Cardiovascular Drugs in ACLS / BLS

VALERIE ZARZA-GERON, M.D.

Internal Medicine – Cardiology
MAKATI MEDICAL CENTER
 Intravenous Access
Central Line
◼ Subclavian vein
◼ Internal jugular vein
◼ Needs interruption
◼ Increase peak
concentration
◼ Central circulation time
◼ Complications
Peripheral Line
◼ Antecubital vein
◼ External jugular vein
◼ No interruption
◼ Slow concentration
peaks
◼ Central circulation time
◼ Complications
 Peripheral IV site

Administer drugs by Bolus

20 cc of saline or distilled water

Elevate the extremity for 10 to 20 seconds

 Tracheal Drug Administration

• Epinephrine, Lidocaine and Atropine

(Diluted in 10 ml NSS or distilled water)
• Administer 2 to 2.5 times the
recommended IV dose
 Pharmacology

Agents used to Agents used to treat

Optimize Cardiac Arrhythmias
Output and Blood
Pressure
Agents used to Optimize Cardiac Output and
Blood pressure
3 Dimensions of the Cardiovascular System
➢ Peripheral vascular tone
➢ Inotropic state of the heart
➢ Chronotropic state of the heart
Agents used to Optimize Cardiac Output and
Blood pressure
Clinically used in ➢ Acute ischemic heart disease
➢ Acute and chronic heart failure
➢ Shock
➢ Cardiac arrest
Agents used to Optimize Cardiac Output and
Blood pressure
Epinephrine
➢ Alpha-adrenergic receptor-stimulating
properties and Beta adrenergic effects
➢ Dose: 1 mg (10ml of a 1:10,000 solution) every
3 to 5 minutes
➢ High dose (0.1mg/kg/IV)
➢ Escalating dose (1mg-3mg-5mg) (Class IIb)
Agents used to Optimize Cardiac Output and
Blood pressure
Epinephrine
➢ Pt not in Cardiac Arrest : 1mg in 500 cc of
D5 W or normal saline by continuous infusion.
Initial dose: 1mcg/min (2-10 mcg/min)

