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ED, ICU and Anesthetics > Anesthetics > Flashcards

Anesthetics Flashcards

1
Q
  1. Definition - anesthesia.

2. Type of agents used

A

Inducing reversible comma

Inducing and maintenance agents

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2
Q

Anxiolysis

Examples

A

Treatment of patients anxiety before the treatment

Examples include diazepam and midazolam

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3
Q

Amnesia and why

A

Delivery of the agent causes the patient to forget the experience of surgery

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4
Q

Areflexia agents and why

A

Muscle relaxants - suxamethonium (depolarizing agent) or rocuronium (non-depolarizing agent)

Used for muscle relaxation - easier manipulation of airway for intubation, relaxation of abdominal muscles for laparotomy, and prevention of generalized tonicity if electroconvulsive therapy

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5
Q

Autonomic stability

A

Monitoring stats (HR, BP, Temp) before, during, and after anesthesia

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6
Q

Analgesia

A

Treatment of pain or induction of numbness

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7
Q

Anesthetics - post-op management

A

Post-op pain, nausea/vomiting, confusion, and cardiovascular/respiratory complications

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8
Q

Acute pain - non-pharmacological management

A
  1. Cognitive - mindfulness-based stress reduction, relaxation training, CBT, sleep education, and hygiene
  2. Physical - exercise, ice/heat, massage
  3. Spiritual - finding purpose in life
  4. Others - acupuncture, osteopathy
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9
Q

Definition - Regional anesthesia

Types of regional anesthesia

A
  1. administration of a local anesthetic at a point along the length of a nerve from the level of the spinal cord or above→reduced impulse transmission along with the nerve→anesthesia along the entire distribution of that nerve/spinal level. The patient remains conscious during anaesthesia and intervention, and there is no CNS depression.
  2. Types - neuraxial and peripheral nerve blocks
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10
Q

Definition - Neuraxial anesthesia

A

Spinal and epidural anaesthesia. Both are performed under sterile conditions with the patient attached to vitals monitoring and IVC in-situ with fluids running.

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11
Q

Spinal anesthesia - definition and preocedure

A

Description
▪ Injection of anaesthetic into the subarachnoid space→Anaesthetisation of the spinal roots passing at that point

o Procedure
▪ Sterilisation of the desired area of the back
• Patient in left lateral position curled into a ball, or sitting on the end of the bed with back arched forward
▪ Use local anaesthetic (e.g. 1% lidocaine) at the desired area prior to block insertion
▪ Insert a 25G needle into the L4/5 space
▪ Confirm entry by flow of CSF out and rotate the needle by 180 degrees
▪ Inject desired anaesthetic agent
• Commonly bupivacaine + glucose 1-3mL
▪ Monitor for a drop in BP and give pressors/fluids as necessary

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12
Q

Effects of spinal anesthesia

A
  1. Sympathetic blockade (vasodilation and degree of hypotension)
  2. Sensory blockade
  3. Motor blockade
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13
Q

Complications of spinal anesthesia

A
  1. Severe hypotension
  2. Apnoea or LOC
  3. Headache - usually secondary to CSF leak
  4. Urinary retention
  5. Permanent nerve damage
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14
Q

Epidural anesthesia - definition and procedure

A

Description
▪ Insertion of an indwelling catheter for an infusion of local anaesthesia into the extradural space

o Procedure
▪ Sterilisation of the area and patient positioning
• As per spinal block
▪ Local anaesthetic prior to block insertion
▪ Insert 16G Touhy needle into the ligamental flavum (2-3cm deep) at the L3/4
space
• Positioning is determined by a loss of resistance to insertion and injection
▪ Threading of an epidural catheter into the epidural space and withdrawal of the needle
▪ Administer a 2mL test dose of anaesthetic and assess response after 3 minutes
▪ Secure the catheter in place and inject the desired amount
▪ Ongoing monitoring of BP (5 minutely for the first 15 minutes)

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15
Q

Complications - epidural anesthesia

A
  1. Dural puncture - accidental spinal anesthesia
  2. Vessel rupture
  3. Epidural hematoma or abscess
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16
Q

Spinal vs Epidural

A

Spinal
o Immediate onset
o More reliable
o Dose cannot be titrated (no catheter placement)
o Injection into subarachnoid space
o Smaller needle and smaller dose
o May be used in obstetrics, but also used in lower limb surgery where a GA is contraindicated

Epidural
o Delayed-onset
o Effect can be variable
o Dose can be titrated and allows for an infusion (catheter in-situ) 
o Injection into the epidural space
o Larger needle and larger dose
o Most commonly used in obstetrics
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17
Q

Contraindications to neuraxial anesthesia

A
  1. Anticoagulant use or coagulopathy
    o Risk of bleeding→pressure on the spinal cord→
    neurological damage
  2. Sepsis
    o Risk of introducing pathogens into the CSF
  3. Shock or hypovolaemia
  4. Raised intracranial pressure
    o Risk of coning/herniation
  5. Unwilling patient
  6. Fixed-output states
  7. Mitral or aortic stenosis - due to its sympatholytic effect, potentially causing loss of vascular tone and ultimately diminished cardiac output
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18
Q

