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Epinephrine increases SVR, BP, HR, vascular resistance and blood

contractility, automaticity pressure


increases blood flow to the heart Epinephrine increases SVR, BP, HR,
and brain, AV conduction contractility, automaticity
velocity increases blood flow to heart
Norepinephrine Naturally occurring potent and brain, AV conduction
vasoconstrictor and inotropic velocity
agent alpha adrenergic effects can
usually induces renal and increase coronary and cerebral
splanchnic vasoconstriction perfusion during CPR
Dopamine Catecholamine, alpha and beta Digoxin Enhances central and peripheral
adrenergic receptor agonist and vagal tone
peripheral dopamine receptor Slows SA node discharge rate
agonist Shortens atrial refractorines
Dobutamine synthetic sympathomimetic Prolongs AV nodal
amine with positive inotropic refractoriness through ANS
action and minimal positive effect
chronotropic activity at low Nitroglycerine Increases venodilation
doses (2.5 ug/kg per min) but Decreases preload
moderate chronotropic activity Decreases oxygen consumption
at higher doses Dilates coronary arteries
Sodium reverses acidosis caused by Increases collateral flow
Bicarbonate global hypo perfusion
Furosemide potent diuretic
direct venodilating effect in NE Severe hypotension
patients with acute pulmonary Low total peripheral resistance
edema Dopamine Hypotension
Adenosine Depresses AV node and sinus Symptomatic significant
node activity bradycardia
CCB slow conduction Dobutamine Severe systolic heart failure
increase refractoriness in AV Sodium Hyperkalemia
node Bicarbonate tricyclic or phenobarbital
may control ventricular overdose
response rate in patients with Patients with pre-existing
AF, Flutter or MAT metabolic acidosis
Verapamil effective in stable narrow Furosemide Diuretic
complex PSVT Adenosine used if SVT is suspected
Beta Blockers Class I in ACS CCB control ventricular response rate
slow ventricular response in AF, Flutter, MAT
(AF/flutter, MAT) Verapamil Alternative drug for Adenosine
convert SVT Beta Blockers second line after adenosine
Amiodarone affects Na, K, Ca channels, as Amiodarone after defibrillation and
well as alpha and beta epinephrine in cardiac arrest with
adrenergic blocking properties persistent arrhythmias in severely
prolongs action potential impaired LV function
duration, refractory period, Lidocaine VF/ Pulseless VT that persist after
decreases AV node conduction defibrillation
and sinus node function Control of hemodynamically
Atropine parasympatholytic action compromising PVCs
accelerates rate of sinus node Magnesium effectively terminates torsades de
discharge pointes
improves AV conduction Atropine symptomatic bradycardia (Class I)
reverses cholinergic mediated AV block Nodal level
decreases in heart rate, systemic use with caution in MI
Digoxin Supraventricular Arrhythmias CCB slow conduction Alternative
(AF/Flutter) increase drug for
Nitroglycerine ACS, CHF, hypertensive urgency refractoriness in Adenosine
with ACS AV node
may control
ventricular
Epi increases SVR, BP, Severe response rate in
HR, contractility, hypotension patients with AF,
automaticity Low total Flutter or MAT
increases blood peripheral Verapamil effective in stable second line
flow to the heart resistance narrow complex after adenosine
and brain, AV PSVT
conduction velocity Beta Blockers Class I in ACS after
NE Naturally occurring Hypotension slow ventricular defibrillation
potent Symptomatic response and
vasoconstrictor and significant (AF/flutter, MAT) epinephrine in
inotropic agent bradycardia convert SVT cardiac arrest
usually induces with persistent
renal and arrhythmias in
splanchnic severely
vasoconstriction impaired LV
Dopamine Catecholamine, Severe systolic function
alpha and beta heart failure Amiodarone affects Na, K, Ca Severe
adrenergic receptor channels, as well as hypotension
agonist and alpha and beta Low total
peripheral adrenergic blocking peripheral
dopamine receptor properties resistance
agonist prolongs action
