late sept Flashcards
ca ionized normal range
1.1-1.3 mmol/L.
K role
brandis p15
hyperkalaemia ECG cahnge Cx
less neg RMP–>excitable and slow
myoctye RMP
-90
antiarrhytmics
Pek and Hill adds classifies SVT (slow AV) -BB, CCB, adenosine, digoxin Ventricular (decreased myocyte velocity but AV normal) -lignocaine Both SVT and Ventricular -amiodarone, flecainide, procainamide, -sotalol-effect beyond Betat Digoxin tax -phenytoin (1b)
digoxin
less Ca efflux!
adenosine
CORE
-nucleoside
3mg/ml
dose 3mg
within 10 for 20s Q1min
FLUSH, TACHYPNOEA, CHEST DYSCOMFORT, BRADY-VF, HB
met: There are two important metabolic fates for adenosine. Most importantly, adenosine is rapidly transported into red blood cells (and other cell types) where it is rapidly deaminated by adenosine deaminase to inosine, which is further broken down to hypoxanthine, xanthine and uric acid, which is excreted by the kidneys.
esmolol
CORE
RBC esterases weakly active met witha 3hr t/2
on in <10 of in<20min
cocaine
Approximately 30-50% of cocaine is metabolized by hepatic esterases and plasma pseudocholinesterase,
yes NAd and DA RUI–>seizure then coma
1-4%
20min DoA
toxic dose 3mg/kg
r squared ratio
- 4 is 100%
3. 5 is 0% saO2
laser
gground state–>absorb energy–>excitable–>stimulated emmision
excited gets stim–>spont emmision
conent CO2 and O2/l
520/200
fast twitch slow twich
fast–>glhycolysis
slow–>OP with myoglobin
regional BF
Having Sex usually brings man kids later
dynamic airway compression
- During forced expiration, after the initial effort dependent rise in flow rate to maximum, the flow rate becomes effort independent, ie ↑ effort does not result in ↑ flow rate
- This is due to dynamic compression of the airways
- During passive expiration, the driving pressure for gas flow is (alveolar P – mouth P)
- During forced expiration, the high intrathoracic (or intrapleural) pressure that surrounds the airway will at some point equal then exceed the pressure within the airway lumen as pressure drops from alveolus towards the mouth due to conversion to kinetic energy for gas flow – this is the equal pressure point (EPP)
Thus, flow rate depends only on the elastic recoil property of the lung and the lung volume
Hz to VF
50Hz worst
diathermy Hz
1megaHz
y axis is voltage
heat diathermy
curretn squared.resistance
diathermy no shock
Monopolar diathermy
200 kHz -> 6 MHz
neutral and active
neutral = large conductive area -> low current density and minimal heat
active = small contact area + high current density
Bipolar diathermy
lower power output
output between 2 points on forceps -> high local current density
no current passes through rest of body
danger of diathermy
burn, electric, trigger defib, smoke is cancer, interfere with monitoring
N20 make
NH4NO3
poynitng
bubbles–>pseudocrit temp
NOTthe idea that below -5C–>liquid vapour interface–>hypoxic mix so HEAT IT UP
N20 SE
nil cofactor for methionine synthetase–>nil folate
–Demyelinating Dx (subacute combine degenrattion of cord.
–megaloblastic–>agranulocytosis
teratogenic in rats
venturi
CORE
if p drops due to opening Vincreases–>entrail
increased flow–>increased entrailment –>consistent FiO2
turbulent flow and densiy
For turbulent flow, resistance is proportional to fluid density and is less dependent on
viscosity
stewarts approach
CORE
Dependent variables:
H+ OH– HCO3– CO32- HA (weak acid) A– (weak anions) Independent variables:
pCO₂
ATOT (total weak non-volatile acids)
SID (net Strong Ion Difference)
SID
core
SID = [strong cations] – [strong anions]
apparent SID = SIDa = (Na+ + K+ + Ca2+ + Mg2+) – (Cl– – L-lactate – urate)
Abbreviated SID = (Na+) – (Cl–)
In normal human plasma the SID is 42 mEq/L
flow meter
core
evernote
pressure measurement
core
barometer vs manometer
strain gauge diaphram
bourdon gauge
BP cuff
core
sphygmometer
SI base units
cor
Sec Meter Mole Ampers Candella Kg Kelvin
standard BE
pH ‐ Measured directly
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.
