Vivas July Flashcards
ideal breathing system
- Simple and safe to use.
- Delivers the intended inspired gas mixture.
- Permits spontaneous, manual and controlled ventilation in all age groups.
- Efficient, requiring low FGF rates.
- Protects the patient from barotrauma.
- Sturdy, compact, portable and lightweight in design.
- Permits the easy removal of waste exhaled gases.
- Ability to conserve heat and moisture.
- Easy to maintain with minimal running costs.
simple safe-o2 in CO2 out, accurate save-cheap system, low flow, efficeint spont strong small baro heat
N20 bottle
For a cylinder that contains liquid and vapour, e.g. nitrous oxide, initially the pressure remains constant as more vapour is produced to replace that which was used. Once all the liquid has been used, the pressure in the cylinder starts to decreases. The temperature in such a cylinder can decrease because of the loss of the latent heat of vaporization leading to the formation of ice on the outside of the cylinder.
test bottle manufacturere
look
bend
pressurise
strip
mark bottle
chemical
test date
test p
tare weight (of empty bottle)
cylinder valve system
yoke (whole) with its pins
bodok washer
valve to turn on and off
PIping system
Cu-non rusting antibacterial
colour and hape matched
flexible hoses
pulltest
risk of fire frome warn hose and connection
cylinder manifold
series of cylinders
As nitrous oxide is only available in cylinders (in contrast to liquid oxygen), its manifold is larger than that of oxygen.
In either group, all the cylinders’ valves are opened. This allows them to empty simultaneously.
- The supply is automatically changed to the secondary group when the primary group is nearly empty. The changeover is achieved through a pressure-sensitive device that detects when the cylinders are nearly empty.
- The changeover activates an electrical signalling system to alert staff to the need to change the cylinders.
VIE
#cu coil #superheater #-160C ie less than -118C crit temp 1000x vol at room temp nil active cooling #LHV
entenox
pseudocritical temp -5C
therefore at -5.1C can be compressed to liquid–>poynting effect
N20 with 20% O2 on bottome with high O2 above
so >10C for 24hours before use, invert and shake, dip to take bottom before becomes hypoxic
only flows when sucked on (2 stage Pressure:demand regulator
renal feedback
macular densar are sensars of Na and release Adenosine
gRanular cells generate Renin
mesangial cells contract
N20 CBF
increased CMRO2
N20 production
NH4NO3–>H20 +N2O with impurities of NO and NO2
N20 SE resp
nil Change in MV despite small decrease in TV
N2O toxicitiy
oxidises the cobalt in B12 which means B12 can’t be a cofactor for methionine synthitase which makes methionine to produce activated folate and DNA
- ->BM suppression–>agranulocytosis
- ->subacute combined degreneration of spinal cord
N20 causing PTx
1) N2 is highly insoluble therefore TRAPPED IN THESE SPACES
2) N20 while insoluble vs other agents is more soluble in blood than N2
3) N20 out of blood into gas filled spaces (down conc gradient) much quicker than N2 exiting that space into blood
N20 lungs
PHTN-increased SNS
apheresis
Apheresis is a medical technology in which the blood of a person is passed through an apparatus that separates out one particular constituent and returns the remainder to the circulation
diasterioisomers
> 1 chiral centre
CO reduced Vd
V1 smaller i believe
t/2=
In2/k
k is rate constant for elimination
isomers definitions
structural=different bonds
stereoisomer=same bonds, different 3D arrangement
strucutural isomers
positional: butane vs isobutane
chain-iso vs enflurane
iso vs enflurane
all agent draw
chloride on diff carbon
similar O:G yet ENFLURANE has higher mac
Iso strong
Flouride stable, impotent increase VP less flammable decreased sol
- halo 3 and old school Br (potent)
- iso/en 5 and CHF2—>CO
- sevo 6 and nil CHF2, has CF3, but compound A
- des 7 and fuck it CHF2 but no compound A
Non polar and small—>high VP
geometric isomer
differ from each other in the arrangement of groups with respect to a double bond, ring, or other rigid structure.
S vs R structure
chiral centre, lowest behind, then flat plane on pace ascending clokwise is Right Rectus vs Serious
high first pass
GTN, morphine, midaz,
prodrug
codeine, clopidogrel
midaz elim
pee out inactive met so CKD no biggy as per oxford
fat
increased alpha1 acid GP
roc offset factors
Rb elderly and femal due to decreased m mass
rememeber Li
Amingoglyco and frusemide–>decreased AcH
aminolgycocyde also CCB
fenytoin speeds up recovery by increasing PrB to alpha 1 A GP and upreg of rec
Rb volatile inhibits NaCHR
clondine PK
99% OBA
50% hep 50% renal elimunchanged
MoA
presynaptic a2 stim–>decreased Nad
B stem–>decreased SNS out
DH–>opiate release and moduclate descening pain
role BBB
core
1) chemical #kenicturus
2) immune # MS
3) ph
4) ion and glucose #manitol not effective in stroke
5) nt #ice abuse
BBB structure
tight junction of endo cells
BM
foot processesses podocytes
enyzmes MAO AchE
Preg cvs
Oestrogen RAAS (all women are tense)
Progesterone ->prostaglandin->vd->improve perfusion
SSx
most common is
- hyperreflexia
- clonus
OHBD shift right
CORE AS FUCK
23dpg is PRODUCED IN hypoxia–>to release O2
23dpg is produced in pregancy
increase–>right shift (release O2)
23DPG is produced in alternative pathway for one of the steps of glycolysis (less efficient-consumes 1ATP inseatd of producing it)
decreased glycolysis in storage–>decreased 23DPG
deadspace preg
The lack of gradient is attributed to the reduction in alveolar dead space (increased blood perfusion from an increase in maternal CO).
