ACLS Cheat Sheet
Electrical Conduction Through the Heart
Pathway Steps
1) SA (sinoatrial) Node
2) AV (atrioventricular) Node
3) The Bundle of His
4) The Left and Right Bundle Branches
5) The Purkinje Fibers
Blood Flow Through the Heart
Steps
1) Inferior and Superior Vena Cava (deoxygenated)
2) Right Atrium (deoxygenated)
3) Right Ventricle (deoxygenated)
4) Pulmonary Artery (deoxygenated)
5) Pulmonary Vein (oxygenated)
6) Left Atrium (oxygenated)
7) Left Ventricle (oxygenated)
8) Aorta (oxygenated)
Seven Steps to Interpret an EKG
Analyze Rate
Analyze Rhythm
Analyze Axis
● Normal Adult Heart Rate: 60-100 beats/minute
● Tachycardia: > 100 beats/minute
● Bradycardia: < 60 beats/minute
● Regular Rhythm: distance from R-R or P-P intervals is the same
● Irregular Rhythm: distance from R-R or P-P intervals differs
Look at lead I and aVf and determine which direction the waves deflect (up or down)
Analyze Intervals
P-R Interval
● Prolonged P-R interval > 0.2 seconds
● Prolonged P-R interval suggests the presence of AV block
● Shortened P-R interval may suggest ventricular preexcitation, a junctional rhythm, or enhanced AV nodal conduction
Analyze P Wave
Are P waves present?
● Flat line/no P waves → no atrial activity
● Hidden/partially hidden P waves → indiscernible atrial activity and/or reentrant tachycardia
Do the P waves look normal?
● Sawtooth baseline → flutter waves
● Chaotic baseline → fibrillation waves
Analyze QRS Complex
Analyze ST Segment - T wave
Width
● Narrow (< 0.12 seconds): typically suggestive of supraventricular arrhythmia
● Wide (> 0.12 seconds): typically suggestive of ventricular arrhythmia
Height
● Small complexes
● Tall complexes
Morphology
● Monomorphic
● Polymorphic
● ST-Elevation: suggestive of myocardial infarction
● ST-Depression: suggestive of myocardial ischemia
● T waves:
○ Tall/peaked T waves: suggestive of hyperkalemia or hyperacute STEMI
○ Inverted T waves: generally non-specific
○ Biphasic T waves: suggestive of ischemia and hypokalemia
○ Flattened T waves: generally non-specific; may represent ischemia or electrolyte imbalances
Main Components of an EKG
QRS
Complex
R
T
P
PR Interval
Q
S
Baseline
QT Interval
Normal Sinus EKG Composition
Interpretation
Simpler Terms
P-Wave
Depolarization of the atria in response to signaling from the SA node
Atrial Contraction
QRS Complex
Depolarization of the ventricles in response to signaling from the AV node
Ventricular Contraction
T wave
Repolarization of the ventricles and the completion of a standard heart beat
Ventricular Relaxation (to allow blood
filling in the ventricles)
Size
Interval
1 small square
3 small squares
1 box (5 small squares)
0.04 seconds
0.12 seconds
0.2 seconds
ACLS Rhythm Recognition
Heart Rhythm
Normal Sinus
EKG
Helpful Tips/Distinct Features
● P wave, QRS complex, and T wave all
present and normal
● Rate is between 60-100 beats/min at rest
● Appropriate duration between T wave
and P wave
● Rhythm is regular in nature
ACLS Rhythm Recognition
Heart Rhythm
EKG
Helpful Tips/Distinct Features
Sinus
Bradycardia
● P wave, QRS complex, and T wave all
present and normal
● Rate is less than 60 beats/minute
● Prolonged duration between T wave and
P wave
● Rhythm is regular in nature
