Exam III Flashcards
(204 cards)
1
Q
Starting with the chamber that receives blood from the vena cavae, put these structures in the order that blood passes through them: right ventricle, aorta, pulmonary veins, left atrium, pulmonary arteries, right atrium, left ventricle
A
Right atrium ->
Right ventricle ->
Pulmonary arteries ->
Pulmonary veins ->
Left atrium ->
Left ventricle -> Aorta
2
Q
Valve located between the right atrium and right ventricle.
A
Tricuspid valve
3
Q
Valve located between the left ventricle and the aorta
A
Aortic valve
4
Q
Valve located between the left atrium and the left ventricle.
A
Mitral valve
5
Q
Valve located between the right ventricle and the pulmonary trunk.
A
Pulmonary valve
6
Q
Which type of cardiac cells do not have a true resting membrane potential?
A
Pacemaker cells
7
Q
In pacemaker cells, which ion is responsible for:
Bringing the membrane potential to threshold.
A
Funny currents, which cause funny channels to open
8
Q
In pacemaker cells, which ion is responsible for:
The depolarization of the action potential.
A
Influx of Na+ ions through funny channels (pacemaker potential) Ca2+ also begins to flow into cell, heightening depolarization
9
Q
In pacemaker cells, which ion is responsible for:
The repolarization of the action potential.
A
K+ channels open and K+ ions leave the cell
10
Q
In contractile cells, which ion is responsible for:
The depolarization of the action potential.
A
Fast sodium channels open causing quick influx of Na+ ions, slow Ca2+ ion channels also open
11
Q
In contractile cells, which ion is responsible for:
The plateau phase of the action potential.
A
Calcium and K+ ion channels remain open, causing stable charge of membrane
12
Q
In contractile cells, which ion is responsible for:
The repolarization of the action potential.
A
Calcium channels slowly close, and K+ flows out of the cell, calcium transported out and back to SR
13
Q
Why is the plateau phase of contractile action potentials important?
A
The plateau phase allows for the contraction to be longer, which is important to push all the blood out of the heart chambers. This also causes the refractory period to be longer, ensuring that the muscle doesn’t succomb to summation or tetanus.
14
Q
Why is it important that the electrical signal is delayed as it moves through the AV node?
A
It ensures that the atria will be able to fully empty the blood into the ventricles before the ventricles begin their contraction.
15
Q
What are systole and diastole?
A
Systole- contraction of the heart
Diastole- relaxation of the heart
16
Q
Is the duration of systole longer or shorter than the duration of diastole?
A
The duration of diastole is longer than systole
17
Q
Atrial diastole
A
Deoxygenated blood enters the right atrium
18
Q
Atrial systole
A
The atria will contract to push the remaining amount of blood (10-20%) into the ventricles
19
Q
Isovolumetric contraction
A
Both valves are closed, and tension increases while no muscle length is changed. No blood will leave, only pressure in the chamber will rise.
20
Q
Ventricular ejection
A
The process by which the heart squeezes out the blood in the ventricles out to the body
21
Q
Isovolumetric relaxation
A
All valves will close again the heart is in a resting state without blood within.
22
Q
Ventricular filling
A
Occurs when high pressure forces the blood to enter the heart’s expanding ventricles.
23
Q
What does the cardiovascular system do?
A
-Oxygen nutrients and water enter the body and need to get to every cell, also waste products that need to leave the cells and be removed from the body
-Cardiovascular system integrated in basically every physiologic process
24
Q
Components of cardiovasc system-
A
Blood: transporter, contained in network of tubes, all vertebrates have closed circulatory system, need something to generate flow of pressure gradient
Heart: pump
Blood vessels: tubes
25
Targets of blood: (2 main cats)
Respiratory surfaces: pulmonary circulation (lungs, unless fish then gills, and lungs and skin for amphibians)
Systemic tissues: systemic circulation (everything else in body that needs blood)
26
Do hearts vary much among vertebrates?
Yes, hearts have changed dramatically through different classes of vertebrates, mainly due to transition form water to land. Or going back and forth between the 2
-pulmonary circuit has had to change a lot.
27
Fish heart: how many chambers?
What's the other unique thing about this heart?
2 chambers in heart
-Heart of fish never sees oxygenated blood, only sees deoxy blood
28
Describe fish heart (see screenshot as well or slides 09 5)
Atrium collects deoxygenated blood from systemic tissues
Ventricle pumps deoxygenated blood to gills
Atrium- chamber received blood from body, could be deoxy from systemic, could by oxy blood from pulmonary tissues
Ventricles- pumping chambers, distribute blood back out through the body to lungs or systemic tissues.
29
With the circulatory system, blue represents deoxygenated blood BUT
the blood still has a lot of oxygen, however it is less than fully oxygenated blood
30
Amphibian heart: how many chambers, and what's unique about this one?
Amphibians: 3 chamber heart
Amphibians: blood mixing in the right atrium and ventricle, both get oxy and deoxy blood
31
Work of the atria of amphibian heart-
-left atrium: collects oxygenated blood from lungs
Right atrium: collects deoxygenated blood from systemic tissues, oxygenated blood from skin (blood from systemic tissues is deoxy blood)
Ventricle: pumps oxygenated blood to systemic tissues, deoxy blood to lungs and skin
(animals left and right in these diagrams, not yours I think)
-Coming into right atrium have sinus venosus vessel (SV) getting blood from the skin and systemic tissue
32
Work of the ventricles of amphibian heart-
-Coming into left atrium, pulmonary bank (from the lungs)
-coming out of ventricle is split and branches (from each??)
Bottom vessel is pulmonary arch to lungs and the skin
Upper one is systemic arch which goes to systemic tissues
-Left atrium collects oxygenated blood from the lungs (coming into pulmonary veins)
33
How do amphibians have mixing of oxy and deoxy blood in their chambers?
