VIVA august Flashcards
Closed system neg
Long time to prime system
semiclosed define
Semi-closed systems have a full boundary with the surrounding atmosphere, and use a controlled source for fresh gas flow. Intake of ambient air is prevented, but excess fresh gas is vented into the surrounding atmosphere. Partial rebreathing of exhaled gas can occur. They are commonly subdivided using the Mapelson classification (see below).
Closed systems have a totally closed boundary across which no gas enters or is vented, meaning that complete rebreathing takes place. The commonest example is the circle system.
circle system
Circle system RB bag
CO2 ab is in line
monitoring NDMR
acceleromyography
-peizoelectric crystal
DBS
-if nil twitch then wait
-fade–>neo give neo 0.02mg-0.05mg/kg
no fade–>occurs when TOFCR =0.6 (so may be no DBS fade despite inadequate reversal!) so wait or Neo 0.02mg/kg as per up2date table 2
I presume if nil titch cant reverse with neo
ie only useful for assessing shallow block
TFOC
Tofc (prop dreams) loss of... 4th at 75% occupancy 3rd 80% 2nd 90 1st almost 100%
normal volumes
RV=15 ER=15 TV=10 IR=45 VC=70 TLC=85
so normal VC=5L
normal FEV1=3.5
normal FEV1/FVC=70%
NACHR types
aabde is adult NACHR
aabdg is fetal
stim of nerves–>mature
NMJ terms
sarcollemma is the membrane around the muscle fibre
sarcomere is a muscle unit
myosin is thick centre
actin is thin margin
Ca binds troponin –>move tropomyosin to expose my sin binding site on actin
sux MoA
NDMR bind 1 of alpha of NACHR sux binds 2 -accomation block -bind-->conformational cange in NACHR-->depol-->end plate continually depolarisied-->M gate of near by NaCH opened but H gate can't reset -also increased K perm-->hyperpol -also decreased sens of NaCHR
yes phase I is sux
Sux doesnt cause fade as purely post synaptic
fade
fade
- NDRM block presynaptic rec
- the normal presynaptic NACHR–>positive feedback to release more Ach
- blocked presynaptic–>fade as less Ach available for subsequent contractions
- contraversion as snake venum which is purely postsynaptic causes fade.
Cx of anion gap
HCO3 Alb NH4
H3PO4
phosphoric acid
handling acids
buffer
compensate ie eliminate
Rx cx
ph
-log10H
pka
ka= A.H/AH
more stronger high ka–>low pKa
pka=-log10Ka
BIB which is ionized
B + H+–>BH+
BH+ is ionized (charge)
increase H–>ionized #BIB
A-.H+–>A- + H+
why propofol emulsified but thio not (yes)
pka propofol 11 hence cant make suffiently basic to ionized so emulsify
pka of thio 7.6 so by making solution pH 11 can ionize in water
ALSO enol form in alkaly form in vial
keto form at physiological pH
midazolam ph and why
3.5 as tautomerism to closed loop lipid sol at pH4
keto-enol tautomerism
THIOPENTON
enol form in alkaly form in vial
keto form at physiological pH
LACTATE DEHYDROGENASE
PYRUVATE TO LACTATE
lactate prod
nil mitochondria eg RBC
high demand low supply–renal medulla
lactate destination
–>pyruvate–>glucose with H+ consumed in process
procainamide
amide (2 I’s) antiarrhthmic
NH4 system
glutamine from protein metabolism then further metabolised in PCT cells
–>2NH4 and 2 HCO3
NH4 swapped for Na HCO# reab
NH3 als secreted in descedning LoH from medulla–>bind H+
BIGGER impact vs HPO4
min urinary ph
4.4 because active H transport enzymes ineffective beyond this pt
carbonic anhydrase
CO2–>carbonic acid
H+ in plasma
36nmol/L
renal acid Mx why required
shit tone of CO2 production=shit tone of resp loss so nil contribution normally
40-80mmol of fixed acids/day (small vs CO2 20K! yet still lots)–>renal requirement
CO2 0.03
SOLUBILITY CONSTANT
IC cells principal cells
principla a SALTED student
intercallated is interrelated h:K H
CO2 MV and MV vs CO2
MV as determinent –>hyperbola at both extremes
CO2 as derterminent–>linear until max and min platues
Smooth vs cardiac and sketal
cardiac and skeletal SR, ryanonide, T tubules, troponin.
cardiac has gap juctions skeletal doesnt
cardiac skeletal
inductor vs capacitor
evernote
voltage
potential difference
impedance
obstruction to flow
inductance
property of changing current in a conductor–>EMF–>change in current in another conuctor
capacitor
2 conductors and an insultor
micro macro shock
0.1ma vs 100ma
electrical safety touch active or neutral wire
patho of least resistance
accidental induction
capacitive coupling and stray capactitance
RCD
coil around active and nuetral if current difference–>leak–>trip 5-10mA
floating circuit
LIM alarm at 5mA
Hz from power socket and why
Why 50Hz?
The lower the frequency, the more efficient the delivery of electricity - less energy is lost from the system
Apparently 50Hz is the lowest frequency where flickering of lightbulbs is not noticeable, so this was chosen as the standard
Why do I care about this for the exam?
AC 50Hz is the most dangerous type of electrical current, in terms of causing ventricular fibrillation!
neutral to earth role
protect the electrical wires on streat from delivering huge current to houses with lightening strike complete curcuit from neutral to earth
case to earth
casing has wire–>earth socket–>closed system with low resistance if faults
soda lime
CO2+H20–>H2CO3
H2CO3 + NaOH–>H20 and heat and NaCO3
NaCO3+CaOH–>caCO3 and NaOH
water and heat speed up and NaOH is a fast reactor to mop CO2 quickly.
amsorb
CaCl instead of NaOH holds water so no base so less CO and compound A
FYI — Amsorb (we use)
Amsorb consists of calcium hydroxide lime (70%), water (14.5%), calcium chloride (0.7%), and two agents to improve hardness (calcium sulfate and polyvinylpyrrolidine). Amsorb has half the absorbing capacity of soda lime and costs more per unit. Calcium chloride serves as a moisture-retaining agent to allow for greater water availability. As a result, there is no need for alkali agents like NaOH or KOH. Without these strong monovalent bases, calcium hydroxide lime has fewer adverse reactions associated with the breakdown of inhalation agents (such as the formation of compound A or carbon monoxide [CO]).
cardiac reflexes
COntract
-Increased SVR—>increased contraction
BOWDITCH force frequency relationship
- increased HR—>increased contractility
- Bowed Box in a ditch—>little kid gets heart rate up and then it contracts to nothing
Bainbridge
Atrial stretch—>baro—>decreased HR
-Bain barorec
Group
screen
Xmathc
screen is patient plasma vs lab RBC (loooking for patient plasma antigen/antibodies)
Xmatch
-will body reject donor RBC
INCUBATION
WASH
glutination
IOP
As the globe has typically poor compliance, a small increase in volume can cause a large increase in intraocular pressure. Factors affecting volume include:
Volume of aqueous humor
Aqueous humor is a clear fluid that fills the anterior and posterior chambers of the eye, and provides avascular tissues with nutrients and oxygen whilst still allowing light to pass freely between the lens and retina. Volume of aqueous humor is a function of:
Production
Aqueous humor is produced by secretion and filtration from capillaries in the ciliary body in the posterior chamber, and circulates through into the anterior chamber.
