Glossary of pHYS

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what causes driving force for unidirectional movvement of blood throughout body
pumpin of heart
site of exchange
cap. almost all cells in body are within a few cell diameters of the cap
two major components of circulartory system
pulmaonary and systermic
CO of brain
650 ml/min about 13% of total
CO of heart
215 ml/min 4% of total
CO of skeletal muscle
1030 mL/min about 20% of total
Skin CO 430 mL/min
9 % of total
Kidney CO
950 ml/min or 20% of total CO
Abdominal CO
1200 ml/min or 24% total CO
total CO per min
5000 mL/min
What happens to O2 and CO2 at perephereal system?
O2 leaves the blood and enters the interstitial space and CO2 leaves the interstial space to enter the blood
What happends to O2 and CO2 in pulmonary system?
Blood flowing through lungs picks up O2 from alveoli and CO2 leaves blood and enters alveoli
Describe blood flowing through GI
pu nutritens and delivers them to the interstial space. Metabolic waste entersthe blood from the interstial sapce and is delived to organs for elimination
How does blood flow?
from a region of higher hydrostatic pressure to a region of lower hydrostatic pressure. the difference between the higher and lower pressure is the pressure gradient
pressure gradient
difference between hi hydrostatic pressure and lo hydrstatic pressure
What happens if increase pressure gradient
increase the blood flow
2 things blood flow must overcome
viscosity and resistance
What causes resistance to blood flow?
shear forces that exist between the blood and the vessel wall and viscosisity of blood
Resistance equation
R=(nL/r4) (8/pie)

n is viscosity is L is blood vessel length, r is radius of blood vessel
Must important factor of blood flow resistance
the radius of blood vessel because it is raised to the fourth in the equation. A little change in the blood vessel radius casue a large change in the blood flow
what happens with blood O2 at lungs?
picks up O2 from alveoli and CO2 leaves the blood and enters the alveoli
What happens with blood O2 at the periphery?
Describe blood through the GI system
PU nutriets in GI and delivers them to the interstitial space.Metabolic waste products enter the blood from the interstidal space and are delivered by the blood to many organs for elimination from body
Where are nutrients picked up by the blood stream?
in the GI, mainly the SI, delivers nutrients to periphereal tissue
increase BP does what to blood flow
increases blood flow
what does ventricles do to hydrostatic pressure?
hyrostatic pressure of blood is increased by ventricle action
driving force of blood flow to perephei and lungs
pressure increase casued by ventricle contraction
how is blood flow measured?
units of vol/time
Does blood viscosity change under normal conditions?
no the length of the blood vessel doesnt either
Basic equation that related blood flow to pressure and resistance
F= P/R

Flow is directly porportional to pressure
gradient and inversely proportional to the vascular resistance
four chambers of heart
left atrium, left ventricle, right atrium, and right ventricle
what composes wall of heart?
cardiac muscle cells called myocardium
inner surface of the cardiac chambers
endothelial cells
mitral valve
between the left atrium and the left ventricle. allows blood to flow from the atrium into the ventricle. The valve opens passively when blood pressure in left atrium is higher than the BP in the left ventricle. if blood tries to move back from the left ventricle into the left atrium the valve closses
what prevents the mitral and tricuspid valve from being pushed back and causing blood to go back into the left atrium
papillary muscles
ouflow valves
pulmonic valve on R and aortic valve on L
tricuspid valve
located between right atrium and right ventricle and only allow blood to go from atrium to ventricle. Valve open when more pressure in right atrium than ventricle.
aortic valve
between left ventricl and aorta. only open when blood pressure is higher in L ventricle than aorta opens passively and allows blood out of aorta. valve closes if pressure increases in aorta
Pulmonic valve
located between right ventricle and pulmonary trunk and nly allows blood to go from venticles into pulmonary trunk. Valve opens when BP in right ventricle is higher than the BP in pulmonary trunk. If blood tries to move back from the pulmonary trunk int the R vnetricle, the valve closes passively
AV valves
mitral and tricuspid valve
Describe cardiac muscle
striated like skeletal m but indiviual cells are shorter than skeletal m.
