ACLS Study Guide

This purpose of this study guide is to assist you in successfully completing

the AHA ACLS course. It includes sections on:
ECG Rhythm Interpretation
ACLS Drugs
ACLS Algorithms

ECG Rhythm Interpretation

Electrical Conduction System
SA Node. Primary pacemaker. Rate 60-100
The impulse travels through the Intraatrial Pathways to innervate
the atria
The impulse reaches the AV Node where electrical activity is delayed
to allow for more complete filling of ventricles.
AV Junction is comprised of the AV Node and the Bundle of His.
Secondary pacemaker. Rate 40-60
The impulse then travels into the Right and Left Bundle branches.
Conducts electrical activity from Bundle of His to Purkinje Network.
The Purkinje Network are fibers that spread throughout the
ventricles, that carry impulses directly to ventricular muscle cells. Our
last pacemaker site. Rate 20-40

P wave:
PRI:

QRS:

T wave:

Represents Atrial depolarization

Represents the time it takes the impulse to travel from the SA Node through the
intraatrial pathways in atria to the AV junction and the delay at the AV node.
Interval from start of P wave to start of QRS, measures 0.12-0.20 sec
Represents conduction of impulse from Bundle of His through the ventricular
muscle. Represents ventricular depolarization.
Should measure less than 0.12 sec
Follows ST segment. Slightly rounded, positive deflection
Represents ventricular repolarization, resting phase of cardiac cycle

Absolute Refractory Period:

No outside stimulus can cause cells to depolarization
From beginning of the QRS complex to the middle of the T wave
Relative Refractory Period:
A dangerous period. A strong outside stimulus can initiate
depolarization of the only partially recharged cells. Possibly causing a
lethal arrhythmia
From the middle of the T wave to its end

5 Steps for Analyzing a Strip:

Heart Rate:
Bradycardia <60, Normal 60-100, Tachycardia >100
Count the # of R waves in a 6 second rhythm strip, then multiply by 10
Find an R wave that lands on a bold line. Count the # of large boxes to the next R
wave. If the second R wave is 1 large box away the rate is 300, 2 boxes - 150, 3
boxes - 100, 4 boxes - 75, 5 boxes 60
Divide 300 by the number of large boxes separating the R waves
Heart Rhythm:
Look at the R R distances, are they regular or irregular
P Wave:
Are there P waves?
Do the P waves all look alike?
Do the P waves occur at a regular rate?
Is there one P wave before each QRS
PR Interval:
Is the PRI between 0.12-0.20?
Is it consistent across the strip?
If it varies is there a pattern?

QRS Complex:
Do all of the QRS Complexes look alike?
Are they regular?
Is the duration 0.04 0.12

Normal Sinus Rhythm

This rhythm represents the normal state with the SA node functioning
as the lead pacer with normal conduction through the heart.

The

intervals should all be consistent and within normal ranges.

Looking at the ECG you'll see that:

Rhythm - Regular

Rate - (60-100 bpm)

QRS Duration - Normal

P Wave - Visible before each QRS complex

P-R Interval - Normal (<5 small squares. Anything above and

this would be 1st degree block)

Indicates that the electrical signal is generated by the sinus node

and travelling in a normal fashion in the heart.

Sinus Bradycardia
The sinus beats are slower than 60 BPM. The origin may be in the
SA node or in an atrial pacemaker. This rhythm can be caused by
vagal stimulation leading to nodal slowing, or by medicines such as
beta blockers, and is normally found in some well-conditioned
athletes. The QRS complex, and the PR interval may slightly widen
as the rhythm slows below 60 BPM. However, they will not widen
past the upper threshold of the normal range for that interval. For
example, the PR interval may widen, but is should not widen over
the upper of 0.20 seconds

Looking at the ECG you'll see that:

Rhythm - Regular

Rate - less than 60 beats per minute

QRS Duration - Normal

P Wave - Visible before each QRS complex

P-R Interval - Normal

Usually benign and often caused by patients on beta blockers

Sinus Tachycardia
It is an excessive heart rate above 100 beats per minute (BPM)
which originates from the SA node. Causes include stress, fright,
pain, dehydration, and exercise. Not usually a surprise if it is
triggered in response to regulatory changes (e.g. shock).

Looking at the ECG you'll see that:

Rhythm - Regular

Rate Usually between 100 150 beats per minute

QRS Duration - Normal

P Wave - Visible before each QRS complex

P-R Interval - Normal

The impulse generating the heart beats are normal, but they are
occurring at a faster pace than normal. Seen during exercise

Atrial Flutter
A single irritable focus in the atria fires in a rapid repetitive fashion at
a rate of 150 350 beats/min. The F waves appear in a saw toothed
pattern such as those in this ECG. The QRS rate is usually regular and
the complexes appear at some multiple of the P-P interval.

