Lecture 8, Cardiovascular Regulation and Integration Flashcards

1
Q

Blood Pressure

A

systolic blood pressure
- blood pressure during left ventricular contraction (systole)
- estimate of the work of the heart against the arterial walls

diastolic blood pressure
- blood pressure during cardiac relaxation (diastole) - pressure when heart is relaxed
- with high peripheral resistance pressure will remain high for longer

mean arterial pressure (MAP)
- slightly lower than the actual “average” pressure
- weighted to account for the fact that the heart remains in diastole (relaxation) longer (in regards to how long your heart spends relaxed or contracted)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Total Peripheral Resistance

A

TPR = MAP + CO
increased MAP
- increase muscle force
- increased cardiac output
- vasoconstriction
decreased MAP
- we can change the resistance the blood encounters by changing the contraction of the vessel that the the blood goes through
- small increase in radius will cause an increase in flow that is 16 times larger - very small changes will cause a big increase in how much blow can flow into it
- more muscle force against the arteries then we are going to have a higher pressure that our body has to overcome
- constrict the blood vessels which is going to increase the pressure
- decrease pressure by vasodilating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Blood Pressure during Exercise

A

*depends on the type of exercise you are doing
- no change in diastolic pressure
- systolic pressure is going to go up when the heart is pumping
- as exercise intensity increases diastolic pressure stays the same or declines ever so slightly
- systolic goes up and up - as we need more and more blood to increase our VO2 pretty linear increase after the start of exercise
- vasodilation may cause a decrease in diastolic BP

resistance exercise
- both systolic and diastolic go up
- heavy leg press: biggest blood pressure responses, more muscle mass activating more blood pressure response
◦ VO2 does not go up during resistance exercise
◦ blood pressure goes up
◦ bicep shortening that tissue mass has to go somewhere and changes shape which leads to a force that equals to the force you are pulling with the muscle
◦ cardiovascular system has to overcome that and our blood pressure goes way up

extra video notes:
- at rest usually blood pressure is 120/80 mmHg - during exercise we see changes in peripheral resistance so changes in resistance a heartbeat has to overcome - increases in systolic BP (proportional to exercise intensity - running faster and faster and cycling closer to our VO2 max) while diastolic stays the same ands can even go down a little bit with very intense exercise
- the largest blood pressure is where we have resistance exercise as our muscles create force and that force is transferred to the bones but muscles change in shape and a forceful contraction leads to forceful change in shape (both systolic and diastolic go up)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Normal Route for Impulse Transmission Within the Myocardium

A

areas of the cell that depolarize faster than the rest of the cells
- SA node (pacemaker of the heart - controls the heart rate): on its own it will depolarize beat at 100 beats per minute when that happens speed that heartbeat to the adjacent cells and will follow down the atria and reach the AV node (80 beats per minute)
- downstream from the SA node is the AV node which contracts at slightly slower rate closer to 60-80 bpm and normal cardiac muscle cells located elsewhere and in ventricles will contract on their own but at a much much lower rate
- since depolarization and contraction spreads throughout the heart whatever contracts the fastest sets the heart rate
- the heart is a muscle that is made up of cardiac cells as opposed to skeletal muscle and in order to pump blood around the body the cells have to change length (shorten and create force)
- the biggest distinction between a cardiac muscle cell and a skeletal muscle cell is that a cardiac muscle cell is constantly depolarizing so it is constantly contracting at set rate on its own
- skeletal muscle cell will only contract if you use a chemical substance or an electrical stimulation
- cardiac muscle cells are linked together through gap junctions so if one cell contracts then adjacent cells will also contract together
- different cells in the heart have different intrinsic rates that they will contract at on their own and there are different nodes in the heart that can help to set the heart rate
- autonomic nervous system helps to control the heart rate and can directly stimulate the SA node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Cardiac Conduction

