Advanced Cardiac Life Support

Algorithm

Drugs

Class I: definitely helpful, excellent

Class II:
Class II a -probably helpful;
good to very good
Class II b -possibly helpful; fair
to good
Class Indeterminate: insufficient evidence; no harm,
but no benefit
Class III:
possibly harmful

 Epinephrine - Why? How? What?

Vasopressin - Why? How? What?

Amiodarone
Magnesium
Procainamide

Lidocaine

WHY?
Natural catecholamine with and -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

-adrenergic activity controversial b/c myocardial work
WHEN?
VF/VT, asystole, PEA, bradycardias

WHEN?
Alternative to epinephrine for shock-refractory VT/VF
WHY?
Natural antidiuretic hormone
Potent vasoconstrictor by stimulation of SM -V1 receptors :

BP & SVR; CO, HR, myocardial O2 consumption and contractility

Does not myocardial oxygen consumption

Not affected by severe acidosis
Class IIb for shock-refractory VF
Class Indeterminate for PEA, asystole
Half life = 10-20 minutes
Dose?
40 Units IVP - one time only!!!

Class

Drug

Ia

Quinidine
Procainamide
Disopyramide

Ib

Lidocaine
Mexiletine
Tocainide

Ic

Conduction
Velocity

Refractory Period

Automaticity

Ion Block
Sodium

Sodium
(fast on-off)

0/

Flecainide
Propafenone
Moricizine

Sodium
(slow on-off)

II

Beta-Blockers

Calcium

III

Amiodarone
Bretylium
Sotalol

Potassium

IV

Verapamil
Diltiazem

0
Calcium

WHY?
Class III antiarrhythmic (characteristics of all classes)
Na, K and Ca channel blocker & & -adrenergic blocker
Prolongs AP and RP
Decreases AV conduction velocity & SN function

New Recommendations (WHEN?):

pulseless VT or VF (IIb)
hemodynamically stable VT (IIb), polymorphic VT (IIb), widecomplex tachycardia uncertain origin (IIb)
refractory PSVT (preserved function, IIa; impaired function IIb)
atrial tachycardia (IIb)
cardioversion of AF (IIa)

HOW?
Cardiac arrest (PVT/VF) - 300mg IVP diluted in 2030ml, may repeat with 150mg in 10 minutes, or
start infusion (max=2..2 g/24h)
Atrial & ventricular arrhythmias in impaired hearts

150mg IVP over 10 min

May repeat q10-15 min, or start gtt 1mg/min x 6 hours,
then 0.5mg/min x 18 h

WHAT?
Hypotension, bradycardia (slow rate, fluids)

WHY?

Magnesium deficiency causes arrhythmias

Facilitates ventricular repolarization by
enhancing intracellular potassium flux, dilates
coronary arteries

WHEN?

Suspected hypomagnesemia, pulseless VT/VF,

torsade de pointes

HOW?

Class IIa in suspected hypomagnesemia, TdP,

and Class IIb in VF/VT: 1 - 2gm slow IVP in
100ml

WHAT?

Hypotension at large doses

WHY?

Type IB antiarrhythmic
Affects fast Na+ channels, shortens refractory period
Suppresses spontaneous depolarization
Local anesthetic, increases fibrillation threshold
Suppresses ventricular ectopy post-MI
Without effecting myocardial contractility, BP or AV nodalconduction

WHEN?
SECOND-CHOICE agent
VT/VF refractory to electrical countershock and epinephrine
(Indeterminate)
Control of PVCs (Indeterminate)
Hemodynamically stable VT (IIb)
Not for routine prophylaxis post-MI, however, accepted in high-risk
patients (hypokalemia, myocardial ishchemia, LV dysfunction)

HOW?

Class IIa: 1 - 1.5 mg/kg IVP q5 - 10 min (max=3mg/kg)

Infusion (with pulse): 1 - 4 mg/min (if pulse is regained)
Therapeutic Levels: 1.5-6 g/ml
ET Dose: 2-2.5 times IV dose
Preparation: 1-2 gm/250 ml D5W or NS

WHAT?

Hepatic metabolism, renal elimination

Bradycardia, cardiac arrest, seizures
Lidocaine toxicity/neurotoxicity - twitching, LOC,
seizures, coma
Lidocaine levels persist in low CO states

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)

WHY?

Blocks inward flow of Ca and Na, slows conduction, RP in

AVN Terminate reentrant arrhythmias requiring AVN
conduction Control ventricular response rate in AF/AFl
Coronary vasodilation May exacerbate CHF

Verapamil:

Negative inotrope & chronotrope (good anti-ischemic)

Class I for acute and preventative SVT

Diltiazem:

Direct negative chronotropic effect, mild negative inotrope

Highly effective in controlling ventricular response in A Fib

WHEN?

Control ventricular response rate in patients with AF/Fl, or

MAT
Verapamil: PSVT not requiring cardioversion

HOW?

WHAT?

Verapamil:

2.5 - 5 mg IVP, over 2 min

(max=30mg)
Inf @ 5-10 mg/hr

Diltiazem:

0.25 mg/kg IVP, may repeat with

0.35mg/kg in 15 min
Infuse @ 5-15 mg/hr

Contraindicated in wide QRS complex tachycardias and

ventricular tachycardias, exacerbation of CHF in
patients with LV dysfunction
Transient decrease in BP
Avoid in sick sinus syndrome of AV block (w/out pacer)
May potentiate digoxin toxicity.

Incompatible with bicarbonate, epinephrine, furosemide

WHY?

