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Quality of CPR with three different ventilation:compression ratios
Resuscitation 58 (2003) 193 /201 www.elsevier.com/locate/resuscitation
Quality of CPR with three different ventilation:compression ratios E. Dorph a,b,*, L. Wik c, T.A. Strømme b, M. Eriksen b, P.A. Steen d a
Norwegian Air Ambulance, N-1441 Drøbak, Norway Institute for Experimental Medical Research, Ulleva˚l University Hospital, N-0407 Oslo, Norway c National Centre of Competence for Emergency Medicine, Ulleva˚l University Hospital, N-0407 Oslo, Norway d Division of Emergency Medical Services, Ulleva˚l University Hospital, N-0407 Oslo, Norway b
Received 29 January 2003; received in revised form 26 March 2003; accepted 31 March 2003
Abstract Current adult basic cardiopulmonary resuscitation (CPR) guidelines recommend a 2:15 ventilation:compression ratio, while the optimal ratio is unknown. This study was designed to compare arterial and mixed venous blood gas changes and cerebral circulation and oxygen delivery with ventilation:compression ratios of 2:15, 2:50 and 5:50 in a model of basic CPR. Ventricular fibrillation (VF) was induced in 12 anaesthetised pigs, and satisfactory recordings were obtained from 9 of them. A non-intervention interval of 3 min was followed by CPR with pauses in compressions for ventilation with 17% oxygen and 4% carbon dioxide in a randomised, crossover design with each method being used for 5 min. Pulmonary gas exchange was clearly superior with a ventilation:compression ratio of 2:15. While the arterial oxygen saturation stayed above 80% throughout CPR for 2:15, it dropped below 40% during part of the ventilation:compression cycle for both the other two ratios. On the other hand, the ratio 2:50 produced 30% more chest compressions per minute than either of the two other methods. This resulted in a mean carotid flow that was significantly higher with the ratio of 2:50 than with 5:50 while 2:15 was not significantly different from either. The mean cerebrocortical microcirculation was approximately 37% of pre-VF levels during compression cycles alone with no significant differences between the methods. The oxygen delivery to the brain was higher for the ratio of 2:15 than for either 5:50 or 2:50. In parallel the central venous oxygenation, which gives some indication of tissue oxygenation, was higher for the ratio of 2:15 than for both 5:50 and 2:50. As the compressions were done with a mechanical device with only 2 /3 s pauses per ventilation, the data cannot be extrapolated to laypersons who have great variations in quality of CPR. However, it might seem reasonable to suggest that basic CPR by professionals should continue with ratio of 2:15 at present if it can be shown that similar brief pauses for ventilation can be achieved in clinical practice. # 2003 Elsevier Ireland Ltd. All rights reserved. Keywords: CPR; Ratios; Gas exchange; Oxygen delivery
Resumo A Reanimac¸a˜o cardio-pulmonar ba´sica corrente do adulto recomenda uma relac¸a˜o ventilac¸a˜o: compressa˜o 2:15, embora a relac¸a˜o o´ptima seja desconhecida. Este estudo foi delineado para comparar as alterac¸o˜es nos gases sanguı´neos arterial e venoso misto, a circulac¸a˜o cerebral e o aporte de oxige´nio com relac¸o˜es ventilac¸a˜o: compressa˜o de 2:15, 2:50 e 5:50 num modelo de RCP ba´sica. Foi induzida Fibrilhac¸a˜o Ventricular (FV) em 12 porcos anestesiados, e foram obtidos registos satisfato´rios em 9 deles. Apo´s um intervalo sem intervenc¸a˜o de 3 minutos, realizou-se RCP com pausa nas compresso˜es para ventilar com Oxige´nio a 17% e dio´xido de carbono a 4% num estudo cruzado, randomizado, com cada relac¸a˜o ventilac¸a˜o: compressa˜o a ser utilizado durante 5 minutos. As trocas gasosas pulmonares foram claramente superiores com uma relac¸a˜o ventilac¸a˜o: compressa˜o de 2:15. A saturac¸a˜o do oxige´nio arterial ficou acima dos 80% ao longo da RCP com relac¸a˜o de 2:15, enquanto que esta desceu abaixo dos 40% durante parte do ciclo de ventilac¸a˜o: compressa˜o para as outras duas relac¸o˜es. Por outro lado, a relac¸a˜o 2:50 produziu 30% mais compresso˜es tora´cicas por minuto que qualquer um dos outros dois me´todos. Isto resultou num fluxo carotı´deo me´dio que foi significativamente mais elevado com a relac¸a˜o 2:50 do que 5:50, enquanto que a relac¸a˜o 2:15 na˜o condicionou alterac¸o˜es significativamente diferentes de ambas. A microcirculac¸a˜o cerebrocortical me´dia foi aproximadamente 37% dos nı´veis pre´-FV
* Corresponding author. Tel.: /47-230-16813; fax: /47-230-16799. E-mail address: [email protected] (E. Dorph). 0300-9572/03/$ - see front matter # 2003 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/S0300-9572(03)00125-4
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durante os ciclos de compressa˜o sem nenhuma diferenc¸a significativa entre os me´todos. O aporte de oxige´nio ao ce´rebro foi mais elevado para a relac¸a˜o2:15 do que para as outras duas relac¸o˜es 5:50 ou 2:50. Em paralelo a oxigenac¸a˜o venosa central, que da´ alguma indicac¸a˜o da oxigenac¸a˜o tecidular, foi mais elevada para a relac¸a˜o 2:15 do que para as outras duas. Estes resultados na˜o podem ser extrapolados para a RCP realizada por leigos que teˆm grande variac¸a˜o na qualidade da RCP, uma vez que as compresso˜es foram realizadas com um aparelho mecaˆnico com apenas 2-3 s de pausa para a ventilac¸a˜o. Contudo parece ser razoa´vel sugerir que a RCP ba´sica realizada por profissionais deve continuar com uma relac¸a˜o de2:15, se for possı´vel obter na pra´tica clı´nica pausas breves similares para a ventilac¸a˜o. # 2003 Elsevier Ireland Ltd. All rights reserved. Palavras chave: RCP; Relac¸a˜o Ventilac¸a˜o:Compressa˜o; Trocas gasosas; Aporte de oxige´nio
Resumen Las actuales guı´as de reanimacio´n cardiopulmonar ba´sica (RCP) recomiendan una relacio´n ventilacio´n: compresio´n de 2:15, en circunstancia que la relacio´n o´ptima es au´n desconocida. Este estudio fue disen˜ado para comparar los cambios en gases arteriales y en sangre venosa mezclada, en la circulacio´n cerebral y en la entrega de oxı´geno con distintas relaciones ventilacio´n compresio´n de 2:15, 2:50 y de 5:50 en un modelo ba´sico de RCP. Se indujo fibrilacio´n ventricular (VF) en 12 cerdos anestesiados, y se obtuvieron registros satisfactorios de 9 de ellos. Despue´s de un intervalo de no intervencio´n de tres minutos se realizo´ RCP con pausas en la compresio´n para realizar la ventilacio´n con oxı´geno al 17% y 4% de dio´xido de carbono en un disen˜o cruzado, randomizado siendo cada me´todo usado por 5 minutos. El intercambio gaseoso pulmonar fue claramente superior con una relacio´n ventilacio´n compresio´n de 2:15. Mientras la saturacio´n de oxı´geno se mantuvo sobre 80% a lo largo de la RCP 2:15, cayo´ bajo 40% durante parte del ciclo ventilacio´n compresio´n en ambas de las relaciones restantes. Por otro lado, la relacio´n 2:50 produjo 30% mas compresiones por minuto que cualquiera de los otros me´todos. Esto resulto´ en un flujo carotı´deo medio que fue significativamente mas alto con la relacio´n 2:50 que con 5:50 mientras que 2:15 no fue significativamente diferente de ninguno de los otros me´todos. La microcirculacio´n cerebral media fue aproximadamente 37% de los niveles previos a la VF durantes los ciclos de solo compresio´n sin diferencias significativas entre los distintos me´todos. La entrega de oxı´geno al cerebro fue mayor para la relacio´n de 2:15 que para ya sea 5:50 o´ 2:50. Paralelamente la oxigenacio´n venosa central, que da alguna indicacio´n de oxigenacio´n tisular, fue mas alta para la relacio´n 2:15 que para ambas 5:50 y 2:50. Como las compresiones fueron realizadas con un aparato meca´nico con solo 2-3 pausas para ventilacio´n, los datos no pueden ser extrapolados a personas que tienen gran variacio´n en calidad de RCP. Sin embargo, pareciera razonable sugerir que la RCP ba´sica por profesionales debiera seguir con relacio´n2:15 en este momento si se puede mostrar que en la pra´ctica clı´nica pueden lograrse pausas para ventilacio´n similarmente cortas. # 2003 Elsevier Ireland Ltd. All rights reserved. Palabras clave: RCP; Relacio´n ventilacio´n compresio´n; Intercambio gaseoso; Entrega de oxı´geno
1. Introduction The optimal ratio of ventilations to chest compressions during cardiopulmonary resuscitation (CPR) is unknown. Current guidelines for adult CPR by one or two lay rescuers is based on a combination of chest compressions and mouth-to-mouth ventilations with a 2:15 ventilation:compression ratio [1]. Recently, the issue of the most advantageous ventilation:compression ratio has been the focus of renewed attention because both lay and professional rescuers are reluctant to perform mouth-to-mouth ventilation mainly due to concerns of contracting infectious diseases [2 /4]. In addition, standard basic CPR is a complex psychomotor task difficult to learn and perform without such complications as gastric inflation [5,6]. Moreover, the relatively long pauses in chest compression required for ventilation result in disturbingly long interruptions in circulation during CPR, which appear potentially to compromise the success of cardiac resuscitation [7 /9]. Consequently, some researchers have begun to explore other ventilation:compression ratios with much
longer series of uninterrupted compressions such as 5:50 [7,10] or even chest compression only CPR [11 /13]. During longer periods of CPR it has been stated that some ventilatory support is critical for successful resuscitation outcomes [14]. It therefore seems appropriate to investigate alternative ventilation:compression ratios with longer sequences of chest compressions, and the present study was designed to determine haemodynamics and oxygen delivery with three different ratios of ventilation and chest compressions in an experimental porcine model of basic CPR.
