Effects of propofol on H-reflex in humans.

BACKGROUND: Depression of spinal cord motoneuron excitability has been proposed to contribute to surgical immobility. The H-reflex, which measures alpha-motoneuron excitability, is depressed by volatile anesthetics, whereas the action of propofol is unknown. The objective of this study was to determine the effects of propofol anesthesia on the H-reflex. METHODS: In 13 patients (group 1), H-reflex was measured before (T0), 3 min after (T1), and 10 min after (T2) a 2-mg/kg bolus dose of propofol, followed by an infusion of 10 mg x kg(-1) x h(-1). Ten patients (group 2) were studied when propofol was given via a programmable pump set to a propofol blood concentration of 6 microg/ml, and 10 patients (group 3) were studied with the pump set to 9 microg/ml. Latencies and amplitudes of H-reflexes (H0, H1, H2) and M-responses (M0, M1, M2) of the soleus muscle were recorded, and H/M ratios (H0/M0, H1/M1, H2/M2) were calculated. RESULTS: In group 1, H-reflex amplitudes and the H/M ratio were diminished after induction with propofol (H0 vs. H1, P = 0.033; H0/M0 vs. H1/M1, P = 0.042). After 10 min of propofol infusion, the H2/M2 ratio was still decreased versus H0/M0 (P = 0.031). In group 2, no difference was detected. In group 3, propofol depressed H-reflex amplitudes at T2 (H0 vs. H2, P < 0.01), and amplitudes were also lower at T2 than at T1 (H1 vs. H2, P < 0.01). In this group, the H/M ratio decreased from T0 to T2 (H0/M0 vs. H2/M2, P < 0.002). CONCLUSIONS: During steady state conditions using propofol as the sole agent, a depression of the H-reflex is observed only at a high blood concentration of 9 microg/ml. The authors suggest that immobility during propofol anesthesia is not caused by a depression of spinal motoneuron circuit excitability.

[Treatment of acute clinical stroke]. / Akute klinische Schlaganfallbehandlung.

Stroke is an emergency. Treatment must begin as soon as possible because significant sustained neurological improvement has been demonstrated when thrombolytic treatment, mainly with recombined tissue plasminogen activator (rtPA) is initiated within the first hours of stroke onset. On the other hand in the acute phase of stroke it is critical that patients get adequate management for the prevention of early complications. Management of the acute phase of stroke is the target of this article. Preclinically started treatment must be continued in the neurological emergency unit. Clinical examination is followed by technical investigations: cerebral computer tomography (CCT) is the most useful radiological investigation in the acute phase. It allows to distinguish between ischemia and hemorrhagic lesions and also to rule out nonstroke brain conditions. Multimodal magnetic resonance imaging (mMRI) may provide data on viable versus irreversibly damaged tissue. Sufficient stroke treatment is based on well managed in-hospital infrastructure. Thrombolysis is the only causative treatment of stroke in selected patients. Complications of acute stroke comprise changes of blood pressure with hemodynamically relevant effects on cerebral perfusion pressure, acute post- ischemic brain edema, and intracerebral bleedings.

Stroke--a medical emergency.

Stroke is the third leading cause of death and number one cause of disability in industrialised countries. A number of new therapeutic approaches are currently in development for use in the acute phase of ischaemic stroke and all trials have, to date, demonstrated the importance of early diagnosis and subsequent initiation of treatment. It is well known that, for most patients, there is a long delay between the onset of symptoms and the start of treatment. A number of factors are responsible for this time delay: signs and symptoms often go unrecognised by patients, relatives, and bystanders and, unlike trauma or myocardial infarction, stroke is not given a high priority by medical staff. Studies into the pathophysiology of acute ischaemic stroke have indicated that treatment options are likely to be optimised when early signs of stroke are recognised and treatment is initiated within six hours of symptom onset. Although a small number of stroke patients are treated as emergencies and attended to by the emergency medical services within this time window, this number could easily be increased by intensified public and emergency personnel education. In the future, it is hoped that treatments which must be administered within the first few hours of acute stroke will be able to be initiated by the emergency medical services. In the same way that hospitals are notified and prepared in advance to receive trauma victims, early notification by the emergency medical services about stroke patients would enable stroke teams to be present at admission, thus improving the likelihood of a better outcome for patients.

