Day 4: Fluids and Vasoactive drugs Flashcards
why is it important to check blood products
Medicolegally
Risk of transfusion reactions
Risk of infection
Must be checked at several levels
What is the protocol for accepting blood products upon arrival?
Do not accept blood products without the accompanying form detailing specific information.
What crucial information does the form accompanying blood products contain?
The form includes the following details:
-Patient’s NAME
-Patient’s HOSPITAL NUMBER
-TYPE OF BLOOD -PRODUCT and BLOOD GROUP (if relevant)
-UNIQUE SERIAL NUMBER OF BLOOD PRODUCT
-EXPIRY DATE AND TIME
How does the information on the form compare with that displayed on the blood product?
The same information displayed on the form should also be present on the blood product itself.
Why is it important to verify the information on both the form and the blood product?
Verification ensures accuracy and helps prevent errors in patient identification and blood product administration.
What is the first step in the verification process for blood products?
Check both the products and the accompanying form separately against the patient’s name and folder number from the patient’s own folder.
Why is it important to verify against the patient’s own folder number?
Why is it important to verify against the patient’s own folder number?
After verifying against the patient’s folder number, what is the next step in the verification process?
Check the form against the blood products to see if the details match.
What is the ideal method for conducting this verification process?
Ideally, one person reads the form while another person goes through the blood products.
What action should be taken in the event of any discrepancy between the form and the blood products?
If any discrepancy is found, do not use the product; instead, return it to the blood bank.
How does the verification process differ for emergency issued blood?
Emergency issued blood is not crossmatched and may have limited details. However, the blood type, expiry date, and serial number must still be checked against the form.
what products must be checked?
ANY blood product from blood bank
-Packed red cells
-Fresh frozen plasma
-Whole blood
-Cryoprecipitate
-Platelets
-Whether issued as emergency or not
division of the CNS
brain
spinal cord
division of the PNS
Somatic
Autonomic
Division of the somatic
motor
sensory
division of the autonomic
sympathetic
parasympathetic
function of the autonomic NS
Responsible for the involuntary control of automatic body functions
Each organ system has autonomic control working all the time
We are not in conscious control of this
sympathetic autonomic NS
Thoracolumbar outflow
Postganglionic neurotransmitter is Noradrenaline
Αlpha and Beta receptors
parasympathetic autonomic NS
Craniosacral outflow
Postganglionic neurotransmitter is Acetylcholine
Nicotinic and muscarinic receptors
function of the sympathetic
Sympathetic: “FIGHT or FLIGHT”
Temperature, glucose, vascular responsiveness, ventilation, cardiac output and GIT
Stress response
function of the parasympathetic
Parasympathetic: HOMEOSTATIC
Maintains normal physiological functioning and energy levels
Digestions and Metabolism
the stress response pyramid
-humoral: HORMONAL
-Nueral: HAEMODYNAMIC
-stress response
stress response
Series of Neurohumoral responses to optimise the bodily defence mechanisms for short-term survival ….. “fight or flight
neural: HAEMODYNAMIC
-Increased sympathetic outflow
-Blood flow
*Increased: heart, lungs, brain and muscle (β)
*Decreased: GIT, kidney, liver (splanchnic circulation) and skin (α)
Humoral: HORMONAL
-Defence of blood volume
*Increased: aldosterone and ADH - salt and water retention
-Mobilisation of glucose stores to supply vital organs with energy
*Insulin inhibited
the adrenaline medulla
-specialized sympathetic ganglion with no postganglionic fibres
- postganglionic fiberes are secretory cells
which hormonal that the medulla secrete when stimulated
- noradrenaline- 70%
-adrenaline - dopamine in small amounts
neurotransmitters in the ANS
acetylcholine
noradrenaline
2 types of receptors in the ANS
cholinergic- bind acetylcholine
noradrenergic- bind noradrenaline
cholinergic receptors: distribution
- all autonomic ganglia (including the adrenal medulla)
- all parasympathetic postganglionic nerve terminals
-sympathetic postganglionic nerve terminals in sweat glands (exception)
-somatic NS- neuromuscular junction
cholinergic receptors: subtypes
nicotinic
muscarinic
nicotinic
-At skeletal NMJ and ALL autonomic ganglia (incl adrenal medulla)
-Stimulated by nicotine and Ach
-Inhibited by Neuromuscular blocking agents
muscarinic
-At parasympathetic postganglionic fibres
-Stimulated by muscarine and Ach
-Inhibited by atropine, glycopyrrolate
parasympathetic excess: the rule of B’s
Blindness (ptosis)
Bronchial secretions
Bronchospasm
Bradycardias
“B”- eristalsis (peristalsis)- vomiting, diarrhoea
Bile secretion
Bladder contraction
adrenergic receptors distribution
only found at the sympathetic postganglionic nerve terminals
adrenergic receptors subtypes
alpha
beta
alpha 1
post-synaptic – smooth muscle vasoconstriction (e.g. blood vessels)
Increases the BP ± reflex bradycardia
alpha 2
pre-synaptic – inhibits further NA release (central) –sedation, analgesia, hypotension
beta 1
increased contractility, HR, AV node conduction, refractory period, renin secretion and lipolysis
beta 2
increased skeletal muscle vessel dilatation, bronchial relaxation, uterine relaxation, bladder relaxation, glycogenolysis
autonomic pharmacology
To create an effect, we can block one side of the autonomic system or stimulate the other
For example, to increase heart rate we can stimulate sympathetic (adrenaline) OR block parasympathetic (atropine)
neostigmine: stimulation of PNS
-Blocks acetylcholinesterase, therefore natural concentration of Ach increases
-This will displace neuromuscular blocking agents (NMBs) and facilitates reversal of these drugs
-BUT… this also results in parasympathetic stimulation of muscarinic receptors (which are not blocked by NMBs)
-This causes side-effects!
