Cardiovascular system Flashcards
what are the three major components of the CV system
blood, blood vessels, heart
what is the main function of the blood
transport nutrients, waste, hormones, gas
what is the main function of the heart
to pump
what is the pathway of deoxygenated blood (in the simplest terms)
body to heart via vena cava, heart to lungs via pulmonary artery
what is the pathway of oxygenated blood (in the simplest terms)
lungs to heart via pulmonary veins, heart to body via aorta
what does it mean for the heart to be a closed system
what’s pumped out comes back in
what does pulmonary mean
to and from the lungs
what does systemic mean
to and from the body
what are the blood vessels that carry deoxygenated blood
superior and inferior vena cava, pulmonary trunk, coronary sinuses
what are the blood vessels that carry oxygenated blood
pulmonary veins and aorta
what is atherosclerosis
buildup of plaque in vessels
what is coronary artery disease
buildup specifically in the heart blood vessels
what is a result of coronary artery disease
heart tissue dies from lack of blood
what is a heart attack
heart tissue dies (takes time)
what is cardiac arrest
immediate electrical issue in the heart
what is the order of how blood flows in the heart
sup/inf vena cava –> right atrium –> right ventricle via tricuspid valve –> pulmonary trunk to lungs –> lungs to be oxygenated –> pulmonary veins –> left atrium –> left ventricle via bicuspid valve –> aorta to body
in the relaxed state of the heart, what two valves are open, and what two valves are closed
tricuspid and bicuspid (mitral) valve are open, aortic and pulmonary valve are closed
what state is the chordae tendineae loose and the papillary muscles relaxed
relaxed state
what is happening to the left ventricle in the relaxed state
it’s relaxed so blood can fill it
in the contracted state of the heart, what two valves are open, and what two valves are closed
tricuspid and mitral valve are closed, and aortic and pulmonary valves are open
what state is the chordae tendineae tensed and the papillary muscles contracted
contracted state
what is the inner layer membrane of the heart called
epicardium (visceral layer)
what is the outer layer membrane of the heart called
pericardium (parietal layer)
what are the two parts of the pericardium
fibrous layer, serous layer (mesothelium)
what type of tissue is the pericardium made up of
areolar (peri - are rhymes)
what does the myocardium contain
cardiac muscle cells and connective tissue
what does the endocardium contain
endothelium and areolar tissue
what is pericarditis
inflammation of the pericardium
what are some potential complications of pericarditis
fluid build up and pressure (cardiac tamponade)
how is force produced in the heart (in reference to two types of cells)
The electrical cells trigger the mechanical cells to produce and action potential
what is another name for electrical cells
autorhythmic cells
what type of cell in the heart have sarcomeres
contractile/mechanical cells
what channel is used in autorhythmic cells
HCN channels
what type of heart cells produce an action potential spontaneously
autorhythmic
where can autorhythmic cells be found
nodes of the heart
when are HCN channels opening
when the membrane potential is hyperpolarized
what do HCN channels generate
“funny” pacemaker current (If)
how do electrical impulses travel to ventricle
signal starts at SA node and moves through AV node branches to purkinje fibers which contract the ventricle
how is a pacemaker action potential threshold reached
HCN channels depolarize using If channels
how is pacemaker action potential depolarized
Ca2+ influx (Ca in cell - actin myosin - to pace myself running)
how is pacemaker action potential repolarized
K+ efflux
what depolarizes the cell to threshold in autorhythmic/pacemaker cells
If (funny) channels; Na+ flows in
what happens during rapid depolarization in autorhythmic cells
Ca2+ flows into cell (same as pacemakers - pacemakers are automatic)
what happens during repolarization in autorhythmic cells
K+ flows out of cell to bring it back to resting membrane potential
what causes contractile cells to reach threshold
action potential (because the pacemaker cells send ; Na+ influx
what is the peak in autorhythmic cells
K+ channels opening (Kaleigh you peaked)
what is the reason for the straight line/no change in contractile cells
delay in Ca2+ influx
what is the peak in contractile cells
Ca2+ released from SR causes influx
what causes slow repolarization in contractile cells
Ca2+ channels start closing
what causes rapid repolarization in contractile cells
K+ channels open and K+ moves out of cell; Na+ efflux
why can’t pacemaker action potentials ever meet resting membrane potential
constant slow inflow of Na+
which node fires faster
SA node
why does the SA node fire faster
it has more HCN channels
what is a result of the AV node being slow
there is a delay in the electrical impulses in the inter ventricular septum
what does an electrocardiogram display
the action potentials in the myocardium
describe the P wave
SA node fires and spreads across the atria to depolarize it
what happens in the PR segment
signal goes to AV node
what happens in the QRS complex
the ventricles depolarize and contract
what happens in the ST segments
action potential plateau
what happens in the T wave
ventricles repolarize and relax
what is one heart beat on an ECG
R to R
what is bradycardia
slow heart rate
what is tachycardia
fast heart rate
what is a heart block defined as
interruption in conduction
what is fibrillation
rapid, irregular contractions
what does an amplified P-wave result in
enlarged atria
what does a flatter T-wave result in
insufficient oxygen to myocardium
what does elevation of the ST segment result in
myocardial infarction
how does the AV valve open
atria pressure is greater than ventricular pressure
why are both the AV and aortic valves closed
ventricular pressure is greater than atria pressure, but ventricular pressure is less than aortic pressure
how does the aortic valve open
ventricular pressure is greater than aortic pressure, and blood moves from ventricle to aorta
what is the 1st step of the cardiac cycle
atria contracts