What joins cardiac muscle cels end to end
intercalated disks
what is adjacent to intercalated disks in cardiac muscles?
gapjunctions permits cell to cell conduction of action potentias
what innervates heart?
PS and Symp
primary sympathetic NT and receptor
Norepi and Beta receptors
primary PS NT and receptro
ACH to M receptor
BF to Cardiac muscle
Coronary A.
BF away from heart
coronay sinus which enters in right atrium
two things that must occur for effective heart pumping
Both sides of the heart must be activated to beat in some sort of regular fashion and on each side of heart, the atrial pump must be activated befor ventricular pump is activated
SA node
cardiac cell with pacemaker activity that spontaneously depolarizes/repolarizes. locarted in R atrium near SVC. it produces Cardiac AP causing contracton
What sets heart rate?
SA node, pacemaker of heart
what initiates heart beat?
SA node
Conduction of contracton
SA node depolarizes and causes both atria to depolarized and contract simultanelously. AV node depolarizes at base of R atrium and cases ventricles to depolarize. Budle of His splits to pukinje fibers at apex cause rapid contraction
only electrical connection between atriia and ventricles
AV node
Conduction of AP through AV node
V. slow allowing the atrial contractions to be completed before ventricular depolarization occurs
bundle of His
divides into L and R. at apex purkinje fibers get AP and rapid contracton occurs
fasted part of conduction
slowest at AV node, fastest at Bundle of His
resting membrane potential of cardiac muscle cells
- 90 mV
What does action potential consist of?
A period of rapid depolarization and a period of rapid repolarization.
distinctive feature of cardiac aaction potential
plateu phase exists between depolarization and repolarization causing a long action potential
five named phases of cardiac action potential
phase4 resting memebrane potential
phase0 rapid depolarization
phase1 initial repolarization
phase2 plateau
phase3 final repolarization
what does rapid depolarizaton of cardiac muscle cell cause?
opening of voltage gated sodium channel when increase sodium permeabiity and siultaneous decrease in potassium permeabiity.
What is plateur phase?
result of potassium channels remaining closed to inhibit repolarization and the voltage gated calcium L type channels open at the end of depolarization allowing calcium ions to enter the cell
What allows final repolarization of the cell?
Calcium channels closing and Potassium channels opening
Excitatin of SA node
no stable resting membrane potential but exhibit a slow depolarization during the resting stage causing cell to slowly reach threshold causing AP. NO plateu phase in SA
deos SA require nerves
NO! it is intrinsic of heart
what is slow depolarization a result of?
two ionic permeablilty changes
Volgage Na channels open as a result of previous repolarizion and T type Ca chanel open to cause positive charge in the cell.
What happens once SA cell reaches threshold due to slow depolarization?
voltage gated Ca channnel L type opens to bring more Ca in.
intrinsic rate of fining of SA node
Why is heart rate 70beats/min even though intrinsicrate of firing of Sa node is 100\min?
bc PS activiy supply SA node predominates over symp activity
What happens without SA node?
other regions of heart still have pace maker actiivgy but slower than SA node bc it is the fastet. IF SA node gone use AV node
P wave
Atrial depolarizaton
QRS complex
ventricular depolarization
T wave
venticle repolarizaition
Flat pt between P and Q on EKG
due to delay at AV node becuase it is slow to depolarize
Why cant we see atria repolariztion on EKG?
Bc very small and occurs ame time as ventricular depolarization which is freaking huge
provides a means of recording the electrical activity of the heart from externally applied electrodes
What does EKG look for?
electrical abnormalities NOT mechanical
PR interval
measure of time from P to Q it is the prolongation of conduction of AP through the AV node
QT interval
amount of time ventricle is contracting. Q starts contracton and T is relaxing
ultimate stimulus for cardiac muscle contraction is
increase in cytosolic Ca concentration
How is cardiac contraction carried out?
depolarization of membrane
causes opening of plasma membrane Ca channels in T tuble. Ca flows into cytosol. Ca binds to Ca recepotor to SR. causing opeing of intrinic Ca channels so more Ca flows into cytosol further increaseing Ca cytosolic conc. causing contraction
How is cardiac muscle repolarized
removal of Ca from cytosol and put back into SR by Ca ATPase and removed from cell to exterior by Ca ATPase and Ca/Na exchanger
What is amount of fee Ca avaible to trigger cross bridge formation a direct deterinant of ?