[Preclinical treatment of patients with stroke]. / Präklinisches Management des Patienten mit Schlaganfall.

Stroke is the third leading cause of death and number one cause of disability in industrialised countries. Studies into the pathophysiology of acute ischaemic stroke have indicated that treatment options are likely to be optimized when early signs of stroke are recognized and treatment is initiated within 3 hours from symptom onset. Therefore, new conceptions heading towards early diagnosis, fast preclinical treatment, structured diagnostics, immediate initiation of acute therapy as well as early initiation of rehabilitation are required. It is well known that, for most patients, there is a long delay between the onset of symptoms and the start of therapy. Many factors are responsible for the time delay:signs and symptoms often go unrecognized and/or are minimized by patients, relatives and bystanders. Unlike trauma or myocardial infarction, stroke is not given a high priority by medical staff and/or emergency medical services (EMS). Although a small number of stroke patients is treated as emergency and attended to by the emergency medical services within this time window, this number could easily be increased by intensified public and emergency personnel education. At present the standard of care by the EMS personnel includes adequate cerebral oxygenation, treatment of cardiac arrhythmia, management of hypertension as well as therapy of hyperglycemia and hyperthermia. For the future, we hope that emergency medical services will be able to initiate therapies which must be administered within the first few hours of acute stroke after onset of symptoms. Early notification of hospitals would enable a particular stroke team to be present at the patient's admission.

Tropisetron or ondansetron compared with placebo for prevention of postoperative nausea and vomiting.

In a prospective, randomized, double-blind, placebo-controlled, multicentre study, the efficacy of prophylactic tropisetron (2 mg) or ondansetron (4 mg) for the prevention of post-operative nausea and vomiting after abdominal or non-abdominal surgery with general balanced anaesthesia was studied in 842 ASA I-III patients. In patients undergoing abdominal surgery, ondansetron and tropisetron reduced the frequency of emetic episodes compared with the placebo (29%, 30% vs. 42% respectively). In men, neither tropisetron nor ondansetron had an effect different from the placebo, whereas in women both drugs led to lower rates of emetic episodes and nausea. In comparison with abdominal surgery, fewer patients in the non-abdominal surgery subgroup had emetic episodes (42% vs. 23% in the placebo group). However, neither tropisetron nor ondansetron was significantly different from the placebo in this patient subgroup. In conclusion, for patients at increased risk of post-operative nausea and vomiting, a prophylactic therapy at the lowest effective dose with tropisetron or ondansetron may be useful.

High dose naloxone does not improve cerebral or myocardial blood flow during cardiopulmonary resuscitation in pigs.

In a prospective, randomized, placebo-controlled, double-blind trial we tested the hypothesis that naloxone given during cardiopulmonary resuscitation (CPR) enhances cerebral and myocardial blood flow. Twenty-one anesthetized, normoventilated pigs were instrumented for measurements of right atrial and aortic pressures, and regional organ blood flow (radiolabeled microspheres). After 5 min of untreated fibrillatory arrest, CPR was commenced using a pneumatic chest compressor/ventilator. With onset of CPR, an i.v. bolus of 40 micrograms/kg b.w. of epinephrine was given, followed by an infusion of 0.4 micrograms/kg per min. After 5 min of CPR, either naloxone, 10 mg/kg b.w. (group N, n = 11) or normal saline (group S, n = 10) was given i.v. Prior to, and after 1, 15, and 30 min of CPR, hemodynamic and blood flow measurements were obtained. After 30 min of CPR, mean arterial pressure was significantly higher in group N (26 +/- 5 vs. 13 +/- 3 mmHg, P < 0.05). Groups did not differ with respect to myocardial perfusion pressure or arterial blood gases at any time during the observation period. Regional brain and heart blood flows were not different between N and S at any point of measurement. We conclude that high-dose naloxone does not augment cerebral or myocardial blood flow during prolonged closed-chest CPR.

