Paediatric Cardiac Respiratory Arrest and CPR
Introduction
Introduction to pediatric cardiac arrest and cardiopulmonary resuscitation Cardiopulmonary resuscitation (CPR) refers to the use of emergency medical means to restore interrupted respiratory and circulatory functions. It is the most important and critical rescue measure in emergency rescue techniques. Cardiac and respiratory arrest are often causal and concomitant. Therefore, the first aid work needs to be taken into consideration at the same time, otherwise the recovery is difficult to succeed. The ultimate goal of cardiopulmonary resuscitation is not only to reconstruct breathing and circulation, but also to maintain brain cell function, not to leave behind the sequelae of the nervous system, to ensure the value of survival, with the deepening of the understanding of the importance of protecting brain function and brain resuscitation, it is better to resuscitate the whole process Called cardiopulmonarycerebralresuscitation (CPCR), the criteria for successful cardiopulmonary resuscitation in children are: cardiopulmonary function returns to pre-disease levels, no convulsions, feeding difficulties and physical movement disorders, normal language expression, intellectual accessibility. basic knowledge The proportion of illness: 0.001% Susceptible people: children Mode of infection: non-infectious Complications: metabolic acidosis, convulsions in children
Cause
Pediatric heartbeat respiratory arrest and cardiopulmonary resuscitation
(1) Causes of the disease
1. Causes of cardiac arrest
(1) Conditions secondary to respiratory failure or respiratory arrest: such as pneumonia, asphyxia, drowning, and tracheal foreign body, are the most common causes of cardiac arrest in children.
(2) surgery, treatment operations and anesthesia accidents: cardiac catheterization, fiberoptic bronchoscopy, endotracheal intubation or incision, pericardial puncture, cardiac surgery and anesthesia can occur during cardiac arrest, possibly with hypoxia, anesthesia Too deep, arrhythmia and vagus reflex are related.
(3) Trauma and accidents: Children more than 1 year old, such as craniocerebral or chest trauma, burns, electric shock and drug allergy.
(4) Heart disease: viral or toxic myocarditis, arrhythmia, especially A-S syndrome.
(5) Poisoning: In particular, potassium chloride, digitalis, quinidine, bismuth preparations, fluoroacetamide rodenticides and other drug poisoning are more common.
(6) severe hypotension: severe hypotension can cause coronary perfusion and tissue perfusion, resulting in ischemia, hypoxia, acidosis, etc. can lead to cardiac arrest.
(7) imbalance of electrolyte balance: such as hyperkalemia, severe acidosis, low blood calcium.
(8) Sudden infant syndrome.
(9) excessive vagal tone: not the main cause of cardiac arrest in children, but if the child is in a state of severe hypoxia due to inflammation of the throat, use the tongue depressor to check the pharynx, can cause heart beat, respiratory arrest .
2. Causes of respiratory arrest
(1) Acute upper and lower airway obstruction: more common in pneumonia, stagnation of children with respiratory failure, tracheal foreign body, gastroesophageal reflux, throat, laryngeal edema, severe asthma persistent state, strong acid, strong alkali-induced airway burn , diphtheria membranous occlusion, etc., in recent years, infants with respiratory tract infections (such as respiratory syncytial virus) caused by airway hyperresponsiveness-induced apnea cases have an increasing trend.
(2) Severe lung tissue disorders: such as severe pneumonia, respiratory distress syndrome.
(3) Accidents and poisoning: such as drowning, neck twisting, drug poisoning (sleeping pills, arrow poison, cyanide poisoning, etc.).
(4) central nervous system inhibition: craniocerebral injury, inflammation, tumor, cerebral edema, cerebral palsy and so on.
(5) Thoracic injury or bilateral tension pneumothorax.
(6) Muscle neurological disorders: such as infectious polyradiculitis, muscle weakness, progressive spinal muscular dystrophy, and advanced dermatomyositis.
(7) secondary to convulsions or cardiac arrest.
(8) metabolic disorders: such as neonatal hypocalcemia, hypoglycemia, hypothyroidism and so on.
