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ISBM > Spring Exam 2 > Flashcards

Spring Exam 2 Flashcards

1
Q

what happens when temp is about 41C

A

Temp. regulation is impaired

heat stroke, brain lesions

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2
Q

what happens when temp is 36-41C

A

Temp regulation efficient in febrile disease and health and exercise

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3
Q

what happens when temp is 34-30C

A

Temp regulation is impaired

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4
Q

what happens when temp is 30-24C

A

Temp regulation is lost

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5
Q

what happens when temp is 27-25C

A

prone to cardiac arrhythmias

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6
Q

what is the normal range for temperature

A

36-38C

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7
Q

body temperature constancy (or body thermal mass) is a function of what?

A

heat production and heat lost to the surroundings

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8
Q

mechanisms by which we LOSE heat to the environment

A
  1. Radiation
  2. Convention
  3. Conduction
  4. Evaporation
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9
Q

movement of heat to one body that is in contact to another

A

conduction

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10
Q

heat loss from ____ is insensible or sensible to us

A

evaporation

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11
Q

example of what type of heat loss?

Breathing= instantly saturating breath with water.

A

evaporation

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12
Q

transfer of heat from warm body to the medium surrounding the body

A

convention

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13
Q

body radiates heat to any surrounding

A

radiations

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14
Q

radiant heat loss is ___% of heat loss

A

40%

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15
Q

factors that contribute to radiant heat loss

A
  • body SA
  • radiant characteristics of the environment
  • skin/radient temp of environment
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16
Q

convention is ___% of heat loss

A

20%

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17
Q

why do infants lose heat pretty readily

A

bc they have a large SA relative to their mass

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18
Q

conduction is ___% of heat loss

A

40%

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19
Q

evaporation is __% of heat loss

A

20%

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20
Q

in order for evaporation to occur, what must be present?

A

heat (energy in the form of heat must be absorbed by water)

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21
Q

for each liter of water evaporated, how much heat is lost from our systems

A

580kcal

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22
Q

what part of the NS controls sweat glands?

A

cholinergic- sympathetic control

ACh release stimulates muscarinic cholinergic R–> stimulates sweating

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23
Q

describe the solution of sweat

A

hypo-osmotic (hypotonic) due to active reabsorption of ions

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24
Q

mechanisms by which we PRODUCE heat

A
  1. basal metabolic rate (~75kcal/hr)
  2. extreme muscular activity (15 fold increase)
  3. shivering (3-5 fold increases)
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25
Q

describe the non-shivering thermogenesis mechanism

A

endogenous uncoupling of the ETS in brown fat via thermogenin. (creates a pore in the ETS and allows constant flow of H+ do reduce EC gradient–> reduces ATP synthetic rate–> decreases AC–> increase catabolic enzymes= increase metabolic activity)

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26
Q

what is thermogenesis under the control of?

A

T3 and T4

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27
Q

thermogenin is restricted to what?

A

brown fat (in infants and lower animals)

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28
Q

how does vasoconstriction promote heat conservation?

A

impacts blood flow to the skin and shunts blood away from the skin surface to reduce radiant and conductive heat loss and to reduce the cooling of deep venous blood–> shunts blood through a path of lesser resistance

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29
Q

describe blood flow during vasoconstriction

A

warm blood leaving the system will enter the deeper systems and exchange between slightly warmer blood (returns to core through deeper veins)

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30
Q

mechanisms by which we CONSERVE heat (4)

A
  1. vasoconstriction
  2. drinking warm drinks
  3. adding layers
  4. turning up the heat
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31
Q

vasoconstriction is due to an increase in ___ tone (which results in)

A
  • SNS

- increased SmM contractility = increased resistance to flow

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32
Q

increasing blood flow to skin promotes what

A

radiant and convective loss

promotes heat loss

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33
Q

vasodilation of vascular beds promotes what

A

conductive/convection heat loss

promotes heat loss

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34
Q

net heat production/loss is a function of what

A

hypothalamic temperature

**BUT heat production is constant (~20cal/sec at base)

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35
Q

Characteristics of thermoreceptors

A
  • warm and cold receptors are always firing (at an overall slower rate)
  • work in a limited temp range
  • poorly adapting receptors (w/ graded response–> frequency modulation)
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36
Q

what is the “heat loss center”

A

POAH (preoptic anterior hypothalamus)

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37
Q

what is the “heat gain center”

A

posterior hypothalamus

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38
Q

what stimulates the POAH?

