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758 Cards in this Set

  • Front
  • Back
Route of blood flow through the heart
Enters from SVC & IVC=> R. Atrium=>Tricuspid Valve=>R.Ventricle=> Pulmonary Valve=> Pulonary arteries => Lungs=> Pulmonary Veins=> L. Atrium=> Mitral/Bicuspid Valve => L. Ventricle => Aortic Valve => out Aorta
Stenosis is? possible problems it causes?
Narrowing of Valve.
=> Problem with fluid getting through
Regurgitation? Possible problems it causes?
Leaky vessels
=>Proble with back flow of the valves
What do atrioventricular valves do?/ purpose of valve?
Prevent backflow from ventricles to atria during systole.
What are the 2 atrioventricular valves?
1. Tricuspid valve
2. Bicuspid (mitral) valve
What is the 1st sound of the heart?
- Closure of Atrioventricular valves
What is the purlose of Semilunar valves/ what do they do?
Preven back flow from arteries to ventricals during diastole. (-separate ventricles from arteries).
What are the 2 types of semilunar valves?
1. Pulmonary Valve
2. Aortic Valve
What is the 2nd sound of the heart?
Closure of semilunar valves.... ((Turbulance of flow??))
What are the 2 types of Cardiac Myocytes (muscle cells)?
1. Contractile Muscle Fibers/Cells (atrial & ventricular myocytes)
2. Conductive m. fibers (excitatory, autorhythmic)
Types of Cardiac Myocytes -2
1. Contractive m. Fibers/cells
- 2 types? Which is th largest?
1. atrial myocytes
2. Ventriclular Myocytes
-Ventricular Myocyes aremuch bigger= More sarcomeres, myosin, actin, mitochondria.
The contractile cardiac myocite: Ventricular Myocytes uses how much of the oxygen it it receives on contraction/ with every heartbeat? - importance/
- Use 70-80% of Oxygen
- This is far more % of oxygen use than any other tissue/ cell in th body
Types of Cardiac Myocytes- 2
2. Conductive Muscle fibers- 2 types?
- examples of what nodes/ cells?
Excitatory and Autorythmic cells.
SA NODE, VA NODE, AUTORYTHEMIC CELLs
Conductive Muscle FIbers of the cardiac myocytes_
What kind of contraction? How does this contribute to cardiac cyce?
Conductive muscle fibers do have som myosin& actin, but not alot, therefore they have WEAK contractions & Doesn't really contribute to cardiac cycle.
Why can heart continue to beat when taken out of place and put into k+ na+ ... etc.....
Bc the heart has more autorythemic cells than any other tissue in body... and bc of the COMPONENTS of the CONDUCTIVE MUSCLE FIBERS
What is the appearance of Cardiac muscle?
How does it differ from skeletal muscle in appearance?2
Looks a lot like skeletal muscle.
-Differs in 2 ways:
1. Connectivity of own fibers
2. Branching
What is key for myosin to biind to actin?
CA++ binds to troponin and removes trypomiysion to allow actin and myosin to bind... etc
______ Muscle is a Syncytium.
CARDIAC Muscle is a syncytium
Cardiac Muscle is a Syncytium. bc??
[Intercalted disc connect cardiac myocytes 1 to another (usually end-toend).]
1. Intercalated Disc
2.Diff. types of cardiac myocyes have diff. intercalted dics ( autorythmic, atrial & ventrricular)
Cardiac Muscle is a Syncytium
1. A.Intercalted discs are?
B.What are the 2 important junctions?
A. Specialized cell membranes containing (gap junctions & desmosomes)
B. 1.Gap Junctions--> allow for rapid communication and excitation from 1 cell to another.
2.Desmosomes- Pulls cells together to transmit/transfer force to the next cardomyotes... which is importabt in the whole co
Cardiac Muscle is a Syncytium.
2. Different types of cardiac myocytes have differences in intercalated dics.
A. Autorythemic cells - type of transmission. (ex)
A. Autorythemic Cells (conductive)- End-to end transmission...
Ex. SA, VA, Purkunji fibers- only have this transmission... BC OF gap junctions.
Cardiac Muscle is a Syncytium.
2. Different types of cardiac myocytes have differences in intercalated dics.
B.Atrial Myocytes - type of transmission. (ex)
B. Atrial Myocytes-(contractile)- Have both 1.End-to-end & 2. Side-to-side transmission. => bc Gap junctions on all sides.
Cardiac Muscle is a Syncytium.
2. Different types of cardiac myocytes have differences in intercalated dics.
C. Ventricular myocytes- type of transmission. (ex)
-C. Ventricular myocytes
- ENd to End transmission
What cardiac myocyte intercalted discs are the fastest? slowest?
By Far the fastest- Autoryhtemic Cells
2nd- atrial
3rd- slowest- ventrical
Fastest conduction of velocity of cardiac myocytes (top??) ??
AUTORYTHEMIC CELLS
Do the atria and ventricles fx as a single syncytium?
NO< The atria and ventricles fx as SEPARATE Syncytiums.
The atria and ventricles fx as SEPARATE Syncytiums bc?
Bc of the thick fibrous tissue separating the ATRIA from the VENTRICLES.
( Works as restrictors makes sure communication goes through conduction pathways.)
The atria and ventricles fx as SEPARATE Syncytiums Bc of the thick fibrous tissue separating the ATRIA from the VENTRICLES.
This does what 2 things>
1. Prevents any inappropriate communication between the compartments outside of the conductive pathways. ( The atria doesnt tell the ventrical what to do).
2. Protects a brief Break in time btw contraction of atria & ventricles.= allows for blood to move from atria to ventricles.
(Slows down signal from Atria to Ventricle)
What is Wolfparkinsons White?
Extra autorythemic pathway in heart and causes passing out of young adults after a night of benge drinking.
Break in contraction of atra and ventricles is important bc...Purpose of atria contraction is filling ventricle with blood. If atria contracted at the same time the ventricle contracted what would happen? so this break is important bc????
The atria wouldnt be be able to fill ventricle with blood.
-Break important bc ENSURES TIME for ATRIAL CONTRACTION to FILL VENTRICLE w/Extra BLOOD!
Fast AP in Contractile Cardiac Muscle=
Fast repsonse- referred to as "Fast Response action potential " in cardiomyocytes
How much longer/shorter time does the AP of Cardiac muscles lasts than skeletal muscles?
- Last~ 15 times as long as skeletal m. AP.. (so longer than skeletal m.)
What are the important ionic condctances in Cardiac muscles?3
1. Na+ - same as skel m.
2. Ca++- (L-Type- )
3.K+- same as skel m.
What does Ca++/ L-type Ca++ do to the AP of Cardiac muscles?
-HELPS WITH CONTRACTION OF MUSCLE- UNIQUE
AP in cardio Myocyte- 0-4 stages start at 4.
4- Resting membrane
0- Rapid Depolarization of Cells (just like neurons in skeletal m.- bc of VG-Na+ channels opening.) --> COnductance of Na+ = Rapid which corraleates to rapid depol.
1-Rapid Repolarization- but rather transient.- Closing of Na+ & opening of K+
2-(Expanding of AP)- Plato- stabelizes bc at this point both VG-K+ & VG-Ca++ channels areopen, so K+ moving out of cell & Ca++ moving into the Cell= Balanced- losing & gaining charges.
3-Rapid repolarization - bc VG-Ca++ channels have closed -K+ reflux
In Cardiomyocytes what causes the unsually long refractory periods?
The PLATEAU
What happens during the Absolute Refractory Period (ARP) of cardiomyocytes?
-imposible to fire an AP.. type- ERP
What is an effective refractory period (ERP).part of what?
ERP- type fo ARP
-Individual even can fire an AP,but can't "tell" anyone else about it... not enough positive AP to hit threshold...
What is a the Relative Refractory Period (RPR) of a cardiomyocyte?
Doesn't extend far.
- Can get an AP,but need a much larger than normal EPSP to get one.
What is a Supranormal Period (SNP) in a cardiomyocyte?
-Type of refractory period .
= MORE excitedable, so- easier to fore an AP here.
- opposite from RRP.
Promblem fxionally: Weak contraction.
Both the RRP and SNP of a cardiomyocyte can produce a _______ Contraction. Reason it is ______ is bc?
both can produce a WEAK Contraction.
-Reason it is weak is bc of the time - If you have short amount of time between AP in the heart then can't fill ventricle w/ blood and that means not much flows out.. so weak contraction
What is the reason the AP in a Cardiomyocyte is longer than that of a skeletal muscle?
BC OF THE L-type Ca++
During the almost the entire length of AP of a Cardiomyocyte it is impossible to fire another AP, however there is a very brief amount of time which it can fire an AP, but not good comes from it... this is called what period?
Effective Refractory Period (EFP)
Why is the long ARP (& erp) of Cardiac myocytes vital physiologically?
To prevent Tetany
- If heart stays contracted then blood couldn't flow through.
What are the 2 main differences in the relationship betw AP of Cardiac contractile & skelteal m. and length of contraction/relaxation?
1. Time scale- skel short AP- almost over berfore contraction occurs& can summate
2. Cardiac ARP last almost entire length of contraction & relaxation.
Excitation and contraction coupling of Cardiac myocytes.. How does the AP travel along the membrane?
t- tubules down the center of the myocyte- more here than in skeletal m.
Where are t tubles more plentiful in myocytes?
rare?
absent?
Plentiful- Ventricular myocytes myocytes- Ca+ to contract
Rare- Atrial Myocytes
Absent- Autorhythemic cells
Why are ttubules absent in autorhtymic cells of cariac myocytes?
Bc you dont need them to contract. - so don't need t tubules.
What are the steps of Ca++ entering the SR in cardio myocytes?4
1. Ca+ enters from the extracellular space through L-type Ca Channels. ( -T-tubules have lots of mucopolysaccharides that bind ca++- keeping an extracellular store near & ready)
2.Calcium endters from the SR (only if #1 happens)-->(Ca+ released via ca+induced ca++ release through ryanodine receptor channels && SR is FAR LESS Developed in Cardiac m. compared to skeletal m.)
3. Calcium - in presence of ATP- initiates contraction.-->(Get ca++ from outside cell so don't solely depend on ca from sR)
4.*** The STRENGTH of CARDIAC Contraction is GRADED Based on Extracellular Ca++ content --> Decrease Ca++ in extracellular space the contraction also DECREASES. ( that doesn't happen in skel m)
To have rigor in cardiac cross bridge cycle need prescence of what and absences of what?
Presence of Ca++
Absence fof ATP
For Relaxation in cardiomyocytes what must you do? and what are the 2 mechanisms to do it?
Must remove CA++ ( just like skel m.)
-Done by:
1. Ca+ ATPase- 1' active transporter
2. NA+/Ca++ Exchanger- 2' active transporter... Na+ moves out and Ca++ moves in.
Digitalis is a cardiac glycoside that inhibits what?
Effects on heart in little doses?
large doses?
the NA+/K+ ATPase.
Little doeses?- min effect.
Large dose- Kills you. bc can increase cardiac contraction 50-100% infailing heart.
Digitalis is a cardiac glycoside that inhibits Na+/K+ ATPase. It can increase the strength of Cardiac contraction 50-100% in failing heart.
***WHY would blocking Na+/K+ ATPase increase cardiac contraction????*****
It is NOT a Direct effect.
It is bc of an INdirect effect- Decrease in Na+ gradient so the power of the Na+/Ca++ exchanger is decreased and that means more Ca+ in cell. More Ca++ in cell= greater contraction.
Cardiac Cycle- Whatever happens on r. side is also happening on L. side w/ very slight differences.
Fact
Cardiac Cycle:
Atrial Cycling-
1. Atrial filling is ____ (active, passive??)
2.Ventricular filling mostly occurs during ____ ____
3. 20% of ventricular filling comes from _____ _____ ( __ ___)
1. Atrial filling is __PASSIVE__.
2. Ventricular filling mostly occurs during _ATRIAL DIASOTOLE (at rest)___
3. 20% of ventricular filling comes from _ATRIAL SYSTOLE (ATRIAL KICK)__
Cardiac Cycle:
Ventricular Cycle:
1. When do they fill? what valves are open or closed?
2. When do they empty? what valves are open or closed?
1. Fill during DIASTOLE when AV VALVES are OPEN.
2.Empty during SYSTOLE when SEMILUNAR VALVES are OPEN
Cardiac Cycle:
Ventricular Cycle
3. Changes in ventricular pressure determines what?
4.What are the 2 stages of Ventricular systole? and Ventrical Diastole?
3. Changes in ventricular pressure determines- STATE OF VALVES
4.Ventricular systole-
1.Isovolumic Contraction
2. Ejection
Ventricular Diastole
1. Isovolumic Relaxation
2. Ventricular Filling
How does blood flow in Cardiac Cycle? what determines pressure>?
Blood flows from high to low pressure ( in relation to atria & ventricles. Diastole (rest) and Systole (contraction) DETERMINE PRESSURE! P
How do ytou know if the valve is open or closed in cardiac cycle?
Pressure of chambers determine if open or closed.
How does volume change in each compartment of cardiac cycle?
High to low pressure & valves open follow pressure gradient.
In the Cardiac cycle the majority of the time what valves are open and which are usually closed?
- AV valves OPEN
-Semilunar Valves- almost always closed except during EJECTION- This is the only time that ventricle pressure is higher(??)
In the EKG what does the pwave stand for? when does it occur?
pwave= 1st increase in atrial pressure- contracts & pressure increases.
- occurs right after Atria Depolarizes
Cardiac Cycle- l. Ventrricular Function.
P wave=
QRS=
T Waves-
P Wave= Atria Depolarization
QRS= Depolararization of ventricle. Ventricle pressure increases above atrial.
T wave= repolarization of Ventricles
1st Heart sound=
2nd Heart sound=
3rd Heart sound=
1st=Closure of AV Valves
2nd=Closure of Semilunar Vavlves
3rd=Turbulent filling of ventricle. (Max filling of venricle)
What is the consequence if 2 heart valves are open simultaneously.. for example the AV valve doesn't close when it is supposed to?
REGURGITATION
Dicotic notch is?
- Blimp in pressure & it is secondary to the closure of semilunar valves increases pressure..
What's responsible for this is -?? 1st atrial contration ....2nd closing of av valves
In the Cadiac Cycle (left ventricular fx)
The Aortic Pressure is always pretty _____. The Artial pressure is always pretty ____. And the Ventricular pressure _______ _ ___.
The Aortic Pressure is always pretty _HIGH_. The Artial pressure is always pretty _LOW_. And the Ventricular pressure _VARIES_ A _LOT_.
What is the end of (ventricular) contraction signalled by?
The closing of the aortic valves
Summary of Ventricular Cardiac Cycle... Start at rest. What are the 4 stages after starting at rest- briefly ( hint- 1st stage has 3 sub divisions)
1. Ventriculular Filling
a. Rapid Ventricular Filling
b.Diastasis
c.Atrial Contraction
2. Isovolumetric Contraction
3.Ejection
4.Isovolumetric Relaxation
Summary of Ventricular Cardiac Cycle..4 stages
1.Ventricular Filling-->
a.Rapid Ventricular Filling-
1.Ventricular Filling--> Passive
a.Rapid Ventricular Filling- Follows opening of AV Valves, Blood enters v
Summary of Ventrcular Cardiac Cycle:
1.Ventricular Filling
b.Diastasis-
b.Diastasis- Slow changes in ventricular pressure & volume.
Summary of Ventricular Cardiac Cycle:
1.Ventricular Filling
c.Atrial Contraction-
c. Atrial contraction- Follows P wave of ECG (atrial depolarization
Summary of Ventricular Cardiac Cycle:
2.Isovolumetric Contraction-
--Follows QRS of ECG & closing of AV Valves. LARGE increase in ventricular pressure. (When ventricle pressure exeeds atrial pressure then ventricle contracts, and AV valves are closed._
-(1st component of ventricular contraction)
Summary of Ventricular Cardiac Cycle:
3.Ejection
-Follows opening of semilunar valves, Blood enters arterie
Summary of Ventricular Cardiac Cycle:
4.Isovolumetric Relaxation-
(occurs after contractoin)- Follows closing of semilunar valves (Dicrotic Notch), LARGE decrease in Ventricular pressure.
(Semilunar valves close, AV still close.. Heart relaxes until next step.
Summary of Ventricular Cardiac Cycle.
How long does the heart stay at rest/ how long does the pressure in the VENTRICLES drop.. with both valves shut after Isovolmetric relaxation??
Heart relaxes- PRessure DROPS until it is BELOW Atrial pressure and thats when AV Valves open!
Summary of Ventricular Cardiac cycle:
What is the dicrotic noth and what is is SOLELY associated with?
Dicrotic notch- when semilunar valves cause 2nd force in blood flowing- so increase pressure before it decreases (in ventricles)...
-->SOLEY associated with the CLOSING of the Semilunar Valves
What is Stroke Volume (SV)? and what is the equation?
--> Ventricular contraction- Colume that leaves the heart. The difference in volume in the ventricle at the end of relaxition & end of contraction.(The volume of blood pumped from 1 ventricle of the heart w/each beat.)
SV= EDV-ESV
(End Diastolic Volume - End Systolic Volume)
What happens to volume & pressure during: Ventricular Filling?
Volume-Increase in volume
Pressure-Slight decrease/constant pressure until atrial kick)
What happens to volume & pressure during: Isovolumetric Contraction.
-Volume- No increase or decrease/ change in Volume
-Pressure- Increase in Pressure
What happens to volume & pressure during: Period of EJECTION of ventricle of cardiac.
-Volume- Decreases until end
-Pressure-Pressure Increases
What happens to volume & pressure during: Isovolumetric Relaxation
-Volume- Stays the same
-Pressure- Decresses
End systolic volume is marked by?
The End of RELAXATION!(marked before the following happens Mitral valves opening which starts the ventricular filling
EDV is important for _______ which is what?
PRELOAD= Max Volume!!
- bc load on cardiac muscle before contraction.
EDV is important for Preload.
It is the _____ in the _____in the ventricles at the end of diastole.
BLOOD in the VENTRICLES
EDV is reflective of ______ fx & important detrminant of _____ _______.
EDV is reflective of _DIASTOLIC_ fx & important detrminant of _VENTRICULAR CONTRACTION_.
EDV is reflective of diastolic fx & an important determinant of ventricular contraction.
-->WHAT DOES THE FRANK-STARLING MECHANISM of the HEART DESCRIBE?
The ability of a healthy ventricle to eject the amount of blood that enters the ventricle (venous return) w/each cardiac cycle. Venous return= SV
Venous Return=
SV
Venous REturn = Stroke Volume.. WHy is this of clinical importance?
B/c if the length of the cardiac myocyte increases, the Force of Contraction increases.
EDV is reflective of diastolic fx & an important determinant of ventricular contraction.
--> SOOOO... IF EDV INCREASES, WHAT HAPPENS TO THE VOLUME OF BLOOD EJECTED FROM THE VENTRICLE??
It increases. An increase in EDV should also Increase SV
What is the relation between atrial pressure and ventricular output?
The greater the max atrial pressure (correlates w/venous return), the greater the ventricular output (preload).
(Increase atrial output= inc. ventricular output/preload)
Why is the R. Ventricle have a smaller increase in pressure/output than the L. Ventricle?
BC the right pumps blood to the lungs..
1. low energy
2.lungs close to heart so don't want to pump high pressure to lungs..
** The LEFT has a bigger job- so THICKER and Larger increase in pressure.
What are the determinants of EDV? 8- main one?
1. Preload- EDV & Venous return
2.VENOUS RETURN= MAINLY!
3.Blood Volume Change-amt of vol.- dehydrated/over hydrated
4.Atrial Contraction- appropriate contraction
5.Ventricular Myocytes- if cant contrack= blood backup= INCREASE in EDV.
6.Distrubution of Blood Vol.-posture- ex-lay back pt
7.HR & Rythm= faster HR or abnormal rhythm= DECREASE inVenous Return
8. Atrioventricle-Valve Fx- Stenosis& Regurgitation
IF EDV is very large what happens?
Volume Overload
What is Volume Overload?
Increase vol. so large that cardio myocytes can't pump blood= HEART FAILURE= ECCENTRIC HYPERTORPHY
What is Eccentric hypertophy?
Stretch in length of mm but not width.
-REducd ability to maintain force in contraction.
(This is a result in heart failure from volume overload from a very large EDV)
Is it health to increase your EDV?
IF you are HEALTHY, then yes, but too much is BAD!
What is a good average for ESV?? think what when hear ESV??( End Systolic VOlume)
40-50 ml
- Think Arterial Pressure and Valve fx
What is ESV influenced by?? 3 things?
1. AFTERLOAD- The Pressure the ventricle must overcome.(inorder to ejcet blood, ventricle pressure must be higher than arterial pressure).
2. PRELOAD
3.Ventricular contractility
What is a good average for SV? WHat is sv?
70ml
SV= EDV - ESV
What is Ejection Fraction and what should it be? Whats too low?
Ejection Fraction: SV / EDV
- SHould be ~60%
- 40% = Heart Failure
When the mitral valve opens & closes what happens?
opens- Ventricular filling
closes- Isovolumetric contraction
What happens when the Aortic Valve Opens and Closes?
Opens- Ventricular Ejection (end of isovolum contract)
Closes- Isovolumetric Relaxation
How does an Increase in Preload effect the (L.) Ventricular Pressure-Volume Loop? (good or bad?)
-Increases Ventricular filling and Ejection.
W/o doing more work- can do the same thing.. just by adding more fluid .. GOOD Thing.
-=> It lengthens ventricular filling and ventricular ejection... the time before EDV
How does an Increase in Afterload effect the (L.) Ventricular Pressure-Volume Loop? (good or bad?)
- More pressure in heart. must inc. ventricular pressure to get a contraction. Heart spends more time in isovolumetric contraction and less time for contraction.. Heart doing more bc heart working harder but doing less.
BAD thing ( ex hypertenstion)
How does an Increase in Contractility effect the (L.) Ventricular Pressure-Volume Loop?(good or bad?)
Increase force of contraction bc amt. of Ca++ in cell Incr.
=>** Solely- Increase in SV bc Decrease in EDV.
Good thing
What are the 2 most important properties that determine the ability of cardiac myocytes to increase tension & velocity of contraction (cardiac performance)?
1. Initial sacromere Length. Preload or EDV
2. Force the contracting myocyte must overcome. Afterload, arterial pressure.
What is Cardiac Output (CO or C.O.) ? What is normal CO?
CO= SV x HR
Normmal= 4-6 L/min... Good CO- 5L/M both R. & L.
How do you regulate CO?
1. Lots of determinants- 4?
1. Metablism- amt of Oxygen using & CO2 produicing - @ REST C.O.= LOw
2.Exercise= Increase C.O.-->Aesome shape 30l/m while working out
3.Age- Increases C.O. up to 10 years, THEN decreases
4. Size of Body- Larger you are the greater C.O. needs to be.
What are the REFLEX DETERMINAANTS of Cardiac Output? 5
1.Venous Return/Preload (Frank Starling Mech)
2.Afterload
3.Changes in Contractility
4. Autonomic Nervous System- symp and parasymp
5.Other Qualifiers- Temp, Changes in ion concentration, Extreme Tachycardia, Cornoary artery blockage, Cardiac Tamponade, Valvular heart disease/
REFLEX DETERMINAANTS of C.O.-
1. Venous Return/ Preload (Frank-Starling Mechanism)
a. Increase in Venous return- _________ Contractility/SV**?
b. Increase in Venous return ________ HR, by : ____??????
a. Increase in Venous return- _INCREASES_ Contractility/SV**?
b. Increase in Venous return _INCREASES_ HR, by: STRETCHING the SA NODE & Via Autonomic Innervation.
