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216 Cards in this Set

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Mallampati Class I
visualise soft palate, uvula, tonsillar pillars
Mallampati Class II
visualise soft palate, uvula but NOT tonsillar pillars
Mallampati Class III
only visually soft palate and BASE of uvula
Mallampati Class IV
only soft palate (uvula cannot be seen)
American Society of Anaesthesiology (ASA) classification for predictor of overall outcome.
6 classes
ASA 1: health, fit
ASA 2: mild systemic disease e.g controlled DM/HTN
ASA 3: severe systemic disease that limits activity e.g angina, COPD
ASA 4: incapacitating disease that is a constant threat to life e.g CHF, renal failure
ASA 5: moribund - not expected to survive 24h with or without surgery e.g ruptured AAA, head trauma with raised ICP
ASA 6: organs harvested
Add E for emergency
Malignant hyperthermia:
mechanism
decr reuptake of Ca++ by sarcoplasmic reticulum=> i/c Ca++ accumulation => muscle contraction => incr aerobic + anaerobic metabolism
Malignant hyperthermia:
triggering drugs
suxamethonium
+
potent volatile agents
Does previous uneventful anaesthesia preclude Malignant hyperthermia?
no
75% have had anaesthesia before
Malignant hyperthermia:
2 early signs
incr end tidal CO2
tachycardia
Malignant hyperthermia:
14 late signs
1. incr temp
2. rhabdo
3. myoglobinuria
4. metabolic + resp acidosis
5. muscle rigidity
6. dysrhythmias
7. HTN
8. cardiac arrest
9. masseter spasm
10. hypoxia
11. hyperkalaemia
12. high CK
13. renal failure
14. DIC
What might be the first indication of a previously unsuspected Dx of Malignant hyperthermia ?
masseter muscle spasm after being given sux
Malignant hyperthermia:
drug Rx
What is it?
How does it work?
DANTROLENE
muscle relaxant
interferes with release of Ca++ from SR => uncouples the excitation contraction of skeletal m
Malignant hyperthermia:
Rx (4)
hyperventilate with 100% FiO2
dantrolene
sodium bicarb for acidosis
cool patient with IV fluids, lavage in stomach + bladder
Can patients with Malignant hyperthermia ever get an anaesthetic?
yes, use a "safe technique" and avoid sux and volatile agents
There are 'vapour free' machines that can be used
What does GORD do to gastric emptying of food?
slows solids
no effect on liquid emptying
Pts with GORD: what meds can be used before induction?
Antacid: sodium citrate - just before induction

or
PPI/H2 blocker - night before and 2hr before op
If a Pt is at high risk of cardiac event during surgery, what can they prophylactically be put on?
What is the aim?
beta-blockers
cardioselective: atenolol/metoprolol
aim: PR 70
Which antihypertensives should patients withhold/continue taking perioperatively?
ACEi - STOP 1/7 before unless severe HTN (intraop hypotension with anaesthetic agents)
Diuretics: stop that day, unless CHF
B-blockers, CCB: CONTINUE
At what stage of the day should diabetics have their surgery scheduled?
morning
Metformin is assoc w/ development of ________ ___________ under GA => stop night before op and monitor BSL
metabolic acidosis
Pts with insulin-dependent DM should be commenced on __________________
IV infusion regime
Pre-op fasting guidelines for adults with no RFs for aspiration
8h meat, fatty foods
6h solid food (incl milk)
2h clear fluids
1-2h for pre-op meds w/ sips of H2O
What does trauma do to gastric emptying?
delays
What do opioids do to gastric emptying?
delays
What med can be given to increase gastric emptying (in a healthy Pt)
metoclopramide
(dopamine antagonist = pro-kinetic)
Which agents should be given to a pregnant woman to avoid aspiration? (2)
Ranitidine
Sodium citrate (antacid)
3 aims of GA
1. unconsciousness (anaesthesia)
2. analgaesia
3. loss of reflexes (muscle relaxants)
3 stages of GA
1. induction
2. maintenance
3. emergence/recovery
Usually, which sorts of GA agents are used for induction and maintenance
induction: IV agents
maintenance: volatile
Conscious sedation: rousable?
yes
independently maintain airway and response to appropriate physical stimulation and verbal command
Making a Pt unrousable by use of propofol/volatile gases still have reflexes, both motor and autonomic (coughing, motor reflexes, eyelash flutter)
=> what is given to decrease motor reflexes?
autonomic reflexes?
motor: muscle relaxants