A
  • shows how electrical impulses travel throughout the heart to allow it to contract in a predictable way - the impulses arise from the SA node in the right atrium and then it spreads across the atria causing them to contract - in order to have useful heartbeat the atria have to contract first
  • atria contracts and then ventricles
  • it is important that this is all done in predictable way or else cardiac muscles can contract but they are not effective at pumping blood throughout the body
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

ECG Waves

A
  • P wave: depolarization of atria before atria contract (seen first)
  • QRS complex: Signals electrical changes from ventricular depolarization before ventricles contract
    ◦ atrial repolarization follows P wave, but produces a wave so small that QRS complex usually obscures it
  • T wave: Represents ventricular repolarization that occurs during ventricular diastole
  • as the heart contracts depolarization or changes in potential occur throughout the cardiac muscles and we can measure these
  • predictable pattern with every heart wave
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Different Phases of the Normal ECG from Atrial Depolarization to Ventricular Repolarization

A
  • at p wave we see polarization or contraction of the atria which is much less muscular then ventricular so the wave is small (the repolarization of the atria just occurs at some point during the QRS complex)
  • then we get a QRS complex which is depolarization or firing of the ventricles and because the ventricles are big and muscular we get this big signal and then we have the T wave which is the repolarization of the ventricle
  • counting r to r interval is how we get accurate heart beat (the time between the r wave on consecutive heart beats and that is the way we can get heart rate)
  • the ST segment - elevation or depression of it (higher or lower can be indication that someone is having reduced blood flow to heart during exercise or that they have had a heart attack)
  • this is one of many views that we can look at of the heart through the placement of one electrode but there are many other views
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Distribution of Sympathetic and Parasympathetic Nerve Fibres Within the Myocardium

A

autonomic nervous system (most important way we control heart rate and contractility of our heart)
- parasympathetic (rest and digest) *cranial nerve and vagus notes and innervates the SA and AV node
◦ slows down heart rate which
acts through cranial nerve
- sympathetic (fight or flight) *come from the spinal cord at cardiac accelerator nerve and integrate them at many points (acts through spinal nerves called cardiac accelerator nerve which acts on SA nodes and other areas of heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Sympathetic Influence

A
  • stimulation of sympathetic cardioaccelerator nerves releases epinephrine and norepinephrine
    ◦ cause chronotropic (increased heart rate) and inotropic (increased force of contraction - increasing stroke volume) effects on heart
  • sympathetic stimulation also produces generalized vasoconstriction except in coronary arteries (since we need to send heart to blood so coronary arteries are not affected)
    ◦ norepinephrine, released by adrenergic fibres, acts as a vasoconstrictor
    ◦ dilation of blood vessels under adrenergic influence occurs from decreased adrenergic activity (decreased sympathetic nervous system stimulation)
  • activated during stressful situations like exercise however we need to increase blood flow to active tissues but the sympathetic nervous system cause vasconstriction for the whole generalized body (smooth muscles to tighten up - decrease in blood flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Autonomic Nervous System

A
  • most tissues have innervation by both nervous systems (the heart is innervated by both the sympathetic cardioaccelerator nerves and parasympathetic vagus nerves)
  • spinal nerve activates the sympathetic nervous system and the cranial nerve activates the parasympathetic nervous system
  • norepinephrine is the main neurotransmitter used in the sympathetic division whereas ACh is the main neurotransmitter used in the parasympathetic nervous system (ACh is also used in motor nerves in the neuromuscular junction)
  • there is sympathetic stimulation of the adrenal glands which sets on top of the kidney which releases both epinephrine and norepinephrine into the systemic circulation so if we activate our autonomic sympathetic nervous system we can get systemic affects through release of these hormones
  • many of our organs (stomach, pancreas, small intestine) all have parasympathetic innervation and when we are in relaxed mode (rest and digest) we can get release on ACh which helps blood flow reach those organs which helps us digest and direct more blood flow there rather than muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Parasympathetic Influence

