ICU personnel have inaccurate perceptions of their patients' experiences.

BACKGROUND: Intensive care unit (ICU) patient care bases - among others - upon the staff's assumptions about each patient's subjective preferences and experiences. However, these assumptions may be skewed and thus result in client-professional gaps (cp-gaps), which occur in two subtypes, hyperattention and blind spots to certain burdens. cp-gaps typically reduce quality of care. We investigated whether cp-gaps of either subtype exist in a 36-bed ICU of a university hospital. METHODS: Observational study on 82 consecutive patients of a 36-bed university ICU, who voluntarily answered a psychometric questionnaire focusing on patients' experiences during an ICU stay. The questionnaire was reliable and valid (Cronbach's alpha, factor analysis). It consisted of 31 Likert-scaled items, which represented three scales of perception (communicative, intrapersonal, somatic) supplemented by 55 binary items for more specific information. Details of the questionnaire are given in the text. Demographic, educational, and medical data were registered too. Patients reported their subjective ICU experience 2-7 days after ICU discharge. Analogously, 60 staff members (physicians and nurses) reported their assumptions about patients' experiences. After correction for a general bias, group differences indicated cp-gaps. RESULTS: Twelve cp-gaps were found. Hyperattention was found in four communicative and three intrapersonal items. Blind spots appeared in two communicative, two intrapersonal, and one somatic item. The pattern of cp-gap subtypes (hyperattention/blind spots) goes well with self-attributional bias - a model of social interaction. CONCLUSIONS: cp-gaps in ICUs can be identified using analogue questionnaires for patients and staff. Both subtypes of cp-gap occur. cp-gaps are substantially influenced by self-attributional bias.

Endogenous nitric oxide reduces the efficacy of the endothelin system to maintain blood pressure during high epidural anaesthesia in conscious dogs.

BACKGROUND AND OBJECTIVE: During high epidural anaesthesia, endothelin only contributes minimally to blood pressure stabilization. This phenomenon could result from the inhibitory action of nitric oxide on the endothelin system. To clarify this, we studied the interaction between nitric oxide and endothelin during high epidural anaesthesia in conscious dogs, in comparison to the interaction of nitric oxide and vasopressin. METHODS: Six animals were used in 45 individual experiments randomly arranged as follows: N-omega-nitro-arginine-methylester 0.3-10 mg kg-1 under physiological conditions or during high epidural anaesthesia (lidocaine 1%) and N-omega-nitro-arginine-methylester (l-NAME) 0.3-10 mg kg-1 after preceding endothelin (Tezosentan(R)) or vasopressin (beta-mercapto-beta,beta-cyclo-penta-methylene-propionyl-O-Me-Tyr-Arg-vasopressin) receptor blockade under physiological conditions or during high epidural anaesthesia. During control experiments normal saline was injected either intravenously (n = 5) or into the epidural space (n = 4). RESULTS: N-omega-nitro-arginine-methylester increased mean arterial pressure dose-dependently in all groups. However, this effect was substantially reduced in the presence of the endothelin receptor antagonist compared to N-omega-nitro-arginine-methylester alone, both under control conditions (7 +/- 3 vs. 21 +/- 3 mmHg; P < 0.05) and during high epidural anaesthesia (17 +/- 3 vs. 30 +/- 1 mmHg; P < 0.05). Blockade of vasopressin showed no similar relationship with N-omega-nitro-arginine-methylester. CONCLUSIONS: The diminished increase in mean arterial pressure after injection of N-omega-nitro-arginine-methylester only during endothelin receptor blockade indicates that endogenous nitric oxide inhibits the action of endothelin during high epidural anaesthesia and might thus explain the reduced efficacy of endothelin in maintaining blood pressure during high epidural anaesthesia.

Desflurane increases heart rate independent of sympathetic activity in dogs.

