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
2
Q
capacitance
A
ability to hold/store blood
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
4
Q
capillary compliance & capacitance
A
- low capacitance
- low compliance
- if V ↑ ➔ P ↑
- good for filtration (e.g. kidneys)
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
6
Q
what determines flow into elastic arteries
A
in-flow: CO
- HR
- SV
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
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
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
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
11
Q
reactive hyperemia
A
previously occluded tissue had ↓ in bf ∴ ECF has temporary ↑ in metabolites to vasodilate & bring blood back to occluded tissue
12
Q
venoconstriction
A
when peripheral veins contract
- resistance is unchanged
- alters stretchiness of vein ➞ ↓ apparent compliance ➞ stiffer = ↑ venous P
- ↑ venous P = ↑ venous return
13
Q
flow rate out of the heart is proportional to:
A
cumulative flow rate
14
Q
stroke volume dependent on
A
- changes w/ activity/metabolic demand usually SNS-mediated: ↑ SNS activity ➞ ↑ SV
- 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)
- EDV determines SV (frank-starling rule): volume stretches ventricular wall
- ↑ optimal overlap btwn existing thick & thin filaments
- geometric advantage ↓ distance existing btwn myosin heads & thin filaments
- Ca interaction w/ troponin ➞ ↑ Ca affinity
- EDV in ventricles is dependent on passive filling & atrial contraction (pre-load = 135mL)
15
Q
CO
A
CO = HR x SV
- flow out of the heart
- can vary from 5-25 L/min
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
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
18
Q
peripheral vein venous return mechanisms
A
- smooth muscle contraction in response to ↑ SNS allows us to ↑ peripheral venous P w/ no effect on radius: alters compliance ➞ stiffer
- skeletal muscle pump: muscle contracts ➞ squeezes peripheral veins ➞ ↑ venous P ➞ drives bf out to CVP
- venous valves: 1 way valves ensure 1-way flow
- cardiac suction & respiratory pump: ventricles relax ➞ V ↑ ➞ ventricle P↓ ➞ suction
- inspiration ➞ ↑ thoracic V ➞ ↓ intrapleural P ➞ SVC & IVC V↑ ➞ SVC & IVC P↓
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:
- L-type Ca channels ➞ ↑ Ca influx
- SERCa pumps ➞ ↑ rate of Ca removal ➞allows quick relaxation
- troponin ➞ ↑ off rate of tropomyosin ➞ allows thin filament to bind to myosin head
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
21
Q
HR regulation of CO
A
- HR depends on:
- rate of depolarization in the SA node (during phase 4)
- duration of nodal delay in AV node
- 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
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
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
24
Q
↑ SNS input to conduction pathways
A
↑ in conduction velocity → faster impulses
25
↓ SNS + ↑ PNS input to pacemaker SA node
- 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)
26
↓ SNS + ↑ PSNS stimulation to AV node
N region becomes slower to rise → ↓ velocity of pacemaking AP through the node → ↑ AV nodal delay
27
change of contractility & effect on PV loop
- ↑ 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
28
↓ SNS + ↑ PNS stimulation to conduction pathways
slows conduction velocity → slower impulses (slower HR)
29
change in EDV & PV loop
- w/ an ↑ in EDV due to ↑ in venous return → larger SV
- change in SV due to change in EDV from vasoconstriction
30
exercise & PV loop
- 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
31
cardiac fx curve
relates ventricular muscle stretch to the force the muscles can generate
32
combined cardiac & vascular fx curves
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
33
vascular (venous) fx curve
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
34
vascular fx curve: blood volume
- ↑ volume = ↑ mean systemic filling pressure
- ↓ volume = ↓ mean systolic filling pressure
- sweat
- dehydration
- hemmorrhage
35
vascular fx curve: vasoconstriction/vasodilation
- 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
36
mean systemic venous pressure
avg pressure in periphery (~7 mmHg)
* peripheral P varies based on location & forces of gravity
37
vascular fx curve: venoconstriction
↑ SNS changes compliance ➞ stiffer walls ➞ ↑P in peripheral veins
38
MAP
- 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
39
TPR
total peripheral resistance
- affected by:
1. Δ in SNS activity
2. local metabolites
3. local signal factors (i.e. histamines, N.O.)
