Liverpool Health Service

Intensive Care Unit

Self Directed Learning Package:

Inotropes

Written by: Gary Forrest

How to use this package

This package is designed to be used in the clinical area

as a self directed learning tool. At the start of the
package is a pre test which covers the information
contained inside. You should read through the pretest
and answer the questions. If you have any problems
with any of the questions, this will provide you with
some guidance as to the areas that you should focus
on in the package.

The package is divided into sections. At the end of

each section is a self test to determine how well you
have understood the information contained in that
section. You will need to complete the self tests at the
end of each section and ensure that you have
mastered the content before moving on to the next
section.

If you have any trouble with the self test, go back over
the section and revise the content. If you are still
unsure then you will need to speak with one of the
educators in your area.

Once you have worked through the entire package,

you should complete the post test. The answers to the
post test are contained at the end of the package. If
you have any trouble with the post test, go back to the
section in the package and revise it. If you are still
unsure, contact the educator in your area.

GOOD LUCK!!!
Learning package objectives

By the completion of this package, the registered nurse

will be able to:

1. Discuss the indications for the administration of

inotropes in the Intensive Care Unit.

2. Define the relevant terminology used when

discussing inotropic therapy.

3. Discuss the physiological effects elicited when the

following receptor sites are stimulated:

i. Alpha
ii. Beta 1
iii. Beta 2
iv. Dopaminergic

4. Discuss the pharmacological effects and dosage

ranges for the following inotropes:

i. Adrenaline
ii. Noradrenaline
iii. Dobutamine
iv. Dopamine

5. Discuss the complications and nursing care issues

relevant to the administration of the above
mentioned drugs.
Pretest

1. Define shock.

2. List the three factors that need to occur for

tissues to be oxygenated

3. What effect do inotropes have on myocardial rate

and contractility?

4. Complete the following haemodynamic equations:

• Cardiac output = ? x ?
• Mean arterial pressure = ? x ? x?

5. Define:

• Cardiac output
• Preload
• Afterload
• Stroke volume
• Inotropy
• Chronotropy

6. Discuss the response elicited when the following

receptors are activated:

• Alpha
• Beta 1
• Beta 2
• Dopaminergic
7. Perform the following drug calculations:

You have a 50 ml syringe with 16 mg of

noradrenaline running at 8 ml/hr. The patient
weighs 80 kg. What dose (in mcg/kg/min) is the
patient receiving?

You are asked to commence an adrenaline

infusion at 0.02 mcg/kg/min. Your unit policy
requires the adrenaline be made up as 4mg in 50
ml and administered via a syringe pump. The
patient weighs 75 kg. What rate (in ml/hr) would
you commence the infusion?

8. Outline the receptors activated by the following

inotropes:

• Adrenaline running at < 0.02 mcg/kg/min

• Adrenaline running at > 0.02 mcg/kg/min
• Noradrenaline running at 0.3 mcg/kg/min
• Dobutamine running at 8 mcg/kg/min
• Dopamine running at < 2 mcg/kg/min
• Dopamine running at 2 – 10 mcg/kg/min
• Dopamine running at > 10 mcg/kg/min
9. Discuss the effects of tachycardia on myocardial
oxygen demands.

10. Discuss the effects of increased afterload on

myocardial oxygen demands.
11. Discuss the effects of tachycardia on stroke
volume and cardiac output.

12. Explain why dobutamine may be a useful inotrope

following a myocardial infarction.

13. Explain why noradrenaline may be a useful

inotrope in septic shock.

14. What is the unit policy on purging inotropes?

Introduction

Inotropes are powerful drugs that are used in Intensive

Care to regulate a patient’s heart rate, blood pressure
and the force of contraction of the heart. They do this
by working on specific receptors throughout the body.

Because of their strength, they are able to exert their

effects at very low doses. Increasing this dosage can
activate other receptors and result in undesired effects
which may be detrimental to the patient.

It is imperative that nurses caring for patients who are

receiving inotropes are aware of the specific dosage
ranges and the receptors activated, the desired effects
of the drugs and the complications associated with
their administration.

This self directed learning package is designed to

assist registered nurses caring for patients receiving
inotropes. It can be completed at the bedside and will
assist with the safe and effective administration of
inotropic agents.
Indications for inotropes

Inotropes may be needed when a patient is in shock.

Shock is generally associated with a low blood
pressure but the definition of shock is much more
than that.

Shock is defined as “inadequate tissue oxygenation”.