Strectch in SA Nodes does what to HR?
Increases HR
Reflex Determinants of CO-
2. What does an Increase in Afterload to to SV?
Increase Afterload= Decrease SV
-Heart has to do more work to push blood into high pressure vessels
Reflex Determinants of CO-
3.Changes in COntractility does what to C.O. and S.V.
Why is this inmportant for C.O?
Changes in Contractility can Increase C.O. --> IF Inc. in Ca++ coming in = Inc. in SV.
-Important for Inc. in C.O. bc-- Inc. SV & HR due to AP firing at a Faster Rate
Reflex Determinants of CO-
4. Autonomic Nervous system
a. Symp Stimulation ( Beta 1 Recptorts) does what to HR & Contractility?
b. Parasympathertic stimulation (Muscarinic receptors) do what to HR & COntractility?
a. Symp Stimulation (Beta 1 receptors) - Increase HR & Contractility 2-3 times
***HOW TO REALLY INCREASE CO- BY MAX SYMP STIMULATION
b. Parasympathetic Stimulatio (muscarinic receptors)- Decrease HR, BUt No change in contractility
Reflex Determinants of CO-
5.Other Qualifers
1. Temp Changes affect HR?
- increase/ decrease temp.
Increase in temp= Increase in HR
- For every 1degree F increased temp= INcrease in HR by 10 bpm
-Decrease in temp= decrease HR
Reflex Determinants of CO-
5.Other Qualifers
2. Changes in Ion concentration: effects on C.). &/or HR
a. If inc.Ca++ =
b. If Inc. K+ =
a. Increase Ca++ = Increase C.O. ...Decr. Ca++ = Dec. HR= weak heart
b.Increase K+ = Inc. extracellylar K+ = Inc. Hypokalemia= DECREASE HR & C.O.
Reflex Determinants of CO-
5.Other Qualifers
3.Extreame Tachycardia- problems and increase HR what happens to CO if too fast?
-If Increase HR then Increase C.O.- to point too fast= NOT GOOD.
- Problem relative to amt of time spent in systole vs. diastole- more time in systole so heart can't fill w/ blood bc less time indiastoly. = DECREASE IN VENOUS RETURN & SV.
Reflex Determinants of CO-
5.Other Qualifers
4. Cornary Artery Blockage??
Decrease Oxygen delieverd to muscles
Reflex Determinants of CO-
5.Other Qualifers
5. Cardiac Tamonade-
Pericardium a lot of fluid.
-Heart usually some fluid but not a lot... bad for heart when fluid is too high= hard to contract heart
Reflex Determinants of CO-
5.Other Qualifers
6.Valvular Heart Disase= what happens to SV and C.O.
Decrease in SV & C.O.
If you want to Increase C.O. - Want to Incease what??
Stroke VOLUME! SV
What is Myocardial Autorhymicity?
- Ability of heart to maintain regular rhythm. Conducts own excitation.
How must one ensure (myocardial) autorhythmicity? -2
1. Heart must initiate electrical ecvitation
2. Excitation must be rapidly conducted through the heart
What is the route of autorhymic cells? (Excitatory & Conductive System of the Heart (Autorhythmic Cells))
SA node=> AV Node=> Purkinje Fibers=> Bundle of His=> L.&r. Bundle Branches ( l. splits larger- activates more fibers than right)=> Distal Purkinje Fibers
Excitatory & Conductive System of the Heart (Autorhythmic Cells):
1. Sinoatrial Node (SA Node)- location? (sinus node)
R. Atrium - posteriolateral to to SVC
Excitatory & Conductive System of the Heart (Autorhythmic Cells)
2. Atrioventricular Node (AV Node)
R. Atrium- - NEAR the AV VALVE
-inf. to SA Node.
Excitatory & Conductive System of the Heart (Autorhythmic Cells)
- SA NODE and AV NODEs are??
and how do they connect?
Classic Autorythmic Cells
dif. from purkinji
=> SA Node connects to AV node via Internodal Pathways
Excitatory & Conductive System of the Heart (Autorhythmic Cells))
3. Purkinje Fiber system?
Conduction velocity is much faster than SA or AV Nodes.
=> traditionally though to be end terminal fibers of Autorhymic cells, but not true they go all the way through bundle of his and distal purkinje finers.
What really is the SA Node? whats therir speed?
SA Nodes are:
1. The smallest electrical region of the heart ( vs. any other autorhythmic cells)
2. Fastest Normal PACEMAKER ( 60-80 AP/min).
( just like HR - 60-80 bpm0`
- What 2 functionalluy distinct group of cells make up the SA Node?
1. Autorhythmic/Pacemaker cells
a. Connect via 3 internodal pathwayus to the AV Node ( much faster pathway than conduction pathway)
2. COnductive Cells-
a. Begin depolarization of Atrial contraction cells:
* Conductive cells/ Conduction pathway --> Connect via gap juntions to R & L. Atrial Contractile Cells
Autorythmic Cells- Resting potentional?? explain?
_ NO True resting potential bc charge is never stagnet, always changing... ALSO- much more (+) than other AP even at the lowest bc start out at much more depolarized state.
AP of SA Node:
1. Resting>
2. Depolarization
1. "REsting" Vm is more depolarized than in contractile myocytes
2. Slow Depolarization due to open Na or Ca leak channels (If Current) Which depolarized Vm to threshold voltage.. Always open bc leak changnels ( If= ionic funny current)
AP of SA Node
(after rest *& depolarization)
3. Voltage -gated Na+/Ca++ Channels are activated at
Threshold Voltage
AP of SA Node
(after rest, depolarization and VG-Na/Ca activation)
4. Peak of AP??
5. Repolarization due to??
4. At peak of AP:
a. VG Na+/Ca++ channels inactivate
b. VG K+ channels Open
5. Repolarization is due to: K+ CURRENT
What is the AP of the SA Node sensitive to? ( hormones, elemenets, chem?? 4
ACh, EPI, NE, Ca++ Channel Agonists & Antaagonists
Refractory Periods of SA Nodal Cells are more straight forward than Ventricular myocytes..
2
1. Relative Refractory Period- extends beyond end of repolarization;post-repolarization refractoriness.
2. IF an AP begins during RRP, conduction velocity is slowed.
RRP of SA Nodal Cells
- Post- Repolarization Refractoriness-
--> Extends into 4 regions of AP... so can't fire for a bit of the AP, does at the beginning then conduction velocity is slowed.
What happens in a SA node if AP fire during RRP bc it is so fast..
Bc so fast- The speed it takes for a reaction is a longer amount of time---> this helps protect heart from FIBRILATION!( Fibrilation- heart filling too fast & can't fill)
What are the AV Nodes? Whats their response potential?
Pacemaker cells, Slower -response to AP
What are AV nodes AP almost always stimulated by?
Frequency?
- Stimuated by Internodal pathways, not intrinsically by the AV node.. (mostly the SA Node controls most APs in AV Node)
- Slower pacemaker frequency comparted to Sa Node- ~ 40-60 Ap/min
AV Nodal Delay.
How long does it take for excitation to arrive at AV node?
0.03 Secconds
AV nodal Dealay
Only takes 0.03 seconds for Excitation to arrive at AV node, but _____ ______ are required for the signal to pass through the AV node - to the bundle of his/branges.
0.13 Seconds
What does the AV Nodal Delay allow?
Allows the ATRIA to Contract & empty blood into the ventricles before the ventricle contract.
What is the AV nodal Delay caused by?
Caused by a Decrease in the # of Gap Junctions connecting the successive cells in the AV Node.
( Cells of AV node= not as many gap junctions- so slows down electrical pathway of heart)
AV Nodal Delay:
There is a fibrouse barrier that completely separates the Atria from the Ventricles EXCEPT at the ___ ______. - what does this ensure?
AV BUNDLE!!!!
-ensures that all electrical actiavity (signals) passing through this autorhythmic path havs no other path to take.
What do AV Nodes ultimately control?
Ventricle COntraction
In many conductive cells, the Faster the HR= what lengh of refractory period and what AP frequency?
Faster HR= Shorter (decreased) Refractory Period. and Increase AP.
Refractory period of AV Nodal Cells:
IN AV Nodal Cells the length of the effective refractory period ____________ over normal range of HR
Does NOT Change over the Normal range of HR
Effective refractory period length doesn't change over the normal range of HR.
a. Length of RP of AV Nodal cells will ______ if HR is execceively High. WHy does it do this?
a. Length of RP of AV Nodal cells will _INCREASE_ if HR is execceively High.
This protects the ventricles from excessively high freq. of contraction in instances such as atrial fibrillation.
What are Ectopic Pacemakers/ what do they do???
(Ability of cells outside normal pathways to conduct)
-If Cells in AV node, Purkinje Fibers, or even atrial or ventricular contactile m. discharge rhymically at a faster rate than the SA node. (SAFTETY MECHANISM)
Ectopic Pacemakers
- Results in an abnormal sequence of contraction; can signifcantly....
- Can Significantly DIMINISH the EFFECTIVENESS of the HEART as a PUMP.
Ectopic pacemakers

ex. in ischemia.. heart attack.
Refering to different regions of the heart (sometimes appropriately, must of the time inappropriately) stimulating contraction of the heart
What all is part of the Bundle of His?
Purkinje Cells, F & L Bundle Branches & distal Purkinje fibers
Purkinje Fiber Systerm
- Have large ____ but _____ are absent.
- Have Large SACROMERES, but T-TUBLES are absent.
Purkinje Cells are the _______ instrinsic pacemakers, but have the _______ conduction velocity.
Purkinje Cells are the _SLOWEST_ instrinsic pacemakers, but have the _FASTEST_ conduction velocity.
Purkinje Cells are the Slowest instrinsic pacemakers, but have the Fastest conduction velocity Bc of 2 reasons:
1. Have more gap junctions
2. Size of Purkinje FIber (big a fat, but not myleinated)
Where is the slowest region in Autorhythmic cells in the order of excitation...
-> Between the AV Nodes & Bundle of HIS.
What is the bigest difference in starting resting potentials in autorhythmic cells comparted to ventricular m. fibers?
Autorhythemic cells starting potential are far more positive than ventriuclar m. fibers are.
Which Atrium contracts and depolarizes 1st?
Right atrium before left atrium
The sequence of depolarzation in cardiac tissue is kind of like doing what?
( hint- futrure dentist.. think teeth/ teeth products)
Squeezing tooth Pate -> squeeze from bottom up. ... Start at septum, then squeeze from bottom up - helps for optimal contraction.
The sequence of depolarzation in cardiac tissue 1-6
1. Depolarize Atria ( R then L)
2. Depolarize Septum from Left to Right)
3 Depolarize anteroseptal region of myocardium toward the apex.
4.Depolarize bulk of ventricular myocardium to epicardium.
5. Depolarize posterior portion of base of the left ventricle
6. The ventricles are now depolarized
1st area of depolarization if ventricles follow the ventricle septum which ventricle is depolarized 1st?
Left ventricle is little before right ventricle.
What are conduction blocks? what are they due to?
problem in communication between SA node and Purkinji fibers.
- Due to CAD (Cornary artery ds) or degeneration associated w/agging.
Autonomic innervation of Pacemaker cells:
Sympatheric efferent neurons innervate what parts of the heart?
ALL OF THE HEART
Autonomic innervation of Pacemaker cells:
Parasympathetic efferent neurons innervate what parts of the heart?
The SA & AV Nodes & a few contractile cells
Autonomic innervation of Pacemaker cells:
ACh activates muscarenic receptors which does what the K+ permeability?? which does what 2 things?
Increase K+ permeability
1. Slows AP Frequecny in nodal Cells
2.Slows transmission through the AV node
What does a vasovagal do?
It is activated by parasympathetics & can stop heart from beating for 15-20secs.
What causes vasovagal?
due to Pain -severe pain reason sometimes.. but bc of ACH.???
Autonomic innervation of Pacemaker cells:
NE- Actiavation of B1 receptor does waht to Na+ and Ca+ permeability>
Increases permeablity.. Cells depolarize more quickly.
Autonomic innervation of Pacemaker cells:
NE. Activation of B1 receptors incr. Na+ & Ca++ permeabilty which does:
a. ______ the rate of SA node Firing
b. _______ the rate of conduction throught the heart
c. ______ the force of contraction (atrial & ventricular)
a. _INCREASE_ the rate of SA node Firing
b. _INCREASE_ the rate of conduction throught the heart (SO Shorter time to contract & move quicker to contract force)
c. _INCREASES_the force of contraction (atrial & ventricular
HOw can the Autorhythemic cell firing be changed? 3
1. Altered by changing the SLOPE of If
2.SLOPE OF the Ica CURRENT
3.Changing thethreshold of Activation
4. Changing the threshold of resting Vm.
Summary of Autonomic Effects on Cardiac Cells:
SA Node
a.Fx:
b.B-Adrenegic Effect:
c.Cholinergic Effect:
a.Fx: Primary Pacemaker
b.B-Adrenegic Effect:
1.Increase Conduction Velocity
2. Increase Pacemarker Rate
c.Cholinergic Effect:
1. Decreases Pacemaker rate
2. Decreases Conduction Velocity
Summary of Autonomic Effects on Cardiac Cells:
Attial Muscle
a.Fx:
b.B-Adrenegic Effect:
c.Cholinergic Effect:
a.Fx: Expel Blood from Atria
b.B-Adrenegic Effect: Increase Contractility
c.Cholinergic Effect: Little effect
Summary of Autonomic Effects on Cardiac Cells:
AV Node
a.Fx:
b.B-Adrenegic Effect:
c.Cholinergic Effect:
a.Fx: Secondaty Pacemaker
b.B-Adrenegic Effect:
1.Increase Conduction Velocity
2. Increases Pacemarker Rate
c.Cholinergic Effect:
1. Decreases Pacemarker Rate
2. Decreases Conduction Velocity
Summary of Autonomic Effects on Cardiac Cells:
Purkinge Fibers
a.Fx:
b.B-Adrenegic Effect:
c.Cholinergic Effect:
a.Fx: 1. Rapid conduction of AP
2.Tertiatry Pacemaker
b.B-Adrenegic Effect: Increases Pacemaker Rate
c.Cholinergic Effect: Decreases Pacemaker Rate
Summary of Autonomic Effects on Cardiac Cells:
Ventricular Muscle
a.Fx:
b.B-Adrenegic Effect:
c.Cholinergic Effect:
a.Fx: Expel Blood from Ventricles
b.B-Adrenegic Effect: Increase Contractility
c.Cholinergic Effect: Little effect
Effects of Autonomic Stimulation on Cardiac Output:
Parasympathetic only effects?
HR
Effects of Autonomic Stimulation on Cardiac Output:
Sympathetic effects:
SV and HR simultaneously
What is the ECG use? and what does it do>
ECG-Uses electrodes placed on the skin of different body surfaces to record the electrical activity of the heart.
What is the ECG a valuable tool for clinically? 2
1. Examining the heart's electrical activity
2. Interpreting Cardiac Fx, Structure, & pathology.
What happens in the intracellular fluid of the ECG when the cell depolarizes?
The intracellular fluid switches from Negative to Positve.
Tips for understanding the ECG-
When Cell Depolarizes, the intrracellular fluid switches from negative to positive.
1. What happens when bc of depolarization and where does it go
2 What is a Vector?
1. The depolarization, which stimulates contraction, spreads through adjacent cells.
2. VECTOR: The direction of the depolarization
The electrical current of ECG is measure between _____ & ______ surface electrodes.
The electrical current of ECG is measure between _POSITIVE_ & _NEGATIVE_ surface electrodes.
The electrical current of ECG is measure between (+) & (-) surface electrodes.
-What does an UPWARD DEFLECTION represent??
Upward Deflection--> Depolarization moves toward Positive Electrode
The electrical current of ECG is measure between (+) & (-) surface electrodes.
-What does an DOWNWARD DEFLECTION?
Downward Deflection--> Depolarization moves toward the Negative Electrode
The electrical current of ECG is measure between (+) & (-) surface electrodes.
What if both electrodes read the same change>
Flat baseline
The electrical current of ECG is measure between (+) & (-) surface electrodes.
What depolarization moves toward the (-) electrode?
Downward Deflection
The electrical current of ECG is measure between (+) & (-) surface electrodes.
What depolarization moves toward the (+) electrode?
Upward Deflection
Waves formed onthe ECG depend on what?
The Position of (+) & (-) electrodes relative to the Vector created by the Heart's activity.
Waves formed on the ECG depend on the position of the (+) & (-) electrodes relative to the vector created by the heart's activity.
--> THe GREATER the MAGNITUDE of the DEFLECTION = what to happen in what direction?
The Greater the Magnitude of the Deflection= The GREATER the MAGNITUDE of the ELECTRICAL VECTOR in that DIRECTION.
(so (+) would be upward, etc. ??)
What are the steps/procedures in the Classic 3-Lead ECG method for recording ECG?
1. Electrodes are placed on R.arm, L.arm,& L. Leg
2.Each limb has a pair of electrodesd to make 3 leads between the limbs.
3. LEad configuration Leads to Einthoven's Triangle.
What are the 3 leads in Einthoven's Triangle? (Bipolar Limb Leads)
1. Lead 1 (horizontal): R. Arm (- ) to L. Arm (+)
2l. Lead 2: R. Arm (-) to L. Leg = The one most often looked at bc it follows the direction of the heart.
3. Lead 3: L. Leg (+) to R. arm (-)
The Bipolar Limb Leads bring lines of triangle together... MOve to intersect at
Move to intersect at a CENTER POINT
The AV Leads (Augmented Voltage Leads) are another mechanism to record _____
ECG
What is an AV Lead stand for?
Another name is _____?
What is the advantage to this lilead?
AV Lead= Augmentd Voltage Lead
=> AkA- UNIPOLAR Lead
=>Advantage- Combine 2 different leads for common ground or common (-)
-AVF-stands for?
-AVR-stands for?
-AVL-stands for?
-AVF= Augmentd Voltage FOOT (Left leg= where + electrode is placed)
-AVR= AugmentVoltage RIGHT (right arm = where + electrode is placed)
-AVL= Augmented Voltage LEFT (left arm= where + electrode is placed)
AV Leads
Why is where the (+) electrode is important?
Bc it orients you to the direction the depolarization is going.
What is AVF? where is the postiive electrode? where is the common negative?
+ Electrode= on Left Leg
(-) Common= Combination of both R.&L. Arms to form the vector . - Combination of Lead 2 & 3 bc going down.
AV Leads
2. What is AVR? Where is the (+) Electrode? where is the combine negative ground?
+ Electode= Placed on Right Arm.
SO, the L. Arm & L. Leg are combined to form the vector from the L to the R. (negative common ground)
AV Leads
3. What is the AVL? Where is the (+) electode placed>? what makes up the common neg ground?
(+) Electrode= Left Arm
(-) common ground= combination of the R.Arm & L. Leg
Limb & AV Leads
-Each lead looks at electicity of the heart from a particular perspective and tells how the heart is??
Depolarizing & if there is a pathology in a particular region of the heart.
Chest Leads are another mechanism to record ____
ECG
In recording ECG using the Chest Lead mechanism, you would place electrodes where?
Anterior Chest, directly over heart
In recording ECG using the Chest Lead mechanism, the PLANE of Recording is _______
HORIZONTAL
In recording ECG using the Chest Lead mechanism, the V1 & V2 are closer to the Base & the R. side of heart, thus their QRS recordings are ____ _______
DOWNWARD DEFLECTIONS
In recording ECG using the Chest Lead mechanism, QRS are Downward Deflections why?
BC V1 & V2 are closer to the Base & R.side of the Heart
In all 3 methods for recording ECG ( Classic 3-Lead/Limb, AV Lead, & Chest Lead) Each Individual LEAD REFLECTS the HEART's ______ activity from it's own ______.
Each individual lead reflects the heart's _ELECTRICAL_ activity from it's own _PERSPECTIVE_.
Is there a potential recordes in ECG when Ventricle is completely depolarized? WHat about when ventricle is completely Repolarized??
NO NEITHER! All you see is transitions when portions are in different electrical states
Atrial Depolarization/ Depolarizatoin of the atria is represented by what in the ECG?
P Wave
What has already happened at the point of Atrial Depolarization? (hint what has already fired an AP?)
SA NODE has already fired. (but can't measure SA node bc too small)
When Looking at LEAD 2 in ECG. (Atrial Depolarization)
- The cardiac dipole points at the ??
The cardiac dipole points at the (+) electrode of lead 2. (Points in direction of depolarized charge in same direction as (+) electrode.
In atrial depolarization WHAT is the RESULT of the cardiac dipole pointing at the (+) electrode of Lead 2?
Result: A (+) Deflection of P Wave on Lead 2
(Atrial Depolarization lead2)
Repolarization of the ATtria occurs when??
At the same time w/ Ventricular Depolarizatoin, thus is obscured by the QRS complex. ( Ventricle depolarizes at the same time Atria is Repolarizing)
Septal Depolarization (of Lead 2??)
A.- Which side of the interventricular septum is depolarized 1st? Left or Right?
B.The Cardiac Dipole points ____ __ the (+) electrode of Lead 2.
C. What is the 1st complex recoded on ECG? Wave & (+) or (-)?
A. LEFT SIDE (from L to R)
B. The Cardiac Dipole points _AWAY_ _FROM_ the (+) electrode of Lead 2.
C.Q Wave (-)
How does the Septum Depolarize? (Septal Depolarization)
-The Left side of interventricular septum is depolarized 1st. (from L to R)
-The Cardiac Dipole points away from the (+) electrode of Lead 2.
- (-) Q Wave recorded on ECG
(From L to R 1st complex is (-)
Apical Depolarization (Lead 2)
A. Depolarization direction is from?
B. The cardiac dipole points ___ the (+) electrode of Lead 2
C.What deflection is recorded on Lead 2? What is this an early part of?
A. Direction: Endocardium to Epicardium
B. The cardiac dipole points _TO_ the (+) electrode of Lead 2
C. A (+) Deflection is recorded on Lead 2
- The Early part of the (+) R Deflection
Ventricular Depolarization (Lead 2)
A.What is the LV Mass compared to RV mass?