A

Major: local brain temp/ECF
Minor: cut. warm receptors and cut. cold receptors (inhibitory)

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39
Q

what stimulates the posterior hypothalamus?

A

Major: inhibition from POAH, cut. cold receptors
Minor: inhibition from cut. warm receptors

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40
Q

what are the effects of POAH stimulation?

A

vasodilation (increase blood flow–> increase radiant heat loss)

  • sweating, panting, salivation
  • *Heat loss!!
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41
Q

what are the effects of the posterior hypothalamus

A

vasoconstriction (heat conservation)

  • shivering, piloerection (trap heat)
  • *Heat gain!!
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42
Q

what acts upon thermoreceptors in the hypothalamus during a fever?

A

IL-1

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43
Q

what is IL-1

A

endogenous pyrogen that changes the set point in a dose dependent manner (fxn of amount of triggers)

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44
Q

what does IL-1 promote?

A
  • ACTH release (cortisol increases)
  • protein catabolism in muscle (increase gluconeogen. beta oxid., etc)
  • redistribution of trace metals (promotes lactoferrin synthesis in neutrophils)
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45
Q

what does lactoferrin do?

A

chelates/binds free Fe2+, which inhibits bacterial growth due to reduced free [Fe2+] **Beneficial in fever!

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46
Q

what is going on during the onset of a fever

A

IL-1 levels rise, body shivers and vasoconstricts to generate heat to achieve a new set point (exicite post. hypo and inhibit POAH)
*exists for however long the pyrogens exist

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47
Q

what is going on when a fever breaks

A

stimulus for set point diminishes and you sweat/vasodilate to lose heat (excited POAH, inhibit post. hypo)

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48
Q

what is the point of a fever?

A

to create an environment that is less conductive to bacterial growth

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49
Q

How does ASA and NSAIDS help reduce a fever?

A

inhibits COX 1 and 2 which are used in the synthesis of PGE2 , which alters set points to produce a fever

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50
Q

what are the costs of a fever with each 1C?

A

13% increase in O2 consumption

  • increase caloric intake
  • increase fluid requirements
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51
Q

what are the overall effects of a fever

A
  • increase muscle catabolism
  • decrease mental acuity, delirium, stupor
  • increase seizure possibility (esp. kids)
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52
Q

what is the primary determinant of cardiac cycle length?

A

diastole period (ventricles are refilling) ~2/3rd of time of cycle

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53
Q

what are the position of ALL the valves during diastole

A

AV and PV are closed, MV and TV are open

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54
Q

what do glycosides target?

A

myocardial contractility

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55
Q

what NS regulates myocardial contractility

A

ANS

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56
Q

what is preload

A

diastolic filling of ventricles

- greater degree of filling/V. stretch= greater force generated

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57
Q

what is afterload

A

aortic pressure

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58
Q

what are diuretics aimed at?

A

reducing preload

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59
Q

describe blood flow through the heart

A

RA–> TV–> RV–> PV–> pulmonary arteries–> lungs–> pulmonary veins–> LA –> MV–> LV–> AV –> Aorta–> body–> veins –> IVC–> RA

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60
Q

describe the pressure and resistance in each circulatory systesm

A

pulmonary- low pressure/low resistance (0-25mmHg)
systemic- high pressure/high resistance (80-120mmHg)
**pressure is on the arterial side!

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61
Q

why does we see a pulsatile flow with a venous laceration?

A

bc there is no oscillation of pressure in the venous system (only in arterial) and there is less overall pressure in venous system

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62
Q

____ is on the arterial side while ___ is on the venous side

A

pressure- arterial,

volume- venous (2/3rds)

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63
Q

describe the SNS innervation on the heart

A

B1, B2, and alpha1 Receptors– NE (and epi) NTs,

  • innervates predominately ventricles
  • mediates + inotropic (force) and chronotropic (increase rate of depolar.)
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64
Q

describe the PSNS innervation on the heart

A

Muscarinic (M2) receptors– ACh

  • innervates predominately atria
  • M2 is inhibitory and works to down regulate free cAMP to decrease HR
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65
Q

PSNS innervation is primarily through what nerve?