autonomic: opioids
LMA: what does the cuff surround?
glottic structures
4 IV induction agents?
propofol
thiopental
ketamine
benzos
What are the two types of inhaled anaesthetics agents?
1. volatile: ____flurane. these are liquids that are vapourised
2. gas: NO - usually given with volatile; reduces amount of volatile needed
What can occur if Pt extubated too early (during twilight zone b/t unconsciousness + wakefulness)
laryngospasm
What does MAC stand for?
What does it mean?
It is inversely proportional to what?
Minimal Alveolar Concentration
= conc reqd to abolish the response to surgical incision in 50% of subjects
inversely proportional to potency
Mech of action: most anaesthetics enhance the activity of _________
inhibitory GABA(A) receptors
anaesthetic agents:
__________ cardiac contractility
broncho___________
________________respiration
_______________ arterial PCO2
decrease
dilation
decrease (increase RR and decr tidal vol => decr net minute ventilation)
increase
What class of drugs does thiopental belong to?

MOA?
barbituate
(it's an induction agent)

decrease time Cl channels open facilitating GABA and suppressing glutamic acid
How does propofol work?

What is the class of drug?
inhibitory at GABA synapse
prolongs GABA Cl- channel opening => hyperpolarisation and neuronal inhibition

Alkylphenol - hypnotic
Induction dose of propofol?
2.0-2.5 mg/kg
What does propofol do to peripheral resistance?
decreases
What other good property other than anaesthesia does propafol have?
anti-emetic
What is used as premedication to provide anxiolysis and sedation before GA or local/regional anaesthetic?
MOA?
benzo: midazolam
increased freq of Cl- channel opening time, facilitating GABA
For anaesthesia induction; dose of midazolam?
0.1-0.2mg/kg IV
What is suxamethonium (succinylcholine)?
How does it work?
muscle relaxant
Depolarising blocking drug --> activates AChR => muscle depol => continued presence at motor endplate desensitises AChR => cease to respond to nerve impulses
Membrane remains depolarised -> neuromuscular transmission blocked --> voltage dependent Na channels inactivated due to sustained depol
4 SEs of sux
1. fasciculations
2. increased ICP
3. hyperkalaemia
4. malignant hyperthermia
Patients are considered "non-fasted" if there has been <____hr b/t last meal and operation => are at risk of _______________ and require ______________
6
aspiration
RSI
Anything that ______________ abdo pressure such as pregnancy, obesity, emergency abdo trauma are at risk of aspiration
increases
To intubate, patient position = head _________ and neck _________
extension
flexion

