窒息性心脏骤停心电变化特点及复苏疗效与应激激素变化的关系
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摘要
研究背景
窒息性心脏骤停(Cardiac arrest, CA)可见于溺水、麻醉意外和中毒等。因窒息发展至CA的过程相对缓慢而渐进,长时间缺氧后,机体全身代谢性酸中毒、心脑肺等重要器官的损害发展至高峰,故窒息性CA的复苏成功率相对较低。
不同原因的CA复苏效果不尽相同,为了提高窒息性CA的复苏成功率,对其病理生理的深入研究必不可少。观察从窒息性CA开始到CPR前实验动物的心电图改变,有助于了解在窒息性CA过程中动物心电变化的类型和时程,对后续心肺复苏(Cardiopulmonary resuscitation, CPR)策略及复苏药物的选用有重要指导意义;正确应用血管收缩类药物是提高自主循环恢复(Return of spontaneous circulation, ROSC)率的一个关键,单用肾上腺素和血管加压素在不同动物的窒息性CA模型中显示出不同的复苏疗效,两者对窒息性CA复苏疗效的比较目前尚无定论。在幼年家猪VF模型中,联合肾上腺素和加压素显示出显著优于单用药物的复苏效果,那么在窒息性CA中联合药物是否也可产生较单用药物更好的复苏疗效,从而成为CPR新的药物策略?值得验证。CA可引起机体最严重的应激反应,大量神经内分泌因子参与了该过程,并与复苏成功率密切相关。在人类心源性猝死及动物VF模型中,促肾上腺皮质激素(Adrenocorticotropic hormone, ACTH)、皮质醇和血管紧张素Ⅱ(Angiotensin II, AngⅡ)等应激激素的浓度高低与CA的ROSC率呈正相关,但在窒息性CA中,上述激素如何变化、对复苏预后产生何种影响、以及血管收缩类药物的应用对应激激素的影响如何等问题在窒息性CA和CPR的研究中均无明确的结论。
本研究分三部份,分别比较三种不同实验动物在窒息性CA诱导过程中心电变化的异同;比较联合用药与单用肾上腺素或加压素对于窒息性CA复苏效果的异同;比较不同的复苏药物在CPR过程中对ACTH、皮质醇和AngⅡ等应激激素的影响,旨在探索窒息性CA的心电生理变化、适宜的复苏药物策略及应激激素与复苏疗效的关系。
第一部分窒息性心脏骤停心电变化特点
目的:通过建立大鼠、家兔和成年家猪等窒息性CA模型,观察窒息CA中不同种属动物心电变化特点。
方法:选取30只SD大鼠、30只家兔和20头成年家猪,采用夹闭气管插管法制备窒息性CA模型,达CA标准后5min开始CPR,CPR后3min予肾上腺素0.045mg/kg静脉注射,5min后重复一次。记录循环停止发生时间(TCA)、自主循环恢复时间(TROSC)和ROSC率;记录各组动物在达到CA标准即刻和CPR前的心电节律类型,包括心室颤动(Ventricular fibrillation, VF)/无脉性室速(Pulseless ventricular tachycardia, Pulseless VT)、无脉性电活动(Pulseless electrical activity, PEA)和全心停搏。
结果:3组动物的TCA、TROSC和ROSC率分别是:大鼠4.48±0.38min、2.44±0.98min和33.3%;家兔6±1 min、5.95±0.75min和30%;家猪13.14±2.7 min、16.14±1.2min和15%。
各组动物不同时点的心电节律类型:
CA即刻:大鼠组中29只表现为PEA,余下1只为VF;家兔组中29只表现为PEA,余下1只为VF;家猪组中12头表现为PEA,4头为VF和4头为全心停搏。
CPR前:大鼠组中6只PEA和24只全心停搏;家兔组中25只PEA和5只全心停搏;家猪组中13只VF、3头PEA和4头全心停搏。大鼠组全心停搏的发生率显著高于家兔和家猪组(P<0.05);家兔组PEA的发生率显著高于大鼠和家猪两组,(P<0.05));而家猪组VF的发生率高于大鼠和家兔组。
结论:不同种属的动物在窒息性CA中呈现不同的心电节律。达到CA标准即刻,大鼠、家兔和成年家猪的心电节律以PEA为主,随着CA状态的延长,3组动物的心电节律发生明显变化,家猪大部分转变为VF,大鼠绝大多数转变为全心停搏,而家兔仍主要表现为PEA。
第二部分联合肾上腺素和加压素在成年家猪窒息性心脏骤停模型中的疗效观察
目的:通过建立成年家猪窒息性CA模型,观察联合肾上腺素和血管加压素对窒息性CA的复苏疗效,是否与单用药物存在差别。
方法:选用24头雄性成年家猪,通过夹闭气管插管法制备窒息性CA模型,达CA标准后5min开始常规CPR,CPR3min后将家猪随机分成3组,每组8头动物,分别静脉注射肾上腺素0.045mg/kg(肾上腺素组)、加压素0.4U/kg(加压素组)和肾上腺素0.045mg/kg+加压素0.4U/kg(联合用药组),5min后重复注药。记录三组家猪的TCA、TROSC和ROSC%。记录基线状态、CPR2min、注药后90s、注药后5min及ROSC后30min等时点的平均动脉压(Mean artery pressure,MAP)、冠脉灌注压(Coronary perfusion pressure,CPP)、血气分析和呼气末二氧化碳分压( Pressure of end-tidal Carbon dioxide,PETCO2)。
结果: 3组家猪的TCA、TROSC和ROSC%分别是:肾上腺素组为16.24±2.31 min、17.14min和12.5%,1头家猪复苏成功;加压素组为15.75±1.45min、16.89min和12.5%,1头家猪复苏成功;联合用药组为16.98±2.05min、13.56±2.14min和100%,8头家猪复苏成功。
联合用药组在注射药物后MAP和PaO2显著高于CPR2min时,而PaCO2则显著低于CPR2min时;联合用药组在注射药物后90sec和5min的MAP及PaO2均显著高于同时点的肾上腺素组(P<0.05)和加压素组(P<0.05),而PaCO2则显著低于同时点的肾上腺素组(P<0.05)和加压素组(P<0.05)。
