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]
