Cardiovascular Pharmacology

Medication
Oxygen

Mechanism of Action
Increases oxygen tension
Increases hemoglobin
saturation if ventilation is
supported
Improves tissue oxygenation
when circulation is
maintained

Nitroglycerin
(Nitrostat,
Nitrobid [SL
forms]; Tridil [IV]

Relaxes vascular smooth

muscle; including dilation of
the coronary arteries
(particularly in the area of
plaque disruption), the
peripheral arterial bed, and
venous capacitance vessels
Dilation of postcapillary
vessels promotes
peripheral pooling of blood
decreases venous return to
the heart
decreases
preload

Morphine sulfate
(Duramorph,
Infumorph, MS
Contin, MSIR,
Oramorph)

Arteriolar relaxation reduces

systemic vascular resistance
and arterial pressure
(afterload)
Reduces pain of ischemia
Reduces anxiety
Increases venous capacitance
(venous pooling) and
decreases venous return
(preload)
Decreases systemic vascular
resistance (afterload)
Decreases myocardial oxygen
demand

Indications
Medications Used In
Cardiac or pulmonary arrest
Suspected hypoxemia of
any cause
Any suspected
cardiopulmonary
emergency, especially
complaints of shortness of
breath and/or suspected
ischemic chest pain
Sublingual tablets or spray:
Prophylaxis, treatment, and
management of patients
with angina pectoris
Pulmonary congestion due
to LV failure
IV:
Ongoing ischemic chest
discomfort
Management of
hypertensive emergencies,
particularly if related to
volume overload.
Management of pulmonary
congestion due to LV failure

Analgesic of choice for

continuing ischemic chest
discomfort unresponsive to
nitrates
Pulmonary vascular
congestion complicating
acute coronary syndromes
(SBP > 90 mm Hg)

Adult Dosage
Acute Coronary Syndromes
Nasal cannula (1 to 6 L/min)
Simple face mask (8 to 10
L/min)
Partial rebreather mask (6 to
10 L/min)
Nonrebreather mask (10-15
L/min)
Cardiac arrest positivepressure ventilation with
100% oxygen
Sublingual tablets - 1 tab
repeated at 5-minute
intervals to max of 3 doses.
Sublingual Spray - Spray on
or under the tongue for 0.5
to 1.0 second at 5-minute
intervals (delivers 0.4 mg per
metered dose).
IV infusion: Begin infusion at
5 mcg/min and increase dose
in increments of 5 mcg/min
every 5-10 min to desired
hemodynamic or clinical
response.

2 to 4 mg (give in 2 mg
increments) slow IV push.
Give additional doses of 2 to
8 mg IV at 5- to 15-minute
intervals.

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Precautions
Obstructive lung disease
Do not withhold oxygen if
signs of hypoxia present
Be prepared to intubate
and assist ventilation as
necessary
Toxicity with prolonged
administration of high flow
oxygen - rarely a concern
in the emergent situation
Primary side effect is
hypotension.
Other side effects include
tachycardia, bradycardia,
headache, palpitations,
and syncope.
Give with extreme caution
(if at all) to patients with
suspected inferior wall MI
with possible right
ventricular MI

Watch closely for:

Bradycardia
CNS depression
Nausea/vomiting
Respiratory depression
(most serious side effect reversible with naloxone or
nalmefene)
Hypotension

Special Notes
Pulse oximetry is
inaccurate in low
cardiac output states or
with vasoconstriction

Do not use in patients

with hypotension
(systolic BP <90 mm
Hg or more than 30
mm Hg below
baseline), extreme
bradycardia (<50
bpm), or tachycardia
(>100 bpm).
Do not give to patients
who have received a
medication for erectile
dysfunction within the
last 24 hours (longer
for some preparations).

Make sure naloxone

and airway equipment
is within reach before
giving.

Medication
Naloxone
(Narcan)

Acetylsalicylic
acid (aspirin)

Fibrinolytic
Agents

Mechanism of Action
While the mechanism of
action of naloxone is not fully
understood, evidence
suggests naloxone
antagonizes the effects of
opiates by competing for the
same receptor sites.

