Download presentation
Presentation is loading. Please wait.
1
Cardiopulmonory Cerebral Resusciatation (CPCR) mashehabat@just.edu.jo
2
Cardiaopulmonary arrest Cardiaopulmonary arrest is the sudden, unexpected cessation of respiration and functional circulation. During respiratory and cardiac arrest, CPCR may be successful if performed before biological death of vital tissue develops.
3
Survival of the patients depends on : 1. Degree of preexisting hypoxia of the cells. 2. The whether circulatory or respiratory arrest occurs first. 3. The brain depends totally on oxygen and is the organ least able to withstand hypoxia.
4
In case of circulatory arrest, the pupils dilate in 45 sec and respiration stops within 1 min due to medullary depression. In the adult, the brain may be damaged within 4-6min. However, if respiratory arrest occurs first, the circulation may continue for 5 min, with decreasing effectiveness, and damage to the brain may not become irreversible for 3-6min.
5
First life support (FLS): Airway, Breathing, Circulation, Drug (Defibrillation ) Advanced life support (ALS): Airway, Breathing, Circulation, Drug (Defibrillation), ECG, Fluid, Gauge, ICU
6
Cardiac arrest: A. Cardiac asystole. B. Ventricular fibrillation Electrical defibrillation is required to reestablish spontaneous and effective cardiac electrical activity. C. Electromechanical dissociation may be caused by anesthetics, hypoxia, or arrhythmia. Artificial respiration and external cardiac compression: must be begun at the same time, efforts must be made to correct the inciting or underlying disease.
7
Ⅱ.Etiology: A. The etiologic factors of cardiac arrest are many and complex. In all patients, the treatment is directed toward correcting hypoxia. In some cases, e.g., electrocution, coronary occlusion, or overdose of isoproterenol, arrhythmia and fibrillation occur first, then hypoxia.
8
B. Causes of respiratory failure 1. Airway obstruction by vomitus, foreign body, blood, secretions, solid mate rial, mucous plugs, laryngeal or bronchial spasm, or tumor. 2. CNS depression: caused by stroke, head trauma, hypercapnia, barbiturates,narcotics, tranquilizers, or anesthetics. 3. Neuromuscular failure secondary to poliomyelitis, muscular dystrophy, myasthenia, or muscle relaxant drugs.
9
C. Primary causes of cardiac or respiratory arrest. 1.Flail chest. 2.Pneumothorax. 3.Massive atelectasis. 4.Acute pulmonary embolism. 5. Congestive heart failure. 6. Overwhelming pneumonia. 7. Gram-negative septicemia. 8. Lung burns. 9. Carbon monoxide poisoning. 10. Massive blood loss.
10
D.Causes of cardiac arrest 1. Low cardiac output. 2. Hyparcapnia. 3. Hyperkalemia. 4. Hypoxia and vagal stimulation. 5. Stimulation of the heart. 6. Coronary occlusion. 7. Overdosage. 8. Hypothermia. 9. Hyperthermia. 10. Acidosis. 11. Electrocution. E. Cardiac arrest: 1. Induction of anesthesia. 2. Surgery. 3. Postanesthseia recovery period.
11
F. Cardiac arrest is more frequent: 1, In geriatric or pediatric patients. 2. In patients with a history of arrhythmias, heart block, digitalis toxicity, myocarditis, myocardial infarction, congestive heart failure, electrolyte imbalance,or dehydration. 3. In massive hemorrhage. 4. During or following heart surgery.
12
Ⅲ.Prevention: The majority of the situations that tend to promote cardiopulmonary arrest are preventable. Points of importance are: A. Identification of high-risk patients. B. Collecting adequate information and correcting serious omissions. B. Avoid hazardous maneuvers. D. Induction of anesthesia must always be done very carefully.
13
Ⅳ.Diagnosis: A. Early symptoms and signs of hypoxia and/or heart failure, including: 1.CNS. Restlessness, anxiety, and disorientation. A cooperative patient who becomes difficult to manage in the recovery room is more likely to be hypox emic than psychotic. 2.Respiratory. Dyspnea, tachypnea,cgasping, laryngeal stridor, pallor, and cyanosis. 3.Cardiovascular. Cyanosis,venous distention, irregular pulse, hypotension, and profuse diaphoresis.
14
B. Late symptoms and signs of cardiopulmonary arrest: 1. Absence of carotid or femoral pulse. The radial pulse is not dependable. 2. Heart sound is not obtainable. 3. Respiratory sdandstill or gasping respirations.Circulatory arrest is followed within 45-60sec by respiratory arrest. 4. Pupillary dilation occurs within 45sec following cardiac arrest. This indicates beginning damage to the anoxic brain. 5. Absence of bleeding and dark-colored blood in the surgical field. 6. Flaccidity. 7. Convulsions. 8. The ECG shows cardiac asystole or ventricular fibrillation.
15
Ⅴ.Therapy: A. The initial goal of therapy is oxygenation of the brain. The second goal is restoration of circultion. In addition, the underlying condition must be corrected. 1.CPCR is not indicated for all patients. Natural death in the aged or in the terminal stages of a chronic illness should not be reversed in this manner. 2. CPCR should be performed in cases of reversible unexpected death that occur as a result of myocardial infarction, general and local anesthetic drugs, electric shock, adverse reaction to drugs, cardiac catheterization, or suffocation.
16
B. Emergency CPCR includes the following ABCD steps, which should always be started as quickly as possible. 1. A, airway. 2. B, breathing. 3. C, circulation. 4. D, drugs and definitive therapy. 5. In a witnessed cardiac arrest (when treatment can be initiated within 1 min of the onset of arrest), the ABCD sequence should include use of a precordial thump.
17
C. Pulmonary resuscitation 1. Airway (A). Time is the critical factor. Establishment of an airway as soon as possible is vital in a successful resuscitation. Artificial ventilation and artificial circulation must be initiated within 2-4 min.
18
a.Immediate opening of the airway. This can be done easily and quickly by tilting the patient ’ s head backward as far as possible. Many times, this maneuver is all that required for breathing to resume spontaneously.
19
To carry out the head tilt, the patient must be lying on the back. The operator places one hand beneath the victim's neck and the other hand on the victim's forehead. Then the neck is raised by the operator with one hand (neck lift), and the head is tilted backward by the pressure with the other hand on the forehead.
20
This effort flexes the neck, extends the head, and raise the tongue away from the back of the throat. Thus anatomic obstruction of the airway, created by the tongue dropping against the back of the throat, is relieved (chin lift).
21
b. The head-tilt technique is satisfactory in most victims. If head tilt is not successful in opening the airway satisfactorily, additional forward displacement of the lower jaw thrust may be necessary.
22
c. This can be done by a triple airway maneuver. l) The physician places the fingers behind the angle of the patient's jaw and forcefully displaces displaces the mandible forword. 2) tilt the head forward and (3) uses the thrumbs to retract the lower lip to allow the patients to breathe through mouth and nose.
23
Breathing (B). If the patient does not promptly resume spontaneous breathing after the airway is opened, artificial ventilation must be started immediately by mouth-to mouth, mouth to nose, or mouth to mask breathing. There is enough oxygen (16%) in expired air to ensure oxygenation of a patient ’ s circulating blood. By doubling normal tidal volume, the rescuer increases the expired oxygen to 18%.
24
a. A self-filling, nonrebreathing bag and well fitting anesthesia mask with oxygen supplied from a cylinder of compressed oxygen may be used as soon as they are available. b. Endotracheal intubation must be carried out at the earliest possible moment.
25
c. An emergency tracheotomy is indicated when an adequate airway can not otherwise be effective. Alternative methods to tracheotomy are: (1) cricothyreotomy, (2) transtracheal catheter ventilation, and (3) esophageal obturator airway. d. In a patient with a laryngectomy, direct mouth-to-stoma artificial respiration must be carried out. The head tilt and jaw-thrust maneuvers are unnecessary for mouth-to- stoma resuscitation.
26
e. During artificial ventilation, the following adverse effects may take place: (1) Inflation of the patient's stomach with air, followed by regurgitation and/or transmission of infection to the operator. These may occur when there is no endotracheal tube in place. (2) Rupture of the patient's lungs. (3) Aspiration of gastric contents.