-spongy walls reduce mixing in chambers
-spiral valve sends oxygenated to systemic circuit, deoxy to pulmocutaneous circuit
-when ventricle contracts, all blood ejected, mostly deoxy out of pulmonary arch, and oxy to go out to systematic arch to systematic tissues
-spiral valve does magical separation of oxy and deoxy blood
34
Which vertebrate uses a spiral valve to separate their mixed oxy and deoxy blood?
Amphibians in their cute lil hearts
35
(most) Reptiles have how many chambers in heart?
3 chambers
-Reptile bask and breath air so look like this. However if it’s hanging out a lot underwater, we have some modifications during a dive
36
Reptile heart general blood flow:
Left atrium: collects oxy blood from lungs (input from pulmonary vein)
Right atrium: collects deoxy blood from systemic tissues (input from SV)
Ventricle: pumps oxygenated blood to systemic tissues, deoxygenated blood to lungs (multiple outputs, pulmonary artery, and systemic arches)
-reptiles not absorb O2 through skin
37
Reptile ventricle has 3 what?
3 subchambers: cavum arterosum (CA_ Cavum venosum (CV) and cavum pulmonale (CP) separated by muscular ridges (subchambers to collect blood)
Deoxy blood from right atrium goes to CV to CP to pulmonary artier, right side of heart
Oxy blood from left atrium go into CA, pump into CV and then head out systemic arches
38
In reptile heart, all the chambers except ______________ are generally keeping oxy and deoxy blood separate
middle chamber CV
39
Most reptiles: diving
What heart do?
-no need to send blood to lungs
-deoxy blood in CV doesn’t go to CP
-all blood exits via systematic arches
-all blood here kinda purpleish, but blood from systemic tissues into left atrium, down into ventricle, into CA, from CA to CV
On right side blood come into right atrium, then go down into CP
-main difference is shunt put into place to change where blood goes to, reduces amount that goes from CB into CP and out the pulmonary artery, most blood just goes out the systemic arches
-shunting blood away from pulmonary circuit to systemic circuit
-send blood to where it needs to be, not where it doesn’t
39
Is the reptile dive response like our mammal dive response?
Np, very different from dive response in lab bc we mammals who returned to water. Mammals do not have a shunt like this. There’s a series of valves that allow for this diving reptile shunt
40
Crocodilians have how many heart chambers?
4 chambers
41
What do them croc heart chambers do?
Left atrium: collects oxy blood from lungs
Right atrium: collects deoxy blood from systemic tissues
Left ventricle: pumps oxy blood into systemic tissues
Right ventricle: pumps deoxy blood to lungs
42
Croc heart-
Input to right atrium (sinus venosus) bringing deoxy blood form systemic tissues
-output from right ventricle (pulmonary artery)
-input to left atrium, pulmonary vein, bringing
-Aorta, structurally different from mammalian and bird, one part comes out left ventricle, another section also comes out right ventricle. Left seems like coming out right ventricle but isn’t??
-deoxy blood into right atrium and into right ventricle, contracts, send deoxy blood out pulmonary artery to lungs. Not through aorta bc it has valve closed
-right side- oxy blood entering left atrium through pulmonary vein into left ventricle, pumps out aorta from both sides (foramen of pentise?? It’s the little split in aorta, lets oxy blood to go from right aorta to left as well.)
-Shunt for crocs when diving, deoxy blood will enter right atrium into right ventricle, oxy blood coming into left side. Valve closed during air breathing will open up, and on pulmonary artery, structures (cogti?) will close, shutting off pulmonary artyery from taking away blood from right ventricle
-from left ventricle oxy blood going out mostly right aorta, but some through foramen and out left aorta
-blood in right ventricle wont go out pulmonary artery and valve on left aorta opened up so blood can exit out left aorta
(shunting blood away from lungs, not total shunt from lungs, but most flow to lungs reduced, rest of blood focused on being sent to systemic tissues.)
Right & left aorta are connected by foreman of panizza
43
Air breathing in crocs-
-valve in left aorta closed, oxy blood enters right and left aorta, deoxy enters pulmonary arteries
44
Diving in crocs-
-Cog teeth close pulmonary arteries
-Blood from right ventricle goes to systemic circulation via left aorta
45
Birds & Mammals: How many heart chambers?
4 chambers (much simpler)
Left atrium: collects oxy blood form lungs
Right atrium: collect deoxy blood form systemic tissues
Left ventricle: pumps oxy blood to systemic tissues
Right ventricle: pumps deoxy blood to lungs
46
Do birds and mammals have a shunt like the crocs?
Do they mix oxy and deoxy blood?
-no structural modifications that can shunt blood away from lungs (during dive for aquatic mammals)
-complete separation of oxy and deoxy blood
47
Left atrium:
collects oxy blood form lungs
48
Right atrium:
collect deoxy blood form systemic tissues
49
Left ventricle:
pumps oxy blood to systemic tissues
50
Right ventricle:
pumps deoxy blood to lungs
51
Flow of blood through mammalian heart
-The right atrium receives deoxy blood form systemic circuit via superior (blood from above heart) and inferior vena cava (blood from below heart)
-pushed blood out pulmonary artery to lungs, oxy blood returned to left atrium via pulmonary veins
-drains into left ventricle, oxy blood pumped out of aorta into tissues
52
4 one-way valves-
-2 atrioventricular (AV) valves
Tricuspid (right) & (bicuspid) Mitral (left)
-2 semilunar valves
Pulmonary (right) & aortic (left)
53
2 atrioventricular (AV) valves-
who are and respond to what
(respond to pressure above the valves)
Tricuspid (right)- controls blood flow between the right atrium and right ventricle
Bicuspid mitral (left)- located between the left atrium and left ventricle
54
2 semilunar valves-
who are and respond to what
(respond to pressure below the valves) as blood pushes against bottom of valve they open and blood relaxes, when blood drains toward top of valve they close
Pulmonary (right)- regulates blood flow between the right ventricle and the pulmonary artery
Aortic (left)- opens to let blood flow from your left ventricle to your aorta
55
Why are valves in heart important?
to ensure blood flows in one direction through cardiovascular system
56
How does heart valve pressure work?
