GNUR 156 exam #3

what does the cardiovascular system contain

the heart, blood vessels and blood

what is the order of the system

heart, arteries, arterioles, capillaries, venules then veins

erythrocytes transport what

transport oxygen and carbon dioxide

leukocytes do what

defend body against pathogens

platelets

important in formation of blood clots

pulmonary circuit

right heart, blood vessels from heart to lungs, lungs to heart

systemic circuit

left heart, blood vessels from heart to systemic tissue and from tissue to heart

pulmonary capillaries: blood entering lungs

deoxygenated

pulmonary capilaries: blood leaving lungs

oxygenated

systemic capillaries: blood entering tissue

oxygenated

systemic capillaries: blood leaving tissues

deoxygenated

normal direction of flow

atria to ventrcles and ventricles to arteries

AV valves

right = tricuspid

left = bicuspid - mitral

semilunar valves

aortic and pulmonary valve

autorhythmicity

ability to generate own rythm

autorythmic cells

provide a pathway fro spreading excitation through heart

pacemaker cells

depolarize membrane potentials generate action potentials

coordinate and provide rhythm to heartbeat (SA and AV node)

conduction fibers

rapidy conduct action potentials initiated by pacemaker cells to myocardium (internodal pathywas, bundle of his, purkinje fibers)

spread of excitation through cells

atria contract then ventricles contract, corrdination is there because of gap junction and conduction pathways

initiation and conduction of impulse 1

1. action potential initiated in SA node; signals spead through atrial mucle via interatrial pathways

initiation and conduction of impulse 2

signal travels to AV node via internodal pathway; AV nodal delay

initiation and conduction of impulse 3

bundle of his

initiation and conduction of impulse 4

splits into left and right bundle of branches

initiation and conduction of impulse 5

purkinje fibers

P wave

atrial depolarization

QRS complex

ventricular depolarization and atrial repolarization

T wave

ventricular repolarization

PQ segment

av nodal delay

QT segment

ventricular systole

QT interval

ventricular diastole

first degree heartblock

slowed diminished conduction through AV node occurs in varying degrees

increases PQ segment duration

increases delay between atrial and ventricular contraction

second degree heart block

slowed sometime sstopped conduction throguh AV node

loses 1 to 1 with P wave and QRS complex

loses 1 to 1 between atrial and ventriicular contraction

third degree heart block

loss of conduction through AV node

P wave becomes independent of QRS

Atrial and ventiricular contractions are independent

systole

ventricle contraction

diastole

ventricular relaxation

what valve opens when atrial pressure is greater then ventricular pressure

AV valve

what valve opens when ventricular pressure is greater then atrial pressure

semi lunar valve

ventricular filling

av valve opens

blood moved from atria to ventricle

pulmonary and aortic valves are closed

middle of ventricular diastole

isovolumetric contraction

start of systole

ventricle contracts increasing pressure

av and sl valves closed

no blood entering or exiting

ventricular ejection

remainder of systole

pressure in ventricles is greater then pressure in arteries the semilunar valve opens

pressure in aorta is greater then pressure in ventricules semilunar valves close

isovolumetric relaxation

diastole

ventricle relaxes decreasing pressure

av and sl valves closed

no blood entering or exiting

stroke volume

volume of blood ejected from ventricle each cycle

EDV - ESV

ejection fraction

fraction of end distolic volume ejected during a heartbeat

SV/EDV

factors that can affect cardiac output

change in heart rate, changes in stroke volume

what is cardiac output

volume of blood pumped by each ventricle per minute

CO = SV x HR

average is 5L

extrinsic control of cardiac output

neural and hormonal

intrinsic control of cardiac output

auto regulation

what neurotransmitter beats your heart faster

epinephrine and glucagon

factors affecting stroke volume

ventricular contractility, end distolic volume, after load

epinephrin binds to..

B1 adgrenergic receptors

what hormones can increase force of contraction

thyroid hormones, insulin, glucagon

starlings law

the hearts storke volume increases as the end distolic volume increases

factors affecting end distolic volume

filling time, atrial pressure and central venous pressure

after load

pressure in aorta during ejection

flow equation

P/R

bulk flow

flow due to pressure gradients

factors affecrting resistence to flow

radius of vessel, length of vessle and viscosity of fluis

vasocontriction (2 things)

decreased radius leads to increased resistance

vasodilation

increased radius leads to decreased resitance

total peripheral resistance

combines resistance of all blood vessels within the systemic circuit

arteries

carry blood away from the heart

veins

return blood to the heart

compliance

measure of how the pressure of a vessel will change with a change in volume

pulse pressure equation

SP - DP

BP equation

SP/DP

MAP equation

SP + (2 x DP)/3

vasoconstriction: increased contraction…

decreased radius

vasodilation: decreased contraction…

increased radius

changes with increased metabolic activity generally cause vasodilation

carbon dioxide, oxygen, hydrogen ions

changes with decreased metabolic activity generally cause vasocontriction

oxygen

active hyperemia

increased blood flow in response to increased metabolic activity

with active hyperemia in a steady state…

O2 is delivered as fast as it is consumed

CO2 is removed as fast as it is produced

when active hyperemia is in an icreased metabolic rate

O2 is consumed faster than it is delivered

CO2 is produced faster than it is removed

what repsonds to low O2 and CO2

vasodilation

reactive hyperemia

increased blood flow in repsonse to previous reduction in blood flow with activitys such as crossing your legs

mygenic response

change in vascular resistence in response to stretch of blood vessels in the absence of external factors

what is the purpose of myogenic autoregulation

keep blood flow constant

norepinephrine binds to

A adrenergic receptors (vasoconstriction)

ADH does vasoconstriction or dilation

vasoconstriction

metaarterioles

directly connect arterioles to venules

intermediate between arterioles and capillaries

exchange across capillary walls

diffusion

factors affecting filtration and absorption across capillaries

standing on feet, injuries, liver desease, kidney disease and heart disease

increased blood volume

increased venous pressure

decreased blood volume

decreased venous pressure

regulation of mean arterial pressure

neural and hormonal control

if normal is higher then MAP

hypotension

if MAP is higher then normal

hypertension

short term regulation seconds to minutes

regulates CO and TPR, involves the heart and blood, primarily nerual control

long term control minutes to days

regulates blood volume, involves the kidneys, primarily hormonal control

vasopressin and angiotensin II

vasoconstriction, increases TPR and increases MAP

when breathing in

raises sympathetic activity and raises heart rate

when breathing out

raises parasympathetic activity and lowers heart rate

average blood volume

women = 5.0L men = 5.5L

erythrocytes

no nucleus, organelles, mitocondria, or anerobic glycolysis

what do erythrocytes transport

transport O2 and CO2

Heme is

an iron containing group that greatly increases oxygen transport

when are erythrocytes synethesized

in red bone marrow

where are erythrocytes filtered

by the spleen (and liver)

eryrocyte synthesis is stimulated by what

erythropoetien

what removes old erythrocytes

the spleen