preg resp
Cx 3
1) mech
2) humeral
3) MRO2 60%
Consumption Drive-progesterone Airway #BD due to progesterone Compliance and work Vol FRC decreased 20% #IC mild increase in preg VQ-shunt, DECREASED DS OHDC measurement
fetal maternal CO2 levels
arterial gap of 15 venous gap of 5 essentially mum takes 5 off baby mum artery 37 (MEMORABLE alkalotic)-->42 fetal arter 52 (memorable acidodic)-->47
REMEMBER MOTHER IS ON BOTTOM (more O2)
haldane effect wiki
deoxyHB binds H+
shift H2CO3 eqn to right with more CO2 soaked up
bohr wiki
H+ stabilizes Hb in Tense state–>release O2
essentially higher CO2–>more H+–>bump O2 off Hb
CVS changes in preg
core
1) humeral
2) mech
3) MRO2
HR.SV.SVR
plus clotting and albumin and HCT
plus regional
plus transport OHDC
Hysteresis
1) surfactant -on expiration as volume decreases surfactant more concentrated to remaining volume—>reduced surface tension—>remains open for longer (less compliant)
2) visicoelastic properties
3) recruitement
4) dynamic compliance effected by airway resistance
deadspace effects
decreased AV
-increased CO2, decreased O2
hypoxia easily reversible with Fio2 vs if shunt a cause.
resistance airway generation
moderate, high, +++low
17 division conductive including terminal bronchioles
17-23 respiratory including respiratory brioles
alv ventilation/min
5000ml/min =5L of BF=VQ=1
CO2 vs AV eqn CORE AF
PACO2=CO2 prod/AV.k
DS eqn
CORE AF
expired Co2 in douglas bag diluted
cardiac arrest
PACO2-PECO2/PACo2
Shunt eqn
CORE AF
Content o2 not Partial pressure
ContentAlv o2-Content arterial/(Content Alv-mixed venous)
Diffusion capacity measurement
Flow=P.Diffusioncapictyoflung
Diffusion cap=P/flow
measure the uptake of something that is diffusion not perfusion limited ie CO
D of CO=sol/MW.A.P/T
CO uptake=diffusion capacity.Palv
PAlv=CO uptake/diffusion capacity of lung
SINGLE BREATH METHOD
measure insp with IR
hold for 10s then measure exp with IR
increases with exercise due to recruitment–>increased area
diffusion limitation axis
Partial pressure not diffusion %
things that are sol or sucked up by Hb–>dont build up an opposing partial P and keep sucking more and more in.
O2 flux eqn
flux is delivery!!!!!
Hb per L is 120
sol per L= 0.03
Hb per 100ml is 12
sol per 100ml is 0.003
diffusion limitation 2 components
diffusion to RBC
O2 and CO2 reaction in RBC
both contribute 50%
diffusion capacity error
VQ mm will fuck with things yet not a diffusion problem
Fick principle
Uptake=Qt(CaO2-CvO2)
measure PBF
fick prinicple uptake measure by measuring conc of expired O2
or indicator dillution method
why shunt cant be compensated
well oxygenated alveoli even with +++PAO2 can’t carry much more O2 due to Hb maxed out #plateu of OHDC
asthma
airway obstruction–>shunt–>hyperventilate–>decreased PaCO2–>EXHAUSTED–>increased PaCO2
BC–>autopeep
copd
shunt+deadspace–>hypoxia and HYPERCAPNIA
treat with PEEP to reduce shunt
hufners constant
each GRAM of Hb takes 1.34 ml of O2
OHDC figures
100: 100
90: 60
p50: 28
75: 40 venous
Myoglobin 50point is 2.8mmHg
teach
central venous vs mixed venous
yes confirmed
central is from atria normal is 70-80%
mixed venous is from Pulm artery
Central is RA
Mixed is pulmonary arter
Coronary sinus drains into RV so mixed is more hypoxic
myocardial oxygen consumption (given that the source of the discrepancy is probably blood washing out of the coronary sinus
can derive
- OER to guide diag and Mx
- CO from ficks prinicple
- shunt eqn
respiratory compliance curve
recoil P on x axis
wheatstone bridge
galvinometer
aorta vs radius
Aortic incisura
Radius diastolic hump
glucose handling graph
glucose flux vs plasma glucose (x)
Warfarin met
Cyp450 CYP3A4
Met induced by STP And carbemazepine
Met inhibited by amiodarone and cimetidine
Warfarin reversal
Remember prothonvinex
Hb BD
haem +globin
haem–>fe and biliverdin–>bilirubin
bili–>urobilinogen–>stercobilin
Conj vs uncong
uncong=prehepatic or hepatic eg cirrhosis
conj=hepatocellular or post hepatic
if any bili in urine=hyperconj
tryptase
1,4,24 peaks, dropping, baseline. baseline will factor into interp
anaphylaxis
Hist leukotreine-chemotractic-->delayed effect PG bradykinin TNFa 5HT NO Tryptase-->activate comp system, coag-->thombus and DIC
serum vs plasma
serum is what is left after blood has clotted ie plasma without coag factors
role of plasma proteints
clings to... water pH drugs cations clots invaders enzyme function energy reserve
reticulocytes
new production of RBC
still have RNA fracgments
dibucaine number
is an amide LA that inhibits Butylcholinesterase
% of butylcholinesterase uneefected after challenge gives number
normal is 80%
genetic dx–>only 20% remain
%effective butylcholinesterase effective
Esterases #amanda diaz
hydrolyse esteres (BD by reaction with H2O)
non spec-remi and emsolol and atrac and cisatrac
butylesterease sux and miv and ester LA cocaine and heroine
achetylcholinesterase-Ach
RBC esterases esmolol and remi (small for remi)
hoffman
spont degen in pH and temp
cleave of quarternary nitrogen link to central chain
local anaesthetic structure function
GOLD
COO is ester
NHCO is amide #amine
aromatic lipophilic group
hydrophilic group
Mepivacaine, bupivacaine, and ropivacaine are characterized as pipecoloxylidides (see Fig. 10-2). Mepivacaine has a methyl group on the piperidine nitrogen atom (amine end) of the molecule. Addition of a butyl group to the piperidine nitrogen of mepivacaine results in bupivacaine, which is 35 times more lipid soluble and has a potency and duration of action 3 to 4 times that of mepivacaine. Ropivacaine structurally resembles bupivacaine and mepivacaine, with a propyl group on the piperidine nitrogen atom of the molecule.
