Cardiovascular System Flashcards
apex of heart
bottom of heart
contractions spread from here then upwards
interventricular septum
wall separating left and right side
cusps
pockets that fill with blood causing them to expand and close
lub dub
lub-AV valves closing
dub-aortic and pulmonary valves closing
heart murmurs
valves don’t close properly (valve regurgitation)
whoosing sound may be heard
heart arrhythmias
irregular heart contractions
cardiomyocytes
cardiac muscle cells
-contractile and nodal
contractile cells
pumps blood through heart
-communicate between 2 cells using gap junctions
-ions from gap junction go to other cells then causes depolarization
nodal/conducting cells
spread electrical activity/AP through heart
self-excitable >make own AP
minimal actin and myosin
don’t contract
intercalated discs
helps connect cardiomyocytes
locked together by desmosomes (protein)
where gap junctions are found
gap junctions
allows Na, Ca and other small molecules together to allow communication
-on intercalated discs
nodal/conducting cells examples
AV nodes
SA nodes
Atrio-ventricular bundle
subendocardial branches
SA node
sinoatrial node
in upper right atrium
pacemaker determines heart rate
receives input from PSNS and SNS
intrinsic rate
100 AP/min
1 AP every 0.6s
nodal cells AP
no stable RMP
reaches threshold by Na and Ca moving in
keep K in-no leaking
Steps pace maker potential
1) positive charge/graded potential is created by Na and Ca entering cell using their own ion channels (Ca and Na in, K out)
2)Depol- caused by opening Ca channels at threshold
-Ca moves down concentration gradient
3)repol- K leaves cell through K channels
more negative
no hyperpolarization
what happens when SA node fails
AV node acts as pacemaker b/c it is the 2nd fastest AP creation
bradycardia
too low HR
dizzy, faint
HR lower than 100 bpm
-PSNS
ACh communicates with heart by binding to receptors on SA node cells/ muscarinic R
-slow HR decreases slop of pacemaker potential, >slower hit of AP
-when ACh binds to muscarinic R, decrease Ca and Na permeability (slower coming in), increase K permeability
HR increasing
-SNS
adrenergic receptors bind with (nor)epinphrine
threshold hit fast to get quicker AP
increase Na and Ca coming in SA node
ECG
electrocardiogram
-looks at electrical activity in heart
-using electrodes, APs moving through heart can be detected on surface of skin
-body fluid conducts electricity
p wave
result of depolarization of atria
QRS wave
result of depolarization of ventricles
larger than P wave b/c ventricles have a larger mass
T wave
result of repolarization of ventricles
atria repolarization
at same time as QRS wave
so small, masked by ventricles depolarization
systole
period when cardiomyocytes are contracting
diastole
period when cardiomyocytes are relaxing
cardiac cycle
isovolumetric ventricular systole
ventricular systole
isovolumetric ventricular diastole
late ventricular diastole
atrial systole
isovolumetric ventricular systole
ventricles start contracting, blood isn’t being pumped out of heart
ventricular systole
ventricles are contracting
blood moves out of heart and into aorta or pulmonary artery
isovolumetric ventricular diastole
ventricles start relaxing and not filled with blood
late ventricular diastole
ventricles are relaxing and start filling with blood from atria
atrial systole
atria contracting and blood moving in ventricles
isovolumetric ventricular systole graph
ECG: QRS> started at atrial contraction
Volume: no change
Valves: closed
Pressure: increase ventricular P
aortic P > vent P
ventricular systole graph
ECG: no new -QRS
Volume: decrease ventricular volume
Valves: aortic open, AV closed
Pressure: vent P > aortic P
isovolumetric ventricular diastole graph
ECG: T wave in phase 2
Volume: no change
Valves: closed
Pressure: lower vent p, higher aortic p
late ventricular diastole graph
ECG: no new-T
Volume: increase ventricular volume
Valves: AV open, aortic closed
Pressure: higher atria P, lower vent P
atrial systole graph
ECG: p wave
Volume: increase ventricular volume
Valves: AV open, aortic closed
Pressure: lower vent p, higher atrial p
ESV
end systolic volume
amount of blood in ventricle at end of systole after ventricle contract
-decrease ESV means more effective heart
EDV
end diastolic volume
amount of blood in ventricle before ventricular contraction
SV
stroke volume
amount of blood ejected by ventricle with each heart beat
SV= EDV-ESV
influence cardiac output
cardiac output
amount of blood the heart pumps each minute
=HRxSR
at rest 5-6L/min
in L
how to adjust SV
ANS innervation
preload on heart/EDV
ventricular muscle
some muscarinic and lots of adrenergic receptors
Ca’s role in contraction
more in cytoplasm, stronger contraction
increase excitation contraction coupling
preload
load on heart prior to contraction
-blood that has filled ventricle=EDV
larger EDV/fuller heart, more stretch
Frank Starling’s Law of the heart
more EDV= more SV
this protects heart from over filling then bursting
total blood volume + % based on systems
4-6L
15% of blood between pulmonary circuit and heart
85% of blood in systemic circuit
general blood vessel structure
have 3 tunics except capillaries
> tunic externa, media, interna
tunica externa
outermost layer
-composed of connective tissue > protection and maintains structure
-has neurons of SNS to communicate with tunica media
tunica media
middle layer
-has smooth muscle to contract or relax >changes diameter
-elastin>elastin fiber, allows for stretch
-collagen
-different amount of contains for different vessels
tunica interna
innermost layer
-has endothelial cell> special cells that line blood vessels
-important for vessel function
arteries
blood away from heart
distribution vessel
larger diameter 25%
alot of elastin to stretch during vent. diastole
-pulsatile pressure
take BP here
pulsatile pressure
the difference between systolic and diastolic blood pressure
arterioles
thick walls>50%
