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C K Spiss

Publications and source records attributed to C K Spiss.

At least 55 records · Page 3Linked to original sources

Comparative analysis between epidural (Gaeltec) and subdural (Camino) intracranial pressure probes.

The new fiberoptic Camino system has recently been introduced for clinical intracranial pressure (ICP) monitoring. We compared the subdural Camino system with the well-established epidural Gaeltec system in both in vitro and clinical conditions. In the in vitro experiments the intracranial vault was simulated by a tightly closed, fluid-filled box (0.9% sodium chloride) with the two probes inside. We simulated pulsating waveforms with a jet ventilator. No difference between the simulated curve patterns and values could be detected. In the clinical studies, both probes were implanted in 10 patients who had either head injuries, subarachnoid hemorrhage, or intracerebral hemorrhage. The in vivo comparison revealed no significant difference between the two systems in the recorded pressures in group 1 (ICP less than 20 mm Hg). The subdurally placed Camino probe showed insignificantly lower ICP values than did the extradural Gaeltec probe. Although group 2 (ICP greater than 20 mm Hg) waveforms were nearly identical, significant differences (p less than 0.01) in pressure measurements (systolic, diastolic, and mean) occurred (Camino, 18 +/- 3 mm Hg; Gaeltec, 27 +/- 3 mm Hg). Correlation coefficients for mean ICP values were 0.82 in group 1 and 0.49 in group 2. Problems with the Camino probe were usually mechanical and occurred in 2 patients. The problems were either easy to recognize or manifested as an ostensibly pathologic curve. No infection occurred with either system during or following implantation. The dissimilar characteristics of the two probes can be ascribed to their different extradural and subdural implantation sites. The Gaeltec probe was more durable over the period of implantation, which averaged 98 hours and ranged from 44 to 298 hours.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Porcine model for studying the passage of non-depolarizing neuromuscular blockers through the blood-brain barrier.

A method has been developed for blood-brain barrier disruption to provide reproducible access to the cerebrospinal fluid of the cerebello-medullary cistern. The technique was used successfully to investigate transfer of pancuronium to the cerebral CSF compartment in pigs. After osmotic disruption of the blood-brain barrier, pancuronium concentrations increased significantly in the cerebrospinal fluid.

Animals↗

Sufentanil decreases cerebral blood flow velocity in patients with elevated intracranial pressure.

Recent investigations revealed that sufentanil increases cerebral blood flow (CBF) and intracranial pressure (ICP) in dogs and man. The aim of our study was to evaluate the impact of sufentanil on cerebral blood flow velocity and ICP in neurosurgical patients. Eight neurosurgical ICU patients with elevated ICP (> 20 mmHg) were examined. Sufentanil was given in incremental doses of 0.5, 1.0 and 2.0 micrograms kg-1. Cerebral blood flow velocity decreased significantly from 54 +/- 4 cm s-1 to 48 +/- 3 cm s-1 with the dose of 1.0 microgram kg-1 sufentanil and 47 +/- 3 cm s-1 with 2.0 micrograms kg-1, respectively (mean +/- SEM). ICP values did not increase with any of the doses studied. Thus, changes of mean arterial pressure which fell with 1.0 microgram kg-1 and 2.0 micrograms kg-1 reflect cerebral perfusion pressure alterations. Although changes of cerebral blood flow velocity revealed changes in vascular tone, ICP remained unaltered.

Anesthesia, Intravenous↗

[Preclinical management of patients with intracerebral hemorrhage].

The prehospital treatment of patients with intracerebral hemorrhage must be aimed at prevention of secondary brain damage and provision of an optimal physiologic environment to maximize the potential of recovery. Adequate cerebral oxygenation and the prevention of hypercarbia is a priority. This can only be managed by early intubation and artificial ventilation in patients with a Glasgow-coma-scale below eight, together with the restoration of normal hemodynamics to guarantee adequate cerebral perfusion.

Brain Damage, Chronic↗

Effect of sufentanil on intracranial pressure in neurosurgical patients.