Peripheral nerve blocks - definition

A

Local anesthetic on a local nerve or plexus to induce anesthesia on specific nerve/plexus distribution
Usually done with the help of ultrasound peripheral nerve stimulator

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19
Q

Peripheral nerve blocks - agents used

A

Similar to local anesthetics
1. Lidocaine, bupivacaine, ropivacaine
2. Adrenaline is often given with the anesthetic to decrease systemic absorption and hence increase the efficacy of the localized effect
▪ NB: contraindicated in penile and digital blocks due to risk of vasoconstriction-induced ischemia

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20
Q

Peripheral nerve blocks - examples

A

Cervical Plexus Block
▪ Used for carotid endarterectomy surgery

Intrascalene/Brachial Plexus block
▪ Used for shoulder surgery

Axillary Block
▪ Hand/forearm surgery

Lumbosacral Plexus Block
▪ Hip surgery

Ilioinguinal-Iliohypogastric Nerve Block
▪ Inguinal hernia repair

Sciatic and/or Femoral Block
▪ Knee, leg, and ankle surgery

Bier’s Block
▪ IV local anesthesia given through the peripheral vein whilst the limb (usually arm) is occluded with a tourniquet/blood pressure cuff to minimize systemic absorption

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21
Q

Peripheral nerve blocks - contraindications

A
  1. Nerve injury - rare
  2. Bleeding
  3. Local anesthetic toxicity
  4. Seizures - This may be because peripheral nerve blocks are associated with injection of larger volumes of local anesthetic than other regional techniques.
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22
Q

Steps of WHO analgesic ladder

A

Step 1 = Non-opioid +/- adjuvant therapy
o E.g. regular NSAIDs and Paracetamol

• Step 2 = Weak opioid + Step 1
o Weak opioids = codeine and tramadol
o Commonly doctors will skip this step and opt to use lower doses of step 3 drugs as they are more commonly prescribed and can be more easily titrated up

• Step 3 = Strong opioid + Step 1
o Strong opioids = oxycodone(Endone), morphine, and fentanyl

• Step 4 = Interventional treatments + Step 1
o Interventions = peripheral/neuraxial nerve blocks and PCAs (Patient-Controlled Analgesia)

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23
Q

Ibuprofen - MOA, route, dosage and drug interaction

A
  1. COX inhibitor - Inhibits conversion of arachidonic acid into thromboxanes, prostaglandins, and prostacyclins.
  2. 200 - 400mg QID PO
  3. Decrease the antiplatelet effect of aspirin and combination with codeine is not recommended
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24
Q

Naproxen - MOA, route, dosage and drug interaction

A
  1. Similar to ibuprofen
  2. 250-500mg PO BD / 750-1000mg PO OD
  3. Can reduce the antiplatelet effect of aspirin
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25
Q

Celecoxib - MOA, route, dosage and drug interaction

A
  1. Selective COX-2 inhibitor

2. 100mg PO BD

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26
Q

Paracetamol - MOA, route, dosage and cautions

A
  1. Analgesia and antipyretic, not anti-inflammatory. Central inhibition of prostaglandin synthesis
  2. 1-gram QID PO (usually comes in 500mg tablets)
  3. Caution in abnormal liver function
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27
Q

Aspirin (as an analgesia) - MOA, route, dosage and cautions

A
  1. COX inhibitor
  2. 600-900mg QID PO (dose different for cardiac pt)
  3. Caution in renal impairment and severe liver disease
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28
Q

Opioids - adjustments and cautions

A

Adjustment based on patient comfort

Cautions - hepatic and renal functions

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29
Q

Morphine - MOA, side effects and precautions

A
  1. MOA - Bind and activate mu-opioid receptors in the CNS → reduced transmission of the pain
    impulse
  2. Side effects -
    a. Sedation
    b. Respiratory depression
    c. Constipation
    ▪ Due to decreased gut motility secondary to binding
    of mu-opioid receptors there
    ▪ May be given with naloxone (opioid antagonist) to
    minimise these effects
    d. Nausea and vomiting
    e. Itching (secondary to histamine release)
    f. Tolerance and dependence
    g. Euphoria or dysphoria
  3. Precautions:
    a. Reduce dose if GFR <50 due to accumulation of active
    metabolites
    b. Avoid in bowel obstruction and ileus
    c. Avoid in respiratory failure
    d. Avoid in hepatic failure
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30
Q

Oxycodone and fentanyl have similar MOA and side effect profile as morphine. However, what are the main differences in terms of precautions?

