Long-term effects of a perioperative safety checklist from the viewpoint of personnel.

BACKGROUND: While positive short-term effects of the use of safety checklists have previously been reported by personnel, it is unclear to which extent these effects are maintained for a long-term period. The aim of the present study was to evaluate perioperative safety standards and the quality of interprofessional cooperation from the viewpoint of the involved personnel for up to 2 years following the introduction of a safety checklist. METHODS: A survey of 99 co-workers in the departments of anaesthesiology and traumatology was conducted using a 19-point questionnaire concerning perioperative safety-relevant aspects and the quality of interprofessional cooperation before and at 3, 18, and 24 months after the introduction of a safety checklist. RESULTS: Verification of written consent for surgery (P < 0.01), clear marking of the surgical site (P < 0.01), and time management (P < 0.05) were rated more positively over time by the anaesthesiologists and nurses. Items involving communication were rated less positively after 18 and 24 months than at 3 months. Orthopaedic surgeons rated being better informed about the patients (P < 0.05), the planned operation (P < 0.01), and the assignment of tasks during surgery (P < 0.01) progressively more positively over the time. CONCLUSIONS: Some positive effects concerning the perioperative organisation and management were rated more positively even 2 years after checklist implementation. However, interprofessional communication and cooperation did not show long-term improvement from staff members' point of view. Probably longer lasting effects for the latter aspects could be achieved by repeated instruction and communication training.

The implementation of a perioperative checklist increases patients' perioperative safety and staff satisfaction.

BACKGROUND: The implementation of the 'Surgical Safety Checklist' caused a significant reduction in the incidence of complications and mortality among patients undergoing surgery. The aim of the present study was to evaluate perioperative safety standards and the quality of interprofessional cooperation before and after the introduction of a safety checklist from staff members' point of view. METHODS: Employees' attitude concerning safety-relevant aspects of the perioperative period, work processes, and quality of interprofessional cooperation was surveyed before and 3 months after introducing an adapted form of the 'Surgical Safety Checklist' by a 19-item questionnaire. RESULTS: After the implementation of the checklist, the cognizance of the names and functions of the individual operating room (OR) staff members, verification of the patient's written consent for surgery, indication for antibiotics before the surgical incision, and the quality of interprofessional cooperation were rated more positively. Traumatology physicians were more convinced that all artifacts had been removed from the surgical field. Finally, communication about intraoperative complications had improved. CONCLUSIONS: Our attitude surveys demonstrate that from the OR staff's perspective, in the perioperative setting, safety-relevant factors can be handled significantly better and with greater awareness by implementing a safety checklist as proposed by the World Health Organization.

Storage of neutrophil granulocytes (PMNs) in additive solution or in autologous plasma for 72 h.

Neutropenia may necessitate polymorphonuclear (PMN) transfusion, but among other reasons, PMN short shelf-life complicates realization of innovative transfusion strategies. In 18 donors, PMNs were mobilized using rHuG-CSF + dexamethasone. (8.3 +/- 1.6) x 10(10) PMNs were harvested in 203 +/- 8.7 mL. PMNs were stored undiluted (1, n = 18) and diluted 1-in-2, 1-in-4, 1-in-8 using T-Sol (2, n = 6), T-Sol + 1% HSA (3, n = 6), or autologous plasma (4, n = 6) for 72 h. Haemograms, pH values, phagocytosis, oxidative burst, and interleukin (IL)-1beta, IL-8 and tumour necrosis factor (TNF)-alpha levels were assessed every 24 h. PMN count decreased from (4.3 +/- 0.8) x 10(10) to (2.2 +/- 1.0) x 10(10), and pH value dropped from 6.4 +/- 0.3 to 5.4 +/- 0.2 within 72 h (1), whereas 1-in-4 and 1-in-8 dilutions exhibited consistent haemograms and pH values above 6.0. 1-in-8 dilution (4) stabilized pH at 7.1 +/- 0.4 after 72 h. Function deteriorated to about 50% within 24 h (1), but 1-in-8 (3), 1-in-4 and 1-in-8 diluted PMNs (4) kept it >90% for 72 h. In all collectives, cytokine levels increased during storage. After all, IL-1beta ranged between 31.0 +/- 16.3 (1-in-4, 4) and 100.0 +/- 21.4 (1-in-4, 2), IL-8 from 513 +/- 454 (1) to 3180 +/- 760 (1-in-8, 2), and TNF-alpha between 3.8 +/- 1.7 (1-in-2, 2) and 23.2 +/- 11.8 (1-in-8, 4) (pg mL(-1)). PMN function may be preserved for 72 h in vitro by dilution of PMN apheresates with, preferably, autologous plasma.

