Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Block 2 Week 3 > Exercise Effects on HR & Circulation > Flashcards

Exercise Effects on HR & Circulation Flashcards

1
Q

What is the initial cardiac response at onset of exercise?

A
  • initial cardiac response to increased workload is to increase HR and SV to account for the need for an increased CO
  • HR increases more so than SV (only ~15%)
  • HR increases linearly w/ O2 consumption (work done by body) up until hit the max HR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does the autonomic nervous system effect exercising heart?

A

-at rest PNS & vagal nerve act on heart to decrease SA node intrinsic firing from 100bpm to 70bpm
-when begin exercising, withdraw PNS initially until hit 100bpm, then need to activate SNS to increase HR up to max
-

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

What does SNS augmentation act on in the heart? What is the role of B-1 receptors & blockers?

A
  • SNS innervates SA node, AV node, and cardiac myocytes to increase rate of contraction& contractility
  • SNS acts on B-1 receptors and only activated when exercising
  • means at B-1 blockers have no effect on Resting HR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How does an athletes heart differ from an average persons heart?

A
  • athletes have an increased SV compared to avg pop, is why resting HR is ~50bpm but CO is sufficient
  • when exercise HR has same max as everyone else, but SV increases so have more CO at a specific HR than a non-ahtelte at the same HR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does a patient w/ CHF heart differ from an avg persons heart?

A
  • venticle can’t create enough force to eject a normal preload level regardless of SNS augmentation
  • require an increased pre-load, ventricle can eject a lower SV but one that will allow body to not go into hypovolemic shock
  • this means that very low SV and require higher HR at rest to maintain MAP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the cardiovascular adjustments to exercise?

A

1) increased SV
2) increased CO
3) increased HR
4) MAP remains relatively constant (MAP= CO x SVR)
5) SVR decreases
6) whole body O2 consumption increases

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

How does SVR relate to body’s O2 consumption?

A
  • SVR is inversely proportional to O2 consumption

- due to local metabolite vasodilation systemically (active hyperemia)

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

How do CO and SVR relate?

A
  • CO is inversely proportional to SVR (MAP= CO x SVR)
  • as resistance increases, less Co can occur
  • reflects baroreceptor heart regulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is Cardiac output limited by? (equation of CO?)

A
  • the stoke volume and heart rate

- CO= SV + HR

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

How does Mean arterial pressure change during exercise?

A

-it remains relatively constant since elevated CO made up for by decreased SVR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is increased cardiac output matched with an increased venous return?

A
  • SNS venoconstriction due to baroreflex
  • sk. muscle pumps
  • respiratory pumps
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does the Frank-Starling curve change during exercise?

A
  • shifts up and to the left
  • the ESV decreases (due to greater contractility), while EDV remains same increasing the PP
  • SV increases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the main function of the pulmonary circulation?

A
  • CO2 and O2 gas exchange

- to bring cardiac output into close proximity to the atmospheric air that fills the alveoli

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

What is main difference between pulmonary and cardiac circulation?

A
  • main difference is that pulmonary circulation is a low pressure- low resistance system
  • cardiac circulation is a high pressure-high resistance system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does blood flow into lungs?

A
  • deoxygenated blood arrives to the lung via the pulmonary artery and enters into capillaries that act as mesh around the alveoli
  • leave alveoli well oxygenated and go to through pulmonary vein into the LA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does Cardiac output and the lungs relate?

A
  • all CO has to flow through the lungs & systemic circulation
  • means all factors that effect CO will affect blood flow to the lungs
  • pulmonary capillaries hold ~75mL of blood, CO is ~75mL; so pulp capillaries refill w/ each heart beat
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what are alveoli?

A
  • smooth, very thin walled vessels

- contain layer of surfactant to decrease the surface tension and help them expand when inspiring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does it mean that the pulmonary circulation is optimized for diffusive exchange?

A
  • that pulmonary system has all key features (seen by Fick’s Law of Diffusion) to have rapid diffusion
  • air/plasma barrier very thin, short diffusion distance, large concentration gradient, O2/CO2 diffuse across membrane rapidly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the path of oxygen from the alveoli to the hemoglobin in RBC? How long take to this?

A

1) surfactant layer
2) alveoli epithelial
3) basal lamina
4) alveoli endothelial
5) air/plasma space
6) RBC–> Hemoglobin
- takes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What would happen if the blood/air barrier was NOT super thin?

A

-would have a slower diffusion

21
Q

What does it mean that pulmonary circulation is low pressure & low resistance?

A
  • pulmonary arteries/arterioles have low resistance to blood flow & transmit all CO under low (hemodynamic) pressure
  • this system ensures fluid absorption in pulp capillaries
22
Q

Why do CHF patients have pulmonary edema>

A
  • failing LV can’t develop sufficient contraction at any degree of stretch
  • LV needs to operate at high filling pressure & volume to have a SV that satisfies baroreceptors
  • high filling pressure backs up into pulmonary cap, increases its pressure and causes fluid pushed out into interstium= pulomary edema
23
Q

effects of pulmonary edema?

A

-decreases cardiac function and impairs gas exchange

24
Q

How do perfusion(Q) and ventilation (V) change with gravity and location in the lung?

A

when standing amount of gravity(hydrostatic pressure) effects distribution of blood flow

  • more hydrostatic pressure at base of lung than at lung apex (top)
  • when standing blood flow to lungs is unequal with 10x more going to base than apex
25
Q

Apex vs base of lung blood flow?

A

at base: cap are thin wall & distensible; increased hydrostatic pressure causes vasodilation, reduces resistance, and increases flow
-at apex: reduced hydrostatic causes capillaries to collapse during diastole so only perfused during systole

26
Q

What happens when have local ischemia/hypoxia in the lungs?

