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NPB 113 > exam 2 > Flashcards

exam 2 Flashcards

1
Q

compliance

A

ability of a vessel to adjust the BP & ↑ the V of blood that it can hold

  • stretchiness in arterial walls
  • compliance = ΔV/ΔP
  • rigid (non-stretch) = low compliance
  • stretchy = high compliance
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2
Q

capacitance

A

ability to hold/store blood

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3
Q

venous capacitance & compliance

A
  • veins have capacitance
  • exhibit high apparent compliance: arises from geometric changes as blood flows in (not stretchiness)
  • can add V w/out ↑P
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4
Q

capillary compliance & capacitance

A
  • low capacitance
  • low compliance
    • if V ↑ ➔ P ↑
    • good for filtration (e.g. kidneys)
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5
Q

elastic arteries compliance & capacitance

A
  • low capacitance ➞ not designed to store blood
  • stretchy ∴ high compliance
  • if we put blood into elastic arteries we ↑P ➔ pressure resevoir
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6
Q

what determines flow into elastic arteries

A

in-flow: CO

  • HR
  • SV
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7
Q

what determines flow out of elastic arteries

A

MAP

  • elastic recoil during both systole & diastole but most important during diastole
  • vasoconstriction/vasodilation in arterioles
  • baroreceptor reflex: ↓ in MAP ➔ ↑ SNS activity ➔ vasoconstriction ↓ outflow ➞ maintains blood in elastic arteries ➞ maintains ↑ BP
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8
Q

resistance

A
  • resistance to flow impedes movement of blood down length of pathway
  • mainly related to radius
  • R = 8ηℓ/𝜋r^4
    • ℓ = length: as ℓ↑ R↑
    • η = viscosity: as viscosity↑ R↑
      • # of RBCs: as RBC↑ viscosity ↑
      • e.g. erythropoietin or dehydration
    • r = radius: as radius ↑ R↓
      • arterioles only vessels that dramatically change radius ➞ major resistance vessels
      • if r↓ by 1/2: R ↑ 16x
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9
Q

arteriolar vsm regulated by:

A

vasoconstriction:

  • SNS-mediated vasoconstriction: ↑SNS activity to arterioles ➞ ↑ arteriolar R due to NE-binding to ⍺-adrenergic receptors
  • vasopressin (AVP/ADH) from neurohypophysis

vasodilation:

  • SNS-mediated vasodilation: small portion of SNS neurons release ACh ➞ vasodilation
    - ↑ SNS activity for same arterioles ➞ ↓ arteriolar R due to ACh binding β-adrenergic receptors on vsm in some skeletal muscle region
    - only small subset of arterioles ∴ not mechanism of action
  • EPI ➞ binds to β2-adrenergic receptors → vasodilation
  • local metabolites: anty chemical signal factors released in immediate vicinity by tissues that influence adjacent arterioles ➞ override SNS vasoconstriction ∴ induces vasodilation
    • [K]
    • PCO2
    • PO2
    • ↓ pH: active tissue undergoes glycolytic metabolism resulting in lactic acid build-up & CO2 production
  • nitric oxide = gas released by tunica intima endothelium during sheer stress causes vasodilation to other vessels to redirect bf instead of forcing it through single stressed vessel to ↓ rubbing
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10
Q

active hyperemia

A

↑bf to active tissue due to release of local metabolites causing vasodilation

  • high blood flow to meet active muscles’ increased need for oxygen
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11
Q

reactive hyperemia

A

previously occluded tissue had ↓ in bf ∴ ECF has temporary ↑ in metabolites to vasodilate & bring blood back to occluded tissue

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12
Q

venoconstriction

A

when peripheral veins contract

  • resistance is unchanged
  • alters stretchiness of vein ➞ ↓ apparent compliance ➞ stiffer = ↑ venous P
  • ↑ venous P = ↑ venous return
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13
Q

flow rate out of the heart is proportional to:

A

cumulative flow rate

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14
Q

stroke volume dependent on

A
  1. changes w/ activity/metabolic demand usually SNS-mediated: ↑ SNS activity ➞ ↑ SV
  2. venous return: blood flows passively from peripheral veins to central veins & ventricles → venous filling
    • peripheral veins (7 mmHg) ➔ central veins (2 mmHg) ➔ ventricles (0 mmHg)
  3. EDV determines SV (frank-starling rule): volume stretches ventricular wall
    1. ↑ optimal overlap btwn existing thick & thin filaments
    2. geometric advantage ↓ distance existing btwn myosin heads & thin filaments
    3. Ca interaction w/ troponin ➞ ↑ Ca affinity
  • EDV in ventricles is dependent on passive filling & atrial contraction (pre-load = 135mL)
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15
Q

