|
This article summarizes, the ALS component
of the advisory statements, with particular
reference to their use in the Arabic
countries, under the aegis of the Arab
Resuscitation Council (ARC) [1-10].
 General
principles
The commonest cause of adult sudden cardiac
arrest is ischemic heart disease. The
majority of individuals who die from
an acute coronary syndrome do so before
reaching the hospital. A small, but
important, group of patients develop cardiac
arrest in special circumstances; examples include
trauma, hypothermia, immersion, drug overdose,
anaphylaxis, hypo-volemia, etc. While
the ALS guidelines are universally
applicable, in these situations specific
modifications may be needed to increase
the chances of success.
TRANSTHORACIC
DEFIBRILLATION
The commonest primary arrhythmia in
adult cardiac arrest is ventricular fibrillation
(VF). In some patients, this is preceded
by a short period of ventricular tachycardia
(VT) which deteriorates in waveform to
VF. Early detection and treatment of these
rhythms is central to the chances of successful
outcome. The majority of eventual survivors
of cardiac arrest come from this group.
The more rapidly a patient can be defibrillated in
these circumstances, the greater the chance
of obtaining a cardiac rhythm and the
higher the ultimate success rate.
It has been estimated that the chances
of successful defibrillation
decline by approximately 2-7% with each
minute that a patient remains in cardiac
arrest. This decline reflects rapid
depletion of myocardial high-energy phosphate
stores, and is mirrored in the deterioration
of the amplitude and characteristics of
the VF waveform. Basic life support (BLS)
can slow the rate of decline but does
not reverse it. As a consequence, the
priority is to reduce the delay between
the onset of cardiac arrest and defibrillation.
Irrespective of the type of machine
used, the correct defibrillation technique
is important to reduce transthoracic impedance
and maximize the chance of success. Only
a small proportion of the delivered electrical
energy traverses the heart during transthoracic
defibrillation so that efforts to maximize
this are important. Common faults include
inadequate contact of the paddles or self-adhesive
pads with the chest wall, failure
or inadequate use of couplants to aid
current passage between the paddles and
chest wall, and faulty paddle positioning
or size. One paddle should be placed to
the right of the upper part of the
sternum below the clavicle, the other
just outside the position of the normal
cardiac apex (V 4-5 position). Placement
over the breast tissue in female patients
should be avoided to reduce transthoracic
impedance. Other positions, such as apex-posterior,
can be considered if the standard
position is unsuccessful.
CPR
TECHNIQUES
Simultaneous compression and ventilation,
high impulse external chest compression, interposed
abdominal compression, vest CPR and active
compression/decompression CPR have been shown
experimentally to improve the hemodynamic
state associated with CPR and in some
cases to improve survival in animal
models. There are no data showing improved
outcome in large-scale
human studies with any of these techniques.
These guidelines do not recommend any
change in the technique of closed
chest compression.
AIRWAY
MANAGEMENT AND VENTILATION
After cardiac arrest and during CPR, normal pulmonary
physiological characteristics are altered.
There is an increase in dead space and
a reduction in lung compliance because
of the development of pulmonary edema.
These changes may compromise gas exchange
and serve to focus attention on the delivery
of oxygenation and ventilation of the patient's
lungs. The aim should be to provide a
fractional inspired oxygen concentration
(FiO2) of 1.0. The relatively low
cardiac output achieved during CPR limits
carbon dioxide delivery to the pulmonary
circulation. As a consequence, high tidal
volumes are unnecessary to achieve adequate
carbon dioxide excretion and the prevention
of hypercapnia. This situation may require modification
if carbon dioxide producing buffers are
administered and relative increases in minute
ventilation are required to prevent carbon
dioxide build-up and the development of hypercapnic
acidosis.
DRUG
DELIVERY DURING CPR
The optimal method of drug administration during CPR is still per venous
route. Obviously, if a central venous
cannula is already in situ, it should
be used. Otherwise, for an individual
patient, the decision to attempt central
venous cannulation depends on the skill
of the operator, availably equipment,
nature of the surrounding events and time
scale. If the decision is made to
perform central venous cannulation it
must never delay defibrillation attempts,
performance of CPR or securing of the
airway. Where a peripheral venous route
is used, a flush of 20- 50 ml of
0.9% saline is given after drug administration
to expedite entry to the central
circulation. Administration of drugs by
the tracheal route is theoretically attractive, particularly
if there is no immediate access to the
systemic circulation. During the management of
cardiac arrest, tracheal intubation frequently
precedes venous cannulation, particularly
in patients where venous access is
rendered difficult by obesity or previous
drug use. This route remains a second
line approach. Drugs given by this route
are also limited, to adrenaline, lignocaine
and atropine. It is recommended that doses
of 2- 3 times the standard i. v. dose
are given, diluted up to a total
volume of at least 10 ml in 0.9% saline.
After administration, five ventilations
are given in an attempt to maximize absorption
from the distal bronchial tree. Theoretically,
administration of the agent by deep endobronchial
application would be advantageous.
This would necessitate the use of a catheter
inserted via the tracheal tube. Surprisingly,
for lignocaine, no advantage was demonstrated
from deep endo- bronchial administration.
