By

MAURICE BAROODY

 Abstracted from :

The sudden and unexpected cessation of respiration and functional circulation is cardiopulmonary arrest or what is commonly referred to as "Sudden Death". The causes of cardiac arrest are multiple but the prompt initiation of effective cardiopulmonary resuscitation (CPR) cannot be overemphasized no matter what the cause is. The viability of the vital centers of the body, particularly the brain, cannot be maintained more than few minutes without adequate functional circulation. Irreversible brain damage may occur when the cessation of circulation lasts longer than 4-6 minutes. Unconsciousness supervenes in 7-8 sec, and the E.E.G. tracing becomes flat within 20-30 sec of arrest. Therefore it is of utmost importance to start effective CPR within this "grace period" between clinical death, which is apparent few seconds following the arrest and biological death, when irreversible brain damage occurs. Whether the arrest is witnessed or unwitnessed, the victim should be given a second chance to live by initiating CPR.

There are many causes of cardiac arrest occurring in and outside the hospital. Cardiac arrest can be primary or secondary. In primary cardiac arrest, the cause is the heart itself and the most common is ventricular fibrillation (VF) following myocardial ischemia. Secondary cardiac arrest can develop following other causes and the most common of them are asphyxia and exsanguination.

Diagnosis of Cardiac Arrest

Phases of CPR

Phase I -Basic Life Support, is the phase where emergency artificial ventilation and cardiac compressions are performed to oxygenate the victim and keep the circulation going until further advanced life support is available.

Here speed is of utmost importance. Recognition of cardiac arrest should be quick, and CPR should be started promptly. Call for help quickly without interrupting CPR or with minimal interruption if you have to. Continue CPR for I hr or until medical help arrives. This phase includes the ABC (Airway, Breathing, Circulation) of CPR.

Phase II. Advanced Life Support. At this stage spontaneous circulation is restarted and the cardiopulmonary system is stabilized. This is the phase where definitive treatment is given following a successful phase 1. Definitive treatment is in the form of drugs and fluids (D), electrocardiographic monitoring (E) and fibrillation treatment (F) by electric defibrillation.

Phase III-Prolonged Life Support. Here the victim is under intensive care. The cause of arrest is assessed and treated. The brain function is given a lot of care by new brain resuscitation measures. The body as a whole is assessed for multiple organ failure and their intensive care. This phase should be continued until the patient regains consciousness, brain death is certified or hope is given up completely because of the underlying disease.

AIRWAY CONTROL (Step A)

Causes of Airway Obstruction

Airway obstruction can be complete or partial. Complete airway obstruction is silent and leads to asphyxia and cardiac arrest within 5-10 min. Partial obstruction is noisy and can result in hypoxic brain damage or pulmonary edema. It can also lead to exhaustion, apnea and cardiac arrest.

Diagnosis of Airway Obstruction

Complete obstructiotion - if victim is awake, he cannot breath, speak or cough. Retraction of supraclavicular and intercostal muscles occur during attempt at inspiration. In the apneic patient, difficulty is encountered to inflate the lungs when attempting to ventilate the patient.

Partial airway obstruction is recognized by the noisy breathing accompanied by retractions.

As a result of airway obstruction clinical signs and symptoms of hypoxia and hypercarbia become immediately apparent.

In an arrest, attention should first be directed at the airway for emergency oxygenation of the patient. Recognition of acute airway obstruction must go hand in hand with therapeutic action.

The unconscious patient should be placed horizontally in a supine position. Head down with side tilt can be placed for a short while to drain any fluids in the oropharynx.

Manual clearing of airway can be performed, if there is particulate matter, by forcing the Mouth open and making a sweeping movement in the mouth and pharynx with one or two fingers.

This maneuver is used to expel a large foreign body completely obstructing the glottis. Since the patient cannot take a breath to cough the FB out, the back blows create vibrating moves that might loosen it and relieve the obstruction. If this fails the abdominal thrusts cause increase in the intrathoracic pressure and expel the FB Out. Of Course the effectiveness of these maneuvers is not 100%, but in emergency situation that is what is available.

