Emergency Drugs

The collapse or sudden deterioration of a patient in a clinical environment can have a

number of possible causes. If it is identified as being due to a cardiac arrest, the survival
chances of the patient will be increased by following guidelines established by the
Resuscitation Council (UK) (2005). These describe the sequence of actions that should
be undertaken at the various stages of the resuscitation attempt.

This article will consider the pharmacological treatment of cardiac arrest. The full
guidelines can be found at the Resuscitation Council website (www.resus.org.uk). To
follow these guidelines accurately it is necessary to be able to identify the various heart
rhythms associated with a cardiac arrest. An explanation of these can be found in basic
textbooks such as The ECG Made Easy (Hampton, 2003).

Adrenaline

This is the first drug given in all causes of cardiac arrest and should be readily available
in all clinical areas. Adrenaline concentrates the blood around the vital organs,
specifically the brain and the heart, by peripheral vasoconstriction. These are the
organs that must continue to receive blood to increase the chances of survival following
cardiac arrest. Adrenaline also strengthens cardiac contractions as it stimulates the
cardiac muscle. This further increases the amount of blood circulating to the vital
organs, and also increases the chance of the heart returning to a normal rhythm.

Adrenaline can be given repeatedly during a cardiac arrest until the condition of the
patient improves. The Resuscitation Council recommends that it is given as soon as
possible once a cardiac arrest has been identified. This can be repeated every 3-5
minutes.

The suggested administration route is by a central line, as it will then reach the cardiac
tissue more rapidly (Resuscitation Council UK, 2005). If this is not available it may be
administered through a cannula in a peripheral vein. If so, the cannula should be
flushed with at least 20ml of 0.9% sodium chloride. This will ensure the entry of the drug
into the circulation.

If venous access cannot be obtained and the patient is intubated, adrenaline can be
given via the endotracheal tube directly into the lungs. Manufacturers suggest that
adrenaline may be injected directly into the heart through the chest wall if no other route
is available (eMC, 2006). This can be a difficult procedure and should only be attempted
by a competent clinician and when all other attempts to gain access have failed.
Once an organised rhythm has been established the use of adrenaline must be
reassessed as excess amounts can precipitate ventricular fibrillation. It is also important
to note that adrenaline reacts with sodium bicarbonate to produce solid material. For
this reason these two drugs should not be administered through the same IV route
without adequate flushing with 0.9% sodium chloride.

Amiodarone

This drug is given during cardiac arrest to treat specific cardiac arrthymias, mainly
ventricular fibrillation and ventricular tachycardia. The Resuscitation Council
recommends that the first treatment for ventricular fibrillation or ventricular tachycardia
should be electrical defibrillation. If this is unsuccessful after three attempts amiodarone
should be given.

Amiodarone has a complex effect on the heart but the main effect is to slow down the
metabolism of cardiac tissue. The drug also blocks the action of hormones that speed
up the heart rate. The overall effect is to slow the heart. This is important in a cardiac
arrest when the heart is beating too fast to produce a normal circulation.

Manufacturers guidelines state (eMC, 2006) that there should be an interval between
bolus doses of amiodarone of at least 15 minutes. This can be continued by an infusion
over 24 hours. Amiodarone is not compatible with sodium chloride and must at all times
be diluted in 5% dextrose.

It can be administered through a cannula situated in a peripheral vein but localised

irritation and discomfort are a common problem and are more likely to occur if the drug
is given as a continuous infusion. This is not quite so important in the emergency
situation but if the patient requires a prolonged infusion then central venous access
should be considered.

The side-effect of this drug most relevant to cardiac arrest is severe bradycardia. For
this reason a patient receiving an infusion of IV amiodarone should be monitored in a
critical care environment such as a coronary care or intensive care unit. This reduced
heart rate can be reversed by atropine and this drug should be available when
amiodarone is being administered intravenously.

Lidocaine

This drug is similar to amiodarone in that it is given to treat specific cardiac arrythmias,
again mainly ventricular fibrillation and ventricular tachycardia. It reduces the electrical
activity of cardiac tissue and so is able to slow down a very fast heart rate.
The Resuscitation Council recommends that lidocaine only be given in situations where
amiodarone is not available. It should not be given at the same time as amiodarone,
and should not be given if amiodarone has already been administered.

It is recommended that IV lidocaine is given as a bolus dose over 2-4 minutes. The
manufacturer recommends (eMC, 2006) at least a five-minute interval between
subsequent doses and there will also be a recommended maximum dose over an hour
(see local guidelines).

Bolus intravenous infusions have a short duration of action (15 to 20 minutes), so if the
patients condition demands it a repeat bolus should be given within this time period and
then a continuous infusion commenced. It is not normally recommended that the
infusion be continued for longer than 24 hours. As with amiodarone, the side-effects of
this drug are bradycardia together with hypotension, and continual cardiac monitoring is
recommended.

Atropine

The action of this drug is to block the effect of the vagus nerve on the heart. This nerve
normally slows heart rate and, during cardiac arrest, is a common cause of asytole.
Atropine also acts on the conduction system of the heart and accelerates the
transmission of electrical impulses through cardiac tissue.

In cardiac arrest it is given to reverse asystole and severe bradycardia. The

Resuscitation Council recommends that atropine be given for pulseless electrical
activity with a rate of less than 60 beats per minute or in complete asystole.

This drug should be administered intravenously and the dose depends on the heart
rhythm. For bradycardia a dose of 0.5mg should be given and repeated every five
minutes until a satisfactory heart rate is achieved. In asystole a single dose of 3mg
should be given and this should not be repeated unless the cardiac rhythm changes to
bradycardia or pulseless electrical activity.

If IV access cannot be obtained then atropine can be given by an endotracheal tube at a

dose two to three times as high as that given intravenously.

Additional drugs

The previously mentioned drugs are administered either as soon as the cardiac arrest
has been diagnosed (adrenaline) or once the electrical activity of the heart has been
assessed on a cardiac monitor (amiodarone or atropine). The following drugs are given
once the above have been tried and there is no improvement in the patients condition.
Their administration requires a knowledge of the patients past medical history or a
history of the circumstances of the arrest.

A list of the drugs recommended by the Resuscitation Council for use during a cardiac
arrest is given in Table 1 (p25). Below is a description of the specific applications of
some of the more commonly used drugs.