CPR过程中,3组动物的CPP和PETCO2在注药后均有所升高,注药后90sec达到峰值。联合用药组最高,重复注药后能保持两者高值,直至复苏成功。虽然加压素组的CPP和PETCO2在注药后高于肾上腺素组,但重复注药后无法维持上述指标在高值,随后逐渐下降。肾上腺素组在复苏全程上述指标均处于低值。
结论:对于成年家猪窒息性CA模型,联合肾上腺素和加压素显著提高CA动物ROSC率,明显改善复苏过程中通气/血流比值,缓解高碳酸血症,复苏疗效显著优于单用药物。
第三部分窒息性心脏骤停复苏疗效与应激激素变化的关系
目的:通过建立成年家猪窒息性CA模型,观察联合用药、单用肾上腺素和单用加压素对应激激素ACTH、皮质醇和AngⅡ在复苏过程中不同时点的影响。
方法:采用24头雄性成年家猪,动物模型的制备和实验分组同第二部分。在基线状态、CPR2min、注药后90s、注药后5min及ROSC后30min等时点抽取3组动物右心房血液检测ACTH、皮质醇和AⅡ的血液浓度,并比较复苏成功动物和死亡动物在CPR过程中3种激素浓度的变化。皮质醇测定采用化学免疫发光分析法,ACTH测定采用免疫放射分析法,AngⅡ测定采用放射免疫分析法。
结果:3组动物的TCA、TROSC和ROSC率见第二部分。3组动物在CPR过程中各时间点ACTH、皮质醇和AngⅡ的浓度变化:
ACTH:3组动物在CPR2min后ACTH的血浆浓度与窒息前相比无显著性差异。联合用药组和单用加压素组在注射首剂药物后,ACTH浓度迅速升高,90sec后显著高于CPR2min(P<0.05)。联合用药组在注射首剂药物后5min, ACTH浓度有所下降,但重复注药后激素浓度回升,并且从第二次注射药物后至ROSC后30min,激素浓度保持在高值,无明显变化。加压素组在注射首剂药物后90sec, ACTH的血浆浓度达到峰值,随后下降,重复注药后激素浓度无回升。肾上腺素组在注射药物后ACTH的血浆浓度逐渐降低。联合用药组在注射首剂药物后的各检测时点,ACTH的血浆浓度显著大于加压素组(P<0.05)和肾上腺素组(P<0.05),加压素组在注射首剂药物后90sec,ACTH浓度显著大于肾上腺素组(P=0.027),肾上腺素组的激素浓度最低。
皮质醇:3组家猪在CPR2min皮质醇的浓度显著低于窒息前状态(P<0.05)。联合用药组和加压素组在注射首剂药物后皮质醇浓度迅速升高,90sec后显著大于CPR2min(P<0.05)。联合用药组在注射首剂药物后5min,皮质醇浓度有所下降,但重复注药后激素浓度回升,并且从第二次注射药物后至ROSC后30min,激素浓度均保持在高值。加压素组在注射首剂药物后90sec,皮质醇浓度达到峰值,随后下降,重复注药后激素浓度无回升。肾上腺素组注射药物后,皮质醇血浆浓度与CPR2min时比较无明显差异,重复注射药物并没有提升皮质醇血浆浓度。联合用药组在注射首剂药物后的各检测时点,皮质醇的血浆浓度显著大于加压素组(P<0.05)和肾上腺素组(P<0.05),加压素组在注射首剂药物后90sec,ACTH浓度显著大于肾上腺素组(P=0.018),但此后与肾上腺素组相比激素浓度无显著差异。
AngⅡ:3组家猪CPR2min的AngⅡ血浆浓度比窒息前状态略有升高,但无统计学意义。3组家猪在注射首剂药物后AngⅡ浓度迅速升高,90sec后显著大于CPR2min(P<0.05)。重复注射药物后联合用药组激素浓度逐渐升高,单用药物组则逐渐下降。联合药物组在注射药物后各时间点测定的激素浓度值均显著大于加压素组(P<0.05)和肾上腺素组(P<0.05);肾上腺素组自二次注射药物后90sec起,激素浓度显著大于加压素组(P<0.05)。
复苏成功动物组的ACTH、皮质醇和AngⅡ在CPR过程中给药后各检测时点的浓度,均显著高于复苏失败动物组(P<0.01)。
结论:窒息性CA复苏过程中ACTH、皮质醇和AngⅡ血浆浓度的高低与动物ROSC率相关,上述3种激素浓度越高,ROSC率越高。在复苏过程中,联合用药组注射药物后各时点ACTH、皮质醇和AngⅡ的浓度均显著高于单用药物组。显著提高复苏过程中应激激素的分泌可能是联合用药在窒息性CA中获得良好复苏疗效的机制之一。
Background:
Asphyxial cardiac arrest (CA) are caused by a diversity of pathophysiological processes leading to asphyxia, which preclude movement of gas from the upper airway to the alveoli and ultimately to the tissues, the cell, and then to the mitochondria, thereby sustaining oxidative metabolism in vital organ, including drowning, drug-induced apnea, allergic disease of the airways, et al. In comparison with the sudden cardiac death caused by ventricular fibrillation(VF), the process from asphyxia developing into CA is longer and more aggressive. The severity and persistence of hypoxemia and hypercarbia characterized by asphyxial CA completely destroy the function of important organs and make the successful resuscitation difficult.
