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This self managed learning package was developed by Roz Elliott, Clinical Nurse
Name :
Unit:
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Medication information and learning package, ICU, RNSH - December 2008
Version 2: Expiry 2009.12.19
Document Authorisation
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Version 2: Expiry 2009.12.19
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Table of Contents
Document Authorisation........................................................................................................... 2
Disclaimer..................................................................................................................................... 3
Feedback ...................................................................................................................................... 4
Introduction................................................................................................................................. 4
LEARNING OUTCOME OBJECTIVES ......................................................................................................................... 4
PREREQUISITES ....................................................................................................................................................... 4
ASSESSMENT PROCESS ........................................................................................................................................... 4
RECOGNITION OF PRIOR LEARNING ...................................................................................................................... 5
Pre self test ............................................................................................................................... 6
Information about medications commonly administered on level 6 ICU.................. 8
THE CORE VASOACTIVE MEDICATIONS USED ON LEVEL 6 ICU ............................................................................ 8
MUSCLE RELAXANTS .............................................................................................................................................. 12
ANALGESIA AND SEDATION .................................................................................................................................. 15
ELECTROLYTES ........................................................................................................................................................ 22
DIURETICS .............................................................................................................................................................. 24
PEPTIC ULCER PROPHYLAXIS................................................................................................................................... 25
ANTICOAGULANTS ................................................................................................................................................. 27
REVERSAL AGENT FOR HEPARIN ............................................................................................................................. 28
ANTI-ARRHYTHMICS.............................................................................................................................................. 29
INSULIN ................................................................................................................................................................. 31
Post self-test .......................................................................................................................... 34
References and supporting literature .............................................................................. 35
Disclaimer
This learning package has been prepared by a health care professional employed in
the intensive care unit at the Royal North Shore Hospital. While all care has been
taken, the intensive care unit at the Royal North Shore Hospital cannot guarantee
that the information contained within the learning package is accurate. Therefore
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Feedback
This learning package has been added to the intensive care unit intranet for all to
view. We appreciate feedback and encourage you to contact the primary author via
e mail (this is located in the authorisation table on the previous page). The primary
author may also be prepared to provide further information and insights to the
topic.
Introduction
This learning package is to be used in conjunction with the level six medication
Prerequisites
In order to complete this package the Registered Nurse must have completed the
hospital:
Assessment process
When you have completed this package please give it to an accredited assessor for
review. Once this has occurred the Registered Nurse can complete the ICU
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Recognition of prior learning
Relevant post graduate qualification will be acknowledged e.g. Graduate Certificate
competency assessment will not have to complete this package or the level 6
ICU competency
If you feel that you hold relevant qualifications please speak with the CNE in your
area.
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Pre self test
Complete the following assignments without consulting texts:
intravenous medications)
Describe the mechanism of action of adrenaline that would lead to its use in
What is the reversal agent for opioid medication and how is it administered?
in Ventricular Fibrillation)?
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What is the mechanism of action of lignocaine?
insulin on IIMS?
ICU?
Ensure you are familiar with the Royal North Shore Hospital medication
administration policy. Other guidelines which may help you successfully complete
the neurosurgical intensive care unit (6C) and the post-operative cardiothoracic
guideline located in the cardiothoracic intensive care unit (6H). Read the following
information about the main medication groups and consult the reading list for
further information.
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Information about medications commonly administered on
level 6 ICU
Adrenaline
Mechanism of action
Sympathomimetic amine which mimics the sympathetic nervous system.
A positive ionotrope and chronotrope which acts on alpha and beta
receptors. It causes
increased heart rate
increased stroke volume/cardiac output.
powerful peripheral vasoconstriction.
dilation skeletal muscle beds at lower doses.
relaxation smooth muscle bronchial tree.
mixed Alpha vasoconstriction and B2 vasodilation usually increases
systemic vascular resistance (SVR) at higher doses.
Usage
Cardiac arrest
Inotropic agent e.g. cardiogenic shock
Anaphylaxis
Life threatening asthma
Administration guide
Cardiac arrest - give 1 mg IV (Minijet) every 3-5 minutes prn. May
be given peripherally in emergencies (flush well).
Infusion - Add 4 mg to 100 mls D5W or N/S. Infuse via a central
line using a volumetric pump. Titrate dosage according to Medical
Orders and clinical response.
Presentation
Ampoules, 1 mg/mL (1:1,000, clear, colourless solution)
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Adverse Effects
Hypertension/cerebral haemorrhage, anxiety, peripheral
vasoconstriction, tremor, palpitations, myocardial ischaemia,
arrhythmias, reduction in renal blood flow.
Precautions
Caution in patients with Ischaemic heart disease, diabetes,
hyperthyroidism.
Dobutamine
Mechanism of action
Synthetic catecholamine. Stimulates B1 receptors causing:
increased myocardial contractility.
increased stroke volume and cardiac output.
decreased preload and afterload (vasodilation).
Also produces mild chronotropic, hypotensive and arrhythmogenic
effects.
Usage
Short term cardiac failure due to:
acute cardiac disease
cardiac surgery
Administration guide
Reconstitute 250 mg with 10 mls H2O or D5W, then add to 100 mls
of D5W, N/S or Hartmanns.
Infuse via a large vein at approximately 2.5 - 10 mcg/kg/min. May be
given peripherally (if necessary). Use a volumetric pump.
Presentation
Single dose vials (sterile aqueous solution), 250 mg/20 mL:
Adverse Effects
Increase in heart rate, which responds to dose reduction (may
worsen myocardial ischaemia).
Hypotension (lower doses due to vasodilation).
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Ventricular ectopic activity.
Precautions
Correct hypovolaemia prior to administration.
Mechanism of action
Vascular smooth muscle relaxant
Venodilation
Arterial dilation at higher doses
Coronary artery dilatation, increasing myocardial oxygen delivery
Usage
Unstable angina - reduces oxygen demand and increases oxygen
supply. hypertension.
Myocardial infarction.
CCF reduces preload and afterload
Administration Guide
Use glass bottles and non-PVC set and change every 24 hours.
Dilute either 50 mg in 500 mls (100 mcg/ml), 200 mg in 500 mls
(400 mcg/ml) or 50 mg in 100 mls (500 mcg/ml). Titrate dose to
desired response.
Presentation
50 mg/10 mL.
Adverse effects
Headache, hypotension, sinus bradycardia, reflex tachycardia, syncope,
nausea, vomiting, dizziness, restlessness, muscle twitching.
Precautions
Avoid in patients with marked anaemia, head trauma, cerebral
haemorrhage. Caution in hypovolaemic patients and RV infarcts. (sudden
hypotension).
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Metaraminol bitartrate
Mechanism of action
Sympathomimetic amine that causes peripheral vasoconstriction,
increasing both systolic and diastolic blood pressure. Also has positive
inotropic actions.
Usage
Emergency to treat hypotension
Administration Guide
IV Bolus -- Dilute 10 mg in 10 mls or 20mls NS. Administer 0.5 to 1
mg IV initially. Repeat as required.
Administer via a large vein.
Presentation
10 mg/1 ml ampoule.
Adverse Effects
Anxiety, tremor, flushing, sweating, nausea, reflex bradycardia.
Overdose may result in hypertension, cerebral haemorrhage,
convulsions, pulmonary oedema, cardiac arrest/arrhythmias.
Precautions
Hypovolaemia should be corrected before administration.
Metaraminol bitartrate is only used as a temporary supportive
measure.
Precautions
Correct blood volume depletion before administering noradrenaline.
Avoid hypertension
Sodium Nitroprusside
Mechanism of action
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Powerful vasodilator of both arterioles and veins. Reduces systemic
pressures and improves cardiac performance.
Usage
Hypertension
Heart failure - reduces preload and afterload, improves cardiac
output and lowers myocardial oxygen requirements.
Administration guide
Central Infusion - Reconstitute 50 mg with 2-3mls or D5W and add
to 100 mls D5W.
Peripheral Infusion - Dilute 50 - 100 mg in 500 mls. Wrap in foil to
protect from light. Administer alone. Titrate dose to desired
effect. Maximum dose 10 mcg/kg/min.
Presentation
Vials, 50 mg (sterile lyophilised powder for reconstitution)
Adverse effects
Hypotension, metabolic acidosis, nausea, vomiting, palpitations,
tachycardia.
Precautions
In high dose SNP or in prolonged therapy. toxic metabolites
accumulate. Cyanide toxicity leading to air hunger, confusion, lactic
acidosis. Caution in those patients with impaired liver or renal function.
