[Resuscitation room management for trauma patients]. / Schockraummanagement bei traumatologischen Patienten.

Resuscitation rooms in central emergency admissions are the first point of contact for potentially severely or multiply injured patients. Here priority is given to the interdisciplinary treatment of these patients, which includes the structured and standardized hospital admission as well as the appropriate initial diagnostics and treatment of potentially life-threatening conditions. The resuscitation room is a central vital link between the prehospital and internal hospital treatment chain. This article describes the core tasks of the resuscitation room team as well as concepts and strategies of initial treatment of severely injured and polytrauma patients.

Severity of polymicrobial sepsis modulates mitochondrial function in rat liver.

Mitochondrial dysfunction is assumed to be an important contributor to multi organ dysfunction syndrome. Here, the effects of varying degrees of sepsis on hepatic mitochondrial function were investigated. Moderate or more severe sepsis was induced in rats using a colon ascendens stent peritonitis (CASP)-model (16 G and 14 G stent respectively). Respiratory control ratio (RCR) was significantly higher in the 16 G-group and unchanged in the 14 G-group compared with healthy controls. The ADP/O ratio was similar in all groups. Our results indicate that different severities of sepsis differently influence the mitochondrial function, which could be a sign of adaptive reaction.

Hypothermia improves oral and gastric mucosal oxygenation during hypoxic challenges.

BACKGROUND: Therapeutic hypothermia, used primarily for protective effects after hypoxia, improves oral and gastric mucosal microvascular oxygenation (µHbO2) during additional haemorrhage. Therefore, we questioned whether hypothermia likewise improves µHbO2 during hypoxic challenges. Since both hypothermia and hypoxia reduce cardiac output (e.g. by myofilament Ca(2+) desensitization), and modulate vasomotor tone via K(+) ATP channels, we hypothesized that the Ca(2+) sensitizer levosimendan and K(+) ATP channel blocker glibenclamide would support the cardiovascular system. METHODS: The effects of mild hypothermia (34°C) on µHbO2 during hypoxia [Formula: see text] were analysed in a cross-over study on five anaesthetized dogs and compared with normothermia (37.5°C) and hypoxia. During hypothermia, but before hypoxia, glibenclamide (0.2 mg kg(-1)) or levosimendan (20 µg kg(-1)+0.25 µg kg(-1) min(-1)) was administered. Systemic haemodynamic variables, gastric and oral mucosal microvascular oxygenation (reflectance spectrophotometry), and perfusion (laser Doppler flowmetry) were recorded continuously. Data are presented as mean (sem), P<0.05. RESULTS: Hypoxia during normothermia reduced gastric µHbO2 by 27 (3)% and oral µHbO2 by 28 (3)% (absolute change). During hypothermia, this reduction was attenuated to 16 (3)% and 13 (1)% (absolute change). This effect was independent of microvascular flow that did not change during hypoxia and hypothermia. Additional administration of levosimendan during hypothermia restored reduced cardiac output but did not change flow or µHbO2 compared with hypothermia alone. Glibenclamide did not exert any additional effects during hypothermia. CONCLUSIONS: Hypothermia attenuates the decrease in µHbO2 during additional hypoxic challenges independent of systemic or regional flow changes. A reduction in cardiac output during hypothermia is prevented by Ca(2+) sensitization with levosimendan but not by K(+) ATP channel blockade with glibenclamide.

The differential effects of recombinant brain natriuretic peptide, nitroglycerine and dihydralazine on systemic oxygen delivery and gastric mucosal microvascular oxygenation in dogs.

Brain natriuretic peptide has vasodilatory properties and may thus increase splanchnic perfusion and oxygenation. We compared the effects of recombinant brain natriuretic peptide on gastric mucosal microvascular haemoglobin oxygenation (reflectance spectrophotometry) and systemic variables with those of equi-hypotensive doses of two other vasodilators (nitroglycerine and dihydralazine). Chronically instrumented, healthy dogs were randomly allocated to receive on different days, one of the three drugs (nitroglycerine and dihydralazine doses titrated to reduce mean arterial pressure by ∼20%). Brain natriuretic peptide significantly increased gastric mucosal microvascular haemoglobin oxygenation selectively, i.e. without concomitant haemodynamic effects. In contrast, the other vasodilators either did not increase gastric mucosal microvascular haemoglobin oxygenation at all (nitroglycerine), or did so only with marked increases in other systemic haemodynamic variables (dihydralazine). Our data suggest a potential role of recombinant brain natriuretic peptide selectively for increasing microvascular mucosal oxygenation. Studies are required to extend these findings to the clinical setting.

