Cardiac Arrest and CPR
Introduction
Introduction to cardiac arrest and cardiopulmonary resuscitation Cardiac arrest refers to the sudden stop of the heart caused by various reasons, the effective pumping function disappears, causing severe hypoxia and ischemia in the whole body. The clinical manifestations are that the aortic pulsation and heart sound disappear; after the loss of consciousness, the breathing stops, Dilated pupils can cause death if not rescued in time. It is generally believed that cardiac arrest can cause dizziness or syncope after 5 to 10 seconds, and coma and convulsions may occur after more than 15 seconds. If the heartbeat is stopped for more than 5 minutes, the brain may be seriously injured or killed, even if it is repeated. There are different degrees of sequelae left behind. Therefore, cardiac arrest is the most critical emergency in the clinic, and it must be raced against time to actively rescue. basic knowledge The proportion of illness: more common in patients with drowning and original heart disease 0.005%-0.008% Susceptible people: no special people Mode of infection: non-infectious Complications: hypotension, coma, arrhythmia, cerebral edema, atelectasis, hyperkalemia, urinary tract infection
Cause
Cardiac arrest and cardiopulmonary resuscitation
(1) Causes of the disease
Cause
(1) Coronary artery disease:
1 coronary atherosclerotic heart disease: coronary heart disease is the most common cause of sudden cardiac death, clinical data reported that coronary heart disease sudden death accounted for 42% to 75% of all cardiac death, a group of 463 cases occurred within 12h of sudden death At autopsy, coronary heart disease was found to be as high as 91%, of which about half died of acute myocardial infarction. The sudden death of coronary heart disease was related to the severity of coronary and myocardial lesions. The more severe the vascular involvement, the higher the incidence of sudden death, acute coronary artery disease. Such as plaque rupture, platelet aggregation, acute thrombosis is an important cause of sudden cardiac death. In recent years, coronary angiography, angioscopy and autopsy studies have considered plaque rupture and hemorrhage based on the original intraluminal thrombosis. Acute injury leads to acute myocardial infarction, and is also associated with unstable angina and sudden cardiac death. It has recently been noted that asymptomatic myocardial ischemia is most common in patients with definite coronary artery disease, stable or unstable angina and previous myocardial infarction. Asymptomatic myocardial ischemia can occur in patients with infarct history, and heart accidents including sudden cardiac death Sexuality is also increased. It is believed that in patients with coronary artery disease, asymptomatic or symptomatic myocardial ischemia may have no myocardial scar or almost no myocardial scar, which may be a reversible cause of polymorphic ventricular tachycardia. Infarcted patients may be the trigger for monomorphic ventricular tachycardia.
2 Coronary artery spasm: Nearly Fellows et al reported that 4 of 260 cardiac arrest survivors (1.5%) were due to coronary artery spasm, but lacked significant, well-defined coronary lesions, which are now more certain, severe coronary Arterial spasm is sufficient for ST-segment elevation, and can be asymptomatic or severe arrhythmia. Spontaneous ST-segment elevation and severe arrhythmia occur simultaneously in patients with variant angina, often suggesting a poor prognosis, Miller Reported in patients with variant angina, 42% of the above-mentioned manifestations were sudden death, and only 6% of those without arrhythmia died.
Corrado reported 200 sudden deaths in the Veneto region of Italy, with an average age of 29.4 years (18 to 35 years). Only 27% of the patients had obstructive plaques, and most (89%) young patients died of single-vessel disease. And the left anterior descending artery lesions are mainly composed of intimal smooth muscle cell proliferation without acute thrombosis and normal fibrous plaque in the middle layer. Such plaques have strong reactive contraction and may induce sudden death.
3 Others: If the origin of the coronary artery is abnormal, a group of young athletes died suddenly during exercise, a total of 22 cases, 2 cases of autonomic examination found abnormal origin of coronary artery.
