The field of resuscitation has been evolving for more than two centuries [ 1 ]. The Paris
Academy of Science recommended mouth-to-mouth ventilation for drowning victims in 1740
[ 2 ]. In 1891, Dr. Friedrich Maass performed the first documented chest compressions on
humans [ 3 ]. The American Heart Association (AHA) formally endorsed cardiopulmonary
resuscitation (CPR) in 1963, and by 1966, they had adopted standardized CPR guidelines for
instruction to lay-rescuers
Advanced cardiac life support (ACLS) guidelines have evolved over the past several
decades based on a combination of scientific evidence of variable strength and expert
consensus. The American Heart Association (AHA) developed the most recent ACLS
guidelines in 2010 using the comprehensive review of resuscitation literature performed
by the International Liaison Committee on Resuscitation. Guidelines are reviewed
continually, but are formally released every five years, and published in the journals
Circulation and Resuscitation
PRINCIPLES OF MANAGEMENT
Excellent basic life support and its importance
Excellent cardiopulmonary resuscitation (CPR) and early defibrillation for treatable
arrhythmias remain the cornerstones of basic and advanced cardiac life support (ACLS).
Although the 2010 American Heart Association (AHA) Guidelines for ACLS (2010 ACLS
Guidelines) suggest several revisions, including medications, electrical therapy, and
monitoring, .
We emphasize the term “excellent CPR” because anything short of this standard does not
achieve adequate cerebral and coronary perfusion
In the past, clinicians frequently interrupted CPR to check for pulses, perform tracheal
intubation, or obtain venous access. The 2010 ACLS Guidelines strongly recommend that every
effort be made NOT to interrupt CPR; other less vital interventions (eg, tracheal intubation or
administration of medications to treat arrhythmias) are made either while CPR is performed or
during the briefest possible interruption. Interventions that cannot be performed while CPR is
in progress (eg, defibrillation) should be performed during brief interruptions at two minute
intervals (after the completion of a full cycle of CPR)
Studies in both the in-hospital and prehospital settings demonstrate that chest compressions
are often performed incorrectly, inconsistently, and with excessive interruption .
Chest compressions must be of sufficient depth (at least 5 cm, or 2 inches) and rate (at least
100 per minute), and allow for complete recoil of the chest between compressions, to be
effective.
A 30 to 2 compression to ventilation ratio (one cycle) is recommended in patients without
advanced airways
ventilations at 8 to 10 per minute are administered if an endotracheal tube or extraglottic
airway is in place
Resuscitation team management
Two principles provide the foundation for CRM(Crisis Resource Management): leadership and
communication
The team leader should avoid performing technical procedures
the team leader may be required to perform certain critical procedures. In these situation
When the team leader determines the need to perform a task, the request is directed to a
specific team member, ideally by name
In CRM, communication is organized to provide effective and efficient care
Initial management and ECG interpretation
In the 2010 ACLS Guidelines, circulation has taken a more prominent role in the initial
management of cardiac arrest.
(C-A-B)
Rescue breathing is performed after the initiation of excellent chest compressions and
definitive airway management may be delayed if there is adequate rescue breathing without
an advanced airway in place
In the non-cardiac arrest situation, the other initial interventions for ACLS include
administering oxygen, establishing vascular access, placing the patient on a cardiac and
oxygen saturation monitor, and obtaining an electrocardiogram
Unstable patients must receive immediate care, even when data are incomplete or
presumptive
Stable patients require an assessment of their electrocardiogram in order to provide
appropriate treatment consistent with ACLS guidelines
Is the rhythm fast or slow?
Are the QRS complexes wide or narrow?