CO

A

CO = HR x SV

  • flow out of the heart
  • can vary from 5-25 L/min
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16
Q

intrinsic property of the heart

A

↑ pre-load/EDV = ↑ contractile strength

  • built into heart ➞ happens automatically
  • dose not require any hormones, drugs, neurotransmitters
  • muscle is stretched ➔ automatic greater response
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17
Q

venous return

A

de-oxygenated blood returning to central venous pool

  • like a flow rate
  • dependent on ΔP btwn peripheral veins & central venous pool
    • SVC & IVC (large V, lots of capacitance, low P)
    • RA
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18
Q

peripheral vein venous return mechanisms

A
  1. smooth muscle contraction in response to ↑ SNS allows us to ↑ peripheral venous P w/ no effect on radius: alters compliance ➞ stiffer
  2. skeletal muscle pump: muscle contracts ➞ squeezes peripheral veins ➞ ↑ venous P ➞ drives bf out to CVP
  3. venous valves: 1 way valves ensure 1-way flow
  4. cardiac suction & respiratory pump: ventricles relax ➞ V ↑ ➞ ventricle P↓ ➞ suction
    • inspiration ➞ ↑ thoracic V ➞ ↓ intrapleural P ➞ SVC & IVC V↑ ➞ SVC & IVC P↓
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19
Q

contractility

A

Δ in contractile strength due to extrinsic forces

  • act on muscle independently of intrinsic factors (can even act simulataneously e.g. exercise)
  • SNS input to heart will ↑ contractile force
    • in the atria: ↑ EDV
    • in the ventricles: ↑ force of contraction ➞ ↑P ➞ ↑SV
    • independent of EDV
    • SNS neurons release NE ➞ binds to β-adrenergic receptors ➞ activates GPCR (Gs ⍺ subunit) ➞ PKA phosphorylates:
      1. L-type Ca channels ➞ ↑ Ca influx
      2. SERCa pumps ➞ ↑ rate of Ca removal ➞allows quick relaxation
      3. troponin ➞ ↑ off rate of tropomyosin ➞ allows thin filament to bind to myosin head
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20
Q

CO during exercise

A

CO ↑ due to ↑ HR & ↑ SV

  • during exercise venoconstriction & skeletal muscle pump cause venous fx curve to shift ↑
  • still work at CVP ≈ 1.8-2 mmHg
  • ESV is smaller than normal ∴ ESP is smaller which facilitates ventricular filling
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21
Q

HR regulation of CO

A
  • HR depends on:
    1. rate of depolarization in the SA node (during phase 4)
    2. duration of nodal delay in AV node
    3. conduction velocity in all conductive pathways
  • an ↑ in HR is caused by ↑ SNS input + ↓ in PNS input
    • myocytes only have sympathetic input but pacemaker & conduction pathways have both ANS & PNS
    • SNS input from thoracic region
    • SNS post-ganglionic neurons release NE
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22
Q

↑ SNS input to SA node:

A
  • NE binds to β1-adrenergic receptors
  • activation of L-type Ca channels
    • steepens phase 0
    • changes threshold value: makes channels easier to open
  • activation of HCN: activating β1-adrenergic receptors in SA node activates cAMP → activates HCN channel more effectively ➞ steepens phase 4 & 0
  • quicker depolarization to threshold
  • threshold is more electronegative
  • can get to threshold much faster & can get more AP per time
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23
Q

↑ SNS input to AV node:

A
  • in N region (& maybe AN region): AP becomes steeper
  • faster conduction through AV node ∴ shorter AV nodal delay
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24
Q

↑ SNS input to conduction pathways

A

↑ in conduction velocity → faster impulses

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25
Q

↓ SNS + ↑ PNS input to pacemaker SA node

A
  • ACh binds to muscarinic cholinergic receptors → binds K channels
  • background K current hyperpolarizes → ↓ max diastolic potential (MDP becomes more electronegative)
  • phase 0 & 4 are less steep (flatter)
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26
Q

↓ SNS + ↑ PSNS stimulation to AV node

A

N region becomes slower to rise → ↓ velocity of pacemaking AP through the node → ↑ AV nodal delay

