Vasoactive

agents
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in shock

By Carrie L. Griffiths, PharmD, BCCCP; Mark L. Vestal, BS; and

Kristie A. Hertel, MSN, RN, CCRN, ACNP-BC

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Abstract: Shock is a condition in which the cardiovascular system fails to provide adequate blood supply
throughout the body. Depending on the severity of shock, vasoactive agents, such as vasopressors and ino-
tropes, are frequently needed to manage the patient and prevent adverse outcomes of shock. This article
reviews the vasoactive agents used in shock, summarizing what critical care nurses need to know about
these important drugs.
Keywords: dobutamine, dopamine, epinephrine, inotropes, milrinone, norepinephrine, shock, vasoactive
agents, vasopressin, vasopressors

Shock is defined as the failure of is in a vasoconstrictive state.2,3 Cardiogenic shock is a low-cardiac-

the cardiovascular system to sup-
ply adequate tissue perfusion,
which results in insufficient cel-
lular oxygen utilization.1,2 It is
crucial that treatment of a patient
in shock is started immediately
because shock is associated with
high mortality and morbidity.3
Clinical manifestations
of shock
When diagnosing shock, it is
important to note that shock is
based on three parameters that
include clinical, hemodynamic,
and biochemical signs.2 First,
systemic arterial hypotension
(defined as a mean arterial pres-
sure [MAP] of less than 70 mm
Hg) and tachycardia are generally
present. Second, clinical signs of
tissue hypoperfusion will be
seen.2 The patient’s skin will be
cold and clammy, and the nurse
will see decreased capillary refill
of the nail beds because the body
Urine output will decrease to less
than 0.5 mL/kg/h (oliguria), and
altered mental status, disorienta-
tion, and confusion will be pres-
ent because the brain is not being
adequately perfused.2,3 Last, one
biochemical marker that indi-
cates atypical cellular oxygen
metabolism, lactate, is generally
elevated (over 1.5 mmol/L) in
shock and should be monitored
throughout the treatment course
to determine whether interven-
tions are successful.2
Four different forms of
shock exist, and it is crucial to
identify which type of shock
the patient is experiencing to
determine the best course of
treatment. Hypovolemic shock is
excess loss of plasma or blood
volume that is initially compen-
sated by increases in heart rate
(HR) and systemic vascular
resistance (SVR) but typically
requires resuscitation.2,4
output state with abnormal myo-
cardial contractility caused by
myocardial infarction (MI), dys-
rhythmias, valvular disease,
end-stage cardiomyopathy, and
conduction defects and appears
clinically similar to hypovolemic
shock. However, compared with
hypovolemic shock, patients with
cardiogenic shock generally pres-
ent with pulmonary edema and
jugular venous distension.2,4
Obstructive shock is an extra-
cardiac process cutting off circu-
latory flow that can be caused by
tension pneumothorax, cardiac
tamponade, or massive pulmo-
nary embolus. Clinically, because
cardiac output is decreased in
obstructive shock, signs and
symptoms resemble hypovolemic
and cardiogenic shock.2,4
Distributive shock (which includes
septic shock) initially presents
as elevated cardiac output and
decreased SVR, as the peripheral

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 Vasoactive agents in shock

vasculature is vasodilated after an Ventilatory support with oxy- tive shock.2,5 In a patient with
inflammatory response.2,4 gen should begin immediately hemorrhagic shock (hypovolemic
to increase oxygen delivery.2 shock from rapid blood loss),
Managing shock Depending on the patient’s sta- crystalloid fluids and blood prod-
Once a patient has been diag- tus, ventilatory support can be ucts would be used to resuscitate
nosed with shock, resuscitation achieved noninvasively through a the patient. However, the treat-
should be initiated immediately to mask or invasively with mechani- ment of shock including the
prevent progression of organ dys- cal ventilation.2 amount of fluid given to the
function or failure.2 Using a mne- Next, fluids are infused to patient must be carefully chosen
monic known as the “VIP rule” improve blood flow to the micro- based on the type of shock.2
can help determine how to pro- vasculature and to increase cardi- Adverse reactions such as fluid