Sinus
Tachycardia
● P wave, QRS complex, and T wave all
present and normal
● Rate is greater than 100 beats/min
● Shortened duration between T wave and
P wave
● Rhythm is regular in nature
First-Degree
Heart Block
● Sinus rhythm with a PROLONGED P-R
interval > 0.20 seconds
● Generally due to a delay in transmission
from the atria to the ventricles
Second-Degree
AV Heart Block
(Mobitz Type I)
● Progressive lengthening of the P-R
interval until a QRS complex is dropped
● Longer Longer Longer Drop = Type I/
Wenckebach
ACLS Rhythm Recognition
Heart Rhythm
EKG
Helpful Tips/Distinct Features
Second-Degree
AV Block
(Mobitz Type II)
● Intermittent dropped QRS complex
WITHOUT progressive lengthening of the
P-R interval
Third-Degree
Heart Block
● No relationship between P and QRS waves
● QRS complexes may be normal or wide
● P-waves have constant P-P interval
without any relation to QRS complex
● P-waves may occur on the S-T segment
● If the P’s and Q’s don’t agree then you’ve
got a 3rd degree
Supraventricular
Tachycardia
● Very narrow QRS complex suggesting
supraventricular arrhythmia
● P-waves are often hidden
● Heart rate generally > 150 beats/minute
Atrial Fibrillation
● Absence of visible P waves
● Irregularly irregular QRS complex
● Ventricular rate is frequently fast
ACLS Rhythm Recognition
Heart Rhythm
EKG
Helpful Tips/Distinct Features
Atrial Flutter
● Saw-toothed flutter that represents
multiple P waves for each QRS complex
Ventricular
Tachycardia
● Widened QRS complexes
● P-waves generally absent
● Heart rate typically >100 beats/minute
Ventricular
Fibrillation
● Chaotic wave pattern
● Fibrillation waves of varying amplitude and
shape
● No identifiable P waves, QRS complexes, or T
waves
● Heart rate typically > 150 beats/minute
● No pulse is present
● Flat-line
● No electrical activity seen on the cardiac
monitor
● No pulse is present
Asystole
Pulseless
Electrical
Activity
Can Be ANY ECG Rhythm
● Can be ANY ECG rhythm
● Main difference is patient is usually
unresponsive with lack of a palpable pulse
Important Considerations for Quality CPR
● Push the chest at least 2 inches (5 cm) deep
● Allow chest to completely recoil
Chest Depth
CPR Rate
● Perform CPR at a rate of 100-120 compressions/min
Compressions-Ventilation Ratio
● If no advanced airway, 30:2 compression-ventilation ratio
How Often to Change Compressors
● Change compressors every 2 minutes, or sooner if fatigued
● Minimize interruptions in compressions
● Avoid excessive ventilation
● Quantitative waveform capnography
Other Important Factors
Cardiac Arrest - Pulseless Arrhythmias
Non-Shockable Rhythms
Shockable Rhythms
Asystole
Ventricular Fibrillation
Pulseless Electrical Activity (PEA)
Pulseless Ventricular Tachycardia (pVT)
Cardiac Arrest Treatment Algorithm
1) Start CPR
Rhythm
Shockable?
Yes
5) VF/pVT
No
2) Asystole/PEA
IV/IO Epinephrine 1 mg
ASAP
6) Shock
7) CPR for 2 minutes
Rhythm
Shockable?
3) CPR for 2 minutes
● Repeat Epinephrine 1 mg every 3 to 5 minutes
● Consider advanced airway capnography
No
Yes
Rhythm
Shockable?
8) Shock
Yes
No
9) CPR for 2 Minutes
4) CPR for 2 Minutes
● IV/IO Epinephrine 1 mg every 3
to 5 minutes
Rhythm
Shockable?
● Treat reversible causes
No
No
Rhythm
Shockable?