Effects of fenoldopam on intracranial pressure and hemodynamic variables at normal and elevated intracranial pressure in anesthetized pigs.

Fenoldopam (FE), a dopamine DA1-receptor agonist, has been introduced for treatment of arterial hypertension and heart failure and for preservation of renal function. Vasodilators are generally assumed to affect all vascular beds including the cerebral circulation. We have evaluated effects of FE-induced (4 micrograms.kg-1.min-1) arterial hypotension on intracranial pressure (ICP) and intraocular pressure (IOP) under conditions of normal and increased intracranial elastance. ICP and IOP responses to hypertension were tested by infusion of angiotensin II (15 micrograms.kg-1.min-1), and the response to hypercapnia was tested by elimination and reintegration of soda lime canisters in the breathing circuit. Intracranial elastance was increased by infusing mock cerebrospinal fluid (CSF) into the lateral ventricle (20 +/- 3 ml.h-1). Arterial hypotension induced with FE did not increase ICP. With increased intracranial elastance, the infusion rate of mock CSF had to be reduced while administering FE to avoid a rise in ICP (p < 0.05 compared with preinfusion value); this indicates a shift on the volume-pressure curve to the right. There were no indicators that cerebral autoregulation or CO2 reactivity of the cerebral vasculature were affected by FE in this anesthetized porcine model, as speculated from analysis of the time course of delta ICP. There are, however, indicators of increased intracranial elastance, most likely caused by vasodilation. Caution should hence be exercised when FE is administered to patients with increased intracranial elastance.

[The preclinical efficacy of emergency care. A prospective study]. / Die präklinische Effektivität der notärztlichen Versorgung. Eine prospektive Studie.

Quality assurance has become an important issue in emergency medicine. At present, no prospective studies are available that quantify the efficacy of interventions performed by emergency doctors. The development and implementation of a rapid, yet simple scoring system, allowing preclinical assessment of all emergency medicine patients, is required. Once the scoring system is implemented, evaluation of the prehospital intervention, based upon objective parameters, is possible. METHODS. The Mainz Emergency Evaluation Score (MEES) is based on seven parameters: level of consciousness, heart rate, heart rhythm, arterial blood pressure, respiratory rate, partial arterial oxygen saturation and pain. A coded value is assigned to each parameter, with the normal physiological condition securing a score of 4, while a life-threatening condition receives a value of 1. For the parameter of pain there is no life-threatening condition, so the lowest value allowed is 2 (Table 2). Addition of the respective values from the seven parameters yields the MEES value, which objectively reflects the patients' condition (minimum = 8, maximum = 28). Comparing the MEES value before (MEES1) and after the intervention (MEES2) allows an objective evaluation of the efficacy of the preclinical care (delta-MEES = MEES2-MEES1). A difference of > or = +2 is considered an improvement, +1, +/- 0, -1 are rated as unchanged and < or = -2 is considered a deterioration in the patients condition. For more detailed evaluation the patients were allocated to 16 diagnosis groups (Table 3). Statistical evaluation utilized analysis of variance, the rank sum test (Wilcoxon) and the correlation coefficient (Kendall-Tau). RESULTS. In 356 patients the condition of 187 (52%) patients improved during the preclinical treatment; the condition of 156 (44%) patients did not change. In 13 patients (3%) the condition became worse (Table 5, Fig. 2). Allocation to 16 diagnosis groups revealed that the improvement in the patient's condition depended on the underlying disease (Table 3); the disease-specific parameter improved in all cases (Table 7). CONCLUSIONS. With the MEES score one can assess the patient's prehospital condition and monitor any improvement or deterioration during subsequent intervention and transport. The MEES was found to be easy to use, reliable and not an additional burden to emergency doctors. The MEES provides a means of assessing the efficacy of preclinical treatment. This score does not allow outcome prediction; this requires the inclusion of hospital data. Assessment of the efficacy of prehospital intervention is an important first step in the inclusion of quality assurance in emergency medical systems.