A
  • they vasoconstrict
  • so that the blood flow goes to alveoli with sufficient O2 to saturate blood
  • provides optimal gas exchange, better matches flow (Q) with ventilation (V)
27
Q

What happens when have local ischemia/hypoxia in the systemic tissue?

A

-causes increased vasodilator metabolites and get vasodilation to get hyperemia or increased blood flow

28
Q

What is ventilation perfusion matching?

A
  • blood will take the most direct route to become fully saturated with O2 by air-filled alveoli
  • they bypass O2 deficient alveoli by capillary vasoconstriction in response to hypoxia
29
Q

What is HAPE?

A
  • high altitude pulmonary edema
  • its a positive feedback cycle instigated by widespread hypoxic vasoconstriction (ex when mountainclmbing and P02 is very very low)
  • widespread hypoxia causes increased pulomary pressure since only a few cap route are open to blood
  • increased pressure promotes filtration over absorption so get Pulmonary Edema
  • pulmonary edema impairs gas exchange which leads to more hypoxic vasoconstriction (+ feedback cycle)
30
Q

What happens if HAPE is initiated? How prevent HAPE?

A
  • death can come quickly if the climber is not immediately brought down to lower elevation and given 100% O2
  • best way to treat is to prevent by slowly acclimated before climbing everest
31
Q

Why do you get pulmonary edema in CHF?

A
  • heart is operating at a very high pressure to eject a small SV
  • high pressure back sup into pulmonary capillaries and is enough to switch from absorption to filtration preference
  • **check notes Starling curve
32
Q

What are causes of pulmonary edema originated in the pulmonary artery?

A
  • pulm artery deoxygenated blood go to lungs
  • pulmonary hypertension due to high altitude, hypoxemia (COPD) hypoventilation
  • results in vasoconstriction in hypoxic capillary beds & greater flow/pressure to other capillary beds
33
Q

What are causes of pulmonary edema originated in the pulmonary vein?

A
  • oxygenated blood going to the heart
  • CHF (left heart failure) or stenotic mitral valve
  • get pulmonary venous hypertesion which clogs up the capillary bed, increases pressure and get leakage of fluid out
34
Q

What is a pulmonary embolism?

A
  • another cause of pulmonary edema
  • when an embolism (blood clot, cell debris or bubble) develop in systemic veins & flow into the lungs where can occlude smaller pulmonary arterioles blocking their blood flow
  • leads to pulmonary hypertension & pulmonary edema
35
Q

What are symptoms/signs of PE?

A
  • dyspnea(difficulty breathing)
  • chest pain on inspiration
  • low blood O2 saturation
  • tachypnea (rapid breathing)
  • cough/hemoptysis (cough up blood)
  • tachycardia
36
Q

what is a thrombus?

A
  • aggregate of platelets in a meshwork of fibrin
  • blood coagulates whenever not toughing the endothelial cells surface
  • can lead to pulmonary embolism & edema
37
Q

What is the cutaneous circulation?

A

the blood circulation to the skin

  • main function is to remove heat from exothermic (releasing heat) metabolic reactions occurring in the body from the surface of the skin
  • once blood moves heat to skin, it can be released by conduction, convection, radian, sweating/evaporation
38
Q

What is the skins main function?

A
  • to remove the heat byproducts of cellular metabolism

- rate of heat

39
Q

what is the global thermal regulation?

A

-the idea that heat loss=rate of heat production so that the core temp in body remains constant regardless of ambient/local temperature

40
Q

How does the body handle too high of a core temp?

A
  • thermostat in the hypothalamus activates cooling mechanisms, decreases SNS vasoconstrictor innervation
  • arterioles and AVA dilate, dermal papillae capillaries & venous plexus fill w/ warm blood
  • get warm (red) skin , like when you plush
  • sweat glands activated to increase evaporative cooling
41
Q

How does the body handle too high of a core temp?

A
  • thermostat in the hypothalamus activates cooling
  • hypothalmus increases SNS vasoconstrictor system
  • arteriorles & AVA vasoconstrict
  • dermal papillae and venous plexus collapse
  • get cold, pale skin
  • sk muscles activated so start shivering to generate more heat
42
Q

What happens when have cardiogenic hypovolemic shock?

A
  • is when have poor perfusion/low blood volume
  • have cold, pale skin since not enough blood to feed the skin so is becoming cold/pale
  • similar to when body has too high of a core body temp and responses are activated
43
Q

What happens in distributive shock?

A
  • causes loss of SVR due to cytokine release so have systemic vasodilation & patients have warm-red skin similar to the response of the body when core temp is too low
44
Q

What are dermal papillae?

A
  • they are projections close to the skin that increase SA for capillary loops
  • they are loaded with capillaries, so highly vascular
45
Q

What is the venous plexus?

A
  • a very distensible reservoir for warm blood near the skin surface
  • has 2 components the distensible plexus (Reservoir) and the arterial plexus (for constriction/dilation)
46
Q

What are some characteristics of the skin?

A
  • 2nd largest organ maintains 1/3 of BW
  • low workload/energy consumption so has low nutritional blood flow demand
  • cutaneous flow not dependent on local metablolism but the hypothalmus and SNS nerves
47
Q

What happens in the skin during hypotension?

A
  • baroreflex gets activated causes strong cutaneous vasoconstriction and prevents blood flow to the skin so it can be redirected to more important places
  • vasocostrciton important also for thermal regulation
48
Q

What are AVA?

A
  • arteriovenous anastomoses
  • connect arteries and veins to help move blood between them
  • vasoconstrict/dilate to increase or decrease blood flow
  • help dissipate heat

Block 2 Week 3 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions