Cardiopulmonary Resuscitation (CPR)

PERHAPS YOU MAY HAPPEN TO BE NEAR
someone who falls to the ground and stops breathing.
You may be alone or someone summons you to help. Can
you help? If you have never learned how to do CPR, you
will not know what to do to save a life. Thus it is wise for
all individuals to attend a practical course in CPR or at
least read and practice the drill until it becomes automatic.
Since its description more than 43 years ago, the
fundamentals of CPR have undergone minimal changes.
The technique is quite simple. The main goal in applying
CPR is trying to get oxygen to the individual’s brain to
keep it alive until expert help arrives. Mouth-to-mouth
ventilation oxygenates the blood, and chest compressions
cause forward flow of blood, albeit a small flow, that results
in some cardiac output into the circulation so that
oxygenated blood reaches vital organs.

In this chapter the relevant points of CPR are summarized
so that if you are faced with an individual who has
‘‘dropped dead’’ or appears to have lost consciousness in
your presence, you may be able to render assistance.

I. CAUSES OF LOSS OF CONSCIOUSNESS
Patients may lose consciousness and fall because of several
reasons such as syncope, seizure, stroke, or cardiac arrest.
A. Syncope/Fainting
With syncope the patient has a pulse, does not stop breathing,
and has no shaking of the limbs. Simply keeping the
head down, preferably with the individual lying flat, and
raising the legs up in the air above the patient’s hips will
cause blood to flow from the legs. In about one minute the
individual will recover completely.

B. Seizure/Epilepsy
During a seizure the patient’s limbs exhibit jerky, movements,
the limbs get rigid, or there is a combination of
rigidity and jerking of one or more limbs. The patient is
breathing, but saliva and foam bubble from the mouth.
Some individuals pass urine or stool. Recovery is typical.

C. Stroke
During a stroke, circulation to part of the brain is cut off
because of a blood clot in an artery in the brain. Strokes
usually occur in individuals over age 60. It is rare for the
patient to fall suddenly to the floor without some warning.
The patient will have a pulse and breathing will be present.
There is no reason to do CPR because the heartbeat,
circulation, and respirations have not stopped.

D. Cardiac Arrest
During cardiac arrest, the heart stops beating completely
and is at a standstill (asystole) in about 25% of individuals.
In about 60–75%, cardiac arrest is due to ventricular
fibrillation. Ventricular fibrillation can be treated by an
electrical shock, which defibrillates the heart and replaces
the ventricular fibrillation with a normal heartbeat.
In standstill or asystole, there is no electrical current in
the heart, and using electrical shock is of no value. In a few
cases, the heart may commence beating on its own. This
condition is called a Stokes-Adams attack, named after the
doctors who first described it. A few individuals can be
saved by the insertion of a pacemaker if the attack occurs
in the hospital.

It is wise for a family member of a heart patient to know
how to give CPR. It reassures the patient that something
can be done. The knowledgeable individual also feels some
sense of confidence, which promotes hope.
Each year approximately a quarter million individuals
die suddenly in the United States from coronary artery
disease before reaching a hospital; more than half a
million have a cardiac arrest and receive CPR during
hospitalization.
II. CARDIAC ARREST RHYTHMS
There are only two cardiac arrest rhythms to consider:
ventricular fibrillation and pulseless ventricular tachycardia
(VF/VT).

A. Ventricular Fibrillation/Pulseless
Ventricular Tachycardia
VF is defined as a pulseless chaotic disorganized rhythm
with an undulating irregular pattern that varies in size and
shape and has a ventricular waveform greater than 150 beats
per minute. VT is an irregular wide QRS complex tachycardia
(see the chapter Arrhythmias/Palpitations). Patients
with V Tmay remain stable, alert, and have a pulse. Patients
with unstable ventricular tachycardia are hemodynamically
unstable with a blood pressure of less than 90 mmHg, chest
pain, shortness of breath, clouding of consciousness, or
rapid loss of consciousness.

The American Heart Association (AHA) Guidelines
2000 for CPR and emergency cardiovascular care advises
that in patients with cardiac arrest it is advisable to always
assume that the rhythm is VF or pulseless VT. Because
individuals who can be saved from cardiac arrest are
usually in VF or pulseless VT, the earliest possible delivery
of defibrillation is the single most effective intervention.
A recent study in Norway, however, indicates that the use
of three minutes of CPR prior to defibrillation, rather than
immediate defibrillation, resulted in better outcomes
among VF patients who received attention more than
five minutes after symptom onset. In patients who received
defibrillation immediately, 46% achieved a spontaneous
palpable pulse on admission versus 56% of those within
three minutes of CPR. Further studies are necessary to
clarify this finding.

