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Drugs in ACLS

The routine use of any vasopressor
during human cardiac arrest
increases survival to hos-pital
discharge, although improved
short-term survival has been
The primary goal of CPR is to re-

establishblood flow to vital organs

Adrenaline (epinephrine) versus no
Standard-dose adrenaline was associated

withsignificantly higher rates of prehospital
ROSC (relative risk [RR]2.80 [95% CI 1.78–
4.41], p < 0.00001) and survival to hospital
admis-sion (RR 1.95 [95% CI 1.34–2.84], p =
0.0004) when compared toplacebo
There was no difference in survival to hospital
discharge(RR 2.12 [95% CI 0.75–6.02], p =
0.16) or good neurological outcome, defined
as Cerebral Performance Categories (CPC) 1 or
2 (RR 1.73,[95% CI 0.59–5.11], p = 0.32)

Our current recommendation is to continue the

use ofadrenaline during CPR as for Guidelines
2010. We have consid-ered the benefit in shortterm outcomes (ROSC and admission to hospital)
We have decided not tochange current practice
until there is high-quality data on long-term
Use. Adrenaline is available most commonly in
two dilutions:
1 in 10,000 (10 ml of this solution contains 1 mg
of adrenaline)
1 in 1000 (1 ml of this solution contains 1 mg of
Both these dilutions are used routinely in Europe.

The first drug used in cardiac

arrest of any cause: it is included
inthe ALS algorithm for use every
3–5 min of CPR.
Preferred in the treatment of
A second-line treatment for
cardiogenic shock

Anti Arrhythmics Drugs
Adenosine slows transmission

across the AV node but has little
effect on other myocardial cells or
conduction pathways.
It is highly effective for terminating
paroxysmal SVT
It has an extremely short half-life
of 10–15 s
The smallest dose likely to be
effective is 6 mg

Refractory VF/pVT
Haemodynamically stable

ventricular tachycardia (VT) and
other resistant tachyarrhythmias
We recommend that an initial
intravenous dose of 300 mg
amiodarone, diluted in 5% glucose
to a volume of 20 ml

Lidocaine is recommended for use

during ALS when amiodarone is
It decreases ventricular
Suppresses ventricular ectopic
It is effective in suppressing
arrhythmias associated with

Lidocaine is indicated in refractory

VF/pVT (when amiodarone is unavailable)
When amiodarone is unavailable,
consider an initial dose of 100 mg (1–1.5
mg kg−1) of lidocaine for VF/pVT
Give an additional bolus of 50 mg if
The total dose should not exceed 3 mg kg

Has effects on sodium,
potassium and calcium channels
as well as alpha and beta
adrenergic blocking properties

Control of haemodynamically stable

monomorphic VT, polymor-phic VT
and wide-complex tachycardia of
uncertain origin.
Paroxysmal SVT uncontrolled by
adenosine, vagal manoeuvres or AV
nodal blockade;
Unsuccessful electrical cardioversion

Give amiodarone, 300 mg intravenously,

over 10–60 min, depending on the
circumstances and haemodynamic
stability ofthe patient
Followed by an infusion of 900 mg over 24
Additional infusions of 150 mg can be
repeated asnecessary for recurrent or
resistant arrhythmias
a maximum manufacturer-recommended
total daily dose of 2 g

Verapamil and Diltiazem
Calcium channel blocking drug

sthat slow conduction and increase
refractoriness in the AV node
These actions may terminate reentrant arrhythmias and control
ventricular response rate in
patients with a variety of atrial

Stable regular narrow-complex

tachycardias uncontrolled orunconverted
by adenosine or vagal manoeuvres
To control ventricular rate in patients with
AF or atrial flutter and preserved
ventricular function
Initial dose of verapamil is 2.5–5 mg
intravenously given over 2 min
Give repeated doses of 5–10 mg every15–
30 min to a maximum of 20 mg.

Diltiazem at a dose of 250mcg/kg

intravenously, followed by a second
dose of 350mcg/kg
Diltiazem may decrease myocardial
contrac-tility and critically reduce
cardiac output in patients with severe
LV dysfunction

Beta-adrenergic blockers
Reduce the effects of circulating

catecholamines and decrease heart
rate and blood pressure
They also have cardioprotective
effects for patients with
acutecoronary syndromes

Narrow-complex regular

tachycardias uncontrolled by
vagalmanoeuvres and adenosine in
the patient with preserved ventricular function
To control rate in AF and atrial
flutter when ventricular functionis

The intravenous dose of atenolol (beta1) is

5 mg given over 5 min, repeated if
necessary after 10 min
Metoprolol (beta1) isgiven in doses of 2–5
mg at 5-min intervals to a total of 15 mg
Propranolol (beta1 and beta2 effects),
100mcg kg, is given slowly in three equal
doses at
2–3min intervals
Intravenous esmolol is a short-acting (halflife of 2–9 min) beta1-selective beta-blocker.
It is given as an intravenous loading dose of
500mcg kg over 1 min, followed by an
infusion of 50–200mcg kg/min

Side effects of beta-blockade

include bradycardia, AV conduction delay and hypotension
Contraindications to the use
ofbeta-adrenergic blocking drugs
include second- or third-degree
heart block, hypotension, severe
congestive heart failure and lung
disease associated with

Is the first line treatment for

polymorphic ven-tricular
tachycardia (torsades de pointes)
and ventricular orsupraventricular
tachycardia associated with
Give mag-nesium sulphate 2 g (8
mmol) over 10 min. This can be
repeated once if necessary.

Intravenous fluids
Ensure normovolaemia
Use intravenous fluid to flush

peripherally injected drugs into the
central circulation