Calcium chloride

Calcium is essential for the contraction of muscular tissue throughout the body, and is
especially important for the strength of contraction of cardiac tissue. If given during
cardiac arrest it can stabilise the contraction of cardiac tissue after metabolic changes
have caused instability and arrythmias (Hollander-Rodriguez and Calvert, 2006).

It has been suggested that calcium can improve weak or inefficient myocardial
contractions when adrenaline has failed. This is especially the case following open-
heart surgery (eMC, 2006).

Calcium can also be used to protect against a number of metabolic conditions that
cause pulseless electrical activity, including raised blood potassium levels, lowered
blood calcium levels and overdose of magnesium or calcium channel blocking drugs.

Calcium chloride must be administered intravenously and must not be injected directly
into tissue due to the high risk of tissue necrosis. It should be given through a small-
bore cannula placed in a large vein, again to reduce the risk of damage to the
surrounding tissue. Due to a chemical interaction calcium chloride should not be given
through the same venous access point as sodium bicarbonate.

There are two main side-effects of calcium that are important in the emergency cardiac
arrest situation. The first is that repeated injections can increase blood acidity and
should be used with caution in patients who have lowered blood pH. As this is found in
a large number of patients following a cardiac arrest frequent monitoring of arterial
blood pH is advised. Second, IV administration of calcium chloride can cause
hypotension due to peripheral vasodilation and, less commonly, bradycardia and
cardiac arrhythmias.
Magnesium sulphate

Magnesium is an important electrolyte involved in the contraction of muscular tissue,

including cardiac muscle. A reduction in blood levels of this element can frequently
cause cardiac arrhythmias, often leading to cardiac arrest.

Common causes of excessive magnesium loss from the body include long-term use of
potassium-losing diuretics, alcohol misuse or diarrhoea. It has also been suggested that
magnesium can help stabilise arrhythmias caused by low potassium levels and digoxin
toxicity (eMC, 2006).

The Resuscitation Council recommends that magnesium be administered intravenously

if there are suggestions that a low magnesium level has contributed to the cardiac
arrest.

When giving magnesium intravenously it is important that there is close monitoring of

blood pressure, urine output and respiratory rate.

Miscellaneous drugs

The remaining drugs recommended by the Resuscitation Council should be readily

available during the resuscitation process but will not be required immediately. They are
used to treat specific medical conditions that may have caused the cardiac arrest, for
example an acute asthmatic episode. They are also used to treat complications
frequently associated with cardiac arrest such as fluid overload due to heart failure.

These drugs should be administered as directed by the clinician managing the cardiac
arrest and are not specifically included in the Resuscitation Council guidelines.
Cardiopulmonary Resuscitation (CPR) in Adults
By Robert E O'Connor, MD, MPH, University of Virginia School of Medicine

Cardiac Arrest and CPR

Cardiac Arrest
Cardiopulmonary Resuscitation (CPR) in Adults
Cardiopulmonary Resuscitation (CPR) in Infants and Children

CPR is an organized, sequential response to cardiac arrest, including

Recognition of absent breathing and circulation

Basic life support with chest compressions and rescue breathing
Advanced cardiac life support (ACLS) with definitive airway and rhythm control
Postresuscitative care

Prompt initiation of uninterrupted chest compression and early defibrillation (when

indicated) are the keys to success. Speed, efficiency, and proper application of CPR
with the least possible interruptions determine successful outcome; the rare exception is
profound hypothermia caused by cold water immersion, when successful resuscitation
may be accomplished even after prolonged arrest (up to 60 min).

Overview of CPR
(See also the American Heart Association's guidelines for CPR and emergency
cardiovascular care.)

Guidelines for health care professionals from the American Heart Association are
followed (see Figure: Adult comprehensive emergency cardiac care.). If a person has
collapsed with possible cardiac arrest, a rescuer first establishes unresponsiveness and
confirms absence of breathing or the presence of only gasping respirations. Then, the
rescuer calls for help. Anyone answering is directed to activate the emergency response
system (or appropriate in-hospital resuscitation personnel) and, if possible, obtain a
defibrillator.

If no one responds, the rescuer first activates the emergency response system and then
begins basic life support by giving 30 chest compressions at a rate of 100 to 120/min
and then opening the airway (lifting the chin and tilting back the forehead) and giving 2
rescue breaths. The cycle of compressions and breaths is continued (see Table: CPR
Techniques for Health Care Practitioners) without interruption; preferably each rescuer
is relieved every 2 min.

When a defibrillator (manual or automated) becomes available, a person in ventricular

fibrillation (VF) or pulseless ventricular tachycardia (VT) is given an unsynchronized
shock (see also Defibrillation). If the cardiac arrest is witnessed and a defibrillator is on
the scene, a person in VF or VT is immediately defibrillated; early defibrillation may
promptly convert VF or pulseless VT to a perfusing rhythm. It is recommended that
untrained bystanders begin and maintain continuous chest compressions until skilled
help arrives.

Adult comprehensive emergency cardiac care.

*If an adequate number of trained personnel are available, patient assessment, CPR, and
activation of the emergency response system should occur simultaneously.
Based on the Comprehensive Emergency Cardiac Care Algorithm from the American
Heart Association.
The techniques used in basic 1- and 2-rescuer CPR are listed in Table CPR Techniques
for Health Care Practitioners. Mastery is best acquired by hands-on training such as that
provided in the US under the auspices of the American Heart Association (1-800-AHA-
USA1) or corresponding organizations in other countries.
CPR Techniques for Health Care Practitioners

Age Group One-Rescuer CPR* Two-Rescuer CPR Breath Size

Adults and 2 breaths (1 sec 2 breaths (1 sec each) Each breath about
adolescents each) after every 30 after every 30 chest 500 mL (caution
chest compressions compressions at 100 against
at 100120/min 120/min hyperventilation)
Age Group One-Rescuer CPR* Two-Rescuer CPR Breath Size
Children (1 yr 2 breaths (1 sec 2 breaths (1 sec each) Smaller breaths than
puberty) each) after every 30 after every 15 chest for adults (enough to
chest compressions compressions at 100 make chest rise)
at 100120/min 120/min
Infants (< 1 yr, 2 breaths (1 sec 2 breaths (1 sec each) Only small puffs from
excluding each) after every 30 after every 15 chest the rescuers cheeks
newborns) chest compressions compressions at 100
at 100120/min 120/min
*For a single lay rescuer, compression-only CPR is recommended in adults and
adolescents.