BASE EXCESS = Amt of Acid or Base that must be added to the blood
sample to restore the pH back to 7.40 if the pCO2 is N (40mm)
STANDARD BASE EXCESS = As for BE but equilibrated with a
specimen of anaemic blood – Hb = 5,0
normal V:Q
0.8 due to some shunt at bases
neonat 0.4 due to more shunting
anaerobic threshold
The anaerobic threshold is the highest exercise intensity that you can sustain for a prolonged period without lactate substantially building up
pulse ox plethysograph
photdiodes
500Hz
5% CO in smokers
12s delay to get average R2 over several beats
functional vs fractional Hb
sats prob functional OHb/OHb+deoxHb
blood gas fractional OHB/all Hb including met and COHb
cooximetry can do this too
cockraft gault
Core
(140-age).LBW/Crx72
U:Cr
https://litfl.com/urea-creatinine-ratio/
fixed acid per day
70mmol/day
HCO3 22x180L=4000/day
renin secretion trigger
core
Renin secretion from the juxtaglomerular apparatus granular cells is stimulated by renal sympathetic
nerve activity, by a direct β1 effect. Also, the fall in
GFR induced by sympathetic nerves reduces the
flow of sodium and chloride to the macula densa,
and this stimulates renin release.
pressure diuresis
Therefore, when the blood
pressure increases blood is diverted from the cortical nephrons to the juxtamedullary nephrons
and the vasa recta capillaries. This tends to wash
solutes (Na, Cl and urea) from the medulla and
reduces the concentrating ability of the kidney,
leading to an increase in urinary loss of water and
solutes. This phenomenon is sometimes known as
pressure diuresis
tubuologlom feedback
An increase in GFR raises the protein concentration in glomerular capillary plasma. This proteinrich plasma enters the peritubular capillaries and
increases the oncotic pressure in them, which
enhances the movement of solutes and water from
the lateral intercellular space into the peritubular capillaries.
Adenosine receptor antiplatelet
Adenosine is an important regulatory metabolite and an inhibitor of platelet activation.
Dipyridamole has two known effects, acting via different mechanisms of action:
Dipyridamole inhibits the phosphodiesterase enzymes that normally break down cAMP (increasing cellular cAMP levels and blocking the platelet aggregation response[4] to ADP) and/or cGMP.
Dipyridamole inhibits the cellular reuptake of adenosine into platelets, red blood cells, and endothelial cells, leading to increased extracellular concentrations of adenosine.
Rx HITS
Use of fondaparinux, a selective factor Xa inhibitor, is common for treatment of HIT
histamine rec
1 eg T1HS IgE mast cell
2 is parietal cell
propoton pump
H:KATPAase
Cl passive flow
K that sucked out of stomach passivly flows back in.
ion trapping
evernote
H2 antag
cimetidine, ranitidine
PCV vs VCV
evernote cram
ICP
5-15mmHg
Porphyrin
BG
- Porphyrin is a precurser of haem and haem containing p450
- acquired or genetic—>deficiency of enzyme that transform 1 porphyrin to another form—>excess of one of these
- Haem precursor is toxic (lack of haem not really a prevalent problem)
Porphyric crisis due to build up of porphyrins—>skin and nervous system effects
- abdo and chest pain
- vomiting fever
- HTN tachy
- Confusion
- Blisteres
Complication
- seziure
- Paralysis
- Fatal
Rx
* IV haem or glocuse—>decreased haem synth—>less precursor accumulating
Triggers
- barbituates
- halothane
- lignocaine
- Cociane
how capo IR works
- The remaining infrared radiation falls on the thermopile detector, which in turn produces heat. The heat is measured by a temperature sensor and is proportional to the partial pressure
PTC and TOF correlation
PTC of <5—>16min to TOFC of 1 and 66min to TOFCR 0.9
PTC of 9=TOFC of 1
ester LA met
core
esterases
–>paraamino benzoic acid–>allergy
procaine
amethocaine
Na Ch state and LA
high affinity to the open state, and weaker binding to the closed resting state. Slow binding of high affinity for the inactivated state
ECG y axis
0.1mv
GOLDEN osmolarity osmolality tonicity
SUMMARY:
NaCl is definitely has the same osmolality as blood 308*.93=287 and is isotonic
CSL definitely has less osmolality than blood278X0.93=258 (yet for reasons that mess with my head is widely (but not universally) reported as isotonic-despite the fact that the osmolality is less AND that lactate is taken up into cells as an ineffective osmol)
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
closing capacity
GOLD
This is clinically relevant during preoxygenation, as it will limit the denitrogenation that can occur.
