physiology 2 Flashcards
what are the basic leads
standard limb leads
what planes to the limb leads work in
vertical or frontal plane
coronal plane
what are the 3 standard limb leads
I
II
III
what does SLL I record
left arm with regard to right arm
what does SLL II record
left leg with regard to right arm
what dose SLL III record
left leg with regard to left arm
what is transmitted well to the ECG
fats events - depolarisation and repolarisation of the action potentials
what is not transmitted well to the ECG
slow events - the plateau of the action potential
what causes a upward going blip
a move of approaching depolarisation
or a wave of repolarisation going away
what 3 limbs have electrodes on them
the left leg
left arm
right arm
what has the positive electrode on it
the limb being recorded with regards to another limb
what happens if a wave of depolarisation goes away from the limb being measured
a downward blip will occur
what happens when a wave of repolarisation approaches the limb being measured
a downward blip will occur
what does the time for QRS tell us
time for whole ventricle depolarisation
how ling dose the QRS complex take to complete - abnormal
about 0.08 secs
abnormal is greater than 0.12 seconds
what is the PR interval showing
time from atrial depolarisation to ventricular depolarisation
how long is the PR interval - why
normally = 0.12 - 0.2 seconds
due to wave having to pass through slow AV node
what does the QT interval show
the time spent were the whole ventricle is depolarised
what is the normal QT interval
about 0.42 seconds at 60bpm
depends on HR
can you see atrial repolarisation - why
NO
as the possible signal coincides with the ventricle depolarisation
it gets ‘‘drowned out’’
why is the QRS complex so complex
different parts of the ventricle depolarise at different times in different directions:
what causes the Q wave - and the downward blip
the interventricular septum depolarising from left to right
away from the left leg = blip down
what causes the R wave - why the upward spike
the bulk of the ventricle depolarises
upward blip = goes from endocardial to epicardial surface (inside to out)
what causes the S wave
why the downward blip
the upperpart of the intraventricular septum depolarises
it goes from bottom to top
why is the t wave positive
as the action potential is longer on the endocardial cells then the epicardial cells - the wave of repolarisation runs the other way (ALMOST LIKE DOWN A CONC GRADIENT)
why is the R wave bigger on SLL 2
as the heart is tilted it follows the direction of SLL 2 the best
what would happen if heart rotated
you would see a decreased SLL 2 R wave and see either an increase or decrease in the other SLL depending on direction
what would happen during Right/left ventricular atrophy/hypertrophy
atrophy wastes away
hypertrophy - builds up
the side that wastes away would be weaker i.e. left atrophy would lead to weaker SLL 1 R wave being smaller
what are Augmented limb leads
it leads to two limb leads being combined ang giving an extra direction to the positive electrode
why are they useful
give 3 new perspectives
what are the names of the augmented limb leads - where do they lead
aVR - right arm
aVL - left arm
aVF - foot (left)
combining SLL and augmented limb leads gives you what
6 different vies of the vertical (coronal plane)
. What extra information do the precordial (chest) leads give you
look at the same events of the other leads, but in the horizontal (or transverse) plane
where are the precordial (chest) leads laced
front of the chest
what are all precordial chest leads
positive
what is normal for a precordial chest lead
negative blip on 1
by the end is a positive blip on 6
how may precordial leads are there
6
what way dose the wave of depolarisation go through the heart in the transverse plane
towards the midclavicular line
what does the rhythm strip tell us (5)
heart rate
is there a P wave before QRS
is PR to short/long
is QRS to wide
is QT to long
what is the calibrating pulse
0.2sec - l large square - 5mm
what speed should the rhythm strip go
run at 25mm/second
how is HR measured
could the R waves in 30 large squares (= 6 seconds) and multiply by 10
what is the term for below 60
bradycardia
what is the term for above 100
tachycardia
what is STEMI used for
hear attack classification
STEMI is worse than NSTEMI
what is a STEMI
ST elevated myocardial infarction
what is a NSTEMI
non-ST elevated myocardial infarction
what happens in a STEM