B. Automated External Defibrillator
The distribution of automatic external defibrillators has
been widespread. The AHA recommends that all firstresponding
emergency personnel such as physicians,
nurses, emergency medical technicians, paramedics, firefighters,
and volunteer emergency personnel be trained
and permitted to operate a defibrillator. The defibrillator
should be available in all emergency ambulances that
engage in the care or transit of cardiac patients.
The automated external defibrillator automatically
interprets the cardiac rhythm and, if VF is present, advises
the operator to provide a shock. Because most cardiac
arrests occur in the home, a case can be made for home
defibrillators for patients at high risk. Their size, that of
a notebook laptop computer, and costs of approximately
$3000 should both decrease considerably over the next
decade.

III. CARDIOPULMONARY RESUSCITATION
CPR is only a temporary measure. The aim is to get blood
containing a fresh supply of oxygen to the brain.
Therefore, it is necessary to breathe enough air into the
patient’s lung, then compress the chest to cause the
nonbeating heart to expel blood into the arteries. This
produces circulation of the blood to the brain. Rarely, the
patient may be revived, and the heart begins to beat
spontaneously. In patients with ventricular fibrillation,
death will occur unless the heart is defibrillated. The hope
is that the ambulance has a portable defibrillator and a
team that can defibrillate the patient.

A. How to Recognize Cardiac Arrest
First, the patient’s level of responsiveness must be determined.
If the patient is unresponsive, he is unconscious
and oblivious to shaking or commands. Second, determine
if the patient is breathing. Within 30 seconds you should
have arrived at a conclusion that a cardiac arrest has
occurred. Speed of diagnosis is critical. Within three to
four minutes of cardiac arrest, irreversible brain damage
can occur because of lack of oxygen. The intention is to
provide basic life support until advanced life support in the
form of expert technical help arrives. When CPR is started
within four minutes after collapse, the probability of
survival doubles.

In a King’s County survey, 46% of patients with VF
survived CPR versus only 7% for presumed asystole and
pulseless electrical activity (PEA). The incidence of VF in
that survey was 45% and asystole/PEA 41%. Thus close to
50% of patients with VF can be resuscitated with efficient
CPR, but less than 10% with other rhythms can be
resuscitated.

B. The Steps of CPR
AHA Guidelines provide the following steps for CPR
(see Fig. 1):

Check responsiveness

Open the airway

Check breathing

Give two effective breaths

Access the circulation

Compress the chest (see Fig. 2)
1. Responsiveness — Airway
CPR should be commenced immediately. First, turn the
victim flat on the back on a hard surface (preferably the
floor). Quickly assess head tilt for responsiveness and loss
of consciousness. Figure 2 shows the use of the head tilt/
chin lift maneuver to open the airway. One hand is placed
on the victim’s forehead and firm backward pressure is
applied with the palm to tilt the head back. The index and
middle finger of the other hand are placed under the bony
parts of the lower jaw. The chin is lifted forward and the
jaw is supported. Avoid pressing the fingers into the soft
tissue under the chin. This maneuver should bring the
teeth almost together and maintain dentures in position.

2. Breathing
Place your ear over the victim’s mouth and nose. If you do
not hear or feel the flow of air escaping and the chest does
not rise and fall, the victim is not breathing. Pinch the
victim’s nostrils closed, using your thumb and index finger
of the hand on the forehead. Then take a deep breath,
make a tight seal over the victim’s mouth with your
mouth, and blow into the victim’s mouth. Blow air into
the victim’s mouth to fill the lungs (ventilate) rapidly two
times allowing the chest to deflate totally between each
breath.

C. Circulation
1. The Pulse
There is no pulse if cardiac arrest has occurred. Check for a
pulse by feeling the carotid artery in the neck. The right
carotid artery is felt one inch from the angle of the jaw.
Place the index finger in a straight line parallel with the
wind pipe (trachea) so that the entire length of the first
finger pad is touching the skin. The tip of the index finger
should be approximately opposite the Adam’s apple. Start
by feeling the most prominent part of the Adam’s apple
with the tips of two fingers, then slide the finger outward
to reach the groove between the hard cartilage of the wind
pipe and the muscle of the neck. The carotid artery lies
only a few millimeters under the skin, and the pulsation is
easily felt. Practice feeding this pulse so that you can find it
in a hurry, taking no more than 10 seconds.

Evidence has accumulated from the European Resuscitation
Council and other international expert panels that
the pulse check is not a good diagnostic test for the
presence or absence of a beating heart. The pulse is not a
satisfactory check for lay responders and they should check
for signs of circulation such as any movement including
swallowing or breathing that consists of more than an
occasional gasp.