Breaths are given without stopping chest compressions.

Puberty is defined as the appearance of breasts in females and axillary hair in males.
Airway and Breathing
Opening the airway is given 2nd priority (see Clearing and Opening the Upper Airway)
after beginning chest compressions. For mechanical measures regarding resuscitation
in children, see Table: Guide to Pediatric ResuscitationMechanical Measures.

Mouth-to-mouth (adults, adolescents, and children) or combined mouth-to-mouth-and-

nose (infants) rescue breathing or bag-valve-mask ventilation is begun for asphyxial
cardiac arrest. If available, an oropharyngeal airway may be inserted. Cricoid pressure
is no longer recommended.

How To Do Bag-Valve-Mask Ventilation

If abdominal distention develops, the airway is rechecked for patency and the amount of
air delivered during rescue breathing is reduced. Nasogastric intubation to relieve
gastric distention is delayed until suction equipment is available because regurgitation
with aspiration of gastric contents may occur during insertion. If marked gastric
distention interferes with ventilation and cannot be corrected by the above methods,
patients are positioned on their side, the epigastrium is compressed, and the airway is
cleared.

When qualified providers are present, an advanced airway (endotracheal tube or

supraglottic device) is placed without interruption of chest compression as described
under Airway Establishment and Control. A breath is given every 6 sec (10 breaths/min)
without interrupting chest compression. However, chest compression and defibrillation
take precedence over endotracheal intubation. Unless highly experienced providers are
available, endotracheal intubation may be delayed in favor of ventilation with bag-valve-
mask, laryngeal mask airway, or similar device.

How to Insert a Laryngeal Mask Airway

Circulation

Chest compression

How to do Cardiopulmonary Resuscitation (CPR) in Adults

In witnessed cardiac arrest, chest compression should be done until defibrillation is
available. In an unresponsive patient whose collapse was unwitnessed, the trained
rescuer should immediately begin external (closed chest) cardiac compression, followed
by rescue breathing. Chest compressions must not be interrupted for >10 sec (eg, for
intubation, central IV catheter placement, or transport). A compression cycle should
consist of 50% compression and 50% release; during the release phase, it is important
to allow the chest to recoil fully. Rhythm interpretation and defibrillation (if appropriate)
are done as soon as a defibrillator is available.

The recommended chest compression depth for adults is between 2 and 2.4 in (about 5
to 6 cm). Ideally, external cardiac compression produces a palpable pulse with each
compression, although cardiac output is only 20 to 30% of normal. However, palpation
of pulses during chest compression is difficult, even for experienced clinicians, and
often unreliable. End-tidal carbon dioxide monitoring provides a better estimate of
cardiac output during chest compression; patients with inadequate perfusion have little
venous return to the lungs and hence a low end-tidal carbon dioxide. Restoration of
spontaneous breathing or eye opening indicates restoration of spontaneous circulation.

Mechanical chest compression devices are available; these devices are no more
effective than properly executed manual compressions but can minimize effects of
performance error and fatigue and can be helpful sin some circumstances, such as
during patient transport or in the cardiac catheterization laboratory.

Open-chest cardiac compression may be effective but is used only in patients with
penetrating chest injuries, shortly after cardiac surgery (ie, within 48 h), in cases of
cardiac tamponade, and most especially after cardiac arrest in the operating room when
the patients chest is already open. However, thoracotomy requires training and
experience and is best done only within these limited indications.

Complications of chest compression

Laceration of the liver is a rare but potentially serious (sometimes fatal) complication
and is usually caused by compressing the abdomen below the sternum. Rupture of the
stomach (particularly if the stomach is distended with air) is also a rare complication.
Delayed rupture of the spleen is very rare. An occasional complication, however, is
regurgitation followed by aspiration of gastric contents, causing life-
threatening aspiration pneumonia in resuscitated patients.

Costochondral separation and fractured ribs often cannot be avoided because it is

important to compress the chest deeply enough to produce sufficient blood flow.
Fractures are quite rare in children because of the flexibility of the chest wall. Bone
marrow emboli to the lungs have rarely been reported after external cardiac
compression, but there is no clear evidence that they contribute to mortality. Lung injury
is rare, but pneumothorax after a penetrating rib fracture may occur. Serious myocardial
injury caused by compression is very unlikely, with the possible exception of injury to a
preexisting ventricular aneurysm. Concern for these injuries should not deter the
rescuer from doing CPR.

Defibrillation
The most common rhythm in witnessed adult cardiac arrest is ventricular
fibrillation (VF); rapid conversion to a perfusing rhythm is essential. Pulseless ventricular
tachycardia (VT) is treated the same as VF.

How To Do Defibrillation In An Adult

Prompt direct-current cardioversion is more effective than antiarrhythmic drugs;
however, the success of defibrillation is time dependent, with about a 10% decline in
success after each minute of VF (or pulseless VT). Automated external defibrillators
(AEDs) allow minimally trained rescuers to treat VT or VF. Their use by first responders
(police and fire services) and their prominent availability in public locations has
increased the likelihood of resuscitation.

Defibrillating paddles or pads are placed between the clavicle and the 2nd intercostal
space along the right sternal border and over the 5th or 6th intercostal space at the
apex of the heart (in the mid-axillary line). Conventional defibrillator paddles are used
with conducting paste; pads have conductive gel incorporated into them. Only 1 initial
countershock is now advised (the previous recommendation was 3 stacked shocks),
after which chest compression is resumed. Energy level for biphasic defibrillators is
between 120 and 200 joules (2 joules/kg in children) for the initial shock; monophasic
defibrillators are set at 360 joules for the initial shock. Postshock rhythm is not checked
until after 2 min of chest compression. Subsequent shocks are delivered at the same or
higher energy level (maximum 360 joules in adults, or 10 joules/kg in children). Patients
remaining in VF or VT receive continued chest compression and ventilation and
optional drug therapy.
Monitor and IV
ECG monitoring is established to identify the underlying cardiac rhythm. An IV line may
be started; 2 lines minimize the risk of losing IV access during CPR. Large-bore
peripheral lines in the antecubital veins are preferred. In adults and children, if a
peripheral line cannot be established, a subclavian or internal jugular central line
(see Procedure) can be placed provided it can be done without stopping chest
compression (often difficult). Intraosseous and femoral lines (see Intraosseous Infusion)
are the preferred alternatives, especially in children. Femoral vein catheters
(see Procedure), preferably long catheters advanced centrally, are an option because
CPR does not need to be stopped and they have less potential for lethal complications;
however, they may have a lower rate of successful placement because no discrete
femoral arterial pulsations are available to guide insertion.