It influences denitrogenation of the FRC. Collapsed lung units will not have nice fresh oxygen wafting into them while you preoxygenate your patient prior to induction. Factors which decrease the FRC (obesity, etc) or increase the closing capacity (old age) increase this effect, whereas techniques which increase the FRC (eg. the use of PEEP) ameliorates it.
SUMMARY
1) FRC is generally unchanged with age. Closing capacity will exceed this, meaning you can’t blow the nitrogen out of some of the basal alveoli during preoxygenation but you’d get into a pickle, i believe, arguing that the FRC has disappeared above the age of 66. (they still a have a residual volume and expiratory reserve in their lungs) and closing capacity just means that a few basal alveoli have started to collapse.
2) enoxaparin can be given IV in STEMI and PCI
CSL is hep failure
Strong ions: These are fully dissociated at a normal pH and exert no buffering effect. They include Na+, Cl–, Ca2+, Mg2+, and organic acids, e.g. β-hydroxybutyrate, lactate
SID of zero–>acidosis and nil HCO3 production from lactate
and ph 6.5
Platelet assessment
Platelet function analyser (PFA-100)
HME
During expiration, the HME picks up some of the moisture from the expired humid air.
These water droplets retain some of the heat from the gas which has carried them.
During inspiration, the incoming torrent of air collects these warm water droplets, and carries them as vapour into the lungs of your patient.
humidity units
g/m^3
ECG
lead three positive electrode is limb not LA
fuel cell
Cathode electrons consumed (RIG) in presence of O2—>more current
Cath has a great rig and consumes lots of O2 and energy
liver acid base balance
The lactate ions are removed, principally by the liver–>HCO3 production
INR why?
PT or/and INR explore the extrinsec pathway of coagulation that involves all vitamin K dependent coagulation factors. Factor 7 is more sensitive to vitamin K deficiency (nutritional or by oral anticoagulants). It’s T1/2 is shorter than for factor 2 for example.
aPTT PT
Core
activated partial thromboplastin time table tenis intrinsix XIII etc
prothrombin time. extrinsic ie TF!
HABR volatile
Volatile anaesthetics
All volatile anaesthetics reduce cardiac output and mean arterial pressure and thereby reduce liver blood flow. Isoflurane, sevoflurane, and desflurane undergo minimal hepatic metabolism and can be regarded as safe.8 Desflurane is probably the ideal volatile agent, being the least metabolized and providing the quickest emergence from anaesthesia. It also relatively preserves hepatic blood flow (it has minimal effects on the hepatic arterial buffer response) and cardiac output.