Sevoflurane and propofol anaesthesia differentially modulate the effects of epinephrine and norepinephrine on microcirculatory gastric mucosal oxygenation.

BACKGROUND: Adequate gastrointestinal mucosal oxygenation is regarded to be crucial in the prevention and therapy of critical illness. Epinephrine and norepinephrine are used for perioperative haemodynamic support. However, their per se effects on gastromucosal haemoglobin oxygenation (µHbO(2)) remain unclear. Moreover, respective effects of epinephrine and norepinephrine may be affected by the type of underlying anaesthesia. Thus, we studied the effects of epinephrine and norepinephrine during anaesthesia with sevoflurane or propofol on regional gastromucosal µHbO(2) and systemic O(2)-derived variables. METHODS: In a double-randomized cross-over study, chronically instrumented dogs (n=6 per group) were anaesthetized randomly with sevoflurane or propofol, ventilated, and then randomly received either epinephrine or norepinephrine (0, 0.05, 0.1, and 0.2 µg kg(-1) min(-1)). We measured gastromucosal µHbO(2), systemic haemodynamics, and O(2)-derived variables. RESULTS: During sevoflurane anaesthesia, norepinephrine markedly increased µHbO(2) (P<0.0001) and systemic oxygen transport (DO(2)) (P=0.0006). In contrast, epinephrine failed to increase µHbO(2), despite doubling DO(2) (P=0.0002). During propofol anaesthesia, in contrast to sevoflurane, neither epinephrine nor norepinephrine affected µHbO(2), although epinephrine, but not norepinephrine, again resulted in markedly increased DO(2) (P<0.0001). CONCLUSIONS: The effects of epinephrine and norepinephrine depended on the type of anaesthesia. In addition, regional effects (i.e. µHbO(2)) were not predictable from systemic effects (i.e. DO(2)).

[Financing problems of capital goods. Part 2: procedure for investment appraisal]. / Finanzierungsproblematik von Investitionsgütern. Teil 2: Verfahren der Investitionsrechnung.

In part 1 of this series about problems of financing capital goods the multiple and partly diametric economic effects of financing instruments were presented using the leasing procedure as an example. The result indicated that due to the complexity of these effects the choice of a specific financing instrument requires an individual consideration. Therefore, part 2 of the series introduces the method of dynamic capital budgeting which allows the instruments discussed in part 1 to be compared with each other and helps to evaluate their economic benefits. More precisely this paper focuses on a comparative analysis of the most common alternatives, leasing, credit financing and investment financing by the state. In this context, after having identified the total costs of ownership of anesthesia devices, the final asset values of the three financing instruments can be compared with each other using the method of dynamic capital budgeting. In contrast to the prevailing opinion, the results show that from a purely fiscal perspective leasing anesthesia devices is the most expensive alternative. Given the fact that no financial support is available from the state, the option of credit financing turns out to be the most preferable alternative from a relatively limited pool of possibilities. However, it still remains to be answered whether credit financing can defend this position against further, innovative forms of debt financing (e.g., factoring, asset-backed securities, hedge funds, mezzanine capital, etc.).

[Financing problems of capital goods: part 1: leasing as a solution?]. / Finanzierungsproblematik von Investitionsgütern: Teil 1: Leasing als Ausweg?

The provision of financial support of hospitals by States for buying capital goods is becoming increasingly more limited. In order to still make investments, alternative forms of financing such as leasing must be considered in hospitals. However, the change from the classical form of dual financing and the decision to opt for a leasing model involves much more than just a question of costs. Leasing results in easily manageable expenditure, flexibility and adaptability for the choice of model but the leasing installments must be directly financed by the turnover from diagnosis-related groups and so lead to a reduction in the annual profit. In this article the authors try to give the reader an overview of the complex and sometimes counter-productive effect of financial instruments for investments in hospitals using leasing financing as an example. In the follow-up article the decision-making procedure using dynamic investment calculations will be demonstrated using a concrete example.

Liver protection in the perioperative setting.

With recent advances in surgical and anaesthetic management, clinical medicine has responded to societal expectations and the number of operations in patients with a high-risk of perioperative liver failure has increased over the last decades. This review will outline important pathophysiological alterations common in patients with pre-existing liver impairment and thus highlight the anaesthetic challenge to minimise perioperative liver insults. It will focus on the intraoperative balancing act to reduce blood loss while maintaining adequate liver perfusion, the various anaesthetic agents used and their specific effects on hepatic function, perfusion and toxicity. Furthermore, it will discuss advances in pharmacological and ischaemic preconditioning and summarise the results of recent clinical trials.