2. Materials and methods 2.1. Animal preparation The experiments were conducted in accordance with ‘Regulations on Animal Experimentation’ under The Norwegian Animal Welfare Act and approved by Norwegian Animal Research Authority. Twelve healthy domestic swine of either sex were fasted over night
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except for free access to water. The animals were sedated with ketamine (20 mg kg 1) and atropine 1 mg intramuscularly and then placed supine in a U-shaped cradle with an external heating blanket interposed between the back and the cradle. The limbs were secured to prevent body displacement during the performance of CPR. A catheter was placed in an ear vein and bolus injections of sodium pentobarbital (15 mg kg 1) and morphine 10 mg were given intravenously (i.v.) followed by an infusion at a rate of 10/15 and 0.4 /0.5 mg kg 1 h 1, respectively to maintain adequate anaesthesia as judged by heart rate, blood pressure, spontaneous respiration, and the canthal reflex. The ear vein catheter was also used for infusion of 25 ml kg 1 h 1 warmed Ringer acetate throughout the preparation period. A midline incision was made in the anterior neck and an 8.0 mm tracheal tube secured within the trachea via a tracheostomy incision. Prior to CPR the pig was ventilated with a volume-controlled ventilator (Servo Ventilator 900 B, Siemens-Elema AB, Solna, Sweden). Initial tidal volume was 15 ml kg 1, the respiratory rate 16 breaths min 1 and the inspired oxygen fraction 0.5. Tidal volume was adjusted to maintain the end-tidal carbon dioxide (ETCO2) at 59/0.5 kPa as measured by the gas monitor (Datex Capnomac UltimaTM, Helsinki, Finland). Urine was drained continuously through a cystostoma, and the intra-abdominal temperature was maintained at 399/0.5 8C throughout the experimental period. A 7F micro-tip pressure transducer catheter (Model SPC 470, Millar Instruments, Houston, TX, USA) was inserted through the right femoral artery and advanced to the descending aorta at the level of the heart for arterial pressure recordings. Another 7F micro-tip pressure transducer catheter (Millar Instruments) was introduced to the left ventricle through the left common carotid artery to measure the left ventricular pressure. A 7F Swan-Ganz† catheter (model 131HF7, Baxter Healthcare Corporation, Irvine, CA, USA) was advanced through the right femoral vein and flow directed into the right atrium for pressure recordings and mixed venous blood sampling. A 7.5F Swan-Ganz† CCOmbo catheter (model 744HF75, Edwards Lifesciences LLC, Irvine, CA, USA) was inserted into the descending aorta for arterial blood sampling and for continuous recording of arterial oxygen saturation. After ligation of all visible branches of the right common carotid artery except the internal carotid artery a transit time perivascular flowprobe (model 3SB880, Transonic Systems Inc, Ithaca, NY, USA) was placed on the artery. All invasive catheters were introduced using a cut-down technique. To monitor cerebral perfusion the technique of laserDoppler flowmetry (LDF) was applied. This method allows continuous measurement of focal microcirculatory blood flow and the LDF readings are expressed in arbitrary perfusion units (PU) [15,16].
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The right parietal region of the skull was exposed. A burr hole of 12/15 mm in diameter was drilled in the cranium using an electric drill (Dremel† Minicraft, Germany) at low speed. A gentle saline drip (0.9%, 25 8C) over the drilling site prevented thermal injury to the cortex. The centre of the hole was located 12/15 mm lateral to the sagittal suture and 12/15 mm caudal to the coronal suture. The dura was opened and the laserDoppler probe (model 407. Perimed AB, Stockholm, Sweden), connected to a perfusion monitor (PeriFlux System 5000, Perimed AB, Stockholm, Sweden), with probe holder (model PH 07-4, Perimed AB, Stockholm, Sweden) was secured in a position carefully chosen to avoid visible pial vessels. The Swan-Ganz catheter in the right atrium and the side port lumen of the micro-tip transducer catheter in the descending aorta were connected to fluid filled transducers (Statham† P23Dd, Gould Instruments, Hato Rey, Puerto Rico). Tidal volumes, respiratory pattern and ETCO2 were measured continuously using a combined differential pressure pneumotach flow sensor and solid state CO2 sensor in combination with a respiratory profile monitor (CO2SMO Plus! Model 8100, Novametrix Medical System Inc., Wallingford, CT, USA). The flow/CO2 sensor was inserted in the breathing circuit between the ventilator and a bacterial filter connected to the tracheal tube. The monitor was connected on-line to a computer (Omnibook 6000, Hewlett Packard Company, Cupertino, CA, USA) into which the data were downloaded, stored and analysed using Analysis Plus! version 3.0 Software package (Novametrix Medical System Inc.). Pressures, carotid flow signals and laser-Doppler flow signals were sampled using PC-based real time data acquisition hardware (DaqBoardsTM Model 200A, IOtech, Inc., Cleveland, OH, USA) supported with software for DASYLab version 5.1 (Datalog, National Instruments company, Moenchengladbach, Germany) and printed on an eight-channel thermal array recorder model TA 11 (Gould Instrument Systems, Inc., OH, USA). Arterial oxygen saturation was recorded using the Swan-Ganz† CCOmbo catheter connected to a continuous oximetry monitor (Vigilance† , Edwards Critical-Care Division, Irvine, CA, USA). Specimens for arterial blood gas analysis were obtained from the descending aorta, for mixed venous blood gas analysis from the right atrium, and measured directly with a blood gas analyser (AVL OMNITM 9, Graz, Austria).
2.2. Machinery Standard chest compression was achieved using a modified automatic hydraulic battery driven chest compression device (Heartsaver 2000† , Medreco, Bodø, Norway) with equal compression /relaxation
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phases. The piston movement was photoelectrically controlled. Compression depth was set at 4 cm. 2.3. Experimental protocol After collecting all necessary baseline (pre-VF) data, pancuronium (Pavulon† , N.V. Organon, Oss, Netherlands) 0.2 mg kg1 was administered to prevent spontaneous gasping during the CPR period. After three minutes the i.v. infusion, heating, i.v. anaesthesia and ventilation were discontinued and ventricular fibrillation (VF) induced by a trans-thoracic 90 V alternating current for 3 s and confirmed by an abrupt fall in aortic pressure. After 3 min of VF without intervention, standard mechanical precordial compressions were commenced at a rate of 100 min 1 for 30 s to allow the initial changes in chest configuration to occur before the zero point for the piston was set. Ventilation was provided with an adult-sized manual bag (Laerdal, Stavanger, Norway) using a gas mixture of 17% oxygen and 4% carbon dioxide, consistent with expired air from a rescue breather [17]. An impedance threshold valve (ITV Resusci-Valve, provided by CPRx LLC, Minneapolis, USA) in impedance mode was placed between the Laerdal valve and the flowsensor to prevent passive inspiratory airway flow generated by precordial compressions. Chest compression cycles were interrupted for delivery of the ventilations. CPR was performed in each pig with three different ventilation:compression ratios; 2:15, 2:50 or 5:50; varied in a randomised, cross-over design with each ratio being used for 5 min. The randomisation list was written so that performance of the different methods was evenly spread as the first, second and third method. Carotid flow, focal cerebrocortical microcirculation, all pressures, respiratory variables and arterial oxygen saturation were recorded continuously throughout the experimental period. Arterial and mixed venous blood gases were sampled at 4.5 min with each ratio. After completion of the experiment, CPR was stopped and the pig died. An autopsy was performed in all pigs to check for damage to the rib cage and internal organs and for verification of catheter placements. 2.4. Calculations All haemodynamic pressures, focal cerebrocortical microcirculation and carotid flow values were analysed by exporting the raw data into a specially constructed program designed in a mathematics software package (MATLAB† , The MathWorks Inc., Natick, MA, USA). The chest compression rate during CPR was set at 100 min 1. The sampling frequency for the pressure and flow signals were 200 Hz, hence there were 120 sampling points for each compression:decompression cycle. As
the duty cycle was 50:50, the decompression phase was defined as the period 9/30 sampling points from the middle point between two peak compressions. Early, mid and late decompressions were then defined as being the first, mid and last 20 sampling points of this period. Mean decompression represents the mean of all sampling points in the decompression phase. Coronary perfusion pressure (CPP) was calculated as the difference between thoracic aortic and right atrial pressures in the decompression phase using an electronic subtraction unit. Brain oxygen delivery (ml min 1) was computed by multiplying arterial oxygen content (Cao2) times the carotid blood flow (ml min 1). The product % PU min 1 times Cao2 was calculated as a measure of cerebrocortical oxygen supply. 2.5. Statistical analysis Statistical analysis was carried out using the statistical software package SPSS (SPSS Inc., Chicago, IL, USA). Data are presented as mean9/S.D. when normality tests were passed and median (25 /75 percentile) when these failed. Comparisons were made between the three CPR methods. Each pig served as its own control and for normally distributed continuous data of equal variance the one-way ANOVA repeated measures with pair wise multiple comparison procedures was used. For nonparametric data, and data failing the test for homogeneity of variance the Kruskal/Wallis test was used. A P value of less than 0.05 was regarded as significant.
