Ball, P.

Bekemeyer, U.

Djonlagic, H.

Hauptmann, A.

Heidbüchel, K.

Müller-Esch, G.

Osswald, P. M.

Peters, A.

Scriba, Peter Christian

Tybussek, R.

Wood, W. G.

English

Peters, Achim

Open Access LMU

Computers in Critical Care and Pulmonary Medicine Edited by P. M. Osswald in Cooperation with O. Prakash, H.-J. Härtung and H. J. Bender With 197 Figures and 29 Tables Springer-Verlag Berlin Heidelberg New York Tokyo Table of Contents Application of Computer Systems in Critical Care K . GEIGER 1 On-line Cardiovascular Applications of Microcomputers in Intensive Care C. PRYS-ROBERTS 8 Organizing and Analyzing Clinical Information Using Table-Based, Graphics-Oriented, Interactive Computer Systems B . J . R A N S I L 17 A n Attempt to Solve the "Information Explosion" in an Intensive Care Ward D. J. PRICE, J. MASON, and S. SNOWDEN 23 Towards a Coherent Structure of the Anesthetist - Computer Interface S. TRISPEL, H . KLOCKE, G. R A U , and R. SCHLIMGEN 29 Effect of Different Ventilation Patterns on the Intracranial Pressure in Neurologic Patients with Mechanical Ventilation Κ. M . EiNHÄuPL, C. GARNER, G. SCHMIEDER, G. KERSCHER, and R. WIECZOREK 38 Computer Applications in Pulmonary Function Testing M . H E I T Z 43 The Assessment of Gas Exchange by Automated Analysis of 0 2 and C 0 2 Alveolar to Arterial Differences: 3 Years Experience in Respiratory Clinical Physiology P. PAOLETTI, E. FORNAI, A. G. NETO, R. PREDILETTO, S. RUSCHI, and C. GIUNTINI 57 Computers in Experimental Pathophysiological Research R. SCHOSSER, H.-P. ENGEL, and K . MESSMER 66 Data Bases in Acute Medicine T. J. STAFFORD, and R. BURNEY 75 Computerized Clinical Records in the Neurosurgical ICU with Self-updating of Some Biological Data R. URCIUOLI, M . KNAFLITZ, G. BALESTRA, M . A . ARBINOLO, M . L . BELLERO, R. BERTINO, C. FRANCO, M . GESSA, and A . GUARNACCIA 78 V I Table of Contents Organization and Analysis of Data from Patients with Trauma and Hemorrhage W . KELLERMANN, Κ . PETER, U . JENSEN, Y . SUMMA, and D. NEUMEIER 82 Computer Assisted ICU Monitoring Τ. OYAMA, H . ISHIHARA, A . MATSUKI, M . YAMASHITA, K. ISOZAKI, and T. SUZUKI 96 Automatic Signal Analysis and Prediction in Intensive Medical Care A.SWOBODA, andE .EppLE 100 Artifact Processing in a Computerized Intensive Care Unit W . BLEICHER, E . E P P L E , M . KOPP, and H . JUNGER 107 Personal Computers for Gas Exchange Measurements in the ICU G . WIESSPEINER,S.SCHUY,H. METZLER, and W . LIST 116 Integration of a New Computer HP 9816S in the Pulmonary Calculator System HP 47804S. Advantages of Using the Screen for Graphic Presentation of Flow-Volume Curves K. ERDMANN, and J.-P. JANTZEN 123 Measurement of Oxygen Uptake with a New Method H . METZLER, G. WIESSPEINER, and W . F. LIST 130 A Microcomputerassisted System for the Monitoring of Cardiorespiratory Variables in the Critically 111 K. HANKELN, and H . MICHELSEN 134 Selective Lung Ventilation H.-J . HÄRTUNG, P.