W0.5 - ANAESTHETICS: Flashcards
Understand the mechanism, action and pharmacological kinetics of: local anaesthetic
agents
directly into tissue, provides analgesia and partially relaxation
- lignocaine, bupivacaine= analgesia nil hypnosis via blocking Na+ channels and preventing axonal propagation
!toxic risk
+benefit of avoiding reliance on opiods
Describe the “triad of anaesthesia” and discuss how this relates to the concept of
balanced anaesthesia.
1) HYPNOSIS
2) ANALGESIA
3) RELAXATION
*finding right dose that provides appropriate amounts of these three elements whilst AVOIDING TOXICITY.
- risk of polypharm., artificial ventilation w/ relaxation = airway control, separation of relaxation & hypnosis
Discuss the physiological effects of general and regional anaesthesia and how these may
interact with patients’ underlying illness.
Regional anaesthesia provides analgesia and if optimum can solely rely or supplement general
- regional can provide reasonable relaxation too via motor nerve blocking
- regional plays vital role in intraop. anaesth. by. suppressing reactions to pain stimuli which may wake the patient
= this allows further supplementation of GA.
- generally resp-sparing compared to GA thus. regional preferred over GA in Pt. w/ resp issues.
- overall regional alongside local avoids global effects of GA but produces phyiological effects
Understand the mechanism, action and pharmacological kinetics of: general anaesthetic agents,
- provides hypnosis and general relaxation
- inhaled and intravenous
- hyperpolarise neurones
- inhaled agents produce direct effect
- intravenous agents = allosteric binding of GABA R opening chloride channels
=> COMBINATION OF IV induction and INHALED maintenance
- topdown loss of cerebral function, LOC -> senses etc.
reflexes spared
> long. resus. via ABC
airway mgmt
cardiovascular impact
Understand the mechanism, action and pharmacological kinetics of: opiates
- analgesia, partially hypnosis
- use in intra-operative anaesth. to. contribute to hypnotic effect of GA
- fentanyl: intra-op
- morphine
- remifentanil: high potency, short acting = supplement inhaled and IV anaesth. allowing lower dosage and faster recovery
Understand the mechanism, action and pharmacological kinetics of: muscle relaxants.
- provides relaxation
administered with unconscious inducer.
indicated inventilation and intubation, immobility required, body cavity access
!awareness
! incomplete reversal= airway obstruction postop
! apnoea dt dependence on airway support
Regional Anaesthesia: how
Nerve and plexus blocks including central neuraxial block (spinal and epidural). Essence is that the anaesthetic agent is applied to the nerve anywhere from the spinal cord to the periphery and anaesthesia produced in a distal site served by that nerve,
therefore effect is remote from the injection.
ASA Scoring
ASA1 = fit healthy
ASA2 = Mild systemic
ASA3 = Severe systemic
ASA4 = Sever +thrat to life
ASA5 = Moribund pt, not expected. to survive, Sx in desperation
ASA6 = Brain. dead, organ retrieval
*
Thiopentone or Propofol
IV anaesthetics, general
- fast unconsciousness, fat soluble => cross BBB.
- rapid onset thus rapid recovery
Inhaled Anaesthetics
general
* diffuse. down concentration gradient, from lungs to blood to brain
- slow. induction, easy maintenance flexible
-awakening: via washout gas.
MAC = concentration of drug required in alveoli to produce anaestheisa
therefore the lower the. MAC the more potent.
Effects of GA
CVS = depression of outflow, negative effect on HR, dilation, venodiltion
Resp = resp depressant, paralyse cilia,
postoperative depression of lungvolumes = thus postop oxygen to ensure V/Q matching
Appreciate the importance of the role of history taking, examination and routine investigations in assessing and preparing patients for surgery.