A
  • parasympathetic neurons release acetylcholine, which delays rate of sinus discharge to slow HR (act on SA node to slow heart rate)
  • bradycardia (slow heart rate) results from stimulation of vagus nerve from medulla’s cardio-inhibitory centre (withdrawing parasympathetic is important right when we start exercising)
  • parasympathetic stimulation excites some tissues and inhibits others (most of the exercise responsive tissues like heart and muscle will decrease activation)
  • at start and during low/moderate intensity exercise, HR increases largely by inhibition of parasympathetic stimulation
  • HR in strenuous exercise increases by additional parasympathetic inhibition and direct activation of sympathetic cardioaccelerator nerves
  • we can regulate HR and contractility in 2 ways: to increase stimulation of sympathetic nervous system and to decrease stimulation of the parasympathetic system (these 2 effects of the autonomic system are working together)
  • during low intensity exercise there is typically a bigger effect of just removing or inhibiting the parasympathetic nervous system and as exercise intensity gets higher sympathetic nervous system must be active in order to give us increase in HR that we require
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

when measuring arterial oxygen saturation would it matter if you sampled blood from the arteries supply active vs inactive muscle?

A

do not have gas exchange in arteries so we should have same amount of oxygen saturation going to every tissue (blood oxygenated in lungs is completed diffused to arteries) but it would matter if we wanted to get oxygen saturation from the venous blood (larger avO2 difference when active muscle is extracting more oxygen due to its low partial pressure of oxygen whereas with inactive muscles the oxygen is able to go past it recognizing that it is not in need of oxygen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how would the heart behave without chemical or neural inputs?

A

SA node (pacemaker of the heart) is going to maintain the heart at 100 beats per minute where the depolarization is transferred to adjacent cells to move down to AV node and eventually to all ventricles, where each cardiac cell is going to beat on its own a little slower than SA node (all of the other cells will synchronize with it because it is the fastest thing on its own) / if the SA node is damaged then the AV node can kick in and the heart would beat at the next fastest cell which would be 80 beats per minute / if both of these pacemakers are gone it can still beat but much much slower

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

why does blood pressure increase during exercise? how does the type of exercise effect this?

A

with resistance training our muscles contract which change shape and so any force generated is being reflected in the muscle and going to need higher blood pressure to overcome the constriction (both systolic and diastolic are affected since you are squeezing the vasculature whether your heart is relaxed or contracting, resistance training increases pumping and relaxed BP) / during aerobic exercise as we work at a higher and higher intensity, systolic pressure increases where diastolic either stays the same or decreases very slightly (higher cardiac output for systolic where we need to get more oxygen to tissue so we pump more blood through the body which increases overall pressure whereas for diastolic pressure, pressure goes down because we want to get more blood to active muscles so our arteries are going to relax and so there is less resistance to flow because we have larger vessels during exercise - vasodilation)
◦ during resistance vasodilation does not matter because we are squeezing it with our muscle, so even if vessel is a bit more relaxed if we are squeezing it down that is a much bigger effect as opposed to vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

explain how each branch of the autonomic nervous system can increase HR

A

inhibit the parasympathetic nervous system / pull back the stimulation because parasympathetic typically decreases HR, increase the sympathetic (NE to increase HR directly which is the the most important at high intensity exercise as at low we can just decrease parasympathetic but once we want to get above 100 beats per minute we have to add sympathetic)

17
Q

Neural Mechanisms for Cardiovascular Regulation Before and During Activity

A
  • input: information from body going to cardiovascular system and we have output: our sympathetic nervous system which we send to heart ro increase or decrease HR and increase contractility or how hard it is pumping
  • send information to the muscles that modulates vasodilation or vasoconstriction (blood vessels) which can happen neurally or chemical signals
  • inputs: higher brain areas (motor cortex) sending signals to low cardiovascular system and we also have input from our barol reflex which a negative input and from our skeletal muscles directly (mechanoreceptors - force and movement and metaboreceptor that sense chemicals or metabolites)
  • the control of heart
  • baroreceptors are located in the aortic arch / mechanoreceptors are in the heart / metaboreceptors receptors in skeletal muscle that are sensitive to movement (these signals will affect the HR and contractility of the heart)
18
Q