Indications
Coma of unknown etiology
to rule out (or reverse)
opioid-induced coma

Blocks synthesis of
thromboxane A2, inhibiting
platelet aggregation

Chest pain or other

signs/symptoms suggestive
of an acute coronary
syndrome (unless
hypersensitive to aspirin)
Unstable angina
ECG changes suggestive of
acute MI

Initial dose of 162325 mg

non-enteric formulation
followed by 75160 mg/day
of an enteric or a non-enteric
formulation

Fibrinolytics work by altering

plasmin in the body, which
then breaks down fibrinogen
and fibrin clots.

Improvement of ventricular
function following STelevation MI with onset of
symptoms of 12 hours and
ECG findings consistent with
STEMI
tPA may be used in acute
ischemic stroke, after
intracranial hemorrhage has
been excluded by CT scan
or other diagnostic imaging
Acute pulmonary
thromboembolism

Consult a reputable drug

reference for complete dosing
information.

Opiate induced respiratory

depression

Adult Dosage
IV, IM, SubQ Narcotic
Overdose-Known or
Suspected:
Initial dose 0.4 mg to 2 mg.
May repeat at 2 to 3 minute
intervals. If no response after
10 mg, reevaluate diagnosis.

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Precautions
Abrupt reversal of narcotic
depression may result in:
Nausea, vomiting
Sweating
Tachycardia
Increased blood pressure
Tremulousness
Seizures
Cardiac arrest
Asthma (relative
contraindication)
Active ulcer disease
(relative contraindication)

Pay careful attention to all

potential bleeding sites
(including catheter
insertion sites, arterial and
venous puncture sites,
cutdown sites, and needle
puncture sites)

Special Notes
Effects of narcotics are
usually longer than
those of naloxone;
thus, respiratory
depression may return
when naloxone has
worn off. Monitor
closely.
Use with caution in the
patient with a history of
asthma, nasal polyps,
or nasal allergies.
Anaphylactic reactions
in sensitive patients
have occurred.
Consult a reputable
drug reference for
specific information
about contraindications
for use of fibrinolytics.

Medication
Heparin
(Sodium Heparin,
Liquaemin
Sodium)

Mechanism of Action
Anticoagulant
Indirectly inhibits thrombin,
acting at multiple sites in the
normal coagulation system.
It is not a fibrinolytic; it does
not dissolve existing clots.

Glycoprotein
IIb/IIIa Inhibitors

Prevent fibrinogen binding

and platelet aggregation

Abciximab
(ReoPro)
Eptifibatide
(Integrilin)
Tirofiban
(Aggrastat)

Indications
Patients undergoing
percutaneous or surgical
revascularization
Patients undergoing
reperfusion therapy with
alteplase, reteplase, or
tenecteplase
Patients treated with
nonselective fibrinolytic
agents (streptokinase,
anistreplase, urokinase)
who are at high risk for
systemic emboli (large or
anterior MI, atrial
fibrillation, previous
embolus, or known LV
thrombus)
In patients with high-risk
stratification unstable
angina/NSTEMI, treatment
should begin as soon as
possible in conjunction with
aspirin, heparin, and
clopidogrel and a strategy of
early PCI

Adult Dosage
60 U/kg (maximum 4000 U
for patients weighing >70 kg)
followed by an infusion of 12
U/kg/hr (maximum 1000
U/hr for patients weighing
>70 kg) initially adjusted to
maintain activated partial
thromboplastin time (aPTT) at
1.5 to 2.0 times control
(about 50 to 70 seconds) for
48 hours or until angiography

Precautions
Discontinue heparin
administration promptly if
a patient develops new
thrombosis in association
with a reduction in platelet
count

Special Notes
When heparin is given
by continuous IV
infusion, the
coagulation time should
be determined about
every 4 hours in the
early stages of
treatment. Follow
institutional heparin
protocol.

Consult a reputable drug

reference for complete dosing
information.