A

vagus (x)

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66
Q

what is an intrope?

A

an agent that alters the force or energy of muscular contractions. (-) inotropic= weaken the force of muscular contractions. (+) inotropic= increase the strength of muscular contraction

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67
Q

what are chronotropic effects?

A

change the heart rate by affecting the nerves controlling the heart

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68
Q

what is diastole?

A

relaxation of ventricles(filling)

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69
Q

what is systole?

A

onset of ventricular contraction

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70
Q

What does the p wave represent?

A

atrial depolarization (atrial contraction during diastole)

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71
Q

what does the QRS complex represent?

A

ventricular depolarization (contraction of ventricles)

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72
Q

what does the T wave represent?

A

ventricular repolarization (relaxation of ventricles)

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73
Q

what are the position of the valves during atrial depolarization (p-wave)?

A

AV and PV are closed, MV and TV are open

*S4

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74
Q

what are the position of the valves during ventricular repolarization (T wave)?

A

TV and MV are open

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75
Q

what causes S1 and S2

A

S1- MV/TV closing

S2- AV/PV closing

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76
Q

Why do we see spike in LA pressure during systole?

A

pressure regurgitation = pressure increase in LV so high that it can transduce through the AV and register as LA pressure increase

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77
Q

when do we see the greatest increase in ventricular pressure?

A

onset of systole

78
Q

what is EF?

A

percent of blood leaving the heart with each contraction (indicator of myocardium sufficiency)
EF= (EDV-ESV)/EDV

79
Q

wht is stroke volume?

A

amount of blood ejected by the LV w/ each contraction

EDV-ESV

80
Q

what is EDV?

A

volume capacity of LV at the end of diastole (~120mL)

81
Q

what is ESV?

A

volume capacity of LV at end of systole (~40mL)

82
Q

what is an isovolumetric contraction period (ICP)

A

there is no change in volume bc you can’t compress blood and it has no where to go bc all valves are closed

83
Q

when do we see an ICP?

A

onset of systole

84
Q

when do we see an IRP?

A

end of systole (where we have closure of AV bc pressure in aorta>pressure in LV

85
Q

what happens to LV pressure during an ICP?

A

increases bc its contracting against fluid (until pressure in LV>pressure in aorta and AV opens)

86
Q

what happens to LV pressure during an IRP?

A

decreases bc its relaxing and we have closure of AV bc pressure in Aorta>pressure in LV (MV and TV are still closed)

87
Q

what is the dicrotic notch?

A

a slight increase in aortic pressure after the AV/PV valves close due to the compliance of the aorta when Aortic p>LVp

88
Q

how do cardiac glycosides work?

A

glycosides inhibit Na/K ATPase pump which results in increased intracellular Na. Thus decreasing the drive to get Ca out and then there is longer period of Ca availability =better contractility

89
Q

what is an intrinisic CO factor?

A
  1. preload concept= greater degree of V. filling/sacromere length= greater force generated
90
Q

the longer the sacromere length/strength……

A
  • the greater the peak tension/force generated

- an increased sensitivity to intracellular Ca (requires less Ca to generate a strong contractile force)

91
Q

what happens to velocity with increased afterload?

A

velocity of muscle shortening is SLOWER and rate is slower (as seen in CHF)

92
Q

why is uncontrolled HTN dangeroug

A

HTN = increased afterload = increased strain on the heart = increase the work of the heart to overcome increase peripheral resistance

93
Q

how do diuretics work to help improve CO

A

reduce overall fluid volume to reduce the after load

-reduced afterload= increased CO

94
Q

what is phospholamban?

A

transmembrane protein in the SR that slows/inhibits SERCA pump (it is subject to phosphorylation by PKA ((NE)))

95
Q

what happens when phospholamban is phosphorylated?

A

becomes inactive–> cannot inhibit SERCA–> quicker relaxation–> more Ca in myoplasm–> primes myocardium for a more robust/forceful contraction

96
Q

what can PKA phosphorylate?