(9) sudden infant death syndrome (SIDS): SIDS is a common cause of death in neonatal infants in developed countries, accounting for 40% to 50% of infant deaths from 1 month to 1 year old.
(two) pathogenesis
1. Hypoxia and metabolic acidosis Hypoxia is the most prominent problem of respiration and cardiac arrest. Once the heartbeat stops, the effective circulation of oxygenated blood is interrupted, oxygen supply is immediately terminated, and metabolic acidosis occurs. Hypoxia inhibits myocardial conduction, causing arrhythmia and bradycardia. At the same time, intracellular potassium release also inhibits myocardial contraction. Myocardial ischemia is 3 to 10 minutes, ATP is reduced by more than 50%, and myocardium is lost. Hypoxia is more sensitive, heartbeat stops for 30s, neuronal metabolic disorder; 1~2min, brain microcirculation autoregulation function is lost due to acidosis, cerebral vascular bed is dilated; anaerobic metabolism of brain cells can only be maintained for 4 to 5 minutes Death, therefore, it is generally believed that heartbeat breathing stops at normal temperature for 4-6 minutes, that is, there is irreversible damage to the brain. Even if the recovery is successful, there must be a neurological sequelae. In the case of recovery, the heart stops for 10 minutes, and the brain cell membrane sodium pump function is lost. , causing brain cell edema.
2. Carbon dioxide retention and respiratory acidosis When respiratory arrest is stopped, carbon dioxide increases at a rate of 0.4 to 0.8 kPa (3 to 6 mmHg) per minute. Carbon dioxide retention in the body can inhibit the excitation and conduction of sinus node and atrioventricular node. Excited cardiac arrest, causing bradycardia and arrhythmia, but also directly weakening myocardial contractility, and dilating cerebral blood vessels, increased cerebral blood flow after dilated heart, resulting in excessive perfusion of cerebral blood flow, intravascular fluid Hydrostatic pressure increased, while hypoxia and acidosis increased capillary permeability, which promoted the formation of cerebral edema, carbon dioxide continued to increase or even cause carbon dioxide anesthesia, directly inhibiting the respiratory center.
3. Energy metabolism, water and electrolyte disorders When glucose is anaerobic glycolysis, the ATP produced is only 1/18 or 1/19 of the aerobic oxidation of glucose, so the energy supply is greatly reduced, membrane pump dysfunction, membrane The ion channel is inactivated, causing changes in the internal and external ionic homeostasis of brain cells, such as a sharp increase in extracellular potassium ions, a gradual decrease in calcium, sodium, and chloride ions, intracellular calcium overload, sodium retention, edema, and acidosis.
4. Cerebral ischemia-reperfusion injury The so-called ischemia-reperfusion injury refers to the tissue and organ of ischemia for a certain period of time. After re-infusion of blood, its function not only fails to recover, but structural damage and dysfunction are aggravated. Found in the brain, also seen in the heart, lung, liver, kidney and other organs, because the brain is the most sensitive organ for ischemia and hypoxia, the performance of ischemia-reperfusion injury is particularly prominent, and its mechanism has not been fully elucidated, mainly with the following Relevant aspects:
(1) Intracellular calcium overload: In normal physiological state, the intracellular and extracellular calcium ion concentration difference is 1/10,000. The cells pass the energy-consuming calcium pump or 3Na /Ca2 exchange system, and the calcium concentration is discharged from the cell by reverse concentration gradient. During reperfusion injury, calcium pump function cannot be maintained due to energy metabolism disorder, calcium ions are transferred to the cells, and mitochondria and endoplasmic reticulum retain calcium, which leads to increased calcium release. Intracellular calcium overload directly leads to protein and fat. In addition, calcium ions entering the smooth muscle around the small arteries can cause vasospasm. At the same time, due to cerebral ischemia and hypoxia, local arachidonic acid production increases, resulting in a large amount of thromboxane, which is a strong smooth muscle contracture substance, further aggravating vasospasm. Increased vascular resistance reduces cerebral perfusion pressure and enters delayed hypoperfusion cerebral ischemia. At this time, although the supply of cerebral blood flow is restored, some intracranial microvessels cannot be reperfused by blood flow, which is also called no recirculation phenomenon. "This stage generally lasts for 48-72 hours, which makes brain cell damage become more and more serious, and even necrosis. It is currently considered that calcium influx is activated after reperfusion." The initial factors of other reactions are also the last way to cause irreversible necrosis of cells.