Production is accelerated by β22 agonism
Production is inhibited by α2 agonism
Carbonic anhydrase inhibitors decrease aqueous humor production probably by decreasing sodium secretion into the eye
Reabsorption
Aqueous humor is reabsorbed into venous blood in the canal of Schlemm.
The trabeculae meshwork is the main source of resistance to reabsorption
If this is blocked, a significant reduction in reabsorption can occur and IOP will increase.
Reabsorption is affected by:
Haemorrhage
Blocks trabecular meshwork.
Muscarinic antagonism
Dilates pupil, which brings the iris closer to canal and decreases absorption.
α1 agonism
Dilates the pupil, decreasing absorption.
PGF2α
Relaxes ciliary muscle, increasing absorption.
Volume of blood within the globe
Affected by:
MAP
Venous obstruction
External factors
Other factors affecting volume or compliance of the globe:
Extraocular muscle tension
Extraocular compression
CSF in stroke
SAH–>block arachnoid villir reab (arachnoid projections through dura
SDH not an issue
#
monroe kelly
liquids are incompressible
CSF production in constnat
Reabsorption is pressure dependant and increases linearly above 7mmHg
Prod in lateral vent chorocoid plexus and in ependymal cells of 3rd and 4th ventricle
150ml constant
500ml prod/day (3x cycle per day)
Ultra filtrate and secretions from fenestrated endothelial cells
Na active glucose fascilitated
Co2 higher pH lower glucose lower
TEG PL change
MA change indep of K and alpha
TEG fibrinolysis
imediate drop in MA once formed
PL function analyser
- Citrated whole blood is drawn through a hole in a collagen-coated membrane which is bound to adrenaline or ADP
- Under the shear stress influences, platelets aggregate and seal the hole
- This is sensed by a pressure transducer
- The time taken for platelets to occlude the hole is referred to as the closure time
MAC requirement at everest
double the MAC as half the barometric pressure
2% of half instead of 2% of the whole.
increased MAC
P+K p 107
propofol to LoC
2.5
to loss of motor respon 14
MAC ANS
MAC BAR
sens and spec
A burglar alarm is highly sensitive if it goes off every time someone breaks in.
It is highly specific it is rarely triggered by possums on the front porch (my thoughts)
The result is that sensitivity is a measure of the probability of getting a positive result out of all the positive cases, and that specificity is a measure of the probability of getting a negative result out of all the negative cases.
- Sensitivity (also called the true positive rate, the epidemiological/clinical sensitivity, the recall, or probability of detection[1] in some fields) measures the proportion of actual positives that are correctly identified as such (e.g., the percentage of sick people who are correctly identified as having the condition). It is often mistakenly confused with the detection limit,[2][3] while the detection limit is calculated from the analytical sensitivity, not from the epidemiological sensitivity.
- Specificity (also called the true negative rate) measures the proportion of actual negatives that are correctly identified as such (e.g., the percentage of healthy people who are correctly identified as not having the condition).
The positive and negative predictive values (PPV and NPV respectively) are the proportions of positive and negative results in statistics and diagnostic tests that are true positive and true negative results, respectively
Can O2 measurement be done with IR
no need two different atoms to absorb IR
IR set up
filter to select freq through
reference chamber
TEG
R/V
main stream vs side stream
Side stream:
fixed volume of gas continuously sampled from the circuit
aspirated through tubing, released to atmosphere or returned to circuit
rate adjusted between 50-500ml/min
errors:
sampling as close to patient as possible to minimize circuit dead space
sampling rate exceeds expiratory flow rate & inspired gas sampled
hypoventilation is sampling exceeds fresh gas flow
water vapour condensed in sample tubing/accumulates in measurement chamber – erroneous readings (filters and water traps in systems)
may have gas leakage, CO2 diffusing out
Main stream:
incorporate the infrared sensor into the circuit very close to the endotracheal tube.
Directly measure in circuit, no gas subtracted
Effects of breathing circuit and sample tubing dead space minimized, response time faster
Problems/errors:
Need to be warmed to prevent condensation
Avoid skin contact (warm, burns)
Heavy, risk circuit kinking of ETT
Requires frequent calibration
Prone to soiling with saliva, mucus
mass spectrometry
postively charged not neg!
Clinical use of mass spectrometry for expired gas analysis began in respiratory care units in the mid-1970s. They were introduced into operating rooms and anesthesia practice shortly thereafter. Because of their size and complexity, hospitals often connected many operating rooms to a single spectrometer and had the results relayed back to the anesthesiologist. The convenience plus low cost of infrared analyzers has largely phased mass spectrometry out of clinical use.
power alpha beta
Alpha value: value chosen (convention alpha = 0.05) for ‘acceptable’ level of Type 1 error. Thus accept 5% chance of incorrectly rejecting the null hypothesis (i.e. stating that there is a difference between the groups when there is not). This is important in medicine as stating that there is a difference between two drugs may cause harm to patients by incorrectly changing practice.
Beta value is a chosen value (convention 0.2) that relates to the chance of making a Type 2 error. This means that we accept a 20% chance of incorrectly accepting the H0 and stating that there is no difference between the two groups, when actually there is a difference. This is less important as although may result in delay of discovery of important advances in medicine, it is less likely to harm the patient population as would be with Type 1 error.
Power = 1 – beta, usually 80%.
- What are the determinants of sample size?
- What are the determinants of sample size?
a) Chosen alpha value: smaller value requires larger sample size
b) Chosen beta value: smaller B (higher power) means larger sample size
c) Effect size ie Delta value: if looking for small difference between two groups, sample size increases
d) Theta: underlying variance in population tested (cannot control) – large variance will increase sample size.
thermo dilution
AUC Cl dose
not ficks prinicple
ficks principle
CO = 250ml / (200ml – 150ml)
HER
High HER
-metabolises free drug so quickly that PrB releases bound drug to maintain equilibrium hence PrB % irrelevant for high HER but ++ RELEVANT for low HER #P+H
(a-v)/a
The hepatic extraction ratio is determined largely by the free (unbound) fraction of the drug and by the intrinsic clearance rate
With increasing hepatic blood flow, hepatic extration ratio will decrease for all drugs
drugs with low intrinsic clearance:
Hepatic extraction ratio will drop more rapidly with increasing hepatic blood flow
Hepatic clearance will not increase significantly with increasing blood flow
The last point is important. Consider a drug which is completely absorbed and undergoes 95% clearance by first pass metabolism, making its systemic bioavailability 5%. With enzyme inhibition, a minor 5% drop in hepatic enzyme activity will result in a doubling of systemic bioavailability (to 10%), which could represent a toxic concentration for drugs with a narrow therapeutic index.
verapamil as a stereotypic drug with high individual variability due to high first pass
ALSO MORPHINE
The liver also forms a reservoir of blood with a volume of 450 mL (30 mL/100 g liver tissue), half of
which may be mobilized if hypovolaemia occurs.
The portal blood can bypass the sinusoids as blood
is shunted from portal venules to hepatic venules
by the relaxation of hepatic venule sphincters.
Catecholamines can mobilize blood from the sinusoids. The liver can also buffer against an increase
in blood volume. Hepatic compliance (i.e., distensibility) is higher at high venous pressures than at
low venous pressures.