B-adrenergic blockade, slows conduction and

increases refractory period in AV node

WHEN?

AMI (reduces rate of reinfarction), reduces

recurrent ischemia and incidence of VF in postMI patients, USA

HOW?

Atenolol:
Metoprolol:
Propranolol:
Esmolol:

WHAT?

2.5-5 mg IV over 5 min

5 - 10 mg IVP q 5 min
0.1 mg/kg IV divided into 3
doses @ 2 - 3 min intervals
500 mcg/kg over 1 min
Inf @ 50 mcg/kg/min

Hypotension, bradycardia, AV block, overt

heart failure or severe bronchospasm/COPD

 PEA no pulse with + electrical activity (not VF/VT)

Reversible if underlying cause is reversed (5 Hs, 5 Ts)

Hypovolemia, hypoxia, hydrogen ion (acidosis), hyper/hypokalemia,
hyper/hypothermia
Tablets, tamponade, tension pneumothorax, thrombosis (ACS),
thrombosis (PE)

Problem

Search for the probable cause and intervene

(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)

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)
Incompatible with bicarbonate, epinephrine & norepinephrine

 Vagal stimulation
Adenosine

WHY?

Endogenous nucleoside, slows conduction through the

AV node and can interrupt AV nodal reentry pathways

WHEN?

PSVT (half-life=10 sec)

If PSVT persists may want longer acting agent
(verapamil or diltiazem)

HOW?

6 mg rapid IV over 1 - 3 sec, followed by 20 ml

NS flush. May repeat in 1-2min with 12 mg dose.
Max.=30 mg

WHAT?

Flushing, dyspnea, chest pain, post-conversion

bradycardia
Drug interaction with theophylline, dipyridamole

Atropine
Dopamine
Epinephrine

WHY?

NE precursor
Stimulates DA, & -adrenergic receptors (doserelated)
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

Oxygen
Nitroglycerin
Morphine Sulfate
Aspirin
Clopidogrel
Thrombolytics
Heparin
Beta-blockers
Glycoprotein IIb/IIIa receptor antagonists
ACE inhibitor
HMG CoA reductase

Why?
increases hemoglobin saturation, improves tissue
oxygenation
supply to ischemic tissues
16-17% oxygen from mouth-to-mouth
When?
Must give supplemental oxygen in ACLS
Always for MI
How?
NC 4 L/min, intubation, etc
Goal - Osat=97-98%
Confirm tube placement

WHY?
binds to receptors on vascular smooth muscle

vasodilation (venous > arterial)

venous BF to heart (preload) & O2 consumption
dilates coronary arteries - myocardial blood supply
antagonizes vasospasm
increases collateral flow to ischemic myocardium
inhibits infarct expansion
decreases pain

WHEN?
Ischemic chest pain; pulmonary edema (when SBP>100); AMI
SL NTG -drug of choice for angina
IV NTG - drug of choice for unstable angina or AMI
Congestive heart failure with ischemia
HOW?
IV: 10-20 mcg/min, increase by 5-10 mcg/min q5-10 min
until desired effect or hemodynamic compromise
SL: 1 tablet (0.4mg) SL q5min times 3
Spray: 1 spray onto oral mucosa

Preparation:

50 mg/250 ml D5W or NS

Cautions:
hypotension - treat with fluids, and rate reduction/elimination
bradycardia - vasovagal reflex to hypotension
treat with fluids, rate reduction, atropine
reflex tachycardia also a concern
headache, dizziness - may be diminished by laying down
patients develop tachyphylaxis to effects - promote nitrate-free
periods, intermittent dosing and lowest-possible doses

WHY? (Pain can catecholamines - BP, HR, O2 demands)

Opiate analgesic
pain, preload and afterload, SVR, anxiety
Relieves pulmonary congestion, myocardial oxygen demand
WHEN?
Pain, pulmonary edema, BP > 90 mm Hg
HOW?
1-3mg IVP (2-15 mg IVP q15-30 min prn)
CAUTION?
Respiratory & CNS depression, bradycardia, hypotension, N/V

 Volume:

fluids, blood, vasopressors

Pump:
s/s of shock - vasopressors; no s/s shock -

dobutamine
BP (>100 mm Hg) - NTG, Nitroprusside
pulmonary edema -furosemide 0.5-1mg/kg,
morphine 1-3mg, NTG SL, oxygen/intubate

Rate: see algorithms

Action:

Alpha & -adrenergic stimulation, increases

contractility and HR, vasoconstriction, improves
coronary blood flow

Indication:

Shock refractory to fluid replacement, severe

hypotension

Dose:

0.5 - 1 mcg/min
refractory shock = 8 - 30 mcg/min

Preparation:

4-8mg/250 ml D5W or NS

Caution:

Hypertension, myocardial ischemia, cardiac

arrest, palpitations

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:

tachyarrhythmias,worsens myocardial ischemia

Action:

Antihypertensive, peripheral vasodilator,

reduces afterload, increases CO and relieves
pulmonary congestion

Indication:

Hypertension, AMI, CHF

Dose:

0.1 - 5 mcg/kg/min, and titrate up to

10mcg/kg/min

Preparation:

50 mg/250 ml D5W

Caution:

Cyanide and thiocyanate toxicity, hypotension

WHY?

Enhances sodium shift intracellularly, buffers acidosis,

decreases toxicity of TCAs, increases clearance of acidic drugs

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
Incompatible with calcium, epinephrine, atropine,
norepinephrine, isoproterenol