The outcomes of resuscitation are different according to the specific etiologies of CA. It’s necessary for the increasing rate of return of spontaneous circulation (ROSC) to understand the process of pathophysiology characterized by asphyxial CA. The timing and spectrum of change of cardiac rhythm from the onset of asphyxial CA to the initiation of CPR is important information, based on which we can decide the optimal strategy of the subsequent CPR and proper vasopressors. It’s crucial of the application of vasopressors during CPR to improve the rate of ROSC. The application of epinephrine or vasopressin in different animal models of asphyxial CA demonstrated varying outcomes of resuscitation, which implied that there is no confirmed conclusion about which one of epinephrine and vasopressin would bring better effect to the asphyxial CA. The combination of epinephrine and vasopressin showed significantly higher rate of ROSC in a pediatric pig model of VF than epinephrine or vasopressin alone, which inspired us that whether epinephrine administrated with vasopressin in asphyxial CA would bring out better outcome of resuscitation just as in the VF model, and therefore would it be a new pharmacologic strategy of asphyxial CA? It’s necessary to verify it in adult pig model of asphyxial CA. CA could evoke the severest stress response of human, in which large amount of stress hormones involved, and affected the outcome of resuscitation. The concentrations of adrenocorticotropic hormone (ACTH), cortisol and angiotensinⅡ(AngⅡ)are positively correlative with the rate of ROSC in the sudden cardiac death and the animal model of VF. However, in the asphyxial CA, how the concentration of the above three stress hormones changes, what effect they have on the outcomes of resuscitation, and how they response to the vosopressors remain unclear.
The research consists of three parts. Firstly, to observe the cardiac rhythms of rats、rabbits and pigs during the asphyxial CA; Secondly, to explore the effect of combination of vasopressors and vasopressor alone in the asphyxial CA; finally, to determine what effect of different vasopressors have on ACTH、 cortisol and AngⅡduring the asphyxial CA.
Part one: The change of cardiac rhythms in the asphyxial CA Objective: to observe the change of cardiac rhythms during the asphyxial CA in different species of animals via establishing the asphyxial CA model of rats、rabbits and pigs.
Method: 30 rats、30 rabbits and 20 pigs were acutely asphyxiated by endotracheal tube clamping until 5min after coming to the criterion of CA. CPR was then provided. Epinephrine was administrated to the three species of animals after 3min of CPR and repeated intravenously every other 5min. Record the time from the initiation of clamping endotracheal tube to the onset of CA (TCA), the time from the start of CPR to the ROSC(TROSC) and the rate of ROSC in three groups; the cardiac rhythms in rats、rabbits and pigs were recorded at the onset of CA and prior to CPR, including VF/pulseless ventricular tachycardia( Pulseless VT), pulseless electrical activity(PEA) and asystole. Result: TCA、TROSC and the rate of ROSC were 4.48±0.38min、2.44±0.98min and 33.3% in rats, 6±1min、5.95±0.75min and 30% in rabbits, 13.46±2.7min、16.14±1.2min and 15% in pigs.
Cardiac rhythms of three groups of animals at the different time point: The moment of onset of CA: 29 rats showed PEA and the rest one present VF; 29 rabbits demonstrated PEA and the rest one showed VF; 12 pigs indicated PEA, VF in 4 and asystole in 4.
Prior to CPR: there are PEA of 6 and asystole of 24 in 30 rats. 25 rabbits showed PEA and the rest 5 present aystole. 13 pigs demonstrated VF, PEA in 3 and aystole in the rest 4. The incidence of asystole in rats was significantly highe -r than the rabbits and the pigs (P<0.05). The rate of PEA in rabbits was sign -ificantly higher than the rats and the pigs. The rate of VF in pigs was highest among three groups of animals.
Conclusion: the different species of animals demonstrated different cardiac rhythms during the asphyxial CA. At the onset of CA, most of rats、rabbits and pigs showed PEA, however, as the asphyxia prolonged, the obvious changes happened in three groups of animals: most of pigs converted to VF、most of rats altered to asystole and most of rabbits still in PEA.
Part two: The effect of epinephrine combined with vasopressin in adult pig model of asphyxial CA
Objective: to observe the effect of combination of epinephrine and vasopressin in the asphyxial CA, and decide what difference between the combination of vasopressors and the vasopressor alone in resuscition via producing the adult pig model of asphyxial CA.
Method: Clamping of the endotracheal tube was applied on 24 adult male pigs to establish the model of asphxial CA. After 3 minutes of CPR, 24 animals were randomly assigned to receive either epinephrine (epinephrine group, 45μg/kg, n=8), vasopressin (vasopressin group, 0.4U/kg, n=8), or epinephrine combined with vasopressin (vasopressin/epinephrine combination group;μg/kg and U/kg: 45 and 0.4, n=8). All drugs were diluted to 10 ml with normal saline and injected separately intravenously at 5-minute intervals. Record the TCA, the TROSC and the rate of ROSC in the three groups; Mean artery pressure(MAP)、blood-gas analysis、Coronary perfusion pressure (CPP) and the pressure of end-tidal Carbon dioxide (PETCO2) were measured before induction of cardiac arrest, at 2 minutes of CPR, and at 90 seconds and 5 minutes after the first-dose drug administration.