the ST segment is raised up high and this is very prominent on a ECG
what dose myocardial infarction mean
myo = muscle cardial = cardiac infarction = death of tissue (necrosis) due to obstruction of blood
what is diastole
diastole occurs when the heart relaxes after contraction
what is systole
Systole occurs when the heart contracts to pump blood out
what are the 5 phases of the cardiac cycle
late diastole
atryial systole
isovolumic ventricular contraction
ventricular ejection
isovolumetric ventriculare relaxiation
what is the fancy name for listening to heart sounds
phonocardiogram
what generates the LUB sound
mirtal (bicuspid) and tricuspid valves closing
what generates the DUB sound
aortic and pulmonary vales closing
what sound indicates an abnormality or further investigation
a murmur = hissing, ssshhhh sound
when would you hear a murmur between the LUB and DUB
Stenosis of either Stenosis of either atrioventricular valves
OR
incontenance/ regurgitaion of the mitral and tricuspid valves
what would give arise to a constat murmur sound
a spetal defect
what would give arise to a murmur after the DUB and before the LUB
incontanace or regurgitation therough the Stenosis of either atrioventricular valves
or
stenosis of the mitral and/ or tricuspid valves
what causes the dicotic notch
the elastic energy of the ventricle
how long is systole roughly compared to diastole
1/3 systole
2/3 diastole
what is isometric contraction
the contraction of the ventricle that doesnt open the aortic valve due to the
what is at the start and then the end of the isometric contraction phase
mitral valve closes
aortic valve opens
after the aortic valve opens what is this phase called
the rapid ejection phase
what happens after the rapid ejection phase - why
the slower ejection phase
its slower as the pressure built up by the blood vol/isometric contraction has subsided
what does the aortic valve open
as the pressure in the ventricle is grater than in the aorta
what is the difference between systolic and diastolic called
pulse pressure
what does the 3rd heart sound relate to
rapid filling phase
when would you hear a healthy 3rd heart sound
in someone young/ or who has a healthy heart - with good elasticity
what is stroke volume
the difference between end systolic volume and end diastolic volume `
what is the ESV roughly
60ml
what happens when HR increases
it shortens diastole
when does preload start to get effected by HR
at about 120bpm
reduces slow filling phase - encroaching on rapid filling phase
what does the sympathetic nervous system release
noradrenaline
and circulating adrenaline from the adrenal medulla
what does noradrenaline/ adrenaline act on
the beta 1 receptors on sinoatrial node
what does the sympathetic nervous system do
increase the slope of the pace maker potential - get closer to the threshold
what does the parasympathetic nervous system release
vagus releases
acetylcholine
what does ACh act on
the muscarinic receptors on sinoatrial node
what does the parsympathetic do
hyperpolarises cells and decreases the slope of pacemaker potential
what is starlings law
the energy of contraction is proportional to the initla length of the cardiac muscle volume
what is preload affected by
end diastolic volume
what are the dominos after increased venous return
increased diastolic volume
therefore increasing the stroke volume
what are the dominos after decreased venous return
decreased end diastolic volume
and decreasing the stroke volume
what is afterload
the load against which the muscle tries to contract
what does TPR
total peripheral resistance
what happens if total peripheral resistance increases
aortic pressure will increase
ventricle will have to work harder - less energy for ejecting blood (stroke volume)
what happens to stimulated beta 1 receptors on the myocytes
increase contractility
ionotropic effect
stronger but shorter contraction
move the graph up
more stroke volume for the same diastolic volume
does parasympathetic NS effect stroke volume
no
valgus does not innervate ventricular muscle
how can cardiac out put increase by 4-6 times
increased HR
increased contractily
increased venous return
TPR falls
what causes increased venous return
venoconstriction
skeletal/respiratory pumps
cardiac out put =
stroke volume x heart rate
what is hypercalcemia - pathological response
more calcium - shifts curve up
ischemia does what to ‘‘the curve’’
shifts it down
what is the ejection fraction
the stroke volume/EDV
the stuff squirted out/stuff left in
