INTRAVENOUS MEDICATIONS · Insulin preparations are classified as rapid-acting, short-acting, intermediate-acting, or long-acting, depending on the onset of action, the peak effect,

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INTRAVENOUS MEDICATIONS

Dana Bartlett, RN, BSN, MSN, MA

Dana Bartlett is a professional nurse and author. His

clinical experience includes 16 years of ICU and ER

experience and over 20 years of as a poison control center

information specialist. Dana has published numerous CE

and journal articles, written NCLEX material and textbook

chapters, and done editing and reviewing for publishers

such as Elsevier, Lippincott, and Thieme. He has written

widely on the subject of toxicology and was recently named a contributing editor,

toxicology section, for Critical Care Nurse journal. He is currently employed at the

Connecticut Poison Control Center and is actively involved in lecturing and mentoring

nurses, emergency medical residents and pharmacy students.

ABSTRACT

It is important to provide nurses with up-to-date and complete data. However, for

some drugs and for certain aspects of their use, i.e., pharmacokinetics and

dosages, in certain clinical situations the data is limited and/or incomplete. A

complete list of adverse effects and side effects for each medication would be

quite lengthy, impractical, to include in this study; and, for most of the drugs

their frequency is not known. Yet, nurses need to be concerned about and familiar

with some of the more common medication adverse effects and side effects, such

as are explained. Intravenous compatibility as it pertains to the medications

discussed in this study module will be discussed. If commonly known and used,

brand names for the drugs are also provided.


Continuing Nursing Education Course Director & Planners:

William A. Cook, PhD, Director; Douglas Lawrence, MA, Webmaster;

Susan DePasquale, CGRN, MSN, FPMHNP-BC, Lead Nurse Planner

Accreditation Statement:

This activity has been planned and implemented in accordance with the policies of

NurseCe4Less.com and the continuing nursing education requirements of the

American Nurses Credentialing Center's Commission on Accreditation for

registered nurses.

Credit Designation:

This educational activity is credited for 4.5 hours. Nurses may only claim credit

commensurate with the credit awarded for completion of this course activity.

Course Author & Planner Disclosure Policy Statements:

It is the policy of NurseCe4Less.com to ensure objectivity, transparency, and best

practice in clinical education for all continuing nursing education (CNE) activities.

All authors and course planners participating in the planning or implementation of

a CNE activity are expected to disclose to course participants any relevant conflict

of interest that may arise.

Statement of Need:

Although information on infusion therapy can vary, there are basic guidelines that

nurses are expected to know in order to meet knowledge needs and practical

experience requirements in the performance of infusion therapy. All nurses,

whether they are certified in infusion therapy or not should understand the basic

principles of administering certain infusion medications, benefits and risks.

Course Purpose:

To provide nurses with the knowledge needed to safely administer some of the

more common intravenous medications.


Learning Objectives:

1. Identify two benefits and two risks specific to IV infusion of medications.

2. Identify two precautions for administering IV insulin

3. Identify two precautions for administering IV heparin.

4. Identify two precautions for administering IV vasopressors and inotropes.

5. Identify two precautions for administering beta-blockers and calcium

channel blockers.

6. Identify two precautions for administering vasodilators.

7. Identify two precautions for administering antiarrhythmics.

Target Audience:

Advanced Practice Registered Nurses, Registered Nurses, Licensed Vocational

Nurses, and Associates

Course Author & Director Disclosures:

Dana Bartlett, RN, BSN, MA, MSN, William S. Cook, PhD,

Douglas Lawrence, MA, Susan DePasquale, CGRN, MSN, FPMHNP-BC –

all have no disclosures.

Acknowledgement of Commercial Support: There is none.

Activity Review Information:

Reviewed by Susan DePasquale, CGRN, MSN, FPMHNP-BC.

Release Date: 3/3/2015 Termination Date: 3/3/2018

Please take time to complete the self-assessment Knowledge Questions before

reading the article. Opportunity to complete a self-assessment of knowledge

learned will be provided at the end of the course.


1. Which of the following are benefits of IV administration of drugs?

a. Rapid onset of action and 100% bioavailability.

b. No risk of tissue damage and precise titration of dosage.

c. Simpler to administer than PO route, steady state drug concentrations.

d. Less expensive than PO preparations, fewer adverse effects.

2. Which of the following are risks specific to IV administration of drugs?

a. Slow onset of action, decreased bioavailability.

b. Imprecise dose titration, easier to administer than PO route.

c. Tissue damage from infiltration/extravasation, complicated administration.

d. Thrombophlebitis, higher frequency of allergic reactions.

3. Which of the following are adverse effects caused by IV insulin?

a. Hypocalcemia and hyperglycemia.

b. Hypokalemia and hypoglycemia.

c. Hyperkalemia and metabolic acidosis.

d. Hypercalcemia and metabolic alkalosis.

4. Which of the following are relatively common adverse effects caused

by IV heparin?

a. Bradycardia and hypotension.

b. Hepatotoxicity and renal damage.

c. Bronchospasm and Stevens-Johnson syndrome.

d. Bleeding and thrombocytopenia.

5. The vasopressors and inotropes may cause:

a. Peripheral vasoconstriction and dysrhythmias.

b. Bleeding and hypoglycemia.

c. Bronchospasm and hypokalemia.

d. Thrombocytopenia and seizures.


6. When using a vasopressor or an inotrope it is critical to periodically

assess:

a. Serum magnesium and serum calcium.

b. Urine output and mental status.

c. Serum glucose and aPTT.

d. Pulmonary capillary wedge pressure and temperature.

7. IV infusion of a beta-blocker can commonly cause:

a. Hypertension.

b. Thrombocytopenia.

c. Hypotension.

d. Seizures.

8. IV infusion of a calcium channel blocker can commonly cause:

a. Tachycardia.

b. QTc prolongation.

c. Hypoglycemia.

d. Hypotension.

9. IV infusion of nitroprusside can cause:

a. Bronchospasm.

b. Cyanide poisoning.

c. Bleeding.

d. Dysrhythmias.

10. IV infusion of an antiarrhythmic is contraindicated if the patient has:

a. Severe heart block.

b. Asthma.

c Hyperglycemia.

d. A bleeding disorder.


INTRODUCTION

This study module will discuss commonly used medications that are delivered by

intravenous (IV) infusion: insulin, heparin, vasopressors and inotropes, beta-

blockers, calcium channel blockers, vasodilators, and antiarrhythmics. The

manufacturers’ package inserts and several widely used and accepted drug

information databases have been used for information about dosages,

pharmacokinetics, administration, IV compatibility, precautions and

contraindications, and adverse effects and side effects. Labeled uses and adult

dosages will be covered. Off-label uses will be discussed when it is considered

appropriate and useful, however, pediatric dosages will not be provided.

INTRAVENOUS INFUSION: BENEFITS, RISKS AND DISADVANTAGES

Intravenous (IV) infusion is often the preferred route of medication

administration, and for certain drugs it is the only route by which they can be

given. Knowing these benefits and risks and how they apply to each medication is

necessary for safe and effective IV drug administration. The benefits, risks and

disadvantages of IV medications are shown in Table 1 below.

Table 1: Benefits, Risks and Disadvantages of IV Medications

BENEFITS

Alternate route of administration

Bioavailability is 100%

Precise titration of dose

Rapid onset of action

Steady state drug concentrations

RISKS AND DISADVANTAGES

Complicated administration

Cost

Infection: Local and systemic

Infiltration

Monitoring issues

Pain/irritation at the infusion site

Phlebitis

Thrombophlebitis

Time and labor intensive

Tissue damage


Nurses must also understand that the indications for medication usage, dosages,

and pharmacokinetics are specific to the IV route of administration. Some of the

common infusion medications are shown below, and in the following sections.

Nitroglycerin

Nitroglycerin relaxes smooth muscle, causes peripheral and coronary artery

vasodilation, and reduces cardiac after-load and pre-load.

1. Oral Nitroglycerin:

Oral nitroglycerin is prescribed for the treatment and prevention of angina

pectoris. The time to onset of action is approximately 60 minutes, the

duration of action is 4 – 8 hours, and the starting dose is 2.5 - 6.5 mg.

2. Intravenous Nitroglycerin:

Intravenous nitroglycerin is prescribed for the treatment and prevention of

angina pectoris, but it is also used to treat acute decompensated heart

failure, peri-operative hypertension, and for the induction of intra-operative

hypotension. The time of onset of action is approximately 3 - 5 minutes and

the starting dose is 5 mcg/minute.

Insulin

Mechanisms of Action and Pharmacokinetics

Insulin is a hormone and its most important function is to facilitate the movement

of glucose across cell membranes so that it can be used for energy or stored as

glycogen. Insulin binds to insulin receptors on cell membranes and this binding

activates glucose transporter molecules that facilitate the movement of glucose

into the cells. Insulin is the primary hormone required for glucose metabolism.

Insulin preparations are classified as rapid-acting, short-acting, intermediate-

acting, or long-acting, depending on the onset of action, the peak effect, and the

duration of action. Regular insulin is the insulin used for IV infusions. It is short-

acting insulin. The onset of action for regular insulin is 30 minutes, the peak


effect is between 2.5 - 5 hours, and the duration of action is between 4 - 12

hours.1

Why is Insulin Used?

The labeled use for insulin is for the treatment of type 1 or type 2 diabetes but

there is considerable clinical experience that supports the use of insulin infusion in

the following clinical situations:1-11

1. Diabetic ketoacidosis (DKA)

2. Hyperosmolar hyperglycemic state

3. Surgery (before, during, and after)

4. Patients receiving total parenteral nutrition

5. Treatment of hyperglycemia during sepsis

6. Treatment of hyperglycemia after trauma

7. Treatment of hyperglycemia after myocardial infarction or cardiac surgery

8. Treatment of hyperglycemia in patients with an acute neurological insult,

i.e., ischemic stroke, subarachnoid hemorrhage

9. Gestational diabetes

10. Hyperkalemia

11. Hyperglycemia caused by steroid therapy

12. Treatment of beta-blocker or calcium channel blocker overdose

Administration

During IV insulin therapy, blood glucose levels should be measured frequently,

usually every hour. Many facilities have protocols for titrating the insulin infusion

based on the hourly blood glucose level. A sample-dosing chart is shown below.

Insulin is measured in units (u) and dosed in units per hour (u/hr). A typical

infusion range is 1 to 20 units per hour.


Blood glucose level Insulin u/hr

< 110 0

111-130 2

131-150 4

151-170 6

171-190 8

191-210 10

211-230 12

231-250 14

251-270 16

Compatibility

Insulin is Y-site compatible with amiodarone, dobutamine, esmolol, heparin,

milrinone, nitroglycerin, nitroprusside, sodium bicarbonate, and vasopressin.1

Insulin is Y-site incompatible with dopamine.1 In certain circumstances insulin

may be compatible with diltiazem, labetalol, and norepinephrine.1

Precautions and Contraindications

Frequent blood glucose checks are mandatory. Signs and symptoms of

hypoglycemia include confusion, headache, dizziness, diaphoresis, and

tachycardia. Intravenous administration of insulin causes movement of potassium

from the extracellular space to the intracellular space. Patients receiving IV insulin

must be closely monitored for hypokalemia.1

The nurse must always check compatibility before running medications together

and ensure that the insulin will not be “bolused” (a large dose of medication

infused over a short period of time) if another medication is being titrated as this

may cause hypoglycemia.


Heparin


Heparin is an anticoagulant that interrupts the clotting cascade by increasing the

action of antithrombin and inactivating thrombin and the clotting factors Xa, IXa,

XIa, and XIIa.12 The onset of action of IV heparin is immediate. The duration of

action is dose dependent.12

Why is Heparin Used?

The labeled uses for heparin are: 1) the prevention and treatment of

thromboembolic disorders; and, 2) as an anticoagulant during extracorporeal and

dialysis procedures. There is considerable experience for using IV heparin in the

following clinical situations:13-19

1. Anticoagulation during percutaneous coronary intervention in patients

having an ST-segment elevation myocardial infarction.

2. Treating patients who are having unstable angina and/or non-ST segment

elevation coronary events.

3. Prior to electro-cardioversion in patients who have atrial fibrillation.

4. Anticoagulation in patients who have atrial fibrillation and are taking

warfarin but in whom warfarin therapy must be briefly interrupted.

5. Anticoagulation in critically ill patients.

6. Anticoagulation in patients undergoing abdominal surgery, cardiac surgery,

major orthopedic surgery, or spinal surgery.

7. Anticoagulation for patients who have suffered major trauma, traumatic

brain injury, acute spinal injury, or traumatic spine injury.

8. Treatment of disseminated intravascular coagulation (DIC). The risks and

benefits of heparin as a treatment for DIC are not completely understood,

but it is prescribed if DIC is caused by certain, specific etiologies.20-21


Administration

Heparin doses are measured in units (u) and dosages are typically prescribed as

units per kilogram per hour (u/kg/hr). The dosage is adjusted based on the

activated partial thromboplastin time (aPTT). The aPTT should be checked prior to

initiating heparin therapy, six hours after the heparin therapy has been started,

and six hours after any adjustment in dosage.22 The treatment goal is an aPTT

1.5 - 2 times the laboratory control time and when two consecutive aPTT

measurements are within the desired therapeutic range; the aPTT can be checked

every 24 hours.

Learning Break:

Specific heparin dosage protocols will not be discussed in this study module because: 1) the

protocols differ depending on the source; 2) the protocols differ depending on the clinical

situation; 3) the patient-to-patient response to heparin can vary quite a bit; and, 4) there is a

phenomenon called heparin resistance in which some patients require unusually high doses of

heparin.

Compatibility

Ideally, heparin would be infused through a dedicated IV site (this can be a

peripheral site) alone or only with maintenance fluids.