Result: TCA、TROSC and the rate of ROSC were 16.24±2.31min、17.14min and 12.5% (1 ROSC) in the epinephrine group; 15.75±1.45min、16.89min and 12.5%(1 ROSC) in the vasopressin group; 16.98±2.05min、13.56±2.14min and 100%(8 ROSC) in the epinephrine/vasopressin combination group.
MAP and PaO2 after first-dose drug administration in the combination group were significantly higher than 2min after CPR (P<0.05), while PaCO2 was significantly lower than 2min after CPR (P<0.05). MAP and PaO2 at 90 sec and 5min after first dose drug administration were significantly higher than the epinephrine group (P<0.05) and the vasopressin group (P<0.05), while PaCO2 was significantly lower than the other two groups.
Both CPP and PETCO2 of the three groups increased after administration of vasopressors, coming to the climax at the 90sec after drug administration. The combination group maintained the highest level of the above two parameters after the vasoprissors repeated during the rest of the resuscitation. CPP and PETCO2 of the vasopressin group were higher than the epinephrine group, but they couldn’t maintain high level even after repeating the vasopressin. The epinephrine group remained the lowest level among the three groups during the whole process of CPR.
Conclusion: the combination of epinephrine and vasopressin significantly incre- ased the rate of ROSC in the adult pig model of asphyxial CA, and improved obviously ventilation/perfusion and hypercarbia during the resuscition. The effect of epinephrine administrated with vasopressin is better than the vasopressor alone in the CPR.
Part three: The correlation of the stress hormone and the outcome of asphyxial CA
Objective: to observe what impact of epinephrine, vasopressin or both of them have on the concentration of ACTH, cortisol and AngⅡat the different time point during the resuscitation via establishing the adult pig model of asphyxial CA. Method: 24 adult male pigs were elected to produce the model of acute asphxial CA. The preparation of animal and the grouping were same to the part two. ACTH、cortisol and AngⅡmeasured for three groups of pigs( epinephrine group、vasopressin group and epinephrine/vasopressin combination group)were measured before inducing cardiac arrest, at 2 minutes of CPR, at 90 seconds and 5 minutes after the drug administration, and at 30minutes after ROSC. ACTH was measured by immunoradiometric assay (IRMA), cortisol by chemiluminesc -ence immunoassay(CIA), and AngⅡby radio immunoassay (RIMA).
Result: TCA, TROSC and the rate of ROSC in the three groups can be found in the part two.
The concentration of ACTH, cortisol and AngⅡof the three groups during CPR:
ACTH: the concentrations of ACTH at 2min of CPR in the three groups resembled before the asphyxia. After the first-dose of drug administration, ACTH of the combination group and the vasopressin group increased, 90sec significantly higher than CPR2min (P<0.05). The combination group remained the highest level of ACTH until ROSC 30min. ACTH in the vasopressin group came up to the climax at 90 sec after the first-dose of drug administration, but fell after drug repeated. The epinephrine group remained the lowest level of ACTH among the three groups. The concentration of ACTH in the combination group at the different time points after drug were significantly higher than the orther two groups (P<0.05). The vasopressin group was significantly higher than the epinephrine group (P=0.027) at the 90sec after the first-dose drug.
Cortisol: the concentrations of cortisol at 2min of CPR in the three groups were a little higher than before the asphyxia. After the first-dose of drug administration, cortisol of the combination group and the vasopressin group increased, 90sec significantly higher than CPR2min (P<0.05). The combination group remained high level of cortisol until ROSC 30min. Cortisol in the vasopressin group came up to the climax at 90 sec after the first-dose of drug administration, but fell after drug repeated. Cortisol in the epinephrine group after drug administration resembled CPR2min, and repeating administration can’t increase the concentration of cortisol. The concentration of cortislo in the combination group at the different time points after drug were significantly higher than the other two groups (P<0.05). The vasopressin group was significantly higher than the epinephrine group (P=0.018) at the 90sec after the first-dose drug.
AngⅡ: AngⅡof the three groups at CPR 2min was a little higher than before asphyxia. After the first-dose of drug, the three groups increased, 90sec significantly higher than CPR2min (P<0.05). Repetition of drug administration increased the concentration of AngⅡin the combination group, but descent in the epinephrine group and the vasopressin group. The concentration of AngⅡin the combination group at the different time points after drug were significantly higher than the orther two groups (P<0.05). The epinephrine group was significantly higher than the vasopressin group (P=0.018) since the 90sec after the second-dose drug (P<0.05).
The concentration of ACTH, cortisol and AngⅡin the pigs with ROSC were significantly higher than the pigs without ROSC at the different time points after drug in the CPR (P<0.01).
Conclusion: the concentrations of ACTH, cortisol and AngⅡduring the asphyxial CA were correlative with the rate of ROSC. The higher concentrations of hormores showed, the higher the rate of ROSC. The concentration of ACTH, cortisol and AngⅡin the combination group at the different time points after drug in the CPR were significantly higher than the epinephrine group and the vasopressin group, suggesting that increasing the concentrations of stress hormones may be one of mechanisms responsible for the better resuscitative effect of combined vasopressors.
窒息性心脏骤停(Cardiac arrest, CA)可见于溺水、麻醉意外和中毒等。因窒息发展至CA的过程相对缓慢而渐进,长时间缺氧后,机体全身代谢性酸中毒、心脑肺等重要器官的损害发展至高峰,故窒息性CA的复苏成功率相对较低。
不同原因的CA复苏效果不尽相同,为了提高窒息性CA的复苏成功率,对其病理生理的深入研究必不可少。观察从窒息性CA开始到CPR前实验动物的心电图改变,有助于了解在窒息性CA过程中动物心电变化的类型和时程,对后续心肺复苏(Cardiopulmonary resuscitation, CPR)策略及复苏药物的选用有重要指导意义;正确应用血管收缩类药物是提高自主循环恢复(Return of spontaneous circulation, ROSC)率的一个关键,单用肾上腺素和血管加压素在不同动物的窒息性CA模型中显示出不同的复苏疗效,两者对窒息性CA复苏疗效的比较目前尚无定论。在幼年家猪VF模型中,联合肾上腺素和加压素显示出显著优于单用药物的复苏效果,那么在窒息性CA中联合药物是否也可产生较单用药物更好的复苏疗效,从而成为CPR新的药物策略?值得验证。CA可引起机体最严重的应激反应,大量神经内分泌因子参与了该过程,并与复苏成功率密切相关。在人类心源性猝死及动物VF模型中,促肾上腺皮质激素(Adrenocorticotropic hormone, ACTH)、皮质醇和血管紧张素Ⅱ(Angiotensin II, AngⅡ)等应激激素的浓度高低与CA的ROSC率呈正相关,但在窒息性CA中,上述激素如何变化、对复苏预后产生何种影响、以及血管收缩类药物的应用对应激激素的影响如何等问题在窒息性CA和CPR的研究中均无明确的结论。
本研究分三部份,分别比较三种不同实验动物在窒息性CA诱导过程中心电变化的异同;比较联合用药与单用肾上腺素或加压素对于窒息性CA复苏效果的异同;比较不同的复苏药物在CPR过程中对ACTH、皮质醇和AngⅡ等应激激素的影响,旨在探索窒息性CA的心电生理变化、适宜的复苏药物策略及应激激素与复苏疗效的关系。
第一部分窒息性心脏骤停心电变化特点
目的:通过建立大鼠、家兔和成年家猪等窒息性CA模型,观察窒息CA中不同种属动物心电变化特点。
方法:选取30只SD大鼠、30只家兔和20头成年家猪,采用夹闭气管插管法制备窒息性CA模型,达CA标准后5min开始CPR,CPR后3min予肾上腺素0.045mg/kg静脉注射,5min后重复一次。记录循环停止发生时间(TCA)、自主循环恢复时间(TROSC)和ROSC率;记录各组动物在达到CA标准即刻和CPR前的心电节律类型,包括心室颤动(Ventricular fibrillation, VF)/无脉性室速(Pulseless ventricular tachycardia, Pulseless VT)、无脉性电活动(Pulseless electrical activity, PEA)和全心停搏。
结果:3组动物的TCA、TROSC和ROSC率分别是:大鼠4.48±0.38min、2.44±0.98min和33.3%;家兔6±1 min、5.95±0.75min和30%;家猪13.14±2.7 min、16.14±1.2min和15%。
各组动物不同时点的心电节律类型:
CA即刻:大鼠组中29只表现为PEA,余下1只为VF;家兔组中29只表现为PEA,余下1只为VF;家猪组中12头表现为PEA,4头为VF和4头为全心停搏。
CPR前:大鼠组中6只PEA和24只全心停搏;家兔组中25只PEA和5只全心停搏;家猪组中13只VF、3头PEA和4头全心停搏。大鼠组全心停搏的发生率显著高于家兔和家猪组(P<0.05);家兔组PEA的发生率显著高于大鼠和家猪两组,(P<0.05));而家猪组VF的发生率高于大鼠和家兔组。
结论:不同种属的动物在窒息性CA中呈现不同的心电节律。达到CA标准即刻,大鼠、家兔和成年家猪的心电节律以PEA为主,随着CA状态的延长,3组动物的心电节律发生明显变化,家猪大部分转变为VF,大鼠绝大多数转变为全心停搏,而家兔仍主要表现为PEA。
第二部分联合肾上腺素和加压素在成年家猪窒息性心脏骤停模型中的疗效观察
目的:通过建立成年家猪窒息性CA模型,观察联合肾上腺素和血管加压素对窒息性CA的复苏疗效,是否与单用药物存在差别。
方法:选用24头雄性成年家猪,通过夹闭气管插管法制备窒息性CA模型,达CA标准后5min开始常规CPR,CPR3min后将家猪随机分成3组,每组8头动物,分别静脉注射肾上腺素0.045mg/kg(肾上腺素组)、加压素0.4U/kg(加压素组)和肾上腺素0.045mg/kg+加压素0.4U/kg(联合用药组),5min后重复注药。记录三组家猪的TCA、TROSC和ROSC%。记录基线状态、CPR2min、注药后90s、注药后5min及ROSC后30min等时点的平均动脉压(Mean artery pressure,MAP)、冠脉灌注压(Coronary perfusion pressure,CPP)、血气分析和呼气末二氧化碳分压( Pressure of end-tidal Carbon dioxide,PETCO2)。
结果: 3组家猪的TCA、TROSC和ROSC%分别是:肾上腺素组为16.24±2.31 min、17.14min和12.5%,1头家猪复苏成功;加压素组为15.75±1.45min、16.89min和12.5%,1头家猪复苏成功;联合用药组为16.98±2.05min、13.56±2.14min和100%,8头家猪复苏成功。
联合用药组在注射药物后MAP和PaO2显著高于CPR2min时,而PaCO2则显著低于CPR2min时;联合用药组在注射药物后90sec和5min的MAP及PaO2均显著高于同时点的肾上腺素组(P<0.05)和加压素组(P<0.05),而PaCO2则显著低于同时点的肾上腺素组(P<0.05)和加压素组(P<0.05)。
