I. Overview
Cardiopulmonary resuscitation (CPR): is a rescue procedure to resuscitate cardiac and respiratory arrest with the aim of restoring cardiopulmonary function. It is mainly used for patients who can maintain better cardiopulmonary function and survive for a longer period of time after resuscitation. The aim is to prevent and save sudden and unexpected death, not to prolong meaningless life. It includes basic life support (BLS), further life support (ACLS) and extended life support (PLS) for the process of cerebral resuscitation. 1973 to 2005, the American Heart Association (AHA) has developed CPR standards six times. Currently, the “chain of survival” is proposed to improve the success rate of resuscitation, that is, “four early”: early access; early freehand CPR; early pulse defibrillation, early advanced CPR. Early activation of EMS system.
Etiology
1.Cardiac arrest: mostly occurs in coronary artery disease, but many non-cardiac diseases such as shock, electrolyte disorders, hypoxia, acidosis, etc. can induce cardiac arrest. The main pathophysiology of cardiac arrest is reduced cardiac function, rhythm disorders, insufficient coronary blood supply and reduced cardiac output.
2, respiratory arrest: including central and peripheral. The former is seen in severe disease and damage to the respiratory center and its conduction system, while the respiratory organs are normal. Such as stroke, traumatic brain injury, poisoning and severe hypoxia. The latter is mainly weak water various causes of airway obstruction right infarction. The heartbeat can be maintained for 30 minutes and the brain can show irreversible damage brain death in 4-6 minutes of cardiac arrest. Patients with clinical causes of respiratory and cardiac arrest, such as acute heart attack, severe trauma, electric shock injury, crush injury, trampling injury, poisoning, etc. are common.
III. Clinical manifestations and diagnosis
1, sudden loss of consciousness.
2.Disappearance of large arteries (carotid artery, femoral artery).
3, respiratory arrest; cyanosis of lips and mouth.
4, dilated pupils, no reflex to light.
5. inaudible heart sounds.
6, the ECG shows ventricular fibrillation (flutter), ventricular quiescence (as a straight line or only heart waves), myocardial electro-mechanical separation (although the ECG has a wider and deformed, higher frequency, more complete QRS wave group, but does not produce effective mechanical contraction of the myocardium.)
The diagnosis can be made with the two points 1 and 2 above, and CPR is performed immediately. Respiratory arrest is often produced 15 to 20 seconds or more after cardiac arrest, and pupil dilatation occurs after several 10 seconds of arrest and is fixed for 1-2 minutes. Artificial respiration is started as soon as the patient is found to have stopped breathing. Loss of aortic pulsation means that effective voluntary circulation has been lost, i.e., chest compressions are performed.
IV. Resuscitation measures
Complete CPR includes BLS and ACLS parts. The main goal of BLS is to supply oxygen to the myocardium and vital organs of the body, including opening the airway (A), artificial ventilation (B), chest compressions (C), and defibrillation (D).
ACLS is mainly for the application of auxiliary equipment and drugs, etc. on the basis of BLS to maintain voluntary breathing and heartbeat.
(A) Basic life support (BLS)
is the key to resuscitation, the earlier it starts the higher the survival rate, those who perform resuscitation in 4 minutes may have 50% survival, those who start resuscitation in 4-6 minutes have about 10% success rate, those who are more than 6 minutes only 4%, those who are more than 10 minutes, the survival may be less.
1, rapid determination of respiratory cardiac arrest: including the determination of respiration (a look; two listen; three feel) cardiac arrest, loss of consciousness, loss of aortic pulsation
2, loudly call for help
3.Position: turn the patient into a supine position and place on a hard plane
4, open the airway (A): clean the mouth foreign body or vomit. Its techniques.
(1) head tilt – chin lift: one hand on the patient’s forehead, backward pressure, so that the head is tilted back the 2nd and 3rd fingers of the other hand on a jaw to lift the forehead up. Make the jaw angle and earlobe line 90 degrees perpendicular to the ground.
(2) Jaw resting technique. This method is used for those with neck trauma. (3) Head tilt-jaw lift maneuver. Forbidden for people with head and neck trauma.
5, artificial respiration (B): no respiratory organs are judged that mouth-to-mouth artificial respiration blowing 2 times. Pinch the patient’s nose with the thumb and index finger of the forehead hand, take a deep breath, and slowly and continuously blow the gas around the lips of the patient with both lips (blowing time is about 1 second) tidal volume of 6~7ml/kg frequency of 110~12 times/min (about 5 seconds once), 16 times/min for children. (about 4 seconds once).
6.External chest compressions (C)
(1) Determine the presence or absence of a heartbeat: listen to the heart sounds and touch the carotid artery. Use one hand to show and place the middle fingers together on the anterior midline of the patient’s neck, slide outward to the depression between the thyroid cartilage and the sternocleidomastoid muscle, and touch with slight force.