2. Chest Compression
Place the heel of one hand over the lower half (see Fig. 1)
of the breastbone, but at least one inch (2 cm or two
fingerbreadths) away from the end of the breastbone
(xiphoid process). Position the heel of your other hand on
the top of the first. Keep the fingers off the rib cage. If your
hands are too high, ineffective chest compression may
result, and fracture of the ribs may occur. Keep your arms
straight at the elbow (locked elbows) and apply pressure as
vertically as possible. Your shoulders should be directly
above the victim’s breastbone. Chest compressions are then
easily carried out by forceful movements of the shoulders
and back, thus the maneuver is less tiring. Depress the
breastbone one to two inches (3–5 cm) toward the spine;
alternately compress and relax.

The compression rate should be about 90–100 compressions
per minute. At the end of the 15th compression
two full breaths are given. CPR should never be interrupted
for more than five seconds, and it should be continued
until skilled help arrives. Endotracheal intubation
should be accomplished within 30 seconds of cessation
of CPR.

Note that the victim’s mouth should be almost completely
closed, however, depress the lower lip a bit so that
the mouth remains slightly open. If dentures cannot be
managed in place, remove them after first giving the very
important first two breaths. You must see the chest rise and
fall. If the first two breaths meet with resistance and the
chest fails to rise when you breathe air into the patient’s
mouth, make sure that the airway is properly opened by
the head tilt/chin lift method and that the seal around the
mouth is airtight. Then clear the airway with your fingers
if necessary. The fact that the patient suddenly dropped to
the ground and was not choking while eating is sufficient
to persuade you not to waste time searching for meat or
vomitus.

IV. DEFIBRILLATION
The first shock setting should be 200 joules followed by
a second shock of 300 joules. One defibrillator paddle
is positioned to the right of the sternum below the clavicle.
The other paddle is placed to the left of the left nipple
with the center of the paddle in the mid-axillary line.
An appropriate gel is one that has a low impedance.
Because gel spreads during chest compression, shocks may
arc across the chest surface thus, the gel must be toweled
off. Conducting gel pads should be used but must be
changed between shocks. Heavy arm pressure should be
applied to each paddle applied to the chest and
defibrillation should take place when the victim’s phase
of ventilation is in full expiration. In the UK the lower
paddle is placed over the points designated as V4 and V5
for the ECG, that is, a little outside the position of the
normal apex beat. The paddle should be placed at least five
inches away from a pacemaker generator.

The area around the patient should be checked so that
no personnel are directly or indirectly in contact with the
patient. The operator must not touch the patient when
the shock is delivered. Deliver countershock by depressing
both paddle discharge buttons simultaneously. If
no skeletal muscle contraction is observed, check the
equipment.

After countershock reassess the cardiac rhythm. If VF
persists repeat the shock as soon as possible and continue
CPR during any delays. If an organized rhythm is restored,
check immediately for a pulse. If no pulse is present
resume CPR.

Ventricular asystole causing cardiac arrest indicates
a poor prognosis. After CPR is initiated epinephrine
is given. Occasionally VF may masquerade as asystole.
The monitoring electrodes should be repeated from the
original positioned to ensure that VF is not present.
Asystole or electromechanical dissociation is usually caused
by irreversible myocardial damage that is extensive with a
poor prognosis.

A. Errors in Defibrillation
Eisenberg and Mengert emphasized the following common
errors in CPR. Defibrillation errors may occur if the
synchronized mode is accidentally selected before defibrillation
is attempted, thus no shock is delivered. Asystole
may be falsely displayed when the selection is set for
paddles and the rescuer believes that rhythm lead II is
being displayed. In addition, if a vast amount of chest hair
is present it should be shaved off where the paddles are to
be placed; smeared gel across the chest should be toweled
off before defibrillation.

Oxygen at 100% concentration is given as soon as
possible through a bag-valve mask or endotracheal tube.
Plastic face masks may provide 50–60% oxygen with an
oxygen flow rate of 10 L/min.

V. DRUGS FOR CARDIAC ARREST
A. Epinephrine (Adrenaline)
For more than 40 years epinephrine has been a key agent
used during cardiac arrest. Epinephrine is both an alphaand
beta-adrenergic agonist; therefore, it stimulates spontaneous
cardiac contractions, increases systemic vascular
resistance resulting in an increased aortic diastolic perfusion
pressure, and improves coronary blood flow. It is
relevant that epinephrine constricts peripheral vessels but
preserves flow to vital organs causing coronary artery
dilation.

Epinephrine is indicated for fine VF, which is rendered
more amenable to removal by countershock and for VF
that does not respond to electrical countershock. Asystole
and pulseless idioventricular rhythms and electromechanical
dissociation may respond to this drug, albeit rarely.
A dose of 1 mg IV push every 3–5 minutes (0.01 mg/kg)
is recommended. A 20-ml IV fluid flush should be administered
to ensure delivery of the drug centrally. A dose of
1 mg/10 ml of a 1:10,000 solution may be given via the
tracheobronchial tube.