Mismatch of local blood flow and oxidative metabolism in stunned myocardium.

Myocardial blood flow is spatially heterogeneous, reflecting nonuniform oxygen supply. Also, myocardial oxidative metabolism is spatially heterogeneous. The effects of acute ischemia and reperfusion on the relationship between local myocardial blood flow (LMF) and oxidative metabolism are still unknown. LMF was measured in isolated, blood-perfused rabbit hearts using colored microspheres and oxidation water labeled with 18O2 (H2(18)O). Three protocols were performed: 18O2-perfusion during normoxia (N; n=7), during early reperfusion (ER; 10 min, n=6), and late reperfusion (LR; 40 min, n=6) following 20 min no-flow ischemia. LMF and local H2(18)O residues were determined within defined myocardial samples (105+/-15 mg). For interindividual comparison, values were normalized to the mean of the individual experiment and expressed as percentages. LMF ranged from 18 to 193% (N), 12 to 250% (ER), and 11 to 180% (LR). The H2(18)O tissue residue ranged from 63 to 132% (N), 73 to 142% (ER) and 32 to 148% (LR). The correlation between LMF and local oxidative metabolism during N (r=0.77; n=56) was lost in the postischemic heart during ER and LR. LMF during N and ER were only weakly correlated (r=0.24; n=48), whereas LMF during N and LR correlated well (r=0.87; n=48). It is concluded that the heterogeneous LMF pattern at baseline is maintained in the stunned myocardium whereas that of local oxidative metabolism is not. Apart from the established mechanisms underlying myocardial stunning, a mismatch between local flow and oxidative metabolism might also contribute.

Correlation between heterogeneous myocardial flow and oxidative metabolism in normoxic and stunned myocardium.

Myocardial blood flow exhibits considerable heterogeneity. Consequently, oxygen supply to the myocardium is also heterogeneous, as is myocardial metabolism. Many lines of evidence show a close correlation between local flow and local metabolism in the normoxic myocardium. So far, myocardial metabolism has predominantly been assessed indirectly by using labeled substrates. We used the (18)O isotope, permitting analytical separation of H2(18)O from the (18)O isotope, as well as quantification of regional oxidative metabolism by measuring the tissue residue of oxidation water in the rabbit myocardium. Correlation of local flow with oxidative metabolism was significant in the normoxic myocardium. This correlation was lost in the postischemic/reperfused myocardium. Apart from the established mechanisms underlying myocardial stunning, a mismatch between local flow and oxidative metabolism might thus also contribute to the postischemic dysfunction. In the normoxic myocardium, function should correlate with metabolism and blood flow. For technical reasons, function has not been assessed on a very local scale. Nevertheless, some considerations are presented on the heterogeneity of function as well as on the scale on which heterogeneity should be investigated to convey physiologically meaningful information on regulatory cardiac mechanisms.

Heterogeneity of local myocardial flow and oxidative metabolism.

In mammalian hearts, local myocardial flow (LMF) varies between 20 and 200% of the mean. It is not clear whether oxidative metabolism has a similar degree of heterogeneity. Therefore, we investigated the relation between LMF and local oxidative metabolism in isolated rabbit hearts. Buffer oxygenation with (18)O(2) resulted in labeled myocardial oxidation water (H(2)(18)O). In four hearts, myocardial oxygen consumption (MVO(2)) was calculated from the H(2)(18)O production and compared with that calculated according to Fick. In eight additional hearts, LMF was measured using microspheres. Coronary venous H(2)(18)O kinetics and local H(2)(18)O residues were determined and analyzed by mathematical modeling. MVO(2) recovery from H(2)(18)O was >93% compared with that according to Fick. LMF ranged from 1.91 to 11.24 ml. min(-1). g(-1), and local H(2)(18)O residue ranged from 0.41 to 1.04 micromol/g. Both variables correlated (r = 0.62, n = 64, P < 0.001). Measurements in nine hearts were fitted by modeling using capillary permeability-surface area products (PS(c)) from 2 to 10 ml. min(-1). g(-1). With flow-proportional PS(c), a 3.33-fold difference in LMF was associated with a 6.45-fold difference in local MVO(2). Both LMF and local oxidative metabolism are spatially heterogeneous, and they correlate to one another.

[Myocardial hibernation: another view]. / Myokardiale Hibernation: eine andere Sicht.