(2) Non-coronary artery disease:
1 primary cardiomyopathy: hypertrophic cardiomyopathy often occurs sudden death, more than half of which occurred before the age of 20, but can also occur at any age, the risk of sudden death in patients with ventricular septal hypertrophy 25mm, the degree of left ventricular outflow tract stenosis Whether it is related to the risk of sudden death, there is data showing that there is no significant difference between the sudden death rate and the left ventricular outflow tract stenosis group without the left ventricular outflow tract stenosis or the pressure gradient of the surgical outflow tract. It is more positive. Family history patients have a high incidence of sudden death, and the incidence of sudden death in dilated cardiomyopathy is also high, about 30%. The pathogenesis of sudden death is still unclear, mostly due to ventricular tachyarrhythmias (including ventricular tachycardia and ventricular fibrillation). A small number of deaths from slow arrhythmia may cause these arrhythmias: extensive subendocardial scar formation and focal fibrosis, causing repolarization unevenness and reentry formation; hemodynamic factors such as afterload And left ventricular end-diastolic volume increased; other may also have electrolyte changes (low potassium, low magnesium), neurohumoral factors, Martini in the analysis of 6 young people without significant heart disease The clinical examination data of patients with tremors found that 5 of them had obvious idiopathic fibrosis and right ventricular abnormalities. It is considered that the occult type of right ventricular cardiomyopathy is much more than usual, and should be considered for young patients with fatal arrhythmia. Equal attention is paid to the diagnosis of left and right ventricular cardiomyopathy.
2 valvular disease: rheumatic heart disease patients with aortic stenosis about 25% can cause sudden death, which may be related to coronary artery insufficiency caused by ventricular fibrillation, heart block, etc., chronic rheumatic heart disease in heart failure or Sudden death is associated with acute or subacute endocarditis.
Primary mitral valve prolapse is often due to mucoid changes in the mitral valve, accompanied by excessive or loose valves. The mitral leaflets may protrude into the left atrium during the systolic phase of the left ventricle to form prolapse and/or regurgitation. And produce the corresponding systolic murmur - click sound, due to increased myocardial stress and early stage of left ventricular systolic dysfunction, often causing tachyarrhythmia, such as short-term atrial tachycardia or ventricular tachycardia, about 10% Sudden death, the following signs often appear before sudden death: ventricular premature contraction, syncope episodes, late systolic and full systolic murmurs, most cases of ventricular tachycardia or ventricular fibrillation, analysis of a group of 15 cases of sudden death of mitral valve Patients with sputum: younger (39 ± 17 years), more women (67%), fewer mitral regurgitation (7%), fewer chordae rupture (29%).
In patients with valvular heart disease undergoing valve replacement, sudden cardiac death is a fairly common complication. Alvarez reported 831 patients with Bjorkshiley prosthetic valves, with an average follow-up of 68.2 months, and 24 sudden deaths, accounting for 16% of deaths. The ventricular premature contraction was significantly more than the survivor and died of other causes. The authors believe that ventricular premature contraction is associated with sudden death.
3 congenital heart disease: tetralogy of Fallot in congenital heart disease, especially in patients with severe pulmonary stenosis before surgery, followed by sudden death, followed by Aishengmanger syndrome, in recent years, arrhythmia Right ventricular dysplasia is a cause of sudden death, and arrhythmogenic right ventricular dysplasia often appears as a "healthy" adult. It has discomfort or palpitations during activities. Activities can often cause ventricular tachycardia. About 50% of patients are originally The physical examination is normal, some patients have more extreme right ventricular enlargement, the chest wall is asymmetrical, and young people develop ventricular tachycardia after exercise, including polymorphic ventricular tachycardia, multiple ventricular tachycardia and primary Ventricular fibrillation, clinical manifestations of syncope or cardiac arrest resulting in sudden death.
4 Others: Myocarditis often occurs in children and adolescents. Acute diffuse myocarditis causes a high risk of sudden death. Among a group of athletes aged 13 to 30 years, myocarditis is the second cause of sudden death. The pathological changes of myocarditis are mainly myocardial inflammation. Cell infiltration, myocardial cell edema, necrosis, involving the conduction system can cause severe arrhythmia such as atrioventricular block, severe myocarditis can easily cause cardiogenic shock and sudden death, multi-systemic sarcoidosis is not uncommon, about 20% of cases can be Cardiac involvement is a cause of sudden death. Cardiac hypertrophy can be caused by cardiac hypertrophy. When the lesion is extensive, various conduction blocks can occur, frequent ventricular tachycardia, ventricular tachycardia and reentry complex arrhythmia, etc. Sudden death can occur, and other sudden deaths such as cardiac tumors (myxomas) can also occur.