Heparin is Y-site compatible with dopamine, epinephrine, esmolol, insulin

(regular), isoproterenol, lidocaine milrinone, nitroprusside, norepinephrine, and

procainamide.12 It is also Y-site incompatible with amiodarone.12 In certain

circumstances heparin may be compatible with diltiazem, dobutamine, labetalol,

nicardipine, and nitroglycerin.12



Heparin is contraindicated in patients who have thrombocytopenia or severe

bleeding.12

Adverse Effects, Side Effects, and Complications

The two most common and potentially serious adverse effects caused by heparin

are hemorrhage and heparin-induced thrombocytopenia type II. The incidence of

hemorrhage caused by heparin varies but it can be significant.23,24 The risk of

bleeding increases as the dose of heparin is increased, and recent surgeries,

trauma, age (greater than 60 years), hepatic dysfunction, recent invasive

procedures, and co-morbidities also increase the risk of bleeding.25

Heparin-induced thrombocytopenia type II occurs when antibodies bind to

heparin-platelet complexes, activate the platelets, and produce a state of

hypercoaguability.26 The immune system-mediated thrombocytopenia and

thrombosis that result can cause significant incidences of morbidity and

mortality.27 Heparin-induced thrombocytopenia type II typically occurs within five

to ten days after initiation of heparin therapy.26,27 The frequency of this adverse

effect has been reported to be between 1% - 5%, and it occurs most often in

women and in post-operative patients.26,27 Heparin-induced thrombocytopenia

type II is difficult to treat successfully: discontinuation of the heparin and

administration of a vitamin K antagonist may not be sufficient to prevent the

development of thrombosis.26

Learning Break: Heparin-induced thrombocytopenia type I is more common than type II. It is

mild and self-limiting and the condition will correct even if heparin therapy is continued.


Severe bleeding caused by heparin or a heparin overdose can be treated with

protamine sulfate. Protamine sulfate binds to and inactivates heparin. One

milligram (mg) of protamine sulfate will inactivate 100 units of heparin, but

heparin has a short half-life so only the amount of heparin that has been given in

the previous 2 - 2.5 hours should be considered when calculating the dose of

protamine. Treatment of a heparin overdose would also depend on the time that

has elapsed since the overdose has been given.

VASOPRESSORS AND INOTROPES

Vasopressors and inotropes are used when there is an urgent or emergent need

to increase blood pressure and/or cardiac output. The vasopressors increase

blood pressure, systemic vascular resistance, and mean arterial pressure (MAP).

The inotropes increase the force of cardiac contraction, increasing cardiac output

and MAP. Some of these drugs can also act as a chronotrope and increase the

heart rate. Each of the vasopressors and inotropes has its particular mechanism

(or mechanisms) of action that is mediated by specific receptor binding and

agonism. Many of them bind with multiple receptor types and can have

vasopressor and inotropic effects, and a chronotropic effect as well.28

General Principles for the Use of Vasopressors and Inotropes

Many of these drugs bind to multiple receptors and can act (to a lesser or greater

degree) as an inotrope, a vasopressor, and a chronotrope. The specificity by

which they can vary depends on the dosage and the patient.28 These drugs can

cause peripheral vasoconstriction, increase myocardial oxygen consumption, and

cause dysrhythmias. Considering the clinical circumstances in which they are

used and the patients who need vasopressors and inotropes these effects can be

a significant risk.29 Fluid resuscitation is critical in order for vasopressors to be

effective.29


Measuring hemodynamic parameters is important when using vasopressors and

inotropes as these indices provide unequivocal evidence that the drugs are

working. However, the goal of treatment with the vasopressors and inotropes is

not to improve cardiovascular function but to attain and sustain good organ and

tissue perfusion. Monitoring mental status, urine output, and signs of perfusion is

as important as measuring blood pressure.29

The dosages of vasopressors and inotropes must be titrated to achieve

therapeutic goals and a second or even a third drug may be needed. The

vasopressors and inotropes should be delivered through a central venous

catheter. If that is not possible, a well-secured peripheral IV line can be used but

it must be carefully monitored.29

In high doses many of the vasopressors and inotropes can decrease or increase

heart rate to an undesired level, increase myocardial oxygen consumption, or

cause vasoconstriction. In patients who have septic shock, a decreased sensitivity

to catecholamines can occur.

If a vasopressor or an inotrope infiltrates the injection site significant tissue

damage called extravasation can occur. Basic treatment for extravasation of a

vasopressor or an inotrope consists of these steps:30

1. Stop the infusion.

2. Do not flush the IV line.

3. Aspirate whatever drug can be removed.

4. If the IV line is not needed for local antidotal treatment, remove it.

5. Elevate the extremity. Do not apply cold or heat.

6. The affected area may need to be injected with diluted phentolamine.


Local injection with terbutaline or topical nitroglycerin paste can also be used.

Phentolamine is no longer manufactured in the United States and obtaining it may

be difficult.

Incompatibility with other medication infusions is important for the nurse to

know. Many of these drugs are incompatible with sodium bicarbonate.

Dobutamine


Dobutamine binds to and stimulates the β1 receptors in the heart and acts

primarily as an inotrope. It has similar actions but to a lesser degree on the α1

and β2 receptors, acting as a weak chronotrope and vasodilator.28 Systemic

vascular resistance (SVR) is usually decreased with administration of dobutamine.

Occasionally, minimum vasoconstriction has been observed.

The onset of action of dobutamine is within one to ten minutes and the peak

effect is seen 10-20 minutes after the infusion has begun.31

Why is Dobutamine Used?

Dobutamine is used for the short-term management of patients who have cardiac

decompensation due to heart failure.28,32. It has also been used to treat

myocardial dysfunction related to sepsis but the evidence for its effectiveness in

this situation is conflicting.33,34

Dosing and Administration

The initial dosage of dobutamine is 0.5-1 mcg/kg/minute, and it should be

titrated at intervals of several minutes.31 The maintenance dosage is 2-20

mcg/kg/minute.28 The maximum dosage is typically considered to be 20

mcg/kg/minute but up to 40 mcg/kg/minute has been used. 31-33


Administration of dobutamine via a central line is preferred, but it can be given

peripherally if central access is not available.

Compatibility

Dobutamine is Y-site compatible with amiodarone, diltiazem, dopamine,

epinephrine, insulin (regular), labetalol, lidocaine, milrinone, nicardipine,

nitroglycerin, norepinephrine, and vasopressin.31 In certain circumstances

dobutamine may be Y-site compatible with heparin.31


Manufacturers of dobutamine recommend that patients who have atrial fibrillation

with rapid ventricular response should be treated with a digitalis preparation

before therapy with dobutamine is started.31 Dobutamine should be used with

extreme caution in patients who are taking a monoamine oxidase (MAO)

inhibitor.31 In patients who have idiopathic hypertrophic subaortic stenosis,

dobutamine is contraindicated.31


Adverse effects, side effects or complications include hypotension, hypokalemia,

elevations of blood pressure and heart rate; and, increased ventricular response

in patients who have atrial fibrillation, and dosage-related ventricular ectopi.31

Dopamine

Mechanism of Action and Pharmacokinetics

Dopamine binds to and stimulates β1 receptors, α1 receptors, and dopamine

receptors in the cerebral, coronary, mesenteric, and renal vasculature.35 The

clinical effects of dopamine are dosage dependent. Low dosages (0.5 - 3

mcg/kg/min) may increase renal blood flow but the clinical usefulness of this

effect has been questioned.28,36,37 In moderate dosages, 3-10 mcg/kg/min,

dopamine functions as an inotrope by stimulating β1 receptors and causing the


release of endogenous norepinephrine.28 In high doses, 10-20 mcg/kg/min,

dopamine stimulates α1 receptors and functions as a vasopressor as well as an

inotrope.28

The onset of action of dopamine is approximately 5 minutes. Dopamine has a

short half-life and the duration of action is approximately 10 minutes.35

Why is Dopamine Used?

The labeled use for dopamine is as an adjunct for the treatment of shock that is

unresponsive to fluid replacement therapy.35 The American College of

Cardiology/American Heart Association recommends dopamine for the following

conditions:

maintaining systemic perfusion and preservation of end-organ performance

in patients who have cardiogenic shock;

patients who have stage D heart failure who are waiting for a heart

transplant or mechanical circulatory support;

short-term management of patients who have severe systolic dysfunction,

low blood pressure, and significantly depressed cardiac output;

palliative care for patients who have stage D heart failure but are not

candidates for a heart transplant or mechanical circulatory support.32

Dopamine can be used to treat septic shock but only if the patient has a low risk

of tachyarrhythmias; and, only if norepinephrine cannot be used.28,33

Administration

Dosage must be individually titrated to the desired hemodynamic response. The

dosage range is typically considered to be 0.5-2-0 mcg/kg/min,28 but dosages of

50 mcg/kg/min and higher have been used.35,38 When discontinuing the infusion,

it may be necessary to gradually decrease the dose of dopamine as abrupt

sudden cessation may cause hypotension.


Compatibility

Dopamine is Y-site compatible with amiodarone, diltiazem, dobutamine,

epinephrine, esmolol, heparin, labetalol, lidocaine, milrinone, nicardipine,

nitroglycerin, nitroprusside, norepinephrine, vasopressin, and verapamil.35 It is

also Y-site incompatible with insulin (regular).35


Dopamine should be used cautiously in patients who have shock, a recent

myocardial infarction, cardiac arrhythmias, or occlusive cardiac disease.35

Dopamine should be used with extreme caution in patients who are taking a MAO

inhibitor.35


Adverse effects of dopamine include (but are not limited to) tachyarrhythmias,

ectopic beats, and increased myocardial oxygen consumption. These adverse

effects typically happen at high dosages.35

Isoproterenol (Isuprel®)

Mechanism of Action and Pharmacokinetics

Isoproterenol is a non-selective β agonist. Its primary effect is as a positive

chronotrope and positive inotrope but, because it stimulates the β2 receptors and

causes vasodilation, cardiac output is not increased.28 The onset of action of

isoproterenol is almost immediate and the duration of action is approximately 10-

15 minutes.39

Why is Isoproterenol Used?

The manufacturer’s labeled uses for isoproterenol are as follows:39

1. Mild or transient episodes of heart block that do not require electric shock

or pacemaker therapy; significant heart block and Adams-Stokes attacks

(except when caused by ventricular tachycardia or fibrillation).


2. Treatment of cardiac arrest until electric shock or pacemaker therapy is

available.

3. Treatment of bronchospasm during anesthesia.

4. An adjunct to fluid and electrolyte replacement therapy and other drugs and

procedures in the treatment of hypovolemic or septic shock and low cardiac

output states.

Off-label uses of isoproterenol include: treatment of beta-blocker overdose;

treatment of electrical storm associated with Brugada syndrome; overdrive pacing

for refractory torsade de pointes; tilt table testing for syncope; temporary control

of bradycardia in denervated heart transplant patients unresponsive to atropine;

and, treating ventricular arrhythmias caused by atrioventricular nodal block.39

Administration

The dosage of isoproterenol is 0.01 - 0.02 mcg/kg/min, but the specific dosage

used will depend on the clinical situation.28,39 Isoproterenol should not be used in

patients who have angina, digitalis intoxication, tachyarrhythmias, or ventricular

arrhythmias.39

Compatibility

Isoproterenol is Y-site compatible with amiodarone, heparin, milrinone, and

nitroprusside.39


Isoproterenol should be used cautiously in patients who have cardiovascular

disease, diabetes, or hyperthyroidism.39 It is contraindicated in patients who have

angina, digitalis intoxication, tachyarrhythmias, or ventricular arrhythmias.39



Isoproterenol can cause a wide range of cardiovascular effects including, but not

limited to, Adams-Stokes attacks, angina, arrhythmias, hypotension and

hypertension, and tachycardia.39

Norepinephrine (Levophed®)


Norepinephrine is a strong α1 receptor agonist and it has modest β1 agonist

activity.28 These mechanisms of action make norepinephrine a potent vasopressor

and to a lesser degree, a positive inotrope. Chronotropic effects are minimal.28

Norepinephrine is also thought to dilate coronary arteries, increasing coronary

circulation.40 The onset of action of norepinephrine is almost immediate and the

duration of action is approximately 1 - 2 minutes.41

Why is Norepinephrine Used?

Norepinephrine is the vasopressor of choice for the treatment of septic shock.28,30

It is also used for the treatment of shock and for treatment of severe cardiogenic

shock caused by myocardial infarction.28,38

Administration

Norepinephrine dosages are prescribed based on the clinical circumstances.38

Specific clinical conditions and norepinephrine dosage ranges are described below.

1. Septic shock:

The dose is 0.01-3 mcg/kg/minute.42 The dosage should be titrated to

attain a MAP of 65 mm Hg. 43,44

2. Shock:

The dose is 8 - 12 mcg/minute, titrated to desired response. The usual

maintenance dosage is 2 - 4 mcg/minute.41

3. Post-cardiac arrest:


Involves ACLS (Advanced Cardiac Life Support) dosing range (weight-based

dosing); Post cardiac arrest care: Initial dose: 0.1 - 0.5 mcg/kg/minute (7 -

35 mcg/minute in a 70 kg patient), and titrate to desired response.45

Compatibility

Norepinephrine is Y-site compatible with amiodarone, diltiazem, dobutamine,

dopamine, epinephrine, esmolol, heparin, labetalol, milrinone, nicardipine,

nitroglycerin, nitroprusside, and vasopressin.41

Precautions and contraindications

Norepinephrine should be used with extreme caution in patients who are taking a

MAO inhibitor.41 Norepinephrine is contraindicated in the following clinical

conditions or situations: hypotension from hypovolemia except as an emergency

measure to maintain coronary and cerebral perfusion; mesenteric or peripheral

vascular thrombosis unless the drug is a lifesaving procedure; during anesthesia

with cyclopropane or halothane; and, during anesthesia due to the risk of

ventricular arrhythmias.41

Adverse Effects, Side effects, and Complications

Adverse effects of norepinephrine are arrhythmias, bradycardia, and peripheral

ischemia.41

Phenylephrine (Neo-Synephrine®)


Phenylephrine is a powerful vasopressor that increases systemic vascular

resistance by direct α1 agonism.28 Vasoconstriction is more prolonged than that

produced by epinephrine. The onset of action of phenylephrine is almost

immediate and the duration of action is approximately 15 - 20 minutes.46

Why is Phenylephrine Used?


Phenylephrine is used to treat hypotension caused by shock.46 Phenylephrine

should not be used to treat hypotension caused by septic shock unless: 1) the

use of norepinephrine may cause serious arrhythmias; 2) the cardiac output is

known to be high and the blood pressure is low; or, 3) as a salvage therapy.28

Administration

The dosage of phenylephrine used to treat severe hypotension is 0.5 - 2

mcg/kg/min, but higher and lower doses have been used.28,45-47

Compatibility

Phenylephrine is Y-site compatible with amiodarone and vasopressin.46


Phenylephrine should be used cautiously in patients who have cardiovascular

disease. In these patients phenylephrine may cause reflex bradycardia, decreased

cardiac output, or precipitate angina and/or heart failure.46 Nurses should also

know that acidosis may reduce the efficacy of phenylephrine.46

Phenylephrine is contraindicated in patients who have severe hypertension or

ventricular tachycardia.46


Adverse effects, side effects or complications are reflex bradycardia,

hypertension, peripheral vasoconstriction, precipitation of angina and/or heart

failure, and reduced cardiac output.46

Epinephrine



Epinephrine is an α1, β1, and β2 agonist. Epinephrine is a positive chronotrope and

a positive inotrope, and it dilates the bronchial passages. Depending on the

dosage, epinephrine can cause vasodilation or vasoconstriction.48

The onset of effects is almost immediate, and epinephrine has a half-life of less

than 5 minutes.48

Why is Epinephrine Used?