The type and volume of fluids or drugs given depend on the clinical circumstances.
Usually, IV 0.9% saline is given slowly (sufficient only to keep an IV line open); vigorous
volume replacement (crystalloid and colloid solutions, blood) is required only when
arrest results from hypovolemia (see Intravenous Fluid Resuscitation).

Special Circumstances
In accidental electrical shock, rescuers must be certain that the patient is no longer in
contact with the electrical source to avoid shocking themselves. Use of nonmetallic
grapples or rods and grounding of the rescuer allows for safe removal of the patient
before starting CPR.

In near drowning, rescue breathing may be started in shallow water, although chest
compression is not likely to be effectively done until the patient is placed horizontally on
a firm surface, such as a surfboard or float.

If cardiac arrest follows traumatic injury, airway opening maneuvers and a brief
period of external ventilation after clearing the airway have the highest priority because
airway obstruction is the most likely treatable cause of arrest. To minimize cervical
spine injury, jaw thrust, but not head tilt and chin lift, is advised. Other survivable causes
of traumatic cardiac arrest include cardiac tamponade and tension pneumothorax, for
which immediate needle decompression is lifesaving. However, most patients with
traumatic cardiac arrest have severe hypovolemia due to blood loss (for which chest
compression may be ineffective) or nonsurvivable brain injuries.

Drugs for ACLS

Despite widespread and long-standing use, no drug or drug combination has been
definitively shown to increase survival to hospital discharge in patients with cardiac
arrest. Some drugs do seem to improve the likelihood of restoration of spontaneous
circulation (ROSC) and thus may reasonably be given (for dosing, including pediatric,
see Table: Drugs for Resuscitation*). Drug therapy for shock and cardiac arrest
continues to be researched.

Drugs for Resuscitation*

Drug Adult Dose Pediatric Dose Comments
Adenosine 6 mg initially, then 0.1 mg/kg initially, Rapid IV push is followed
12 mg 2 then 0.2 mg/kg 2 by flush (maximum single
dose 12 mg).
Amiodarone For VF/pulseless For VF/pulseless For VF/pulseless VT: Give
VT: 300 mg VT: 5 mg/kg as IV push over 2 min.
For perfusing VT: For perfusing VT: 5 For perfusing VT: Give
Loading dose: mg/kg over 2060 initial dose as IV push over
150 mg min, repeated to a 10 min.
maximum of 15
Infusion (drip): 1 mg/kg/day
mg/min 6 h,
then 0.5
mg/min 24 h
Amrinone Loading dose: Loading dose: 0.75 500 mg in 250 mL 0.9%
0.75 mg/kg over 1 mg/kg over 5 min saline gives 2 mg/mL.
23 min (may be repeated
up to 3 mg/kg)
Infusion (drip): 5
10 mcg/kg/min Infusion: 510
mcg/kg/min
Atropine 0.51 mg 0.02 mg/kg Repeat q 35 min to effect
or total dose of 0.04 mg/kg
(minimum dose 0.1 mg).
Calcium chloride 1 g 20 mg/kg 10% solution contains 100
mg/mL.
Calcium 0.66 g N/A 22% solution contains 220
gluceptate mg/mL.
Calcium 0.6 g 60100 mg/kg 10% solution contains 100
gluconate mg/mL.
Dobutamine 220 mcg/kg/min Same as adult dose 500 mg in 250 mL 5% D/W
(starting at 25 gives 2000 mcg/mL.
mcg/kg/min)
Dopamine 220 mcg/kg/min Same as adult dose 400 mg in 250 mL 5% D/W
(starting at 25 gives 1600 mcg/mL.
mcg/kg/min)
Epinephrine Bolus: 1 mg Bolus: 0.01 mg/kg Repeat q 3 to 5 min as
needed.
Infusion: 210 Infusion: 0.11.0
mcg/min mcg/kg/min 8 mg in 250 mL 5% D/W
gives 32 mcg/mL.
Drug Adult Dose Pediatric Dose Comments
Glucose 25 g 50% D/W 0.51 g/kg Avoid high concentrations
in infants and young
children.

5% D/W: Give 1020

mL/kg.

10% D/W: Give 510

mL/kg.

25% D/W: Give 24 mL/kg.

For older children, use a

large vein.
Lidocaine 11.5 mg/kg; 1 mg/kg loading In adults, lidocainemay be
repeat q 510 min dose, then 2050 considered after ROSC for
to a maximum of mcg/kg/min infusion VF/VT.
3 mg/kg
In children, lidocainemay
be used instead
of amiodarone for
refractory VF/VT.
Magnesium 12 g 2550 mg/kg to a Give over 25 min.
sulfate maximum of 2 g
Milrinone Loading dose: 50 Loading dose: 50 50 mg in 250 mL 5% D/W
mcg/kg over 10 75 mcg/kg over 10 gives 200 mcg/mL.
min min

Infusion: 0.5 Infusion: 0.50.75

mcg/kg/min mcg/kg/min
Naloxone 2 mg intranasal or 0.1 mg/kg if patients Repeat as needed.
0.4 mg IM are < 20 kg or < 5 yr
Norepinephrine Infusion: 216 Infusion: Starting 8 mg in 250 mL 5% D/W
mcg/min with 0.050.1 gives 32 mcg/mL.
mcg/kg/min
(maximum dose 2
mcg/kg/min)
Phenylephrine Infusion: 0.11.5 Infusion: 0.10.5 10 mg in 250 mL 5% D/W
mcg/kg/min mcg/kg/min gives 40 mcg/mL.
Procainamide 30 mg/min to Same as adult dose Procainamide is not
effect or a recommended for
maximum of 17 pulseless arrest in children.
mg/kg
Drug Adult Dose Pediatric Dose Comments
Sodium 50 mEq 1 mEq/kg Infuse slowly and only
bicarbonate when ventilation is
(NaHCO3) adequate.