3. Results Ventricular fibrillation (VF) was obtained in 11 pigs by the first trans-thoracic shock, while one pig needed two shocks due to insufficient electrode-skin contact. Three pigs were excluded from further analysis; one due to inadequate flow and pressure recordings, and two due to major intrapulmonary haemorrhage. In the remaining nine pigs (weight, 309/4 kg) no gross liver, lung, heart or other visceral damage was found at post mortem autopsy. ETCO2, tidal and minute ventilation were not recorded for the ratios of 2:15 and 2:50 in one pig due to malfunction of the respiratory profile program (Analysis Plus!). Arterial oxygen saturation was not obtained in two pigs. 3.1. Blood flows and oxygen delivery Mean carotid flow was significantly lower with the ratio of 5:50 than with 2:50 while 2:15 was not significantly different from either. Mean carotid blood flow during the chest compression cycles alone (exclud-
E. Dorph et al. / Resuscitation 58 (2003) 193 /201 Table 1 Internal carotid artery blood flow (ml min 1), cortical cerebral blood flow (CCBF) (% PU) and estimated oxygen delivery pre-VF and with ventilation /compression ratios 2:15, 2:50 and 5:50 including and excluding the the periods when compressions were interrupted for ventilations
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Table 2 Calculated coronary perfusion pressure, aortic, right atrial and left ventricular pressures (mmHg) with ventilation /compression ratios 2:15, 2:50 and 5:50 during standard CPR with the inspiratory impedance valve 2:15
Pre-VF Flow during compression cycles Carotid flow 1579/35 CCBF 100 Average flow per minute Carotid flow 1579/35 CCBF 100 Oxygen delivery per minute Carotid 19.29/3.8 CCBF 11759/43 a b c
2:15
2:50
2:50
5:50
42 (29 /47) 689/11 289/12
40 (25 /45) 709/10 269/11
389/11 1399/32 11 (8 /12)
359/8 1279/20 9 (2 /11)
359/10 1229/29 89/4
339/7 1159/16 89/5
20 (13 /29)
22 (12 /27)
5:50
alone 539/11 389/19
569/18 389/18
499/19 359/13
349/8 229/11
489/15c 329/16
339/13a 249/9
3.59/0.9 2539/125
2.39/0.7c 2209/126
1.89/0.8b 1739/94
P B/0.05 vs. 2:50. P B/0.05 vs. 2:15. P /0.07 vs. 2:15.
ing the periods when compressions were interrupted for ventilations) was approximately 34% of pre-arrest control with no significant difference between the methods (Table 1). Mean focal cerebrocortical microcirculation was approximately 37% of pre-VF values during compression cycles alone with no significant differences between the methods. Carotid oxygen delivery min 1 was significantly higher for the ratio of 2:15 vs. 5:50 and there was a strong trend towards the same vs. 2:50. No significant difference between methods was found concerning estimated cerebrocortical oxygen supply. 3.2. Measured pressures Mean aortic pressure was 1039/9 mmHg pre-VF and fell to approximately 38% of this level during chest compression sequences, with no significant differences between the three methods for mean and peak compression or mean decompression phase (Table 2). Mean right atrial pressure was 59/5 mmHg pre-VF and increased to 359/14 mmHg during the compression phases with ratio 2:15. There were no significant differences between the methods for mean and peak compression or mean decompression phase. Mean left ventricular pressure was 579/6 mmHg preVF and fell by 40% during CPR compression sequences with no significant differences the three methods for mean and peak compression or mean decompression phase.
Aortic pressure Mean 34 (33 /37) Peak compression 629/17 Mean decompression 259/6 Right atrial pressure Mean 359/14 Peak compression 1239/44 Mean decompression 10 (4 /12) Left ventricular pressure Mean 339/12 Peak compression 1119/36 Mean decompression 99/7 Coronary perfusion pressure Mean decompression 16 (10 /22)
All pressures are taken from the compression cycles (excluding the pauses for ventilation). Mean9/S.D. or median (25 /75 percentile).
Table 3 End-tidal CO2 (ETCO2), arterial and mixed venous blood gases during pre-VF and the three different CPR ratios (mean9/S.D.) Pre-VF
2:15
ETCO2 (kPa) 4.89/0.1 6.29/0.4 Arterial blood gas pH 7.429/0.05 7.219/0.08 5.69/0.3 7.19/0.7 pCO2 (kPa) PO2 (kPa) 38.39/6.4 8.99/1.4 BE (mmol 1) 2.29/3.7 /6.99/4.9 Mixed venous blood gas pH 7.379/0.05 7.109/0.08 pCO2 (kPa) 6.39/0.4 11.19/1.3 pO2 (kPa) 6.59/0.6 3.09/0.8 BE (mmol 1) 2.39/3.9 /6.09/5.1 a b c
2:50
5:50
7.29/0.4a
6.99/0.4a
7.149/0.07c 9.69/1.1a 5.79/0.8a /6.59/3.9
7.169/0.06 9.09/08a 5.59/1.1a /6.29/4.1
7.089/0.08 12.09/1.4 2.39/0.5c /6.49/4.4
7.089/0.07 12.29/1.5 2.29/0.5b /5.89/4.1
P B/0.001 vs. 2:15. P B/0.05 vs. 2:15. P B/0.08 vs. 2:15.
3.4. Expired CO2 concentrations, blood gases and arterial oxygen saturation The arterial pO2 and oxygen saturation were significantly lower and the end-tidal CO2 and arterial pCO2 significantly higher for ratios 2:50 and 5:50 compared with ratio 2:15. Mixed venous pO2 was significantly lower for 5:50 compared with 2:15 with a trend toward the same for 2:50 vs. 2:15 (Table 4, Fig. 1).
3.3. Calculated pressures (Table 2)
3.5. Ventilation and chest compressions (Table 4)
There were no significant differences in coronary perfusion pressure during the chest compression cycles between the three methods (Table 3).
Pauses for ventilation were 4.99/0.3 and 13.59/0.8 s for two and five breaths, respectively. There were no differences in tidal volumes between the ratios. The
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Table 4 Ventilation and chest compressions with different ventilation /compression ratios
Tidal volume (ml) Breaths per minute Minute ventilation (l) Actual compressions per minute
2:15
2:50
5:50
6949/98 8.69/0.2 6.09/0.6 649/2
6969/103 3.49/0.04a 2.49/0.3a 869/1a
6819/73 6.99/0.2 4.79/0.2 669/2
Mean9/S.D. a P B/0.001 vs. 2:15 and 5:50.
Fig. 1. Arterial oxygen saturation during compression cycles for different CPR ratios at the time of arterial and venous blood gas sampling. Median (25 /75 percentile).
number of breaths per minute and the minute ventilation were significantly greater with ratio 2:15 than with the two other ratios. The number of chest compressions minute was significantly higher with ratio 2:50 compared to ratios 2:15 and 5:50.