(2) Free radical increase: In the early stage of cardiac arrest, due to ischemia, hypoxia, free radical scavenging system is affected, but at this time, oxygen supply is insufficient, lacking the necessary substrate for generating free radicals, so the free radical formation is corresponding Less, the body is not enough to cause serious damage, after reperfusion, because the oxygen supply is improved, providing free radical-generating raw materials, and the free radical scavenging substances in the blood have not yet formed, resulting in explosive growth of free radicals, free radicals It binds to enzymes, receptors and other components on the cell membrane, affecting the structure, function and antigen specificity of the cell membrane. The malondialdehyde (MDA), a peroxidized product of unsaturated fatty acids, can enlarge the pores of the cell membrane and increase the permeability. Lead to further damage to the cells, aggravating brain edema, and high blood pressure.
(3) Intracellular acidosis: Accumulation of lactic acid during cardiopulmonary resuscitation and inappropriate use of sodium bicarbonate can cause severe intracellular acidosis. Intracellular acidosis reduces ATP production by inhibiting mitochondria, leading to energy metabolism failure. Causes membrane failure.
(4) Excessive release of excitatory amino acids: Excitatory amino acids mainly refer to glutamate and aspartic acid, which are the main neurotransmitters of excitatory synapses in the central nervous system. When ischemia-reperfusion, presynaptic glutamate Increased release and/or decreased reuptake, resulting in overstimulation of postsynaptic excitatory amino acid receptors, when glutamate and its receptor -aminohydroxymethylpropionic acid, N-methyl-D-endo When combined with amino acid (NM-DA), it promotes the influx of sodium and chloride ions and water, resulting in acute swelling of neurons. At the same time, NMDA regulates the opening of calcium channels, massive influx of extracellular calcium ions, intracellular calcium overload, and free radicals. Produced, eventually leading to cell membrane destruction, neuronal damage.
Prevention
Pediatric cardiac arrest and cardiopulmonary resuscitation prevention
Prevent iatrogenic accidents, strictly follow various medical procedures, carefully operate, avoid accidents, and prevent drug poisoning.
Complication
Pediatric heartbeat respiratory arrest and complications of cardiopulmonary resuscitation Complications, metabolic acidosis, convulsions in children
Can be complicated by hyperkalemia, severe acidosis, hypocalcemia, convulsions, mental, mental retardation, physical movement disorders, language disorders, and even "vegetative".
Symptom
Pediatric heartbeat respiratory arrest and cardiopulmonary resuscitation symptoms Common symptoms Loss of consciousness complexion gray dark skin faint light reflection disappears heart sound and pulse disappears cardiac arrest pupil abnormal convulsion ventricular fibrillation
Sudden coma
General cardiac arrest occurs after 8 to 12 seconds, and some cases may have a transient convulsion.
2. Pupil enlargement
After 30 to 40 s of cardiac arrest, the pupils began to expand, and the light reflex disappeared. The size of the pupil reflected the degree of damage of brain cells. Some resuscitation drugs such as atropine affected the observation of the pupil.
3. The aorta beat disappears
After the heartbeat and respiratory arrest, the carotid artery and femoral artery beat disappeared. If the body surface still touches the vascular pulsation, it means that there is still some blood perfusion in the vital organs in the body. The young child has a short neck and the carotid artery is difficult to palpate. You can directly touch the apex to determine if there is a heartbeat.
4. Heart sound disappears
The heart sound disappears or the heart does not stop, but the heart sound is very weak, and the heart rate is slow. For example, the heart rate of the older child is <30 beats/min, the newborn is <80 beats/min, and the newborn in the delivery room is <60 beats/min. .
5. Breathing stops
After the heart stops for 30~40s, the breathing stops. At this time, the chest-abdominal breathing movement disappears. The auscultation has no breathing sound, and the complexion is gray or blemish. It should be noted that the breathing is too weak, slow or inverted gas, and no effective gas can be used. The pathophysiological changes caused by the exchange are the same as the respiratory arrest, and artificial respiration is also required.