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.

Effects of thoracic epidural anaesthesia on microvascular gastric mucosal oxygenation in physiological and compromised circulatory conditions in dogs.

BACKGROUND: The effects of thoracic epidural anaesthesia (TEA) on gastric mucosal microvascular haemoglobin oxygenation (microHbO(2)) are unclear. At the splanchnic level, reduction of sympathetic tone may promote vasodilation and increase microHbO(2). However, these splanchnic effects are counteracted by systemic effects of TEA (e.g., decreased cardiac output (CO) and mean arterial pressure (MAP)), thus making the net effect on microHbO(2) difficult to predict. In this respect, effects of TEA on microHbO(2) may differ between physiological and compromised circulatory conditions, and additionally may depend on adequate fluid resuscitation. Furthermore, TEA may alter the relationship between regional microHbO(2) and systemic oxygen-transport (DO(2)). METHODS: Chronically instrumented dogs (flow probes for CO measurement) were anaesthetized, their lungs ventilated and randomly received TEA with lidocaine (n=6) or epidural saline (controls, n=6). Animals were studied under physiological and compromised circulatory conditions (PEEP 10 cm H(2)O), both with and without fluid resuscitation. We measured gastric mucosal microHbO(2) by reflectance spectrophotometry, systemic DO(2), and systemic haemodynamics (CO, MAP). RESULTS: Under physiological conditions, TEA preserved microHbO(2) (47 (3)% and 49 (5)%, mean (sem)) despite significantly decreasing DO(2) (11.3 (0.8) to 10.0 (0.7) ml kg(-1) min(-1)) and MAP (66 (2) to 59 (3) mm Hg). However, during compromised circulatory conditions, TEA aggravated the reduction in microHbO(2) (to 32 (1)%), DO(2) (to 6.7 (0.8) ml kg(-1) min(-1)) and MAP (to 52 (4) mm Hg), compared with controls. During TEA, fluid resuscitation completely restored these variables. TEA preserved the correlation between microHbO(2) and DO(2), compared with controls. CONCLUSIONS: TEA maintains microHbO(2) under physiological conditions, but aggravates the reduction of microHbO(2) induced by cardiocirculatory depression, thereby preserving the relationship between gastric mucosal and systemic oxygenation.

Comparison of the role of endothelin, vasopressin and angiotensin in arterial pressure regulation during sevoflurane anaesthesia in dogs.

BACKGROUND: In this study we aimed to clarify the role of endothelin in arterial pressure regulation during anaesthesia with increasing concentrations of sevoflurane (1-3 MAC) and compare it with those of vasopressin and angiotensin. METHODS: After an awake control period, on different days, six dogs underwent each of the following four interventions: sevoflurane anaesthesia alone (1-3 MAC), sevoflurane after block of either endothelin receptors using tezosentan (3 mg kg(-1) followed by 3 mg kg(-1) h(-1)), vasopressin V(1a) receptors using [d(CH(2))(5)Tyr(Me(2))]AVP (40 micro g kg(--1)) or angiotensin receptors using losartan (6 mg kg(-1) h(-1)). Plasma concentrations of endothelin, big endothelin, vasopressin and renin were measured. Effects of sevoflurane in the presence and absence of the respective receptor block were analysed and compared using analysis of variance for repeated measures (ANOVA followed by Fisher's PLSD (protected least significant difference) (P<0.05)). RESULTS: Mean arterial pressure decreased in a dose-dependent manner with sevoflurane during all interventions. At 1 MAC, this decrease was greatest during angiotensin receptor block (mean (SEM), -41 (3) mm Hg), intermediate during vasopressin and endothelin receptor block (-31 (4) and -30 (2) mm Hg respectively), and least during sevoflurane alone (-24 (3) mm Hg). The course of systemic vascular resistance mirrored the course of arterial pressure, while cardiac output did not differ between groups. Plasma concentrations of endothelin, big endothelin and renin did not change during any intervention, whereas vasopressin concentration increased from approximately 0.5 to 40 ng litre(-1) at 3 MAC as arterial pressure decreased in all groups. CONCLUSIONS: At 1 MAC, angiotensin attenuated the decrease in arterial pressure during sevoflurane anaesthesia more than endothelin and vasopressin. However, at higher MAC only vasopressin was specifically activated to partly compensate for the arterial pressure decrease.

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.

Nitric oxide synthases in vagal neurons are crucial for the regulation of heart rate in awake dogs.