-M. OSSWALD, and H . J . BENDER 138 Automated Anesthetic Record Keeping N . T Y SMITH 147 Computer Aided Methods to Predict Perioperative Risks U . FELDMANN , Ρ . - Μ . OSSWALD , Η . - J . HÄRTUNG , and Η . LUTZ 162 New Tasks for Medical Informatics? C. O .KÖHLER 184 Artificial Intelligence: the Expert Systems Approach to Medical Consultation Ε. H . SHORTLIFFE, andL. M . FAGAN 190 Expert Consultation Systems in Medicine P. L . MILLER 198 The Importance of Using a Computer to Provide Pediatric Anesthesia and Emergency Drug Information and Treatment Regimens in the Clinical Setting D. J . ESSIN, D . L . WARNER, M . JAGODOWICZ, and S. N . STEEN 207 Computer Systems in Artificial Ventilations (New Techniques) W . KOLLER, A . A L O Y , N . M U T Z , and G. PAUSER 212 Table of Contents V I I Series Dead Space Volume Assessed as the Mean Value of a Distribution Function G . W O L F F , and J . X . BRUNNER 2 2 1 Evaluation of Indices for Respiratory Mechanics from an Automated System B. FRIBERG, M . FORSSBLAD, S. BAEHRENDTZ, J. HULTING, K . EKENBÄCK, Μ . JOHANSSON, and G . M A T E L L 228 Mathematical Modelling for Prediction of Optimal Ventilator Settings R. RUDOWSKI, G. MATELL, K . EKENBÄCK, C. SPANNE, and Β . OSSMER 235 Indications for the Application of Closed Loop Systems in Perioperative Medicine R. D . WESTENSKOW 247 Glucose-Insulin-Potassium Therapy Guided by a Glucose-Controlled Insulin Infusion System in Acute Myocardial Infarction G. MÜLLER-ESCH, P. B A L L , U . BEKEMEYER, H . DJONLAGIC, A . HAUPTMANN, Κ. HEIDBÜCHEL, A . PETERS, R. TYBUSSEK, W. G. WOOD, and P. C. SCRIBA . . . . 252 Changes in Monitoring Methods Caused by the Use of Intelligent Bedside Equipment E. EPPLE, W.BLEICHER, M . KOPP, and H . JUNGER 259 Automated Arrhythmia Detection in Intensive Care C. ZEELENBERG, S. H . M E I J , M . R. HOARE, and P. G. HUGENHOLTZ 265 Monitoring Intracranial Pressure - Nuisance to, or Advantages for, Ward Personnel K . WIEDEMANN, G. SCHMIDT, and M . MÜLLER 280 Computerized Neuromonitoring M . R . G A A B 290 Computer-Assisted Monitoring of Intracranial Pressure in Stroke A . HAASS, T. MADLER, and K . SCHIMRIGK 307 Microprocessor-Controlled Registration and Evaluation of Respiratory Pressure-Volume Diagrams in ICUs W. KELLERMANN , Y. SUMMA , and Κ. PETER 3 1 1 NAPROS - A semiautomatic and easy to use anaesthetic record system D. WINTER, and P.-M. OSSWALD 3 1 9 A Real Time Pattern Recognition Program for Continuous Processing of Cardiovascular Biosignals Μ . M A I W A L D 329 Microcomputer-Assisted ICP Monitoring in Neurological Patients G. SCHMIEDER, C. GARNER, Κ. M . EINHÄUPL, Κ. SIEGL, and G. KUFNER 334 Glucose-Insulin-Potassium Therapy Guided by a Glucose-Controlled Insulin Infusion System in Acute Myocardial Infarction G . M Ü L L E R - E S C H , P . B A L L , U . BEKEMEYER, H . DJONLAGIC, A . H A U P T M A N N , Κ . HEIDBÜCHEL, A . PETERS, R . TYBUSSEK, W . G . W O O D , and P . C. SCRIBA A number of hormonal and metabolic alterations have been observed during acute myocardial infarction ( A M I ) : There is a rapid increase of catecholamine and Cortisol secretion; free fatty acid (FFA) serum levels are markedly elevated (Gupta et al. 1969; Januszewicz et al. 1971; Vetter et al. 1974); and insulin secretion may be inappropiately low. These alterations result in a disturbance of glucose utilization, so-called stress hyperglycemia. Moreover, under these conditions and due to the accumulation of free fatty acids in the ischemic myocardium, severe ventricular arrhythmias as well as a progression of myocardial cell damage are likely to occur (Kurien and Oliver 1970; Kurien et al. 