Homs Practical Flashcards
High pass
Allows higher frequencies and low pass is vice versa
Occluding both arteries
Brachial pulse
Nernst equation
Ek = 58log10 ([outside]ref/[inside]test)
Membrane circuit representation
Resistor, capacitor and voltage source in parallel
Membrane time constant
T = Rm x Cm
Voltage capacitance relationship
V= QC
Adding capacitor
Drops current to 0 then allows it to rise again as charged- reaches Vmax when fully charged
Time constant percentage charged
At time t, voltage is 63% of final voltage
Frequency of UK mains
50Hz
How is a partial short circuit formed
If tissue between two electrodes has low electric resistance- smaller potential difference than expected will be recorded
Stimulus artefact
Stimulating current directly to recording electrodes through body or liquid on surface
Earth electrode
Channels some unwanted stimulating current
AP unaffected
Swapping around recording electrodes
Upside down APs
Intracellular recording convention
Ext electrode= reference
Internal is test (therefore test relative to ext = negative)
Normal electrode set up
Reference electrode closer to stimulating cathode
Stim anode; stim cathode, earth, recording ref (external); recording test (internal)
Anode block
Having stim anode after stim cathode - leads to hyperpolarisation preventing impulse passing onwards
Recruitment
Adding lateral fibres- respond to stimulus- lateral fibre has higher frequency and longer latency than medial fibre
Direction of AP in medial and lateral fibres
Cranial- caudal in MGF, caudal-cranial in LGF
Temperature effect on APs
Affects kinetic properties of channel gating mechanisms- cooling slows rate of sodium channels opening therefore slower conduction velocity
Repolarisation slower and sodium channels inactivate slower and potassium channels open slower
Compound AP
Many muscle fibres response
Latency
Time between first stimulus and first sign of a response
Short PR interval
Wolff Parkinson white syndrome- extra rapid path for signals to pass from atria to ventricles
Long PR value
First degree AV block
Long QRS interval
Bundle branch block
Long QT interval
Long QT syndrome- genetic mutation
Electric systole
Time between Q wave to end of T wave (rest is diastole)
Exercise effect on systole and diastole pressures
Systole pressures increase, diastole pressures fall
Heart rate increase effects
Increases slope of pacemaker potential
Adrenergic stimulation B1 increases current through VGKC= more rapid repolarisation of cell after plateau = shorter cardiac AP
B1 stimulation = calcium pumps in SR work harder quicker removal of Ca2+ from cytosol= rapid relaxation
Respiratory sins arrhythmia
Increase in HR on inspiration, decrease in HR in expiration
Normal
Mean arterial pressure
D + 1/3(S-D)
Active hyperaemia
From of metabolic auto regulation
Demand outpaces supply changing metabolic levels leading to vasodilatation
Increasing exercise intensity on breathing rate
Increases proportionallly then disproportional as exercise becomes anaerobic (low pH)
Exercise effect on Pulse rate
Increases over first minute then stabilises at steady state
Exercise effect on %SpO2
No change - body not reliant on negative feedback for gas levels
Alveolar ventilation equation
VA= (VECO2/PACO2) xK
Cardiac output- fick
CO= rate of CO2 production/ (venous-arterial CO2)
RQ
Amount of CO2 produced/ amount of O2 taken in
how to avoid aliasing
set sampling rate at more than twixe frequency of origimal signal
potential of membrane recorded as…
potential always reported as test relative to ref
capacitive current
flow of electrons onto left plate and off of right plate- looks like current flowing through capacitor
how to increase capacitance
larger surface area of plates, plates closer together (thinner insulating layer)
capacitance key points
stores charge
capacitor takes time to charge and discharge- slows change in voltage
capacitance of excitable cell membrane affects velocity of AP conduction
how does myelination increase conduction velocity
not through T=RC as myelination increases R but also decrease C- not much change
but increased R increases length constant (lambda)
colours of electrodes
cathode (black)
anode (red)
earth (green)
latent period
time taken for AP to travel from stim cathode to 1st recording electrode
conduction velocity through absolute method and reeason why its not great
use single distance (D) and latent period (LP)
v=D/LP
delay with initiating AP in first place and AP peak measuring to occurs after first sign of electrical activity- gives v slighlty lower than true conduction v
if use strong stim current, AP generated further from cathode therfore v too high
accurate conduction v
compare equivalent APs on two traces, obtained when recording at 2 diff distances -difference method
v= (D2-D1)/(LP2-LP1)
ST segment
ventricular muscle all depolarised
what does a bio amp do
electrically isolated device for increasing size of v small voltage (safe)
aorta bp compared to pulm artery bp
5-6 x greater
how to increase systolic p
more blood pushed out arteries stiffer (less compliant)
misdiagnose hypertension using pressure cuff if…
if cuff v narrow relative to arm- gives falsely high bp (misdiagnose hypertension)- ie obese subject with larger arms
misdiagnose hypotension if..
cuff wide relative to arm- falsely low bp
recommended width of cuff
40% circumference of midpoint of arm
bp slighlty higher in which arm
right- use this as standard
cause of functional and reactive hyperaemia
hypoxia
accumulation of vasodilator metabolites (ie increase in PCO2, lactic acid, adenosine, K+ and temp, fall in pH)
how do pulse oximeters work
measures colour of blood to determine percentage saturation of arterial blood (more saturated = brighter red)
gives peripheral oxygen saturation (%SpO2)
end expiratory sample
first gas similar to atmospheric air (dead space)
terminal stages=exhalation from alveoli(arterial blood)
resp gas analyser measures
Dried O2 and CO2 percentages
measurements made in douglas bag(CO) exp
arterial blood gas concs amount of gas exhaled in 5 mins no. of breaths in 5 mins conc of O2 nad CO2 in exhaled gas last 3 measuremtns = tidal vol, rate of CO2 and O2 consumption
why shouldnt you hyperventilate in douglas bag exp
blows off a lot of stored CO2- gives abnormally high values for CO
haemorrhage events
BV falls -> decrease in VR -> decrease MSP -> decrease atrial P -> decrease CO -> HR increases to try to restoore MAP -> increase in TPR -> decrease in splanchnic flow
normal glucose levels
4-7mmol/l
cephalic phase of digestion
parasympathetic stimulation of beta cells via vagal ACh = anticipatory insulin release
what potentiates insulin release in response to oral glucose
incretins- GIP and GLP-1
How is insulin release inhibited in exercise
sympathetic stimulation of alpha-2 receptors - increases blood glucose
most common source of error in RQ
hyperventilation- increases amount of CO2 unloaded from blood (should be aiming for an expired %O2 od 14-17%
how much heat does each gram of sweat take
2.45kJ
