Nursing Flashcards
Dehydration
Fluid lost slowly from extravascular compartment. Patient unable to keep up with ‘ins’ and ‘outs’.
Water loss equal from all compartments.
Intravascular volume assessment
Heart rate Pulse quality CRT and mucous membranes colour Blood pressure Mentation Temp
Extravascular volume assessment
Moistness of MM Skin turgor Weight Globe position Urine output
What clinicopathological features will be affected by patients hydration status
PCV / Total solids
Urea and creatinine
Urine specific gravity
Hypovolaemia fluid administration
Rapid fluid resuscitation
Dehydration fluid recovery
Correct slowly
What are fluids trying to achieve
Change in volume status
Change in content
Change in distribution
Crystalloids
Solutions containing solutes
Solutes and water move freely between membranes
Distributed through all body compartments by 1hour
Cheap
Isotonic / Hypertonic / Hypotonic
Isotonic crystalloids
Mostly used
Same tonicity as plasma
Treatment of hypovolaemia and dehydration
Replacement fluids
Mimic intravascular electrolyte conc (high sodium and low potassium)
0.9% NaCl and Hartmanns
Hypertonic crystalloids
More common in large animals
Tonicity larger than plasma
Prolongs intravascular volume expansion
Hypotonic crystalloids
Very rarely used Tonicity lower than plasma 0.18% saline and 4% glucose Glucose metabolised Monitor fir electrolyte disturbances
What co morbidities need to be considered when prescribing fluid therapy
Cardiac disease and heart failure Renal disease Respiratory disease Those that can balance ins and outs as suffer from volume overload Be more cautious
Signs of volume overload
Pulmonary Odense
Venous engorgment
Peripheral Odema formation
Cagily effusions
Per os
Fluid by mouth
Absorption in intestinal tract, relatively slow and body can be selective
Subcut fluids
Injected under skin
Slowly absorbed into regional capillaries and distributed equally beteeen fluid compartments
IV fluids
Into intravascular compartment
Central venous access fluids
Common in large animals
Catheters directly into larger vessels usually jugular vein
Intra Osseus fluids
Into medullary cavity of long bone. This is highly vascularised so rapidly absorbed.
Pain
Unpleasant sensory and emotional experience associated with actual or potential tissue damage
How patient interprets nociception
Nociception
The neural process of encoding noxious stimuli
Nociceptive pain
Pain that arises from actual or threatened damage to non neural tissue and is due to the activation of nociceptors.
Neuropathic pain
Pain caused by a lesion or disease of the somatosensory nervous system
Harder to treat
Hyperalgesia
Increased pain from a stimulus that normally provokes pain
Reduced pain threshold
Allodynia
Pain due to stimulus that doesn’t normally provoke pain
Acute pain
Short period of time
Miniutes / hours / weeks
Can be protective at first
Can be one chronic if not treated
Chronic pain
Pain that lasts longer than a few weeks
Physiological signs associated with pain
Increased heart rate blood pressure abs temp
Altered resp
Stress hormones
NRS
VAS
SDS
CSOM
Numerical rating scale
Visual analogue scale
Simple descriptive Scale
Client specific outcome measures
Pharmacokinetics
What the body does to the drug
Pharmacodynamics
What the drug does to the body
What are the targets for drug action
Receptors
Enzymes
Transporters
Ion channels
Full agonist
Able to generate a maximal response after binding to receptor
High affinity and high intrinsic activity
Affinity
How well drug binds ti receptor
Intrinsic activity / efficacy
Magnitude of effect once bound
Partial agonist
Drug that has an intrinsic activity of less than 1
Receptor occupancy produces submaximal effect
Inverse agonist
Drug binds and has opposite effec to agonist
Antagonist
Exhibits affinity but no intrinsic activity
Therapeutic index
Maximum non toxic dose / minimum effective dose
ADME
Absorption
Distribution
Metabolism
Excretion
Bioavailability
The fraction of a dose reaching the systemic circulation after administration compared to the dose administer iv
Factors determining drug distribution
Protien binding Tissue binding Organ blood flow Membrane permeability Brig solubility
Preventive analgesia
Administration of analgesia before during and after procedure to prevent in regulation of the nervous system. Should reduce intensity and duration of acute pain and reduce chronic pain.
Multi modal analgesia
Uses different classes of analgesic agents to overcome pain. More effective abs often can use lower doses.
Lower doses = less side effects.
Types of analgesic agents
Opioids
NSAIDs
LA
NSAID
Non steroidal anti inflammatory drug
Opioids
Controlled drug.
Act at the endogenous opioid receptors primarily in brain and spinal cord.
Usually administered IV ( not pethidine)
Some administered buccally.
Side effects - resp depression sedation bradycardia nausea decrease in GI motility
NSAIDs
Prostaglandins are an inflammatory mediator.
Metabolised in liver.
Can’t use two of these at once.
Side effects - GI ulceration renal ischhemia
Local anaesthetics
Enter nerve fibres abs block the voltage operated Na+ channel. This blocks nerve conduction.
Metabolism depends on if it’s an ester or amide.
Epidural
Anaesthetic injected into epidural space via catheter
Spinal anaesthesia
Aesthetic is injected directly into cerebrospinal fluid with small needle.
Baricity
Is the weight of one substance compared with the weight of an equal volume of another substance.