B. The cardiac dipole points ___ the (+) electrode of Lead 2
C. Why does it go more Left than right?
D. What deflection is recorded on ECG?
A. LV mass=~ 3-fold RV mass
B. The cardiac dipole points _TO_ the (+) electrode of Lead 2 (Continues in same direction)
C.Bc mass is 3 fold larger in Left ventricle than right ( see A), which means more (+) charge in L. than R. Ventricle so continues upward deflection (see D)
D. The Whole (+) deflection is recorde on ECG
Late LV Depolarization (Lead 2)
A.The cardiac dipole points ___ _____ ___ the (+) electrode of Lead 2
B. What deflection & Wave are recorded on ECG?
A.The cardiac dipole points _SLIGHTLY AWAY FROM_ the (+) electrode of Lead 2
B. The DOWNWARD R Deflection & S WAVE are recorded on ECG
Complete Ventricular Depolarization of (lead 2)
A. Cardiac Dipole-
B. What is recorded on ECG?
A. NO Cardiac Dipole
B. An Isoelectric ST Segment is recorded on ECG (should be Flat Line. (50:50)
Ventricular Repolarization of Lead 2
A.Repoloarization takes place in what direction?
B.The Direction of charge is what? (how does this compare to depolarization of the ventricle?
C. What is the result of the direction/ Cardiac dipole points ?
D.What is the deflection on ECG?
A. Repolarization takes place in OPPOSITED Direction of Depol. * APEX TO BASE* (cells @apex= longer AP =plato so (D.). )
B.Direction of charge CHANGES: (+) to (-)... Not (-) to (+) like in depol
C. Result: Cardiac dipole pointing TO the (+) electrode of lead2
D. A (+) delection of T WAVE is recorded on ECG
Complete Repolarization of Ventricles of Lead2
A. Cardiac Dipole
B. Recording on ECG?
A. NO Cardiac Dipole Exists
B.Isoelectric (flat) line recorded on ECG
The whole ECG reading of Lead 2 From P- the T..8
. NEED TO LOOK BACK THROUGH ECG LECTURE slides 15-22
1. Atrial Depol. => P Wave(+) Deflection
2. Atrial Repol= same time as Ventricle Depol- QRS
3. Septal Depolarization=> (-) Q Wave
4.Apical Depolarization=>(+) deflection R Wave
5. Ventricular Depolarization=>Whole (+) deflection R
6.Late LV Depolarization=> Downward (-) deflection of R & S waves
7. Complete Depolarization=> Isoelectric ST = flat line
8.Ventricular Repolarization=> (+) deflection T WAVE
8. Complete REpolarization of Ventricles=>Isoelectirc (flat)line
Review of Normal ECG (Lead 2)
A. P Wave:
B. P-R Interval:
C.QRS Complex
D. Isoelectric ST Segment
E. T Wave:
F. Q-T Interval:
(ECG Lec- Slide From P- the 23)
A. P Wave: Atrial Depolarization.
- R. Arm (-) -->Left Leg (+)
B. P-R Interval: A-V Conduction Time
C.QRS Complex: Ventricular Depolarization (beginning of upward stoke)
D. Isoelectric ST Segment: Time during which all ventricles are depolarized & correspond to the plateau phase of the AP
E. T Wave:Ventricular Repolarization
F. Q-T Interval: The time for both ventricular depolarization & repolarization to occur
An ECG tracing runs at _____/____
ECG tracing runs at 25mm/sec
25mm= 1 sec
How to measure HR??
HR (beats/min)= (60sec/min) / # Sec/beat...
HR= 60/RR Intervals
or
HR= 300/ #large boxes, so 300/5
What is the sharpest component of the ECG?
The HR= R interval.
Common Abnormalities seen in ECG:
1. Vector Analysis - can be used to determine the
Electrical Axis of the heart
Common Abnormalities seen in ECG:
1. Vector Analysis - can be used to determine the Electrical Axis of the heart:
Which can be influenced by 2 things.
1. Body Type- can shift axis: obesity or tall and lanky
2.If a ventricle is hypertophied, the axis of heart shifts toward the hypertorphied ventricle. (bc alot more tissue to depolarize)
Common Abnormalities seen in ECG:
1. Vector Analysis - can be used to determine the Electrical Axis of the heart:
Which can be influenced by 2 things
1. BODY TYPE CAN SHIFT AXIS
A. Obesity-->
B. Tall , Lanky-->
A. Obesity--> Left Axis Deviation ( also preggers.. bc abs contents in left axis)
B. Tall, Lanky--> Right Axis Deviation- Ex. Trey Anderson
Common Abnormalities seen in ECG:
2. CHanges in Voltages of the ECG - 3 things
1. M. Hypertophy will INCREASE the voltage of QRS complexes
2. Infarctions lead to atrophy
--> Decreased M. mass
3. Fluid in Pericardium (lessening in voltages of ECG)
Common Abnormalities seen in ECG:
2. CHanges in Voltages of the ECG - 3 things
1. M. Hypertorphy will _____ the voltage of QRS complexes
1. M. Hypertophy will INCREASE the voltage of QRS complexes
Common Abnormalities seen in ECG:
2. CHanges in Voltages of the ECG - 3 things
2. Infarctions lead to atrophy--> ______ in M. mass
2. Infarctions lead to atrophy
--> Decreased M. mass
Common Abnormalities seen in ECG:
2. CHanges in Voltages of the ECG - 3 things
3. Fluid in pericardium - leades to lessing of what in ECG?
3. Fluid in Pericardium (lessening in voltages of ECG)
Common Abnormalities seen in ECG:
1. Vector Analysis--> Body type can shitt axis
A. LEFT Axis Deviation= Lead ___
B. RIGHT Axis Deviation = Lead ____
A. LEFT Axis Deviation= Lead _1_
B. RIGHT Axis Deviation = Lead _2__
Common Abnormalities seen in ECG:
3. Changes in Duration of QRS Interval- by 2 ways?
1. Hypertophy of Ventricles ( takes longer for signal to travel through , extra tissue, so it takes longer to depolarize it.
2. Zofan- Increases the duration of QRS interval
Common Abnormalities seen in ECG:
4. Changes in ST Segment-
A. how should it look?
B. How should it look if Acute MI?
A. Should be flat (isoelectric) (only point that is isoelectric??)
B. Acute MI- Elevated ST segment.
Common Abnormalities seen in ECG:
5. Arrhythmias-4types
1. Bradycardia-
2. Tachycardia-
3.Atrial Ventricular Fibrillation- 4. Heart Block
Common Abnormalities seen in ECG:
5. Arrythmias- 4types
-1. Bradcardia-
1. Bradycardia- abnormal slow HR ( <60bpm)
Common Abnormalities Seen in ECG:
5. Arrhthemias-4types
2. Tracardia
2. Tachycardia- abnormally fast HR- >100bpm @rest. = Sinus problem in SA Node
Common Abnormalities Seen in ECG:
5. Arrhthemias-4types
3.Atrial Ventricular Fibrillation
3.Atrial Ventricular Fibrillation--
ATRIAL-uncordinated contraction in atruium= Decrese ventricular Filling & SV => If blood stays for long time- inc. risk for clot- need anticollagent)
Common Abnormalities Seen in ECG:
5. Arrhthemias- 4types
4.Heart Block
a. 1st Degree-
b. 2nd Degree-
-Type1-
-Type2-
c. 3rd Degree-
4. Heart Block- Problem of conduction from Atria to ventricle
a. 1st Degree- "Slow conduction." - Longer than normal P-R Interval(takes longer to send single depoalrization of atria and depol of ventricle)
b. 2nd Degree-' Intermettin'
-Type1-"Mobitz type1"- Changes in P-R Interval- where it each PR interval progressively gets longer& longer between the 2& eventually drops a QRS.
-Type2- "mobitz type 2" Regular PR intervalbut only see PWave ( p wave-sometimes it works, sometimes it doesn't)
c. 3rd Degree- "COMPLETE HEART BLOCK"- Atria NOT communicating w/ventricle.. So P waves not elicit a QRS wave.
What is a complete heart block
Heart block 3rd degree of arrythemias
Common Anti-Arrhthmic Medications- what do the mostly target? what are the 4 classes?
- Mostly target tachyarrythmias ( or too rapid/fast HR)
4 Classes:
1. Class 1- Block Na+ channels
2. Class 2- Block Beta Adrenergic Receptors
3.Class 3- Block K+ Channels
4. Class4- Block L-Type Ca+ Channels
Common Anti-Arrthymic Medications- 4 Classes:
1. Class 1- Block Na+ Channels.
A. Na+ channels are important for what??
B.SO blocking Na+channels does what
C. What is that result in?2
A. Na+ channels- important for Depol
B. SO- blocking Na+ channels = SLOWING of Depol at the beginning of AP & mostly in Fast Contracting Cells
C. Results: 1.Slow down contraction
2. Slow down conduction between cells bc of lack of communication of Gap Junctions
Common Anti-Arrthymic Medications- 4 Classes:
2. Class2- Block Beta Andrenergic Receptors
-What Target? & 2 results?
-Target BETA1
-Antagaonist/ Blockers of BETA1 Result in: Decreased HR & Conduction (slow signals beween cells)
Common Anti-Arrthymic Medications- 4 Classes:
3.Class 3 Block K+ Channels
A. about?
B. What does blocking K+ Channels do?
C. Bc of ^(B)^ what is the result?
A. FAVORED TREATMENT
B. Slow Repolarization
C. ^ ^ Which Leads to INCREASE in LENGTH of AP, so SLOW CONDUCTION
Common Anti-Arrthymic Medications- 4 Classes:
4. Class4: Block L-Type Ca++ Channels
A.What cells are targetted here?
B. What is the result?
A. Autorhythmic Cells-->
B. DEPOLARIZATION Rate of Autorhythmic cells are SLOWED & SLOW CONDUCTION between Cells.
Smooth m. cells are ______ smooth m. cells.
- They are Normally ______ ( have "___"), but can____________________
Smooth m. cells are _TONIC_ smooth m. cells.
- They are Normally _CONTRACTED_ (have "_TONE_"), but can_ALTER Their FORCE of CONTRACTOIN_
( Tonic sensitive entire time in skeltal)
Smooth M. Contraction comparted to SKeletal& Cardiac contractions??
Smooth M. Contraction is FAR SLOWER to DEVELOP & LASTS Much LONGER than Skeletal& Cardiac contractions.
What do Smooth Muscle Fibers
A. Contain?
B. Lack?
C. Require for Contraction?
1.
2.
A. Contain: Actin& Myosin
B. Lack: Troponin & Tropomyosin
C. Require for Contraction?
1. Ca++
2. ATP
What do Smooth Muscle Fibers
C. Require for Contraction?
1. CA++ - what does it bind to?
1. Ca++ (binds to Calmodulin) - for (to stimulate) contraction
What do Smooth Muscle Fibers
C. Require for Contraction?
2. ATP - IN 2 Plaves
a.
b.
2.ATP
a. For Ca++ Stimulated Contraction ??(??_)
B. Myosin Head ATPase
How can smooth muscle contraction be stimulated? -3 ways:
1. Stretch
2. Ligands
3. Pacemaker Cells
How do smooth Muscles Increase Contractile force?
- AP is ****NOT***Required for increase in contractile forces*
-GRADED Potentials can open Ca+ Channels which in turn can initiate ca++-induced Ca++ release from SR (once it is in the cell that is (IP3)-Interacellular Ca++ binds to Calmodulin
Smooth muscles can use Graded potentials to increase Contractile forces by:
A. Opening ___ Channels which in turn can intiate ____ -_______ ____ Release from __
B.-Intracellular Ca++ binds to _______
A. Opening _CA++_ Channels which in turn can intiate _CA++-INDUCED_ _CA++_ Release from _SR_ ( Once in the cell that is (IP3)
B.-Intracellular Ca++ binds to _CALMODULIN_
Cross Bridge Cycling in Smooth M.:
- Attachement of Myosin to actin depends on ??
The Phosphorylation of Cross-Bridge By Myosin Light Chain Kinase (MLCK).
Cross Bridge Cycling in Smooth M.:
- Attachement of Myosin to actin depends on the Phosphorylation of Cross-Bridge by MLCK.
=> WHAT is MLCK Activated by??
Calcium-Calmodulin
Cross Bridge Cycling in Smooth M.:
Phosphorylated Crossbridges continue to cycle ( Myosin ATPase is active) until ??
Myosin Phosphatase Dephosphorylates the Myosin Head
Cross Bridge Cycling in Smooth M.:
Phosphorylated Crossbridges continue to cycle - How does it do this?
Bc myosin ATPase is still active
Cross Bridge Cycling in Smooth M.:
IN the presence of ATP MLCK stimulates?
Cross Bridge Cycling
Cross Bridge Cycling in Smooth M.:
Need ATP for 2 reasons?
1. Stimulates Crossbridge cycling
2.Allow for rationing(???) of Myosin head
Excitation-Contraction Coupling in Smooth M.:
When myosin is dephosphorylated, myosin & actin form Latch Bridges. Tension is maintained although Ca++ & ATP are absent. This is CALLED?
LATCH STATE
Excitation-Contraction Coupling in Smooth M.:
Latch State is when myosin is dephosphorylated, myosin & actin form ____ _____. Tension is maintained although ___ & ___ are absent.
When myosin is dephosphorylated, myosin & actin form _LATCH BRIDGES_. Tension is maintained although _Ca++_ & _ATP_ are absent.
Excitation-Contraction Coupling in Smooth M.:
When myosin is Phosphorylated, Corss bridges repeatedly ___ & ____ if ____ is present.
When myosin is Phosphorylated, Corss bridges repeatedly _FORM_ & _BREAK_ if _ATP_ is present.
Excitation-Contraction Coupling in Smooth M.:
Why is the Latch state so cool/ unique???
Because smooth muscle becomes latched together= SUSTAIN CONTRACTION W/Out any more Energy Used ( no more ATP used).
In smooth muscle- What is a TONIC COntraction?
A sustained contraction at low cost
Tonic CONtractions in smooth muscles do what?
** Smooth M. Contracts a _FORCE_ & that _FORCE_ is maintained at the _SAME RATE__
Common Abnormalities Seen in ECG:
5. Arrhthemias-4types
2. Tracardia
2. Tachycardia- abnormally fast HR- >100bpm @rest. = Sinus problem in SA Node
Common Abnormalities Seen in ECG:
5. Arrhthemias-4types
3.Atrial Ventricular Fibrillation
3.Atrial Ventricular Fibrillation--
ATRIAL-uncordinated contraction in atruium= Decrese ventricular Filling & SV => If blood stays for long time- inc. risk for clot- need anticollagent)
Common Abnormalities Seen in ECG:
5. Arrhthemias- 4types
4.Heart Block
a. 1st Degree-
b. 2nd Degree-
-Type1-
-Type2-
c. 3rd Degree-
4. Heart Block- Problem of conduction from Atria to ventricle
a. 1st Degree- "Slow conduction." - Longer than normal P-R Interval(takes longer to send single depoalrization of atria and depol of ventricle)
b. 2nd Degree-' Intermettin'
-Type1-"Mobitz type1"- Changes in P-R Interval- where it each PR interval progressively gets longer& longer between the 2& eventually drops a QRS.
-Type2- "mobitz type 2" Regular PR intervalbut only see PWave ( p wave-sometimes it works, sometimes it doesn't)
c. 3rd Degree- "COMPLETE HEART BLOCK"- Atria NOT communicating w/ventricle.. So P waves not elicit a QRS wave.
What is a complete heart block
Heart block 3rd degree of arrythemias
Common Anti-Arrhthmic Medications- what do the mostly target? what are the 4 classes?
- Mostly target tachyarrythmias ( or too rapid/fast HR)
4 Classes:
1. Class 1- Block Na+ channels
2. Class 2- Block Beta Adrenergic Receptors
3.Class 3- Block K+ Channels
4. Class4- Block L-Type Ca+ Channels
Common Anti-Arrthymic Medications- 4 Classes:
1. Class 1- Block Na+ Channels.
A. Na+ channels are important for what??
B.SO blocking Na+channels does what
C. What is that result in?2
A. Na+ channels- important for Depol
B. SO- blocking Na+ channels = SLOWING of Depol at the beginning of AP & mostly in Fast Contracting Cells
C. Results: 1.Slow down contraction
2. Slow down conduction between cells bc of lack of communication of Gap Junctions
Common Anti-Arrthymic Medications- 4 Classes:
2. Class2- Block Beta Andrenergic Receptors
-What Target? & 2 results?
-Target BETA1
-Antagaonist/ Blockers of BETA1 Result in: Decreased HR & Conduction (slow signals beween cells)
Common Anti-Arrthymic Medications- 4 Classes:
3.Class 3 Block K+ Channels
A. about?
B. What does blocking K+ Channels do?
C. Bc of ^(B)^ what is the result?
A. FAVORED TREATMENT
B. Slow Repolarization
C. ^ ^ Which Leads to INCREASE in LENGTH of AP, so SLOW CONDUCTION
Common Anti-Arrthymic Medications- 4 Classes:
4. Class4: Block L-Type Ca++ Channels
A.What cells are targetted here?
B. What is the result?
A. Autorhythmic Cells-->
B. DEPOLARIZATION Rate of Autorhythmic cells are SLOWED & SLOW CONDUCTION between Cells.
Vascular smooth m cells are ___ smooth m. cells. Theyare normally ______ (have "__"), but can alter their ____ of _____.
Vascular smooth m cells are _TONIC_ smooth m. cells. They are normally _CONTRACTED_ (have "_TONE_"), but can alter their _FORCE_ of _CONTRACTION_. ( tonic sensitive entire time in skel m.) (NOT AT MAX CONTRACTION)
How does smooth m, contraction compare to skeletal & cardiac muscle contractions?
Smooth M. Contraction is FAR Slower to DEVELOP & Last much LONGER than skeletal & cardiac contractions.
Smooth muscle:
A. Contain:2
B. Lack:2
C. Require:2
A. Contain- Actin & Myosin
B. Lack- Troponin & Tropomyosin
C. Require:
1. Calcium (Bind calmodulin) (to stimulate) for contraction
2. ATP for contraction (mupsion head has an ATPase)
Smooth m. contraction can be stimulated by 3 things:
1. Stretch
2. Ligands
3 Pacemaker Cells
Are action potentials required for increases in contractile force in smooth m.?
NO!
APs are NOT required for increases in contractile force in smooth m.. What can be used? and where does the component bind?
1. Graded potentials can open Ca++ channels which in turn can initiate Ca++ induced ca release from SR (once it is in the cell that is IP3)
Intracellular Ca++ binds to calmodulin.
Cross bridge cycling in smooth m.:
Attachment of myosin to actin depends on the :
Phosphorylation of the crossbridge by myosin light chanin kinsase (MLCK)
Cross bridge cycling in smooth m.:
Attachment of myosin to actin depends on the phosphorylation of the crossbridge by (MLCK).
-How is MLCK activated?
by Ca+ Calmodulin
Cross bridge cycling in smooth m.:
After myosin actin attaches, phosphorylated cross-bridges continue to cycle (myosin ATPase is active) until when?
Unil Myosin phosphatase dephosphorylates the myosin head.
What stimulates cross bridge cycling/?
MLCK... Which has to be in the pressence of ATP to stimulate it.
Ecitation -contraction Coupling in smooth m.:
When Myosin is dephosphorylated, myosin & actin form _____ ____. Tension is maintained althought ___ & ___ are absent.
Ecitation -contraction Coupling in smooth m.:
When Myosin is dephosphorylated, myosin & actin form _LATCH BRIDGES_. Tension is maintained althought _ATP_ & _CA++_ are absent.
Ecitation -contraction Coupling in smooth m.
Ecitation -contraction Coupling in smooth m.:
When Myosin is dephosphorylated, myosin & actin form Latch Bridges. Tension is maintained althought ATP & Ca++ are absent. This is called??
LATCH STATE
Why is the Latch state unique to smooth muslces? why is it important?
Bc the muscles become latched together
THey can sustain contraction w/out using any additional energy (ATP).
Ecitation -contraction Coupling in smooth m.:
When myosin is PHosporylated, corss bridges repeatedly do what? in the pressence of what?
Cross birdges repeatedly FORM & BREAK if ATP is present .. when myosin is phosphorylated
Tonic Contractions are?
-smooth muscles contracts what happens in thesetonic contractions?
Sustained Contractions ar a low cost.
-As smooth m contracts force.. FORCE maintained at SAME RATE!!!
Latch state can save up oto how much ATP that would normally be used ?
- what stops latch state?
up to 300 times
-unsure what stops latch state, but might be ca++ levels dropping
Arteries
1. size of vessel
a. what muscle type
b. walls are ??
2. ____ pressure Vessels
3. ____ Velocity Blood Flow
1. Thick Vessel Walls- Largest Vessels
a. LOTS of Vascular SMOOTH m. (in arterial wall)
b. Walls are COMpliant/distensible (able to stretch/ eleasticity)
2. _HIGH_ pressure Vessels
3. _HIGH_ Velocity Blood Flow
Arterioles
1.Branch off of ____
2. Vessels with the Largest ____ in the ______
3.They are _____ muscles bc?
a. ____ sphincters
Arterioles
1.Branch off of _ARTERIES_
2. Vessels with the Largest _RESISTANCE_ in the _CIRCULATION_
3.They are _CONTROL_ muscles bc? of Resistance
a. _PRECAPILLARY_ sphincters -BANDS OF SMOOTH MUSCLES SPEARTETE
Capillaries
1. ____ of Blood Vessels; bc made up of ____ &____ _____
2.______ Velocity of Blood Flow
3.____ Blood Volume
a. precap shpincters
4. Fx:
1. _SMALLEST_ of Blood Vessels; bc made up of _ENDOTHELIUM CELLS_ &_BASEMENT MEMBRANE__
2._SLOWEST_ Velocity of Blood Flow
3._LOW_ Blood Volume
a. precap shpincters
4. Fx: EXCHANGE W/INTERSTITIAL FLUID
Metarteriole
- what does this vessel do?
Bypase between arterioles & venules to connect to??
Types of Capillaries:
1. Continuous capillaries?
Most common- Found in BBB, tighter and tight junctions small passage ways
Types of Capillaries:
2. Fenestrated Capillaries-
Opening in endothelial cells.
- In Endocrine organs, glomerus, and intestines,
- Lots of secreation and absorption
Types of Capillaries:
3. Sinusoidal caps-
Fenstrated - large and LEAKY!
- Found in Spleen, liver & lymph nodes
- Inc movement of cells into and out of vessels
Venules
-early venulues allow for? fx?
- What important thing singals start here?
Early venules allow for EXchange across vessel walls
- signals of ANGIOGENISS start HERE
Veins
1. _____ Vessels: ____ blood volume of all vessels
2._____ Pressure of all vessels
a.1 way flow depnds on ___
b. ____ ____ necessary for flow, particualarly against gracitational pressure
3.Vascular smooth muscle can ____ & _____ to alter venous return to heart
Veins
1. _CAPACITANCE_ Vessels: _HIGHEST_ blood volume of all vessels
2._LOWEST_ Pressure of all vessels
a.1 way flow depnds on _VALVES_
b. _VENOUS PUMPS_ necessary for flow, particualarly against gracitational pressure
3.Vascular smooth muscle can _CONSTRICT_ & _DILATE_ to alter venous return to heart
-SUPER STRETCHY
Circulatory Characteristics:
1. Blood volume:
- Big= ___ L bloodvol.
=>Distribution of blood ( via %) in diff. parts of body?
a. Pulmonary Circ-
b. Systemic Cir-
c. Veins,Venules & venous sinuses
d. Arterioles & caps
e. Arteries
f. Heart
LARGEST??