How to perform it:

When a patent airway is established and the victim is still not breathing, then emergency artificial ventilation should be started immediately; it should never be delayed by attempts to find and apply adjuncts. Mouth-to-mouth or mouth-to-nose ventilation is the technic to use. Direct exhaled air ventilation is always readily available. In acute apnea, immediate ventilation with exhaled air does more good than air or oxygen becoming available seconds later. Exhaled air, containing 16-18% oxygen is adequate for resuscitation if the patient's lungs are normal and the operator uses about twice normal T.V. It results in a. PaO₂ of over 75 Torr (SaO₂ over 90%) in the patient.

When mouth-to-mouth ventilation is not possible due to certain reasons such as: meeting obstruction; mouth not easily accessible as with resuscitation started in water, trauma. trisnius, as during convulsions, etc... switch to mouth-to-nose ventilation which is as efficient.

12. Take a deep breath; encircle the patient's nose with your mouth (avoid pinching his nose with your lips), and blow. Open his mouth during exhalation.

When adjuncts are available, then there are several options to choose from in order to ventilate the patient:

- Mouth-to-adjunct ventilation

Mouth-to-airway

Mouth-to-mask with oxygen

- Bag-valve-mask with oxygen (Ambu Bag)

- Mannually-triggered oxygen-powered ventilators

- Automatic ventilators.

The sequence of steps A,B,C, after having established unresponsiveness, are as follows:

- Secure patent airway.

- Apply 3 to 5 rapid, deep lung inflations without allowing full exhalations.

- Feel for the pulse.

12. If pulse is present, continue with one inflation every 5 seconds. In children, a rate of one inflation about every 3 sec. is desirable.

CIRCULATION SUPPORT (Step C)

External cardiac compressions and its combination with airway control and artificial ventilation have made it possible for any trained person to initiate attempts at reversal of clinical death, even outside the hospital.

The heart occupies most of the space between the lower sternum and the spine. Squeezing the heart between the sternum and the spine by chest compressions can readily produce artificial circulation. External cardiac compressions seem to move blood by 2 mechanisms: (1) direct compression of the heart and (2) overall intrathoracic pressure fluctuations (chest pump), which can be augmented by simultaneous IPPV.

Sternal compressions can produce systolic pressure peaks of 100 mmHg and more, but the diastolic pressure is usually not more than 10 mm Hg. The systolic CVP is almost as high as the arterial pressure leaving only a minimal cerebral perfusion pressure. External cardiac compressions usually result in a cardiac output and carotid blood flow which is 30% or less of normal.

For artificial circulation to be effective, pressure should be applied at exactly the lower half of the sternum in the midline. This also avoids the occurrence of injury.

The patient must be in a horizontal position preferably with raised legs to promote venous return. He must be on a firm surface (ground, floor, hard litter, or with a hard board under his back if in bed).

Compress the sternum with enough force to produce a good carotid or femoral pulse which must be checked by another person. Your arms should be vertical, and the compressions should be smooth, regular and uninterrupted.

In adults, use your entire body weight, keeping your arms straight, to avoid fatigue. After each compression, release pressure completely but do not lift your hands off the sternum. Use the heel of the hands only, keeping your fingers away from the chest wall to avoid rib fracture. Do not press on or below the xyphoid to avoid liver injury or regurgitation.

In small children, use one hand only to compress the sternum; in infants the tips of two fingers will be enough to do the job. In small infants you may encircle the chest with the two hands and compress the sternum with your two thumbs.

In infants and small children apply pressure at the midsternun because the heart lies higher up in the chest.

Press down about 1-2 cm in infants and 21/2-4 cm in small children. A rate of 100 to 120 compressions is recommended for small children and infants.

The recommended sequence of CPR steps is as follows:

It is important to master this technic because you rarely find another skilled person at the scene of the accident at first to help you.

With two operators the chest compressions are performed uninterrupted, one per second. Lung inflations are interposed one at the upstroke of each fifth compression.

This technic provides 60 heart compressions and 12 lung inflations each minute. The operators should position themselves on opposite sides of the patient for easy switching of roles in case of fatigue.

First operator interposes one quick lung inflation after every fifth sternal compression.

The ventilating operator should intermittently palpate the carotid pulse to check the effectiveness of cardiac compressions and the return of spontaneous pulse.

The pupils should be examined periodically. Continue cardiac compressions until spontaneous breathing is resumed.