A
  1. Ca channels (promote incresaed Ca influx)
  2. tropinin I
  3. phospholamban
  4. Ca ATPase (promotes Ca extrusion)
97
Q

what happens when troponin I is phosphorylated by PKA?

A

leads to enhanced blockage of actin inhibition –> contributes to rapid relaxation

98
Q

describe the conduction pathway in the heart

A

spontaneous depol. of SA in RA–> spreads via gap jxns–> AV node (can also spontan. depol but slower)–> common bundle of His–> R and L bundle branches–> purkinje fibers–> V. depol= contraction

99
Q

when is the heart considered in sinus rhythm?

A

when the SA node serves as the “pacemaker”

100
Q

what is the importance of the AV node

A

it slows down the cardiac impulse traveling from the atria to the ventricles to allow the atria to empty its blood into the ventricles before the V start to contract

101
Q

describe the flow of ions in the AP phases in the ventricle

A

0- rapid depol. (Na floods in)
1- brief repol. (transient outward of K+)
2- sustained depol. (influx of Ca**, K still going out)
3- repol. (K out–> no HYPERpol.)
4- RMP (Na/K channels maintain gradients)

102
Q

what K current?

  • maintains resting potential, closes w/ depolarization
  • prolongs the plateau
  • decrease in conductance w/ depol
A

inward rectifying K current

103
Q

what K current?

  • opens at tend of the plateau
  • initiates repol
  • key for triggering phase 3
A

outward rectifying K current

104
Q

what K current?

  • activated by Gi in response to vagal stimulation and adenosine
  • hyperpolarizes resting hear cells
  • slows SA nodal cells
  • shortens atrial AP
A

acteylcholine-activated K current

*mediated by M2 receptors and decrease in cAMP in cells

105
Q

what is isoproterenol and what are its effects on transient Ca currrent

A

pure beta agonist (synthetic catecholamine) that increase the permeability of Ca= faster depol.= more Ca gets in–> but not much longer in duration

106
Q

what effects does ACh have on the heart?

A

released via PSNS stimulation to decrease HR and force

107
Q

how does ACh decrease HR and force?

A
  1. hyperpolarizing membranes- makes the more leaky to K (which flows out=hyperpol.)
  2. decrease cAMP via M2 receptor = less PKA phosphorylation = more slower Ca channels and Ca ATPase
108
Q

what are the effects of adding a Ca channel blocker like diltazem on V. AP

A

imitates adding ACh bc both down regulate Ca influx!!

- more dilt. = less plateau phase and decreased muscle force (- inotropic effect)

109
Q

what cells have fast response cells

A

atria, ventricles and purkinje fiber cells

110
Q

what do fast response cells have

A

Em at phase 4

  • ERP where you cannot stimulate and it gives rise to RRP where u need above normal stimulus to induce
  • due to Na influx= steep change in M.P.
111
Q

what cells have slow response cells?

A

nodal cells (SA node)

112
Q

what is responsible for spontaneous depolarization of nodal cells?

A

inward “funny” current driven by Na+ influx. (phase 4)

-HCN-gated channels open with hyperpolarization of the membrane

113
Q

how do extrinisic factors change the rate of spontaneous depolarization?

A
  1. slowing phase 4= longer to reach threshold= decrease HR (ex. ACh/muscarine- decrease, Epi- increases rate)
  2. change MDP or threshold potential = delayed reaching of threshold= slower
114
Q

how does ACh/muscarine slow phase 4?

A

reduces cAMP= slows inward funny current= slower to reach threshold=decrease HR

115
Q

how does epi increase rate of phase 4

A

enhances funny current = get threshold faster= makes Na more leaky = faster depol.

116
Q

why can cardiac muscle not summate?

A

ARP and RRP extends for the entire duration of the AP, therefore the contraction is done by the time the myocyte is ready to engage in another AP (aka- due to prolonged depolarization)

117
Q

what effects does PKA have? (6)

A
  1. increase intracellular Ca (phosph. Ca channels in SR)
  2. increase flux across HCN channels (p HCN)
  3. increase HR and force (increase cAMP)
  4. increase Ca uptake effiency in SR (p. phosplamban–>no inhibition on SERCA)
  5. greater acheivement of pressure w/ respect to time
  6. increase CO
118
Q

what are the 3 fundamental layers in vascular

A
  1. Intima (endothelial layer w/ elastic tissue)
  2. Media (mostly SmM)
  3. Adventitia (lymph vasc)
119
Q

what is compliance?