1971; Oliver et al. 1968). Glucose-insulin-potassium infusions (GIK) in A M I have been used in a number of clinical trials in order to overcome these deleterious effects (Mantle et al. 1981; Rogers et al. 1976,1979; Sodi-Palleres et al. (1962)). Some of the postulated benefits of GIK treatment in A M I are: a decrease of FFA, a reduction of potassium efflux, a repletion of intracellular potassium stores, an enhancement of myocardial glucose utilization, a reduction of myocardial oxygen consumption, and an improvement in coronary perfusion. These changes should reduce severe life-threatening arrhyth-mias, limit infarct size, improve left ventricular function, and reduce hospital mortal-ity (von Arnim and Bolte 1980; Brachfeld 1973; Kurien et al. 1971; Manke et al. 1981; Oliver 1973). With an "open loop" fixed GIK regime as in the studies mentioned above, severe hyperglycemia as well as hypoglycemia were not infrequently seen, because the degree of impairment of the insulin sensitivity could not be predicted. We therefore decided to use a glucose - controlled insulin infusion system (GCIIS); this involves applying "closed-loop" control during treatment with GIK according to the individual insulin sensitivity and thereby studying hormonal and metabolic patterns in A M I . Methods Nine patients (eight male, one female; age 61.8 ± 8.8 years) with A M I admitted to our intensive care unit within 12 h after onset of chest pain received GIK for 24 h. The solution contained 430 g glucose, 166 U porcine regular insulin, and 133 mEq KCl per liter. The infusion rate was 0.9 ml/kg/h. Additional feedback - controlled insulin and/ or glucose was given by the GCIIS (Biostator-Controller). The following constants were chosen: Mode 3:1, Var 100, BI80, BD 60, and FI 500-1000. Insulin concentra-Glucose-Insulin-Potassium Therapy Guided 253 D E X T R O S E OILUTEO BLOOD INSULIN PATIENT INFUSION PUMP ANALYZER PUMP COMPUTER MODULE)-GLUCOSE ANALYZER 1. G C I I S I N T E R F A C E PRINTER P R O C E S S O R K E Y B O A R O MONITOR F L O P P Y - D R I V E Fig. 1. Schematic diagram of device used for processing of GCIIS data COMPUTER MANUAL INPUT OF COMMENTS tion of the GIK solution was increased when blood glucose could not be kept below 250 mg/dl. Insulin, C-peptide, Cortisol, GH, prolactin, and lactate were determined at 6-h intervals. FFAs were measured by gas-liquid chromatography (Tserng et al. 1981). Figure 1 shows a schematic diagram of the technical equipment. The patient is connected to the GCIIS. By means of an interface all data for blood glucose (BG), insulin infusion rate ( IR), and dextrose infusion rate (DR) are transferred directly from the Biostator to a microcomputer for further processing (Muller-Esch et al. 1984). The microcomputer fulfils several functions: 1. Monitoring: BG, IR, and DR are plotted continuously 2. Manual input: comments concerning, for example, the actual therapy can be entered via the keyboard 3. Calculations: a BASIC computer program has been developed for the calculation of the glycemic indices mean blood glucose (MBG), M-value, and M A G E (Mul-ler-Esch et al. 1984) 4. Printer and floppy disks: all values for BG, IR, and DR, as well as comments which appear in their time - related positions, and calculated parameters are plotted and documented on 5-in. floppy disks. 