Is the rhythm regular or irregular
AIRWAY MANAGEMENT DURING ACLS
Ventilation is performed during CPR to maintain adequate oxygenation and to eliminate
carbon dioxide, although this is less important. Nevertheless, during the first few minutes
following sudden cardiac arrest (SCA), oxygen delivery to the brain is limited primarily by
reduced blood flow. Therefore, in adults, the performance of excellent chest compressions
takes priority over ventilation during the initial period of basic life support. In settings with
multiple rescuers or clinicians, ventilations and chest compressions are performed
simultaneously
we know that hyperventilation is harmful, as it leads to increased intrathoracic pressure,
which decreases venous return and compromises cardiac output
ACLS Guidelines recommend 8 to 10 breaths per minute with an advanced airway in plac
but we believe 6 to 8 breaths are adequate
Elements of BLS (4 of 8)
The System Components of
CPR (1 of 2)
Source: American Heart Association
Coronary Perfusion
Pressure (mm Hg)
Survival is related to arterial pressures
generated by chest compressions
35
30
25
20
15
10
5
0
Not the pH
Not the oxygen content
It’s all about Coronary
Perfusion Pressure !
24-hour
Survivors
Resuscitated
But
Expired
Could
Not
Resuscitate
Survival better with compression rate of
100 – 120 compressions/minute
Mean rate, ROSC group
90 ± 17 *
Number of 30 sec segments
210
p=0.003
Mean rate,
no ROSC group
79 ± 18 *
180
150
No ROSC
ROSC
120
90
60
30
0
10-20
20-30
30-40
40-50
50-60
60-70
70-80
80-90
90-100 100-110 110-120
Chest compression rate (min-1)
Abella et al, 2005
>120
Shock success, percent
Shock success by compression depth
p=0.02
n=10
n=13
n=14
n=5
Compression depth, inches
Edelson et al, 2006
Shock success, percent
Shock success by pre-shock pauses
100
80
90%
60
p=0.003
64%
55%
40
20
10%
0
≤10.3
(n=10)
10.5-13.9
(n=11)
14.4-30.4
(n=11)
≥33.2
(n=10)
Pre-shock pause, seconds
Edelson et al, 2006
Assessing ABCs (14 of 18)
Assessing ABCs (18 of 18)
When to Stop BLS (1 of 2)
• Once you begin CPR, continue until (STOP
acronym):
– S Patient Starts breathing and has a pulse
– T Patient is Transferred to another trained
responder
– O You are Out of strength
– P Physician directs to discontinue
When to Stop BLS (2 of 2)
• “Out of strength” does not just mean tired,
but physically unable to continue.
ACLS Survey
• A––Airway
•
■ Maintain patent airway.
•
■ Maintain proper head position.
•
■ Use oropharyngeal or nasopharyngeal airway if indicated.
•
■ Use advanced airway if indicated (laryngeal mask airway [LMA],
•
laryngeal tube, esophageal-tracheal tube, endotracheal tube [ET]).
• ■ B––Breathing
•
■ Perform bag-mask ventilation.
•
■ Provide supplemental oxygen.
•
■ Monitor adequacy of ventilation and oxygenation.
•
• Ensure adequate chest rise.
•
• Use CO2 detector or quantitative waveform capnography.
•
• Measure oxygen saturation.
•
• Avoid excessive ventilation.
ACLS Survey
• ■ C––Circulation
•
■ Provide high-quality CPR.
•
■ Monitor cardiac rhythm.
•
■ Initiate prompt defi brillation/cardioversion when indicated.
•
■ Establish IV/IO access.
•
■ Administer medication when indicated.
•
■ Administer volume resuscitation when indicated.
•
■ Assess for ROSC.
• D––Differential Diagnosis:
•
■ Identify and treat potentially reversible causes.
Hypokalemia
Hypokalemia should be suspected in patients on diuretics,
those
with a recent history of vomiting or diarrhea, and malnourished
patients, especially alcoholic and elderly patients.
ECG:
flattened T waves and prominent U waves, in leads V2–V3, ST
depression, QT prolongation, There could be increased
PVCs,(NSVT).
Emergent treatment
for a potassium level <2.5 mEq/L or signifi cant ventricular ectopy
includes potassium repletion with potassium chloride IV, maximum
20 mEq/hr by central line, or 10 mEq/hr by peripheral line.
