First, CPR
Cardiac arrest is also a circulatory arrest. It refers to sudden arrest of the heart caused by various causes. It is accidental and unexpected death. It is also called sudden death. In the United States, 400,000 people die of myocardial infarction every year . If the CPR measures are timely and effective, the survival rate is as high as 70 % to 80 %. Common causes are acute myocardial infarction (AMI) , hypokalemia, and severe myocarditis. There are also cardiomyopathy, mitral valve prolapse, pulmonary embolism, electrolyte imbalance, drug allergy or poisoning, anesthesia, trauma, electrocution, drowning, snake bites, asphyxia, acute pancreatitis, vagal reflexes, and other types of heart. Lung disease. Clinical manifestations of sudden cardiac arrest loss of consciousness ( usually accompanied by convulsions ) , respiratory arrest, heart sounds stopped and the disappearance of aortic beats, mydriasis, purpura obvious. According to the general rule, cardiac arrest for 15 seconds of loss of consciousness, 30 seconds of respiratory arrest, 60 seconds of mydriasis, 4 minutes of anaerobic metabolism of sugar, 5 minutes of brain ATP depletion, energy metabolism completely stopped, so lack of oxygen 4 ~ 6 Minor brain neurons can undergo irreversible pathological changes.
To explore the efficacy of CPR in the recovery process , the death diagnosis is divided into clinical death and biological death. The former showed signs of heartbeat, respiratory arrest, loss of consciousness, dilated pupils, but the respiratory cycle interruption time did not exceed the limit of irreversible damage of brain cells. It was generally considered as complete ischemic and hypoxic for 4 minutes, but recent studies have found that brain cell damage is irreversible In the heartbeat, breathing stops for more than 6 minutes. Diagnostic methods rely mainly on clinical and electrocardiographic performance
( A ) Cardiac arrest ECG
1. ventricular fibrillation
It accounts for 30 % of clinical deaths , but it accounts for 90 % of sudden deaths . At this time, the ventricular muscles are inconsistent, rapid and disordered continuous tremors. The electrocardiogram showed that the QRS complex disappeared and replaced by continuous and irregular ventricular fibrillation with varying amplitude. However, care should be taken not to misinterpret the interference clutter as a tremor wave. Ventricular flutter is also a manifestation of death electrocardiogram, because the simple ventricular flutter is very rare, and soon turned into a ventricular stretch or both, called impaired ventricular flutter or ventricular flutter - tremor. The electrocardiogram of the ventricular flutter showed the same amplitude, fast and slow rule, and the top and bottom were all blunt and round, and could not distinguish between QRS and ST-T waves.
2. Ventricular quiescence ( with or without atrial quiescence )
Ventricular static is a common manifestation of death. There was no ventricular activity wave on the electrocardiogram, showing a flat line or only atrial P wave. Common sinus, atrial, and knot impulses can not reach the ventricle, and the heart rhythm in the room when the auxiliary rhythm point can not be timely when the impulse is expressed as ventricular static. It can occur either during rapid carotid sinus massage or after DC shock, or after ventricular flutter or tremor and severe escape rhythm.
3. Electrocardiographic mechanical separation
Often the heart is in "extreme pump failure" and the myocardium has no contractility. Although the electrocardiogram can be slow (20 to 30 beats per minute ) , short, and wide malformation of the ventricular autonomous rhythm, there is no stroke volume, even if cardiac pacing is used. Treatment can often not be effective. It is an electrocardiographic manifestation of extremely high mortality rate. Do not mistakenly believe that the heart is still beating.
According to statistics from the United States, about 60 % of patients with coronary heart disease died of sudden death, and most of them died before the hospital. Sudden death caused by other causes, death due to lack of timely and proper resuscitation, or strict ( b ) Basic Life Support (BLS) Once the breathing and heartbeat are stopped, immediately attack the precordial area ( lower sternum ) and remove the cause. 1 , 2 and 3 steps for CPR .
l. often use the method of raising the head up to ensure that the airway is open and determine whether there is breathing
(1) Untie the tops;
(2) expose the chest;
(3) release the trousers;
(4) The first aider is on the side of the patient;
(5) Insert one hand behind the neck;
(6) Lift up;
(7) Pressing the forehead with one hand causes the head to retreat;
(8) Neck hyperextension;
(9) With hands
Refers to the removal of foreign substances in the pharynx and removal of active dentures;(10) Put the ear close to the patient's mouth and nose and face the chest;
(11) Listen to the sound of breathing and watch the chest rise and fall;
(12) Confirm that breathing has stopped.
2. mouth-to-mouth breathing
1 The first-aid person will press the frontal hand's thumb and forefinger to close the patient's nostrils;
2 another hand care jaw;
3 Open the patient's mouth;
4 take a deep breath;
5 Use mouth tightly and cover the patient's mouth to blow air;
6 See the patient's chest rise as effective;
7 from the patient's mouth;
8 Relaxation pinches the nostrils of the thumb and index finger;
9 see thorax restoration;
10 feel the patient's mouth and nose exhaled;
(11) Continuous air-blowing two times to fully ventilate the patient's lungs.
3. Determine whether the heartbeat is stopped or not, and whether the patient's carotid artery is pulsed with chest cardiac compression:
1 with the palm of one hand on the 1/3 of the patient's sternum at the junction;
2 The other hand presses on the back of the hand of the hand, and the fingers of both hands should be raised and cannot be pressed against the chest wall;
3 double elbow joints straight;
4 Use the body weight and shoulder arm strength to press vertically downwards;
5 subsidence of the sternum 4cm ;
6 Relax in situ after a slight pause;
7 But the palm root cannot leave the anchorage point of the chest wall;
8 15 consecutive cardiac presses;
9 Press the heart 15 times after blowing the air twice . So repeated.
4. Pediatric examination
1 pediatric pressure can be used single finger pressure;
2 Newborns can be pressed with two fingers;
3 Press frequency, adult 80 to 100/ minute;
4 children 100 beats / minute, newborn 120 beats / minute;
5 Press depth, newborn 2cm , children 3cm .
When the CPR operation is repeated four times, the effect needs to be checked, but the pause time should not exceed 5 seconds.
5. Check whether the recovery is effective
1 The carotid artery beats;
2 The pupils shrink from large;
3 purpura decreased, spontaneous breathing recovery;
4 systolic blood pressure 60mmHg (8kPa) or more.
( III ) Further Life Support (ALS)
The success of CPR depends on the BLS and ALS . The former are mostly on pre-hospital and on-site rescue, while the latter often perform CPR on the emergency room or ICU ( intensified care unit ) and CCU ( coronary care unit ) . The two are closely linked.
1. oxygen therapy
Respiratory and circulatory arrest, occurrence of hypoxic acidosis, metabolic disorders and other changes in the body, and the implementation of mouth-to-mouth artificial respiration, the oxygen content of 16 % to 17 %, the maximum alveolar oxygen tension can only reach 10.7kPa (80mmHg) , and Normal is 13.3kPa (100mmHg) . According to the characteristics of oxyhemoglobin dissociation curve, high concentration oxygen inhalation can increase arterial oxygen tension, increase hemoglobin oxygen saturation, and improve tissue hypoxia, so it is advisable to inhale pure oxygen in the short term, and it is believed that the lung will not be caused within 6 hours. damage. Oxygen therapy in ALS uses the " S " type airway tube, balloon valve mask and endotracheal tube to strengthen oxygen. Artificial machine-assisted breathing is an ideal method of effective ventilation, often using intermittent positive pressure ventilation (IPPV) or continuous positive airway pressure (CPAP) , once spontaneous breathing is performed with synchronized intermittent command breath (SIMV) or simultaneous pressure support breathing. If acute respiratory distress syndrome (ARDS) occurs, end-expiratory positive pressure breathing (PEEP) should be used . The ideal indicator for artificial ventilation: the partial pressure of carbon dioxide ( Paco2 ) drops to 4.63 to 6.00 kPa (35 to 45 mmHg) , and the partial pressure of oxygen (Pao2) increases to more than 10.7 kPa (800 mmg) .
2. Cardioversion
Sudden cardiac arrest in the central nervous system accounts for 90 %. When the onset does not exceed 1 minute, there is no apparent lack of oxygen in the heart muscle. At this time, giving pre-cardiac sniper, can produce 5J electrical energy equivalent , which can restore some patients with ventricular fibrillation, such as If the pause time exceeds several minutes, then the effectiveness of sniping is poor. You should use 200 , 30O , 360J ( children's first 2J/kg , later 4J/kg , calculated ) to perform asynchronous shock defibrillation. If the ventricular fibrillation is small, epinephrine can be injected, causing the ventricular fibrillation valve to rise significantly. Recently, it was suggested that an increased dose (2 to 5 mg) had a certain effect on intractable ventricular fibrillation. Verapamil ( equipotential stop ) could reduce the incidence or severity of myocardial injury after electric shock, and this prevented the accumulation of calcium ions in the mitochondria. It can increase the success rate of defibrillation. In addition, bromobenzylamine, lidocaine, procainamide, amiodarone, and heart rate can be applied during ventricular arrhythmia. Electrocardiographic separation is less common, but the prognosis is poor. There is currently no special treatment and atropine can be used. In the animal experiments, the use of Mesacon's new life to obtain better results can be used.
( IV ) Precautions in CPR
1. Prevent complications
Resuscitation complications include acute gastric dilatation, rib or sternal fracture, rib cartilage separation, pneumothorax, hemothorax, lung injury, hepatic rupture, coronary puncture ( intracardiac injection ) , pericardial tamponade, and intragastric reflux error Suction or inhalation of pneumonia, etc., it requires accurate judgment, strict monitoring, timely processing, and regular operation.
2. Heart resuscitation
The ratio of compression time to relaxation time and frequency of compression in the past used to be considered as one third of each compression and relaxation cycle, and relaxation accounted for the remaining 2/3 . Experimental studies have confirmed that when the time for cardiac compression and relaxation is 1/2 , Maximal hemodynamic effects were achieved with cardiac ejection. Moreover, it is advocated that the compression frequency can be increased from 60 to 80 beats / minute to 80 to 100 beats / minute to increase blood pressure in the short term by 60 to 70 mmHg , which is beneficial for cardiac resuscitation.
3. Comparison of chest cardiac compression and intrathoracic heart compression
Since the advent and promotion of chest cardiac compression in 1960 , it has almost replaced intrathoracic cardiac compression or chest trauma alone, chest bleeding, multiple rib fractures, tension pneumothorax, pericardial tamponade, thorax or spinal deformity, and severe Emphysema in cardiac arrest patients CPR first aid. In recent years, a large number of clinical data indicate that the final chest chest compressions only 10% to 14% full recovery, but long-term survival chest cardiac massage
The rate is as high as 28 %. It was confirmed that the intracoronary heart pressure was higher than the extracorporeal heart pressure. In some cases, transthoracic cardiac compression failed to change the intrathoracic heart compression may be successfully rescued, therefore, chest cardiac compression has been re-emphasized.4. Resuscitation of medications and routes of administration
Regarding the route of administration, it was compared with the average time from the injection to the heartbeat recovery of intracardiac, intravenous or intratracheal administration, and the effects of the three were similar. Intracardiac injection can cause pneumothorax and myocardial injury, and the need to suspend CPR measures such as chest cardiac compression and artificial respiration during puncture , which is not conducive to systemic blood supply and cardiac resuscitation, it is not advocated intracardiac injection, only as too late to establish intravenous The intracardiac administration is only considered when there are emergency measures at the time of the drug route or if the heartbeat does not recover after intravenous or tracheal administration. At present, a reliable intravenous infusion channel should be established when CPR is advocated, and it should be administered intravenously ( preferably via the cubital vein into the central vein ) . Based on the adverse effects of the so-called "three-point needle", it has been agreed that the conventional use of the "three-pronged needle" must be abolished. Adrenaline is generally recognized as the drug of choice for cardiac arrest. In recent years. A new perspective was put on the use of epinephrine and sodium bicarbonate.
5. The application of large doses of adrenaline
Epinephrine mainly excites alpha receptors, contraction of peripheral blood vessels increases the aortic diastolic pressure, increases coronary perfusion and cardiac blood flow, while contraction of the external carotid artery increases the blood supply to the brain, which is conducive to resuscitation of the heart; can improve myocardial stress, When ventricular fibrillation makes fine tremors tremble, increasing the success rate of electrical defibrillation, therefore, it is the first choice for all cardiac arrest. It is recommended that CPR use a standard amount of adrenaline of 1 mg/ time for intravenous injection. In recent years, domestic and foreign scholars have used high-dose epinephrine to rescue cardiac arrest by series of animal experiments and clinical observations, confirmed that the main driving force of CPR myocardial blood flow is aortic diastolic pressure, at this time no use of vasoconstrictor drug aortic diastolic blood pressure Very low ( via 2.67kPa) , but the increase in aortic diastolic pressure measures can effectively improve myocardial ischemia, cardiac arrest after the concentration of catecholamines in vivo can rise several dozen times, but this time the body does not respond to endogenous catecholamines Exogenous catecholamines react, therefore, exogenous adrenaline must be given when the heart is stopped. After the circulation is stopped, human cells are hypoxic and hypoxia, the function of cell metabolism is decreased, the sensitivity of receptors to epinephrine is decreased ( receptor effect is low ) , and low concentration of epinephrine can not make the receptor excited or fail to achieve the effect of cardiac resuscitation. This is the theoretical basis for advocating the use of large doses of adrenaline for CPR and poor efficacy with low doses. Regarding the dose of epinephrine, most people nowadays advocate that CPR and standard doses of epinephrine are not effective. Early use of large doses of epinephrine, 3 to 5 mg per day for adults , may be reasonable.