A

Common precautions

  1. Avoid in bowel obstruction and ileus
  2. Avoid in respiratory failure
  3. Avoid in hepatic failure

Differences
1. Morphine - Reduce dose if GFR <50 due to accumulation of active metabolites
2. Oxycodone - Consider dose reduction if GFR <30
and decrease dosage with age
3. Fentanyl - Not renal-dependent, so can be used in renal disease and avoid in serotonin syndrome or co-prescription with a MAOI

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31
Q

Morphine - Route and dosages for acute, chronic and breakthrough pains

A
  1. Acute pain - titrate boluses of IV 1 – 2.5mg every 5 minutes or SC 5 – 10mg 2-hourly
  2. Chronic pain - calculate morphine equivalent dose of all opioids used in 24 hours and deliver as a controlled release preparation over 24 hours
  3. Breakthrough pain - additional dose equivalent to 1/6 the daily dose titrated
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32
Q

Codeine - Route and dosage

A

200mg oral codeine = 10mg SC morphine

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33
Q

Oxycodone (Endone) - Strength compared to morphine, route and dosages for acute and chronic pains

A
  1. It is 1.5X stronger than morphine
  2. Acute pain - 5-10mg PO every 4-hours
  3. Chronic pain - highly variable (30-60mg q4h PO)
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34
Q

Fentanyl - Strength compared to morphine, route and dosages for acute and chronic pains

A
  1. 100 micrograms fentanyl = 10mg IV morphine (100X stronger)
  2. Acute pain → careful boluses of 25 micrograms with cardiorespiratory monitoring
  3. Breakthrough pain → 200 microgram lozenge PO
  4. Chronic pain → not usually used until the patient is stabilized on another opioid, in which case a patch may be used
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35
Q

Enteral vs parenteral

A
  1. Enteral - when not to give

a. Impaired GIT absorption (Active IBD, pancreatitis, bowel obstruction, ileus, etc.)
b. Enteral preparation of the medication is not available (e.g. adrenaline)
c. Precision in dosing is required (enteral absorption is far more variable)
d. Immediate onset of action is required (many enteral drugs require absorption
into the bowel wall and liver prior to inducing an effect)
e. An infusion is required

  1. Downside of parenteral
    a. Hospitalization - pain and discomfort
    b. Poses a risk for infection
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36
Q

Perform simple dilution calculations when drawing up analgesic medications to ensure appropriate dosing as the bed-side

  1. The conversions - g,mg and mcg/ug
  2. Ordered 100mg. Available 2mg / 3 ml. Calculate the dosage
  3. 20kg. Acepromazine - Dose rate: 0.04mg/kg and Concentration: 2mg/ml
A
  1. 1g = 1000mg, 1mg = 1000mcg/ug
  2. 100/2 X 3 = 150
  3. Dose rate: 0.04mg/kg = 0.04 x 20(kg) = 0.8mg required.
    Concentration: 2mg/ml
    Dose to be given = 0.8/2 = 0.4ml
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37
Q

Opioids - partial agonist, mixed agonist/antagonist and antagonist

A
  1. Patial agonist - Buprenorphine - high affinity but poor efficacy, thereby inducing a degree of analgesia but also acting as a deterrent for opioid abuse
  2. Mixed agonist / antagonist - pentazocine, nalbuphine, butorphanol - less commonly used
  3. Antagonist - naloxone and naltrexone
    a. Competitive antagonists at the mu, kappa, and delta receptors that act centrally and peripherally
    b. Rapid onset of action but a short half-life, and so should be used with caution as the antagonist may wear-off before the narcotizing agent does
    c. Combined with buprenorphine as Suboxone in patients being treated for opiate addiction.
38
Q

Opioids based on origin

A
  1. Endogenous opioids - Beta endorphin, enkephalin, dynorphin
  2. Opiates (derived from opium poppy) - Morphine and codeine
  3. Semi-synthetic opioids - Heroin/diamorphine, buprenorphine, oxycodone
  4. Synthetic opioids - Fentanyl, methadone, hydromorphone
39
Q

Opioid pharmacology - Types of receptors, MOA and side-effects

A
  1. Types of receptors- Mu, delta, and kappa
  2. Activation of these receptors causes reduction in synaptic transmission of pain signals via various mechanisms:
    o Presynaptic closure of Ca channels → hyperpolarization → reduced release of ACh, NA, serotonin, GLUT, NO, and substance P → reduced pain sensation
    o Postsynaptic opening of K channels → hyperpolarization
  3. Side-effects
    o Anti-diarrhoeal/constipation
    o Sedation
    o Antitussives (commonly used in palliative care for this reason)
    o Anti-cholinergic effects(pupil constriction,urinary retention)
    o Nausea and vomiting
    o Pruritis

• Strong opioids, such as fentanyl and morphine, act as agonists at all 3 receptors, whereas other agents may only act at one or two of the opioid receptor types

40
Q

Principles of safe prescribing

A
  1. Reason - treatment/ symptomatic relief/ prevention
  2. Accurate drug hx
  3. Concise medical hx - pregnancy/ co-morbidities / liver or renal impairment
  4. Discuss with pt
  5. Right dose, route, pt, medication
  6. Documentation
  7. Ask for help if needed
41
Q

Common drugs associated with challenges in renal disease

A

▪ Pre-renal – diuretics, ACE inhibitors, anti-hypertensives
▪ Intra-renal – NSAIDs, PPIs, lithium
▪ Post-renal – acyclovir and allopurinol
o The most common medications used in hospital that require dose reduction in renal disease are insulin and clexane

