Sauerstoffangebot und -aufnahme unter Reanimation mit dem neuen Beatmungsmuster Chest Compression Synchronized Ventilation im porcinen Modell

Einleitung: Zur Verbesserung von Perfusion und Sauerstoffversorgung unter Reanimation wurde das neue kompressionssynchrone, druckkontrollierte Beatmungsverfahren Chest Compression Synchronized Ventilation (CCSV) entwickelt und im Tiermodell untersucht. Messwerte dieser Studie dienten der vorliegende...

Full description

Saved in:
Bibliographic Details
Main Author: Imhof, Tobias Sebastian
Contributors: Kill, Clemens (Prof. Dr. med.) (Thesis advisor)
Format: Doctoral Thesis
Language:German
Published: Philipps-Universität Marburg 2017
Subjects:
Online Access:PDF Full Text
Tags: Add Tag
No Tags, Be the first to tag this record!

Introduction: The novel pressure-controlled ventilator mode Chest Compression Synchronized Ventilation (CCSV) was invented with the objective of improving perfusion and oxygen supply during CPR. Measurements from a study applying CCSV to a pig model provided the basis for the work in hand. Its aim was to investigate the effects of the novel ventilator mode on oxygen delivery (DO2), oxygen consumption (VO2) and related parameters during resuscitation compared to changes with the use of the recommended standard ventilation (Intermittent Positive Pressure Ventilation, IPPV). Material and methods: After approval by local authorities 44 pigs under continuous anesthesia and analgesia were endotracheally intubated and connected with measuring equipment. Following iatrogenic induction of ventricular fibrillation (t = 0 min) animals were randomized either to receive CCSV (Tinsp 265 ms, Pinsp 60 mbar, steep ramp) or IPPV (respiratory rate 10/min, VT 7 ml/kg body weight, Pmax 45 mbar, I:E 1:1.5). After three minutes of untreated VF ventilation was connected and chest compression was started by LUCAS™. Arterial and venous blood samples were taken and CO was measured at t = 4 min, 8 min, 12 min, 16 min, 20 min and 24 min. Heart rhythm analysis and – if indicated – defibrillations were performed at t = 13 min, 15 min, 17 min, 19 min, 21 min and 23 min. Animals receiving ROSC were carried into a separate aftercare. Resuscitation was accompanied by drug administrations at t = 7 min, 14 min, 18 min, 22 min (epinephrine 1 mg i.v.) and t = 11 min (vasopressin 0.8 IU/kg body weight i.v.). With the aid of using the resulted measured values, CaO2, DO2, DO2I, CvO2, avDO2, VO2, VO2I and O2ER and were calculated. Changes during resuscitation until t = 12 min were calculated starting from baseline values. Statistical analysis was performed by U-test comparing CCSV and IPPV within the total population (TP) and separately within the following subpopulations: A) animals receiving ROSC after one defibrillation (Primary Responder, PR); B) animals receiving ROSC after more than one defibrillation or not receiving ROSC (Primary Non-Responder, PNR). The focus of consideration and discussion was laid on TP and PR. Subsequently PR and PNR were opposed and investigated with regard to possible characteristics. Results were presented as median (Q0,25/Q0,75), p < 0,05 was considered to be significant. Results: ROSC was achieved in 15 animals under CCSV and 20 under IPPV (p = .065), average time of occurrence and quantity of PR for each method were identical (CCSV vs. IPPV): ROSC t [min]: 13 (13/15) vs. 13 (13/16.5), p = .542; PR for each method: 11 vs. 11, p = 1. Within TP the following differential values could be determined (CCSV vs. IPPV): DO2 [ml/min]: -297.98 (-404.71/-241.56) vs. -211.11 (-324.69/-135.82), p = .052; VO2 [ml/min]: 4.55 (-55.53/46.29) vs. 8.62 (-46.4/82.73), p = .528; CaO2 [ml/l]: 27.02 (14.97/42.57) vs. 14.76 (-10.18/23.87), p = .019; CO [l/min]: -2.4 (-3.25/-2.02) vs. -1.58 (-2.73/-1.26), p = 0.53. Further differences were not significant. Analysis of PR resulted in the following (CCSV vs. IPPV): DO2 [ml/min]: -256.44 (-387.47/101.93) vs. -185.28 (-284.57/-138.44), p = .3; VO2 [ml/min]: 30.16 (4.55/240.41) vs. 12.82 (-57.03/66.02), p = .519; CaO2 [ml/l]: 32.78 (24.25/45.82) vs. 15.68 (4.91/23.16), p = .007; avDO2 [ml/l]: 76.09 (70.92/82.7) vs. 62.36 (51.65/72.06), p = .005; CO [l/min]: -2.4 (-3.3/-0.43) vs. -1.5 (-2.17/-1.27), p = 0.243. All others were not significant. Discussion: By significantly improving CaO2, CCSV provides the capability to strongly optimize oxygen delivery and oxygen consumption during resuscitation. However, a lowering of cardiac output over the course of CPR, as it could be observed in comparable studies, still represents a crucial limitation. As a result, future studies regarding cardiopulmonary resuscitation should focus on improvements of cardiac output. With a view to CCSV, further research is needed concerning its utilization during resuscitation following longer-term untreated cardiac arrest and in combination with preceding CPR consisting of alternating chest compression and ventilation at a ratio of 30:2.