ie atlanto-occipital extension; C-spine flexion
___________________ pressure (aka _______________ manoevre) is applied during RSI to obstruct the _________________ between cartiladge and C__ to prevent aspiration of gastric contents
cricoid; Sellick's
oesophagus
C6
LMA is positioned __________________________ so does not protect against pulmonary aspiration to the same degree as LMA
supraglottic
When using direct laryngoscopy before intubating, you visualise the pt's glottis through their mouth be aligned the axes of... (3)
1. oral cavity
2. pharynx
3. larynx
Why are diabetics at increased risk of aspiration?
delayed gastric empying
Sux is usually used during RSI to facilitate intubation, except in burns patients are spinal cord injury patients where __________________ is used to avoid hyperkalaemia
rocuronium
RSI: do they do face mask ventilation?
no
to avoid stomach distension
Airway risk is LOW if thyromental distance >_____ finger breadths
3
What condition is associated with instability of the atlanto-occipital joint => may make a difficult airway
Rheumatoid Arthritis
Sizing the guedel
corner of mouth to angle of mandible
LMA inserted into ____________________________ within the pharynx
piriform fossa
True or false: LMA protects against aspiration
false
Ideal position for intubation
Pt supine with head on pillow, head flexed, neck extended (sniffing position)
Typical size ETT for men
8-8.5
Typical size ETT for women
7-7.5
What will you see (2) if you accidentally intubate the oesophagus?
1. capnography may show initial burst of CO2 from gas in stomach, but then nothing
2. abdo will rise
What happens if you insert ETT too far?
goes into R main bronchus
ventilate only one lung => ventilate only 1 lung
stats start to fall
When extubating, what two things do you have to remember to do first?
1. suction oropharynx
2. deflate cuff
Rapid pulse or high BP while under may indicate 2 things
1. ineffective analgaesia
2. emersion from anaesthesia
Why is temp monitored during long op?
1. detect malignant hyperthermia
2. prevent hypothermia which often happens b/c of cool OT, evaporative heat loss, conduction of heat to cooler instruments that touch the body
--- prevent with body warmers, blankets, warm IV fluids
Aim for U/O?
0.5mL/kg/hr
Most common type of periop eye injury?
corneal abrasion
When an operation is happening in supine position (most common), the arm position should be less than 90 deg; why?
minimise brachial plexus injury from pressure of humerus head in the axilla
What position can you make the theatre bed in case of hypotension?
Trendelenberg
(head down) - increases venous return

Risk = raised ICP

This also decreases lung compliance due to abdo viscera pressure against diaphragm
2 risks of anaesthetic in sitting position
1. venous embolism
2. air embolism
4 contraindications to mechanical devices used for VTE prophylaxis
1. severe peripheral arterial disease
2. recent skin grafts
3. severe peripheral neuropathy
4. severe leg deformity
Duration of VTE prophylaxis:
high risk Pts
10 days
Duration of VTE prophylaxis:
knee replacement
14 days
Duration of VTE prophylaxis:
hip replacement/#
28-35 days
Blood transfusion appropriate when Hb < ____g/L
70
Which blood group is the universal recipient?
AB
Which blood group is the universal donor?
O
Blood group A can receive blood from who?
A
O
Blood group B can receive blood from who?
B
O
Blood group AB can receive blood from who?
A
B
AB
O
Blood group O can receive blood from who?
O
Plt transfusion is required if platelet levels are <______x10^9/L and they are having a procedure with associated blood loss or major blood loss (>500mL expected loss)
50
6 indications for FFP
1. warfarin OD
2. DIC
3. massive transfusion rxn
4. isolated coag def
5. TTP
6. HUS
Define massive blood transfusion
replacement of >1 blood volume (5L) is <24h
OR
>50% blood volume in 4h
5 causes of DIC
1. tissue damage
2. hypoxia
3. acidosis
4. sepsis
5. haemolytic transfusion
4 things that may require massive blood transfusion
1. dilution/consumption (e.g replacement with flids lacking coag factors of plts e.g crystalloids)
2. DIC
3. systemic fibrinolysis: assoc with liver disease in partiuclar (causes rapid lysis of thrombi at surgical sites)
4. platelet dysfn
What do you think of 4-30 days post transfusion, p/w fever, diarrhoea, liver fn abnormalities, pancytopaenia

Which cells are involved
graft vs host disease

T cells
Acute haemolytic blood transfusion rxn:
what causes it
when does it occur
ABO incompatibility ==> intravascular haemolysis
occurs immediately
Febrile non-haemolytic blood transfusion rxn:
what causes it
when does it occur
alloAbs to WBC, plt or other donor plasma Ag + release of cytokines from blood products
within 0-6h
Allergic non-haemolytic blood transfusion rxn:
what causes it
how does it present?
Rx?
alloAbs (IgE) to proteins in donor plasma --> mast cell activation --> histamine

p/w urticaria, sometimes as anaphylaxis with bronchospasm, laryngeal oedema, hypotension (but this is usually with IgA def Pts)