4. Discussion In this experimental model of basic CPR a ventilation:compression ratio of 2:15 was clearly superior to the ratios 2:50 and 5:50 regarding pulmonary gas exchange (arterial oxygenation and carbon dioxide removal), while 2:50 tended to give the best circulation. Thus while the arterial oxygen saturation stayed above 80% throughout CPR for 2:15, it dropped below 40% during part of the ventilation:compression cycle in both the other two ratios. On the other hand, the ratio of 2:50 produced 30% more chest compressions per minute than either of the two other methods, with a parallel higher carotid blood flow per minute than 5:50 and there was a tendency to the same vs. 2:15 (P /0.07), and for the brain microcirculatory minute flows. The main purpose of basic CPR is to deliver oxygenated blood to the brain and heart until spontaneous circulation can resume. The oxygen delivery depends both on the blood flow and its oxygen content. The optimum ventilation:compression ratio therefore
cannot be determined from one of these factors alone. Well-oxygenated blood is of no help if it does not reach the tissues. While the oxygen content appears best with 2:15, and the cerebral circulation best with 2:50, the oxygen delivery calculated from both factors therefore might indicate the optimal CPR method best. The oxygen delivery to the brain was highest with the ratio of 2:15, significantly higher than for 5:50 with a strong trend vs. 2:50 (P /0.07). In parallel, the central venous oxygenation, which gives some indication of tissue oxygenation [18], was higher for 2:15 than for both 5:50 and 2:50. Clinically, the optimum method for coordinating mouth-to-mouth ventilation and chest compressions has not been established. Early experimental studies suggested a ventilation:compression ratio of 1:4 [19,20]. The presently recommended ventilation:compression ratio of 2:15 [1] was initially based on a study [21] in anaesthetised patients with normal circulation where two inflations every 15 s with exhaled air gave a mean PaO2 of 79 mmHg (10.5 kPa). Results from dogs with a chest compression rate of 60 per minute and a clamped tracheal tube with pauses when the tube was opened for ‘quick’ ventilations with air were reported in the same paper [21]. A ventilation/compression ratio of 3:15 gave a mean arterial oxygen saturation of 90 vs. 75% for a ratio of 6:30. These data fit well with ours with the 6:30 saturation being intermediate between ours for 2:15 and 5:50. In contrast, computer simulations of blood flow and gas exchange during CPR have indicated that the ratios 2:15 and 5:50 should be approximately equivalent in terms of gas exchange and predicted noticeably less severe hypoxia and hypercarbia than seen in our experiment [22]. This discrepancy could be explained by the fact that computer simulation models do not include the increased physiological shunting caused by pulmonary contusion, deflation or congestion, or the thoracic configurational changes seen in actual resuscitations [14,23,24]. Our data on carotid and cerebrocortical blood flows agree with the simulation prediction that cardiac output would be approximately equal for 2:15 and 5:50 ratios [22]. Recently, a three-staged approach to CPR has been suggested [7]. The first involves chest-compression-only CPR, the second introduces rescue breaths with a ventilation:compression ratio of 5:50, and the third is a conversion to standard ratio (2:15) CPR. This idea was supported by findings by Chamberlain et al. [10] of about 50% more compressions per minute for 5:50 compared with 2:15 for single rescuer CPR on manikins. In the present study 5:50 gave worse gas exchange with no better circulation than 2:15, and the gas-exchange was no better for 5:50 than for 2:50, which gave better circulation. It is important to note that our results came under ideal circumstances that cannot automatically be
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extrapolated to the clinical situation with lay rescuers, and the difference in results from Chamberlain et al. [10] might be explained by this. In their study [10] the mean duration of pauses between compressions was 16 and 30 s for two and five ventilations respectively (or 8 and 5 s per ventilation). This combined with a lower ventilation:compression ratio of 5:50 explained the reported overall 50% gain in the number of chest compressions per minute vs. 2:15. In the present study, accurate compressions were given by a mechanical device that does not tire, and the pigs were ventilated via a tracheal tube with no time lost changing between compressions and ventilations. Thus although the time interval for two ventilations of mean 4.9 s in the present study and 649/2 compressions given per minute comply well with the guidelines [1], many publications, in addition to the one by Chamberlain et al. [10], indicate that persons trained in basic CPR are unable to follow these guidelines even a few months after taking a course [5,6,25]. At the same time recently, and well trained, individuals have been able to follow the guidelines and achieved 50 /64 compressions and 7 /8 rescue breaths per minute even with single rescuer 2:15 CPR on manikins [26 /28]. Therefore it might seem reasonable to suggest that well trained professional personnel should continue with 2:15 at present. The findings in the present study that 5:50 provided the same gas exchange but significantly less chest compressions and blood flow than 2:50 can indicate that the suggested staged approach to CPR might benefit from changing the second stage 5:50 ratio to 2:50. This is also in accordance with a recent mathematical analysis suggesting that a 2:50 ventilation:compression ratio is adequate for one- and two-rescuer basic CPR [29]. What about ratio 2:15 compared with 2:50? If a layperson requires a 16 s break in the compressions for two mouth-to-mouth ventilations, there will be no circulation for 60% and 35% of the total resuscitation time for the ratios 2:15 and 2:50, respectively. Although CPR is a compromise between provision of blood flow and ventilation, 60% of the time without circulation seems unacceptably low. At the same time the mean blood oxygen content with 2:50 or 5:50 was only a little more than half of the content achieved with 2:15. It could be speculated that 2:30 might be a better compromise. The oxygen saturation data in the present study indicate that the drastic drop in blood oxygenation takes place after approximately 30 compressions, and Babbs et al. [29] have predicted that 2:30 might be the optimal ratio based on theoretical considerations. If this is the case there would be no need for the third stage suggested by Assar et al. [7]. First stage continuous compressions without ventilation, second stage 2:30, and with advanced CPR in intubated patients contin-
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uous compressions with interposed ventilations could be advocated. There are many previous experimental studies of gas exchange and acid /base status during CPR, but differences in species, non-intervention time intervals, modes of ventilation, gas mixture used for ventilation, coordination of ventilation to compression, compression method, and timing of blood gas determinations make comparisons difficult. Only studies with a gas mixture mimicking exhaled air seem appropriate for basic life support with mouth-to-mouth or mouth-to-mask ventilation [11,30/32]. For standard ratio CPR these experimental studies report PaO2 values of 10.2 /13.4 kPa after 5.5 /9 min of CPR, with PaCO2 2.8 /4.4 kPa, pHa 7.4 /7.5, mixed venous blood PvO2 1.9 /2.7, PvCO2 7.6 / 9.3, and pHv/7.21 /7.25. All the above studies allowed chest compression induced and gasping ventilations, which must have occurred with ambient air to explain why their PaCO2 values were at the same level or lower than the 4 kPa in the gas mixture used for active ventilation on those studies. Our study was designed to eliminate the influence of both gasping and a patent airway during CPR, thus mimicking closely the most common real life cardiac arrest scenario with upper airway obstruction precluding chest compression induced ventilation [19] and no gasping respiration [33,34]. These differences in model design can explain why our animals had more hypoxic, hypercapnic and acidotic arterial and central venous blood gases compared with the results reported above for the same 2:15 ventilation to compression ratio. The blood gases for the ratios 5:50 and 2:50 are rather disturbing as a number of animal and human studies indicate that arterial hypercapnic and metabolic acidosis, as well as arterial hypoxemia have adverse effects on resuscitation from cardiac arrest [35 /40]. On the other hand, several animal studies suggest that the addition of ventilation during the initial minutes after cardiac arrest does not improve the outcome [11 /13,30]. In the study by Kern et al. [11] nonventilated animals had no better blood gases than those that we found with the 2:50 and 5:50 ratios, and much worse than in their animals receiving ventilation. The optimal ventilation /compression ratios for various durations of basic CPR are therefore unknown. The end-tidal CO2 (ETCO2) value was significantly lower for ratio 2:15 compared with both other ratios. Since the ETCO2 can be affected by ventilation as well as perfusion [18,41,42], it is difficult to analyze this difference further. The higher ETCO2 with ratio 5:50 than 2:15 could represent a combined effect of a tendency to better blood flow and less ventilation, whereas for 2:50 it might be due to the reduction in ventilation alone. The mean ETCO2 value of 6.2 kPa with ratio 2:15 in this study is much higher than the 3.6 kPa reported by Kern et al. for the same 2:15 ratio with
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the same inhalation gas which included 4 kPa CO2 [11]. As for the blood gases, the fact that the ETCO2 values were lower than in the inhaled air mixture used, must be due to ambient air ventilation occurring with chest compressions through the open airway in their study. In conclusion, a ventilation:compression ratio of 2:15 in this experimental model of ideal basic CPR gave better pulmonary gas exchange and cerebral oxygen delivery than both the ratios 2:50 and 5:50. Continuous arterial oxygen saturation tracings indicated that ratio 2:30 might be an even more optimal ventilation:compression ratio. Further investigations are needed to define the best method for coordinating ventilation and chest compressions during real CPR.
[11]
[12]
[13]
[14]
[15]
Acknowledgements This work was supported by grants from the Laerdal Foundation for Acute Medicine, the Jahre Foundation and the Norwegian Air Ambulance.
[16]
[17]
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E. Dorph et al. / Resuscitation 58 (2003) 193 /201 [30] Berg RA, Kern KB, Hilwig RW, Ewy GA. Assisted ventilation during ‘bystander’ CPR in a swine acute myocardial infarction model does not improve outcome. Circulation 1997;96:4364 /71. [31] Berg RA, Kern KB, Hilwig RW, Berg MD, Sanders AB, Otto CW, et al. Assisted ventilation does not improve outcome in a porcine model of single-rescuer bystander cardiopulmonary resuscitation. Circulation 1997;95:1635 /41. [32] Sanders AB, Kern KB, Berg RA, Hilwig RW, Heidenrich J, Ewy GA. Survival and neurologic outcome after cardiopulmonary resuscitation with four different chest compression /ventilation ratios. Ann Emerg Med 2002;40:553 /62. [33] Van Hoeyweghen RJ, Bossaert LL, Mullie A, Calle P, Martens P, Buylaert WA, et al. Quality and efficiency of bystander CPR. Belgian Cerebral Resuscitation Study Group. Resuscitation 1993;26:47 /52. [34] Clark JJ, Larsen MP, Culley LL, Graves JR, Eisenberg MS. Incidence of agonal respirations in sudden cardiac arrest. Ann Emerg Med 1992;21:1464 /7. [35] Idris AH, Wenzel V, Becker LB, Banner MJ, Orban DJ. Does hypoxia or hypercarbia independently affect resuscitation from cardiac arrest? Chest 1995;108:522 /8.
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Quality of CPR with three different ventilation:compression ratios E. Dorph a,b,*, L. Wik c, T.A. Strømme b, M. Eriksen b, P.A. Steen d a
Norwegian Air Ambulance, N-1441 Drøbak, Norway Institute for Experimental Medical Research, Ulleva˚l University Hospital, N-0407 Oslo, Norway c National Centre of Competence for Emergency Medicine, Ulleva˚l University Hospital, N-0407 Oslo, Norway d Division of Emergency Medical Services, Ulleva˚l University Hospital, N-0407 Oslo, Norway b
Received 29 January 2003; received in revised form 26 March 2003; accepted 31 March 2003
Abstract Current adult basic cardiopulmonary resuscitation (CPR) guidelines recommend a 2:15 ventilation:compression ratio, while the optimal ratio is unknown. This study was designed to compare arterial and mixed venous blood gas changes and cerebral circulation and oxygen delivery with ventilation:compression ratios of 2:15, 2:50 and 5:50 in a model of basic CPR. Ventricular fibrillation (VF) was induced in 12 anaesthetised pigs, and satisfactory recordings were obtained from 9 of them. A non-intervention interval of 3 min was followed by CPR with pauses in compressions for ventilation with 17% oxygen and 4% carbon dioxide in a randomised, crossover design with each method being used for 5 min. Pulmonary gas exchange was clearly superior with a ventilation:compression ratio of 2:15. While the arterial oxygen saturation stayed above 80% throughout CPR for 2:15, it dropped below 40% during part of the ventilation:compression cycle for both the other two ratios. On the other hand, the ratio 2:50 produced 30% more chest compressions per minute than either of the two other methods. This resulted in a mean carotid flow that was significantly higher with the ratio of 2:50 than with 5:50 while 2:15 was not significantly different from either. The mean cerebrocortical microcirculation was approximately 37% of pre-VF levels during compression cycles alone with no significant differences between the methods. The oxygen delivery to the brain was higher for the ratio of 2:15 than for either 5:50 or 2:50. In parallel the central venous oxygenation, which gives some indication of tissue oxygenation, was higher for the ratio of 2:15 than for both 5:50 and 2:50. As the compressions were done with a mechanical device with only 2 /3 s pauses per ventilation, the data cannot be extrapolated to laypersons who have great variations in quality of CPR. However, it might seem reasonable to suggest that basic CPR by professionals should continue with ratio of 2:15 at present if it can be shown that similar brief pauses for ventilation can be achieved in clinical practice. # 2003 Elsevier Ireland Ltd. All rights reserved. Keywords: CPR; Ratios; Gas exchange; Oxygen delivery
Resumo A Reanimac¸a˜o cardio-pulmonar ba´sica corrente do adulto recomenda uma relac¸a˜o ventilac¸a˜o: compressa˜o 2:15, embora a relac¸a˜o o´ptima seja desconhecida. Este estudo foi delineado para comparar as alterac¸o˜es nos gases sanguı´neos arterial e venoso misto, a circulac¸a˜o cerebral e o aporte de oxige´nio com relac¸o˜es ventilac¸a˜o: compressa˜o de 2:15, 2:50 e 5:50 num modelo de RCP ba´sica. Foi induzida Fibrilhac¸a˜o Ventricular (FV) em 12 porcos anestesiados, e foram obtidos registos satisfato´rios em 9 deles. Apo´s um intervalo sem intervenc¸a˜o de 3 minutos, realizou-se RCP com pausa nas compresso˜es para ventilar com Oxige´nio a 17% e dio´xido de carbono a 4% num estudo cruzado, randomizado, com cada relac¸a˜o ventilac¸a˜o: compressa˜o a ser utilizado durante 5 minutos. As trocas gasosas pulmonares foram claramente superiores com uma relac¸a˜o ventilac¸a˜o: compressa˜o de 2:15. A saturac¸a˜o do oxige´nio arterial ficou acima dos 80% ao longo da RCP com relac¸a˜o de 2:15, enquanto que esta desceu abaixo dos 40% durante parte do ciclo de ventilac¸a˜o: compressa˜o para as outras duas relac¸o˜es. Por outro lado, a relac¸a˜o 2:50 produziu 30% mais compresso˜es tora´cicas por minuto que qualquer um dos outros dois me´todos. Isto resultou num fluxo carotı´deo me´dio que foi significativamente mais elevado com a relac¸a˜o 2:50 do que 5:50, enquanto que a relac¸a˜o 2:15 na˜o condicionou alterac¸o˜es significativamente diferentes de ambas. A microcirculac¸a˜o cerebrocortical me´dia foi aproximadamente 37% dos nı´veis pre´-FV
* Corresponding author. Tel.: /47-230-16813; fax: /47-230-16799. E-mail address: [email protected] (E. Dorph). 0300-9572/03/$ - see front matter # 2003 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/S0300-9572(03)00125-4
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durante os ciclos de compressa˜o sem nenhuma diferenc¸a significativa entre os me´todos. O aporte de oxige´nio ao ce´rebro foi mais elevado para a relac¸a˜o2:15 do que para as outras duas relac¸o˜es 5:50 ou 2:50. Em paralelo a oxigenac¸a˜o venosa central, que da´ alguma indicac¸a˜o da oxigenac¸a˜o tecidular, foi mais elevada para a relac¸a˜o 2:15 do que para as outras duas. Estes resultados na˜o podem ser extrapolados para a RCP realizada por leigos que teˆm grande variac¸a˜o na qualidade da RCP, uma vez que as compresso˜es foram realizadas com um aparelho mecaˆnico com apenas 2-3 s de pausa para a ventilac¸a˜o. Contudo parece ser razoa´vel sugerir que a RCP ba´sica realizada por profissionais deve continuar com uma relac¸a˜o de2:15, se for possı´vel obter na pra´tica clı´nica pausas breves similares para a ventilac¸a˜o. # 2003 Elsevier Ireland Ltd. All rights reserved. Palavras chave: RCP; Relac¸a˜o Ventilac¸a˜o:Compressa˜o; Trocas gasosas; Aporte de oxige´nio
Resumen Las actuales guı´as de reanimacio´n cardiopulmonar ba´sica (RCP) recomiendan una relacio´n ventilacio´n: compresio´n de 2:15, en circunstancia que la relacio´n o´ptima es au´n desconocida. Este estudio fue disen˜ado para comparar los cambios en gases arteriales y en sangre venosa mezclada, en la circulacio´n cerebral y en la entrega de oxı´geno con distintas relaciones ventilacio´n compresio´n de 2:15, 2:50 y de 5:50 en un modelo ba´sico de RCP. Se indujo fibrilacio´n ventricular (VF) en 12 cerdos anestesiados, y se obtuvieron registros satisfactorios de 9 de ellos. Despue´s de un intervalo de no intervencio´n de tres minutos se realizo´ RCP con pausas en la compresio´n para realizar la ventilacio´n con oxı´geno al 17% y 4% de dio´xido de carbono en un disen˜o cruzado, randomizado siendo cada me´todo usado por 5 minutos. El intercambio gaseoso pulmonar fue claramente superior con una relacio´n ventilacio´n compresio´n de 2:15. Mientras la saturacio´n de oxı´geno se mantuvo sobre 80% a lo largo de la RCP 2:15, cayo´ bajo 40% durante parte del ciclo ventilacio´n compresio´n en ambas de las relaciones restantes. Por otro lado, la relacio´n 2:50 produjo 30% mas compresiones por minuto que cualquiera de los otros me´todos. Esto resulto´ en un flujo carotı´deo medio que fue significativamente mas alto con la relacio´n 2:50 que con 5:50 mientras que 2:15 no fue significativamente diferente de ninguno de los otros me´todos. La microcirculacio´n cerebral media fue aproximadamente 37% de los niveles previos a la VF durantes los ciclos de solo compresio´n sin diferencias significativas entre los distintos me´todos. La entrega de oxı´geno al cerebro fue mayor para la relacio´n de 2:15 que para ya sea 5:50 o´ 2:50. Paralelamente la oxigenacio´n venosa central, que da alguna indicacio´n de oxigenacio´n tisular, fue mas alta para la relacio´n 2:15 que para ambas 5:50 y 2:50. Como las compresiones fueron realizadas con un aparato meca´nico con solo 2-3 pausas para ventilacio´n, los datos no pueden ser extrapolados a personas que tienen gran variacio´n en calidad de RCP. Sin embargo, pareciera razonable sugerir que la RCP ba´sica por profesionales debiera seguir con relacio´n2:15 en este momento si se puede mostrar que en la pra´ctica clı´nica pueden lograrse pausas para ventilacio´n similarmente cortas. # 2003 Elsevier Ireland Ltd. All rights reserved. Palabras clave: RCP; Relacio´n ventilacio´n compresio´n; Intercambio gaseoso; Entrega de oxı´geno
1. Introduction The optimal ratio of ventilations to chest compressions during cardiopulmonary resuscitation (CPR) is unknown. Current guidelines for adult CPR by one or two lay rescuers is based on a combination of chest compressions and mouth-to-mouth ventilations with a 2:15 ventilation:compression ratio [1]. Recently, the issue of the most advantageous ventilation:compression ratio has been the focus of renewed attention because both lay and professional rescuers are reluctant to perform mouth-to-mouth ventilation mainly due to concerns of contracting infectious diseases [2 /4]. In addition, standard basic CPR is a complex psychomotor task difficult to learn and perform without such complications as gastric inflation [5,6]. Moreover, the relatively long pauses in chest compression required for ventilation result in disturbingly long interruptions in circulation during CPR, which appear potentially to compromise the success of cardiac resuscitation [7 /9]. Consequently, some researchers have begun to explore other ventilation:compression ratios with much
longer series of uninterrupted compressions such as 5:50 [7,10] or even chest compression only CPR [11 /13]. During longer periods of CPR it has been stated that some ventilatory support is critical for successful resuscitation outcomes [14]. It therefore seems appropriate to investigate alternative ventilation:compression ratios with longer sequences of chest compressions, and the present study was designed to determine haemodynamics and oxygen delivery with three different ratios of ventilation and chest compressions in an experimental porcine model of basic CPR.