(3) Electrophysiological abnormalities:
1 congenital or acquired long QT syndrome: patients with primary QT prolongation syndrome often have a family history, most patients with congenital deafness, some patients with complete hearing, strenuous exercise or emotional susceptibility Fainting accompanied by prolonged QT interval, electrocardiogram can have severe arrhythmia such as torsade ventricular tachycardia, ventricular fibrillation or occasional ventricular arrest, short-term fainting episodes can recover spontaneously, longer duration can be sudden death, hypokalemia, Myocarditis, coronary heart disease, etc. can lead to the extension of secondary QT interval, complicated by polymorphic ventricular tachycardia, in addition to quinidine, amiodarone, propiamine and other drugs can prolong the QT interval, vulnerable period Prolonged, when the ventricular contraction falls in the vulnerable period, it is easy to fold back to form a torsade ventricular tachycardia. If it develops into ventricular fibrillation, sudden death can occur.
2 Pre-excitation syndrome: When pre-excitation syndrome with atrial fibrillation, the time limit of the bypass refractory period has a positive relationship with the ventricular rate. The shorter the refractory period of the atrioventricular accessory pathway, the more likely the atrial fibrillation will become a malignant arrhythmia. Sudden death, Klein reported 25 patients with ventricular fibrillation in atrial fibrillation, bypass refractory period of at least <250ms, so patients with short refractory period should pay attention to prevent sudden death.
3 conduction system lesions: some patients with sudden death are related to abnormalities in the structure of the heart conduction system and the involvement of the disease, abnormalities in the structure of the cardiac conduction system, cases of ventricular fibrosis in the Maham fiber, and ectopic tachycardia appear, and the electrocardiogram appears left. Bundle conduction block, Bharati et al observed ventricular tachycardia with left bundle branch block, James fiber as a bypass of the heart conduction system into the atrioventricular node and bundle junction, because it participates in the heart conduction system impulse The reversal, and bypassing the atrioventricular node, thus disturbing the normal rhythm of the heart, and accelerating the transmission of some impulses, which in turn causes tachycardia, the presence of James fiber in the atrioventricular conduction system, and the impediment to the dying Play an important role, the atrioventricular node and the bundle in the central fiber, such as maintaining the fetal period of dissociation state, people with this histological structure are prone to sudden death, which may be due to a large number of heart impulses into the scattered in the center of the fiber body isolated from each other Conducting a beam, causing a fatal arrhythmia.
Some diseases involve the heart conduction system, and sudden death of patients with cardiomyopathy has been as described above. In infants with cardiomyopathy, swollen vacuole-containing adipose cells are interwoven in the sinus node and atrioventricular node, and it is also found in the heart. Left bundle branch and Purkinje fiber, subventricular and interventricular septum, patients with sudden vomiting and tachycardia with right bundle branch block and sudden death, invasive cardiomyopathy such as myocardial sarcoma, atrioventricular Knot, Xizhizhi was infiltrated by granulomatous heart conduction block, ventricular arrhythmia, and even sudden death, heart amyloidosis especially in the elderly, sinus node is extremely susceptible, manifested as atrial fibrillation, sinus heartbeat, I degree atrioventricular block and severe ventricular arrhythmia lead to sudden death, fat infiltration of the myocardium involving the conduction system to cause conduction dysfunction leading to sudden death, the sinus node of the cardiac conduction system of patients with equine syndrome, and atrioventricular node Membrane hyperplasia, stenosis or even occlusion of the lumen, rupture of the mid-membrane elastic fibers, fibrosis of the two knot cells with fat infiltration, impaired pacing function of the knot can lead to severe arrhythmia and ventricular fibrillation
Predisposing factors
(1) Behavioral stress and sudden cardiac death: Modern studies have shown that behavioral stress increases ventricular vulnerability, induces malignant arrhythmia, and epidemiological studies of the relationship between type A behavior and death patterns. The pathophysiological mechanism associated with type A behavior may be that type A behavioral individuals have a strong sympathetic response to environmental stress stimuli. This high sympathetic response makes the heart prone to ventricular fibrillation, and studies also reflect "passive" peripheral nerve tension. Insufficient changes to trigger ventricular arrhythmias, but impulses from the high-level nerve center can increase the frequency and level of premature ventricular arrhythmia, and analyze a high level of neurological activity and arrhythmia in a group of 117 patients with frequent fatal arrhythmias. Relationship, the results show that 25 of them (21%) arrhythmia is triggered by mental factors, most of which occur within 1 hour before the onset of fatal arrhythmia, interpersonal conflict, anger, sadness and other psychological factors can become triggers of arrhythmia factor.
Excessive physical activity, especially exercise, after a meal or when the climate is cold, a large amount of catecholamines are released, myocardial oxygen consumption is increased, blood supply and oxygen consumption are imbalanced, resulting in acute myocardial ischemia-induced arrhythmia, clinically ischemic heart disease patients It is not uncommon for exercise tests to induce frequent ventricular tachycardia and ventricular tachycardia. There are also reports of induced ventricular fibrillation. For example, a group of 22 young athletes died suddenly. Among them, 18 sudden deaths occurred during exercise and shortly after exercise, and 17 deaths may be caused by Arrhythmia caused by cardiac arrest, strenuous exercise is the cause.
(2) Electrolyte disorders: ventricular tachycardia and ventricular fibrillation can occur in hyperkalemia or hypokalemia. Patients with refractory heart failure with low sodium and low chlorine syndrome are prone to sudden death. A large number of studies in the last 30 years have shown that Magnesium deficiency is associated with sudden death, and sudden death is common in areas with magnesium deficiency in water; and myocardial magnesium levels are reduced at autopsy in patients with sudden death; magnesium deficiency can cause arrhythmias (including early, ventricular or supraventricular arrhythmias) and coronary artery spasm Intravenous magnesium supplementation reduces the risk of arrhythmias and sudden death after acute myocardial infarction.
(3) heart failure: heart failure patients are prone to sudden death, in the ventricular muscle with scar and poor compensation, depolarization, repolarization unevenness can lead to ventricular arrhythmia, especially in the blood catecholamine and heart failure The product can cause ventricular fibrillation caused by ECG instability. The use of digitalis and diuretics in heart failure can lead to hypokalemia, arrhythmia and decreased ventricular fibrillation threshold. Mild myocardial ischemia may induce severe arrhythmia and cause sudden death.
(4) Side effects of antiarrhythmic drugs: It is well known that many antiarrhythmic drugs have arrhythmogenic side effects, such as quinidine, amiodarone, acetamidamine, etc., which may cause torsion when selected for the treatment of arrhythmia Sedation and ventricular fibrillation.
(two) pathogenesis
1. Ventricular arrhythmia: The main cause of sudden cardiac death is fatal arrhythmia. According to the dynamic electrocardiographic record of 61 patients with sudden cardiac death, fatal arrhythmia occurred: 26 cases (43%) Sexual ventricular tachycardia, 15 (25%) polymorphic ventricular tachycardia, 5 (8%) torsades de pointes, 3 (5%) primary ventricular fibrillation and 1 (2%) atrial tachycardia Speed with 1:1 conduction, slow arrhythmia 11 cases (18%), the mechanism of ventricular tachyarrhythmia is not fully understood, may be the result of interaction of various factors and pathological structure and function abnormalities of various diseases The interaction between the heart and the autopsy of the heart that reported sudden cardiac death found that 75% of the original old myocardial infarction, pathologically confirmed the presence of acute myocardial infarction only 20.9% to 30%, in recent years between ventricular hypertrophy and cardiac death More and more attention is paid to the ventricular hypertrophy in addition to the complex chronic ventricular arrhythmia as a risk factor, and as an independent risk factor for fatal arrhythmia, coronary heart disease with secondary ventricular hypertrophy, primary Sexual ventricular hypertrophy (hypertrophic cardiomyopathy) Sudden or ventricular fibrillation and sudden death account for more than half of the total number of deaths, patients with chronic myocardial disease with dilated and diffuse fibrosis, the incidence of severe polymorphic ventricular arrhythmia is high, and half of them are sudden death.
Most of them are due to ventricular tachycardia or ventricular fibrillation. From the available data, long-term left ventricular hypertrophy can cause regional differences in focal fibrosis and action potential, and ventricular fibrillation is more likely to occur during acute ischemia. Sexual functional changes such as transient ischemia (reperfusion), systemic metabolic and hemodynamic abnormalities, changes in neurochemistry (neurological physiology), and effects of harmful substances on the myocardium may interact with structural abnormalities. Fatal arrhythmia, coronary artery structural lesions cause regional myocardial blood flow stability is reduced, the cells are in a state of significant electrical instability, such as acute thrombosis, oxygen supply / demand balance changes, myocardial metabolism or electrolyte light Degree fluctuations and neurophysiological instability can lead to regional membrane instability, which may be the mechanism of exercise-induced arrhythmia and sudden death. Electrophysiological studies show that Purkinje fiber is self-disciplined and transmitted during acute myocardial ischemia. The speed is slowed down, and the repolarization and recovery time between the connected cardiomyocytes are not synchronized, so the current of the potential difference is easily generated, and a reentry pathway is formed to cause the chamber. Coronary artery spasm with collateral circulation can cause the myocardial to suffer from both transient ischemia and reperfusion. In triggering fatal arrhythmias, both platelet aggregation and thrombosis may be key events in triggering Platelet activation based on thrombus produces a series of biochemical changes that may increase the susceptibility to ventricular fibrillation through vasomotor regulation. In metabolic reactions, interstitial potassium concentration increases during acute ischemia, whereas potassium in the marginal cells of old infarcts The concentration is regionally reduced, the resting membrane potential is lost and the rapid reaction rate is reduced, the lactate and free fatty acids are increased, the action potential time is shortened, and the tissue CAMP is increased, which induces a slow reaction, which may destroy the myocardial in some regions and overall. The integrity of the membrane makes it susceptible to electrical triggered ventricular tachycardia or ventricular fibrillation.
2. Electromechanical separation: Electro-mechanical separation is about 3% to 22% of the cause of sudden cardiac death outside the hospital. It is also a common cause of sudden cardiac death in the hospital. Patients often experience sudden loss of consciousness and no previous heart or respiratory symptoms. Heart sounds and pulse disappeared. There is an electrocardiogram waveform of the atrioventricular system on the ECG, but the ventricle has no effective blood discharge function. This is common in heart rupture, acute pericardial tamponade, rupture of aortic sinus aneurysm, acute myocardial infarction, etc., electro-mechanical The mechanism of separation is thought to be closely related to calcium, triggering the loss of calcium flux, calcium cannot be released from the sarcoplasmic reticulum, and the sensitivity of the contraction process to calcium is reduced. Ischemic acidosis can change the affinity of calcium for contractile proteins. Myocardial contractility is reduced. On the other hand, it is thought that there is a role played by the autonomic nervous system. The sharp increase in parasympathetic activity or the sharp decrease in sympathetic activity may be the trigger mechanism for electromechanical separation, and the heart rate and blood pressure decreased due to Bezolel-Jarisch reflex. Common in the inferior wall infarction, which may play a role in the occurrence of electromechanical separation.
Prevention
Cardiac arrest and cardiopulmonary cerebral resuscitation prevention
1. The success rate of cardiopulmonary resuscitation after cardiac arrest and sudden cardiac death is very low, so it is mainly active prevention. First aid intervention (on-site first aid) is mainly to strengthen the popularization of cardiopulmonary resuscitation training for the public and improve public emergency. Consciousness; strengthen the construction of the first aid system, expand the emergency network and shorten the time from the call to the scene, so that patients can be treated in time to reduce the sudden death rate.
2. Strengthen the monitoring of environmental factors, genetic factors of common cardiovascular diseases, follow a reasonable lifestyle, and avoid the causes of sudden death such as overeating, overeating, strenuous exercise and emotional agitation.
3. Familiar with the identification of high-risk patients with cardiac arrest, the following situations are prone to cardiac arrest:
1 has a history of primary ventricular fibrillation.
2 patients with coronary heart disease, had a history of rapid ventricular tachycardia.
3 Within 6 months after the recovery of acute myocardial infarction, ventricular premature systolic grading was above Grade II, especially with severe left ventricular dysfunction (EF < 40%) or significant heart failure.
4 There is an increase in QT interval and QT interval dispersion, especially in patients with syncope.
4. Prevention of recurrent cardiac arrest
For survivors of persistent ventricular tachycardia or ventricular fibrillation, antiarrhythmic drugs may be used to prevent recurrence of potentially fatal arrhythmias; if not, newly performed surgical treatment or implantation of anti-tachycardia And anti-ventricular fibrillation devices can be considered.
Complication
Cardiac arrest and complications of cardiopulmonary cerebral resuscitation Complications, hypotension, coma, arrhythmia, cerebral edema, atelectasis, hyperkalemia, urinary tract infection
Due to hypoxia caused by cardiac arrest, carbon dioxide retention and acidosis, electrolyte imbalance has not been corrected, the function of the vital organs of the body has not recovered after injury, and cardiovascular function and blood flow are often found after spontaneous circulation recovery. Disorders such as learning, often have shock, arrhythmia, cerebral edema, renal insufficiency and secondary infections and other complications.
1. Hypotension and shock: hypoxia and carbon dioxide accumulation can affect myocardial function; intrathoracic heart compression or intracardiac puncture injection of too many times, all affect the function of the heart muscle, so that the heart beat volume is reduced, resulting in hypotension, heart and lung The heart pump function of patients with resuscitation changes, the early cardiac output during resuscitation is mostly low, because the heart rate increases, the cardiac output can still be compensated, but the left ventricular per beat function index and peripheral vascular resistance increase, the myocardial contractile function decreases significantly. The heart index is reduced.
2. Heart failure: the heart relapses for too long, the myocardium is in a state of ischemia and hypoxia for a long time, causing damage to the heart; the application of a large number of vasoconstrictor drugs in the rescue, so that the peripheral vascular resistance increases, correspondingly increase the burden of the heart, plus heart rhythm Abnormalities, excessive fluid input, too fast and electrolyte imbalance and acid-base balance disorders, etc. damage the heart muscle, increasing the burden on the heart can easily lead to acute left heart failure.
3. Arrhythmia: The causes of arrhythmia mainly include myocardial hypoxia damage after cardiac arrest, severe electrolyte or acid-base balance disorder, the effect of resuscitation drugs, some drugs are misplaced into the myocardium during intraventricular injection, excessively low temperature, etc. Because the above pathophysiological and biochemical changes directly affect the myocardium, the stress of the myocardium increases and causes various arrhythmias.
4. Respiratory insufficiency: During the rescue of cardiopulmonary resuscitation, the patient is in a coma, the cough reflex disappears, the airway secretion cannot be cleared in time, the atelectasis is easily caused, the ventilation/blood flow ratio is imbalanced, and the intrapulmonary shunt increases, resulting in low Oxygenemia; simultaneous inhalation of sputum and reflux of stomach contents, as well as dehydration, hibernation drugs, low-temperature and high-dose corticosteroids, can cause lung infection; therefore, adult respiratory distress can occur in the early stage of resuscitation Sign.
5. Nervous system complications: patients with cardiac arrest are successful in initial resuscitation, but the rate of morbidity in the nervous system is extremely high, ranging from focal to diffuse brain damage, from temporary to permanent damage. Mild dysfunction to irreversible coma and death, so brain resuscitation not only needs to quickly improve and correct the immediate effects of cerebral ischemia, but also actively prevent secondary cerebral ischemia and hypoxia damage after sudden arrest, and promote brain function. Can be restored as soon as possible.
6. Renal failure: due to cardiac arrest and hypotension, renal blood flow stops or decreases, causing renal cortical ischemia and renal vasoconstriction. When blood pressure is lower than 8.0 kPa (60 mmHg), glomerular filtration stops. Increases angiotensin and renin activity, further causing renal vasoconstriction and renal ischemia, which lasts for too long and can cause renal failure.
7. Water and electrolyte imbalance: In the process of rescue of patients with cardiac arrest, water and electrolyte disorders are prone to occur, such as hyperkalemia, hypokalemia, high sodium and hyponatremia.
8. Acid-base metabolism imbalance: During myocardial arrest and resuscitation, tissue acidosis and the resulting acidosis are dynamic processes due to hypoventilation and hypoxia metabolism, which depends on cardiac arrest time. The length of blood flow and the level of blood flow during CPR.
9. Infection: The cause of secondary infection after resuscitation is not only related to the invasion of pathogenic bacteria, but more importantly, in the process of resuscitation, due to the weakening of the body's defense ability, the pathogens take advantage of it, especially in the human body or the environment. Non-pathogenic bacteria or weak pathogens have become important pathogens of infection, such as pneumonia, sepsis, urinary tract infections and other infections.
10. Digestive system complications: After successful resuscitation in patients with cardiac arrest, the microvascular hypoxic zone persists, and the hypoxic zone stimulates and enhances the immune response, thereby increasing oxygen demand and oxygen uptake, resulting in increased hypoxemia. Due to the fragile intestinal mucosal tissue, it is extremely poorly tolerant to hypoxia, and is prone to low perfusion injury, and intestinal failure and upper gastrointestinal bleeding may occur.
