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Cardiopulmonory
Cerebral Resusciatation
(CPCR)
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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.
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.
• 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.
• First life support (FLS):
• Airway, Breathing, Circulation, Drug
(Defibrillation )
• Advanced life support (ALS):
Airway, Breathing, Circulation, Drug
(Defibrillation),
ECG, Fluid, Gauge, ICU
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
• 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.
• 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).
• 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.
• 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.
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%.
• 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.
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-tostoma resuscitation.
• 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.
4. Pulmonary ventilation
• is not adequate during external
cardiac compression, so artificial
ventilation must be carried out
concurrently by any means available.
D. Artificial circulationexternal 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 circulationexternal 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.
• 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.
• 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.
• 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.
• 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.
• 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.
• 8. Under optimum conditions,
external heart compression
produces only 30-40% of the
normal amount of blood flow.
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.
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
• 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.
• 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.
• 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.
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.
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.
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.
• 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.
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.
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.
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.
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.
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.
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.
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.
B. Signs of central nervous
system death
• 1.
2.
3.
4.
5.
Unresponsiveness.
No movements.
No breathing.
Absence of reflexes.
Fixed and dilated pupils unresponsive
to a direct light.
6. An isoelectric EEG.
C. Results of CPCR:
• Recovery, Coma, Death.
• 1. Persistent vegetative state
(PVS): < 1 month
• 2. Permanent vegetative state
(PVS): > 1 month
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