Looking at the ECG you'll see that:

Rhythm Usually regular

Rate Usually fast 110-150 beats per minute

QRS Duration - Usually normal

P Wave - Replaced with multiple F (flutter) waves, usually at a

ratio of 2:1 (2F - 1QRS) but sometimes 3:1

P Wave rate - 300 beats per minute

P-R Interval - Not measurable

Atrial Fibrillation
Atrial fibrillation is the chaotic firing of numerous atrial pacemaker cells
in a totally haphazard fashion.

The result is that there are no

discernible

QRS

waves.

And

the

complexes

are

innervated

haphazardly in an irregularly irregular pattern. The ventricular rate is

guided by occasional activation from one of the pacemaking sources.
Because the ventricles are not paced by anyone site, the intervals are
completely random.

Looking at the ECG you'll see that:

Rhythm - Irregularly irregular

Rate - usually 100-160 beats per minute but slower if on

medication

QRS Duration - Usually normal

P Wave - Not distinguishable as the atria are firing off all over

P-R Interval - Not measurable

The atria fire electrical impulses in an irregular fashion causing

irregular heart rhythm

Supraventricular Tachycardia (Narrow complex Tachycardia)

(SVT)
SVT is a narrow complex tachycardia originating above the ventricles.
SVT can occur in all age groups.

Looking at the ECG you'll see that:

Rhythm - Regular

Rate - > 150 beats per minute

QRS Duration - Usually normal

P Wave - Often buried in preceding T wave

P-R Interval - Depends on site of supraventricular pacemaker

1st Degree AV Block

1st Degree AV block is caused by a conduction delay through the AV
node but all electrical signals reach the ventricles. This rarely causes
any problems by itself and often trained athletes can be seen to have
it. The normal P-R interval is between 0.12s to 0.20s in length, or 3-5
small squares on the ECG.

Looking at the ECG you'll see that:

Rhythm - Regular

Rate - Normal

QRS Duration - Normal

P Wave - Ratio 1:1

P Wave rate - Normal

P-R Interval - Prolonged (>5 small squares)

2nd Degree Block Type 1 (Wenckebach)

Mobitz Type I is also know as Wenckebach (pronounced WEEN-keybock).
period.

It is caused by a diseased AV node with a long refractory

The result is that the PR interval lengthens between

successive beats due to increasing delayed conduction through the AV

junction until a beat is dropped. At that point, the cycle starts again.

Looking at the ECG you'll see that:

Rhythm - Regularly irregular

Rate - Normal or Slow

QRS Duration - Normal

P Wave - Ratio 1:1 for 2,3 or 4 cycles then 1:0.

P Wave rate - Normal but faster than QRS rate

P-R Interval - Progressive lengthening of P-R interval until a QRS

complex is dropped

2nd Degree Block Type 2

In 2nd degree Type 2, the impulse either passes through the AV
junction normally or it is blocked completely.

It is an all or nothing

type of thing. Beats are intermittently nonconducted and QRS

complexes dropped, usually in a repeating cycle of every 3rd (3:1
block) or 4th (4:1 block) P wave

Looking at the ECG you'll see that:

Rhythm - Regular

Rate - Normal or Slow

QRS Duration - Prolonged

P Wave - Ratio 2:1, 3:1

P Wave rate - Normal but faster than QRS rate

P-R Interval - Normal or prolonged but constant

3rd Degree Block

3rd degree block or complete heart block occurs when the impulse
travels through the atria normally but is blocked completely at the
junction.

The atria and ventricles are firing separately each to its

own drummer, so to speak.

normal or tachycardic.

The atrial rhythm can be bradycardic,

The escape beat can be junctional (normal

QRS) or ventricular (wide QRS).

Looking at the ECG you'll see that:

Rhythm - Regular

Rate - Slow

QRS Duration Usually wide, but if ventricular impulse is

generated low in the junction it could be normal.

P Wave - Unrelated

P Wave rate - Normal but faster than QRS rate

P-R Interval - Variation

Differentiation of Second- and

Third-Degree AV Blocks
More Ps than QRSs
yes
yes
PR fixed?

2nd degree
Mobitz type II

no
QRS alike
and regular?

yes

3rd degree AV block

2nd degree Mobitz type I

no

Wenckebach

Wide Complex Tachycardia (usually monomorphic ventricular

tachycardia) Abnormal
Ventricular tachycardia is simply the presence of three or more ectopic
ventricular complexes in a row with a rate above 100. Originates from
one irritable focus so the rhythm is regular.