Minimize arterial and

venous punctures, IM
injections, and use of
urinary catheters,
nasotracheal intubation,
and nasogastric tubes.
When establishing IV
access, avoid noncompressible sites (e.g.,
subclavian or jugular
veins).

High-risk features
include persistent pain,
hemodynamic or
rhythm instability,
diabetes, acute or
dynamic ECG changes,
and any elevation in
cardiac troponins
attributed to cardiac
injury.
Abciximab should not
be given unless PCI is
planned

ry edema

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Medication
Angiotensin
Converting
Enzyme (ACE)
Inhibitors
Captopril
(Capoten);
Enalapril
(Vasotec);
Lisinopril (Prinivil,
Zestril); Ramipril
(Altace)

Adenosine
(Adenocard)

Mechanism of Action
In general, prevent
conversion of angiotensin I to
angiotensin II (a potent
vasoconstrictor). As a result,
blood vessels relax, reducing
the pressure the heart must
pump against, and decreasing
myocardial workload.
By increasing renal blood
flow, help rid the body of
excess sodium and fluid
accumulation.

Slows sinus rate

Slows conduction time
through AV node
Can interrupt reentry
pathways through AV node
Can restore sinus rhythm in
PSVT

Indications
Recommended within the
first 24 hours after onset of
symptoms in STEMI patients
with pulmonary congestion
or LV ejection fraction
<40%, in the absence of
hypotension (SBP <100 mm
Hg or more than 30 mm Hg
below baseline)
Also recommended for all
other patients with acute MI
with or without early
reperfusion therapy

Adult Dosage
Consult a drug reference for
complete dosing information.

Drugs Used for Control of Heart Rhythm and Rate

Peripheral IV dose: 6 mg
Stable, narrow-complex AV
rapid IV push over 1-3
nodal or sinus nodal reentry
seconds.
tachycardias
For unstable reentry SVT
while preparations are made If no response within 1-2
minutes, administer 12 mg.
for cardioversion
May repeat 12 mg dose once
Undefined, stable, narrowin 1-2 minutes.
complex SVT as a
combination therapeutic and
Follow each dose immediately
diagnostic maneuver
with 20-mL normal saline
Stable, wide-complex
tachycardias in patients with flush.
a recurrence of a known
reentry pathway that has
been previously defined

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Precautions
Adjust dose in patients
with renal impairment or
renal failure

Special Notes

May cause a profound

drop in BP following the
first dose or if used with
diuretics

Use with caution in

patients with emphysema,
bronchitis, asthma

Recommended IV site is
the antecubital fossa.
Use injection port
nearest hub of IV
catheter. Constant ECG
monitoring is essential.

Discontinue in any patient

who develops severe
respiratory difficulty

Onset of action 10 to
40 seconds; duration 1
to 2 minutes

Dysrhythmias at time of
rhythm conversion

Medication
Amiodarone
(Cordarone)

Mechanism of Action
Possesses characteristics of
all four classes of
antiarrhythmics. Blocks
sodium channels (class I
action), inhibits sympathetic
stimulation (class II action),
and blocks potassium
channels (class III action) as
well as calcium channels
(class IV action).
Suppresses SA node function
Prolongs PR, QRS, and QT
intervals
Slows conduction at the AV
junction

Atropine sulfate

Increases heart rate by

accelerating SA node
discharge rate and blocking
vagus nerve
Little or no effect on force of
contraction
May restore cardiac rhythm in
asystole or bradycardic
pulseless electrical activity
(PEA)

Indications
Pulseless VT/VF (after CPR,
defibrillation, and a
vasopressor)
Polymorphic VT
Wide-complex tachycardia
of uncertain origin
Stable VT when
cardioversion unsuccessful
Adjunct to electrical
cardioversion of SVT/PSVT,
atrial tachycardia
Pharmacological conversion
of atrial fibrillation
Rate control of atrial
fibrillation or flutter when
other therapies ineffective

First-line drug for

symptomatic narrow-QRS
bradycardia
Asystole (after epinephrine)
Slow PEA (after
epinephrine)

