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Human Anatomy Model - Open Chest Cardiac Compression

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Human Anatomy Model - Open Chest Cardiac Compression

release date:2021-12-29 author: Click:

Human Anatomy Model - Open Chest Cardiac Compression


As early as 1898, Tuffier's successfully applied open chest compressions for CPR. In 1960, Kouwenhoven et al reported that the application of chest compression was successful. Because this method is non-invasive and easy to operate, it has basically completely replaced open chest compression for many years. However, a large number of clinical data show that the effect of chest compression is unsatisfactory, and only 10% to 14% fully recover in the end; while the long-term survival rate of open chest compression is as high as 28%. The experiment also confirmed that the cardiac output of the open-chest method was about double that of the chest-thoracic method, and the cardiac-cerebral perfusion was also higher than the latter. Therefore, open chest compressions have received renewed attention. Indications: ① Those who are ineffective after conventional chest compression for 10-15 minutes (maximum no more than 20 minutes); ② Under the condition of intra-arterial pressure measurement, the diastolic blood pressure during chest compression is less than 5.332kPa; ③ External defibrillation fails. Methods: The left anterolateral fourth intercostal incision was used to enter the chest with the right hand. After entering the chest, the thenar muscle of the right hand and the thumb are placed in front of the heart, and the other four fingers and palms are placed behind the heart, and the heart is squeezed rhythmically at a speed of 80 beats per minute. Two manipulations can also be used, placing both hands on the left and right ventricles and squeezing at the same time.

人体解剖模型

Extended life support, as early as 1962, vladimir's attention and put forward the concept of post-resuscitation diseases (Postresuseitationdiseases). It is believed that a variety of irreversible damage to the body, especially the damage to the brain, occurs not only in the process of clinical death, but also in the post-resuscitation stage. The brain is closely related to the function of the organs of the whole body. Recent studies have shown that brain resuscitation is the fundamental condition for restoring breathing, circulation, metabolism and visceral functions. The resuscitation of the brain, especially the cerebral cortex, can accelerate the recovery of other living organs and systems. Therefore, brain protection should be carried out at the beginning of CPCR, and the focus should be on brain resuscitation and other organ damage during the extended life support stage. The brain is an organ with high blood flow, vigorous metabolism and high oxygen demand. The adult cerebral blood flow is about 50mL/min.100g, accounting for about 15% of the cardiac output; the oxygen metabolism rate is about 3.2-3.8mL/min.100g, and its energy is almost entirely dependent on the oxidative metabolism of glucose. After 2-4 minutes of cessation of circulation, the brain's glucose and glycogen stores are depleted, and 4-5 minutes later, adenosine triphosphate (ATP) is depleted. After the systemic circulation is completely stopped, if there is no reperfusion (if no resuscitation is performed), the myocardium and brain cells can tolerate almost 60 minutes without dying; however, if cardiopulmonary resuscitation is performed 5 minutes after complete ischemia to rebuild the circulation, some patients Brain and other organ damage will occur after resuscitation. When reperfusion injury occurs in the brain, multifocal brain reperfusion absence, i.e. no reflow phenomenon, first appears, followed by global cerebral congestion lasting about 15-30 minutes, and then delayed onset lasting more than 6 hours. Whole brain hypoperfusion, and eventually brain death or improvement, recovery, but most of the poor prognosis.


Treatment measures include: 1. Basic measures, that is, to maintain the original homeostasis of intracranial and extracranial. Including the use of diuretic dehydration drugs, moderate hypothermia and hyperventilation to control intracranial pressure (ICP less than 0.66kPa), and maintain the mean arterial pressure (MAP) of 18kPa with drugs immediately after the heartbeat is restored for 1-5 minutes. It was then maintained at around 12 kPa throughout the coma. The original hypertension can be as high as 13-16kPa; maintain PaO2 above 13.3kPa, PaO2 field between 3.3-4.6kPa. pHa between 7.30-7.45; maintain plasma colloid osmotic pressure above 2kPa, serum osmolality between 280-330mmol/L; blood sugar between 5.5-16mmol/L; actively control convulsions; 2. Specific measures, including Apply measures such as reducing brain metabolism, improving brain blood supply, preventing inflow, reducing the generation and scavenging of oxygen free radicals. The main channel blockers used for cerebral resuscitation are dofluzine, flubenazine, nimodipine, verapamil, and magnesium sulfate. It can reduce the formation of oxygen by acting on the hypoxanthine oxidase pathway. Deferoxamine can block the reaction by chelating iron ions, thereby preventing or reducing the generation of -OH. Mannitol and dexamethasone also play a role. In addition, in addition to reducing brain metabolism and scavenging oxygen free radicals, nizofinol has the functions of stabilizing biofilm, antithrombotic and promoting prostacyclin production. The latter is a natural antagonist of thromboxane. In the PLS stage, in addition to active cerebral resuscitation treatment, the functions of the heart, lung, liver, kidney, coagulation and digestive organs should be closely monitored, and targeted treatment should be taken once abnormality is found.

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相关标签:HumanAnatomyModel,HumanAnatomyModelCompany,HumanAnatomyModelManufacturer

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