Yes
Yes
10) Shock
11) CPR for 2 Minutes
● IV/IO Amiodarone 300 mg once: consider
additional 150 mg once
● IV/IO Lidocaine 1-1.5 mg/kg once, then
0.5-0.75 mg/kg every 5-10 minutes (max
cumulative dose: 3 mg/kg)
12)
● If no signs of ROSC, go
to step 3 or 4
● If signs of ROSC, begin
post-cardiac arrest care
Go to Step 8 or 10
Reversible Causes to ALWAYS Consider in Cardiac Arrest (H’s & T’s)
H’s
Clinical Pearls
T’s
● Patients at risk for hypovolemia: sepsis, hemorrhage,
malnourishment, burn
Hypovolemia
Clinical Pearls
Tension
Pneumothorax
● Air is trapped in the pleural space under
positive pressure
● Requires urgent needle decompression
Hypoxia
● SpO2 <88% prior to cardiac arrest
Tamponade,
Cardiac
● Accumulation of fluid in the pericardial space
● Requires urgent pericardiocentesis
Hydrogen Ion
● Acidosis; pH <7.35 prior to arrest
Toxins
● Common Toxins: acids, pesticides,
organophosphates, sedatives, opioids, alcohol,
serotonergic agents, cocaine, amphetamines,
potassium efflux blockers, CCBs, digoxin
Hypo/
Hyperkalemia
● Hypokalemia: K+ < 3.5 mEq/L
● Hyperkalemia: K+ > 5.3 mEq/L
● Patients at risk for K+ imbalances: burn, ESRD, fall/trauma,
heart disease, certain medications, malnourishment
Hypothermia
● Body temperature < 35 C (95 F)
Thrombosis
● Coronary thrombosis
● Pulmonary thrombosis
Medications Used for the Treatment of Non-Shockable Rhythms: Asystole/Pulseless Electrical Activity
Place in
Therapy
Drug
Route
Dose
1st-line
Epinephrine
(0.1 mg/mL)
IV/IO
1 mg every 3-5 minutes until ROSC is
achieved
2nd-line
(off-label)
Epinephrine
(1 mg/mL)
Endotracheal
2 to 2.5 mg every 3-5 minutes until IV/IO
access established or ROSC is achieved
Mechanism of Action
Benefit in Cardiac Arrest
Stimulates Alpha-1, Beta-1,
and Beta-2
Increases cardiac stimulation and
tissue perfusion
Medications Used for the Treatment of Shockable Rhythms: Ventricular Fibrillation/Pulseless Ventricular
Tachycardia
Place in
Therapy
Drug
Route
Dose
Mechanism of Action
Benefit in Cardiac
Arrest
1st-line
Epinephrine
(0.1 mg/mL)
IV/IO
1 mg every 3-5 minutes until
ROSC is achieved
Stimulates Alpha-1, Beta-1, and Beta-2
Increases cardiac
stimulation and
tissue perfusion
If VF/pVT Continues Despite Defibrillation Attempts and Epinephrine Administration, START:
2nd-line
2nd-line
Amiodarone
Lidocaine
IV/IO
300 mg bolus once; consider
additional 150 mg bolus
once
Inhibits adrenergic stimulation, by affecting sodium,
potassium, and calcium channels thus prolonging the action
potential and refractory period in myocardial tissue;
decreases AV conduction and sinus node function
Provides rhythm
control to try and
stabilize the heart
IV/IO
1-1.5 mg/kg bolus. Repeat
0.5-0.75 mg/kg bolus every
5-10 minutes (max
cumulative dose: 3 mg/kg)
Suppresses automaticity of conduction tissue by increasing
electrical stimulation threshold of ventricle, His-Purkinje
system, and spontaneous depolarization of the ventricles
during diastole by a direct action on the tissues; decreases
neuronal membrane’s permeability to sodium ions
Provides rhythm
control to try and
stabilize the heart
Pharmacokinetics of Drugs Used in Cardiac Arrest
Drug
Onset of
Action
Half-Life
Duration of
Action
Metabolism
Excretion
Hepatic
Adjustment
Renal Adjustment
Special Population
Consideration
IV/IO
Epinephrine
1-2
minutes
<5 minutes
~5-10
minutes
MAO, COMT,
and Hepatic
Metabolism
Urine
None
None
None
IV/IO
Amiodarone
~60
minutes
9-36 days
2 weeksmonths
Hepatic via
CYP2C8 and
CYP3A4
Feces
(in the setting of
cardiac arrest)
IV/IO
Lidocaine
45-90
seconds
~8 minutes
10-20
minutes
Hepatic via
CYP1A2 and
CYP3A4
Urine
(in the setting of
cardiac arrest)
None
None
None
(in the setting of
cardiac arrest)
None
(in the setting of
cardiac arrest)
Types of Common Bradyarrhythmias
Sinoatrial (SA) Node Dysfunction
Atrioventricular (AV) Node Dysfunction
Sinus Bradycardia
First-Degree Heart Block
Sinoatrial Block
Second-Degree Heart Block (Mobitz Type I)
Sinus Pause
Second-Degree Heart Block (Mobitz Type II)
Sick Sinus Syndrome
Third Degree Heart Block
None
None
Bradycardia With Pulse Treatment Algorithm
Bradyarrhythmia (HR <50 beats/min)
Identify and Treat Underlying Cause
● Maintain patent airway; administer oxygen if hypoxemic
● Cardiac monitor to identify rhythm
● Establish IV access
● 12-lead ECG
● Consider possible hypoxic and toxicologic causes
Persistent Bradyarrhythmia Causing:
● Hypotension?
● Acutely altered mental status?
● Signs of shock?
● Ischemic chest discomfort?
● Acute Heart Failure?
Yes
Administer IV Atropine
First Dose: 1 mg bolus. Repeat 3-5 minutes
Maximum Dose: 3 mg
If Atropine is Ineffective:
Transcutaneous pacing
and/or
IV Dopamine infusion:
5-20 mcg/kg/minute: titrate slowly to patient response
or
IV Epinephrine Infusion:
2-10 mcg/minute: titrate to patient response
No
Monitor & Observe
Consider:
● Expert consultation
● Transvenous pacing
Medications Used for the Treatment of Symptomatic Bradycardia (HR <50 bpm) with Pulse
Place in
Therapy
Drug
Route
Dose
Mechanism of Action
Clinical Pearls
1st-line
Atropine
IV
First Dose: 1 mg bolus; may
repeat every 3-5 minutes
Maximum Total Dose: 3 mg
Blocks the action of acetylcholine at
parasympathetic sites in smooth muscles leading
to increased heart rate and cardiac output
Atropine is likely NOT effective
for type II second-degree or
third-degree AV node block
If Atropine is Ineffective, START:
2nd-line
Transcutaneous Pacing
AND/OR
2nd-line
Dopamine
IV
Continuous Infusion: 5 mcg/kg/
minute; increase every 2
minutes until desired effect
Maximum Dose: 20 mcg/kg/min
Stimulates both adrenergic and dopaminergic
receptors leading to cardiac stimulation resulting
in increased inotropy and chronotropy
Doses between 5-10 mcg/kg/
min: primarily beta-1 agonist
Doses > 10 mcg/kg/min:
primarily alpha-1 agonist with
some beta-1 agonist
OR
2nd-line
Epinephrine
Infusion
IV
Continuous Infusion: 2-10 mcg/
minute; titrate to desired effect
Usual Dose Range: 0.1-0.5 mcg/
kg/min
Stimulates Alpha-1, Beta-1, and Beta-2 leading to
increased chronotropy, inotropy, and
vasoconstriction
Beta-2 agonism leads to
relaxation of smooth muscle of
the bronchial tree
Refractory Symptomatic Bradycardia Despite Adequate Interventions, CONSIDER:
3rd-line
Transvenous Pacing
Pharmacokinetics of Drugs Used in Symptomatic Bradycardia with Pulse
Drug (IV)
Onset of
Action
of
Half-Life Duration
Action
Atropine
Immediate
~3 hours
2-5 hours
Hepatic via
enzymatic
hydrolysis
Urine
None
None
Ineffective in heart transplant patients
due to lack of vagal innervation
Epinephrine
1-2
minutes
<5
minutes
~5-10
minutes
MAO, COMT,
and Hepatic
Metabolism
Urine
None
None
For obesity with BMI >30 kg/m2, use
IBW for initial dose calculations
Dopamine
~5
minutes
~2
minutes
<10 minutes
Renal, hepatic,
and plasma
Urine
None
None
For obesity with BMI >30 kg/m2, use
IBW for initial dose calculations
Metabolism
Hepatic
Renal
Excretion Adjustment
Adjustment Special Population Consideration
Regular Narrow vs Wide QRS Complex Tachyarrhythmias
Regular Narrow Complex (<0.12 second)
Wide QRS Complex (≥0.12 second)
Supraventricular Tachycardia
Ventricular Tachycardia
Tachycardia with Pulse Algorithm
Tachyarrhythmia (HR≥ 150 beats/min)
Identify and Treat Underlying Cause
● Maintain patent airway; assist breathing if necessary
● Oxygen (if hypoxemic)
● Cardiac monitor to identify rhythm; monitor blood pressure and oximetry
● Establish IV Access
● 12-lead ECG
Persistent Tachyarrhythmia Causing:
● Hypotension?
● Acutely altered mental status?
● Signs of shock?
● Ischemic chest discomfort?
● Acute heart failure?
No
Yes
Wide QRS?
