USE OF VASOACTIVE DRUGS IN THE CRITICALLY ILL PATIENT
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Transcript USE OF VASOACTIVE DRUGS IN THE CRITICALLY ILL PATIENT
Dr Bronwyn Avard, July 2010
To understand the basic
physiology of shock
To understand the pharmacodynamics and
pharmacokinetics of vasoactive drugs used
in ICU
To know the indications for the
administration of different inotropes and
vasopressors in the critically ill patient
To know the complications of administering
these vasoactive drugs, and relevant
patient care issues
Please complete pre-test before
progressing with learning package.
Click on this link :
http://www.surveymonkey.com/s/vasoactivepretest
SHOCK
Cardiac output = stroke volume x heart rate
amount of blood ejected
from the ventricle in systole
depends on :
- preload
- afterload
- contractility
Cardiac output = stroke volume x heart rate
› Preload = end-diastolic ventricular volume
› Afterload = resistance against which ventricle
contracting
› Contractility = strength of muscle activity
Cardiac index = cardiac output / BSA
Oxygen delivery =
cardiac output x arterial oxygen content
stroke volume x heart [haemoglobin]
rate
x SaO2
preload
afterload
contractility
Blood pressure =
cardiac output x systemic vascular resistance
Hypovolaemic
Cardiogenic
Distributive / vasodilatory
Obstructive
Inotropes
Vasopressors
global
oxygen
delivery
cardiac
output
arterial
oxygen
content
mean
arterial
pressure
cardiac
output
systemic
vascular
resistance
RECEPTOR TYPE
EFFECT
alpha
vasoconstriction
beta-1
↑ heart rate &
contractility
vasodilation &
bronchodilation
vasodilation (renal &
mesenteric)
beta-2
dopamine
Adrenaline
Noradrenaline
Dobutamine
(Dopamine)
Metaraminol
Phenylephrine
Ephedrine
aka ephinephrine
Low dose = ↑ heart rate & contractility
High dose = vasoconstriction
•Adrenaline infusion 0.01mcg/kg/minute
•HR 110 bpm
•MAP 70mmHg
•Warm peripherally
• Infusion increases to 0.03mcg/kg/minute
•HR now 150bpm
•MAP now 65mmHg
•Cool peripherally
WHY?
As heart rate rises,
less time available for cardiac filling,
hence stroke rate falls
MAP falls rather than rising
as you would have expected
aka norepinephrine
Low doses = mainly ↑ HR & SV
High doses = mainly vasoconstriction
•Nordrenaline infusion 0.05mcg/kg/minute
•MAP 55mmHg
•Warm peripherally
• As infusion increases
•Cool peripherally
•Lactate rising
WHY?
Vasoconstriction caused by higher
dose noradrenaline redistributes
blood flow to essential organs
Even though MAP rises, splanchnic
perfusion falls & rising lactate can
indicate gut ischaemia
Acts on both beta 1 and 2 receptors
Net effects are
› Increased contractility
› Increased heart rate
› Mild vasodilation
Effect on MAP variable and not always
predictable – may increase or decrease
• 76 year old woman post NSTEMI
•HR 84bpm
•MAP 64mmHg
•Cool peripherally
• Begun on dobutamine 7.5mcg/kg/minute
•MAP falls to 60mmHg
WHAT WOULD YOU DO?
She was probably vasoconstricted
prior to infusion.
Beginning dobutamine caused
vasodilatation hence MAP fell.
Fluid bolus or noradrenaline would
be appropriate.
mcg/kg/min = rate (mL/h) x concentration (mcg/mL)
weight (kg) x 60
You are caring for a 60 year old man, weighing
approximately 90kg, admitted after a non-ST
elevation myocardial infarction.
He is receiving adrenaline at 5mL/h. The 100mL
bag has 8mg adrenaline in it.
What dose of adrenaline
is he receiving ?
(in mcg/kg/min)
mcg/kg/min = rate (mL/h) x concentration (mcg/mL)
Weight (kg) x 60
ANSWER : 0.07 mcg/kg/min
mcg/kg/min = rate (mL/h) x concentration (mcg/mL)
weight (kg) x 60
mcg/min = concentration (mg/mL) x 1000 x rate (ml/h)
60
You are looking after a 25 year old woman who
has been admitted with sepsis.
She has 6mg noradrenaline in 100mL bag of
normal saline, which is running at 5mL/hour.
How many mcg/minute is she receiving?
mcg/min = concentration (mg/mL) x 1000 x rate (mL/h)
60
ANSWER : 5mcg/min
This is why we use the concentration of
6mg/100mL as the “mL/h” equals “mcg/min”
(she was on 5mL/h noradrenaline)
Adrenaline
Noradrenaline
Ephedrine
Metaraminol
Phenylephrine
Inotropes :
› Milrinone
› Levosimenden
Vasopressor :
› Vasopressin
Accurate measurement of vital signs &
invasive blood pressure
Check vasoactive drugs at start of shift
Ideally administered centrally
Labelling critical
Change bag every 24 hours
Local necrosis with extravasation
Tachycardia & arrhythmias
Increased myocardial oxygen
consumption
Ischaemia of gut &/or extremities
SHOCK
adrenaline
hypovolaemic
cardiogenic
distributive
obstructive
noradrenaline
dobutamine
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