Adult Dosage
Cardiac arrest Pulseless
VT/VF
Initial bolus 300 mg IV/IO
bolus. Consider repeat dose
of 150 mg IV/IO bolus once
in 5 minutes
If return of spontaneous
circulation, consider
continuous IV infusion (1
mg/min infusion for 6 hours
and then a 0.5 mg/min
maintenance infusion over 18
hours).
Other indications:
Loading dose 150 mg IV
bolus over 10 minutes (15
mg/min). May repeat every
10 min as needed. After
conversion, follow with a 1
mg/min infusion for 6 hours
and then a 0.5 mg/min
maintenance infusion over 18
hours
Symptomatic bradycardia
0.5 mg IV push every 3 to 5
min to a total dose of 3.0 mg
Asystole/slow Pulseless
Electrical Activity ({PEA)
IV/IO: 1.0 mg every 3 to 5
minutes to a total dose of 3
mg
ET: 2 to 2.5 times IV/IO dose

Precautions
Hypotension and
bradycardia are most
common side effects. Slow
infusion rate or
discontinue if seen.
Forms a precipitate when
mixed with sodium
bicarbonate or heparin.

Do not push slowly or in

smaller than
recommended doses.
Small doses (under 0.5
mg) produce modest
paradoxical cardiac
slowing that may last two
min.
May worsen ischemia or
induce VT or VF.
Use with caution in
second-degree AV block
type II and third-degree
AV block with a new wide
QRS may be ineffective
or cause paradoxical
slowing.

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Special Notes
Like all antiarrhythmic
agents, amiodarone
may cause a worsening
of existing arrhythmias
or precipitate a new
arrhythmia.

Give oxygen before

giving atropine.
Use with caution in
acute MI. Excessive
increases in heart rate
may further worsen
ischemia or increase
size of infarction

Medication
Beta-blockers

Mechanism of Action
Slow sinus rate

Atenolol
(Tenormin)

Depress AV conduction

Esmolol
(Brevibloc)
Labetalol
(Normodyne,
Trandate)
Metoprolol
(Lopressor)
Propranolol
(Inderal)

Digoxin (Lanoxin)

Reduce blood pressure

Decrease myocardial oxygen
consumption
Reduce the incidence of
dysrhythmias by decreasing
catecholamine levels
Reduce risk of sudden death
in patients with an acute
coronary syndrome

Slows conduction through AV

node (prolonging PR interval)

Indications
For rate control in:
Narrow-complex
tachycardias that originate
from either a reentry
mechanism (reentry SVT) or
an automatic focus
(junctional, ectopic, or
multifocal tachycardia)
uncontrolled by vagal
maneuvers and adenosine
in the patient with no signs
of heart failure
Atrial fibrillation and atrial
flutter in the patient with no
signs of heart failure
Control of blood pressure in
hypertensive emergencies
Use in the postresuscitation
setting is reasonable if there
are no contraindications
Limited use in emergency
cardiac care

In atrial flutter or fibrillation,

decreases number of atrial
impulses reaching the
ventricles, thus decreasing
the ventricular response

Control ventricular response

rate in patients with atrial
fibrillation or atrial flutter

Increases force and velocity

of myocardial contraction

Heart failure due to poor left

ventricular contractility

Adult Dosage
Consult a reputable drug
reference for complete dosing
information.

Precautions
Avoid concurrent use with
calcium channel blockers,
because of potential
bradycardia and
hypotension.
Should be used with
caution in patients with
pulmonary disease or
congestive heart failure

Consult a reputable drug

reference for complete dosing
information.

PSVT

Narrow toxic-totherapeutic ratio

May result in toxicity in
patients with hypokalemia
or hypomagnesemia
May cause severe sinus
bradycardia or SA block in
patients with pre-existing
sinus node disease
May cause complete AV
block in patients with preexisting incomplete AV
block

Increases cardiac output

Avoid in WPW because of

possible ventricular
dysrhythmias

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Special Notes
Monitor BP, heart rate,
and ECG closely.
Oral beta-blocker
therapy should be given
promptly for acute
coronary syndromes of
all types unless
contraindications are
present, regardless of
the need for
revascularization
therapies.