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27
Q

change of contractility & effect on PV loop

A
  • ↑ SNS causes ↑ in contractile strength independent of EDV
  • pressure at which semilunar valves open dependent on afterload
    • point D determined by pressure in aorta (MAP) not contractile force
  1. force of contraction (∴ P developed) has ↑ at every point during contraction
  2. SV ↑
  3. ESV ↓ (∴ ↓ ESP) w/ ↑ contractility → start diastole w/ smaller pressure → advantageous for ventricular filling
  4. rate of pressure development ↑ ∴ faster contractions
  5. rate of relaxation ↑ due to SERCa pump activation
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28
Q

↓ SNS + ↑ PNS stimulation to conduction pathways

A

slows conduction velocity → slower impulses (slower HR)

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29
Q

change in EDV & PV loop

A
  • w/ an ↑ in EDV due to ↑ in venous return → larger SV
  • change in SV due to change in EDV from vasoconstriction
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30
Q

exercise & PV loop

A
  • during exercise we ↑ SNS output to heart
  • contractility ↑
  • ↑ SNS to veins → ↑ venous return → ↑ EDV
  • contracting skeletal muscles ↑ venous return → ↑ EDV
  1. ↑ contractility + ↑ venoconstriction & venous return = ↑ EDV (venoconstriction = no change in contractility → making veins stiffer)
  2. ↑SV
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31
Q

cardiac fx curve

A

relates ventricular muscle stretch to the force the muscles can generate

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32
Q

combined cardiac & vascular fx curves

A

CO is matched by peripheral venous return at point A: @ 5 L/min CVP pressure = 2 mmHg

  • always have to match venous return w/ CO (CO of 5 L/min = venous return of 5 L/min)
  • CVP pressure must be higher than ESV in order for blood to flow
  • pressure at 2 mmHg facilitates blood coming out of CVP into ventricle & also facilitates blood coming out of peripheral veins into CVP
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33
Q

vascular (venous) fx curve

A

relates amount of blood coming out of peripheral veins & pressure in venous pool

  • IVC, SVC, RA
  • CVPP: central venous pool pressure
  • CVP acts as back-pressure → prevents venous return
  • CVP influences ventricular filling → P that pushes blood into ventricles
    • ventricular filling dependent on CVP pressure & ESV
    • CVP — ESP
    • ESP acts as back-pressure stopping CVP pool from filling
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34
Q

vascular fx curve: blood volume

A
  • ↑ volume = ↑ mean systemic filling pressure
  • ↓ volume = ↓ mean systolic filling pressure
    • sweat
    • dehydration
    • hemmorrhage
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35
Q

vascular fx curve: vasoconstriction/vasodilation

A
  • mean systemic venous pressure stays constant: equal amount of blood flowing in/out
  • vasoconstriction: less blood coming from cap ➔ veins = slower venous return
  • vasodilation: more blood flows faster
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36
Q

mean systemic venous pressure

A

avg pressure in periphery (~7 mmHg)

  • peripheral P varies based on location & forces of gravity
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37
Q

vascular fx curve: venoconstriction

A

↑ SNS changes compliance ➞ stiffer walls ➞ ↑P in peripheral veins

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38
Q

MAP

A
  • homeostatically regulated
    • P too low: blood does not perfuse to necessary tissues → loss of O2 & nutrients for cell resp → tissue damage
    • P too high: neurons & capillaries damaged (e.g. eyes)
  • normotensive = 70-100 mmHg
  • measured in elastic arteries
  • MAP is proportional CO x TPR
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39
Q

TPR

A

total peripheral resistance

  • affected by:
    1. Δ in SNS activity
    2. local metabolites
    3. local signal factors (i.e. histamines, N.O.)
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40
Q

high-pressure baroreceptors

A

detect BP in elastic arteries (areas of high pressure flow)

  1. carotid sinus: walls of carotid arteries
  2. aortic arch
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41
Q

low-pressure baroreceptors

A

detect BP in places that are low pressure (representative of venous side) ∴ monitor venous BP ➞ important b/c affects venous return & EDV

