Effect of different compression–decompression cycles on haemodynamics during ACD–CPR in pigs

Resuscitation 36 (1998) 123 – 131

Effect of different compression–decompression cycles on haemodynamics during ACD–CPR in pigs Kjetil Sunde a,b,*, Lars Wik b, Pa˚l Aksel Naess b,c, Arnfinn Ilebekk b, Gunnar Nicolaysen d, Petter Andreas Steen e a

Norwegian Air Ambulance, Department of Research and Education in Acute Medicine, N-1441 Drøbak, Norway. b Ulle6aal Uni6ersity Hospital, Institute for Experimental Medical Research, N-0407 Oslo, Norway c Ulle6aal Uni6ersity Hospital, Department of Surgery, N-0407 Oslo, Norway d Department of Physiology, Uni6ersity of Oslo, PO Box 1103, Blindern, 0317 Oslo, Norway e Ulle6a˚l Uni6ersity Hospital, Department of Anaesthesiology, N-0407 Oslo, Norway Received 28 August 1997; received in revised form 24 November 1997; accepted 4 December 1997

Abstract The haemodynamic effects of variations in the relative duration of the compression and active decompression (4 cm/2 cm) during active compression–decompression cardiopulmonary resuscitation (ACD – CPR), 30/70, 50/50 and 70/30, were tested in a randomized cross-over design during ventricular fibrillation in seven anaesthetized pigs (17 – 23 kg) using an automatic hydraulic chest compression–decompression device. Duty cycles of 50/50 and 70/30 gave significantly higher values than 30/70 for mean carotid blood flow (32 and 36 vs. 21 ml min − 1, transit time flow probe), cerebral blood flow (30 and 34 vs. 19 , radionuclide microspheres), mean aortic pressure (35 and 41 vs. 29 mmHg) and mean right atrial pressure (24 and 33 vs. 16 mmHg). A higher mean aortic, mean right atrial and mean left ventricular pressure for 70/30 were the only significant differences between 50/50 and 70/30. There were no differences in myocardial blood flow (radionuclide microspheres) or coronary perfusion pressure (CPP, aortic-right atrial pressure) between the three different duty cycles. CPP was positive in both the early and late compression period and during the whole decompression period. The expired CO2 was significantly higher with 70/30 than 30/70 during the compression phase of ACD–CPR. Beyond that no significant differences in the expired CO2 levels was observed. In conclusion a reduction of the compression period to 30% during ACD – CPR reduced the cerebral circulation, the mean aortic and right atrial pressures with no effect on the myocardial blood flow of varying the compression – decompression cycle. © 1998 Elsevier Science Ireland Ltd. All rights reserved. Keywords: Active compression–decompression; CPR; Duty cycle; Blood flow; Coronary perfusion pressure; ETCO2

1. Introduction Active compression – decompression cardiopulmonary resuscitation (ACD – CPR) has been reported to increase both coronary, carotid and cerebral blood flow [1–4], coronary perfusion pressure [3,5,6], velocity time integral (an analog of cardiac output) [5,7] endtidal CO2 [2,3,8] and arterial blood pressure [3 – 7] com* Corresponding author. Tel.: + 47 22 117800; fax: + 47 22 117799; e-mail: [email protected]

pared with standard CPR (S-CPR). In all these experimental studies [1–8] compression–decompression duty cycles of 50/50 have been used. This is the presently recommended duty cycle [9], but we are unaware of studies comparing the effects of various duty cycles during ACD–CPR. In two recent studies from two different EMS systems paramedics trained in manual ACD–CPR with the Cardiopump® (Ambu International, Glostrup, Denmark) were unable to adhere to this recommendation. In both studies the compression time was only 31%

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K. Sunde et al. / Resuscitation 36 (1998) 123–131

[10,11]. If this is a common trend also in other EMS systems, and such variations in duty cycle affect the results of ACD–CPR, this might explain why the results of clinical ACD – CPR studies so far [12 – 16]are less convincing than would be expected from the laboratory studies [1–8]. Therefore, we have examined the effects of three different duty cycles (30/70, 50/50 and 70/30) on cerebral, myocardial and other organ blood flow and various blood pressures including the coronary perfusion pressure in anaesthetized pigs. To be able to control and rapidly change the compression and decompression periods in each animal we used an automatic hydraulic compression–decompression device (Heartsaver 2000®, Medreco, Bodø, Norway).