In patients with atrial

fibrillation or atrial
flutter, IV calciumchannel blockers or
beta-blockers are
generally more effective
than digoxin for initial
control of ventricular
rate.

Medication
Diltiazem
(Cardizem)

Verapamil
(Isoptin, Calan)

Mechanism of Action
Inhibits movement of calcium
ions across cell membranes in
the heart and vascular
smooth muscle, resulting in:
Relaxation of coronary
vascular smooth muscle
Dilation of both large and
small coronary arteries
Decreased sinoatrial and
atrioventricular conduction
Decreased myocardial oxygen
demand
Produces antihypertensive
effects primarily by relaxation
of vascular smooth muscle
and a resultant decrease in
peripheral vascular resistance
Inhibits movement of calcium
ions across cell membranes in
the heart and vascular
smooth muscle, resulting in:
Relaxation of coronary
vascular smooth muscle
Dilation of both large and
small coronary arteries
Decreased sinoatrial and
atrioventricular conduction
Decreased myocardial oxygen
demand

Indications
Stable narrow-QRS
tachycardias if the rhythm
persists despite vagal
maneuvers or adenosine
To control the ventricular
rate in patients with atrial
fibrillation or atrial flutter

Adult Dosage
Initial dose 0.25 mg/kg IV
bolus over 2 min. If needed,
follow in 15 min with 0.35
mg/kg over 2 min.
Subsequent IV bolus doses
should be individualized for
each patient.

Precautions
Avoid in patients with
wide-QRS tachycardia
unless it is known with
certainty to be
supraventricular in origin
(may precipitate VF)
Should not be given to
patients with a SBP of <90
mm Hg

Special Notes
Monitor BP, heart rate,
and ECG closely.
Concurrent use of
amiodarone and
diltiazem can result in
bradycardia and
decreased cardiac
output by an unknown
mechanism.
Should not be given to
patients with atrial
fibrillation or atrial
flutter associated with
known preexcitation
(WPW) syndrome.

Stable narrow-QRS
tachycardia due to reentry if
the rhythm persists despite
vagal maneuvers or
adenosine
Stable narrow-QRS
tachycardia due to
automaticity (junctional,
ectopic atrial, multifocal
atrial tachycardia) if the
rhythm persists despite
vagal maneuvers or
adenosine
To control the ventricular
rate in patients with atrial
fibrillation or atrial flutter

2.5 to 5.0 mg slow IV bolus

over 2 min (administer over 3
to 4 min in elderly or if BP is
within the lower range of
normal).
May repeat with 5 to 10 mg
in 15 to 30 min (if no
response and BP remains
normal or elevated)
Max dose 20 mg

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Avoid in patients with

wide-QRS tachycardia
unless it is known with
certainty to be
supraventricular in origin.
(may precipitate VF)
Should not be given to
patients with a SBP of <90
mm Hg.
Should not be given to
patients with impaired
ventricular function or
heart failure.

Monitor BP, heart rate,

and ECG closely.
Should not be given to
patients with atrial
fibrillation or atrial
flutter associated with
known preexcitation
(WPW) syndrome.

Medication
Epinephrine
(Adrenalin)

Lidocaine
(Xylocaine)

Magnesium
sulfate

Mechanism of Action
Stimulates alpha, beta-1, and
beta-2 receptors
Alpha-agonist constricts
arterioles in the skin,
mucosa, kidneys, and viscera
increased systemic
vascular resistance
Beta-1 agonist increases
force of contraction (+
inotropic effect), increases
heart rate
increased
myocardial workload and
oxygen requirements
Beta-2 agonist relaxation of
bronchial smooth muscle,
dilation of vessels in skeletal
muscle; dilation of cerebral,
pulmonary, coronary, and
hepatic vessels
Suppresses ventricular ectopy
In therapeutic doses,
lidocaine does not affect BP,
cardiac output, or myocardial
contractility.