  • sends sensory info to NTS & hypothalamus
  1. pulmonary artery
  2. jxn between veins & atria
  3. R & L atria
  4. R ventricle
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42
Q

baroreceptors

A

detect BP & innervate wall of vessels or chambers

  • when blood fills the vessel/wall will stretch
  • dendrites detect Δ in wall stretch (squeezes against dendrites)
  • as vessel V↑ (P↑) → AP freq ↑
43
Q

sensory processing of high-pressure baroreceptors

A

info processed by brain stem

  1. nucleus tractus solitarius (NTS) receives input from baroreceptors & sends output to the following:
  2. DMNX: dorsal motor nucleus of the 10th cranial nerve (vagus nerve): PSNS nuclei excited by NTS input
  3. nucleus ambiguous (NA): PSNS nuclei excited by NTS input
  4. rostral ventrolateral medulla (RVLM): SNS nuclei that receive inhibitory input from NTS ➞ regulates SNS output to arterioles & heart
  • input from carotid receptors travels via glossopharyngeal crania nerve
  • input from aortic arch travels via vagus cranial nerve
44
Q

baroreceptor response to a rise in MAP

A
  1. high pressure baroreceptors ↑ firing rate from baseline activities
  2. input goes to NTS
    • ↑ neuronal firing rate to the DMNX & NA ➞ ↑ PNS activity → slows heart
    • ↑ activity to RVLM ➞ ↓ SNS → slows heart, ↓ contractility, ↓ venous return, causes arteriolar vasodilation
45
Q

chemoreceptors influences on CO

A

peripheral chemoreceptors found in aortic arch & carotid bodies (above carotid sinus) monitor blood pH, arterial PCO2, & arterial PO2

  • exert a positive drive on vasomotor center causing vasoconstriction
46
Q

in response to hypoxia

A

hypoxia = PO2 &laquo_space;60 mmHg
- peripheral chemoreceptors ↑ firing rate → input to NTS
- activates SNS output → vasoconstriction (selective to drive bf to necessary areas)
- tachycardia (↑ HR = ↑ CO) can help to perfuse to important vessels (eg cerebral circulation, coronary circulation, kidneys)

47
Q

baroreceptor response to sudden ↓ in MAP

A
  • from hemorrhage or ↓ in V
  • ↓ bf to critical places
  • ↓ MAP detected by high pressure baroreceptors → ↓ rate of firing
    • to the DMNX & NA of the PSNS: ↓ activation ➞ ↑ HR
    • to the RVLM of the SNS: ↓ activation (of inactivation) ∴ allows activation of SNS ➞ ↑ HR, ↑ contractility, ↑ venous return, causes arteriolar vasoconstriction
  • ↑ SNS & ↓ PSNS
48
Q

↑ in SNS output stimulates:

A

1.↑ contractility in ventricular muscle → ↑ SV
2. venoconstriction of veins → ↑ venous return → ↑ EDV (frank starling = ↑ contractility)
3. pacemaker cells & conductive pathways → ↑ HR (chronotropy)
4. arteriolar vasoconstriction → ↓ bf out of elastic arteries → ↓ blood V leaving elastic arteries → ↑ V in elastic arteries → ↑ MAP

49
Q

↓ PSNS output stimulates

A
  1. pacemaker cells (SA node) → ↑ HR (↑ chronotropy)
  2. conductive pathways → ↑ HR (↑ chronotropy)
50
Q

blood flow in an upright standing position:

A

~66-70% of TBV is in veins ➞ many of them are below the level of the heart

  • blood in lower extremities fights against gravity in order to flow back to the part
  • gravity exhibits hydrostatic pressure
51
Q

blood flow in a supine position:

A

laying down on back: gravity plays a minimal effect on preventing bf back from peripheral veins to CVP

  • force of gravity in respect to veins is unilaterally exhibited
52
Q

in response to an erect position:

A
  • above heart: blood drains easily → P ≈ 0 mmHg
  • blood pools at bottom of legs & arms (below heart) → P ≈ 5-100 mmHg
    • veins in lower extremities exhibit a lower compliance compared to veins in the upper extremities
      • skeletal muscle pump: postural/static muscles always contracting → push against vessels = most important component for venous return
      • venous valves prevent backwards flow of blood
  • going from supine → standing position:^^ MAP ∴ need to activate baroreceptor reflex
  • in heat: vasodilation to skin for cooling ∴ more likely to pass out
53
Q

orthostatic hypotension

A

↓ in MAP from supine → standing

54
Q

CV goal for exercise

A

↑ bf to specific organs:

  • exercising muscle
  • coronary circulation
  • pulmonary circulation
  • cerebral circulation
  • cutaneous circulation (for active cooling)
55
Q