42
Q

Common drugs associated with challenges in liver disease

A

Paracetamol, amiodarone, azathioprine→hepatitis
▪ Tetracyclines→fatty change
▪ Augmentin and nifedipine→cholestasis

43
Q

Definition - High risk prescribing

Examples

A

Definition
o Prescription of medication by health professionals where there is evidence of significant risk of harm to patients, and should therefore either be avoided or closely monitored
and regularly reviews for ongoing appropriateness

• Examples of high-risk medications = A PINCH

o Anti-infectiveagents
▪ Antibiotics/antivirals, especially broad spectrum agents and agents with a narrow therapeutic range (e.g. aminoglycosides)

o Potassium and other electrolytes
▪ Potential for inducing arrhythmias, especially in patients with co-existent renal disease and on certain medications

o Insulin
▪ Especially in sick patient with multiple comorbidities

o Narcotics and sedatives
▪ Opioids, benzos, and anaesthetic agents

o Chemotherapeutic agents
▪ Methotrexate, azathioprine, etc.

o Heparin and anti-coagulants
▪ Warfaring, DOACs, clexane, etc.

44
Q

Management of opioid tolerance

  1. Non-pharmalogical and pharmalogical
  2. Prophylaxis
A

Non-pharmacological interventions
▪ Drug education
▪ Psychological/psychiatric support

Pharmacological interventions
▪ Opioid maintenance therapy
Use of agents that bind to opioid receptors with less efficacy (producing less of a euphoric effect) than the addictive drug and have a longer half-life
• Methadone – oral preparation
• Buprenorphine – commonly administered as a transdermal patch or as a preparation combined with naloxone to prevent IV administration (suboxone)
▪ Anti-depressive/anti-anxiety medications if indicated
▪ Management of comorbidities associated with IV drug use • E.g. HIV, hepatitis C, endocarditis, etc.

o Prophylaxis
▪ Avoidance of inducing opioid dependence when prescribing opiates can be aided with the use of screening tools such as the ‘Opioid Risk Tool’

45
Q

Chronic pain

  1. Formal risk assessment tool
  2. Investigations
  3. Management
A
  1. PEG (scale - pain on avg, enjoyment of life and general activity)
  2. Investigations
    - Imaging
    - Diagnostic nerve blocks
    - nerve conduction studies - done by specialist
    - Appropriate blood tests
  3. Management
    - Referal to a pain specialist for MDT is ideal
    - Management of other co-morbidities that may contribute to the pain (depression, anxiety)
    - Psychological intervention if indicated
46
Q

Biopsychosocial model of pain

A

Biological pain, psychological factors (mental health and perception of pain) and social factors such as cultural practices around pain and degree of support around the management of pain

47
Q

Psychological interventions in chronic pain

A
  1. CBT - Perception of pain and skills to cope with pain
    Examples: Pain conditioning, discouraging pain/illness behavior and breathing techniques
  2. Mind-body therapies
    Common interventions include relaxation, breathing techniques, meditation, and hypnosis

Psychological interventions have the greatest effect when used as an adjunct to pharmacotherapy
(when indicated) and other non-pharmacological interventions, such as sleep hygiene, regular exercise, socializing, and a healthy diet

48
Q

Regional anesthesia equipment - needles and their uses

A
  1. Block needles - To enter deep tissues
  2. Short bevel needles - for IV injection
  3. Insulated needles - nerve stimulators
  4. Echogenic needles - better ultrasound detection
49
Q

regional anesthesia

  • Purpose
  • Inside or outside needle?
A
  1. Ongoing infusion of local anesthesia

2. Inside

50
Q

Manifestations of local anesthetic toxicity

and time taken for effect

A
  1. Time taken - 5 min to 1 hour
  2. Side effects

CNS:

a. Circum-oral numbness
b. Tongue paresthesia
c. Visual and Auditory
d. Diziness
e. Muscle twitching
f. tremor, convulsion, coma and death

CVS

a. Initial hypertension and tachycardia followed by vasodilation, bradycardia
b. Conduction defects - PR/QRS anomalies
c. VT/VF, cardiac arrest

  • Lignocaine can inhibit coagulation
  • Local neurological symptoms
  • Allergic reaction common with esters but rare with amides
51
Q

Local anesthetic toxicity

  • MOA
  • Agent given with local to reduce the chance of toxicity and MOA
  • Preventions
A

Usually occurs with high doses

  1. Systemic absorption of the local anesthetic at supratherapeutic level
  2. Blockage of Na channel in the CVS and CNS
    a. CNS - Biphasic sequence - with initial excitation (due to blockade of inhibitory pathways), followed by inhibition (due to blockade of both inhibitory and excitatory pathways)
    b. CVS - sodium blockade in the pacemaker and electrical conduction cells in the heart → re-entrant arrhythmias and potential heart block
  3. Agent used alongside - Adrenaline - Vasoconstriction - decreased systematic absorption - decreased toxicity
  4. Prevention
    a. Be aware of dosing - supratherapeutic doses
    b. Give small, divided doses rather than large boluses, and regularly assess symptoms
    c. Treat causes that exacerbate and predispose to toxicity
    ▪ Acidosis, hypoxia, and hypercapnia
52
Q