Evidence exists that

magnesium:
Produces systemic and
coronary vasodilation
Possesses antiplatelet activity
Suppresses automaticity in
partially depolarized cells
Protects myocytes against
calcium overload under
conditions of ischemia by
inhibiting calcium influx
especially at the time of
reperfusion

Indications
Cardiac arrest (IV bolus)
VF, pulseless VT, asystole,
pulseless electrical activity
(PEA)
Symptomatic bradycardia
(IV infusion)

Adult Dosage
Cardiac arrest IV/IO:
1 mg (10 mL) of 1:10,000
solution, follow with 20 mL
fluid flush and elevate
extremity. May repeat every
3 to 5 min.

Precautions
Increases myocardial
oxygen demand
Avoid mixing with sodium
bicarbonate

ET dose: 2 to 2.5 mg diluted

in 10 mL NS

Initial dose: 1 to 1.5 mg/kg

IV/IO bolus. Consider repeat
dose (0.5 to 0.75 mg/kg) in 5
to 10 minutes.
Maximum IV/IO bolus dose 3
mg/kg

Polymorphic VT with
prolonged QT interval
(Torsades de Pointes)
For rhythm control of atrial
fibrillation 48 hours
duration

ET dose: 2 to 3 mg/kg (2 to
2.5 times IV dose)
Torsades (pulseless): 1 to 2 g
(2 to 4 mL of 50% solution)
IV push diluted in 10 mL
Torsades (with pulse) or atrial
fib with a rapid ventricular
response: 1-2 g IV in 50 to
100 mL D5W over 5 to 60
min. Give the infusion slowly
if the patient is stable and
more rapidly if the patient is
unstable

Give epinephrine
infusion via infusion
pump
Check IV site frequently
for evidence of tissue
sloughing

Continuous IV infusion in
symptomatic bradycardia
Dose 2-10 mcg/min

Pulseless VT/VF that

persists after defibrillation
and vasopressor
administration

Special Notes
Should not be given in
same IV line as alkaline
solutions

IV/IO route
recommended in
cardiac arrest over ET
route

Lidocaine may be lethal in

a bradycardia with a
ventricular escape rhythm
Maintenance infusion 1 to
4 mg/min.

Use with caution in:

Patients receiving digitalis
Patients with impaired
renal function
Patients with preexisting
heart blocks

Only bolus therapy is

used in cardiac arrest.
Signs and symptoms of
lidocaine toxicity are
primarily CNS related

Signs and symptoms of

magnesium overdose
include:
Hypotension
Flushing, sweating
Bradycardia, AV block
Respiratory depression
Drowsiness, decreasing
level of consciousness
Diminished reflexes or
muscle weakness,
flaccid paralysis
Antidote = calcium

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Medication
Procainamide
(Pronestyl)

Mechanism of Action
In therapeutic doses,
decreases conduction velocity
in the atria, ventricles, and
His-Purkinje system
Prolongs the effective
refractory period of the atria
Shortens the effective
refractory period of the AV
node
Decreases automaticity in the
His-Purkinje system and
ectopic pacemakers
Prolongs the PR and QT
intervals
Exerts a peripheral
vasodilatory effect

Indications
Stable monomorphic VT in
patients with no signs of
heart failure
Control of rapid ventricular
rate in atrial fibrillation or
atrial flutter in patients with
no signs of heart failure
Control of rapid ventricular
rate in atrial fibrillation or
atrial flutter in patients with
known Wolff-ParkinsonWhite (WPW) syndrome and
no signs of heart failure
AV reentrant narrowcomplex tachycardias such
as reentry SVT if no
response to vagal
maneuvers and adenosine
and if no signs of heart
failure

Adult Dosage
20 mg/min IV infusion until
one of the following occurs:
Dysrhythmia resolves
Hypotension
QRS widens by >50% of
original width
Total dose of 17 mg/kg given
Maintenance infusion 1 to 4
mg/min.