Muscle relaxants
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Compete with acetylcholine for receptor sites at the neuromuscular
junction. Their action may be reversed with anticholinasterases such as
neostigmine. The group can be divided into two groups:
Aminosteriod group eg pancuronium, rocuronium, vecuronium
Benzylisoquinolinium group eg atracurium, cisatracurium
Vecuronium
Dose
IV for intubation 80-100mcg/kg and 20-30 mcg/kg for maintenance.
Onset
Within 3 minutes
Side effects
Aminosteriods have minimal histamine release and therefore very few
have potential for anaphylactic reactions. Care with hepatic or renal
impairment, as this is the elimination route
Pancuronium
Dose
IV for intubation 50-100mcg/kg and 10-20 mcg/kg for maintenance.
Onset
Within 4 minutes
Side effects
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Again, care for hepatic impairment, use a lower dose or different
medication
Atracurium
Dose
IV for intubation 400500/kg and 80-100 mcg/kg for maintenance.
Onset
Within 2 minutes
Side effects
Avoid in Myasthenia gravis.
Reduce dose when inhalation anaesthetics are used simultaneously.
Mild histamine release is possible therefore cardiovascular effects
i.e. hypotension are possible.
Benzylisoquinoluniums cause more histamine release and therefore
have more cardiovascular related side effects
Suxamethonium
Dose
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IV for intubation 0.6-1.2 mcg/kg and larger doses for operation 2.5-
4.3 mg/kg (a test dose of 0.1mg/kg should be given to rule out
prolonged block).
Onset of action
1-2 minutes and lasts only 4-6 mins in normal NMJs (ideal for brief
procedures such as intubation).
Side effects
Again care for hepatic and renal impairment. First dose often results in
tachycardia and repeated doses may cause bradycardia. Atropine
premedication is advised. Avoid in hyperkalaemia. People with low levels
or atypical plasma cholinesterase should not receive suxamethonium.
Suxamethonium should not be administered to debilitated patients who
have reduced muscle movement.
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Opioids
The opioids are useful for critically ill patients because they have
sedative, euphoric and analgesic effects. These drugs act on receptors
sites normally activated by endogenous beta-endorphin and encephalin.
There are five main subgroups of opioid receptor (,, , and ).
receptor is the main site of action of opioids for their analgesic,
euphoric and dependency effects. receptors mediate dysphoria,
mydriasis and respiratory stimulation and receptors mediate
sedation, spinal analgesia and dependence. Side effects of the opioids
are related to there action on these receptors and are dose related:-
nausea and vomiting
dysphoria
decreased gut motility
ventilatory depression
cardiovascular depression
some patients report hallucinations and many experience
disorientation
Fentanyl
Fentanyl is a synthetic potent opioid derived from the pethidine group.
It is 100 times more potent than morphine. It has a rapid onset of
action because it crosses the blood brain barrier easily. When first
administered fentanyl is a short-acting opioid however it soon
accumulates in the bodys fat stores and clearance is similar to
morphine when given as an infusion. Because it is short acting an initial
loading dose of the drug is required to achieve analgesia. It has no
active metabolites.
Fentanyl is said to have fewer cardiovascular effects compared to
morphine as it induces less histamine release. It accumulates in the
fatty deposits in the body so it can produce prolonged respiratory
depression once the infusion is discontinued. Dependence and
withdrawal symptoms are not uncommon after > 9 day infusion.
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Doses for mechanically ventilated adult patients:
Infusion: 25 to 100 mcg/hr as patient requires (conc. 10mcg/ml or
500mcg in 50mls normal saline) Bolus: 25 to 50mcg every 5minutes or
until analgesia is achieved
Morphine
Morphine has a high affinity for receptors making it a highly potent
analgesic. It has a lower degree of lipid solubility than fentanyl and
diffuses over the blood brain barrier more slowly than fentanyl. This
gives it a delayed onset of action. Morphine produces active
metabolites such as morphine-6 glucuronide which can prolong its
clinical effects. Patients with reduced renal and/or liver function are
more likely to have impaired clearance of the drug and its metabolites
and therefore experience prolonged effects. Morphine also causes
histamine release which can increase the likelihood of hypotension
especially if the patient is volume depleted, elderly or/and has renal
failure.
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Naloxone hydrochloride - reversal for opioid overdose
Mechanism of action:
Narcotic antagonist.
Usage:
Reversal of narcotic agonists.
