Treatment of acute left heart failure using dobutamine and intraaortic counterpulsation

Ten anesthetized mongrel dogs had a left anterolateral thoracotomy; the left anterior descending coronary artery was then ligated. After 60 min five animals each were treated either with dobutamine (4 g/min/kg; for 10 min), or with dobutamine and intraaortic counterpulsation. Combined treatment of cardiogenic shock proved superior. Those five dogs had significantly lower heart rates and dp/dt/pvalues. Due to IABP the non-ischemic parts of the left ventricle were better perfused; there was no difference in treatment with regard to ischemic parts. The combined treatment was successfully inaugurated in two patients with cardiogenic shock.     

小剂量多巴酚丁胺负荷超声心动图试验对可逆性功能障碍心肌预测的新指标

目的：探讨小剂量多巴酚丁胺负荷超声心动图（DSE）试验中左心室功能EF值的变化,即ΔEF这一量化指标预测急性心肌梗死（AMI）后患者的功能障碍心肌是否可逆及其可恢复程度。方法：入选患者25例, 接受小剂量DSE检查,测定负荷试验各阶段的收缩功能EF值,25例患者亦接受冠脉造影,并择期行经皮经腔太动脉成形术（PTCA）治疗,根据病变血管的情况植入支架,在术后3．5－13个月之间复查小剂量DSE试验。结果：以小剂量DSE过程中EF增加值,即ΔEF大于等于15％作为衡量标准,预测可逆性功能障碍心肌的敏感性,特性和准确性分别为70．6％,75％和72％,此预测改善值与无改善值之间的差异有显著性意义（P＜0．05）,结论：ΔEF可以作为准确评价可逆性功能障碍心肌的指标,并且是一种定量测定方法。     

Comparison between dobutamine and levosimendan for management of postresuscitation myocardial dysfunction

OBJECTIVE: To investigate the effects of levosimendan, a nonadrenergic inotropic calcium sensitizer, in comparison with adrenergic dobutamine for the management of postresuscitation myocardial dysfunction following resuscitation from prolonged cardiac arrest. DESIGN: Randomized prospective animal study. SETTING: Animal research laboratory. SUBJECTS: Male Yorkshire-cross domestic pigs INTERVENTIONS: Ventricular fibrillation was induced in male domestic pigs weighing between 35 and 40 kg. Cardiopulmonary resuscitation, including precordial compression and mechanical ventilation, was started after 7 mins of untreated cardiac arrest. Electrical defibrillation was attempted after 5 mins of cardiopulmonary resuscitation. Each animal was successfully resuscitated without pharmacologic intervention. Resuscitated animals were randomized to treatment with levosimendan, dobutamine, or saline placebo. The inotropic agents or an equivalent volume of placebo diluents was administered 10 mins after restoration of spontaneous circulation. Levosimendan was administered in a loading dose of 20 microg.kg over 10 mins followed by a 220-min infusion of 0.4 microg.kg.min. Dobutamine was infused into the right atrium in an amount of 5 microg.kg.min. Treatment was continued for a total of 230 mins. MEASUREMENTS AND MAIN RESULTS: Levosimendan and dobutamine produced comparable increases in cardiac output. However, levosimendan produced significantly greater left ventricular ejection fraction and fractional area changes compared with dobutamine and saline placebo. CONCLUSIONS: Levosimendan has the potential of improving postresuscitation myocardial function. It is likely to serve as an alternative to dobutamine as an inotropic agent for management of postresuscitation myocardial dysfunction.     

Pharmacological postconditioning with sevoflurane after cardiopulmonary resuscitation reduces myocardial dysfunction

Introduction

In this study, we sought to examine whether pharmacological postconditioning with sevoflurane (SEVO) is neuro- and cardioprotective in a pig model of cardiopulmonary resuscitation.

Methods

Twenty-two pigs were subjected to cardiac arrest. After 8 minutes of ventricular fibrillation and 2 minutes of basic life support, advanced cardiac life support was started. After successful return of spontaneous circulation (N = 16), animals were randomized to either (1) propofol (CONTROL) anesthesia or (2) SEVO anesthesia for 4 hours. Neurological function was assessed 24 hours after return of spontaneous circulation. The effects on myocardial and cerebral damage, especially on inflammation, apoptosis and tissue remodeling, were studied using cellular and molecular approaches.

