Elastin

Collagen

Smooth muscle

endothilial cells

Vessels

Elastic (windkessel)

Resistive

Exchange

Capacitance

elastic (windkassel vessels: abundent elastic fibers, smooth muscle and collagen

Resistive vessels: arterioles & precapilary sphyncters, highest wall thickness, high ability to control blood flow

Exchange Vessels: capilarys, 1 layer endothelial, good diffusion of substrates

Capacitance Vessels: veins, high colagen fibers, some smooth muscle.  thin walls.  regulate volume rather than pressure

effects on pressure

arteriolar constriction

arteriolar dilation

arteriolar constriction: high pressure in arteries, low pressure in veins (big ΔP)

Arteriolar dilation: low pressure in arteries, high pressure in veins (small ΔP)

Compliance

what

which vessels

what bornes the load

Δv/Δp higher the slope, more compliance

Veins have high compliance, arteries have low complance, high resistance

load on vessel walls first borne by elastin and smooth muscle, and lastly by colagen

Peripheral runoff:

Systolic pressure:

Diastolic Pressure:

Pulse Pressure:

Peripheral runoff: transfer of blood from arterial circulation to capilaries & veins during diastole

Systolic pressure: peak aortic pressure

Diastolic pressure: lowest arteriolar pressure before ventricular ejection.  Dependent on arterial compliance & residual arterial volume

Pulse Pressure: SP-DP

Mean Arterial Pressure

average pressure of blood profusing capilaries during cardiac cycle

MAP = DP + PP/3

Q= ΔP/R

Q= Cardiac output

ΔP= Mean Atrial Pressure-Right Atrial Pressure

R= TPR (Total Peripheral Resistance)

MAP= (HR X SV)X TPR

Qh>>Qr

Qh<<Qr

Qh>>Qr=high atrial pressure

Qh<<Qr=low atrial pressure

Qh=cardiac output

Qr=runoff

ΔP=ΔV/C

ΔP: change in pulse pressure

ΔV: ejection of stroke volume

C: complicance

low stroke volume: effect on PP and SP

high stroke volume: effect on PP and SP

high compliance: effect on PP and SP

low compliance: effect on PP and SP

low SV:low PP, low SP

high SV: high PP, high SP

high C: low SV, low SP

low C: high SV, high SP

<from supine to upright>

Δvein and artery pressure:

bloodflow:

Δvein and artery pressure: no change

bloodflow: from thorax to feet

nuscle contraction of feet squeeze veins to release blood

muscles squeeze vains to release blood to heart, facilitates ventricular filling, increase stroke volume

also increases blood flow through capilary bed

Arterial Baroreceptors: sense arterial BP

Arterial Stretch receptors: sense Volume

fast acting, respond to low BP (MAP)

senses MAP and Pulse Pressure

sensors at arch of aorta and carotid sinus

Afferent: aorta->vagus->brainstem.  caroted sinus->glosopharyngeal nerves-> brainstem

Integration: info enters brainstem via NTS

Efferent: to heart: vagus, to others: adrenal medulla nto relese NE for sympathetic

increase fireing of baroreceptors

Body: decrease sympathetic, result in vasodilation. lower TPR

Heart: increase vagal tone (PNS), reduce sympathetic to SA node.  lower HR, less CO

lower fireing of Baroreceptors

Body:increase sympathetic to arterial vasculature and splanchnic veins.  vasoconstriction, splanchnic venoconstriction, raise TPR

Brain: decrease vagal tone (parasympathetic), increase Sympathetic to SA and cardiac muscle.  increased HR and SV, raised CO

peripheral chemoreceptors at carotid bodies get most blood/area of body. 

activated by low pO₂ high pCO₂ low PH

receptor->glossopharyngeal->brainstem->NTS

efferent: via vagus or sympathetic

sense low O₂ high CO₂ low PH

Body: increase sympathetic to raise TPR to raise BP

Heart: increase ventilation, increase sympathetic to heart, raise HR and CO to increase BP

Atrial Stretch receptors at atria and junctions of veins with atria

sense atrial filling.  high venous volume: high fire

high stretch receptor response

inhibit sympathetic nerve to kidney (more water loss).  inhibit (vasopressin conserves water)

increase release of ANP so lose more Na & H₂O

increase sympathetic to kidney

more vasopressin release

less ANP release

low BP: P_c decreases, fluid moves from interstitial to capillaries

High BP: P_c increases, fluid moves out of capillaries into interstitial

renin (from kidney) turns angiotensinogen (from liver) into angiotensin1.