Rx: anti-histamine (diphenhydramine)
Transfusion related acute lung injury (TRALI):
what causes it
when does it occur
how does it present?
binding of donor Abs to WBC of recipient and release of mediators --> incr capillary permeability in lungs
2-4h
p/w acute resp distress, APO
Delayed haemolytic blood transfusion rxn:
what causes it
when?
p/w
alloAbs to minor Ag e.g Rh, kell, duff, kidd (level of Ab at time of transfusion too low to cause haemolysis, then later increases and --> extravascular haemolysis)
5-7d post-infusion
p/w anaemia, mild jaundice
Where is the chemoreceptor triggering zone for vomiting?
base of 4th Ventricle
Which NTs work at the chemoreceptor triggering zone for vomiting (2)
5HT3
D2
MOA: metoclopramide
D2 receptor antagonist
MOA: Ondansetron/Tropisetron
5HT3 receptor antagonist
MOA: prochloroperazine (anti-emetic)
D2 receptor antagonist
What is scopolamine, what is it used for?
anticholinergic agent that blocks binding of ACh => blocks neuronal pathways from vestibular system
acts as an anti-emetic
What is dolasetron?
MOA?
anti-emetic
5HT3 receptor antagonist
Which corticosteroid has an anti-emetic property?
dexamethasone
Which receptors in the CNS do opioids work on?
µ agonist
MOA tramadol
weak µ receptor agonist
+ inhibits reuptake of serotonin and NAd
What is the advantage of using tramadol over opioid?
doesn't --> resp depression or decr GI motility
MOA ketamine
NMDA antagonist
What are 5 differences between morphine and fentanyl?
1. morphine = hydrophilic; fentanyl = lipophilic
2. morphine = delayed onset; fentanyl = rapid onset
3. morphine = longer duration; fentanyl = shorter duration
4. N+V -> higher incidence in morphine
5. pruritis -> higher incidence in morphine
What does morphine O.D do to pupils?
constrict: pinpoint pupils
What can be given in morphine O.D if clinically significant resp or CV depression?
Naloxone
Dose: Fentanyl
30-75mcg IV
Dose: Morphine
2-5mg IV
2.5-10mg S/C
Dose: Oxycodone
2.5-15mg PO q4h
Dose: Ibuprofen
200-400mg PO q8h
Dose: Paracetamol
1g PO q4-6h
max 4g/d
Under normal physiological conditions, how much water is lost?
30-35mL/kg/day
Rule for maintenance fluids
4-2-1:

1st 10kg: 4mL/kg/hr
2nd 10kg: 2mL/kg/hr
Next kg over 20kg: 1mg/kg/hr
What is the difference (in placement) of a spinal vs epidural anaesthetic?
spinal: local injected directly into subarachnoid space

epidural: local diffuse into the subarachnoid space from the epidural spcae
Which layers do you have to get through (in order) before reaching the epidural space (5)
1. skin
2. s/c tissue
3. supraspinous lig
4. interspinous lig
5. ligamentum flavum
How do local anaesthetics work?
blocking conduction of afferent nociceptive impulses
What, other than analgaesia, do you get by using epidural?
motor nerve block
What is the opioid of choice for epidural infusion?
Fentanyl

(best used in combo with local; improves the quality of epidural analgesia compared to local anaesthetic alone)
Which 2 local anaesthetics are most commonly used in an epidural infusion
bupivacaine and ropivacaine

- often in combo w/ fentanyl
____________ _____________ plus ___________ in a patient who has recently had an epidural block represents a medical emergency.
Could indicate an _________________ ______________
What Ix do you do?
Who do you refer to?
back pain
fever