4.2% contains 0.5

mEq/mL; 8.4% contains 1
mEq/mL.
Vasopressin No longer Not recommended Vasopressin is no more
recommended effective than epinephrine.
*For indications and use, see text.

IV or intraosseous.

ROSC = restoration of spontaneous circulation; VF = ventricular fibrillation;

VT = ventricular tachycardia.
In a patient with a peripheral IV line, drug administration is followed by a fluid bolus
(wide open IV in adults; 3 to 5 mL in young children) to flush the drug into the central
circulation. In a patient without IV or intraosseous access, naloxone, atropine,
and epinephrine, when indicated, may be given via the endotracheal tube at 2 to 2.5
times the IV dose. During administration of a drug via endotracheal tube, compression
should be briefly stopped.

First-line drugs
The main first-line drug used in cardiac arrest is

Epinephrine

Epinephrine may be given 1 mg IV q 3 to 5 min. It has combined alpha-adrenergic and

beta-adrenergic effects. The alpha-adrenergic effects may augment coronary diastolic
pressure, thereby increasing subendocardial perfusion during chest
compressions. Epinephrine also increases the likelihood of successful defibrillation.
However, beta-adrenergic effects may be detrimental because they increase oxygen
requirements (especially of the heart) and cause vasodilation. Intracardiac injection
of epinephrine is not recommended because, in addition to interrupting precordial
compression, pneumothorax, coronary artery laceration, and cardiac tamponade may
occur.

Amiodarone 300 mg can be given once if defibrillation is unsuccessful

after epinephrine, followed by 1 dose of 150 mg. It is also of potential value if VT or VF
recurs after successful defibrillation; a lower dose is given over 10 min followed by a
continuous infusion. There is no persuasive proof that it increases survival to hospital
discharge.
A single dose of vasopressin 40 units, which has a duration of activity of 40 min, is an
alternative to epinephrine (adults only). However, it is no more effective
than epinephrine and is therefore no longer recommended in the American Heart
Association's guidelines. However, in the unlikely case of a lack of epinephrine during
CPR, vasopressin may be substituted.

Other drugs
A range of additional drugs may be useful in specific settings.

Atropine sulfate is a vagolytic drug that increases heart rate and conduction through
the atrioventricular node. It is given for symptomatic bradyarrhythmias and high-degree
atrioventricular nodal block. It is no longer recommended for asystole or pulseless
electrical activity.

Calcium chloride is recommended for patients

with hyperkalemia, hypermagnesemia, hypocalcemia, or calcium channel blocker
toxicity. In other patients, because intracellular calcium is already higher than normal,
additional calcium is likely to be detrimental. Because cardiac arrest in patients on renal
dialysis is often a result of or accompanied by hyperkalemia, these patients may benefit
from a trial of calcium if bedside potassium determination is unavailable. Caution is
necessary because calcium exacerbates digitalis toxicity and can cause cardiac arrest.

Magnesium sulfate has not been shown to improve outcome in randomized clinical
studies. However, it may be helpful in patients with torsades de pointes or known or
suspected magnesium deficiency (ie, alcoholics, patients with protracted diarrhea).

Procainamide is a 2nd-line drug for treatment of refractory VF or VT.

However, procainamide is not recommended for pulseless arrest in children.

Phenytoin may rarely be used to treat VF or VT, but only when VF or VT is due to
digitalis toxicity and is refractory to other drugs. A dose of 50 to 100 mg/min q 5 min is
given until rhythm improves or the total dose reaches 20 mg/kg.

Sodium bicarbonate is no longer recommended unless cardiac arrest is caused by

hyperkalemia, hypermagnesemia, or tricyclic antidepressant overdose with complex
ventricular arrhythmias. In children, sodium bicarbonate may be considered when
cardiac arrest is prolonged (> 10 min); it is given only if there is good ventilation. When
sodium bicarbonate is used, arterial pH should be monitored before infusion and after
each 50-mEq dose (1 to 2 mEq/kg in children).

Lidocaine is not recommended for routine use during cardiac arrest. However, it may
be helpful as an alternative to amiodarone for VF or VT that is unresponsive to
defibrillation (in children) or after ROSC due to VF or VT (in adults).

Bretylium is no longer recommended for management of cardiac arrest.

Dysrhythmia Treatment
VF or pulseless VT is treated with one direct-current shock, preferably with biphasic
waveform, as soon as possible after those rhythms are identified. Despite some
laboratory evidence to the contrary, it is not recommended to delay defibrillation to
administer a period of chest compressions. Chest compression should be interrupted as
little as possible and for no more than 10 sec at a time for defibrillation. Recommended
energy levels for defibrillation vary: 120 to 200 joules for biphasic waveform and 360
joules for monophasic. If this treatment is unsuccessful, epinephrine 1 mg IV is
administered and repeated q 3 to 5 min. Defibrillation at the same energy level or higher
is attempted 1 min after each drug administration. If VF persists, amiodarone 300 mg IV
is given. Then, if VF/VT recurs, 150 mg is given followed by infusion of 1 mg/min for 6 h,
then 0.5 mg/min. Current versions of AEDs provide a pediatric cable that effectively
reduces the energy delivered to children. (For pediatric energy levels, see Defibrillation;
for drug doses, see Table: Drugs for Resuscitation*.)

Asystole can be mimicked by a loose or disconnected monitor lead; thus, monitor

connections should be checked and the rhythm viewed in an alternative lead. If asystole
is confirmed, the patient is given epinephrine 1 mg IV repeated q 3 to 5 min.
Defibrillation of apparent asystole (because it might be fine VF) is discouraged
because electrical shocks injure the nonperfused heart.

Pulseless electrical activity is circulatory collapse that occurs despite satisfactory

electrical complexes on the ECG. Patients with pulseless electrical activity receive 500-
to 1000-mL (20 mL/kg) infusion of 0.9% saline. Epinephrine may be given in amounts of
0.5 to 1.0 mg IV repeated q 3 to 5 min. Cardiac tamponade can cause pulseless
electrical activity, but this disorder usually occurs in patients after thoracotomy and in
patients with known pericardial effusion or major chest trauma. In such settings,
immediate pericardiocentesis or thoracotomy is done (see Figure: Pericardiocentesis.).
Tamponade is rarely an occult cause of cardiac arrest but, if suspected, can be
confirmed by ultrasonography or, if ultrasonography is unavailable, pericardiocentesis.