The effects of sufentanil on intracranial pressure, mean arterial pressure, cerebral perfusion pressure and heart rate were studied in 20 neurosurgical intensive care unit patients. Epidural intracranial pressure probes were implanted in patients who suffered head injury, intracerebral haemorrhage or underwent tumour resection. Sufentanil was given intravenously in sequential doses of 0.5, 1.0 and 2.0 micrograms/kg. Fifteen minutes elapsed after each dose. The patients were allocated to either group 1 (baseline intracranial pressure less than 20 mmHg) or group 2 (baseline intracranial pressure greater than 20 mmHg). Intracranial pressure did not change significantly in either group. Therefore the falls in mean arterial pressure with the highest dose in both groups and with 1.0 micrograms/kg in group 2, closely reflect corresponding reductions in cerebral perfusion pressure. As sufentanil in itself exerts no effects on intracranial pressure, concomitant haemodynamic changes are the critical factor for an adequate cerebral perfusion pressure.

Adult↗

[Requisite muscle relaxation using vecuronium for tracheobronchial suction in neurosurgical intensive care patients].

Coordination of respiratory care with protection of the brain is critical in neurosurgical intensive care. Therefore, in addition to hyperventilation, adequate sedation and muscle relaxation are applied to mitigate the difficulties with control of intracranial pressure (ICP) during routine tracheobronchial suctioning (TBS). Although hypnotics have been shown to be effective in mitigating increases in ICP in response to endotracheal suctioning in paralyzed patients, brisk bucking and coughing with further increases in ICP may occur without muscle relaxation. Long-term neuromuscular (nm) paralysis may be undesirable in neurosurgical critical care because clinical evaluation with early detection of neurological deterioration will be impossible in the paralyzed patient. Therefore, the effects of TBS without and after nm blockade with an intermediate-acting nondepolarizing muscle relaxant on ICP were studied. PATIENTS AND METHODS. Nine patients with moderate increases in mean ICP of 19.2 +/- 8 mmHg due to head injuries and spontaneous subarachnoid hemorrhage were investigated. All patients were on-line sedated with midazolam and sufentanil and controlled ventilation was adjusted to maintain a paCO2 of 30 +/- 2 mmHg. Respiratory and hemodynamic parameters and ICP (epidural probe) were continuously monitored and recorded on an integrated data bank. After a bolus dose of propofol, routine TBS was performed without the use of muscle relaxants. Before the next TBS, nm monitoring was initiated and train-of-four (TOF) stimulation was imposed at the ulnar nerve using supramaximal pulses. The response of the adductor pollicis muscle was recorded by accelerometry. After supramaximal stimulation had been achieved, a bolus dose of 2 times the ED95 of vecuronium (0.12 mg/kg) was given. Depth of nm blockade was quantified by the posttetanic count (PTC). ICP and CPP were measured before, during, and after TBS. Diaphragmatic movement, bucking, and coughing were registered by visual observation and graded as absent, slight, moderate, or severe. STATISTICS. Student's t-test and the Wilcoxon test for paired data (P less than 0.05; values as mean +/- SD) were used. RESULTS. (see Table and Figure). Despite adequate sedation, moderate to severe diaphragmatic movements in response to carinal stimulation with significant increases in ICP (18.2 +/-7 to 24 +/- 8 mmHg) an d subsequent decreases in cerebral perfusion pressure (CPP) (68.9 +/- 2 to 62.4 +/- 8 mmHg) could be observed without muscle relaxation. After a bolus of vecuronium, profound nm paralysis quantified by a PTC of 5 was observed after an onset time of 4.2 +/- 1 min. ICP (20.2 +/- 8 vs. 20.1 +/- 8 mmHg) and CPP (64.0 +/- 13 vs. 64.8 +/- 13 mmHg) remained unchanged. Slight diaphragmatic movements could be elicited in only two patients during TBS. DISCUSSION. TBS is a potent trigger of diaphragmatic movement, bucking, and coughing by reflex activation of the phrenic nerve. A major determinant of the magnitude of ICP increase during TBS is the transmission of the cough-induced increase in intrathoracic pressure to the cerebral venous system. Vecuronium was utilized for nm blockade because of its proven lack of cerebral and cardiovascular side effects, its relatively short onset, and its intermediate duration of action. Despite the postulated faster onset of nm blockade in the diaphragm, suppression of thumb-twitch response to TOF stimulation does not necessarily predict absence of diaphragmatic movement elicited by excessive tracheal stimulation. As demonstrated, intense nm blockade quantified by a PTC of 5 is necessary to rule out any bucking and coughing, i.e., to ensure total diaphragmatic paralysis in response to tracheal stimulation. On-line neurological evaluation, one of the essentials in the approach to the neurosurgical patient, will not be prevented by the intermittent bolus regime utilized in this study.