Deliberate arterial hypotension does not reduce intraocular pressure in pigs.

Among the accepted advantages of general anesthesia in ophthalmic surgery is improved control of intraocular pressure (IOP). Although standard textbooks advocate deliberate arterial hypotension to facilitate intraocular surgery by reducing IOP, scientific proof of such an effect is lacking. The authors investigated effects of induced arterial hypotension on IOP in an anesthetized porcine model. Forty-two piglets were anesthetized with piritramide, were placed in the prone position, and had the anterior chamber of one eye punctured with a small Teflon cannula to measure IOP. Six pigs were used in a pilot study to establish dose-response relationships for the hypotensive agents; 36 pigs were randomly allocated to one of three groups (n = 12) to receive nitroprusside, adenosine, or isoflurane to reduce mean arterial pressure (MAP) by 50%. Measurements were made after initial stabilization of hemodynamic variables and IOP (control), when a stable MAP of 0.5x control was maintained for 10 min or longer, and after return of MAP to a posthypotensive steady state. The median of differences between time intervals was analyzed statistically for all variables. Nitroprusside and adenosine produced hyperdynamic hypotension (cardiac index increased); isoflurane-induced hypotension was hypodynamic. Control IOPs were 12.9, 12.5, and 11.1 mmHg in the nitroprusside, adenosine, and isoflurane groups, respectively. Median change in IOP during hypotension was -1.5, +1.5, and 0 mmHg in the nitroprusside, adenosine, and isoflurane groups, respectively. The IOP during adenosine-induced hypotension was significantly higher than that during either nitroprusside- or isoflurane-induced hypotension. Return of MAP to control levels was frequently associated with intraocular rebound hypertension when arterial hypotension had been induced with adenosine or nitroprusside.(ABSTRACT TRUNCATED AT 250 WORDS)

[The effect of muscle relaxants on masseter tone. An experimental study in an MH-susceptible swine model]. / Zur Wirkung von Muskelrelaxanzien auf den Massetertonus. Eine experimentelle Studie am MH-disponierten Schweinemodell.