Hyperkalemia
should be suspected in patients with a history of renal
failure, diabetes with hyperglycemia, recent dialysis, metabolic
acidosis, or use of potassium-sparing medications such as
spironolactone, ACE inhibitors, or angiotensin-receptor blockers
ECG:Tall&peaked T waves; small P waves or loss of P waves; and QRS widening.
Patients are at risk for fatal arrhythmias. With severe hyperkalemia, patients may
present in cardiac arrest with sine waves (the P wave disappears and the QRS and
T wave merge in an oscillating pattern) on the ECG.
Emergent treatment includes administration of IV calcium chloride to stabilize
myocardial cell membranes, and IV sodium bicarbonate to shift potassium out of the
vascular space and into body cells. In the
absence of cardiac arrest, other treatments include IV insulin plus
glucose or nebulized albuterol to shift potassium into cells, and IV
furosemide, sodium polystyrene sulfonate (Kayexalate), or dialysis
to increase potassium excretion.
Hypovolemia
The ECG may be normal with a rapid heart
rate.
Resuscitation measures in cardiac arrest
will be ineffective unless intravascular
volume is replaced rapidly.
Hypoxia:
Hypoxia (low arterial and tissue oxygen) should be suspected
in patients with a history of asthma, COPD, or CHF. Causes of hypoxia
include airway obstruction, pulmonary embolus, pulmonary edema,
signifi cant pleural effusions, pneumothorax or hemothorax, severe
asthma attack, COPD exacerbation, or respiratory infection.
Hypothermia:
A central body temperature of
34°–36°C (93.2°–96.8°F) is mild hypothermia; 30°–34°C (86–93.2°F) is
moderate hypothermia; <30°C (<86°F) is severe hypothermia.
ECG:
sinus bradycardia with prolonged PR and QT intervals ,& a J or Osborne
wave may be noted,in inf.leads&V4-V6 ,VT,VF
Mild hypothermiawarm room
Moderate hypothermiahot-water bottles
Severe hypothermia warm IVfl uids
and warm oxygen.
Hydrogen ion (acidosis)
Tension pneumothorax
Thrombosis (pulmonary or
coronary)
Tamponade
Toxins
.
.
.
37
Multifocal Atrial Tachycardia (MAT)
38
39
SVT
40
41
NSRSVT
42
43
Atrial Flutter (A-flutter)
44
45
AF
46
47
Junctional Arrhythmias
48
49
Idioventricular Rhythm
50
51
Premature Ventricular
Contraction: Multiform
52
53
SMVT
54
55
SPMVT
56
57
TDP
58
59
VF
60
61
CHB
62
63
Mobitz II
64
65
Mobitz I
66
Overview of ACLS
Pharmacology
and
Update on New ACLS
Guidelines
Objectives
• Pharmacists should be able to identify:
Why?
…we use an agent
When?
…to use an agent
How?
…to use an agent
What?
...to watch for
• To familiarize the pharmacist with the ACLS
algorithms
• To help the pharmacist become comfortable
with the crash cart
• To introduce the needless delivery system
Routes of Administration
Intravenous
• Preferred route
Endotracheal
·
·
·
·
2-2.5 X’s IV dose in 10ml volume
Each dose is followed by 10 ml NS flush down the ET
tube
(Ex. epinephrine, atropine, lidocaine, diazepam,
naloxone)
Absorption occurs at alveolar capillary interface
Intraosseous (active bone marrow)
· Pediatric patients without IV access
Other: Sublingual, intracardiac, IM, SC (poor
absorption)
Epinephrine
WHY?
• Natural catecholamine with  and ß-adrenergic agonist activity
•
Results in:
•  flow to heart and brain
•  SVR, SBP, DBP
•  electrical activity in the myocardium & automaticity ( success
with defibrillation)
• myocardial contraction (for refractory circulatory shock (CABG))
•  increases myocardial oxygen requirements
• Primary benefit: -vasoconstriction
• ß-adrenergic activity controversial b/c  myocardial work
WHEN?
• VF/VT, asystole, PEA, bradycardias
Epinephrine
HOW?
• High dose versus standard dose?
