Human ECGs corrupted with real CPR artefacts in an animal model: generating a database to evaluate and refine algorithms for eliminating CPR artefacts.

AIM: For the analysis of ECG rhythms during ongoing CPR, single- or two-channel methods have been proposed to eliminate artefacts from the CPR-corrupted ECG. To refine, test and evaluate these algorithms with a realistic data set, we introduce an animal model with which we created an extended database of human ECGs with real CPR artefacts. MATERIAL AND METHODS: In a pig model real CPR-related artefacts were added to annotated human emergency ECGs. Via a special catheter placed in the oesophagus, ECG sequences (duration>10s) were fed in close to the dead pig's heart. The resulting surface potential was recorded on the thorax without and during ongoing chest compressions, which were monitored using a miniature force sensor. RESULTS: The animals served as a vehicle for human ECGs, making it possible to create a database in which 918 real human ECG sequences (437 shockable and 481 non-shockable) were corrupted with CPR-induced artefacts. The achieved signal-to-noise ratios (SNR) ranged from -17 to +15 dB, sensitivity was 93.5% and specificity was 50.51%. The fed-in ECG and the uncorrupted surface ECG correlated almost perfectly (r=0.926+/-0.081; n=918), indicating negligible signal distortion due to the dead pig itself. CONCLUSION: As the generated database includes both the original and the corrupted ECG covering a wide range of SNRs as well as the compression force signal, it provides an extended data set to evaluate the reconstruction performance of CPR artefact-removal algorithms.

Effects of SZ1677, a new non-depolarizing steroidal neuromuscular blocking drug, and rocuronium on two laryngeal muscles and the anterior tibial muscle in guinea pigs.

BACKGROUND: SZ1677 is a new neuromuscular blocking drug structurally related to rocuronium. We compared the effect of an ED(90) of SZ1677 (25 microg/kg) with that of rocuronium (100 microg/kg) in guinea pig laryngeal and peripheral muscles. METHODS: Electromyography was used to quantify neuromuscular blockade at the posterior cricoarytenoid muscle, the thyroarytenoid muscle and the anterior tibial muscle after SZ1677 (n = 10) and rocuronium (n = 9). RESULTS: Maximum neuromuscular blockade was similar after SZ1677 and rocuronium (83 +/- 11% vs. 89 +/- 11%; thyroarytenoid muscle: 91 +/- 8% vs. 97 +/- 3%; anterior tibial muscle: 91 +/- 15% vs. 96 +/- 3%, respectively). Onset time of neuromuscular blockade at the laryngeal muscles was similar for the two neuromuscular blocking drugs; it was shorter at the thyroarytenoid muscle (67 +/- 32 s vs. 42 +/- 40 s) than at the posterior cricoarytenoid muscle (101 +/- 26 s vs. 102 +/- 108 s). Onset time at the anterior tibial muscle was longer after SZ1677 (114 +/- 34 s) than after rocuronium (68 +/- 46 s); P < 0.05. Neuromuscular recovery was faster after SZ1677 (interval 25%-75%: posterior cricoarytenoid muscle: 222 +/- 66 s; thyroarytenoid muscle: 192 +/- 92 s; tibial muscle 149 +/- 55 s) than after rocuronium (450 +/- 148 and 464 +/- 183 s, 292 +/- 86 s, respectively); P < 0.05. CONCLUSIONS: In guinea pigs, SZ1677 offers a rapid onset of neuromuscular blockade at a laryngeal adductor muscle with a shorter duration than rocuronium. Regardless of the drug used, the course of neuromuscular blockade differs not only between peripheral muscles and the larynx but also between antagonistic laryngeal muscles. The differences seem to be species specific.

Does ester hydrolysis change the in vitro degradation rate of cisatracurium and atracurium?

BACKGROUND: We assessed the role of ester hydrolysis as an additional degradation mechanism to Hofmann elimination in the breakdown of cisatracurium and atracurium. METHODS: Cisatracurium and atracurium were incubated in phosphate buffer (pH 7.4, 37 degrees C) with and without the addition of carboxylesterase. Control measurements with an added esterase inhibitor were performed separately. Cisatracurium/atracurium and their degradation products, laudanosine and monoquaternary acid, were analysed using high-pressure liquid chromatography. RESULTS: Degradation of cisatracurium and atracurium proceeded exponentially, and after addition of carboxylesterase, no significant differences in the degradation rates were found. Neither an increase in carboxylesterase activity nor the addition of esterase inhibitor showed any effect. However, areas under the peaks of the chromatogram representing monoquaternary acid increased during incubation with esterase. CONCLUSION: The rate-limiting step in the degradation of cisatracurium/atracurium is Hofmann elimination. Ester hydrolysis is involved in the second degradation step that forms monoquaternary acid, but its contribution to the total elimination rate is negligible.

Carbon monoxide formation in dry soda lime is prolonged at low gas flow.

UNLABELLED: When exposed to volatile anesthetics containing a CHF(2)-group, such as isoflurane, desiccated absorbents produce carbon monoxide (CO). In the anesthesia circuit, the anesthetic flow that passes through the absorber varies with the minute ventilation. We sought to determine CO formation at different levels of test gas flow. Isoflurane 0.5% (series A) or 0.5% isoflurane + 5% CO(2) (series B) in pure O(2) was passed through dry soda lime samples (600 g, Draegersorb 800((R))) at flows of 1, 3, 5, 7, and 10 L/min. Each experiment was performed three times. At the outlet, CO concentration, isoflurane concentration and temperature were continuously recorded. In both series, the duration of CO formation was inversely related to the test gas flow. In series B, mean CO concentrations and the calculated amount of CO formation decreased significantly with increasing flow rates, which was not the case in series A. In both series, the higher the flow rate, the higher was the temperature and the shorter the time until the isoflurane concentration increased to the set level. We conclude that anesthetic degradation in dry soda lime is finite and, as long as no CO(2) is added, will produce roughly the same amount of CO regardless of inflow rate. The inflow rate influences the duration of CO formation such that at lower minute ventilation longer CO formation can be expected. IMPLICATIONS: CO formation from isoflurane degradation in dry soda lime was determined at different rates of test gas flow. The duration and, in the presence of CO(2), the total amount of CO formation were inversely related to the flow rate.

Absorption of carbon dioxide by dry soda lime decreases carbon monoxide formation from isoflurane degradation.

UNLABELLED: This study was performed to determine whether the absorption of carbon dioxide (CO(2)) influences the formation of carbon monoxide (CO) from degradation of isoflurane in dry soda lime. Isoflurane (0. 5%), CO(2) (5%), a combination of the two in oxygen, and pure oxygen were separately passed through samples of 600 g of completely dried soda lime (duration of exposure, 60 min; flow rate, 5 L/min). Downstream of the soda lime, we measured concentrations of CO, isoflurane, and CO(2) as well as the gas temperature. CO(2) increased the peaks of CO concentration (842 +/- 81 vs 738 +/- 28 ppm) and shortened the rise time of CO to maximum values (12 +/- 2 vs 19 +/- 4 min). However, CO(2) inhibited total CO formation (99 +/- 10 vs 145 +/- 6 mL). At the same time, CO(2) absorption by the soda lime decreased in the presence of CO formation (from 21.4 +/- 0. 8 to 19.4 +/- 0.9 g). The temperature of the gases increased during the passage of both isoflurane and CO(2) (to 32.6 +/- 2.0 degrees C and 39.4 +/- 4.0 degrees C, respectively), but the largest increase (to 41.5 +/- 2.1 degrees C) was recorded when isoflurane and CO(2) simultaneously passed through the dry soda lime. We assume that the simultaneous reduction in CO formation and CO(2) absorption is caused by the competition for the alkali hydroxides present in most of soda lime brands. IMPLICATIONS: We determined, in vitro, that carbon monoxide (CO) formation from isoflurane by dry soda lime is reduced by carbon dioxide (CO(2)). We believe that the potential for injury from CO is less in the clinical milieu than suggested by data from experiments without CO(2) because of an interdependence between CO formation and CO(2) absorption.

