Study On Correlated Clinical Factors Of Cardiogenic And Non-cardiogenic Cardiac Arrest In Intensive Care Unit

Research on cardiac arrest has been constantly considered as a great topic in medical science. According to statistics,in America , there are about 400-500 thousand cardiogenic sudden deathes every year. Cardiogenic cardiac arrest is usually caused by severe Electrophysiology disorders of heart ,which is always expressed as ventricular fibrillation in electrocardiogram and its incidence rate can reach to 72% left and right[4] 。Little correlated research has been done on non-Cardiogenic cardiac arrest 。Therefore we designed this research,and performed analysis and investigation on cardiac arrest patients induced by various etiological factors in our ward . Objective : Through discussion and investigation on the variability of correlated clinical factors of cardiogenic and non-Cardiogenic cardiac arrest patients, to elevate recognition to cardiac arrest caused by different etiological factors and to provide corresponding guidance for preventing cardiac arrest and elevating achievement ratio of resuscitation。Methods: All cardiac arrest patients were received from January to December in 2004 and be treated with cardiopulmonary resuscitation , to amount to 47 patients with males 31 ,female 16 and aged from 6 to 92 years .According to causes of cardiac arrest they were divide into two groups: cardiogenic group:20 patients with acute myocardial infarction 14 patients , other ischemic heart disease 4 patients, rheumatic valvular disease of heart 1 patients , dissection of aorta 1 patients ; non-cardiogenic group:27 patients with 6 patients treated with operations for severe pancreatitis,intestinal obstruction,abdominal trauma , 5 patients of severe infection , 6 patients of chronic obstructive pulmonary disease ,8 patients of craniocerebral trauma , 2 patients of cerebral thrombosis。All of blood samples were obtained before or during resuscitation,and were detected for blood biochemical indicators ,including creatine kinase isoenzyme, blood glucose, serum potassium , sodium ion and so on。At the same time of resuscitation , bedside contiguous electrocardio-monitoring was undertaken , and the electrocardiograms before and during cardiopulmonary resuscitation were reviewed continuously through central monitoring station。Statistical analyses were performed with the SPSS statistical package . To measurement data we adopt mean±standard deviation for statistical description,and t-test to compare two sets; To numeration data we adopt Mann-Whitney test (one of non-parametric tests) for multiple comparison 。The diference of P≤0.05 is significant。Results:Non-Cardiogenic group had higher incidence rate of hyperglycaemia ,hypernatronemia ,kaliopenia obviously than cardiogenic group ,and the extent of change had also significant statistical difference 。Cardiogenic group had higher myocardial enzymology obviously than non-Cardiogenic group .In the electrocardio-changes , cardiogenic arrest showed higher incidence rate of ventricular fibrillation and higher recovery rate of autonomic circulation。Non-Cardiogenic group took on higher incidence rate of brady-arrhythmia and lower of recovery rate of autonomic circulation。Discussion:In general intensive care unit ,most patients are critical ones from other correlated divisions,so the incidence rate of cardiac arrest and cardiopulmonary resuscitation is higher than other departments。From clinical observation ,we discover that patients of cardiac arrest induced by different causes have different blood biochemistry, different electrocardiogram,and different recovery rateof autonomic circulation . When internal environment disorder is concerned , non-cardiogenic cardiac arrestgroup took on higher incidence rate of hypernatremia,kaliopenia,and stress hyperglycemiastress hyperglycemia obviously .Data suggests that the incidence rate of hypernatremia, is 6%in America and 16.55%in domestic [20,21]。The hypernatremia incidence rate of our patients treated by resuscitation is 18.5%, and all of them were patients of craniocerebral injury for various causes,consistent with another report [22] 。Hypernatremia is common in deparment of cerebral surgery .It is related to insufficient intake of fluid for coma , using a great quantity of osmotic diurtc to treat cerebral edema, non-dominancy dehydration induced by insufficient humidification at the process of mechanical ventilation,loss fluid caused by central high fever .Meanwhile ,it may have more closer relationship with antidiuretic hormone dyssecretosis from craniocerebral injury [23]. At the earlier period of craniocerebral injury , the secretion of antidiuretic hormone reduces ,and then central diabetes insipidus occurs with the result of hypernatremia。Hypernatremia usually cause conspicuous hyperosmosis state,resulting in cell dehydration .Nerve cell dehydration leads to nervous malfunction ,aggravation of coma and even death .Significant hypernatronemia may result in bradycardia and bundle branch block。