ceed with resuscitation: Ventilate ac output.2 For example, crystal- overload can occur, and the patient
(administer oxygen), Infuse (fluid loid fluids, such as 0.9% sodium should be monitored closely.2 If
resuscitation including crystalloids chloride (normal saline), should hypotension persists after fluid
or blood products), and Pump be infused quickly (at a volume resuscitation, the administration
(administer vasoactive agents).2 of at least 30 mL/kg) for distribu- of vasoactive agents is required.2
1,6-10,12-17
Overview of vasopressors and inotropic agents
Alpha1- Beta1- Beta2-
adrenergic adrenergic adrenergic Dopaminergic
Drug effect effect effect effect Important facts
Decreases blood flow to splanchnic circulation
Could increase lactate levels
Epinephrine ++++ +++ ++ 0
Can cause cardiac toxicity
May cause extravasation
Vasopressor of choice
As dose increases, stimulation of alpha1
Norepinephrine ++++ +++ 0 0
increases and renal perfusion decreases
May cause extravasation
Stimulates V1 receptor leading to vasoconstriction
Vasopressin 0 0 0 0
May cause extravasation
Can cause severe bradycardia and decrease
cardiac output
Phenylephrine ++++ 0 0 0
Decreases renal perfusion
May cause extravasation
Alternative vasopressor for septic shock
Precursor to norepinephrine
Dopamine Effects on renal blood flow decrease as dose
++ +++ + ++
(moderate dose) increases
Can cause tachydysrhythmias
May cause extravasation
Can cause tachydysrhythmias
Dobutamine + +++ + 0 Patients with hypertension could have an
increased effect
Phosphodiesterase-3 inhibitor
Milrinone 0 0 0 0 Kidney function should be monitored
Inotropic effects can cause dysrhythmias
Consult the manufacturer’s prescribing label for complete prescribing information including dose recommendations and
dose adjustments for each drug.

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Hypovolemia should be corrected
before the administration of any
vasoactive agents.2
This article reviews the
following vasopressors and
inotropes that may be adminis-
tered to treat shock: epineph-
rine, norepinephrine, vasopressin,
phenylephrine, dopamine,
dobutamine, and milrinone
(see Overview of vasopressors
and inotropic agents).
Vasopressors
Epinephrine. A potent alpha-
and beta-adrenergic agonist,
epinephrine increases MAP by
increasing cardiac output and
vascular tone.6 At low weight-
based doses, epinephrine heavily
stimulates the beta1 and beta2
receptors, increasing cardiac out-
put and HR; at higher doses,
epinephrine heavily stimulates
the alpha receptors, leading to
vasoconstriction and an inotropic
effect.1 Epinephrine has a quick
onset of less than 5 minutes and
a half-life of less than 5 minutes.7
Although epinephrine is an
effective vasopressor, it may lead
to detrimental adverse reactions.
Epinephrine has been shown to
decrease blood flow to the
splanchnic circulation and may
increase lactate levels.5 At high
doses and prolonged infusion
administration of epinephrine,
direct cardiac toxicity can occur
through damage to arterial walls
by cardiac myocyte necrosis and
apoptosis.8 Epinephrine, along
with other vasopressors, can
cause significant tissue damage,
skin sloughing, and dermal necro-
sis. If extravasation occurs, the
I.V. infusion must be changed to
another site and the area of necro-
sis treated with phentolamine,
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an alpha-receptor antagonist,
which is injected into the area of
necrosis and reverses ischemic
changes.9 To prevent extravasation,
vasopressors should be infused
through a central venous cathe-
ter using an infusion pump.10
Additional adverse reactions of
epinephrine include hyperglyce-
mia from the beta1 receptor
stimulation and tachycardia.7
Despite the adverse reactions,
epinephrine remains an effective
vasopressor that is generally
reserved for second-line treat-
ment and is the preferred vaso-
pressor for refractory shock.1,5
Norepinephrine. The mediator
of the sympathetic nervous sys-
tem, norepinephrine is a potent
alpha1- and alpha2-receptor ago-
nist with beta1-adrenergic agonist
effects and no beta2 effects,
which leads to robust vasocon-
striction with little to no inotropic
effects.10 Through the stimulation
of alpha1 and alpha2 receptors
and limited beta-adrenergic recep-
tors, norepinephrine increases
