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127 Cards in this Set

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CO equation
HR x SV

HR=phase 4 depolarization
SV=Pl, AL, CTY
MAP equation
CO x SVR
Flow
Q = Delta P / R
Conduit Vessels and asscoiated pressure.
Aorta and Fems
Pressure ~100 to 90
Not much change in diameter.
Resistance vessels and assc pressure
Small arteries and Arterioles

P=45mmHg
Greatest amount of control applied to these vessels, via metabolic, myogenic, and hormonal means.
Exchange vessels
Caps

P=25
Greatest total surface are, therefore smallest velocity which facilitates filtration and resorption.
Capitance vessels
Venous system

P=10 to near 0 at vena cavae
60-70% of BV stored here.
3 Pressures transmitted against vessels?
Transmural,
Intra-vascular,
and Hydrostatic.
Atrial contraction accounts for what percentage of vent filling?
~15%
Atrial systole is represented by which structure on an ECG?
PR segment
S4 is heard when
"spurt" of blood (the 15%) from atrial contraction.
May be a sign of LVH or RVH and inc CTY.
Sign of artrial hypertension.
LVEDP and LVEDV are indices of what?
PL = 140mL in 70kg.
S1 is heard when
The onset of Vent contraction by the closing of mitral and tricuspid.
Isovolumetric contraction is?
After AV valves close, the building of pressure, with all valves closed, to overcome pulmonary and aortic pressures.
SV equals
LVEDV - LVESV

140-65=75mL
Ejection Fraction
SV / LVEDV

75 / 140 =60%
S2 is heard when
The pressure in the ventricles fall below aortic and pulmonary, thus A and P valves close.
Pulmonary valve closes 1st, aortic 2nd, a split may be heard.
S3 may be heard
From rapid filling of atria. Noticable in youth b/c of thin chest, elongated ventricles, and therfore stretched chordae tendinae.
Innocent murmer.
S1 split is audible in patients with...
A Right bundle block, this would also delay P valve closing, therefore an S2 split may also be audible.
S2 split may be heard in normal individuals, it may however be a sign of...
VSD can lead to increased S2 split b/c LV blood is moving into RV, and RV is trying to move much more Volume than it is used to.
Valve cycle during heart beat starting with A and P valves just closing.
MT open - vents fill - AP fires
MV closes
TV closes
PV opens
AV opens
AV closes
PV closes
MT open
atrial waves can be used in conjx with jugular distention to measure?
CVP
CVP is a determinent of PL.
A wave
Atrial contraction
An increase in the A wave signifies a tricuspid stenosis
C wave
Contraction of the heart
An increase in C wave means tricuspid insuff or VSD.
V Wave
Thoracic Venous filling
An increase in V wave is seen with increase in C wave to signify tricuspid insuff.
What is the most important determinant of CV function?
MAP
3 determinants of CVP
Venous SM tone
BV
Body position
Increase venous SM tone
Inc CVP
Inc PL
Inc SV
Dec BV
Dec CVP
Dec PL
Dec SV
3 patholgies increasing AL
HTN, Arteriosclerosis, AV stenosis.
3 determinants of AL
Diastolic Pressure = major
CPL
Aortic valve resistance
What is CTY
Contractile force at a give PL and AL
What effects CTY
Cardiac efferents and Cats
Do changes in AL and PL effect CTY
NO!
PL can alter the force of contraction, but not CTY.
What is the truest index of CTY?

Where is that located on a Pressure-Volume curve?

What would an inc in CTY look like on PV curve?
ESP (AV closure) is truest index of CTY.

Located on the upper left of curve.