Central Command: Input from Higher Centres

A
  • impulses originating in brain’s higher somatomotor central command centre continually modulate medullary activity
  • central command provides greatest control over HR during exercise
  • heart rapidly “turns on” during exercise by decreasing parasympathetic inhibitory input and increasing stimulating input from central command
  • central command in cardiovascular regulation explains how emotional state can affect cardiovascular response (thus, creating difficulty obtaining “true” resting values for HR and BP)

my notes:
- most important one as it has the biggest affect
- HR correlates well with exercise intensity but because the main driver is the brain, emotions have to be taken into account as we are susceptible to it (HR is not perfect because so much is determined by our brain)
- our brain turns on HR by pulling parasympathetic stimulation that we had at rest and adding more sympathetic stimulation as we get to higher and higher intensity
- this can happen before exercise, increase as we do not need chemical or neural input to increase HR- before stimuli (feedforward mechanism)
- the greatest control comes from the motor cortex that sends descending signals to the medulla that then acts through the autonomic nervous system
- heart rate rapidly turns on during exercise but increasing parasympathetic stimulation and sympathetic but the biggest effect is the central command (feedforward stimulation - before any input we are feeding forward information)
- our emotions can affect CV system (higher BP or HR during stress

19
Q

Influence of Central Command on Heart Rate when Movement Begins

A
  • heart rate increase over the race but they do not start the race with 50-60bpm rather they know the gun is going to go off (anticipation) where there is an emotional response and so when gun goes off the heartbeat is 120-140bpm (which would be considered a relatively high exercise intensity heart rate)
  • feedforward mechanism is not dependent on us exercising rather thinking that we are going to start exercising
  • body knows that you have to increase cardiac output during exercise to move blood around the body - heart rate goes up beforehand in trained athletes - happens more readily in short sprint events where it needs to be up faster
  • if you are starting line of marathon your HR may not go up because the body does not anticipate need to have a high quick increased HR as with marathons you often start off slow opposite to a sprint
20
Q

Peripheral Input

A

three mechanisms continually assess the nature and intensity of exercise and muscle mass activated:

  1. reflex neural input from mechanical deformation of type III afferents within active muscles (from our mechanorecepetors (afferents) that send information from body back to brain - sense deformation as we have more movement it stimulates the nerve endings and provides that input to the brain)
    - stretch and activity of the muscle is being sent to the medulla to help regulate CV system
  2. chemical stimulation of type IV afferents within active muscles (metaboreceptors which respond to chemical signals from the muscle - ph, CO2, acetyl coA)
  3. feed-forward outflow from motor areas of central command
    *do not want to spike our HR before exercise way too high
    - our brain can get it wrong sometimes so we need other mechanisms to control our CV system as well
21
Q

Peripheral Input, cont.

A
  • specific mechanoreceptor feedback governs central nervous system’s regulation of blood flow and BP during dynamic exercise
    ◦ aortic arch and carotid sinus contain pressure-sensitive baroreceptors
    ◦ negative feedback
    ◦ cardiopulmonary receptors assess mechanical activity in the left ventricle, right atrium, and large vein
  • second set of mechanoreceptors that provide negative feedback which when stimulate send signal back to brain to calm down and reduce HR and BP (baroreceptors which are located in the aortic arch (gives us a whole body average of BP) and in the carotid arteries that are going up to brain because we do not want high BP in the brain)
  • need mechanisms to send blood to right spots as it is inefficient to increase HR and SV without it going to right spot
  • baroreceptors are sensitive to stretch and blood flow so if blood pressure gets too high or there is too much force on the arteries, the baroreceptors will act negatively decreasing BP and HR
  • can activate urself but palpating the carotid arteries on your neck (do not want to do it post exercise as we may not get accurate values or drop BP a little too much which would decrease amount of blood going to the brain)
22
Q

Distribution of Blood: Physical Factors Affecting Blood Flow, cont.