MAP by increasing BP and SVR
with a slight impact on cardiac
output.1,8,10 Norepinephrine has a
rapid onset of action, within 1 to
2 minutes, and has a duration of 1
to 2 minutes.11 Currently, norepi-
nephrine is the recommended
first-line vasopressor by the
Society of Critical Care Medicine
Guidelines for Management of
Sepsis and Septic Shock.5
Although norepinephrine is con-
sidered a first-line vasopressor for
shock, a variety of precautions,
warnings, contraindications, and
adverse reactions should be taken
into consideration when adminis-
tering.2 Prolonged administration
of norepinephrine could result in
myocardial ischemia because of
March l Nursing2018CriticalCare l
cardiotoxic effects on the cardiac
myocytes.8 Like epinephrine, nor-
epinephrine can cause significant
tissue damage, skin sloughing, and
dermal necrosis that is treated with
phentolamine. Administration of
norepinephrine through a larger,
central vein, diluted at an appro-
priate concentration, will also
help prevent extravasation.9,10
Norepinephrine should be used
cautiously in patients taking anti-
depressants (such as monoamine
oxidase inhibitors [MAOIs], tricy-
clic antidepressants [TCAs], or
imipramine type antidepressants)
because concomitant administra-
tion has been shown to lead to
severe, prolonged hypertension.12
Contraindications to norepi-
nephrine treatment include
concomitant use with inhaled
anesthetics such as cyclopropane
(no longer used in the United
States) and halothane because it
can increase cardiac autonomic
irritability, leading to ventricular
tachycardia and fibrillation. Avoid
the use of norepinephrine in
patients with mesenteric or
peripheral vascular thrombosis,
and those who are hypotensive
from blood volume deficits, except
for emergency therapy to maintain
perfusion until blood replacement
therapy can be administered.12
Adverse reactions to norepineph-
rine include ischemic injury from
tissue hypoxia, brady- or tachydys-
rhythmias, anxiety, transient head-
aches, dyspnea, nausea/vomiting,
and extreme hypertension.10,12
Vasopressin. Also known as
antidiuretic hormone, vasopres-
sin is a hormone that is naturally
released by the posterior pituitary
gland in response to decreased
blood volume and increased
plasma osmolality that leads to
9
 Vasoactive agents in shock
vasoconstriction.10 Vasopressin
acts via the V1 receptor, which
leads to constriction of the vascu-
lar smooth muscle and the V2
receptor. This leads to enhanced
water reabsorption in the renal
collecting duct, resulting in an
increase in SVR and little to no
impact on cardiac output.8
Vasopressin has a rapid onset
of action, with a peak effect
occurring within 15 minutes and
a half-life of 10 minutes or less.13
Currently, vasopressin is recom-
mended as an adjunct therapy to
norepinephrine when monother-
apy with norepinephrine does
not achieve the target MAP over
65 mm Hg.5
Although vasopressin is an
endogenous hormone, many
warnings, precautions, adverse
reactions, and interactions should
be taken into consideration before
administration. Vasopressin has
been reported to cause dysrhyth-
mias, chest pain, MI, and asysto-
le.10 Although uncommon,
vasopressin also has been
shown to cause extravasation
when administered through a
peripheral line; administration of
vasopressin through a central line
could avoid this complication.9
Vasopressin should be cautiously
used in patients who are taking
medications that may cause the
syndrome of inappropriate antidi-
uretic hormone secretion such as
TCAs, selective serotonin reuptake
inhibitors, haloperidol, enalapril,
methyldopa, and pentamidine,
because concomitant use may
increase the pressor and antidi-
uretic effect of vasopressin.13
Patients who are taking medica-
tions that could cause diabetes
insipidus (such as demeclocycline,
lithium, foscarnet, and clozapine)
10 l Nursing2018Critical Care l Volume 13, Number 2
Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
could experience a decreased
pressor effect of vasopressin.13
Adverse reactions of vasopressin
include gastrointestinal disorders
(mesenteric ischemia), increased
bilirubin, acute kidney insufficien-
cy, hyponatremia, bronchial con-
striction, and diaphoresis.10,13
Phenylephrine. A pure alpha1-
adrenergic agonist, phenylephrine
causes rapid peripheral vasocon-
striction resulting in increased BP.