Big= _5_ L bloodvol.
a. Pulmonary Circ- 9%
b. Systemic Cir- 84%
c. Veins,Venules & venous sinuses- 64%
d. Arterioles & caps-7%
e. Arteries-13%
f. Heart-7% (right side)
Largest= Systemic Circulation
Circulatory Characteristics:
1. Blood Volume
-Where are the blood resivors> like need extra blood would get it from??
LARGE ORGANS
such as large ab veins, liver, spleen, etc.
Circulatory Characteristics:
2. Cross Sectional Area of following Vessels:
a. Aorta-
b. Arterioles-
c. Capillaries-
d. Venules-
e. Vena Cava-
a. Aorta- 2.5 cm(^2)
b. Arterioles- 40 cm(^2)
c. Capillaries- 2500 cm(^2)
d. Venules- 250 cm(^2)
e. Vena Cava- 8 cm(^2)
Circulatory Characteristics:
3. Velocity of Blood Flow
- Velocity of Blood Flow is ____ proportional to cross-sectional area. Thus flow is:
- Fx advantage?
- Velocity of Blood Flow is _INVERSELY_ proportional to cross-sectional area.
(Velocity = {Flow} / {Cross-sectional area} )
-Thus flow is: SLOWEST through the CAPILLARIES (vessel w/ largest X area= slowest velocity)
-Fx advantage- INCREASE in Nutrient Exchange
Circulatory Characteristics:
4.Pressure
- Pressures must ______ throughout the vascular circuit.
- Pressures must _DECREASE_ throughout the vascular circuit.
( See smoothing in flow in caps bc important for max exchange)
Blood Flow:
1. Volume of blood passing a given period of time ( __/__)
1. Volume of blood passing a given period of time (_mL_/_MIN_)
Blood Flow:
1. Volume of blood passing a given period of time (_mL_/_MIN_)
a. Ohm's Law F= (flow=)
b. Thus, flow is driven by the ____ _____ & impeded by ___ ____
A. Ohms Law : F= }D{ (P)/ (R
Flow = (Change in) Pressure between 2 points / resistance
B. Thus, flow is driven by the _PRESSURE GRADIENT & impeded by VASCULAR RESISTANCE
Blood Flow:
1. volume of blood
Increase in blood flow= 2 things? initial and end pressure
Resistance is always???
Increase in Blood Flow=
1. Increase in initial Pressure
2. Decrease End Pressure
=>Resistance= Always oppoostion of pressure
Blood Flow:
2. 2 types of flow in Vessesls ( not including No flow)
1. Laminar Flow
2. Turbulent flow
Blood Flow:
2. 2 types of flow in Vessels
1. Laminar Flow
2. Turbulent flow
1. Laminar Flow- Straigh- moves more cells through vessel stays in line - highest velocity in middle. Edges have a bit more resistance to them.
2. Turbulent flow- just like on an airplane bumpy... hit a point and turn back on itself.
Blood FLow
2.Types of flow-2
1. Laminar Flow
a. When vessels are _____., endotheium is _____ , ___ (size) vessels
b. Velociy of flow is always _____ in the _____ of the vessel compared to the outside.
- Parbolic profile of flow=
a. When vessels are _STRAIGHT_., endotheium is _HEALTHY_ , _SMALLER_ vessels
b. Velociy of flow is always _GREATER_ in the _CENTER_ of the vessel compared to the outside.
- Parbolic profile of flow= always seen in particular distribution of w/in vessel ( central flow fastest)
Blood FLow
2.Types of flow-2
2. Turbulent flow
a. ____ Flow
b. More likely if: 4 things
c.Creates ____ _____ which ____ resistance & friction in vessel
d. problem?
a. _DISORERLY_ Flow (not straight)
b. More likely if:
-High velocity of BF, Obstructed Vessels, Sharp turns in vessels, Endothelium is rough/damaged.
c.Creates _EDDY CURRENTS_ which _INCREASE_ resistance & friction in vessel
d. problem? Increase friction & empides flow
Blood FLow
2.Types of flow-2
2. Turbulent flow
-What is Reynolds number? What is the standard?
Reynold's Number (Re)= Calculation of FLOW Turbulence.
- If Re is > 2000 flow is most likely turbulent. >3000 , always turbulent.
Blood FLow
2.Types of flow-2
2. Turbulent flow
how is Re calculated? / what is turbulence directly and indirectly propotional to?
Re= [ (V) (d) (p) ] / [ n]
- Turbulence Directly propotional to:
a. V- velocity of Blood Flow
b. d- Diameter of Vessel
c. p- DENSITY of Blood
INDIRECTLY to:
a. n- Viscosity of blood
Blood FLow
2.Types of flow-2
2. Turbulent flow
a. If increase viscosity of blood what happens to turbulence?
a. Turbulence Decreases
Blood FLow
2.Types of flow-2
2. Turbulent flow
What is Turbulent Flow a problem??
4 reaseons?
1. Increases the energy required for flow
2. Increases the risk of endothelial injury
3. Increases the possiblity of Thromic events (clots) & embiotic events (Detatchment of clots)
4. Increases the Energy required to Dirve Flow
Resistance
A. Total Peripheral Vascular Resistance (TPR)
B. Poisuuille's Equation =
B. Poiseulle's Equation
R=*nl/ pi r^4
(resistance= [ 8 x Viscosity x Length] / (pi) x Radius (raised to the 4th)
Resistance
B. Poisuuille's Equation =
A. Increase in viscosity = ____ Resistance & ___ Flow
B.Increase in Vessel Length= ____ resistance & that ___Flow
C. Increase in Radius= greatly ____ Resistance & which ____ Flow
A. Increase in viscosity = _INCREASE_ Resistance & _DECREASE_ Flow
B.Increase in Vessel Length= _INCREASES_ resistance & that _DECREASE_ Flow
C. Increase in Radius= greatly _DECREASES_ Resistance & which _INCREASES_ Flow
Hematocrit has a _____ affect on Blood Viscosity
-what is hematocrit?
-what is a normal hematocrit?
Hematocrit has a _DIRECT_ affect on Blood Viscosity
- Hematocrit= Ratio of RBC to BLOOD VOLUME= % of RBV
- Normal 38-42
Hematocrit has a Direct Affect on Blood Viscosity..
SO, Anemia would be expecto to ____ Resistance & ___ Flow.
=>WHAT type of Flow would MOST likely be associated with anemia?
Hematocrit has a Direct Affect on Blood Viscosity..
SO, Anemia would be expecto to _DECREASE_ Resistance & _INCREASE_ Flow.
=>iNCREASES TURBLENT FLOW
Small changes in Vessel Diameter induce Large Changes in ____ ______
BLOOD FLOW
What is the most powerful determinant of cascular resistance?
RADIUS
Radius is the most powerful determinant of vasculature resistance. This is convenient because?
This is convenient since RADIUS is the ONLY Variable that the SYSTEM has CONTROL over!
How can body alter vascular system?
by ALTERING the RADIUS of the VESSELS!
(not by viscosity or lengthening)
A man suffers a stroke caused by partial occlusion of his left int. carotid A. Eval of man's carotid artery shows a 75% reduction in its radius. Assuming that blood flow through the left carotid artery is 400ml/min prior to the occlusion, what is blood flow through artery after the occlusion?
Low would DECREASE signifcantl bc increase in resistnace so it would increase by 256 folds. Radius is decreased by 1/4, so resistance is increased by 1/ (1/4 (raised to the 4th))
So flow (f= DP/R ) = 39 % of normal vafoule..... JUST KNOW IT IS A DECREASED ALOT!!
How is smooth m. cells diff from other muscle cells in contraction how the L .state?
The latch state= can use 300 times less ATP than skeletal or cardiac m. cells.
Which is called a TONIC CONTRACTION.... WHich Vascular Smooth Muscles do tonic contractions.
How is Ca+ diff in smooth m. than other m.?
maintains contraction.. binds comaudulin and enzyme MLCK which allows actin myosin binding
Other than ca++ and latch state how is smooth m. diff from cardiac or skeltetal muscle?
think rate of contration, force, AP
- slow to contract
- Less force
- Don't need AP to elicit contraction, just need a graded potentional
Which vessels store the largest vol. of blood?
Veins
Which vessels have the largest cross sectional area?
smallest?
importance?
Largest- Capillaries
Smallest- Arteries
Importance- for velocity
Where is velocityof blood flow the fastest?
slowest?
Fastest= Arteries
SLowest= Capillaries
Vessels with highest pressure are?
Lowest pressure?
Highest= Arteries
Lowest= Veins
Very simply, what are the determinants of blood flow (and how quick it flows)?
- 2
1. Resistance=
a. RADIUS**
b. Length of Vessel
c. Viscosity
2.Pressure Gradient =
F= dP (between 2 points) / R
An increase in arterial pressure does what to blood flow?
INCREASES Blood Flow
Increase in Arterial Pressure increases Blood Flow
a. Directly by:
b. Indirectly bc:
a. Directly by: INCREASING PRESSURE GRADIENT
b. Indirectly bc: the INCREASED PRESSSURE DISTENDS VESSELS, DECREASING RESISTANCE
Calculation of Resistance to Blood Flow:
- 2 flow types
1. Series Flow
2. Parallel flow.
Calculation of Resistance to Blood Flow:
1. Series Flow:
a. Blood travels from A.->
b.Total resistance to blood flow is:
c. Rtotal=
d. In a series, the total flow through each leve is _____
a. Blood travels from A.-> Arteriolie -> cap. ( add up individual resistance)
b.Total resistance to blood flow is: EQUAL to the SUM of INDIVDUAL RESISTANCES
c. Rtotal= R1 + R2 +R3....
d. In a series, the total flow through each leve is _EQUAL_ (Amt. of blood enters into heart same as it is>>??)
Calculation of Resistance to Blood Flow:
1.Series Flow- In a series, the total flow through each level is Equal.
=> IF this is true, what must change when resistance Increases in order to maintain constant flow??
Have to change pressure gradient in order to maintain constant flow.
Calculation of Resistance to Blood Flow:
Which vessel has the highest resistance and therefore has the greatest drop in pressure?
ARTERIOLES
Calculation of Resistance to Blood Flow:
C.O. is distributed unevenly between different organs. Blood Flow through each parallel branch is ____ equal. Resistance in each branch is ___ equal. But pressure in each branch is _____ equal.
C.O. is distributed unevenly between different organs. Blood Flow through each parallel branch is _NOT_ equal. Resistance in each branch is _NOT_ equal. But pressure in each branch is _RELATIVELY_ equal.
Calculation of Resistance to Blood Flow:
2. Parallel Blood Flow
a. Travels from A =>
b. Total resistance of a parallel circuit is ___ than the ressistance of an individual vessel bc??
c. 1/ Rtotal=
d. Adding a blood vessel in a parallel circuit will ____the totalresistance of the system. which means?
a. Travels from A => multiple arterioles
b. Total resistance of a parallel circuit is _LESS_ than the ressistance of an individual vessel bc: OF PHYSICS.. (causes d)
c. 1/ Rtotal= 1/R1 + 1/R2 + 1/R3...
d. Adding a blood vessel in a parallel circuit will _REDUCE_the total resistance of the system. which means: THAT Iit Becomes Easier for BLOOD to FLOW Through the CIRCUIT as a WHOLE.
Calculation of Resistance to Blood Flow:
2.Parallel Blodd Flow
What happens to the resistance of the system (TPR) when an individual vessel's resistance increases?
Increase in individual vessel = increase in resistance around..
_____ is the volume of blood can hold at a given pressure.
COMPLIANCE
Compliance is the vol. of blood can hold at a given pressure.
Compliance =
Compliance= (change in) Volume / (change in) pressure
Compliance is the vol. of blood can hold at a given pressure.
At higher compliances, what happens to the amount of vol. that can be stored?
- A lot more vol. can be stored for each mmHG change in pressure.
Compliance is the vol. of blood can hold at a given pressure.
Veins- see Increase in ___ but not in ___
Veins - see Increase in _ VOLUME_ but not in PRESSURE very much like you do in A.
Compliance is the vol. of blood can hold at a given pressure.
Arteries- as you age what changes??
There is a decrease in vol as pressure increases compared to younger
Vascular Capacitance /compliace is ??
The ability to stretch and store blood
Veins are ___ times ___ distensible than arteries
Veins are _8_ times _MORE_ distensible than arteries
Veins contain _____ ___ _____ ( bc pressure very low); Large ____ under _____ pressure.
Veins contain _UNSTRESSED BLOOD VOLUMES_ (bc pressure very low); Large _VOLUME_ under _LOW_ pressure.
Arteries contain _____ ____ ____; Low ____ under ____ Pressure
Arteries contain _STRESSED BLOOD VOLUMES_; Low _VOLUME_ under _HIGH_ Pressure
Changes in compliance cause ____ ____
BLOOD SHIFTS (usually venule)
Changes in compliance cause blood shifts.
1. Venoconstriction-
1. Venoconstriction- Not change in total ressistance or pressure,but change in volume
- push more blood into heart
and INCREASE SV. ( by increasing (EDV??)
Changes in compliance cause blood shifts.
2. Aging of arteries
- like artherosclerosis- [hardening of vasculature wall (increase collagen, decrease elastin).]---> as arteries become more stiff, can't streach, so need higher pressure for blood to go in.
Changes in compliance cause blood shifts.
3. Sympathetic innervation
- decreases compliance.. helpful in hemmoarage
Volume -Pressure Curves of Systemic A & V.
For a massive hemmoarge u want to??
Get all vol you can from any resiovore, so DECREASE vol. of vessels from Sympathetics
Volume -Pressure Curves of Systemic A & V.
=>Sympathetic Stimulation does what??? how does it affect hemorrage?
- DECREASES Compliance.
- HELPFUL ( inparticurlarly) during hemorrage.
Volume -Pressure Curves of Systemic A & V.
=> When vol changes in arterial system does pressure change?
B. Veins?
A. Arteries- YES, A LOT!
B. Veins- a little bit, but it is marginal.
Volume -Pressure Curves of Systemic A & V.
- What is the imporacne of sympathetic stimulation?
- Better able to maintain arterial pressure inspite of blood volume loss.
Volume -Pressure Curves of Systemic A & V.
=> would you rather loose blood in arteries or veins? why>
VEINS! Bc if drop vol. in veins not much pressure is lost.
Compliance of Healthy Arteries Helps Ensure __ ____ ____
Continuous Capillary Flow
Compliance of Healthy Arteries Helps Ensure Continuous Capillary Flow:
1. Systole?
Arterial blood flows through the capillaries throughout systole.
Compliance of Healthy Arteries Helps Ensure Continuous Capillary Flow:
2. Diastole"
Arterial blood continues to flow through the capillaries throughout diastole.
Compliance of Healthy Arteries Helps Ensure Continuous Capillary Flow:
When the arteries are nomally compliant, a substantial fraction of the SV is stored in the arteries during?>??
Ventricular systole
Compliance of Healthy Arteries Helps Ensure Continuous Capillary Flow:
When are the previously stretched arteies recoiled? the vol of blood is displaced by the recoil ensures continuous cap flow throughout this stage?
Ventricular diastole
What happens to capillary flow w/severe arteriosclerosis (where walls become rigid)?
Capillary flow Increases & becomes pulsitile b/c what happens is that there is a loss of ability for vessels to stretch & hold extra bit of blood that they release during diastole, the blood just shoots through the the arteries all the way into capillaries everytime the ventricle contracts. SO Get a MUCH more PULSITILE Delivery of BLOOD which means NOT GOOD for EXCHANGE!
What is the driving force of blood flow throughout the circulatory system?
the PRESSURE GRADIENT
Pressures in the ARTERIAL VESSELS is ______, producing _____ & _____ Pressures.
Pressures in the ARTERIAL VESSELS is _PULSATILE_, producing _SYSTOLIC_ & _DIASTOLIC_ Pressures.
If not for _______ ________, blood would flow almost instantaneously from the heart through the vessels to the capillaries.
If not for _ARTERIAL VESSELS_, blood would flow almost instantaneously from the heart through the vessels to the capillaries.
Pressures in the Arterial Vessels is _Pulsatile_, producing _Systolic_ & _Diastolic_ Pressures.
=> WHERE does PUSATION Disappear?
By the CAPILLARIES!!! BECOMES SMOOTH
Arterioles have the greatest change in ______ and the highest _______.
Arterioles have the greatest change in _PRESSURE_ and the highest _RESISTANCE_.
Pulse Pressure=
Pulse Pressure= Systolic Pressure - Diastolic Pressure.
IF pulse pressure is big than SV=
BIG
The 1' determinants of Pulse Pressure are?? 2
1. SV output ( the bigger the SV, the bigger the PP)
2. Compliance of the Arterial Tree=> Decrease in compliance = Increase in PP
A decrease in compliance= what must the ventricle to pulse pressure?
INCREASE
Mean Arterial Pressure (MAP) =? 2 equations
MAP = Diastolic Pressure + (1/3) Pulse Pressure
(?? relative time in systole compared to diastole (longer)).

MAP = C.O x TPR
Why is important to understand/ what does the following equations tells us?? How does workload (co and resistance vasculatrure affect the bp?>
MAP = C.O. x TPR
Tells max force on arteries by 2
- If change workload of heart (C.O) then BP increases .
- Change resistance vasculatrure= INcrease BP
Map is what???
The average pressure in a complete cardiac cyce ( overtime)
What causes the dip in arterial pressure ( dicrotic notch)- ( pic on slide 32/33 in SMooth m. ppt.)
- ?
Closing of Semilunar valves
When does aortic stenosis occur? and why?
When the aortic valve is stenosis. bc it is very ridged and hard to force blood through it.
In Aortic stenosis what happens to Mean pressure? ( Map>??) why?
It decreases bc can move through .. so down stream less pressure
In aoritc stenosis what happens to ventricular pressure?
IT INCREASES
Venous Pressure:
1. Usually less than ____ mmHG
2. Central Venous Pressure (CVP) is a closte estimate of ___ ____ ____- which is a nice gage about what? and tells about what?
a. important estimate of ___ ___
1. Usually less than _10_ mmHG
2. CVP is a closte estimate of _RIGHT ARTERIAL PRESSURE_ (RAP)= Nice gage of EDV - tells about preload.
a. Important estimate of _BLOOD VOLUME_.
Venous Pressure is Regulated by: -4 things
Regulated by:
1. Tricuspid Valve Fx
2. R. Ventricular Fx.
3. Pulmonary Circulatory Fx.
4. C.O.
Venous Pressure:
-Common Causes of Increased CVP-3
most common??
Common causes of Increased CVP?
1. Heart Failure => Most Common! (Mostly R. Heart Failure. = Ventricular Failure.. Can't eject blood into arteries. Causes blood to go backwards.
R. Heart Failure= CVP= HIGH. disentsion in jucgular and lots of edema in tissue
2. Tricuspid Disorders
3. Pulmonary artery hypertension.
Venous Pressure:Common Causes of DECREASED CVP
Hypovolemia- bc most blood is in veins.
Venous Pressure:
Most important systemic venous pressure =???
RIGHT SIDE OF HEART... ( good tricuspid value, want able to close??
Regulation of Blood FLow????
- BY Changes in vessel radius, via both local & humoral mechanisms.
Regulation of blood flow by changes in radius- by:
1. Local Flow-
Is regulated acutely ( secs/mions) - w/in a particular tissue (muscle)
(-linked very closely to metabolic rate.)
Regulation of blood flow by changes in radius- by:
1. Local Flow- INCREASES proportionally with?
MEtabolic Rate
Regulation of blood flow by changes in radius- by:
1. Local Flow- mechanisms:
a.
b.
c.
a. tissue factors
b. vascular smooth muscle (VSM)
c.Endothelial factors
Regulation of blood flow by changes in radius- by:
1. Local Flow- mechanisms:
a.Tissue Factors -3
1.Increases in ADENOSINE, CO2, K+, H+ Stimulates what? and is associated with what?
Stimulates VASODILATION of Vascular Smooth Muscle
- Also associated w/ INCREASED Metabolism, when Blood Flow needs to reflexively Increase.
Regulation of blood flow by changes in radius- by:
1. Local Flow- mechanisms:
a. Tissue Factors-3
2. Oxygen Lack
- When Oxygen concentration decreases locally, VSM _______
- Less oxygen=
2. Oxygen Lack
- When Oxygen concentration decreases locally, VSM _VASODILATES__
- Less oxygen= LESS FUEL for VSM CONTRACTION = DIRECT RELAXATION.
Regulation of blood flow by changes in radius- by:
1. Local Flow- mechanisms:
a. Tissue Factors-3
3. Local Autoregulation of Blood Flow: When arterial pressure Increases, blood flow ??? doing wahat?
- When arterial pressure Increases, Blood Flow Increases, washing out Vaso dilators ( effect VSM
Regulation of blood flow by changes in radius- by:
1. Local Flow- mechanisms:
a. Tissue Factors-3
3. Local Autoregulation
- Lack of Dilators=
-lack of dilatiors= jvasocontriction flow retruns to normal = feedback
( effect of VSM)
- Metabolic autoreg
Regulation of blood flow by changes in radius- by:
1. Local Flow- mechanisms:
b. VSM- is sensitive to ___ bc?
VSM- Has mechanical receptors to be SENSITIVE to STRECH.
-Stretch if more blood flow through vessels Decrease in blood flow = NEG FEEDBACK
Regulation of blood flow by changes in radius- by:
1. Local Flow- mechanisms:
b.VSM
- if blood flow through a vessel increases, the wall ( & VSM) ____ =
- if blood flow through a vessel increases, the wall ( & VSM) _STRETCH_ = REFLEX VASOCONSTIRCITON
Regulation of blood flow by changes in radius- by:
1. Local Flow- mechanisms:
b.VSM
- MYOGENIC REGULATION=
= Another form of blood flow AUTOREG
Regulation of blood flow by changes in radius- by:
1. Local Flow- mechanisms:
c. Endothelial factors.
-important for?
- main ex?
Important for Larger Arteries
- major ex Nitrc Oxide (NO
Regulation of blood flow by changes in radius- by:
1. Local Flow- mechanisms:
c, Endothelial Factors
-NO
- Released from:
-Synthesized from:
-Synthesis of the enzyme:
-NOS stimulated by:
-If Endothelium is damaged (chronic hypertension) it may be unable to _____ ___
-NO
- Released from: HEALTHY Endothelial Cells
-Synthesized from: L-arginine & oxygen
-Synthesis of the enzyme: Nitrc Oxide Synthase (NOS)
-NOS stimulated by: INcrease in Shear Stress on the endothelial surface. ( Angiotensin 2 can also stimulate NOS- weird bc it vasconstrictor)
-If Endothelium is damaged (chronic hypertension) it may be unable to _synthesize NO_
Regulation of blood flow by changes in radius- by:
1. Local Flow- mechanisms:
c, Endothelial Factors
What is shear stress and what does an increase in it on the endothelial surface do?
Shear stress= Blood flowing through vessel hits at a higher rate..
= is a measure of the force of friction from a fluid acting on a body in a path of that fluid. (turbulent flow hypertension Increases shear stress. )
Increase in shear stress= synthesis of NOS ( = HIGHER BP, ETC)
Regulation of blood flow by changes in radius- by:
1. Local Flow- mechanisms:
c, Endothelial Factors
-NO
-Synthesis of NOS & NO stimulates VSM & Blood flow to do what?