2. Materials and methods 2.1. Animal preparation The experiments were conducted in accordance with ‘Regulations on Animal Experimentation’ under The Norwegian Animal Welfare Act and approved by Norwegian Animal Research Authority. Twelve healthy domestic swine of either sex were fasted over night
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except for free access to water. The animals were sedated with ketamine (20 mg kg 1) and atropine 1 mg intramuscularly and then placed supine in a U-shaped cradle with an external heating blanket interposed between the back and the cradle. The limbs were secured to prevent body displacement during the performance of CPR. A catheter was placed in an ear vein and bolus injections of sodium pentobarbital (15 mg kg 1) and morphine 10 mg were given intravenously (i.v.) followed by an infusion at a rate of 10/15 and 0.4 /0.5 mg kg 1 h 1, respectively to maintain adequate anaesthesia as judged by heart rate, blood pressure, spontaneous respiration, and the canthal reflex. The ear vein catheter was also used for infusion of 25 ml kg 1 h 1 warmed Ringer acetate throughout the preparation period. A midline incision was made in the anterior neck and an 8.0 mm tracheal tube secured within the trachea via a tracheostomy incision. Prior to CPR the pig was ventilated with a volume-controlled ventilator (Servo Ventilator 900 B, Siemens-Elema AB, Solna, Sweden). Initial tidal volume was 15 ml kg 1, the respiratory rate 16 breaths min 1 and the inspired oxygen fraction 0.5. Tidal volume was adjusted to maintain the end-tidal carbon dioxide (ETCO2) at 59/0.5 kPa as measured by the gas monitor (Datex Capnomac UltimaTM, Helsinki, Finland). Urine was drained continuously through a cystostoma, and the intra-abdominal temperature was maintained at 399/0.5 8C throughout the experimental period. A 7F micro-tip pressure transducer catheter (Model SPC 470, Millar Instruments, Houston, TX, USA) was inserted through the right femoral artery and advanced to the descending aorta at the level of the heart for arterial pressure recordings. Another 7F micro-tip pressure transducer catheter (Millar Instruments) was introduced to the left ventricle through the left common carotid artery to measure the left ventricular pressure. A 7F Swan-Ganz† catheter (model 131HF7, Baxter Healthcare Corporation, Irvine, CA, USA) was advanced through the right femoral vein and flow directed into the right atrium for pressure recordings and mixed venous blood sampling. A 7.5F Swan-Ganz† CCOmbo catheter (model 744HF75, Edwards Lifesciences LLC, Irvine, CA, USA) was inserted into the descending aorta for arterial blood sampling and for continuous recording of arterial oxygen saturation. After ligation of all visible branches of the right common carotid artery except the internal carotid artery a transit time perivascular flowprobe (model 3SB880, Transonic Systems Inc, Ithaca, NY, USA) was placed on the artery. All invasive catheters were introduced using a cut-down technique. To monitor cerebral perfusion the technique of laserDoppler flowmetry (LDF) was applied. This method allows continuous measurement of focal microcirculatory blood flow and the LDF readings are expressed in arbitrary perfusion units (PU) [15,16].
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The right parietal region of the skull was exposed. A burr hole of 12/15 mm in diameter was drilled in the cranium using an electric drill (Dremel† Minicraft, Germany) at low speed. A gentle saline drip (0.9%, 25 8C) over the drilling site prevented thermal injury to the cortex. The centre of the hole was located 12/15 mm lateral to the sagittal suture and 12/15 mm caudal to the coronal suture. The dura was opened and the laserDoppler probe (model 407. Perimed AB, Stockholm, Sweden), connected to a perfusion monitor (PeriFlux System 5000, Perimed AB, Stockholm, Sweden), with probe holder (model PH 07-4, Perimed AB, Stockholm, Sweden) was secured in a position carefully chosen to avoid visible pial vessels. The Swan-Ganz catheter in the right atrium and the side port lumen of the micro-tip transducer catheter in the descending aorta were connected to fluid filled transducers (Statham† P23Dd, Gould Instruments, Hato Rey, Puerto Rico). Tidal volumes, respiratory pattern and ETCO2 were measured continuously using a combined differential pressure pneumotach flow sensor and solid state CO2 sensor in combination with a respiratory profile monitor (CO2SMO Plus! Model 8100, Novametrix Medical System Inc., Wallingford, CT, USA). The flow/CO2 sensor was inserted in the breathing circuit between the ventilator and a bacterial filter connected to the tracheal tube. The monitor was connected on-line to a computer (Omnibook 6000, Hewlett Packard Company, Cupertino, CA, USA) into which the data were downloaded, stored and analysed using Analysis Plus! version 3.0 Software package (Novametrix Medical System Inc.). Pressures, carotid flow signals and laser-Doppler flow signals were sampled using PC-based real time data acquisition hardware (DaqBoardsTM Model 200A, IOtech, Inc., Cleveland, OH, USA) supported with software for DASYLab version 5.1 (Datalog, National Instruments company, Moenchengladbach, Germany) and printed on an eight-channel thermal array recorder model TA 11 (Gould Instrument Systems, Inc., OH, USA). Arterial oxygen saturation was recorded using the Swan-Ganz† CCOmbo catheter connected to a continuous oximetry monitor (Vigilance† , Edwards Critical-Care Division, Irvine, CA, USA). Specimens for arterial blood gas analysis were obtained from the descending aorta, for mixed venous blood gas analysis from the right atrium, and measured directly with a blood gas analyser (AVL OMNITM 9, Graz, Austria).