CPR过程中,3组动物的CPP和PETCO2在注药后均有所升高,注药后90sec达到峰值。联合用药组最高,重复注药后能保持两者高值,直至复苏成功。虽然加压素组的CPP和PETCO2在注药后高于肾上腺素组,但重复注药后无法维持上述指标在高值,随后逐渐下降。肾上腺素组在复苏全程上述指标均处于低值。
结论:对于成年家猪窒息性CA模型,联合肾上腺素和加压素显著提高CA动物ROSC率,明显改善复苏过程中通气/血流比值,缓解高碳酸血症,复苏疗效显著优于单用药物。
第三部分窒息性心脏骤停复苏疗效与应激激素变化的关系
目的:通过建立成年家猪窒息性CA模型,观察联合用药、单用肾上腺素和单用加压素对应激激素ACTH、皮质醇和AngⅡ在复苏过程中不同时点的影响。
方法:采用24头雄性成年家猪,动物模型的制备和实验分组同第二部分。在基线状态、CPR2min、注药后90s、注药后5min及ROSC后30min等时点抽取3组动物右心房血液检测ACTH、皮质醇和AⅡ的血液浓度,并比较复苏成功动物和死亡动物在CPR过程中3种激素浓度的变化。皮质醇测定采用化学免疫发光分析法,ACTH测定采用免疫放射分析法,AngⅡ测定采用放射免疫分析法。
结果:3组动物的TCA、TROSC和ROSC率见第二部分。3组动物在CPR过程中各时间点ACTH、皮质醇和AngⅡ的浓度变化:
ACTH:3组动物在CPR2min后ACTH的血浆浓度与窒息前相比无显著性差异。联合用药组和单用加压素组在注射首剂药物后,ACTH浓度迅速升高,90sec后显著高于CPR2min(P<0.05)。联合用药组在注射首剂药物后5min, ACTH浓度有所下降,但重复注药后激素浓度回升,并且从第二次注射药物后至ROSC后30min,激素浓度保持在高值,无明显变化。加压素组在注射首剂药物后90sec, ACTH的血浆浓度达到峰值,随后下降,重复注药后激素浓度无回升。肾上腺素组在注射药物后ACTH的血浆浓度逐渐降低。联合用药组在注射首剂药物后的各检测时点,ACTH的血浆浓度显著大于加压素组(P<0.05)和肾上腺素组(P<0.05),加压素组在注射首剂药物后90sec,ACTH浓度显著大于肾上腺素组(P=0.027),肾上腺素组的激素浓度最低。
皮质醇:3组家猪在CPR2min皮质醇的浓度显著低于窒息前状态(P<0.05)。联合用药组和加压素组在注射首剂药物后皮质醇浓度迅速升高,90sec后显著大于CPR2min(P<0.05)。联合用药组在注射首剂药物后5min,皮质醇浓度有所下降,但重复注药后激素浓度回升,并且从第二次注射药物后至ROSC后30min,激素浓度均保持在高值。加压素组在注射首剂药物后90sec,皮质醇浓度达到峰值,随后下降,重复注药后激素浓度无回升。肾上腺素组注射药物后,皮质醇血浆浓度与CPR2min时比较无明显差异,重复注射药物并没有提升皮质醇血浆浓度。联合用药组在注射首剂药物后的各检测时点,皮质醇的血浆浓度显著大于加压素组(P<0.05)和肾上腺素组(P<0.05),加压素组在注射首剂药物后90sec,ACTH浓度显著大于肾上腺素组(P=0.018),但此后与肾上腺素组相比激素浓度无显著差异。
AngⅡ:3组家猪CPR2min的AngⅡ血浆浓度比窒息前状态略有升高,但无统计学意义。3组家猪在注射首剂药物后AngⅡ浓度迅速升高,90sec后显著大于CPR2min(P<0.05)。重复注射药物后联合用药组激素浓度逐渐升高,单用药物组则逐渐下降。联合药物组在注射药物后各时间点测定的激素浓度值均显著大于加压素组(P<0.05)和肾上腺素组(P<0.05);肾上腺素组自二次注射药物后90sec起,激素浓度显著大于加压素组(P<0.05)。
复苏成功动物组的ACTH、皮质醇和AngⅡ在CPR过程中给药后各检测时点的浓度,均显著高于复苏失败动物组(P<0.01)。
结论:窒息性CA复苏过程中ACTH、皮质醇和AngⅡ血浆浓度的高低与动物ROSC率相关,上述3种激素浓度越高,ROSC率越高。在复苏过程中,联合用药组注射药物后各时点ACTH、皮质醇和AngⅡ的浓度均显著高于单用药物组。显著提高复苏过程中应激激素的分泌可能是联合用药在窒息性CA中获得良好复苏疗效的机制之一。
Background:
Asphyxial cardiac arrest (CA) are caused by a diversity of pathophysiological processes leading to asphyxia, which preclude movement of gas from the upper airway to the alveoli and ultimately to the tissues, the cell, and then to the mitochondria, thereby sustaining oxidative metabolism in vital organ, including drowning, drug-induced apnea, allergic disease of the airways, et al. In comparison with the sudden cardiac death caused by ventricular fibrillation(VF), the process from asphyxia developing into CA is longer and more aggressive. The severity and persistence of hypoxemia and hypercarbia characterized by asphyxial CA completely destroy the function of important organs and make the successful resuscitation difficult.