- Known co-morbidities
Severity
Control - Unknown co-morbidities
Systemic enquiry
Clinical examination - Ability of withstand stress
Exercise tolerance; Cardiopulmonary exercise testing
Reason for limitation
Cardio-respiratory disease
Rarities / Family history
Malignant hyperpyrexia
Cholinesterase deficiency
Smoking – respiratory complications and wound healing
Alcohol – risk of infection and septic shock - Cessation of alcohol – no re3duction in mortality but reduction in complications (dose dependant)
Discuss the possible effect of concurrent medical disease on the progress of anaesthesia and surgery and how this should tailor further investigation.
a
Discuss the role of routine preoperative investigation and list the advantages and disadvantages of this practice
- Ability of withstand stress
Exercise tolerance; Cardiopulmonary exercise testing
Reason for limitation
Cardio-respiratory disease
Describe the basic phases of general anaesthesia (eg, induction, maintenance and
recovery).
pre-oxygenation
______
INDUCTION
- analgesic
- hypnotics
- relaxants
*airway mgmt: oropharyngeal airway, LMA
* breathing:spont., controlled, supported
* hemodynamics: vaasoactive drugs
MAINTENANCE
- multi-modal analgesia and anti-emesis
- documenting
EMERGENCE
- waking. significant risk
- sign-out, reversal of neuromuscular blockade
- stopping agents
RECOVERY
- ABC continuous, management
- nausea
- handover to ward
______
post-op
Risks during anaesthesia and monitoring
AWARENESS = depth of aneasthesia monitoring
EYE INJURY = eye care
!prone position
HYPOTHERMIA
PRESSURE INJURY
!prone position
VTE
NERVE INJURY
Planes of. Anaesthesia
stages
1) analgesia and amnesia
2) delirium and unconsciousness
3) surgical anesthesia
4) apnoea to death
- Describe the reasons why pain should be treated and the consequences of not doing.
66% of people attending A & E seeking help with pain had made around 3 visits to HCP in proceeding weeks
Person living with pain has poor quality of life as bad as other neurological diseases
Low Back Pain is the number 1 disease for years lost to disability worldwide
alleviated pain = better prognosis & outcome
Describe the differences between the different types of pain that a patient may experience and describe how each may best be managed
ACUTE: recent onset w/ limited duration
CHRONIC: 3mos+, after normal healing, nil identifiable cause
CANCER PAIN: progressive, mix of acute and chronic
NON-CANCER PAIN: diff causes, acute or chronic
NOICICEPTIVE PAIN: protective function, sharp+/- dull, localised
NEUROPATHIC PAIN: NS dmg/abn.
-burning, shooting numbness, pins and needles
- not well localised
- Give an outline of the different therapies available for the management of pain.
Simple analgesics:
PARACETAMOL
NSAIDs:diclofenac, ibuprofen
OPIODS:
- weak: codeine, tramadol
- pos: morphine, oxycodone, fentanyl
+antidepressants:amitryptyline, duloxetine
+ anticonvulsants: gabapentin
+ ketamine: NMDA r antagonist
- Describe the practicalities involved in the delivery of pain relief in the clinical setting.
- WHO pain ladder = acute
weak => stronger - acute, chronic, cancer pain
Mild
Paracetamol (± NSAIDs)
Moderate
Paracetamol (± NSAIDs) + codeine/ alternative
Severe
Paracetamol (± NSAIDs) + morphine
-reverse with intense pain, uncontrolled chronic pain, acute crisis,
- Discuss the role of scoring systems in the practical delivery of analgesia.
Verbal Rating Score
Numerical Rating Score
Visual Analogue Scale
Smiling faces
Abbey Pain Scale (for confused patients)
Functional assessments
- Understand the differences between acute and chronic pain states.
a
Periphery - Steps of Pain
tissue injury, mediated by prostaglandins, subtance P
stimulate nociceptors
signals travel in Adelta or C nerve to SC
> non-drug treatments
NSAIDs
local anaesthetics
SC - Steps of Pain
Dorsal horn - relay station
Ad or C nerve synapses w/ second nerve
=> up opposite side of spinal cord
> non-drug: acupuncture, massage, TENS
local anaesthtics
opiods
ketamine
Brain - Steps of Pain
Thalamus is second relay station
connects to many parts of the brain
-cortex, limbic system, brainstem
pain perception occurs in cortex
> psych
drug: paracetamol, opiods, amitryptiline, clonidine
Modulation - Steps of Pain
Descending pathway from brain to dorsal horn
Usually decreases pain signal
Neuropathic Pain
NS dmg/abn.