It has minimal beta-adrenergic
activity, and therefore minimal
chronotropic or inotropic activity.10
Phenylephrine has a rapid
onset that typically occurs within
minutes and has a half-life of
approximately 5 minutes.14
Currently, little to no clinical data
exist on phenylephrine use in
sepsis and its use in patients with
sepsis should be limited.5
Although phenylephrine is an
effective vasoconstrictor, many
warnings and precautions, adverse
reactions, and interactions should
be taken into consideration before
administration. Phenylephrine has
been linked to severe bradycardia
and decreased cardiac output,
which could be detrimental in a
patient with shock.14 Like other
vasopressors, phenylephrine
causes significant tissue damage,
skin sloughing, and dermal necro-
sis that could be treated with
phentolamine. However, this
adverse reaction can be avoided
by administering phenylephrine
through a larger, central vein,
diluted to an appropriate concen-
tration.9,10 I.V. phenylephrine con-
tains sodium metabisulfite, which
could lead to life-threatening ana-
phylactic symptoms in individuals
with sulfite sensitivity. However,
according to the package insert,
the prevalence of sulfite sensitivi-
ty is unknown and is probably
low.14 Next, oxytocic drugs, such
as oxytocin, increase the pressor
effect of phenylephrine and could
potentially lead to hemorrhagic
stroke; BP should be monitored
closely in patients receiving both
drugs.14 Phenylephrine has been
shown to cause renal toxicity;
renal function should be moni-
tored closely.14
Adverse reactions to phenyl-
ephrine include bradycardia,
atrioventricular (AV) block,
myocardial ischemia, nausea,
vomiting, chest pain, headache,
excitability, nervousness, and
tremor.14 Phenylephrine has
many drug interactions that
should be taken into consider-
ation; for example, MAOIs,
TCAs, centrally acting sympatho-
lytic agents (such as guanfacine),
alpha2-adrenergic agonists (such as
clonidine), steroids, and atropine
increase the pressor effect of phen-
ylephrine. Adversely, phenyleph-
rine can block medications such
as alpha-adrenergic antagonists.14
Dopamine. A naturally occur-
ring precursor to norepinephrine,
dopamine is a potent vasocon-
strictor that has many different
dose-dependent effects on the sys-
temic vasculature.15 At very low
doses, once known as renal doses,
dopamine primarily activates
dopaminergic receptors, leading
to vasodilation in the renal,
splanchnic, mesenteric, and coro-
nary vasculature.1 Administering
dopamine at a higher rate for
renal protection is not recom-
mended because there are no
available data to support this
treatment solely to maintain
kidney function.5 At moderate
(inotropic) doses, dopamine
primarily activates the beta1-
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adrenergic receptors, leading to
an increase in MAP, HR, stroke
volume, and cardiac output.1 At
high doses, dopamine begins to
stimulate the alpha1-adrenergic
receptors, increasing MAP.1
Dopamine has a quick onset of
action that occurs within 5 min-
utes and has a short half-life of 2
minutes.15 Norepinephrine is a
more potent vasopressor than
dopamine to correct hypotension
in patients with shock, but dopa-
mine could be an acceptable
alternative to norepinephrine in
patients with a low risk of
tachydysrhythmias and absolute
or relative bradycardia.5
Although dopamine is an
acceptable alternative to norepi-
nephrine, many contraindications,
warnings and precautions, adverse
reactions, and interactions must
be taken into consideration.
Dopamine is contraindicated in
patients with pheochromocytoma
(a rare neuroendocrine tumor that
originates in the adrenal gland)
and should not be administered to
patients with tachydysrhythmias
because infusion of dopamine
may worsen these conditions.
Sodium metabisulfite is embed-
ded within the drug and could
lead to life-threatening anaphy-
lactic reactions.15
Precautions should be taken
into consideration with adminis-
tration of dopamine. When titrat-
ing the infusion during discontinu-
ation, hypotension can occur. To
avoid this problem, consider coad-
ministering I.V. fluids to expand
the patient’s intravascular vol-
ume.15 Like other vasopressors,
dopamine has been known to
cause extravasation, which can be
prevented by administering dopa-
mine through a larger, central
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When titrating dopamine
during discontinuation,
hypotension can occur,
so coadminister I.V. fluids
to expand the patient’s
intravascular volume.