Local anesthetic toxicity - Management

A

As a junior, call for help

  1. Mild symptoms - Perioral numbness and tongue paresthesia - cessation of the agent and boluses of IV midazolam (to reduce seizure threshold)
  2. Severe local anesthetic toxicity

a. Stop giving the agent
b. Call for help
c. IV lipid emulsion therapy (absorb the local anaesthetic from the systemic circulation due to the anaesthetic agents being lipid-soluble) - Give an initial bolus of 20% lipid emulsion IV at 1.5mL/kg, then start an ongoing infusion at 15mL/kg/hour. Repeat up to 2X based on response
d. IV midazolam - thiopentone or propofol (avoid large doses) if no effect
e. ABCDE - 100% O2, prevent hypoxemia, hypercarbia and acidosis
f. Manage arrhythmia and cardiac arrest as per ALS except
- Reduce epinephrine to 1mcg/kg
- Avoid vasopressors, beta-blockers, CCBs
- Amiodarone is the first drug of choice as anti-arrythmic
g. Cardio-pulmonary bypass last resort

53
Q

Safe single dose limits for lignocaine, ropivacaine, and bupivacaine

A
  1. Lignocaine - 5mg/kg - 7mg/kg (medium potency)
  2. Ropivacaine - 2.5mg/kg - 3mg/kg (high potency)
  3. Bupivacaine - 2.5mg/kg - 3mg/kg (high potency)
54
Q

Airway assessment - predictor of intubation difficulty

A
  1. C-spine stability and mobility - Sniffing position
2. Assessment of Mallampati score
I - Full view of uvula
II - 50% of uvula
III - Only the base of uvula
IV - Hard palate and tongue. Other structures not visible
  1. 3-2-1 assessment
    The presence of any of the following is associated with a difficult intubation
    • Thyromental distance (from mentum to thyroid cartilage) <3 finger breadths
    • Mouth opening <2 finger breadths
    • Anterior jaw subluxation <1 finger breadth
55
Q

ASA

  • What it is
  • Scoring system
A
  1. Gross prediction of general outcome after anesthesia
  2. ASA 1 = healthy, fit patient with no known disease
    o ASA 2 = patient with mild systemic disease that is well controlled
    ▪ E.g. controlled T2DM or hypertension, obesity, smoker o ASA 3 = severe systemic disease that limits activity
    ▪ E.g. stable angina, COPD, T1DM, morbid obesity
    o ASA 4 = incapacitating disease that is a constant threat to life
    ▪ E.g. unstable angina, CKD, acute respiratory failure
    o ASA 5 = moribund patient not expected to survive 24 hours without surgery
    ▪ E.g. ruptured AAA or head trauma with raised ICP
    o ASA 6 = declared brain dead and organs are being removed for donation

NB: an ‘E’ is put after the ASA status to indicate the procedure is an emergency

56
Q

Drugs to be ceased prior to surgery

A

Anticoagulants
▪ Important to know why the patient is anticoagulated as this may influence whether some form of blood thinning is required in the meantime
▪ If crucial the patient is anticoagulated, then admit the patient 2 days before surgery and switch the oral anticoagulant for temporary heparin therapy until post-operatively and monitor INR

  1. Aspirin
    ▪ Controversial
  2. Prasugrel,ticagrelor,andclopidogrel
    ▪ Cease 5-7 days before surgery
  3. Patient on dual anti-platelet therapy
    ▪ Postpone the surgery until one-year post-stent insertion if possible
    ▪ Consult cardiology
  4. NSAIDs - Discontinue
  5. Diuretics - Discontinue usually; assess for hypokalaemia and hypovolaemia
  6. Insulin
    ▪ Continue basal/long-acting insulin on the day of surgery ▪ Omit oral hypoglycaemic agents
  7. Oral contraceptive pill and HRT
    ▪ Cease 4-weeks before major surgery if possible due to VTE risk
    ▪ Restart at 2-week post-op if mobilizing well
    ▪ Use thromboprophylaxis with clexane and stockings
  8. Ophthalmic drugs
    ▪ Cease anticholinesterases, beta-blockers, and alpha-blockers
57
Q

Pre-operative medications commonly given

A
  1. Gastric reflux prophylaxis → metoclopramide or ranitidine
  2. Gastrointestinal or genitourinary surgery → antibiotic prophylaxis (commonly cefazolin)
  3. Pre-operative anxiety/agitation → midazolam
  4. Coronary artery disease→consider nitroglycerin and beta blockers
58
Q