• Higher ROSC with high dose, but no change in survival
• High doses may exacerbate postresuscitation myocardial dysfunction
Recommendations:
•
•
•
•
Class I: 1 mg IV q 3 - 5 min
Class IIb: 2-5mg IVP q3-5min, or 1mg-3mg-5mg
Class Indeterminate: high-dose 0.1mg/kg IVP q3-5min
Infusion for  HR & BP (IIb)
• 1mg in 250ml NS or D5W - infuse @ 1-10 mcg/min
• ET Dose=2-2.5 times IV dose
What to watch for?
•
Tachycardia, hypertension, myocardial ischemia, acidosis
Pulseless Ventricular
Fibrillation
or Tachycardia
• In ACLS, always assume VF - most common
• 85%-95% of survivors have VF
• Survival dependant on early defibrillation
• Medications indicated only after 3 failed
shocks
Drugs for VF/PVT
• Epinephrine - Why? How? What?
• Vasopressin - Why? How? What?
• Amiodarone
• Magnesium
• Procainamide
• Lidocaine
Drugs Used to Improve Cardiac Output and Blood
Pressure
Sodium Bicarbonate
WHY?
decreases
drugs
Enhances K+ shift intracellularly, buffers
acidosis,
toxicity of TCA’s, increases clearance of acidic
WHEN?
Class I - hyperkalemia
Class IIa - bicarbonate-responsive acidosis metabolic
acidosis secondary to loss of bicarb (renal/GI);
overdoses (TCAs, phenobarbital, aspirin)
Class IIb - protracted arrest in intubated patients
Class III - hypoxic lactic acidosis
HOW?
1 mEq/kg IVP, 0.5mEq/kg q10 min prn
WHAT?
May worsen outcome if not intubated/ventilated.
Metabolic alkalosis, decreased O2 delivery to
tissues, hypokalemia,
CNS acidosis, hypernatremia,
hyperosmolarity
Tachycardia - Atrial
Fibrillation/Flutter
4 Clinical Features:
• Unstable?
• Impaired cardiac function?
• WPW?
• Duration? <48h, or > 48h?
• Focus - treat unstable patients urgently
• Control ventricular response  convert 
anticoagulate
Drugs Used in Afib/AFlutter
•
•
•
•
•
•
Calcium channel blockers
Beta-blockers
Digoxin
Amiodarone
Procainamide
Flecainide (IV form in ACLS -not available
in US)
• Propafenone (IV form in ACLS -not
available in US)
• Sotalol (IV form in ACLS -not available in
US)
Stable Monomorphic Ventricular Tachycardia
Preserved
Cardiac
Function
NOTE!
May go directly to
cardioversion
Medications: any one
•Procainamide (IIA)
•Sotalol (IIA)*
•Amiodarone (IIB)
•Lidocaine (IIB)
*Not yet available in the US.
Impaired
LV
EF<40% or
CHF
Amiodarone (IIB)
•150 mg IV bolus over 10 min
•may repeat 150mg q1015min or start infusion
OR
Lidocaine (IIB)
•0.5 to 0.75 mg/kg IV push
Then use
•Synchronized
cardioversion
Narrow-Complex Supraventricular
Tachycardia
• Vagal stimulation
• Adenosine
• Junctional
• 1. EF > 40% - Amiodarone, B-blocker, CCB
• 2. EF <40%, CHF - Amiodarone
• PSVT
• EF>40% - CCB, BB, digoxin, DC cardioversion
(procainamide, amiodarone, sotalol)
• EF<40%, CHF - DC cardioversion; digoxin,
amiodarone,
• MAT
• EF>40% -No DC cardioversion; CCB, BB,
amiodarone
• EF<40% -No DC cardioversion; amiodaonre,
diltiazem
Wide-Complex Tachycardia
• “Wide” …. Prolonged QRS or QRST interval
• HR > 120 bpm (ex. VT, sinus tachycardia,
A.flutter)
• Establish diagnosis - 12-lead ECG
• Adenosine if SVT- slows AV conduction.