If kaliopenia occurs on patients after abdominal surgery or craniocerebral injury ,it is due to taking food too late after operations ,gastrointestinal decompression,intestinal juice drainage or osmotic diurtc .On partial patients of craniocerebral injury,it may be also attributed to functional injury of pituitary gland after surgical trauma,resulting in central diabetes insipidus for reduction of antidiuretic hormone secretion and poor supply of potassium .Hypopotassemia can account for making resting membrane potential absolute value of myocardial cell diminish , excitability increase and membrane permeability to potassium drop , forming relative augmentation of the inward current ,and accelerating the rate of automatic depolarization of myocardial cell at the active potential 4 phase , leading to the increase of autorhythmicity .Clinical manifestation show increased incidence rate of tachycardia and ectopic excitement [25].The boundary value of stress hyperglycemia is fasting plasma glucose≥6.1mmol/L or random blood sugar;RBS≥11.1mmol/L[26]. Higher rate of stress hyperglycemia in non-cardiogenic cardiac arrest is due to more irritable factors,which result in increase of decomposition stimulating hormone .Meanwhile ,at critical state , there is phosphorylation disturbance of various signaling transduction channels'moleculars activated by insulin,which makes the function of corresponding glucose transporter decrease , results in dysfunction of glucose transport mediated-by-insulin [27],and makes the clearance rate of glucose decrease obviously . The loss of equilibrium of producting/ clearing glucose is account for hyperglycaemia . If blood glucose keeps on fluctuating at a high level for a long time ,some pathological change will happen ,and it does harm to organism similar to diabetes [30],resulting in hyperosmotic anhydration, osmotic diuresis, functional disturbance or electrolyte disturbances like hypernatremia and kaliopenia. Cardiogenic arrest group had more serious myocardial damage .It was because that most of this group were acute myocardial infarction patients .In the blood-supply areas of acute coronary angiemphraxis , ischemia and necrosis of myocardial cells takes place ,releasing the content of these myocardial cells and makingcardiac creatase in serum increase .At the same time ,the change of myocardial enzymology is in direct proportion to area of necrosis .When the area reaches to more than 40%of the left ventricle, pumping function failure 。Myocardiolysis and cardiac failure always supply a basis for astable electric potential of myocardial cells ,initiating various kinds of malignant arrhythmia easily . Non-cardiogenic cardiac arrest group had also increased myocardial enzymology ,which may be caused by the effects on myocardial cells of secondory general hypoxia,shock,acidosis and other factors like myocardial depressant factor,TNF-αand so on ,at the basis of primory diseases . Simultaneously ,it should be paid attention to that the primary diseases and subsequent SIRSof non-cardiogenic cardiac arrest patients may initiate the incidence of acute coronary artery syndrome . In the electrocardiographic changes , ventricular fibrillation was often seen in cardiogenic cardiac arrest group .It may be because that acute ischemia and necrosis of the myocardial cells could induce different length of different parts'refractory periods, reentry excitement is formed ,and when ectopic excitement is enough high or drops to ventricular vulnerable period , ventricular tachycardia,ventricular fibrillation or ventricular flutter will happen .Non-cardiogenic cardiac arrest group had higher incidence rate of brady-arrhythmia .This may be caused by that oxygen demand of critical patients increased for trauma,infection,sepsis and so on ,and when shock,respiratory failure and congestive heart failure happened , oxygen ventilation and oxygen consumption would be injured,leaving organism tissue in severe "oxygen debt"state [37],in which condition ,organism would obtain energy for cell metabolism through anaerobic metabolism and in this progress, product a large quantity of endogenous adenosine that had negative muscle power and negative chronotropic effect inducing sinus bradycardia and atrial ventricular block [33]. Severe hypoxia,acidosis,metabolic product-myocardial depressant factor and so on have also a depressant effect on cardiac rhythm .When it's coming to recovery rate of autonomic circulation after resuscitation ,cardiogenic arrest group is higher than non-cardiogenic cardiac arrest group .The reason may be that internal environment only changed slightly,and when cardiac arrest happened , ventricular fibrillation is the major pattern of manifestation of electrocardio-activity ,and can be treated quickly by lightning stroke defibrillation after finding abnormality of electrocardiogram,and recover to normal cardiac rhythm . When patients of non-cardiogenic cardiac arrest group happened to cardiac arrest , most of the internal environment had obvious disorder .Even given standard cardiopulmonary resuscitation and drug treatment,causes of cardiac arrest could nor be removed quickly.When drugs were not ineffective on brady-arrhythmia , bedside temporary pacing isthe optimal chose ,but existing medical condition constraint its wide application , therefore the recovery rate of autonomic circulation is low。Conclusion:Patients of non-cardiogenic cardiac arrest group had conspicuous internal environment disorders,which may participate in the progress of inducing non-cardiogenic cardiac arrest , and cause low recovery rate of autonomic circulation with high incidence rate of brady-arrhythmia simultaneously .Severe myocardial ischemia and injury is the basis of cardiac electrophysiological abnormality of patients who happened to cardiogenic arrest. High incidence rate of ventricular fibrillation and treated with lightning stroke...