Adult↗

Sufentanil does not increase cerebral blood flow in healthy human volunteers.

The effect of sufentanil on human cerebral blood flow (CBF) was studied in seven unpremedicated, healthy volunteers 31 +/- 3.5 yr of age (mean +/- SD) and either sex. CBF (ml.100 g-1.min-1) was measured noninvasively with the 133Xe clearance technique and a scintillation camera before and after sufentanil 0.5 micrograms/kg administered intravenously. This technique provides values for global blood flow and for gray and white matter blood flow, and from 13 preselected regions in one hemisphere. After the administration of sufentanil, the volunteers were stimulated verbally in order to prevent their loss of consciousness and hypercarbia. Heart rate (HR), arterial pressure, oxyhemoglobin saturation, and end-tidal CO2 (ETCO2 were recorded during the measurements. Neither global CBF (46.1 +/- 1.6 control and 43 +/- 1.9 after sufentanil, mean +/- SEM) nor gray (76.5 +/- 3.2 and 70.9 +/- 6.1) or white (22.7 +/- 1.5 and 24.2 +/- 1.6) matter blood flow changed significantly after sufentanil administration. As well, no significant differences in HR (72 +/- 4 control and 79 +/- 4 beats per min after sufentanil) and ETCO2 (39.8 +/- 1.4 and 41.1 +/- 1.1 mmHg) were observed. It is concluded that sufentanil has no significant effect on CBF in healthy human volunteers.

Adult↗

[Tube-free translaryngeal superposed jet ventilation].

Microsurgical operations on the larynx require sufficient space for the surgeon in order to achieve the best surgical result. After preliminary experimental studies we integrated two jets of a specific size into the Kleinsasser tube. Simultaneously, we developed a "superimposed jet-ventilation system", which consists of a low-frequency jet ventilation and superimposed high-frequency jet ventilation. Respiration was maintained with a mixture of oxygen and air, whereby an additional increase in air and volume via the Kleinsasser tube, which is open on the outside, can be sustained on account of the Venturi effect. We tested this tubeless translaryngeal superimposed jet-ventilation system in 48 patients. Anesthesia was carried out by continuous intravenous administration of Propofol and intermittent doses of Sufentanil and Vecuronium as required. The clinical results showed optimal ventilation without hypercapnia. The arterial pC0(2) levels were below 42 mmHg. The arterial p0(2) levels were above 120 mmHg with a FIO2 of 40%. No complications were observed with regard to respiration during any of the operations. The surgeon had optimal conditions to carry out the operation. Because of the absence of a plastic tube, inhalation anesthetics and nitrous oxide, laryngeal laser surgery is another field of application for which this form of tubeless jet ventilation is excellently suited. We tested it with 12 patients, and no complications due to laser anesthesia were observed. We consider this form of a tubeless superimposed translaryngeal jet ventilation to be a great improvement in microlaryngeal surgery.

Adult↗

[The effects of propofol bolus administration on the intracranial pressure in craniocerebral trauma].