This phenomenon is termed the “hepatic arterial buffer response”. Halothane impairs this response and decreases HBF secondary to reductions in both PBF and hepatic arterial blood flow in animals
halothane tox
type 1-decreased BF–>anaerobic met
type 2-oxidative met–>TFA acts as haptan–>AB bind–>AI hepatitis
reflexes in heart
etc
The Bainbridge reflex, also called the atrial reflex,
H+ measurement
http://www.partone.lifeinthefastlane.com/blood_gases.html
Rx central antichol
physostigmine
hyoscine
Hyoscine hydrobromide (1st) P+H and Petkov only reference this one. -scopalaine—.AE with antichol Symptoms
Hyoscine butybromide (buscaban) -butyl added (semisynthetic)—>buscapan—>better as safer as nil central antichol
atoprine and glyco offset
hepesterase vs minimal met and renal clearance
LPBR
CORE
Low pressure receptors are baroreceptors located in large systemic veins, in the pulmonary arteries, in the walls of the atria, and ventricles of the heart.[2] They are also called volume receptors. These receptors respond to changes in the wall tension, which is proportional to the filling state of the low pressure side of circulation (below 60mmHg). Thus, low pressure baroreceptors are involved with the regulation of blood volume. The blood volume determines the mean pressure throughout the system, in particular in the venous side where most of the blood is held. Increasing stretch of the receptors stimulates both an increase in heart rate and a decrease in vasopressin (ADH) secretion from posterior pituitary, and renin and aldosterone. The decrease in vasopressin secretion results in an increase in the volume of urine excreted, serving to lower blood pressure. In addition, stretching of atrial receptors increases secretion of atrial natriuretic peptide (ANP), which promotes increased water and sodium excretion through the urine.[1]
CMRO and CBF
ketamine and NO2 increased both CBF and requirement
autoreg CBF
Although the brain comprises only 2% of the body
weight, it uses 20% of the total body’s resting oxygen consumption. e lack of storage of substrates
and the high metabolic rate of the brain account
for the organ’s sensitivity to hypoxia.
Regional cerebral blood ow (CBF) varies with
the metabolic rates of local areas of the brain. CBF
and cerebral metabolism are said to be coupled.
Various regulatory mechanisms maintain the CBF
at physiological levels. Local metabolic factors are
involved in ow–metabolic coupling, and these
include H+, K+, adenosine, phospholipid metabolites, glycolytic metabolites and nitric oxide.
Autoregulation refers to the phenomenon in
which CBF is kept constant over a mean arterial
blood pressure range of 50–150 mmHg (6.7–20 kPa).
diathermy distance
6 inch rule!
GTN
50mg in 1000ml–>50mcg per ml
special giving set (not Polyethyline)
hepatic nitrate reductase
elim t/2 1min IV
Sodium nitopruside
brown glass admin.
cocaine
MAOi, RUI,LA
atropine neo glyco dose
- Atropine dose 20/kg, glycolic dose 50/kg. Neostigmine 50 (2.5mg is 50kg)
*
ECG 25mm/s
So 5mm big box is 0.2s
So small 1mm is 0.04s
10mm->1cm
1000ms->1s
phenylepherine met
MAO
hence only direct!!!!!!
hypokalaemia
Effects of hypokalaemia on the ECG
ECG changes when K+ < 2.7 mmol/l
Increased amplitude and width of the P wave
Prolongation of the PR interval
T wave flattening and inversion
ST depression
Prominent U waves (best seen in the precordial leads)
Apparent long QT interval due to fusion of the T and U waves (= long QU interval)
With worsening hypokalaemia…
Frequent supraventricular and ventricular ectopics
Supraventricular tachyarrhythmias: AF, atrial flutter, atrial tachycardia
Potential to develop life-threatening ventricular arrhythmias, e.g. VT, VF and Torsades de Pointes
QT prolonged
Antipsychotics Chlorpromazine Haloperidol Droperidol Quetiapine Olanzapine Amisulpride Thioridazine Type IA antiarrhythmics Quinidine Procainamide Disopyramide Type IC antiarrhythmics Flecainide Encainide Class III antiarrhythmics Sotalol Amiodarone Tricyclic antidepressants Amitriptyline Doxepin Imipramine Nortriptyline Desipramine Other antidepressants Mianserin Citalopram Escitalopram Venlafaxine Bupropion Moclobemide
glyco dose
10mcg
atropin
20mcg
neo
50mcg
damping
Damping is the decrease in the amplitude of an oscillation or wave motion with time
PHTN Cx
evernote
PEEP renal effects
stim stretch rec in atria–>increased ANP–>inhibited RAAS
CCF Rx
digoxin
funny channel blocker
esmolol indication
not HTN crisis–>high afterload +neg ino–>BAD
HOCM with Hypotension
BB renal
inhibit RAAS
BB eyes
increased outflow
?decreased prod
heart mechanical help
A ventricular assist device (VAD) is an electromechanical device for assisting cardiac circulation, which is used either to partially or to completely replace the function of a failing heart.
ohms assumption
rigid pipes, lamina, neutonians fluid
Pao2 predicted
CORE
Aa gradient (age+10)/4 10 y.o=5mmHg
shunt
CORE
Normal shunt
Anatomical shunt
Thebesian veins, which drain directly into the left cardiac chambers
Bronchial circulations, which drain into the pulmonary veins
Functional shunt
Blood draining through alveoli with a V/Q between 0 and 1.