Termination of Resuscitation
CPR should be continued until the cardiopulmonary system is stabilized, the patient is
pronounced dead, or a lone rescuer is physically unable to continue. If cardiac arrest is
thought to be due to hypothermia, CPR should be continued until the body is rewarmed
to 34 C.

The decision to terminate resuscitation is a clinical one, and clinicians take into account
duration of arrest, age of the patient, and prognosis of underlying medical conditions.
The decision is typically made when spontaneous circulation has not been established
after CPR and ACLS measures have been done. In intubated patients, an end-tidal
carbon dioxide (ETCO2) level of < 10 mm Hg is a poor prognostic sign.
POSTRESUSCITATIVE CARE
Restoration of spontaneous circulation (ROSC) is only an intermediate goal in
resuscitation. The ultimate goal is survival to hospital discharge with good neurologic
function, which is achieved by only a minority of patients with ROSC. To maximize the
likelihood of a good outcome, clinicians must provide good supportive care (eg, manage
blood pressure, temperature, and cardiac rhythm) and treat underlying conditions,
particularly acute coronary syndromes.

Postresuscitation laboratory studies include ABG, CBC, and blood chemistries,

including electrolytes, glucose, BUN, creatinine, and cardiac markers. (Creatine kinase
is usually elevated because of skeletal muscle damage caused by CPR; troponins,
which are unlikely to be affected by CPR or defibrillation, are preferred.) Arterial
PaO2 should be kept near normal values (80 to 100 mm Hg). Hct should be maintained
at 30 (if cardiac etiology is suspected), and glucose at 140 to 180 mg/dL; electrolytes,
especially potassium, should be within the normal range.

Coronary angiography
When indicated, coronary angiography should be done emergently (rather than later
during the hospital course) so that if percutaneous coronary intervention (PCI) is
needed, it is done as soon as possible. The decision to do cardiac catheterization after
resuscitation from cardiac arrest should be individualized based on the ECG, the
interventional cardiologist's clinical impression, and the patient's prognosis. However,
guidelines suggest doing emergency angiography for adult patients in whom a cardiac
cause is suspected and who have

ST-segment elevation on the ECG

Coma with no ST-segment elevation

Neurologic support
Only about 10% of all cardiac arrest survivors have good CNS function (cerebral
performance index 1 or 2) at hospital discharge. Hypoxic brain injury is a result of
ischemic damage and cerebral edema (see pathophysiology of cardiac arrest). Both
damage and recovery may evolve over 48 to 72 h after resuscitation.

Maintenance of oxygenation and cerebral perfusion pressure (avoiding hypotension)

may reduce cerebral complications. Both hypoglycemia and hyperglycemia may
damage the post-ischemic brain and should be treated.

In adults, targeted temperature management (maintaining body temperature of 32 to

36 C) is recommended for patients who remain unresponsive after spontaneous
circulation has returned (1, 2). Cooling is begun as soon as spontaneous circulation has
returned. Techniques to induce and maintain hypothermia can be either external or
invasive. External cooling methods are easy to apply and range from the use of external
ice packs to several commercially available external cooling devices that circulate high
volumes of chilled water over the skin. For internal cooling, chilled IV fluids (4 C) can
be rapidly infused to lower body temperature, but this method may be problematic in
patients who cannot tolerate much additional fluid volume. Also available are external
heat-exchange devices that circulate chilled saline to an indwelling IV heat-exchange
catheter using a closed-loop design in which chilled saline circulates through the
catheter and back to the device, rather than into the patient. Another invasive method
for cooling uses an extracorporeal device that circulates and cools blood externally then
returns it to the central circulation. Regardless of the method chosen, the goal is to cool
the patient rapidly and to maintain the core temperature between 32 C and 36 C.
Currently, there is no evidence that any specific temperature within this range is
superior, but it is imperative to avoid hyperthermia.

Numerous pharmacologic treatments, including free radical scavengers, antioxidants,

glutamate inhibitors, and calcium channel blockers, are of theoretic benefit; many have
been successful in animal models, but none have proved effective in human trials.

Blood pressure support

Current recommendations are to maintain a mean arterial pressure (MAP) of > 80 mm
Hg in older adults or > 60 mm Hg in younger and previously healthy patients. In patients
known to be hypertensive, a reasonable target is systolic BP 30 mm Hg below prearrest
level. MAP is best measured with an intra-arterial catheter. Use of a flow-directed
pulmonary artery catheter for hemodynamic monitoring has been largely discarded.

BP support includes

IV 0.9% saline
Sometimes inotropic or vasopressor drugs
Rarely intra-aortic balloon counterpulsation

Patients with low MAP and low central venous pressure should have IV fluid challenge
with 0.9% saline infused in 250-mL increments.

Clinical Calculator: Mean Vascular Pressure (systemic or pulmonary)

Although use of inotropic and vasopressor drugs has not proved to enhance long-term
survival, older adults with moderately low MAP (70 to 80 mm Hg) and normal or high
central venous pressure may receive an infusion of an inotrope (eg, dobutamine started
at 2 to 5 mcg/kg/min). Alternatively, amrinone or milrinone is used (see Table: Drugs for
Resuscitation*).

If this therapy is ineffective, the inotrope and vasoconstrictor dopamine may be

considered. Alternatives are epinephrine and the peripheral
vasoconstrictors norepinephrine and phenylephrine(see Table: Drugs for
Resuscitation*). However, vasoactive drugs should be used at the minimal dose
necessary to achieve low-normal MAP because they may increase vascular resistance
and decrease organ perfusion, especially in the mesenteric bed. They also increase the
workload of the heart at a time when its capability is decreased because of
postresuscitation myocardial dysfunction.
If MAP remains < 70 mm Hg in patients who may have sustained an MI, intra-aortic
balloon counterpulsation should be considered. Patients with normal MAP and high
central venous pressure may improve with either inotropic therapy or afterload reduction
with nitroprusside or nitroglycerin.

Intra-aortic balloon counterpulsation can assist low-output circulatory states due to left
ventricular pump failure that is refractory to drugs. A balloon catheter is introduced via
the femoral artery, percutaneously or by arteriotomy, retrograde into the thoracic aorta
just distal to the left subclavian artery. The balloon inflates during each diastole,
augmenting coronary artery perfusion, and deflates during systole, decreasing afterload.
Its primary value is as a temporizing measure when the cause of shock is potentially
correctable by surgery or percutaneous intervention (eg, acute MI with major coronary
obstruction, acute mitral insufficiency, ventricular septal defect).