≥0.12 second
No
Yes
Synchronized Cardioversion
Consider
● Consider sedation
● If regular narrow complex: consider
IV adenosine 6 mg IV push; may
repeat a second dose of 12 mg
● IV Adenosine only if regular
or monomorphic
● Antiarrhythmic infusion
● Expert consultation
If Refractory, Consider
● Vagal maneuvers (if regular)
● IV Adenosine (if regular)
● Beta-Blocker or Calcium Channel Blocker
● Consider expert consultation
● Underlying cause
● Need to increase energy level for next cardioversion
● Addition of anti-arrhythmic drug
● Expert consultation
Medications Used for the Treatment of Tachycardia with Pulse
Place in Therapy
Drug
Route
2nd-line
Adenosine
IV
1st-line ONLY IF
REGULAR AND
MONOMORPHIC
Adenosine
IV
1st-line
Amiodarone
IV
1st-line
Procainamide
IV
1st-line
Sotalol
IV
1st-line
Dose
Mechanism of Action
Clinical Pearls
Symptomatic Tachycardia (HR ≥150 bpm)
Synchronized Cardioversion
If Regular Narrow Complex, CONSIDER
First Dose: 6 mg
Given half-life of <10 seconds,
rapid IV push
Slows conduction time through AV node, interrupting
must follow adenosine
Second Dose
the re-entry pathways through the AV node
administration with a RAPID
(if needed): 12 mg
20 mL NS flush
Asymptomatic Tachycardia with a Wide QRS Complex (≥0.12 second)
First Dose: 6 mg
Given half-life of <10 seconds,
rapid IV push
Slows conduction time through AV node, interrupting
must follow adenosine
Second Dose
the re-entry pathways through the AV node
administration with a RAPID
(if needed): 12 mg
20 mL NS flush
CONSIDER one of the following Antiarrhythmic Infusions:
First Dose: 150 mg
Inhibits adrenergic stimulation, by affecting sodium,
Long-term use associated
over 10 minutes
potassium, and calcium channels thus prolonging the
with increased risk of
Maintenance Infusion: action potential and refractory period in myocardial
pulmonary
and hepatic
1 mg/min for the
tissue; decreases AV conduction and sinus node
toxicity
first 6 hours
function
Decreases myocardial excitability and conduction
Prolonged use may lead to
Initial: 20-50 mg/min
by increasing electrical stimulation threshold
drug-induced lupus
Maintenance Infusion: velocity
of ventricle, His-Purkinje system, and through direct erythematosus-like syndrome
1-4 mg/min
cardiac effects
and blood dyscrasias
Bolus: 1.5 mg/kg or
Beta-blocker which contains both beta-adrenoceptorDo NOT initiate sotalol if
100 mg over 5 minutes blocking and cardiac action potential prolongation
baseline QTc > 450 msec
Pharmacokinetics of Drugs Used in Tachycardia with Pulse
Drug (IV)
Onset of Half-Life Duration
Action
of Action
Adenosine
Rapid
Amiodarone
~60
minutes
Vascular
<10
endothelial cells
seconds Very Brief and
erythrocytes
9-36
days
10-30 2-5 hours
Procainamide minutes
Sotalol
Metabolism
5-10
minutes 12 hours
2 weeksHepatic via
months CYP2C8 and 3A4
3-12
hours
12-16
hours
Hepatic via
acetylation
None
Excretion
Hepatic Adjustment
Renal Adjustment
Special Population
Consideration
Urine
None
None
None
Feces
If hepatic enzymes >3x
normal; consider decreasing
dose or discontinuing therapy
None
Caution major drug
interactions
Urine &
Feces
Child-Pugh score 8-10:
reduce by 25%
Child-Pugh score >10:
reduce by 50%
CrCl 10-50 mL/min:
reduce by 25-50%
CrCl <10 mL/min:
reduce by 50-75%
Caution major drug
interactions
Caution in patients
with preexisting
marrow failure or
cytopenia of any type
None
CrCl>60 mL/min:
every 12 hours
CrCl 30-60 mL/min:
every 24 hours
CrCl 10-29 mL/min:
every 36-48 hours
CrCl <10 mL/min:
AVOID USE
Caution major drug
interactions
Do NOT initiate
sotalol if baseline
QTc > 450 msec
Urine as
unchanged
drug