This may not be true shunt, as blood may have some oxygen content but not be maximally oxygenated
Pathological shunt
Pathological shunting can be anatomical (e.g congenital cardiac malformations), or physiological (e.g. pneumonia causing alveolar consolidation).
Intra-cardiac e.g. VSD
Extra-cardiac
e.g. Pulmonary AVM, PDA
DS
The total dead space (also known as physiological dead space) is the sum of the anatomical dead space plus the alveolar dead space.
shunt equation
CORE
GOLDEN
content of arterial oxtygen=content of shunted O2 +content of nonshunted oxygen.
one lung ventilation shunt approach
CORE
Fio2 wont do much
PEEP to good lung wont do much-perhaps optimises the PVR
CPAP to bad lung–>good option
clamp
HPVC anaesthetic
propofol doesnt effect
NO
Epoprostenol
tirofibin
GP2b3a
endothelial fucntion clotting
Healthy endothelial cells express antiplatelet and anticoagulant agents that prevent platelet aggregation and fibrin formation, respectively.
dabagatran
double Moa
double duration
dialyis
Dual reversal
heparin selectivity
In commercially prepared UH the ratio of anti-IIa activity to anti-Xa activity is approximately 1:1
enoxaparin
Depending on the molecular size distribution, this ratio will typically vary from 4:1
protamine doa
Because the action of protamine is shorter than that of heparin, follow-up coagulation tests should be performed to detect a “heparin rebound” effect
t/2 life rubbish
clopidogrel irreverible effect
gent post ABx effect
alpha vs beta t/2
warfarin MoA
CORE
Warfarin inhibits epoxide reductase (specifically the VKORC1 subunit), thereby diminishing available vitamin K and vitamin K hydroquinone in the tissues, which inhibits the carboxylation activity of the glutamyl carboxylase.
diffusion limitation
CORE
CO is diffusion limited as nil back pressure established to restrict further diffusion
test
uptake=Diffusionconstant.PACO
single breath of CO with 10s hold and measure insp vs exp for difference.
liver and PL
Thrombopoietin
Thrombocytopenia is a common complication of chronic liver disease, characterised by decreased TPO synthesis, reduced haematopoiesis and increased platelet destruction in the spleen
Haematopoiesis refers to the commitment and differentiation processes that lead to the formation of all blood cells from haematopoietic stem cells. In adults, haematopoiesis occurs mainly in the bone marrow (medullary), but it can also occur in other tissues such as the liver, thymus and spleen (extramedullary).
liver coags
Within the liver, hepatocytes are involved in the synthesis of most blood coagulation factors, such as fibrinogen, prothrombin, factor V, VII, IX, X, XI, XII, as well as protein C and S, and antithrombin, whereas liver sinusoidal endothelial cells produce factor VIII and von Willebrand factor.
prothrombin X
heparin present
heparin
Within the liver, hepatocytes are involved in the synthesis of most blood coagulation factors, such as fibrinogen, prothrombin, factor V, VII, IX, X, XI, XII, as well as protein C and S, and antithrombin, whereas liver sinusoidal endothelial cells produce factor VIII and von Willebrand factor.
heparin dose
Within the liver, hepatocytes are involved in the synthesis of most blood coagulation factors, such as fibrinogen, prothrombin, factor V, VII, IX, X, XI, XII, as well as protein C and S, and antithrombin, whereas liver sinusoidal endothelial cells produce factor VIII and von Willebrand factor.
colloid
a homogeneous non-crystalline substance consisting of large molecules or ultramicroscopic particles of one substance dispersed through a second substance. Colloids include gels, sols, and emulsions; the particles do not settle, and cannot be separated out by ordinary filtering or centrifuging like those in a suspension.