-Synthesis of NOS &NO stimulates _RELAXATION_ of VSM. => _INCREASED_ Blood Flow.
Does NO constrict blood vessels?
So Angiotensin in this is a
No, NO relaxes Blood Vessels
So Angiotensin 2 is a Protector in this.
Regulation of blood flow by changes in radius- by:
1. Local Flow- mechanisms:
c, Endothelial Factors
An Increase in cGMP will _____ the Ca++ senstitivity of MLCK, This then ____ Contraction!
An Increase in cGMP will _DECREASE_ the Ca++ senstitivity of MLCK, This then _DECREASES_ Contraction!
Pharmaceutically the Importance of NO?
ex: for anginia, etc
Like Nitroglycerin, Amyl Nitrates.
Nitroglycerin - for release of chest pain un angina. =
= IMPORTANCE- Acute treatment for any type of arterial occlucsion bc increases vasodilation.
Pharmaceutically the Importance of NO?
For Sildenafil (Viagra)- what does it do>
-> Sildenafil (VIagara) inhibits cGMP specific phosphodiesterase-5 (PDE-5).
** THUS, Inhibitining degradation of cGMP& prolonging the action of NO
(so cGMP stays areound longer,& and MLCK stays away longer)
What if an unfortunate pt takes a viagra and has a heart attack... do you give them a nitroglycerin? why or why not?
NO- bc they could have a very major drop in BP to be very low. get dilation in arterials and veins.. Pull in veins so it also cause blood to not feed back into heart therefore - DROPPING R. Arterial Pressure, Dropping L.EDV, Dropping SV, & Drop in C.O. = very severe seniero.
Regulation of blood flow by changes in radius- by:
1. Local Flow- mechanisms:
c, Endothelial Factors
-ENDOTHELIN->
-Powerful _____
- Secreation Increases if ____ cells are ____ ____. Advantage:
-ENDOTHELIN->
-Powerful _VASOCONSTRICTOR_
- Secreation Increases if _ ENDOTHELIAL_ cells are _PHYSCIALLY INJURED_- B(damaged vessel=bleeding). (DIRECT Contrast to NO) Advantage: You vasoconstrict & hopefully Decrease BF to Hemorrage.
Regulation of blood flow by changes in radius- by:
1. Local Flow- mechanisms:
c, Endothelial Factors
- ENDOTHELIN
-Unfortunately, endothelin secreation _____ response to endothelial damage Secondary to ______ (shear stress) = ___ BP even more.
- ENDOTHELIN
-Unfortunately, endothelin secreation _INCREASES_ in response to endothelial damage Secondary to _HYPERTENSION_ (shear stress) = _INCREASE_ BP even more.
Long-term Local Regulation of Blood Flow
1. Angiogenesis=
Angiogensis= creation of new blood veessls in response to overactive metabolism w/in tissue. ( so can increase blood flow to other places/tissures)
Long-Term Local REg. of Blood Flow:
1. Angiogensis
A. __ _____ is an important signal (for: B)
B. ___ _____:vascular endothelial growth factor, fibroblast growthfacto, angiogenin ( stimulates ______ happens at ____ &___)
C. Vascularity (____ ______) is determined by _____ ___ ___ ___ _____. ( not the ...)
A. _LOW OXYGEN_ is an important signal (for: B)
B. _GROWTH FACTORS_: vascular endothelial growth factor, fibroblast growthfactors, angiogenin (stimulates _ANGIOGENSIS_ happens at _Arterials_ &_Caps_)
C. Vascularity (_ANGIOGENIC GROWTH_) is determined by _MAX BLOOD FLOW NEED OVERTIME_. ( Not the Average blood flow need!!)
**MAX NEED STIMULATES ANGIOGENSIS.
Long-Term Local REg. of Blood Flow:
VASODILATORS => Increase _______
- 8 (abc order)
VASODILATORS => Increase _METABOLISM_
1. Adenosine
2. Bradykinin (parakaeryin)
3. CO2
4. Decreased Oxygen
5. Histamine (parakaeryin)
6. H+
7.NO
8. K+
Long-Term Local REg. of Blood Flow:
VASOCONTRICTORS:
5 (abc order
VASOCONSTRICTORS
1. angiotensin2 (potent VC - tensing bv)
2.Endothelin
3. Increased Blood Flow ( Autoreg.)
4. NE/EPI
5. Vasopressin (pressing vessel)
Control of arterial blood pressure - 3 things/ equations:
1. Map= C.O x TPR
2. Flow = (delta) Pressure / Resistance
3.(delta) Pressure= (delta) Volume / Compliance
crossbridge cycling continues until 2 things
1. myosin phosphatase removes myosin head
2. ca is removed
If valve doesn't work=
varocosities
What slows blood flow down in laminar flow on edges?
Leukocytes slow on edge- make it sticky.
Faster , larger the diameter or the denser the vessel is directly proprotional to what type of blood flow?
TUrbulent blood flow= Re number

increase viscosity= decrease in blood.
Anything that increases resistance does what to flow?
Decreases Flow
Anything that increases pressure will do what to flow?
Will increase flow
Arterial Barorector Reflex: is what
Overall body control for BP- really really fast working.
Arterial Baroreceptor Reflex:
1. Very effective for ____ _____ arterial pressure when necessary
2. Receptors: Mechanical receptors in ____ ___ & ___ ___ sensitive to change in arterial Pressure.
3. Brainstem cardiovascular centers in the ________ and ____ and control the ____ & ____ efferent neurons that can alter 3 things?
1. Very effective for _RAPIDLY INCREASING_ arterial pressure when necessary
2. Receptors: Mechanical receptors in _CAROTID SINUS_ & _AORTIC ARCH_ sensitive to change in arterial Pressure.
3. Brainstem cardiovascular centers in the _MEDULLA_ and _PONS_ and control the _SNS_ & _PNS_ efferent neurons that can alter 3 things? 1. HR., 2. VASCULAR RESISTANCE, 3. cARDIAC CONTRACTILITY.
Inscreas radius =
increase flow and decrease reistance
Arterial Baroreceptor Reflex:
4. Setpoint for "normal" BP will reset if
BP elevation is maintianed for a period of days
Arterial baroreceptor reflex response to a Decrease in ARTERIAL PRessure causes
1. _____strech on carotid sinus baroreceptors = > ____ firing rate of Carotid sinus nerve
Decrease Arterial Pressure=> DECREASE stretch on Carotid Sinus Baroreceptors => DECREASE FIRING Rate of Carotid Sinus Nerve
Decrease Arterial Pressure=> DECREASE stretch on Carotid Sinus Baroreceptors => DECREASE FIRING Rate of Carotid Sinus Nerve
WHICH CAUSES the Parasymathetic and sympathetic to do what>?
Parasympatheic Acitvity= DECREASE Para activity to heart = INCREASE HR to INCREASE Pa (arterial pressure) back to normal
SYMPATHEIC- INCREASE in SYMP activity to HEART & BV = Increase in: HR, Contractility, Constrictio nof arteriloes ( TPR), Constriction of Veins, & venous return and DECREASE in UNSTRESSED VOLUME TO INCrease Pa toward normal
Arterial Baroreceptor reflex works:
What is the valsalve maneuver?
Expire against a slosed glottis.
Arterial Baroreceptor reflex works: under VALSALVE MANEUVER
A. Thoracic pressure Increases which will ____ venous return.
B. IF Venous return dECREASES__, preload _____, CO _____ , & Pa ______, which does what to HR?
A. Thoracic pressure Increases which will _INCREASE_ venous return.
B. IF Venous return _DECREASE_, preload _DECREASE_, CO _DECREASES_ , & Pa _DECREASES_, which does what to HR? INCREASS HR
Arterial Baroreceptor reflex works:
Once the maneuver is released what will happen to venous return? CO? Pa? and Reflex response of HR?
Venous return= Big Increase
CO= BIG INCrease
Pa= Increase
HR= Deep down below normal
Veins are ___ and ____ vessels?
Veins are COMPLIANCE & VOLUME Vessels
How is the Cardiopulmonary Baroreceptor reflex different from the Arterial barorector reflex? ( obvious)
It is on the VENOUS side.. not on arterial side
Cardiopulmonary Baroreceptor Reflex:
1. Low pressure recepotors in the ____, ____, & ______ ______ are sensitive to changes in blood Volume.
2.If Blood Volume is Increased
a. Atrial Natriuretic Peptide (ANP) is ______
ANP stimulates =>
1. Low pressure recepotors in the _VEINS_, _ATRIA_, & _PULMONARY ARTERIES_ are sensitive to changes in blood Volume.
2.If Blood Volume is Increased
a. Atrial Natriuretic Peptide (ANP) is _INCREASED_
ANP stimulates => VasoDilation & REnal exvretion of Na and H2O
Cardiopulmonary Baroreceptor Reflex:
2.If Blood Volume is Increased
b. Antidiruetic Hormone (ADH) secretion is ______
ADH Stimulates:
b. Antidiruetic Hormone (ADH) secretion is _DECREASED_
ADH Stimulates=> VasoConstriction & Water Retention
Cardiopulmonary Baroreceptor Reflex:
2.If Blood Volume is Increased
c. Renal Arterioles ____
c. Renal Arterioles _VasoDilate-_ (inc. in vasodilation renal excretion of Na & H2O ( more blood goes into kidney = secretes more fluid to get back to the heart?
Cardiopulmonary Baroreceptor Reflex:
2.If Blood Volume is Increased
d. HR ______ =____ _____
-Purpose:
d. HR _INCREASES_ =_BAINBRIDGE REFLEX_
-Purpose: Increase HR to Increase CO to Increase Renal Perfusion & Renal Excretion of Na & h2o
Humoral Mechs for BP & Vol. Control:
1. Renin-Angiotensin Aldosterone System
A. Secreted in (activated by) response to Decrease in ___ & ___.
B. Angiotensin 2 _____ BP & Volume
- causes 3 things?
A. Secreted in (activated by) response to Decrease in _BP_ & _VOLUME_.
B. Angiotensin 2 _INCREASES_ BP & Volume
~Causing: 1. Increased Renal Na+ & H2O Retnenion (more blood in kidney)
2.Vasoconstriction
3. Increased Sympathetic output ( fb to INcrease BP)
Humoral Mechs for BP & Vol. Control:
2. ADH/Vasopressin (AVP)
A. Secreted in response to 2 things:
B. ADH more than any other horomone is mostpotent to ____ __. which stimulates some 2 things
A. Secreted in response to:
1. DECREASE in BV or Pressure
2. Incresases in plasma osmolarity.
B. ADH more potent to INCREASE BP than any other hormone.. = Increases BP & vol.
1. Stimulates Renal H2O retention & Vasocontriction
Only way to increase Blood Volume is if you ??
consume something.
The control point in renin angiotensin 2-alderstone system is???
RENIN
look at slide 48 in Smooth muscle ppt
Microcirculation.
Capillaries are responsible for?
From caps perception what describes change?
Filtration -
Absorption-
Caps responsible for: TRANSPORT & EXCHANGE BETWEEN TISSUE AND BLOOD
-Describe exchange: Filtration: Blood-> Tissue
& Absorbtion: Tissue-> blood.
Microciculation:
Blood flow through capillaries is ____ bc?
-What are the 3 things that excahnge?
Blood flow through capillaries is _INTERMITTENT_ BC of Precap Sphincter Contraction & relaxation(blood doesn't always flow through at all times)
3 Things that Exchange:
a. Gases= Simple diffusion
b. Solute= Lipid Diffusion
c. Fluid Movement- depnds on 2 types of forces: HYDROSTATIC & COLLOID OSMOTIC (Oncotic pressure)
Fluid Movement is a thype of exchange in capilaries that depends on 2 types of forces:
1. Hydrostatic Pressure/force-
Due to the force of a fluid w/in a compartment ( cap vs interstitium). Pushes water (fluid) away from compartment. (like soaker hose)
-Hydrostatic Cap pressure (Pc)
-Hydrostatic Intersitial Fluid pressure (Pif)
--( pushing away from initial site)
Fluid Movement is a thype of exchange in capilaries that depends on 2 types of forces:
2. Colloid Osmotic Pressure/Force:
Due to osmotic forces within a compartment (cap vs. interstitium) Pulls water toward the compartment.
-Plasma collloid osmotic pressure (pi c)- pulls fluid to cap forc plasma proteins absorption.
-interstitual fluid colloid osmotic pressure ( pi if)
High concentration of___ & pulls)
Starling Forces, Filtration & Absorption.
What are filtration forces?
What are Absorption forces?
exceptions?
Filtration forces: Pc, Pi If, & - Pif
Absorption forces: Pi c & + P if
Exceptions Hydrostatic fluid in intersitual fluid**
Net Filtration Pressure =
Net Filtration Pressure= Filtration(+) - Absorption (-)
= Pc + pi if - pi c - (+/-) P if
The Staling equation also accounts for the _____ ____ of the capillary
- colllectively, systemic caps produce a net filtration of ___L/Day
The Staling equation also accounts for the _WATER PERMEABILTY_ of the capillary (KF)
Net Filtration Pressure= Kf [Pc + pi if - pi c - (+/-) P if]
- colllectively, systemic caps produce a net filtration of _2-3_L/Day
The lymphatic system returns fluid & solute to the vascular compartment ( ~2-3L/day)
- where does the lymphatic system being>
with the terminal capillaries in the tissue
How do lymphateic cessels ensure one way flow of lempatic fluid?
1. 1 way flap valves
2. myogenic reg, skelatal m. pumps , & nearby pulsing arteries - help maintian flow
3. lympatic pump is so effecitive that intersitial fluid hydrostatic presssure (Pif) is (-)
Before emptying into the venoud system, lymphatic vessels 1st carry fluid through ___ ______.
If intersitial fluid colume exceeds the drainage capacity of the lymphatics, _____ develops.
Before emptying into the venoud system, lymphatic vessels 1st carry fluid through _LYMPH NODES_.
If intersitial fluid colume exceeds the drainage capacity of the lymphatics, _EDEMA_ develops.
Cause of Edma= Increased Pc (hydrostatic pressure)- Fluiod pressure is highin cap.
Examples?
1. Arteriolar Dilation
2.Venous Constriction

3. Increased Venous pressure
4. Heart failure
5. Extracellular fluid volume expansion
THe following are examples of edema formation caused by what??
1. Decreased plasma protein
2. Severe liver failure (lack of plasma protein(
3. Protein malnutrition
4. Nephrotic syndrome
Cause of Edema formation:
Decreased pi c- (colloid osomotic pressure)
The following are examples of Edema formation caused by???
1. Due to Burns
2. Inflammation
INCREASED Capillary Permeability
Impaired lymphatic drainage can cause the edema formation of what?
ex:
1. Increase standing
2. removal of lymph nodes
3. Infection of Lymph nodes
What is the primary purpose of cutaneous circulation? (skin)
To regulate temp btw the blood and skin.
Cutaneous circulation
1. At rest- receives __ % of CO
2. When Temp changes, cutantous bloof flow changes in the ____ direction.. ( increase temp = ______ Cuteaneous BF)
a. Under _____ nervous system contral via __ & __ receptors, Arteriole & venule smooth muscle cells
b. _______ ________ nerves to sweat glands may also aid vasodilation by what?
Cutaneous circulation
1. At rest- receives _5_ % of CO
2. When Temp changes, cutantous bloof flow changes in the ____ direction.. ( increase temp = ______ Cuteaneous BF)
a. Under _SYMPATHETIC_ nervous system contral via _ALPHA_ & _BETA_ receptors, Arteriole & venule smooth muscle cells
b. _CHOLINERGIC SYMPATHETICS_ nerves to sweat glands may also aid vasodilation by what? SYMPATHETIC TO MUSCRERNIC RECEPTORS - ACH- WHICH STIMULATES NO TO VASODILATE
Cutaneous Circulation
3. Local Responses to cooling= _______
Local responses to warming = ______
Exception=
Cutaneous Circulation
3. Local Responses to cooling= _VASOCONSTRICTION_
Local responses to warming = _VASODILATAION_
Exception= COLD- INDUCED VASODILATION- occurs as protection measure= Rosey cheeks in COLD> due to 1. vasodilation- so increase in diameter
2. decreatse in metabolic rate but oxygen is still attached to hemoglobin, therefore it is red.
Cutaneous Circulation
4. What occurs with warming following a period of cold?? this happens in all vesselse, but esp. in skin?
REactive Hypermia
Reactive Hyperemia is bloof flow that is ??
- occurs?
Way past normal BF.
- local reg of blood flow - regional bf is controllled by local as well as neural and humoral factors.
-Occurs when bf is reestablished after occlusion. Buildup of vasodilatory metabolites like CO2, H, K , Lactiv acid and adenosine results in relazation of arterioles & precap sphincters directly exposed to these substances. Hence, a period of increased blood flow (hyperemia) occurs upon reperfusion.H
How much CO does Cerebral circulation receive at rest? how much of the oxygen it receives does it use?
15% of CO at Rest- Cerebral circ.
- Uses about 70% of ox delivered to it.
Cerbral blood flow is carefully regulated!
Why? How? Type of Regulation> Neuron involvement?
1. It's a vital metabolic tissue
2.It's encased in a hard shell
3. SO, can't be too high or too low= AUTOREGULATION is Very Importatn
4.Neurons depend on blood flow for delievery of (NUTRIENTS) - Glucose & Oxygen for metabolism
(30% can severely alter fx)
WHat type of regulation helps maintain a constant rate of blood flow over MAP between 50 mmHG & ~180 mmHG?
Myogenic regulation
How is myogeni regulation overcome?
HOw is sympathetic stimulation involved
In EXTREME Ischemic situations
- if vasomotor centers of the brain become ischemic , sympathetic stimulation GREATLY INCREASE!!!.. Cerebral bloodflow stays constricted
Metabolic regulation is also important for maintence of normal _____
Cerebral blood flow ( amount of activity w./in tissue)
= CO2 & Oxygen : Hypoxia
Metabolic Regulation-
1. CO2- Increases in CO2 will ____ H+ ion concentraion.
a. High concentractions of H+ ions greatly _______ neuronal activity.
b. Thus it is forturnate that H+ ions _______ smooth m. to ______ cerebral flow up to __ times normal.
1. CO2- Increases in CO2 will _INCREASE_ H+ ion concentraion. (Acidic capacity)
a. High concentractions of H+ ions greatly _DEPRESS_ neuronal activity.
b. Thus it is forturnate that H+ ions _VASODILATE_ smooth m. to _INCREASE_ cerebral flow up to _2_ times normal.
Metablolic Regulations-
2.Oxygen:hypoxia
a. Cerebral Oxygen utilization is ___ _____in physiologic conditions.
b. If Oxygen concentration is insufficient, there is a large ____ response in _______ vessels
2.Oxygen:hypoxia
a. Cerebral Oxygen utilization is _FAIRLY CONSTANT_in physiologic conditions.
b. If Oxygen concentration is insufficient, there is a large _VASODILATORY_ response in _CEREBRAL_ vessels!
Metabolic Regulation
3. Astrocytes may release _____ substances
4. What about hormones that are vasoactive in systemic vasculature?
5.Neuronal activity can be very closely linked to changes in ___ ___ __.
3. Astrocytes may release _VASOACTIVE_ substances
4.Hormones that are vasoactive in systemic vasculature? CAN'T PASS THE BBB-> EX. ANGIOTENSIN
5.Neuronal activity can be very closely linked to changes in _CEREBRAL BLOOD FLOW_.
Coronary Circulation- At rest, recieves how much % of C.O?
-Which Coronary artery is more important for CAD?
~5%
Left - base of aorta= more important than Right CA
Flow through the cornary vessels varies with the ___ ____.
-Coronary Blood Flow is Lowest during _______. BC??
Flow through the cornary vessels varies with the _CARDIAC CYCLE_.
-Coronary Blood Flow is Lowest during _SYSTOLE_. BC= of CONTRACTION of CARDIOMYOCYTES= Squeezing & compressing -> so influences cornary vessels.
Cornary blood flow during diastole is important bc?
that is when it is provided with blood
What happens to coronary blood flow if ventricular compliance decreases?
IF tissue is not compliant, makes it harder for blood to get through bc it is more ridged.
Differences in coronary blood flow during cardiac cycle are much greater in the _____ ventricle compared to ____ ventricle. BC? COnsequences?
Differences in coronary blood flow during cardiac cycle are much greater in the _LEFT_ ventricle compared to _RIGHT_ ventricle.
-B/c- L. ventrricular pressure is much higher and the diminishment of pressure during systolye so restricts blood flow doesnt't have as much pressure as in r. ventricle. R. is highest during systole... not as much of a change
-COnsequences? Usually fx ok, not aproblem with blood flow in right. May have some in left bc more in demand.
A.When is aortic Pressure the Highest?
B. When is L. Ventrical- coronary blood flow the highest?
C. When is R. Ventricular Coronary blood flow the highest?
A. Aortic Pressure Highest= Systole
B. L. Ventriular -Coronary BF Highest= At beginning of Diastole- B/c when blood flow highest
C.R. Ventriular -Coronary BF Highest= Systole, but not as much of a change once in diastole.
What is the Primary driving force for Coronary blood Flow?
AORTIC PRESSURE
Most Control of Coronary blood flow is At the ____ level 1' via Changes in ____ ____.
=> Coronar y blood flow very closely mirrors ____ demand.
Most Control of Coronary blood flow is At the _TISSUE_ level 1' via Changes in _METABOLIC DEMAND_. (Changes in CO2 ...)
=> Coronary blood flow very closely mirrors _OXYGEN_ demand.
Coronary blood flow very closely mirrors oxygen demand is important clinically bc of _____ ____ __ - which is?
Important clinically bc of MYOCARDIAL OXYGEN CONSUMPTION= AMt of O2 consumed by cardiac work per min. ( amt of O2 that heart consumes at any point in time)
-> MvO2= Coronary Blood Flow x A-V (<-max) O2 difference
Myocardial Oxygen Consumption is the amt of O2 consumed by heart at any time.
=> THe 1' Determinants of Myocardial Oxygen Consumption are ???4
1. HR ( # of contractions)
2. Myocardial Contractility = 1' determinant of this= the AMT. of Ca++ in the CELL.
3.EDV- ED pressure - changes constriction on left wall= preload
4. Afterload= Increase Pressure= Increase Work on HEart
Coronary blood flow should be between ___ -___ ml/min/100g. in comparison to Myocardial Oxygen consumption
80-90
Controlof Coronary BF is 1' via changes in metabolic demand. cornary bf very closely mirrors O2 demand.
1. At Rest the heart utilizes ___% of O2 delivered.
2. Anytime acardiac utilization of oxygen increases, the coronary vessels reflexively vasodilate to _____ resistance & ____ flow.
1. At Rest the heart utilizes _70_% of O2 delivered.
2. Anytime a cardiac utilization of oxygen increases, the coronary vessels reflexively vasodilate to _DECREASE_ resistance & _INCREASE_ flow.
Controlof Coronary BF is 1' via changes in metabolic demand. cornary bf very closely mirrors O2 demand.