After the initiation of CPR, prompt efforts should be made to restore spontaneous circulation which provides more adequate blood flow to the brain and heart than CPR. This usually requires I.V. drugs and fluids (Step D); ECG diagnosis (Step E), and fibrillation treatment (Step F). Although all these steps are usually followed in sequence from A to F, there are occasions where you can start with any of them. For example, if a monitored patient suddenly goes into VF, and a defibrillator is at his bedside, you can start directly by defibrillation (Step F). Furthermore, if spontaneous pulse returns promptly after initiation of CPR then, steps D.E. and F might not be needed. In other words, what should be done depends on the circumstance of the arrest. Needless to say, you should maintain CPR while trying to restore spontaneous circulation.

DRUGS AND FLUIDS

Peripheral veins - dorsum of hand, arm, dorsum of foot – either by cannulation or cut down. This is the preferred method.

Central vein - External jugular or internal jugular.

E.J. vein could be easily cannulated; but the I.J. vein could be more difficult and dangerous to cannulate while the patient is being bounced by cardiac compressions.

In intubated patients this route can be used to instill certain drugs that are easily absorbed and do not cause tissue damage. Such drugs as epinephrine, atropine and xylocaine, using 1-2 times the I.V. dose and diluted by 10 ml of water. Bicarbonate, however, should not be used transtracheally because it causes damage to the mucosa.

This is not recommended during closed chest cardiac compression. It might cause pneumothorax, injury to coronary artery, injection into cardiac muscle, and prolonged interruptions of cardiac compressions. Consider IC adrenaline only when no vein is available and no endotracheal tube is inserted. During open cardiac massage, IC injection is safe and effective if performed under direct vision.

In general the drugs that are used in CPR can be divided into 4 groups depending on their pharmacologic action:

Among all of them above, epinephrine and sodium bicarbonate are the two drugs used in every cardiac arrest during cardiac compression. The other drugs described are for the pre- or post-arrest period.

Sodium Bicarbonate: This is the second drug (after epinephrine) to be given during CPR. Its purpose is to combat the metabolic acidosis occurring during arrest and which reduces the effect of epinephrine and causes vasodilatation, myocardial depression and capillary leakage. The recommended initial dose of sodium bicarbonate is 1 mEq/K I.V. Repeated doses of 0.5 mEq/Kg are given every 5-8 minutes of CPR. Ideally, Subsequent doses should be guided by arterial pH, aiming for values between 7.3 and 7.5. The optimal approach for the use of sodium bicarbonate is to correct base deficit according to the following formula:

Give half of this dose as a bolus I.V., and titrate the rest only if needed, to reduce base deficit to 5 mEq/lt. or less.

Epinephrine: In asystole, epinephrine helps restart spontaneous cardiac action, as it increases myocardial contractility and elevates perfusion pressure. In cases of VF it converts fine VF into course VF. which is more amenable for defibrillation. The dose for an adult is 0.5-1mg I.V. repeated every 5 minutes during resuscitation.

Calcium Chloride: Calcium increases myocardial contractility but is not superior to epinephrine. It is recommended for electromechanical dissociation, when epinephrine fails to restart cardiac action. It is used also when cardiac depression is caused by certain drugs like barbiturates. The dose is 5 ml/70kg of the 10% CaCl₂ and repeated if necessary at 10 minute intervals.

Isoproteranol: This sympathomimetic amine with pure beta-receptor stimulant action usually has no place during cardiac compressions, except perhaps in the case of asystole or severe atropine resistant bradycardia from heart block.

If administered, it should be by I.V. drip using 1mg in 500 ml and titrating the dose at 2-20 micrograms per minute. The infusion is adjusted to keep the heart rate at about 60 per minute.

Dopamine: In CPR cases, dopamine is useful for supporting arterial perfusion pressure after restoration of spontaneous circulation, once the more potent norepinephrine is no longer required. It is administered by I.V. drip using 200 mg in 250 ml of 5% D/W. Its cardiovascular effect depends on the dose. In low doses (2-10 micg/kg/min) its inotropic effect is associated with renal vasodilatation. In high doses (10 micg/kg/min), it exerts additional vasoconstriction effect. In doses above 20 micg/kg/min., even the renal and mesenteric vessels may be constricted.

Lidocaine: This is the antiarrhythmic agent of choice for the treatment of premature ventricular contractions (PVCS) and for preventing progression to VT or VF. Lidocaine increases the electrical stimulation threshold of the ventricle during diastole, and depresses cardiac irritability where successful defibrillation repeatedly reverts to VF.