254 G. Müller-Esch et al. Results The insulin sensitivity - as measured by blood glucose concentrations and total insulin requirements during GIK - varied markedly. Figure 2 a is an example from a patient with high insulin requirements. Initial BG is about 110 mg/dl, rising to more than 250 mg/dl after starting GIK infusion. Despite submaximal additional feedback-control-led insulin by the GCIIS, BG did not fall below 200 mg/dl. In contrast, in the patient shown in Fig. 2b, euglycemia during GIK could be obtained with only minor addi-tional feedback-controlled insulin administration. And in another patient, additional feedback-controlled dextrose had to be given to prevent hypoglycemia during GIK, MBG being in the range of about 80 mg/dl (Fig. 2c). According to these data we can divide our patients into two groups: in five patients (group A ) , a total of 309 ± 52 U insulin/24 h was sufficient to maintain fair glycemic control (Table 1, top). In four patients, however (group B), insulin concentration of GIK had to be partially multiplied because of marked hyperglycemia: insulin require-ments were 1193 ± 258 U/24 h; despite this, we did not achieve nearly normal BG values or nearly normal glycemic indices (Table 1, bottom). When compared to the "low insulin" group, the "high insulin" group presented with higher serum insulin levels before GIK treatment. During therapy, this group had higher values for C-peptide, Cortisol, prolactin, and lactate. GH and glucagon did not differ significantly (Table 1). Table 1. Insulin, C-peptide, glucagon, Cortisol, GH, prolactin, and lactate serum levels during GCIIS-guided GIK therapy in patients with low insulin requirements (group A) and high insulin requirements (group B). The glycemic indices MBG, MAGE, and M-value are also shown. (P < 0.05 vs. group A) Group A (309 ± 52 U insulin/24 h, η = 5) Oh 6h 12 h 18 h 24 h Insulin (mU/1) 11.3 ± 7 . 5 191 ± 48 227 ± 181 289 ± 198 316 ± 219 C-peptide fag/l) 2.6 ± 1.8 1.0 ± 0 . 7 0.6 ± 0.5 2.5 ± 4 . 1 2.1 ± 2 . 5 Glucagon (ng/l) 140 ± 25 158 ± 53 160 ± 84 176 ± 82 164 ± 74 Cortisol (ng/ml) 233 ± 131 172 ± 98 196 ± 95 212 ± 112 188 ± 92 GH (ng/ml) 2.1 ± 1.5 4.4 ± 2.9 4.2 ± 2.0 3.5 ± 2 . 5 2.1 ± 1.6 Prolactin (uU/ml) 398 ± 131 258 ± 64 242 ± 72 225 ± 79 248 ± 51 Lactate (mmol/1) 1.4 ± 0 . 5 2.0 + 1.0 1.6 ± 0.8 1.3 ± 0 . 6 1.1 ± 0 . 3 MBG: 94 ± 28 MAGE: 51 ± 8 Μ -value: 17 ± 7 Group Β (1193 ± 258 U insulinl24 h, η = 4) Oh 6h 12 h 18 h 24 h Insulin (mU/1) • 43 ± 22 • >500 • >500 • >500 • >500 C-peptide (yugfl) 8.0 ± 7.5 • 13.4 ± 12.9 • 15.0 ± 14.3 21.6 ±22.9 12.3 ± 15.6 Glucagon (ng/l) 152 ± 77 87 ± 6 2 90 ± 7 3 124 ± 140 15.1 ± 169 Cortisol (ng/ml) 301 ± 224 • 418 ± 135 • 418 ± 174 • 412 ± 203 • 418 + 186 GH (ng/ml) 3.1 ± 2.4 6.1 ± 2 . 4 3.0 ± 1.8 1.7 + 1.4 1.5 ± 1.2 Prolactin (μυ/ml) 590 ± 281 • 549 ± 182 • 489 ± 150 • 532 ± 135 • 681 ± 191 Lactate (mmol/1) • 2.7 ± 1.3 • 3.5 ± 0 . 8 2.7 ± 0.9 • 2.7 ± 1.2 • 3.5 ± 1.4 • MBG: 234 ± 42 • MAGE: 159 ± 57 • M-value: 46 ± 15 Glucose-Insulin-Potassium Therapy Guided 255 D.E. 9 74y acute myocardial infarction (AMI) GIK K30gm glucose, 166U insulin, 133 mEq KC L / t ; infusion rate 0.9ml/ kg /h ) Fig. 2a 500-4)0-300-B G . c ? 