what is the 2nd step of the cardiac cycle
atria moves blood to ventricle
what is the 3rd step of the cardiac cycle
AV valve closes; atrial systole ends
What is the 4th step of the cardiac cycle
isovolumic contraction
what causes isovolumic contraction
ventricle pressure rises, but isn’t higher than aortic pressure
what is the 5th step of the cardiac cycle
blood is pumped out of the ventricle into the aorta
why does the ventricle pump out blood
ventricle pressure is greater than aortic pressure
what is the 6th step of the cardiac cycle
aortic valve closes
what is the 7th step of tech cardiac cycle
isovolumic relaxation
what causes isovolumic relaxation
ventricular pressure is less than aortic pressure, but greater than atria pressure
1st step of the pressure volume loop (starting on the right bottom corner)
isovolumic contraction
2nd step of the pressure volume loop
ventricles eject blood into aorta
3rd step of the pressure volume loop
AV valve closes and vents repolarize
4th step of the pressure volume loop
isovolumic relaxation
5th step of the pressure volume loop
AV valve opens and passively fills ventricles
when is end diastolic volume read
after passive filling of vents and before isovolumic contraction
when is end systolic volume read
after isovolumic relaxation and before passive filling
what is the slope in the pressure volume loop
relationship between ESV and afterload
the slope constructed using the ESV in the PV loop indicates
contractility
what is stroke volume
volume of blood pumped out in one beat
what is ejection fraction
systolic volume divided by EDV x 100
what is preload
the length of the muscle of ventricles before contraction
what is afterload
the force that goes against the heart when it has to contract (vent pressure > aortic pressure)
what is contractility
the ability for the heart to pump blood against a specific load
what is preload related to
EDV
what is the equation for cardiac output
CO = HR x SV
how is cardiac output defined
volume of blood pumped through the heart in 1 minute
what factors affect stroke volume
EDV and ESV
how are SV and EDV related
directly
how are SV and ESV related
inversely
what factors affect heart rate
autonomic innervation (PNS and SNS) and hormones
how is blood being pumped impacted by exercise
it increases when intensity increases
what determines amount of blood being pumped
venous return
what is venous return
veins bringing blood back to the heart
what is the frank starling principle
force-length relationship
what prevents muscle overstretching
CT, cardiac skeleton, and pericardium
where does the electrical signal start in the parasympathetic part of the autonomic innervation
cardioinhibitory center
what does the signal travel through in the parasympathetic part of the autonomic innervation
vagus nerve
where do the ganglionic fibers synapse in the parasympathetic part of the autonomic innervation
cardiac plexus
what is the main goal of the PNS nerves in the heart
slow heart rate and hyperpolarize
where does the electrical signal start in the sympathetic part of the autonomic innervation
cardioacceleratory center
where do the ganglionic fiber synapse in the sympathetic part of the autonomic innervation
sympathetic ganglia
do the SNS or PNS nerves integrate the ventricles more
SNS
what is the main goal of the SNS nerves in the heart
speed up HR and depolarize
how does depolarization occur via sympathetic nerves
Nor-epi opens Na+ and Ca2+ channels
how does hyerpolarization occur via parasympathetic nerves
ACh opens K+ channels and K+ leaves SA node
how does the cardiac center monitors detect changes in blood composition
chemo and baroreceptors
what do baroreceptors do
detect changes in blood pressure
what does it mean if there is a higher degree of hyperpolarization in parasympathetic stimulation
it’s harder to reach threshold = decreased heart rate from delay
what causes hyperpolarization in parasympathetic NS
K+ channels and open and it leaves cell
what hormone is in charge of opening K+ channels in PNS stimulation
ACh
what causes rapid depolarization in sympathetic stimulation
Na+ and Ca+ channels open
what hormone is in charge of opening HCN (Na+ and Ca+ channels)
Nor-epi
does rapid depolarization occur in PNS or SNS stimulation
sns
what is the point of the SNS contracting peripheral vessels
to take away blood flow to unimportant things and give it to brain and vital organs
what is does it mean to dilate the bronchioles
to give more oxygen to tissues
what factors influence blood flow and resistance
blood viscosity, blood vessel length, blood vessel diameter
what is blood viscosity influenced
plasma proteins and temperature
how does blood vessel length affect blood flow
it’s like drinking out of a longer straw - it takes a long time to flow to the necessary areas
what happens to the blood vessels during systolic pressure
they branch out to a larger cross sectional area
what does the branching of blood vessels lead to
decreases in BP
when does the greatest decreases in blood pressure occur
when blood moves from arterioles to capillaries
does deoxygenated blood move through arteries or veins
veins (they both start with NOT a vowel)
what do capillaries do to blood
they facilitate gas exchange in the blood
what is the outermost layer of arteries and veins
tunica externa
what is the middlemost layer of arteries and veins
tunica media
what is the innermost layer of arteries and veins
tunica intima
do arteries or veins have thicker walls
arteries
what are arteries made of
smooth muscle
what keeps back flow from occurring in veins
valves - can only move one way
how do varicose veins come about
the valves weaken, and blood is able to pool in certain areas
how are diameter and cross-sectional area related
inversely
when does the speed of blood moving decrease the most
arteries to arterioles to capillaries
what happens after the P wave
ventricle fills
what’s another name for the serous layer of the pericardium
mesothelium
what binds to calcium in the smooth muscle contraction
calmodulin
what is attached to myosin in smooth muscle contraction
RLC
what does calmodulin activate
myosin light chain kinase
what leads to phosphorylation of smooth muscle cross bridges
myosin light chain kinase