Pre-operative fasting

  • Reason
  • Evaluation and considerations
A
  1. Reason - avoid risk of aspiration. NBO before surgery
  2. Oral intake
    - no clear fluid 2hrs pre-operative
    - everything else 6 hrs pre-operative.
    - Emergency - everything 6 hrs pre-operative ideally
  3. HTN - <180/110 before surgery
  4. CAD
    - 60 days between an MI and surgery
    - Beta-blockers intra-operatively
  5. Respi
    - Smoking - ideally 8-weeks prior surgery. 24hrs minimum
    - Asthma -Moderately severe asthma
    a. Consider a 1-week of steroid and SABA (decrease the risk of intra-operative bronchospasm)
    b. Avoid the use of non-selective beta-blockers (labetalol, carvedilol, propranolol, nadolol)
    c. Delay surgery by at least 6-weeks in patients with moderately severe asthma that develop an URTI
    - COPD
  6. Hematology - evaluation of FBC and coags
  7. Endocrine
    - Diabetes
    a. Assessment of HbA1c and signs of end damage (UECs, LFTs, albumin creatinine ratio, etc.)
    b. Develop a plan for intra-operative glycaemic control – e.g. insulin infusion
    - Thyroid disease - risk of thyroid storm
    - Addison’s disease - Intraoperative steroid supplementation
59
Q

Anesthesia: Intra-operative monitering

A
  1. Most important- presence of anesthetist all the time
  2. Respiratory
    - O2 monitoring - pulse oximetry, capnography and RR
    - CO2 monitoring - End-tidal volume of CO2 monitoring by capnography. Maintain ventilation through mechanical, volume control or pressure support ventilation
  3. CVS
    - ECG
    - Non-invasive BP monitoring - Hypotension is the most common side effect of most anesthetic drugs. Use metaraminol if hypotension caused by meds
  4. Urinary output - Monitored hourly in catheterized patients
  5. Temperature
    - Hypothermia - common due to OT temp. Use forced-air warming blankets and warm IV fluids
    - Hyperthermia - uncommon - other causes + rarely malignant hyperthermia
  6. Fluids - Total = maintenance fluids + deficit fluids + ongoing losses
- Maintenance = 4-2-1 rule (N. saline/ Hartmann's)
o 4mL/kg/hr for first 10kg
o 2mL/kg/hr for second 10kg
o 1mL/kg/hr for every kg above 20kg
o E.g. 70kg person = (4x10) + (2x10) + (1 x50) = 100mL/hr
- Electrolyte replacement
o 100 mmol/day of Na
 o 70-90mmol/day of K
  • Deficit - Should be hydrated before the surgery
  • Ongoing losses during surgery - suctioning, drainage, hemorrhage, evaporation from skin
  1. Sedation - Varies. Check for movements, sympathetic activation (increase in BP & HR, lacrimation, dilated pupils) and laryngospasm (Coughing, possible rise in end-tidal CO2)
60
Q

Extubation - Definition, considerations and complications

A
  1. Definition - Weaning off the ventilator and relying on the patients own respiratory drive to oxygenate and ventilate themselves
  2. Considerations
    - Paralytic agent worn off (consider nerve stimulation monitoring) and administer a paralytic reversal agent (neostigmine +/- glycopyronium)
    - Breathing effort is seen
    - Provide 100% O2 for 3-5 minutes prior to extubation (thought to reduce risk of atelectasis)
    - Suction the secretions around the cuff-end of the ETT before deflating the cuff and removing it (to protect against potential aspiration)
  3. Complications
    - Aspiration
    - Trauma to airways
    - Laryngospasm
    ▪ secondary to late removal of ETTs, blood, or airway secretions
    ▪ Absence of laryngospasm occurs when patients are adequately sedated
61
Q

Anesthesia - Post-op management

A
  1. Pain - Analgesia (usually panadol and fentanyl)
  2. Confusion and agitation
  3. Nausea and vomiting - metoclopramide (avoid in bowel obstruction) or ondansetron. Sometimes dexamethasone
  4. Respiratory complications - Aspiration and airway obstruction
  5. Blood pressure - Hypotension (Fluids +/- ionotropes) or hypertension (ACE-I, BB or CCB)
62
Q

Propofol - Use, MOA, onset, and consideration

A
  1. Both induction and maintenance
  2. Central GABA-A receptor agonist - Decreased cerebral metabolism and blood flow, decreased cardiac output, and decreased respirations
  3. Very rapid onset and short half-life
  4. Significant BP drop
63
Q

Sodium thiopental - Use, MOA, and onset

A
  1. Short-acting agent used for induction only
  2. GABA modulation centrally
  3. Has barbiturate like effect (useful for status epileptics)
64
Q

Etomidate - Use and MOA

A
  1. Induction agent only - for poor cardiac functions and uncontrolled HTN
  2. MOA similar to propofol
  3. Minimal cardiac/ respiratory depression
65
Q

Ketamine - Use and MOA

A
  1. Has induction, maintenance, analgesic, and amnesic properties making it a common adjunct to many general anaesthetics. Due to its sympathomimetic effects, it is commonly used in trauma and massive
    hemorrhage
  2. MOA - NMDA antagonism in addition to opioid agonist → increased HR/BP/SVR, increased coronary artery perfusion, respiratory depression, and bronchiole
    smooth muscle relaxation
66
Q

Benzodiazepines - Use and reason why it is rarely used

A
  1. Used as an adjunct to induction/maintenance agents, commonly given prior to surgery in the anaesthetics bay
  2. Significant respiratory depression, longer onset of action and unpredictable half-life
67
Q