epidural abscess
MRI
neurosurgeon
For a spinal anaesthesia, how do you confirm that the placement is in the subarachnoid space?
free flow of CSF out of the hub of the needle
What can you add to a local anaesthesia to decrease the rate of absorption and therefore prolong the duration of the anaesthetic?
vasoconstrictor; adrenaline
What is the difference between hyperbaric and hypobaric solutions used in local anaesthetics?
hyperbaric: spreads to dependent areas eg. if head is down, the anaesthetic moves up spine; if sitting up, it moves down spine
hypobaric (less commonly used): does opposite and floats up
MOA: local anaesthetics
inhibit sodium channels --> membrane unable to depolarise sufficiently to reach the threshold potential and generation of an AP is prevented
S.Es of local anaesthetic (split into systems)
CNS: numb tongue, peri-oral tingling, metallic taste, tinnitus, visual dysfn, tremors, LOC, seizure, resp depression
CVS: bind to myocardial Na channels --> arrthymia, decr contractility, cardiac arrest
Neurotoxicity: "Transient Neurological Symptoms {TNS}" = hyper/paraesthesias, motor weakness legs/bum - usually resolve w/i 3d
Hypersensitivity/allergy
Ventilatory support (oxygen) indicated if RR > ____
30
Ventilatory support (oxygen) indicated if PaO2 <____kPa on FiO2 > ______
11
0.4
Ventilatory support (oxygen) indicated if PaCO2 high with significant resp distress (e.g pH <______)
5 other indications for O2
7.2

1. exhaustion
2. confusion
3. severe shock
4. severe LVF
5. raised ICP
Type I Respiratory Failure
What is it?
Failure of ____________
Causes:
Rx:
hypoxia (PaO2 < 60mmHg) with normal or low PaCO2
oxygenation
acute diseases of lung (fluid filling of collapse of alveolar units): cardiogenic/noncardiogenic pulmonary oedema, pneumonia, pulmonary haemorrhage
O2 therapy
Type II Respiratory Failure
What is it?
Failure of ____________
Causes:
Rx:
hypoxia AND hypercapnoea (>50mmHg)
ventilation + oxygenation (cost alveolar vent is inversely prop to PCO2)
drug OD, neuromuscular disease, chest wall abno, severe airway disease (eg COPD)
Rx: ventilatory assistance + S' O2
Symptoms of cerebral hypoxia (3)
anxiety
agitation
depression consciousness
What happens to BV during hypoventilation?
dilate
Other than malignant hyperthemia, what is another familial disease that can cause adverse anaesthetic rxns?
atypical cholinesterase (prolonged duration of muscular blockade)
Fasting guidelines: meat, fried or fatty foods, how many hours can they be eaten before surgery?
8
If someone is taking regular opioids (e.g MS contin) for chronic pain, can they keep taking them before the surgery?
Why?
yes
keep dose consistent to prevent withdrawal
At the beginning of a GA, what happens to the eyes and when can you say the Pt is properly unconscious and ready for surgery?
What happens to pupils when ready?
eyes initially are rolling
then become fixed when ready

dilate
What do volatile anaesthetic agents (e.g --fluranes) do to ICP?
raise
What does propofol do to ICP
decrease
Can you use thiopental for maintenance anaesthetic?
no - it accumulates with increased dosing
How long does propofol last for?
4-6mins
Antagonist for Benzos
Flumazenil
Which of the inhalation agents has the most rapid onset?
N.O
In a semi-conscious Pt, is guedel (oropharyngeal) or nasopharyngeal airway better tolerated?
nasopharyngeal
2 contraindications to nasopharyngeal airway
1. c-spine injury
2. base of skull #
At least how many ppl required to do an intubation of a trauma pt with potential C-spine injury?
What does each do?
3:
1. pre-oxygenate + intubate
2. cricoid pressure
3. manual in-line immobilisation of head and neck (counters forces made by moving laryngoscope)
What drug can you give to decrease salivation and bronchial secretions?
Atropine
= muscarinic antagonist
What are the two different sorts of muscle relaxants, how do they work? E.g of each?
DEPOLARISING: Suxamethonium
- mimics ACh and binds to ACh-Rs => prolonged depol.