In the following, three newer concepts are brought together: myocardial hibernation, heterogeneity in myocardial blood flow and oxidative metabolism, and effects of hibernating animal serum on non-hibernators. Myocardial hibernation is viewed as a protective mechanism that helps to maintain myocardial integrity and viability by down-regulating contractile function as an adaptation to reduced blood flow. Myocardial flow is considerably heterogeneous. Consequently, oxygen supply to the myocardium is also heterogeneous. Many lines of evidence show a close correlation between regional flow and regional metabolism. In low-flow/low-metabolism areas, myocardial function must be reduced, since the myocardium would otherwise undergo necrosis. Thus, others and we hypothesize that function must be down-regulated to induce hibernation in low-flow areas. Because no regional histologic differences exist (the mitochondria are uniformly distributed within the myocardium), the pattern of heterogeneity seems to shift over time. Hence, we hypothesize that such very regional hibernation presents an evolutionary, protective mechanism, permitting subsequent myocardial areas to rest within the ceaselessly working heart. We also hypothesize that this mechanism ensures the down-regulation of function following myocardial ischemia in order to induce myocardial hibernation on a broader level. Surprisingly, a substance (opioid in nature) contained in hibernator serum both induced hibernation-like state in non-hibernators and suppressed myocardial oxygen consumption. Thus, we lastly hypothesize that myocardial hibernation is a remnant of the early stages of evolution and is closer to physiologic hibernation than traditionally viewed.

Does ischemic preconditioning require reperfusion before index ischemia?

BACKGROUND: Ischemic preconditioning (IP) is initiated through one or several short bouts of ischemia and reperfusion which precede a prolonged ischemia. To test whether a reperfusion must precede the prolonged index ischemia, a series without reperfusion (intraischemic preconditioning: IIP) and a series with gradual onset of ischemia, i.e. ramp ischemia (RI), which is possibly related to the development of hibernation, was compared to conventional IP (CIP). METHOD: Experiments were performed an 27 blood-perfused rabbit hearts (Langendorff apparatus) that were randomized into one of four series: (1) control (n = 7): 60 min normal flow - 60 min low flow (10%) ischemia - 60 min reperfusion. (2) CIP (n = 7): 4 times 5 min zero flow with 10 min reperfusion each - 60 min low flow (10%) - ischemia 60 min reperfusion. (3) IIP (n = 7): 50 min normal flow - 10 min no flow - 60min low flow (10%) ischemia -4 60min reperfusion. (4) RI (n=6): gradual reduction to 10% flow during 60min - 60min low flow (10%) ischemia - 60min reperfusion. At the end of each protocol, the infarcted area was assessed. RESULTS: The infarct area in control hearts was 6.7+/-1.4% (means+/-SEM) of LV total area, in CIP hearts 2.6+/-0.8%, in IIP hearts 3.1+/-0.5%, and in RI hearts 3.0+/-0.3% (all p<0.05 vs. control). The differences between the three protection protocols were statistically not significant, and no protective protocol reduced post-ischemic myocardial dysfunction. CONCLUSION: The preconditioning effect (infarct size reduction) appears not to depend on intermittent reperfusion. Thus, the protective mechanism of IP develops during the initial ischemia that precedes the index ischemia. Alternatively, low-flow ischemia is effectively a sort of reperfusion.

Pharmacologic heart rate reduction: effect of a novel, specific bradycardic agent on the heart.

Because heart rate (HR) is a major determinant of myocardial oxygen consumption (MVO2) a decrease in HR could prevent ischemia or reduce its consequences. We examined the effects of a novel bradycardic agent of the benzazepinone type, DK-AH 269 (DK), on ventricular function and perfusion in 12 isolated, blood-perfused rabbit hearts. HR was significantly reduced by 1mumol/L DK (160 +/- 28 vs. 124 +/- 23 min-1); diastole lengthened from 235 +/- 69 to 334 +/- 85 ms. Aortic flow tended to fall after DK (50.0 +/- 29.6 vs. 35.6 +/- 21.5 ml/min), but stroke volume remained unchanged (0.29 +/- 0.16 vs. 0.28 +/- 0.17 ml) following DK. Peak left-ventricular pressure (LVPmax) (106 +/- 29 vs. 92 +/- 35 mmHg) and dp/dtmax (1482 +/- 582 vs. 1247 +/- 644 mmHg/s) were decreased. dp/dtmin, as a measure of early relaxation, was also decreased (-1361 +/- 362 vs, -1125 +/- 488 mmHg/s), whereas the end-diastolic pressure (LVPed) was increased (20 +/- 12 vs. 25 +/- 17 mmHg). Coronary blood flow (CBF) per beat was not affected by DK: 0.07 +/- 0.02 vs. 0.07 +/- 0.02 ml. However, the coronary resistance increased with DK from 0.76 +/- 0.29 to 1.13 +/- 0.66 mmHg/(ml/min/100 g). The MVO2 was decreased (6.8 +/- 3.4 vs. 5.9 +/- 2.8 ml/min/100 g). The relation between subendocardial and subepicardial flow (colored microspheres) was unchanged after DK (1.12 +/- 0.22 vs. 1.13 +/- 0.16). Using electrical pacing to restore the control HR, dp/dtmax, LVPed, and MVO2 were nearly restored to predrug levels. In contrast, stroke volume, LVPmax, dp/dtmin and CBF per beat were less than control. In summary: DK effectively reduces heart rate and increases diastole. In parallel with the moderately reduced contractile function, MVO2 is reduced whereas CBF per beat is preserved. These results suggest that this novel bradycardic agent could be useful in treating unwanted tachycardia in the experimental setting, postoperative tachycardia in patients with heart disease or be useful even in treating coronary heart disease.