Epinephrine IV infusion is used as a second-line agent for the treatment of

hypotension caused by septic shock.28 It is used for the treatment of hypotension

caused by shock; and,48 for the treatment of symptomatic bradycardia

unresponsive to atropine.49

Administration

The dosages for IV epinephrine in certain resuscitation scenario are outlined

below.

1. The dosage for the treatment of septic shock is 0.05 – 2 mcg/kg/min. The

dosage may be increased every 10 - 15 minutes by 0.05 – 2 mcg/kg/min

until the desired blood pressure has been reached. Epinephrine should be

weaned slowly, preferably over 12 - 24 hours.48

2. The dosage for severe, fluid resistant shock is 0.1 - 0.5 mcg/kg/min,

titrated to the desired response.45

3. The dosage for bradycardia that is symptomatic and unresponsive to

atropine is: 2 to 10mcg/minute or 0.1 to 0.5 mcg/kg/minute.49

Compatibility


Epinephrine is Y-site compatible with amiodarone, diltiazem, dobutamine,

dopamine, heparin, labetalol, milrinone, nicardipine, nitroglycerin, nitroprusside,

norepinephrine, and vasopressin.48


Epinephrine should be used with caution in patients who have cardiovascular

disease, cerebrovascular disease, diabetes, Parkinson’s disease, or thyroid

disease.48

There are no absolute contraindications to the use of epinephrine in an

emergency situation.48


Cardiac, gastrointestinal, and central nervous system adverse effects or side

effects including but not limited to angina, hypertension, tachycardia, nausea,

vomiting, anxiety, dizziness, and headache may be noted during IV infusion of

epinephrine. The frequency of these is not known.48

Vasopressin


Vasopressin is a synthetic form of an endogenous hormone. Vasopressin binds to

the V1 vasopressin receptors in the vascular smooth muscle, causing

vasoconstriction. It also binds to the V2 vasopressin receptors in the renal

collecting tubules, and this increases the collecting duct permeability and water

reabsorption. These effects increase the mean arterial pressure and systemic

vascular resistance and maintain intravascular volume.28

The onset of effects is less than or equal to 15 minutes, and the duration of action

is less than or equal to 20 minutes.50

Why is Vasopressin Used?


The labeled use for IV infusion of vasopressin is for the treatment of shock that is

unresponsive to IV fluids and catecholamines.50 Vasopressin is indicated for

treatment of hypotension caused by septic shock and it appears to be particularly

useful for this when used in conjunction with norepinephrine.28,51 Vasopressin is

not recommended to be used as the single vasopressor when treating

hypotension caused by septic shock, but dosages up to 0.03 units/minute can be

given to patients who are receiving norepinephrine.33 Dosages higher than 0.03 -

0.04 units/minute should only be used for salvage therapy, i.e., when an

adequate mean arterial pressure cannot be achieved by other vasopressors.33

Vasopressin can be used to treat cardiac arrest caused by anaphylaxis that is

unresponsive to epinephrine.52 This is an off-label use. Other off-label uses of

vasopressin include the treatment of pulseless cardiac arrest or pulseless

electrical activity, and the treatment of bleeding esophageal varices.50

Administration

The recommended dosage of vasopressin for shock is 0.03 units/minute.50

Vasopressin should be titrated by 0.005 units per minute at 10- to 15-minute

intervals to a maximum dose of 0.1 units per minute to achieve the target blood

pressure. When the target blood pressure has been maintained for 8 hours

without the use of catecholamines, vasopressin should be tapered by 0.005

units/minute every hour as tolerated.50

Hypotension caused by septic shock can be treated by infusing vasopressin

starting at 0.03 units per minute, used concurrently with norepinephrine, to

attain the desired mean arterial pressure or to decrease norepinephrine dose.33

Doses greater than 0.03 units per minute may have more cardiovascular side

effects and should only be used for salvage therapy.33 Also, hypotension occurring

after discontinuation of vasopressin has been reported.53 Vasopressin dosages

should be slowly tapered after other vasopressors or inotropes have been

discontinued.


Compatibility

Vasopressin is Y-site compatible with amiodarone, diltiazem, dobutamine,

dopamine, epinephrine, heparin, insulin (regular), lidocaine, milrinone,

nitroglycerin, norepinephrine, and phenylephrine.50


Vasopressin should be used with caution in patients who have asthma,

cardiovascular disease, goiter with cardiac complications, migraines, renal

disease, seizure disorder, or vascular disease. 50


Adverse effects, side effects, or complications are angina, arrhythmias,

bradycardia, and vasoconstriction. The frequency of these is not defined.50

Milrinone (Primacor®)

Mechanisms of Actions and Pharmacokinetics

Milrinone is a selective phosphodiesterase inhibitor that inhibits the conversion of

cAMP to AMP in the heart and the vasculature.28,54 Milrinone is a positive inotrope

and a vasodilator that increases cardiac output and decreases systemic vascular

resistance.28

The onset of action of milrinone is between 5 - 15 minutes and it has a half-life of

approximately 2.5 hours.54

Learning Break: Phosphodiesterase is an enzyme that breaks down intra-cellular second


messengers such as cyclic adenosine monophosphate (cAMP). Adrenergic drugs such as

epinephrine cannot directly affect target organs. They bind to adrenergic receptors and

activate cAMP and cAMP in turn increases the activity of intra-cellular enzymatic processes.

Mirinone and similar medications increase intra-cellular concentrations of cAMP and by doing so

increase heart rate and cause vasodilation.

Why is Milrinone Used?

Milrinone is used for the short-term therapy of patients who have acute,

decompensated heart failure.32 Off-label uses of milrinone IV infusion include:

inotropic therapy for patients unresponsive to other therapies; palliative therapy

for patients who have end-stage heart failure and who are not transplant

candidates; and, rescue therapy for term infants who have pulmonary

hypertension.54,55

Administration

The American College of Cardiology Foundation/American Heart Association

recommends a maintenance dosage is 0.125 mcg/kg/min - 0.75 mcg/kg/min.32

Higher maintenance dosages have been used,54 and some sources recommend a

loading dosage of 50 mcg/kg administered over 10 minutes followed by a

maintenance dose titrated to the clinical response.54 There is some evidence that

starting milrinone without a loading dose is more effective.56 Milrinone may be

effective in treating acute heart failure following myocardial infarction but the

dosage and effectiveness of the drug for this purpose have not been

established.57

If the patient has atrial flutter or fibrillation, rate control before starting milrinone

is recommended. Milrinone may increase the ventricular response in these

patients.54

Compatiblity


Milrinone is Y-site compatible with amiodarone, diltiazem, dobutamine, dopamine,

heparin, insulin (regular), isoproterenol, labetalol nicardipine, nitroglycerin,

nitroprusside, norepinephrine, sodium bicarbonate, vasopressin, and verapamil.54

Additionally, milrinone is Y-site incompatible with procainamide.54


Certain precautions should be observed when using milrinone.54 Hypokalemia and

hypomagnesemia should be corrected before treatment with milrinone is started.

Milrinone should be used with caution in patients who have renal impairment.

Concurrent use of milrinone and inamrinone is contraindicated.54

Adverse Effects, Side Effects and Complications

Adverse effects, side effects, or complications are ventricular arrhythmias,

especially in patients who have renal dysfunction.54,58 These may occur even after

milrinone has been discontinued.54

BETA-BLOCKERS

Beta-blockers competitively antagonize the effects of catecholamines at the β

receptors. They can be selective or non-selective. Some beta-blockers have

adrenergic receptor antagonist effects and a few have intrinsic sympathomimetic

activity, as well. They are primarily given as oral preparations for the treatment of

angina, hypertension, and certain arrhythmias, but some can be given as an IV

bolus or a continuous IV infusion, and there are many off-label uses for the beta-

blockers.

Several types of beta-blockers are outlined in the section below, which includes

drug action and expected treatment outcomes.

Esmolol (Brevibloc®)



Esmolol is a β1 selective beta-blocker. Esmolol has no intrinsic sympathomimetic

or membrane-stabilizing activity. At high doses esmolol will inhibit the β2

receptors in the peripheral vasculature and the bronchial tree.59,60

The onset of action is 2 - 10 minutes. The duration of action is approximately 10 -

30 minutes, but this can be extended after cumulative doses or extended use.59

Learning Break: Membrane-stabilizing refers to the inhibition of action potentials by the

interruption of ion movements across cell membranes. Certain drugs “stabilize” cell membranes,

making them less able or unable to depolarize and preventing the cell from initiating a

contraction or transmitting a nerve impulse.

Why is Esmolol Used?

The labeled uses or esmolol are:59-61

1. Treatment of supraventricular tachycardia (SVT) and controlling ventricular

rate in patients who have atrial fibrillation or flutter;

2. Treatment of intraoperative and postoperative tachycardia and/or

hypertension;

3. Treatment of noncompensatory sinus tachycardia.

Administration

In cases of supraventricular tachycardia or non-compensatory sinus tachycardia

the loading dose (optional) is 0.5 mg/kg over 1 minute followed by an infusion of

50 mcg/kg/minute for 4 minutes. The infusion may be continued at 50

mcg/kg/minute and, if the response is inadequate, it can be titrated in 50


mcg/kg/minute increments to a maximum of 200 mcg/kg/minute; however, the

dosage should not be increased at intervals less than every 4 minutes.

For a more rapid response after the loading dose and the continuous infusion,

another 0.5 mg/kg bolus dosage can be given over 1 minute and the

maintenance dosage can be increased to 100 mcg/kg/minute for 4 minutes. A

third bolus dose can be given if needed, 0.5 mg/kg, and the infusion can be

increased to 150 mcg/kg/minute after 4 minutes at that rate. Additionally, the

infusion can be increased to 200 mcg/kg/minute, and no fourth bolus dose given

before the increase to 200 mcg/kg/minute.59

In cases of intraoperative or post-operative tachycardia and/or hypertension, the

nurse may initiate infusion rates to achieve immediate or gradual control. For

immediate control, an initial bolus of 1 mg/kg over 30 seconds is given, followed

by an infusion of 150 mcg/kg/minute. The infusion rate may be titrated as

needed, and the maximum dosage is 300 mcg/kg/minute. For gradual control, an

initial bolus of 0.5 mg/kg over 1 minute is given, and then an infusion of 50

mcg/kg/minute infusion for 4 minutes. The infusion can be titrated in increments

of 50 mcg/kg/minute; however, the dosage should not be increased at intervals

less than every 4 minutes to a maximum dosage of 300 mcg/kg/minute. A bolus

dose of 0.5 mg/kg over 1 minute prior can be given before each increase in the

infusion rate.59

Controlling the ventricular rate in patients who have atrial fibrillation or flutter

involves a loading dose of 0.5 mg/kg given over 1 minute. This is followed by an

IV infusion at 50 mcg/kg/minute for 4 minutes and, if needed, the infusion can be

continued at that rate. If the initial response to the bolus and the IV infusion is

not optimal, another bolus of 0.5 mg/kg over 1 minute can be given and the

infusion rate can be increased to 100 mcg/kg/minute for 4 minutes and these

steps can be repeated until the desired heart rate is reached or hypotension

begins to occur.59 At that point, the infusion rate should be decreased to less than


or equal to 25 mcg/kg/minute. If the safety endpoint is exceeded, the infusion

should be stopped, reassessed, and restarted at a reduced dose.59

Esmolol is contraindicated if the patient has severe sinus bradycardia or sick sinus

syndrome; if there is second or third-degree heart block (except in patients with

a functioning ventricular pacemaker); in patients who have cardiogenic shock or

decompensated heart failure; and, in patients who have pulmonary hypertension.

Esmolol should not be used in conjunction with IV administration of a calcium

channel blocker or if the pharmacologic effects of the drugs will overlap.59

Compatibility

Esmolol is Y-site compatible with amiodarone, diltiazem, dopamine, heparin,

insulin (regular), labetalol, nicardipine, nitroglycerin, nitroprusside, and

norepinephrine.59 In certain circumstances esmolol may be Y-site compatible with

sodium bicarbonate.59


Certain precautions should be observed when using esmolol.59 Infusion into small

veins or through a butterfly catheter should be avoided because of the risk for

thrombophlebitis. There should be close monitoring of blood pressure during

administration as hypotension is common. Additionally, hyperkalemia can occur in

patients who have renal failure.

Esmolol is contraindicated if the patient has severe sinus bradycardia or sick sinus

syndrome; if there is second or third-degree heart block (except patients with a

functioning ventricular pacemaker); in patients who have cardiogenic shock or

decompensated heart failure; and, in patients who have pulmonary hypertension.

Esmolol should not be used in conjunction with IV administration of a calcium

channel blocker or if the pharmacologic effects of the drugs will overlap.59

Adverse Effects, Side Effects and Complications


Adverse effects, side effects or complications of esmolol are hypotension,

dizziness, nausea and vomiting.59

Labetalol


Labetalol is an α1, β1, and β2 antagonist. The ratio of alpha to beta blockade in

the IV form of the drug is 1:7. Labetalol has weak intrinsic sympathomimetic

activity and does not stabilize the cardiac membrane.62 Labetalol is a negative

chronotrope, a negative inotrope, and it dilates peripheral vasculature.

The onset of action is 2 - 5 minutes. The duration of action depends on the dose

and the method of infusion.

Why is Labetalol Used?

