IU P225 Physiology Exam 3

3 main components of cardiovascular system

heart, blood vessels, blood

the heart

generates the pressure

blood vessels

highway system (the route)

blood

vehicles (cars on the highway)

3 types of blood vessels

arteries, capillaries, veins

arteries

take blood away from the heart

veins

take blood to the heart

capillaries

site of exchange

trick question: all veins are oxygen poor and all arteries are oxygen rich

typically true BUT there are exceptions; not always true

plasma

92% water, 7% electrolytes, proteins

albumin (plasma protein)

from liver; colloid oncotic pressure

globulin (plasma protein)

from liver and lymphoid tissue; clotting factors

fibrinogen (plasma protein)

from liver; forms fibrin threads for clotting

transferrin

from liver and other tissues; iron transport

erythrocytes

red blood cells; bi-concave disks that carry oxygen

leukocytes

white blood cells; irregularly shaped and fight infections

platelets

round or oval shaped and facilitate clotting

hematocrit

portion of your blood make of red blood cells; men have higher % than women due to no menstruation (42-52% vs 37-47%)

pacemaker cells

affect heart rate; sets the pace for heart rate

3 phases of pacemaker cell action potentials

1. drift: sodium influx

2. depolarization: calcium influx

3. repolarization: potassium efflux

(always voltage-gated channels!)

drift phase of cardiac pacemaker action potential

allows for generation of spontaneous action potential; most important phase

SA node

true pacemakers; signals AV node & contracts right atrium; fires every 1 second

AV node

accepts signals from SA node, signals bundle of His; fires every 2 seconds

bundle of His

pathway from AV to ventricles, signals bundle branches and purkinje fiber; fires every 3 seconds

purkinje fibers

sends signals through ventricles, causes ventricular contractions; fires every 3 seconds

SNS effect of cardiac pacemaker cells

norepinephrine binds to beta 1 adrenergic --> increases sodium permeability and drift phase slope --> threshold reached sooner --> increased HR

PNS effect of cardiac pacemaker cells

acetylcholine binds to muscarinic receptors --> increases potassium permeability --> decreases drift phase slope --> threshold reached later --> HR decreases

how many channels are open at rest during drift phase?

three; ligand-gated sodium and potassium, voltage-gated sodium

what causes drift?

sodium influx

what happens if someone is given atropine, a muscarinic cholinergic antagonist?

increased HR due to increased potassium flow

4 phases of cardiac muscle cell action potential

1. depolarization: Na+ influx

2. early repolarization: K+ efflux

3. plateau: Ca2+ influx, K+ efflux

4. repolarization: K+ efflux

plateau phase

lengthens time of action potential; allows for relaxation of heart and ventricles to fill up before subsequent contraction (prevents overwork)

ryanodine receptors

action potential activates voltage-gated calcium receptors; Ca2+ influx from SR --> more cross-bridges --> more force of contraction

SNS effect of cardiac muscle cells

causes more Ca2+ influx into SR --> reduces refractory period --> allows more frequent/stronger contractions

sympathetic pacemaker

sodium

parasympathetic pacemaker

potassium

sympathetic cardiac muscle

calcium

two primary variables of the heart

strength and speed of contractions

isovolumic

constant volume!!! all valves closed!!!

4 phases of cardiac cycle

1. filling: volume increases

2. iso.vol. contraction: no change in volume

3. ejection: volume decreases

4. iso.vol. relaxation: no change in volume

5 variables of wiggers diagram

1. pressure 2. volume 3. heart sounds 4. EKG 5. vavles open/closed

ejection volume changes

volume decreases because SL valve opens

isovolumic relaxation volume changes

constant because all valves closed

filling volume changes

volume increases because AV valve opens

isovolumic contraction volume changes

constant because all valves closed

when are both sets of valves open together?

never; would cause chaotic blood movement

valve opening and closing

each valves only open for one phase, track -- will be closed for next phase

causes of pressure changes in left ventricle

contraction: pressure up

relaxation: pressure down

add more blood: pressure up

blood leaves: pressure down

what causes ventricular pressure to change during isovolumic contraction?

increased contraction

what causes ventricular pressure to change during filling?

increased blood volume

ejection pressure changes

increases then decreases; ventricle contracting entire time but 2nd half blood volume decreases (so pressure decreases)

isovolumic relaxation pressure changes

decreases because ventricle is relaxing

filling pressure changes

increases because blood volume increases

isovolumic contraction pressure changes

increases because ventricle is contracting

cardiac output

amount of blood pumped from the heart per 1 minute

according to frank-starling law, as venous return increases...

stroke volume increases

what phase of the cardiac cycle shows pressure increases but blood volume remaining constant

isovolumic contraction

ejection EKG/waves

none

isovolumic relaxation EKG/waves

t-wave because ventricles repolarizing

filling EKG/waves

p-wave because atria depolarizing

isovolumic contraction EKG/waves

QRS complex because atria repolarizing and ventricles depolarizing

what causes valves to close?

changes in pressure

end of ejection

SL valve close because aorta pressure > ventricular pressure; dub heart sound

end of isovolumic relaxation

AV valve open because atrial pressure > ventricular pressure; no sound

end of filling

AV valve close because ventricular pressure > atrial pressure; lub heart sound

end of isovolumic contraction

SL valve open because ventricular pressure > aorta pressure; no sound

between what 2 phases does lub sound occur?

between filling and isovolumic contraction

between what 2 phases does dub sound occur?

between ejection and isovolumic relaxation

only time when ventricular pressure exceeds aortic pressure?

ejection

only time atria is contracting

during filling

cardiac output equation

cardiac output = heart rate x stroke volume

PNS effects on heart heart

acetylcholine to muscarinic receptor on SA node --> potassium efflux during drift --> decrease HR and cardiac output

PNS efforts on stroke volume

none

SNS effects on heart rate

norepinephrine to B1 receptor on SA node --> sodium influx during drift --> increase HR and cardiac output

SNS effects on stroke volume

norepinephrine to B1 receptor on ventricular cells --> calcium influx during plateau --> increase SV

beta blocker effect on HR and SV

decreases because blocks sodium and calcium influx

what causes systolic blood pressure?

blood leaving the left ventricle

what causes diastolic blood pressure?

elastic recoil of arteries

blood pressure generally refers to what aspect of cardiovascular system?

arteries

what factors cause increased blood pressure?

part rate, stroke volume, cardiac output

does end diastolic volume affect preload or afterload?

preload

preload

amount of pressure in the ventricle prior to contraction

afterload

pressure the ventricle has to contract against

end-diastolic volume

amount of blood in the ventricle prior to contraction

end-systolic volume

amount of blood in the ventricle after contraction

pressure equation

pressure = flow x resistance

flow equation

flow = pressure / resistance

factors that influence resistance

radius (arteriole radius), viscosity (thickness of fluid; increased = greater resistance), vessel length (longer = greater resistance)

what are the resistance vessels?

arterioles; have the greatest effect on mean arteriole pressure (MAP)

vasoconstriction

decreased radius

vasodilation

increased radius

local factors that affect vasodilation

temperature, oxygen, carbon dioxide, blood flow

hormonal factors that affect vasodilation

renin, angiotensin, vasopressin, atrial natriuretic peptide (ANP)

neural factors that affect vasodilation

amount of sympathetic activity

cardiac output equation

MAP / TPR

MAP equation

HR x SV x TPR

decreasing radius by half will cause resistance to increase by a factor of...

16

vessel diameter

distance accros diameter; decreased = increased resistance

cross-sectional area

area of sliced portion of vessel; decreased CSA = increased resistance

blood pressure

force exerted by the blood