BACKGROUND AND OBJECTIVE: Desflurane has been shown to increase sympathetic activity and heart rate (HR) in a concentration-dependent manner. Nevertheless, desflurane, like all other volatile anaesthetics, increased HR in parallel to vagal inhibition in a previous study. Therefore, our hypothesis is that desflurane elicits tachycardia by vagal inhibition rather than by activation of the sympathetic nervous system. METHODS: Six dogs were studied awake and during desflurane anaesthesia (1 and 2 MAC) alone, after pretreatment with propranolol (2 mg kg(-1) followed by 1 mg kg(-1) h(-1)), or after pre-treatment with atropine (0.1 mg kg(-1) followed by 0.05 mg kg(-1) h(-1)). The effects on HR and HR variability were compared by an analysis of variance (P < 0.05). HR variability was analysed in the frequency domain as power in the high-(0.15-0.5 Hz, vagal activity) and low-frequency range (0.04-0.15 Hz, sympathetic and vagal activity). RESULTS: HR increased during 2 MAC of desflurane from about 60 (awake) to 118 +/- 2 beats min(-1) (mean +/- SEM) in controls and to 106 +/- 3 beats min(-1) in dogs pre-treated with propranolol. In contrast, pretreatment with atropine increased HR from 64 +/- 2 to 147 +/- 5 beats min(-1) (awake) and HR decreased to 120 +/- 5 beats min(-1) after adding desflurane. High-frequency power correlated inversely with HR (r2 = 0.95/0.93) during desflurane alone and in the presence of beta-adrenoceptor blockade, with no significant difference between regression lines. There was no correlation between these variables during atropine/desflurane. CONCLUSIONS: The increase in HR elicited by desflurane mainly results from vagal inhibition and not from sympathetic activation.

Accuracy of feedback-controlled oxygen delivery into a closed anaesthesia circuit for measurement of oxygen consumption.

BACKGROUND: Oxygen consumption (V*O2) is rarely measured during anaesthesia, probably because of technical difficulties. Theoretically, oxygen delivery into a closed anaesthesia circuit (V*O2-PF; PhysioFlex Draeger Medical Company, Germany) should measure V*O2. We aimed to measure V*O2-PF in vitro and in vivo. METHODS: Three sets of experiments were performed. V*O2-PF was assessed with five values of V*O2 (0-300 ml min(-1)) simulated by a calibrated lung model (V*O2-Model) at five values of FIO2 (0.25-0.85). The time taken for V*O2-PF to respond to changes in V*O2-Model gave a measure of dynamic performance. In six healthy anaesthetized dogs we compared V*O2-PF with V*O2 measured by the Fick method (V*O2-Fick) during ventilation with nine values of FIO2 (0.21-1.00). V*O2-PF and V*O2-Fick were also compared in three dogs when V*O2 was changed pharmacologically [102 (SD 14), 121 (17) and 200 (57) ml min(-1)]. In patients during surgery, we measured V*O2-PF and V*O2-Fick simultaneously after induction of anaesthesia (n=21) and during surgery (n=17) (FIO2 0.3-0.5). RESULTS: Compared with V*O2-Model, V*O2-PF values varied from time to time so that averaging over 10 min is recommended. Furthermore, at an FIO2 >0.8, V*O2-PF always overestimated V*O2. With FIO2 <0.8, averaged V*O2-PF corresponded to V*O2-Model and adapted rapidly to changes. Averaged V*O2-PF also corresponded to V*O2-Fick in dogs at FIO2 <0.8. V*O2 measured by the two methods gave similar results when V*O2 was changed pharmacologically. In contrast, V*O2-PF systematically overestimated V*O2-Fick in patients by 52 (SD 40) ml min-1 and this bias increased with smaller arteriovenous differences in oxygen content. CONCLUSION: V*O2-PF measures V*O2 adequately within specific conditions.

Xenon increases total body oxygen consumption during isoflurane anaesthesia in dogs.