2. Materials and methods

2.1. Animal preparation The study was approved by the Norwegian Council for Animal Research. Ten domestic healthy pigs of either sex (17–23 kg) were anaesthetized with Ketalar 30 mg kg − 1 and Atropine 1 mg i.m. A catheter was placed in an ear vein for infusion of 30 ml kg − 1h − 1. Ringer acetate and a target mean aortic pressure was set at 75 mmHg BMAP B120 mmHg. The pigs were placed supine with the chest in a U-shaped trough and the limbs secured to prevent lateral displacement of the chest during the ACD – CPR. A specially constructed pig mask was used for initiation of inhalation anaesthesia with desflurane (Suprane®, Pharmacia & Upjohn, end-tidal 15%), before a tracheotomy was performed. Anaesthesia was maintained with Suprane end-tidal 10% which is the reported MAC-level for pigs [17], measured sidestream by a Datex Capnomac Ultima (Helsinki, Finland), and adjusted if needed for each individual pig. Ventilation was performed with a Siemens Servo Respirator 900 B, with FiO2 of 0.5, a frequency of 16/min and an initial tidal volume of 15 ml kg − 1 adjusted to maintain end-tidal CO2 (ETCO2) at 5.09 0.5 kPa as measured by the Datex Capnomac Ultima. The urine was drained continuously through a cystostoma, and the rectal temperature was kept at 37.09 1.5°C, using a heating pad. One 7F microtip pressure transducer catheter (Millar Instruments, Model PC 470, Houston, TX) was introduced into the right femoral artery and advanced to the descending aorta, at the level of the heart, for arterial pressure recordings. Another 7F microtip pressure transducer catheter (Millar Instruments) was introduced into the left ventricle through the left carotid artery for measuring of the left ventricular pressure and for infusion of radionucleotide labelled microspheres into the ventricle through the sideport. For measuring

tissue blood flow : 6.0×105 microspheres (109Cd, 57 Co, 46Sc or 95Nb) (NEN-TracTM; DuPont) with a diameter of 15.5 mm diluted in 8 ml saline were infused at a rate of 3 ml min − 1 for 130 s, starting 20 s after the start of each ACD–CPR method. After each microsphere infusion the catheter was flushed with 10 ml of saline. Arterial blood was continuously withdrawn by a calibrated withdrawal pump (Harvard Instruments, Cambridge, MA) from the aorta during and after each microsphere infusion at a rate of 1.5 ml min − 1 via a 7F Swan–Ganz® catheter (Baxter, Anasko, Puerto Rico) with multiple sideholes advanced 15 cm in the left femoral artery from the inguinal ligament. The balloon was filled with 0.3 ml saline to ensure that the catheter tip was free in the vessel lumen. We measured the aortic pressure immediately before and after this saline inflation, and it did not affect any recorded haemodynamic variable. Two other 7 F Swan–Ganz® catheters (Baxter) were placed in the right atrium, one via the right femoral vein and one via the left external jugular vein for pressure recordings and mixed venous blood sampling. A polyethylene catheter was introduced into the right axillary artery for arterial blood sampling. After ligation of all visible branches of the right common carotid artery except the internal carotid artery, a transit time flow probe (Transonics, Ithaca, NY) was placed on the carotid artery. The oesophageal pressure at the level of the heart was measured by a cylindrical air-containing rubber balloon; 5 cm long and 3.4 cm in diameter glued to the end of a 7F stiff catheter with an open end and multiple side holes in the section inside the balloon [1,2]. Pressures were measured by Statham® P23Dd transducers (Gould Instruments, Hato Rey, Puerto Rico) and the microtip pressure transducer catheters. Pressures and carotid flow were recorded on an eight channel galvanometric recorder model 7758B (Hewlett Packard, Waltham, MA). A 4.0× 8.0 cm hard rubber plate was fastened with six screws to the sternum [1,2]. All catheter placements were verified by pressure tracings and post mortem examination.

2.2. Machinery ACD–CPR was achieved using a modified automatic hydraulic battery driven double-acting chest compression/decompression device (Heartsaver 2000®, Medreco, Bodø, Norway) with the possibility to change the compression–decompression duty cycle between 30/ 70, 50/50 and 70/30. The piston movement was photelectrically controlled. Active decompression was accomplished by attaching the piston to the hard rubber plate secured to the sternum.