In the presence of portosystemic shunts, some portal blood bypasses first pass clearance and therefore bioavailability of drugs with a high first pass clearance will be increased
low HER
phenytoin
methadone
HIGH HER
Glyceryl trinitrate Verapamil Propanolol Lignocaine Morphine Ketamine Metoprolol Propofol
HER
High lipid sol—>good GI ab and high HER #bblockers P+H
osmolality measured in lab
Measured by: Movement of a stick on thawing solution, 1 mole will depress freezing point by 1.86 Kelvin.
mosmol
meq
measure of osmols
measure of osmols*valency of that osmol
osmoloarity
avagadros number of molecules/L
solvent solute
vent is the water
ute is the salt
How to remember ‘solute & solvent’ in a solution: A thief broke into a building and filled a bag with loot. Then the police came. The thief hid the loot in a vent, so he wouldn’t get caught. The solute goes into the solvent
how does hyperglycaemia cx low Na
hypersomolar–>draw fluid in (and i assume trigger ADH)
psuedo hyponatraemia
- normally plasma contains 93% water, 7% solids (5.5% proteins, 1% salts, 0.5% lipids)
- hyperlipidaemia & other disorders increase solid phase up to 10%
- [Na+] in aqueous phase
- most methods for plasma [Na+] measure Na+ content of fixed volume of plasma, yield misleadingly low [Na+] as lipid accounts for larger than normal % of plasma
- concentration of sodium in plasma water is unchanged, but there is less water and therefore less sodium in a given volume of plasma
- osmolality will be normal
ineffective osmoles
glucose and urea
hep BF
evernote
HER Prb
p10 P+H
low metabolic capacity–>Prb relevant as free drug overwhlems system and then ER reduced after brief Mx–>narrow window so test.
Intrinsic Cl, unbound drug
HER big 2 determinants
Intrinsic Cl, unbound drug
SHC water
4.2Kg/kg/C
ITR margins
sweat=effective
VC=effective
Autonomic response
ITR lower margin term
threshold temp
TNZ lower margin term
Critiical temp
VC and VD can occur here as don’t really fuck with metabolic rate (regulated by controlling heat loss not producing heat)
The thermoneutral zone is defined as the range of ambient temperatures where the body can maintain its core temperature solely through regulating dry heat loss, i.e., skin blood flow.
temp rec path
Ad delta cold <25
c warm raffini 30-46
STT
post HT Poles cold efferent
LHV number
2.4kj?kg at 37C
thiazide
block Na reab–>hyponatraemia
prod of aqueous humer
B2 increase
a2 inhibit
Drainage of aqueous humur
haemorrhage blocks
formular name thermodilution
stewart hamilton
?law of conservation of energy?
Loop diuretic
Na-K-Cl cotransporter in the thick ascending limb of the loop of Henle, by binding to the chloride transport channel, thus causing sodium, chloride, and potassium loss in urine.
thiazide
Thiazide diuretics control hypertension in part by inhibiting reabsorption of sodium (Na+) and chloride (Cl−) ions from the distal convoluted tubules in the kidneys by blocking the thiazide-sensitive Na+-Cl− symporter
spironolactone
causes less K secretion ie potassium sparing diuretic
aldosterone
Na:KATPase PRINICPLE ASSAULTED DCT AND CD
HATPas INTERCALATED CELLS CD
HK ATPase INTERCALATED CD
GFR EQUATION
GFR=kf.NFP NOTE: afferent Cap pressure hydrostatic is 60mmHg ie MAP oncotic is 24
low pressure baro
IVC SVC atrial Pulm art and vein
calculate Hep BF
Like CO AUC (ficks prinicple is more complex with a fixed infusion)
ICG has a known HER 0.74
AUC (measured)=x (known)/cl
AUC=x/(Q.0.74)
HER is 0.74 for ICG
Cl is vol cleared per min=Q.HER ie Q.0.74
renal clearance calc
Renal clearance can be calculated by dividing the
amount of a substance in urine (collected over a
given time) by the plasma concentration, P:
P
Renal clearance =
Amount of substance in
urine per unit time
Plasma concentration of
substance,
The amount of a substance in urine over a given
time is the volume of urine produced in that time,
V, multiplied by the urinary concentration of the
substance, U. Thus, for any substance,
U V
P = × Renal clearance
(plasma volume/unit time; mL/min,L/day
CrCl vs GFR
Creatinine is filtered by the renal tubule and is not
reabsorbed. Creatinine clearance is used routinely
as a method of estimating GFR. However, a small
amount of creatinine is secreted by the tubules
into the lumen so that the creatinine clearance is
slightly greater than the true GFR.
GFR calc
RENAL CL and GRF
Clearance= amount removed so what do you need vol, conc urine and conc plasma
Renal clearance can be calculated by dividing the amount of a substance in urine (collected over a given time) by the plasma concentration, P: P Renal clearance = Amount of substance in urine per unit time Plasma concentration of substance, The amount of a substance in urine over a given time is the volume of urine produced in that time, V, multiplied by the urinary concentration of the substance, U. Thus, for any substance, U V P = × Renal clearance (plasma volume/unit time; mL/min,L/day
Renal BF calc
RENAL BF
Clearance of a drug that is peed out every time
PAH is filtered at the glomerulus, and any remaining in the peritubular capillaries is secreted into the lumen by proximal tubules. When the PAH concentration is low, all the plasmaperfusing, -filtering and -secreting parts of the kidney (the effective renal plasma flow is 85%–90% of the total renal plasma flow) are completely cleared of PAH. The renal clearance of PAH is therefore equal to the effective renal plasma flow, from which the effective renal blood flow can be calculated: = − Effective renal blood flow Effective renal plasma flow 1 Blood haematocrit
GFR vs eGFR
eGFR is simple plasma Cr with nitl urine monitoring
plasma cr is inversely proprotional to CrCl (requires urine monitoring) which is similar to GFR (requires inuline)
HCT normal
45%
%BF organs
Having Sex usually brings man kids later
oncotic pressure normal
24mmHg #half to hydrostatic as a rule of thumb
60-15-24=21 at afferent
fluid shift in haemorrhagic shock
decreased hydrostatic out increased oncotic in–>autotransfuse
high dose ADH renal
decreased RBF and gfr as constrict afferent
intralipid
fat emulsion soya and egg phosphatatide and glycerol
1.5ml/kg of 20%
risk of LA tox drug factors
VD or VC!
pathomneumonic of bupivocaine tox
refractory VT or VF
motor neuron
AALPHA
ONSET LA AND LIPID SOL
Slower
LA tox ration neuro and cardiac
Cardiac collapse:CNS
nerve block onset by nerve type
1st C fibres are large unmyelinated (ache and SNS fibres) blocked at same time as A delta pain and cold (small myelinated)
-stoelting “Both types of pain-conducting fibers (myelinated A-δ and unmyelinated C fibers) are blocked by similar concentrations of local anesthetics, despite the differences in the diameters of these fibers.”