Results

Animals treated with SEVO had lower peak troponin T levels (median [IQR]) (CONTROL vs SEVO = 0.31 pg/mL [0.2 to 0.65] vs 0.14 pg/mL [0.09 to 0.25]; P < 0.05) and improved left ventricular systolic and diastolic function compared to the CONTROL group (P < 0.05). SEVO was associated with a reduction in myocardial IL-1β protein concentrations (0.16 pg/μg total protein [0.14 to 0.17] vs 0.12 pg/μg total protein [0.11 to 0.14]; P < 0.01), a reduction in apoptosis (increased procaspase-3 protein levels (0.94 arbitrary units [0.86 to 1.04] vs 1.18 arbitrary units [1.03 to 1.28]; P < 0.05), increased hypoxia-inducible factor (HIF)-1α protein expression (P < 0.05) and increased activity of matrix metalloproteinase 9 (P < 0.05). SEVO did not, however, affect neurological deficit score or cerebral cellular and molecular pathways.

Conclusions

SEVO reduced myocardial damage and dysfunction after cardiopulmonary resuscitation in the early postresuscitation period. The reduction was associated with a reduced rate of myocardial proinflammatory cytokine expression, apoptosis, increased HIF-1α expression and increased activity of matrix metalloproteinase 9. Early administration of SEVO may not, however, improve neurological recovery.     

复苏后心功能不全与炎症因子关系的实验研究

目的:观察犬心跳骤停复苏后血流动力学和细胞因子的变化及其关系。方法:体外电击诱发犬室颤,3min后复苏,12只犬随机分为2组,常规治疗组(CPR组)和正常对照组,每组6只,采用Swan-Ganz漂浮导管监测复苏前和复苏后6h的心输出量(CO)和肺动脉楔压(PAWP),同时抽血检测血清肿瘤坏死因子-α(TNF-α),白介素-6(IL-6)和白介素-10(IL-10)水平(放免法)。结果:两组各血流动力学指标在心跳骤停前差异无统计学意义,CPR组的MAP在复苏成功即时高于正常对照组,随后开始下降,在复苏后4、6h低于正常对照组。CPR组的PAWP从心跳骤停前的(5.0±1.26)mmHg一直上升,到复苏后达高峰(28.83±4.79)mmHg,各观察点均高于正常对照组,CO在复苏成功后随时间延长而下降,6h降至最低,复苏后各观察点均低于正常对照组和电击前。TNF-α、IL-6浓度在复苏后即时和2h开始出现明显的升高,并随时间的延长而增高,与本组电击前及同时间的正常对照组比较差异有统计学意义。在整个实验过程均未能检测到IL-10的浓度。细胞因子TNF-α和IL-6与CO之间呈负相关。结论:电击诱发室颤犬复苏成功后存...     

Abdominal counterpulsation in cardiopulmonary resuscitation: animal models and theoretical considerations

Abdominal counterpulsation improves blood flow during otherwise standard CPR in animal models and in electronic models of the circulation. The method generates both central aortic and central venous pressure pulses. Success depends upon maximizing the former and minimizing the latter. Solution of a simple, first-order, differential equation may provide insight into proper technique. The equation suggests that the central arteriovenous pressure difference is maximized when pressure is applied directly over the abdominal aorta and when fluid loading is avoided. Proper technique may be critical in generating the largest possible arteriovenous pressure difference.     

Cardiopulmonary resuscitation ameliorates myocardial mitochondrial dysfunction in a cardiac arrest rat model

