Acls

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