BACKGROUND: This study was designed to examine whether the coupling between oxygen consumption (VO2) and cardiac output (CO) is maintained during xenon anaesthesia. METHODS: We studied the relationship between VO2 (indirect calorimetry) and CO (ultrasound flowmetry) by adding xenon to isoflurane anaesthesia in five chronically instrumented dogs. Different mixtures of xenon (70% and 50%) and isoflurane (0-1.4%) were compared with isoflurane alone (1.4% and 2.8%). In addition, the autonomic nervous system was blocked (using hexamethonium) to study its influence on VO2 and CO during xenon anaesthesia. RESULTS: Mean (SEM) VO2 increased from 3.4 (0.1) ml kg(-1) min(-1) during 1.4% isoflurane to 3.7 (0.2) and 4.0 (0.1) ml kg(-1) min(-1) after addition of 70% and 50% xenon, respectively (P<0.05), whereas CO and arterial pressure remained essentially unchanged. In contrast, 2.8% isoflurane reduced both, VO2 [from 3.4 (0.1) to 3.1 (0.1) ml kg(-1) min(-1)] and CO [from 96 (5) to 70 (3) ml kg(-1) min(-1)] (P<0.05). VO2 and CO correlated closely during isoflurane anaesthesia alone and also in the presence of xenon (r2=0.94 and 0.97, respectively), but the regression lines relating CO to VO2 differed significantly between conditions, with the line in the presence of xenon showing a 0.3-0.6 ml kg(-1) min(-1) greater VO2 for any given CO. Following ganglionic blockade, 50% and 70% xenon elicited a similar increase in VO2, while CO and blood pressure were unchanged. CONCLUSIONS: Metabolic regulation of blood flow is maintained during xenon anaesthesia, but cardiovascular stability is accompanied by increased VO2. The increase in VO2 is independent of the autonomic nervous system and is probably caused by direct stimulation of the cellular metabolic rate.

Endogenous endothelin and vasopressin support blood pressure during epidural anesthesia in conscious dogs.

UNLABELLED: We studied whether endogenous endothelin, like endogenous vasopressin, helps to maintain blood pressure during high epidural anesthesia when efferent sympathetic drive is diminished. On different days, six awake dogs underwent each of the following five interventions: blockade of vasopressin V(1a) receptors using [d(CH(2))(5)Tyr(Me(2))]AVP, (40 microg/kg) or endothelin receptors using tezosentan (3 mg/kg followed by 3 mg. kg(-1). h(-1)) with or without epidural anesthesia (1% lidocaine, intraindividual dose did not differ between experiments), and epidural saline (n = 5). The effects of endothelin- or vasopressin-receptor blockade were analyzed (means +/- SEM) and compared by an analysis of variance for repeated measures (paired Student's t-test, alpha-adjusted, P < 0.05). Vasopressin-receptor blockade decreased blood pressure (10 +/- 2 mm Hg) only in the presence of epidural anesthesia, whereas endothelin-receptor blockade reduced blood pressure both in the presence and absence of epidural anesthesia (12 +/- 3 versus 10 +/- 1 mm Hg). During baseline and each intervention, plasma concentrations of vasopressin and big-endothelin were measured and compared by a Wilcoxon's rank sum test; P < 0.05. Vasopressin concentrations increased during epidural anesthesia and after additional endothelin receptor blockade, but big-endothelin concentrations remained unchanged during each intervention. We conclude that vasopressin acts as a reserve system, as it stabilizes blood pressure specifically during epidural anesthesia, whereas the unchanged concentrations of big-endothelin indicate that the endothelin system is not specifically activated to support blood pressure during epidural anesthesia. IMPLICATIONS: We studied in awake dogs whether endogenous endothelin, like endogenous vasopressin, helps to maintain blood pressure during resting conditions and epidural anesthesia. Only vasopressin was specifically activated to support blood pressure during epidural anesthesia, whereas endothelin supported blood pressure to the same extent during epidural anesthesia and during resting conditions.