A higher dose of epinephrine was advocated by the AHA
in 1992 based on studies. If the 1-mg IV dose was
ineffective, escalating doses of 3 and 5 mg or 5 mg per dose
rather than 1 mg were advised; the result of 8 large
randomized trials in patients with cardiac arrest however,
showed no significant benefit. The higher dose regimen is
no longer recommended.

B. Vasopressin
Vasopressin, a clonal substance antidiuretic hormone,
becomes a powerful vasoconstrictor when used at much
higher doses than normally present in the body. This drug
possesses effects that duplicate the positive effects of
epinephrine, but does not duplicate the adverse effects of
epinephrine. Only one dose of vasopressin is required.
This is less frequent than epinephrine because the 10- to
20-minute half-life of vasopressin is much greater than
the 3- to 5-minute half-life of epinephrine. Vasopressin
is recommended only for VF/VT; there is no evidence to
support its usefulness in asystole or PEA.

Vasopressin is to be administered IV single-dose one
time only. If there is no response 5–10 minutes after a
single dose of vasopressin, it is advisable to resume
epinephrine 1 mg IV push every 3–5 minutes.

C. Amiodarone
Amiodarone is a complex drug which effects sodium,
potassium, and calcium channels as well as alpha- and
beta-adrenergic blocking properties (see the chapter
Arrhythmias/Palpitations). This drug is recommended
after defibrillation and epinephrine in cardiac arrest with
persistent VT or VF.

The recommended dose is 300 mg IV push. If VF/
pulseless VT recurs, consider administration of a second
dose of 150 mg IV.

D. Beta-Adrenergic Blocking Agents
The actions and beneficial effects of beta-blockers are given
in the chapter Beta-blockers. Atenolol, metoprolol, and
propranolol have been shown to reduce the incidence
of VF significantly in post-MI patients who did not
received fibrinolytic agents. Beta-blockers have been shown
to prevent recurrent VF. VF is unique among cardiac
arrhythmias because management with immediate countershock
antifibrillatory drugs can be useful. Beta-blockers
increase VF threshold and have been shown to be useful in
patients who have repetitive VF precipitated by electrocution.
Although these agents have a negative inotropic
effect, they are not helpful in patients in cardiac arrest.
Metoprolol is administered 5 mg by slow IV push
over 5 minutes, at 5-minute intervals for a total 15 mg.
Propranolol has been used worldwide and its use continues
at a dose of 0.1 mg/kg by slow IV push divided into three
equal doses at 2- to 3-minute intervals. The rate of
administration should not exceed 1 mg/minute. Esmolol is
a short-acting beta-blocking agent with a short half-life of
2–9 minutes. The drug is metabolized by erythrocyte
esterases and requires no dose adjustment in patients with
renal or hepatic impairment. The dosing regimen is
complex and requires an IV infusion pump (see the
chapters Beta-Blockers and Arrhythmias/Palpitations).

E. Sodium Bicarbonate
This agent is no longer recommended for routine use
except for pre-existing hyperkalemia. Prompt ventilation of
the lungs is essential for excretion of carbon dioxide and is
the most effective method for combating acidosis.
Sodium bicarbonate may be used to combat bicarbonate
responsive acidosis, tricyclic overdose, and after about 10
minutes of ventilation including intubation, defibrillation,
and use of epinephrine. If CPR is still necessary, sodium
bicarbonate may be used. The drug may also be used on
return of circulation after long cardiac arrest, but its
use should be guided by arterial pH measurements.
The recommended dose is an IV bolus of 1 mEq/kg
( 50 mEq).

F. Atropine
This drug is of value in the management of severe
bradycardia associated with cardiac arrest. Patients with
asystole or PEA may respond to atropine while preparations
are made for pacing. Patients with a high degree
atrioventricular block, slow idioventricular rates, and severe
sinus bradycardia with hypotension should be given a trial
of atropine IV.

A dose of 1 mg IV repeated in 3–5 minutes is recommended.
If asystole persists, the maximum of 3 mg can be
administered (0.04 mg/kg).
G. Magnesium Sulfate
Magnesium sulfate is reported to expedite ventricular
defibrillation and is indicated for polymorphic ventricular
tachycardia, torsades de pointes, and management of
hypomagnesemia. A dose of 1–2 mg IV is recommended.

H. Bretylium
Bretylium has been dropped from the VF/pulseless VT
algorithm. This drug was used in the 1980s and 1990s for
recurrent VF, but was only partially successful and never
proven. In the late 1990s, severe problems with obtaining
the raw materials curtailed manufacture. The world sources
of bretylium appear to be nearly exhausted. Bretylium has
a high incidence of side effects including hypotension. It
has been replaced by amiodarone and beta-blocking
agents.


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