59y acute myocardial infarction (AMI) - GIK ( i»30gm glucose, 166U insulin, 133 mEq KCL / I ; infusion rate 0.9ml/kg/h ) Constants: Var r 100 Bl =80 Fl = 1000 RD = 50 BD = 60 FD = 390 Fig. 2b Fig. 2a-c. Blood glucose (BG), insulin infusion rate (IR), and dextrose infusion rate (DR) during GCIIS-guided GIK therapy in three patients with A M I 256 G. Müller-Esch et al. Constants Μ Κ σ* U9y acute myocardial infarction! AMI ) • GIK (430gm glucose, 166U insulin, 133mEqKCL /1 . infusion rate 0 9ml/kg/h ) Var = 100 Bl = 80 Fl = 1000 RD = SO BD -- 60 FD = Ο » Table 2. Insulin, C-peptide, glucagon, Cortisol, GH, prolactin, lactate, and blood glucose (BG) levels in seven conventionally treated patients with A M I as compared to four patients under GCIIS-guided GIK therapy (group Β). · Ρ < 0.05 vs. controls) Controls (n = 7) Oh 6h 12 h 18 h 24 h Insulin (mU/1) 35 ± 17 18 ± 11 26 ± 2 4 26 ± 2 4 39 ± 3 4 C-peptide ^g/ l) 5.4 ± 2.9 4.9 ± 3.3 4.7 ± 3 . 2 6.4 ± 3 . 3 8.6 ± 6.2 Glucagon (ng/l) 323 ± 446 373 ± 537 348 ± 412 431 ± 497 443 ± 407 Cortisol (ng/ml) 239 ± 145 266 ± 192 218 ± 108 247 ± 171 229 ± 163 GH (ng/ml) 2.1 ± 3 . 1 2.9 ± 3.8 2.4 ± 2.7 3.3 ± 6.5 2.6 ± 2.6 Prolactin (μυ/ml) 834 ± 895 445 ± 256 273 ± 106 228 ± 50 306 ± 74 Lactate (mmol/1) 2.1 ± 2 . 1 2.1 ± 1.8 1.7 ± 1.1 1.4 ± 0 . 5 1.4 ± 0.4 BG (mg/dl) 147 ± 38 157 ± 49 122 ± 23 144 ± 48 162 ± 72 Group Β (1193 ± 258 U insulin/24 h, η = 4) Oh 6h 12 h 18 h 24 h Insulin (mU/1) 43 ± 2 2 >500 >500 >500 >500 C-peptide ^g/l) 8.0 ± 7.5 13.4 ± 12.9 • 15.0 ± 14.3 21.6 ± 22.9 12.3 ± 15.6 Glucagon (ng/l) 152 ± 77 87 ± 6 2 90 ± 7 3 124 ± 140 151 ± 169 Cortisol (ng/ml) 301 ± 224 418 ± 135 • 418 ± 174 412 ± 203 418 ± 186 GH (ng/ml) 3.1 ± 2 . 4 6.1 ± 2.4 3.0 ± 1.8 1.7 ± 1.4 1.5 ± 1.2 Prolactin (μυ/ml) 590 ± 281 549 ± 182 • 489 ± 150 • 532 ± 135 • 681 ± 191 Lactate (mmol/1) 2.7 ± 1.3 3.5 ± 0 . 8 2.7 ± 0 . 9 • 2.7 ± 1.2 • 3.5 ± 1.4 MBG: 234 ± 42 MAGE: 159 ± 57 M-value: 46 ± 15 Glucose-Insulin-Potassium Therapy Guided 257 Fig. 3. Free fatty acids (FFA) during GCIIS-guided GIK therapy in two patients with A M I Seven conventionally, treated patients with A M I served as controls (Table 2). In comparison with these patients without GIK, group Β had higher serum levels for C-peptide, Cortisol, prolactin, and lactate. Serial FFA measurements in two patients show a decrease of FFA under G I K below the arrhythmia threshold (Oliver et al. 1968) of 1200 μηιοΐ/ΐ (Fig. 3). Discussion Because of the small number of patients we are not yet able to decide whether the observed hormonal-metabolic differences between the groups are directly correlated to the infarct size or wheter they reflect different systemic reactions, different hor­monal-metabolic patterns, during A M I . In conclusion, these preliminary data indicate that the impairment of insulin sensitivity and glucose utilization during A M I varies markedly. FFA can be reduced below the arrhythmia threshold. Further studies should compare metabolic, hemody­namic, and antiarrhythmogenic effects of GCIIS-guided GIK support in patients with A M I . References Von Arnim Τ, Bolte HD (1980) Therapie mit Glukose-Insulin beim kardiogenen Schocksyndrom. In: Brückner JB (ed) Kreislaufschock. Springer, Berlin Heidelberg New York, pp 500-505 Brachfeld Ν (1973) The glucose-insulin-potassium (GIK) regimen in the treatment of