2nd touch and pressure Abeta
3rd motor A alpha
—>D,C,B,A
lipid sol of LA number
octenol: water coeff
lig 350
rop 700
bup 3000
pka LA
7.9 and 8.1
ester LA met
CORE
rapid organ indep hydrolysis by butlycholinesterase
metabolite is PABA–>hypersens reaction
cocaine has hepatic hyrolysis –>inactive–renal ecretion
amide LA
amidase–>hydroyxlation and N-de-alkylation
dep on liver
minimal renal excretion of unchanged drug
prilocaine
–>o toludeine—>metHb (oxidized Fe2+–>Fe3+ –>metHb–>cant carry O2)–>Rx with methylene blue
ester example
procaine
tetracaine
cocaine
dibucaine number
INHIBITS BUTYLCHOLINESTERASE
Inhibits normal allel but hardly touches mutant allel
So more inhibition with Normal enzymes
hence
Normal number >80
Homogenous atypical is 20. (Less inhibition. Less change. Lower number)
BIB equation
B + H+—>BH+ BH+ is IONIZED B Is unionized
AIA EQquaion
- AH—>A- + H+. NOTE THAT BASE AND ACID HAVE NO CHARGE AH AND B
Hb structure #evernote
If Fe3+—>methaemoglobinaemia—>can’t carry O2
O-tolulene from prilocaine in EMLA causes this
Fuel cell
Cathode electrons consumed (RIG) in presence of O2—>more current
Cath has a great rig and consumes lots of O2 and energy
At the anode: Pb + 2(OH) → PbO + H 2 O + 2e –
(OIL) oxidation of lead at anode (spits of electron)
Pulse ox absorption
660 deoxy absorbs RED 660nm (990nm is IR on right)
beer lambert not strictly applied due to scatter hence calibrate with pop study so…
A copy of this correction calibration graph is available inside the pulse oximeters in clinical use. When doing its calculations, the computer refers to the calibration graph and corrects the final reading displayed.
LED pattern different to 50Hz to minimize interference
pulse ox memorable errors
dye, MetHb, COhb
nail pollish
arrhythmias
anaemia irrelavnt
PATHOLOGY, PATIENT, PROGRAMME, PROBE
draw pulse ox curve for 75% sats
half way between oxy and deoxy ;)
pulse ox AC DC
So the final signal picture reaching the pulse oximeter is a combination of the “changing absorbance” due to arterial blood and the “non changing absorbance” due to other tissues.
LED benedit
Are cheap ( so can be used even in disposable probes)
Are very compact (can fit into very small probes)
Emit light in accurate wavelengths
Do not heat up much during use (low temperature makes it less likely to cause patient burns)
LED pattern
LED pattern different to 50Hz to minimize interference
lights off–>detect baseline interference
red on–>change
IR on–>change
R ratio
R absorbance AC/DC red / AC/DC IR
modulation ratio. gives the ratio of change to both EM ranges in relation to one another. this number is then clinically correlated with study pop
R is derrived from population study. different population–>different R value in different brands–>difference
R = (ac absorbance/dc absorbance) red / (ac absorbance/dc absorbance )IR
R corresponds to SaO2
— SaO2 100% = R 0.4
— SaO2 85% = R 1
— SaO2 0% = R 3.4
Cvs changes in obesity mak95
evernote
laplaces law and PPV
P=4T/r
if T stable then decreasing r–>increasing pressure inwards to collapse
(P, ventricular pressure; r, ventricular radius; h, wall thickness).
Decreased afterload due to a reduction in LV end-systolic transmural pressure and an increased pressure gradient between the intrathoracic aorta and the extrathoracic systemic circuit
Mechanisms affecting the right ventricle and the pulmonary circulation are:
Increased intrathoracic pressure is transmitted to cenral veins and the right atrium, decreasing right ventricular preload
Increased intrathoracic pressure is transmitted to pulmonary arteries
Transmitted alveolar pressure increases pulmonary vascular resistance
Increased pulmonary vascular resistance increases right ventriular afterload
Thus, increased afterload and decreased preload has the net effect of decreasing the right ventricular stroke volume.
Mechanisms affecting the left ventricle and the systemic circulation are:
Decreased preload by virtue of lower pulmonary venous pressure
Decreased afterload due to a reduction in LV end-systolic transmural pressure and an increased pressure gradient between the intrathoracic aorta and the extrathoracic systemic circuit
Thus, decreased LV stroke volume
The consequences of this are:
Decreased cardiac output
Decreased myocardial oxygen consumption
Closing collapse-why base
base of lung smallest due to gravity
FRC in ovese GA
Under anesthesia, the FRC of the obese patient decreases about 50% as compared to 20% reduction for the nonobese patient.
CLOSING CAPACITY UNCHANGED
closing capity changed with
effort, flow
age
COPD
not obesity
WOB graph
Elastic work
About 65% of total work, and is stored as elastic potential energy. Energy required to overcome elastic forces:
Lung elastic recoil
Surface tension of alveoli
Resistive work
About 35% of total work, and is lost as heat. This is due to the energy required to overcome frictional forces:
Between tissues
Increased with increased interstitial lung tissue
Between gas molecules
ARP
Phases 0, 1, 2 and most of 3 are refractory to stimulation. In fact, until the membrane reaches -50 mV the myocyte cannot contract again. This is the ABSOLUTE REFRACTORY PERIOD.
Ca keeps them above the reset point Na Ch are time dep
Nerve refractory period 2ms
Myocyte 200ms+50ms RRP (due to ca ch)
antiplatelets
dipyridamole potentiaties ie augments adeonisine not inhibit–>increased cAMP it alsoe is PDEi to increase cAMP–>send messangers–>PLi
clopidogrel p2y12 subunit of ADP rec
also -prasugrel
-ticagrelor
tramadol met
desmethyl tramadol active
renally cleared
CYP2D6–>genetic variability
tapentadol
nil active met
minimal but some renal clearance
PL granules
alpha
fibronectin, fibrinogen, vWF, PDGF, and Thrombospondin, platelet factor 4.
δ-granules
Contain 5-HT, ATP, ADP, and Ca2+.
platelet storage duration
5 days
Pl stroage treatment
wiki
Platelet aphoresis vs pooled whole blood platelets
- aphoresis–>sufficient dose from a single donor–>better
- pooled–>from whole blood in insuffient dose from any single donor so pool together–>more risk of bacteria and virus
Both apheresis and pooled platelets are leucodepleted during or soon after collection and are also irradiated before release from Lifeblood, unless other specific arrangements have been made with the receiving laboratory/institution.
Platelets can be stored for 5 days after collection at 20 - 24º C with gentle agitation. Platelets can be irradiated at any stage during their 5 day storage and thereafter can be stored up to their normal shelf life of 5 days after collection.
The first advantage is that the whole-blood platelets, sometimes called “random” platelets, from a single donation are not numerous enough for a dose to give to an adult patient. They must be pooled from several donors to create a single transfusion, and this complicates processing and increases the risk of diseases that can be spread in transfused blood, such as human immunodeficiency virus.[citation needed]
Collecting the platelets from a single donor also simplifies human leukocyte antigen (HLA) matching, which improves the chance of a successful transfusion. Since it is time-consuming to find even a single compatible donor for HLA-matched transfusions, being able to collect a full dose from a single donor is much more practical than finding multiple compatible donors.
