Lecture 11: CV response to exercise 1 Flashcards

1
Q

closed loop design of circulatory system
- what does the heart do? (aka what?)
- what are the 3 circulations ish –> do they have low or high resistance and conductance?

A

HEART = the pump
- creates pressure needed to move blood through circulatory system
1. SYSTEMIC ARTERIAL CIRCULATION:
- large, low resistance (high conductance) tubes conducting blood from left heart to various organs
2. MICROCIRCULATION:
- small tubes, high resistance, low conductance vessels
3. SYSTEMIC VENOUS CIRCULATION:
- large, low resistance (high conductance) tubes conducting blood back to the right heart

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

what are the 3 components of the microcirculation?
- describe tubes + function ish

A
  1. ARTERIOLES: small tubes within tissue that control tissue blood flow –> high resistance (low conductance) vessels
  2. CAPILLARIES: thin tubes allowing exchange of substances (O2, CO2, nutrients) btw blood and tissue
  3. VENULES: small tubes within tissue for collection of blood from capillaries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is arterial blood pressure?
- determined by relationship btw (2)

A

force exerted by blood against arterial walls
- cardiac output and total vascular conductance!

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

what is systolic vs diastolic blood pressure?

A

SYSTOLIC: pressure generated as blood is ejected from the heart during ventricular systole/contraction (120 ish)
*influenced by body size, sex
DIASTOLIC: pressure during ventricular diastole/relaxation (when heart is filling up) (80 ish)

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

what is MAP?
- determines what?
- formula? + derive its components

A
  • Mean Arterial Pressure is the average pressure during a cardiac cycle
  • it determines the rate of blood flow through the systemic circulation = pressure required for blood flow to muscles, organs and tissues
  • MAP (mm Hg) = CO/TVK
    MAP = HR * SV * (length * viscosity)/r^4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is the formula for CO?
for TVK?

A

Cardiac output:
CO = heart rate x stroke volume (volume of blood pumped out at L ventricle at each systolic contraction)

total vascular conductance:
TVK = 1/SVR (systemic vascular resistance)
SVR = (length * viscosity)/r^4
*small change in r = HUGE impact!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is the relationship btw conductance and resistance?

A

low resistance = high conductance
high resistance = low conductance

bc TVK = 1/SVR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the major regulated variable if you want to increase systemic circulation?

A

mean arterial pressure (MAP)!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  • MAP represents the _______ ________ for blood flow through all the organs
  • what is CO
  • what is TVK
  • CO and TVK determine ______ _______ ______, and thus, MAP
A
  • the driving force (pressure reservoir in the arteries *schéma)
  • CO is the rate of blood pumped from the heart into the systemic circulation in L/min (ie how much blood goes into the bucket *schéma)
  • TVK is the sum of conductance to flow provided by all systemic blood vessels (ie how wide the arterioles are)
  • CO and TVK determine arterial blood volume and thus MAP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

formula of blood flow and its components
- what happens to flow if decrease arteriole radius by 1/2?

A

flow = delta(P) x K
- delta (P) = pressure gradient
- K = 1/R
- R = (length * viscosity)/r^4

  • if decrease r by 0.5 –> 16 fold increase in resistance or decrease in conductance = decrease flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the primary way in which cardiovascular system regulates tissue blood flow to a particular vascular bed?

A

through changes in conductance given a vascular bed –> which is secondary to changes in arteriole radius (vasodilation, vasoconstriction)
- where vasodilation comes from ie contraction of muscles (bc signals for more blood to come/feedforward)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the formula for VO2?

A

CO x arterial-mixed venous O2 content difference (C(a-v)DO2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

C(a-v)DO2 is determined by (2) + describe subthings

  • is it good to have a big or small C(a-v)DO2?
A
  1. O2 carrying capacity of arterial blood:
    - hemoglobin concentration (Hb)
    - partial pressure of O2 in arterial blood (PbO2)
    - affinity of Hb to O2, which is affected by PaO2, temperature and pH (O2 dissociation curve)
  2. muscle O2 utilization/extraction: capillary density, mitochondrial density and function, adequacy of tissue perfusion and diffusion
  • big! that means more O2 in blood and more O2 is utilized by muscles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

sex and training related differences in maximal exercise CO are due primarily to differences in which variable?

A

in stroke volume!
- during max exercise, everyone will probably reach a max heart rate (ie 200 bpm for everyone)
- therefore, it’s the SV that changes
- men have higher SV then women (110 vs 90 for untrained, and 180 vs 125 for trained)
- trained have bigger SV than untrained (180 vs 110 for men and 125 vs 90 for women)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  • which nodes are contacted by which nervous systems for HR regulation?
  • explain how the nervous system regulates HR before, at onset and during exercise
A
  • both PNS and SNS innervates both SA and AV nodes
    1. when stimulated, PNS nerves (ie vagus nerve)release the neurotransmitter acetylcholine –> decreases HR by decreasing SA and AV node activity
    2. at the onset of exercise, there is a rapid PNS withdrawal, which increases HR UP to 100 bpm
    3. as exercise intensity increases, SNS stimulation causes release of neurotransmitter norepinephrine –> increases HR + increases force of myocardial contractility (from increasing action potentials) by increasing SA and AV node activity
  • SNS stimulation is responsible for increasing exercise HR above 100 bpm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

which 3 variables regulates SV at rest and during exercise?

A
  1. end-diastolic volume (EDV) or pre-load
  2. mean arterial blood pressure (MAP) or after-load
  3. myocardial contractility (force of contraction)
17
Q
  • what is EDV?
  • what is the Frank-Starling law of the heart?
  • how does EDV increase SV? (4 little things)
A
  • represents volume of blood in ventricles at the end of diastole (ie before systolic contraction)
  • frank-starling law of heart (elastic recoil model) predicts that the strength of ventricular contraction increases as EDV increases (ie if EDV is low/not a lot of blood in heart, don’t need much contraction/strength to pump it out)
  • increase in EDV
    1. lengthens cardiac muscle fibers
    2. increases # of actin-myosin cross-bridge interactions
    3. increases Ca2+ sensitivity of troponin C
    4. increases velocity of cardiac muscle fiber shortening
  • all combining to increase the force of contraction, and therefore, SV
18
Q

EDV is determined by what? which is influenced by (2)

A
  • by venous return!
    1. venoconstriction: decrease venous blood volume = increase venous return = increase EDV
    2. skeletal muscle pump: compress veins and push blood back towards heart = increase EDV
19
Q
  • in order to eject blood, what is needed for the pressure? ish
  • as MAP increases, what happens to SV? healthy subject vs heart failure patient with left ventricular dysfunction
A
  • in order to eject blood, pressure generated by left ventricle must exceed MAP –> afterload is the amount of pressure that the heart needs to exert to eject the blood during ventricular contraction
  • as MAP increases, SV decreases! (at first, until compensation)
    HEALTHY: slow decrease in SV as MAP increases, will reach a plateau
    HEART FAILURE: rapid decrease bc less effective blood pumping –> so HR needs to compensate more
20
Q

What increases myocardial contractility? what is the relationship btw myocardial contractility and SV? how?

A
  • force of contraction/myocardial contractility is enhanced by increased SNS stimulation, with increased circulating catecholamines (ie epinephrine and norepinephrine) –> which increases entry of Ca2+ into cardiac muscle fibers –> which increases cardiac SV
  • at any given EDV, increase in myocardial contractility will increase cardiac SV
    *graph: the line with sympathetic stimulation will always have higher SV at a given EDV than control
21
Q

what happens to muscle blood flow at onset of exercise? vs to MAP? at low vs high intensity

A

MBF: immediate vasodilation (feedforward), then plateau. if higher intensity, plateau will be at a higher MBF (L/min)

MAP: a small decrease/dip at onset, then increases and plateaus. if higher intensity, plateau will be at a higher MAP

22
Q
  • MAP = CO/TVK –> we can also think of it as what?
  • why is there a decrease in MAP at onset of exercise?
A
  • MAP = arterial inflow (CO) / arterial outflow/peripheral tissue perfusion (into capillary beds)
  • because there is an increase in arterial outflow (which would decrease MAP) and CO hasn’t increased yet.
    *MAP regulation requires CO to increase during exercise
23
Q

since the onset of exercise results in immediate (________ dependent) increase/decrease in exercising muscle blood flow, MAP regulation requires (WHAT) to increase/decrease during exercise
- MAP regulation may or may not also require reductions/increases in _______ _______ to non-exercising tissues, potentially restraining of exercising _______
- restrains of exercising _____ has important implications for (3)

A
  • immediate (intensity dependent) increases in MBF, MAP regulation requires cardiac output to increase during exercise (IMPORTANT!)
  • reductions in blood flow to non-exercising tissues –> potentially restraining of exercising MBF
  • restraining of exercising MBF = important implications for muscle oxygenation, contractile function and exercise performance!
24
Q

what happens to THESE during exercise: (graph)
HEART RATE
SV
CARDIAC OUTPUT
SVR
TVK
MAP

A

HEART RATE: increase!
SV: mini decrease (barely) then plateaus, then increases
CARDIAC OUTPUT: increase slowly
SVR: decrease
TVK: increase as SVR decreases

MAP: overall impacted by all the above! –> decrease at first, then increases

25
Q

HEMODYNAMIC RESPONSE TO EXERCISE (1)
- at the onset of constant-load exercise, MAP initially increases/decreases
- why?

A

MAP decreases initially!
- can only be explained by an imbalance between CO and TVK (or SVR), where the immediate increase in TVK (or decrease in SVR) (bc more arterial outflow) is greater than the increase in CO (CO = HR x SV). THUS, both arterial blood volume and MAP decrease

26
Q

HEMODYNAMIC RESPONSE TO EXERCISE (2)
- why is there an immediate increase/decrease in CO at onset of exercise?
- at around ___sec into exercise, MAP begins to increase/decrease, indicating what?

A
  • increase in CO due to immediate increase in HR (parasympathetic withdrawal) with little or no change in SV
  • around 12sec, MAP begins to increase, indicating that CO (arterial inflow) is greater than TVK (arterial outflow). increases in CO are due to SNS-mediated increases in HR and SV
27
Q

HEMODYNAMIC RESPONSE TO EXERCISE (3)
- MAP continues to increase/decrease to a new ______-_______ over the next __-___ min.
- during this time (2) continue to increase/decrease, while (2) increase/decrease
- what needs to be greater than what for MAP to increase/decrease?

A
  • increase to a new steady-state over next 1-2min
  • exercising muscle VK (conductance) and blood flow continue to increase, while VK and blood flow to non-exercising tissues decrease
  • increase in CO must be greater than increase in muscle VK in order for MAP to increase