colloid
dextrans, gelafusion, starch, alb, RBC
vasopressin threshold
- thirst alone at 290 decause max urine reab
SID IVF
SID of Resuscitation Fluids :‐ Effect on Plasma HCO3‐ levels
= 27 NEUTRAL
< 27 ACIDAEMIA ( ⇓ Plasma HCO3)
> 27 ALKALAEMIA ( ⇑ Plasma HCO3)
plasmalyte
acetate, gluconate
MH test
The standard procedure is the “caffeine-halothane contracture test”
genetic
sufent
1000x potency of morphine petkov #synthetic
pethidine
10x less potent vs morphin
anti chol
interat with MAO–>seretonin sx
methadone
also 5HT and NAd reuptake
recemic opioid and NMDA
40% excreted renally unchanged full ago t/2 2 days interpatient variability less sedating vs morphine
esterases
acid and ETOH
butyl-sux, miv, ester, cocaine, heroine Acetyl NSTE-remi, Cis, atrac RBCesterase-esmol ALP
dibucaine
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)
DA, NA Ad structure
x
meteraminol met
liver
hydralazine
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)
digoxin antiarrhythmic
increased IC K–>slow AV phase 4
amiodarone OBA and SE
variable ++ approx 50%
PK
(altered PrB and met)
PD
methylxanthine
PDEi
fixed external upper airway
exp fix and insp fixed
echo PHTN
bernouli princip and RAP and TR velocity
glucose CSF
low
CSF drainage
monroe
sylvia
why roc quick
bowman principle
COX2i
less bleeding, less GI ulcers
CI for drug
allergy, refusal
tramadol
yes racemic
yes metabolites is more potent at Mu
gabapentin
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)
clop rec
P2Y12
hyperkalaemia ECG
essentially CCB
–>increased PR, QRS, sinus brady, heartblock arrest.
N2O stats
SVP 50bar
O:G 1.4 (low potency)
hepatic reservoir mechanism
The sinusoids
form a low-pressure microcirculatory system of
the acinus with sphincters at the hepatic arteriole,
the hepatic venous sinusoid and arteriolar–portal
shunts. Thus, the sinusoids act as a significant
reservoir for blood, depending on the tone of the
sphincters
change mac catagories
normal, disease, drug
placenta metabol
butylcholinesterase
MAO, COMT, bHCG, lactogen, proge,est
triple point water
The triple point is at A where these three lines intersect and where water, water vapour and ice can exist in equilibrium. The temperature at which this occurs is defined as 273.16 K on the thermodynamic temperature scale. (The triple point is not exactly at 0 oC because under the pressure of its own vapour ice melts at about 0.0075 oC.)
SHC
j/kg/C
humidity at 37C
The SVP of water at 37°C is 47mmHg and contains 44mg/l of water whereas at room temperature (20°C) it is 20mmHg and contains only 18 mg/l).
CSHT remi
3-8min
cis trans define
Geometric isomerism or cis-trans isomerism describes the orientation of functional groups within the molecule
ECY axis
.1mv per mm square
TR CVP
In tricuspid regurgitation, the backflow of blood out of the right ventricle obliterates the normal x descent. The c wave becomes accentuated and fuses with the v wave, as both are the results of right ventricular contraction (and the v wave peak pressure is often the same as the right ventricular peak systolic pressure).
big a wave
Prominent a waves: tricuspid stenosis, or reduced right ventricular compliance
protein C
Activated protein C exerts its anticoagulant activity primarily through inactivation of coagulation factors Va and VIIIa, which are required for factor X activation and thrombin generation.
the 5-8 inhibits the backling movement
resp change preg
CORE
loose 350 can of cook in FRC
gain 150ml in TV
most MV is due to TV
CO and MV change in preg
50% increase in both
CO is linear
MV peat at 20weeks
isobastic
reference point
R2
R corresponds to SaO2
— SaO2 100% = R 0.4
red/IR
VIE temp
a temperature of -150oC (critical temp -119oC)
bohr effect
allosteric modulation–>T state stabilization (less CO2 affinity)
placenetal tf drugs
A variety of nutrients, waste products and toxins
cross the placental barrier by simple diusion,
facilitated transport, active transport, endocytosis
and bulk ow.