The outcomes of resuscitation are different according to the specific etiologies of CA. It’s necessary for the increasing rate of return of spontaneous circulation (ROSC) to understand the process of pathophysiology characterized by asphyxial CA. The timing and spectrum of change of cardiac rhythm from the onset of asphyxial CA to the initiation of CPR is important information, based on which we can decide the optimal strategy of the subsequent CPR and proper vasopressors. It’s crucial of the application of vasopressors during CPR to improve the rate of ROSC. The application of epinephrine or vasopressin in different animal models of asphyxial CA demonstrated varying outcomes of resuscitation, which implied that there is no confirmed conclusion about which one of epinephrine and vasopressin would bring better effect to the asphyxial CA. The combination of epinephrine and vasopressin showed significantly higher rate of ROSC in a pediatric pig model of VF than epinephrine or vasopressin alone, which inspired us that whether epinephrine administrated with vasopressin in asphyxial CA would bring out better outcome of resuscitation just as in the VF model, and therefore would it be a new pharmacologic strategy of asphyxial CA? It’s necessary to verify it in adult pig model of asphyxial CA. CA could evoke the severest stress response of human, in which large amount of stress hormones involved, and affected the outcome of resuscitation. The concentrations of adrenocorticotropic hormone (ACTH), cortisol and angiotensinⅡ(AngⅡ)are positively correlative with the rate of ROSC in the sudden cardiac death and the animal model of VF. However, in the asphyxial CA, how the concentration of the above three stress hormones changes, what effect they have on the outcomes of resuscitation, and how they response to the vosopressors remain unclear.
The research consists of three parts. Firstly, to observe the cardiac rhythms of rats、rabbits and pigs during the asphyxial CA; Secondly, to explore the effect of combination of vasopressors and vasopressor alone in the asphyxial CA; finally, to determine what effect of different vasopressors have on ACTH、 cortisol and AngⅡduring the asphyxial CA.
Part one: The change of cardiac rhythms in the asphyxial CA Objective: to observe the change of cardiac rhythms during the asphyxial CA in different species of animals via establishing the asphyxial CA model of rats、rabbits and pigs.
Method: 30 rats、30 rabbits and 20 pigs were acutely asphyxiated by endotracheal tube clamping until 5min after coming to the criterion of CA. CPR was then provided. Epinephrine was administrated to the three species of animals after 3min of CPR and repeated intravenously every other 5min. Record the time from the initiation of clamping endotracheal tube to the onset of CA (TCA), the time from the start of CPR to the ROSC(TROSC) and the rate of ROSC in three groups; the cardiac rhythms in rats、rabbits and pigs were recorded at the onset of CA and prior to CPR, including VF/pulseless ventricular tachycardia( Pulseless VT), pulseless electrical activity(PEA) and asystole. Result: TCA、TROSC and the rate of ROSC were 4.48±0.38min、2.44±0.98min and 33.3% in rats, 6±1min、5.95±0.75min and 30% in rabbits, 13.46±2.7min、16.14±1.2min and 15% in pigs.
Cardiac rhythms of three groups of animals at the different time point: The moment of onset of CA: 29 rats showed PEA and the rest one present VF; 29 rabbits demonstrated PEA and the rest one showed VF; 12 pigs indicated PEA, VF in 4 and asystole in 4.
Prior to CPR: there are PEA of 6 and asystole of 24 in 30 rats. 25 rabbits showed PEA and the rest 5 present aystole. 13 pigs demonstrated VF, PEA in 3 and aystole in the rest 4. The incidence of asystole in rats was significantly highe -r than the rabbits and the pigs (P<0.05). The rate of PEA in rabbits was sign -ificantly higher than the rats and the pigs. The rate of VF in pigs was highest among three groups of animals.
Conclusion: the different species of animals demonstrated different cardiac rhythms during the asphyxial CA. At the onset of CA, most of rats、rabbits and pigs showed PEA, however, as the asphyxia prolonged, the obvious changes happened in three groups of animals: most of pigs converted to VF、most of rats altered to asystole and most of rabbits still in PEA.
Part two: The effect of epinephrine combined with vasopressin in adult pig model of asphyxial CA
Objective: to observe the effect of combination of epinephrine and vasopressin in the asphyxial CA, and decide what difference between the combination of vasopressors and the vasopressor alone in resuscition via producing the adult pig model of asphyxial CA.
Method: Clamping of the endotracheal tube was applied on 24 adult male pigs to establish the model of asphxial CA. After 3 minutes of CPR, 24 animals were randomly assigned to receive either epinephrine (epinephrine group, 45μg/kg, n=8), vasopressin (vasopressin group, 0.4U/kg, n=8), or epinephrine combined with vasopressin (vasopressin/epinephrine combination group;μg/kg and U/kg: 45 and 0.4, n=8). All drugs were diluted to 10 ml with normal saline and injected separately intravenously at 5-minute intervals. Record the TCA, the TROSC and the rate of ROSC in the three groups; Mean artery pressure(MAP)、blood-gas analysis、Coronary perfusion pressure (CPP) and the pressure of end-tidal Carbon dioxide (PETCO2) were measured before induction of cardiac arrest, at 2 minutes of CPR, and at 90 seconds and 5 minutes after the first-dose drug administration.