27
4. Pulmonary ventilation is not adequate during external cardiac compression, so artificial ventilation must be carried out concurrently by any means available.
28
D. Artificial circulation- external cardiac compression 1. Circulation (C). In a case of sudden, unexpected cardiac arrest, all the ABCs of basic life support must be applied in rapid succession. This includes artificial ventilation and artificial circulation- external cardiac compression. 2. Artificial circulation can be carried out by external cardiac compression, which must be started at once. The exact instant of cardiac arrest is seldom known, and anoxia may cause irreversible damage to the brain after 4 min. After that interval, if resuscitation is successful, the patient will probably remain decerebrate.
29
3. Proper application of external cardiac compression requires that the patient be in a horizontal position and on a firm surface. 4. Application of pressure must be restricted to the lower half of the sternum, but not over the xiphoid process, to obtain maximum compression of the heart and to minimize the dangers of fractured ribs and damage to the liver.
30
5. The heel only of one hand is placed in the center of the chest over the lower half of the sternum, and the heel of the other hand is placed on top of the heel of the first hand. It is very important that the fingers be kept elevated at all times and not allowed to touch the chest wall, If pressure is incorrectly applied directly over the xiphoid, it may drive this bony process into the liver, which can result in fatal rupture of this vascular organ.
31
Adequate force must be exerted vertically downward to move the lower sternum 4-5 cm toward the vertebral column, forcing blood into the pulmonary and systemic arteries. This requires 35-45 kg of pressure on the chest of an adult.
32
7. Following sternal compression, the sternum is released, and one cycle is repeated. When the pressure is released, the chest expands and the heart fills with oxygenated blood, which is circulated through the tissues with the next compression of the heart.
33
For one worker alone, the compression and relaxation cycle of external chest compression should be repeat at a rate of 80 per minute; 15 compressions alternate with 2 quick lung inflations. If there are two rescuers, it should be repeated at a rate of 60 per minute for compressions, which is a 5:1 ratio, with no interruption in compressions for ventilation. If the patient's trachea has been intubated, the compression rate can be 80 per minute.
34
8. Under optimum conditions, external heart compression produces only 30-40% of the normal amount of blood flow.
35
9. For infants and young children less pressure is required. Pressure with the fingertips alone on the middle third of the sternum is recommended for infants. For children up to 9-10 years of age, the use of one hand is considered adequate. The compression rate should be 100 per minute with ventilation every five compressions. There should be a ratio of 5:1 whether there are one or two rescuers.
36
E. Drug therapy 1. Intracardiac or IV-injected positive inotropic and vasoactive agents are of great help in stimulating heart contraction and in increasing perfusion pressure during external cardiac compression. a. The intracardiac route may be used when there has been a delay in starting an IV infusion. b. Intracardiac injections necessitate interruption of cardiac compression and ventilation, and there is the additional risk of laceration of a coronary artery, pneumothorax, or cardiac tamponade. Also, intramyocardial injection may precipitate intractable fibrillation
37
2. The drugs that may be used under any condition of cardiac arrest are sodium bicarbonate and epinephrine. 3. Ventricular fibrillation a. The specific therapy includes epinephrine ( adrenalin ) (to convert a fine fibrillation to a coarse fibrillation, to improve the perfusion pressure, and to increase myocardial contractility). b. Sodium bicarbonate ( to facilitate the fibrillation, to enhance the effects of epinephrine, and to treat metabolic acidosis). c. Electrical defibrillation.
38
d. If the preceding therapeutic measures are not successful, make sure that ventilation and external cardiac compression are being performed as optimally as possible, and repeat the epinephrine and sodium bicarbonate. If defibrillation is still unsuccessful, add lidocaine (1 mg/kg IV bolus) and repeat the above regimen. If still unsuccessful, substitute procainamide (1 mg/kg IV bolus) for lidocaine and repeat defibrillation.
39
e. If still unsuccessful, add propranolol (0.5-1 mg IV) and repeat defibrillation. f. The principal indication for isoprotereflol (2-20 ug/min drip rate, not bolus) is immediate control of hemodynamically significant bradycardia to get the heart started again and/or to boost the rate to about 60 beats/min.