To explain this further, you can have a normal blood

pressure and not have the tissues being oxygenated so
this would be defined as shock. Alternatively you can
have a low blood pressure and still have the tissues
being oxygenated so this wouldn’t be defined as shock.
Inotropes and tissue oxygenation

For tissues to be oxygenated, 3 factors need to be

considered:

1) Oxygen transfer across the alveolar-capillary

membrane
2) Oxygen attachment to haemaglobin
3) Adequate cardiac output (CO) to move the
oxyhaemaglobin molecule to the tissues

In relation to this last point, there are several ways of

increasing CO:

1) Enhancing circulating volume through fluid

resuscitation (increasing preload)
2) Enhancing myocardial contractility with inotropes
(their inotropic effect)
3) Manipulating heart rate with inotropes (their
chronotropic effect)

You can see how inotropes are useful in the

management of shock and tissue oxygenation.
Haemodynamic equations

Inotropes are used in shock mainly to manipulate

cardiac output and afterload (systemic vascular
resistance (SVR)). In order to understand this,
consider the following simplified haemodynamic
model:

Cardiac output (CO) = Heart Rate (HR) x Stroke

Volume (SV)

Where SV is the volume of blood ejected by the left

ventricle (approximately 70ml)

Normal CO = 4 to 8 Litres/minute

Generally we measure Blood Pressure (BP) not CO so

how do these relate?

Mean Arterial Pressure (MAP) = CO x SVR (afterload)

Therefore:

MAP = SV x HR x SVR

Can you see how inotropes may be useful?

Before you go any further, try the following self
test.

Self test 1.

1. Define shock.

2. List the three factors that need to occur for

tissues to be oxygenated

3. What effect do inotropes have on myocardial rate

and contractility?

5. Complete the following haemodynamic equations:

• Cardiac output = ? x ?
• Mean arterial pressure = ? x ? x?
Haemodynamic terminology

Before we move on it might be useful to revise some

definitions.

• Cardiac output

The amount of blood ejected from the left ventricle

during systole over a period of one minute. Cardiac
output is determined by multiplying heart rate by
stroke volume

• Preload

The volume of blood in the ventricle at the end of

diastole

• Afterload

The resistance that the heart must pump against in

order to eject the blood. This resistance is provided
by the arterial system

• Stroke volume

The amount of blood ejected by the left ventricle

• Inotropy

Increased strength of contraction

• Chronotropy

Increased rate of contraction

Receptor activation

Inotropes work by targeting specific receptor sites in

the body. The degree of effect depends upon the dose
of the inotrope and the receptor it targets. The
following table summarises the receptor type and the
effect seen.

Receptor Type Effect

Alpha Vasoconstriction

Beta 1 Increased heart rate and

contractility
Beta 2 Bronchodilation;
vasodilation of skeletal
and coronary blood
vessels
Dopaminergic Vasodilation of renal and
mesenteric blood vessels
Calculating drug dosages

When choosing an inotrope to treat shock, the

haemodynamic values can be manipulated by selecting
a drug and dose that affects the receptor type. As the
receptor activation is dependent on the dose of the
drug given, it is necessary to be able to calculate drug
dosages in micrograms per kilogram per minute
(mcg/kg/min). The following discussion will show you
how this is done.

To calculate mcg/kg/min for a given infusion rate:

mcg/kg/min = rate (ml/hr) x concentration (mcg/ml)

divide by weight (kg) divide by 60

For example:

A patient is receiving an adrenaline infusion at 5

ml/hr. The infusion is 4 mg in 50 ml (80mcg/ml). The
patient weighs 90 kg. You need to calculate the dose
that the patient is receiving in mcg/kg/min.

mcg/kg/min = 5 x 80 divide by 90 divide by 60

= 0.07 mcg/kg/min
To calculate infusion rate for a specific dose

ml/hr = dose (mcg/kg/min) x patient’s weight (kg) x 60

x volume (ml) divide by (strength (mg) x 1000)

For example:

You want to give a patient who weighs 75 kg a dose of

5 mcg/kg/min of dobutamine. The bag of 500 ml of
5% dextrose contains 250 mg of dobutamine. You need
to calculate the rate of the infusion

ml/hr = (5 x 75 x 60 x 500) divide by (1000 x 250)

= 45 ml/hr
Before you go any further, try the following self
test.