The labeled use of IV labetalol is for the treatment of hypertensive emergencies.62

Off-label uses are for the treatment of hypertension during ischemic stroke,

pediatric hypertension, treatment of a patient with subarachnoid hemorrhage,

and chronic hypertension during pregnancy.62-65

Administration

1. Hypertensive emergencies:

The bolus dose is 20 mg IV push given over 2 minutes. This can be followed

as needed with 40 - 80 mg bolus doses (Some sources recommend 20 – 80

mg) every 10 minutes to a total of 300 mg.62,66 The constant infusion rate

dose is 0.5 - 2 mg/minute.66 However, there is limited information on how

long a constant infusion can be used. The manufacturer’s recommendation

is not to exceed a total dose of 300 mg and to discontinue the infusion after

2.5 hours at 2 mg/minute, but there is clinical experience using higher

doses and for much longer periods of time.59

2. Ischemic stroke:


Controlling blood pressure during and after reperfusion treatment to

maintain a blood pressure less than or equal to 180/105 mm Hg. If the

systolic blood pressure is greater than 180 to 230 mm Hg or diastolic

greater than 105 to 120 mm Hg, labetalol 10 mg over 1 to 2 minutes

should be given followed by an infusion of 2 to 8 mg/minute.64

3. Chronic hypertension during pregnancy:

To treat a hypertensive emergency in pregnancy (systolic BP greater than

or equal to 160 mm Hg or diastolic BP greater than or equal to 110 mm Hg)

an initial IV dose of labetalol 20 mg should be given. If the blood pressure

does not respond the dose can be increased every 10 minutes in increments

of 20 to 40 mg. The maximum single dose is 80 mg.63,67 A continuous

infusion of 1 -2 mg per minute may be used if needed.63 After the initial

dose a continuous infusion of 1 to 2 mg/minute can be used instead of

intermittent dosing.63

Compatibility

Labetalol is Y-site compatible with amiodarone, diltiazem, dobutamine, dopamine,

epinephrine, esmolol, lidocaine, milrinone, nicardipine, nitroglycerin,

nitroprusside, and norepinephrine.62


The following precautions should be observed when using labetalol:62 excessive

administration of labetalol can cause prolonged hypotension and/or bradycardia;

labetalol should be used with caution in patients who have diabetes, hepatic

impairment, depression, peripheral vascular disease, asthma, heart failure, or

myasthenia gravis. Labetalol should not be used patients with hyperadrenergic

states, i.e., amphetamine or cocaine intoxication, unless α adrenergic blockade

has been accomplished.62


Labetalol is contraindicated if the patient has severe bradycardia or second or

third-degree heart block, unless the patient has a functioning ventricular

pacemaker. Additionally, it is contraindicated in patients who have cardiogenic

shock or uncompensated heart failure, asthma, and, if there is severe and

prolonged hypotension.62


Dizziness and orthostatic hypotension are common after administration of

labetalol.62

CALCIUM CHANNEL BLOCKERS

Calcium channel blockers decrease the influx of calcium through voltage-gated

calcium channels in the myocardium, the cardiac impulse forming and conduction

tissues, and the peripheral vasculature. Calcium influx is needed for vascular

smooth muscle and cardiac muscle contraction and for sinoatrial node and

atrioventricular node depolarization; and, by inhibiting calcium influx the calcium

channels blockers produce negative chronotropic, dromotropic, and inotropic

effects, and relax the smooth muscle tissue of the peripheral vasculature. Heart

rate and blood pressure are lowered, coronary blood vessels are dilated, and

oxygen delivery to the myocardium is increased.

There are three classes of calcium channel blockers used in the US:

benzothiazepine (i.e., dialtiazem), dihysropyridines (i.e., nicardipine), and,

phenylalkylamine (i.e., verapamil). Each of these affects the myocardium, the

sinoatrial node and the atrioventricular node, the coronary circulation, and the

smooth muscle of the peripheral vasculature to a greater or lesser degree.

The calcium channel blockers are primarily used for the treatment of angina and

hypertension.


Diltiazem (Cardizem®)


Diltiazem blocks the movement of calcium through calcium ion channels in the

myocardium, the atrioventricular node and sinoatrial node, and the peripheral

vasculature. Diltiazem causes coronary vascular dilation and peripheral

vasodilation, lowering blood pressure and increasing myocardial blood flow.68

The onset of action is 3 minutes. The duration of action is 0.5 - 10 hours.68

Why is Diltiazem Used?

IV infusion of diltiazem is used to treat patients who have atrial fibrillation or

atrial flutter and a rapid ventricular rate and for conversion of paroxysmal

supraventricular tachycardia (PSVT).68 The off-label use for IV diltiazem is

treatment of stable narrow-complex tachycardia uncontrolled or unconverted by

adenosine or vagal maneuvers or for recurrent supraventricular tachycardia.49

Administration

1. For treatment of rapid ventricular response atrial fibrillation or atrial flutter

or PSVT:

Initial bolus dose is 0.25 mg/kg actual body weight over 2 minutes. A

repeat bolus dosage of 0.35 mg/kg can be given 15 minutes after the initial

dose if the response is inadequate. The continuous IV infusion dosage is 10

mg/hour; this can be increased in increments of 5 mg/hour up to 15

mg/hour.

Continuous IV infusions of greater than 15 mg/hour for more than 24 hours

are not recommended.68,69


2. Treatment of stable narrow-complex tachycardia uncontrolled or

unconverted by adenosine or vagal maneuvers or treatment of recurrent of

SVT:

Initial dose is 15 - 20 mg (or 0.25 mg/kg) IV over 2 minutes. Additional

doses of 20 - 25 mg (0.35 mg/kg) can be given every 15 minutes if

needed. The continuous infusion rate should be 5 -15 mg/hour.49

Compatibility

Diltiazem is Y-site compatible with dobutamine, dopamine, epinephrine, esmolol,

labetalol, lidocaine, milrinone, nicardipine, nitroglycerin, nitroprusside, and

norepinephrine.68 Diltiazem is Y-site incompatible with heparin.68


Diltiazem is contraindicated if patients have any of the following conditions:68 sick

sinus syndrome (except in patients with a functioning artificial pacemaker);

second- or third-degree heart block (except in patients with a functioning artificial

pacemaker); severe hypotension (systolic less than 90 mm Hg); cardiogenic

shock; administration concomitantly or within a few hours of the administration of

IV beta-blockers; atrial fibrillation or flutter associated with accessory bypass

tract (i.e., Wolff-Parkinson-White syndrome); or, ventricular tachycardia.


Adverse effects, side effects, or complications are bradycardia, headache,

hypotension, and precipitation of heart failure.49,68

Nicardipine (Cardene®)


Nicardipine blocks the movement of calcium through calcium ion channels in the

myocardium and the peripheral vasculature. It decreases systemic vascular

resistance and blood pressure and dilates the coronary vasculature. It has no


appreciable effect on the sinoatrial node, the atrioventricular node or the His-

Purkinje system.70,71

The onset of action is 10 minutes and the duration of action is approximately 20

minutes.71

Why is Nicardipine Used?

Parenteral nicardipine is used for the short-term treatment of hypertension when

the use of oral medications is not possible.70 The off-label use for IV nicardipine is

for the control of blood pressure in patients who have had an acute ischemic

stroke.64

Administration

Short-term treatment of hypertension:

Nicardipine 5 mg/hour, increased in increments of 2.5 mg/hour every 5 minutes,

is recommended if rapid correction is needed, or every 15 minutes. The maximum

dosage is 15 mg/hour. If the dosage is rapidly increased, reducing it by 3

mg/hour should be considered once the target blood pressure has been

achieved.71

Compatibility

Nicardipine is Y-site compatible with dobutamine, dopamine, epinephrine,

esmolol, labetalol, milrinone, nitroglycerin, nitroprusside, and norepinephrine. In

certain circumstances it may be compatible with heparin.71


Nicardipine should be used with caution if the patient has heart failure, hepatic

impairment, hypertrophic cardiomyopathy, renal impairment, or a mild degree of

aortic stenosis.71 Nicardipine is contraindicated if the patient has advanced aortic

stenosis.71


Adverse Effects, Side effects, and Complications

Headache, hypotension, nausea and vomiting, and tachycardia are the most

common side effects.70

Verapamil

Verapamil blocks the movement of calcium through calcium ion channels in the

myocardium, the SA node, the cardiac conducting system, and the peripheral

vasculature. Verpamil acts as a negative inotrope, it prolongs the refractory

period in the atrioventricular node, it decreases systemic vascular resistance and

blood pressure, and it dilates the coronary vasculature.72,73

Why is Verapamil Used?

Verapamil is used to treat supraventricular tachycardia and for rate control in

patients who have paroxysmal supraventricular tachycardia or atrial fibrillation.72

Administration

1. Supraventricular Tachycardia:

The recommended initial dose of verapamil is 2.5 - 5 mg over 2 minutes. A

second dose of 5 - 10 mg may be given 15 to 30 minutes after the initial

dose if tolerated by the patient, and if the patient does not respond to the

initial dose. The maximum total dose is 20 - 30 mg.72

2. Atrial fibrillation rate control:

The recommended initial dose of verapamil is 0.075 - 0.15 mg/kg given as

a bolus over 2 minutes. An additional 10 mg can be given after 30 minutes

if there is no response, followed by a continuous infusion of 0.005

mg/kg/minute.69

Compatibility

Verapamil is Y-site compatible with dobutamine, dopamine, and milrinone.72



Verapamil should be used with caution if the patient has hepatic impairment,

renal impairment, myasthenia gravis, Duchenne’s muscular dystrophy,

hypertrophic cardiomyopathy, or is being treated with a beta-blocker or digoxin.72

Verapamil can slow the recovery from non-depolarizing neuromuscular blocking

agents.72

Verapamil is contraindicated if patients have any of the following conditions:

severe left ventricular dysfunction; hypotension (systolic pressure less than 90

mm Hg) or cardiogenic shock; sick sinus syndrome (except in patients with a

functioning ventricular pacemaker); second or third-degree atrioventricular block

(except in patients with a functioning ventricular pacemaker); atrial flutter or

fibrillation and an accessory bypass tract (Wolff-Parkinson-White [WPW]

syndrome, Lown-Ganong-Levine syndrome).72

Adverse Reactions, Side Effects, and Complications

Adverse effects, side effects, and complications are confusion, dizziness, and

hypotension.72

VASODILATORS

The primary effect of the two drugs discussed in this section, nitroglycerin and

nitroprusside, is vasodilation. They have similar mechanisms of action but they

are used for different clinical situations.

Nitroglycerin


Nitroglycerin stimulates the formation and release of nitric oxide, an endogenous

compound that relaxes vascular smooth muscle in the peripheral veins and to a

lesser degree, the peripheral arteries. This effect decreases venous return to the

heart, pre-load and to a lesser degree, after-load, myocardial oxygen


consumption, systemic vascular resistance and mean arterial pressure; and,

lowers blood pressure and dilates coronary arteries.74,75

The onset of action of IV nitroglycerin is immediate and the duration of action is 3

- 5 minutes.

Why is Nitroglycerin Used?

Intravenous nitroglycerin is used to treat the following conditions and prevention

strategies:74

1. The prevention and treatment of angina pectoris.

2. Acute decompensated heart failure, especially when associated with acute

myocardial infarction. Peri-operative hypertension, especially during

cardiovascular surgery.

3. Induction of intra-operative hypotension.

The off-label uses of IV nitroglycerin are the treatment of pulmonary hypertension

and treatment of unstable angina or non-ST-segment myocardial infarction.74,76

Administration

1. Treatment of angina pectoris:

The initial dosage is 5 mcg/minute. This can be increased in increments of 5

mcg every 3 - 5 minutes up to 20 mcg/minute. If there is no response at

that point the dosage may be increased by 10 – 20 mcg/minute every 3 - 5

minutes. The generally accepted maximum dosage is 400 mcg/minute.74

2. Treatment of unstable angina or non-ST-segment myocardial infarction: The

initial dosage is 10 mcg/minute. It should be increased by 10 mcg/minute

every 3 - 5 minutes until relief of symptoms or the desired blood pressure

response is attained. If there is no response at 20 mcg/minute, the dosage

should be increased by 10 - 20 mcg/minute.76

Compatibility


Nitroglycerin is Y-site compatible with amiodarone, diltiazem, dobutamine,

dopamine, esmolol, epinephrine, insulin (regular) labetalol, lidocaine, milrinone,

nicardipine, nitroprusside, norepinephrine, and vasopressin. In certain situations

nitroglycerin may be Y-site compatible with heparin.74


Nitroglycerin binds to soft plastics so it should be administered in glass bottles

and with the IV infusion set supplied by the manufacturer.74

Nitroglycerin is contraindicated for patients who have any of the following

conditions: hypersensitivity to nitrates, corn, or corn products; constrictive

pericarditis; pericardial tamponade; or, restrictive cardiomyopathy.74


Adverse effects, side effects, and complications are bradycardia, headache,

hypotension, syncope, and tachycardia.74

Nitroprusside (Nitropress®)


Nitroprusside stimulates the formation and release of nitric oxide, an endogenous

compound that relaxes vascular smooth muscle in the peripheral veins and to a

lesser degree, the peripheral arteries. This effect decreases peripheral resistance

and after-load, and lowers blood pressure.77

The onset of action of nitroprusside is less than 2 minutes. The duration of action

is between 1 - 10 minutes.77

Why is Nitroprusside Used?

Nitroprusside is used for the following situations and conditions:66,77

1. Treatment of hypertensive crisis


2. Treatment of acute, decompensated heart failure

3. Controlled hypotension to reduce bleeding during surgery.

Nitroprusside has an unlabeled use for the treatment of hypertension in patients

who are having an acute ischemic stroke.64

Administration

1. Hypertensive crisis:

The dosage of nitroprusside is 0.25 - 5 mcg/kg/minute. This can be titrated

in increments of 0.5 mcg/kg/minute up to a maximum dosage of 10

mcg/kg/minute.66,77

2. Acute decompensated heart failure:

The starting dosage is 5 - 10 mcg/minute. The dosage can be titrated every

5 minutes and the dosage range that is typically effective is 5 - 300

mcg/minute. Dosages greater than 400 mcg/minute are not recommended

because there is little additional benefit and an increased risk for cyanide

toxicity.77

3. Nitroprusside has a labeled use for controlled hypotension to reduce

bleeding during surgery but there is no specific dosing information for this

use.