PurposePrevious studies implicate that the mitochondrial injury may play an important role in the development of post-resuscitation myocardial dysfunction, however few of them are available regarding the ultrastructural alterations of myocardial mitochondria, mitochondrial energy producing and utilization ability in the stage of arrest time (no-low) and resuscitation time (low-flow). This study aimed to observe the dynamic changes of myocardial mitochondrial function and metabolic disorders during cardiac arrest (CA) and following cardiopulmonary resuscitation (CPR).MethodsA total of 30 healthy male Sprague-Dawley rats were randomized into three groups: 1) VF/CPR: Ventricular fibrillation (VF) was electrically induced, and 5 min of CPR was performed after 10 min of untreated VF; 2) Untreated VF: VF was induced and untreated for 15 min; and 3) Sham: Rats were identically prepared without VF/CPR. Amplitude spectrum area (AMSA) at VF 5, 10 and 15 min were calculated from ECG signals. The rats' hearts were quickly removed at the predetermined time of 15 min after beginning the procedure to gather measurements of myocardial mitochondrial function, high-energy phosphate stores, lactate, mitochondrial ultrastructure, and myocardial glycogen.ResultsThe mitochondrial respiratory control ratios significantly decreased after CA compared to sham group. CPR significantly increased respiratory control ratios compared with untreated VF animals. A significant decrease of myocardial glycogen was observed after CA, and a more rapid depletion of myocardial glycogen was observed in CPR animals. CPR significantly reduced the tissue lactate. The mitochondrial ultrastructure abnormalities in CPR animals were less severe than untreated VF animals. AMSA decayed during untreated VF; however, it was significantly greater in CPR group than the untreated VF group. In addition, AMSA was clearly positively correlated with ATP, but negatively correlated with myocardial glycogen.ConclusionImpairment of myocardial mitochondrial function and the incapability of utilizing glycogen were observed after CA. Furthermore, optimal CPR might, in part, preserved mitochondrial function and enhanced utilization of myocardial glycogen.     

Comparison of serum creatine kinase and creatine kinase MB activities post marathon race versus post myocardial infarction

Serial total creatine kinase (CK) and CK MB activities were determined in the serum of seven runners following a marathon race and compared to enzyme activities in the sera from five patients following acute myocardial infarction (AMI). In the runner's sera, total CK and CK MB activities were significantly elevated at 1, 24, 48 and 72 hours post marathon race when compared to the 1 hour pre-marathon samples (p < 0.01). Serum CK MB activities peaked at 24 hours in both groups of subjects. The MB activities 24 hours following the marathon were substantially higher (91 ± 30 U/l; mean ± SD) than the MB activities 24 hours following AMI (46 ± 38 U/l). However, the percentages of CK MB 24 hours following the marathon and AMI were almost identical (7.0 ± 2.4% and 7.2 ± 2.3%, respectively). Furthermore, CK and CK MB clearances were significantly prolonged (p < 0.02 and p < 0.001, respectively) following the marathon race (T $\text{1}\text{2}$ CK, 49 hours; T $\text{1}\text{2}$ CK MB, 29 hours) as compared to following AMI (T $\text{1}\text{2}$ CK, 27 hours; T $\text{1}\text{2}$ CK MB, 12 hours). These results suggest release of CK MB from the skeletal muscle of marathon runners. Therefore, we recommend that elevation of CK MB in the range indicative of myocardial damage be interpreted with caution in long-distance runners.     

Differences of postresuscitation myocardial dysfunction in ventricular fibrillation versus asphyxiation

PurposeThis study aims to characterize postresuscitation myocardial dysfunction in 2 porcine models of cardiac arrest (CA): ventricular fibrillation cardiac arrest (VFCA) and asphyxiation cardiac arrest (ACA).MethodsThirty-two pigs were randomized into 2 groups. The VFCA group (n = 16) were subject to programed electrical stimulation, and the ACA group (n = 16) underwent endotracheal tube clamping to induce CA. Once induced, CA remained untreated for 8 minutes. Two minutes after initiation of cardiopulmonary resuscitation (CPR), defibrillation was attempted until return of spontaneous circulation (ROSC) was achieved or animals died.ResultsReturn of spontaneous circulation was 100% successful in VFCA and 50% successful in ACA. Cardiopulmonary resuscitation duration in VFCA was about half as short as in ACA. The survival time of VFCA was significantly longer than that of ACA. Ventricular fibrillation cardiac arrest had better mean arterial pressure, cardiac output, and left ventricular ± dp/dt_max after ROSC than ACA. Echocardiography revealed significantly lower left ventricular ejection fraction in ACA than in VFCA. Myocardial perfusion imaging using single-photon emission computed tomography demonstrated that myocardial injuries after ACA were more severe and widespread than after VFCA. Under a transmission electron microscope, the overall heart morphologic structure and the mitochondrial crista structure were less severely injured in the VFCA group than in the ACA group. Moreover, the percentage of apoptotic cardiomyocytes was higher in ACA than in VFCA.ConclusionsCompared with VFCA, ACA causes more severe cardiac dysfunction associated with less successful resuscitation and shorter survival time.     

Enoximone very low-dose dobutamine stress echocardiography: a new test for detecting viability in severe myocardial dysfunction after acute myocardial infarction.