Previous investigations have revealed that propofol has a beneficial effect on intracranial dynamics in patients undergoing elective neurosurgery. In the present study we evaluated the impact of propofol in patients with normal or compromised intracranial compliance. METHODS. Epidural ICP probes were implanted in 14 patients with head injury. The heart rate, mean arterial pressure (MAP), intracranial pressure (ICP) and end-tidal CO2 were recorded continuously, and propofol was given in doses of 0.5, 1.0 and 2.0 mg/kg; there were 15 min between each application. The data were evaluated 1, 2, 5 and 10 min after each application. The patients were allocated to group I (ICP less than 20 mmHg) or group II (ICP greater than 20 mmHg) according to their ICP baseline level. A statistical analysis was performed by one-way ANOVA. A P value of less than 0.05 was regarded as significant. RESULTS. In group I decreases in MAP at all measuring points were detected with 1.0 and 2.0 mg/kg propofol; ICP with 1.0 and 2.0 mg/kg and CPP with 2.0 mg/kg fell significantly. In group II MAP decreased with all doses studied, as did ICP with 1.0 and 2.0 mg/kg; however, CPP was not particularly influenced. CONCLUSION. Propofol decreased ICP in patients with normal and compromised intracranial compliance, particularly with 2.0 mg/kg. As the responses to the hypotensive effects of propofol were mild and almost similar in both groups, no inadvertent CPP drops were observed with any of the doses studied. Thus, propofol as a bolus can be used safely for the sedation of ICU patients with head injury and normal or compromised intracranial compliance.

Adult↗

[Atrial arrest and intraventricular conduction disorders due to accidental hyperkalemia during kidney transplantation].

Besides anemia, coagulopathies, and hypertension, electrolyte disturbances are among the most significant features of end-stage renal disease. Although plasma potassium represents only 1.5%-2% of the whole-body content, hyperkalemia has definite effects on cardiac pacemaker cells and myocardial conduction. The typical ECG findings and therapeutic management will be discussed. Case report. A 64-year-old man with chronic renal failure due to phenacetin abuse was scheduled for transplantation of a 41-h-old cadaver kidney. The preoperative laboratory check revealed BUN 51 mg% and creatinine 11.5 mg%; serum sodium and potassium were within normal limits (sodium 141 mmol/l, potassium 5.11 mmol/l). A central-venous blood gas sample after induction of anesthesia and intubation revealed pH of 7.32, pCO2 43 mmHg, HCO3 22.1 mmol/l, base excess - 3.4 mmol/l, and venous oxygen saturation 84%. Plasma potassium (5.22 mmol/l) was within the normal range. As an endarterectomy of the left common and external iliac arteries had to be performed, the arterial cross-clamping time was longer than normal (73 min). After declamping an ECG pattern (modified V5 lead) typical of hyperkalemia (atrial arrest, idioventricular rhythm, right bundle-branch block-like QRS, AV dissociation, AV block I) was observed. Plasma potassium had increased to 6.77 mmol/l (+1.55 mmol/l). Immediate treatment was started with a bolus injection of 20 ml 10% calcium gluconate, rapid infusion of 200 ml 8.4% sodium bicarbonate, and glucose-insulin infusion (glucose 33 1/3%, 15 U regular insulin). After 25 min sinus rhythm was restored and potassium levels decreased to normal. Despite the observed ECG changes the cardiovascular status remained stable.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias, Cardiac↗

[Traumatic spinal cord lesion. An interdisciplinary challenge--a synopsis of the early trauma phase].

Increased morbidity and mortality in patients with spinal cord injuries present the anesthesiologist with many problems. The extent of neuronal damage is determined not only by the initial trauma, but also by subsequent activation of lipid peroxidation and lipase reactions due to local ischemia of the spinal cord. Complete transection of the spinal cord is characterized by impairment of diaphragmatic function and cardiovascular depression due to functional sympathectomy. Since hypoxemia is a common finding in high tetraplegics, immediate, careful intubation is mandatory at the trauma site. Because of rotational instability of the cervical spine, any brisk movement of the neck must be avoided. Therefore, orotracheal intubation may be performed only after sufficient stabilization of the spine in a neutral position has been guaranteed. Functional sympathectomy of the cardiovascular system is responsible for the hypotension frequently seen in high tetraplegics. Adequate volume replacement is provided based on central venous and pulmonary capillary wedge pressures. Reduced sympathetic tone causes increased sensitivity to volatile and intravenous anesthetics, so that myocardial depressants (e.g. halothane) should preferably be avoided. Opioid-induced anesthesia and nondepolarizing muscle relaxants should, therefore, be the anesthetic technique of choice.

Combined Modality Therapy↗

Total artificial heart bridging: a temporary support for deteriorating heart transplantation-candidates--methods and results.