Most drugs and respiratory gases cross by
simple diusion. e rates of transfer of these
substances follow Fick’s law. Substances such as
glucose cross through the placenta more rapidly
than predicted by Fick’s law, because of facilitated diusion. Amino acids, calcium, iron and
vitamins A and C are transported by active transport of substances against a concentration gradient. Bulk ow of water by osmotic and hydrostatic
forces may transport small molecules, whereas
large molecules such as IgG cross the placenta by
endocytosis.
CHST prop at 8
The CSHT for propofol after a 8 hour infusion is around 50 minutes.
propofol
CORE
glycerol isotonic
NaOH
propofl allergy
The propofol is mixed in a liquid containing soybean oil and a substance called egg lecithin. Lecithin is a fatty substance found in some plant and animal tissues. Patients who are allergic to foods, including soy and egg, are allergic to proteins in the foods and are not allergic to the oils or fats in the foods.
propofol
egg emulsifies
Soy sticks
Soybean oil holds the bulk of the propofol in a medium that can be stabilized and dispersed; lecithin serves as an emulsifier to stabilize the small propofol–soybean oil droplets in aqueous dispersion, and glycerol maintains the formulation isotonic with blood.34The pH of the emulsion is adjusted with the base, sodium hydroxide, to around 7.0–8.5 for optimal emulsion stability.
BE
They defined base excess as the amount of strong acid (in mmol/L) that needs to be added in vitro to 1 liter of fully oxygenated blood in order to return the sample
hamburger effect
GOLD
It increases the unloading of oxgyen, because of the allosteric modulation of the haemoglobin tetramer by chloride (it stabilises the deoxygenated T-state)
Chloride entering the cell draws water in along its osmotic gradient, increasing the haematocrit of venous blood relative to arterial blood
CBF for ischaemia
normal is 50ml/100g/min
<20–>ischaemia
<10–>dead
allosteric
x
haldane
HbO+H–>HbH+O2
hypersen types
1 Ige
2 Ig:A eg ABO incomp
3 IgA nephropathy complex
4 delay T cell MS
QT
It is advisable not to give succinylcholine if at all possible, as it is known to prolong the QTc
phenylepherine
100mch push
partial pressure
CORE
the pressure that would be exerted by one of the gases in a mixture if it occupied the same volume on its own.
Daltons law
Henry’s law amount dissolve
buffer
imidazole groups of histidine residues
HI HI HI HI HI HI HI
diffusion perfusion limited
Both oxygen and carbon dioxide exchange is perfusion-limited.
back pressure
SAGM
SAG-M2 (saline adenine glucose mannitol)
50% sats point
p50 is the oxygen tension when hemoglobin is 50 % saturated with oxygen
MG GBS
Myasthenia=muscle weakness Gravis= grave
AI antibodies block or destroy NAChR at NMJ
-Think Myastenia—>muscle
GBS
-AI attach of peripheral nerves
—>raised potassium with SUX
-think Succy Syndrome
damping role
Frequency response
With optimal damping, it is possible to maximise the frequency response along the “flat range” of frequencies (the range of frequencies over which the natural frequency does not amplify the signal by very much). This optimal level of damping corresponds to a “damping coefficient” of 0.7, damping coefficient being an index of the tendency of the system to resist oscillations.
The optimal damping coefficient of a system therefore depends on the natural frequency. With a very low natural frequency, the flat range is very narrow, and no amount of damping can prevent the distortion of the measured waveform by resonant amplification. On the other hand, with a very high natural frequency the system will never distort any waveforms within a clinically relevant range, and it doesn’t matter what your damping coefficient is.
elimination
Elimination is removal from plasma (met and distrib and excretion)
LA ionization
However the proportions vary between the drugs: lignocaine has a pKa of 7.9 and is approximately 25% unionised at pH 7.4 . Bupivacaine has a pKa of 8.1 and hence less of the drug is unionised at pH 7.4 (about 15%).
hepatic artery
Constriction (α), then dilation (β)
portal vein inflow
splenic
sup mesenteric
ie the splachnic circ