K. Sunde et al. / Resuscitation 36 (1998) 123–131

2.3. Experimental protocol After instrumentation baseline (pre-VF) measurements were obtained for all variables. The i.v. infusion, the heating and the inhalation anaesthesia were thereafter discontinued. Ventricular fibrillation (VF) was induced by a trans-thoracic current (90 V AC) for 3 s and confirmed by ECG changes and an abrupt fall in arterial pressure. Ventilation was then discontinued. After 3 min of VF, 4 cm standard mechanical chest compressions without active decompressions were initiated at a rate of 80 min − 1 for 30 s to allow the initial changes in chest configuration before the zero point for the compressions and active decompressions was set. The experiment was then started with 4 cm compression and 2 cm decompression choosing one of three different compression – decompression duty cycles; 30/ 70, 50/50 or 70/30, picked at random from a list. Manual bag valve ventilation with 100% O2 was performed during every fifth decompression without interruption of the compression – decompression cycle. The person ventilating the pig was blinded for the ETCO2 values. Carotid flow and all pressures were recorded at 120 and 240 s after the start of each compression/decompression cycle. Arterial and mixed venous blood gases were measured between 180 and 240 s. ETCO2 during manual ventilation, and partial pressure of endo-tracheal CO2 generated with each chest compression cycle were also recorded and tissue blood flow measured as described above. After 300 s the duty cycle was changed to one of the other two patterns, and all measurements were repeated with the same time schedule. After 600 s the duty cycle was changed to the last pattern, and all measurements were again repeated. The randomization list was written so that the different duty cycles were evenly spread between being performed as the first, second or third method. After completion of the experiment, the ACD –CPR and ventilations were stopped, and the pig died. All pigs were autopsied to check for damage to the internal organs and for verification of the catheter placements. Samples of the following organs were obtained, weighed and placed into counting vials: heart (four regions), brain (six regions), kidneys (two regions), liver, small intestine and diaphragma.

2.4. Calculations Left ventricular transmural pressure was calculated as the difference between left ventricular and oesophageal pressures, and coronary perfusion pressure (CPP) as the difference between thoracic aortic and right atrial pressures. Tissue blood flow was measured with radiolabelled microspheres according to the technique described by Heymann et al. [18] with modifica-

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tions as described by Iversen and Nicolaysen [19], and evaluated during CPR by others [1–4]. Radioactivity of tissue and arterial blood was measured in a gamma counter (Auto-Gamma 5220, Packard, IL) and corrected for overlap. Regional blood flow per gram was calculated based on the radioactivity in the tissue and in the reference arterial blood and the reference sample flow [19].

2.5. Statistical analysis Data are presented as mean9 S.D. Comparisons were made between the three different ACD–CPR methods. Each pig served as its own control and for continuous parametric data the One Way ANOVA Repeated Measures with pairwise multiple comparison procedures was used. For non-parametric data the Friedman One Way ANOVA Repeated Measures was used. Statistical significance was considered to be at the PB 0.05 level.

3. Results Ventricular fibrillation (VF) was obtained in nine pigs by the first trans-thoracic electric shock, while one pig needed three electric shocks because of electrode displacement. Three pigs were excluded. One had severe hypertension with MABP\ 120 mmHg despite adequate anaesthesia (no movement in unparalyzed animal), one had thrombotic emboli and a large cardiac infarction and one had air-embolus, probably occurring during instrumentation in connection with an intrapleural bleeding from a lung. In the remaining seven pigs no gross liver, lung, heart or other visceral damage was observed. One minute after start of ACD–CPR, and each change in the ACD–CPR duty cycle, both blood pressures, carotid flow and ETCO2 had stabilized. Total ACD–CPR time was 1691 min. Tracings of left ventricular pressure, aortic pressure, carotid flow and oesophageal pressure during each of the three different duty cycles as obtained in one pig, are shown in Fig. 1.

3.1. Blood flows Mean carotid blood flow was 145935 ml min − 1 pre-VF and was 219 3 ml min − 1 during ACD–CPR with the 30/70 duty cycle (Table 1). With duty cycles of 50/50 and 70/30 mean carotid arterial blood flow was 52 and 71% higher respectively with no significant difference between the two latter. Mean cerebral blood flow was 83 9 35 ml min − 1 100 −1 g pre-VF and was 19 9 6 ml min − 1 100 g − 1 during ACD–CPR with duty cycle 30/70 (Table 2). In parallel with the changes in the carotid blood flow, cerebral