ACE (in lung/kidney) turns Angiotensin 1 into angiotensin2.

angII stimulates aldosterone release

final result: Na/H2o reabsorption

Kidney and cardiovascular systemm

by adjusting water/salt loss

Hypovolemic shock

low resistance shock

cardiogenic shock

hypovolemic shock: loss of volume/hemorrhage

low resistance shock: Distributive shock.  septic infection

Cardiogenic Shock: extreme type

MAP drops since low venous return,SV,CO

compensate: baroreceptors unloaded-> withdraw vagal tone-> activate sympathetic-> increased HR/TPR/venous constriction

rteries sense-> release vasopresin-> more angiotensinII-> aldosterone

"venous pooling"

sense less venous return,less CO, less BP

baroreceptor activated-> sympathetic response-> more HR. TPR

Vasovagal syncope

fainting

ICF

(intracellular)

ECF

(extracellular cell fluid)

interstitial

Plasma

ECF: 1/3 main cation is Na

Interstitial: 3/4 of ECF or (1/4 of total)

Plasma: 1/4 of ECF or (1/12 total)

number of particles.

water goes from low osmolarity to high osmolarity

pressure to stop water flow

high osm, high osm pressure

hyponatrimic

hypernatrimic

hyponatrimic: plasma Na<135

hypernatrimic: plasma Na >145

volume of blood ejected in one contraction

SV=EDV-ESV

EDV: end dystaloc volume (volume after fillng)

ESV: end systolic volume (volume after ejection)

Cardiac output

Cardiac Index

blood flow/time

CO=SV X HR

Cardiac Index

cardiac output/BSA

work of the heart for 1 contraction

SW=VPP X SV

VPP: ventricule pulse pressure, peak pressure - end diastolic pressure

comparing left and right

SV

CO

SW

left SV =r ight SV

Left CO = right CO

left SW > right SW

Preload

what is it?

how is it measured?

what influences it?

what tension in ventricle walls at the end of diastole

(tension of the walls at the most relaxed state)

determines resting fiber length.

measure ventricular EDV or EDP

effectors: filling time, compliance, filling pressure, atiral contractility, pericardial restraint

pressure gradient between introthorasic pressure and central venous pressure

affects right ventricle gradient

Drug treatment for the heart

Cardiac Inotropic drugs:

Vasodilators

ACE inhibitors

Beta Blockers

Cardiac Inotropic: increase contractility, digitalis

Vasodilators: lowers BP, so less P for heart to pump against.  isosorbine, hydralizine

ACE Inhibitors:type of vasodilator.  lower BP->help heart.  Captopril, Benazepril

Beta Blockers: blcok beta adrenergic receptor, limits sympathetic stimulation.  Propranalol, metoprolol

upper 8 segments of thorasic

conects to SA,AV,and myocardium

right side: HR

Left side: contractility

brainstem-> vagus nerve

SA,AV,Myocardium

right= SA heart rate left=AV conduction

uses Acetylcholine (muscarinic, cholinergic)

small effect on ventricles b/c fewer receptors

most β₁ some β₂

small effect on coronary vascular smooth muscle

main effect: increased HR, contractility,relaxation

NE->cAMP->activates protein kinase-> phosphorylates stuff to allow

1.) L type Ca channels (+ inotropic)

2.) phospholambam increase SR to uptake Ca (faster relax, faster fire)

3.)contractile proteins Troponin+P less Ca sensative

main receptor is M-2

ACH->G protein-> activate signaling pathway

1.) inhibits adenyl cyclase to lower cAMP

2.) Stimulate Guanylate Cyclase to increase cGMP to counter cAMP resulting in less Ca current

3.) activate K channels in Atrial only.  effects HR, not contractility

increase HR because cAMP stimulates Ca channels and cation channels "funny current"

increase slope of pacemaker potential (faster depolarization)

Small Arteriole

Terminal arteriole

Metarteriole

capillaries

postcapillary venules

Small Arteriole:precapilary systemic control, highly innervated, vascular smooth muscle.  alter diamater of lumen for control

Terminal Arteriole: less inervation, greater local control, smooth muscle, alter diamater for control, branches into capillaries

Metarterioles: "thoroughfare" conect small arterioles to venules.  branches into capilaries, blood bypasses capilary by going through metarteriole. 

