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CARDIOVASCULAR SYSTEM :heavy_heart_exclamation_mark_ornament: (CARDIAC…
CARDIOVASCULAR SYSTEM :heavy_heart_exclamation_mark_ornament:
CARDIAC MUSCLE TYPES
PACEMAKERS :stopwatch:
parts of the heart
ATRIOVENTRICULAR NODE (AV)
fire less frequently that the SA node (50% less frequently)
SINOATRIAL NODE (SA)
fire at regular frequency = your pulse
MYOGENIC
can generate their own action potential
aka cells depolarize spontaneously
specialized pacemaker cells - depolarize the fastest
pacemaker and contractile/ conductive cells are connected by gap junctions
pacemaker action potential
prepotential = pacemaker potential
SA and AV cannot maintain stable resting membrane potentials
I f channels (funny channels)
= open at negative membrane potentials open at negative membrane potential
(aka hyperpolarization) = equally permeable to K and Na
VG K channel
= repolarization
VG L - type Ca channel
open = depolarization
(there's also a
T - type channel
- open quickly right before the threshold and closes quickly)
I f opens again
-> restart the cycle / no hyperpolarization
parasympathetic tone control HR
muscarinic receptor keep the heart rate down
close T-type Ca channels of nodal cells
=> slope in the rising phase is not steep
activation of VG K channels
hyperpolarization of the pacemaker cells
harder to reach the threshold
CONDUCTIVE :racing_car:
parts of the heart
internodal pathway
AV bundle
bundle branches
Purkinje fiber
physical advantage explained
few gap junctions at AV node
around the AV node have small diameter fibers
reasons: no electronic current spreading from SA node to AV node at the same time
no gap junction between ventricle and atria
reason: blood won't be able to backflow from ventricle to atria
CONTRACTILE :construction_worker:
ACTION POTENTIAL
comparing to skeletal muscle contraction
longer repolarization phase
longer absolute refractory period
prevent summation/ tetanus in the heart
depolarization phase is the same
what AP looks like
phase 0 = depolarization
= Na channels =
sodium flows in
phase 1 = some repolarization
= Na channel inactivated / VG K To opens =
some K flows out
phase 2 = plateau
= VG Ca channels (L - type Ca channel) =
Ca enters, K still leave
phase 3 = repolarization
= VG Ca channels close / K Dr open =
K flows out
phase 4 = many leak K channels open
= more K flowing out, reestablish membrane potential
parts of the heart
atria
ventricles
CARDIAC CYCLE :two_hearts:
EKGs
general idea
lead 1 - current flows from the left arm (positive electrode) to the right arm (negative electrode)
measure the potential difference outside of all the contractile cells of the heart
record electricity activity from of the heart from the surface of the skin
what it looks like
P wave
atrial depolarization
less cells in the atria = lower magnitude
PR interval
start at atrial depolarization
ends at ventricle depolarization
ex: blockage between the SA node and AV node
or cardiac cells get negative dromotropic
:arrow_right: longer PR interval
formal definition - atrial depolarization and A/V node conduction time
QRS complex
ventricle depolarization
steep = happens quickly
T wave
contractile ventricle repolarization
diffuse = less magnitude
QT interval
starts at ventricle depolarization
ends at ventricle repolarization
P/V LOOPS
GENERAL IDEAS
stroke volume
EDV - ESV
volume of blood that pumped by the ventricle
systole
contraction
ESV
end systolic volume
amount of blood in ventricles after contraction
afterload comes before ESV
how much tension you need before you actually start to reduce ventricular volume
aka how much resistance you need to overcome systemically
point at which aortic valves swings open
these systems include
aka aorta
blood systems leaving the heart
diastole
relaxation
EDV
end diastolic volume
amount of blood in ventricles before contraction
pre-load
how much cardiac myocyte stretch before contract
FRANK-STARLING EFFECT
increase blood volume returning to the heart
put sarcomere in position to generate more force per contraction
note: at rest, the heart sarcomere is not very long
LENGTH-TENSION RELATIONSHIPS
passive tension
like elastic