Relying on the synergistic action on contractility of enoximone and dobutamine when concomitantly infused, 25 patients with their first acute Q-wave anterior myocardial infarctions underwent conventional low-dose dobutamine echocardiography (LDE) and enoximone very-LDE to assess myocardial viability in severely dysfunctioning areas. Images were recorded at peak of pharmacodynamic effect of drugs and 4 months after revascularization. At peak-dose stage of LDE and enoximone very-LDE the regional infarct zone wall-motion score significantly decreased from the basal value of 25.6 +/- 2.9 to 16 +/- 6.0 (P <.001) and to 14.5 +/- 5.2 (P <.001), respectively. A high correlation was found by comparing the wall-motion score of each patient calculated at peak effect of combined drug administration with follow-up values (r(s) = 0.9). Enoximone very-LDE has proven to be a new test useful to evaluate viability in asynergic segments especially when the results of conventional tests are questionable.     

Noninvasive assessment of myocardial dysfunction in patients with chronic aortic regurgitation

Chronic aortic regurgitation may have minimal symptoms until severe myocardial dysfunction is apparent. Multiple preoperative indicators of postoperative prognosis have been sought. It appears that an elevated left ventricular end systolic dimension on echocardiography or elevated end systolic volume on radionuclide ventriculography in combination with depressed LV function and substantially increased calculated systolic wall stress may present an indicator for aortic valve replacement. Response of ejection fraction to stress may not be as reproducible, but when combined with a depressed resting ejection fraction may also be an indicator for aortic valve replacement. Even patients with severely depressed left ventricular ejection fraction may improve with surgery; however, the risks of a poor postoperative outcome is substantial increased. Appropriate management of a patient with chronic aortic regurgitation requires monitoring of multiple parameters during the patient's clinical course for optimal timing of valve replacement surgery.     

Preventing sudden cardiac death in post myocardial infarction patients with left ventricular dysfunction

Cardiovascular nurses play a key role in caring for the post myocardial infarction (MI) patient. That role includes reducing the risk of MI recurrence and the progression to heart failure. Equally important is evaluating for the risk of sudden cardiac death (SCD). Although drugs such as beta blockers and angiotensin converting enzyme (ACE) inhibitors are typically indicated to help reduce the risk of SCD, data continue to show that using implantable cardioverter defibrillators (ICDs) saves lives compared with using medications alone. This article focuses on the problem of SCD, the findings of recent clinical trials, the implant criteria for defibrillators, new Centers for Medicare & Medicaid Services (CMS) decisions regarding reimbursement, and postoperative care for the defibrillator patient. Included are 2 case studies demonstrating the nurses' role in identifying asymptomatic patients who are indicated for ICD therapy. It is critical that cardiovascular nurses be aware of the latest scientific evidence showing improved outcomes for post-MI patients, particularly those with left ventricular dysfunction.     

Pre- and postconditioning effect of Sevoflurane on myocardial dysfunction after cardiopulmonary resuscitation in rats

Post-resuscitation myocardial dysfunction is an important cause of death in the intensive care unit after initially successful cardiopulmonary resuscitation (CPR) of pre-hospital cardiac arrest (CA) patients. Volatile anaesthetics reduce ischaemic–reperfusion injury in regional ischaemia in beating hearts. This effect, called anaesthetic-induced pre- or postconditioning, can be shown when the volatile anaesthetic is given either before regional ischaemia or in the reperfusion phase. However, up to now, little data exist for volatile anaesthetics after global ischaemia due to CA. Therefore, the goal of this study was to clarify whether Sevoflurane improves post-resuscitation myocardial dysfunction after CA in rats.     

Post-resuscitation right ventricular dysfunction: delineation and treatment with dobutamine

Newly qualified doctors are ill equipped to deal with pre-hospital trauma emergencies. There is a public perception that medical education provides both experience and knowledge in this field. In Birmingham, United Kingdom (UK), committed doctors and nurses trained in pre-hospital care have evolved a specific course designed to equip the medical undergraduate to deal with pre-hospital trauma scenario. The pre-hospital trauma course for medical students has run annually from 1993 to 2000. The course caters for 200 students with a faculty of 30 instructors. Successful completion of the course which is rigorously assessed grants a certificate awarded by the Faculty of Pre-hospital Care at the Royal College of Surgeons of Edinburgh. Most importantly it equips the undergraduate with essential theoretical knowledge and practical skills to handle a pre-hospital trauma emergency.