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103 - Heart, Lungs, Blood
Theme 1: Cardiovascular System
T1 L9: Cardiac pressure-volume cycle & ion action potentials
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Cerebral Circulation - Special Aspects
Brain maintains all vital functions, so needs constant flow and pressure.
Auto-regulation
to achieve this.
Circle of Willis
: arteries of brain's inferior surface organised into a circle. redundancy of blood supply. 'back-up system of blood supply'
Renal Circulation - Special Aspects
Portal system
: glomerular capillaries to peritubular capillaries
20-25% or cardiac output
makes both
ACE
and
RENIN
:
endocrine functions
controlling blood volume
responding to renal blood pressure
Skeletal Muscle - Special Aspects
Adrenergic input causes
vasodilatation
Can use 80% of cardiac output during strenuous exercise
Major site of peripheral
resistance
Muscle pump
: augments venous return
Skin Circulation - Special Aspects
Role in
thermoregulation
(perfusion can increase 100x)
Arterio-venous anastomoses
: direct connection between small arteries and small veins without capillaries. Primary role in thermoregulation
Sweat
glands: role in thermoregulation, produce sweat (plasma ultrafiltrate)
Response to
trauma
: red reaction, flare, wheal
Four stages of the Cardiac cycle / "Pressure-Volume Loop"
Ventricular filling
Isovolumic ventricular contraction
Ejection
Isovolumic ventricular relaxation
Valve Sounds: S1 & S2
S1 'lub': heard during
isovolumic contraction
(
mitral
valve closes)
S2 'dub': heard during
isovolumic relaxation
(
aortic
valve closes)
Isovolumic contraction and relaxation only occur when both
aortic
and
mitral
valves are
closed.
PV loop for mitral stenosis: decreased
preload
and
afterload
.
PV Loop for Aortic stenosis:
increased afterload
.
PV loop for mitral regurgitation:
increased
preload, decreased afterload
.
PV loop for aortic regurgitation:
increased preload
.
Auscultation: valve sounds
Systolic murmur:
fluid leaves ventricle
so AV
regurgitation
or SL valve
stenosis
Diastolic murmur:
fluid enters ventricle
so AV
stenosis
or SL
regurgitation
K+ channels
Delayed rectifier
K+ Channels: open when membrane depolarises with a delay.
Inward rectifier
K+ channels: open when Vm goes below -60mV (when cells are at rest). Clamps membrane potential at rest, preventing depolarisation
Ventricular myocyte action potential phases:
0.
Depolarisation
: Na+ gates open in response to wave of excitation from pacemaker
Transient outward current
: tiny amount of
K+
leaves cell
Plateau phase
: inflow of Ca2+ just about balances outflow of K+, until membrane potential becomes too negative and the Ca2+ channels close
Rapid repolarisation phase
: Vm falls as K+ leaves cell
Back to
resting potential
QRS complex shows:
ventricular depolarisation
T wave shows:
ventricular repolarisation
Action potentials in SA node and AV node
spontaneously
depolarise at rest: not stable because there is no
inward rectifier
channels
upstroke of action potential due to a brief increase in
Ca2+
current - not Na+!
Only has 3 phases:
Depolarisation
(influx of Ca2+)
Repolarisation
(K+ exiting)
Pacemaker (diastolic) potential
Pacemaker potential
Resting
membrane potential of myocytes in SA and AV node
it is in a slope bc lack of
inward rectifier
channels
Slope
of pacemaker potential determines rate of firing
Funny current If
makes the SA node channel
spontaneously
active
HCN
channel (non-specific cation): opens upon
hyperpolarisation
and closes upon
depolarisation
leads to a net inward current; lots of
Na+
going in and tiny
K+
going out
Depolarises
cell towards 0mV
Ivabradine
partially inhibits funny current, which
slows
heart rate in angina and heart failure
Blocking ion channels of cardiac action potentials
Na+
channel block:
decreases
conduction velocity
: changes the organisation of firing in different regions of the heart
does NOT prevent depolarisation or affect heart rate
used to treat
arrhythmias
Ca2+
channel block:
decreases
heart rate
decreases
contractile
force
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