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NPB 113 > FINAL > Flashcards

FINAL Flashcards

1
Q

contractile force vs resting length

A

↑ EDV due to ↑ venous return → ↑ developed force

  • resting length = EDV
  • mechanisms:
  1. maybe as we ↑ EDV we ↑ # of cross-bridges
  2. ↑ EDV (stretching walls of ventricle) ↑ geometric advantage: distance between thick & thin filaments decreases as the sarcomere is stretched ➔ as sarcomeres lengthen, they get smaller in diameter → develops force
  3. ↑ Ca affinity to troponin-C: stretch of muscle ↑ affinity of troponin-C to Ca → greater amount of time Tn-C is bound to Ca allows greater crossbridge cycling → greater force (depends on [Ca] & affinity)
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2
Q

frank-starling rule of the heart

A

as EDV ↑, ventricular force ↑

  • ↑ venous return → ↑ EDV
  • increased Ca sensitivity occurs at longer muscle fiber lengths
  • more EDV = more preload = more SV = more forceful contractions
    • preload: volume in ventricles (=EDV)
    • afterload = back-pressure in the elastic arteries keeping semilunar valves closed (bad)
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3
Q

vessel layers

A

tunica adventitia/externa: outermost layer

  • strong connective tissue, collagen, elastin, & fibroblasts to help create overall structure
  • anchors vessels’s w/in tissue

tunica media: smooth muscle cells & connective tissue

  • could be continuous in a distinct layer or discontinuous
  • changes diameter of vessel

tunica intima/interna: endothelium

  • sometimes can find elastin or connective tissue
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4
Q

elastic arteries

A

fill w/ blood, stretch (storing potential energy), & recoil ➔ squeezes blood ➔ ↑ pressure

  • pressure reservoir allows us to drive bf during diastole
  • has all 3 tissue layers
  • mean arterial pressure (MAP): driving force for bf from arteries ➞ capillaries
    • homeostatically regulated but parameters can shift after years of consistency
    • MAP = 1/3 SP + 2/3 DP or MAP = DP + 1/3 (SP−DP)
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5
Q

muscular arteries

A

distribution arteries: directs blood to certain regions

  • changes proportion of bf allocated
  • downstream of elastic arteries
  • smaller than elastic arteries
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6
Q

arterioles

A

major resistance vessels

  • vasoconstrict in response to ↑ SNS input
  • vasodilate in response to ↓ SNS input & signal factors (local metabolites)
  • varying number of tissue layers
    • larger arterioles hav eall 3 layers w/ continuous SM
    • smaller arterioles have discontinuous bands of SM
  • avg diameter ~30 microns
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7
Q

vasoconstriction of arteriolar vsm:

A
  1. SNS-mediated vasoconstriction: ↑SNS activity to arterioles ➞ ↑ arteriolar R due to NE-binding to ⍺-adrenergic receptors
  2. vasopressin (AVP/ADH) from neurohypophysis
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8
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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9
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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10
Q

vasodilation mechanisms in arteriolar vsm:

A
  1. 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
  2. EPI ➞ binds to β2-adrenergic receptors → vasodilation
  3. local metabolites: anty chemical signal factors released in immediate vicinity by tissues that influence adjacent arterioles ➞ override SNS vasoconstriction ∴ induces vasodilation
    • [adenosine]
    • [K]
    • PCO2
    • PO2
    • ↓ pH: active tissue undergoes glycolytic metabolism resulting in lactic acid build-up & CO2 production
  4. 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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11
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 down a pressure gradient → venous filling
  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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12
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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13
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: ↓ 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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14
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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15
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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16
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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17
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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18
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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19
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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20
Q

combined cardiac & vascular fx curves

A

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

  • CVP pressure must be higher than ESV in order for blood to flow
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21
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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22
Q

vascular fx curve: blood volume

A
  • ↑ volume = ↑ mean systemic filling pressure
  • ↓ volume = ↓ mean systolic filling pressure
    • sweat
    • dehydration
    • hemmorrhage
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23
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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24
Q

vascular fx curve: venoconstriction

A

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

25
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.)
26
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 ↑
27
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
28
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
29
Q

chemoreceptors influences on CO

A

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

  • exert a positive drive on vasomotor center causing vasoconstriction
30
Q

CV response to hypoxia

A
  1. peripheral chemoreceptors ↑ firing rate → input to NTS
  2. activates SNS output → vasoconstriction (selective to drive bf to necessary areas)
  3. tachycardia (↑ HR = ↑ CO) can help to perfuse to important vessels (eg cerebral circulation, coronary circulation, kidneys)
31
Q

baroreceptor response to sudden ↓ in MAP

A
  • ↓ 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
32
Q

↑ in SNS output effect on CO:

A
  1. ↑ contractility in ventricular muscle → ↑ SV
  2. venoconstriction of veins → ↑ venous return (lower compliance) → ↑ EDV
  3. stimulate pacemaker cells & conductive pathways → ↑ HR (chronotropy)
  4. arteriolar vasoconstriction → ↓ bf out of elastic arteries → ↓ blood V leaving elastic arteries → ↑ V in elastic arteries → ↑ MAP
33
Q

↓ PSNS output effect on CO

A
  1. ↓ pacemaker cell activity (SA node) → ↑ HR (↑ chronotropy)
  2. conductive pathways → ↑ HR (↑ chronotropy)
34
Q

CV response to exercise

A

↑ SNS output & ↓ PSNS output

  1. ↑ SNS:
    • ↑ venous return → ↑ EDV → ↑ SV
    • ↑ HR
    • vasoconstriction of arterioles = ↑ TPR (↑ TPR would ↓ bf ➞ need local metabolites to vasodilate certain arterioles)
  2. active tissues release local metabolites into interstitium that vasodilate vessels supplying exercising muscles/organs
    • 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
  3. thermoregulation induduces ↑ bf to skin → sweat ➞ vasodilation to cutaneous tissue
35
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
36
Q

autoregulation of cardiovascular system

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
37
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
38
Q

what determines gas extraction rate

A

bf rate & O2 utilization by tissues

  • also depends on distance → shorter distances facilitate gas exchange
39
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 a membrane
    • 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
40
Q

compensatory response to a drop in MAP

A
  • ↑ SV
  • ↑ HR
  • ↑ venous return (venoconstriction)
41
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

42
Q

autonomic input to bronchiolar SM

A
  • autonomic input changes radius & primarily affects static resistance
  • SMC contract → makes bronchioles smaller in diameter (bronchoconstriction) → ↑ R
  • SMC relax = bronchodilation → ↓ R
  • bronchioles = primary resistance sites
    1. response to ↑ PSNS input = bronchoconstriction → matching bf to lungs w/ air flow
    2. response to ↑ SNS input = bronchodilation & ventilate portions of lung not previously ventilated (β-adrenergic response)
    3. ↑ histamine release from immune cells causes constriction of bronchioles & alveolar ducts (although alveolar ducts do not have SM)
43
Q

airway resistances

A
  1. static resistance from radius
  2. dynamic resistance from airflow & the renold’s number
  3. autonomic input to bronchiolar sm
  4. lung volume
  5. luminar & interstitial gases
44
Q

lung volume effect on resistance

A

as lung V↑ → R in bronchioles ↓

  • alveoli ↑ in size & are mechanically tethered to the bronchioles
    • enlarged alveoli pull on the wall of the bronchiole → ↑ radius
    • maybe allows bronchioles to overcome collapsing transmural forces
45
Q

luminar & interstitial gases effect on resistance

A
  • as interstitial PCO2 ↑ → causes causes SMC to relax ∴ bronchodilation ➞ R↓ → ↑ airflow
    • more predominant effect than PO2
  • as interstitial PO2 falls → bronchodilation (SMC relax) ➞ R↓ → ↑ airflow
  • matching ventilation to perfusion
46
Q

resistance to pulmonary bf factors

A

resistance is low

  1. as perfusion ↑ (due to an ↑ CO) the resistance ↓ → recruitment & distention of bv↓ resistance
  2. lung volume induces changes in resistance to blood vessels (effects on septum capillaries, extra-alveolar blood vessels, and zones of the lung)
  3. lung interstitial/parenchyma PCO2 content
47
Q

resistance to pulmonary bf from recruitment & distention

A

↑ perfusion due to↑ CO:

  1. recruitment of blood vessels: ↑ in bf to closed/unused blood vessels ➞ ↓R
  2. distention of pulmonary bv due to ↑ pulmonary arterial BP → ↓R
48
Q

resistance to pulmonary bf from lung volume

A
  • bv sitting in between alveoli/in septum get squished during inspiration → ↑ R
  • extra-alveolar blood vessels are not in septum ∴ do not get squished during inspiration, but actually expand due to transmural force ➞ ↓R
49
Q

resistance to pulmonary bf from lung volume based on zones

A
  • in an upright indiv: blood perfuses zone 3 > zone 2 > zone 1
  • selectively perfusing bottom 1/2 - 2/3
  • at apex: ↓ in bf due to gravity + bv are squished down by larger alveoli
    - transmural force expanding bv is weaker than squishing force of lung tissue ∴ bv at top get squished
  • at base: blood selectively perfuses lower bv + lung tissue is not as expanded so not much squishing force on bv ∴ more overall blood flow into the lower vessels
50
Q

resistance to pulmonary bf from lung interstitial/parenchyma PO2/PCO2 content

A
  • local effect
  • low O2 content w/in parenchyma causes local vasoconstriction of the pulmonary arterioles → shunts blood away from region that is poorly ventilated
  • high PO2 content → vasodilation of pulmonary arterioles → ↑ bf to that ventilated region
  • allows us to match blood flow to ventilation
  • PCO2 effects are not as influential as PO2
    • high CO2 causes local vasoconstriction
    • low CO2 causes vasodilation
51
Q

ventilation-perfusion ratios

A
  • ideal lung VA (alveolar ventilation) should match bf to that alveolus
  • VA/QC should be 1 → ratio is actually ≈ 0.8 (in middle)
  • apex is over-ventilated compared to blood flow (1.2)
  • base is under-ventilated compared to blood flow (0.6)
52
Q

factors contributing to O2 unbinding

A
  1. tissue is producing CO2 → ↑ PCO2 causes ↓ in affinity of Hb to O2 which causes causes Hb-O2 to unbind O2 (R shift of dissociation curve = ↓ affinity ➞ Bohr effect)
  2. in tissue: ↓pH from CO2 → H2CO3 (↑H+) + lactic acid ➞ R shift in Hb-O2 saturation curve causes Hb-O2 to unbind O2 (Bohr effect)
  3. ↑ temp at active tissue ➞ heat causes R shift in Hb-O2 saturation curve which causes Hb-O2 unbinding of O2
  4. tissue & interstitial 2-DPG (diphosphoglycerate) produced during metabolic activity ➞ R shift in Hb-O2 saturation curve which causes Hb-O2 unbinding of O2
53
Q

Hb binding in the lungs

A

↑ affinity of Hb to O2 (lower saturation at lungs) → left shift of curve

  • interstitial CO2 is low
  • pH is more neutral (7.4)
  • temp is cooler
54
Q

peripheral chemoreceptors

A
  • in aortic bodies & carotid bodies
  • stimulated by:
    1. ↓ arterial PO2 → fall below 60 mmHg activates ventilation
    2. arterial acidity (↓pH/↑[H+]) usually due to ↑ activity/CO2 → ventilation ↑
      • rapid response
      • pH homeostasis response
      • partial compensation of pH disturbance
    3. CO2 in arterial blood → rise in arterial PCO2 due to ↑ metabolism &/or a ↓ in ventilation stimulates ventilation (weak response)
55
Q

central chemoreceptors

A
  • found in the brain stem in the medulla
  • primary sensor, strong response
  • detects [H+] which is proportional to blood PCO2
  • ↑ brain ECF [H+] stimulates ventilation
56
Q

pulmonary stretch receptors

A
  • peripheral sensory afferents
  • in lung parenchyma
  • monitor volume of lungs
  • inspire: lung volume ↑ → AP freq ↑ → brainstem NTS → inhibits ventilation
  • expire: ↓ lung volume ➞ AP freq ↓ → brainstem NTS → activates ventilation
  • can influence respiration independently of gas content
57
Q

irritant receptors

A
  • peripheral sensory afferents
  • monitor noxious stimuli in lungs/airways
  • itch, pain, temp
  • induce sneeze, cough, or forced expiration
  • induces bronchoconstriction → protective effect
58
Q

metaboreceptors

A
  • peripheral sensory afferents
  • chemoreceptors found in tissues
  • monitor ECF chemicals (CO2, pH)
  • ↑ tissue metabolism releases CO2 that metaboreceptors detect → activates ventilation
  • contributes to fine-tuning respiration
59
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

NPB 113 (5 decks)

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