6. Sodium bicarbonate
Recent studies on the adverse effects of sodium bicarbonate on CPR . It was confirmed that premature and excessive administration of sodium bicarbonate can lead to: increased acidosis in myocardial cells and decreased myocardial contractility; direct dilatation of arteries reduced the aortic diastolic pressure and reduced coronary perfusion pressure by 43.50 %; caused metabolic alkalosis; The oxyhemoglobin dissociation curve left, affect the release of oxygen hemoglobin; hyperkalemia caused by hyperkalemia into the cells, hypokalemia prone to arrhythmia, is not conducive to the correction of ventricular tachycardia and ventricular fibrillation; use of large doses of sodium bicarbonate can cause Hypernatremia, hyperosmolaremia, increased blood viscosity, and thrombotic tissue necrosis. It can be seen that improper application of sodium bicarbonate will bring potential danger to CPR . As a result , the theory and method for the application of sodium bicarbonate in CPR have been significantly revised. The current claim is that sodium bicarbonate is not used as an immediate drug for resuscitation, and it is believed that the acid-base imbalance in the short-term cardiac arrest is mainly due to respiratory acidosis caused by ventilation disorders, and the principle of treatment depends on ventilation to balance. It is advocated that sodium bicarbonate can only be used for patients with metabolic acidosis before cardiac arrest; in CPR , if there is no basis for the diagnosis of metabolic acidosis, only use of effective ventilation, cardiac compression, electrical defibrillation and drug treatment can be used. sodium bicarbonate, typically in the CPR 10 minute-by 1mmol / kg administered 5% sodium bicarbonate, half every 15 minutes thereafter administered once every 2 to 3 times the amount of total <300ml, post-resuscitation should be measured arterial blood pH and carbonate to guide Paco2 Use of sodium hydrogen. Before and after the decomposition of sodium bicarbonate into water and CO2 , it is necessary to ensure ventilation, in order to facilitate CO2 discharge to prevent acidosis.
7. calcium and calcium antagonists
Calcium can increase myocardial contractility, prolong systole, and increase ventricular autonomic and myocardial conduction velocity. It is often used in CPR . Recently, it was thought that the cell membrane was damaged during cardiac arrest. Intracellular Ca++ overload was accompanied by a series of damages. At this time, calcium-induced hypercalcemia was harmful to cells and organs, and calcium may also be the brain without reperfusion after the onset of CPR . Because of the precipitating factors of the phenomenon , the use of calcium in CPR is still controversial. Some people think that calcium antagonists can reduce the Ca++ influx of vascular smooth muscle , relieve coronary and cerebral vasospasm, and can improve myocardial and cerebral ischemic damage.
Second, brain recovery
The recovery of brain function after cardiopulmonary resuscitation is the key to measuring successful resuscitation. Cerebral resuscitation is a fundamental condition for restoring respiratory, circulatory, metabolic, and splanchnic functions. It has been reported that about 20 % to 40 % of patients have permanent neurological impairment after successful CPR . In view of the importance of cerebral protection and cerebral resuscitation, ischemic in recent years The mechanism of brain injury has been studied extensively. The brain is an organ with a large blood flow and a high metabolic rate and a large amount of oxygen, and its energy is almost entirely dependent on the oxidative metabolism of glucose. Cardiac arrest if the brain is completely ischemic for 5 minutes to perform CPR reconstruction cycle, because the Ca++ influx and excessive free radical formation and other factors on the damage of the brain is called perfusion damage, Ca++ into the cell causes vascular smooth muscle spasm, on the other hand Activated cytosolic phospholipase A2 , so that arachidonic acid release, under the action of enzymes into thromboxane (TXA2) so that blood vessels contraction platelet aggregation caused by cerebral hypoperfusion further damage the brain tissue blood supply and oxygen. There are also toxic effects of oxygen radicals that cause damage to brain cells and eventually lead to brain death. Some people think that this phenomenon is blocked by calcium antagonists. It has also been found