Since 1975 at the 2. Dept. of Surgery, University of Vienna, Austria, artificial circulation devices and artificial hearts have been constructed and in experimental use. We started a clinical heart transplantation (HTX) program in 1984, and up to now more than 40 HTXs have been performed. Since May 1986, 3 patients--all suffering from end stage dilatative cardiomyopathy--received total artificial heart (TAH) as a temporary support until HTX was possible. Two of them were transplanted after 9 and 10 days. The third patient, who additionally suffered from a postinfarctial lung abscess and had to undergo an indispensable lobectomy contemporary with TAH implantation, could not be transplanted due to an incurable infection, which he died of after 22 days on TAH. The temporary TAH implantation proved to be a valuable measure preventing life-threatening circulatory deterioration. After restoration of a sufficient circulation by the implanted system, the patients' general conditions improved and the concomitant dysfunctions of kidneys, brain, and other vital organs, due to cardiogenic shock, could be rectified in those two patients, who underwent transplantation. Thromboembolic complications were observed only in the third patient, who developed a small infarction in the anterior lobe of the left hemisphere caused by cerebral embolism after 3 weeks of TAH pumping. The use of TAH is liable to severe, even lethal, complications. At present it should be used only as a last resort. If a donor heart is not available, this measure can be a real chance to save the patient's life.

Adult↗

Effects of ischemia on the canine myocardial beta-adrenoceptor-linked adenylate cyclase system.

Several studies indicate that myocardial ischemia causes a redistribution of beta-adrenergic receptors from a presumably intracellular compartment to the cell surface. However, a decreased adenylate cyclase and contractile responsiveness to beta-adrenergic stimuli has also been reported. The aim of the present study was to investigate possible ischemia-induced changes in myocardial beta-adrenoceptor coupling to adenylate cyclase. Myocardial ischemia was induced by hydraulic occlusion of the LAD in mongrel dogs anesthetized with isoflurane. After 90 min of ischemia, tissue samples were removed from the ischemic and nonischemic regions for tissue catecholamine determinations and for the preparation of particulate fractions from tissue homogenates. Saturation experiments on microsomal fractions obtained from the ischemic and control areas did not reveal any significant changes in the calculated dissociation constant for (-)[125I]iodocyanopindolol binding nor in the calculated receptor density. Likewise, the relative numbers of beta 2-adrenergic receptors were comparable in both preparations (approximately 20%). On the other hand, the proportion of beta-adrenoceptors stabilized in the high-affinity state by (-)isoproterenol was significantly reduced in the ischemic region when compared with the control myocardium (17 +/- 5 vs. 41 +/- 4%). This change was accompanied by a significant decrease in the intrinsic activity of (-)isoproterenol in stimulating adenylate cyclase activity. We propose that the initial uncoupling of the beta-adrenoceptor from its effector is a physiologically important, protective mechanism which guards the ischemic myocardium against the deleterious effect of excessive sympathetic stimulation.

Adenylyl Cyclases↗

Epinephrine infusion induces hyporesponsiveness of vascular smooth muscle.

Exposure to vasoactive drugs may lead to desensitization of vascular smooth muscle responsiveness. We have explored this phenomenon by infusing epinephrine into awake rabbits for 2h and then assessing smooth muscle contraction, both in vivo and ex vivo. Epinephrine was infused at a rate of 1 microgram X min-1 which resulted in a 15-fold increase in the plasma epinephrine concentration. The dose of phenylephrine required to cause a 25 mmHg increase in mean arterial pressure significantly increased from 109 +/- 56 micrograms prior to the infusion to 261 +/- 143 at the end of the 2h infusion (p less than 0.01). The sensitivity to phenylephrine remained decreased when reassessed 2h later. Untreated rabbits displayed no change in alpha-adrenergic responsiveness when assessed at 2 hourly intervals over the time-course of the experiment. Contraction of aortic rings removed from both epinephrine-treated and control rabbits was determined in vitro in tissue baths. The EC50 of norepinephrine-induced contraction increased from 31 +/- 6 to 210 +/- 20 nM while there was also a 30% decrease in the maximal force of contraction (EMax) in treated vessels. The EC50 only partially recovered after 4h of incubation ex vivo, while the EMax was restored to the control value. The EC50 for histamine in the aortic rings from epinephrine-treated rabbits was not different from controls although there was a 25% reduction in the EMax at 2h. We conclude that desensitization of alpha-adrenergic mediated vascular contractility develops rapidly in vivo and is only slowly reversible after removal of the agonist.