(2) Mechanism: “chest pump” and “heart pump” theory. Chest pump refers to the increase in intrathoracic pressure during external chest compressions, and the blood is squeezed out by the same intrathoracic pressure in the large blood vessels and left ventricle. Because the thoracic entrance out of the large vein indentation and the role of the jugular vein valve to prevent the reflux of blood, coupled with the arterial wall is thicker than the vein wall, the lumen is relatively small, anti-vascular atrophy can be greater than the vein, and therefore remain open, the blood can only flow forward from the arterial pulsometer when the pressure is pressed, the aortic pressure rises significantly, pushing the blood outside the thoracic artery flow. When the compression is relaxed, the intrathoracic pressure returns to that before the compression, the vein is relaxed and the lumen is opened, the blood of body circulation can return to the heart from the vein, but the arterial blood is blocked by the aortic valve and cannot return to the heart, part of it flows into the coronary artery and is discharged to the artery. After the pressure is relaxed, the venous blood is sucked back to the heart when the heart is restored to its original state.
(3) Position: The patient is in the supine position, and the resuscitator is located on the right (or left) side of the patient.
(4) Compression site: the middle of the chest, the lower half of the sternum, i.e., the intersection of the line of the double nipples with the sternum, is the compression area. After positioning, the root of the left hand stays in the position, place the palm of the other hand on it with fingers crossed, and lift the end of the fingers. Touch the sternum with the palm root only.
(5) compression position: upper body leaning forward, arms straight, relying on the upper body weight of the rescuer, shoulders, arms, muscle strength vertical downward rhythmic compressions.
(6) compression frequency and depth: frequency 100 times / min, so that the sternum sinks 4-5cm. children frequency 100-120 times / min, depth 3-4cm. compression and relaxation time is equal. The root of the palm of the hand does not leave the sternum when relaxing.
(7) compressions and artificial respiration with: chest compressions and artificial respiration ratio of 30:2, 5 cycles of compressions (30:2) after checking the patient’s carotid artery breathing pupil changes and electrocardiogram, no then continue compressions.
(8) Defibrillation: 80% of the causes of cardiac arrest are ventricular fibrillation. Defibrillate only once with an energy of 360j. then perform CPR). If the ECG shows ventricular quiescence or electro-mechanical separation, in principle, defibrillation cannot be performed and electrical pacing can be used. The use of portable automated external defibrillators (AEDs) has been promoted.
(II) Further life support (ACLS)
Including drugs and cardiac monitoring: drug therapy, drug administration route, mainly intravenous route, if the tracheal intubation has been completed, but not established static pulse meter channel, can use endotracheal drug administration, but the drug dose should be 2 times larger than intravenous, diluted with 5ml of saline or distilled water, quickly sprayed into the trachea. Intracardiac administration is not advocated. Epinephrine: The most important and preferred drug during CPR, especially its a property increases aortic diastolic pressure and coronary perfusion pressure and peripheral vascular resistance, which increases myocardial and cerebral blood flow and is considered to be the initial determinant affecting the outcome of resuscitation. b receptor effect increases heart rate during CPR, myocardial oxygen consumption, but the overall effect is to increase endocardial and epicardial blood flow and thicken ventricular fibrillation waves. Recommended small dose: 1 ml IV every 3-5 minutes. Although high-dose epinephrine has been reported to increase the recovery rate of autonomic circulation, there is no statistically significant increase in its neurological prognosis in terms of survival to discharge compared with conventional doses.
Atropine: Reduces cardiac vagal tone, increases sinus node firing rate, and improves atrial conduction. It is primarily used to treat patients in cardiac arrest. The commonly used dose is 0.5-1 mg, repeated once in 5 minutes.
Lidocaine: During CPR, intravenous application of lidocaine facilitates the heart to maintain electrical stability. It is primarily used for persistent and recurrent ventricular fibrillation or ventricular tachycardia. The first 50-100mg is administered intravenously and can be repeated after 5 minutes. Or administered intravenously at 2-4mg/min. 2005 resuscitation guidelines recommend up to daptone.
Sodium bicarbonate: Acidosis may attenuate the hemodynamic effects of epinephrine. However, its use in cases where artificial ventilation or autonomic ventilation is not established may increase HCO- and increase PaCO2. As CO2 easily crosses the blood-brain barrier, the acidosis of brain tissue is aggravated. Excess blood base shifts the oxygen dissociation curve of hemoglobin to the left, inhibits oxygen dissociation, aggravates tissue hypoxia, and is not conducive to cardiopulmonary resuscitation. However, artificial ventilation has been established, or resuscitation has been pending for a certain period of time before the establishment of autonomic circulation is still available. There are conditions according to blood gas analysis. It can be given intravenously at a dose of 0.5-1mmol/kg.
Respiratory triplet (kolamine, lopressor, back sulking). Has not been used; because of aggravated cerebral hypoxia and oxygen consumption, can cause convulsions, convulsions. But after successful resuscitation or shallow, slow spontaneous breathing can be used in moderation.
Naloxone: can specifically antagonize morphine receptors, can effectively reverse hypotension and restore consciousness. Because it can improve hemodynamics, increase mean arterial pressure, increase cardiac output, strengthen myocardial contraction, and reduce platelet aggregation in the lungs to release free radicals and stabilize capacitor membranes. It is possible to administer 0.4-0.8 mg. Cardiac monitoring, etc.