strength of cardiac contraction.
refractory period of cardiac m.
no further muscle contractions can be elicited last as long as contraaction itself. Caused by long plateu phase
Is it possibe to produce tetanic contractions in cardiac muscle?
no bc long refractory period due to long plateu phase
two phases of cardiac cycle
diastole and systole
cardiac ventricles are relaxing and filling with blood from atria
cardiac ventricles contract and eject blood into the aorta and pulmonary arteries
rapid filling phase
early in diastlole when pressure gradient is relatively large
slow filling phase
diastole prgresses and pressure gradient decreases causing ventricle filling to be slower
atrial contraction phase
as result of elecrrical activity the left atrium contracts and pushes a little more blood into the ventricle
total volume of blood at end of diastle
steps of diastole
rapid filling
slow filling
atrial contraction
how much blood is ejected from hert during normal contraction
only 50-60%
describe ventricular contraction
mitral valve closes stopping the flow of blood back into the atrium and at this time the aortic valve is still close bc pressure in the aorta os way higher. as the contraction continues, the ventricle pressure increases to exceed aortic pressure to aortic valve opens and blood goes thrhough rapidly
isovolumic contraction phase
so ventricle initially contracing and both mitral and aortic valve are closed at this point both the valves and the walls of the closed chamber are contracting
Mitral valve problem
causes atrial hypertrophy
period of time between closing aortic falve and opening mitral valve
isovolumic relaxingation period
what causes slow filling phase of ventricle
atrial pressure wquals ventricular pressure
end systolic volume
amount of blood in ventrilce at the end of the ejuecttion phase
Stroke vol
Ejection fraction
amount of blood ejected during a contraction

Strokvol/End Diastolic vol
Ejection fracton in normal individulas
During diastlole what happens to aortic pressure?
it decreases from a peak value of 120 mmHg to a pressure of 80 mmHg. Decrease in pressure is due to blood leaving aorta and going to periphery
major diffenence in right and left side of heart
peak prssure in R is 24 mmHg and diastolic is 8 mmHg while left pressure is 120 mmHg/70 mmHg
What causes Pressure difference between R and L sides of heart?
vascular reisstanc in systemic is much higher than pulmonary
what produce heart soundsS?
passive closing of cardiac valves
First heart sound
lub is result of closing of the mitral and tricupsid valve at the end of diastole
Second heart soundd
dub is result of closing the aortic and pulmonic valves at the end of systole
Heart murmur
caused by blood flowing through abnormally small opening or in narrowed blood vessel. Valves dont open or close properly
What is splitting of second heart sound caused by/
respiratory cyle? Take break decrease intra thoracic pressure so lungs expand, descending the diaphragm increases vol in thoracic cavity and decreases pressure so increasing pressure gradiend for blood to flow through IVC adding more blood on the right.
When inhale what side of heart gets more blood?
Right. causing delay of pulmonic valves

When exhale get more load on Left
The volume of blood pumped by each ventricle per minute
cardiac output
what is cardiac out put for an average adult
5 L/min
Stroke volume
amount of blood ejected by each ventricle with each beat
Cardiac output equation
CO = Stroke volume X Heart
Diffence in CO between R and L heart
no difference they are in series so the CO is equal on both sides
Parasympathetics effect on SA node
decrease rate of fining and decrease in heart rate
sympathectic effect of firing on SA node
increase the rate of firing and increases heart rate
If heart rate increases what happens to stroke volume?
it decreases.
How does increasing sympathetics on SA increase the heart rate?
Increasing sympathetics increases the number of Na and Ca T channels that open which causes the membrane potential to reach threshold faster causing more SA node AP and increasing the HR.
How does incrasing parasympathetic on SA decrease the heart rate?
decreases the number of Na and Ca T type channels that normally open in the membrane so it takes longer to reach threshold. Fewer SA AP occur so heart rate decreases
What is responsible for changes in the slope of diastolic depolarization?
the opening or closing of the special Na and Ca T type channels in the SA membrane
Epinephrine effect on the heart
releases from the adrenal medually and it increases the heart rate by interacting with the same beta rector as noperp
Other factors beside parasymp and symp and effect the heart rate
body temp, serum electorlyte conc. and adenosine
increseases heart rate. Released during excercise
What happens if you increse the left ventricular end diastolic vol?
Increase stroke volume of pump because you increase he volume and therefore increase the fiber length
What happens to stroke volume as ventrucular diastolic volume increases?
stroke volume increases. because as heart fills the muscles stretch, increasing fiber length and causing a more forceful contraction
Frank starling mechanism
Stroke vol vs Ventricular end diastoic vol. basically as end diastolic volume increases, stroke volume increases too. this is an intrinsic property of cardiac muscle
Consequence of Frank starling mechansim
CO of both ventricles are equal
What does sympathetic activity do to frank starling graph curve
shifts it up and left bc increase in symp causes an increase in stroke volume due to increase cardiac conductivity
three mechanisms that are responsible for increases in cardiac contractility
1. opening more plasma membrane Ca L type channels during plateu phse
2. stimulating Ca reabsorbion into SR
3. altering the binding of Ca to troponin
what is an increase in cardiac contractily a result of?
increase in the amount of free calcium in the cytool during contraction and the rate of removal of Ca from the cytosol durnig relaxation
PS effect on cardiac contractility
ventricles receive little PS so no effect on cardiac contractility
magnitude of the aortic pressure or pulmonary artery pressure against which the ventricle must eject its blood
What does and increase in afterload do to Stroke volume
causes stroke volume to decrease bc it is applying the same force but there isgreater resistance
What happens if you block L type Ca channels
decrease both conductivity and stroke vol
when does systole start?
when aortic valve opens, diastole is when aortic valve closes
dicrotic notch
point in time when aortic valve closes
systolic pressure
diastolic pressure
pulse pressure, basically the change in the pulse in a single ejection
what happens to BP with age?
as you age BP increases due to changes in compliance. vessels get stiffer.
Mean arterial pressure
diastloic pressure + 1/3PP
what is magnitude of pulse pressure determined by?
amount of blood ejected by ventricle per beat (stroke vol)
rate of ejection of blood from ventricle
compliance of the arterial system
what happens if ventricle ejects blood too rapidly?
arteries cant adapt so it takes longer to fill
indicates how easlity an elastic structure can be stretched

describe central aorta ejecting blood
blood ejected from ventricle is greateer that amount of blood that goes into peripheral. aortic wall stretches and excess blood ejected into aorta is stored making it large and storing energy. during diastole when ventricle is not ejecting blood, the aorta contracts and the stored elastic enery provides additional driving pressure to help the movements of blood in the peripheral circulation
BV with most pressure
BV with least pressure
importance of arerioles
detemine the relative blood flow to various organs and play a major role in the MAP
major site of resistance in periphereal vascular system
Ohms law
what determines vascular resistance?
arterioles radius (because to the fourth power)
What surrounds arterioles?
smmoth muscle with intrinsic tone. the muscle is controlled by sympathetic nerve activity
potent vasodialators
potassium and adenosine. cause increase Blood flow
Active hyperemiea
increased blood flow as a result of increased metabolic activity. reslt of production of loss of certain materials in immmediate vicinity wi the vascular bed. Ex. increased Oxygen of CO2, adenosine or potassium causes an increae in BF
flow autoregulation
maintain blood flow in face of changesin MAP. occurs by increasing BP, cause BF to increase but organ doest need it so constrict the arteriole to the organ
what happens if you increase metabolic activity of the tissue
automatically increase BF to that tissue
NT to arterioles
sympathetics norepi NT and alpha receptors. only symp present in arterioles. If NT release and binds to recepotor cause constriction of arterioles and decreases BF
Why does changing sym not effective to controlling BF to specific organ?
bc the effects of symp discharge occur throughout the body
Most common way to control BF to specific organ
reguating the arterial blood pressure
What neurons release NO?
noncholinergic and nonadrenergic
vasodialatore. they control BF in GI and penis.