Animals↗

Prolonged hyporesponsiveness of vascular smooth muscle contraction after halothane anesthesia in rabbits.

Halothane diminishes smooth muscle contractility in vascular tissue. In order to further characterize this phenomenon we undertook a series of in vivo and ex vivo experiments. Pressor dose-response curves to the selective alpha 1-adrenergic agonist, phenylephrine, were constructed in groups of rabbits before, during and 2 hr after halothane anesthesia and the dose of phenylephrine that induced a 25 torr increase in mean arterial pressure (ED25) was derived by polynomial regression analysis. ED25 torr increased significantly during halothane anesthesia, and rabbits remained in this insensitive state when the ED25 was assessed 2 hr after anesthesia. The halothane-induced loss of responsiveness was corroborated by ex vivo experiments utilizing aortic rings from halothane-anesthetized rabbits. The maximal contraction to norepinephrine (NE) was significantly lower in halothane-treated aortic rings and only slowly returned to normal by 4 hr. The EC50 (the dose causing a 50% maximal contraction) for NE was significantly greater in aortic rings from halothane-anesthetized rabbits. This loss of sensitivity, reflected by the higher EC50 was not restored by 4 hr of ex vivo incubation in a halothane-free medium. We conclude that halothane induces loss of sensitivity to adrenergic agonists that persists for several hours after termination of the halothane anesthetic.

Anesthesia↗

[Adrenoreceptors].

With the development of techniques for the qualitative and quantitative assessment of receptor function and knowledge of the biological responsiveness of neurotransmitter-mediated pathways, it is now quite clear that the response of a patient to a drug does not only involve the concentration of the drug in blood and tissue. Number and function of receptors are also important factors. A perturbation in which the receptor number is elevated is called "up-regulation", whereas "down-regulation" refers to the uncoupling between receptor and effector and the consecutive decrement in the receptor concentration. In general, there is an inverse relationship between the ambient concentration of the agonist and the number of its receptors and, therefore, the sensitivity of the target organ. The demarcation between alpha- and beta-adrenergic receptors has long been appreciated. Recent advances in the understanding of adrenergic receptors have led to the subdivision of beta-receptors; beta 1-adrenoceptors mediate the stimulation of rate and force of cardiac contraction and stimulate lipolysis. beta 2-adrenoceptors mediate smooth muscle relaxation and facilitate glycogenolysis and the release of insulin, glucagon and renin. The alpha-adrenergic receptors may also be divided into two subgroups. The alpha 1-adrenoceptors are postsynaptic located and facilitate smooth muscle constriction. Presynaptic located alpha 2-adrenoceptors mediate feedback inhibition of norepinephrine-release, while postsynaptic alpha 2-adrenoceptors facilitate smooth muscle contraction in selected vascular beds and stimulate the inhibition of various metabolic processes (insulin and renin secretion, lipolysis). The stage is now set for the application of the new knowledge of receptor function and regulation to the advancement of the practice of anaesthesia and intensive care.

Adrenal Cortex Hormones↗

[Non-invasive pulse oximetry for the measurement of oxygen saturation in intensive care patients].

Non-invasive measurements of oxygen saturation are attractive because they provide continuous information which may result in improved patient care. We evaluated a new finger pulse oximeter as a measure of arterial oxygen saturation in critically ill patients with respiratory distress. In 12 patients studied, 133 simultaneous comparisons between in vivo (Pulse-Oximeter, Nellcor, Hayward, California) and in vitro (IL CO-Oximeter 282) oxygen-haemoglobin saturation were made. Linear regression analysis of these pooled data yielded on excellent correlation (r = 0.97, p less than 0.001, 0.3% accuracy). The results demonstrate that non-invasive oxygen monitoring of patients with respiratory failure is feasible and can reliably detect potential life-threating arterial oxygen desaturation.

Carbon Dioxide↗