effects of propranolol during coronary artery surgery were investigated in 26 patients who chronically took propranolol and who received a standardized morphine/diazepam/pancuronium/halothane anesthetic. Effects were shown by correlating logarithm of the plasma propranolol concentrations versus percentage change in hemodynamics following stressful events (induction, intubation, skin incision, sternotomy, and sternal retraction). Log propranolol and hemodynamics following cardiopulmonary bypass also were correlated. A broad range of propranolol levels were observed. Levels (range and mean +/- SD) were preinduction 0-96 (25.6 +/- 21.6) ng/ml; preincision 0-86 (27.2 +/- 24.4) ng/ml; and sternal retraction 0-92 (28.2 +/- 25.4) ng/ml. The range of hemodynamic responses to stressful events also was broad. Representative changes between preincision control and sternotomy were (range and mean +/- SD): HR-8-30 (7 +/- 10) beats/min; PCWP 1-21 (8.5 +/- 4.6) mmHg; CI -0.2-1.1 (-0.2 +/- 0.7) 1 X min-1 X m-2, and SVR -244-1,288 (310 +/- 388) dyn X s X cm-3. By the time of sternal retraction, CI had declined from preincision values in 14 patients. Linear regression analysis demonstrated an inverse correlation between log propranolol and magnitude of HR, MAP, PCWP, and CI response to stressful stimulation. A direct but statistically weaker correlation with SVR also was seen. Significant correlations between log propranolol versus hemodynamic response to anesthetic induction and versus postcardiopulmonary bypass hemodynamics were not observed.

Adult↗