changing length and C attachments–>changed lipid sol DoA metabolism etc
piperadine nitrogen:
1) Methyl->4)butl–>bupivocaine ++lipid sol and doa
Butyl–>3)propyl–>ropivocaine
methyl ethyl propoyl butyl
LA pH
Local anesthetics are poorly soluble in water and therefore are marketed most often as water-soluble hydrochloride salts. These hydrochloride salt solutions are acidic (pH 6), contributing to the stability of the local anesthetic. An acidic pH is also important if epinephrine is present in the local anesthetic solution, because this catecholamine is unstable at an alkaline pH.
remifentanil vs fent potency
can simplistically be thought of as equipotent
classically remi called 2x more potent
pethidine
high sol low potency renal and fetal accum with active metabolite reacts with MAOi
action and SE antichol and SSRI and morphine
not reversed with naloxone
methadone
C-full opioid agonist, NMDA antag, SSRI
U-pain addition good for neuropathic pain
P-PO
A-opiate and NMDA
D-1/4 morphine (more potent)
O-relatively fast 2.5hrs (lipid sol) offset long due to large Vd
R-PO/IV
S
- less sedation, euphoria, addiction
- Qt prolongation in high dose
D -PrB 90% highly lipid sol A -good OBA 75% due to low first pass met M -hep met (has large reserve) with inactive met E inactive peed out T/2 24 hours
Low cost
Individual unpredictable PK and PD so slow titration
naloxone naltrexone
naloxone crosses BBB, low OBA and fast and short effect–>IV reversal (yet also with targin as low OBA means it stops GI Sx without blocking neuro Sx)
Naltrexone
-good OBA nil BBB crossing
Opiate classification
Endogenous -encephalin, endorphine Natural -morphine -codeine -thebaine Semi syth -codiene changed to oxycodone -morphine changed to heroine Synthetic -phenylpiperidine -morphine deriv -thebaine change-->naloxone and naltrexone
lafent offset
small Vd due to less lipid sol–>more rapid elimination despite less clearance
opiate change
incomplete cross tolerance
fent CSHT
better than alfent until2 hr infusion
quantal vs
graded
opiate rec
NOP is supraspinal
Cortex, Thal, BG, PAG, Resp centre, SC, periph
white vs grey matter
white is fat so middle of brain and outter tracts of SC
ANS
sympathetic spinal colum grey matter and peripheral ganglio
PSNS
CN nuclei
Sacral Rami
content O2 of blood Normal
200ml/L
bohr reason
H stab
Hb binding
ttttttoo boooooohring
Hamburger effect RV RV RV GOLDEN
venous blood lower Cl vs arterial.
CO2 into RBC–>HCO3–>swapped from Chloride
Effect: mittigation of acidity in venous
increased CO2 carry cap in venous
increased offloading of O2 as Cl causes T state stabilization #allosteric change
henderson
ph=pka +log HCO/CO2x0.003
pka+log A-/HA
HCO3 in resp acidosis
INCREASES in acute and chronic 3x more in chronic
Predicted CO2
HCO3x1.5+8
Bicarb types
standard with real CO2
actual if CO2 normal
BE if real CO2
BExxx if normal Hb
NAG
10-16
CATMUDPILES
Cyanide, CO, aminoglycosides
measure osmolarity
2xNa +urea+glucose
Blood gas interp steps
met or resp or mixed
HAG or NAG
osmol gap
delta gap for HAG+other
HAG NAG renal
RTA is HCO3 loss hence NAG
ureamia is HAG
La Place
CORE
P=2T/r
surfactant and hysteresis
collapsing–>surfactant pressed together–>resist further collapse
Resp compliance
1/RC=1/L+1/Thoracic cage =1/100
surfactant
Prevention of fluid transudation. As the surface
tension forces are generally reduced by surfactant,
less interstitial fluid is sucked into the alveolus.
dynamic airway compression relevance
more apparent in lung Dx to restrict exp flow rate due to loss of lung elastic recoil and radial traction.
