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ACLS
ACLS
Norepinephrine Nitroglycerine
-severe hypotention -ACS, CHF, hypertensive urgency with ACS
-low total peripheral resistance
Epinephrine increases SVR, BP, HR,
Dopamine contractility, automaticity
-hypotension increases blood flow to the heart
-symptomatic significant bradycardia and brain, AV conduction
velocity
Dubutamine Norepinephrine Naturally occurring potent
vasoconstrictor and inotropic
-severe systolic heart failure
agent
usually induces renal and
Sodium bicarbonate splanchnic vasoconstriction
-hyperkalemia Dopamine Catecholamine, alpha and beta
-tricyclic or phenobarbital overdose adrenergic receptor agonist and
-patients with pre-existing metabolic acidosis peripheral dopamine receptor
agonist
Furosemide Dobutamine synthetic sympathomimetic
-diuretic amine with positive inotropic
action and minimal positive
Adenosine chronotropic activity at low
-used if SVT is suspected doses (2.5 ug/kg per min) but
moderate chronotropic activity
CCB at higher doses
Sodium reverses acidosis caused by
-control ventricular response rate
Bicarbonate global hypo perfusion
Furosemide potent diuretic
Verapamil direct venodilating effect in
-alternative drug for Adenosine patients with acute pulmonary
edema
Beta blockers Adenosine Depresses AV node and sinus
-Second line after adenosine node activity
CCB slow conduction
Amiodarone increase refractoriness in AV
-after defibrillation and epinephrine in cardiac arrest node
with persistent arrhythmias in severely impaired LV may control ventricular
function response rate in patients with
AF, Flutter or MAT
Lidocaine Verapamil effective in stable narrow
-VF/ Pulseless VT that persist after defibrillation complex PSVT
Beta Blockers Class I in ACS
-Control of hemodynamically compromising PVCs
slow ventricular response
(AF/flutter, MAT) Verapamil -alternative drug for Adenosine
convert SVT Beta blockers -Second line after adenosine
Amiodarone affects Na, K, Ca channels, as
well as alpha and beta Amiodarone -after defibrillation and epinephrine in
adrenergic blocking properties cardiac arrest with persistent arrhythmias in severely
prolongs action potential impaired LV function
duration, refractory period,
decreases AV node conduction
Lidocaine -VF/ Pulseless VT that persist after
and sinus node function
defibrillation, Control of hemodynamically
Atropine parasympatholytic action
accelerates rate of sinus node compromising PVCs
discharge
improves AV conduction Magnesium -effectively terminates torsades de
reverses cholinergic mediated pointes
decreases in heart rate, systemic Atropine -Symptomatic bradycardia (Class I), AV
vascular resistance and blood block Nodal level, use with caution in MI
pressure Digoxin -Supraventricular arrhythmias (AF/flutter)
Epinephrine increases SVR, BP, HR, Nitroglycerine -ACS, CHF, hypertensive urgency
contractility, automaticity with ACS
increases blood flow to heart
and brain, AV conduction EPINEPHRINE
velocity -increases SVR, BP, HR, contractility, automatic
alpha adrenergic effects can
-increases blood flow to the heart, brain
increase coronary and cerebral
perfusion during CPR -increases AV conduction velocity
Digoxin Enhances central and peripheral
vagal tone Epinephrine increases SVR, BP, HR,
Slows SA node discharge rate contractility, automaticity
Shortens atrial refractorines increases blood flow to the heart
Prolongs AV nodal and brain, AV conduction
refractoriness through ANS velocity
effect Norepinephrine Naturally occurring potent
Nitroglycerine Increases venodilation vasoconstrictor and inotropic
Decreases preload agent
Decreases oxygen consumption usually induces renal and
Dilates coronary arteries splanchnic vasoconstriction
Increases collateral flow Dopamine Catecholamine, alpha and beta
adrenergic receptor agonist and
Norepinephrine -severe hypotension, low total peripheral dopamine receptor
peripheral resistance agonist
Dobutamine synthetic sympathomimetic
amine with positive inotropic
Dopamine –hypotension, symptomatic significant
action and minimal positive
bradycardia chronotropic activity at low
doses (2.5 ug/kg per min) but
Dubutamine -severe systolic heart failure moderate chronotropic activity
at higher doses
Sodium bicarbonate –hyperkalemia, tricyclic or Sodium reverses acidosis caused by
phenobarbital overdose, patients with pre-existing Bicarbonate global hypo perfusion
metabolic acidosis Furosemide potent diuretic
direct venodilating effect in
Furosemide -diuretic patients with acute pulmonary
Adenosine -used if SVT is suspected edema
CCB -control ventricular response rate Adenosine Depresses AV node and sinus
node activity
CCB slow conduction
increase refractoriness in AV
node
may control ventricular
response rate in patients with
AF, Flutter or MAT
Verapamil effective in stable narrow
complex PSVT
Beta Blockers Class I in ACS
slow ventricular response
(AF/flutter, MAT)
convert SVT
Amiodarone affects Na, K, Ca channels, as
well as alpha and beta
adrenergic blocking properties
prolongs action potential
duration, refractory period,
decreases AV node conduction
and sinus node function
Atropine parasympatholytic action
accelerates rate of sinus node
discharge
improves AV conduction
reverses cholinergic mediated
decreases in heart rate, systemic
vascular resistance and blood
pressure
Epinephrine increases SVR, BP, HR,
contractility, automaticity
increases blood flow to heart
and brain, AV conduction
velocity
alpha adrenergic effects can
increase coronary and cerebral
perfusion during CPR
Digoxin Enhances central and peripheral
vagal tone
Slows SA node discharge rate
Shortens atrial refractorines
Prolongs AV nodal
refractoriness through ANS
effect
Nitroglycerine Increases venodilation
Decreases preload
Decreases oxygen consumption
Dilates coronary arteries
Increases collateral flow