K. Sunde et al. / Resuscitation 36 (1998) 123–131

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Fig. 1. Reproduction from typical tracings of left ventricular pressure (LVP), aortic pressure (AP), carotid blood flow and oesophageal pressure during ACD – CPR with different duty cycles on a pig.

blood flow was 58 and 79% higher for the 50/50 and 70/30 duty cycles respectively with no significant difference between the two latter. With small individual differences, the same pattern was found in all six regions of the brain (not tabulated). The mean cerebral blood flow was 23% of the pre-VF value with 30/70, 36% with 50/50 and 41% with 70/30. Mean myocardial blood flow was 1159 52 ml min − 1 100 g − 1 pre-VF and 27 – 37% of this value during ACD–CPR with no significant difference between the three duty cycles (Table 2). The same changes in blood flow tended to occur both in the epi- and endo-cardium of the left ventricle and in the right ventricular wall. The endocardial/epicardial ratio was 1.18 9 0.12 preVF, and changed to 0.6290.24, 0.7290.43 and 0.739 0.32 for 30/70, 50/50 and 70/30 respectively with no significant differences between the three different duty cycles. Both kidney, liver and small intestine blood flow tended to be higher with 50/50 and 70/30 compared with 30/70 (Table 2), but the difference was not statistically significant. In contrast to the other measured organs, the blood flow in the diaphragm was not reduced from the pre-VF value during ACD – CPR (Table 2). Table 1 Internal carotid artery blood flow during active compression–decompression cardiopulmonary resuscitation (ACD–CPR) with different duty cycles Carotid flow (ml min−1)

30/70

50/50

Mean Peak compression Early decompression Mid decompression

2193 1609 39 −839 63 69 8

329 10* 36 9 6* 1979 55 206 9 28 −97960 −909 49 195 −119 31

Data presented as mean 9S.D. * PB0.05 vs. 30/70.

70/30

3.2. Measured pressures Mean aortic pressure was 899 20 mmHg pre-VF and 299 10 mmHg during ACD–CPR with duty cycle 30/70 (Table 3). This was 21 and 41% higher for 50/50 and 70/30 respectively with a significant difference between the two latter. This occurred in parallel with the increased duration of the high pressure compression phases as there were no significant differences in the pressure obtained during the different phases of compression and decompression between the three methods. The mean right atrial pressure was 16 9 6 mmHg with duty cycle 30/70, and was 50 and 106% higher for 50/50 and 70/30, respectively (Table 3). For this pressure also the difference between 50/50 and 70/30 was significant. Again there were no significant differences in the pressure obtained during the different phases of the compression and decompression between the three methods, as the difference in mean pressures correlated with the difference in compression duration (Table 3). The same pattern was true for the mean left ventricular pressure, but here the peak compression pressure Table 2 Mean regional blood flow generated with active compression–decompression cardiopulmonary resuscitation (ACD – CPR) with different duty cycles Blood flow (ml min−1 100 g−1)

Pre-VF

30/70

50/50

70/30

Brain Heart Kidney Liver Small intestine Diaphragmatic muscle

83 9 35 115 952 221 923 53 918 56 9 26 12 9 6

19 96 36 922 14 9 10 793 13 97 22 916

30 912* 42 935 24 913 12 95 23 9 11 24 9 14

34 9 8* 31 9 16 29 925 16 912 20 913 18 914

Data presented as mean 9S.D. * PB0.05 vs. 30/70

K. Sunde et al. / Resuscitation 36 (1998) 123–131 Table 3 Aortic, right atrial, left ventricular and oesophageal pressures during active compression – decompression cardiopulmonary resuscitation (ACD– CPR) with different duty cycles Pressure (mmHg)

30/70

50/50

Table 4 Calculated coronary perfusion pressure (aortic-right atrial pressure) and transmural left ventricular pressure (left ventricular – oesophageal pressure) during active compression – decompression cardiopulmonary resuscitation (ACD – CPR) with different duty cycles

70/30 Pressure (mmHg)

Aortic pressure Mean Peak compression End compression Lowest decompression Mid decompression

29 910 70 924 70 924 15 9 13 23 9 7

Right atrial pressure Mean Peak compression End compression Lowest decompression Mid decompression

16 96 79 9 33 79 9 33 −1297 7 94

24 9 6* 859 20 28 98 −15910 49 7

21 9 7 94 9 33 94 9 33 4 97 11 95

309 8* 1039 23 35 9 7 096 79 6

−29 5 309 14 30 9 14 −1197 −89 5

1 9 5* 31 913 139 7 −1795 −1395

Left 6entricular pressure Mean Peak compression End compression Lowest decompression Mid decompression Oesophageal pressure Mean Peak compression End compression Lowest decompression Mid decompression