CV response to exercise

A

↑ SNS output & ↓ PSNS output

  • ↑ SNS:
    • ↑ venous return → ↑ EDV → ↑ SV
    • ↑ HR
    • vasoconstriction of arterioles = ↑ TPR (↑ TPR would ↓ bf ➞ need local metabolites to vasodilate certain arterioles)
  • active tissues release local metabolites into interstitium that vasodilate vessels supplying exercising muscles/organs
    • localized w/in the tissue that has the greatest activity
    • H+ (↓ pH)
    • ↓ PO2
    • ↑ PCO2
    • ↑ K+
    • ↑ adenosine
    • ↑ lacate
    • overrides the SNS-induced ↑ in TPR in the local spot
      • global ↑ in TPR except in the exercising muscle
    • thermoregulation induduces ↑ bf to skin → sweat
      • vasodilation to cutaneous tissue
  • continued ↓ in TPR allows us to drive bf to particular exercising tissues
56
Q

blood distribution during exercise

A

proportion of bf changes during exercise

  • at rest: 5L/min
  • during exercise: 17.5L/min
  • skin & coronary circulation same percentage but larger V
    • skin: 12% = 500mL/min ➞ 12% = 1.4L/min
    • coronary: 4% = 250mL/min ➞ 4% = 750mL/min
  • splanchnic circulation % & proportion ↓
  • skeletal muscle % & proportion ↑
57
Q

control of exercise response

A

central command = prefrontal motor cortex (associative cortical region) of cerebral cortex

  1. talks to spinal cord to control skeletal muscle
  2. talks to BS: ↑ SNS & ↓ PSNS
58
Q

BP during exercise

A
  • SP: initial ↑ until plateau
  • DP: very slight change, slight drop ➞ local metabolites cause vasodilation in skeletal muscle vessels
  • MAP: slight ↑ at very beginning

with heavy sweating:

  • sweating = losing blood V
  • ↓ venous return ➞ ↓ EDV ➞ ↓ SV ➞ ↓CO ➞ SP↓
  • SP starts to fall
  • DP: slight decrease (mainly constant)
  • MAP: fairly constant
59
Q

regulation of microcirculation

A
  • arterioles & capillaries
  • ↑ SNS → precapillary sphincters contract
  • ↓ SNS & local metabolites → pre-capillary sphincters vasodilate
    • EDRF = endothelium-derived relaxation factor: causes arteriolar sm vasodilation & relaxes precapillary sphincters released in response to shear stress (e.g. NO)
    • histamines can also cause vasodilation as inflammatory response
  • ↑ bf into cap = Pcap↑
  • bf in capillary is proportional to ΔP between arteriole & vein
60
Q

EDRF

A

endothelium-derived relaxation factor: causes arteriolar sm vasodilation & relaxes precapillary sphincters

  • released in response to shear stress
  • NO
61
Q

autoregulation

A

yields constant bf in the face of changes in BP

  • due to VSM cells of arterioles that supply those cap
  • in order to maintain constant pressure to specific capillary beds
  • if MAP ↑ → vsm cells automatically vasoconstrict
  • if MAP ↓ → vsm cells automatically vasodilate
  • myogenic response: muscle cells contract in response to stretch
62
Q

capillary exchange

A
  • moving blood-borne solutes from blood to interstitium or vice versa
  • through pores or through endothelium
  • exchange always occurs w/ interstitium then tissues (not directly with tissues)
63
Q

exchange items:

A
  1. solutes that are dissolved in water plasma (glucose, wastes, AA, proteins)
  2. gases (O2, CO2, anaesthetics)
  3. water
64
Q

gas exchange

A
  • transcellular: plasma to/from interstitium
  • across the endothelium (thin)
  • requires ΔPgas (partial pressure gradient: PP gas = dissolved gas)
  • ex: O2
    • arteriolar PO2 = 100 mmHg
    • interstitial PO2 varies according to tissue activity ≈ 60-40 mmHg
65
Q

↑ capillary O2 extraction by:

A
  1. ↑ tissue metabolism (cellular respiration)
  2. ↓ bf rate
    • ↓ in O2 extraction when bf rates ↑ (↑ MAP or exercise)
    • soln: perfuse more capillaries w/in a given exercising tissue
66
Q

what determines gas extraction rate

A

bf rate & O2 utilization by tissues

  • also depends on distance → shorter distances facilitate gas exchange
67
Q

exchange of water-soluble mol & ions

A
  • water-soluble compounds & ions cannot easily cross endothelial cell membranes (hydrophilic cannot cross hydrophobic lipid bilayer)
  • must cross via pores ➞ pores influence larger mol movement (proteins → must be neutral or ⊕ charged)
  • Cl, Na, K, Ca, HCO3- → super tiny ∴ can fit through pores easily even with charge ➞ transport via Δ[gradient]
  • proteins are impeded due to size & charge → move via [gradient]
68
Q

water-soluble mol & ions solute exchange depends on:

A
  1. [gradient] between blood & interstitium
  2. permeability → influenced by size of pore
  3. surface area → ↑ SA = ↑ # of pores
  4. size of pores → mainly influences protein movement
  5. charge of protein → basement membrane surrounding capillary only allows neutral & ⊕ charged proteins through
  • for continuous capillaries (with no pores) → ions & water-soluble mol must use endothelial transport mechanisms
69
Q

basal lamina effect on protein exchange

A

basement membrane surrounding capillary = proteinaceous layer that endothelial cells sit on → provides structure

  • made up of lots of ⊖ charged AA ∴ ⊖ charged AA & sm peptides are excluded from passing through pores
  • neutrally charged AA & sm peptides can cross fairly easily
  • ⊕ charged AA & sm peptides cross easiest → don’t stick like magnets, just force pulling them along
70
Q

H2O movement across endothelial wall

A
  • proteins are osmotically active: influence water movement across capillary wall
  • via fenestra/pores = paracellular transport
  • via aquaporins → AQP1 = transcellular transport
  • alterable → affect hydraulic conductivity
71
Q

paracellular H2O transport

A

H2O movement via fenestra/pores

72
Q

transcellular H2O transport

A

H2O movement via aquaporins → AQP1

73
Q

forces influencing H2O movement:

A

pressure gradient (V of blood w/in cap): generates hydrostatic pressure: as blood moves along the capillary, fluid moves out through its pores and into the interstitial space

osmotic pressure: pressure exerted to oppose the force of water/liquid movement

  • due to albumin, fibrinogen, & globulins
  • attract water back into the cap
74
Q

starling law of fluid transfer:

A
  • J = flux of water occurring across the vasculature
  • Jv = water flux across a cap
  • SA = surface area
  • Lp = hydraulic conductivity: a measure of how easily water can pass through soil or rock
    • more pores or AQP = ↑ Lp
  • Pcap = BP in cap → pushes water out of vessel
  • PIF = P in interstitium/interstitial fluid: pushes water into vessel
  • σ = reflection coefficient: varies from 0 → 1
    • when σ = 1: wall of cap does not allow proteins to move across capillary → maintains capacity for filtration
    • when σ = 0: capillary wall is permeable to proteins → dangerous (e.g. burns having edema)
  • 𝜋cap = oncotic pressure in blood due to proteins: attracts water into cap → opposes hydrostatic pressure
  • 𝜋IF = oncotic pressure in interstitium that pulls water out of capillary
  • hydrostatic pressure difference: net force of water moving out of blood because of BP → hydrostatic force pushing water out
  • oncotic/osmotic pressure difference: net force of water moving out of blood because of blood proteins
75
Q

filtration & net reabsorption across the cap

A
  • filtration = cap loses H2O
  • reabsorption = cap gains H2O
  • fluid movement proportional to Jv (sterling’s law of fluid transfer - water flux across a cap)
    • at start of cap: filtration
    • at end of cap: net reabsorption
  • ⊕ value = fluid leaves cap, pushing water out of capillary ➞ net filtration
  • ⊖ value = causes fluid to move into cap, sucking water back in ➞ net reabsorption
  • net filtration exceeds net reabsorption
    • tend to have more net filtration occurring across the capillary compared to net reabsorption
      • exception in kidneys where there is no net reabsorption
    • this is how we create interstitial fluid
  • fluid is reabsorbed in a balanced manner by lymphatic capillaries
    • runs parallel to blood
    • 1 way valves: as fluid pushes in, valves open then close
    • drains into venous system into subclavian veins
    • lymphatic blockages can cause edema
    • important in immune response
76
Q

solute movement depends on:

A
  1. [gradient]
  2. # of pores
  3. kinetic force → movement of solvent moving solute = solvent drag
77
Q

solvent drag

A

movement of solvent moving solute: as H2O is osmotically moving, it drags a solute across a cap independent of [gradient] associated with that solute

  • aka convection movement
  • σ for solute ≈ 0 (closer to 0) ∴ pore is big or doesn’t impose a charge restriction
78
Q

what would decrease venous filling of the heart?