equal pressure point moves deeper into lungs on exp as airways get smaller in collapsing lung
determined by AlvP-Pleural pressure not mouth pressure
spiro dx
FEV1 decrease to GREATER EXTENT in COPD
FEV1 decreased to LESSER extent
west says in both FRC is decreased
i believe can be increased hence barrel chest copd
RR and TV and WoB in Dx
trap=elastic
curve=frictional (80% airway and 20% tissue)
in PF elastic work big and frictional work low so breath small TV with high RR
in COPD elastic work reduced and airway res increased–>take big breathes and low RR
static compliance
oeophageal pressure measure
adding to alpha cardbon
BLOCKS MAO
classification of sympathomimetics
evernote gold
COMT mech
add a methyl group
MAO
oxidative deamination ie uses O2 to cleave amine
Sotalol
add salt to everything class I,II, III
low lipid bblocker
poor ab but minimal first pass met–>good OBA and long halflife as minimal met
adenosine
C-nat purine nucleoside U-SVT reentry and diag P 3mg/ml clear A- 1)adenonsine sense K ch open -->hyperpol 2) inhibit cAMP excitation in ventricles 3)infusion-->drop SVR D O 10-20s doA S -CI in 2nd or 3rd degree heart block or SSSx -can cx VF/VT as brady increases excitabiliy -can Cx AF of Aflutter as decreased atrial refractory period -can cx brady requiring pacing Met-RBC and vasc endo to AMP no dose change in renal or hep
why ohms law imperfect for lungs
elastic, non lamina, non-newtonian fluid
F=P/R yet increase increase P–>decreased resistance
admix
“venous admixture is the amount of mixed venous blood
required to mix with pulmonary capillary blood
to produce the observed alveolar–arterial Po2 difference.” (includes true shunt AND VQ scatter)
mixed venous blood is the venous blood drained from bronchi (via bronchial veins) and LV (via thesbian veins) to LA AND VQ SCATTER AND CARDIAC DEFECT R–>LSHUNT
Sources of venous admixture include:
“True” intrapulmonary shunt, blood which passes through lung regions where V/Q = 0
V/Q scatter, blood which passes through lung regions where V/Q < 1.0
Thebesian veins, which contribute myocardial venous blood with low oxygen content
Bronchial veins, which drain the bronchial walls
Intracardiac right-to-left shunts
Normal shunt fraction in healthy adults is 4-10%
!!!!SO TRUE SHUNT IS ZERO OXYGENATION
yet decreased VQ contributes to admix!!!!
shunt
Shunt is the blood which enters the systemic arterial circulation without participating in gas exchange
anatomical shunt CORE
just 2! P+K and derranged phys
thesbian which go to coronary sinus –>LA
bronchial Veins–>LA
OLV CPAP
if blood going through may as well try add some O2 to it.
Pulm HTN Mx
1) O2
2) NO donor (sodium nitropruside or GTN)
3) CCB
4) PDEi
- PDE3i cGMP inhibited BD Silden
- PDE35i CAMP inhibited BD milrinone
5) Prostaglandins–>VD
silden
milrinone
S=5
M=3
visually looks that way
3->cAMP–>contractility
peripheral chemo rec
CO2 and O2 CB and AoA
pH only in CB
rotem
GOLD
clotting–>fibrin blocks–>platelet strength
CT–>CFT–>MCF–>plasmin
vasopressin
VwF
hypoplasmin
leukaemia, thrombolysis, bradykinin, ESLD due to impaired clearance of plasminogen activator
Trauma, DIC, thombolytic therapy, placenta acreta–>plasminogen activator from placeta–>lots of lysis
resp centre
CORE
Medullar resp centre
Di
Ve
Be
pons
- pneumotaxic-taxes slow
- apneustic centre-aps speed up efficientcy
HYperbaric Rx
CO poisoning
decompression
gas gangreen
pendeluf and RR
worse with high RR as need prolonged exp oause to balance
daltons law clinic sig
P=P1 +p2
so at everest less PP of O2
avagadros law
at equal temp, vol and pressure different gases contain the same number of molecules
dilution of O2 in trachea–>decreased PP of O2
henry’s law
conc proportional to pressure of gas in a liquid.
gibbs donnan
KPr intracell KCL out
CL comes in K comes in water comes in
osmotic p
the pressure that would have to be applied to a pure solvent to prevent it from passing into a given solution by osmosis,
oncotic
osmotic p exerted by colloids ie protein
albumin tonicity and effect
I agree albumin 20% (and 4%) are hypotonic and hyposmolar which as a fluid would mean they wouldn’t effectively expand much volume.
But
1) albumin remains much more intravascular without spreading interestitial fluid as fast as IVF
2) album 20% is 200g/l vs 45g/l in healthy patient, 4% is 40g/l so if giving it to someone will low albumin then it will increase the oncotic pressure despite the decreased osmotic pressure (colloid + electrolyte contribution). This will mean the starling forces (defined by oncotic pressures not osmotic) will pull fluid into blood and prevent peeing out at kidney
3) Gibbs donnan effect–>albumin pulls more water into IV space that would be expected
albumin 20% tonicity
Alb 130mmol/L Na 130mmol –>260mmol–>hypotonic
normal plasma osmolarity
280mols/L
TWB splitts
60% TBW
1/3 EC
1/4 IV
5% of weight is plasma vol =3.5L then add cells
Stewart theory
!!!!Strong, weak nonvolatile, weak volatile!!!!
Stewart theory from Melbourne course
H+/HCO3 are dependant on 3 variables
1. SID #electrical neutrality
1. Na + K-Cl =42
2. Other Strong ions Ca Mg, lactate, ketones,
3. Weak ion HCO3, Albumin
2. Weak inorganic acids
1. Alb
1. IVF—>dilute albumin (an acid)—>increased HCO3
2. (Note in SID decreased Alb—>increased HCO3
2. Phosphate
3. CO2
benefit Acknowledges - hydration status effects -Albumin conc effects -identifies SID as MOST IMPORTANT FACTOR
G+S+Xmatch
- ABO (what Antigens are present on RBC)
- Forward test
- Recipient RBC vs control
- Backward test (confirm forward)
- Recipient plasma vs control RBC
- Forward test
- Screen for non ABO antigens (these are not on RBC! So patients serum is tested for antigens!!!!!)