Effects of vecuronium and rocuronium in antagonistic laryngeal muscles and the anterior tibial muscle in the cat.

BACKGROUND: Adequate vocal cord paralysis and full recovery of laryngeal muscle function are important when muscle relaxants are used perioperatively. This study was designed to compare the effects of vecuronium and rocuronium at the vocal cord abductor and adductor muscles and the anterior tibial muscle in cats. METHODS: Twelve adult cats were studied under pentobarbitone-N2O/O2-anesthesia. After supramaximal electrical stimulation of the peroneal nerve and the recurrent laryngeal nerve (0.1 Hz and intermittent train-of-four) evoked electromyographic responses were obtained from the anterior tibial muscle, the posterior cricoarytenoid muscle (vocal cord abductor) and two vocal cord adductor muscles, the lateral cricoarytenoid and the vocal muscle. Six cats received bolus doses of increasing size of vecuronium (ED90 22.5 microg x kg(-1)) and six cats rocuronium (ED90 90 microg x kg(-1)). RESULTS: Equipotent doses of vecuronium and rocuronium caused a similar degree of paralysis in all muscles (vecuronium ED90: 70% blockade at the posterior cricoarytenoid, 83% at the lateral cricoarytenoid, 84% at the vocal muscle and 90% at the anterior tibial muscle; rocuronium ED90: 71% at the posterior cricoarytenoid, 67% at the lateral cricoarytenoid, 78% at the vocal muscle and 90% at the anterior tibial muscle; vecuronium 2 x ED90: 93% blockade at the posterior cricoarytenoid, 95% at the lateral cricoarytenoid, 97% at the vocal muscle and 99% at the anterior tibial muscle; rocuronium 2 x ED90: 89% blockade at the posterior and lateral cricoarytenoid, 93% at the vocal muscle and 100% at the anterior tibial muscle). Onset time was significantly shorter at the posterior cricoarytenoid muscle (290 s) compared to the lateral cricoarytenoid muscle (400 s) after vecuronium ED90 and to the vocal muscle (150 s versus 210 s) after rocuronium ED90. Compared to the anterior tibial muscle (interval 25-75%: 6.5 min after vecuronium 2 x ED90 and 3.3 min after rocuronium 2 x ED90 and to the posterior cricoarytenoid muscle (interval 25-75%: 7 min after vecuronium 2 x ED90 and 4.3 min after rocuronium 2 x ED90), recovery of laryngeal adductor muscle function was markedly delayed with both neuromuscular blocking drugs (interval 25-75% at the lateral cricoarytenoid and vocal muscle: 14 min and 15.8 min after vecuronium 2 x ED90 and 10.3 min and 11.6 min after rocuronium 2 x ED90 respectively). CONCLUSION: In cats, the time course of neuromuscular blockade after vecuronium and rocuronium differs in antagonistic laryngeal muscles. The protective laryngeal function of glottis closure recovers later than vocal cord abduction after both vecuronium and rocuronium.

Chest injuries after active compression-decompression cardiopulmonary resuscitation (ACD-CPR) in cadavers.

In a prospective study of 38 cadavers of patients older than 18 without previous chest injury or cardiopulmonary resuscitation (CPR), active compression-decompression (ACD) resuscitation manoeuvres were performed to determine possible factors influencing sternal and/or rib fractures. ACD was performed for 60 s, with compression and decompression forces being continuously recorded. A stepwise logistic regression analysis was applied. Factors analyzed were age, gender, use of a compression cushion beneath the piston of the ACD device (Ambu CardioPump), and maximal compression and decompression forces. After ACD, the cadavers were autopsied and thoracic injuries were assessed. There was a significant correlation between sternal fractures and gender (P = 0.008), and between rib fractures and age (P = 0.008). Women were found to have a higher risk for sternal fractures, whereas older patients had a higher risk for rib fractures. Maximal compression force was another factor in sternal and/or rib fracture (P = 0.048). Even though a significantly higher incidence of sternal fractures was observed when the compression cushion was used (P = 0.045), inclusion of this variable in the regression analysis only marginally improved the prediction for correct classification of sternal fractures. In conclusion, when well controlled ACD-CPR is performed in cadavers, age is the most important factor determining the incidence of rib fracture. Sternal fractures were more common in female cadavers.

Measuring forces and frequency during active compression decompression cardiopulmonary resuscitation: a device for training, research and real CPR.

Active compression decompression (ACD) cardiopulmonary resuscitation (CPR) is possibly a superior alternative to standard (STD) CPR, but an optimal compression and decompression pattern has to be ensured. ACD-CPR can be evaluated during CPR training sessions using commercially available manikins; however devices for recording compression and decompression forces or frequency during real CPR are lacking. Using the Ambu CardioPump without changing its mechanical characteristics, two force transducers were integrated into the ACD device. Using specially designed electronics and a portable computer, compression and decompression forces were measured and displayed continuously and compression frequency and the compression decompression phase are calculated on-line during real CPR action. All measured parameters were stored on a hard disk for later retrieval and analysis. Linearity of force measurement was better than 6% within a -250- +500 N range. The error in repeatability was below 5% thus outperforming the original mechanical force measurement system of the Ambu CardioPump. Compression frequency was calculated very accurately (error < 1%). The system has been successfully used during CPR training, during ACD-CPR in 37 corpses under research conditions and in five out-of-hospital CPR casualties. Simple and safe in use, our modified CardioPump with integrated electronics provides an important, technically advanced solution for monitoring ACD-CPR on-line. It warrants quality assurance during ACD-CPR training and in real CPR scenarios and guarantees accurate recording of compression and decompression forces and compression frequency.

Effects of half the tidal volume during cardiopulmonary resuscitation on acid-base balance and haemodynamics in pigs.

The effects of half the tidal volume during cardiopulmonary resuscitation (CPR) on haemodynamics, acid-base balance, and oxygenation were studied in anaesthetized pigs. The animals were ventilated with a mean tidal volume of 12.5 +/- 0.5 ml/kg at a rate of 14/minute resulting in a mean arterial pCO2 of 40 +/- 3 mmHg. They were randomly assigned to two groups: in one group ventilation was performed with half the pre-arrest tidal volume (50% group; n = 9), in the other group ventilation remained unchanged during CPR (100% group; n = 10). After 8 minutes of CPR attempts were made to restore spontaneous circulation with epinephrine and countershocks. There were no differences in advanced life support requirements, haemodynamic parameters, and resuscitability between the two groups. During CPR up to 5 minutes after restoration of spontaneous circulation (ROSC) dead space ventilation was significantly higher in the 50% group compared with the 100% group (p < 0.05). During CPR (at 3 and 7 minutes) arterial pO2 values were significantly lower (218 +/- 136 and 221 +/- 120 mmHg vs. 381 +/- 130 and 352 +/- 147 mmHg; FiO2 1.0) and hyperventilation was less pronounced (34.4 +/- 7.3 and 31.3 +/- 7.7 mmHg vs. 26.2 +/- 5.6 and 26.9 +/- 6.3 mmHg) in the 50% group. Our results suggest that half the tidal volume during CPR is likely to establish a more physiological acid-base balance and has no adverse effects on haemodynamics in intubated pigs ventilated with pure oxygen.

Performance of proportional and continuous nitric oxide delivery systems during pressure- and volume-controlled ventilation.

We have evaluated the effect of delivering nitric oxide using a continuous flow system (CFS) or two commercially available proportional gas injection systems (PGIS), Nodomo (Dräger, Lübeck, Germany) and Pulmonox-Mini (Messer Griesheim Austria, Gumpoldskirchen, Austria) on measured and simulated concentrations of nitric oxide. Nitric oxide concentration was measured in a bench test at five sites in the inspiratory breathing system during volume- or pressure-controlled ventilation and mathematically simulated using a mixing chamber model. For a target concentration of 10 parts per million (ppm) at the "Y" piece, simulated nitric oxide concentrations were 1.9-139 ppm for CFS, 0.3-22 ppm for the Nodomo and 0.0-31 ppm for the Pulmonox-Mini near the nitric oxide administration site. However, peak concentrations decreased rapidly along the inspiratory system. Measured and simulated variations depended on the nitric oxide delivery system, site of measurement and tidal volume. Measured variations were four times smaller in the Nodomo than in the Pulmonox-Mini and CFS. As inappropriate mixing may occur even with PGIS, nitric oxide should probably not be administered near the "Y" piece.