Nitric oxide synthase (NOS) inhibitors elicit bradycardias independent of the endothelium (e-NOS) or increases in blood pressure. Therefore, this bradycardia could be mediated by other NOS isoforms, most likely that of the nervous system (n-NOS). If so, heart rate variability (HRV) as a measure of vagal activity should be an indicator of the activity of n-NOS in vagal neurons. To test this, we studied the dose-effect relations of L-NAME (0.3 - 50 mg x kg(-1)) on heart rate (HR), HRV and systemic vascular resistance (SVR) in seven awake dogs. HRV was analyzed in the time domain as standard deviation of the RR-intervals (SDNN) and in the frequency domain as power in the high (0.15 - 0.5 Hz) and low (0.04 - 0.15 Hz) frequency range. The effects of HR and SDNN reached their maxima at a dose of 3 mg x kg(-1) and had their ED50 at 0.27 +/- 0.03 mg x kg(-1) and 0.43 +/- 0.1 mg x kg(-1), respectively, whereas SVR had its maximum at 10 mg x kg(-1) and ED50 at 0.86 +/- 0.11 mg x kg(-1) (p < 0.05). HF-power (vagal activity) predominated compared to LF-power (mainly sympathetic activity) during baseline as well as after L-NAME. The effects on HR and HRV were absent after ganglionic blockade (hexamethonium), whereas the effects on SVR remained unchanged. Thus, NO exerts a powerful restraining activity on vagal neurons and plays a key role in the adjustment of heart rate in awake resting animals with prevailing vagal activity.

Determination of total blood volume by indicator dilution: a comparison of mean transit time and mass conservation principle.

OBJECTIVE: Using indocyanine green (ICG), blood volume can be determined within minutes according to the mass conservation principle by back-extrapolation of the concentration/time curve to the time of injection (BVTinj) or by the transit time approach (BVMTT) as the product of cardiac output and mean transit time (MTT) of ICG through the circulation. To see which factor accounts for the difference between the two methods we measured cardiac output and MTT independently and compared the volumes with those obtained by dilution of Evans blue (BVEB). DESIGN: Prospective animal study. SETTINGS: University department of experimental anaesthesiology. ANIMALS: Six anaesthetised, spontaneously breathing dogs with chronically implanted ultrasound flow probes around the pulmonary artery. MEASUREMENTS AND RESULTS: BVMTT and BVTinj agreed closely (48 +/- 2 ml.kg-1 and 49 +/- 2 ml.kg-1), but underestimated blood volume by about 40% compared with BVEB (75 +/- 1 ml.kg-1). Transit times measured were 33 +/- 1 s and should be about 50 s as calculated from the quotient of BVEB and cardiac output. CONCLUSIONS: Both methods underestimate blood volume by about the same extent compared with BVEB, probably because slowly perfused compartments are not detected during the short measurement period of 4 min. In the case of the transit time approach, rather short transit times result and in the case of the mass conservation principle, back-extra-polation yields rather high plasma concentrations of ICG at the time of injection. Accordingly, the two methods seem to be equivalent for measuring blood volume rapidly, although the absolute volume is underestimated by about 40%.

[Coupling of cardiac output or systemic O2 transport and metabolism during catecholamine therapy]. / Kopplung von Herzzeitvolumen bzw. systemischem O2-Transport und Metabolismus unter Katecholamintherapie.

Catecholamines increase cardiac output (CO) and thus systemic oxygen delivery, but they also increase the tissue's oxygen demand (thermogenic or calorigenic effect). Therefore, it is of particular interest for the choice of a catecholamine as to what extent CO is increased in relation to oxygen demand (VO2), because the tissue's oxygen balance is improved only if CO and thus oxygen delivery increases more than oxygen demand. For this purpose we reviewed the literature and analysed the relation between CO and VO2 during physiological as well as during pathological conditions. In particular, we compared the slopes of the regression lines of the individual CO/VO2-relation for each catecholamine. Dependent on study conditions, the extent of the increases in CO and VO2 varies substantially already for one and the same agent. During physiological conditions, the synthetic agents dobutamine and dopexamine primarily increase CO, whereas the endogenous ones epinephrine and particularly norepinephrine increase both CO and VO2 to about the same extent. During pathological conditions the literature is inconsistent, but it appears that the CO/VO2-relations do not differ substantially from those observed under physiological conditions. With due caution the current information implies that the synthetic catecholamines dobutamine and in particular dopexamine might be preferred in the treatment of low cardiac output states because they increase CO and thus oxygen delivery above the increase in metabolic demand.