Capillaries: slowest flow, autonomic, neural, and local metabolic control.

Postcapillary Venules: some gas exchange may happen

non nutritive flow

nutritive flow

non nutritive: through metarterioles, low metabolic exchange

Nutritive: high exchange, flow controled by arteriole and precapillary sphyncters

continuous capillaries:

Fenestrated capillaries:

Discontinuous capillaries:

Continuous: in muscle, skin, lung,fat,CT,and neural.  intercellular clefts between endothelials, hydrophylic molecules pass through, not in blood-brain, fenesterae.

Fenesterated: suround epithelial, kidney, intestine, endocrine glands.  endothelial cells have fenesterae large pores.  hydrophylics molecules pass through

Discontinuous: in sinusoid like bone marow, liver, spleen.  big gaps between endothelials, permiable to large and small hydrophylics.  gaps have basement membranes

capilary recruitment: increase SA, decrease diffusion distance

increase conc gradient: as tissue use more substrate, bigger gradient

increase bloodflow: greater delivery of substrate maintains gradient.

<capillary hydrostatic pressure>

small post/pre pressure

big post/pre pressure

small post/pre=small Pc favors absorption

big post/pre=big P/c favors filtration

arteriolar vasodilation

arteriolar vasoconstriction

arteriolar vasodilation: histamine release raises Pc, so favors filtration

arteriolar vasoconstriction: SNS activation, lowers Pc favor absorption

drops in plasma protein concentration

congestive heart failure

adding an IV

drops in plasma protein: liver disease or burns, lowers capillary osmotic pressure, favors filtration

CHF: raises Pc favors filtration

adding IV: lowers Pc, favors absorption

Metabolic theory: when flow increases, and perfusion pressure increases, vasodilator metabolites from tissue are washed away, so vasoconstriction happens.  when flow/profusion decreases, vasodilator metabolites build up again.

Myogenic Theory: increased pressure causes increased wall tension, so smooth muscle contract to raise resistance

Flow Limited

high local control (trumps hormonal)

aortic pressure provides driving force for flow

coronary BF is praportional to Myocardial O₂ consumption (MVO)

use vasodilator Adenosine

only 20% of bloodflow in systole

neural control dominates at rest

metabolic control dominates when exercising

functional hyperemia

sympathetic releases blood from liver

parasympathetic causes motility so functional hyperemia

low autoregulation.  mostly metabolic

strog tonic activity

constricts arterio venous anastomes  to release blood

sweat glands: sympathetic cholinergic release bradykinin

Venous plexus: greatest blood reservoir

autoregulates and reactive hyperemia

high autoregulation

functional hyperemia

if low CO₂ bloodflow to brain will lessen

if low O₂ dilation.  high O₂ no effect

high K causes vasodilation

Adenosine vasodilation

NO vasodilation

tumor: sympathetic vasoconstriction

under basal conditions maintains blood flow

adjust flow for metabolic needs

Tone

basal tone:

resting state:

Tone: contractile state of resistance on a vessel

basal tone: partial contraction, independent of neuronal and metabolic mechanisms, result of intrinsic properties of vessel

resting state: at rest.  most arteriolar vessels are constricted more than basal b/c tonic sympathetic nerve activity.  so if no SNS, vessels will pasively dilate/relax.

endothelium mediated control

flow induced:

flow induced: high blood flow increases sheer stress on endothelium, endothelium releases NO/PGI2 (dilators), decreases  endothelim (constrictor), so vasodilation

a subject is given a medication that:

Increases LV stroke volume

Decreases HR

Does not change cardiac output or TPR

the result of the drug is...

this blood vessel has

smooth muscle

reacts to synpathetic and vasoactive metabolites

controls distribution of CO of tissues & organs

a drug is administered that:

decreases systolic volume

and does not effect diastolic volume, diastolic pressure, and P-P interval

the drug acts by...

A drug has the effect of

Increasing HR

no change for stroke volume

TPR doesnt change

as a result of this...

during exercise, a patient's

MAP remains constant

CO increaed from 5 to 15

this can occur because of..

a drug is administered that:

decreases end-systolic volume

but no change to end-diastolic volume, end diastolic pressure, P-P interval