359 13* 75 9 17 36 96 13 9 17 20 99

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419 14** 82 9 23 329 5 13 9 15 199 9 33 97** 1029 36 239 7 −1298 295 36 9 10** 1149 36* 28 9 4 −496* 395* 69 8* 29 918 1296 −189 7 −1898*

Data presented as mean 9 S.D. * PB0.05 vs. 30/70. ** PB0.05 vs. 50/50.

with 70/30 was significantly higher and the decompression pressures significantly lower than with 30/70 (Table 3). The mean oesophageal pressure was significantly higher with 50/50 and 70/30 than with 30/70 (Table 3). The oesophageal pressure was positive during compression and negative during active decompression with all the three duty cycles, and significantly lower with 70/30 than with 30/70 during the mid decompression phase (Table 3).

30/70

Coronary perfusion pressure Mean 11 95 Peak compression −8918 End compression −8918 Lowest decompression 27 913 Mid decompression 13 95 Left 6entricular transmural Mean Peak compression End compression Lowest decompression Mid decompression

pressure 24 9 8 63 925 63 925 15 97 19 96

50/50

70/30

997 −11914 8 9 10 26 915 18 9 13

896 −149 21 1199 20 9 10 149 9

29 99 72 926 22 99 15 9 12 15 9 15

29 9 9 86937* 1695 15 9 8 18 96

Data presented as mean 9S.D. * PB0.05 vs. 30/70.

There were no differences in the left ventricular transmural pressure with the three methods, except for a significantly higher peak compression pressure with 70/30 (86 937 mmHg) than with 30/70 (63 925 mmHg) (Table 4).

3.4. Expired CO2 concentration ETCO2 was 4.49 0.3 kPa pre-VF (Table 5). There were no significant differences in ETCO2 with the different methods for the manual ventilations, but the peak expired CO2 generated by the compression–decompression cycle was significantly higher with 70/30 than with 30/70 (Table 5).

3.5. Blood gases Blood gases are presented in Table 6. There were no systematic variations between periods with the different ACD–CPR duty cycles.

3.3. Calculated pressures There were no significant differences in mean and phasic coronary perfusion pressures between the three different duty cycles, with a positive CPP throughout the decompression phase, and for 50/50 and 70/30 also at the end of the compression phase (Table 4). Fig. 2 is a reproduction of an original tracing of the aortic and right atrial pressure during ACD – CPR with a 50/50 duty cycle, indicating a positive CPP in the early and late compression phase and throughout the decompression.

Fig. 2. Reproduction from an original tracing of the aortic and right atrial pressure during ACD – CPR with a 50/50 duty cycle on a pig, showing positive coronary perfusion pressure as a shaded area.

K. Sunde et al. / Resuscitation 36 (1998) 123–131

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Table 5 End-tidal CO2 (ETCO2) with ventilation and peak expired CO2 level generated by chest compressions and decompressions during active compression – decompression cardiopulmonary resuscitation (ACD – CPR) with different duty cycles ETCO2 (kPa)

Pre-VF

30/70

50/50

70/30

Manual ventilation Compression/ decompression cycle

4.4 90.3

1.49 0.6

1.79 0.3

1.8 9 0.7

0.59 0.2

0.89 0.2

1.19 0.4*

Data presented as mean 9 S.D. * PB0.05 vs. 30/70.

4. Discussion In the present study in anaesthetized pigs with ventricular fibrillation (VF), the brain circulation was much lower during ACD – CPR with a 30 vs. 50 or 70% compression phase, while the relative duration of the compression phase did not affect myocardial blood flow, the coronary perfusion pressure or the flow to other organs. Previous reports of positive hemodynamic effects of ACD–CPR compared to standard CPR (S-CPR) in pigs [1–3], dogs [4,5] and human [6 – 8] all report the use of a 50% compression phase. This agrees with the recommendations of the first European pre-hospital ACD–CPR workshop [9], but both are probably based upon the recommendations for S-CPR [20,21], as the effects of varying the relative duration of the compression phase during ACD – CPR have to our knowledge not previously been reported. Taylor et al. [22] found a two to three times higher carotid blood flow measured by transcutaneous unidirectional Doppler with 50–60 vs. 30–40% compression time during mechanical STable 6 Arterial and mixed venous blood gas values during active compression–decompression cardiopulmonary resuscitation (ACD – CPR) with different duty cycles Blood gas