Pressure in one direction opens valve, pressure in other direction closes it (like standing on one side of a door)
57
2 types of myocardial cells-
1) Pacemaker (auto-rhythmic) cells- set heart rate (BPM)
2) Contractile cells- -perform mechanical work of the heart
58
1) Pacemaker (autorhythmic) cells
-generate spontaneous action potentials
-establish heart rate.
-unique, most electrically excitable cells have stable resting membrane potential which wont change without external cell input
-these cells have unstable membrane potential that spontaneous depolarizes so it has action potentials regularly and spontaneously, has its own control mechanism.
59
Activity of pacemaker cells establish
heart rate, nervous system can influence them but they don’t need them
-Indiana Jones and the temple of doom. Pulls out heart continues to beat until burst into flames, this is a lil bit true as long as the pacemaker cells have ATP
60
Contractile cells, describe the general make-up of them
-organized into sarcomeres
-cells branch & are joined end to end
-intercalated disks
-gap junctions & desmosomes
-functional syncytium
-contractions and relaxations allow for all to happen
61
How does cardiac muscle differ from skeletal muscle fiber?
-share similarity with skeletal muscle fiber, organized into sarcomeres (thin and thick filaments, cycle of contraction/relaxation)
-cardiac muscle very different from skeletal fiber, have more of a branching structure to them
62
How are contractile cells joined together?
-contractile cells are joined end to end not all laying out next to each other in rows
-intercalated disk is where these join (little dark lines in pic on slide)
-In intercalated disks 2 important proteins, Gap junctions and desmosomes
-desmosomes are rivets in jean pocket so doesn’t tear at corner, important in maintaining connection between 2 contractile cells
63
How are action potentials spread through contractile cells?
-action potential spread across membrane and pass through gap junctions, so theoretically need one stimulation of one contractile cell in heart and will spread to whole heart for them to act in unison and synchrony (crazy!!) will contract and release all at the same time
63
Which cell uses funny channels, and what do they do? [the channels]
Pacemaker cells
I^f channels: Na+ and K+ (I for current, F for funny bc response different from anything they’d ever seen lol)
(only open for short period of time)
Allows calcium in cell, further depolarizes cell and gets us to threshold
64
Pacemaker cells-
Pacemaker potential is what
unstable, depolarizing membrane potential
65
What is the process that opens funny channels? (I^f channels)
(other hint pacemaker cells)
I^f channels: Na+ and K+ (I for current, F for funny bc response different from anything they’d ever seen lol)
(I^F start by opening to allow Na+ into the cell, K+ leaves but less so initial depolarization occurs)
-next step is opening of T-type calcium channels (only open for short period of time)
Allows calcium in cell, further depolarizes cell and gets us to threshold
66
Contractile cells form a functional syncytium, what does this mean?
They're functionally connected to each other, action potential can pass through all cells (skeletal insulated from one another)
67
What are Gap junctions, and why are they important for contractile cells?
(is a protein) they are basically tunnels that cause cytoplasm of these cells to be continues so ions and small molecules in one cell can travel into other cell, allows electrical signals to pass form one to another
68
Describe what ions drive Action potentials in pacemaker cells-
-Rising phase is produced by more calcium entry through different set of calcium channels (L-type calcium channels, L for long, open for longer)
K+ channels: repolarization when potassium channels open, K+ leaves cell
Process then repeats
69
The pace of action potentials firing in pacemaker cells determines
the pace of the heartbeat
Pacemaker cells fire regular rhythmic action potentials
70
Contractile cell action potentials general facts:
Similar to neural and skeletal muscle AP except for plateau
-decreased K+ permeability
-increased Ca2+ permeability (L-type channels)
-stable resting membrane potential, once get signal from pacemaker cells fire action potetential
71
Contractile cell action potentials process via ion channels-
-starts with rising phase where sodium comes in through normal voltage gated channels
-repolarizing phase gonna look like opening up of L type calcium channels
-K+ leaving cell through Potassium channels, calcium coming in so cancels out, change in membrane potential pretty small and slow, forms plateau phase
-L type channels close so K+ only one still exiting
72
Mechanical events that need to occur in heart, what are and why?
Need a flow of electrical activity to go through heart in a very specific pathway
Atria to contract, exit points at bottom through AV valves into ventricles
-Need atria to contract first and top down
-Needs to be followed by contraction of the ventricles (after atria are done contracting)
-Need ventricles to contract from the bottom up bc exit sites are at the tops
72
Is the AP the same duration as twitch in heart contractile cells?
Yes
(very different from skeletal muscle)
73
Atria to contract, exit points at bottom through AV valves into ventricles
What way do they contract?
Need atria to contract first and top down
74
Followed by contraction of the ventricles (after atria are done contracting)
What way do they contract?
-Need ventricles to contract from the bottom up bc exit sites are at the tops
75
Pacemaker cells aren’t neurons, and contractile cells are more what?
branching type cells that join end to end with other contractile cells, gap junctions so action potentials can spread to their neighbors
76
Pacemaker cells and contractile cells have a connection, which forms electrical connection needed to get
contractile cells going
77
Does the order of contraction of cells throughout the heart matter?
