浅谈急性心肌梗死患者的护理和保健指导

急性心肌梗死属冠心病的严重类型，男性多于女性，多发生于40岁以后。该病起病急，病情重，并发症较多，死亡率高。因此，临床护理人员恰当地做好护理和保健指导，对急性心肌梗死患者的治疗康复起着十分重要的作用。     

青少年Pilon骨折的治疗

目的探讨青少年Pilon骨折的特点、治疗方法及其并发症。方法对1990年4月～2003年12月期间治疗的13例青少年胫骨Pilon骨折病例进行随访分析。按Merv—Letts分型：Ⅰ型5例，Ⅱ型6例，Ⅲ型2例。骨牵引治疗2例，有限内同定8例，有限内固定结合外固定支架3例。结果所有患者平均随访24个月，按Helfet踝关节功能评价：优8例，良4例，差1例，优良率92．3％。并发症：皮肤坏死2例，创伤性关节炎4例，骨骺早闭3例，畸形愈合1例，骨延迟愈合1例，外固定支架钉道感染1例，总体并发症38．5％。结论青少年Pilon骨折应根据其分型采用不同的治疗方案：疗效与创伤程度有关：Ⅲ犁骨折有较高的并发痹。     

Cerebral Cortical Aquaporin-4 Expression in Brain Edema following Cardiac Arrest in Rats

OBJECTIVES: Brain edema occurs following clinical as well as experimental cardiac arrest (CA) and predicts a poor neurologic outcome. The objective of this study was to determine the expression of cerebral cortex aquaporin (AQP)-4, a member of a family of membrane water-channel proteins, in brain edema formation following normothermic or hypothermic CA. METHODS: Twenty-four rats were subjected to time-matched normothermic (N-Sham, 37.5 degrees C +/- 0.5 degrees C, n = 6) or hypothermic (H-Sham, 34 degrees C +/- 0.5 degrees C, n = 6) sham experiments and normothermic (N-CA, n = 6) or hypothermic (H-CA, n = 6) CA induced by asphyxiation for 8 minutes. Hypothermia was induced before CA. The animals were resuscitated with cardiopulmonary resuscitation, ventilation, and epinephrine administration. Brain edema was determined by brain wet-to-dry weight ratio at one hour of resuscitation. AQP4 immunoactivity in the cerebral cortex was determined using immunohistochemical staining and was semiquantified as an intensity of staining with an automated cell imaging system. RESULTS: Mild hypothermia in the sham experiments did not alter cerebral cortex AQP4 immunoactivity (mean +/- SD) (55.0 +/- 3.7 in H-Sham vs. 53.3 +/- 1.7 in N-Sham, p > 0.05). N-CA resulted in a significant increase in AQP4 immunoactivity (61.8 +/- 4.5) compared with N-Sham (p = 0.01) and H-Sham (p = 0.03). H-CA attenuated AQP4 compared with N-CA (53.4 +/- 1.3, p = 0.01). Brain wet-to-dry weight ratios were 4.41 +/- 0.07 in N-Sham, 4.40 +/- 0.08 in H-Sham (p > 0.05 vs. N-Sham), 4.55 +/- 0.04 in N-CA (p = 0.004 vs. N-Sham; p = 0.005 vs. H-Sham), and 4.43 +/- 0.09 in H-CA (p = 0.02 vs. N-CA; p > 0.05 vs. N-Sham and H-Sham). CONCLUSIONS: Cerebral cortical AQP4 expression is up-regulated after normothermic CA, which is attenuated by hypothermia induced before CA.     

What Are the Etiology and Epidemiology of Out‐of‐hospital Pediatric Cardiopulmonary Arrest in Ontario,Canada?

Background: Pediatric cardiopulmonary arrest (CPA) outside of the hospital has a very high mortality rate. Objectives: To evaluate the etiology and initial compromise of pediatric CPA cases in hopes of developing strategies to improve out‐of‐hospital resuscitation. Methods: The Ontario Prehospital Advanced Life Support (OPALS) study was a large multicenter initiative to evaluate the impact of emergency medical services (EMS) programs on 17 communities with 40,000 critically ill and injured patients who were older than 11 years. As part of this study, the authors conducted a retrospective observational cohort study that included all children younger than 18 years of age with out‐of‐hospital CPA, during an 11‐year period from 1991–2002. CPA was defined as patient being pulseless, apneic, and requiring chest compressions. Data were collected from ambulance call reports and centralized dispatch data and were reviewed by two independent investigators. Results: There were 503 children with CPA in the sample. Mean age was 5.6 years (range, 0–17 yr); 58.4% of patients were male, and 37.8% were younger than 1 year of age. Cardiopulmonary resuscitation (CPR) first was started by a bystander in 32.4% of cases, whereas 66.0% were unwitnessed arrests. Initial rhythms were asystole 77.2% of the time, pulseless electrical activity 16.4% of the time, and ventricular fibrillation or ventricular tachycardia 4% of the time. Annual incidence was 9.1/100,000 children. CPA was witnessed in 34.0% of cases; 80.7% of these were bystander‐witnessed, and 18.1% were EMS‐witnessed. Primary pathogenic cause of arrest was medical in 61.2% of cases, trauma in 37.2% of cases, and indeterminate in 1.6% of cases. Initial underlying physiologic compromise of witnessed arrests was judged to be respiratory in 39.8% of cases, sudden collapse (presumed electrical) in 16.4% of cases, progressive shock in 1.2% of cases, and indeterminate in 42.6% of cases. Presumed etiology was trauma, 37.6%; sudden infant death syndrome (SIDS), 20.3%; and respiratory disease, 11.6%, most commonly. Survival to hospital discharge was 2.0%. Conclusions: This is one of the largest population‐based, prospective cohorts of pediatric CPA reported to date, and it reveals that most pediatric arrests are unwitnessed and receive no bystander CPR. Those that are witnessed most often are caused by respiratory arrests or trauma. Trauma, SIDS, and respiratory disease are the most common etiologies overall. These data are vital to planning large resuscitation trials looking at specific interventions (i.e., increasing bystander CPR) and highlight the need for better strategies for prevention and early recognition.     