Anticholinergic drugs: muscarinic blockade of the PNS
-Postganglionic PNS receptors are muscarinic (Ach)
-Blockade inhibits muscarinic effects (e.g. atropine)
-Unmasks background effects of sympathetic nervous system
-Glycopyrroloate is an anticholinergic that does not cross the blood brain barrier
stimulants
direct or indirect stimulation of adrenoreceptor
antagonists
block receptors (both alpha and beta)
What is the pharmacological effect of drugs that have β1 effects?
Drugs with β1 effects are termed inotropes as they increase the force of cardiac contraction.
Name a drug that exhibits inotropic effects.
Dobutamine is an example of an inotrope.
What is the pharmacological effect of drugs that have α1 effects?
Drugs with α1 effects are termed vasopressors as they cause vasoconstriction, leading to an increase in blood pressure.
Give examples of drugs that act as both inotropes and vasopressors.
Adrenaline (epinephrine) and Noradrenaline (norepinephrine) are both inotropes and vasopressors.
What drug is primarily a vasopressor and not an inotrope?
Phenylephrine is a vasopressor but does not have significant inotropic effects.
Sympathomimetics
also known as adrenergic drugs, are a class of drugs that mimic the effects of the sympathetic nervous system. This system is responsible for the “fight or flight” response, which includes increased heart rate, dilation of pupils, and increased blood flow to muscles. Sympathomimetics act on adrenergic receptors, which are receptors that respond to adrenaline (epinephrine) and noradrenaline (norepinephrine).
classification of sympathomimetics
direct acting
indirect acting
direct acting sympathomimetics
Adrenaline (αll α & β))
Noradrenaline (α1, α2, β1)
Phenylephrine (α1 only)
Isoprenaline
Dobutamine
(Dopamine)
indirect acting sympathomimetics
Ephedrine
-releases NA from sympathetic terminals, as well as direct (α β) effects
Direct-acting sympathomimetics mechanism
These drugs directly stimulate adrenergic receptors
Indirect-acting sympathomimetics: mechanism
These drugs work by increasing the levels of noradrenaline (norepinephrine) at the synaptic cleft, either by inhibiting its reuptake or by promoting its release
a agonists
Phenylephrine
α1 only vasoconstrictor
Clonidine
Dexmedetomidine
α2
Sedative, analgesic
b agonists
Isoprenaline
β1 and 2 effects
Salbutamol
β2
Bronchodilatation
Uterine relaxation
alpha receptor antagonists (blockers)
Occasionally used as antihypertensives but are agents of choice in phaeocromocytoma
-Phentolamine – α1 and 2
-Phenoxybenzamine - α1 (noncompetitive)
-Prazosin and Doxazosin - α1
beta blockers
- all competitive with varying B1 and B2 effects
- bradycardia, antiarrythmics, sedative, lower BP
- decrease cardiac mortality
- bronchospasm in asthmatics
- inhibit gluconeogenesis in liver and lipolysis
Combined α and β antagonists
Labetalol – racemic mixture but predominantly a β blocker
ephedrine
Drug of choice for management of hypotension in most cases – given as 5-10 mg boluses IV
Raises blood pressure but tends to cause tachycardia (Beta effects predominate)
phenylephrine
-Preferred vasopressor in obstetric spinal anaesthesia
-Extremely potent a1 agonist reflex bradycardia
-MUST BE DILUTED (comes in 10mg ampoules dose is only50-100 µg!!
10 mg is diluted into 200 mL N saline to give 50 µg / mL
-UNDILUTED PHENYLEPHRINE IS FATAL
use of inotropes
-Generally given via INFUSION via a central line
-Adrenaline, noradrenaline
-For critically ill patients who need inotropic support (e.g. sepsis, cardiac failure)
-Adrenaline boluses are only given as part of resuscitation or as management of anaphylaxis