➢ Pt in Cardiac Arrest: continuous infusion

1mg in 250 cc normal saline or D5 W to infuse
at 1 mcg/min (3 – 4 mcg/min)
Agents used to Optimize Cardiac Output and
Blood pressure
Norepinephrine
➢ Naturally occurring potent vasoconstrictor and
inotropic agent
➢ Usually induces renal and splanchnic
vasoconstriction
➢ Indications: Severe hypotension
( systolic BP < 70mm Hg)
Low total peripheral resistance
➢ Dose: 0.5 – 1.0 mcg/min
Agents used to Optimize Cardiac Output and
Blood pressure
Vasopressin (Class Indeterminate)
➢ Vasopressor used as alternative to epinephrine
for the treatment of adult shock – refractory VF
➢ Patient with asystole or pulseless electrical
activity
➢ Patients who remain in cardiac arrest after
treatment of epinephrine
➢ Vasodilatory support in septic shock
Agents used to Optimize Cardiac Output and
Blood pressure
Dopamine:
➢ Catecholamine, alpha and beta adrenergic
receptor agonist and peripheral dopamine
receptor agonist.
➢ Indication: Hypotension with bradycardia
After ROSC (Return Of
Spontaneous Circulation)
Agents used to Optimize Cardiac Output and
Blood pressure
Dopamine
➢ Doses: 5 – 20 mcg/kg per minute
2 – 4 mcg/kg/min : primarily dopaminergic agonist, little
inotropic effect and renosplanchnic
augmentation
5 – 10 mcg/kg/min B1 and B2 inotropy predominates
10 – 20 mcg/kg/min: alpha receptors predominates
with systemic and splanchnic
arteriolar vasoconstriction
Agents used to Optimize Cardiac Output and
Blood pressure
Dobutamine
➢ Synthetic catecholamine and a potent inotropic
agent
➢ Used in severe systolic heart failure
➢ Predominant beta receptor agonist
➢ Dose: 5 – 20 mcg/kg/min
> 20mcg/kg/min : increase the HR >10%
Agents used to Optimize Cardiac Output and
Blood pressure
Calcium
➢ Retrospective and prospective studies in the
cardiac arrest setting have not shown benefit
(Class lll)
➢ Used in hyperkalemia, hypocalcemia or calcium
channel blocker toxicity (Class llb)
➢ Dose: 10% solution Calcium chloride 2 – 4
mg/kg
Agents used to Optimize Cardiac Output and
Blood pressure
Digitalis
➢ Limited use as as inotropic agent
➢ Decrease ventricular rate in some patients
(AF / Flutter)
➢ Narrow toxic-to-therapeutic ratio
Agents used to Optimize Cardiac Output and
Blood pressure
Nitroglycerin
➢ Used for their ability to relax vascular smooth
muscle
➢ First choice in ischemic type of pain or
discomfort
➢ IV form permits better titration in patients with
acute coronary syndromes, hypertensive
emergencies and CHF
Agents used to Optimize Cardiac Output and
Blood pressure
Sodium Nitroprusside
➢ Rapid-acting direct peripheral vasodilator
➢ Indications:
Severe heart failure
Hypertensive emergencies
➢ Dose: 0.1 – 5 mcg/kg per minute
50 mg in 250 cc normal saline or
D5W
Agents used to Optimize Cardiac Output and
Blood pressure
Sodium Bicarbonate
➢ Little data indicates that therapy with buffers
improves outcome
1. Does not improve ability to defibrillate or
improve survival rates in animals
2. Can compromise coronary perfusion pressure
3. May cause adverse effects due to extracellular
alkalosis,including shifting the oxyhemoglobin
saturation curve
Agents used to Optimize Cardiac Output and
Blood pressure
Sodium Bicarbonate
➢ Little data indicates that therapy with buffers
improves outcome
4. May induce hyperosmolality and hypernatremia
5. Produce carbon dioxide
6. May inactivate simultaneously administered
catecholamine
7. Exacerbates central venous acidosis
Agents used to Optimize Cardiac Output and
Blood pressure
Sodium Bicarbonate
➢Indications:
◼ Patients with pre-existing metabolic acidosis

◼ Hyperkalemia

◼ Tricyclic or phenobarbital overdose

◼ After a protracted arrest or long resuscitative

efforts
➢Dose: 1 mEq/kg
 Antiarrhythmic Drugs
Adenosine
➢ Depresses AV node & sinus node activity
➢ Short-lived pharmacologic response
➢ Half-life is < 5 seconds (degraded in the blood
& periphery)
➢ Should be used only if SVT is suspected
➢ Dose: 6 mg IV followed by 20 ml of saline
flush. If no response may give 12 mg
after 1-2 minutes
 Antiarrhythmic Drugs
Amiodarone
➢ Useful in treatment of atrial & ventricular
arrhythmias
➢ Ventricular rate control of rapid atrial arrhythmias in
severely impaired LV function
➢ After defibrillation and epinephrine in cardiac arrest
with persistent VT or VF
 Antiarrhythmic Drugs
Amiodarone
➢ Control of hemodynamically stable VT (Class IIb),
polymorphic VT (Class IIb)
➢ Adjunct to electrical cardioversion in refractory
PSVT’s (Class IIa), atrial tachycardia (Class IIb), &
pharmacologic cardioversion of AF (Class IIa)
➢ Side effects are hypotension and bradycardia
➢ Dose: 150 mg IV over 10 mins, followed by
1 mg/ kg/min infusion for 6 hours, and then
0.5mg/ kg/min.
 Antiarrhythmic Drugs
Atropine
➢ Reverses cholinergic-mediated decreases in heart
rate, systemic vascular resistance, & blood pressure
➢ Should be used with caution in the presence of AMI
➢ Symptomatic sinus bradycardia (Class I)
➢ AV block Nodal level or ventricular asystole
(Class IIa)
 Antiarrhythmic Drugs
Atropine
➢ Should not be used in Mobitz type II block
➢ Dose: Asystole & PEA - 1 mg IV every 3- 5 mins
Bradycardia – 0.5 – 1 mg every 3 – 5 mins
for a total dose of 0.04 mg/
kg. A total dose of 3 mg
(0.04 mg/kg) results in full
vagal blockade in humans
 Antiarrhythmic Drugs
B-Adrenergic Blockers
➢Class I in acute coronary syndromes