- Recipient plasma vs control RBC
- Xmatch (Will the recipient reject this offering)
- Is screen and Hx negative for ABs then 2 options
- Algorithm based on data—>choice
- Immediate saline spin (check screen really right with real donor sample)
- Recipient plasma vs donor RBC
- Screen positive or sig hx
- Indirecirect Antiglobulin test (IDAT) to see if ABO and other antigens present
- Incubation of recipient plasma and donor RBC
- Wash this combo to remove any plasma Ig not bound to RBC (this would react with the anti-human immunoglobulin about to be added
- Glutination-add anti-human-IG to bind the Ig that is bound to antigens—>little clumps—>positive result (bad thing: means recipient has antibodies against donor RBC that then clump when bound by antihuman Ig)
- Indirecirect Antiglobulin test (IDAT) to see if ABO and other antigens present
- Is screen and Hx negative for ABs then 2 options
immunoglob
Role of immunoglobulins
- Labelled for NK to destroy
- Labelled for phagocytosis #opsinization of viruses
- Compliment activation
- Bound to Bcell wall—>make a befell an Antigen presenting cell
Immunoglobulins tip is variable so specific to antigens
immune system pneumonic
Innate PGN Cs
Addaptive immune BAT
complement cascade
Complement
- proinflamatory proteins activated by classic: Ig:Antigen or alternative or proteolytic enzymes—>inflammation, lysis
- reaction in ABO incompatability
- inhibited by C1 esterase
collegiate
increase BP, osmotic P
decreased freezing point and SVP
actual and standard HCO3
pCO2 – Measured directly
Actual HCO3 – Measures pH and pCO2 from blood sample and then
calculates HCO3 from the H‐H Equation
Standard HCO3 – Calculated parameter when the blood sample is
equilibrated with a gas mixture with PCO2 level of 40mmHg – attempt
to represent the True metabolic component in patients with dual Acid –
Base AbN.
BE and standard base excess
Hb 50 (anaemic–>standardized)
Mannitol
RV adme and PD
Des PD
Decreased TV Increased RR
Nil neg into more VD more hypotensive more tachy
Frusemide
Pulm and systemic VD
Cl channel block can’t conc medulla
SNP met
OHb–>met–>cyanomet
Rhodanase adds sulfur group
B12–>cyanocobalamine
Bicobolt chelates
Heparin
mucopoly
ACS
REVERSIBLE BINDING TO
ATIII
9,10,11,12,13
PL
8000 SC TDS/BD
T/2 1.5hrs
bleeds, HITS, osteoporosis, ald inhib
Vd 100ml/L Ab same SC M hep and liver and ER system-->de polymerated -slowed in hypothermia E-renal fine
target APTT 2x normal
HITTS RX
direct thrombin inhibitor
4Ts
timing 5-10days
oTher Cx
thombosis
thrombocytopenia
CYP450 types
3A4 midaz warfarin, clopid
2D6 tramadol
Naturalf freq stiffness eleasticity
on top
damping effect
yes does decreased freq a little and increase freq response window (ie the range of frequency of before resonance occurs)
damping anzca text
- To determine the optimum damping of the system, a square wave test (fast flush test) is used ( Fig. 11.9 ). The system is flushed by applying a pressure of 300 mmHg (compress and release the flush button or pull the lever located near the transducer). This results in a square waveform, followed by oscillations:
a. in an optimally damped system, there will be two or three oscillations before settling to zero
b. an overdamped system settles to zero without any oscillations
c. an underdamped system oscillates for more than three to four cycles before settling to zero.
resonant freq
The lowest resonant frequency of a vibrating object is called its fundamental frequency. Most vibrating objects have more than one resonant frequency and those used in musical instruments typically vibrate at harmonics of the fundamental.
Resonant Frequency is the Oscillation of a system at its natural or unforced resonance.
damping coeff
reflection of freq response of system
actual damping/critical damping
zero damping=o
optimal damping=0.64
critical damping =the point at which there is just no overshhoot =1
overdampe=no overshoot and takes more time than critical damping to get there >1
HM
HM6G is INACTIVE but neuroexcitatory and accum in renal
more lipid sol vs moprhine–>faster onset vs morph
smaller Vd vs fent–>longer DoA vs fent
Morphine met
CYP450 demethylation and glucornidation
M3G–>neuroexcitatory
M6G–>13x more potent
octenol:water coeff
morph=1
fent=600
oxcodone met
noroxycodone inactive
and oxymorpphone–>WEAKLY active
3A4 → inactive
noroxycodone
2D6 → active
oxymorphone
Naloxone is an “Nalkyl derivative of
oxymorphone”
buprenorphine
partial ag
slow dissocaition from rec–>long action and unpredictable reversal and low dependancy
-resp dep not completely reversed by naloxone
biliary excretion
25x potency of morphine
SL BA=50%
PO is well ab but high FPM
Vd 4l?kg
CYP450–>bile
severe resp dep with high midaz
elim T/2 5hrs
Mannitol
decreased CSF produ
cross glom and not reab–>wash out medulla–>no reab
nil met
small Vd
HTN transiently
target osmol 300-320
hypokalaemia
Hypertonic saline
ICP rhabdo preserve renal function start diuresis in renal transplant bowel prep glaucoma
titrate to target Na 155 benefit nil osmolar testing cheap available antioxidant less likely to cause hypovolaemia 10min on for 1 hr
Disad hypernatraemia hyperchlo acid hypokalaemia central pontine demiolosis renal failure phlebitis, necrosis hypervolaemia seizure encephalopathy rebound raised ICP
porphyrin
porphyrin ring of Hb
precurser of Hb
req p450 to change forms
genetic or acquired dysrufption–>accum–>toxic
skin and nervous system
- tachy, HTN
- fever
- confusion
- seizure, paralysis
- death
- abdo, chest pain,
- blisters
parietal cell stim and inhibition
Highly specialised
Mitochondria ++
Proton pump (apical H+/K+-ATPase) moves H out of cell againstsignificant gradient
3 agonists:
Gastrin
ACh
Histamine
Inhibited by: Somatostatin B-adrenergic activity High acidity PGE2
filling ratio N2O
0.75 or 0.66 in tropics
yoke pins etc
yoke is the outside c grip with pins as 1 componenet and fresh gas flow outlet
washer
valve is part of cylinder
Heat vs temp
Heat is potential and kinetic energy that is transferred from a substance of higher temp to lower temp.
J or Cal
Temperature is not energy but a measure of the hotness or coldness of a substance (measure of average kinetic energy of a single particle in a system per degree of freedom)
K or C
heat can be added to increased the temp OR change the state.
SHC
The amount of heat energy required to increase one Kg of a substance by one Degree Centigrade/Kelvin
Renal BF reg
Autoreg
SNS Renin ATII ANP PGs
Tubulorglomerular balance
glucose
increased oncotic P in pertubular cap–>increased reab
oliguria mech
osmorec HP baro LP baro renal Baro renal autoreg
cardiovascular centre
HTN–>…
NTS stims Nambig stims PSNS
NTS inhibits RVLM hence decreased SNS
how is medulla gradient created
LoH
ACSENDING pulls NaCL into interstium (reab) H20 impermeable.
DESCENDING pulls allows H20 to be pulled out by NaCl
300 osmole–>400 in desc and 200 in ascending
play over until 1400 in loop pin
Vasa recta
water out as descending replaced as ascending
potassium Ch blocker antiarrhythmic
rb sotalol
digoxin tox
phenytoin
SVT and VT options
amiod, flacainide, sotalol
sotalol
class 1,2,3
Rx VT
prevent SVT
adensoisne rec
Where are the adenosine receptors?
A1: Gi, in SA/AV node, cause decrease in HR.
A2A: Gs, coronary arteries (vasodilatation)
A2B: Gs, bronchiole smooth muscle (bronchospasm)
A3: Gi, cardioprotective in ischaemia, inhibits neutrophils degranulation
Cardiac SE adenonsine
decreased atrial refractory–>AF or flutter
adenosine met
plasma and RBC esterase
digoxin
25% PrB-->large Vd minimal hep met largely excreted unchanged in urine narrow TI level 1-2mcg/L OBA 70%
increase Ach releaseat M rec
ECG
- PR prologn
- ST dep reverse tick
- t wave flatterening
- Short Q T
anorexia,N/V/D
Rx digoxin tox
ABC electrolytes brady Rx Phenytoin Dig ABs if >20mcg/L 2 weeks to steady state post PO half line alph 1 day beta 3 weeks
Ester vs amide structure
COOR
vs
NHCO
nerve block onset types
B>Ad>Ab>C
ANS>sens>motor
neuro tox common LA
CIRCUMORAL TINGLING
thiopentone vial
500mg in 20ml
25mg/ml
NaCO3 NOT HCO3
thio vs prop CVS
Sodium thiopental generally produces less hypotension than an equivalent dose of propofol when used for induction of anaesthesia. This is partly because both drugs decrease systemic vascular resistance, but thiopentone (as opposed to propofol) tends to preserve the reflex tachycardia seen in states of acute hypotension, which can restore cardiac output.
Adx
Htn brady–>pulmonary oedema seizure
Nil betablcoeker
Muscle relaxants class SE
Aminosteroids anaphylaxis
Benzylisoquinoliniums histamine release
Hoffman
Cleave nh4 from central structure
Laudenosine
Temp and oh dep
Butylecholinesterase prod
Liver
Leg block monitor
Post tibial nerve
Plantaflexion of big toe
Onset muscle
See Evernote
FRC as o2 buffer
constant o2 supply. stops swing of insp O2 with none on exp
full body plethysomgraphy
V1.P1=(V1-changeV).P2 of box
V2.P3=(V2+changeV).P4 of lung
gauge pressure =alv pressure when zero flow
estimate pao2 by age
100-a/3
po2 tissue
5
mitochondria 1
Hep BF and volatiles
It is generally accepted that all the inhalational anesthetics alter hepatic blood flow and oxygenation that may lead to changes in hepatocellular functions [22-24]. The decrease in total hepatic blood flow (THBF) is primarily because of decreased cardiac output and imposes various compromising effects on hepatic oxygen supply [22]. Sevoflurane, like isoflurane, preserved THBF at up to 1 MAC, but THBF was reduced in tandem with increased MAC [23]. However, desflurane is shown to better preserve THBF than halothane or isoflurane in animal studies
hepatic unit
acina
central hepatic venules
peripheral bile duct, heaptic arterioles and portal venules
- portal triad
- ->sinusoids
3 zones
1) periportal-high O2 protein synth
2) mediolobular
3) Centrilobular-CYP450 low O2.
hepatic failure first effected
synthetic function
enzyme function ++late
coags made by liver
fibringoen, ATIII, prothrombin,2,7,9,10
osmolarit of blood and NACL
tonicity of NACL
290 vs 308 (close enough)
blood is not a perfect fluid so NaCL doesn’t completely dissociate so 308 x osmotic coef of 0.93=286
tonicity define
effective osmotic pressure
normal osmolar gap
10 due to normal unmeasured osmoles
osmolar gap cx
mannitol, ethanol, methanol
colligiate properties
osmotic pressure, depressed freezing point
solute vs solvent
U—>V
how to measure (not calc) osmolarity
osmometer: HP vs osmotic
vapour pressure depression
FP depression with platue pressure using thermister
pendulum chest
Seen in flail chest when several ribs are fractured at multiple sites so that a portion of the
Chest wall moves independently
• The negative intrathoracic pressure during inspiration causes the fractured ribs to be
sucked in, thereby preventing expansion of the lung and during expiration, this segment
moves outwards.
• When the injury is unilateral, air from the affected lung passes into the opposite healthy
lung during inspiration and air moves back from the normal lung into the affected lung
during expiration = “Pendulum breathing”.
why PTx resolves
O2 absorbed down conc gradient
N2 absorbed down conc gradient
- 593 in atm
- 573 in blood as alv air is humidifed and then equillibrates with blood
second gas effect as O2 absorption–>conc further
slow vs fast twitch
slow is Type I
RAP normal
0-5
fluid bolus starling curve
increased RAP and MSFP
cefazolin allergy or MRSA Abx
clina/ticoplanin
vanc for MRSA
GI absorption
mor lipid sol–>more absorption
Most drugs are weak organic acids or bases, existing in un-ionized and ionized forms in an aqueous environment. The un-ionized form is usually lipid soluble (lipophilic) and diffuses readily across cell membranes. The ionized form has low lipid solubility (but high water solubility—ie, hydrophilic) and high electrical resistance and thus cannot penetrate cell membranes easily.
bacterial wall
g+ve thick PG wall (peptidoglycan)
g ive thin PG wall with lipopolyysacharide layer
ABx moa anaesthetics
evernote
all renal clearance except metronidazole which has an active met–>renal Cl
contamination class and ABx
clean elective (nil ABx)
clean contam emergency anything or elective hernia
contam NONPURULENT penetrating <4
dirty PURULENT penetrating >4. or bowel p
give <24 hours
nerve block
Supraclav: commet with subclavian artery
interscalene: between scalenes
infraclavicular: surrounds axillary artery cephalad
axillary: surrounds axillar
metabolic alkalosis
https://litfl.com/metabolic-alkalosis/
H loss
1) GI
2) renal
- diuretics
HCO3 gain
-Antacid HCO3 iatrogenic
So easy to piss away HCO3 so something has to maintain the HCO3 reab issue
1) low Cl
-diuretics
-HCL vomit
2) dehyd
aldosterone–>reab Na. nut not as much chloride saved.
3) low K due to high minercorticoids
–>minerocorticoids–>aldosterone–>reab Na and spit out K and H+
Sx resp -cling to O2 -resp comp-->hypovent impaired contractility decreased CBF confusion, obtunded
LA tox
circum oral tingling and numbness tinitus vertigo NOT TASTE or VISION EXCITABLE TWITCHING seziure coma
HTN tachy
VD prolonged QRS and PR and brady
semiopen
mapelson
T extended freq disabled A for efficeincy Bain for BRAIN MRI
closed benefit and loss
slow onset
warm
how does afterload affect contractility
The increased afterload causes an increased end-systolic volume. This increases the sarcomere stretch. That leads to an increase in the force of contraction.
withdraw reflex
afferent–>several interneuron–>alpha motor neuron
–>flexor stim extensor relax.
- interneurons from pathway that cross the spinal cord can stimulate the extensor motor neurons on the opposite side of the body to produce the cross-extensor reflex
SNS cell bodies and structure
lateral grey col (since cell body has no myelin)
and in peripheral ganglion
preganglionic is myelinated yes–>NaCHR
paravertebral ganglia
exit from grey collum (unmyelin)–>white rami COMMUNICANS
–>synapse with paravertebral ganglion OR
–>up or down to other paravertebral ganglia # cervical sympathetic ganglia OR
–>skip and create more distal ganglia
So… blocking on white rami communicante–>effects at multiple levels
ANS structure
SNS and PSNS
- efferent: visceral and somatic
- afferent (just visceral): organ sens, reflex loop, refered pain
A delta vs C fibre lamin
A delta lamina 1,5 #15As rugby team pain
C is lamina 1 2 3
as per ANZCA talk and a model answer
pain fibre rec modulation
evernote pain pathway goldne
once NMDA stim
cations in
changed gene transcription
activate kinases
central sensitization
peripheral sensitation
at nociceptor
central is at DH and brain
central sens
1) wind up
- increased no of action potentials per noxious stim
2) Long term potentiation
- C fibres activated to transmit pain
3) altered gene transcription
- persistant neural inflam
4) abnormal connection between cells in DH
spinoreticular tract
spine to reticular formation then thalamus and hypothal–>emotion
neuropathic pain mech
dysfunction of nervous system
1) changed NaCH–>spont depol
2) changed K –>less breaks
3) changed Ca –>more NT
due to changed gene transciption and phsphorylation of ion ch
paracetamol meta
phase I (cyp450)–>NAPQI–>neutralized by glutathione (replenished by NAC)
phase II (simultneous) non toxic
NSAID in IHD risk
both selective and nonselective CI
paracoxib benefit
less asthma
less PLi (PL is cox1)
less GI
pain Mx options
- Simple
- Opiate
- Neuropathic #ducktape
- Duloxetine
- Clonidine
- Ketamine
- Tramadol/talent
- Amitriptyline
- Pregabalin
- Adduvent ie psych immobilize enviro
- Regional
decrease ascedending -nsaid, paracetamol -opiate -LA NaCH -gabapentinoids CCB -ketamine -clonidine -regional increased descending -SNRIs -tramadol
gabapentinoids soa and SE
VGCCB at DH
Gabapentinoids prevent VGCC getting to presynaptic membrane in dorsal horn. inhibit alpha2delta subunit (the tugboat that pulls VGCC to membrane)
drowsy and fat
Other SoA
-NMDA rec antag #neuropathic
Gabapentin vs pregabalin
Gabapentin
A -active uptake, changes with dose–>unreliable
-non linear dose response curve
M-neither is metabolised!!!!!!