Dobutamine synthetic Hyperkalemia potential duration,
sympathomimetic tricyclic or refractory period,
amine with positive phenobarbital decreases AV node
inotropic action and overdose conduction and
minimal positive Patients with sinus node function
chronotropic pre-existing Lidocaine VF/ Pulseless
activity at low metablic VT that persist
doses (2.5 ug/kg acidosis after
per min) but defibrillation
moderate Control of
chronotropic hemodynamica
activity at higher lly
doses compromising
NaHCO3 reverses acidosis Diuretic PVCs
caused by global Magnesium effectively
hypo perfusion terminates
Furo potent diuretic used if SVT is torsades de
direct venodilating suspected pointes
effect in patients Atropine parasympatholytic symptomatic
with acute action bradycardia
pulmonary edema accelerates rate of (Class I)
Adenosine Depresses AV node control sinus node AV block
and sinus node ventricular discharge Nodal level
activity responsive in improves AV use with
AF, Flutter, conduction caution in MI
MAT reverses
cholinergic refractory VT/VF
mediated decreases Magnesium 1-2 gm (8-16 mEqs) mixed in 50-
in heart rate, 100 ml D5W given over 15-60 mins
systemic vascular followed by 0.5 to 1 gm IV infusion
resistance and Atropine 0.5 mg every 3-5 mins
blood pressure Epi 2-10 mcg/ min
Epi increases SVR, BP, (1 mg in 500cc of D5W or NS by
HR, contractility, continuous infusion)
automaticity Digoxin acute loading dose 0.5 to 1 mg IV
increases blood or PO
flow to heart and 0.004 to 0.006 mg/kg initially over
brain, AV 5 min
conduction velocity then 0.002 to 0.003 mg/kg at 408 hr
alpha adrenergic interval
effects can increase total of 0.008 to 0.012 mg/kg
coronary and divided to 8 to 16 hrs
cerebral perfusion Nitroglycerine IV bolus 12.5 to 25 mcg (if no SL
during CPR or spray given)
Digoxin Enhances central Supra infusion-10 mcg/min titrate to effect
and peripheral ventricular increases by 10 mcg/min every 3-5
vagal tone Arrhythmias min until desired effect
Slows SA node (AF/Flutter) max dose 200 mcg/min
discharge rate Sublingual tablet (0.3-0.4) 1 tab
Shortens atrial every 5 min
refractoriness Spray 1-2 sprays for 0.501 sec
Prolongs AV nodal every 5 min, max of 3 doses
refractoriness
through ANS effect NE Severe hypotension
Nitroglycerine Increases ACS, CHF, Low total peripheral resistance
venodilation hypertensive Dopamine Hypotension
Decreases preload urgency with Symptomatic significant
Decreases oxygen ACS bradycardia
consumption After ROS (return of spontaneous
Dilates coronary circulation)
arteries Dobutamine Severe systolic heart failure
Increases collateral
Sodium Hyperkalemia
flow
Bicarbonate tricyclic or phenobarbital
overdose
Epi 1 mg IV bolus Patients with pre-existing
metabolic acidosis
NE 0.1-0.5 mcg/kg/min
Furosemide Diuretic
Dopamine 2-20 mcg/kg/min
Adenosine used if SVT is suspected
Dobutamine 2-20 ug/kg/min
CCB control ventricular response rate
NaHCO3 1 mEq/kg in AF, Flutter, MAT
Furo 0.5-1 mg/kg Verapamil Alternative drug for Adenosine
Adenosine 6 mg, 12 mg Beta Blockers second line after adenosine
Verapamil 2.5-5 mg IV Amiodarone after defibrillation and
Amiodarone VT with pulse 150 mg IV over 10 epinephrine in cardiac arrest with
mins followed by 1 mg/min persistent arrhythmias in severely
infusion for 6 hrs then 0.5 mg/min impaired LV function
Lidocaine Initial bolus 1-1.5 mg/kg IV Lidocaine VF/ Pulseless VT that persist after
additional bolus 0.5 to 0.7 mg/kg defibrillation
can be given over 3-5 mins for Control of hemodynamically
compromising PVCs Magnesium
Magesium effectively terminates torsades de -effectively terminates torsades de pointes
pointes
Atropine symptomatic bradycardia (Class I) Atropine
AV block Nodal level -Symptomatic bradycardia (Class I)
use with caution in MI -AV block Nodal level
Digoxin Supraventricular Arrhythmias -use with caution in MI
(AF/Flutter)
Nitroglycerine ACS, CHF, hypertensive urgency Digoxin
with ACS
-Supraventricular arrhythmias (AF/flutter)

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

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