➢Metoprolol Dose:5 mg IV every 5 minute interval for total of 15 mg

➢Propranolol Dose: 0.1 mg/ kg IV every 2-3 minute interval

➢Esmolol Dose: 0.5 mg/ kg loading dose

50 mcg/ kg per minute maintenance infusion
2nd bolus of 0.5 mg/ kg infused in 1minute
repeated every 4 minutes for a total maximum
of 300 mcg/ kg per minute
 Antiarrhythmic Drugs
Calcium Channel Blockers
➢ Slow conduction & increases refractoriness in the AV
node
➢ May also control ventricular response rate in patients
with AF, Flutter, or MAT
➢ Verapamil: Effective in narrow complex PSVT
Should not be given in patients with
impaired ventricular function or
heart failure
➢ Dose: 2.5 – 5 mg IV given in 2 minutes. Administered
every 15 – 30 mins to a maximum of 20 mg.
 Antiarrhythmic Drugs
Flecainide
➢ Not approved for use in the USA
➢ Potent sodium channel blocker with significant
conduction slowing effects
➢ Effective for atrial flutter and AF, ectopic atrial
tachycardia, AV nodal reentrant tachycardia, and SVTs
associated with accessory pathway (WPW)
➢ Dose: 2 mg/ kg body weight at 10 mg/ min
 Antiarrhythmic Drugs
Lidocaine
➢ Routine use in AMI is not recommended
➢ Acceptable for:
▪ VF/ pulseless VT that persist after defibrillation and
administration of epinephrine (Class Indeterminate)
▪ Control of hemodynamically compromising PVC’s
(Class Indeterminate)
▪ Hemodynamically stable VT (Class IIb)
➢ Delicate toxic-to-therapeutic balance
➢ Dose: Initial bolus of 1 – 1.5 mg/ kg IV. Additional bolus of 0.5 to 0.75
mg/ kg can be given over 3 – 5 minutes for refractory VT/ VF.
 Antiarrhythmic Drugs
Magnesium
➢ magnesium associated with arrhythmias, cardiac
insufficiency, & sudden cardiac death
➢ Precipitates refractory VF & hinder intracellular potassium
replenishment
➢ Treatment of drug induced torsades de pointes (Anecdotal)
➢ Not recommended in cardiac arrest except when arrhythmias
are suspected to be caused by magnesium deficiency
➢ Dose: 1 – 2 gm (8-16meqs) mixed in 50 – 100 ml D5W given over 5 to
60 mins. Followed by 0.5 to 1gm IV infusion
1 to 2 gm diluted in 100 ml D5W administered over 1 – 2 mins in
emergency situations
 Antiarrhythmic Drugs
Sotalol
➢ Vaughn Williams Class Ill Antiarrhythmic
➢ Prolongs action potential duration & increases cardiac tissue
refractoriness
➢ Nonselective B-blocking properties
➢ Dose: 1 to 1.5 mg/ kg body weight at 10 mg/ min
(relatively slow infusion for emergency situations)
Management of
Cardiac Arrest
Access for Medications:
Correct Priorities
◼ Central vs Peripheral Infusions
◼ Central Infusion
◼ Not needed in most resuscitation attempts

◼ Peripheral Infusion
◼ Peak drug concentrations are lower
◼ Longer circulation time (1-2 min)
◼ Administer drug by bolus injection & follow with 20 ml
bolus IV then elevate the extremity for 10-20 sec
Access for Medications
◼ Other routes
◼ Intraosseous (IO)
◼ Safe and effective for fluid resuscitation, drug delivery
& blood sampling