vein; if extravasation occurs, it can
be treated with phentolamine.9,15
Adverse reactions of dopamine
include ventricular dysrhythmias,
atrial fibrillation, ectopic beats,
tachycardia, hyper/hypotension,
headache, and nausea/vomiting
and should be monitored for and
treated appropriately.15
Many medications interact with
dopamine. Because dopamine is
metabolized by monoamine oxi-
dase, MAOIs could potentiate the
effects of dopamine, and patients
taking MAOIs should receive
no more than one-tenth of the
usual initial dose of dopamine.15
Coadministration with dopa-
mine and cyclopropane (no longer
used in the United States) or
March l Nursing2018Critical Care l
halogenated hydrocarbon inhaled
anesthetics can increase the risk
of ventricular dysrhythmias and
should be coadministered with
extreme caution. Medications
such as TCAs and oxytocin could
lead to extreme hypertension, and
haloperidol could block the dopa-
minergic effect.15
Inotropes
Dobutamine. A synthetic cate-
cholamine, dobutamine is a
potent inotrope that increases
cardiac output by strongly
stimulating the beta1-adrenergic
receptor, and mild-to-moderate
stimulation of the beta2-adrenergic
and alpha1-adrenergic receptors.1
At low doses, dobutamine has
been shown to increase stroke
volume without significant tachy-
cardia; with high doses, tachycar-
dia worsens, leading to decreased
diastolic filling time, which
results in smaller increases in
cardiac output.1
Dobutamine’s onset of action
occurs within 1 to 2 minutes and
has a half-life of 2 minutes.16 This
makes dobutamine the preferred
inotrope in unstable patients with
cardiogenic shock, and it is rec-
ommended in patients with hypo-
perfusion in septic shock when
appropriate fluid loading and
vasopressors do not achieve nor-
mal end-organ function.1,5
Although dobutamine is an
effective inotropic agent, many
contraindications, precautions
and warnings, interactions,
and adverse reactions exist.
Dobutamine is contraindicated
in patients with idiopathic
hypertrophic subaortic stenosis.
Because dobutamine promotes
conduction, patients with atrial
fibrillation are at increased risk
11
 Vasoactive agents in shock
of developing rapid ventricular
response, and patients with
hypertension are at increased
risk of an increased pressor
effect. Dobutamine could precip-
itate or exacerbate ventricular
ectopic activity and hypersensi-
tivity reaction, and elicit an ana-
phylactic reaction from patients
who have a sulfite sensitivity. In
animal studies, the concomitant
use of a beta-antagonistic medi-
cation led to a lesser dobutamine
effect. Hypotension can also be a
result of dobutamine administra-
tion, but is mainly seen when
titrating the agent down or off.16
Adverse reactions of dobutamine
include nausea, angina, dyspnea,
headache, decreases in serum
potassium, and phlebitis.16
Milrinone. A selective
phosphodiesterase-3 inhibitor,
milrinone is a potent inotrope
and vasodilator that increases
intracellular calcium and myocar-
dial contractions, and relaxes the
pulmonary and systemic vascula-
ture, lowering SVR and pulmo-
nary vascular resistance.1,17
Milrinone is indicated for short-
term management of patients
with acute decompensated heart
failure.17 When infused I.V., mil-
rinone peaks within 2 minutes
and has a half-life of 1 to 3
hours.11
Although milrinone has a
different mechanism of action
than dobutamine, there are
many contraindications, precau-
tions and warnings, interactions,
and adverse reactions that must
be taken into consideration.
Milrinone is contraindicated in
patients with severe obstructive
aortic or pulmonary vascular
disease or hypertrophic subaor-
tic stenosis. Because milrinone,
12 l Nursing2018Critical Care l Volume 13, Number 2
Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.
Lack of understanding of
vasoactive medications
may lead to patient
compromise and
possibly a sentinel
event.
like dobutamine, increases
myocardial contractions, supra-
ventricular and ventricular
dysrhythmias may occur,
and patients should be closely
monitored during infusions.
Milrinone also slightly shortens
the AV node conduction time,
and patients with atrial fibrilla-
tion or flutter may experience an
increased ventricular response
rate. It should be used with cau-
tion in patients with hypoten-
sion. Patients with kidney
impairment (creatinine clearance
of 50 mL/min/1.73 m2 or less)
will require a renal dose adjust-
ment.17 Few interactions with
milrinone exist, but it can form a
precipitate with furosemide and
bumetanide when administered
into the same I.V. line; therefore,
coadministration of these medi-
cations should be avoided.