Plateletpheresis products are also easier to test for bacterial contamination
leukodeplete and irradiation role
Irradiated blood components are used to prevent Transfusion-associated graft-versus host disease (TA-GVHD) the primary cause of which is proliferation and engraftment of transfused donor T-lymphocytes
The leucocytes present in donated blood play no therapeutic role in transfusion and may be a cause of adverse transfusion reactions. Removal of leucocytes may therefore have a number of potential benefits for transfusion recipients, including:
Reduced risk of platelet refractoriness
Reduced risk of febrile non-haemolytic transfusion reactions (FNHTR)
Reduced risk of CMV transmission
Reduction in storage lesion effect
Reduction in the incidence of bacterial contamination of blood components
Possible reduced risk of transfusion-associated graft vs host disease (TA-GVHD)
Possible reduction in transfusion related immunomodulatory (TRIM) effects, including cancer recurrence, mortality, non-transfusion transmitted infection
Possible reduced risk of transmitting variant Creutzfeldt-Jakob Disease (vCJD)
betablocker BSL
decreased BSL cellular uptake as less glucose and less insulin to facilitate uptake and less response.
BSL can go high or low (low is more classical)
CV phys: B1-glycogenolysis and pancreatic release of glucagon, which increases plasma glucose concentrations. β1-adrenoceptor
pub med: Specific beta(2)-agonist effects on the pancreatic beta cell result in increased insulin secretion, yet other mechanisms, (b1)such as increased glucagon secretion and hepatic effects, cause an overall increase in serum glucose and an apparent decrease in insulin sensitivity.
nerve type onset
—>D,C,B,A
lignocaine met
hep–>MEG–>lower sezirue threshold
>600mg–>methhb–>impaired O2 transport
10% renally eliminated
adenosine hepatic arterial
It is suggested that this buffer response is due to intrahepatic levels of adenosine. With reduced portal blood flow, a build-up of adenosine occurs that vasodilates the hepatic artery.
TUBULOGLOMERULAR FEEDBACK In the juxtaglomerular apparatus, the macula densa lies in the wall of the ascending limb of the loop of Henle, close to the renal arterioles. The contraction of the smooth muscle of the afferent arteriole to the glomerulus is controlled by a vasoconstrictor, adenosine, from the macula densa (although the vasoconstrictor was previously thought to be renin). The macula densa releases more adenosine if the renal perfusion pressure rises and reduces production if the pressure falls. Adenosine production by the macula densa is determined by the composition of the fluid in the ascending loop of Henle. If the perfusion pressure increases, the glomerular capillary pressure and glomerular filtration also increase. The macula densa senses the increased flow of sodium and chloride in the ascending limb of the loop of Henle and releases more adenosine, which constricts the afferent arterioles, reducing the glomerular capillary pressure and the GFR. The vasodilator nitric oxide may be produced by the macula densa when the renal perfusion pressure falls.
laser
light amplification by stimulated emission of radiation; an optical device that produces an intense monochromatic beam
ant STT
The anterior spinothalamic tract, also known as the ventral spinothalamic fasciculus, is an ascending pathway located anteriorly within the spinal cord, primarily responsible for transmitting coarse touch and pressure. The lateral spinothalamic tract (discussed separately), in contrast, primarily transmits pain and temperature.
chronic opioid use
In addition, chronic opioid exposure can lead to hypogonadism, opioid-induced hyperalgesia, sleep-disordered breathing, and potentially increased risk of cardiovascular disease and neurocognitive impairment.
classify inhalational anaesthetics
gas and volatiles
Xenon bad
PONV Low O2 Cost raised ICP dense-->increased Wob
volatile define
Volatile anaesthetic agents share the property of being liquid at room temperature, but evaporating easily for administration by inhalation.
anatomical DS measure and changes
fowlers
-size, large insp–>traction, position/posture
CVS change with PEEP in CCF
depends if dehydrated or overfilled
resp q
derived from ration of CO2 prod per O2 consumed
Carbs is 1
lipid is 0.7
ANS BP control question
HR.SV.SVR alpah1 B1 B2 rec
Pulse pressure determ
HR.SV.SVR
WIDENED: Increased stroke volume, and stiff arterioles or Run off due to Aortic dissection of CVM—>wide
- SV: exercise, preg, AR
- increased SVR: atherosclerosis, hyperthyroidism
Narrow
- SV:hypovol, CCF, AS
- compliant arteries
winkessell
elasticity of aorta allows damping of the pressure wave–>
Decreased AL in systole as aorta compliant
AND flow in diastole.
peripheral arteries less compliant–>resistance–>stored volumed to be more evenly released to allow flow in diastole
regional BF left and right heart wiggers
frown in systole for both
tramadol classification
centrally acting synthetic PARTIAL opioid AGONIST
also NMDA rec antag and SNRI
met desmethyl-tramadol
descedning pain pathway
from brain stem nuclei–>DH
tract unclear in my mind
Serotonin Sx
hyperreflexia, tremor, rigidity, hyperthermia, tachy, sweat–>seizure
Rx with cyproheptadine +/-benzo and activated charcoal
potentiate attenuate
x
USS CO
limitation
Hr.SV=CO
SV=VTI.LVOTarea
limitation
- nonuniform flow
- arrhyhtmias
- theta
- heart moves
- only measures flow in DESCEDNING aorta=70% of CO
doppler shift eqn
changed freq proprtional to changed velocity.Costheta
USS wavelength
20mHz
definition is 20kHz
receptor theory of drug effect
The main points to describe receptor theory are:
Drugs interact with receptors in a reversible manner to produce a change in the state of the receptor
This interaction can be modeled mathematically and follows the Law of Mass Action
The binding of drug and receptor determines the quantitative relationship between dose and effect.
Mutual affinity of drugs and receptors determines the selectivity of drug effects
Competition of mutually exclusive molecules for the same receptors explains agonist, partial agonist and antagonist drug activity
law of mass action
Gold
Law of mass action:
Rate of reaction is proportional to conc of reactants
A+R—>AR
V1=V2 at equillibrium
V1=D.R.k1
V2=DR.k2
So D.R/DR=K2/K1=Dk
Kd=dissociation constant also called Ka= K2/K1=A.R/AR
KA=association constant and is reciprical (strenght of sticking on once bound)
pharm
The main points to describe receptor theory are:
- Drugs interact with receptors in a reversible manner to produce a change in the state of the receptor
- This interaction can be modeled mathematically and follows the Law of Mass Action
- The binding of drug and receptor determines the quantitative relationship between dose and effect.