◼ Endotracheal route
◼ if IV and IO access cannot be established
Access for Medications
◼ Other routes
◼ Endotracheal route
◼ Resuscitation drugs which may be administered by this
route
◼ Epinephrine, atropine, naloxone & vasopressin
◼ Typical dose is 2 to 2 ½ times the recommended IV dose
◼ Medications should be diluted in 5 -10ml water / normal
saline
◼ Epinephrine & lidocaine should be diluted in water for
better absorption
Access for Medications
◼ Other routes
◼ Endotracheal
◼ Disadvantage: lower
epinephrine
concentrations
◼ May produce transient
B- adrenergic effects
ACLS Pulseless Arrest Algorithm
 Ventricular Fibrillation/ Pulseless
Ventricular Tachycardia
◼ Deliver 1 shock then resume CPR
immediately ( 5 cycles or 2 min)
◼ 200 J for the first shock and an equal or higher
shock dose for the 2nd & subsequent shocks
◼ Check rhythm
◼ Continue CPR while defibrillator is charging
◼ Deliver shock
 SHOCK
RHYTHM
CPR CHECK CPR

Providers should give 1 shock rather than 3 successive shocks

which were previously recommended

First shock success rate is high

 ACLS Pulseless Arrest Algorithm

Copyright ©2005 American Heart Association

 Ventricular Fibrillation/ Pulseless
Ventricular Tachycardia
◼ If VF / pulseless VT persists after delivery of
1-2 shocks plus CPR
◼ Give a vasopressor (epinephrine every 3-5 min)
or one dose of vasopressin

◼ When VF/ pulseless VT persists after 2-3

shocks plus CPR & vasopressor
◼ Consider anti-arrhythmics such as amiodarone or
lidocaine
 Ventricular Fibrillation/ Pulseless
Ventricular Tachycardia
◼ Minimize interruptions in chest compressions
because they reduce coronary perfusion
pressure

◼ Establishing IV access should not interfere

with CPR & delivery of shocks

◼ Drugs should be administered ASAP before or

after shock delivery
 Ventricular Fibrillation/ Pulseless
Ventricular Tachycardia
◼ Drug doses should be prepared before the
rhythm check

◼ Rhythm checks should be very brief

◼ Pulse checks should generally be performed

if an organized rhythm is established. If there
is any doubt, resume CPR
Asystole & Pulseless Electrical
Activity (PEA)
◼ Pulseless electrical activity (PEA)
◼ Encompasses pseudo-electromechanical
dissociation, idioventricular rhythm,
ventricular escape rhythms,
postdefibrillation idioventricular rhythms
and bradyasystolic rhythms

◼ Often caused by reversible causes

Asystole & Pulseless Electrical
Activity (PEA)
◼ Does not benefit from defibrillation attempts
◼ Perform high-quality CPR with minimal
interruptions
◼ Continuous chest compressions 100/min
◼ Two rescuers should change compression
roles every 2 minutes
◼ Epinephrine can be administered every 3-5
min
Medications for Arrest Rhythms
◼ Vasopressors
◼ No placebo-controlled trials have shown
increased rate of neurologically intact survival to
hospital discharge
Medications for Arrest Rhythms –
VF/ Pulseless VT
◼ Epinephrine
◼ Alpha-adrenergic effects can increase coronary &
cerebral perfusion pressure during CPR
◼ Beta-adrenergic effects may increase myocardial
work & reduce subendocardial perfusion
◼ No evidence to show that it improves survival