Asystole from tetanic stimulation of the accessory nerve

An asystolic cardiac arrest is reported which occurred at the same time as supramaximal tetanic stimulation over the accessory nerve in order to evoke contractions in the trapezius and sternocleidomastoid muscles. The cause may have been the inadvertent stimulation of one or more of the cranial nerves of the carotid sheath at the base of the skull: the cranial root of the accessory nerve, the vagus, the sino-carotid branch of the glossopharyngeal nerve or the hypoglossal nerve. The most likely culprit, if not the vagus itself, was the cranial root of the accessory nerve which both functionally and anatomically should be seen as an integral part of the vagus. It is suggested that stimulation of any nerve in the carotid sheath should be approached with caution and that a tetanic stimulus to this area might best be avoided.     

Effects of calcium in continuous cardioplegia on myocardial protection

The effects of calcium (Ca) on a hyperkalemic cardioplegic solution for continuous cardioplegia were examined in an isolated perfused working rat heart model. The coronary arteries were perfused with a modified Krebs-Henseleit bicarbonate buffer (K-H) solution, containing various concentrations of Ca(0.1, 0.6, 1.2, and 2.5 mmol/l) and a high concentration of potassium (20 mmol/l), for 180 min, after which cardiac arrest was induced at 37°C for 180 min. Cardiac function and creatine kinase (CK) were measured. In the control group, K-H solution was infused in place of the cardioplegic solution, and cardiac arrest was not induced. No significant differences were observed between the groups infused with the K-H solution containing Ca concentrations of 0.6, 1.2, and 2.5 mmol/l in the percent recovery of aortic flow (82.1±2.9%, 80.6±2.0%, and 71.5±3.7% (mean±SEM) respectively) or in the recovery of other indices of cardiac function, or in CK leakage. There were also no significant differences in the recovery of cardiac function and CK leakage between these groups and the control group. In the Ca 0.1 mmol/l group, however, the characteristic Ca paradox was observed. These findings suggest that if the Ca concentration in a cardioplegic solution is higher than 0.6 mmol/l during continuous cardioplegia, excellent cardioprotective effects will be achieved.     

以心跳骤停为首发症状的蛛网膜下腔出血共同特征研究

<正>心跳骤停（cardiac arrest,CA）和蛛网膜下腔出血（subarachnoid hemorrhage,SAH）均是急诊科常见的急危重症,CA可见于多种疾病的各个阶段,复苏成功率不高,甚至造成CA的病因不甚明确。SAH典型表现为剧烈头痛、呕吐、脑膜刺激征,诊断并不困难。而以CA为首发症状的SAH,由于心肺复苏无法常规进行头颅CT检查,给诊断增加了困难。本文通过对16例以CA为首发症状的SAH患者进行回顾性研究,来提高SAH-CA的快速病因诊断,避免漏诊误诊。     

Failure of oocyte maturation: possible mechanisms for oocyte maturation arrest

For human IVF, the patient's ovaries are hormonally stimulated to ensure the collection of fully matured oocytes that are at the metaphase II stage. Only these oocytes can be successfully fertilized either when mixed with sperm or after ICSI. Nevertheless, in some cases immature or maturing oocytes are recovered from follicles. Surprisingly, sometimes these oocytes do not complete maturation when cultured in vitro, for unknown reasons. In this article we discuss some possible mechanisms that may be responsible for those atypical arrests.     

Invasive electrophysiological evaluation of patients with sleep apnoea-associated ventricular asystole—methods and preliminary results

SUMMARY  Twelve patients (aged 48 ± 12 y) with ventricular asystole of >3s due to complete atrioventricular (AV) block ( n = 8), sinoatrial (SA) block or sinus node arrest ( n = 3) or both ( n = 1) associated with obstructive sleep apnoea underwent invasive electrophysiological evaluation of sinus node function and AV conduction properties before and after administration of atropine (0.02 mg kg^-1). Ventricular asystole lasted for 5.9 ± 2.8 s (range 3.1–13 s). Sinus node function was assessed by measurement of sinus node recovery time, sinoatrial conduction time, and the response of sinus rate to atropine. Parameters of AV-conduction assessment included AH- and HV-intervals, AV- and VA-Wenckebach periods, and effective refractory period of the AV node before and after atropine. Sinus node function was normal in 11 of the 12 study patients and moderately abnormal in 1 patient. AV-nodal function was normal in 8 patients and moderately abnormal in 4 patients. A slightly prolonged HV-interval (59–63 ms) was present in 6 patients. Intra- or infra His block was not observed in any patient. In conclusion, normal or only moderately abnormal electrophysiological findings in patients with sleep apnoea-associated ventricular asystole suggest that a neurally mediated cardioinhibitory reflex may cause ventricular asystole in these patients. This sleep apnoea-triggered 'vasovagal' reflex may unmask pre-existing mild to moderate structural abnormalities of the AV conduction system.