YES we don’t want random spread throughout heart
-want specific spread throughout spread so mechanical events will work just how they need to
78
Conduction through the heart: two main sets of pacemaker cells to be aware of in mammalian heart
At root of right atrium is SA node, second set floor of right atrium (AV node)
79
Flow of APs:
starts where, and then who's next
Sinoatrial (SA) node
-Interatrial pathway-
(Bachmann’s bundle)-
Pathway from pacemaker cells SA node to contractile cells of the atria starting from the top spreading down so can contract from top spreading down
80
Internodal pathway-
Pathway from pacemaker cells AV node
81
-Atriocentricular (AV) node
**mainly causes delay
These two (internodal pathway and AV node) are connected to synchronize, AV pacemaker cells fire Aps slightly slower
-faster SA node firing makes AV node cells speed up so they go at same rate
-as signal spreads through AV node, slows down a little bit, delay in signal here important to allow atria to finish what they’re doing before ventricles start contracting. Delay synchronizes activity the way it needs to be
-Band of connective tissue electrically insulates atria contractile cells from cells of ventricles
82
AV bundle (bundle of His)
-right and left bundles
Splits into right and left branches who go to tip of heart
83
Perkinje fibers-
spread back up walls of ventricles
Allows ventricle to contract from bottom to the top
84
Each heartbeat-
same electrical spread?
-every heartbeat has same characteristic spread of electrical activities
85
Do contractile cells in the atria depolarize and repolarize at the same time?
Yes, all contractile cells in atria going through depolarization and repolarization at the same time
86
Electrocaridogram (the ECG) measures what?
cardiac activity
Output looks very different because of spread of action potentials through the gap junctions synchronizing everything
87
Electrocaridogram: ECG
Every heartbeat has 3 things to see-
what are they, and what do they measure?
P wave-
-coordinated atrial depolarization of all contractile cells
-QRS complex-
-ventricular depolarization
-atrial repolarization
-T wave-
-ventricular repolarization
88
P wave-
-coordinated atrial depolarization of all contractile cells
89
-QRS complex-
-ventricular depolarization
-atrial repolarization
90
-T wave-
-ventricular repolarization
91
Cardiac excitation-contraction coupling Sequence of events:
1) AP spreads across membrane & down t-tubules
2) Ca2+ in from ECF during contractile action potential
3) Ca2+-induced Ca2+ release from sarcoplasmic reticulum (RyR channels)
4) Sarcomere contraction similar to skeletal muscle
5) Ca2+ removal terminates contraction
(Into SR via Ca2+-ATPase
Into ECF via Na+/Ca2+ antiporter)
92
(Understand timing of mechanical and electrical activity in the cardiac cycle)
anyways, what're systole and diastole?
Systole: contraction, pressure increases, chambers contract pushing blood through and out
Diastole: relaxation, pressure decreases, chambers relax, allow them to refill
93
Blood flows from
high pressure to low pressure, driving force to move blood is alternating series of contractions and relaxations of chambers of the heart
94
Overview of 5 mechanical events in the heart-
1) Atrial & ventricular diastole
(Passive filling of atria & ventricles)
2) Atrial systole
(Atria contract, complete filling of ventricles)
3) Isovolumic ventricular contraction
(Ventricles contract, all valves closed, Atria refilling)
4) Ventricular ejection
Semilunar valves open, ventricles empty
Atria still refilling
5) Isovolumic ventricular relaxation
Ventricles relax, all valves closed
Atria still refilling
95
1) Atrial & ventricular diastole (passive filling of atria and ventricles)
Atrial and ventricular diastole- entire heart is relaxed, neither chamber contracted
-main filling stage of heart, blood coming into relaxed atria, AV valves open, atria pressure higher than ventricles, passively through valves into ventricles, each chamber filled
96
Why is the main physiological focus the volume and pressure changes in the left ventricle?
Focusing on changes in volume and pressure of left ventricle, because in 4 chamber heart it injects blood into systemic circulation, right to pulmonary, left ventricle has much more work to do than right ventricle
-much more resistance left ventricle needs to overcome, left ventricle always focal point for mammalian and bird especially physiology center
97
What is the pressure and volume of the left ventricle during stage 1) Atrial & ventricular diastole ?
-Ventricle relaxed, so pressure is basically low and unchanging
-Volume of ventricle going up, filling with blood significant increase
98
Which stage is the main filling stage of the heart?
Stage 1) atrial and ventricular diastole
blood coming into relaxed atria, AV valves open, atria pressure higher than ventricles, passively through valves into ventricles, each chamber filled
99
2) Atrial systole
-atria contract, complete filling of ventricles
-ventricles still in diastole, completes filling of the ventricles
100
At what point are the atria done being filled? What about the ventricle?
Atria: stage 1, atria and ventricular diastole
Ventricle: stage 2, atria contracting will finish filling of the ventricles
101
What is the pressure and volume of the left ventricle during Stage 2) Atrial systole?
-pressure in ventricle will be increased from squeeze of atria, pressure up a little bit
-Volume will be upped in ventricle a little bit as well
102
When is the end diastolic volume (EDV) for the left ventricle?
think of it as the point of max filling with blood right before contraction
for ventricle *after diastole,* volume after it’s finished filling/right before it’s gonna contract
103
3) Isovolumic ventricular contraction (can also be called be systole instead of contraction)
When it’s contracting, causes valves to close.
-ventricles contract, all valves closed
-Atria refilling
-At very start of this stage, AV valves are closing, and that produces the first partsoun ?? (first sound of beat in heartbeat)
-Atria are relaxed, filling with blood, stays put, no change in volume, big increase in pressure
103
Why doesn't blood volume change during isovolumic ventricular contraction? (stage 3)
Pressure in the ventricles isn’t enough to open semilunar valves, hence isovolumic
Volume inside isn’t changing, bc at start of contraction, all valves in heart closed.
When ventricle contracts, floor valves close so no backflow into atria, aortic valve and pulmonary have been closed this whole tile bc they shoot up and out of ventricle.
103
What happens to blood volume in the 2 isovolumic stages of the cardiac cycle?
Nothing, it stays the same
103
4) Ventricular ejection
-as pressure builds, overcomes pressure in pulomary artery and aorta, semilunar valves open and blood can exit out into circulation and venticles start to empty, only portion of blood will be ejected
-Have blood returning to heart, so atria refill during this stage
103
What is the pressure and volume of the left ventricle during Stage 3) Isovolumic ventricular contraction
-During this period, volume of ventricle unchanged
-Pressure will be increasing due to contractions
103
What is the pressure and volume of the left ventricle during 4) Ventricular ejection
Volume of blood will be going down
-ventricles continuing to contract, so pressure will raise to a point, and then start to decrease
-volume of blood remaining in ventricle will be end systolic volume (ESV)
104
5) Isovolumic ventricular relaxation
-volume not changing, ventricle relaxing
-as ventricles start to relax, semi-lunar valves start to close, all valves are closed,
-AV valves cant open until pressure in ventricle is less than atria (shut here)
105
What is the pressure and volume of the left ventricle during 5) Isovolumetric ventricular relaxation
volume not going to change, the pressure will be decreasing, rapid drop probably back to where it was before previous cardiac cycle
106
The relationship between electrical events, pressure & volume-
-depolarization of and repolarization of atria, then of ventricles that lead to these mechanical events. Each event will be preceded by an electrical event, one of the ECG waves
107
-Wiggers diagram-
-shows you over time relationship between volume pressure and electrical activity
(09 slide 29)
-changes in left ventricle volume and pressure
**see this chart more
-middle part of figure also have changes in left ventricular pressure, atrial and aortic pressure
-Left ventricle pressure corresponds to changes of pressure in entry and exit point of left ventricle
-focus on left ventricular pressure changes
108
ECG action and shit idk
-before atria can contract need p-wave to depolarize
-QRS complex when atria are repolarizing, ventricles depolarizing, right before isovolumetric ventricular contraction (before pressure in ventricle starts to shoot up and volume plateaus
-Relaxation of ventricles same as T waves as repolarization spreads across ventricles, decrease in pressure as they relax
109
-be able to think about the mechanical events, list in order, and what’s happening at each stage. Also visualize over one cycle how the volume in left ventricle is changing, how pressure changing, how does that coindice to each piece, and what is timing of electrical events?
**spend time with that nasty figure *moany face* end there don’t start there tho
110
Heart rate is a function of what two things?
Antagonistic autonomic control
Cardiac output or CO, is a function of two things, the heart rate (BPM) multiplied by stroke volume
-Cardiac output based on each minute how much blood ejected out of the heart
111
stroke volume-
-how much blood is for every contraction, how much blood is ejected during ventricular ejection
-end diastolic volume and end systolic volume
EDV-ESV=stroke volume
-stroke how much blood ejected every beat, then together how much is ejected every minute?
112
Does the heart need autonomic input to work?
-Heart doesn’t need external nervous input to beat, however rate of pacemaker cell firing APs is controlled through autonomic nervous system
113
At rest baseline input from both branches to control heartrate.
Which is higher at resting?
In heart, higher baseline input from parasympathetic at rest.
-If you eliminated any autonomic input to the heart, it would lower the resting heartrate
114
2 ways to increase heartrate (via autonomic control)
for a little decrease parasym, big increase activate sym
115
To decrease heart rate:
-increase parasym input to slow heartrate down
-Antagonistic autonomic control of heart
116
Autonomic regulation of rate:
-Sympathetic (NE and E) increases permability of If and Ca2+ channels
-Parasym (ACh) increases K+ permeability and decrease Ca2+ permeability
117
cardiac output =
heart rate * stoke volume (how many mL of blood ejected each beat, =end diastolic volume- end systolic volume)
Regulation of heart rate from autonomic input
118
Stroke volume control is a bit more complex than heartrate, why?
More factors involved, Intrinsic control (heart itself) vs Extrinsic control (outside of the heart)
119
-Intrinsic control-
Frank-Starling law- Heart has relationship between stroke volume and end diastolic volume
Basically stroke volume increases with EDV (almost linear relationship between these two things)
-If volume increasing more blood into ventricle, so then ventricle has to contract a little stronger
-If more coming in than leaving, ventricle will fill too much over time, or empty out
-Couples 2 things, so every heartbeat as much as ejected will come in
120
Why does the Frank-Starling law have sense?
-Physiology is that cardiac muscle has length tension relationship like skeletal muscle
-Resting sarcomere length of cardiac cells is well short of the optimal length. So cells are producing weaker contraction than they could
-now contract with more force so more ejection if higher volume of blood
121
Extrinsic control-
Sympathetic activity causes: can also influence stroke volume, at any end diastolic volume how much force is produced at given sarcomere length? Sympathetic input will increase that force.
-increased contractility
-increased venous return
-increase in stroke volume with increase of end diastolic volume, stroke volume gonna be stronger if sympathetic transmitters are present (they increase amount of calcium coming into cell during contraction)
122
Extrinsic sympathetic input also causes
-bigger stroke volume and more blood through system
-Veinous return will be increased (how much blood coming back to heart through the veins)
-increase end diastolic volume, which will then increase stroke volume.
-sympathetic input increases contractility to heart, to vessels increase veinous return as well, helpful for overall ramping up blood flow throughout the body in times of panic
123
-Controlling cardiac input figure helpful to review **
slide 09 34
124
Does the parasympathetic nervous system impact the extrinsic control of the stroke volume?
No, only sympathetic
(I think gulp)
125
Overview:
Blood flow to organs (real high to low):
lungs, digestive system, liver, kidneys, skin, brain, heart, skeletal muscle, bone, other
-supplies metabolic needs
-reconditions blood
-Systemic flow can be altered to meet demand
-what percent of total blood flow goes to each organ
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Why do the kidneys and digestive system get so much blood flow?
-Other thing that influences blood flow is if organ reconditions blood flow (changes composition in some way)
-kidney and digestive are metabolically active but act as nutrient drop and filters
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Main equation for blood flow:
relationship q= deltaP/R, Q is flow, delta P and R are the main factors, P pressure gradient, R is resistance
Pressure gradient- flow increases as gradient increases (pressure at start of tube will always be more than pressure at end, longer distance bigger pressure drop at end)
Resistance- influenced most by vessel radius, flow decreases as resistance increases, viscosity, radius
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Radius can also be changed significantly
R= 1/radius^4
-small changes in the radius of vessel will have huge impacts on resistance, smaller radius, bigger resistance, inverse relationship
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What are the main vessels of the body?
Arteries -> arterioles -> Capillaries -> venules & veins
-Arteries- blood vessels leaving the heart (pattern of divergence, big to small tubes)
-Aterioles- branching from arteries
-Capillaries- finest blood vessels
-Venules- (pattern of convergence, small tubes make big tubes)
-Veins
Each vessel type has slightly different composition
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Arteries: function as pressure reservoirs (lot of elastic tissue, greatest ability to expand and contract
-*Arteries expand during systole, relax during diastole*
-serves as a secondary pump, under most pressure in cardiovascular system
-Ensures constant flow through circulatory system
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How do arteries cope with the incredible pressure they're under?
-arteries allow walls to bulge out, pressure relieved during diastole
-squeezing arterial blood helps push out to the cardiovascular system
-secondary pump action of arteries helps smooth out pumps of blood, without they wouldn’t have blood to push bc not enough blood, collapse of arteries helps keep that pressure
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Blood pressure-
What are the 2 metrics we use to measure it?
How do you calculate them?
Systolic vs diastolic
Pulse pressure- basically just the difference between systolic and diastolic (120-80 pp would be 40)
Mean arterial pressure (MAP) MAP= diastolic pressure + 1/3 of the pulse pressure, provides nice average number. Use 1/3 of pulse pressure bc heart spends more time in diastole than systole
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Pulse pressure-
basically just the difference between systolic and diastolic (120/80 pp would be 40)
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Mean arterial pressure (MAP) MAP=
diastolic pressure + 1/3 of the pulse pressure, provides nice average number. Use 1/3 of pulse pressure bc heart spends more time in diastole than systole
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What happens to blood pressure as it gets away from the heart?
-pressure decreases w/ distance, highest pressure at arteries, will decrease through the further vessels
-in ventricle we get huge swings of pressure, in arteries that swing is much less, diastole pressure doesn’t go down to zero bc of elastic nature of arterial walls
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Arterioles-
variable resistance vessels in the body
Most vessels have smooth muscle to change diameter, arterioles have a bunch
-baseline diameter can be changed in 2 directions
-*biggest capacity to change their overall diameter*
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Arteriolar tone (contraction:) can lead to two changes-
-vasoconstriction
-vasodilation
-medium level of contraction gives resting diameter
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Effects of variable resistance- (arterioles)
-blood flow changes with resistance
-adjustments to blood flow based on metabolic need
-this can change in different areas of body depending on current need, dilating in one area, and constricting in another
-lotta flow to digestive, kidneys, muscle, not much to bone
-during exercise changes dramatically, lots of blood to skeletal muscle, not much to liver and digestive tract, significant changes in the arterioles
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Ways to change resistance-
Local (intrinsic) control-
blood vessels themselves have control over their diameter, how much contraction of smooth muscle at any point or time
Mechanisms for this:
1) Myogenic autoregulation
2) Metabolic changes
3) Vasoactive mediators
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Myogenic autoregulation-
mediated by stretch on arterioles, don’t want increases or decreases this good way to do that. Baseline level of flow have certain amount of pressure, arteriole a little stretch. Suddenly increase in flow, unwanted, which will expand arteriole and increase pressure
-stretch causes reflexive contraction of smooth muscle, counteracting increase in flow that would happen otherwise
-if blockage reduced flow, reduced stretch will require a bit of vasodilation to bring it back
-blood vessels are controlling their own diameter making sure weird changes don’t alter blood flow
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Metabolic changes-
may occur due to local change in metabolic activity of a tissue. For example, dominant arm writing, working harder so gonna need more oxygen levels, and may be producing more CO2. At the gym doing one arm curls, lactic acid may be building up dropping pH in area (examples of possible metabolic changes in tissue becoming more active, opposite in going less active)
-walls of blood vessels will then release vasoactive mediators
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Vasoactive mediators-
chemicals that will change the contraction status of the smooth muscle
-nitric oxide or NO an example, is a vasodilator
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Extrinsic control-
-hormones-
-sympathetic activity- main extrinsic control, will cause changes to vascular smooth muscle contraction
-how sympathetic affects blood vessel diameter, varies on types of receptors on those blood vessels
-a adrenergic receptors- (main autonomic control mech)
-greater affinity for NE, but will bind epinephrine
-Beta2 adrenergic- receptors- much more limited
-Prefer E
-When E binds it causes vasodilation so opposite response
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Beta2 adrenergic receptors- much more limited
-cardiac muscle and skeletal muscle (smooth muscle)
-bind NE and E, prefer E
-When E binds it causes vasodilation so opposite response
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a adrenergic receptors-
(main autonomic control mech)
-on all arteriolar smooth muscle (except vessels in the brain)
-greater affinity for NE, but will bind epinephrine
-cause vasoconstriction
-all arterioles get input form sympathetic post-ganglionic neurons, level of activity will establish resting diameter of those vessels, increase input constrict, decrease, dilation
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General rule of thumb for alpha vs beta adrenergic receptors-
because all blood vessels except brain have alpha, sympathetic will cause vasoconstriction, unless it’s activating the beta-2 receptors than can get vasodilation instead
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Capillaries-
-site of gas, nutrient, and waste exchange (only happens with these guys, other vessels have too much stuff surround them)
-thin endothelial cells comprising them
-specializations for exchange
-respiratory gases, waste products, hormones, etc
-goal of cardiovascular system is exchange
-huge surface area for a lotta exchange to occur
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-Exchange mechs-
(for capillaries)
-diffusion simplest way
-bulk flow gonna be everyone else, cells making walls have gaps “pores” which allows for another pathway for exchange
-blood stuff can move to interstitial fluid and vice versa
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Bulk flow-
can go in both directions, from blood to interstitial space, or vice versa
Filtration: out of capillary
Absorption: into capillary
Main factors: 2 main here
1) -Hydrostatic pressure (Pcap) pressure
2) Colloid osmotic pressure
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Hydrostatic pressure (Pcap) pressure-
that fluid exerts on walls of tube its moving through, outward pressure
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Colloid osmotic pressure (pi)-
osmotic difference of fluid in capillary and interstitial fluid, water gonna want to move from more conc to less conc. Plasma contains proteins ITF does not, so colloid osmotic pressure is inward into capillary
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If we have filtration at arteriole end, we have ________ static pressure
higher
Absorption at venous end, osmotic pressure higher
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Pcap > pi =
filtration
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Pcap < pi =
absorption
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Hydrostatic and osmotic pressure over capillary bed-
-Hydrostatic pressure over length of capillary bed, it’s gonna start high and end a bit lower than it was
-osmotic pressure wont change over length of capillary bed, stay the same
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-Aterial end of capillary, hydrostatic pressure higher than osmotic pressure
-veinous end relationship switched to hydrostatic pressure higher, absorption favored to stuff comes in
-both getting movement of fluids, filtration get delivery of nutrients
-absorption removed metabolic waste products
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-Osmotic pressure there bc of the proteins in the plasma, why?
-Proteins cans squeeze through endothelial cell pores, so cant be filtered
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-Net filation > net absorption, excess of interstial fluid build up that needs to be removed
-in addition to blood capillaries, some involved with lymphatic system
-Excess fluid filtered and not reabsorbed into lymphatic vessels who converge and empty into the vena cave
-So excess fluid filtered and not reabsorbed is returned to cardiovascular system through lymphatic system
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Venules & veins- (venules collect from capillaries and give to veins)
-function as volume reservoirs
-venous return can be altered based on demand
-more blood in the veins than in the arteries, they have the majority of blood
-increased venous return = increased EDV (end diastolic volume) = increased stroke volume (SV)
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Altering venous return-
what're the main 3 ways?
1) Sympathetic activity
2) Skeletal muscle pump & valves located within the veins
3) Respiratory pump
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1) sympathetic activity,
they have alpha receptors as well, vasoconstriction reduced volume of blood veins can hold
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2) Skeletal muscle pump & valves located within the veins,
mechanisms to produce more pressure, and ensure one direction flow
-pressure in veins pretty low, so not a whole lot of driving force away from gravity
-veins surrounded by muscles, gonna push blood in both directions away from constriction point
-veins will have series of one way valves that prevent backflow of the blood
-This is why locked knees cause passing out lol bc doesn’t activate skeletal muscle to pump
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3) Respiratory pump-
also helps with venous return, negative pressure in thoracic cavity, inferior vena cava included with that, negative pressure helps pull blood back towards the heart
-respiratory pump also not activated that much
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Cardiovascular priorities: these 2 things need to be happening
-maintaining adequate flow to organs based off metabolic demand
-maintaining adequate pressure also crucial, pressure gradient high at heart and arteries, low at venules and veins, need adequate flow through rest of body, cant be too big bc heart will get overwhelmed and cause excess strain on mechanical components.
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Mean arterial pressure (MAP)- what 2 main things alter it?
MAP α CO x TPR
MAP also influenced by:
Blood volume/viscosity
&
Distribution of blood in arteries & veins
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Baroreceptor reflex
Baroreceptors in aorta & carotids
Medulla
Autonomic response alters CO & TPR
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MAP α CO x TPR
MAP mean arterial pressure
CO is cardiac output
TPR is total peripheral resistance
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Baroreceptor reflex
-physiological mechanism that helps maintain stable blood pressure by rapidly adjusting heart rate and blood vessel diameter in response to changes in arterial pressure
-essentially acting as a negative feedback loop to keep blood pressure within a normal range
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Relationship between baroreceptor and medulla
-baroreceptor is an autonomic mechanism that regulates blood pressure by sensing changes in arterial pressure
-transmitting signals to the medulla oblongata, which then adjusts heart rate and blood vessel tone to maintain stable blood pressure
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Which vertebrate am I?
Oxy & deoxy blood are completely separate, except when I dive
Crocodiles
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Oxy on the left, deoxy on the right- you gotta keep ‘em separated
2) Mammals and birds
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I like to mix it up in my atrium and ventricle
3) Amphibians
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I have a chamber that can hold either oxy or deoxy blood
4) Most reptiles
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List all the heart chambers and major vessels connected to the heart that contain deoxy blood
5) The right atrium and the right ventricle, and the superior and inferior vena cava, and the pulmonary arteries.