◼ Dose: 1 mg every 3 -5 min (2-2.5 mg via

endotracheal route
Medications for Arrest Rhythms –
VF/ Pulseless VT
◼ Vasopressin
◼ Nonadrenergic peripheral vasoconstrictor that
causes coronary & renal vasoconstriction
◼ No statistically significant differences between
vasopressin & epinephrine for return of
spontaneous circulation (ROSC), 24-hour survival
or survival to hospital discharge
◼ Dose: 40 U IV/IO
Medications for Arrest Rhythms –
Asystole & PEA
◼ Vasopressors
◼ May consider giving vasopressin for asystole but
insufficient evidence in PEA
◼ Epinephrine 1mg every 3-5 min
◼ Atropine
◼ Reverses cholinergic-mediated decreases in heart rate,
systemic vascular resistance & BP
◼ No prospective studies to support its use in asystole/ PEA
◼ Dose: 1 mg IV every 3 -5 min ( maximum of 3mg)
Medications for Arrest Rhythms –
Antiarrhythmics
◼ Amiodarone
◼ Affects Na, K and Ca channels as well as alpha
and beta adrenergic blocking properties
◼ May be administered for VF or pulseless VT
unresponsive to CPR, shock & vasopressor
◼ Dose: 300 mg IV/IO followed by 150 mg IV/IO
Medications for Arrest Rhythms –
Antiarrhythmics
◼ Lidocaine
◼ Alternative anti-arrhythmic to Amiodarone
◼ No proven short-term or long-term efficacy in
cardiac arrest
◼ Initial dose: 1-1.5 mg/kg IV, then 0.5 – 0.75
mg/kg IV push every 5 -10 minutes ( maximum
dose of 3 mg/kg)
Medications for Arrest Rhythms –
Antiarrhythmics
◼ Magnesium
◼ Effectively terminates torsades de pointes
◼ Not effective in irregular/ polymorphic VT in
patients with normal QT
◼ Dose: 1-2 g in 10 ml D5W IV/IO push over 5-
20min
◼ When with pulse, 1-2 g in 50-100 ml D5W
Interventions not Supported by
Outcome Evidence
◼ Pacing in arrest
◼ Procainamide in VF and Pulseless VT
◼ Norepinephrine
◼ Precordial thump for VF/ pulseless VT
◼ Electrolyte therapies in arrest rhythms
(Magnesium)
◼ Routine administration of IV fluids during
arrest
ELECTRICAL THERAPIES

◼ Automated External
Defibrillators, Defibrillation,
Cardioversion, and Pacing
Early defibrillation is critical for several
reasons:
1. Ventricullar fibrillation (VF)- most frequent
initial rhythm in sudden cardiac arrest (SCA)
2. Treatment of VF is electrical defibrillation
3. Probability of successful defibrillation
diminishes rapidly overtime
4. VF tends to deteriorate to asystole within a
few minutes
3-4 %- survival rate per minute from
collapse to defibrillation when bystander
CPR is provided.

Immediate CPR- if provided, many adults

in VF can survive with intact neurologic
function especially if defibrillation is
performed within about 5 minutes after
sudden cardiac arrest.
 New Recommendations to
Integrate CPR and Automated
External Defibrillator (AED)
Use

◼ 3 actions must occur within the first

moments of a cardiac arrest:
1. Activation of the emergency medical
services (EMS)
2. Provision of CPR
3. Operation of an AED
SHOCK FIRST VERSUS CPR FIRST
◼ When an out-of-hospital cardiac arrest is not
witnessed by EMS personnel, they may give about 5
cycles of CPR before checking the ECG rhythm and
attempting defibrillation
(class IIb).
( 1 cycle of CPR = 30 compressions and
2 breaths )
In studies, when EMS call-to-arrival intervals were 4
to 5 minutes or longer, victims who received 1 ½
to 3 minutes of CPR before defibrillation showed an
increase rate of initial resuscitation survival to
hospital discharge.
1 year survival- for those who received
immediate defibrillation for VF SCA.