active tension
like skeletal muscle
lacking extreme right
what it looks like
start point A - mitral valve open
point B - EDV - ventricle contraction
mitral valve closes
preload
point C - aortic valve opens
afterload
point D - ESV - aortic relaxation/ ventricle relaxation
point A' - atrial contraction
A to A' - passive filling
B to C - building up contraction for ventricular contraction
INOTROPY
sympathetic nervous system = beta 1 receptor on contractile cells- Gs
cAMP
protein kinase A
increase the slope of total tension curve
less blood in the ventricle after contraction
note you don't really hormonally decrease inotropy, the only way you can do it is to decrease the sympathetic tone/ parasympathetic only acts on the pacemaker cells not the contractile cells
changing inotropy only affects point D - the ESV point
increase inotropy - active tension curve (per length of sarcomere) - steeper slope
decrease inotropy (not physiologically possible) - less steep slope
WIGGER's
VAVLES
AORTIC VALVE
high pressure in ventricle/ low pressure in aorta = open
low pressure in ventricle/ high pressure in aorta = close
MITRAL VALVE
pressure opens valve
valve allows unidirectional flow
NOTES
figure out where on the graph that valves open
CHANGE THE CONTRACTION
INOTROPIC :weight_lifter:
FORCE OF CONTRACTION
mechanism
= :arrow_up: PKA (protein kinase A)
beta 1 adr R
coupled with Gs
= increase AD = increase cAMP
consequences
= :arrow_up: myosin ATPase rate
increased by PKA
able to cycle faster = generate more crossbridges / time = more tension
= :arrow_up: SERCA uptaking Ca into SR
heart
can relax :hearts:
:arrow_up: electromotive force of Ca
:arrow_up: LTCC activity = opens longer = more Ca coming from outside
= :arrow_Up: more Ca released from SR = more crossbridges
property of contractile myocyte
CHRONOTROPIC :watch:
RATE OF CONTRACTION
2 MECHANISMS
change the rate of rise of depolarization
parasympathetic system
slow down heart rate :broken_heart:
receptor : m2 AchR
Gi protein
open K channels
inhibits T type Ca channels
depolarize the cell from the threshold
Or hyperpolarize
coupled with Gs = PKA
:arrow_up: influx of
Na
Ca
open T-type channels longer
I f opens at slightly more (+) value
increase HR :heartpulse:
receptor : beta 1
sympathetic system
present at pacemaker cells (cause the contractile cells have intrinsic property to contract)
DROMOTROPIC
conducting velocity
pertaining to A-V interval
Ex: blockage between SA and AV nodes - slow down the conductivity
CARDIOVASCULAR PRESSURE
RECEPTORS
BARORECEPTORS
CHEMORECEPTORS
FLOW + RESISTANCE AND PRESSURE
R = P/Q
GENERAL IDEA
striated muscle
actin
myosin
organized the same way as in skeletal muscle
RELAXATION
SERCA - pumps Ca back into the SR
NaCaX - Na and Ca pumps
Ca ATPase - use ATP to pump Ca out of sarcoplasm
COUPLING
electronically coupling
allows action potential to spread immediately from one cell to the other
no waiting time between the stimulus and the contraction
gap junction
excitation-contraction coupling
calcium induced, calcium release
RyR is activated by Ca influx, not voltage change and DHP
SERCA pump - pump Ca back in the Sarcoplasmic reticulum
Ca enters through DHP receptor ( L -type Ca channel)
Ca activate RyR
Ca released from the SR
actin pulls myosin - contraction
called
cardiac myocytes
ex: what does PV looks like when increase blood volume returning to the atria and ventricle increase?
point A = same
point B = shift to right
point C = shift with point B
assuming point D stays the same = ESV stays the same
observer Frank-Starling effect
mechanism enables the heart to match its output with its blood input
protect heart from abnormal increase of volume
note: try to mess up with the channels
predict the excitability of the ventricles
half of channels are gone
channels open too long
channels not open
block K Dr channels - examples in class
phase 2 rises because Ca entering cells
much longer absolute refractory period
excitability of the ventricles = not very likely to contract because of long refractory period
long QT syndromes
note
inference from EKG
action potential
conduction errors
predict from the control and pathological AP/ conductive state
draw EKG