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Where does the blood in the left atrium come from and where does it go?
6) The blood comes from the pulmonary veins (oxygenated,) and then goes to the left ventricle out to the aorta to the tissues.
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What would happen if the tricuspid valve was leaky?
7) The valve is on the right side separating the atrium and ventricle. We would expect back flow of the deoxygenated blood, disrupting the unidirectional blood flow.
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Can summation & tetanus occur in cardiac contractile cells? Why or why not? Why is this important?
1) Summation and tetanus likely cannot occur in cardiac contractile cells. This would be prevented due to the long refractory period which will broaden action potential, so by the time you can fire another action potential the muscle is relaxed. Since it can’t be stimulated while contracting, summation can’t occur. If summation or tetanus occurred, the pump function of the heart would be compromised.
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How would a mutation that results in a non-functional T-type Ca2+ channels affect heart function and why?
2) Pacemaker cells would be heavily impacted as they wouldn’t be able to get to threshold so the cells might not fire action potentials. As a result, the contractile cells wouldn’t receive any action potentials and the heart would not be able to contract.
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List all the differences between excitation-contraction coupling in cardiac vs skeletal muscle
3) Where action potential comes from:
Cardiac- from pacemaker cells or other contractile cells
Skeletal- synapse
How calcium released from SR
Cardiac- calcium induced calcium release
Skeletal- RyR and DnD
Shared action potentials between contractile cells (cardiac)
Calcium removal different, both use Ca2+ ATPase in SR, but cardiac muscle also sends some Ca2+ back into the ECM
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Atrial pressure is higher than ventricular.
1) Atrial systole, and Atrial and ventricular diastole (represented by blue color steps)
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Ventricular pressure is higher than aortic.
2) Ventricular ejection (color purple)
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All valves are closed.
3) Isovolumic stages (both) (color green and red)
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Left ventricular volume and pressure are both increasing.
4) Atrial systole (one of the blue)
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Why would these permeability changes cause the heart rate to change?
5) Increasing permeability of ion channels, so membrane depolarization to threshold can happen at a faster rate.
When If channels open, sodium will come in faster, and calcium will come in faster, so threshold achieved faster, speeds up rate of pacemaker cells.
ACh with extra K leaving cell, brings further from threshold, and decreases calcium permeability so taking longer to get to threshold, slows everything down
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Which cardiac cells get parasympathetic input? What about sympathetic?
1) Parasympathetic input- can affect heart rate and changes permeability of ion channels that affect how quickly pacemaker cells reach threshold, does not affect stroke volume, only heartrate.
Parasympathetic only affects heart rate not force, doesn’t affect contractile cells. Sympathetic affects heart rate with pacemaker cells, sympathetic input goes to contractile cells affecting stroke volume.
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Chytrid fungus lowers extracellular Na+ and K+, causing cardiac arrest in frogs. Why would this happen?
2) Since sodium is less available, the cell membranes of pacemaker cells can’t depolarize because the electrochemical gradient is much weaker than before. K+ electrochemical gradient a bit weaker, (inward electrical gradient, concentration grad a bit stronger.) If lower extracellular K+, electrochemical gradient bigger than normal, so more K+ leaving, hyperpolarize membrane
-pacemaker cells might never reach threshold, or just fire too slowly for heart to keep beating
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How does vasoconstriction affect resistance and blood flow?
1) This will increase the resistance of the vessel and decrease blood flow. Small changes in the radius will have big chances in resistance
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How would vasodilation of the arteriole affect bulk flow and why?
2) Vasodilation would result in more hydrostatic pressure, due to increased flow through the capillary. This will result in more filtration, more fluid moving into the interstitial space, so the lymphatic system would have to work harder to move more fluid back. (example occurrence may be due to an injury)
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For an amphibian heart, what does each chamber collect?
What's the oxy status of this blood?
Left atrium: collects oxygenated blood from lungs
Right atrium: collects deoxygenated blood from systemic tissues, oxygenated blood from skin
Ventricle: pumps oxygenated blood to systemic tissues, deoxygenated blood to lungs & skin
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What seperates their oxy from deoxy blood?
Spiral valve
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How do amphibians deal with blood mixing in the heart?
Right atrium and ventricle get both oxygenated and deoxygenated blood
Spongy walls reduce mixing in chambers
Spiral valve sends oxygenated blood to systemic circuit, deoxygenated blood to pulmocutaneous circuit
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For most reptile hearts, which chamber collects which blood?
Left atrium: collects oxygenated blood from lungs
Right atrium: collects deoxygenated blood from systemic tissues
Ventricle: pumps oxygenated blood to systemic tissues, deoxygenated blood to lungs
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Most reptiles how handle blood mixing?
Ventricle has 3 subchambers: cavum arteriosum (CA), cavum venosum (CV), & cavum pulmonale (CP)
Separated by muscular ridge
Deoxygenated blood enters CP via CV, exits via pulmonary artery
Oxygenated blood enters CA, exits via CV and systemic arches
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Most reptiles: diving
No need to send blood to lungs
Deoxygenated blood in CV doesn’t go to CP
All blood exits via systemic arches
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Crocodilians: 4 chambers
Left atrium: collects oxygenated blood from lungs
Right atrium: collects deoxygenated blood from systemic tissues
Left ventricle: pumps oxygenated blood to systemic tissues
Right ventricle: pumps deoxygenated blood to lungs
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Crocodilians: 4 chambers
Right & left aorta are connected by foramen of Panizza
Air breathing
Valve in left aorta is closed
Oxygenated blood enters right and left aorta, deoxygenated enters pulmonary arteries
Diving
Cog teeth close pulmonary arteries
Blood from right ventricle goes to systemic circulation via left aorta