Presentation:
400 mcg / 1 ml. 20 mcg/ml ampoules.
Adverse Effects:
Nausea, vomiting, tremor, tachypnoea, seizures, violent behaviour,
pulmonary oedema, hypotension/hypertension, VT, VF.
Precautions:
Monitor patients carefully as the duration of action of Naloxone
may be less than the narcotic. Additional doses may be required.
Administration to narcotic - dependent persons may precipitate
acute withdrawal symptoms
Other analgesics
Paracetamol
Indications:
Pain and fever
Precautions:
Hepatic (check liver function tests first), renal impairment; restricted
salt intake (Soluble, Rapid tabs)
Adverse Reaction:
Rare: dyspepsia; nausea; allergy; haematological changes
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Dose:
May be taken with or without food. Take with water. Adults, children >
12 yrs: 1-2 tabs every 4 hrs; max 8 tabs/day.
Drug Interactions:
Anticoagulants; chloramphenicol; drugs affecting gastric emptying;
hepatic enzyme inducers including alcohol, anticonvulsants
Sedation
The aims of sedation
The aim of sedation in most circumstances is to provide a comfortable
patient who is responsive to commands. The aims may be summarised as
follows:
PATIENT COMFORT!!!
Anxiolysis
Synchrony with the ventilator
Amnesia (controversial)
Benzodiazepines
Benzodiazepines are the most commonly used sedative agents used for
ICU patients (Murdoch & Cohen, 2000; Soliman, Melot, & Vincent,
2001). They have anxiolytic effects and inhibit central nervous system
activity. They act by binding to a receptor adjacent to the gamma
amino-butyric acid receptor on neuronal cell membranes. This increases
the intracellular flow of chloride ions which ultimately causes the cell
to hyperpolarize and increases the threshold for excitability thus
reducing neuronal cellular activity. Benzodiazepines are lipophilic and
cross the blood brain barrier rapidly. The anxiolytic effects and
corresponding attenuation of the stress response can predispose the
patient to hypotension, especially if intravascular depletion exists.
Lorazepam, midazolam and diazepam are the most commonly
administered benzodiazepines in ICU.
Midazolam
A short acting benzodiazepine. It acts rapidly (1 to 5 minutes) because
it crosses the blood brain barrier very easily because it has a high
affinity for lipoproteins. This means that it accumulates in the body
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fat deposits and is gradually released into the circulation causing
clinical effects even when the drug is no longer administered.
Midazolam has active metabolites, which may contribute to the
cumulative effects. These effects cause concern, particularly in
patients with renal failure and/or hepatic impairment who consequently
take a prolonged amount of time to wake up. Tolerance to midazolam is
common, increasing doses of the drug are required over days and weeks
to produce similar sedative effects. Physical dependence is shown by
the occurrence of withdrawal symptoms; commonly acute anxiety.
Abrupt withdrawal is best avoided.
Diazepam
Very similar in action to midazolam however it is longer acting. It is
even more lipophilic than midazolam, which means it, accumulates in the
body fat stores and takes a lot longer to clear once it is discontinued.
It also has active metabolites which predispose patients to prolonged
clinical effects. For this reason diazepam is difficult to titrate and is
therefore not suitable for administration via an infusion. Diazepam acts
synergistically (has additive effects) when used in combination with
other central nervous system depressants such as opioids and the dose
should be adjusted accordingly.
Propofol
Mechanism of action:
Anaesthetic agent.
Usage:
Sedation of ventilated patients in the ICU. Do not use in children or
adolescents under 16 years.
Induction and maintenance of general anaesthesia
Presentation:
200 mg/20ml.
Adverse Effects:
Apnoea, bradycardia, hypotension, involuntary movements/convulsions
Contraindications
Precautions
Check for propofol, soyabean or egg hypersensitivity.
Patients with fat metabolism disorders.
May need to reduce dose in patients > 55 years of age.
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Do not use for sedation in the ICU for patients under 17 years of
age.
Electrolytes
Occasionally patients require electrolyte balance correction. The most
common electrolytes which require supplementation are potassium and
magnesium.
Potassium
Usage
For treatment and prevention of hypokalaemia.
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Local Administration Guide
ADMINISTER VIA A CENTRAL LINE.
Dilute in NS, D5W, Hartmanns. Administer at a rate no greater than
10-20 mmol/hr. If administered via central line, dilute in 100-
500mls. Maximum concentration is 30 mmol/100mls.