11. Other complications
(1) Hyperglycemia: The body will have an increased blood glucose response after suffering severe traumatic stress.
(2) hyperamylasemia: may be related to pancreatic ischemia after cardiac arrest, hypoxia leads to a large release of pancreatic amylase.
Symptom
Cardiac arrest and cardiopulmonary resuscitation symptoms Common symptoms Palpitation cardiac arrest Carotid pulsation weakened or disappeared Consciousness loss Sudden heart decompensation Anal sphincter relaxation Cochlear ventricular fibrillation
The occurrence of sudden cardiac death has a rhythm change with an increased incidence in the morning. The increase in the morning incidence may be related to the increase in physical strength and mental activity of the patient at this time. The increased risk of myocardial ischemia, ventricular fibrillation and thrombosis is a heart disease in the morning. The possible cause of sudden death, the patient can have no symptoms before the death, or even a history of organic heart disease. About half of the sudden death patients often have chest pain, palpitations, fear, progressive fatigue and other aura symptoms within 2 weeks. .
Cardiac loss is effectively contracted for 4 to 15 s, that is, clinical signs appear, mainly: sudden unconsciousness or convulsions, rapid and shallow breathing, slow or stop, aortic pulsation disappears, heart sounds disappear, pupil dilated, skin cyanosis, nerve reflex Disappeared, some patients died quietly during sleep.
Examine
Cardiac arrest and cardiopulmonary resuscitation
Metabolic acidosis due to hypoxia, decreased blood pH, and increased blood glucose and amylase may occur.
It must be pointed out that the diagnosis of cardiac arrest is mainly based on clinical manifestations, and laboratory and instrumental examinations are secondary.
1. Electrocardiogram: There are three types of ECGs that are performed during cardiac arrest:
1 ventricular fibrillation is the most common, accounting for 77% to 85%; the performance of the QRS wave disappears, replaced by regular or irregular ventricular flutter or tremor wave;
2 ventricular pause: 5%, because the ventricular electrical activity stops, the ECG is in a straight line or there is still atrial wave;
3 electro-mechanical separation: about 15%, showing a slow, wide, low-amplitude QRS wave, but does not produce effective ventricular mechanical contraction, it is generally believed that the success rate of ventricular pause and electromechanical separation recovery is lower.
2. EEG: brain waves are low.
Diagnosis
Cardiac arrest and differential diagnosis of cardiopulmonary cerebral resuscitation
Diagnostic criteria
Electrocardiogram examination revealed that the PQRS wave disappeared and the ventricular fibrillation waveforms of varying thickness were present, or the electrocardiogram showed a slow deformed QRS wave, but did not produce effective myocardial mechanical contraction. The ventricular pacing ECG was straight or only atrial wave.
1. Clinical manifestations
1 sudden loss of consciousness or convulsions;
2 large arterial pulsations (femoral artery, carotid artery) disappeared;
3 can not hear the heart sound, can not detect blood pressure;
4 acute pale or cyanosis, followed by respiratory arrest, dilated pupils, fixed, anal sphincter relaxation.
Among them, 1, 2 are especially important.
2. Laboratory and equipment inspection
Electrocardiogram showed ventricular fibrillation, ventricular arrest or ventricular self-pulsation rhythm; EEG showed low brainwave.
In fact, as long as the patient has acute loss of consciousness and disappearance of the aortic pulsation, it is enough to establish the diagnosis of cardiac arrest without relying on ECG and other examinations, so as not to delay the rescue.
Differential diagnosis
During cardiac arrest, wheezing or cessation of breathing often occurs, but sometimes the breathing is still normal. During the cardiac arrest, if the resuscitation is rapid and effective, the automatic breathing can always be good. When the cardiac arrest occurs, the skin often appears. The mucous membranes are pale and cyanotic, but they are easily overlooked under the light. If there is severe suffocation or hypoxia before cardiac arrest, the cyanosis is often obvious.
Cardiac arrest can cause sudden loss of consciousness and should be differentiated from many diseases such as fainting, epilepsy, cerebrovascular disease, major bleeding, pulmonary embolism, etc., which can sometimes cause cardiac arrest, such as the disappearance of the aorta of these patients. Resuscitation should be performed immediately, and heart compression is not a problem for the beating heart, but it can also help the heart with insufficient cardiac output.
