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 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
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 Conduction Velocity
Refractory Period Automaticity Ion Block
Ia Quinidine Procainamide Disopyramide
Sodium
Ib Lidocaine Mexiletine Tocainide
0/
Sodium (fast on-off)
Ic Flecainide Propafenone Moricizine
0
Sodium (slow on-off)
II Beta-Blockers Calcium
III Amiodarone Bretylium Sotalol
0
0
Potassium
IV Verapamil Diltiazem
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), wide-complex 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 20-
30ml, 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 PVC’s (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 µg/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? 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 WHAT? 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 post- MI patients, USA
HOW? Atenolol: 2.5-5 mg IV over 5 min Metoprolol: 5 - 10 mg IVP q 5 min Propranolol: 0.1 mg/kg IV divided into 3 doses @ 2 - 3 min intervals Esmolol: 500 mcg/kg over 1 min Inf @ 50 mcg/kg/min WHAT? 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 H’s, 5 T’s)
• 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 (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
• 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 & ß-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 TCA’s, 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
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