A

the vessels ability to stretch when pressure is applied

= Change in vessel volume/change is pressure (transmural)

120
Q

what factors decrease compliance?

A
  • high pressures (when max stretched is reached)
  • age
  • arteries are less compliant than veins
121
Q

what factors influence resistance in vessels?

A

Directly proportionate to length and viscosity and inversely proportionate to the radius

122
Q

where is the greatest resistance to flow?

A

in the arterioles because we have a narrowing (SmM) and more resistance (small radius) in the vessel so therefore we have a large change in pressure (Ohm’s law: R = V/I)

123
Q

what are the types of resistance?

A
  1. series resistance ( linked linearly)

2. parallel resistance (offers lower resistance to flow- in our system)

124
Q

where is our body is there series resistance?

A

in the hypothalamus (to allow for diffusion of HR and molecules) and in the kidneys and liver to allow for filtration and decrease flow for glomerulus to fxn

125
Q

how does viscosity influence flow?

A

increase in viscosity= increase in resistance to flow = increase in hematocrite= increase in oxygen carrying capacity (blood doping)

126
Q

The composition of the lymphatics (ie. hydrostatic and oncotic pressure) is basically identical to where?

A

interstitial fluid

127
Q

what are the roles of the lymphatic system?

A
  • return fluid from ECF to circulatory system
  • Fats/nutrients are absorbed in the GI tract
  • *maintain constancy in terms of hydrostatic and oncotic pressure w/in ISF
128
Q

describe the drainage of the lymphatic system

A

1/4th is drained by the Rt. lymphatic duct and 3/4ths is drained by thoracic duct

129
Q

describe the flow of lymph

A

capillary bed–> terminal bulb (drains ISF area)–> afferent lymph. vessel–> Lymph node–> efferent lymph vessel–> vein/venous system

130
Q

how are oncotic pressures maintained?

A

lymph returns 1/4th-1/2 of circulating proteins back into vascular system

131
Q

What structural differences allow the lymphatic capillaries to efficiently take up proteins from the ISF?

A

have tight junction and are much more porous, with larger fenestrations, allowing for macromolecules (proteins) to easily enter
(higher k value due to increased permeability)

132
Q

what are the driving forces of lymph movement from capillaries to lymphatics?

A

differences in hydrostatic and oncotic pressure (passive network)

133
Q

List 4 events that result in increased lymphatic flow

A
  • increase cap. hydrostatic pressure (ie. w/ exercise)
  • increase cap. permeability
  • increase ISF [protein] (ie. increase oncotic pressure- draws fluid into ISF)
  • decrease cap. oncotic pressure
134
Q

Cardiac output is a function of what?

A
  1. Hormonal balance/influence (TH)
  2. metabolic needs
  3. Size of individual (normalized with cardiac index)
  4. STRONGLY influenced by ANS
135
Q

How can cardiac output be determined?

A

Invasively: Fick’s method or Indicator dilution method

Non-invasively: Echo, radionuclide imaging, impedence cardiography

136
Q

what is Fick’s method?

A

CO = (O2 consumed ml/min) / (arterial O2 content- venous O2 content)

137
Q

what are the cardiac and coupling factors that influence cardiac output?

A

cardiac: HR and myocardial contractility
Coupling: preload and afterload
CO= HR x SV

138
Q

what is stroke volume

A

the amount of blood ejected by the left ventricle in one contraction

139
Q

how does preload and afterload affect CO?

A
  • increase in preload= increase SV= increase CO

- increase in afterload = decrease in CO

140
Q

how does contractility affect CO?

A 
increased contractility (via NE and epi) increase CO= increase SV
*positive inotropic state
141
Q

what is the Frank-Starling Relationship?

A

the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the EDV)
*sigmoidal relationship w/ a plateau

142
Q

dP/dt represents what?

A

ventricular force

143
Q

describe the relationship between RA pressure and venous return

A

as RA pressure increases= venous return decreases

take a deep breath= decrease ITP (intrathoracic pressure) decrease pressure= increase venous return

144
Q

how does exercise affect CO and VR?