- Mutual affinity of drugs and receptors determines the selectivity of drug effects
- Competition of mutually exclusive molecules for the same receptors explains agonist, partial agonist and antagonist drug activity
Law of mass action:
Rate of reaction is proportional to conc of reactants
A+R—>AR
V1=V2 at equillibrium
V1=D.R.k1
V2=DR.k2
So D.R/DR=K2/K1=Dk
Kd=dissociation constant also called Ka= K2/K1=A.R/AR = conc of drug in plasma to get 50% rec occupancy in mmol/L
KA=association constant and is reciprical (strenght of sticking on once bound)
L/mmol (which is annoying)
If affinity is high then DR»»>D.R at equilibrium so DR/D.R is high so KA is high so KD (inverse) is low
affinity
50% rec occupied Kd
potency
ED50% 50% max response
efficacy
once bound Emax
IA
ration of Emax:full ag
COHb ab
As the graph show the light profiles in the chosen areas (red = 660 nm and infrared = 940 nm) overlap considerably for carboxyhemoglobin and oxyhemoglobin (as it does for methgb and deoxyhgb). This means that the pulse oximeter will see the reflected light for carboxyhgb and oxyhgb as the same when measuring in the red light spectrum and thereby measure a combined reflection. Carboxyhgb is not reflected/absorbed in the infrared spectrum and therefore does not add to this part in the ratio. Remember, the ratio between these measurements is checked against the pulse oximeters database. This ratio will correspond with the displayed SpO2.
collegiate
Boiling point increases in proportion to the molar concentration of the solutes
Freezing point decreases in proportion to the molar concentration of the solutes
Vapour pressure is dependent on the vapour pressure of each chemical component and the mole fraction of that component in the solution (Raoult’s law)
how drugs work
evernote
pulse ox two types
Pulse oximetry is a noninvasive method for accurately estimating oxygen saturation (SaO2) by reading the peripheral oxygen saturation (SpO2). As SaO2 and SpO2 are sufficiently correlated and pulse oximetry has the advantages of being safe, convenient, inexpensive, and noninvasive, this approach is clinically accepted for monitoring oxygen saturation [1], [2].
Pulse oximetry is simple to carry out; it only uses two different light sources and a photodiode [3], [4], [5]. Depending on the measurement site, either the transmissive or the reflective mode can be used. In the transmissive mode, the light sources and photodiode are opposite to each other with the measurement site between them. Light then passes through the site. In the reflective mode, the light sources and photodiode are on the same side, and light is reflected to the photodiode across the measurement site.
Currently, the transmissive mode is the most commonly used method because of its high accuracy and stability. Nevertheless, the demand for reflective-mode oximetry is continuously increasing because it does not require a thin measurement site. It can be used at diverse measurement sites such as the feet, forehead, chest, and wrists. In particular, if the wrist is the available measurement site, pulse oximeters can be conveniently used in the form of a band or watch. To the best of our knowledge, reflectance pulse oximetry, specifically for monitoring oxygen saturation at the wrist, is currently not practiced clinically. In recent years, many reflectance pulse oximeters have become commercially available, but they are only for personal monitoring of oxygen saturation and for entertainment purposes. Obviously, the focus is on developing oximeters for medical purposes, and research is being carried out in this regard. Furthermore, most research papers discuss only the basic principle of pulse oximetry and its utilization in smart devices; only a few papers discuss the challenges associated with reflective pulse oximetry.
In this study, we developed a reflectance pulse oximeter and addressed the practical issues and limitations associated with its use. Using this oximeter, we investigated the results of AC amplitudes and DC offsets of the red and infrared signals, including modulation ratio, which are critical factors to estimate SpO2. We first tested our device by measuring oxygen saturation at a fingertip and wrist and analyzed its performance. Finally, we summarized all issues and discussed the feasibility of using the device for clinical purposes.
hep met phases
evernote
ester met
The product of phase I has an oxygen species that reacts better with enzymes involved with phase II reactions. Phase II reactions conjugate the metabolites created in phase I to make them more hydrophilic for secretion into blood or bile.
cocaine moa
DA and NARUI
3mg/kg for 30 min
excitatory Sx of any LA
Poynting effect
Bubbling O2 through N20 produces a mix with a lower critical temp than that of O2 #pseudocrit temp temp below which can be compressed-->lamination
sympathomimetic def and cat
compounds that mimics the effect of endogenous agonists of SNS
DIRECT vs mixed vs indirect
Selective vs nonselective
(Catechol is a shitty classification as it doesn’t narrow MoA or use)
-catechol ring benzen and OH at 3,4
Levosimenden
tropC sens and K:atpase open–>VD
acute decomp CCF
milronone
PDE3i
-heart and VD
CCF in cardiac surg
QTc
prolong Cx
QT/square RR risk in tachy
<440
all LOW Hypokalaemia Hypomagnesaemia Hypocalcaemia Hypothermia Myocardial ischemia
TYPE1 AND 3 ANTIARRHYTHMICS
antipysh and TCA
crystalloid vs colloid
Crystalloids are aqueous solutions of mineral salts or other water-soluble molecules. Colloids contain larger insoluble molecules, such as gelatin; blood itself is a colloid.
colloids
https://derangedphysiology.com/main/required-reading/electrolytes-and-fluids/Chapter%20225/colloids-vs-crystalloids-resuscitation-fluids
gelafusin is from pig fat–>coagulopathy and anaphylaxis
starch and dextran–>AKI and anaphylaxis
starch lasts for 5 days
albumin as an antioxidant
NDMA def and rec
N-methyl-D-aspartate receptor
glutamate
glycine
PCP
Ketamine MoA
NMDA rec antag-blocking Ca in
inhibit presynaptic glutamate release
interact with opiate rec
ket met
CYP450–>inactive–>pee hence CKD fine
cori
Lactate–>pyruvate–>glucose (GNG)
key parts of cellular resp
https://www.khanacademy.org/science/biology/cellular-respiration-and-fermentation/overview-of-cellular-respiration-steps/a/steps-of-cellular-respiration
glycoslysis
pyruvate oxidation
kreb cycle
ETC
Eectrontransport is call oxidative phosphorylation
CO2 prod in kreb cycle and pyruvate oxidation
eGFR vs GFR
eGFR is based on an isolated Cr level which is inversely related to CrCl which slightly overestimates GFR
CrCL
cockcroft gault eqn
(140-age).wt/(72.Cr)
less clearance with old, small, females
RBF
Effective renal
blood flow
=Effective renal plasma flow/1- Blood haematocrit
washin factors
drug patient anaesthetic #n20 AND DURATION
o2 tank size
E=emergency J=juganaut
how much O2 in a cylinder
50Bar 4.5L–>50.4.5=225
pipeline pressure O2
4bar
O2 tank 50bar
cylinder pattern
bottles shoulders evernote
Motion sickness
Hyoscine anticholinergic
Cyclizine
Anti hist and ach
Stenetil
Prochloperaxine
DA H ACh
Ondans
Can cx Qt change
Rx epse
Benztropine
Tnr kids
Thethermoneutral zoneis the range across which the basal rate heat production (and oxygen consumption) is balanced by the rate of heat loss
For an adult it istypically 27-31°C
In neonates it is higher,typically 32-34°C.
Phase two heat loss
2.5hr
Critical temp heat
critical temp is for ITR
TNZ lower limit
Laser
PHOTON–>decay to base level
Argo for cataract highest freq
Chlorhex n20
Sugamadex
Hydrophobic ring to bind steroid aminosteroids as per Kate. OxCHB says anionic inner ring binds Amine cationic ends
Hydrophilic–>peed out stable
High association low disassociate
The intermolecular (van der Waals) forces, thermodynamic (hydrogen) bonds, and hydrophobic interactions of the sugammadex-rocuronium complex make it very tight. (stoelting)
- ->fluclox
- ->altered haemostasis (stoelting)
- ->OCP
- ->postoperative nausea/vomiting
BSL
mmol/L
OAG
x
metformin
biguanide
gliclazide
sulfonylurea
Binds and inhibits ATP-sensitive K+
channels on pancreatic β cells
! depolarisation ! open voltage-gated Ca2+ channels !