3. This is particularly beneficial with _______.
= PROMBELMS
a. Increased HR ____ work of heart while ____ diastolic time.
b. This heart is using more _____ & has a greater ____ demand , thus the refelex Vaso____ is particuallry important.
3. This is particularly beneficial with _TACHYCARDIA_.
= PROMBELMS
a. Increased HR _INCREASES_ work of heart while _DECREASING_ diastolic time.
b. This heart is using more _OXYGEN_ & has a greater _OXYGEN_ demand , thus the reflex _VASODILATION_ is particuallry important.
Mechanism of Metabolic Control of Coronary BF.
1.Linkage between ___ ___ use & Coronary BF is not yet settled.
2. Most likely Vasodilator is ______
a. Increase in Contraction _____ the amt of Atp Utilized.
b.More AMP is ultimately produced which eventually ____ to _____.
c._____ leaks into the interstitium & is absorbed by ___ cells.
3. Other possibilities for Vasodilators: 6
1.Linkage between _MYOCARDIAL O2_ use & Coronary BF is not yet settled.
2. Most likely Vasodilator is _ADENOSINE_= As increases- will move out of cells & stimulate vasodilation.
a. Increase in Contraction _INCREASES_ the amt of Atp Utilized. (INC. MORE ADENOSINE)
b.More AMP is ultimately produced which eventually _DEGRADES_ to _ADENOSINE_.
c._ADENOSINE_ leaks into the interstitium & is absorbed by _VSM_ cells.
3. Other possibilities for Vasodilators: 6-
a. K+
b. NO
c. Prostaglandins
d. CO2
e. O2
f. Lactic Acid
---> Need more vasodilators bc they can all work together!
What is the preferred metabolic source of energy for Cardiac myocytes?
- up to 70% of ATP comes from FATTY ACIDs (Oxidation)
-
What is the next preferred metabolic source of energy for cardiac myocytes if going through ischemia"?
but during ischemia, O2 decreases, myocytes will rely on the LESS desirable mech of ANEROBIC GLYCOLYSIS for energy.- 2 lactic Acid & Adenosine
During ischemia-myocytes rely on Anaerobic Glycolsis for energy.
1. Lactic Acid is produced as a _______ -
what fafferent fibers come in>?
- Advantage of latcic acid's presence?
Lactic Acid is produced as a _BYPRODUCT - PAIN (Angina)
- SYMPATHETIC AFFERENT FIBERS have Chemoreceptors that can Transmit Nociceptro activation & result in angina pectoris when ischemia occurs.
- Advatange of latic acid's presence: Vasodilation (increases likely hood of O2)
During ischemia-myocytes rely on Anaerobic Glycolsis for energy.
2. Adenosine- released from cells follwing cardiac ischema.
Advantage?
Advantage= Vasodilation & Nociceptor Activation= pain which is good bc tells person to stop (example - stop shoveling snow)
- Realeased sometimes too quikcly anc dould cause cell to die.
What changes are the most important factor for cornary blood flow?
Local Tisssue Changes
The autonomic (sympatetic) Nervous system also influences Coronary blood Flow.
1.Direct Influences: _____ Stimulation -3 factors
a. ___ receptor
b. __ receptor
c. Indirect - does what to symp and mycardial o2 consump? = vaso_____
1. Direct Influences: SYMPATHERITC Stimulations
a. Alpha 1 receptors
b. Beta 2 receptors (more variable)
c. Indirect Influence bc sympathetic stimulation INCREASES Mycardial Oxygen Consumption= Vasodilation (indirect)
The autonomic (sympatetic) Nervous system also influences Coronary blood Flow.
2. Indirect Influences;_______ Stimulation
a. Decreases in HR ____ Myocardial O2 Consumption, thus coronary vessels ______.
2. Indirect Influences: _PARASYMPATHETIC_ Stimulation
a. Decreases in HR _DECREASES_ Myocardial O2 Consumption, thus coronary vessels _CONSTRICT_.
Coronary vessels alter their diamter in response to what hormones?
2- Vasocontrcitors, 1- vasodilatator
Vasocontrictors: Vasopressin & Angiotensin 2
Vasodilator: ANP
Coronary BF is Determined by:
1. Pressure Gradient-
2. Vessel Radius
( check out chart on slide 18 in special ppt.)
1. Pressure Gradient- Aortic pressure & myocardial compression
2. Vessel Radius - local METABOLISM ( = most important determinant), reural reg, hormone reg.
Does ANS influence Cerebral flow?
=> how is cerebral flow maintained & regulated?
NO
=> Maintained& regulated by Local Tissue ( heart, skin, etc)
What contributes more to restance than any other vessels in the body>
Arteriles found in skeletal blood flow
What is the most common cause of CAD?
Atheroscleoriss
What is Atherosclerosis?
Who is at Risk?
Athrerosclerosis- Disease of Large & intermediate sized arteries where fatty lesions (atheromatous plaques) develop w/in arterial walls
Who is at risk? = bad life style.genetics
1. High LDL, 2. Physical Inactivity, 3. Obesity, 4.DIabetes Mellitus, 5. Hypertension, 6. Cigarette smoking, 7. Genetics, *. women-small side, men large side.
Any risk of atherosclerosis is going to have damage/ disterburances associated with _____
- lose 3 things
THe endothelial cell / endothelial fx:
1. Lose LOCAL CONTROL of Vascular Tone - bc if damages enodtheial cell= release endotheliian= Vasoconstriction... Also not able to release NO2 so have inadequate Vasodilation
2. Lose antithrombic surface of endothelium. - (so stop controlling not clot formation)
3. Lose control of inflammatory cell adhesion and diapesis ( of leukocyte into cell).
What are the vessels at greatest risk for CAD / Atheroscleroticplaque
-Sites of turbulent flow (often branch points in arteries)
How does Atherosclerotic plaque Develop?
1. True starting point is _____ to the ____/___ depostion in the ______ ___.
2.Endothelial cells begin expressing ___ ______ molecules & are ___ able to release ___
3.Macromolecules, platelets, & monocytes can now adhere to endothelium.
a. Circulating monocytes experiencce _____ & enter the vessel wall.
b. ____ continues to accumulate in vessel wall.
1. True starting point is _DAMAGE_ to the _ENDOTHELIUM_/_LIPID_ depostion in the _VASCULATURE WALL_. (SHEAR STRESS)
2.Endothelial cells begin expressing _CELL ADHESION_ molecules & are _LESS_ able to release _NO2_
3.Macromolecules, platelets, & monocytes can now adhere to endothelium.
a. Circulating monocytes experiencce _DIAPEDESIS_ & enter the vessel wall.
b. _LDLs_ continues to accumulate in vessel wall.
(=> aREA= MORE POPULATED - IMMUNE *& FATTY TISSUE)
How does Atherosclerotic plaque develop continued..
After damage endothelium in vessel, & adhesion less able to release NO, monocyes diapedess and LDLS continue to accumulate)
**4. In tissue, Monocytes become ______-which ingest the deposited (selectively) ____ & ___ them. _____ become/change into ____ cells.
5. Macrophages release ____ Mediators & _____ Factors
a. more macrophages ____
b. __ ___ ___ & __ ___ proliferate w/in arterial wall.
6. Unfortante thing- Smooth m. cells & Collagen form a ___ ___ over the ___ core.
7. The plaque accumulates _____ ____ & forms ____ ___ = more ___= ___ compliance where arterial sclerosis compliant is atherosclerosied
a. Calicifications & deposits of CT _____ the ___ walls.
**4. In tissue, Monocytes become _MACROPHAGES_-which ingest the deposited (selectively) _LIPOPROTEINS_ & _OXIDIZE_ them. _MACROPHAGES_ become/change into _FOAM_ cells.
5. Macrophages release _INFLAMMATORY_ Mediators & _GROWTH_ Factors: WHAT THIS DOES IS:
a. more macrophages _ACCUMULATE_
b. _SMOOTH M. CELLLS_ & _FIBROUS TISSUE_ proliferate w/in arterial wall.
6. Unfortante thing- Smooth m. cells & Collagen form a _FIRBROUS CAP_ over the _LIPID_ core.
7. The plaque accumulates _HYDROXYAPATITE MINERALS_ & forms _CA+ DEPOSITS_ = more _RIDGED_= _DECREASE_ compliance where arterial sclerosis compliant is atherosclerosied
a. Calicifications & deposits of CT _STIFFENS_ the _ARTERIAL_ walls.
How does Atherosclerotc plaque Develop... continue the last 3ish steps.
8. The plaque size continually _____. It initially grows _____, ____ fro mthe Lumen. ( size of lumen is ____)
9. VSM cells secrete ___ _________.
a. These can ___ the collagen in the fibrous cap, ____ its likelihood of Rupture.
10. THe prodtruding plaque is expose to _____ BF which can further ____ the endothelum.
a. If blood clots develop, then a ___ & perhaps even a ___ develop.
b. If BF is reduced 50%, there is a limited ability to _____ BF to match cardiac demand. If reduced-__% coronary BF at rest likely insuffiecnt.
( if radius is decreased 50% does that mean BF is reduced 50%?)
8. The plaque size continually _INCREASES_. It initially grows _OUTWARD_, _AWAY from the Lumen. ( size of lumen is _MAINTAINED_)
9. VSM cells secrete _MATRIX METALLOPROTEINASE_. (Start to breakdown fibrous cap found above lipid core. eats away wall that sepatates plaque from lumen)
a. These can _WEAKEN_ the collagen in the fibrous cap, _INCREASING_ its likelihood of Rupture.
10. THe prodtruding plaque is exposed to _TURBULENT_ BF which can further _DAMAGE_ the endothelum.
a. If blood clots develop, then a _THROMBIS_ & perhaps even a _EMBOLUS_ develops.
b. If BF is reduced 50%, there is a limited ability to _INCEASE_ BF to match cardiac demand. If reduced-_80_% coronary BF at rest likely insuffiecnt.
(if radius is decreased 50% DOES NOT tmean BF is reduced 50%)
Very briefly the development of atherosclerotic plaque?
1. Damaged endothelium
2. Monocyte adhered to epitheliym adhears to adhesion molecule.
3. Monocyte migrates from arterial lumen into arterial intma to become macrophage
4.Macrophage binds to receptor lipoprotein particle
5. Macrophage collects lipid droplets and becomes a foam cell.
6. This releases growth /inflammatory factors.
7. Small plaqu- on outside of lumen
8. Large plaque still normal size lumen
9. Thromisis of a ruptured plaque decreases size of lumen
10. THrombis breaks off and becomes embolus
Atherosclerosis = Progressive process (slide 25 in special circ)
Lipid accumulation Increases - stages? ages?
Lipid accumulation increases- Foam cells& fatty streak (these 2 are clinically silent in 20s), intermediat lesion and Atheroma. (inflamatory response)
Increases with age.
Atherosclerosis = progressive process.. after lipid accumulation.. it moves to smooth m. & collagen.. this is when: ____ & ___ happen
- FIbrous plaque= ____ _____
- Plaque raphe not a clot untiL?
Fibrous plaque builds up anc complicated lesion/rupture happens.
Fibrous plaque= Stable Intermittent... then unstable after this part
-Plaque raphe = not a clot until EXPOSED to BLOOD.
Atherosclerosis= Prgressive process. Once Complicated lesion/ rupture.. what can be the result of this> 5ish?
1. ACS=
a. Unstable angina
b. MI
2. Ischemic stroke/TIA
3. Acute Limb Ischemia
4.Cardiovascular Death
5. ANgina Claudication
IFCoronary narrowing is slow, than iIT (atherosclerosis??) is often accompained by developement of ____ ___
- how is it made?
-how long does it take?
Collateral Cessels
- heart can make collateral vessels.. 1 arterial bed connects to aother.. = BYPASS- takes a few weeks
Acute Effects of Caridac Iscemia:
Cardiac Ischemia produces ____ distrubance in contractility that ____ Cardiac Pump fx.
Cardiac Ischemia produces _REGIONAL_ distrubance in contractility that _REDUCE_ Cardiac Pump fx. (If part of heart deprived from O2 - it can die)
Acute Effects of Cardiac ischemia: Cardiac Ischemia produces regional distrubance in contractility that reduce Cardiac Pump fx.
1. _____ of Cardiac muscle fails 1st.
a. can cause ___ ___ ischemia bc of __ ____
2.If involves papillary muscle, ___ ____ _______ can occur
3.Can lead to _____ failure, ____
4. ____ venous volume.
1._RELAXATION_ of Cardiac muscle fails 1st. (1st compromided->heart can't relaz, so stays in contracted state= further dec. o2)
a. can cause _EVEN GREATER_ ischemia bc of _POOR PERFUSION_
2.If involves papillary muscle, _AV VALVE REGURGITAION_ can occur (Ejection from Ventricular Greater Decreases)
3.Can lead to _VENTRICULAR_ failure, _FIBRILLATION_
4. _INCREASED_ venous volume.- B/c if ejection Decreases, so backed up in compliance vessels (veins)
What if the ischemic is in SA Node or AV node?
Massive arrythemias so further decreases Oxygen
What is the goal when treating cardiac ischemia?
- done in 2 ways
RESTORE OXYGEN to the MYOCARDIUM ( both long and short term)
1. Lower (decrease) myocardial oxygen consumption
2. Increase Oxygen Supply to the Myocardium.
To restore oxygen to myocardium to treat cardiac ischemia.
1. Lower/decrease myocardial oxygen consumption: - what 3 things do this? and how?
1. Dec. myocardial O2 condumption= dec. work on heart
a. Beta Blocers= bc decrease contractility & HR
b. Ca++ Channel blockers= 1.Decrease contraction- need less ATP & O2... 2. Decrease Rate of Contractoin (HR)= Decrase O2
C. Nitrates= 1.Decrease afterload bc vasodilate arteries & 2. Decrease Preload bc dec. work of heart
To restore oxygen to myocardium to treat cardiac ischemia.
2. Increase O2 Supply to the Myocardiuym... Can be done in 4 ways (2 surgeries)
1. Organic Nitrates= vasodilate coronary vessels
2.Ca++ Channel Blocekers- Vasodilate coronary Vessels
SURGERIES_=>
3. Ballon Angioplasty- inflated size of lumen
4. Cornary artery bypass graft
Can one recover from an acute mycardial infacrtion? what is it dependant upon?
YES, possible but depends on the amount of tissue of the heart is compromised.
Recovery from an Acute Myocardial Infarction- the steps:
1.Immediately following MI-> If Infacttion is LG, ____ Region is dead. ____ region is Non-functional (unable to contract or conduct)
2.Days after MI, ___ fibers die (will eventually be replaced by ____ tissure)
3.Some of the surrounding fibers may also ___ with time.
4. Most of Nonfunctional muscle ___ (____ are great)
5. Process is usually complete w/in a ___ ___ to __ ___.
6.W/greater time , the fibrous tissue may ____ in area as the surround m. ______ a bit.
- Fx region can ___ in size & dead part ___ in size.
1.Immediately following MI-> If Infacttion is LG, _CENTRAL_ Region is dead (LACK BF). _SURROUNDING_ region is Non-functional (unable to contract or conduct) -->(Degradation - some tissues have partial fx)
2.Days after MI, _CENTRAL_ fibers die (will eventually be replaced by _FIBROUS_ tissue) <-- good bc much stronger than dead fibers
3.Some of the surrounding fibers may also _DIE_ with time.
4. Most of Nonfunctional muscle _RECOVERS_ (_COLLATERALS_ are great)
5. Process is usually complete w/in a _FEW DAYS_ to _3 WEEKS_.
6.W/greater time , the fibrous tissue may _DIMINISH_ in area as the surround m. _HYPERTROPIES_ a bit.
- Fx region can _INCR._ in size & dead part _DECR._ in size.
What is Systolic Stetch?
-When does it occur>
It is the 1st day after MI immediately following..
- The region around the dead fibers are super thin and weak.
--> Everytime blood pumps- pushes on that region.. Bowing out = > CAN RUPTURE = DEATH of PERSON.
But with time these fibers ar replaced.
What are the 3 components of blood cells?
1. Erthrocyhtes/RBC- most clinical
2. LEukocytes/WBC-- largest
3.Thrombocytes/platelets - smallest
Plasma is made up of;
1. _% _-
2. _ %_ -ex.
3._ % __ & __
1. 92% Water- Necessary in capillary for HYDROSTATIC PRESSURE
2. 7%proteins--> Osmotic/oncotic Pressure
a. Albumin, b. Gloublins (alpha,beta, gamma), c.Fibrinogen. ( all made in liver!)
3.1% Inorgainc & Organic Substances ( hormones, Na, K, etc)
What is the difference bettwen serum and Plasma?
Serum takes blood from blood clots... Serum= PLASMA - Clotting Proteins
Plasma= Anticollagent added to blood & centerfuged.
What is Hematocrit?
What is normal for women and men?
% of total blood volume occupied by blood cells (RBC) - relative amt of RB to other compents.
Normal Hematocrit levels
Women- 38-46%- (lower than mens bc few rbc & hemoglobin)
Men- 42- 54%
What is the centerfuges blood look like?
about 58% on top this is the plasma volume and it is less dense
2. midd is the less than 1% white cells/ Buffy coat
3. 42% and that is the Packed RBC vol.
What could be the causes of someone who has a problem with hematorict?- 2
1. Problem with blood volume .. Fluid balance.
2. Problem with RBC Production.. too little or too much
Erythrocytes 3 Fx?
1. Hemoglobin Transport-
a. Major mechanism of O2 in body
b. Minor component in transport of CO2
2.Contains Carbonic Anhydrase- For CO2 transport... Speeds up CO2 + H2O to convert into bicarbonate (HCO3)-> VERY efficent in Blood buffering**
3. Responsible for Majority of Blood's Acid/ Base buffering
What is the structure of a RBC? why is it unque to the Fx?
1. Shape & membrane
a.Allows for what?
b. Facilitates 2 things
1. Biconcave Disc w/Large & Flexible Membrnaes (a lot more than need analagous to 1/2 full plastic bag)
a. Allows Maximal SA: Volume Ration
b. Faciltates Diffusion (gas) & Movement through small Vessels
Structure of RBC
2. Lack ____ & ____, but retain Functional ___ ____
a. Has Capacity to do ?? 6
2. Lack _NUCLEUS & ORGANELLS_ but retain functional _CYTOPLASMIC ENZYMES_.
A. - Metabolixe Glucose,
- Form ATP,
- Maintain membrane pliability, ion transport, & iron in ferrous state,
- Prevent Oxidation of Proteins in the RBCs
Site of RBC Production?
1. Early Gestation : ___ __
2. Later in gestation transitions to ____ , ____, & ___ ____.
3. Prior to Birth transitions to ___ ____
4. Children ( by Age 5) & Adults : ____ ____
(What is responspile for blood cell synthesis??)
1. Early Gestation : _YOLK SAC_
2. Later in gestation transitions to _LIVER_ , _SPLEEN_, & _LYMPH NODES_.
3. Prior to Birth transitions to _BONE MARROW_
4. Children ( by Age 5) & Adults : _BONE MARROW_
A. By age of 5 marrow of long bones has transition to yellow bone marrow.
( Verterbrae is responsible for blood cell synthesiss stem in??)
What is the Primary source for Extra RBC?
RBC Reserves are found in 3 organs?
1' Source for extra RBC= LIVER
=> RBC Reserves are in LIver, Lung, & Spleen. ( found where lot of blood is found)
Blood Cell Genesis
1. All blood starts as ______ _____ _____ Cells.
a. All Circulating blood cells _____ from this cell type.
2. Committed Stem cells
a. Generally referred to ____ ____ ____ ()
b.Growth & reproduction of these cells depends on ___ ____ ( ____) - from _____ ___ ___.
C. CFU-Es are ______ of ____
a. Order of erythrocytes.=
1. All blood starts as _PLURIPOTENT HEMATOPOIETIC STEM_ Cells.
a. All Circulating blood cells _DERIVE_ from this cell type.
2. Committed Stem cells (Replicating & transitioning into->)
a. Generally referred to _COLONY-FORMING UNITS_ (CFUs)
b.Growth & reproduction of these cells depends on _GROWTH INDUCERS_ (_INTERLEUKIN-3_) - from _Outside Bone Marrow_.
C. CFU-Es are _PROGENITORS_ of _ERYTHROCYTES (RBCs)_
a. Order of erythrocytes.=
Proerythroblast=> Basophil Erythroblasts=> Polychromatophil Erythroblasts=> Orthochromatic Erthryoblasts=> Reticulocytes (can circulate in blood & more like RBC) => Erythrocytes
Pro(s) B, P, O, R,E
All blood Cells bgin as PHSCs (___ ____ ___ __) CFUs are committed ___ cells = what do they ultimately produce?
All blood Cells bgin as PHSCs (_PLURIPOTENT HEMATOPOIETIC STEM CELLS_) CFUs are committed _STEM_ cells = what do they ultimately produce? ERYTHROCYTES
PHSC --> LSC ( __ ___ __) = what 2 types of cells?
PHSC--> LSC (_Lymphoid Stem Cells_) =>
1. T Lymphocytes
2. B Lymphocytes
PHSC--> CFU-S(s= __) can form--> 3 things
PHSC-> CFU-s ( s= SPLEEN) can form 3 things:
1. CFU- B (blast)=> more
2.CFU-GM (Granulocytes,monocytes) - more
3. CFU-M (megakaryocytes)
PHSC--> CFU-S ->can form 3 things:
1. =>CFU-B (blast) = > ____ = ______
2. => CFU-GM (Granulocytes, monocytes) => A._____ -a,b,c & B.______-a.
3.CFU-M (Megakaryocytes) => ______ _ ( ___)
1.CFU- B (blast)=> CFU-E (erythrocytes)= RBCs
2. CFU-GM (Granulocytes, monocytes) => A._GRANULOCYTES_ (Neutrophils,Eosinophils, & Basophils) & B._MONOCYTES_ (-> Macrocytes)
3.CFU-M (Megakaryocytes) => _MEGAKARYOCYTES_ ( => Platelets)
Genesis of RBC
Go from _____ Hemoglobin to ____ hemoglobin ( which is best for __ exchange).
Go from _LEAST_ Hemoglobin to _MOST_ hemoglobin ( which is best for _GAS_ exchange).
Genesis of RBC Route?? where is it what does it contain?
1. Proerythoroblasts: formed from CFU-E Stem cells.- Has organelles ( huge nucleus, mitochondria, ER) -W/in Bone Marrow
2. Basophil Erythroblasts -has smaller cells, but still see organells and rather large nucleus.- W/in Bone Marrow
3.Polychromatophil Erythroblasts -Decrease size of nuclues - W/in Bone Marrow
4. Orthochromatic Erythroblast= big change=>Nucleus is expelled ( condensation by macrophage) - W/in Bone Marrow
5. Reticulocyte- Leaves Bone marrow. Simillar structure to RBC. EXCEPT: 1. some organelles still present
2. Smaller amt of hemoglobin
Regulation of RBC Production:
-1' signal/ control of RBC production>?
