Cardiovascular System Flashcards
apex of heart
bottom of heart
contractions spread from here then upwards
lub dub
lub-AV valves closing
dub-aortic and pulmonary valves closing
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
APs have no stabl RMP, reach threshold by Na and Ca moving in cell
intercalated discs
connects cardiomyocytes
locked together by desmosomes (protein)
have gap junctions
gap junctions
allows Na, Ca and other small molecules together to allow communication
-on intercalated discs
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
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 binds to receptors muscarinic receptors on SA node cells
-when ACh binds to muscarinic R, decrease Ca and Na permeability (slower coming in), increase K permeability
-longer time to reach AP threshold, slower HR
HR increasing *
-SNS
adrenergic receptors bind with (nor)epinphrine
AP threshold hit fast which increases HR
increase Na and Ca permeability
ECG
electrocardiogram
-electrical activity in heart
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
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
how to increase excitation contraction coupling
more Ca in cytoplasm, stronger contraction
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 *
distribution vessel
alot of elastin to stretch during vent. diastole
-pulsatile pressure
pulsatile pressure
the difference between systolic and diastolic blood pressure
arterioles *
-resistance vessels
thick walls
-greatest resistance
-higher muscle than elastin
-large drop in pressure
-smooth muscle innervated by SNS
capillaries *
-only single layer of endothelial
-exchanges vessels
venules
low blood pressure
veins *
-capacitance vessels
-large diameter, thin walls
-low P
-uses valves in lumen
-some smooth muscle + elastin for stretch and increase diameter
-innervated by ANS
valves in veins
prevent back flow
-have cusps that fill with blood
venous return *
-amount of blood returned to heart
-SNS cause small contraction, decrease diameter and more blood goes back to heart
-increases EDV, SV, cardiac output
varicose veins
-enlarged, twisted veins
-common in legs and feet
-occur from malfunctioning vein valves causing blood to pool + veins to swell, increasing P
importance of blood flow regulation
to increase blood flow to active tissues
maintain blood supply to vital organs
maintain BP
maintain temp
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 *
-bulk flow
-substance can move between endothelial cells lining capillaries through intercellular clefts
intercellular clefts
have proteins called tight junctions between them
-vary in size and leakiness of cleft
continuous capillaries
most abundant
-varies in permeable
-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
3 major regulatory systems for controlling flow
local regulation, humoral regulation, neural regulation
local regulation *
-intrinsic mechanism
-changes condition inside tissues
most tissues
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 *
-muscles contracts or relaxes to control blood flow
metabolic theory *
metabolic needs
-increase co2, H, adenosine, temp, decrease o2 to increases blood flow by increase radius and vasodilation
vasodilator metabolites
co2, H, adenosine
humoral regulation *
-substance that are travelling in blood through tissues
-substances change radius of BV, usually by binding to receptors
-extrinsic mechanism
vasoconstrictors *
-increase bp
-epinephrine when bind to alpha adrenergic receptors
-angiotensin 2
-ADH
Vasodilators *
-decrease BP
-histamine- released by inflammatory cells
-ANP
epinephrine > beta adrenergic receptors
neural regulation *
neurons from SNS innervate smooth muscle cells in tunica media of
ex. norepinephrine
-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)
baroreceptors *
-regulates MAP
-stretches when change in BP, send signals to medulla oblongata to adjust HR
steps of baroreceptor reflex SNS *
not sup import
-baroreceptors stretch and detect change in BP
-sends sensory info to cardiovascular center in medulla oblongata
-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 *
not sup import
-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
When vasoconstriction occurs, what happens to blood pressure in the sites before and after that constriction?
Increase below, decrease p after