↑intracellular [Ca2+] ! ↑release of insulin vesicles
S/fx – hypoglycaemia, GIT upset
sitaglipton
DPP-4i prevent GLP breakdown
These agents work by activating the GLP-1R, rather than inhibiting the breakdown of GLP-1 as do DPP-4 inhibitors,
Glucagon-like peptide-1 agonist
Glucagon-like peptide-1 agonist inhibit glucagon (it's like it's own negative feedback)
a lower risk of causing hypoglycemia.
SGLT2i mech
eg sergliflozin
By reducing glucose blood circulation, gliflozins cause less stimulation of endogenous insulin secretion or lower dose of exogenous insulin that results in diabetic ketoacidosis
block 180g/day=180 jelly beans
insulin met
liver and kidney
insulin
polypeptide hormone
diathermy
Resistancethrough body-->heat high current density monopolar 10cm away short bursts ICD-->back up external
Volatile stability
Cl stabilizers
ether has O2 bonds–>explode
CSL ton and osmo
hypoosmolar
isotonic as per government website
Cx of Anion gap
So4 po4
Freeze dep
0.003 permmol
Remi hyperalgesia
TLR stim by remifentanil acid longer t/2 vs Remi renslly cleared
Morph met
M3G
TLR neurexcite hyperalgesia
Carvedilol
Indications. Carvedilol is a non-selective adrenergic blocker indicated for the chronic therapy ofheart failurewith reduced ejection fraction (HFrEF),hypertension, and left ventricular dysfunction followingmyocardial infarction(MI) in clinically stable patients.
Propranalol
Old school shitty
B1 AND 2
MEMBRANE STABLE
SALT AND PRPOER
PPL
NOT BLACK OR SALLY
NIL ALPHA NOT LOW LIPID
mole
6*10^23 molecules
tonicity
Tonicity is the measure of the osmotic pressure gradient between two solutions.
NACL AND CSL TONICITY
CORE
Osmolarity=Nax2=308 RRRRREALLY EASY
Osmolality=Osmolarity*0.93 as Nacl 97% dissociates
So NaCL0.9% has osmolarity 308 and osmolality of 287—>isoosmolar and isotonic
Vs CSL osmolarity of 276. So osmolality is 256 (hypoosmolar) THEN the lactate disappear—>hypotonic!!! BAD FOR CEREBRAL OEDEMA OR HYPONATRAEMIA
CSL and CL
increase 1.5mmol/L every L
plasmalye only increase 0.4
(normal level of cloride is 98-105 and plasmalyte has 98)
non electric thermometer
Non-electrical techniques
(1) mercury or alcohol thermometer
- thin column of mercury or alcohol ! expands when heated
- height of column reflects degree of expansion ! proportional to temperature
- mercury solidifies at -39ºC ! not suitable for low temperatures
- alcohol boilds at 79ºC ! not suitable for high temperatures
- disadvantages = takes 3 ~ 5 min to reach thermal equilibrium, glass can break
causing injury
(2) bimetallic strip thermometer
- 2 strips of metal with different thermal expansion coefficients fixed together in
coil ! expands different extent when heated ! moves dial
(3) Bourdon gauge thermometer
- sensing element contains volatile fluid ! content expands when heated !
moves dial
electric thermo
resistance wire linear increase
thermister curved decrease
heat loss
R-50
E-30
C and C-15 tot
resp 5%
AND loop
NTS inhibts RVLM–>less SNS output
midaz dose
.5mg/kg PO
0.1mg/kg IV
ketamine
5mg/lg PO
clonidine
4mcg/kg PO kids
OBA 98%
glucose filtered dayly
180g
defibe I and V
high current (#capacitor) high voltage (2000)
monopolar diath limitation
penis, ears, fingers–>nil collateral
short burst
back up external defiub if ICD
NSAIDS in preg
third trimester terrible!!! DA closure
t/2 2H
Obuprofen met
CYP–>renal elim
ED space contents
fat, nerve roots, blood vessels and
lymphatics.
COXi
PL, endo (cyclin), sm m PGs
LA add to EDB
increase duration without motor block, improve quality of block
pethidine
active met norpeth–>seizure
addiction
ach LA onset 6min for 4hrs
sufent
old school opioid induction and post op analgesia
lipid sol –>rapid onset
hep and renal dep
hypotension, histamine release, tachy brady
minimal change in CSHT
Pneumoperitoneum
resp neuro GI
antifreeze
ethylene glycol
TRUP Sx
glycine tox
CVP in AF, tricuspi path etc
https://derangedphysiology.com/main/cicm-primary-exam/required-reading/cardiovascular-system/Chapter%20783/interpretation-central-venous-pressure-waveform
des vs sevo
des
methy-ethyl
sevo
methyl-isopropyl
both highly F
VOlatile met
Halothan The major metabolite is trifluoroacetic acid (TFA), which is protein-bound and this TFA–protein complex can induce a T-cell-mediated immune response resulting in hepatitis ranging from mild transaminitis to fulminant hepatic necrosis and possibly death.
The production of inorganic fluoride by the metabolism of halogenated agents may cause direct nephrotoxicity. Studies investigating methoxyflurane demonstrated an association between high fluoride levels (serum fluoride >50 μmol litre−1) and polyuric renal failure. Serum fluoride levels peak earlier and decrease more rapidly with enflurane than with methoxyflurane, making enflurane less nephrotoxic. Isoflurane is more resistant to defluorination and can be used for prolonged periods without significant increases in serum fluoride levels. Sevoflurane undergoes significant defluorination
sevo–>3-5% CYP2E1 metabolism to hexafluoroisopropanol and inorganic F- (which may be nephrotoxic)
Hepatic CYP450 (CYP2E1) metabolises C-halogen bonds to release halogen ions (F-, Cl-, Br-), which can be nephrotoxic and hepatotoxic. The C-F bond is minimally metabolised compared to the C-Cl, C-Br, and C-I bonds. All agents undergo hepatic oxidation, except for halothane which is reduced.
CHF2–>CO with soda lime (not present on sevo!
Halothane
Cl,Br–>potentent unstable, metabolismed
CF3–>inflammable
met trifluroacetic acid–>Pr:TFA–>t cell immune hepattis
neg ino, VD, impaired baro, vagal–>brady–>++decreased BP, decreased work and consumption
arrhytmogenic
catechol sens
ester amide linkage
evernote
LA hydophilic side
NH4
lipophilic is aromatic ring
LA S:F
Increasing carbons in hydrocarbon linkage aromatic ring or on the tertiary amine—>increased lipid sol and potency
Methy, propyl butyl group to amine end of molecule
methadone agonist
FULL not partial
Mg
PR prolong and AV SA ERP inhibit excitation of Adrenaline inhibit Ach release at NMJ and NAd in SNS uterine BD PETs MI bleed due to Cablock
minor
-flush, HA, Nausea
–>arrest
Mg level to Sx
googe: magnesium toxicity and plasma conc
Des BP
23C
N20 crit temp
36
prop HR
INITIAL EXCITATORY PHASE then peak effect coincides with drop in HR as tachy reflex inhibited.