myocardial ischemia. Circulation 47: 459-462 Gupta DK, Jewitt DE, Young R, Hartog M , Opie L M (1969) Increased plasma-free-fatty-acid concentrations and their significance in patients with acute myocardial infarction. Lancet 2: 1209-1213 Januszewicz W, Sznajdermann M , Ciswicka-Sznajdermann M , Wocial B, Rymaszewski Ζ (1971) Plasma free fatty acid and catecholamine levels in patients with acute myocardial infarction. Br Heart J 33: 716-718 Kurien VA, Oliver MF (1970) A metabolic cause for arrhythmias during acute myocardial hypoxia. Lancet 1: 813-815 Kurien VA, Yates PA, Oliver MF (1971) The role of free fatty acids in the production of ventricular arrhythmias after acute coronary artery occlusion. Eur J Clin Invest 1: 225-241 FFA (/jmol/l) Oh 6h 12h 18h 2Uh 258 G. Müller-Esch et al. Mantle JA, Rogers WJ, Smith LR, McDaniel HG, Papapietro JE, Russell RO, Rackley CH (1981) Clinical effects of glucose-insulin-potassium on left ventricular function in acute myocardial infarc-tion: results from a randomized clinical trial. Am Heart J 102: 313-324 Müller-Esch G, Peters A , Göhl Μ, Heidbüchel Κ, Scriba PC (1984) Simplified evaluation and documentation of data from glucose controlled insulin infusion systems (GCIIS). Biomed Technik 29: 62-66 Oliver MF (1973) Glucose, insulin, potassium in acute myocardial infarction. Acta Cardiol [Suppl] 17: 257-262 Oliver MF, Kurien VA, Greenwood TW (1968) Relation between serum-free-fatty acids and arrhyth­mias and death after acute myocardial infarction. Lancet 1: 710-715 Rogers WJ, Stanley AW, Breinig JB, Prather JW, McDaniel MG, Moraski RE, Mantle JA, Russell RO Jr, Rackley CE (1976) Reduction of hospital mortality rate of acute myocardial infarction with glucose-insulin-potassium infusion. Am Heart J 92: 441-454 Rogers WJ, Segall PH, McDaniel HG, Mantle JA, Russell RO Jr, Rackley CE (1979) Prospective randomized trial of glucose-insulin-potassium in acute myocardial infarction. Effects on myocardial hemodynamics, substrates and rhythm. Am J Cardiol 43: 801-809 Sodi-Pallares D, Testeiii MK, Fishleder BL, Bisteni A, Medrano GA, Friedland C, DeMicheli A (1962) Effects of an intravenous infusion of a potassium-glucose-insulin solution on the electrocar­diographic signs of myocardial infarction. Am J Cardiol 9: 166-181 Tserng KY, Kliegmann RM, Miettinen EL, Kaihan SC (1981) A rapid, simple, and sensitive procedure for the determination of free fatty acids in plasma using glass capillary columm gas-liquid chromatography. J Lipid Res 22: 852-858 Vetter NJ, Strange RC, Adams W, Oliver NF (1974) Initial metabolic and hormonal response to acute myocardial infarction. Lancet 1: 284-289 

Clinical effects of glucose-insulin-potassium on left ventricular function in acute myocardial infarction: results from a randomized clinical trial. Am Heart J 102: 313-324 Müller-Esch

Therapie mit Glukose-Insulin beim kardiogenen Schocksyndrom. In: Brückner JB (ed) Kreislaufschock.

Glucose-Insulin-Potassium Therapy Guided by a Glucose-Controlled Insulin Infusion System in Acute Myocardinal Infarction

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Glucose-Insulin-Potassium Therapy Guided by a Glucose-Controlled Insulin Infusion System in Acute Myocardinal Infarction

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