Self test 2.
1. Define:

• Cardiac output
• Preload
• Afterload
• Stroke volume
• Inotropy
• Chronotropy

2. Discuss the response elicited when the following

receptors are activated:
• Alpha
• Beta 1
• Beta 2
• Dopaminergic

3. Perform the following drug calculations:

You have a 50 ml syringe with 16 mg of

noradrenaline running at 8 ml/hr. The patient
weighs 80 kg. What dose (in mcg/kg/min) is the
patient receiving?

You are asked to commence an adrenaline

infusion at 0.02 mcg/kg/min. Your unit policy
requires the adrenaline be made up as 4mg in 50
ml and administered via a syringe pump. The
patient weighs 75 kg. What rate (in ml/hr) would
you commence the infusion?
In the next part of our discussion we will look at some
common inotropic drugs and dosage ranges.

Pharmacology

There are four inotropes that we will be considering in

this package:

• Adrenaline
• Noradrenaline
• Dobutamine
• Dopamine
Adrenaline

• Also known as epinephrine in the North American

literature
• Works on alpha, beta 1 and beta 2 receptors
• The net result is increased HR, BP and CO

Low doses

• < 0.02 mcg/kg/min

• primarily beta 1 and beta 2 but beta 1 more
dominant
• increases heart rate (chronotropy)
• increases force of contraction (inotropy)
• increases cardiac output
• dilates bronchi
• dilates skeletal muscle and coronary blood vessels

High doses

• > 0.02 mcg/kg/min

• mainly alpha effects
• increases blood pressure and SVR secondary to
vasoconstriction
Clinical application

You are managing a patient on an adrenaline infusion.

You calculate the dose at 0.01 mcg/kg/min. Your
clinical assessment reveals:

• HR 110/minute (beta 1 effects)

• BP 110/60 (beta 1 effects)
• Warm peripheries (beta 2 effects)

Points for consideration

A tachycardia will increase the amount of workload

and myocardial oxygen requirement of the heart. In
patients who have cardiac disease, the myocardial
oxygen demands may exceed the myocardial oxygen
supply and myocardial ischaemia may result.
Clinical application

The dose of the adrenaline infusion in the first case

scenario is increased to 0.03 mcg/kg/min. Your
clinical assessment now reveals:

• HR 150/minute (beta 1 effects)

• BP 100/60
• Cool peripheries (alpha effects)

Points for consideration

Increasing the dosage has resulted in increased beta 1

effects (tachycardia) and some alpha effects causing
vasoconstriction and cool peripheries. This should
increase the BP but hasn’t. A possible reason for this
is the tachycardia is not allowing the ventricles time to
fill adequately hence less blood is ejected from the left
ventricle (decreased stroke volume). You can see how
important it is to monitor your patient closely and
understand the desired effects and problems
associated with these medications.
Noradrenaline

• Also known as norepinephrine in the North

American literature
• Works on alpha and beta receptors
• The net result is increased CO, SVR and MAP

Low doses

• beta 1 effects predominate

High doses

• alpha effects predominate

Dosage range

• 0.05 mcg/kg/min to more than 0.3 mcg/kg/min

Clinical application

A patient is started on a noradrenaline infusion at

0.05 mcg/kg/min. You are asked to titrate the
noradrenaline to keep the MAP greater than 70 mmHg.
You periodically increase the infusion and stop when
the MAP has stabilised at 70 mmHg. Your clinical
assessment reveals:

• HR 90/minute
• BP 108/52 MAP (71) (alpha effects)
• Cool peripheries (alpha effects)

Points for consideration

As the alpha effects dominate and vasoconstriction

occurs, SVR or afterload increases. This means the
heart will have to work a lot harder in order to eject
the blood from the ventricle. Increased heart workload
means increased myocardial oxygen demands. If this
exceeds myocardial oxygen supply, then ischaemia
may occur. This could have a significant impact on
patients with a cardiac history.
Dobutamine

• Works on beta 1 and beta 2 receptors

• The net effects are increased CO and minimally
increased HR
• Decreased SVR and MAP

As dobutamine works primarily on beta 1 receptors, it

increases the force of myocardial contraction (inotropy)
without significant increases in heart rate
(chronotropy). Mild beta 2 stimulation results in slight
vasodilation which can decrease SVR and MAP.

Dosage range

• 2 – 15 mcg/kg/min
Clinical application

A patient with a myocardial infarction is hypotensive.