A

an ↑ in ESV

79
Q

an increase in CO in a subject who changed from a supine to a standing position occurred because

A

this is an actual compensatory response to a drop in MAP that occurs when a subject changes from supine to standing position

80
Q

major problem that arises from an increased afterload

A

SV is lower than normal

  • must use greater force to overcome higher pressure ∴ less force to get blood out
81
Q

compensatory response to a drop in MAP

A
  • ↑ SV
  • ↑ HR
  • ↑ venous return (vasoconstriction)
82
Q

where are β-adrenergic effects primarily seen?

A

skeletal muscle

83
Q

what can increase TPR?

A
  • adrenergic stimulation
  • vasoconstriction
  • increased viscocity
84
Q

what can decrease TPR?

A
  • PSNS stimulation
  • vasodilation
  • local metabolites
  • local signal factors (histamines, NO)
85
Q

⍺-adrenergic stimulation causes

A

vasoconstriction

86
Q

β-adrenergic stimulation causes

A

vasodilation

87
Q

which vascular beds exhibit vasoconstriction during exercise?

A

the splancnic circulation

88
Q

which vascular beds exhibit vasodilation during exercise?

A
  • cerebral circulation
  • coronary circulation
  • those supplying exercising muscle
89
Q

why is there non-uniform compliance in our venous circulation

A

it reduces the venous pooling effects in the lower legs

90
Q

peripheral chemoreceptors directly respond to

A

changes in plasma CO2

91
Q

what would you expect to observe if the autorhythmic cells were treated with an adrenergic receptor agonist?

A

the L-type Ca2+ channel would be more active than normal

92
Q

what happens if the ventricles are stimulated by a β1-adrenergic agonist?

A

ESV ↓

  • ↑ SA, AV, & ventricular muscular firing ➞ ↑ HR & contractility ➞ ↑ SV & CO
93
Q

if a patient experienced a sudden hemorrhage, where the SV dropped, what would be part of the compensatory response that would allow the cardiac output to return close to normal?

A

A ↓ PNS input to pacemaking cells

94
Q

what trend would you expect to observe during a 90 minunte exercise period with constant effort?

A

HR initially rises, levels out, then falls at the end of exercise

95
Q

baroreceptors versus peripheral chemoreceptors

A

baroreceptors exert a negative drive on vasomotor center causing vasodilation

peripheral chemoreceptors exert a positive drive on vasomotor center causing vasoconstriction

96
Q

if the contractility of the heart ↑ that means that

A

the heart develops pressure more effectively than normal

97
Q

what region of the CNS CV control center is the primary integrator of afferent info?

A

the nucleus tractus solitarius

98
Q

the PSNS centers in the CV control center

A
  1. DMNX: dorsal motor nucleus of the 10th cranial nerve
  2. NA: nucleus ambiguous
99
Q

the SNS centers in the CV control center

A

RVLM: rostral ventrolateral medulla

100
Q

According Poiseuille’s law, if vessel A has a diameter twice as large as vessel B, then the resistance of
vessel A is

A

16x less than B

101
Q

SNS-mediated vasoconstriction

A

↑ SNS activity to arterioles ➞ ↑ arteriolar R due to NE-binding to ⍺-adrenergic receptors

102
Q

SNS-mediated vasodilation

A

small portion of SNS neurons release ACh ➞ vasodilation

  • ↑ SNS activity for same arterioles ➞ ↓ arteriolar R due to ACh binding β-adrenergic receptors on vsm in some skeletal muscle region
  • only small subset of arterioles ∴ not mechanism of action
103
Q

SV, HR, & CO during exercise

A
  1. SV ↑ at onset of exercise then plateaus until sweating causes loss of volume & ↓ SV
  2. HR ↑ at onset then plateaus until ↑ when compensates for ↓SV
  3. CO ↑ then plateaus & maintains consistency until a decrement in performance once HR performs at max for long enough
104
Q

cardiac drift

A

during exercise with constant effort: ↑ in HR to compensate for a ↓ in SV after loss of volume while maintaining a consistent CO

NPB 113 (5 decks)

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