Hence instrument Paeds airway as heart rate just starts to back off
anaphylactoid
Search Results
Featured snippet from the web
Anaphylactoid reactions are defined as those reactions that produce the same clinical picture with anaphylaxis but are not IgE mediated, occur through a direct nonimmune-mediated release of mediators from mast cells and/or basophils or result from direct complement activation.
anaphylaxis crossreaction
NDMR ammoniumgroup coumpound in cosmetic cough and cleaning
NDMR review
evernote
DoA morphine vs fenty why
nil redisp
active met
morphine and fentanyl clearance
similar (infact morphine slightly more!)
yet nil redistrib and active met
bup Moa and PK
NIL NMDA WRONG (methadone only)
peak 80min post IV! kappa blokced-->less resp dep less tol and euphoria high PrB yes renal impairment relevant
anaphylactoid
Anaphylotoxins c3,4,5–>bind to mast or basophil–>anaphylactoid
classic anaphylactoid: trigger–>Ag:Ig->comp–>mast
alternative: no clear trigger–>com–>mast
complement system
protolytic inflam cascade
reg by C1 esterasei 0defecient in angiooedema
comp–>ABO incompat reaction
CI
2STD from mean
adenosine and rec
Adenosine AGONIST
aslo iCamp–>neg inotropy
A1: Gi, in SA/AV node, cause decrease in HR. (k CH OPEN–>HYPERPOL–>neg chrono
A2A: Gs, coronary arteries (vasodilatation)
A2B: Gs, bronchiole smooth muscle (bronchospasm)
A3: Gi, cardioprotective in ischaemia, inhibits neutrophils degranulation
digoxin
digitalis lantana nat occuring cardiac glycoside min hep met non dialysable Rx hyperkalaemia and brady and use phenytoin
half life in textbooks
Each phase has its own halflife; usually the “overall” halflife quoted by textbooks is the halflife for slowest of the phases, which tend to massively ovepredict the “real” halflife of a highly fat-soluble drug
compartment
“A pharmacokinetic compartment is a mathematical concept which describes a space in the body which a drug appears to occupy. It does not need to correspond to any specific anatomical space or physiological volume”.
bi exponential washout phases
The distribution phase is the initial rapid decline in serum drug concentration
The elimination phase is the slow decline in drug concentration, sustained by redistribution of drug from tissue stores.
triexponential
https://derangedphysiology.com/main/cicm-primary-exam/required-reading/pharmacokinetics/Chapter%202.0.1/single-and-multiple-compartment-models-drug-distribution
The distribution phase finishes with the concentrations reaching their peaks in the peripheral compartments.
To call the next phase the “elimination phase” is probably incorrect, but it is a period during which the main effect on drug concentration is in fact elimination. This phase ends when the slow compartment concentration becomes higher than the tissue concentration and the total clearance is slowed down by the gradual redistribution of the drug into the blood compartment.
The last phase is called the “terminal” phase, also sometimes confusingly referred to as the elimination phase. In actual fact during this phase elimination is rather slow because the concentration of the drug in the central compartment is minimal. The major defining factor affecting drug concentration during this phase is the redistribution of stored drug out of the slow compartment.
triexponetial equation
Ae^-alpha.t + Be^beta.t +Ce&gamma.t
triexponential phases
- distribution V1->other compartments
- elimination is main process from V1–>Vo as high conc and NO REDISTRIBUTION FROM V2 OR V3 TO V1 some ongoing distribution V1–V3
- terminal elimination V1–> Vo occurs but is slow as El=Cl.c and c is low. it is further slowed due to redistribution from V3–>V1
limitation of compartment model
1) That the central compartment is the only compartment from which the drug is eliminated. Of course that is not the case, as for example in the case of cisatracurium where the drug degrades spontaneously no matteer where it is in the body, i.e. elimination takes place in numerous compartments simultaneously.
propofol half life
alpha is 2 min
beta ie terminal elimination is 6 hours
salbutamol met
liver inactive
OH 4,5–>nil COMT
nil MAO
anticholinergic in asthma
yes ipratropium
aminophylinne
methylxantine nonselective PDEi
heliox in asthma
79:21 or 60:40
reynolds number
radius!!!!!!!! air in a large tunnel–> turbulent
honey in a straw –>lamina
2r.v.d/viscoistiy
> 2000
why density irrelevant form lamina flow
R=8nl/pir^4
viscosity relevant density irrelvant
lamina vs turbulent flow consequence
lamina V=P.k with nice central fast spike
turbulent V= square root of p.k
naturally occuring levo or dextro
Most naturally occurring molecules are all one isomer (e.g. all levo)
so more potent
microcirc
smallest arterioloes, precap sphincter cap and venules
- ->SVR
- ->cutaneous shunt for temp
- ->exchange
Flow through capillaries is also intermittent, controlled by contraction or vasodilation of precapillary, terminal arterioles. Periodic contraction and vasodilation in microvascular beds (vasomotion) causes the flow through capillaries to increase and subside approximately every 15 sec.
figures for starling forces in microvasc
https://en.wikipedia.org/wiki/Starling_equation#Reflection_coefficient
placenta metabolic
the placenta contains enzymes that synthesize hormones such as oestrogen, progesterone,
chorionic gonadotrophin and placental lactogen.
It also contains pseudocholinesterase, alkaline
phosphatase, monoamine
butylcholinesterase
In humans, cocaine is detoxified to pharmacologically inactive products primarily by butyrylcholinesterase. Butyrylcholinesterase also hydrolyzes aspirin, succinylcholine, mivacurium, and heroin
roles of placenta
TIME
BF to placenta
At term, maternal blood flow to the placenta is approximately 600–700 ml/minute.
time of closure of fetal parts
FO 4-6weeks OR NEVER
DA 14 hrous then 14 days
DV hours #V8
neonatal cardio changes
The cardiovascular changes above can be modified
Elevation of RAP ! persistence of foramen ovale
Decrease PVR ! persistence of ductus arteriosus
Prostaglandins and hypoxia ! inhibit closure of ductus arteriosus
(1) Umbilical vessels are obliterated when the cord is clamped externally ! ↓blood
flow through IVC and ductus venosus
(2) Ductus venosus closes over 3 ~ 10 days
(4) First breath ! negative intrathoracic pressure ! oxygen enters lungs ! opening
of pulmonary vessels + ↓hypoxic pulmonary vasoconstriction ! dramatic fall in
pulmonary vascular resistance
(5) ↓↓pulmonary vascular resistance ! ↑pulmonary blood flow ! ↑venous return to
left atrium ! ↑left atrial pressure ! LAP exceeds RAP ! functional closure of
foramen ovale within minutes to hours of birth ! all RA blood passes into RV
(6) Anatomical closure of foramen ovale occurs over several days
(7) Ductus arteriosus constricts (high PaO2) and complete closure within 48 hours
(8) Other changes take several weeks after birth – ↓RV wall thickness, ↑LV wall
thickness, etc
first breathe
MAKEUP: Describe the first breath
Before birth: 20ml/kg fluid present in the lungs
- Most expelled during passage through birth canal (absorbed / expelled)
- Much is replaced by air with the 1st breath
o ↑compliance lung tissue
First breath: Requires large negative pressures (-50 – -60cmH2O)
Subsequent breaths easier
- establishment of air-liquid interface
- Surfactant action in ↓surface tension
FRC is established quickly
- 10min → 17ml/kg
- 30 – 60 min → 30ml/kg (adult value)
N20 to anaemia
- N2O oxidises Cobalt ion on B12—> co factor for methionine synthesise for folate