Adverse reactions of milrinone
include ventricular dysrhyth-
mias, ventricular ectopic activity,
hypotension, angina, headache,
hypokalemia, and tremor.17
Nursing considerations
Patients presenting to EDs or
ICUs with hemodynamic com-
promise related to any form
of shock are considered high-
acuity patients. Critical care
nurses must know the probable
medications used to treat these
patients and any invasive or non-
invasive monitoring that may be
required. Nurses are responsible
for knowing the adverse reac-
tions of each vasoactive medica-
tion. Lack of understanding of
vasoactive medications may lead
to patient compromise and possi-
bly a sentinel event.
Appropriate and accurate
monitoring of hemodynamic
parameters is required when
titrating continuous infusions of
vasoactive medications. Patients
need an arterial line for continu-
ous BP monitoring.18 An arterial
line allows for optimal titration of
medications with close observa-
tion of patient responsiveness in
real time.
Nurses must monitor the arte-
rial line waveform to ensure
accurate readings are obtained.
The accurate recording of intra-
arterial pressure depends upon
an appropriate dynamic response
of the monitoring system.
The rapid-flush (square wave)
test is the clinical test of choice.
This will determine if the arterial
waveform has overdamped or
www.nursingcriticalcare.com
underdamped characteristics. If
the waveform is overdamped,
mainly caused by air bubbles in
the tubing, the systolic BP has
been underestimated. If the
waveform is underdamped, the
systolic BP has been overestimat-
ed. This can be caused by patient
factors, excessive tubing length,
or connecting tubing with stop-
cocks. If the arterial line wave-
form is inaccurate, nurses should
use noninvasive BP cuff readings
for titration of medications until a
new arterial line can be placed.
When utilizing a noninvasive BP
cuff for titration of vasoactive
medications, obtain readings at
least every 15 minutes, and more
frequently if readings reveal
hypotension.18
Inotropes affect cardiac con-
tractility as well as preload and
afterload. Inotropic medications
require further invasive monitor-
ing of cardiac output along with
preload and afterload. The gold
standard for this monitoring has
been a pulmonary artery (PA)
catheter.19 Based on recent con-
sensus statements on circulatory
shock and hemodynamic moni-
toring, PA catheters should only
be used in complex shock
patients to determine the type of
shock, refractory shock patients,
or patients with severe shock. PA
catheters are not recommended
for routine use in patients with
shock.19 However, noninvasive
devices that calculate these val-
ues have been developed and can
be used as a substitute for PA
catheters with fewer complica-
tions for the patient.
Appropriate education is
required to understand the hemo-
dynamic parameters and titration
of vasoactive and inotropic medi-
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cations based on hemodynamic
measurements. Vasopressors and
inotropic medications are caustic
to veins. Vasoactive medication
should not be administered for a
prolonged period of time through
a peripheral I.V. catheter because
of the possibility of serious tissue
injury by extravasation.20 A cen-
tral venous catheter placed in
the subclavian vein, internal
jugular vein, or femoral vein
is appropriate for vasoactive
medication infusions. In emer-
gent, life-threatening situations,
a brief period of infusion through
a peripheral catheter is accept-
able. Whenever a vasoactive
medication infusion is started,
use an infusion pump to control
the rate of infusion.21 Nurses
need to be familiar with the infu-
sion pumps at their facilities and
how to titrate the medications on
specific infusion pumps.
Conclusion
Once a patient has been diag-
nosed with shock, resuscitation
should be initiated immediately,
which may require the adminis-
tration of vasoactive agents once
the patient has been volume
resuscitated. Each vasoactive
agent exerts its effects differently,
and it is important to select the
correct vasoactive agent for the
type of shock the patient has.
Once the patient has been initiat-
ed on a vasoactive agent, appro-
priate and accurate monitoring
should be enforced to prevent
adverse outcomes. ■
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Carrie L. Griffiths is an assistant professor of phar-
macy at Wingate University School of Pharmacy in
Wingate, N.C.
Mark L. Vestal is a doctor of pharmacy candidate at
Wingate University School of Pharmacy in Wingate, N.C.
Kristie A. Hertel is an advanced practice provider in
trauma and surgical critical care at Vidant Medical
Center in Greenville, N.C.
The authors have disclosed no financial relationships
related to this article.
DOI-10.1097/01.CCN.0000527219.88686.70
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