in arotic arch and corotid arteries - respond to change in BP -> transmit info to CNS via CN IX, and X - dec. BP -> PSNS inhibition and cardiac SNS activation -> increased HR - increased BP -> PSNS activation and SNS inhibition

blood flow and innervation Flashcards by Chelsey Miller

Sympathetic nervous system

innervation widespread to all areas of heart

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Parasympathetic NS

innervation of SA and AV nodes by vagus nerve

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SNS effect

chronotropic: increase HR
dromotropic: increase speed of conduction
inotropic effect: increase force of contraction
iusitropic: relax more quickly
– release of NE, binds to B receptors
— -> increased cAMP

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PSNS effect

decrease HR
decrease speed of action potential conduction
- ACH binds to muscarinic receptors
– inhibits cAMP
– increases K permeability: increased efflux
increase vagal stimulation -> dec. HR
– vasovagal response: dizzy, fainting

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blood flow determined by

driving pressure

vascular resistance

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ohm’s law

increased driving pressure (P) -> increased blood flow (Q)
increased resistance (R) -> decreased blood flow (Q)
Q= P/R

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coronary blood flow: driving pressure

determined by aortic BP and right atrial pressure

inc. aortic BP -> increased coronary blood flow
increased right atrial pressure -> decreased coronary blood flow

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coronary blood flow: vascular resistance

2 determinants

coronary artery diameter
external compression r/t myocardial contraction/relaxation

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vessel autoregulation

intrinsic ability of arteries to adjust bloodflow r/t tissue needs

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SNS and vessel

NE binds to A1-> vasoconstriction

NE binds to B2 -> vasodilation

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CO =

HR x SV

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SV influenced by

preload
contractility
afterload

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preload

volume in heart

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afterload

resistance of vasculature

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SNS activated by

inadequate blood pressure, lack of O2, buildup of metabolic end products

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baroreceptors

in arotic arch and corotid arteries

respond to change in BP -> transmit info to CNS via CN IX, and X
dec. BP -> PSNS inhibition and cardiac SNS activation -> increased HR
increased BP -> PSNS activation and SNS inhibition

Bainbridge reflex

sensory fibers within heart chanbers

respond to chang in intrachamber pressure (blood volume)
over distention -> dec. PSNS and inc. HR

end diastolic volume

blood in ventricles just before contraction

- ventricles usually eject 60-70% , while 30-40 remains in ventricle

Frank starling law (length-tension relationship)

increased preload (blood volume) -> increased stretch -> increased force of contraction

stretching of muscle fiber -> myosin and actin more closely aligned, more cross bridge formation -> stronger contraction
only works to a certain point, then plateaus

contractility 3 factors

amounts of contractile proteins in muscle cell
availability of ATP
availability of free Ca

cardiac workload

hearts O2 requirements/ ATP requirements

Poiseuille’s Law

resistance = viscosity x length x 8/ radius
greatest resistance to blood flow is vessel radius and length
- greatest resistance in the smallest vessels; arterioles

velocity and cross sectional area

branching of arterial vessels increases total cross-sectional area and thus dec. velocity of blood flow

laminar flow

streamlined, blood flows smoothly.
walls slow flow.
fastest in middle

turbulent flow

``` results from pathologic conditions - coarctation (narrowing) - valvular abnormalities - low blood viscosity (anemia) Associated with murmurs or bruits Produces increased pressure gradient ```

S1/ lub

ventricular contraction/ systole | - blood hitting AV valves causes them to close

S2/ dub

atrial contraction ventricular filling - blood against semilunar valves causing them to close.

``` increased blood volume stiff chordae tendineae heart failure "kentucky" gallop - blood hitting other structures within ventricle ```

Atrial Kick turbulent blood flow against stiffened ventricular walls atrial contraction trying to overcome hypertrophic ventricle "tennessee" gallop

Increased contractility

NE not r/t blood volume r/t number of contractile proteins allows for ejection of more blood

increased afterload

ventricle has to overcome more pressure - > decreased SV ejected - aortic valve closes sooner d/t increased BP

Cardiac myocytes

2 types - working cells: mechanical pumping function - electrical cells: transmit electrical impulses

differentiated myocytes

unable to proliferate - increase in size - increase contractile proteins stem cells -> myocyte to create moree

intercalated disk

joins 2 sarcolemmas, contains gap junctions

functional syncytium

separate cells working together

Striation of cardiac cells

d/t structure of proteins (myofibril) of contractile apparatus - myosin - actin - - titin: hold myosin filaments in place

ANP

atrial natriuretic peptide | - released from myocytes in response to atrial stretch (inc. BP)

BNP

B-type natriuretic peptide | - released from ventricular myocytes r/t chronically over distended ventricles

ANP and BNP cause

Na and H2O excretion in kidneys | - renin-angiotensin-aldosterone system antagonist