Malignant hyperthermia (MH) may occur, when a genetically predisposed individual or pig (MHS) is exposed to triggering agents. The increase in free, ionized sarcoplasmic calcium inducing the vicious circle of MH is believed to result from calcium-induced release with volatile anaesthetics, and from depolarization-induced calcium release with succinylcholine (SCH). The administration of SCH to susceptible humans or pigs frequently produces an increase in masticatory muscle tone. This hitherto ill-defined phenomenon is referred to as "masseter spasm" (MS). We have attempted to elucidate the pathophysiology of MS in a porcine model. METHODS. After the protocol had been approved by the state authorities, 6 MHS pigs were investigated. The pigs were mixed breeds (German Landrace and Dutch Pietrain) and were 9 +/- 1 weeks old with an average body weight of 25.5 kg. Premedication consisted of intramuscular injection of azaperone, 7.5 mg.kg-1. Anaesthesia was induced with piritramide, 1.2 mg.kg-1, administered via a cannulated ear vein. Subsequent to laryngoscopic endotracheal intubation, neuromuscular blockade was achieved with 4 mg pancuronium. Ventilation was set at 12 breaths per minute and adjusted to maintain an end-tidal CO2 concentration of 4.7% by adapting the tidal volume (PhysioFlex). Anaesthesia was maintained with piritramide, 2.25 mg.kg-1.h-1, pancuronium, 0.4 mg.kg-1.h-1, and N2O (60% in O2). Instrumentation included an arterial line, a central venous line, and a fiberoptic pulmonary artery catheter (Oximetrix). Masticatory muscle tone (MMT) was assessed with an intermolar balloon, connected to a pressure transducer and calibrated to zero prior to SCH administration. As a reference variable for effects produced by SCH, intraocular pressure (IOP) was measured manometrically in the anterior chamber. After stabilization of haemodynamic variables, the neuromuscular blockade was allowed to wear off. After recovery of the evoked masseter electromyogram, a paralyzing dose of pancuronium was administered (0.5 mg.kg-1). When paralysis was complete, SCH was administered (1.5 mg.kg-1), followed a few minutes later by dantrolene infusion (5 mg.kg-1 over 10 min). RESULTS. The administration of SCH was followed by clinically unequivocal MH episodes in all pigs, indicated by an increase in oxygen uptake (VO2; PhysioFlex; Fig. 1) and end-tidal CO2 concentration and a decrease in oxygen saturation of mixed venous blood (svO2; Fig. 2). Despite complete neuromuscular blockade (monitored with EMG), SCH produced an increase in MMT in all pigs which was reversed by dantrolene (Fig. 3). The time course of MMT paralleled that of IOP, suggesting a similar underlying mechanism. DISCUSSION. Succinylcholine is a trigger of MH in susceptible individuals; onset of the syndrome may be associated with "masseter spasm". SCH increases extraocular muscle tone, probably by means of stimulating multiply innervated fibers; the resulting IOP increase is not prevented by competitive neuromuscular blockade. The existence of multiple innervated fibers has also been shown in muscle spindles in the deep layers of the masseter, with their stimulation resulting in elevation of the jaw. We speculate that the increases in MMT and IOP observed in this study reflect the same process, i.e. a motor response, initiated by SCH-induced stimulation of the intramyocellular contractile system of multiply innervated muscle fibers, that is independent of neuromuscular transmission. Triggering of MH with SCH despite complete neuromuscular blockage suggests a mechanism other than depolarization-induced calcium increase. And, for the semantics, according to neurological terminology MS should be referred to as contracture not as spasm.

[The seated position in patent foramen ovale?]. / Sitzende Position bei offenem Foramen ovale?

Anesthetic management of patients presenting for posterior cranial fossa surgery in the seated position includes detection and treatment of venous air embolism. Atrial positioning of a central venous (cv) line may be verified by either X-ray or an atrial ECG tracing. We report a case where a chest X-ray film proved superior. A 26-year-old white female was scheduled for posterior cranial fossa exploration. A cv line was inserted via the left antecubital vein; the chest X-ray film documented correct positioning of the catheter tip within the atrium but an aberrant course of the superior vena cava. Echocardiography was performed in the induction room and indicated a patent foramen ovale. In view of the risk of paradoxical air embolism, surgery was postponed. Subsequent cardiologic and radiologic examinations revealed a patent foramen ovale and a persisting left superior vena cava draining into a dilated coronary sinus. Surgery was rescheduled and carried out uneventfully in the prone position. This case demonstrates: 1) an advantage of a thoracic-X-ray film compared to atrial ECG tracing as not only the catheter tip position, but also the course of the catheter can be identified; and 2) the usefulness of preoperative screening for a patent foramen ovale in patients scheduled for surgery in the seated position.

[Computed tomography after extracorporeal shockwave lithotripsy (ESWL) of the kidneys. II. A correlation with the histopathologic findings 3 weeks later in an animal experiment]. / Computertomographie nach extrakorporaler Stosswellen-Lithotripsie (ESWL) der Nieren. Teil II: Korrelation mit histopathologischen Befunden nach 3 Wochen im Tierexperiment.

In a pig model, 13 kidneys were treated with a second generation lithotripter and examined by CT immediately and three weeks after ESWL. 9 (69%) acute traumatic lesions were seen in CT without, and 10 (77%) in CT with contrast in the 13 treated kidneys. After 3 weeks only 1 residual lesion persisted in CT contrast studies. On the histopathologic specimens residuals of bleeding were found in 3 (23%) of the 13 kidneys treated, which could not be seen in CT studies. CT is accurate in monitoring acute traumatic renal lesions after ESWL, but appears less reliable in chronic ones. Three weeks after ESWL traumatic renal lesions show marked regression.