Dysrhythmia treatment
Although VF or VT may recur after resuscitation, prophylactic antiarrhythmic drugs do
not improve survival and are no longer routinely used. However, patients manifesting
such rhythms may be treated with procainamide (see Other drugs)
or amiodarone (see First-line drugs).

Postresuscitation rapid supraventricular tachycardias occur frequently because of high

levels of beta-adrenergic catecholamines (both endogenous and exogenous) during
cardiac arrest and resuscitation. These rhythms should be treated if extreme,
prolonged, or associated with hypotension or signs of coronary ischemia. An esmolol IV
infusion is given, beginning at 50 mcg/kg/min.

Patients who had arrest caused by VF or VT not associated with acute MI are
candidates for an implantable cardioverter-defibrillator (ICD). Current ICDs are
implanted similarly to pacemakers and have intracardiac leads and sometimes
subcutaneous electrodes. They can sense arrhythmias and deliver either cardioversion
or cardiac pacing as indicated.
In the hospital setting, emergencies typically occur in emergency departments (EDs)
and intensive care units (ICUs). But many also take place in progressive care units or
general nursing units. And when they do, they can cause marked anxiety for nurses
especially those unfamiliar or inexperienced with the drugs used in these emergencies.
Generally, the goal of using emergency drugs is to prevent the patient from deteriorating
to an arrest situation. This article helps nurses who dont work in ICUs or EDs to
understand emergency drugs and their use.
Under normal circumstances, a registered nurse (RN) needs a physicians order to
administer medications. In emergencies, RNs with advanced cardiac life support
(ACLS) certification can give selected drugs based on standing orders, relying on
algorithms that outline care for certain emergencies. Wherever possible, nurses should
strive to maintain proficiency in basic life support (BLS), as the latest research shows
the importance of effective cardiopulmonary resuscitation. Some non-ICU nurses may
want to pursue ACLS training as well.

Drugs for acute coronary syndrome

Acute coronary syndrome (ACS) refers to a spectrum of clinical manifestations
associated with acute myocardial infarction and unstable angina. In ACS, a plaque in a
coronary artery ruptures or becomes eroded, triggering the clotting cascade. A blood
clot forms, occluding the artery and interrupting blood and oxygen flow to cardiac
muscle.
Many healthcare providers use the acronym MONA to help them remember the initial
medical treatment options for a patient with ACS.
M: morphine
O: oxygen
N: nitroglycerin
A: aspirin.
But keep in mind that while MONA might be easy to remember, the drugs arent given in
the MONA sequence. Theyre given in the order of OANM.

Oxygen
Oxygen (O2) is given if the patients O2 saturation level is below 94%. The heart uses
70% to 75% of the oxygen it receives, compared to skeletal muscle, which uses roughly
20% to 25%.
Aspirin
The standard recommended aspirin dosage to treat ACS is 160 to 325 mg, given as
chewable baby aspirin to speed absorption. Aspirin slows platelet aggregation,
reducing the risk of further occlusion or reocclusion of the coronary artery or a recurrent
ischemic event.

Nitroglycerin
To help resolve chest pain from ACS, nitroglycerin 0.4 mg is given sublingually via a
spray or rapidly dissolving tablet. If the first dose doesnt reduce chest pain, the dose
can be repeated every 3 to 5 minutes for a total of three doses.
A potent vasodilator, nitroglycerin relaxes vascular smooth-muscle beds. It works well
on coronary arteries, improving blood flow to ischemic areas. It also decreases
myocardial oxygen consumption, allowing the heart to work with a lower oxygen
demand. In peripheral vascular beds, nitroglycerin causes vasodilation and reduces
preload and afterload, resulting in decreased cardiac workload.
If chest pain recurs once the initial pain resolves or decreases, the patient may be
placed on a continuous I.V. infusion of nitroglycerin. Because of the drugs vasodilatory
effects, be sure to institute continuous blood-pressure monitoring.

Morphine
If chest pain doesnt resolve with sublingual or I.V. nitroglycerin, morphine 2 to 4 mg
may be given every 5 to 15 minutes via I.V. push. An opioid acting primarily on
receptors that perceive pain, morphine also acts as a venodilator, reducing ventricular
preload and cardiac oxygen requirements.
As with nitroglycerin, the patients blood pressure needs to be monitored continuously. If
hypotension occurs, elevate the patients legs, give I.V. fluids as ordered, and monitor
for signs and symptoms of pulmonary congestion.

Other medications for ACS

Metoprolol may be used in the initial treatment of ACS. A cardioselective
(beta1 receptor) drug, its a beta-adrenergic blocker that dilates peripheral vascular
beds, in turn reducing blood pressure, decreasing cardiac workload, and lowering
cardiac oxygen demands. It also may have a mild analgesic effect in ACS-related chest
pain. The patients blood pressure must be monitored. (See Be cautious with beta
blockers by clicking on the PDF icon above.)
A primary goal of ACS treatment is to minimize muscle cell damage, which necessitates
restoring blood flow to cardiac muscle. Drugs that may be used to reduce expansion of
the arterial occlusion or restore blood flow to cardiac muscle include:
 heparin or enoxaparin (a low-molecular-weight heparin), which helps prevent the
original arterial clot from expanding and allows it to break down on its own; as a
result, the vessel opens and new clot formation is inhibited.
glycoprotein IIB-IIIa inhibitors, such as abciximab (Reopro). These drugs bind to
glycoprotein IIb-IIIa receptor sites on platelets, preventing further aggregation
and stopping expansion of the original clot or formation of new clots.
fibrinolytics, such as reteplase (Retavase) and alteplase (Activase). These
agents break down the original clot, opening the vessel for blood flow. (See
Drugs used to treat acute coronary syndrome by clicking on the PDF icon
above.)

Drugs for arrhythmias

Bradycardias and tachycardias commonly arise during medical emergencies. The
primary goal of drug therapy for these arrhythmias is to return the heart rate and rhythm
to normal, thereby maximizing cardiac pumping and restoring hemodynamic stability. To
achieve this goal, antiarrhythmics are given to slow, speed, or block conduction of the
hearts electrical impulses. A combination of drugs in the proper dosages may resolve
bradycardias and tachycardias. (See Drugs used to treat arrhythmias by clicking on the
PDF icon above.)