40
high-pressure baroreceptors
detect BP in elastic arteries (areas of high pressure flow)
1. **carotid sinus**: walls of carotid arteries
2. **aortic arch**
41
low-pressure baroreceptors
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**
42
baroreceptors
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
sensory processing of high-pressure baroreceptors
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
baroreceptor response to a rise in MAP
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
chemoreceptors influences on CO
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
in response to hypoxia
**hypoxia** = PO2 << 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
baroreceptor response to sudden ↓ in MAP
- 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
↑ in SNS output stimulates:
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
↓ PSNS output stimulates
1. pacemaker cells (SA node) → ↑ HR (↑ chronotropy)
2. conductive pathways → ↑ HR (↑ chronotropy)
50
blood flow in an upright standing position:
~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
blood flow in a supine position:
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
in response to an erect position:
- 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
orthostatic hypotension
↓ in MAP from supine → standing
54
CV goal for exercise
↑ bf to specific organs:
- exercising muscle
- coronary circulation
- pulmonary circulation
- cerebral circulation
- cutaneous circulation (for active cooling)
55
CV response to exercise
↑ 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
blood distribution during exercise
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
control of exercise response
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
BP during exercise
- 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
regulation of microcirculation
- 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
EDRF
endothelium-derived relaxation factor: causes arteriolar sm vasodilation & relaxes precapillary sphincters
- released in response to shear stress
- NO
61
autoregulation
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
capillary exchange
- 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
exchange items:
1. solutes that are dissolved in water plasma (glucose, wastes, AA, proteins)
2. gases (O2, CO2, anaesthetics)
3. water
64
gas exchange
- 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
↑ capillary O2 extraction by:
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
what determines gas extraction rate
bf rate & O2 utilization by tissues
- also depends on distance → shorter distances facilitate gas exchange
67
exchange of water-soluble mol & ions
- 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
water-soluble mol & ions solute exchange depends on:
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
basal lamina effect on protein exchange
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
H2O movement across endothelial wall
- 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
paracellular H2O transport
H2O movement via fenestra/pores
72
transcellular H2O transport
H2O movement via aquaporins → AQP1
73
forces influencing H2O movement:
**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
starling law of fluid transfer:
- 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
filtration & net reabsorption across the cap
- **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
solute movement depends on:
1. [gradient]
2. # of pores
3. **kinetic force** → movement of solvent moving solute = **solvent drag**
77
solvent drag
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
what would decrease venous filling of the heart?
an ↑ in ESV
79
an increase in CO in a subject who changed from a supine to a standing position occurred because
this is an actual compensatory response to a drop in MAP that occurs when a subject changes from supine to standing position
80
major problem that arises from an increased afterload
SV is lower than normal
- must use greater force to overcome higher pressure ∴ less force to get blood out
81
compensatory response to a drop in MAP
- ↑ SV
- ↑ HR
- ↑ venous return (vasoconstriction)
82
where are β-adrenergic effects primarily seen?
skeletal muscle
83
what can increase TPR?
- adrenergic stimulation
- vasoconstriction
- increased viscocity
84
what can decrease TPR?
- PSNS stimulation
- vasodilation
- local metabolites
- local signal factors (histamines, NO)
85
⍺-adrenergic stimulation causes
vasoconstriction
86
β-adrenergic stimulation causes
vasodilation
87
which vascular beds exhibit vasoconstriction during exercise?
the splancnic circulation
88
which vascular beds exhibit vasodilation during exercise?
- cerebral circulation
- coronary circulation
- those supplying exercising muscle
89
why is there non-uniform compliance in our venous circulation
it reduces the venous pooling effects in the lower legs
90
peripheral chemoreceptors directly respond to
changes in plasma CO2
91
what would you expect to observe if the autorhythmic cells were treated with an adrenergic receptor agonist?
the L-type Ca2+ channel would be more active than normal
92
what happens if the ventricles are stimulated by a β1-adrenergic agonist?
ESV ↓
- ↑ SA, AV, & ventricular muscular firing ➞ ↑ HR & contractility ➞ ↑ SV & CO
93
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 ↓ PNS input to pacemaking cells
94
what trend would you expect to observe during a 90 minunte exercise period with constant effort?
HR initially rises, levels out, then falls at the end of exercise
95
baroreceptors versus peripheral chemoreceptors
baroreceptors exert a negative drive on vasomotor center causing vasodilation
peripheral chemoreceptors exert a positive drive on vasomotor center causing vasoconstriction
96
if the contractility of the heart ↑ that means that
the heart develops pressure more effectively than normal
97
what region of the CNS CV control center is the primary integrator of afferent info?
the nucleus tractus solitarius
98
the PSNS centers in the CV control center
1. DMNX: dorsal motor nucleus of the 10th cranial nerve
2. NA: nucleus ambiguous
99
the SNS centers in the CV control center
RVLM: rostral ventrolateral medulla
100
According Poiseuille’s law, if vessel A has a diameter twice as large as vessel B, then the resistance of
vessel A is
16x less than B
101
SNS-mediated vasoconstriction
↑ SNS activity to arterioles ➞ ↑ arteriolar R due to NE-binding to ⍺-adrenergic receptors
102
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
103
SV, HR, & CO during exercise
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
cardiac drift
during exercise with constant effort: ↑ in HR to compensate for a ↓ in SV after loss of volume while maintaining a consistent CO
NPB 113
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