Give a loading dose of 1mg/kg I.V. as a bolus, and immediately follow it by a continuous infusion of 1-4 mg/70 kg per minute. Use a solution of 1mg/ml in 5% D/W. Additional boluses of 0.5-1.0 mg/kg may be given every 5 minutes, if necessary, to a total of 200-300 mg/70 kg.

Procainamide: This drug is an alternative to lidocaine, when the latter has not been effective in suppressing PVCs or VT. The recommended dose is about the same as that of lidocaine.

Atropine: Atropine sulfate reduces vagal tone, enhances A-V conduction, and reduces the incidence of VF in profound bradycardia secondary to M.I. Atropine has essentially no place in CPR, except possibly in refractory asystole. It is indicated when the heart rate decreases to less than 50 beats/min., or there is bradycardia associated with PVCs or hypotension. It also increases the heart rate In case of high A-V block with bradycardia. The recommended dose of atropine is 0.5 mg I.V., repeated as needed but not to exceed 2 mg as a total dose.

Propranolol: This beta-adrenergic blocker has no place in emergency CPR, as it makes the heart difficult to resuscitate. It is of use after spontaneous circulation has been established and when recurrent ventricular arrhythmias (PVCs or VT) and atrial tachyarrhythmias are present, particularly if these arrhythmias are triggered by the excessive use of beta-receptor stimulating drugs. The recommended dose is 1mg/70 kg I.V. repeated up to a total of 3 mg. It is contraindicated in asthmatics and patients with heart failure.

Norepinephrine: This potent vasopressor is used mainly for its alpha-adrenergic stimulating action, but sometimes, owing to its slight beta-adrenergic action, it can be used during CPR in a dose similar to that of epinephrine, but such use is still controversial. Its main use is in the post-resuscitation period when an adequate B.P. cannot be maintained due to peripheral vasodilatation. It should be used only by an I.V. drip under constant monitoring of B.P. Eight mg levophed is added to 500 ml of 5%D/W (16 micrograms per ml). Start with 3 microgms (0.2 ml)/min per 70 kg and adjust rate according to response.

Metaraminol: The action of this vasopressor is mostly by releasing norepinephrine and it is less potent than norepinephrine. It can be given by I.V. bolus of 1-5 mg, or by an I.V. drip of 0.4mg/ml solution (100 mg in 250 ml) and titrated according to the response of the patient.

Morphine: Morphine sulfate is not indicated in CPR emergencies, but it is important in cases of M.I. to relieve pain and anxiety and in the treatment of acute pulmonary edema which may occur before or after cardiac arrest. It is given in individual doses of 2-5 mg/70 kg I.V. every 5-30 minutes as required until the desired effect is reached.

Diuretics: The diuretic action of such drugs as, Furosemide (Lasix) and ethacrynic acid (Edecrin), is indicated in pulmonary edema. They may also reduce intracranial hypertension caused by post-anoxic cerebral edema. Diuresis starts within 5 minutes after I.V. administration, and the peak at about one-half hour and lasts for several hours.

Corticosteroids: These drugs may be used for their anti-inflammatory and anti-edema effects in the immediate postresuscitation period. The use of methylprednisolone sodium succinate

(5-30mg/kg or dexamethasone phosphate (1mg/kg) as a single dose, for prompt treatment of cardiogenic shock, or shock lung occurring as complication of cardiac arrest, is advisable. When cerebral edema is suspected following cardiac arrest, methylprednisolone sodium succinate 1mg/kg every six hours may be beneficial. After 48 hours this dose is gradually tapered over 1-2 weeks. If aspiration is present, dexamethasone phosphate may be used in doses of 4 to 8 mg every six hours.

It is essential to provide an intravenous route for the intermittent or continuous rapid administration of drugs and fluids that may be required to reestablish or support a stable cardiac rhythm and adequate circulation. For this, a large bore cannula is needed.

I.V. fluids should be administered with the following objectives in mind:

During fluid therapy, always make adjustments for increased or decreased diuresis, keeping urine flow over 25 ml/70 kg per hour.

The amount and rate of I.V. infusion depend on the amount and rate of estimated blood volume loss and type of fluid selected. The normal circulating blood volume accounts for 7-8 per cent of body weight (10% for simplification).