Intervening for bradycardia

In bradycardia, the heart rate slows to a critical point and hemodynamic instability
occurs. Usually, bradycardia is defined as a heart rate slower than 60 beats/minute
(bpm). But in some patients, hemodynamic instability may occur at faster rates. This
instability may manifest as dizziness, light-headedness, nausea, vomiting, hypotension,
syncope, chest pain, and altered mental status. Atropine, epinephrine, and dopamine
may be used to treat bradycardia, with dosages depending on the acuity and severity of
hemodynamic instability.
For symptomatic patients, the healthcare team must determine the cause of
bradycardia. In many cases, bradycardia results from use of other drugs, specifically
other antiarrhythmicsfor instance, beta blockers and calcium channel blockers. So
those drugs may need to be withheld temporarily until their effects wear off. Beta
blockers reduce circulating catecholamine levels, decreasing both the heart rate and
blood pressure.
Typically, atropine is the drug of choice for symptomatic bradycardia. An anticholinergic
and potent belladonna alkaloid, it increases the heart rate, which improves
hemodynamic stability.
Epinephrine may be used as a secondary measure if atropine and temporary heart
pacing dont improve hemodynamic stability. Among other actions, epinephrine
stimulates beta1 receptors, causing cardiac stimulation, which in turn increases the
heart rate.
Dopamine also may be used to support hemodynamic status by correcting hypotension.
It enhances cardiac output, minimally increasing oxygen consumption and causing
peripheral vasoconstriction.
If your patient is receiving these I.V. drugs, be sure to monitor for extravasation, which
could lead to tissue damage. If possible, use a central line to deliver epinephrine and
dopamine.

Intervening for tachycardia

Tachycardia, which usually refers to a heart rate faster than 100 bpm, may result from
various cardiac mechanisms. The first step in choosing the right drug is to identify the
origin of the arrhythmia. Most tachycardias are classified as one of two types:

narrow-QRS-complex tachycardias (for instance, atrial fibrillation, atrial flutter, or

atrial or multifocal atrial tachycardia)
wide-QRS-complex tachycardias (for example, ventricular tachycardia or
supraventricular tachycardia with aberrancy).

Each type calls for a slightly different treatment. Narrow-QRS-complex tachycardias

with a regular rate generally are treated with adenosine, along with beta blockers,
calcium channel blockers, and/or amiodarone or ibutilide.
With a wide-QRS-complex tachycardia, the first step is to determine if the arrhythmia is
a ventricular tachycardia or is conducted with aberrancy. Wide-QRS-complex
tachycardias with aberrancy call for the same treatment as narrow-QRS-complex
tachycardias. On the other hand, ventricular tachycardia in a patient with a pulse is
treated with amiodarone alone or with amiodarone in conjunction with synchronized
cardioversion.
Adenosine. This general antiarrhythmic is used mainly as a diagnostic agent to identify
the origin of an underlying narrow-QRS-complex tachycardia. It briefly depresses the
atrioventricular (AV) node and sinus node activity. When given by rapid I.V. bolus, the
drugs primary action is to slow electrical impulse conduction through the AV node. Be
aware that adenosine commonly causes a few seconds of asystole, but because of its
short half-life (6 to 10 seconds), the asystole usually is brief. The drug sometimes
restores a normal sinus rhythm; if it doesnt, calcium channel blockers and beta blockers
may be given immediately to control the heart rate while amiodarone or ibutilide may be
used to help restore a normal sinus rhythm.
Diltiazem. A first-line agent in controlling heart rate in narrow QRS-complex
tachycardias, this drug can be used both in patients with preserved cardiac function and
in those with impaired ventricular function (ejection fraction below 40%) or heart failure.
(Verapamil, another calcium channel blocker, should be used only in patients with
preserved cardiac function.)
A calcium channel blocker, diltiazem slows and/or blocks electrical impulse conduction
through the AV node, reducing the number of impulses that arrive at the ventricular
tissue and slowing the heart rate.
It may cause hypotension secondary to vascular smooth-muscle relaxation. Also, it may
block impulses in some narrow-QRS-complex tachycardias that involve AV nodal
reentry, thereby terminating the rhythm and restoring normal sinus rhythm.
Other drugs. Occasionally, selected beta blockers are used to help control the heart rate
associated with narrow-QRS-complex tachycardias. They include metoprolol, atenolol,
propranolol, and esmolol. Propranolol isnt cardioselective and can affect pulmonary
function, so its used less often. Typically, esmolol is given only in the ICU.
Atenolol is administered as a 5-mg I.V. bolus over 5 minutes. If the patient tolerates the
dose and the arrhythmia persists after 10 minutes, an additional bolus of 5 mg may be
given over 5 minutes. Metoprolol also is administered I.V. in 5-mg increments over 5
minutes; the dose may be repeated twice, to a total of 15 mg.
Dont give beta blockers or calcium channel blockers to patients with narrow-QRS-
complex tachycardias suspected of being pre-excitation arrhythmias, such as Wolff-
Parkinson-White (WPW) syndrome. Such arrhythmias allow impulses to flow from the
atria to the ventricles through an accessory or alternate pathway. Beta blockers and
calcium channel blockers may increase the number of impulses arriving at ventricular
tissue, further speeding the heart rate.
Amiodarone. This drug is used to treat certain narrow- and wide-QRS complex
tachycardias identified as ventricular tachycardia or tachycardias of unknown origin.
Although a class III antiarrhythmic, it has some properties of all antiarrhythmic classes.
Its primary action is to block potassium channels in the cell, but it also prolongs the
action potential duration, depresses conduction velocity, slows conduction through and
prolongs refractoriness in the AV node, and has some alpha-, beta-, and calcium-
channel blocking capabilities.
Dosing depends on circumstances. When used to treat ventricular tachycardia in
patients with a pulse, runs of paroxysmal ventricular tachycardia, or narrow-QRS-
complex tachycardias, amiodarone is given as a bolus of 150 mg over 10 minutes,
followed by a continuous I.V. infusion starting at 1 mg/minute for 6 hours and then 0.5
mg/minute for 18 hours. If the patient is on nothing-by-mouth status for an extended
time, the infusion can be kept running at 0.5 mg/minute. Otherwise, an oral dose usually
is started before the infusion ends.