E -elimination zero order for gabapentin at high doses
tramadol met path
o desmethyltramadol–>opioid rec
CYP2d6 (genetic variability)
ketamine routes
Rb oral 40min
nasal 15min
clonidine vs dex
DH and locus ceruleus and SNS peripheral nerves and reticular n. GiPCR–>changed Na and K ch conductance
dex is full agonist (higher ceiling vs clonidine)
peak at 10min similar
t/2 2 vs 15hrs hence doa 1 vs 6 hrs
severe brady
hi Pr Bound
no renal clearance ok in CKD!
decrease in hep failure
pain pathway
Tissue damage/Nociception/Pain Experience
Buprenorphine
C: partial Mu agonis. Kappa antag. 25xpotency vs morphine hence 200-400microg SL dose (OBA 70%)
U: acute with poor oral, chronic, opiate replacement/wean
P: SL, patch, iv
A:
D
Onset: peak after IV is 80min: due to slow distribution to effect site and other sites
Give doses Q8H for pain IV or SL
Offset: terminal elim 24 hrs, elimination half life 5 hours due to high affinity to rec. binds and doesn’t let go
R
S
-less resp dec as kappa blocked
-less euphoria ?as slow?
-less tolerance And depressiondependance as slow on and off
-antagonise full
-unpredictbale reversal with naloxone
E
T
D-large 3.2L/kg due to high PrB
A-good ab but large first pass met hence SL not PO
M-liver phase I and II—>bile
E-70% in bile with some renal
Elim T/2 is 5 hours
No dosage adjustment is required in patients with renal impairment or mild to moderate hepatic impairment. Patients with severe hepatic impairment may accumulate buprenorphine and Bupredermal patch should be used with caution, if at all, in such patients. (MIMS)
fentanly clearance and effect site term
10% renal excretion unchanged 90% is inactive met
clearance rate and Vd is similar to morphine
t/2Keo 4.5 min vs 4.5 hrs morphine
codeine met
15%–>morphine hence give 6xdose
Poor -2 shitty allells Intermediate -1 shitty allel Extensive (normal -2 normal Ultrameta -multiple repeats of funcitoning allel
aftricans–>ultrafast
poor white man–>poor
nociception
def
substantia geletanosa
The apex of the posterior grey column, one of the three grey columns of the spinal cord, is capped by a V-shaped or crescentic mass of translucent, gelatinous neuroglia, termed the substantia gelatinosa of Rolando (or SGR) (or gelatinous substance of posterior horn of spinal cord). C fibres from primary afferents terminate here with some fibres projected to deeper layers of spinal grey matter, from which arises the spinoreticular tract to the ascending reticular activating system. However, some A delta fibers (carrying fast, localized pain sensation) also terminate in the substantia gelatinosa, mostly via axons passing through this area to the nucleus proprius. Thus, there is cross talk between the two pain pathways.
wind up
Wind-up = repeated stimulus with no change in strength causes an increase in response from dorsal horn neurons mediated by the release of excitatory neuromediators. Wind-up is dependent on activation of NMDA receptor
Ca to NT release
Ca binds calmodulin– calmodulin dep kinases–>doc and release
Ca in second order afferent neuron pain
Ca in due to NMDA, AMPA, NK1
Ca:calmodulin–>changed gene transcription
altered K perm
second messangers–>NO–>neurotoxic
silent nociceptor
unmyelinated primary afferents, normally do not respond, but in presence of inflammation or chemical sensitization may become responsive and discharge vigorously
blood supply to kidney in shock
reduced!
ATII and SNS–>VC afferent and efferent
PG–>VD afferent and effent
normally ANP–>VC efferent and VD afferent–>increase filtration
ADH trigger
high osmol (VOLT etc in Hypothal) >280
low pressure baro rec >5-10% blood vol
-but bumps threshold left and steepens
above 20% BV ADH has caused maximal renal reab and continues to rise and now is its VC effect becomes apparent.
ADH
see evernote
WOB diagram
trapezium=ELASTIC (TISSue and alv ST)
curve=RESTRICTIVE: 80% airway 20% tissue (increased in interesitial Dx)
static vs dynamic
Dynamic compliance=vol/(Pmax-PEEP)
-hence no eosoph
Static Compliance=vol/PlateuP-PEEP)
-hence eosoph
potassium channels cardia AP
K1 RMP
Kto special transient at peak of 1
Kr rectifying
excitatory and inhib NTs
glut, NAd ach, 5HT
inhib
GABA glycine
time constnat
time to complete if rate cont
t=C.R
t=0.63of completion (loner than half life)
t/2= 0.5 completion
t/2=t.0.63
oxycodone met
CYP450
noroxycodone active
15% of parent renally elliminated so imperfect but a fair option for PO renal Dx
pethidine
Mu, SSRI, VGSC, SE Ach
met to norpethadine 50% as potent but renally accumulates
accumulates in renal delerium anticholinergic addictive seziures due to
Na Ch types
resting (closed) –>active–>inactive
ARP due to NaCh in inactive stage (need time and repol to reset both gates)
Botulin etc
botuline stops release of Ach
hemicolinium inhibits Choline recycling
T tubule
invagination of sarcolemna
MEPP
small small small big
cardiac vs smooth vs cardiac
evernote
midaz met
a little bit of active met yet renal excretion no problem
MG vs GBS
GBS succhy syndrome –>K so use NDMR
MG->muscles weak ACHR Dx–> more sens to 10% of NDMR dose or use sux (less sensitive to sux as less agonist rec).