Short-lived hypotension
• Amiodarone (IIa) normal LV function
• Amiodarone (IIb) impaired LV function
• Procainamide (IIa)- terminates SVT due to
altering conduction across accessory pathways
• Lidocaine if VT
• Sotalol, propafenone, flecainide
Pulseless Electrical Activity
• PEA… no pulse with + electrical activity (not
VF/VT)
• Reversible if underlying cause is reversed (5 H’s, 5
T’s)
• Hypovolemia, hypoxia, hydrogen ion (acidosis),
hyper/hypokalemia, hyper/hypothermia
• Tablets, tamponade, tension pneumothorax, thrombosis (ACS),
thrombosis (PE)
Intervention
Comments/Dose
Problem
intervene
Search for the probable cause and
(HCO3)
Epinephrine
1 mg IV q3-5 min.
Atropine
With slow heart rate, 1 mg IV q3-5 min.
(max. dose 0.04 mg/kg)
Atropine
WHY?
Anticholinergic/direct vagolytic
Enhances sinus node automaticity and AVN
conduction
WHEN?
PEA, symptomatic sinus bradycardia, asystole,
HOW?
Bradycardia: 0.5 -1 mg IV q3-5 min
Asystole: 1 mg IV q 3-5 min
Max = 0.04 mg/kg or 3 mg
ET Dose=1-2mg diluted in 10ml
Paradoxical bradycardia with insufficient dose (<0.5mg)
WHAT?
Tachycardia; 2nd or 3rd degree AV block
(paradoxical
slowing may occur), MI (may
worsen ischemia/HR)
Bradycardia
“All Patients Deserve Empathy”
(The sequence reflects interventions for increasingly severe bradycardia)
•
•
Absolute or relative
Serious signs and symptoms (CP, hypotension, mental status changes)
Mnemonic
Intervention
Comments/Dose
All
Atropine
0.04 mg/kg)
0.5-1.0 mg IVP q 3-5 min (max 0.03-
Patients
S/S
Pacing
Use Transcutaneous Pacing if severe
Deserve
Dopamine
5-20 µg/kg/min.
Empathy
Epinephrine
2-10 µg/min.
Dopamine
WHY?
NE precursor
Stimulates DA,  & -adrenergic receptors
(dose-related)
Want  -stimulation, for bradycardia-induced
hypotension
WHEN?
Hypotension/shock
HOW?
renal: 2 - 5 mcg/kg/min
cardiac: 5 - 10 mcg/kg/min (B1 & alpha)
vascular: 10 - 20 mcg/kg/min (alpha)
Preparation:
400 mg/250 ml D5W or NS
WHAT?
Tachycardia, tachyphylaxis, proarrhythmic
If requiring > 20mcg/kg/min consider adding
NE
ACLS Algorithms
Asystole
• Consider possible causes and treat accordingly
(ex.hypoxemia, hyper/hypokalemia, acidosis)
Acronym “TEA”
T
Transcutaneous Pacing (TCP) (Class IIb)
Only
effective with early
implementation along with
appropriate interventions and medications
E
Epinephrine 1 mg IV q3-5 min.
A
Atropine 1 mg IV q3-5 min. (max. dose
0.04 mg/kg)
• Discourage shocking due to excess parasympathetic
discharge
Acute Myocardial Infarction
• “Call first, call fast, call 911”
• Oxygen 4L/min??
• NTG SL, paste or spray; if BP > 90 mm Hg, IV
NTG
• Morphine IV
• ASA PO (I)
• Thrombolytics? (I) - within 6 hours of
symptoms, (II) if > 6hr
• IV heparin Or Enoxaparine
• B-blockers
• Clopidogrel
• Captoprile
Drugs Used to Improve Cardiac
Output and Blood Pressure
Dobutamine
Action:
B1- adrenergic activity
Indication:
Inotrope in heart failure/hypotension
Dose:
2 - 20 mcg/kg/min
Preparation:
250 mg/250 ml D5W or NS
Caution:
ischemia
tachyarrhythmias,worsens myocardial