A decision is made to commence a dobutamine
infusion at 8 mcg/kg/min. Your clinical assessment
reveals:

• HR 84/minute
• BP 110/50

Points for consideration

Dobutamine is often a good drug to use in myocardial

infarction as it doesn’t increase HR (beta 1) and
myocardial oxygen demands or increase SVR (alpha
effects) and myocardial workload. As it does not have
any alpha properties, BP is supported by increased
myocardial contractility only, therefore if hypotension
persists an alpha stimulant may be required.
Dopamine

• Works on dopaminergic, alpha, beta 1 and beta 2

receptors
• The effects are dose dependent
• Can work to increase renal blood flow, CO, HR and
SVR

Dopamine is dose dependent as follows:

Low doses

• 0.05 – 2 mcg/kg/min
• dopaminergic receptors
• increased renal and mesenteric blood flow

Moderate doses

• 2 – 10 mcg/kg/min
• beta 1 receptors
• increased HR and contractility

High doses

• > 10 mcg/kg/min
• alpha receptors
• increased SVR
• dopaminergic effects lost
Clinical application

A patient has a low urine output despite fluid

challenges and a normal blood pressure. A decision is
made to commence low dose dopamine at 2
mcg/kg/min.

Points for consideration

There is much debate about the usefulness of low dose

dopamine for improving urine output and there have
been several research papers which have questioned
its value. For this reason, widespread use of dopamine
at this dosage range is uncommon.
Some final points for consideration….

Purging inotropes.

As a general rule, inotropes should never be purged.

Purging results in uneven doses of the inotrope being
given to the patient and as a result the patient can
have huge changes in their haemodynamic
parameters.

Inotropes need to be regulated by continuous infusion

to maintain a consistent dose delivery and
haemodynamic control. The unit protocol states that
inotropes should never be purged.

Changing a syringe.

Preparing the next syringe should never be left until

the last minute. Inotrope infusions should never run
out. Some patients are very dependent on their
inotropes and will not tolerate them being turned off
for even a short period of time. It is compulsory to
have the next infusion prepared as soon as the current
syringe is connected (have a replacement syringe
prepared regardless of strength & rate of infusion).

Some patients may become haemodynamically

unstable for the short time that the syringe is being
changed. There are two ways to overcome this.
One way is to start the second infusion through a
three way tap while the first is still running. When the
blood pressure starts to rise, cease the first infusion
immediately.

For this method, a three way tap should be connected

into the line when the inotrope is first started. If you
are starting an inotrope, it is good practice to include a
three way tap to facilitate syringe changes.

The second way is to change the syringe quickly and

observe for any changes in your patient’s blood
pressure. If the blood pressure drops, increase the
infusion rate regularly until the blood pressure starts
to climb. Wean the rate slowly back to the original rate
keeping the blood pressure stable.

It is always a good idea to get some help when you are

changing a syringe until you become comfortable with
regulating inotropes.

Choosing a lumen.

Inotropes should always be infused through a separate

lumen to avoid purges of the drug should fluid
challenges be given. For this reason, the proximal
lumen is chosen

Remember, when in doubt – ASK!

Before you go any further, try the following self
test.

Self test 3.
1. Outline the receptors activated by the following
inotropes:

• Adrenaline running at < 0.02 mcg/kg/min

• Adrenaline running at > 0.02 mcg/kg/min
• Noradrenaline running at 0.3 mcg/kg/min
• Dobutamine running at 8 mcg/kg/min
• Dopamine running at < 2 mcg/kg/min
• Dopamine running at 2 – 10 mcg/kg/min
• Dopamine running at > 10 mcg/kg/min

2. Discuss the effects of tachycardia on myocardial

oxygen demands.

3. Discuss the effects of increased afterload on

myocardial oxygen demands.
4. Discuss the effects of tachycardia on stroke
volume and cardiac output.

5. Explain why dobutamine may be a useful inotrope

following a myocardial infarction.

6. Explain why noradrenaline may be a useful

inotrope in septic shock.

7. What is the unit policy on purging inotropes and

on syringe preparation?
Post test

1. Define shock.

2. List the three factors that need to occur for

tissues to be oxygenated

3. What effect do inotropes have on myocardial rate

and contractility?

4. Complete the following haemodynamic equations:

• Cardiac output = ? x ?
• Mean arterial pressure = ? x ? x?