-resistance vessels> higher muscle than elastin
-large drop in pressure
smooth muscle innervated by SNS
regulates blood flow
capillaries
-also called endothelial cells
-only single layer of endothelial
-exchanges vessels
-hormones go capillaries to bind receptors on target cells
low BP
venules
low blood pressure
veins
-blood back to heart
capacitance vessels
-large diameter, thin walls
-low P
-uses valves in lumen
-some smooth muscle + elastin for stretch and increase diameter
valves in veins
prevent back flow
-have cusps that fill with blood
venous return
-amount of blood returned to heart
-ANS can innervate veins
-SNS cause small contraction, decrease diameter and more blood goes back to heart
-increase venous return, EDV, SV, cardiac output
increase venous return by moving
skeletal muscle pump
-contraction of smooth muscle squeezes on veins > decrease diameter to forced to heart
varicose veins
-enlarged, twisted veins
-common in legs and feet
-occur from malfunctioning vein valves causing blood to pool + veins to swell, increasing P
why does blood flow need to be regulated
to increase blood flow to active tissues
maintain blood supply to vital organs
maintain BP
to increase or decrease heat loss
resistance affect on blood flow
decreases flow
what affects blood resistance
-lumen radius (^r, smaller resistance)
-viscosity (^, ^resist)
-length of blood vessels (lined with endothelial cells increase friction> ^resist)
blood pressure equation
pressure gradient x radius to the power of 4
transcellular transport
substance enters and then exits endothelial cell and epithelial cell
paracellular transport
-substance can move between 2 endothelial cells lining capillaries through intercellular clefts
called bulk flow
fluid and anything that dissolved in it that are small enough fit through intercellular cleft
intercellular clefts
have proteins called tight junctions between them
-vary in size and leakiness of cleft
-small slits
-found at borders of where 2 endothelial cells meet
continuous capillaries
most abundant> in muscles, brain lungs, heart
-varies in permeable
-intercellular clefts
ex. brain almost no permeability through intercellular clefts
fenestrated capillaries
found in kidneys and intestines
-intercellular clefts
-more bulk flow than continuous capillaries
sinusoidal capillaries
found in liver and spleen
edema
excessive filtration causing swelling
filtration forces
because capillaries have blood under pressure, molecules in blood will experience filtration through intercellular clefts
forces that push molecules throught intercellular clefts to get filtered
starling forces
promotes or prevent filtration
-hydrostatic forces causing fluid to move
lymphatic system
-filters using bulk flow
-interstitial fluid moves into lymphatic capillaries through lymphatic system then drains it back into circulation
-doesn’t work leads to edema
3 major regulatory systems for controlling flow
local regulation, humoral regulation, neural regulation
local regulation
-intrinsic mechanism
-most tissues
-also called autoregulatory mechanism b/c tissues autoregulates flow
temp, gases pressure
types of local regulation
myogenic theory and metabolic theory
extrinsic mechanism
signal to change blood flow comes from outside the tissue
intrinsic mechanism
stimulus to change blood flow comes from within the tissues that need it
myogenic theory
-muscle stretch
-increase BP leads to increase blood flow
this stretches arterial wall
reflexive contraction of smooth muscle (decrease radius, vasoconstriction)
decrease blood flow and BP in capillaries to protect the capillaries
metabolic theory
metabolic needs
-increase co2, H, adenosine, temp, decrease o2 during metabolically active tissue
this then increases blood flow by increase radius and vasodilation
vasodilator metabolites
co2, H, adenosine
humoral regulation
-mechanism involves substance that are travelling in blood through BV
-substances change radius of BV, usually by binding to receptors
-usually hormones
-extrinsic mechanism
epinephrine causing regulation
-released by adrenal gland when SNS is activated
-binds to adrenergic receptors on smooth muscle cells of BV
-alpha and beta found in same BV
-binds to alpha adrenergic receptor causing vasoconstriction, increase BP
-binds to beta adrenergic receptors causing vasodilation, decrease BP
histamine
chemical released by inflammatory cells like allergic reactions
-not hormone
-binds to receptor on BV causing vasodilation, increase blood flow, decreases BP
neural regulation
neurons from SNS innervate smooth muscle cells found in tunica media of many BV
-neurons release norepinephrine that binds to adrenergic receptors to cause vasoconstriction
-extrinsic
what nervous system innervates blood vessels
SNS
MAP
average BP in arteries during one cardiac cycle
MAP equation
MAP =CO x TPR
or
=DP + 1/3 (SP -DP)
PSNS affect on BP
decreases HR, SV (small amount) decrease BP
indirectly as it doesn’t innervate BV
- using PSNS, use less SNS causes vasodilation b/c no constriction
baroreceptors
mechanoreceptor >sense stretch
found in carotid sinus (neck) and aortic arch
steps of baroreceptor reflex SNS
-baroreceptors stretch and detect change in BP
-sends sensory info to cardiovascular center in medulla oblongata
-then info heart and blood vessels
-the SNS info is sent out to SA node to change heart’s pace by increasing slope of pacemaker potential and change ventricular myocytes
-increase SV by increase contractility
increase HR (SA node), TPR
then increase MAP
steps of baroreceptor reflex PSNS
-baroreceptors stretch and detect change in BP
-sends sensory info to cardiovascular center in medulla oblongata
-then info goes to SA not to blood vessel
-decrease HR, SV (contractility), SNS activation (decrease TPR)
therefore decrease MAP
conducting system: AP conduction
1)SA node
2) atrial cardiomyocytes
3)signals go to AV node
4)atrioventricular bundle
5)bundle branches
6)subendocardial branches-
7)ventricular cardiomyocytes