A. Hypoxia ( ____O2 delivery to ___) _____ RBC Production.
- Tissue oxygenation controls RBC production
A. -Hypoxia (DECREASED O2 delivery to TISSUES) _INCREASES_ RBC Production.
Regulation of RBC Production:
What are the mechanisms of Hypoxia?- 6
Hypoxia Increases RBC Production by:
1. Anemia, 2. Hemorrage, 3. Bonemarrow destruction, 4. High altitudes, 5. lung Ds., 6. Cardiac Ds.
-Hypoxia Increases RBC Production by: INCREASING PRODUCTION of ERYTHROPOIETIN (EPO)
Regulation of RBC Production:
EPO is 1' produced by ____ (90%) & also the ____ (10%).
a. EPO Stimulates production of ______ from____
b. EPO speeds up the maturations of ____
c. EPO reaches max production w/in _____ of ____ stimulus, but it takes _____ days for the new ____ to appear in the blood stream.
d. As long as hypoxia continues, EPO remains _____.
EPO is 1' produced by _KIDNEYS_ (90%) & also the _LIVER_ (10%).
a. EPO Stimulates production of _PROERTHYROBLASTS_ from_CFU-Es_
b. EPO speeds up the maturations of _RBCs_
c. EPO reaches max production w/in _24 HOURS_ of _HYPOXIC_ stimulus, but it takes _5_ days for the new _RBCs_ to appear in the blood stream.
d. As long as hypoxia continues, EPO remains _ELEVATED_.
What is lifespan of RBC?
What is necessary?
W/age the RBC membrand becomes Increasingly _____.
- RBC 120 Days lifespan (short
- Adeguate Vit b12 & foliac Acid are necessary
-W/age the RBC membrand becomes Increasingly _FRAGILE_
W/age the RBC membrand becomes Increasingly _FRAGILE_
A. RBCs ___ as they squeeze through small vessels ( usually seen in ___)
B. RBC is ___ & _____ by macrophages w/in ___ min.s (rapid)
C. _____ is scavenged by the protein haptoglobin, heme by hemopexin & b iron by transferrin.
D. RBC Components are returned to ____, ___ , & ____ for ____.
A. RBCs _RUPTURE_ as they squeeze through small vessels ( usually seen in _SPLEEN_) (smalllest located here 3um convient where it will raphe)
B. RBC is _ENGULFED_ & _DIGESTED_ by macrophages w/in _60_ min.s (rapid)
C. _HEMOGLOBIN_ is scavenged by the protein haptoglobin, heme by hemopexin & b iron by transferrin.
D. RBC Components are returned to _MARROW_, _LIVER_ , & _SPLEEN_ for _REUSE_. ( & A bit for Excreation)
ABnormaaliteis in RBC PRoduction.
1. Polycthemia=
a. _____ RBC production 2ndary to _____
b. ____ RBC Vol. (HCT= __-__%) bc of :
~i. Polycythemia Vera
1. Polycthemia= EXCESS RBC IN SYSTEM
a. _EXCESS_ RBC production 2ndary to _HYPOXIA_ (Higher altitudes)
b. _EXCESSIVE_ RBC Vol. (HCT= _60-70_%) bc of : Excessive Production of RBC Precursors ( usually also Increase WBC & Olatelets)
i. Polycythemia Vera- Genetic- high RBC, WBC, Plateles. - Viscous -greater resistance to BF
Abnormalities in RBC Production
2. Anemia
A. Aplastic Anemia=
B.Megaloblastic Anemia=
C. Hemolytic Anemias=
i. Sickle Cell Anemia
ii. Erythroblastosis Fetalis:
2. Anemia
A. Aplastic Anemia= non Fxing Bone marrow- problem RBC & others
B.Megaloblastic Anemia=Low B12 & Foliac Acid - lots of RBC, but low Venoslow??
C. Hemolytic Anemias= RBC that rupture
i. Sickle Cell Anemia- S shaped- sickle RBC membrane not pliable ( obstruction of vessles
ii. Erythroblastosis Fetalis: - precursor cells released too quickly -lysis of RBC - unfortunate- RH - antibodies association
Blood Types
1. RBCs Express numerous membrane ______ & _____ that serve as antigens.
a. Antigens -are
b. Most antigens are relatively ___
1. RBCs Express numerous membrane _GLYCOPROTEINS_ & _GLYCOLIPIDS_ that serve as antigens.
a. Antigens ( AGGLUTINS)-are PROTEINS Capable of Inducing an Immune Response
b. Most antigens are relatively WEAK!
Blood Types
2. Blood Typing is based on 3 ____ found on the ___ Membrane: _ ,_ & __
a. Pressence or absencse of A & B Antigens determines:
b. Presence or Absence of Rh antigen determies:
2. Blood Typing is based on 3 _ANTIGENS_ found on the _RBCs_ Membrane: _A_ ,_B_ & _Rh (D)_ (Rho Factor)
a. Pressence or absence of A & B Antigens determines: A,B AB, or O blood Type.
b. Presence or Absence of Rh antigen determies: Whether Rh-Positive or Rh-Negative
When blood is transfused, it is not usually whole blood, but _____ _____. So the only rxn. to worry about is between the Recipient's _____ *& the Donor's _____.
When blood is transfused, it is not usually whole blood, but _PACKED RBCs_. So the only rxn. to worry about is between the Recipient's _PLASMA_ (w/ antibodies)*& the Donor's _RBCs_.
Blood Type: A
AG on RBC=
Antibody in Plasma=
Can Donate to=
Can Receive From=
Blood Type: A!
AG on RBC= A
Antibody in Plasma= B
Can Donate to= A, AB
Can Receive From= A, O
Blood Type: B!
AG on RBC=
Antibody in Plasma=
Can Donate to=
Can Receive From=
Blood Type: B!
AG on RBC= B
Antibody in Plasma= A
Can Donate to= B, AB
Can Receive From= B, O
Blood Type: AB
AG on RBC=
Antibody in Plasma=
Can Donate to=
Can Receive From=
Blood Type: AB!!
AG on RBC= A & B
Antibody in Plasma= NO ANTIBODIES = UNIVERSIAL RECIPENT
Can Donate to= AB
Can Receive From= AB, A, B, & O
Blood Type: O!!
AG on RBC=
Antibody in Plasma=
Can Donate to=
Can Receive From=
Blood Type: O!
AG on RBC= NO ANTIGEN (UNIVERSAL DONOR- (really O- is)
Antibody in Plasma= A & B
Can Donate to= O, A, B, & AB
Can Receive From= O
Unlike most immune rxns, a person already has ___ ( ) to the A/B antigens not on their RBCs. BC??
when do they appear? & how?
Unlike most immune rxns, a person already has _ANTIBODIES_ (IgMs ) to the A/B antigens not on their RBCs.
- B/c- These are i the plasma prior to nay exposure- appear 2-8 months after birth.
--> introduced to immune system through FOOD 7 Bacteria
What is the maximum titer? Like when is your immune system at top notch?
- what does this mean with kids?
10 years old, then declines with age.
- this means kids would be more likelhy to have a problem with inappropriate blood transfussion.
What happens if inappropriate A-B-O blood is transfused?
Antibodies (IgMs) attack antigens= lots & lots of blood clotting together to form Agglutination.
What is Agglutination?
1.If perosn receives RBCs w/__ that they have __ against, RBCs will agglutinate.
2. why do multiple RBCs clump together?
3.Cause _____ of ___ BV , (common in) ______ _______ Repsonse.
4. Hours to days later, _Hemolysis_ occurs.
a. due to extreme _____ of RBCs & action of _____ WBCs
b. Possible to have acute ____ , but not likely.
1.If perosn receives RBCs w/_Ag_ that they have _Ab_ against, RBCs will agglutinate.
2. Ag &Ab have multiple binding sites,so RBCs clump together
3.Cause _OBSTRUCTION_ of _SMALL_ BV , (common in) _SYSTEMIC INFLAMMATORY_ Repsonse.
4. Hours to days later, _Hemolysis_ occurs.
a. due to extreme _DISTORTION _ of RBCs & action of _PHAGOCYTIC_ WBCs
b. Possible to have acute _HEMOLYSIS_ (immediately break apart), but not likely.
A. Agglutination Response is usually betweeen the donor's ____ & the Recipient's ___/____.
B. Pathologic effects of aggulation can be extreme & fatal - ex:
C. Where is terrible place for inappropriate transfussion?
A. Agglutination Response is usually betweeen the donor's _RBCs_ & the Recipient's _Ab_/_AGGLUTINS_.
B. Pathologic effects of aggulation can be extreme & fatal - ex: 1.System Inflammatory Response, 2. Kidney Failure, 3. Intravscular Coagulopathy (Bad- blood clots occuring. uses up all pts clotting factors so pt bleeds) ,etc.
C. Terrible place for inappropriate transfussion= KIDNEYS
Components of Blood Typing- The Rh/D Antigen Response is DifferentL
1. A Person is Rh(+) if:
a. ___ Rh-antibodies in the plasma.
1. Rh(+)= Rh ANTIGEN on RBCs.
a. _NO_ Rh-antibodies in the plasma.
Components of Blood Typing- The Rh/D Antigen Response is Different:
2. A person ins Rh(-) if :
- __NO_ Rh-ANtibodies in the Plasma -IF The person has _______ been ____ to ___ ____.
i. May see mild ____ response ____ weeks after Rh(-) perosn receives ____ _____.
ii. usually the 1st exposure (if occurs) =
2. Rh(-) :LACK Rh ANTIGEN on RBC
-_NO_ Rh-ANtibodies in the Plasma -IF The person has _NEVER_ been _EXPOSED_ to _Rh(+) BLOOD_.
i. May see mild _AGGLUTINATION_ response _2-4_ weeks after Rh(-) perosn receives _RH (+) RBCs_.
ii. usually the 1st exposure (if occurs) = MILD!!
Hemolytic Anemia: Erythroblastosis Fetalis: =
Rh Ab ( IgG) can cross the PLACENTA, unlike A/B (Antibodies (IgM)
Hemolytic Anemia: Erythroblastosis Fetalis: Rh Ab ( IgG) can cross Placenta, unlike A/B Ab (IgM)
1. No problem if mom is __ & baby is __.
2. Can be a problem if mom is __ & baby is __.
a. Rh(-) mom has neither Ag on ___ or Aby in ____
b. Rh (+) baby has Rh AG on ____, but no ABY in ____
-With the 1st baby=
-After 1st baby, mom develops ___ to the ____ _____
1. No problem if mom is _RH+_ & baby is _RH-_.
2. Can be a problem if mom is _RH-_ & baby is _RH+_.
a. Rh(-) mom has neither Ag on _RBC_ or Aby in _PLASMA_
b. Rh (+) baby has Rh AG on _RBC_, but no ABY in _PLASMA_
-With the 1st baby= NO PROBLEM! , but at the baby's birth, there is mixing of maternal & fetal blood.
-After 1st baby, mom develops _Aby_ to the _Rh Ag_
-( Rh Aby, unlike the A & B Aby, can cross the placenta)
Hemolytic Anemia: Erythroblastosis Fetalis: Rh Ab ( IgG) can cross Placenta, unlike A/B Ab (IgM)
** If the second baby is also Rh+, mom's Rh- ABy will?
1. Aby cause ____ & ____ in ____ circulation
2. Aby can also attack & ___ other cells of the body.
3. Aby circulate in baby;s blood for ____ _____ after birth.
- Cross the placenta & attack the baby's Rh Antigen & thus RBC
1. Aby cause _AGGLUTINATION_ & _HEMOLYSIS_ in _FETAL_ circulation
2. Aby can also attack & _DAMAGE_ other cells of the body.
3. Aby circulate in baby;s blood for _ 1-2 MONTHS_ after birth.
Hemolytic Anemia: Erythroblastosis Fetalis: Rh Ab ( IgG) can cross Placenta, unlike A/B Ab (IgM)
** 2ND BABY THAT IS RH+ W/ RH- MOM
1.At birth baby are severely ____ & ____
a. ___ & ____ are enlarged as they produce more RBCs
b. Children may be ____ ____ & may ___
c.Treat by ____ w/ ___ __
** 2ND BABY THAT IS RH+ W/ RH- MOM
1.At birth baby are severely _JAUNDICED_ & _ANEMIC_
a. _LIVER_ & _SPLEEN_ are enlarged as they produce more RBCs
b. Children may be _MENTALLY IMPAIRED_ & may _DIE_
c.Treat by _REPLACING_ w/ _RH- BLOOD_
Hemolytic Anemia: Erythroblastosis Fetalis: Rh Ab ( IgG) can cross Placenta, unlike A/B Ab (IgM)
- CAN PREVENT Rh-/+ blood mixiing and baby problems by?
Mom is given a dose of anti- Rh antibodies (Rho-gam) during 1st pregnancy before birth of 1st child that is Rh+.
-Aby preven sensitzation of the D antigen. Bind to the D(Rh) Ag on baby's RBCs that corss the placenta at Birth.
Rho-fam works bc it cover the Rh Ag so that the mother's immube system does NOT see it & thus does not form an Aby to id.
4 types of Orang Transplants?
Which are the bests ones (list best to worst- ish)?
Look at all blood types
1. Autografts- BEST- bc from part of a person to another part of same person.. Ag are your own.
2. Isografts- 2nd best= Identicle twin
3. Allografts- w/in same species = ore ideal proper matching to organ only last 5-15 years- so delay transplant
4, Xenografts- other species... baboons, pigs, apes
Organ Transplants must look at:
1. Tissue Typing
a. Based on the presensce of the ____
b. Each Cell has __ of these Ag ( __ possible Ag= ____ possible combos)
1. Tissue Typing
a. Based on the presensce of the _HLA- HUMAN LEUKOCYTE ANTGENS ( FOUND IN ALL CELLS)_
b. Each Cell has _6_ of these Ag ( _150_ possible Ag= _1 TRILLION_ possible combos)
Organ transplants Depends on
2. Allograts ____ match all HLAs
a. importance
b. Best success is w/ ___
3. What do you do the suppress the immune system to PREVENT ORGAN REJECTION?
2. Allograts _RARELY_ match all HLAs
a. Some of HLAs are not as SEVERELY Anti-Genic as Others
b. Best success is w/ _SIBLINGS OR PARENT-CHILD MATACHES ( Besides identicle twins)_
3. MEDICATIONS - suppress the immune system to prevent organ rejection.. Ex. steroids .. PRoblem= INCREASE risk for INFECTION!!
Dental pt. have the greatest increase in HR, SBP & DBP during which 2 parts of a dental visit?
1. During Extraction
2. Before injection
The Cardiovascular responses of Hypertensive pts are ___ ____ than those of normotensive pts.
If pt is in pain?
The Cardiovascular responses of Hypertensive pts are _EVEN GREATER (to any tuper of stress)_ than those of normotensive pts.
If pt is in pain? INCREASEs Even more Don't need to treat them
Look out for any type of CV ds and use ______ w/ _____ & _____ when numbing pt.
Look out for any type of CV ds and use _PRUDENCE_ w/ _EPI_ & _LIDOCAINE_ when numbing pt.
What are the CV responses of a Dentist?
In response to administering a local anestheric & execution of an extraction the dentist experinces an average of:
12% increase in HR
24% increase in SBP (worse than pt)
18% Increase in DBP
- If pt is calm, dentist is more likely to be calm as well.
Is EDV or ESV bigger?
EDV is bigger- at end of ventrile filling when AV valves close
ESV- At beginning of AV valves opening
Positive Ionotrophic effect=
-What happens to SV & CO for a given EDV?
- What is the Ejection fraction relatively?
-is it good or bad?
- CO & SV Increase for a given EDV
= Larger Ejection Fraction (SV/EDV)
=GOOD THING
Negative Iontropic Effect=
-What happens to SV & CO for a given EDV?
- What is the Ejection fraction relatively?
-is it good or bad?
- CO & SV Decrease for a given EDV.
- Ejection Fraction is smaller ( - to right)
- BAD bc heart is doing more work
What is Increased Preload of EDV?
= Important determinant.
- sacromere have more optimal overlap & eject blood w/every beat
Increased after load= Pressure
- what stage
-SV=
good or bad?
Increase afterload- pressure pumping against heat.
- Isovolumeric Conctraction most of time
= Sig. Decrease in SV
= VERY BAD
If HR is 80BPM the COis? 97.5 ml =sv
CO= SV x HR
= 8 L/min
What is Heart Failure??
What are the 2 1'effects;
Heart Failure= failure of Ventriculular pump- Either filling of ejection sufficently.
2 1' Effects:
1. Decreased CO
2. Damming of Blood in Veins
What are the Symptoms of Heart failure?
Dianosis of Heart failure is associated with?
Symptoms: Dyspena, Fatigue, Edema(in CHF = fluid = edema- only 50% survival - most older ppl)
Diagnosis- Associated w/ REDUCTIONS in Quality of Life & Lifespan ( Low bf & delivery to organs)
What are 6 Common Causes of Heart Failure? (most common one??)
1. Damage to myocardium= Most freq. -> CAD or following MI
2.Failure related to work overload (afterload) - ex. hypertension
3. Failure related to Valve abnromalities - Ex. stenotic or reguritive valves
4.Failure caused by an abnormal cardiac rhythm
5. Failure caused by pericardial abnormalities- ex. tymponade- excess fluid in pericardial sac.
6. Congenital defromities of the heart.
Types of Heart Failure.
Which side heart failure is causes congestion in the pulmonary circulation? pump failure?
LEFT SIded Heart Failure
- bc L. ventricle is workhorse if heart, so not ejecting sujffeint amt of blood to periphery, but right is normal.. L blood backs up in pulmonayr system & Incrases cap pressure, increases hydrostatic pressure and fluid in lungs
iF ytou have a respiratory problem when lie pt back, it is probably which side heart failure?
Left side
What is the type of heart failure that is Cor Pulmonale ?
- Congestion is in the systemic circulation?
Secdonary to other type of heart failure?
RIght sided heart failure is 2ndary to left.
Normally one whould ahv eboth.
Types of heart failure- How it looks:
1. Diastolic failure
- Failure of Rest
- Stiffened walls of wentricle impairs VENTRICULAR FILLING.
- Thich & Fribotic wall- sixe of ventricular compartment is smaller so can't get as much blood out.
Types of heart failure- How it looks:
2. Systolic Failure
- Failure of Volume OVerload
- Large, dilated heart w/impaired EJECTION FRACTION.
-HYPERtrophy in Length
What is the type of heart failure that has normal ejection factor, but lower blood so lower sv?
Diastolic Failure
What is the type of heart failure that has decreased EJection fraction and Heart is large, but weak so can't push out?
Systolic failure
Can Systolic and Diastolic Failure coexist?
NOOO!
Systolic or Diastolic Heart Failure:
1. Large, dialated Heart (eccentric hypertrophy)
2.System hypertenion
3. Normal or near-normal Ejection Fraction
4. Broad agges affected, more common in men.
1. Large, dialated Heart (eccentric hypertrophy)- SYSTOLIC HEART FAILURE
2.System hypertenion- DIASTOLIC HEART FAILURE
3. Normal or near-normal Ejection Fraction- DIASTOLIC HEART FAILURE
4. Broad agges affected, more common in men.- SYSTOLIC HEART FAILURE
Systolic or Diastolic Heart Failure:
1.Small ventricular cavity, thick , stiff wall, (concentric LV hypertrophy) (lumen much smaller
2. Normal or Low BP
3.Low Ejection Fraction
4.More common in eldererly women
1.Small ventricular cavity, thick , stiff wall, (concentric LV hypertrophy) (lumen much smaller - DIASTOLIC HEART FAILURE
2. Normal or Low BP - SYSTOLIC HEART FAILURE
3.Low Ejection Fraction- SYSTOLIC HEART FAILURE
4.More common in eldererly women- DIASTOLIC HEART FAILURE
Systolic or Diastolic Heart Failure:
1.Poor Prognosis
2.Myocardial ischemia is import in select cases
3. Myocardial ischemia is common
4. Which is easeier to treat???
1.Poor Prognosis - BOTH SYSTOLIC & DIASTOLIC HEART FAILURE
2.Myocardial ischemia is import in select cases- SYSTOLIC HEART FAILURE
3. Myocardial ischemia is common- DIASTOLIC HEART FAILURE
4. Which is easeier to treat???
SYSTOLIC IS EASIER TO TREAT.
If increase R. atrial pressrure & Increase Preload = ___ CO
Increase in CO
Look at slide 12 in CV Pathppt
Look at slide 12 in CV Pathppt
When a region of heart fails
CO= ___
Sensed by ______ causing
Sympathetics and parasympathics to do waht?
- humoral changes?
Heart failures= DECREASE 9( 'UNLOADS") CO= Sensed by BARORECTPTORS. Which causes INCREASE in Sympathetic Activation and Loss of Parasympatheric activation... coupled with homoral changes to INcrease BP, Volume & Vascular Resistance.
-Acutely this is (+), but these ame alterations lead to end-organ changes in advanced Heart Failure.
So Heart fail s in some place and Baroreceptor dysfunction => ___ Afferent Inhibitory signals at vasomotor center. cause 2 things
So Heart fail s in some place and Baroreceptor dysfunction => _DECREASE_ Afferent Inhibitory signals at vasomotor center. cause 2 things:
1. Increase Sympathetic NS activity => a. Decreased limb flow or... b. Decreased renal BF, Increase Aldosterone *& Na+ & H20 Reabsorption.... or c. Increase Renin secretion --> increase in Angiotensin 2. which also does b.
2. Increases Vasopressin Secretion.=a. Increases resostamce in vasculatioure...or b.Decreased renal BF, Increase Aldosterone *& Na+ & H20 Reabsorption
So When CO goes back to normal , signals like increase in angiotensin , etc goe back to to normal, except. when?
IF you have CHF then signals stay UPREGULATED.
= Positive feedback loop??
Initially, Neurohomoral compensations are positive, but they result in an large increases in both
BP & BV which have a detrimental effect on Cardiac Fx.
And as heart failure progresses these signals are NOT diminished.
An increase in Venous pressure is (+) bc ?
Increase in Venous Return, Increase Preload, so Increase Contractility
(** CHECK OUT SLIDE 14 IN CV PATH PPT)
Why does CO decrease if Resistance & Arterial Pressure Increase?
Bce there is an increase in afterload.
(** CHECK OUT SLIDE 14 IN CV PATH PPT)
What is the formular that relates TPR to CO?
MAP = TPR x CO
(** CHECK OUT SLIDE 14 IN CV PATH PPT)
Cellular changes that occur in Response to heart failure? name 5
1. Myocyte Hypertorphy - usually associated with vol. overload
2. Srcomere proteins- myosin alter
3. Cell membrane changes- prolonging of AP longer thanb nomal ( Vg Na channel s , k channels, & depletion of ca stores= Decrease force of contraction)
4. Metabolic changes- Greater total oxygen requirement of the heart- but cant pump more oxygen
- oxygen impairment impairs relaxation & weakens contraction. Heart trouble relazing and filliling = diastolic
-decreased concentration of phosphocreatein- heart using more atp than can make.
5. Autonomic receptor adaptations- alpha1 & beta 1- desenstizes and thats bad bnc beta one is good for heart in nromal circumstances.
Name 6ish types of Medications that would be prescribed to a typical CHF patient?