MAC - Definition

A

Minimum alveolar conc required (compared to O2) to induce anesthesia in 50% of the population

68
Q

Halothane -MAC, effect on ICP and CVS

A
  1. MAC - 0.8

2. High ICP (all inhalation agents), decreased CO, BP (risk of arrythmia with adrenaline)

69
Q

Isoflurane -MAC, effect on ICP and CVS

A
  1. MAC - 1.2

2. High ICP, decreased CO, BP, tachycardia

70
Q

Sevoflurane -MAC, effect on ICP and CVS

A
  1. MAC - 2.0

2. High ICP, minimal affect on cardiac function (savior-flurane)

71
Q

Desflurane - MAC, effect on ICP and CVS

A
  1. MAC - 6.0

2. High ICP, decreased CO, BP, tachycardia

72
Q

Bupivacane - benefit and side-effect

A
  1. Slow onset and long half-life, hence it is commonly used for abdominal tap blocks and epidurals
  2. Cardiotoxic (alternative is ropivacaine)
73
Q

Adrenaline vs noradrenaline

A
  1. Adrenaline - Both alpha and beta agonists (predominantly beta). Used in ED/ICU settings for patients with impaired cardiac output
  2. Noredrenaline - Predominantly acts on alpha agonist. Used in septic shock
74
Q

Dopamine

  • Affect of low and high doses
  • Use
A
  1. At low doses → inotropic action and vasodilation in the renal and splanchnic circulation
    ▪ At higher doses → tachycardia, arrhythmias, and vasoconstriction
  2. Mainly used in patients with bradycardia at low risk for arrhythmias
75
Q

Dopexamine vs dobutamine

A
  1. Both are dopamine analogues
  2. Dopexamine: Vasodilatory affect > ionotropic affect
  3. Dobutamine: Ionotropic affect > vasodilatory affect
76
Q

Perioperative - isoprenaline, metaraminol and Ephedrine

A
  1. Isoprenaline - Beta agonism - bradycardia or heart block
  2. Metaraminol - Weak a1 agonist - hypotension
  3. Ephedrine - Both alpha and beta agonists - adjunct for hypotension / bradycardia
77
Q

Suxamethonium - MOA, use and side effects

- Management of malignant hyperthermia

A
  1. MOA - non-competitive polarizing (initial twitch), blocks nicotinic cholinergic receptors - skeletal muscle paralysis, including diaphragm
  2. Use - rapid onset, short life - used for rapid-sequence intubation and less ideal for intra-operative paralysis
  3. Side effects
    - Stimulation of muscarinic receptors → cholinergic effect
    ▪ Hyperkalaemia
    ▪ Raised ICP and intra-ocular pressure
    ▪ Post-operative myalgias and fasciculations (initial twitch)

▪ Malignant hyperthermia
• Tachycardia, tachypnoea, cyanosis, muscle rigidity, and hyperthermia that develops secondary to inhalational anaesthetic agents of suxamethonium
• Management is with cessation of the causative agent, cooling, increased O2 delivery, and administration of dantrolene

78
Q

Rocuronium - MOA, use and reversal agent

A
  1. MOA - Competitive blockade of post-synaptic ACh receptors → prevention of muscle
    depolarisation
  2. Use - Longer onset of action and half-life compared to suxamethonium makes it ideal for paralysis in an intra-operative context
  3. Reversal agent - acetylcholinesterase inhibitors→increased ACh at the NMJ
79
Q

Partial pressure - definition

FiO2 - defnition and application of it

A
  1. The proportion of a particular gas that occupies a given environment. Helps in crossing the alveolar membrane depending on the gradient
    - Greater the gradient difference, the higher the diffusion rate
  2. FiO2 - Fraction of inspired air.
    - increasing rates of flow and changes to the device used to deliver oxygen can alter the FiO2 anywhere up to 100% (i.e. breathing pure oxygen)
80
Q

Oxygen toxicity - over oxygenation

  1. Risk factors
  2. Pathophysiology
  3. Clinical features
  4. Diagnosis
  5. Management
A 
1. Risk factors
o Delivery of FiO2>80%
o Use of PEEP
o Prolonged oxygen therapy
o Oxygen delivery without a clear indication
  1. Pathophysiology - High O2 causes vasoconstriction in coronary, cerebral ad renal vessels + cellular damage due to free radicals
  2. Clinical features
    a. Neurological - seizures, irritability, anxiety, hallucination
    b. CVS - MI, arrythmia
    c. Respiratory
    Absorption Atelectasis - Excessive absorption of gas from the alveolus to the pulmonary capillaries due to excessive PO2 gradient → alveolar collapse
    ▪ Pulmonary O2 Toxicity - substernal pain, cough, dyspnoea, pulmonary oedema/hemorrhage
    ▪ Pulmonary fibrosis - Secondary to prolonged O2 exposure→fibroblast proliferation
    ▪ Ventilator-associated Pneumonia
  3. Management
    Mostly prophylaxis
    - Always examine the need for O2 - <94% and <88% in COPD patients
    - Constantly review the need for O2 in O2 therapy
81
Q