DRUG
THERAPY DURING CPR
Adrenaline was used to produce peripheral
vasoconstriction and re-start
the hearts of animals in asystole. To
date, there has been no randomized, controlled
study in humans comparing standard
dose adrenaline (1 mg every 3 min) with
placebo of sufficient power to provide
an unequivocal result. It is recommended
that the indication, dose and time intervals between
doses of adrenaline remain unchanged. Antiarrhythmic
agents to prevent arrhythmia are well
established. Their use to facilitate defibrillation
is much less clear. There are many agents
recommended like Amiodarone 300 mg iv diluted
in 20-30 ml then 150 mg supplement then
Img/min for 6h then 5 mg/min for 24 h
to a total dose of 2 gm. Also other
drugs which fall out of fashion. It is
recommended that no change be made
in relation to the use of lignocaine for
general antiarrhythmic management. But
bretylium is no longer recommended.
[11]
The use of atropine in the treatment
of hemodynamically compromising bradyarrhythmias
and some forms of heart block is
well established. In healthy human volunteers,
a single dose of 3 mg i. v. is sufficient
to block vagal activity completely and
this dose is recommended if atropine is considered
for asystole.
In the past, administration of sodium
bicarbonate as a buffer was advised to
reverse the potentially deleterious
effects of acidosis. The best method of
reversing acidosis associated with
cardiac arrest is to restore spontaneous
circulation. At present, sodium bicarbonate
remains the buffer of choice. It
is suggested that its use is limited only
to patients with severe acidosis
(arterial pH less than 7.1 and base deficit
less than -10) and to cardiac arrest occurring
in special circumstances, such as hyperkalaemia.
The
universal ALS algorithm
Each step of the algorithm presupposes
that the one before has been unsuccessful.
Basic life support will already have been
started. This must continue while the monitor/defibrillator
is being attached. In patients who have
had a witnessed collapse can have a single
precordial thump administered pending
attachment of the monitor/defibrillator.
Then analysis of the ECG rhythm takes
place. Movement artifact, lead disconnection
and electrical interference can all
mimic cardiac arrest rhythms. For the
rescuer with a manual defibrillator, the
crucial decision is whether or not the
rhythm present is VFNT. If VFNT is suspected, defibrillation
must occur without delay. The first shock
is given with an energy level of 200 J for
a standard monophasic shock, or its equivalent
if a biphasic waveform in used. If the
first defibrillating shock is unsuccessful,
a shock of the same energy (200 J) is
repeated. If still unsuccessful a
third shock is given, this time at 360
J. A check of a major pulse is performed if,
after a defibrillating shock, an ECG rhythm
compatible with cardiac output is obtained.
If, however, the monitor/defibrillator
indicates that VF persists, then the additional
shocks in the sequence of three can
be administered without a further pulse
check. With modern monitor! defibrillators
it is possible, if necessary, to administer
the first three shocks within a period of
60 s, and in the majority of, patients
who are treated successfully, defibrillation
occurs after ~ one of the first three shocks.
If the first sequence of three shocks
: is unsuccessful, the best chance for
restoring a perfusing rhythm. , is
still defibrillation but correction of
reversible causes or , aggravating factors,
and attempts to maintain myocardial and
l cerebral perfusion and viability, are indicated
at this stage.
Potential causes or aggravating factors
leading to persistent VF/VT may include
electrolyte imbalance, hypothermia and
; drugs or toxic agents for which
specific therapy may be required. These
interventions, together with checking
defibrillating, I paddle/electrode positions
and contacts, should occur during
the
1-min period of CPR.
During this time, attempts are made to
secure advanced airway management and
ventilation and to institute venous
access. The first dose of adrenaline is
given. The ECG rhythm is then re-assessed.
If VF is still present, the next sequence
of defibrillating shock is started
without delay. These shocks are all
at 360 J .Provided that resuscitation
was started appropriately, sequential
loops of the left-hand side of the algorithm
are continued, allowing further sequences of
defibrillating shocks, CPR and the ability
to perform/secure advanced airway and
ventilation techniques and drug delivery.
As long as resuscitation has been started
appropriately, it should
not normally be abandoned while the ECG
rhythm is still recognizably VF/VT.
If at the time of initial rhythm analysis,
VF/VT can be positively excluded, clearly
defibrillation is not appropriate. In
this situation, the right-hand side of
the algorithm is followed. These
patients may have asystole or electromechanical
dissociation (EMD). Any electrical
rhythm associated with cardiac arrest
will, if untreated, deteriorate to asystole. The
prognosis for these rhythms is, in general,
much less favorable but nevertheless there
are some situations where they have
been provoked by remediable conditions,
which, if detected and treated promptly,
may lead to success.
Cardiac pacing may be of value in patients
with extreme bradyarrhythmia. Its efficacy
in true asystole is unproved, except
in cases of trifascicular block where
p waves are present. If pacing is
contemplated and delay occurs before its
institution, external cardiac percussion
(fist pacing) may be effective in
producing cardiac output, particularly
in those situations where myocardial
contractility has not been critically
compromised. While the search for, and correction
of, these potential causes of arrest are
underway, basic life support with advanced airway
management and ventilation, venous access,
etc, should occur as before, and adrenaline
is
administered every 3 min.
After 3 min of CPR, the ECG rhythm is
re-assessed. If VF/ VT has developed,
then the left-hand side of the algorithm
is followed. If a non- VF/VT rhythm still
persists, loops of the right- hand
side of the algorithm continue for as
long as is considered appropriate for
resuscitation to continue.
References:
|