Result: TCA、TROSC and the rate of ROSC were 16.24±2.31min、17.14min and 12.5% (1 ROSC) in the epinephrine group; 15.75±1.45min、16.89min and 12.5%(1 ROSC) in the vasopressin group; 16.98±2.05min、13.56±2.14min and 100%(8 ROSC) in the epinephrine/vasopressin combination group.
MAP and PaO2 after first-dose drug administration in the combination group were significantly higher than 2min after CPR (P<0.05), while PaCO2 was significantly lower than 2min after CPR (P<0.05). MAP and PaO2 at 90 sec and 5min after first dose drug administration were significantly higher than the epinephrine group (P<0.05) and the vasopressin group (P<0.05), while PaCO2 was significantly lower than the other two groups.
Both CPP and PETCO2 of the three groups increased after administration of vasopressors, coming to the climax at the 90sec after drug administration. The combination group maintained the highest level of the above two parameters after the vasoprissors repeated during the rest of the resuscitation. CPP and PETCO2 of the vasopressin group were higher than the epinephrine group, but they couldn’t maintain high level even after repeating the vasopressin. The epinephrine group remained the lowest level among the three groups during the whole process of CPR.
Conclusion: the combination of epinephrine and vasopressin significantly incre- ased the rate of ROSC in the adult pig model of asphyxial CA, and improved obviously ventilation/perfusion and hypercarbia during the resuscition. The effect of epinephrine administrated with vasopressin is better than the vasopressor alone in the CPR.
Part three: The correlation of the stress hormone and the outcome of asphyxial CA
Objective: to observe what impact of epinephrine, vasopressin or both of them have on the concentration of ACTH, cortisol and AngⅡat the different time point during the resuscitation via establishing the adult pig model of asphyxial CA. Method: 24 adult male pigs were elected to produce the model of acute asphxial CA. The preparation of animal and the grouping were same to the part two. ACTH、cortisol and AngⅡmeasured for three groups of pigs( epinephrine group、vasopressin group and epinephrine/vasopressin combination group)were measured before inducing cardiac arrest, at 2 minutes of CPR, at 90 seconds and 5 minutes after the drug administration, and at 30minutes after ROSC. ACTH was measured by immunoradiometric assay (IRMA), cortisol by chemiluminesc -ence immunoassay(CIA), and AngⅡby radio immunoassay (RIMA).
Result: TCA, TROSC and the rate of ROSC in the three groups can be found in the part two.
The concentration of ACTH, cortisol and AngⅡof the three groups during CPR:
ACTH: the concentrations of ACTH at 2min of CPR in the three groups resembled before the asphyxia. After the first-dose of drug administration, ACTH of the combination group and the vasopressin group increased, 90sec significantly higher than CPR2min (P<0.05). The combination group remained the highest level of ACTH until ROSC 30min. ACTH in the vasopressin group came up to the climax at 90 sec after the first-dose of drug administration, but fell after drug repeated. The epinephrine group remained the lowest level of ACTH among the three groups. The concentration of ACTH in the combination group at the different time points after drug were significantly higher than the orther two groups (P<0.05). The vasopressin group was significantly higher than the epinephrine group (P=0.027) at the 90sec after the first-dose drug.
Cortisol: the concentrations of cortisol at 2min of CPR in the three groups were a little higher than before the asphyxia. After the first-dose of drug administration, cortisol of the combination group and the vasopressin group increased, 90sec significantly higher than CPR2min (P<0.05). The combination group remained high level of cortisol until ROSC 30min. Cortisol in the vasopressin group came up to the climax at 90 sec after the first-dose of drug administration, but fell after drug repeated. Cortisol in the epinephrine group after drug administration resembled CPR2min, and repeating administration can’t increase the concentration of cortisol. The concentration of cortislo in the combination group at the different time points after drug were significantly higher than the other two groups (P<0.05). The vasopressin group was significantly higher than the epinephrine group (P=0.018) at the 90sec after the first-dose drug.
AngⅡ: AngⅡof the three groups at CPR 2min was a little higher than before asphyxia. After the first-dose of drug, the three groups increased, 90sec significantly higher than CPR2min (P<0.05). Repetition of drug administration increased the concentration of AngⅡin the combination group, but descent in the epinephrine group and the vasopressin group. The concentration of AngⅡin the combination group at the different time points after drug were significantly higher than the orther two groups (P<0.05). The epinephrine group was significantly higher than the vasopressin group (P=0.018) since the 90sec after the second-dose drug (P<0.05).
The concentration of ACTH, cortisol and AngⅡin the pigs with ROSC were significantly higher than the pigs without ROSC at the different time points after drug in the CPR (P<0.01).
Conclusion: the concentrations of ACTH, cortisol and AngⅡduring the asphyxial CA were correlative with the rate of ROSC. The higher concentrations of hormores showed, the higher the rate of ROSC. The concentration of ACTH, cortisol and AngⅡin the combination group at the different time points after drug in the CPR were significantly higher than the epinephrine group and the vasopressin group, suggesting that increasing the concentrations of stress hormones may be one of mechanisms responsible for the better resuscitative effect of combined vasopressors.
引文
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