1. Diuretics= decrease bv
2. Beta blocker= lower sympatheritc activity
3. RAA S Taargets
4. Digoxin- Increase cardiac ca++ levels to increase contractility.
5. Anticoagulants- blood has static quality.. asprin
6. Anti-arrhythmic drugs
(ace inhibitors and angiotensin 2 blockers)
Dental Considerations with classic CHF Pt.
1. Heart failure should be ___ ____.
2. Consider pt positoin during treatment. They will also be more prone to ____ ____ so cant Increase BP quick enough when stand up.
1. Heart failure should be _well controlled (not acute)_.
2. Consider pt positoin during treatment. They will also be more prone to _ORTHOSTATIC HYPOTENTION so cant Increase BP quick enough when stand up.
Symptoms- ANgina suggest ?
Ischemi problem.. Probably CAD obstruction causing most problems.
If Coronary blood flow is insufficient then what happens to the ability of the myocardial cells to work?
Decreases-->Can't pump as much blood out.
Ejection Fraction of .3 inicatess what type of heart failure?
Contractitlity:
SV:
CO:
SYSTOLIC and both l.& r. side
Contractitlity: low
SV: low bc pulse pressure low
CO: low b dizzy bluie cold calmy
When does Ventricular filliling most often occur?
during Atrial diastole
Increased afterload does what for a pressure volume loop digram of the heart?
-Pushes it to:
-SV=
-ESV=
-EDV=
-Intraventricular Pressure=
-Ejection/filling period=
-Pushes it to: up & to the right.. slims it up
-SV= DECREASES
-ESV= INCREASES
-EDV= UNCHANGED
-Intraventricular Pressure= INCREASED
-Ejection/filling period= DECREASED
What describes the ability of a healthy ventricle to eject the amt of blood that enters (venous return) w/each cardiac cyce.
= if EDV/preload Increases, what does the BV ejected from the ventricle do?
1. Frank-Starling Mechanism of the heart
2. it too increases... bc of this mechanism
What percentage of ventricular filling comes from systole? what is this called?
20%
Atrial Kick
(maybbbbbeeee dicrotic notch????? IDK thought)
Pre load is mostly associate with End ____ Volume.
DIASTOLIC EDV
The follow facts describe what???
- The vol. of blood in the ventricles at the end of diastole
-Reflects diastolic fx
-importnat determinant of ventricular contraction.
EDV- aka preload
T/F:
Atrial filling is muscle/activevly driven?
FALSE
- ATRIAL Filling is PASSIVE
Is the SR more developed in Skeletal or cardiac m.?
skeletal
Which Valves prrevent backflow from ventricles into atria during systole?
The Atrioventricular Valves
1. Tricuspid
2. Bicuspid/mitral valve
How does venous return stimulate HR?
Stretch the SA Node & via autonomic innervation
T/F During isvolumetric contraction volume increases, but pressure stays constant?
FALSE!!= (this would more describe ventricular filling)
During Isovolumetric contraction: VOL. Remains Constant while PRESSURE Increases.
Which 3 systems recieve the MOST blood from the Heart at rest? how much %?
1. Renal
2. GI
3. Skeletal Mm
- Each about 25%
What is the progression of Ca generating Contraction in Cardiac myocytes?
1. Ca enters the sarcoplasm from extracellular space through L-type Ca channels (mucopolysacharides here bind Ca & keep it store in extracellular so it is ready when needed)
2. Ca enters from the SR (bc #1 happened)
a.Ca induced ca- releaseases ca through ryanodine receptor channels (SR far less developed in Cardiac m than skel.)
3. Ca, in the presence of ATP intiates contarction
4.The strength of cardiaac contraction is graded based on the extracellular Ca content (not solely based on SR ca)
So if you decrease ca+ in extracellular space what happens to the contraction of a CARDIAC MYOCYTE??
Decreases contraction
What normally determins CO?- 4 things
1. Metabolism - (O2 using, CO2 producing)
2. Exercise= can increase while working out up to 30/L min if in SUPER awesome shape
3. Age= Increase up to 10, then start decrease
4. Size of body- bigger you = greater CO needs to be
Types of Cardiac Myocytes?
1. Contractile
a. Atrial M.
b. Ventricular M.
2. Conductive M. Fibers
a.Excitatory
b.Autorhythmatic
2 stages of Ventricular Diastole?
1. Isovolumic Relaxation
2. Venticular Filling
2 Stages of Ventricular Systole?
1. Isovolumic contraction
2. Ventricular ejection
What 2 things does venous return Incease?
1. Contractility
2. HR
??? (other persons notes)
T/F: The ventricular output of the LEFT VENTRICLE is more dependent on Atrial Pressure than is the RIGHT VENTRICLE
FALSE: VICE VERSA
The R . Ventricle is more Dependent on ATRIAL PRESSURE than the L. Ventricle
Which Valves prevent backflow from arteries to ventricles during diastole?
Semilunar Valves
a. Pulmonary
b. Aortic
Gap junctions and desmosomes are found in this specialized cardiac cell membrane structure called _____ ___
Intercalted disc
Which autonomic receptors control CO?
-->Beta 1 (sympathetic)
-->Muscarinic (parasympathetic)
(?? other notes)
What happens to BP if increase Angiotenisin 2?
BP Decreases
What stimulates the release of Adenosine from muscle cells?
Decreased pO2
During which part of the cardiac cycle is BF the greatest?
Diastole
The following are methods for lowering ____ ___ _____:
1. Beta-adrenergic blockers
2. Organic nitrates that reduce preload ( & afterload, a lil)
3. Ca Channel blockers
The following are methods for lowering _MYOCARDIAL 02 CONSUMPTION_:
What is the MAIN regulatory mech for Coronary BF Reg?
LOCAL MUSCLE CONTROL
______ ____ Causes:
1. Stimulation of Nociceptors ( anginal pain , symp activation)
2. Electrical Conduction Abnormalities & Arrythemias
3. Impaired Contractility (forward failure)
4. Decreased Compliance of Myocardium during diastole (backward failure)
5. Congestion in the Pulmonary Circulation (dyspena & trachypnea)
6. Mitral regurgitation ( due to Increased BP)
These are all caused by MYOCARDIAL ISCHEMIA
Methods to increase O2 supply to heart? 4
1. organic nitrate
2. Ca Channel blockers
3. Ballon angioplasty
4. Surgical revascularization
How does atherosclerosis cause an Acute MI?
Thrombosis of a rubtured atherosclortic plaque leads to embosis, occludes a heart artery
What benefits do nitrates have in ischemic heart disease?
* Dilation of Coronary Arteries
- Thus increasing O2 supply to cardiac m.
What is the deposition of cholesterol beneath the endothelium?
atherosclerosis
T/F: The prominent mechanism of nervous control of coronary BF is the indirect effect.
TRUE
What is the coronary bf in a resting human?
225ml/min ( 4-5% of CO)
What vessels supply the heart itself with blood?
Coronary Ateries
Cardiac Veins
Adenosine,
Adenosine Phosphate compounds,
K ions,
H ions,
CO2,
Prostaglandins,
NO
ARE ALL EXAMPLES OF Vaso ___
VASODILATORS
Where do atherosclerotic lesions most often form? ( where does plaque develop)
Vessels of Turbulent flow- often brant points in arteries
= Sites of bifrurcation in the (conductance vessels??)
What is stenosis and where does it typically occur?
Narrowing of blood vessels
- Typically involves the MITRAL VALVE
What is the most serious form of fibrilllation?
Where there is no coordination of the ventricular m. contraction.
- Unconsciousness w/in 4-5 sec. from lack of blood to brain
- caused by ischemia of cardia m. & or conductive system, or repeptive electrical stimulation to the heart
Ventricular Fibrillation
What is the PR Interval threshold for 1st Degree Heart Block?
- What is 1st degree?
- What happens with QRS?
.21 sec
- Longer than normal PR Invterval.. Takes SA Node longer to stimulate AV Node.
- QRS complex is still present after every P wave
Infarction is?
An Area of tissue death due to Ischemia
What is sinus tachycardia?
> 100 bpm
- fever, sympathetic stimulation
The following things can cause a ____ _____.
1. Abnormal Pacemaker rhythm
2. Shift of Pacemaker to another part of the heart
3. block of conduction system
4. Abnormal pathways of the impulse transmission through the heart
5. Spontaneous generation of abnormal impulse of any part of heart (ectopic focus)
These can all cause a CARDIC ARRHYTHMIA
T/F: Atrial Fibrillation (AF) is not a serious condition, & is fairly common in the elderly & pts with mitral valve ds.
TRUE (??)
What CV pathological condition may occur in healthy people due to lack of sleep??
PACS (Premature Atrial Contractions)
- Characterized by "compensatory pause"
T/F: AF is not as severe as VF?
TRUE
What is Ascites? what can cause it?
Ascites- Accumulation of fluid in the peritoneal cavity
- Can be caused by mitral valve stenosis
What happens to HR in a Sinus Arrythmia?
HR Varies by 5% during quiet respiration & up to 30% during deep respiration
Increased Vasopressin &/or Renin-Angiotenin-aldosterone causes what?
Ultimately VASOCONSTRICTIOn
- Increased Salt & Water retention=> INcreased VENOUS RETURN (GOOD) = VASOCONSTRICTION= Increased AFTERLOAD (???)
What is 3rd Degree Heart Block?
-Atrial and ventricular rhythm?
Complete Heart Block!
- complete block of the impulse from SA Node to the AV node (dissociation of P & QRST waves)
Atrial Rhythm( PWAVE)= normal
Ventricular (QRS)= no relation so there are fewer bc it is set by rade of the AV node instead of the SA Node
What are Premature Ventricular Contractions? (PVCs)
-Results from ectopic focus in the ventricle.
- QRST interval not preeeded by p wave)
Increased endothelin will cause which effects?
vaso?
= > does what? favorable and unfavorable
VASOCONSTRICTION=> Increased Venous REturn (favorable)
& Increased Afterload (unfavorable)
What is fibrillation?
Incoordinated twitching of heart muscle fibers
-can be atrial or ventricular
What causes ectopic foci?
1. local areas of ischemia
2. small calcified plaques at dif points in heart
3. toxic irritaion of AV-node, Purkinje system, or myocardium caused by nicotine, caffeine, or drugs & alcoholism
What causes Heart Failure?
Inappropriate work loade
Myocyte loss
Restricted filling
( mostly in the ventricle)
What is Idioventricular rhythm?
The P-Q interval takes too long, so ventricles start their own beat.
-Atria and ventricles contract out of sync
ACE inhibitors stands for?
What does it inhibit?
- What does it cause?
ACE Inhibitors= Angiotensin Converting Enzyme Inhbitors
==> Inhibits the Renin-Angiotensin-Aldosterone System
==>Causes Reduced salt & water retention, LOWERS BP (??)
This is opposite of renin-angiotensin aldosterone system
Increased interleukins & TNF -alpha causes what effects?
1. Myocyte Hypertorphy (good, kind of)
2. Apoptosis (bad)
What is 2nd Degree Heart Block? - 2 types
- Conduction through the AV node INTERMITTENTly fails so that some but not all P waves are followed by QRS complex ( drop beat)
1. Type 1-PR interveal gets larger between each cycle until a QRS complex doesn't follow (drop beat)
2. Type 2= normal PR interval , then just a P wave= can happen up to 50 % of the time
What is HEART BLOCK?
- what can it cause
-how many degrees?
The conduction from the SA Node to the Ventricle is BLOCKED
- Can cause a WIDE range of arrhythmias
- 1st, 2nd (type 1 & 2) , & 3rd degrees
What will ectopic Foci in the heart cause?
Premature contractions
T/F: Beta-1 Receptor desnsitization results in up-regulation to compensate ( for heart failure????)
FALSe- results in down regulation... (other persons notes...)
What type of Fibrillation is less severe and a person can live for months/years with it.
- IT is characterized by absent P waves or fine high frequency , very low voltage waves that the R-R) interval is irregular ??
ATRIAL FIBRILLATION (AF)
What is an abnormal rhythm of heart beating?
Arrythmia
What are some methods of treatment for CHF? (abc order)
(1-B,2-Cs, 3-Ds, 1-I (or A), 1-V)
1. Beta blockers
2. Cardiac Transplant
3. Correction of Reverisble Causes
4. Diet
5. Digitalis
6. Diuretics
7.Inhibitors of Renin-Angiotensin-Aldosterone System (ACE inhibitors)
8. Vasodilators
What do cellular responses to CHF do to the autonomic receptor adaptations of Alpha 1 receptors?
slight increase in Alpha 1 receptors
What is sinus bradycarida?
bmp
stimulation?
< 60 bpm
- Athleticism, vagal stimulation
What is it called when blood can flow backwards through a valve?
- leaky valves
Regurgitation
What are some consequences of aortic valve stenosis? and order?
1.Elevated L ventricular systolic pressure due to stenotic aortic valve. =>
2. L ventricular hypertrophy. =>
3.L ventricular dilatation =>
4.L ventricular failure=> which can lead to 2 things (5a- leads to nothing else, 5b. does)
5a. Coronary insufficiency(pain), syncope
5b.Elevated L atrial pressure=>
6. Pulmonary congestion=>
7. Dyspnea, pulmonary edema=>
8. R ventricular failure
Depolarization of the atria results in whih wave on the ECG?
P wave
What does the Q-T Interval Represent??
Time for VENTRICULAR CONTRACTION
(0.35 s)
Which direction does repolarization take place? In the heart ( rep on ECG)
APEX to BASE
- this is opposite of Depolarization
What 2 things may ECG leads measure?
1. Difference in electrical potential between 2 different points on the body.
2. 1 point on body & a virtual reference point w/ 0 potenital, located inthe center of the heart
What is a graphic recording of electrical activity (potentials) produced by the conductive system & the myocardium of the heart during its depolarization/repolarization cycle?
ECG ( Electrocardiograph)
PR, ST, and Isoelectric lines are what of the ECG?
Segments of the ECG
Which part/ wave of an ECG indicates repolarization (of ventricle)
T wave
What do the P-Q & P-R Intervals represent?
Time for ATRIAL Deplarization
( 0.16 sec)
List parts of ECG Wave from left to right:
PR Interval -P Wave
QT Interval- Q, -R Peak, -S, -T waves
A persons HR is 100 BPM. What is the ECG cycle Length?
HR= 1/CYCLE LENGTH
Cycle length= 1/HR
Cycle length= 1/100
Cycle Length= .01 min= .6 sec= 600msec
What does the T-P Interval stand for?
Time for Ventricular Relaxation
What does P-P interval represent?
1 Cardiac Cycle
How is an AVL (augmented lead) configuration set up?
Negative leads on R. Arm & L. Leg.
(+) on Left arm
Which Limb is the ground lead usually placed on??
(Right leg)
(other persons notes??)
Which side of the interventricular septum is depolarized 1st?
L. side
How is an AVR (augmented Lead) configuration set up?
Negative leads on Left Leg & Left arm
Postive on Right arm
3 Laws of ECG:
1. A positive (upward) defelction in any lead if the wave of depolarization spreads toward the ____ ___ of that lead
POSITVE POLE
3 Laws of ECG:
2. A Negative Deflection (downward) appears in any lead if the wave of depolarization spreads toward the __ ___ of that lead
NEGATIVE POLE
3 Laws of ECG:
3. If the mean depolarization path is perpendicular to any lead, a ____ ____ ____ is usually seen.
SMALL BIPHASIC DEFLECTION
Apical depolarization results in which part of an ECG?/
......... early part of r wave
not sure about this from other persons notes
What is the most commonly used clinical ECG- system? describe it?
what lead is looked at most?
The 12-lead ECG System
- Leads 1,2,3 = bipolar leads
- Leads AVR,AVL, AVF, & V1-V6 = UNIPOLAR LEADS
- mostly look at LEAD 2- bc follows direction of heart
T/F: An ECG can assist in the dignosis of electroylte distrubances?
TRUE
Einthoven's Triangle=
The Triangle formed between leads 1, 2, & 3 ( r. arm. left leg, Left arm)
How can we determine the HR from the ECG cycle length?
HR= 1/Cycle Length
-Cycle length is the distance between R Waves
Or 300/ # of large boxes
What does the position of electrodes relative to the heart's electrical activity vector influence?
Waves formed on the surface ECG
How is an AVF augumented lead configuration set up?
Neg.= left arm & right arm
Positive- left leg
Where are precordial leads placed?
V1 - 4th intercostal (right)
V2 - 4th intercostal (left)
V3 - Between V2 and V4
V4 - Midclavicular
V5 - 5th intercostal space (anterior axillary line)
V6 - 5th intercostal space (midaxillary line)
What are the intervals of the EKG called?
- PR
-QT
- Wave-segment combos
T/F: Pulsations in BP are larger in the Aorta than anywhere else in the body!
FALSE- THEY ARE LARGEST IN THE LARGE ARTERIES
What type of muscle has the highest amt of ATPase activity?
skeletal m.
What types of complexes link Cardiac m. cells?
Junctional Complexes including GAP JUNCTIONS
What % of blood is held in the heart?
7%
What type of complexes link smooth m. cells?
Gap Junctions
How are enothelial cells joined together in fenestrated caps?
???? tight junctions???)
What compound is DIRECTLY responsible for relaxation of VSM?
cGMP
fx of endothelium in blood vessels? -4
1. Vascular tone reg.
2. VSM cell proliferation
3. Inflammatory response
4. Hemostasis
Where is flow velocityt the greatest?
Arteries
What special fx do fenestrated caps contribute to the choroid plexus?
secretion ( and absorption??)
If the TPR is .7PRU , what will the Pulmonary vasculat resistance be?
about .1 PRU... ( idk why)
In which type of m. are actin & myosin NOT organized into sacromeres?
Smooth m.
What special fx do continuous caps contribute in the CNS?
Contribute to the BBB
2 formulas for flow?
flow= VA ( Velocity x Cross Sectional Area)
Flow= P/R ( Change in pressure (pressure gradient) divided by Resistance ( vascular resistance)
Which vessels have the most collective cross sectional area?
Capillaries ( 2500 square cm)
What VASOCONSTRICTORs do Endothelial cells secrete?
1. Endothelin= Released from damaged cells to prevent extensive bleeding
2. Thromboxane A2
3. Angiotensin2
What part of the circulatory system has the greatest capacitance?
Lowest?
Greatest= Veins
Lowest= Arteries ( esp aging)
What special fx do fenestrated caps contribute in the GI tract?
ABSORPTION
(secretion to some other place -_-----__)
How do fatty plaques from atherosclerosis increase BF resistance??
Turbulent flow
What type of caps have an incomplete basement membrane?
Sinusoidal caps
Systemic circulation accounts for how much of Blood Volume?
Where is most the blood in systemic circ located? what percent?
Systemic Circulation = 84%, ( the most)
Most blood is in:
Veins, Venules, & venous Sinuses- 64%
T/F: Hypercoagulability can cause abnormal blood flow & vice versa.
FALSE- Abnormal bf CAN cause Hypercoagulability, BUTTTTTT Hypercoagulability CANNOT cause abnormal bf.
What % of blood is in systemic circulation at any time?
Pulmonary Circulation?
Heart?
System Circulation- 84%
Pulmonary Circulation- 9%
Heart- 7%
What type of junctions joins endothelial cells of Blood vessels?
Tight Junctions???
What VASODILATORS do ENDOTHELIAL cells Secrete? 3
1. Prostacyclin (PGI2)
2. NO
3. H2O2
The force exerted by the blood against any unit area of the vessel wall is called? ( measureed in mmHG
Blood Pressure
How are T tubules organized in Cardiac m.?
Form dyadic contact with SR near Z lines
Does blood travel faster in small veins or in arterioles?
arterioles
What type of m. doesn't have t tubules?
Smooth m.
T/F: In fenestrated capillaries , the fenestrations are oval-shaped *& located between endothelial cells.
FALSE- THEY OPEN THROUGH THE CELLS THEMSELVES... ( MIGHT BE OVAL THO??)
Which m. type is nonstraited?
smooth
The amt of blood pumped into the aorta by the heart each min is called?
CO
In what m. types does troponin bind to Ca?
Skeletal m. & cardiac m.
( not smooth.. smooth binds to calmodulin)
Special fx of fenestrated caps contribute to kidney glomeruli??
Filtration?
T/F: Arterioles have strong Muscular walls
True
Relationship of Velocity of BF & vascular cross-sectional area?
Inversely proportional
muscle types innervated in electrical syncitia?
Cardiac and smooth m.
Where is BP lowest?
R. Atrium
What serves as the skeletal backbone against which contraction occurs in VSMcells?
Intermediate filamentes
HOw does vessel length relate to blood resistance?
Longer vessel= more resistance ( so therefore is a direct)
What are the biological implications of turbulent flow?
1. Increase probability of endothelial injury
2. Deposit of Ca, Cholesterol, leading to plaque development.
3. Increased possiblity of bacterial infection
4. Increased possibility of thrombotic events
What are 3 important sources of Blood Resistance?
Blood Viscosity
Total length of Vessel
Blood vessel diameter/ Radius
What can pulmonary wedge pressure be used for?
Diagnossi of L. ventricular failure
&
To recognize the degree of mitral valve stenosis & regurgitation
Where is vascular resistance the Greatest??
in Arterioles (?)
The quantity of blood passing a given point in the circulation in a given period & is normally expressed in ml/min =
Blood Flow
why is the latch bridge mech important in VSMCs?
Keeps artereies in a state of partial contraction = vasomotor tone??
Where does the steepest change in BP occur?
Arterioles
Reynold's number= Re=
Re= (vdp)/ n
turbulance
What are some direct consequences of endothelial dysfunction?
1. Impaired vasomotion/tone
2. Prothrombic state
3. Proinflammatory state
4. Proliferation in arterial wall
The total quantity of blood that can be stored in a given portion of the circulation for each mm Hg pressure rise
( THE Ability to hold blood volume)
VASCULAR COMPLIANCE / Capacitance
C= Volume/ Pressure
What are major determinant of peripheral resistance?
small-diameter arterioles
T/F: VSMCs have extensive intracellular Ca-containing vesicles, from which they primairly draw for contraction
FALSE- VSMCs MAINLY get their CA from Extracellular sources
HOW DOES: Total Pulmonary Vascular Resistance Relate to TPR?
It is 1/7 of TPR ( note earlier question)
If pressure dif between 2 points is 66mmHg & the flow is 33ml/sec, what is the resistance in PRU?
2 PRU mmhg *sec/ml
T/F: ENDOTHELIAL injury can cause abnormal blood flow & vice versa
TRUE.. not same for hypercoalagability
T/F: Blood flow is quicker through sinusoidal cap.?
FALSE= slower
Special fx of fenestrated caps contribute to endocrine glands?
Secretion
What is the significance of delayed compliance/ STress- relaxation
It is a valuable mech for the circulation to accomadate much extra blood when needed, such as after too large a tranfusion.
What is the usual response of VSMCs to hormonal stimulation?
- other responses?
usual= Contraction or relaxation
others= growht & or hypertrophy & migration to the intima
Describe the two types of VMC contractions.
Phasic contraction - Initial phase of force development - Depends on the formation of actin-myosin crossbridges in response to acute elevations of intracellular Ca Tonic contraction - Persists even after Ca levels return toward baseline - Maintains vascular tone