Presentation
1 g/10 ml = 13.4 mmol in 10 ml.
Adverse Effects
Hyperkalaemia ECG changes, arrhythmias, hypotension, listlessness,
confusion, paraesthesia of the extremities, muscular weakness
including paralysis, thrombophlebitis.
Magnesium
Usage
Hypomagnesaemia
Cardiac Arrest / Post M.I.
Cardiac Arrhythmias - VF / VT.
Asthma
Seizures associated with epilepsy, pre-eclampsia and eclampsia.
Subarachnoid haemorrhage (see also MASH study on ICU intranet)
Hypomagnesaemia
Dilute 20 mmols (10 mls) in 100 mls D5W, N/Saline or Hartmanns and
infuse over at least 1 hour.
Cardiac Arrest
1 ampoule (10mls) in divided doses of 5 mls. Administer 5mls as an IV
Bolus over 15 mins.
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Asthma
Initial dose 15 mls (30 mmols) over 1 hour then follow with infusion :
Add 35-50 mmol of Mg to 1000mls D5W and administer over 12-24
hours.
Subarachnoid haemorrhage
See MASH study instructions on ICU intranet
Presentation
49.3% solution, 20 mmol in 10 mls
Adverse Effects
Hypotension, Bradycardia, Respiratory paralysis, Flaccid Paralysis,
Overdose may cause A-V Block, Cardiac arrest, Flushing, (administer
Calcium chloride in the event of an overdose)
Contraindications
Hypermagnesemia may occur in impaired renal function:
Calcium may be used to reverse magnesium intoxication
Precautions
Hypotension
Check plasma magnesium levels
Diuretics
Frusemide
Usage
Fluid Overload
CCF/Pulmonary oedema
Renal failure
Maintenance of urine output eg: rhabdomyolysis/myoglobinuria
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Usual dose 20-80 mg IV bolus over 1-2 minutes. Increased dose
may be required if patient normally on high dose diuretic therapy
or has renal failure.
High Dose Therapy : Add 250 mg to 100 mls N/S or Hartmanns.
The rate of Infusion should not exceed 4mg/minute
Presentation
Lasix Ampoules, 20 mg/2 mL: 5's; 40 mg/4 mL: 1's.
Adverse Effects
Fluid and electrolyte imbalances, especially hypokalaemia may
precipitate arrhythmias. (Na, Ca, Cl, Mg imbalances may also occur).
Ototoxicity in high doses.
Precautions
Monitor patient carefully for fluid and electrolyte imbalance.
Pantoprazole
Mechanism of action
Proton-pump inhibitor. Short-term treatment of duodenal, gastric
ulcer; reflux oesophagitis; GI lesions unresponsive to H2-blockers;
Zollinger-Ellison syndrome; maintenance of healed reflux oesophagitis,
prophylaxis
Contraindications
Cirrhosis; severe hepatic impairment
Precautions
Exclude malignancy; prolonged use; hepatic impairment; pregnancy,
lactation, children
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Adverse Reactions
GI upset; eructation; constipation; headache; sweating, dry mouth;
metallic taste; fatigue; asthenia; interstitial nephritis; severe skin
reactions; anaemia; leucopenia; others, see full PI
Drug Interactions
Drugs with pH dependent bioavailability eg ketoconazole; coumarin
anticoagulants
Presentation
Pantoprazole Na; powder for reconstitution; 40mg in amp
Dose
Peptic ulcer, GI lesions refractory to H2-blockers, Zollinger-Ellison
syndrome: 40 mg/day.
Reflux oesophagitis: 20-40 mg/day. Only for use if oral therapy not
appropriate.
Ranitidine
Mechanism of action
H2-receptor antagonist. Short-term treatment of proven duodenal or
gastric ulcer; maintenance treatment to reduce risk of relapse in
duodenal ulcer; maintenance treatment (up to 1 yr) to reduce risk of
relapse where documented healing of benign gastric ulcer; gastrinoma
(Zollinger-Ellison syndrome); short-term symptomatic treatment of
reflux oesophagitis unresponsive to conservative antireflux measures;
maintenance treatment to reduce risk of relapse in reflux oesophagitis;
scleroderma oesophagitis. Injection: where oral treatment is
inappropriate; prophylaxis against recurrent haemorrhage in bleeding
peptic ulceration
Precautions
Exclude malignancy; history of acute porphyria; high dose; intubated
ICU patients; renal impairment; salt restriction or PKU (effervescent
tabs); chronic lung disease, diabetes, immunocompromised, elderly
(increased risk of community acquired pneumonia); pregnancy, lactation,
children
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Adverse Reactions
Headache; GI, CNS disturbances; rash; others rare, see full PI
Drug Interactions
Sucralfate
Dose
IVI or slow IV infusion. 50 mg every 6-8 hrs, or 25 mg/hr for 2 hrs,
every 6-8 hrs
Anticoagulants
Heparin
Mechanism of action
Heparin is a naturally occurring mucopolysaccharide which inhibits the
clotting of blood in vitro and in vivo. It enhances the rate at which
antithrombin III neutralises thrombin and activated factor X (Xa).
Antithrombin III also neutralises other activated coagulation factors,
e.g. factors IX, XI, XII and plasmin.
With low dose heparin therapy, anticoagulation appears to result from
neutralisation of Xa which prevents the conversion of prothrombin to
thrombin. With full dose heparin therapy, anticoagulation appears to
result primarily from neutralisation of thrombin which prevents the
conversion of fibrinogen to fibrin. Full dose heparin therapy also
prevents the formation of a stable fibrin clot by inhibiting activation
of fibrin stabilising factor.
Usage
Treatment and prophylaxis of thromboembolic disorders
Contraindications
Actual, potential haemorrhagic states; threatened abortion;
immediately postpartum; endocarditis; severe hypertension; GI
ulcerative conditions; advanced renal, hepatic disease; major surgery;
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shock; severe thrombocytopenia; previous heparin, pentosan assoc
thrombocytopenia.
Precautions
IM injection; neuraxial anaesthesia, spinal puncture, especially
traumatic, repeated, indwelling epidural catheter, monitor neurological,
haematological status; large doses, prolonged use; asthma; GI tubation;
hepatic, renal disease; hypertension; retinal vascular disease; oral
surgery; elderly; pregnancy, lactation
Adverse Reactions:
Haemorrhage; heparin induced thrombosis/ thrombocytopenia
syndrome; local skin necrosis; others.
Drug Interactions
Other anticoagulants; thrombolytics; NSAIDs; corticosteroids;
hydroxychloroquine; sulfinpyrazone; probenecid; ethacrynic acid;
vitamin K antagonists; cytostatics; cefotetan; valproic acid;
propylthiouracil; antihistamines; digitalis; tetracyclines; nicotine;
vitamin C; quinine; ACTH; insulin; others.
Dose
Complex, depends on rationale, 5000 IU /0.2 mL subcutaneous route
twice a day is frequently prescribed for prophylaxis
Protamine sulphate
Mechanism of action
Protamine is a small basic protein which combines with heparin to form
a stable, inactive complex.
Usage
Reversal of heparin anticoagulation and overdose.
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Local Administration Guide
Slow IV injection diluted or undiluted in D5W/NS. Give over a period
of 5 mg/min.
Note: 1 mg Protamine neutralises 100 units Heparin.
Presentation
Protamine Sulphate 1% 100 mg/10 ml ampoules.
Adverse Effects
Hypotension, cardiovascular collapse, bradycardia, pulmonary
hypertension, dyspnoea
Precautions
Check for Protamine hypersensitivity before administration. Too much
Protamine causes anticoagulant effects.
Anti-arrhythmics
Amiodarone
Mechanism of action
Class III antiarrhythmic. Prolongs the action potential duration and
hence the refractory period of atrial, nodal and ventricular tissues.
Usage
Ventricular dysrhythmias
Atrial fibrillation
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volumetric pump. Infuse up to 15 mg/kg/24 hours and continue for
1-2 days.
In clinical emergencies, 150-300 mg may be diluted in 10-20 mls D5W
and given over 1-2 minutes (see ARC ALS guidelines)
Presentation
50 mg /1 mL or 3 mL
Adverse Effects
Heart block
Negative inotropic action. Hypotension, circulatory collapse,
arrhythmias
Nausea, vomiting, CNS excitation
Hyper/hypothyroidism
Pneumonitis, pulmonary fibrosis
Corneal deposits
Precautions
Care in patients with heart failure/low ejection fraction. Check and
correct electrolyte abnormalities.
Lignocaine
Mechanism of action
Class 1B anti-arrhythmic. (Sodium channel blocker which stabilises
excitable membranes) Affects predominantly ischaemic myocardial
cells.
Usage
Treatment of - ventricular arrhythmias (VT, VF, PVCs).
Local anaesthetic.
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for 1 - 2 hours, then 2 mg/min (30 ml/hr) for up to 24 hours or as
directed by Medical Staff. NB: In a fluid restricted patient use
0.8% (4G in 500 mls D5W).
Presentation
Minijet 2% (100 mg/5mls); Preloaded Infusion 0.4% (2G in 500 mls
D5W); Lignocaine 1000 mg/10 mls (Xylocard 1000).
Adverse Effects
CNS - Paraesthesia, seizures, slurred speech, muscle twitching,
drowsiness, psychosis, agitation, confusion.
Respiratory depression.
Cardiovascular - Hypotension, bradycardia, heart block, arrhythmias.
Precautions
Reduce dose in:
hepatic failure/alcoholics
elderly > 70 years
CCF
Correct abnormal electrolyte levels (especially K/Mg) to ensure
effectiveness of lignocaine.
Insulin
Actrapid
Mechanism of action
Insulin lowers blood glucose levels by binding to insulin receptors on
the cell membrane to increase glucose uptake and inhibit hepatic
glucose output. Actrapid is a short acting human insulin preparation.
The hypoglycaemic effect after subcutaneous administration begins
after approximately 0.5 hours and is at a maximum between 2.5 and 5
hours and terminates after approximately eight hours. Intravenous
administration results in a hypoglycaemic effect after a few minutes
and the duration of action is less than 30 minutes.
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Usage
Diabetes
Hyperglycaemia
Unstable blood glucose levels due to illness and catecholamine usage
Presentation
Neutral insulin (human) (rys); 3 mL cartridge for use in NovoNordisk
insulin delivery device, single use only.
Adverse Effects
Hypoglycaemia
Insulin resistance
Local reactions including lipodystrophy (s/c injection only)
Precautions
BSLs to be checked hourly if:
Catecolamines in use
Cessation/interruption of feeds or TPN
Rapid weaning of catecholamines
Corticosteroid usage
If BSLs, feeding and catecholamine usage stable, BSL may be
monitored every 2 hours. Less frequent BSL checking is not permitted
for patients receiving insulin infusions.
Concomitant illness (eg. Pancreatitis, sepsis)
Renal or hepatic impairment
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Transfer from animal insulin
Be sure to rotate injection site (s/c only)
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Post self-test
Complete the following self test without consulting the preceding
sections. If you score more than 80% you are eligible to complete the
level 6 ICU medication competency. Please approach an ICU CNE to
arrange a date to complete the competency.
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References and supporting literature
This list is not exhaustive but provides an excellent starting point for
further reading.
BMA, & RPSGB. (1996). British National Formulary (Vol. 32). London:
British Medical Association and the Royal Pharmaceutical Society of
Great Britain.
Brook, A. D., Ahrens, T. S., Schaiff, R., Prentice, D., Sherman, G.,
Shannon, W., & Kollef, M. H. (1999). Effect of a nursing -implemented
sedation protocol on the duration of mechanical ventilation. Critical
Care Medicine, 27(12), 2609-2615.
Ely, W. E., Inouye, S. K., Bernard, G. R., Gordon, S., Francis, J., May, L.,
Truman, B., Speroff, T., Gautam, S., Margolin, R., Hart, R. P., & Dittus,
R. (2001). Delirium in mechanically ventilated patients validity and
reliability of the confusion assessment method for the intensive care
unit (CAM-ICU). Journal of the American Medical Association, 286(21),
2703-2710.
Hill, L., Bertaccini, E., Barr, J., & Geller, E. (1998). ICU sedation: A
review of its pharmacology and assessment. Journal of Intensive Care
Medicine, 13, 174- 183.
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ICU intranet: MIMS
Kollef, M. H., Levy, N. T., Ahrens, T. S., Schaiff, R., Prentice, D., &
Sherman, G. (1998). The use of continuous IV sedation is associated
with prolongation of mechanical ventilation. Chest, 114(2), 541- 548.
Soliman, H. M., Melot, C., & Vincent, J.-L. (2001). Sedative and
analgesic practice in the intensive care unit: the results of a European
survey. British Journal of Anaesthesia, 87(2), 186-192.
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