40
F. Establishment of an IV route must be achieved as soon as possible by : (1) percutaneous peripheral puncture, (2) cutdown over the greater saphenous vein at the ankle or another Vein, (3) percutaneous puncture of the subclavian, external jugular, femoral, or internal jugular vein.
41
G. Correction of metabolic acidosis. 1. Profound metabolic acidosis occurs within a few minutes in the presence of cardiovascular collapse, and it persists in spite of efforts at cardiopulmonary resuscitation, which perfuses tissues but at a reduced rate. 2. Sodium bicarbonate should be infused promptly. The IV dose is 1 mEq/kg. Repeat after 10 min. Then give 0.5 mEq/kg every I0 min until arterial blood gases and pH are known. 3. Blood pH and base deficit are useful guides in the maintenance of acid-base balance. 4. A normal pH renders the heart more responsive to circulating and injected catecholamines and defibrillation.
42
H. Therapy in asystole. 1. ECG shows a straight line. 2. Tilt the head to open the airway, and palpate the carotid pulse. 3. If the carotid pulse is absent at any time in any witnessed arrest, it is reasonable to apply a precordial thump with the knowledge that this is usually successful only in fibrillation, not in asystole. 4. If the victim is not breathing, give four quick, full lung inflations. 5. If pulse and breathing are not immediately restored, begin one-rescuer or two-rescuer cardiopulmonary resuscitation.
43
6. Epinephrine (0.5 mg) is injected IV, and the injection is repeated every 5min. 7. Sodium bicarbonate is given by IV bolus only. 8. Isoproterenol, 2-20 ug/min (drip rate, not bolus). 9. Calcium chloride, 5 ml of a 10% solution, administered slowly IV. 10.Prompt insertion of an endocardial electrode, by the transvenous or direct transthoracic route, with artificial pacing may be required.
44
I. Therapy in electromechanical dissociation. In electromechanical dissociation, the ECG shows a rhythmic electrical activity of the heart but no peripheral pulse or blood pressure. The therapy is the same as for asystole.
45
J Therapy in ventricular fibrillation. 1. Tilt the head to open the airway and palpate the carotid pulse. If the pulse is absent, give a precordial thump. 2. The administration of epinephrine and sodium bicarbonate is followed by DC countershock. Use maximum energy, 400 Watt-sec.
46
3. Continued external cardiac compression and artificial ventilation are necessary. 4. If defibrilation with DC countershock is not successful, give: a. Epinephrine, 0.5 mg. b. Sodium bicarbonate. c. Lidocaine, 1 mg/kg IV bolus. d. Repeat DC counterohock. If still not successful: First, substitute procainmide (1 mg/kg IV bolus) for lidocaine; second, try proporanolol (0.5-1 mg IV bolus), but extreme caution must be exercised when using it.
47
Ⅵ.Complications: Include rib fractures, fracture of sternum, costochondral separation, pneumothorax, hemothorax, lung contusions, laceration of the liver, and fat emboli. A check for these conditions must be done in the postoperative period. Also check for intrathoracic and intraabdominal bleeding.
48
Ⅶ. Indications for open chest cardiac massage Thoracotomy and direct cardiac massage are nessesary in the following: A. Penetrating chest wounds. B. Tension pneumothorax. C. Cardiac tamponade. D. Chest deformities,eg., barrel chest and kyphoscoliosis.
49
Ⅷ. Termination of effort: Resusciatation is considered unsuccessful if signs of death of the heart and brain are present after 1 hr of continuous cardiopulmonary resusciatative effort.
50
A. Signs of cardiac death 1. Absence of cardiac electrical activity. 2. Slurring and widening of the QRS Complexes. 3. Persistent fibrillation with slowing and Loss of amplitude.
51
B. Signs of central nervous system death 1. Unresponsiveness. 2. No movements. 3. No breathing. 4. Absence of reflexes. 5. Fixed and dilated pupils unresponsive to a direct light. 6. An isoelectric EEG.
52
C. Results of CPCR: Recovery, Coma, Death. 1. Persistent vegetative state (PVS): < 1 month 2. Permanent vegetative state (PVS): > 1 month
53
Thanks
Similar presentations
© 2025 SlidePlayer.com Inc.
All rights reserved.