Basal metabolism does not account for high O2 consumption in stunned myocardium.

Myocardial O2 consumption (MVo2) in stunned myocardium is relatively high compared with the reduced ventricular function. The mechanism of this "oxygen paradox" could occur at different levels: basal metabolism, excitation-contraction coupling, and energy production. In one previously reported series on 12 isolated, blood-perfused rabbit hearts, left ventricular systolic and diastolic function in stunned myocardium were significantly decreased compared with control, whereas total MVo2 was not. The MVo2 for the unloaded contraction was overproportionately high for the decreased function in stunned myocardium, and contractile efficiency was clearly deteriorated. To assess whether the basal metabolism specifically is elevated in stunned myocardium, a second series (n = 14) with a similar protocol was performed in this study. Basal MVo2 after KCl arrest (0.5 +/- 0.3 ml.min-1.100 g-1) was significantly lower than that measured after KCl arrest (1.2 +/- 0.5 ml.min-1.100 g-1) in an additional series on nonischemic hearts (n = 8). Our conclusion is that basal MVo2 in stunned myocardium is not elevated. Thus this O2-consuming portion of total MVo2 is not responsible for the inefficiency in stunned myocardium. Instead, a "metabolic stunning" occurs at the level of both excitation-contraction coupling and force development by the contractile apparatus.

[Effect of a new bradycardic substance on the isolated rabbit heart]. / Effekt einer neuen bradykarden Substanz auf das isolierte Kaninchenherz.

Beside wall tension and contractility, heart rate is a major determinant of myocardial oxygen consumption. Therefore, a decrease in heart rate could prevent ischemia or reduce its consequences. We examined the effect of a new bradycardic agent of the benzazepinone-type (DK-AH 269) on eight isolated, saline-perfused rabbit hearts, bradycardia resulted from a specific blockade of i(f)-channels in sinus node cells. After control measurements (C), the substance was added in three increasing concentrations (D1: 10(-8) M, D2: 10(-7) M, D3: 10(-6) M). We observed a dose-dependent reduction in heart rate (C: 206 +/- 25, D1: 195 +/- 30, D2: 77 +/- 41, D3: 154 +/- 48/min). In the highest dosage, the duration of diastole was increased by 100%. To characterize systolic function, we measured stroke volume (SV), peak left ventricular pressure (LVPmax) and its first derivative (dP/dtmax). Aortic flow was slightly decreased whereas SV increased to 108% of control after initial reduction at the two lower dosages. LVPmax remained unchanged, and dP/dtmax was dose-dependently reduced to 91, 81, and 70% of control (C: 1885 +/- 376, D1: 1721 +/- 525, D2: 1526 +/- 504, D3: 1327 +/- 337 mm Hg/s); dP/dtmin as a measure of early relaxation was also reduced. The coronary flow per beat did not change compared with control in the presence of the two lower doses of DK-AH 269, but was significantly increased with the highest dose (C: 0.29 +/- 0.06, D1: 0.28 +/- 0.07, D2: 0.29 +/- 0.09, D3: 0.34 +/- 0.11 ml). The myocardial oxygen demand was dose-dependently decreased (C: 10.4 +/- 2.5, D1: 9.6 +/- 2.5, D2: 8.8 +/- 2.6, D3: 7.9 +/- 2.4 ml/min/100 g). The relation between subendocardial and subepicardial flow, assessed with colored microspheres, exhibited no changes in the presence of the highest dose of DK-AH 269 (C: 1.28 +/- 0.09, D3: 1.27 +/- 0.08). DK-AH 269 reduced heart rate in isolated rabbit hearts and increased the duration of diastole. Whereas systolic function was primarily left unchanged, coronary flow per beat and oxygen consumption were decreased. According to our results, this new bradycardic agent could be useful in treating coronary heart disease.