Compatibility

Nitroprusside is Y-site compatible with diltiazem, dobutamine, dopamine,

epinephrine, esmolol, insulin (regular), isoproterenol, labetalol, lidocaine,

milrinone, norepinephrine, nitroglycerin, and procainamide. In certain

circumstances nitroprusside may be compatible with amiodarone. It is compatible

in a syringe with heparin.77



Nitroprusside solutions must be protected from light. The IV bag must be covered

with aluminum foil or another opaque material.77

Nitroprusside is contraindicated for the treatment of compensatory hypertension

(aortic coarctation, arteriovenous shunting); for controlled hypotension during

surgery in patients who have inadequate cerebral circulation or in moribund

patients requiring emergency surgery; for the treatment of high output heart

failure associated with reduced systemic vascular resistance, i.e., septic shock;

and, in patients who have congenital optic atrophy or tobacco amblyopia.77

Nitroprusside and Cyanide Toxicity

Nitroprusside is metabolized to cyanide and cyanide toxicity is possible. Cyanide

toxicity can be avoided by using the lowest possible dose, monitoring for changes

in mental status and lactic acidosis, and avoiding if possible using nitroprusside

for greater than 24 – 48 hours. Dosages of 10 mcg/kg/minute should never be

used for greater than 10 minutes.77


Adverse effects, side effects, or complications are hypotension, headache,

methemoglobinemia.77 Nitroprusside can decrease cerebral, coronary, and renal

perfusion; and, this is a dose-dependent effect.66,78

ANTIARRHYTHMICS

Antiarrhythmics are used to prevent and treat arrhythmias. These drugs have

many complex effects on the heart, i.e., decreasing impulse conduction and

velocity, increasing the refractory period of the myocardium, and increasing the

electrical stimulation threshold of the ventricles. Despite this wide variety of

actions the clinical effectiveness of all of the antiarrhythmics is mediated by their

ability to block the movement of calcium, sodium, or potassium through ion

channels in the heart. The Vaughan Williams classification system divides the

http://www.uptodate.com/contents/nitroprusside-drug-information?source=see_link


antiarrhythmics into four categories based on their electrophysiological effects,

Class I, II, II, and IV. Class I antiarrhythmics are further divided, Class IA, IB,

and IC.

Amiodarone (Nexterone®)


Amiodarone is a Class III anti-arrhythmic. The anti-arrhythmic effect of these

drugs is primarily mediated by affecting the movement of potassium through ion

channels in the myocardium and prolongation of the action potential. Amiodarone

also has electrophysiological properties of the Class I, II, and IV antiarrhythmics;

it acts as α and β adrenergic receptor antagonists; it affects the movement of

calcium, potassium, and sodium through ion channels in the myocardium; and, it

decreases the rate of sinoatrial depolarization and decreases conduction through

the atrioventricular node.79,80 Amiodarone has negative chronotropic, inotropic,

and dromotropic actions, and it also causes vasodilation.80

The pharmacokinetics of amiodarone are complex and there is little information

about the onset and duration of action of IV amiodarone.

Why is Amiodarone Used?

Amiodarone infusion is used for the treatment and prevention of

hemodynamically unstable ventricular tachycardia or ventricular fibrillation that

do not respond to other therapies.79

The off-label uses of IV amiodarone include: treatment of heart failure in patients

who have atrial fibrillation without a pre-excitation syndrome; prevention of post-

operative atrial fibrillation or atrial flutter associated with cardiothoracic surgery;

pharmacologic cardioversion of supraventricular tachycardia; and, the treatment

of atrial fibrillation in critically ill patients who require rate control and do not

have a pre-excitation syndrome.69,79


Administration

1. Pulseless ventricular tachycardia or ventricular fibrillation:

IV or intraosseous (IO) bolus: amiodarone 300 mg rapid IV push, undiluted.

If the arrhythmia persists after the initial dose and after defibrillation,

another dose of 150 mg can be given. When spontaneous circulation

returns, start an amiodarone infusion of 1 mg/minute for 6 hours, then 0.5

mg/minute for 18 hours.49

2. Stable ventricular tachycardia:

In the first 24 hours amiodarone 1050 mg is given using the following

regimen:

Step 1: 150 mg (100 mL) over first 10 minutes (mix 3 mL in 100

mL D5W).

Step 2: 360 mg (200 mL) over next 6 hours (mix 18 mL in 500 mL

D5W): 1 mg/minute

Step 3: 540 mg (300 mL) over next 18 hours: 0.5 mg/minute.79

Note: After the first 24 hours: 0.5 mg/minute utilizing

concentration of 1 to 6 mg/mL. The mL amounts in parentheses

above refer to the amounts of amiodarone and the different

available concentrations of the drug.

Compatibility

Amiodarone is Y-site compatible with diltiazem, dobutamine, dopamine,

epinephrine, esmolol, insulin (regular), isoproterenol, labetalol, lidocaine,

metoprolol, milrinone, nitroglycerin, norepinephrine, phenylephrine,

procainamide, and vasopressin.79 Amiodarone is Y-site incompatible with

heparin.79



Infusions greater than 2 hours must be administered in a non-PVC container. PVC

tubing is should be used regardless of the infusion duration.79

Correct hypokalemia or hypomagnesemia before using amiodarone and

throughout therapy.79

Amiodarone is contraindicated in patients who have any of the following

conditions: sinus-node dysfunction causing marked sinus bradycardia; second and

third-degree heart block (except in patients with a functioning pacemaker);

bradycardia causing syncope (except in patients with a functioning pacemaker),

Wolff-Parkinson-White syndrome; and, cardiogenic shock.79

Adverse effects, side effects, and complications

Adverse effects, side effects, or complications are bradycardia and hypotension,

rate-related.79

Amiodarone has a boxed warning. Liver toxicity is common after administration of

amiodarone. It is usually mild and associated with the oral form of the drug, but

severe hepatotoxicity has been reported and this effect may occur after prolonged

duration of IV amiodarone.79

Lidocaine


Lidocaine is a Class Ib anti-arrhythmic. It is also used as a local anesthetic.

Lidocaine inhibits the movement of sodium through fast-sodium ion channels in

the myocardium and cardiac conducting tissue and in nerve conducting issues.

This effect stabilizes the myocardium, making it less able to depolarize in


response to a stimulus. It prevents spontaneous depolarization of the

myocardium; and, it decreases the automaticity of the His-Purkinje system.81

The onset of action of a bolus dose of lidocaine is within 45 - 90 seconds. The

duration of action is 10 - 20 minutes.81

Why is Lidocaine Used?

Lidocaine is used for the acute treatment of ventricular arrhythmias caused by

myocardial infarction or by cardiac manipulation during surgery.81

Administration

1. Ventricular fibrillation or pulseless ventricular tachycardia (after

defibrillation, CPR, and vasopressor administration, and if amiodarone is not

available:

The initial dosage IV or IO is 1- 1.5 mg/kg. If needed this can be followed

with boluses of 0.5 - 0.75 mg/kg every 5 - 10 minutes up to a maximum

dosage of 3 mg/kg. This is followed by a continuous infusion of 1 - 4

mg/kg/minute after perfusion has been established. Endotracheal (loading

dose only) is 2 - 3.75 mg/kg, diluted in 5 to 10 mL normal saline or sterile

water. Absorption is greater with sterile water and there will be less of a

decrease in the PaO2.81

2. Hemodynamically stable monomorphic ventricular tachycardia:

The initial IV dosage is 1 - 1.5 mg/kg. If needed repeat doses of 0.5 to 0.75

mg/kg can be given every 5 - 10 minutes as needed up to a maximum

dosage of 3 mg/kg. The continuous IV infusion is 1 to 4 mg/minute.81

3. Reduce maintenance infusion in patients with congestive heart failure,

shock, or hepatic disease. Starting dose should be at 10 mcg/kg/minute,

and with a maximum dosage of 1.5 mg/minute or 20 mcg/kg/minute.81

Compatibility


Lidocaine is Y-site compatible with amiodarone, diltiazem, dobutamine,

dobutamine dopamine, heparin, labetalol, nicardipine, nitroglycerin, nitroprusside,

and vasopressin.81


Constant electrocardiographic monitoring is necessary during IV administration of

lidocaine. Lidocaine should be used with caution in patients who have hepatic

impairment, congestive heart failure, hypoxia, severe respiratory depression,

hypovolemia, history of malignant hyperthermia, or shock.81

Lidocaine is contraindicated for patients who have any of the following conditions:

Adam-Stokes syndrome; Wolff-Parkinson-White syndrome; severe degrees of

sinoatrial, atrioventricular, or intraventricular heart block (except in patients with

a functioning pacemaker); and, allergy to corn or corn products (the premixed

injection may contain corn-derived dextrose).81


Agitation, bradycardia, confusion, dizziness, hypotension, and seizures may occur

in high doses or in susceptible patients.82

Procainamide

Mechanisms of actions and pharmacokinetics

Procainamide is a Class Ia anti-arrhythmic that blocks the movement of sodium

through fast-sodium in channels in the heart. Procainamide decreases myocardial

excitability and decreases conduction velocity in the His-Purkinje system. It can

also decrease myocardial contractility. 83,84

There is limited pharmacokinetic information about IV procainamide but

therapeutic drug levels are produced within minutes of administration.84


Why is Procainamide Used?

Procainamide is used for the treatment of life-threatening ventricular

arrhythmias.83

The off-label uses of procainamide include: arrhythmias (i.e., stable monomorphic

ventricular tachycardia, pre-excited atrial fibrillation, and stable wide complex

regular tachycardia [likely ventricular tachycardia] in adults with preserved left

ventricular function; arrhythmias (i.e., tachycardia with pulses and poor perfusion

[probable supraventricular tachycardia unresponsive to vagal maneuvers and

adenosine or synchronized cardioversion], probable ventricular tachycardia

[unresponsive to synchronized cardioversion or adenosine], in children [PALS];

paroxysmal supraventricular tachycardia; and, ventricular tachycardia [to prevent

recurrence]).83

Administration

1. Loading dose:

Procainamide 15 to 18 mg/kg administered as slow infusion over 25 to 30

minutes or 100 mg/dose at a rate not to exceed 50 mg/minute repeated

every 5 minutes as needed to a total dose of 1 g.

2. Maintenance dose:

Procainamide 1 to 4 mg/minute by continuous infusion. Maintenance

infusions should be reduced by one-third in patients with moderate renal or

cardiac impairment and by two-thirds in patients with severe renal or

cardiac impairment.

Compatibility

Procainamide is Y-site compatible with amiodarone, heparin, nitroprusside, and

vasopressin. In certain circumstances procainamide is compatible with diltiazem.

Procainamide is incompatible with milrinone.83 The stability of procainamide in IV

dextrose solutions is varied and a pharmacist should be consulted for more

information.



Procainamide should not be used in conjunction with drugs that prolong the QT

interval.83

Procainamide can increase the ventricular response in people who have atrial

fibrillation or atrial flutter. Hypokalemia and hypomagnesemia should be

corrected before starting therapy with procainamide, and the drug should be used

with caution in patients who have heart failure.83

Procainamide is contraindicated for patients who have any of the following

conditions: complete heart block; second-degree AV block or various types of

hemiblock (without a functional pacemaker); SLE, and, torsade de pointes.83


Bradyarrhythmias, hypotension, and seizures are the major adverse effects

caused by procainamide.85

MEDICATION SAFETY ISSUES

Medication administration is a large component of a nurse’s professional role.

Medication administration is also one of the most potentially dangerous tasks a

nurse can perform. Medication errors, defined as “any preventable event that may

cause or lead to inappropriate medication use or patient harm while the

medication is in the control of the health care professional, patient or consumer,”

are costly from human, economic, and societal perspectives.

Studies show that medication errors affect three to five percent of hospitalized

patients in the US. Patients may suffer discomfort, complications, prolonged

hospitalization, disability, or death. Researchers estimate that medication errors


cause over 7000 deaths in the US each year; though not all medication errors

cause patient harm and not all errors are recognized or reported.

Medication errors are a significant problem in the US and word-wide. The

economic cost of medication errors has been estimated at $5,000 per error or an

annual impact of $2.8 million for an average 700-bed teaching hospital. Patient

length of stay is prolonged by approximately two days when errors occur. This

financial significance is magnified if litigation occurs. Financial judgments are

awarded in 13% of cases related to serious errors and average approximately

$3.1 million per award.

From the human perspective, healthcare professionals and patients are affected

by medication errors. The healthcare professional responsible for an error,

especially errors that cause patient harm, frequently suffer severe emotional

distress. Nurses frequently associate errors with harm to the patient and failure of

their moral and ethical responsibility to “do no harm.” Though all medication

errors are potentially serious, studies have shown that patients who are critically

ill are more likely to have life-threatening consequences to adverse drug events

than any other patient population. Also, intravenous route errors have the

greatest potential for harm.

In 2008, the Institute for Safe Medication Practices (ISMP), a nonprofit research

group that advocates for patient safety, developed a list of medications that are

known to contribute to a significant number of medication errors and are

associated with a risk for poor outcome with improper administration. These

drugs, referred to as high-alert medications, require special safeguards to reduce

the risk of injury to patients. The Institute for Safe Medication Practices warms

that 20 drugs are responsible for 80% of medication error fatalities. Most of the

medications described in this course are included on this list of medications.


The Joanna Briggs Institute is an International not-for-profit Research and

Development Organization specializing in Evidence-Based resources for

healthcare professionals in nursing, midwifery, medicine, and allied health. With

over 54 Centers and groups, servicing over 90 countries, the Joanna Briggs

Institute is a recognized global leader in Evidence-Based Healthcare. In 2009, the

Joanna Briggs Institute published best-practice recommendations related to the

preparation and administration of intravenous medications. These

recommendations included:

Medications should always be prepared in the pharmaceutical setting if

possible.

Administration sets not containing blood, lipids, or blood products can

remain in place for up to 96 hours without increasing the incidence of

infection.

Methods to avoid contamination should be followed, such as accessing the

port with only sterile devices, wiping the port with an appropriate antiseptic

solution and capping stock ports when not in use.

Ensure all components of an IV system are compatible to minimize possible

leaks and breaks in the system.

When utilizing piggyback systems, use care to ensure the rubber membrane

of an injection port is not exposed to air or comes in direct contact with

non-sterile tape to reduce infection risk.

Following these best practice recommendations and taking extra care when

administering the high-alert medications will reduce the risk of medication errors

and increase the safety of patients.

SUMMARY

Intravenous medication administration involves infusion of a medication into a

patient’s vein either slowly or rapidly, and may involve a continuous infusion.

Often, administering a medication by intravenous route is the preferred method


to treat a physical condition, and sometimes the intravenous route is the only

method by which a medication can be given. Another effective method of

administering a medication when venous access is unavailable and rapid injection

is necessary, as during a resuscitation event, is through intraosseous injection.

It’s important for nurses to be informed about and remain up-to-date on the

types of intravenous medications and drug actions, as well as the medication

contraindications and potential side effects. Often medications administered

through an infusion set are compatible with other medications, however, drug

incompatibilities should be known by nurses to avoid potentially adverse

outcomes. Nurses should also know how to administer a drug in the setting of

blood or blood-product transfusions.

There are several helpful resources that offer guidance for nurses when practicing

infusion therapy of medication. The Institute for Safe Medication Practices (ISMP),

in an effort to advance patient safety, has developed a list of “high alert”

medications identified as leading to poor outcomes. High-alert medications

require nurses to observe recommended safety checks to reduce the risk of

serious adverse outcomes as a result of medications administered intravenously.