There is insufficient evidence to support or

refute CPR before defibrillation for in-
hospital cardiac arrest.
1-SHOCK PROTOCOL VERSUS 3-
SHOCK SEQUENCE
◼ In animal studies, frequent or long
interruptions in precordial chest compressions
for rhythm analysis or rescue breathing were
associated with postresuscitation myocardial
dysfunction and reduced survival rates.
◼ Secondary analyses of 2 randomized trials
showed that interruption in chest compression
is associated with a decreased probability of
conversion of VF to another rhythm
◼ In 2005, the rhythm analysis for a 3-shock
sequence performed by a commercially
available AEDs resulted in delays of up to 37
◼ If 1 shock fails to eliminate VF, the
incremental benefit of another shock is low,
and resumption of CPR is likely to confer a
greater value than another shock.
◼ When VF/pulseless ventricular tachycardia is
present, the rescuer should deliver 1 shock
and should then immediately resume CPR,
beginning with chest compressions (class IIa).
◼ After 5 cycles (about 2 minutes) of CPR, the
AED should then analyze the cardiac rhythm
and deliver another shock if indicated (class
IIb)
◼ First shock efficacy for monophasic shocks is
lower than first-shock efficacy for biphasic
◼ A recommendation for higher initial energy
when using a monophasic waveform by expert
consensus with consideration of the potential
negative effects of a high first-shock energy
versus the negative effects of prolonged VF.
◼ Rescuers using monophasic AEDs should give
an initial shock of 360 J: if VF persists after
the first shock, second ansd subsequent
shocks of 360 J should be given.
◼ There was no significant difference in the
percentage of patients who developed
advanced AV block after 1 shock.
◼ AV block was more likely to develop after 2 or
3 shocks of 320 J than after 2 or 3 shocks of
175 J, but the block was transient and did not
affect survival to hospital discharge.
◼ When VF is present for more than a few
minutes, the myocardium is depleted of
oxygen and metabolic substrates.
◼ A brief period of chest compressions can
deliver oxygen and metabloc substrates
, increasing the likelihood that a
perfusing rhythm will return after
defibrillation.
◼ Analyses of VF waveform characteristics
predictive of shock success have
documented that the shorter the time
between a chest compression and
delivery of a shock, the more likely the
shock will be successful.
DEFIBRILLATION WAVEFORMS AND
ENERGY LEVELS
◼ Defibrillation involves delivery of current
through the chest and to the heart to
depolarize myocardial cells and eliminate VF.
◼ Defibrillation ( shock success ) is typically
defined as termination of VF for at least 5
seconds following the shock.
◼ VF frequently recurs after successful shocks,
but this recurrence should not be equated
with shock failure.
◼ No specific waveform (either monophasic or
biphasic) is consistently associated with a
higher rate of return of spontaneous
circulation or rates of survival to hospital
discharge after cardiac arrest.
◼ MONOPHASIC WAVEFORM
DEFIBRILLATORS

- deliver current of one polarity

- monophasic damped sinusoidal waveforms
(MDS) returns to zero gradually, whereas the
monophasic truncated exponential waveform
(MTE) current is abruptly returned to baseline
to zero current flow.
- research indicates that when doses
equivalent to or lower than monophasic doses
are used, biphasic waveform shocks are safe
and effective for termination of VF.
BIPHASIC WAVEFORM
DEFIBRILLATORS
◼ Overall research indicates that lower-energy biphasic
waveform shocks have equivalent or higher success for
termination of VF than either damped sinusoidal or
truncated exponential monophasic waveform shocks
delivering escalating energy (200 J, 300 J, 360 J) with
successive shocks.
◼ Several randomized and observational studies have shown
that defibrillation with biphasic waveforms of relatively low
energy ( less than or equal to 200 J ) is safe and has
equivalent or higher efficacy for termination of VF than
monophasic waveform shocks of equivalent or higher energy
(class IIa).
FIXED AND ESCALATING ENERGY
◼ Current research confirms that it is reasonable to use
selected energies of 150 J to 200 J with a biphasic truncated
exponential waveform or 120 J with a rectilinear biphasic
waveform for the initial shock.
◼ For second and subsequent biphasic shocks, use the same
or higher energy (class IIa).
◼ Nonescalating and escalating energy biphasic waveform
shocks can be used safely and effectively to terminate short
duration and long duration VF ( class IIa).
◼ The safety and efficacy data related to specific biphasic
waveforms, the most effective initial shock, and whether to
use escalating sequences require additional studies in both
the in-hospital and out-of-hospital settings.
AUTOMATED EXTERNAL
DEFIBRILLATORS
-Sophisticated, reliable computerized devices
that use voice and visual prompts to guide
lay rescuers and health care providers to
safely defibrillate VF SCA.
-Recorded information about frequency and
depth of chest compressions during CPR.
◼ LAY RESCUER AED PROGRAM

-Also known as public access defibrillation, or

PAD programs

- Goal is shorten the time from onset of VF

until CPR and shock delivery by ensuring that
AEDs and trained lay rescuers are available in
public areas where SCA is likely to occur.

