Lecture 7: Cardiac Muscle Tissue Flashcards
the blood flow path through the heart
vena cave right atrium tricuspid valve right ventricle pulmonary valve pulmonary artery lungs pulmonary vein left atrium mitral valve left ventricle aortic valve aorta body vena cava
cardiac muscle tissue characteristics
striated mononucleated central nuclei syncytium intercalated discs cells can be branched
define ‘syncytium’
the ability of the heart to act as one giant cell, the AP can rapidly spread so that all cells contract as one
depolarization values of the heart
-85 —-> +20mV
how long does the plateau last?
0.2 seconds
special requirements for cardiac AP
- self-generated
- prolonged
- propagated
what does it mean for the AP to be propagated?
to spread from cell to cell (syncytium)
in proper sequence and rate
cardia AP pathway
generated in SA node atria contract AV node purkinje fibers ventricles contract
automaticity of the heart
some tissues gradually depolarize during phase 4
eventually reaching threshold
automaticity of the heart: tissues affected
SA and AV nodes
but SA reaches threshold first
the SA node is known as the heart’s ?
pacemaker
what determines rhythmicity of heart cells?
depolarization rates
what causes gradual depolarization during phase 4?
special Na channels which open after phase 3
compare skeletal and cardiac muscle fibers: t-tubules, cisternae, and SR
t-tubules are found along Z-lines
1 cisternae per t = diad
SR is less extensive
2 types of cardiac AP
fast and slow
determined by location in the heart
fast AP
heart chambers and purkinje fibers
rapid conduction and contraction
amplitude = 100mV
was is significant about the purkinje fibers?
are conductive only
never contract
slow AP
SA and AV nodes slow conduction no contraction automatic depolarization amplitude = 60mV
phase 4
resting potential
slow depolarization of nodes
phase 0
rapid depolarization
phase 1
initial incomplete repolarization
peak
beginning of plateau
phase 2
plateau
phase 3
repolarization
fast AP factors
large cell diameter
high amplitude
rapid onset of AP
resting potential -90mV
slow AP factors
small diameter
low amplitude
slow depolarization rate due to Ca
resting potential -60mV
ventricular fiber AP
caused by opening of fast Na channels and slow Ca/Na channels
calcium sources in cardiac AP
from SR
From extracellular matrix
ions responsible for plateau
large concentration of K and Ca inside cell
SA node threshold
-40mV
channels at resting potential
slow Na/Ca channels open
K+ channels open
fast Na channels closed
resting potential for ventricles
-85/-90
during resting potential
slow leak of Na into cells
membrane becomes more positive
SA threshold at -40
phase 4 ions
slow Na influx
phase 0 ions
Ca influx
phase 3 ions
K efflux
SA node AP generate the ____ rhythm
sinus rhythm
ectopic rhythm
an action potential that originates anywhere besides the SA node
bad — heart will not sequence correctly
does skeletal or cardiac muscle cells have finer control over Ca concentrations and contractility?
cardiac
Ca pathway in a cardiac muscle cell
AP travels across sarcolemma t-tubules conduct AP DHP receptors allow extra Ca into cytosol increasing intra Ca triggers ryanodine Ca from SR into cytosol Ca threshold reached Ca binds to troponin contraction
Ca transportation during relaxation
SERCA into SR
sarcolemma channels allow Ca into extra matrix
SERCA in cardiac muscle
primary transport to move Ca
Phospholambian helps
Phospholambian
integral protein within the SR
when phosphorylated this protein can stop the SR from preventing the SERCA pump
moving Ca back into the extracellular matrix
secondary transport via Ca/Na channels (antiporter)
[Na] outside cell is maintained via Na/K exchange channels
when looking at graphs of heart pressures and volumes, compare the left and right sides
volumes are the same
but the right side of the heart goes to the lungs which are fragile so pressure is lower
____ of blood flows from atria to ventricles before the atria even contract. atrial contraction moves the _____ blood.
80%
contraction moves the remaining 20% of blood
isovolumic contraction occurs when….?
volume stays the same
pressure builds from ventricle contraction
first 0.02 seconds the aortic valve does not open
blood has no where to go
first third of diastole
rapid filling of ventricles
second third of diastole
small amount of blood flows into ventricles representing the blood that is constantly flowing into the atria
final third of diastole
atria contract
pushing final 20% of blood into ventricles
period of rapid ejection
1/3 of systole left ventricle pressure 80mmHg right ventricle 8 semilunar valves open 70% of blood is ejected
final two thirds of systole
30% of blood is ejected from ventricles
frank-starling law
the greater the heart muscle is stretched, the greater the contractile force, that greater the volume of blood that can be moved
EDV
end diastolic volume —- amount of blood in ventricles after diastole (filling)
rest = 120mL
ESV
end systolic volume —- amount of blood left in ventricles after contraction
rest = 40-50mL normal
SV
stroke volume = how much blood does the ventricle actually pump out
SV = EDV - ESV rest = ~70mL
effective ejection fraction
SV/EDV
at rest ==== 70/120 ~ 64%
how can SV be increased?
increase EDV
decrease ESV
40 cm/sec
mean velocity of blood coming from ventricle to aorta
120 is systole
(-) in diastole
proximal aorta velocity in diastole
negative values
because initial backflow of blood is what causes semilunar valves to close
blood flow in proximal vs distal aorta
proximal – flow is phasic
distal – flow is constantly forward
what allows blood to constantly flow forward in distal aorta, arteries and tributaries?
elastance of vessels walls
what controls blood flow to tissues?
tissues themselves
ANS stimulation
CO
cardiac output
measured in L/Minute
at rest = 5L/min
blood flow to tissues
controlled by tissue itself depending upon it’s current need, will act directly upon near vessels with their needs
Microvessels also help monitor needs
sympathetic blood flow stimulation
results in an CO increase
parasympathetic blood flow stimulation
results in a CO decrease
ANS stimulations can indirectly influence blood flow, how?
changing heart rate
changing contractile strength of heart
active tissues….
require 20x to 30x more blood flow than at rest
cardiac output cannot exceed _____ times resting amount
4-7x resting amount
what helps to keep CO at a constant rate?
ANS stim
tissues
if EDV = 120
ESV = 50
ejection fraction = ?
60%
P wave
atria contraction
QRS complex
ventricle contraction
T wave
repolarization of ventricles
P-Q interval
0.16 seconds
delay of signal from initial origin to onset of ventricular contraction
the AV nodes receives signal from SA node ___ seconds after origin.
0.3 seconds
signal is delayed in the AV node for ____ seconds. due to ?
0.9 seconds
small cell size
low amplitude
slow depolarization rate
a final delay of ___ seconds occurs in the _______.
0.4 seconds in the penetrating bundles
amount of time between SA signal origination and ventricular contraction?
0.16 seconds
excess K in extracellular fluid would have what effect on heart activity?
heart walls become dilated
prior to ventricular isovolumic contraction, there is a slight but marked elevation in atrial pressure. what is responsible for this elevated pressure?
atrial contraction
resting potential of -85mV is characteristic of which phase in the cardiac AP?
phase 4
conductance of which ions is responsible for phase 0?
Ca and Na