Poor cardiac output is

usually associated with this rhythm

Looking at the ECG you'll see that:

Rhythm - Regular

Rate Fast usually 180-190 Beats per minute

QRS Duration - Prolonged

P Wave - Not seen

Results from abnormal tissues in the ventricles generating a

rapid and irregular heart rhythm.

Polymorphic V-Tach (Torsades de Pointes)

Similar to ventricular tachycardia

Morphology of QRS complexes shows variations in width and
shape
Resembles a turning about or twisting motion along base line
May result from hypokalemia, hypomagnesemia, tricyclic
antidepressant drug overdose, the use of antidysrhythmic drugs,
or combination of these
Seen in alcoholics, eating disorders and the debilitated patients

Ventricular Fibrillation (VF)

Disorganized electrical signals cause the ventricles to quiver instead of
contract in a rhythmic fashion. A patient will be unconscious as there is
no cardiac output and blood is not pumped to the brain. Immediate
treatment by defibrillation is indicated. This condition may occur
during or after a myocardial infarct.

Looking at the ECG you'll see that:

Rhythm - Irregular

Rate - 300+, disorganized

QRS Duration - Not recognizable

P Wave - Not seen

This patient needs to be defibrillated!! QUICKLY

Pulseless Electrical Activity (PEA)

PEA occurs when any heart rhythm (other than V-Tach or V- Fib) is
observed on the monitor and does not produce a pulse. PEA can be
any rhythm (sinus, bradycardia, tachycardia). There is organized
electrical activity without a pulse.

Prognosis for PEA invariably is poor unless an underlying cause

can be identified and corrected
The highest priority of care is to maintain circulation for the
patient with basic and advanced life support techniques while
searching for a correctable cause

Asystole Abnormal
Asystole refers to the absence of any electrical cardiac activity. It is
defined by < 10 non-perfusing complexes per minute

Looking at the ECG you'll see that:

Rhythm - Flat or an occasional p wave or QRS complex. The

QRS complexes when they occur are wide and bizarre

Rate - 0 Beats per minute

QRS Duration - None

P Wave - None

ACLS Drugs
Drug

Action

Indication

Adenosine

Slows conduction through

the AV node.
Can interrupt reentry
pathways in the AV node.
Negative
chronotropic/dromatropic.
Very short half live,

Stable narrow complex

SVT unresponsive to
vagal maneuvers.
May consider for
unstable narrowcomplex reentry
tachycardia while
preparations are made
for cardioversion.
Regular and
monomorphic widecomplex tach thought to
be or previously defined
to be reentry SVT.

Amiodarone

Antidysrhythmic
Prolongs duration of
action potential and
effective refractory
period.
Increases PR and QT
intervals.
Decreases sinus rate.

Stable VT (preferably
after expert consult).
Recurrent, unstable VT.
VF/pulseless VT
unresponsive to shock
delivery, CPR and
vasopressors.

Precautions/
Contraindications
Transient side effects
include flushing, chest
pain or tightness, brief
periods of asystole or
bradycardia, ventricular
ectopy.
Less effective in patients
taking theophylline or
caffeine.
May cause
bronchospasm, caution
with asthma patients.
Contraindicated in
poison/drug-induced
tachycardia or second or
third degree heart block.
Will not terminate atrial
fib, atrial flutter or VT.
Rapid infusion may lead
to hypotension.
Do not administer with
other drugs that prolong
QT interval.
*Caution multiple
complex drug
interactions

Dosage
Initial bolus of 6mg
given rapidly over 1 to 3
seconds followed
immediately by a 20ml
saline flush
A second dose of 12 mg
can be given in 1 to 2
minutes if needed
*Reduce initial dose to
3mg in patients
receiving dipyridamole
(persantine) or
carbamzepine
(Tegretol), in heart
transplant patients or if
given by central venous
access.
VT with a pulse: 150mg
IV in 50 ml piggyback
over 10 minutes.
VF/Pulseless VT:
300mg IV push, second
dose if needed 150mg
IV push.

Atropine

Anticholinergic (parasympathetic blocker)

Increase heart rate and
AV conduction.
Dries secretions.
Dilates bronchioles.
Decreased GI motility.