2.2. Machinery Standard chest compression was achieved using a modified automatic hydraulic battery driven chest compression device (Heartsaver 2000† , Medreco, Bodø, Norway) with equal compression /relaxation
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phases. The piston movement was photoelectrically controlled. Compression depth was set at 4 cm. 2.3. Experimental protocol After collecting all necessary baseline (pre-VF) data, pancuronium (Pavulon† , N.V. Organon, Oss, Netherlands) 0.2 mg kg1 was administered to prevent spontaneous gasping during the CPR period. After three minutes the i.v. infusion, heating, i.v. anaesthesia and ventilation were discontinued and ventricular fibrillation (VF) induced by a trans-thoracic 90 V alternating current for 3 s and confirmed by an abrupt fall in aortic pressure. After 3 min of VF without intervention, standard mechanical precordial compressions were commenced at a rate of 100 min 1 for 30 s to allow the initial changes in chest configuration to occur before the zero point for the piston was set. Ventilation was provided with an adult-sized manual bag (Laerdal, Stavanger, Norway) using a gas mixture of 17% oxygen and 4% carbon dioxide, consistent with expired air from a rescue breather [17]. An impedance threshold valve (ITV Resusci-Valve, provided by CPRx LLC, Minneapolis, USA) in impedance mode was placed between the Laerdal valve and the flowsensor to prevent passive inspiratory airway flow generated by precordial compressions. Chest compression cycles were interrupted for delivery of the ventilations. CPR was performed in each pig with three different ventilation:compression ratios; 2:15, 2:50 or 5:50; varied in a randomised, cross-over design with each ratio being used for 5 min. The randomisation list was written so that performance of the different methods was evenly spread as the first, second and third method. Carotid flow, focal cerebrocortical microcirculation, all pressures, respiratory variables and arterial oxygen saturation were recorded continuously throughout the experimental period. Arterial and mixed venous blood gases were sampled at 4.5 min with each ratio. After completion of the experiment, CPR was stopped and the pig died. An autopsy was performed in all pigs to check for damage to the rib cage and internal organs and for verification of catheter placements. 2.4. Calculations All haemodynamic pressures, focal cerebrocortical microcirculation and carotid flow values were analysed by exporting the raw data into a specially constructed program designed in a mathematics software package (MATLAB† , The MathWorks Inc., Natick, MA, USA). The chest compression rate during CPR was set at 100 min 1. The sampling frequency for the pressure and flow signals were 200 Hz, hence there were 120 sampling points for each compression:decompression cycle. As
the duty cycle was 50:50, the decompression phase was defined as the period 9/30 sampling points from the middle point between two peak compressions. Early, mid and late decompressions were then defined as being the first, mid and last 20 sampling points of this period. Mean decompression represents the mean of all sampling points in the decompression phase. Coronary perfusion pressure (CPP) was calculated as the difference between thoracic aortic and right atrial pressures in the decompression phase using an electronic subtraction unit. Brain oxygen delivery (ml min 1) was computed by multiplying arterial oxygen content (Cao2) times the carotid blood flow (ml min 1). The product % PU min 1 times Cao2 was calculated as a measure of cerebrocortical oxygen supply. 2.5. Statistical analysis Statistical analysis was carried out using the statistical software package SPSS (SPSS Inc., Chicago, IL, USA). Data are presented as mean9/S.D. when normality tests were passed and median (25 /75 percentile) when these failed. Comparisons were made between the three CPR methods. Each pig served as its own control and for normally distributed continuous data of equal variance the one-way ANOVA repeated measures with pair wise multiple comparison procedures was used. For nonparametric data, and data failing the test for homogeneity of variance the Kruskal/Wallis test was used. A P value of less than 0.05 was regarded as significant.
3. Results Ventricular fibrillation (VF) was obtained in 11 pigs by the first trans-thoracic shock, while one pig needed two shocks due to insufficient electrode-skin contact. Three pigs were excluded from further analysis; one due to inadequate flow and pressure recordings, and two due to major intrapulmonary haemorrhage. In the remaining nine pigs (weight, 309/4 kg) no gross liver, lung, heart or other visceral damage was found at post mortem autopsy. ETCO2, tidal and minute ventilation were not recorded for the ratios of 2:15 and 2:50 in one pig due to malfunction of the respiratory profile program (Analysis Plus!). Arterial oxygen saturation was not obtained in two pigs. 3.1. Blood flows and oxygen delivery Mean carotid flow was significantly lower with the ratio of 5:50 than with 2:50 while 2:15 was not significantly different from either. Mean carotid blood flow during the chest compression cycles alone (exclud-
E. Dorph et al. / Resuscitation 58 (2003) 193 /201 Table 1 Internal carotid artery blood flow (ml min 1), cortical cerebral blood flow (CCBF) (% PU) and estimated oxygen delivery pre-VF and with ventilation /compression ratios 2:15, 2:50 and 5:50 including and excluding the the periods when compressions were interrupted for ventilations
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Table 2 Calculated coronary perfusion pressure, aortic, right atrial and left ventricular pressures (mmHg) with ventilation /compression ratios 2:15, 2:50 and 5:50 during standard CPR with the inspiratory impedance valve 2:15
Pre-VF Flow during compression cycles Carotid flow 1579/35 CCBF 100 Average flow per minute Carotid flow 1579/35 CCBF 100 Oxygen delivery per minute Carotid 19.29/3.8 CCBF 11759/43 a b c
2:15
2:50
2:50
5:50
42 (29 /47) 689/11 289/12
40 (25 /45) 709/10 269/11
389/11 1399/32 11 (8 /12)
359/8 1279/20 9 (2 /11)
359/10 1229/29 89/4
339/7 1159/16 89/5
20 (13 /29)
22 (12 /27)
5:50
alone 539/11 389/19
569/18 389/18
499/19 359/13
349/8 229/11
489/15c 329/16
339/13a 249/9
3.59/0.9 2539/125
2.39/0.7c 2209/126
1.89/0.8b 1739/94
P B/0.05 vs. 2:50. P B/0.05 vs. 2:15. P /0.07 vs. 2:15.
ing the periods when compressions were interrupted for ventilations) was approximately 34% of pre-arrest control with no significant difference between the methods (Table 1). Mean focal cerebrocortical microcirculation was approximately 37% of pre-VF values during compression cycles alone with no significant differences between the methods. Carotid oxygen delivery min 1 was significantly higher for the ratio of 2:15 vs. 5:50 and there was a strong trend towards the same vs. 2:50. No significant difference between methods was found concerning estimated cerebrocortical oxygen supply. 3.2. Measured pressures Mean aortic pressure was 1039/9 mmHg pre-VF and fell to approximately 38% of this level during chest compression sequences, with no significant differences between the three methods for mean and peak compression or mean decompression phase (Table 2). Mean right atrial pressure was 59/5 mmHg pre-VF and increased to 359/14 mmHg during the compression phases with ratio 2:15. There were no significant differences between the methods for mean and peak compression or mean decompression phase. Mean left ventricular pressure was 579/6 mmHg preVF and fell by 40% during CPR compression sequences with no significant differences the three methods for mean and peak compression or mean decompression phase.
Aortic pressure Mean 34 (33 /37) Peak compression 629/17 Mean decompression 259/6 Right atrial pressure Mean 359/14 Peak compression 1239/44 Mean decompression 10 (4 /12) Left ventricular pressure Mean 339/12 Peak compression 1119/36 Mean decompression 99/7 Coronary perfusion pressure Mean decompression 16 (10 /22)
All pressures are taken from the compression cycles (excluding the pauses for ventilation). Mean9/S.D. or median (25 /75 percentile).
Table 3 End-tidal CO2 (ETCO2), arterial and mixed venous blood gases during pre-VF and the three different CPR ratios (mean9/S.D.) Pre-VF
2:15
ETCO2 (kPa) 4.89/0.1 6.29/0.4 Arterial blood gas pH 7.429/0.05 7.219/0.08 5.69/0.3 7.19/0.7 pCO2 (kPa) PO2 (kPa) 38.39/6.4 8.99/1.4 BE (mmol 1) 2.29/3.7 /6.99/4.9 Mixed venous blood gas pH 7.379/0.05 7.109/0.08 pCO2 (kPa) 6.39/0.4 11.19/1.3 pO2 (kPa) 6.59/0.6 3.09/0.8 BE (mmol 1) 2.39/3.9 /6.09/5.1 a b c
2:50
5:50
7.29/0.4a
6.99/0.4a
7.149/0.07c 9.69/1.1a 5.79/0.8a /6.59/3.9
7.169/0.06 9.09/08a 5.59/1.1a /6.29/4.1
7.089/0.08 12.09/1.4 2.39/0.5c /6.49/4.4
7.089/0.07 12.29/1.5 2.29/0.5b /5.89/4.1
P B/0.001 vs. 2:15. P B/0.05 vs. 2:15. P B/0.08 vs. 2:15.
3.4. Expired CO2 concentrations, blood gases and arterial oxygen saturation The arterial pO2 and oxygen saturation were significantly lower and the end-tidal CO2 and arterial pCO2 significantly higher for ratios 2:50 and 5:50 compared with ratio 2:15. Mixed venous pO2 was significantly lower for 5:50 compared with 2:15 with a trend toward the same for 2:50 vs. 2:15 (Table 4, Fig. 1).
3.3. Calculated pressures (Table 2)
3.5. Ventilation and chest compressions (Table 4)
There were no significant differences in coronary perfusion pressure during the chest compression cycles between the three methods (Table 3).
Pauses for ventilation were 4.99/0.3 and 13.59/0.8 s for two and five breaths, respectively. There were no differences in tidal volumes between the ratios. The
E. Dorph et al. / Resuscitation 58 (2003) 193 /201
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Table 4 Ventilation and chest compressions with different ventilation /compression ratios
Tidal volume (ml) Breaths per minute Minute ventilation (l) Actual compressions per minute
2:15
2:50
5:50
6949/98 8.69/0.2 6.09/0.6 649/2
6969/103 3.49/0.04a 2.49/0.3a 869/1a
6819/73 6.99/0.2 4.79/0.2 669/2
Mean9/S.D. a P B/0.001 vs. 2:15 and 5:50.
Fig. 1. Arterial oxygen saturation during compression cycles for different CPR ratios at the time of arterial and venous blood gas sampling. Median (25 /75 percentile).
number of breaths per minute and the minute ventilation were significantly greater with ratio 2:15 than with the two other ratios. The number of chest compressions minute was significantly higher with ratio 2:50 compared to ratios 2:15 and 5:50.