Autoclaving impairs the connector-tube bond of the laryngeal mask airway but not its airtightness.

The general-purpose laryngeal mask airway (LMA) is re-usable when undamaged, and cleaned and autoclaved correctly. We had found weakening of the silicone adhesive that bonds the connector of the LMA to the tube. We report that repeated autoclaving damaged the adhesive such that the connector could be rotated in the tube after the 12th autoclave cycle in almost all of the LMA tested. The damage to the adhesive did not affect the airtightness of the junction, which appears to be maintained by the material properties of the connector and tube and by the shape of the join.

Dystrophin deficient mdx muscle is not prone to MH susceptibility: an in vitro study.

The association between malignant hyperthermia (MH) and neuromuscular disorders is controversial. An association between MH and Duchenne muscular dystrophy, a common and lethal disorder caused by deficiency of dystrophin, has been reported sporadically but is still not proved. To examine this problem, we performed halothane and caffeine in vitro contracture tests on skeletal muscles from dystrophin deficient mdx mice, an animal model for human Duchenne muscular dystrophy. As neither halothane nor caffeine triggered abnormal responses in mdx muscles, we conclude that dystrophin deficiency per se is not the primary cause of MH-like crises, as reported for patients with Duchenne muscular dystrophy.

Classification of malignant hyperthermia-equivocal patients by 4-chloro-M-cresol.

To clarify the contracture response to 4-chloro-m-cresol (4-CmC) in malignant hyperthermia (MH) equivocal (MHE) muscle, we studied the effect of cumulative concentrations of 4-CmC. In vitro contracture test (IVCT) was performed in 35 probands according to the European MH test protocol. Surplus muscle bundles were exposed to 4-CmC (25-200 micromol/L), maintaining each concentration for 4 and 8 min. After 4 min exposure, the contracture increase of MH susceptible (MHS) (n = 7) muscle specimens was significantly (P = 0.05) greater at 50 micromol/L compared with either MHE halothane sensitive (MHEh) (n = 13) or MH normal (MHN) (n = 15) classified patients. Statistically significant differences (P < 0.05) were also found at 75 micromol/L. Exposure for 8 min yielded significant differences at 50 micromol/L only between MHS and MHEh. MHEh muscles revealed a dose-response curve similar to that found in MHN specimens. MHS muscles showed a significantly higher sensitivity to 4-CmC than either MHEh or MHN, and, in the probands tested so far, MHEh and MHN muscles seem to identically respond to 4-CmC, which seems to indicate a normal response in MHEh probands, implying no MH susceptibility. Therefore, 4-CmC might reduce the frequency of MHEh diagnosis based on standard halothane-caffeine IVCT. However, since MHE individuals may also represent an aberrant genetic status, with MH causing defects linked to unknown mutations, it is premature to consider 4-CmC as a solution to the diagnostic uncertainty of the true status of MHE probands. Presently, 4-CmC may provide supplementary information for a more precise phenotypic categorization of MHE individuals.

[Neostigmine and edrophonium. Antagonism of profound and shallow mivacurium blockade]. / Neostigmin und Edrophonium. Antagonisierung einer tiefen und oberflächlichen Mivacuriumblockade.