A
  • friction between blood and internal vascular wall creates resistance (force) that impedes blood flow
  • three factors determine resistance:
    ◦ 1. blood thickness (viscosity) - if we have thick blood it is going to have more resistance which is not good which can go up as we exercise more as we sweat and lose more fluid / can go up to a dangerous degree with doping (if we took a bunch of blood out and put it back in where we have less plasma and less fluid but too many red blood cells we can make the blood thick) - does not change a whole lot

◦ 2. length of conducting tube - cannot change the length of the tubes, but pre-capillary sphincters can close off where no blood flow is going into them at rest but during exercise they open up and perfuse and where red blood cells travels can become longer

◦ 3. blood vessel radius - smooth muscles in our arteries and arterioles which can increase radius by opening and relaxing where 1 unit change in radius can cause 16 unit change in flow (do not have to see huge change in radius to change big change in flow)

  • want low resistance in vessels that are perfusing muscle but a little higher resistance in places where we do not necessarily need as much blood
  • the last two are more predominant ones which change a lot during exercise
  • when we exercise we need to increase cardiac output to increase oxygen going to the muscle and to take carbon dioxide away from the muscle (but outside of that we need to make sure it is directed to the right place)
  • length of the arterial system (can have longer path for blood to travel - not necessarily physically changing the length)
  • the bigger the radius of the blood vessel the more blood is going to flow through it (smooth muscle around our arterioles can contract or relax and when it relaxes we see big increases of blood flow to increases where it is relaxed)
23
Q

Blood Flow Distribution

A
  • each circle represents how much blood is going to that area
  • 5L cardiac output at rest
  • big metabolic demand in the brain (needs a ton of blood) and in liver and GI tract (digestion, metabolism, filtering blood with our kidney and moving nutrients around with liver and GI) - lots of blood flow goes to these tissues, muscles needs some blood just to stay alive and renew itself and our skin needs a little bit of blood and our heart needs it as we need ATP for it
  • when we go to maximal exercise (VO2 max) we see a big expansion of cardiac output so we need to use maximum amount of oxygen (total cardiac output expands - 5L/min to 20L/min where the circle begins to look a lot different)
  • our brain still looks the same and maybe even slightly more and your heart needs a fair amount more blood as it needs to work a lot harder to pump out 4 times more blood than it was our rest / when you start exercising you are moving blood away from liver, GI tract and kidney (shunting blood away from these visceral organs) but the skin gets more blood due to sweating, the skeletal muscle increases deeply specifically the active one (big circle)
  • not much different in non-athletes and athletes for the smaller things (heart may get a little more and then less to kidney, GI tract and liver as there are better at shunting blood away to go to active muscle) but active muscle increases (a little more for brain cause more power being generated) - need mechanisms to send them to the right spots such as active muscle where it is needed most

extra video notes:
- the brain uses a consistent absolute amount of blood (goes up a little with exercise but very close to rest and does not matter how trained you are)
- at rest our muscles do not need much brain as we are not generating more ATP (just need basil amount)
- heart needs more at exercise as it is a muscle and with more blood it can contract more and harder
- from both absolute and relative perspective the liver, kidney and GI are using less so we can use it in other areas

24
Q

Exercise Effect on Blood Flow

A
  • any increase in energy expenditure requires rapid adjustments in blood flow that impact the cardiovascular system
  • during exercise, local arterioles of active muscles dilate while vessels to tissues that can temporarily compromise their blood supply constrict
  • as we have increased energy demands and increased ATP demands, where we have fast increase in cardiac output so we need to dilate and open up the blood vessels to supply the active muscle while at the same time constricting blood vessels to not go to the tissues that are not working
  • in order to support increase in energy expenditure that occur at the start of exercise we need to generate ATP with which we need more oxygen and for that we need more blood (we can do that through increase in cardiac output and sending cardiac output to places where it is needed)
  • our autonomic nervous system plays a role by generalized sympathetic activation which causes vasoconstriction (tightening of smooth muscle in arteries)
  • local products from active muscles are going to relax everything around active muscle so the systematic vasoconstriction paired with the local vasodilation sends the blood to where it needs to go
25
Q
A