A
  • increase metabolic needs= neuronal and humeral output= increase SNS activity = increase contractility = increase CO and VR
    (increase dP/dt)
  • increase venous constriction = increase MSFP = VR
145
Q

What compensation takes place in CHF with decreased CO?

A
  • increased SNS tone for a little until reservoir used up
  • increase volume (ie. preload and fluid retention) to increase MSFP and VR= increase CO

(but gets to a point where O2 demand increases, increase wall tension [Laplaces law], and the heart cannot generate higher pressures

146
Q

what regulates fluid volume in long term regulation of pressure changes?

A

the kidneys (ADH)

147
Q

what are the physiologic an physical factors that influence BP

A

Physiologic: CO and peripheral resistance (what we can manipulate)
Physical: arterial blood volume and compliance

148
Q

how does arterial compliance promote continuous flow

A

LV systole: increase pressure and blood is pushed into the aorta which extends
LV diastole: pressure in aorta is greater and recoils on itself pushing blood into capillaries

149
Q

A_____ transmural pressure must exist for flow to occur

A

positive

ie. the pressure inside of the vessel must be greater than the pressure surrounding the vessel (interstitial)

150
Q

describe how MAP and PP change in different parts of the body

A

MAP- decreases as we move away from the heart
PP- increases as we move away from the heart
*allows for blood to flow from high pressure –> low pressure

151
Q

the site of regulation of the distribution of flow, is the site of _____. Which is ___

A

greatest resistance to flow

arterioles and terminal arterioles

152
Q

what do Alpha 1 and Beta 2 receptors mediate and how?

A

A1- constriction (increase Ca availability by Gq and IP3 mediated)
B2- dilation (Gs: + AC–> increases cAMP)

153
Q

describe the affinity for A1 and B2

A

A1: highest for NE (some epi)
B2: highest for Epi (none for NE)

154
Q

what happens to vascular SNS response with no receptor blockage

A

flow decrease due to increased resistance and delta p (ie. vasoconstriction)

155
Q

what happens to vascular SNS response with Alpha, Beta, and ACh receptor blockage

A

no flow w/ symp. stimulation

156
Q

what happens to vascular SNS response with Alpha receptor blockage

A

increased flow due to decreased resistance and delta p due to effects of ACh (passive vasodilation)

157
Q

what happens to vascular SNS response with Alpha and ACh receptor blockage

A

small increased flow due to effects of NE binding B2 (small vasodilation)

158
Q

how does ACh affect vascular tone

A

ACh in ECF binds to muscarinic R on endothelium –> metabolizes Arginine–> produces NO–> diffuses across SmM and interacts w/ G cyc. and produce cGMP–> extrudes Ca by phosphorylating SERCA and Ca/ATPase to get Ca out of myoplasm = relaxation

159
Q

what are endothelial factors that promote relaxation?

A
  1. ACH (produces NO = increase cGMP)
  2. Nitroprussides
  3. Local metabolites (adenosine)
  4. Prostaglandins (PGI2= increase cAMP)
160
Q

what are endothelins

A

peptides produced by many cells that promote vasoconstriction (POTENT)

161
Q

how does ED-1 promote contraction?

A

binds Gq–> increase IP3–> binds SERCA–> release Ca–> increase contraction

162
Q

how does ED-1 inhibit itself

A

binds ETb–> increase NOS–> increase NO–> increase cGMP–> phosphorylate SERCA and Ca/ATPase–> extrudes Ca–> inhibits contraction

163
Q

what features of capillaries allow them to be leaky?

A
  1. fenestrations- holes that can open or close
  2. vesicular channels
  3. tight jxns btwn endothilum cells
  4. discontinous endothelium (in liver, BM, spleen)

*only small proteins can fit and diffuse out

164
Q

net filtration pressure is equal to

A

k (outward pressure - inward pressure)

= k ((HPcap+ PiISF) - (Picap+ HPisf))

165
Q

when is there net flow into and out of the capillaries?

A

Inward: on arteriole side
Outward: on venous side, when Pressure inside cap is less than interstitial HP
*oncotic pressure is always stable

166
Q

what is diffusion-limited distribution?