Pre VF

30/70

50/50

70/30

Arterial pH 7.47 90.1 PCO2 (kPa) 5.4 90.5 PO2 (kPa) 30.3 9 5.0 BE (mmol 6.8 95.0 l−1)

7.499 0.1 7.479 0.1 7.41 9 0.1 3.3 90.9 3.79 0.9 3.691.8 28.2 9 22.7 29.0 915.3 31.89 18.9 −3.195.3 −2.295.6 −5.69 7.0

Mixed 6enous pH 7.4290.1 PCO2 (kPa) 6.3 90.5 PO2 (kPa) 6.0 90.8 BE (mmol 6.6 93.0 l−1)

7.189 0.1 8.5 91.9 2.8 9 0.4 −4.89 5.0

Data presented as mean 9S.D.

7.189 0.1 8.8 9 1.0 2.89 0.6 −4.295.4

7.189 0.1 8.89 1.2 2.7 9 1.0 −4.193.4

CPR in eight patients. Better cardiac output (measured with indicator-dilution technique), and myocardial and cerebral blood flow (measured with radioactive microspheres), were found by Halperin et al. [23] when the compression phase of S-CPR was increased from 15 to 45% in dogs. The present study was performed with a mechanical device which allowed controlled variations in the relative duration of the compression phase without interrupting the CPR. The chosen compression-/active decompression length of 4/2 cm were based on previous positive hemodynamic effects of ACD–CPR vs. S-CPR in the same model [2], and we have in two previous studies [1,2] shown that the hemodynamics in the model do not detoriarate as a function of time within the limits of the present study. With the 50% compression phase in the present study the mean aortic pressure was similar to the results with ACD–CPR in other studies [1–8] Both the mean aortic pressure, mean right atrial pressure and mean left ventricular pressure increased with an increase in the compression phase from 30 to 50 to 70%. This was due to the longer duration of the high pressure compression phase as there were no significant differences in any of the pressures between the different duty cycles at any specific time during the cycle. Endtidal CO2(ETCO2) has been reported to reflect cardiac output during standard CPR [24–26], and ACD–CPR to significantly increase ETCO2 vs. S-CPR [2,3,8]. In the present study there was no effect on ETCO2 of different durations of the compression phase, and thus there are no indication that cardiac output varied. The small peaks in expired CO2 secondary to the compressions increased with the relative duration of the compression phase, indicating a better ventilatory effect of the compression–decompression cycle with increased compression duration. Such a correlation between these peaks and the ventilatory effect has been found in a previous study of ACD–CPR with varying compression–active decompression depth [2]. The mean cerebral flow of 30 ml min − 1 100 g − 1 with 50% compression phase in the present study corresponds well with the previously reported 32 ml min − 1 100 g − 1 by Wik et al. [2] and 30 ml min − 1 100 g − 1 by Lindner et al. [3] with 50% compression ACD–CPR in pigs. At the same time the lower mean cerebral blood flow of 19 ml min − 1 100 g − 1 with a 30% compression phase is similar to the cerebral flow found with S-CPR and 50% compression in the same studies, 21 [2] and 15 ml min − 1 100 g − 1 [3]. Although these are animal data that cannot automatically be extrapolated to humans, it is tempting to speculate whether these can explain the apparent discrepancy between the very positive effects of ACD– CPR in well-controlled experiments [1–8] and the more uncertain effects of ACD–CPR on the final outcome of patients in larger clinical studies [12–16].

K. Sunde et al. / Resuscitation 36 (1998) 123–131

In two recent studies on manikins [10,11], trained paramedics in two different EMS systems in Norway were not able to adhere to the recommended guidelines for ACD–CPR [9] when using the hand-held Cardiopump®. In both studies [10,11] the mean compression phase lasted only 31% of the whole duty cycle. If this is also the case in other EMS systems, and the hemodynamic effects of reducing the compression phase are the same in humans as in pigs, the cerebral circulation is not improved with manual ACD – CPR compared to S-CPR. This could at least partly explain why final outcome, which largely depends on cerebral function [27,28] did not improve in most of these clinical studies [12 – 16]. The mean myocardial blood flow of 42 ml min − 1 100 −1 with a 50% compression phase also corresponds g with the findings of Wik et al. [2] (37 ml min − 1 100 g − 1) in the same model, slightly higher than the 30 ml min − 1 100 g − 1 found by Lindner et al. [3]. The relatively large standard deviation in myocardial blood flow compared to cerebral blood flow was due to large inter-individual variations. This could not easily be explained by variations in the venous return to the heart, as there was no significant correlation between the myocardial blood flow and the right atrial pressure (P \ 0.05 and/or Pearson correlation coefficientB 0.80 for all three methods). During VF myocardial blood flow appears to correlate with the pressure gradient between the aorta and right atrium (the coronary perfusion pressure (CPP)) in the decompression phase of CPR [29 – 31]. Increases in CPP therefore account for proportional increases in myocardial blood flow and resuscitability [29 – 31]. The studies comparing ACD – CPR with standard CPR reports increased coronary perfusion pressure during ACD–CPR [3,5,6]. The CPP of 20 – 27 mmHg in the decompression period with the different duty cycles in the present study correspond well with the 16–28 mmHg reported in other studies [3,5,6] of ACD –CPR. In the present study, as previously reported from Schultz [6] and Lurie [32], the CPP was also positive during the early and late compression phase with ACD–CPR. Whether this can partly explain a higher myocardial blood flow with ACD – CPR than with SCPR [2–4] would probably also depend on the myocardial tissue pressure. If this pressure is higher than the right atrial pressure, it seems likely that the myocardial perfusion is a function of the aortic pressure minus the tissue pressure, not the right atrial pressure, in parallel to the case in a brain with a high intracranial pressure. To our knowledge the myocardial tissue pressure has not been measured during CPR, but Chang et al. [33] measuring Doppler coronary flow velocities reported augmentated myocardial blood flow with ACD –CPR vs. S-CPR to occur during the late decompression phase, and not in the compression phase.

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The pattern of the left ventricular myocardial blood flow distribution can be described by the endocardial to epicardial blood flow ratio. We found a pre-VF ratio of 1.18 which correspond well with a previous finding of 1.22 in anaesthetized pigs [34], but lower than 1.64 reported by Lindner et al. [3], also in pigs, and 1.76 by Chang et al. [4] in dogs. This difference could be due to different models and anaesthetic agents. However, the important finding is that the ratio changed during ACD–CPR to 0.73 with the 50/50 duty cycle with no significant difference between the three different duty cycles. This reduction in the endocardial to epicardial blood flow ratio was similar to that found by Lindner et al. [3] and Chang et al. [4] who reported reductions to 0.97 and 0.92, respectively. This indicates a fall of 38% in the present study vs. 41 and 48% in the studies by Lindner and Chang, respectively. In both the studies of ACD–CPR in pigs previously referred to [2,3], and in a similar study performed on dogs [4], the myocardial blood flow was higher with ACD–CPR than with S-CPR. As the myocardial circulation was not significantly affected by the relative duration of the compression phase in the present study, this could indicate that ACD–CPR with a compression phase of 30% should give a better myocardial blood flow than S-CPR. The rate of return of spontaneous circulation (ROSC) after VF improves with increased myocardial blood flow [35,36], and Michael et al. [35]have reported that a myocardial blood flow of at least 20 to 25 ml min − 1 100 g − 1 seems to be necessary for ROSC in experimental animals. These data would fit with findings of an increased rate of ROSC in some clinical studies [12,16], even if it seems difficult to achieve more than 30% compression phase with manual ACD–CPR [10,11]. We should be cautious about extrapolating from animal data to human clinical studies. Three other clinical studies [13–15] failed to find a significant improvement in the ROSC rate with ACD–CPR. Other factors than the compression/decompression duty cycle are affected by the manual performance in clinical CPR. Manual ACD–CPR requires 25% more work than S-CPR [37], and in a clinical study of 1784 patients Stiell et al. [13] reported that 18% of the performers rated ACD–CPR as difficult or very difficult to perform with fatigue, back and hand pain, and balance problems. It can therefore be speculated that the difference in results of the clinical trials may be due to differences in the quality of the ACD–CPR performance. In the study by Plaisance et al. [16], which is the single study published so far which showed a dramatic superiority ACD–CPR vs. S-CPR (ROSC 45 vs. 30% and hospital discharge rate without neurologic impairment 6 vs. 2%), there was constant evaluation, frequent refresher courses and great number of rescuers involved in each case which could limit the risk of fatigue.

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