NON-DEPOLARISING: Rocuronium, Vercuronium
- inhibis postsynaptic ACh Rs => prevent depol.
Is Sux long or short acting?
short (5-10mins)
What effect can sux have on K+?
increase
Some Pts have abnormal or missing plasma cholinesterase therefore have decreased sux metabolism so will be ________________ for longer and need to be ventilated til sux is fully metabolised (what is this called?)
paralysed

sexamethonium apnoea
What drugs are given to reverse neuromuscular blockade?
MOA?
Cholinesterase inhibitors (NEOSTIGMINE)
inhibit enzymatic degrad of ACh => incr ACh at nicotinic and muscarinic Rs which deplace NON-DEPOLARISING muscle relaxants
What does an arterial line measure?
BP
MAP (aim >60)
What sort of monitoring do you need to measure preload?
central venous line
What sort of monitoring do you need to measure afterload?
arterial line
3 locations for central venous cannulation

*Which has highest risk of DVT and bacterial colonisation?
1. internal jugular
2. subclavian
3. femoral (*highest risk)
7 potential complications of central venous cannulation
1. pneumo/haemo/chylothorax
2. venous thrombosis
3. thrombophlebitis
4. infection
5. haemorrhage
6. catheter or guidewire embolisation
7. cardiac arrhythmias
Define Hypothermia
<36 deg
5 adverse effects of hypothermia
1. risk of wound infection (imp immune fn)
2. delayed healing
3. reduced Plt fn and imp activation of coag cascade => incr blood loss
4. incr risk arrhythmia (particularly VT)
5. decr metabolism anaesthetic agents => prolongs post-op recovery
Where in the brainstem are the two centres of vomiting found?
medulla
Mechanism of vomiting
Chemoreceptor trigger detects circulating toxins in blood and CSF and relays stimuli to the Integrative Vomiting Centre which produces the act of emesis
3 ways in which the vomiting centre can be activated
1. nerve impulses from stomach/intestinal tract -> reflexive activation (mechanoreceptors from contraction/dilation, chemoreceptors from chemical stimuli)
2. stimulation from higher brain centres
3. chemoreceptor trigger zone sending impulses (detects toxins)
Which two sorts of surgeries tend to increase post-op N+V?
1. abdo
2. gynae
Which anaesthetic agents (3) increase post-op N+V?
1. inhalational agents (NO>fluranes)
2. opioids
3. neostigmine (large dose)
S.Es ondansetron (3)
1. H/A
2. flushing
3. seizures
Lignocaine, bupivocaine, ropivocaine:
order from time to onset and duration of action
safe dose of each?
1. lignocaine fastest/shortest 5mg/kg
2. bupivocaine 2.5mg/kg
3. ropivocaine lasts longest 3-4mg/kg
Safe dose lignocaine?
max dose w/ adrenaline?
5mg/kg

7mg/kg
Local anaesthetic toxicity: Seizure
What can be given?
diazepam, propofol, thiopental
--> all lower Sz threshold
What is meant by the term "high spinal"?
when spinal anaesthetic drifts up to block thoracic level (T2-T4) => cardiac sympathetic block

(adverse outcome to spinal)
Where is the epidural space?
between the ligamentum flavum and the dura
Nasal prongs:
fixed/variable?
max flow?
max FiO2?
variable
5L/min
40%
Hudson mask:
fixed/variable?
max flow?
max FiO2?
variable
10L/min
55%
Venturi mask:
fixed/variable?
max flow?
max FiO2?
fixed
FiO2 = 24-50% depending on nozzle
Non-rebreather mask:
fixed/variable?
max flow?
max FiO2?
variable
15L/min
70%
Self-inflating Laerdal mask:
fixed/variable?
max flow?
max FiO2?
fixed
15L/min
100%
Define hypoxic hypoxia
decr O2 saturation of Hb
e.g low inspired partial pressure of O2 (high altitude), hypoventilation, V-Q mismatch
Define stagnant hypoxia
blood flow through capillaries is insufficient to supply the tissues e.g poor C.O, vasoconstriction
Define anaemic hypoxia
low [PaO2] due to low [Hb] in blood

e.g bleeding, haemolytic anaemia, iron def, renal failure, BM failure
Histotoxic hypoxia
inability of cells to take up or use O2, despite normal delivery e.g cyanide poisoning
Where does crystalloid soln distribute?

Requires ___:1 replacement
ECF

3:1
(i.e 1L of i/v replacement requires 3L N/S due to distribution into interstitial fluid)
Where does colloid soln distribute?