UNLABELLED: Mivacurium has a short duration of action because it is rapidly hydrolysed by plasma cholinesterase. There is ongoing controversy concerning the antagonism of mivacurium-induced neuromuscular block, firstly because of its short spontaneous recovery time, and secondly because the metabolism of mivacurium may be inhibited by anticholinesterases. We therefore compared neostigmine and edrophonium reversal of deep and moderate mivacurium-induced blocks. METHODS: After approval by the local ethics committee, 48 ASA class I and II adult patients were investigated during nitrous oxide-fentanyl-thiopental anaesthesia using train-of-four (TOF) stimulation and monitoring of the isometric force of adduction of a thumb. The patients received 0.2 mg/kg mivacurium i.v. Neuromuscular transmission was allowed to recover spontaneously in 10 patients (group SP). In 2 other groups the neuromuscular block was antagonised by administration of 0.04 mg/kg neostigmine (group N5; n = 9) or 1.0 mg/kg edrophonium (group E5; n = 10) when T1 had recovered spontaneously to 5% of control. In two other groups the neuromuscular block was antagonised with the same doses of neostigmine or edrophonium in 10 patients (group N25) and 9 patients (group E25), respectively, when T1 had recovered spontaneously to 25% of control. RESULTS: Neostigmine or edrophonium administered when T1 had recovered spontaneously to 25% of control shortened the recovery time (time from administration of ant-agonist to a T4/T1-ratio of 0.7) significantly from 10.7 +/- 2.2 min (mean +/- SD) in the SP group to 5.1 +/- 2.0 and 5.3 +/- 1.5 min in the N25 and E25 groups, respectively (P < 0.05). The corresponding recovery times in the SP, N5, and E5 groups were 15.9 +/- 2.9, 10.0 +/- 1.9, and 7.7 +/- 2.2 min, respectively. The difference between the SP and E5 groups was significant (P < 0.05). The recovery indices (time from 25% to 75% recovery of T1) of 3.0 +/- 1.3 and 1.7 +/- 0.9 min for the E5 and E25 groups, respectively, were shorter than those of the SP group at 6.1 +/- 2.0 min (P < 0.05). CONCLUSIONS: Two theoretical reasons, the very rapid onset time and the fact that it does not inhibit plasma cholinesterase, suggest edrophonium to be the preferred antagonist of a mivacurium-induced blockade. These two characteristics are reflected in our results: only edrophonium was able to shorten the recovery index significantly and, administered at a profound level of mivacurium-induced neuromuscular block, only edrophonium was successful in shortening recovery time significantly. Therefore, edrophonium should be the anticholinesterase of choice to antagonise a mivacurium-induced neuromuscular block.

Active compression-decompression cardiopulmonary resuscitation in standing position over the patient: pros and cons of a new method.

Active compression-decompression cardiopulmonary resuscitation (ACD-CPR) has been introduced to improve outcome of CPR after cardiac arrest. Usually, ACD-CPR is performed with the rescuer kneeling beside the patient (ACD-B), but ACD-CPR with the rescuer in standing position (ACD-S) has been taught and applied in some centres in addition to conventional ACD-CPR (ACD-B). The aim of this randomised and cross-over study was to evaluate the new technique of ACD-S and to compare it with conventional ACD-B. Twelve professional rescuers (aged 30.8 +/- 7.9 years) applied both methods of ACD-CPR on a manikin. We obtained the following results. (1) Duration of CPR performance was comparable for ACD-S (13.2 +/- 7.1 min) and ACD-B (15.5 +/- 10.2 min, P = 0.48). (2) Pain in the upper extremity and pain in the vertebral column were the main reasons for break-off by the rescuers. Exhaustion was judged to be similar during ACD-S (5.3 +/- 2.3) and ACD-B (6.2 +/- 2.1; on a rating scale with 1 = no and 9 = complete exhaustion). (3) Oxygen consumption was significantly higher during ACD-S (P < 0.005), whereas heart rate and lactate levels did not differ. (4) Decompression forces were lower than compression forces. The averaged decompression forces in both methods were similar during the first 2 min and the last min. Compression forces decreased in ACD-S from 55.1 to 48.9 kp (P = 0.002) and in ACD-B from 52.8 to 47.0 kp (P = 0.069). We conclude that ACD-CPR in standing position can be considered equal to ACD-B in view of maximal duration of CPR, exhaustion of the rescuers and decompression forces. The decrease of compression forces in ACD-S and ACD-B as well as the difference between compression forces in ACD-S and ACD-B seem to be of no clinical relevance, and exhaustion was judged to be similar despite oxygen consumption being higher in ACD-S than in ACD-B.