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Precautions
Use with caution with
other medications that
prolong the QT interval
(e.g., phenothiazines,
tricyclic antidepressants,
thiazide diuretics, sotalol)
Reduce maintenance
infusion rate in liver
dysfunction (procainamide
is metabolized by the
liver), renal failure
(procainamide is
eliminated by the kidneys)

Special Notes
Carefully monitor ECG
and BP. If BP falls 15
mm Hg or more,
procainamide
administration should
be temporarily
discontinued.
Observe ECG closely for
increasing PR and QT
intervals, widening of
the QRS complex, heart
block, and/or onset of
TdP.

Medication
Dopamine
(Intropin,
Dopastat)

Norepinephrine
(Levophed,
Levarterenol)

Dobutamine
(Dobutrex)

Mechanism of Action

Indications
Adult Dosage
Precautions
Medications Used To Improve Cardiac Output and Blood Pressure
Volume deficits must be
Hemodynamically significant Continuous IV infusion - dose
Stimulates dopaminergic,
corrected before beginning
range 2 to 10 mcg/kg/min.
bradydysrhythmias that
beta, and alpha-adrenergic
dopamine therapy
have not responded to
receptor sites
Increase infusion rate
atropine and/or when
Gradually taper drug
according to blood pressure
external pacing is
Low dose (dopaminergic
before discontinuing the
and other clinical responses
unavailable
effects) - 0.5 to 2
infusion.
mcg/kg/min (renal dose)
Hypotension that occurs
Medium dose (beta effects) after return of spontaneous
2 to 10 mcg/kg/min (cardiac
circulation
dose)
High dose (alpha effects)
Hemodynamically significant
(pressor dose) - 10 to 20
hypotension in the absence
mcg/kg/min
of hypovolemia
> 20 mcg/kg/min - Produces
effects similar to
norepinephrine
Use with extreme caution
0.5 to 1.0 mcg/min IV
Cardiogenic shock
Norepinephrine functions as a
in patients receiving
titrated to improve blood
peripheral vasoconstrictor
monoamine oxidase
pressure (up to 30 mcg/min)
Severe hypotension
(alpha-adrenergic action), an
inhibitors (MAOI) or
(systolic BP <70 mm Hg)
inotropic stimulator of the
antidepressants of the
Give by continuous IV
not due to hypovolemia
heart, and a dilator of
triptyline or imipramine
infusion.
coronary arteries (betatypes, because severe,
adrenergic action)
prolonged hypertension
may result

Stimulates alpha, beta-1, and

beta-2 receptors
Potent inotropic effect (i.e.,
increased myocardial
contractility, increased stroke
volume, increased cardiac
output), less chronotropic
effect (heart rate), minimal
alpha effect
(vasoconstriction)

Short-term management of
patients with cardiac
decompensation due to
depressed contractility
(e.g., CHF, pulmonary
congestion)

Continuous IV infusion. Usual

dose is 2-20 mcg/kg/min IV,
based on patient response

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2006 Southwest EMS Education
Used with permission

Norepinephrine is a
concentrated, potent
medication that must be
diluted in dextrose
containing solutions before
infusion.
Tachycardia may occur
with high doses, although
this occurs less commonly
than with dopamine.
Use with tricyclic
antidepressants can cause
an increased adrenergic
effect and possibly result
in a severe hypertensive
emergency or cardiac
dysrhythmias

Special Notes
Extravasation may
cause necrosis and
sloughing
Should only be infused
via an infusion pump.
Monitor blood pressure,
ECG, and drip rate
closely.

When discontinuing
infusion, taper off
gradually.

Correct hypovolemia
before treatment with
dobutamine
Continuously monitor
ECG and blood pressure

Medication
Vasopressin
(Synthetic
Pitressin)
Calcium chloride

Mechanism of Action
Increases vasoconstriction
and arterial tone that results
in increased myocardial
perfusion
Essential for functional
integrity of nervous and
muscular systems
Necessary for normal cardiac
contractility
Increases force of cardiac
contraction (positive inotropic
effect)
Antidote for magnesium
sulfate

Indications
Cardiac arrest

Adult Dosage
IV/IO: One time dose of 40
units IV push

Precautions
Tissue necrosis if
extravasation occurs

Known or suspected acute

hyperkalemia
Hypocalcemia
Calcium channel blocker
toxicity/overdose
Pretreatment for calcium
channel blocker
administration
Magnesium toxicity

Hyperkalemia
8 to 16 mg/kg IV over 10
min. Dosage should be
titrated by constant
monitoring of ECG changes
during administration.