A

in CHF, ISF increases which increase the distance things must travel to reach lymph–> increase oncotic p. in interstital = increased edema

167
Q

autoregulation relays heavily on ___ changes

A

resistance

168
Q

how does autoregulation decrease flow?

A

high pressure on vessel walls= increase contraction = increase resistance = decrease flow

169
Q

what are the short term and long term controls of BP

A

short term: vascular tone, HR, force of contraction

long term: ECF volume control (renal influences)

170
Q

what happens to venous pressure when you stand up?

A

feet: increase in Venous p.
head: decrease in venous p.
* due to gravity
* SNS increases to constrict vessels and increase pressure to head

171
Q

how does walking affect venous pressure?

A

causes skeletal muscle to contract which acts like a pump–> decreases venous pressure

172
Q

what receptors sense pressure?

A

baroreceptors which sends signal to medullary (CV centers)

  • cardiopulmonary barorecept.- use vagus or SNS afferent/efferents
  • arterial baro.- poorly adapting recept. that sense stretch and respond to MAP
173
Q

what are the carotid sinus and carotid bodies

A

sinus- most sensitive (has higher AP output)

bodies- least sensitive baroreceptors

174
Q

how does the SNS respond to increase sinus pressure

A

increase in afferent signals and a decrease in efferent firing
Decrease in pressure→ decrease in afferent signals and then an increase in efferent firing
(increase SNS also increases SV)

175
Q

how does the PSNS respond to increased sinus pressure

A

increase in afferent fibers to CV centers –> increases in efferent traffic along the vagal nerve

176
Q

what are the baroreceptors in the kidney

A

granular cells

177
Q

what 2 hormones are pressor agents?

A
  1. ADH

2. Aldosterone

178
Q

how does the kidney regulate BP?

A
  • decreased renal press., renal tubular [Na], or increased renal SNS–> increased renin–> increased angio I and II–> increase aldosterone (water retention and max [na] reabsorption) and vasoconstriction
  • *= increase BV=BP=CO
179
Q

how does the hypothalamus and pituitary regulate BP

A

cardiopulmonary, arterial barorecep, and osmorecept–> hypothalamus–> post. pitu.–> increase ADH–> reabsorb water and vasoconstrict
**= increase BV=BP=CO

180
Q

describe the vasculature of the myocardium

A

a lot of capillaries! in a parallel arrangement

181
Q

where does the fundamental source of ATP for the myocardium come from?

A

Fatty acids

182
Q

describe what happens to the LCA during a contraction

A

the pressure around the LCA increases greatly so that it is greater than the pressure inside the LCA (neg. transmural pressure)–> LCA flattens= no flow during systole

183
Q

how does autoregulation of coronary arteries affect flow in the face of high pressure?

A

senses high pressure–> increase resistance–> decrease flow

184
Q

how does autoregulation of coronary arteries affect flow in the face of a high metabolic demand?

A

high metabolic demand= increased flow

185
Q

what 4 factors influence coronary flow?

A
  1. autoregulation
  2. mechanical factors
  3. neural activity/humoral
  4. metabolic factors*
186
Q

how does SNS and PSNS affect coronary flow

A

both increase flow!

187
Q

how does SNS increase coronary flow?

A
  • increased NE binding to B1= increased HR and force of contraction= increased overall pressure = increase coronary flow
  • Epi bind B2 = vasodilation = increased flow
188
Q

how does PSNS increase coronary flow?

A

ACh binds muscarinic R. = decrease HR and force of contraction via production of NO= decrease pressure (mechanical pressure is relieved)= increase flow

189
Q

O2 consumption by the myocardium is determined by what 4 factors?

A
  1. ventricular wall tension (Law of Laplace)
  2. HR
  3. Velocity of fiber shortening (dP/dt) ((Increased HR)
  4. Peak tension developed
190
Q

what is the impact of stenosis on coronary flow at rest?

A

take about 80% stenosis before flow starts to decrease

191
Q

what is the impact of stenosis on coronary flow during stress/ hyperemic state

A

flow decreases at a lower stenosis percentage

- dramatic decline ~75%

ISBM (8 decks)

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