Nurses often tend to blame themselves when harm results following medication

administration. However, its important for nurses to understand how system

defects can lead to errors and to be part of health safety teams in their

organization that review and address gaps in patient safety that occur.

Please take time to help the NURSECE4LESS.COM course planners evaluate nursing

knowledge needs met following completion of this course by completing the self-

assessment Knowledge Questions after reading the article. Correct Answers: page 56.

1. Which of the following are benefits of IV administration of drugs?

a. Rapid onset of action and 100% bioavailability.

b. No risk of tissue damage and precise titration of dosage.

c. Simpler to administer than PO route, steady state drug concentrations.

d. Less expensive than PO preparations, fewer adverse effects.


2. Which of the following are risks specific to IV administration of drugs?

a. Slow onset of action, decreased bioavailability.

b. Imprecise dose titration, easier to administer than PO route.

c. Tissue damage from infiltration/extravasation, complicated administration.

d. Thrombophlebitis, higher frequency of allergic reactions.

3. Which of the following are adverse effects caused by IV insulin?

a. Hypocalcemia and hyperglycemia.

b. Hypokalemia and hypoglycemia.

c. Hyperkalemia and metabolic acidosis.

d. Hypercalcemia and metabolic alkalosis.

4. Which of the following are relatively common adverse effects caused

by IV heparin?

a. Bradycardia and hypotension.

b. Hepatotoxicity and renal damage.

c. Bronchospasm and Stevens-Johnson syndrome.

d. Bleeding and thrombocytopenia.

5. The vasopressors and inotropes may cause:

a. Peripheral vasoconstriction and dysrhythmias.

b. Bleeding and hypoglycemia.

c. Bronchospasm and hypokalemia.

d. Thrombocytopenia and seizures.

6. When using a vasopressor or an inotrope it is critical to periodically

assess:

a. Serum magnesium and serum calcium.

b. Urine output and mental status.

c. Serum glucose and aPTT.


d. Pulmonary capillary wedge pressure and temperature.

7. IV infusion of a beta-blocker can commonly cause:

a. Hypertension.

b. Thrombocytopenia.

c. Hypotension.

d. Seizures.

8. IV infusion of a calcium channel blocker can commonly cause:

a. Tachycardia.

b. QTc prolongation.

c. Hypoglycemia.

d. Hypotension.

9. IV infusion of nitroprusside can cause:

a. Bronchospasm.

b. Cyanide poisoning.

c. Bleeding.

d. Dysrhythmias.

10. IV infusion of an antiarrhythmic is contraindicated if the patient has:

a. Severe heart block.

b. Asthma.

c Hyperglycemia.

d. A bleeding disorder.

CORRECT ANSWERS


1. A

2. C

3. B

4. D

5. A

6. B

7. C

8. D

9. B

10. A

REFERENCE SECTION

The reference section of in-text citations include published works intended as

helpful material for further reading. Unpublished works and personal

communications are not included in this section, although they may appear within

the study text.

1. Insulin Regular. Lexicomp®. February 24, 2015. Retrieved February 25,

2015 from www.UCHC.edu.

2. Olveira G, Tapia MJ, Ocón J, Cabrejas-Gómez C, Ballesteros-Pomar MD,

Vidal-Casariego A, et al. Parenteral nutrition-associated hyperglycemia in

non-critically ill inpatients increases the risk of in-hospital mortality

(Multicenter study). Diabetes Care. 2013;36:1061-6.

3. Iwakura K. Stress hyperglycemia and microvascular obstruction after acute

myocardial infarction. J Cardiol. 2014 Dec 29. pii: S0914-5087(14)00346-3.

doi: 10.1016/j.jjcc.2014.11.012. [Epub ahead of print].

4. Spanakis EK, Shah N, Malhotra K, Kemmerer T, Yeh H-C, Golden SH. Insulin

requirements in non-critically ill hospitalized patients with diabetes and

steroid-induced hyperglycemia. Hosp Pract (1995). 2014; 42: 23-30.

http://www.uchc.edu/

http://www.ncbi.nlm.nih.gov/pubmed/?term=Olveira%20G%5BAuthor%5D&cauthor=true&cauthor_uid=23223407

http://www.ncbi.nlm.nih.gov/pubmed/?term=Tapia%20MJ%5BAuthor%5D&cauthor=true&cauthor_uid=23223407

http://www.ncbi.nlm.nih.gov/pubmed/?term=Oc%C3%B3n%20J%5BAuthor%5D&cauthor=true&cauthor_uid=23223407

http://www.ncbi.nlm.nih.gov/pubmed/?term=Cabrejas-G%C3%B3mez%20C%5BAuthor%5D&cauthor=true&cauthor_uid=23223407

http://www.ncbi.nlm.nih.gov/pubmed/?term=Ballesteros-Pomar%20MD%5BAuthor%5D&cauthor=true&cauthor_uid=23223407

http://www.ncbi.nlm.nih.gov/pubmed/?term=Vidal-Casariego%20A%5BAuthor%5D&cauthor=true&cauthor_uid=23223407

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Iwakura%20K%5BAuthor%5D&cauthor=true&cauthor_uid=25553870

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Stress+hyperglycemia+and+microvascular+obstruction+after+acute


5. Jacobi J, Bircher N, Krinsley J, Agus M, Braithwaite SS, Deutschman C, et al.

Guidelines for the use of an insulin infusion for the management of

hyperglycemia in critically ill patients. Crit Care Med. 2012;40:3251-76.

6. Kitabchi AE, Hirsch IB, Emmett M. Diabetic ketoacidosis and hyperosmolar

hyperglycemic state in adults: Treatment. UpToDate. October 17, 2014.

Retrieved February 7, 2015 from

http://www.uptodate.com/contents/diabetic-ketoacidosis-and-

hyperosmolar-hyperglycemic-state-in-adults-

treatment?source=search_result&search=hyperosmolar+nonketotic+hypergl

ycemia&selectedTitle=1%7E121.

7. Garazi E, Bridge S, Caffarelli A, Ruoss S, Van der Starre P. Acute cellular

insulin resistance and hyperglycemia associated with hypophosphatemia

after cardiac surgery. A A Case Rep. 2015;4:22-5.

8. Neff K, Donegan D, MacMahon J, O’Hanlon C, Keane N, Agha A, et al.

Management of parenteral nutrition associated hyperglycaemia: a

comparison of subcutaneous and intravenous insulin regimen. Ir Med J.

2014;107:141-3.

9. Simmons D. Safety considerations with pharmacological treatment of

gestational diabetes mellitus. Drug Saf. 2015;38:65-78.

10. Mount DB. Treatment and prevention of hyperkalemia in adults. UpToDate.

December 3, 2014. Retrieved February 7, 2015 from

http://www.uptodate.com/contents/treatment-and-prevention-of-

hyperkalemia-in-

adults?source=search_result&search=hyperkalemia+treatment&selectedTitl

e=1%7E150.

11. Doepker B, Healy W, Cortez E, Adkins EJ. High-dose insulin and intravenous

lipid emulsion therapy for cardiogenic shock induced by intentional calcium-

channel and beta-blocker overdose: a case series. J Emerg Med.

2014;46:486-90.

12. Heparin. Lexicomp®. February 13, 2015. Retrieved February 20, 2015 from

www.UCHC.edu.

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Jacobi%20J%5BAuthor%5D&cauthor=true&cauthor_uid=23164767

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Bircher%20N%5BAuthor%5D&cauthor=true&cauthor_uid=23164767

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Krinsley%20J%5BAuthor%5D&cauthor=true&cauthor_uid=23164767

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Agus%20M%5BAuthor%5D&cauthor=true&cauthor_uid=23164767

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Braithwaite%20SS%5BAuthor%5D&cauthor=true&cauthor_uid=23164767

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Deutschman%20C%5BAuthor%5D&cauthor=true&cauthor_uid=23164767

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/23164767

http://www.uptodate.com/contents/diabetic-ketoacidosis-and-hyperosmolar-hyperglycemic-state-in-adults-treatment?source=search_result&search=hyperosmolar+nonketotic+hyperglycemia&selectedTitle=1~121




http://www.ncbi.nlm.nih.gov/pubmed/?term=Garazi%20E%5bAuthor%5d&cauthor=true&cauthor_uid=25611002

http://www.ncbi.nlm.nih.gov/pubmed/?term=Bridge%20S%5bAuthor%5d&cauthor=true&cauthor_uid=25611002

http://www.ncbi.nlm.nih.gov/pubmed/?term=Caffarelli%20A%5bAuthor%5d&cauthor=true&cauthor_uid=25611002

http://www.ncbi.nlm.nih.gov/pubmed/?term=Ruoss%20S%5bAuthor%5d&cauthor=true&cauthor_uid=25611002

http://www.ncbi.nlm.nih.gov/pubmed/?term=Van%20der%20Starre%20P%5bAuthor%5d&cauthor=true&cauthor_uid=25611002

http://www.ncbi.nlm.nih.gov/pubmed/25611002

http://www.uptodate.com/contents/treatment-and-prevention-of-hyperkalemia-in-adults?source=search_result&search=hyperkalemia+treatment&selectedTitle=1~150






13. Guyatt GH, Akl EA, Crowther M, Gutterman DD, Schuünemann HJ; American

College of Chest Physicians Antithrombotic Therapy and Prevention of

Thrombosis Panel. Executive summary: Antithrombotic Therapy and

Prevention of Thrombosis, 9th ed: American College of Chest Physicians

Evidence-Based Clinical Practice Guidelines. Chest. 2012;141(2 Suppl):7S-

47S.

14. Steinberg BA, Peterson ED, Kim S, Thomas L, Gersh BJ, Fonarow GC, et al.

Use and outcomes associated with bridging during anticoagulation

interruptions in patients with atrial fibrillation: Findings from the Outcomes

Registry for Better Informed Treatment of Atrial Fibrillation (ORBIT-AF).

Circulation. 2015;131:488-94.

15. Rosenthal L. Atrial fibrillation. eMedicine. November 24, 2014. Retrieved

February 10, 2015 from http://emedicine.medscape.com/article/151066-

overview.

16. Lipinski MJ, Lhermusier T, Escarcega RO, Baker NC, Magalhães MA,

Torguson R, et al. Bivalirudin versus heparin for percutaneous coronary

intervention: an updated meta-analysis of randomized controlled trials.

Cardiovasc Revasc Med. 2014;15:315-22.

17. Andrade-Castellanos CA, Colunga-Lozano LE, Delgado-Figueroa N, Magee K.

Heparin versus placebo for non-ST elevation acute coronary syndromes.

Cochrane Database Syst Rev. 2014 Jun 27;6:CD003462. doi:

10.1002/14651858.CD003462.pub3.

18. Alikhan R, Bedenis R, Cohen AT. Heparin for the prevention of venous

thromboembolism in acutely ill medical patients (excluding stroke and

myocardial infarction). Cochrane Database Syst Rev. 2014 May

7;5:CD003747. doi: 10.1002/14651858.CD003747.pub4.

19. Kim L, Schuster J, Holena DN, Sims CA, Levine J, Pascual JL.Early initiation

of prophylactic heparin in severe traumatic brain injury is associated with

accelerated improvement on brain imaging. J Emerg Trauma Shock.

2014;7:141-8.

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Guyatt%20GH%5BAuthor%5D&cauthor=true&cauthor_uid=22315257

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Akl%20EA%5BAuthor%5D&cauthor=true&cauthor_uid=22315257

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Crowther%20M%5BAuthor%5D&cauthor=true&cauthor_uid=22315257

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Gutterman%20DD%5BAuthor%5D&cauthor=true&cauthor_uid=22315257

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Schu%C3%BCnemann%20HJ%5BAuthor%5D&cauthor=true&cauthor_uid=22315257

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=American%20College%20of%20Chest%20Physicians%20Antithrombotic%20Therapy%20and%20Prevention%20of%20Thrombosis%20Panel%5BCorporate%20Author%5D




http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Steinberg%20BA%5BAuthor%5D&cauthor=true&cauthor_uid=25499873

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Peterson%20ED%5BAuthor%5D&cauthor=true&cauthor_uid=25499873

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Kim%20S%5BAuthor%5D&cauthor=true&cauthor_uid=25499873

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Thomas%20L%5BAuthor%5D&cauthor=true&cauthor_uid=25499873

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Gersh%20BJ%5BAuthor%5D&cauthor=true&cauthor_uid=25499873

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Fonarow%20GC%5BAuthor%5D&cauthor=true&cauthor_uid=25499873


http://emedicine.medscape.com/article/151066-overview

http://emedicine.medscape.com/article/151066-overview

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Lipinski%20MJ%5BAuthor%5D&cauthor=true&cauthor_uid=25440505

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Lhermusier%20T%5BAuthor%5D&cauthor=true&cauthor_uid=25440505

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Escarcega%20RO%5BAuthor%5D&cauthor=true&cauthor_uid=25440505

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Baker%20NC%5BAuthor%5D&cauthor=true&cauthor_uid=25440505

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Magalh%C3%A3es%20MA%5BAuthor%5D&cauthor=true&cauthor_uid=25440505

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Torguson%20R%5BAuthor%5D&cauthor=true&cauthor_uid=25440505


http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Andrade-Castellanos%20CA%5BAuthor%5D&cauthor=true&cauthor_uid=24972265

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Colunga-Lozano%20LE%5BAuthor%5D&cauthor=true&cauthor_uid=24972265

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Delgado-Figueroa%20N%5BAuthor%5D&cauthor=true&cauthor_uid=24972265

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Magee%20K%5BAuthor%5D&cauthor=true&cauthor_uid=24972265


http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Alikhan%20R%5BAuthor%5D&cauthor=true&cauthor_uid=24804622

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Bedenis%20R%5BAuthor%5D&cauthor=true&cauthor_uid=24804622

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Cohen%20AT%5BAuthor%5D&cauthor=true&cauthor_uid=24804622


http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Kim%20L%5BAuthor%5D&cauthor=true&cauthor_uid=25114421

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Schuster%20J%5BAuthor%5D&cauthor=true&cauthor_uid=25114421

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Holena%20DN%5BAuthor%5D&cauthor=true&cauthor_uid=25114421

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Sims%20CA%5BAuthor%5D&cauthor=true&cauthor_uid=25114421

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Levine%20J%5BAuthor%5D&cauthor=true&cauthor_uid=25114421

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Pascual%20JL%5BAuthor%5D&cauthor=true&cauthor_uid=25114421



20. Levi M. Diagnosis and treatment of disseminated intravascular coagulation.

Int J lab Hematol. 2014;36:228-36.

21. Wada H, Matsumoto T, Yamashita Y. Diagnosis and treatment of

disseminated intravascular coagulation (DIC) according to four DIC

guidelines. J Intensive Care. 2014 Feb 20;2(1):15. doi: 10.1186/2052-

0492-2-15. eCollection 2014. Review.

22. Landaw, SA, Bauer KA. Approach to the diagnosis and therapy of lower

extremity deep vein thrombosis. UpToDate. July 15, 2014. Retrieved

February 5, 2015 from

http://www.uptodate.com/contents/approach-to-the-diagnosis-and-therapy-

of-lower-extremity-deep-vein-

thrombosis?source=machineLearning&search=deep+vein+thrombosis&selec

tedTitle=1%7E150&sectionRank=1&anchor=H28#H30.

23. Ucar EY, Akgun M, Araz O, Tas H, Kerget B, Meral M, et al. Comparison of

LMWH versus UFH for hemorrhage and hospital mortality in the treatment of

acute massive pulmonary thromboembolism after thrombolytic treatment :

Randomized controlled parallel group study. Lung. 2015;193:121-7.

24. Puymirat É, Aissaoui N, Silvain J, Bonello L, Cuisset T, Motreff P, et al.

Comparison of bleeding complications and 3-year survival with low-

molecular-weight heparin versus unfractionated heparin for acute

myocardial infarction: the FAST-MI registry. Arch Cardiovasc Dis.

2012;105:347-54.

25. Garcia DA, Baglin TP, Weitz JI, Samama MM; American College of Chest

Physicians Evidence-Based Clinical Practice Guidelines. Chest.

2012;141:e24S-43S.

26. Linkins LA. Heparin induced thrombocytopenia. BMJ. 2015 Jan 8;350:g7566.

doi: 10.1136/bmj.g7566.

27. Lovecchio F. Heparin-induced thrombocytopenia. Clin Toxicol. 2014;52:579-

83.

28. Kanter J, DeBlieux P. Pressors and inotropes. Emerg Med Clin N Am.

2014;32:823-34.

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Wada%20H%5BAuthor%5D&cauthor=true&cauthor_uid=25520831

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Matsumoto%20T%5BAuthor%5D&cauthor=true&cauthor_uid=25520831

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Yamashita%20Y%5BAuthor%5D&cauthor=true&cauthor_uid=25520831

http://www.uptodate.com/contents/approach-to-the-diagnosis-and-therapy-of-lower-extremity-deep-vein-thrombosis/contributors

http://www.uptodate.com/contents/approach-to-the-diagnosis-and-therapy-of-lower-extremity-deep-vein-thrombosis?source=machineLearning&search=deep+vein+thrombosis&selectedTitle=1%7E150&sectionRank=1&anchor=H28#H30




http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Ucar%20EY%5BAuthor%5D&cauthor=true&cauthor_uid=25351610

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Akgun%20M%5BAuthor%5D&cauthor=true&cauthor_uid=25351610

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Araz%20O%5BAuthor%5D&cauthor=true&cauthor_uid=25351610

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Tas%20H%5BAuthor%5D&cauthor=true&cauthor_uid=25351610

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Kerget%20B%5BAuthor%5D&cauthor=true&cauthor_uid=25351610

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Meral%20M%5BAuthor%5D&cauthor=true&cauthor_uid=25351610


http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Puymirat%20%C3%89%5BAuthor%5D&cauthor=true&cauthor_uid=22800719

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Aissaoui%20N%5BAuthor%5D&cauthor=true&cauthor_uid=22800719

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Silvain%20J%5BAuthor%5D&cauthor=true&cauthor_uid=22800719

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Bonello%20L%5BAuthor%5D&cauthor=true&cauthor_uid=22800719

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Cuisset%20T%5BAuthor%5D&cauthor=true&cauthor_uid=22800719

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Motreff%20P%5BAuthor%5D&cauthor=true&cauthor_uid=22800719


http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Garcia%20DA%5BAuthor%5D&cauthor=true&cauthor_uid=22315264

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Baglin%20TP%5BAuthor%5D&cauthor=true&cauthor_uid=22315264

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Weitz%20JI%5BAuthor%5D&cauthor=true&cauthor_uid=22315264

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Samama%20MM%5BAuthor%5D&cauthor=true&cauthor_uid=22315264

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=American%20College%20of%20Chest%20Physicians%5BCorporate%20Author%5D

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=American%20College%20of%20Chest%20Physicians%5BCorporate%20Author%5D

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Garcia+DA%2C+Baglin+TP%2C+Weitz+JI%2C+et+al%2C+%E2%80%9CParenteral+Anticoagulants%3A+Antithrombotic+Therapy+and+Prevention+of+Thrombosis%2C+9th+ed%3A+American+College+of+Chest+Physicians+Evidence-Based+Clinical+Practice+Guidelines

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Linkins%20LA%5BAuthor%5D&cauthor=true&cauthor_uid=25569604


http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Lovecchio%20F%5BAuthor%5D&cauthor=true&cauthor_uid=24844576


29. Manaker S. Use of vasopressors and inotropes. UpToDate. July 21, 2014

Retrieved February 14, 2015 from http://www.uptodate.com/contents/use-

of-vasopressors-and-

inotropes?source=search_result&search=Use+of+vasopressors+and+inotro

pes&selectedTitle=1%7E150.

30. Lexicomp®. Management of drug extravasations. January 20, 2015.

Retrieved February 15, 2015 from www.UCHC.edu.

31. Lexicomp®. Dobutamine. February 1, 2015. Retrieved February 15, 2015

from www.UCHC.edu.

32. Yancy CW, Jessup M, Bozkurt B, Butler J, Casey DE Jr, Drazner MH, et al;

American College of Cardiology Foundation/American Heart Association Task

Force on Practice Guidelines. 2013 ACCF/AHA guideline for the management

of heart failure: a report of the American College of Cardiology

Foundation/American Heart Association Task Force on practice guidelines.

Circulation. 2013;128:e240-e327.

33. Dellinger RP, Levy MM, Rhodes A, Annane D, Gerlach H, Opal SM, et al.

Surviving sepsis campaign: international guidelines for management of

severe sepsis and septic shock, 2012. Intensive Care Med. 2012; 39:165–

228

34. Hernandez G, Bruhn A, Luengo C, Regueira T, Kattan E, Fuentealba A, et al.

Effects of dobutamine on systemic, regional and microcirculatory perfusion

parameters in septic shock: a randomized, placebo-controlled, double-blind,

crossover study. Intensive Care Med. 2013;39:1435-43.

35. Dopamine. Lexicomp®. February 26, 2015. Retrieved February 27, 2015

from www.UCHC.edu.

36. Debaveye YA, Van den Berghe GH. Is there still a place for dopamine in the

modern intensive care unit? Anesth Analg. 2004;98:461-8.

37. Marinosci GZ, De Robertis E, De Benedictis G, Piazza O. Dopamine use in

intensive care: Are we ready to turn it down? Transl Med UniSa. 2012;4:90-

4.

http://www.uptodate.com/contents/use-of-vasopressors-and-inotropes?source=search_result&search=Use+of+vasopressors+and+inotropes&selectedTitle=1%7E150






http://www.ncbi.nlm.nih.gov/pubmed/?term=Hernandez%20G%5BAuthor%5D&cauthor=true&cauthor_uid=23740284

http://www.ncbi.nlm.nih.gov/pubmed/?term=Bruhn%20A%5BAuthor%5D&cauthor=true&cauthor_uid=23740284

http://www.ncbi.nlm.nih.gov/pubmed/?term=Luengo%20C%5BAuthor%5D&cauthor=true&cauthor_uid=23740284

http://www.ncbi.nlm.nih.gov/pubmed/?term=Regueira%20T%5BAuthor%5D&cauthor=true&cauthor_uid=23740284

http://www.ncbi.nlm.nih.gov/pubmed/?term=Kattan%20E%5BAuthor%5D&cauthor=true&cauthor_uid=23740284

http://www.ncbi.nlm.nih.gov/pubmed/?term=Fuentealba%20A%5BAuthor%5D&cauthor=true&cauthor_uid=23740284



http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Debaveye%20YA%5BAuthor%5D&cauthor=true&cauthor_uid=14742388

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Van%20den%20Berghe%20GH%5BAuthor%5D&cauthor=true&cauthor_uid=14742388


http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Marinosci%20GZ%5BAuthor%5D&cauthor=true&cauthor_uid=23905068

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=De%20Robertis%20E%5BAuthor%5D&cauthor=true&cauthor_uid=23905068

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=De%20Benedictis%20G%5BAuthor%5D&cauthor=true&cauthor_uid=23905068

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Piazza%20O%5BAuthor%5D&cauthor=true&cauthor_uid=23905068



38. Hanneman L, Reinhart K, Grenzer O, Meier-Hellman A, Bredle DL.

Comparison of dopamine to dobutamine and norepinephrine for oxygen

delivery and uptake in septic shock. Crit Care Med. 1995;23:1962-70.

39. Lexicomp®. Isoproterenol. February 13, 2015. Retrieved February 15, 2015

from www.UCHC.edu.

40. Levophed [Package insert]. Lake Forest, IL: Hospira, Inc.; 2014

41. Lexicomp®. Norepinephrine. February 6, 2015. Retrieved February 12, 2015

from www.UCHC.edu.

42. Hollenberg SM, Ahrens TS, Annane D, Astiz ME, Chalfin DB, Dasta JF, et al.

Practice parameters for hemodynamic support of sepsis in adult patients:

2004 Update. Crit Care Med. 2004;32:1928-48.

43. Rachoin JS, Dellinger RP. Timing of norepinephrine in septic patients: NOT

too little too late. Crit Care. 2014;15:691.

44. Asfar P, Meziani F, Hamel JF, Grelon F, Megarbane B, Anguel N, et al. High

versus low blood-pressure target in patients with septic shock. N Engl J Med.

2014;370:1583-93.

45. Peberdy MA, Callaway CW, Neumar RW, Neumar RW, Geocadin RG,

Zimmerman JL, et al. Part 9: Post Cardiac Arrest Care: 2010 American Heart

Association Guidelines for Cardiopulmonary Resuscitation and Emergency

Cardiovascular Care. Circulation, 2010;(18 Suppl 3):768-86.

46. Lexicomp®. Pheylephrine. February 9, 2015. Retrieved February 16, 2015

from www.UCHC.edu.

47. Neosynephrine [Package insert]. Bastian, VA: General Injectables & Vaccines

Inc; 2010.

48. Lexicomp®. Epinephrine (Systemic, Oral Inhalation). Lexi-Drugs. February

13, 2015. Retrieved February 17, 2015 from www.UCHC.edu.

49. Neumar RW, Otto CW, Link MS, Kronick SL, Shuster M, Callaway CW, et al.

Part 8: Adult advanced cardiovascular life support: 2010 American Heart


Cardiovascular Care. Circulation. 2010;122(18 Suppl 3):S729-67.



http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Astiz%20ME%5BAuthor%5D&cauthor=true&cauthor_uid=15343024

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Chalfin%20DB%5BAuthor%5D&cauthor=true&cauthor_uid=15343024

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Dasta%20JF%5BAuthor%5D&cauthor=true&cauthor_uid=15343024

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Rachoin%20JS%5BAuthor%5D&cauthor=true&cauthor_uid=25672524

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Dellinger%20RP%5BAuthor%5D&cauthor=true&cauthor_uid=25672524


http://www.ncbi.nlm.nih.gov/pubmed/?term=Asfar%20P%5BAuthor%5D&cauthor=true&cauthor_uid=24635770

http://www.ncbi.nlm.nih.gov/pubmed/?term=Meziani%20F%5BAuthor%5D&cauthor=true&cauthor_uid=24635770

http://www.ncbi.nlm.nih.gov/pubmed/?term=Hamel%20JF%5BAuthor%5D&cauthor=true&cauthor_uid=24635770

http://www.ncbi.nlm.nih.gov/pubmed/?term=Grelon%20F%5BAuthor%5D&cauthor=true&cauthor_uid=24635770

http://www.ncbi.nlm.nih.gov/pubmed/?term=Megarbane%20B%5BAuthor%5D&cauthor=true&cauthor_uid=24635770

http://www.ncbi.nlm.nih.gov/pubmed/?term=Anguel%20N%5BAuthor%5D&cauthor=true&cauthor_uid=24635770

http://www.ncbi.nlm.nih.gov/pubmed/24635770?dopt=Abstract&holding=f1000,f1000m,isrctn

http://www.ncbi.nlm.nih.gov/pubmed/?term=Neumar%20RW%5BAuthor%5D&cauthor=true&cauthor_uid=20956225

http://www.ncbi.nlm.nih.gov/pubmed/?term=Geocadin%20RG%5BAuthor%5D&cauthor=true&cauthor_uid=20956225

http://www.ncbi.nlm.nih.gov/pubmed/?term=Zimmerman%20JL%5BAuthor%5D&cauthor=true&cauthor_uid=20956225







50. Lexicomp®. Vasopressin. February 9, 2015. Retrieved February 17, 2015

from www.UCHC.edu.

51. Bihari D, Prakash S, Bersten A. Low-dose vasopressin in addition to

noradrenaline may lead to faster resolution of organ failure in patients with

severe sepsis/septic shock. Anaesth Intensive Care. 2014;42:671-4.

52. Vanden Hoek TL, Morrison LJ, Shuster M, Donnino M, Sinz E, Lavonas EJ, et

al. Part 12: Cardiac arrest in special situations. 2010 American Heart


Cardiovascular Care. Circulation. 2010;122: S829-S861.

53. Bauer SR, Aloi JJ, Ahrens CL, Yeh JY, Culver DA, Reddy AJ. Discontinuation

of vasopressin before norepinephrine increases the incidence of hypotension

in patients recovering from septic shock: A retrospective cohort study. J Crit

Care. 2010 Jun;25(2):362.e7-362.e11. doi: 10.1016/j.jcrc.2009.10.005.

54. Lexicomp®. Milrinone. February 6, 2015. Retrieved February 17, 2015 from

www.UCHC.edu.

55. James AT, Corcoran JD, McNamara PJ, Franklin O, El-Khuffash AF. The effect

of milrinone on right and left ventricular function when used as a rescue

therapy for term infants with pulmonary hypertension. Cardiol Young. 2015

Jan 20:1-10. [Epub ahead of print]

56. Baruch L, Patacsil P, Hameed A, Pina I, Loh E. Pharmacodynamic effects of

milrinone with and without a bolus loading infusion. Am Heart J,

2001;141:266-73.

57. Tang X, Liu P, Li R, Jing Q, Lv J, Liu L, Liu Y. Milrinone for the treatment of

acute heart failure after acute myocardial infarction: A systematic review

and meta-analysis. Basic Clin Pharmacol Toxicol. 2015 Jan 27. doi:

10.1111/bcpt.12385. [Epub ahead of print]; and, Milrinone. [Package

insert]. Lake Forest, IL: Hospira, Inc.; 2014.

58. Anderson JL, Askins JC, Gilbert EM, Menlove RL, Lutz JR. Occurrence of

ventricular arrhythmias in patients receiving acute and chronic infusions of

milrinone. Am Heart J. 1986; 111:466-74.


http://www.ncbi.nlm.nih.gov/pubmed/?term=Bihari%20D%5BAuthor%5D&cauthor=true&cauthor_uid=25233186

http://www.ncbi.nlm.nih.gov/pubmed/?term=Prakash%20S%5BAuthor%5D&cauthor=true&cauthor_uid=25233186

http://www.ncbi.nlm.nih.gov/pubmed/?term=Bersten%20A%5BAuthor%5D&cauthor=true&cauthor_uid=25233186


http://www.ncbi.nlm.nih.gov/pubmed/?term=Yeh%20JY%5BAuthor%5D&cauthor=true&cauthor_uid=19926252

http://www.ncbi.nlm.nih.gov/pubmed/?term=Culver%20DA%5BAuthor%5D&cauthor=true&cauthor_uid=19926252

http://www.ncbi.nlm.nih.gov/pubmed/?term=Reddy%20AJ%5BAuthor%5D&cauthor=true&cauthor_uid=19926252

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Bauer+SR%2C+Aloi+JJ%2C+Ahrens+CL%2C+Yeh+JY%2C+Culver+DA%2C+Reddy+AJ.

http://www-ncbi-nlm-nih-gov.online.uchc.edu/pubmed/?term=Bauer+SR%2C+Aloi+JJ%2C+Ahrens+CL%2C+Yeh+JY%2C+Culver+DA%2C+Reddy+AJ.


http://www.ncbi.nlm.nih.gov/pubmed/?term=James%20AT%5BAuthor%5D&cauthor=true&cauthor_uid=25599873

http://www.ncbi.nlm.nih.gov/pubmed/?term=Corcoran%20JD%5BAuthor%5D&cauthor=true&cauthor_uid=25599873

http://www.ncbi.nlm.nih.gov/pubmed/?term=McNamara%20PJ%5BAuthor%5D&cauthor=true&cauthor_uid=25599873

http://www.ncbi.nlm.nih.gov/pubmed/?term=Franklin%20O%5BAuthor%5D&cauthor=true&cauthor_uid=25599873

http://www.ncbi.nlm.nih.gov/pubmed/?term=El-Khuffash%20AF%5BAuthor%5D&cauthor=true&cauthor_uid=25599873


http://www.ncbi.nlm.nih.gov/pubmed/?term=Pina%20I%5BAuthor%5D&cauthor=true&cauthor_uid=11174341

http://www.ncbi.nlm.nih.gov/pubmed/?term=Loh%20E%5BAuthor%5D&cauthor=true&cauthor_uid=11174341

http://www.ncbi.nlm.nih.gov/pubmed/?term=Tang%20X%5BAuthor%5D&cauthor=true&cauthor_uid=25625413

http://www.ncbi.nlm.nih.gov/pubmed/?term=Liu%20P%5BAuthor%5D&cauthor=true&cauthor_uid=25625413

http://www.ncbi.nlm.nih.gov/pubmed/?term=Li%20R%5BAuthor%5D&cauthor=true&cauthor_uid=25625413

http://www.ncbi.nlm.nih.gov/pubmed/?term=Jing%20Q%5BAuthor%5D&cauthor=true&cauthor_uid=25625413

http://www.ncbi.nlm.nih.gov/pubmed/?term=Lv%20J%5BAuthor%5D&cauthor=true&cauthor_uid=25625413

http://www.ncbi.nlm.nih.gov/pubmed/?term=Liu%20L%5BAuthor%5D&cauthor=true&cauthor_uid=25625413

http://www.ncbi.nlm.nih.gov/pubmed/?term=Liu%20Y%5BAuthor%5D&cauthor=true&cauthor_uid=25625413



59. Lexicomp®. Esmolol. February 17, 2015. Retrieved February 17, 2015 from

www.UCHC.edu.

60. Brevibloc [Package insert]. Deerfield, IL: Baxter Healthcare Corporation;

2014.

61. January CT, Wann LS, Alpert JS, Calkins H, Cigarroa JE, Cleveland JC Jr, et

al. 2014 AHA/ACC/HRS guideline for the management of patients with atrial

fibrillation: a report of the American College of Cardiology/American Heart

Association Task Force on Practice Guidelines and the Heart Rhythm Society.

J Am Coll Cardiol. 2014;64:e1-76.

62. Lexicomp®. Labetalol. February 17, 2015. Retrieved February 20, 2015

from www.UCHC.edu.

63. Magee LA, Pels A, Helewa M, Rey E, von Dadelszen P; Canadian

Hypertensive Disorders of Pregnancy Working Group. Diagnosis, evaluation,

and management of the hypertensive disorders of pregnancy: executive

summary. J Obstet Gynaecol Can. 2014;36:416-441.

64. Jauch EC, Saver JL, Adams HP Jr, Bruno A, Connors JJ, Demaerschalk BM, et

al. Guidelines for the early management of patients with acute ischemic

stroke: a guideline for healthcare professionals from the American Heart

Association/American Stroke Association. Stroke. 2013;44:870-947.

65. Woloszyn AV, McAllen KJ, Figueroa BE, DeShane RS, Barletta JF.

Retrospective evaluation of nicardipine versus labetalol for blood pressure

control in aneurysmal subarachnoid hemorrhage. Neurocrit Care.

2012;16:376-80.

66. Elliot WJ, Varon J. Drugs used for the treatment of hypertensive

emergencies. UpToDate. November 3, 2014. Retrieved February 20, 2015

from http://www.uptodate.com/contents/drugs-used-for-the-treatment-of-

hypertensive-emergencies?source=see_link#H9.

67. American College of Obstetricians and Gynecologists (ACOG). Committee

opinion no. 623: emergent therapy for acute-onset, severe hypertension

during pregnancy and the postpartum period. Obstet Gynecol.

2015;125:521-5.


http://www.ncbi.nlm.nih.gov/pubmed/?term=January%20CT%5BAuthor%5D&cauthor=true&cauthor_uid=24685669

http://www.ncbi.nlm.nih.gov/pubmed/?term=Wann%20LS%5BAuthor%5D&cauthor=true&cauthor_uid=24685669

http://www.ncbi.nlm.nih.gov/pubmed/?term=Alpert%20JS%5BAuthor%5D&cauthor=true&cauthor_uid=24685669

http://www.ncbi.nlm.nih.gov/pubmed/?term=Calkins%20H%5BAuthor%5D&cauthor=true&cauthor_uid=24685669

http://www.ncbi.nlm.nih.gov/pubmed/?term=Cigarroa%20JE%5BAuthor%5D&cauthor=true&cauthor_uid=24685669

http://www.ncbi.nlm.nih.gov/pubmed/?term=Cleveland%20JC%20Jr%5BAuthor%5D&cauthor=true&cauthor_uid=24685669



http://www.ncbi.nlm.nih.gov/pubmed/?term=Jauch%20EC%5BAuthor%5D&cauthor=true&cauthor_uid=23370205

http://www.ncbi.nlm.nih.gov/pubmed/?term=Saver%20JL%5BAuthor%5D&cauthor=true&cauthor_uid=23370205

http://www.ncbi.nlm.nih.gov/pubmed/?term=Adams%20HP%20Jr%5BAuthor%5D&cauthor=true&cauthor_uid=23370205

http://www.ncbi.nlm.nih.gov/pubmed/?term=Bruno%20A%5BAuthor%5D&cauthor=true&cauthor_uid=23370205

http://www.ncbi.nlm.nih.gov/pubmed/?term=Connors%20JJ%5BAuthor%5D&cauthor=true&cauthor_uid=23370205

http://www.ncbi.nlm.nih.gov/pubmed/?term=Demaerschalk%20BM%5BAuthor%5D&cauthor=true&cauthor_uid=23370205

http://www.ncbi.nlm.nih.gov/pubmed/23370205?dopt=Abstract

http://www.ncbi.nlm.nih.gov/pubmed/?term=Woloszyn%20AV%5BAuthor%5D&cauthor=true&cauthor_uid=22528277

http://www.ncbi.nlm.nih.gov/pubmed/?term=McAllen%20KJ%5BAuthor%5D&cauthor=true&cauthor_uid=22528277

http://www.ncbi.nlm.nih.gov/pubmed/?term=Figueroa%20BE%5BAuthor%5D&cauthor=true&cauthor_uid=22528277

http://www.ncbi.nlm.nih.gov/pubmed/?term=DeShane%20RS%5BAuthor%5D&cauthor=true&cauthor_uid=22528277

http://www.ncbi.nlm.nih.gov/pubmed/?term=Barletta%20JF%5BAuthor%5D&cauthor=true&cauthor_uid=22528277


http://www.uptodate.com/contents/drugs-used-for-the-treatment-of-hypertensive-emergencies?source=see_link#H9

http://www.uptodate.com/contents/drugs-used-for-the-treatment-of-hypertensive-emergencies?source=see_link#H9


68. Lexicomp®. Diltiazem. February 20, 2015. Retrieved February 21, 2015

from www.UCHC.edu.

69. January CT, Wann LS, Alpert JS, Calkins H, Cigarroa JE, Cleveland JC Jr, et

al. 2014 AHA/ACC/HRS guideline for the management of patients with atrial

fibrillation: a report of the American College of Cardiology/American Heart

Association Task Force on Practice Guidelines and the Heart Rhythm Society.

J Am Coll Cardiol. 2014;64:e1-76.

70. Cardene. [Package insert]. Deerfield, IL: Baxter Healthcare Corporation;

2014.

71. Nicardipine. Lexicomp®. February 18, 2015. Retrieved February 23, 2015

from www.UCHC.edu.

72. Verapamil. Lexicomp®. February 20, 2015. Retrieved February 22, 2015

from www.UCHC.edu.

73. Verapamil injection [package insert]. Lake Forest, IL: Hospira, Inc.; 2014.

74. Nitroglycerin. Lexicomp®. February 18, 2015. Retrieved February 24, 2015

from www.UCHC.edu.

75. Reeder GS. Nitrates in the management of acute coronary syndrome.

UpToDate. February 14, 2012. Retrieved February 24, 2015 from

http://www.uptodate.com/contents/nitrates-in-the-management-of-acute-

coronary-

syndrome?source=search_result&search=nitroglycerin+drip&selectedTitle=

1%7E150.

76. Anderson JL, Adams CD, Antman EM, Bridges CR, Califf RM, Casey DE Jr, et

al; American College of Cardiology Foundation/American Heart Association

Task Force on Practice Guidelines. 2012 ACCF/AHA focused update

incorporated into the ACCF/AHA 2007 guidelines for the management of

patients with unstable angina/non-ST-elevation myocardial infarction: a

report of the American College of Cardiology Foundation/American Heart

Association Task Force on Practice Guidelines. Circulation. 2013;127:e663-

e828.


http://www.ncbi.nlm.nih.gov/pubmed/?term=January%20CT%5BAuthor%5D&cauthor=true&cauthor_uid=24685669

http://www.ncbi.nlm.nih.gov/pubmed/?term=Wann%20LS%5BAuthor%5D&cauthor=true&cauthor_uid=24685669

http://www.ncbi.nlm.nih.gov/pubmed/?term=Alpert%20JS%5BAuthor%5D&cauthor=true&cauthor_uid=24685669

http://www.ncbi.nlm.nih.gov/pubmed/?term=Calkins%20H%5BAuthor%5D&cauthor=true&cauthor_uid=24685669

http://www.ncbi.nlm.nih.gov/pubmed/?term=Cigarroa%20JE%5BAuthor%5D&cauthor=true&cauthor_uid=24685669

http://www.ncbi.nlm.nih.gov/pubmed/?term=Cleveland%20JC%20Jr%5BAuthor%5D&cauthor=true&cauthor_uid=24685669





http://www.uptodate.com/contents/nitrates-in-the-management-of-acute-coronary-syndrome?source=search_result&search=nitroglycerin+drip&selectedTitle=1%7E150





77. Nitroglycerin. Lexicomp®. February 18, 2015. retrieved February 23, 2015

from www.UCHC.edu.

78. Hottinger DG, Beebe DS, Kozhimannil T, Prielipp RC, Belani KG. Sodium

nitroprusside in 2014: A clinical concepts review. J Anaesthesiol Clin

Pharmacol. 2014;30:462-71.

79. Amiodarone. Lexicomp®. February 23, 2015. Retrieved February 24, 2015

from www.UCHC.edu.

80. Nexterone [package insert]. Deerfield, IL. Baxter Healthcare Corporation;

2014.

81. Lidocaine (Systemic). Lexicomp®. February 17, 2015. Retrieved February

20, 2015 from www.UCHC.edu.

82. Kearney TE. Lidocaine. In: Anderson IL, Benowitz NL, Blanc PD, Clark RF,

Kearmey TE, Osterloh JD, eds. Poisoning & Drug Overdose. 5th ed. New

York, NY: McGraw-Hill;2007.

83. Procainamide. Lexicomp® February 11, 2015.Rretrieved February 21, 2015

from www.UCHC.edu.

84. Procainamide injection [package insert]. Lake Forest, IL: Hospira, Inc.;

2014.

85. Benowitz NL. Antiarrhythmic drugs. In: Anderson IL, Benowitz NL, Blanc

PD, Clark RF, Kearney TE, Osterloh JD, eds. Poisoning & Drug Overdose. 5th

ed. New York, NY: McGraw-Hill; 2007.

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http://www.ncbi.nlm.nih.gov/pubmed/?term=Hottinger%20DG%5BAuthor%5D&cauthor=true&cauthor_uid=25425768

http://www.ncbi.nlm.nih.gov/pubmed/?term=Beebe%20DS%5BAuthor%5D&cauthor=true&cauthor_uid=25425768

http://www.ncbi.nlm.nih.gov/pubmed/?term=Kozhimannil%20T%5BAuthor%5D&cauthor=true&cauthor_uid=25425768

http://www.ncbi.nlm.nih.gov/pubmed/?term=Prielipp%20RC%5BAuthor%5D&cauthor=true&cauthor_uid=25425768

http://www.ncbi.nlm.nih.gov/pubmed/?term=Belani%20KG%5BAuthor%5D&cauthor=true&cauthor_uid=25425768






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