- Survival rate of 41 % to 74 % from out-of-

hospital witnessed VF SCA when immediate
bystander CPR is provided and defibrillation
occurs within about 3 to 5 minutes of collapse.
RECOMMENDED ELEMENTS FOR
COMMUNITY LAY RESCUER AEDs
PROGRAMS:
-A planned and practiced response; typically
this requires oversight by a healthcare
provider
-Training of anticipated rescuers in CPR and
use of the AED
-Link with the local EMS system
-Process of ongoing quality improvement
◼ CPR and AED use by public safety first
responders (traditional and nontraditional) are
recommended to increase survival rates for
SCA (class I).
◼ AED programs in public locations where there
is a relatively high likelihood of witnessed
cardiac arrest (eg,airports,casinos,sports
facilities) are recommended (class I)
◼ Approximately 80 % of out-of-hospital cardiac
arrests occur in private or residential settings
◼ AEDs are of no value for arrest not caused by
VF/pulseless VT and they are not effective for
treatment of nonshockable rhythms that may
develop after termination of VF.
◼ Nonperfusing rhythms are present in most
patients after shock delivery and CPR is
ELECTRODE PLACEMENT
◼ Rescuers should place AED electrode pads on
the victim’s bare chest in the conventional
sternal-apical (anterolateral) position position
(class IIa).
◼ The right (sternal) chest pad is placed on the
victim’s right superior-anterior (infraclavicular)
chest and the apical (left) pad is placed on the
victim’s inferior –lateral left chest , lateral to
the left breast (class IIa).
◼ When an implantable medical device is located
in an area where a pad would normally be
placed, position the pad at least 1 inch (2.5
cm) away from the device (class
indeterminate)
◼ If the victim has an ICD that is delivering
◼ Do not place AED electrode pads directly on
top of a transdermal medication because the
patch may block delivery of energy from the
electrode pad to the heart and may cause
small burns to the skin.
◼ If an unresponsive patient is lying in water or
if the victim’s chest is covered with water or
the victim is extremely diaphoretic, remove
the victim from water and briskly wipe the
chest before attaching electrode pads and
attempting defibrillation
◼ AEDs can be used when the victim is lying on
snow or ice.
◼ Most victims do not need any special
preparation of the chest other than removal of
◼ IN HOSPITAL USE OF AEDs

- Defibrillation may be delayed when patients

develop SCA in unmonitored hospital beds and
in outpatient and diagnostic facilities.

- Despite limited evidence, AEDs should be

considered for the hospital setting as a way to
facilitate early defibrillation ( a goal of less
than or equal to 3 minutes from collapse ),
especially in areas where staff have no rhythm
recognition skills or defibrillators are used
infrequently.
MANUAL DEFIBRILLATION
◼ SHOCK ENERGIES
- Both low-energy and high-energy biphasic
waveform shocks are effective, but definitive
recommendations for the first and subsequent
energy levels for all devices cannot be made
because devices vary in waveform and
reported shock success.
- Although both escalating-energy and
nonescalating-energy defibrillators are
available, there is insufficient data to
recommend one approach over another.
◼ With biphasic defibrillator, it is
reasonable to use selected energies of
150 J to 200 J with a biphasic truncated
exponential waveform or 120 J with a
rectilinear biphasic waveform for the
initial shock.
◼ For second and subsequent shocks, use
the sane or higher energy ( class IIa ).
◼ The 200-J “default” energy level is not
necessarily an optimal dose, but it was
selected because it falls within the
reported range of dose effective for first
and subsequent biphasic shocks.
◼ If a monophasic defibrillator is used,
select a dose of 360 J for all shocks.
If VF is initially terminated by a
shock but then recurs later in the
arrest, deliver subsequent shocks at
the previously successful energy
level.
◼ The most important determinant of
survival in adult VF SCA is rapid
defibrillation by either a monophasic
or biphasic device.
◼ TRANSTHORACIC IMPEDANCE

◼ When transthoracic impedance is too high,

a low-energy shock will not generate
sufficient current to achieve defibrillation.
◼ To reduce transthoracic impedance, the
defibrillator operator should use conductive
materials such as gel pads or electrode
paste with paddles or through the use of
self-adhesive pads.
◼ ELECTRODE POSITION
◼ Self-adhesive monitor/defibrillator electrode
pads are as effective as gel pads or paste and
should be used routinely instead of standard
paddles (class IIa).
◼ When providing cardioversion or defibrillation
for patients with permanent pacemaker or
ICDs, do not place the electrodes over or
close to the device generator, because
defibrillation can cause the pacemaker to
malfunction.
◼ Permanent pacemakers and ICDs should be
reevaluated after the patient recieves a shock
because some of the defibrillation current
flows down the pacemaker leads.
◼ ELECTRODE SIZE

