Phys Unit 3 - Ch 14

cardiac output

volume of blood ejected by each ventricle each minute

CO =

HR x SV

stroke volume

total blood ejected by the ventricles in one heart beat

BP increases during

vasoconstriction

SV is determined by

contractility (EDV)

preload (venous return)

afterload (total peripheral resistance)

increase in sympathetic activity -->

increased CO (because HR increases)

increase afterload -->

decreased SV

decrease SV -->

decrease CO

total peripheral resistance

vasoconstriction and total resistance in entire blood

BP decreases during...

vasodilation

end diastolic volume (EDV)

volume of blood in each ventricle at end of ventricular diastole (filling)

preload

degree of stretch of the cardiac muscle fibers at the end of diastole

"venous return"

afterload

Resistance heart must overcome to eject blood.

EDV

blood in the ventricle after completely filled

increase EDV -->

increase SV

Frank-Starling Law

The greater the stretch, the stronger is the heart's contraction. This increased contractility results in an increased volume of blood ejected (Increased SV)

Increased EDV results in increased contractility and thus increased stroke volume

optimal overlap

SV =

EDV - ESV

end systolic volume (ESV)

volume of blood remaining in each ventricle after systole

increase heart filling by increased EDV -->

increase venous return --> ....

at rest, heart sarcomeres are ________ at optimal overlap

NOT

stroke volume is influenced by

venous return

factors that influence venous return to heart

pressure differences (between arteries and veins)

sympathetic nerve activity (stimulate smooth muscle contraction and lower compliance)

skeletal muscle pumps (increase --> increase venous pressure --> increase EDV)

blood volume (increase --> increase EDV)

body position

urine volume and tissue-fluid volume impact

blood volume

breathing impacts

negative intrathoracic pressure

negative intrathoracic pressure contributes to

venous return

venous return is directly related to

EDV

sympathetic nerve stimulation contributes to

venoconstriction

venoconstriction and skeletal muscle pump contributes to

venous pressure

What is the mechanism of increasing EDV increasing SV?

Frank-Starling

increased afterload...

decreased SV

increased afterload... ESV

increased ESV

TPR increases...

increased afterload (because it is more difficult to eject blood)

increasing SNS

increases SV (as it increases contractility)

contractility

how hard heart contracts

HR is determined by

altering balance of parasympathetic and sympathetic influence on SA node

HR max

220-age

HR max decreases...

with age

HR - sympathetic nervous system

increases excitement

increases HR

faster depolarizations --> more APs sent --> faster HR

HR - parasympathetic nervous system

lower HR than inherent

stimulates greater contractility (release calcium)

ejection fraction

fraction of blood pumped out with each heartbeat

SV/EDV x 100

normal ejection fraction

50-60%

failure to eject blood

lower than 50% ejection fraction

not getting enough water...

taken from blood

blood volume decreases, BP decreases

osmotic forces

control movement of water between interstitial space/blood

-->

affecting blood volume

water moves to areas of...

high osmolarity (salty)

urine formation, water intake...

impact blood volume

dynamic equilibrium

plasma/interstitial exchange of fluid between capillaries and tissues

components that contribute to plasma/interstitial exchange

hydrostatic pressure

osmotic (oncotic) forces

Starling Forces

hydrostatic pressure

blood in capillary; interstitial

water pressure high in vessel, gets pushed out

osmotic pressure

pulls water out of blood

(deals with proteins in blood (albumin))

high osmotic pressure in interstitium

water goes into capillaries

Starling Forces

blood volume regulation

fluid movements across capillaries dependent on balance of these forces

what do Starling Forces predict?

the movement of fluid out of the capillaries at the arteriole end (positive value) and into the capillaries at the venule end (negative value)

arteriole end of capillaries

delivering lots

high hydrostatic pressure

water pushed out

low oncotic pressure

venule end of capillaries

low hydrostatic pressure

high oncotic pressure

is the return of fluids 100%?

no - 10-15% remains in interstitial spaces

enters lymphatic capillaries, ultimately returns to venous system --> prevents edema, swelling

ADH

antidiuretic hormone (vasopressin)

kidney reabsorbs water

decrease blood volume

increase osmolarity

increases water retention

LESS PEE

increases thirst

responds to low blood volume

secreted by posterior pituitary gland

aldosterone

regulates blood volume

secreted by adrenal cortex

in response to low BP and low blood flow to kidneys

regulated by RAAS

increases reabsorption of sodium

RAAS

stimulates vasoconstriction

increases resistance

increases blood pressure

ANP

atrial natriuretic peptide

produced by atria of heart when stretched

promotes salt, water excretion in urine in response to increased blood volume

inhibits sodium reabsorption and thus inhibits water reabsorption

inhibits ADH secretion

antagonist of aldosterone

what inhibits ADH secretion?

ANP

what is an antagonist of aldosterone?

ANP

lots of urine indicates...

ANP high

blood flow is produced by...

pressure difference

blood flow is...

directly proportional to pressure gradient

blood flows from ______ pressure to _____ pressure

high

low

resistance

how difficult for blood to flow at given pressure distance

F

flow rate of blood through a vessel

F= change in P / R

P

pressure gradient

R

resistance of blood vessels

blood flow is more regulated by...

resistance

vasoconstriction -->

increase resistance

decrease flow

vasodilation

decrease resistance

increase flow

determinants of resistance

blood viscosity, vessel length, vessel radius

longer vessels -->

increase resistance

increase radius -->

vasodilation

decrease radius -->

vasoconstriction

what is the major determinant of resistance to flow?

vessel's radius

slight change in radius -->

significant change in blood flow

LA, LV

high pressure

RA

0 pressure

blood pressure

force exerted by blood against a vessel wall

blood pressure depends on

volume of blood

compliance of vessel walls

compliance

stretchability

systolic pressure

Blood pressure in the arteries during contraction of the ventricles.

higher

max arterial pressure

average = <120

pressure entering vessel

diastolic pressure

min pressure in arteries when blood is draining off into vessels downstream

average = <80

pulse pressure

difference between systolic and diastolic pressure

PP = SBP - DBP

if SBP = 120 and DBP = 80

what is pulse pressure (PP)?

40

mean arterial pressure (MAP)

average pressure driving blood forward into tissues during cardiac cycle

(1/3PP) + DBP = MAP

what is the importance of mean arterial pressure?

assessing blood flow to tissues

(maintaining pressure)

what is the greatest change in pressure in systemic circulation?

arterioles

(greatest ability to constrict and dilate)

systemic circulation BP

120-80

HIGH

greater resistance

pumping everywhere

pulmonary circulation BP

<40

LOW

small

pumping to lungs

TPR

sum of all vascular resistance in systemic circulation

regulated by arterioles

major resistance vessels

arterioles

(because of vasconstriction and vasodilation)

(determination of MAP)

arteriole function

distribute CO among systemic organs, depending on vasoconstriction and vasodilation

arterioles are controlled by

intrinsic and extrinsic factors

intrinsic factors for arterioles

promote constant blood flow

- autoregulation

nitric oxide and arterioles

NO produced by endothelial cells

causes smooth muscle relaxation

vasodilation (OVERRIDES)

extrinsic factors for arterioles

sympathetic NS

epinephrine - vasoconstriction

angiotensin II - vasoconstriction

vasopressin - vasoconstriction