Glucose can be added to make solutions heavier.
Addition of vasconstructors
Reduces speed of systemic absorption abs therefore prolong duration of action.
General anaesthesia
State of unconsciousness produced by anaesthetic agents. No pain across body.
Regional anaesthetic
Insensibility caused by interruption of sensory in region
Local anaesthetic
Lack of sensation in localised part if body.
Sedation
Allaying if irritability or excitement
Anxidysis
Reduces anxiety
Analgesia
Reduced sensibility to pain
Narcosis
Sleep like state
Hypnosis
Artificially induced state of passivity
What is premedication
A drug combination given prior to induction of GA.
Calms patient and aids restraint.
Provides preemptive analgesia.
Allows reduction of induction drugs and maintenance drugs. MAC sparing.
Helps smooth induction and recovery.
Preoperative phase
Owner conversation and informed consent. Full history. ASA classification. Getting ready. Set up machine / equipment. Prep drugs / IV catheter. Premed.
Induction phase
Takes patient from conscious to anaesthetised. IV catheter. Pre oxygenation. Premed IM. Admin of induction agent. Securing of airway.
Order of admission phases
Preoperative
Induction
Maintenance
Recovery
Maintenance phase
Maintain anaesthesia.
Placement of local or regional blocks.
Surgery / diagnostic procedure.
Recovery phase
Cessation of gas.
Remove airway device.
Recovery area.
Anaesthetic triad
Analgesia
Narcosis. Muscle relaxation
Reasons for anaesthesia
Facilitate surgery etc
Prevention of pain
Research
Immobility
The CEPSAF inquiry
Overal risk of an animal not waking from sedation
Brachycephalic problems
Airways GOR ocular skin skeletal
What drug can boxers not have
ACP - Acepromazine
MDR1
Collies sheepdog shepherd.
Can’t remove drugs and toxins from brain when this gene is present
Greyhounds problem
Lack of body fat = slow recovery and keep warm.
P4SO clearance mechanism.
Doberman problems
Dialysed cardiomyopathy can be asymptomatic
Von willerbrand factor - BMBT , blood clotting issues
The female dog of what breed is effected with sick sinus syndrome
Mini Schnauzer
Preventative analgesia
Prevent unregulation of nervous system in the face of noxious stimuli.
Should reduce intensity and duration of acute pain and reduce chronic pain.
Muti modal analgesia
Use several agents abs techniques to be effective.
This means lower dose which is less side effects.
Analgesic agents in practice
Opioids Non steroidal anti inflammatory drugs Local anaesthetics Alpha-2 agonists Ketamine
NSAIDs
Non steroidal anti inflammatory drugs
Alpha -2 agonists
Sedatives that are analgesic
Ketamine
Anaesthetic that is analgesic
Opioids factoids
Controlled drugs in UK Schedule 2 Act at the endogenous opioid receptors Can be IV Well absorbed orally subcut im Can cause resp depression sedation bradycardia nausea
NSAIDs
Prostaglandins are inflammatory mediators.
Metabolised in liver. Effective for acute abs chronic pain.
Can’t use two non steroidal as a multi modal anaesthetic regimen.
Can cause GI ulceration renal ischaemia.
GI side effects very common - vomiting diarrhoea.
Local anaesthetics
Enter nerve fibre and block voltage operated Na+ channel which blocks nerve conduction.
Membrane stabilising effect.
Can be esters or amides.
What analgesic is toxic to cats
Paracetamol
Tramadol
Centrally acting analgesic
More evidence in dogs than cats
Metabolism of esters
Metabolised in plasma
Hydrolysis if ester link
Metabolism if amides
Broken down in liver
Baricity
Weight of one substance compared to the weight of equal volume of another substance.
Glucose can be added to make solution heavier
Why would adrenaline be added to a solution
Added as a vasoconstrictor to local anaesthetics to reduce speed of systemic absorption and therefore prolong duration of action
Balanced anaesthesia
Premed
Induction
Maintenance
Recovery
Sedation factoids
Dose dependant up to plateau dose.
Improved by combination with opioid.
Improved when animal left in quiet environment.
Petechia
Blood clots in mouth or stomach
ASA classification
I normal healthy animal II mild systemic disease III systemic disease we’ll controlled by treatment IV severe systemic disease V unlikely to survive 24 hours E emergency
Pre op fasting
Reduce volume of stomach contents
Prevent GOR regurgitation aspiration
Feeding a small canned food 3 hours pre op reduced incidence of GOR.
Prolonged starvation may actually caused an increased of GOR.
What is shock
An imbalance between oxygen delivery to the tissues and oxygen consumption by the tissues.
Cells respire anaerobicly = less oxygen = less energy = more lactate = acidic environment
Types of circulatory shock
Hypovolaemic
Cardiogenic
Obstructive
Distributive
Hypovolaemic shock
Resulting in decreased blood volume.
Result of fluid losses or decreased intake.
Usually due to haemorrhage
Cardiogenic shock
Reduced cardiac output.
Heart failing as pump.
Obstructive shock
Due to physical obstructions in blood flow to or from the heart through the great vessels.
Distributive shock
Due to maldistribution of blood flow.
Usually due to inappropriate or widespread vasodilation.
The minimum database
PCV TS Urea Glucose Lactate Blood smear examination