Analysis of respiratory water--a new method for evaluation of myocardial energy metabolism.

Aerobic ATP synthesis via oxidative phosphorylation causes a proportional production of respiratory water. Thus the amount of respiratory water produced at a given time should be a reliable measure of the current ATP demand of the mammalian myocardium. Respiratory water from isolated rabbit hearts was labeled by using the stable oxygen isotope 18O. The hearts were perfused according to the method of Langendorff (O. Langendorff. Pfluegers Arch. 61: 291-332, 1895) with 18O2-equilibrated Krebs-Henseleit solution. Control hearts were exclusively perfused with carbogen-equilibrated Krebs-Henseleit solution. Myocardial tissue was then lyophilized; the extracted water and samples from the coronary venous effluent were converted to CO2 by using the guanidine hydrochloride technique. The delta 18O values within the CO2 samples were determined by mass spectrometry and related to the standard mean ocean water (SMOW) scale. Compared with control hearts, the 18O-labeled hearts exhibited a significant increase of delta 18O values from tissue water (-47.50 +/- 0.64 vs. -40.35 +/- 2.05% SMOW; P < 0.05). The values were also significantly increased in the coronary venous effluent after a perfusion time of only 50 s (-47.50 +/- 0.64 vs. -43.66 +/- 0.91% SMOW; P < 0.05). Thus this first adaptation of the guanidine hydrochloride technique on microliter samples of myocardial tissue water and coronary venous effluent demonstrates that this method can be used to evaluate both respiratory activity and the kinetics of cardiac metabolic processes.

Utilization of oxygen by the contractile apparatus is disturbed during reperfusion of post-ischaemic myocardium.

UNLABELLED: Post-ischaemic ventricular function remains depressed (= myocardial stunning) despite nearly normal coronary blood flow during reperfusion. In order to illuminate the causes of this phenomenon, we studied the relationship between ventricular function and myocardial oxygen consumption (MVO2tot) in experiments on 15 isolated rabbit hearts perfused with erythrocyte suspension (hct = 30%). Left ventricular systolic function was assessed by measuring aortic flow (ml.min-1), peak systolic pressure (LVPmax), dP/dtmax, and early relaxation in terms of dP/dtmin during control and 30 min after the onset of reperfusion, following 20 min global no-flow ischaemia. The pressure-volume area was calculated as a measure of total mechanical energy. The external mechanical efficiency (Eext) was assessed from stroke work and MVO2tot. Both contractile efficiency (Econ = inverse slope of the MVO2-PVA relationship) and MVO2 of the unloaded contracting heart (MVO2unl = basal MVO2 + MVO2 for excitation-contraction coupling) were calculated using pressure-volume area and MVO2tot. RESULTS: At matched heart rate (149 +/- 30 vs 147 +/- 31 min-1; mean +/- SD) and end-diastolic volume (1.3 +/- 0.2 ml), the systolic variables were significantly decreased in the stunned myocardium: aortic flow: 38 +/- 13 vs 9 +/- 11 ml.min-1, LVPmax: 112 +/- 19 vs 74 +/- 18 mmHg, and dP/dtmax: 1475 +/- 400 vs 1075 +/- 275 mmHg.s-1. Likewise, dP/dtmin was significantly impaired (-1275 +/- 250 vs -975 +/- 250). The decrease in pressure-volume area (570 +/- 280 vs 270 +/- 200 mmHg.ml.100 g-1) was not statistically significant. In contrast, both Eext (0.75 +/- 0.29 vs 0.18 +/- 0.26 arbitrary units) and Econ (31 +/- 18 vs 14 +/- 7%) were significantly decreased, whereas MVO2tot (40 +/- 9 vs 34 +/- 8 microliters.beat-1.100 g-1) and MVO2unl (26 +/- 9 vs 22 +/- 6 microliters.beat-1.100 g-1) were not. SUMMARY: Ventricular function after brief episodes of ischaemia is decreased whereas MVO2tot is maintained, i.e. external efficiency is decreased. MVO2 for the unloaded contraction remained unchanged, indicating that MVO2 for excitation-contraction coupling is inappropriately high for the depressed contractile state. The decreased contractile efficiency indicates further that O2 utilization of the contractile apparatus is disturbed during reperfusion.