First line drug for acute

symptomatic
bradycardia

0.5mg IV every 3 to 5
minutes as needed, not
to exceed total dose of
0.04mg/kg (total 3mg)

To control ventricular
rate in atrial fibrillation
and atrial flutter.
Use after adenosine to
treat refractory reentry
SVT in patients with
narrow QRS complex
and adequate blood
pressure

Use atropine cautiously

in the presence of acute
coronary ischemia or
MI.
Do not rely on Atropine
in Mobitz type II second
or third degree AV
block.
Should not delay
implementation of
external pacing for
patients with poor
perfusion.
Do not use for wideQRS tachycardias of
uncertain origin or for
poison/drug-induced
tachycardias.
Avoid use in patients
with WPW.
Blood pressure may
drop.

Diltiazem

Inhibits calcium ion

influx across cell
membrane during cardiac
depolarization; produces
relazation of coronary
vascular smooth muscles,
dilates coronary arteries,
slows SA/AV node
conduction times, dilates
peripheral arteries

Dopamine

Causes increased cardiac

output: acts on beta 1 and
alpha receptors, causing
vasoconstriction in blood
vessels

Second-line drug for

symptomatic
bradycardia (after
atropine).
Use for hypotension
with signs and
symptoms of shock.

Correct hypovolemia
with volume
replacement first.
May cause
tachyarrhythmias and
excessive
vasoconstriction.

Usual infusion rate is 2

to 20mcg/kg/min
Titrate to patient
response

15-20mg (0.25mg/kg)
IV over 2 minutes. May
give another IV dose in
15 minutes at 20 to 25
mg (0.35mg/kg) over 2
minutes

Epinephrine

Used during resuscitation

primarily for is alpha
adrenergic effects
(vasoconstriction)
increasing coronary and
cerebral blood flow

Cardiac arrest: VF,

pulseless VT, asystole,
PEA.
Symptomatic
bradycardia after
atropine as an
alternative to dopamine.
Severe hypotension
when pacing and
atropine fail.
Anaphylaxis.

Raising BP and
increasing HR may
cause myocardial
ischemia, angina and
increased myocardial
oxygen demand.
High doses do not
improve survival

Cardiac Arrest:
1mg (1:10,000) IV
administered every 3 to
5 minutes during
resuscitation. Follow
each dose with 20 ml
NS flush
Profound bradycardia or
hypotension:
2 to 10 mcg per minute
infusion titrated to
patient response

Magnesium

Reduces SA node
impulse formation.
Prolongs conduction time
in myocardium

Recommended for use

in cardiac arrest only if
torsades de pointes or
suspected
hypomagnesemia is
present.
Life-threatening
ventricular arrhythmias
due to digitalis toxicity

Occasional fall in blood

pressure with rapid
administration.
Use with caution if renal
failure is present

Cardiac arrest (due to

hypomagnesemia or
Torsades de Pointes)
1 to 2 g diluted in at
least 10ml of NS or
D5W over 5 minutes
Trosades de Pointes
with a Pulse of AMI
with hypomagnesemia:
Loading dose of 1 to 2
Grams mixed in 50 to
100 ml NS or D5W over
5 to 60 minutes, follow
with 0.5 to 1 gram per
hour IV (titrate to
control Torsades)

Sodium Bicarb

Vasopressin

Verapamil

Alkalinizing agent
buffers acidosis

Known preexisting
hyperkalemia.
Known preexisting
bicarb responsive
acidosis (DKA,
overdose of tricyclic
antidepressant, ASA,
cocaine or
diphenhydramine).
Prolonged resuscitation
with effective
ventilation; on return of
spontaneous circulation
after long arrest interval
Nonadrenergic peripheral May be used as
vasoconstrictor,
alternative pressor to 1st
increasing blood flow to
or 2nd dose of
heart and brain.
epinephrine in
Vasopressor effects not
VF/pulseless VT,
blunted by severe acidosis asystole or PEA cardiac
arrest.

Adequate ventilation
and CPR, not bicarb, are
the major buffer
agents in cardiac arrest.
Not recommended for
routine use in cardiac
arrest patients.

Potent peripheral
vasoconstrictor.

Cardiac arrest:
One dose of 40 units
may replace first or
second dose of epi

Slows depolarization of
slow-channel electrical
cells
Slows conduction through
AV node

Do not use for wide

QRS tach of unknown
origin, WPW, sick sinus
syndrome or 2nd or 3rd
degree heart block

5 mg IV over 2 min
(over 3 min in older
adults)
May repeat 5 mg every
15 min as needed to
total dose of 30mg

Alternative drug after

Adenosine in SVT
To control ventricular
rate in atrial fibrillation
and atrial flutter.

1 mEq/kg IV bolus
Once ROSC, if rapidly
available, use arterial
blood gas analysis to
guide bicarb therapy
During cardiac arrest,
ABG results are not
reliable indicators of
acidosis.