5. Define:

• Cardiac output
• Preload
• Afterload
• Stroke volume
• Inotropy
• Chronotropy

6. Discuss the response elicited when the following

receptors are activated:

• Alpha
• Beta 1
• Beta 2
• Dopaminergic
7. Perform the following drug calculations:

You have a 50 ml syringe with 16 mg of

noradrenaline running at 8 ml/hr. The patient
weighs 80 kg. What dose (in mcg/kg/min) is the
patient receiving?

You are asked to commence an adrenaline

infusion at 0.02 mcg/kg/min. Your unit policy
requires the adrenaline be made up as 4mg in 50
ml and administered via a syringe pump. The
patient weighs 75 kg. What rate (in ml/hr) would
you commence the infusion?

8. Outline the receptors activated by the following

inotropes:

• Adrenaline running at < 0.02 mcg/kg/min

• Adrenaline running at > 0.02 mcg/kg/min
• Noradrenaline running at 0.3 mcg/kg/min
• Dobutamine running at 8 mcg/kg/min
• Dopamine running at < 2 mcg/kg/min
• Dopamine running at 2 – 10 mcg/kg/min
• Dopamine running at > 10 mcg/kg/min
9. Discuss the effects of tachycardia on myocardial
oxygen demands.

10. Discuss the effects of increased afterload on

myocardial oxygen demands.
11. Discuss the effects of tachycardia on stroke
volume and cardiac output.

12. Explain why dobutamine may be a useful inotrope

following a myocardial infarction.

13. Explain why noradrenaline may be a useful

inotrope in septic shock.

14. What is the unit policy on purging inotropes?

15. What is the unit [policy on syringe preparation?

16. Answers to the Post test

1. Shock is defined as “inadequate tissue

oxygenation”.

2. i) Oxygen transfer across the alveolar-capillary

membrane
ii) Oxygen attachment to haemaglobin
iii) Adequate cardiac output (CO) to move the
oxyhaemaglobin molecule to the tissues

3. Inotropes increase myocardial rate and

contractility.

4. Cardiac output - The amount of blood ejected

from the left ventricle during systole over a period
of one minute. Cardiac output is determined by
multiplying heart rate by stroke volume

Preload - The volume of blood in the ventricle at

the end of diastole

Afterload - The resistance that the heart must

pump against in order to eject the blood. This
resistance is provided by the arterial system

Stroke volume - The amount of blood ejected by

the left ventricle

Inotropy - Increased strength of contraction

Chronotropy - Increased rate of contraction

5. Cardiac output = heart rate x stroke volume
Mean arterial pressure = heart rate x stroke
volume x systemic vascular resistance

6. Alpha – vasoconstriction. Increased blood

pressure and cool peripheries
Beta 1 – increased heart rate
Beta 2 – bronchodilation and vasodilation of
skeletal and coronary blood vessels
Dopaminergic – increased renal and mesenteric
blood flow

7. 0.53 mcg/kg/min

1.1 ml/hr

8. Adrenaline running at < 0.02 mcg/kg/min – beta

Adrenaline running at > 0.02 mcg/kg/min - alpha
Noradrenaline running at 0.3 mcg/kg/min –
alpha
Dobutamine running at 8 mcg/kg/min - beta
Dopamine running at < 2 mcg/kg/min -
dopaminergic
Dopamine running at 2 – 10 mcg/kg/min - beta
Dopamine running at > 10 mcg/kg/min - alpha
9. Tachycardia will increase myocardial oxygen
demands. This can be detrimental if myocardial
oxygen demands exceed myocardial oxygen
supply.

10. Increased afterload will increase myocardial

oxygen demands. As the heart has to work harder
to pump the blood out against constricted vessels,
its workload increases as does its myocardial
oxygen demands.
11. Tachycardia may result in a decreased stroke
volume and cardiac output. As the heart beats
faster it may not have enough time to fill during
diastole. This will result in a decreased stroke
volume. As cardiac output is dependent on stroke
volume, this may decrease also.

12. Dobutamine may be a useful inotrope following a

myocardial infarction as it has beta effects only.
The beta effects will increase the force of
contraction without increasing heart rate and
myocardial oxygen demands. As dobutamine has
no alpha properties, afterload is not increased
hence myocardial workload and oxygen demands
are not increased.

13. Noradrenaline may be a useful inotrope in septic

shock as its alpha effects will increase afterload
and assist with raising systemic blood pressure.

14. Inotropes should never be purged.

15. The replacement inotrope syringe should be
prepared as soon as the current syringe is
connected. There MUST always be a replacement
syringe prepared in the bed area regardless of
strength and rate of infusion.