-burning, shooting numbness, pins and needles
- not well localised
- nerve trauma, diabetic pain
- fibromyalgia, chronic tension headache
dt receptor abn, sensistation abn, chemical changes in dorsal horn, loss of normal inhibitory modulation
Paracetamol: pros and cons
Advantages
Cheap, safe
Can be given orally, rectally or intravenously
Good for:
Mild pain (by itself)
Mod-severe pain (with other drugs)
Disadvantages
Liver damage in overdose
NSAIDs: pros and cons
Aspirin, ibuprofen, diclofenac
Advantages
Cheap, generally safe
Good for nociceptive pain
Best given regularly with paracetamol (Synergism)
Disadvantages
Gastrointestinal and renal side effects plus bronchospasm in some patients with asthma
Codeine: pros and cons
Advantages
Cheap, safe
Good for mild-moderate acute nociceptive pain
Best given regularly with paracetamol
Disadvantages
Constipation
Not good for neuropathic pain
Tramadol: pros and cons
Weak opioid effect plus inhibitor of serotonin and noradrenaline reuptake (modulation)
Advantages
Less respiratory depression
Can be used with opioids and simple analgesics
Less constipating than opioids
Disadvantages
Nausea and vomiting, controlled drug
Morphine: pros and cons
versatile administration
*mod-sever nociceptive pain = post-op
*. ancer pain
CI: neuropathic pain
Disadvantages
Constipation
Respiratory depression in high dose
Addiction and avoidance due to fear of addiction
Controlled drug
Oral dose needs to be increased if changing from IV/ IM or S/C routes as third pass metabolism reduces the amount of morphine available.
Amitriptyline
Tricyclic antidepressant (TCA)
increases inhbitory descending
+
neuropathic pain, depression, insomnia
-
anti-cholinergic sfx: urinary retention, glaucoma
LT =cognitive decline and dementia
Role of anticonvulsant drugs in pain mgmt
- reduce abn firing of nerves thus neuropathic pain
- carbamezapine
- sodium valporate
- gabapentin
Understand the term ‘critical illness’ and discuss.
multi-organ
single organ
=> require support
Identify the patients who may be at risk of developing critical illness.
- septic
- head injuries
- metabolic source of shock
Discuss how these problems may be averted and discuss their early and subsequent
management.
1) resp failure
>HFT nasal cannula, up to 70lof o2. for TYPE 1
- temperature
- humidity
- imparts pressure benefit, will provide set amount of O2.
> Non invasive ventilator, provides pressure and ensures open airways. reduces work of breathing. for TYPE 2
- copd, retainers
> intubation & ventilator: severe resp failure, ensures physical barrier maintaining pressure
- fine tuning etc.
- unable to communicate
- alternatively w/ tracheostomy
2) cvd failure
> arterial line: continuous monitoring and acquiring bloods.
- not rapid delivery, poor. mode of instant resuse.
> vasopressors: metaraminol, NA = increase preload
> inotropes: adrenaline, dobutamine = contractile promotion
3) fluid mgmt - maintenance / resus
> colloids: large osmotic constituents, artificial molecules thus risk to renal insult
> crystalloids: fluids w/ small osmotic constituents, leak into tissue and wide distribution risk
0.8 saline = massive chloride load = metabolic acidosis risk
4) neurological failure:
> ventilation = support raised ICP, decent pressure
Describe the potential consequences of failure to identify and manage these problems.
Resp failure
T1 = oxygenation failure, T2= oxygenation and ventilation failure
CVD failure; shock = mass hypoxia poor perfusion
Discuss the principles involved in the early management of the critically ill patient.
- assessment of fluid and temperature
- urine output marker for fluid resus and maintenance