6. ECG
Common equipotential lines, electromechanical separation or ventricular fibrillation ECG equipotential lines and electromechanical separation are the most common arrhythmias in children with resuscitation, accounting for more than 70%. Electro mechanical dissociation (EMD): refers to various electrocardiograms Different degrees of conduction block or ventricular self-pulsation, even showing the sinus rhythm of the normal wave group, but the heart has no blood discharge function, blood pressure and pulse can not be measured, true electro-mechanical separation (Ture-EMD) refers to complete myocardial Stop contraction and there is still electrical activity on the electrocardiogram. Pseudo-electromechanical separation (pseudo-EMD) refers to recessive myocardial contraction. Aortic blood flow can be seen during ultrasound Doppler examination, but no vascular beats occur. Insufficient blood supply to the coronary arteries, extensive myocardial ischemia, hypoxia, hypovolemia, strong pneumothorax, pulmonary embolism, myocardial rupture and pericardial tamponade, treatment with adrenaline, combined with ideal ventilation and oxygen supply Pressing, atropine treatment effect is not certain, heart rate <60 times / min can try atropine 0.04mg / kg, pseudo-electromechanical separation prognosis is better than true electro-mechanical separation, active rescue has recovery Can, as a worst prognosis ECG equipotential lines, the survival rate of only 2% to 5 discharged%.
7. Fundus changes
The blood flow in the fundus is slow or stagnant, and the blood cell aggregation changes in a color-like manner, suggesting that the cerebral blood flow has been interrupted and the brain cells are about to die.
In order to strive for the rescue opportunity and improve the treatment effect, diagnosis should be made as soon as possible. Any sudden coma with aortic pulsation or heart sound disappearance can be diagnosed. Suspicious cases should be resuscitated first. Do not delay the rescue treatment due to repeated contact with arterial pulsation or heart sound. The newborn baby has no spontaneous breathing for 1 minute and is the indication for recovery.
Examine
Pediatric heartbeat respiratory arrest and cardiopulmonary resuscitation
The results of laboratory tests show that the cause of respiratory heartbeat is different. Various accidents, non-infectious factors, high blood potassium, severe acidosis, low blood calcium, etc.; infection factors such as severe pneumonia There is a clear blood infection, PaO2 declines, and PaCO2 rises. Metabolic diseases such as hypoglycemia, hypothyroidism, etc. may have endocrine disorders.
1. ECG examination can have the following performance:
1 heartbeat slows down.
2 ventricular tachycardia.
3 ventricular fibrillation.
4 ventricular arrest.
In clinical practice, sudden onset of irritability, difficulty in breathing, paleness, cyanosis, weakened pulse and decreased blood pressure, etc., the clinical manifestations before cardiac arrest should be highly valued, as long as there is sudden loss of consciousness and disappearance of aortic pulsation The diagnosis of cardiac arrest can be established. At this time, cardiopulmonary resuscitation should be performed immediately, and repeated auscultation should not be performed for the diagnosis. It should not wait for the ECG examination to avoid delay in the rescue.
2. Ultrasound Doppler examination
Aortic blood flow was seen during ultrasound Doppler examination, but no vascular beats.
3. X-ray chest examination
Visible pneumonia, tension pneumothorax, pericarditis and other abnormalities.
4. Brain CT examination
According to clinical needs, you can do various auxiliary examinations such as brain CT.
Diagnosis
Diagnosis and differential diagnosis of pediatric cardiac arrest and cardiopulmonary resuscitation
1. Sudden loss of consciousness or convulsions.
2. The aorta (neck, femoral artery) beat disappeared, blood pressure could not be measured.
3. The heartbeat stops and the heart sounds disappear.
4. Breathing is irregular, slow and even stop with convulsions.
5. The pupils are scattered.
6. The skin is pale or bruised.
The timely identification of various causes of respiratory arrest is mainly dependent on detailed medical history, physical examination and corresponding laboratory examinations, and auxiliary examinations are clear.