Requires ___:1 replacement
intravascular volume

1:1
(stays within i/v space)
What are the % breakdown of distribution of body water?
2/3 intracellular
1/3 extracellular
- 3/4 interstitial
- 1/4 intravascular (plasma)
Total body water = ____% of total body weight
60%

(i.e in 70kg person = 42L water)
Starling forces:
Capillary hydrostatic pressure - ______ fluid ___________ capillary
Interstitial hydrostatic pressure - _______ fluid ________ capillary
Plasma colloid osmotic pressure - _________ fluid__________ capillary
Interstitial colloid osmotic pressure - ____________ fluid _________ capillary
Starling forces:
Capillary hydrostatic pressure - pushes fluid out of capillary
Interstitial hydrostatic pressure - pushes fluid into capillary
Plasma colloid osmotic pressure - pulls fluid into capillary
Interstitial colloid osmotic pressure - pulls fluid out of capillary
How does CHF cause oedema? (in terms of starling forces)
increase capillary hydrostatic pressure
How does nephrotic syndrome/liver failure cause oedema? (in terms of starling forces)
decrease plasma proteins
How do toxins/infection/burns cause oedema?
increase capillary permeability
How does lymphatic blockage cause oedema? (in terms of starling forces)
increased interstitial colloid osmotic pressure
ADH secretion is influenced by:
1. receptors in hypothal that are sensitive to increasing plasma osmolarity --> __________ ADH secretion
2. stretch receptors in atria of heart; activated by larger than normal volume of blood returning to heart --> ______________ ADH secretion
3. stretch receptors in aorta and carotid aa; stimulated when BP falls --> ______________ ADH secretion
stimulate
inhibit
stimulate
Low BP --> decreased GFR as lower flow through tubule in kidney => _________________ cells --> renin --> _________ --> stimulates the adrenal cortex to produce _______________ => increase sodium reabsorption --> increase H2O reabsorption => conserve volume and raise BP
juxtaglomerular
angiotensin II
aldosterone
What maintenance electrolytes are required for sodium and potassium?
Na: 3mEq/kg/day
K: 1mEq/kg/day
What % body weight is fluid deficit in mild dehydration (dry mucous membranes, thirsty)
3%
What % body weight is fluid deficit in moderate dehydration (skin turgor decr, sunken eyes, oliguric)
5%
What % body weight is fluid deficit in severe dehydration (tachycardic, hypotensive, mottled skin, cap refill reduced)
10%
How do you estimate blood volume in an adult?
estimated blood vol = weight (kg) x average blood vol

average blood vol:
males = 75mL
females = 65mL
Grade I-IV blood loss
%?
I: <15%
II: 15-30%
III: 30-40%
IV: >40%
Grade IV blood loss
HR?
SBP?
U/O?
LOC?
>120
<90
none lethargic
When giving a blood transfusion, should administer it within ____mins of arrival
30
4 types of shock
1. hypovolaemic
2. septic/anaphylactic
3. cardiogenic
4. neurogenic
Rx hypovolaemic shock
fluid resus
Rx cardiogenic shock
improve cardiac perfusion and CO:
NORADRENALINE
What happens to vascular resistance and cardiac output in neurogenic shock?
resistance decreases
C.O increases
Mgmt anaphylactic shock
1:1000 adrenaline 0.3-0.5mg SC
Antihistamines (diphenhydramine or phenergin)
Salbutamol

if severe:
(in addition to above)
ABCs, may need ETT
Steroids
Crystalloid resus
Major fn of alpha 1 Rs
increase vascular smooth muscle contraction
increase intestinal and bladder sphincter contraction
Major fn of alpha 2 Rs
decrease sympathetic outflow
Major fn of beta 1 Rs
increase HR, increase contractility
Major fn of beta 2 Rs
vasodilation
bronchodilation
increase HR
increase contractility
Which adrenoceptors does adrenaline work on
all alpha and beta
Which adrenoceptors does noradrenaline work on
primarily alpha
Which adrenoceptors does dobutamine work on
mainly beta 1
Which adrenoceptors does dopamine work on
alpha 1, alpha 2, beta 1
Which adrenoceptors does Metaraminol work on
alpha 1, alpha 2, beta 1