Function of epinephrine in arterioles
if it binds to alpha receptors causes vasoconstriction. If it binds to beta receptors on arterioles in skeletal m. it causes vasodilation
angiotensin II, vasopressin
vasodilator released by atria of heart
what happens when endothelial cell secrete paracrine agents?
diffuse to nearby vascluar smooth muscle cells and induce either vasoconstricion or vasodialation
PGI2 prostacyclin
not continuously relesed like NO but it is a vasodialator
paracrine vasoconstrictor
precapillary sphincter
vascular smmoth m. around smaller vessels. Controls BF to down stream capillaries
major site of exchange of nutrients and metabolic end products
Typical cap structur
thin walled tube of endothelial cells one layer thick resting on a basement membrane without smooth m.
What is between endotheial cells in cap
intercelluar fluid
what is cap blood flow dependent on?
state of contraction or relaxation of upstream arterioles
What causes constriction or dialation of metarterioles in cap bed?
local metabolites
Blood flow velocity equation
V = F/A
sequence movement of nutrient
Blood plasma through cap wall into Interstial fluid and then into cell.
Purpose of bulk flow
distributing ECF
what governs the fluid across the cap wall
starlings law of capillary
net filtraion pressure equation
(Pc - Pif) - (IIp-IIif)

Pc=cap hydrostatic P
Pif=interstitial p
IIp=osmotic P due to PP
IIif-intertial P due to PP
What does negative net filtration pressure mean?
it is absorbed. goes back into cap
in systemic cap beds, when is there a net movement of fluid out of capalaries?
At arterial end and a net movement of fluid into the capalaries at the venous end
What happens if increase symp to veins?
displace blood to artioles to increase pressure in arterioles bc fluid moves from veins to arterioles
Do veins exchange material?
Driving force for blood flow form veins back to the heart
pressure gradient between the peripheral veins and the R atrium
Function of veins
return blood to heart and to as storage function bc total volume of the peripheral veins can be altered by sympathetic nerve activity on vascular smooth muscle in the walls of the vessels cause vasoconstriction and pushing blood into arterioles
reservoir for blood in systemic circulation
What two things happen in inspiration?
diaphragm descends down increasing th intraabdominal pressure and peripheral venous pressure. the intrathoracic pressure decreases and decreases the veins in the thorax. The increase in ab venous pressure and decrease in thoracic venous pressure increase pressure gradient and increases amount of blood flow to the heart this is the respiratory pump
% of Blood vol in veins
amount of lymph reabsorbed each day
4 L
Why doesnt peripheral interstial space accumulate fluid or proteins?
bc th lymph picks it up and returns it to circulatory system
Venous pooling
standing and not moving therefore not using skeletal muscle so blood goes away from arterilole side to veins so BP decreases and there is not enought oxygen to brain so you pass out
smooth muscle of lymph
exhibits rhythmical contractions and propels the lymph to the heart. Vessles also have valves to allow unidirectional flow
What activates smooth muscle around lymph vessels
stretch. it begins contracting when the vessels are distended. Also sympathetic innervation activates the smooth m. around the vessels along with the respiratory pump
What happens if lymph is blocked?
fluid accumulation in periphereal system, edema
How is absorbed fat carried to cardiovascular system?
baroreceptor action if artial pressure increases
arterial baroreceptors increase fireing reflex via medulary cariovascular center causing decrease sympathetic to heart, arteries causing decrease SV, CO, and vasodialation causes artiole blood to go to venous side. It also causes parasympathetics to the heart to increase so SA and AV node decrease to decresase HR
major cardiovascular regulator
MAP in systemic circulation
MAP equation
What controls MAP over seconds to hours?
baroreceptor reflex and hormonal secretions
special collecion of nerve ending bilaterally in carotid sinus and in aortic arch
Describe baroreceptors
stretch receptors whose rate of firing depends on pressure in aorta carotid sinus. Sends output to heart, arterioles, and veins
If BP increases, stretch increases, baroreceptor firing increases causing decrease symp and increase PS
How is BP regulated long term?
blood volume of kidneys
Cardiac Catherization
measure pressure of heart. Can see ventricles and locate plaques or clots
excericise with EKG see where pt feels pain
non invasiove. see 2D of heart.

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