Bradycardia with rapid IV

injection
Precipitates with bicarb
Do not administer IM or
SubQ - can cause severe
tissue necrosis, sloughing,
or abscess formation.
Use with caution in
patients taking digitalis
increases ventricular
irritability and can
precipitate digitalis toxicity

Sodium
Nitroprusside
(Nipride)

Direct-acting arterial and

venous vasodilator
Relaxes vascular smooth
muscle with consequent
dilation of peripheral arteries
and veins; other smooth
muscle (e.g., uterus,
duodenum) is not affected
Venodilation promotes
peripheral pooling of blood
and decreases venous return
to the heart, thereby
reducing preload
Arteriolar relaxation reduces
systemic vascular resistance
(afterload)
Dilates coronary arteries

Immediate reduction of
blood pressure in a
hypertensive emergency or
hypertensive urgency

Administer via infusion pump

Begin infusion at 0.1
mcg/kg/min and titrate slowly
(every 3 to 5 minutes)
upward (to 5 mcg/kg/min) to
desired clinical response
Average dose is 3
mcg/kg/min; max
recommended infusion rate
10 mcg/kg/min

Alkalinizing Agents/Buffers

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2006 Southwest EMS Education
Used with permission

Can cause precipitous

decreases in BP. In
patients not properly
monitored, these
decreases can lead to
irreversible ischemic
injuries or death.
Monitor for signs of
cyanide toxicity

Special Notes
May be used in place of
first or second dose of
epinephrine in cardiac
arrest
Monitor IV site closely.
Ensure patency of IV
line before giving.
Patient may experience
pain, burning at the IV
site, severe venous
thrombosis, and severe
tissue necrosis if
solution extravasates.
Patient may complain of
"heat waves," tingling,
and/or a metallic taste
if administered too
rapidly.
Nitroprusside is more
active on veins than on
arteries
Solution is sensitive to
certain wavelengths of
light, and must be
protected from light
during clinical use
Effects stop quickly
upon discontinuation of
infusion

Medication
Sodium
bicarbonate

Mechanism of Action
Increases plasma bicarbonate
Buffers excess hydrogen ion
concentration
Raises blood pH
Reverses clinical
manifestations of acidosis

Furosemide
(Lasix)

Inhibits reabsorption of
sodium and chloride in
ascending limb of loop of
Henle, resulting in an
increase in urinary excretion
of sodium, chloride, and
water
profound diuresis
Venodilation - increases
venous capacitance,
decreases preload (venous
return)

Indications
Known preexisting
hyperkalemia
Preexisting metabolic
acidosis
Overdose tricyclic
antidepressants,
procainamide

Adjunctive therapy in acute

pulmonary edema (systolic
BP >90 to 100 mm Hg
without signs and symptoms
of shock)

Adult Dosage
Initial dose 1 mEq/kg IV
bolus. 1/2 the initial dose
may be repeated every 10
min thereafter

Precautions
Extravasation may lead to
tissue inflammation and
necrosis

Special Notes
Do not mix with
parenteral drugs
because of the
possibility of drug
inactivation or
precipitation
Give only after ensuring
adequate ventilation

Diuretics
If the patient is not on oral
furosemide therapy, the
initial dose is 0.5 1.0 mg/kg
(usually 20-40 mg) IV push
given at a rate no faster than
20 mg/minute.

Ototoxicity and resulting

transient deafness can
occur with rapid
administration. Do not
exceed the recommended
rate of infusion.
Can cause excessive fluid
loss and dehydration,
resulting in hypovolemia
and electrolyte imbalance.

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2006 Southwest EMS Education
Used with permission

Patients with
sulfonamide
hypersensitivity or
thiazide diuretic
hypersensitivity may
also be hypersensitive
to furosemide.