◼ For adult defibrillation, both handheld paddle

electrodes and self-adhesive pad electrodes 8
to 12 cm in diameter perform well, although
defibrillation success may be higher with
electrodes 12 cm in diameter rather than with
those 8 cm in diameter.
◼ Small electrodes (4.3 cm) may be harmful
and may cause myocardial necrosis.
CURRENT-BASED DEFIBRILLATION
-Clinical studies using MDS waveform shocks have
tried to identify the range of current necessary to
achieve defibrillation and cardioversion and the
optimal current for ventricular defibrillation appears to
be 30 to 40 MDS.
“OCCULT” VERSUS “FALSE” ASYSTOLE
-There is no evidence that attempting to “defibrillate”
asystole is beneficial.
-In all outcomes studied, including ROSC and survival,
the group that received shocks showed a trend
toward a worse outcome than the group that did not
receive shocks.
◼ FIRE HAZARD
-Severe fires have been reported when ventilator
tubing is disconnected from the tracheal tube and
then left adjacent to the patient’s head, blowing
oxygen across the chest during attempted
defibrillation
-The use of self-adhesive defibrillation pads is
probably the best way to minimize the risk of sparks
igniting during defibrillation.
-If manual paddles are used, gel pads are preferable
to electrode pastes and gels because they can spread
between the 2 paddles, creating the potential for a
spark (class IIb).
-Rescuers should take precautions to minimize
sparking during attempted defibrillation; try to ensure
that defibrillation is not attempted in an oxygen-
enriched atmosphere (class IIa).
SYNCHRONIZED CARDIOVERSION
◼ Synchronized cardioversion is shock delivery
that is timed with the QRS complex.
◼ This synchronization avoids shock delivery
during the relative refractory portion of the
cardiac cycle, when a shock could produce VF.
◼ The energy (shock dose) used for a
synchronized shock is lower than that used for
unsynchronized shocks (defibrillation).
◼ These low energy shocks should always be
delivered as synchronized shocks because if
they are delivered as unsynchronized they are
likely to induce VF.
◼ If cardioversion is needed and it is impossible to
synchronize a shock (eg, the patient’s rhythm is
irregular), use high-energy unsynchronized shocks.
◼ Synchronized shocks indicated to treat:
◼ 1.unstable reentrant SVT
◼ 2.atrial fibrillation

◼ 3.atrial flutter

◼ 4.unstable monomorphic VT

Not used for:

1.VF
2.pulseless VT
3.unstable polymorphic (irregular) VT
SUPRAVENTICULAR TACHYCARDIAS
(Reentrant SVT)
◼ 100 J to 200 J – Atrial fibrillation
◼ 50 J to 100 J- Atrial flutter and other SVT
◼ A recent prospective randomized study that
compared the rectilineal biphasic waveform
(200 J maximum selected energy) with a
biohasic truncated exponential waveform
(360 J maximum energy) for elective
cardioversion found no significant differences
in efficacy between 2 waveforms.
VENTRICULAR TACHYCARDIA
◼ Pulseless VT is treated as VF
◼ Unstable monomorphic (regular) VT with
pulse- synchronized cardioversion
◼ Unstable polymorphic (irregular) VT w/ or w/o
pulse- unsynchronized high-energy shocks
◼ If there is any doubt if monomorphic or
polymorphic VT in unstable patient, DO NOT
DELAY shock delivery, provide high energy
unsynchronized shocks (ie, defibrillation
doses)
PACING
◼ Not recommended for patients in asystolic
cardiac arrest.
◼ Transcutaneous pacing is recommended for
treatment of symptomatic bradycardia when a
pulse is present.
◼ Immediate pacing is indicated if the patient is
severely symptomatic, especially when the
block is at or below the His Purkinjie level.
◼ If does not respond to transcutaeous pacing,
transvenous pacing is needed.