exam 2 Flashcards
compliance
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
capacitance
ability to hold/store blood
venous capacitance & compliance
- veins have capacitance
- exhibit high apparent compliance: arises from geometric changes as blood flows in (not stretchiness)
- can add V w/out ↑P
capillary compliance & capacitance
- low capacitance
- low compliance
- if V ↑ ➔ P ↑
- good for filtration (e.g. kidneys)
elastic arteries compliance & capacitance
- low capacitance ➞ not designed to store blood
- stretchy ∴ high compliance
- if we put blood into elastic arteries we ↑P ➔ pressure resevoir
what determines flow into elastic arteries
in-flow: CO
- HR
- SV
what determines flow out of elastic arteries
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
resistance
- 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
arteriolar vsm regulated by:
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
active hyperemia
↑bf to active tissue due to release of local metabolites causing vasodilation
- high blood flow to meet active muscles’ increased need for oxygen
reactive hyperemia
previously occluded tissue had ↓ in bf ∴ ECF has temporary ↑ in metabolites to vasodilate & bring blood back to occluded tissue
venoconstriction
when peripheral veins contract
- resistance is unchanged
- alters stretchiness of vein ➞ ↓ apparent compliance ➞ stiffer = ↑ venous P
- ↑ venous P = ↑ venous return
flow rate out of the heart is proportional to:
cumulative flow rate
stroke volume dependent on
- 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)
CO
CO = HR x SV
- flow out of the heart
- can vary from 5-25 L/min
intrinsic property of the heart
↑ pre-load/EDV = ↑ contractile strength
- built into heart ➞ happens automatically
- dose not require any hormones, drugs, neurotransmitters
- muscle is stretched ➔ automatic greater response
venous return
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
peripheral vein venous return mechanisms
- 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↓
contractility
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
CO during exercise
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
HR regulation of CO
- 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
↑ SNS input to SA node:
- 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
↑ SNS input to AV node:
- in N region (& maybe AN region): AP becomes steeper
- faster conduction through AV node ∴ shorter AV nodal delay
↑ SNS input to conduction pathways
↑ in conduction velocity → faster impulses