Oxygen toxicity - Oxygen induced hypercapnia

  1. Definition
  2. Management
A
  1. Delivery of O2 in COPD patients - blunting of hypoxic O2 drive - hypercapnia and apnea
  2. Management
    - Identify hypoxic drive - COPD has a high HCO3 baseline
    - Use fixed-O2 delivery systems when O2 therapy is required in these patients (e.g. Venturi masks)
    - Have altered calling criteria for these patients and aim for saturations between 88-92%
82
Q

Oxygen flux equation - definition and equation

A
  1. Amount of O2 delivered to the tissues and the factors responsible for it
  2. DO2 = CO X {(BO2 X ceHB X sO2) + (PaO2 X0.03 )}
DO2 = Rate of O2 delivered
CO = Cardiac output
BO2 = Maximal O2 carrying capacity of the blood 
ceHb = Concentration of effective hemoglobin
0.03 = Solubility constant for O2 at 37 degrees celcius
83
Q

Alveolar gas equation- definition and equation

A
  1. Estimates the partial pressure of O2 in the alveolus given a particular atmospheric pressure and FiO2
  2. PaO2 = {FiO2 [0.21 RA] X (P atm [760mm sea level] - P h2o [27 mm of H2O pressure])} - (PaCO2 [ABG]/RespQ [0.8])

At sea level, the atmospheric pressure is 760mmHg:
▪ O2 constitutes 21% of total concentration of gases at room air, and hence is said to occupy 21% of the atmospheric pressure → 0.21 x 760mmHg = 160mmHg partial pressure of O2 at sea level

84
Q

Hb/O2 dissociation curve

  1. Clinical importance
  2. Factors affecting the curve - left and right shift
A
  1. There is a sharp decline in hemoglobin saturation once SaO2 levels drop below ~85% in a normal situation as seen in the sigmoidal grapgh
2. Left shift - 
Decreased PCO2 – e.g. hyperventilation 
o Hypothermia
o Alkalosis
o Carbon monoxide poisoning
o Methaemoglobinaemia

Right shift
o Increased PCO2 – e.g. hypoventilation, exercise, COPD o Hyperthermia/fever
o Acidosis
o High altitudes

85
Q

Basic O2 delivery systems (4) - Litres and FiO2

A
  1. Nasal prongs - 2 to 4L/min; FiO2 0.25-0.35
  2. Face mask (hudson) - 5 to 10L/min; FiO2 0.35-0.60. Mostly post-op use
  3. Venturi Mask - flow can be adjusted - useful in COPD with strict control of FiO2. FiO2 - 0.25 - 0.60
  4. Non-rebreather mask - 15L/min; FiO2 0.6-0.9
86
Q

Non-invasive ventilation (3)

A
  1. CPAP and BiPAP
  2. High flow nasal cannula - humidified O2 delivery. 1 to 60L/min; FiO2 0.8-1
    - Very useful and well-tolerated, but only really seen in ICU for patients with APO or hypoxic respiratory failure
87
Q

Invasive ventilation (2)

A
  1. Bag valve mask - 100% O2 delivery

2. Endotracheal intubation - 100% O2 ventilation. Risk of aspiration, laryngeal spasm, and damage to vocal cords

88
Q

Demographic findings of REASON study

A
  1. 100% should be expected to stay at least one night in hospital
  2. 20% will have a major complication within 5 days
  3. 10% will require ICU admission, of which half will be unplanned
  4. 5% will die by day 30

Major reasons of mortality - High ASA, hypoalbuminemia, SIRS like reaction and AKI

89
Q

Why 5% glucose is not used in resuscitation? What can we use for resuscitation and why?

A
  1. 5% glucose will readily distribute evenly between all 3 body fluid compartments as we would want the majority of the fluid to remain intravascular
  2. Normal saline 0.9% is predominantly distributed in the extracellular space, with about 1/3 remaining in the intravascular space
90
Q

Perioperative hyponatremia

  1. Importance
  2. Management
A
  1. Used as a predictor for post-operative morbidity and mortality
  2. Management - Identification of the underlying cause and fluid replacement (isotonic vs. hypertonic saline) vs. fluid restriction
Etiology includes
o Dehydration, diarrhoea, vomiting
o Medication-induced
o SIADH secondary to physiological stress of surgery
o Endocrinopathies
o Heart/liver/kidney failure
91
Q

Problems with normal saline

A
  1. Massive Na load - 1 bag is enough for the whole day. Not compatible with renal failure patients who are under sodium restriction
  2. Risk of hyperchloremic acidosis
  3. Risk of hyperchloremic kidney injury
92
Q

Role of IV colloids

A
  1. Increases oncotic pressure, thereby maintaining intravuscular volume
  2. There is little evidence that their use is superior to balanced electrolyte solutions, though there is some evidence that it can reduce oedema and potentially reduce the amount of IV fluids required for resuscitation

ED, ICU and Anesthetics (1 decks)

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