4. Discussion In this experimental model of basic CPR a ventilation:compression ratio of 2:15 was clearly superior to the ratios 2:50 and 5:50 regarding pulmonary gas exchange (arterial oxygenation and carbon dioxide removal), while 2:50 tended to give the best circulation. Thus while the arterial oxygen saturation stayed above 80% throughout CPR for 2:15, it dropped below 40% during part of the ventilation:compression cycle in both the other two ratios. On the other hand, the ratio of 2:50 produced 30% more chest compressions per minute than either of the two other methods, with a parallel higher carotid blood flow per minute than 5:50 and there was a tendency to the same vs. 2:15 (P /0.07), and for the brain microcirculatory minute flows. The main purpose of basic CPR is to deliver oxygenated blood to the brain and heart until spontaneous circulation can resume. The oxygen delivery depends both on the blood flow and its oxygen content. The optimum ventilation:compression ratio therefore
cannot be determined from one of these factors alone. Well-oxygenated blood is of no help if it does not reach the tissues. While the oxygen content appears best with 2:15, and the cerebral circulation best with 2:50, the oxygen delivery calculated from both factors therefore might indicate the optimal CPR method best. The oxygen delivery to the brain was highest with the ratio of 2:15, significantly higher than for 5:50 with a strong trend vs. 2:50 (P /0.07). In parallel, the central venous oxygenation, which gives some indication of tissue oxygenation [18], was higher for 2:15 than for both 5:50 and 2:50. Clinically, the optimum method for coordinating mouth-to-mouth ventilation and chest compressions has not been established. Early experimental studies suggested a ventilation:compression ratio of 1:4 [19,20]. The presently recommended ventilation:compression ratio of 2:15 [1] was initially based on a study [21] in anaesthetised patients with normal circulation where two inflations every 15 s with exhaled air gave a mean PaO2 of 79 mmHg (10.5 kPa). Results from dogs with a chest compression rate of 60 per minute and a clamped tracheal tube with pauses when the tube was opened for ‘quick’ ventilations with air were reported in the same paper [21]. A ventilation/compression ratio of 3:15 gave a mean arterial oxygen saturation of 90 vs. 75% for a ratio of 6:30. These data fit well with ours with the 6:30 saturation being intermediate between ours for 2:15 and 5:50. In contrast, computer simulations of blood flow and gas exchange during CPR have indicated that the ratios 2:15 and 5:50 should be approximately equivalent in terms of gas exchange and predicted noticeably less severe hypoxia and hypercarbia than seen in our experiment [22]. This discrepancy could be explained by the fact that computer simulation models do not include the increased physiological shunting caused by pulmonary contusion, deflation or congestion, or the thoracic configurational changes seen in actual resuscitations [14,23,24]. Our data on carotid and cerebrocortical blood flows agree with the simulation prediction that cardiac output would be approximately equal for 2:15 and 5:50 ratios [22]. Recently, a three-staged approach to CPR has been suggested [7]. The first involves chest-compression-only CPR, the second introduces rescue breaths with a ventilation:compression ratio of 5:50, and the third is a conversion to standard ratio (2:15) CPR. This idea was supported by findings by Chamberlain et al. [10] of about 50% more compressions per minute for 5:50 compared with 2:15 for single rescuer CPR on manikins. In the present study 5:50 gave worse gas exchange with no better circulation than 2:15, and the gas-exchange was no better for 5:50 than for 2:50, which gave better circulation. It is important to note that our results came under ideal circumstances that cannot automatically be
E. Dorph et al. / Resuscitation 58 (2003) 193 /201
extrapolated to the clinical situation with lay rescuers, and the difference in results from Chamberlain et al. [10] might be explained by this. In their study [10] the mean duration of pauses between compressions was 16 and 30 s for two and five ventilations respectively (or 8 and 5 s per ventilation). This combined with a lower ventilation:compression ratio of 5:50 explained the reported overall 50% gain in the number of chest compressions per minute vs. 2:15. In the present study, accurate compressions were given by a mechanical device that does not tire, and the pigs were ventilated via a tracheal tube with no time lost changing between compressions and ventilations. Thus although the time interval for two ventilations of mean 4.9 s in the present study and 649/2 compressions given per minute comply well with the guidelines [1], many publications, in addition to the one by Chamberlain et al. [10], indicate that persons trained in basic CPR are unable to follow these guidelines even a few months after taking a course [5,6,25]. At the same time recently, and well trained, individuals have been able to follow the guidelines and achieved 50 /64 compressions and 7 /8 rescue breaths per minute even with single rescuer 2:15 CPR on manikins [26 /28]. Therefore it might seem reasonable to suggest that well trained professional personnel should continue with 2:15 at present. The findings in the present study that 5:50 provided the same gas exchange but significantly less chest compressions and blood flow than 2:50 can indicate that the suggested staged approach to CPR might benefit from changing the second stage 5:50 ratio to 2:50. This is also in accordance with a recent mathematical analysis suggesting that a 2:50 ventilation:compression ratio is adequate for one- and two-rescuer basic CPR [29]. What about ratio 2:15 compared with 2:50? If a layperson requires a 16 s break in the compressions for two mouth-to-mouth ventilations, there will be no circulation for 60% and 35% of the total resuscitation time for the ratios 2:15 and 2:50, respectively. Although CPR is a compromise between provision of blood flow and ventilation, 60% of the time without circulation seems unacceptably low. At the same time the mean blood oxygen content with 2:50 or 5:50 was only a little more than half of the content achieved with 2:15. It could be speculated that 2:30 might be a better compromise. The oxygen saturation data in the present study indicate that the drastic drop in blood oxygenation takes place after approximately 30 compressions, and Babbs et al. [29] have predicted that 2:30 might be the optimal ratio based on theoretical considerations. If this is the case there would be no need for the third stage suggested by Assar et al. [7]. First stage continuous compressions without ventilation, second stage 2:30, and with advanced CPR in intubated patients contin-
199
uous compressions with interposed ventilations could be advocated. There are many previous experimental studies of gas exchange and acid /base status during CPR, but differences in species, non-intervention time intervals, modes of ventilation, gas mixture used for ventilation, coordination of ventilation to compression, compression method, and timing of blood gas determinations make comparisons difficult. Only studies with a gas mixture mimicking exhaled air seem appropriate for basic life support with mouth-to-mouth or mouth-to-mask ventilation [11,30/32]. For standard ratio CPR these experimental studies report PaO2 values of 10.2 /13.4 kPa after 5.5 /9 min of CPR, with PaCO2 2.8 /4.4 kPa, pHa 7.4 /7.5, mixed venous blood PvO2 1.9 /2.7, PvCO2 7.6 / 9.3, and pHv/7.21 /7.25. All the above studies allowed chest compression induced and gasping ventilations, which must have occurred with ambient air to explain why their PaCO2 values were at the same level or lower than the 4 kPa in the gas mixture used for active ventilation on those studies. Our study was designed to eliminate the influence of both gasping and a patent airway during CPR, thus mimicking closely the most common real life cardiac arrest scenario with upper airway obstruction precluding chest compression induced ventilation [19] and no gasping respiration [33,34]. These differences in model design can explain why our animals had more hypoxic, hypercapnic and acidotic arterial and central venous blood gases compared with the results reported above for the same 2:15 ventilation to compression ratio. The blood gases for the ratios 5:50 and 2:50 are rather disturbing as a number of animal and human studies indicate that arterial hypercapnic and metabolic acidosis, as well as arterial hypoxemia have adverse effects on resuscitation from cardiac arrest [35 /40]. On the other hand, several animal studies suggest that the addition of ventilation during the initial minutes after cardiac arrest does not improve the outcome [11 /13,30]. In the study by Kern et al. [11] nonventilated animals had no better blood gases than those that we found with the 2:50 and 5:50 ratios, and much worse than in their animals receiving ventilation. The optimal ventilation /compression ratios for various durations of basic CPR are therefore unknown. The end-tidal CO2 (ETCO2) value was significantly lower for ratio 2:15 compared with both other ratios. Since the ETCO2 can be affected by ventilation as well as perfusion [18,41,42], it is difficult to analyze this difference further. The higher ETCO2 with ratio 5:50 than 2:15 could represent a combined effect of a tendency to better blood flow and less ventilation, whereas for 2:50 it might be due to the reduction in ventilation alone. The mean ETCO2 value of 6.2 kPa with ratio 2:15 in this study is much higher than the 3.6 kPa reported by Kern et al. for the same 2:15 ratio with
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the same inhalation gas which included 4 kPa CO2 [11]. As for the blood gases, the fact that the ETCO2 values were lower than in the inhaled air mixture used, must be due to ambient air ventilation occurring with chest compressions through the open airway in their study. In conclusion, a ventilation:compression ratio of 2:15 in this experimental model of ideal basic CPR gave better pulmonary gas exchange and cerebral oxygen delivery than both the ratios 2:50 and 5:50. Continuous arterial oxygen saturation tracings indicated that ratio 2:30 might be an even more optimal ventilation:compression ratio. Further investigations are needed to define the best method for coordinating ventilation and chest compressions during real CPR.
[11]
[12]
[13]
[14]
[15]
Acknowledgements This work was supported by grants from the Laerdal Foundation for Acute Medicine, the Jahre Foundation and the Norwegian Air Ambulance.
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