Extra-cellular fluid volume is normally about 25% of body weight in liters (plasma volume 5% and interstitial space 20%). Since electrolyte solutions are distributed throughout both the intravascular and interstitial spaces, therefore such solutions should first be given in four times the quantity of blood volume lost.

It is apparent, that if moderate to severe blood loss is corrected by electrolyte solutions only, the creation of tissue edema is inevitable. Colloid solutions (blood, plasma, albumin, dextran, gelatin, starch) however, remain longer in the intravascular space and should therefore be given first in volumes equal to the blood volume lost.

As soon as possible after the start of CPR, the EKG pattern should be determined primarily to differentiate between the three most common patterns associated with the clinical picture of cardiac arrest, namely:

1. Ventricular fibrillation (or VT with coma)

2. Electric asystole

EKG monitoring is important during resuscitation but the EKG by itself is not an indicator of circulation; it should be coupled with palpation of the pulses, BP measurement and examination of the skin for color, temperature and capillary refill.

Electric defibrillation is indicated for the termination of lethal dysrhythmias of ventricular tachycardia (with coma or without pulse) and ventricular fibrillation. The most rapid effective and accepted method for terminating ventricular fibrillation, is electric countershock which can be delivered either as alternating current (AC) or direct current (DC).

DC has more advantages and is preferred to the high voltage AC countershock. DC countershock is produced by a capacitance discharge-type defibrillator, delivering up to 400 watt second (Joules) in about 0.01 second duration. The defibrillator should have been present for 200-300 Joules energy for the first countershock in an adult. The suggested initial energy dose for external countershock is 3 Joules per kg for adults and 2 Joules per kg for children. The highest repeat dose is 5 J/kg.

The present recommended technic of external countershock is as follows: In witnessed arrest apply countershock immediately (within 30-60 seconds of the onset of VF) without first starting CPR or giving drugs. If unsuccessful, start CPR promptly, administer drugs and repeat countershocks. In unwitnessed arrest apply CPR for about 2 minutes before attempting defibrillation. Technic:

The patient's outcome in terms of survival and overall performance capability (particularly human mentation) depends on the severity and duration of the insult, the speed and quality of emergency restiscitation, and the early start and high quality of brain-oriented, post-resuscitative intensive therapy.

All organ systems are interdependent, and the failure of the extracranial organs influence the brain and add to the insult. Probably all vital organ systems suffer from changes post-CPR.

Following resuscitation the patient usually suffers from multiple organ failure for hours or days. This "post-arrest syndrome" includes acidosis, reduced cardiac Output, disseminated intravascular coagulation and "self poisoning" from renal and hepatic failure. There may be aspiration syndrome, flail chest from sternal compressions, acute pulmonary edema or progressive pulmonary consolidation. All should be managed with the proper measures. Cardiovascular support after CPR must aim at prevention and treatment of life-threatening dysrhythmias and shock state. The cause of shock must be determined. An aggressive approach to the prevention or immediate reversal of shock states is necessary to prevent deterioration to "irreversible shock" and "re-arrest".

There are several accepted measures to control extracerebral organ system function in ways which would benefit the brain; and measures for iiitracranial homeostasis, particularly control of intracranial pressure (ICP).

Most of these measures are new or under re-investigation, and still controversial. One must keep in mind the differences between the kind of injury to the brain produced by ischemia, anoxia, hypoglycemia, anemia, trauma, hemorrhage, metabolic or toxic abnormalities, inflamation, or by different combinations of these processes. Ischemia of the brain can be global as in cardiac arrest or shock states, or it can be focal as in cerebral infarction. In considering therapeutic measures, one must differentiate between protection and resuscitation, i.e. measures instituted before an insult, or taken after an insult to the brain.

Measures that seem to be effective if instituted immediately and during the first few hours of post-ischemia include the following:

The clinician must bear in mind that the depressant effects of large doses of thiopental or pentobarbital are considerable, particularly in patients with heart disease or hypovolemia, and that the risk/benefit ratios of this treatment versus conventional (safe) doses have not yet been determined. In the meanwhile, usual anesthetic doses of thiopental or pentobarbital (2-5 mg/kg I.V., repeated as needed) that do not depress the circulation and require only small amounts of vasopressor, if they do, may be clinically indicated. Even this less controversial treatment should be used early after the insult and only to patients who are comatose.