An inc in CTY will shift curve UP and LEFT. A dec will shift curve DOWN and RIGHT.
What cellular basis is the primary determinant of CTY?
Ca Kinetics
Ca release from SR
Influx across PM
Removal of Ca during relaxation
Do parasymp effect CTY?
NO, there is no parasymp innervation of the ventricles.
Determinants of CTY
Thyroid hormone - coupled to cAMP.
Digitalis/caffine
Sympathetic nerve stimuli - Cats
The largest pressure drop is across these vessels?
Arterioles
The largest X-sectional area is at the level of which vessels?
How flow here fast or slow?
Caps, and flow is very slow to facilitate transfer of materials.
Highest Velocity is where?
Aorta
What is the main concept behind Poiseuill's law?
That radius has the largest physiologic effect on Q and R.
LaPlace in a nutshell.
Tension is directly proportional to P and radius.
Tension is inversly related to wall thickness.
Therefore wall thickness can counteract increases in Pressure and radius (HTN).
LaPlace in a nutshell.
Tension is directly proportional to P and radius.
Tension is inversly related to wall thickness.
Therefore wall thickness can counteract increases in Pressure and radius (HTN).
Pulse pressure equation
Psys - Pdias
Determinants of Systolic Pressure?
SV = major
Pdias = minor
CPL
Determinants of diastolic pressure?
SVR = major
Psys = minor
HR
2 components of CPL
Passive = structural
Active = SM tone
Inc SM tone = dec CPL = inc CVP = inc PL = inc SV.
2 components of CPL
Passive = structural
Active = SM tone
Inc SM tone = dec CPL = inc CVP = inc PL = inc SV.
Main determinants of CVP
1.Constriction of venules and small viens by epi, NE, VP, and AII.
2.CPL
3.BV
4.Gravity
5.CO
What are the the effects of NE, Epi, VP, and AII during sympathoexcitation?
What is there effect on vessel diameter?
Dec CPL to aid in venous return to the heart.
They do NOT decrease vessel diameter, just stiffen wall.
Primary effect of hemorrage?
Dec in BV
Dec CVP
Dec PL
Dec CO
Dec MAP
Secondary compensation for hemorrage?
Barorecptors sense dec MAP
Inc SVR
INC VSM tone=Dec in CPL
Inc CTY
Inc HR
Inc SV
INC CO and INC MAP
Two priamry factors that govern tissue blood flow?
*Perfusion P across tissue and draining vein.
*Diameter of resistance vessels
What percentage of caps are actively participating in exchange of nutrients?
*1/3 or 30%
*Except in cardiac and neuro circ.
Who's Law best defines cap flow?
Laplace
Poiseulle
Faber
Harrell
Poiseulle
*diameter of resistance vessel(r) is main controller of flow.
What are the 2 mechanism used by auto regulation (AR)?
What are 2 principles of AR?
*AR uses myogenic and metabolic mechanisms.
*AR is used to maintain a constant flow.
*AR is found in almost all vascular beds.
Myogenic reg.
What effect does inc MAP have?
Raise myogenic tone and dec diameter.
T/F
Myogenic and metaboic regulation is seen in venous circ.
False.
Principle behind metabolic regulation?
Dependent on local release of vasodialator metabolite(VD) by cells in proportion to their metabolic rate and oxygen use.
Works under 2 conditions
Metabolic regulation, condition 1
*When tissue matabolic rate is constant
*INC in MAP
INC VD washout
Vasoconstriction

DEC in MAP = DEC oxygen
therefor vasodilation
Metabolic reg, Condition 2
*WITH changes in metabolic rate.
INC tissue activity
INC metabolic rate
INC oxygen utilization
INC vasodilation
Functional Hyperemia refers to which metabolic conditon?
Is func hyperemia a form of AR?
*FH is a condition 2 mechanism.
*FH is not an AR mechanism, b/c FH looks to change flow to meet tissue demands.
*AR looks to maintain a constant flow.
Which group of vessels is most sensitive to VD?
Resistance vessels - Term. arterioles.
What are some vasoactive autacoids?
Bradykinin, IL, cytokines
Histimine
NO-high clinical importance
Thromboxane
What are some vasoactive autacoids?
Bradykinin, IL, cytokines
Histimine
NO-high clinical importance
Thromboxane
T/F, symp vasoconstrictors anr continuosuly released on SM cells?
T
*This is the key factor to neurogenic tone.
*Key controller of SVR and MAP.
*NE acting with alpha-ARs
What does the adrenal medulla release during sympathoexcitation?
Where do these act?
*Epi and some NE.
*Epi and NE act on Beta-1s in the heart to inc HR.
*Act on alpha-ARs for peripheral vasoconstriction.
*EPI also acts on bets-2s as a vasodilator in skeletal muscle(good for fight/flight).
Angiotensin...
Renal peptide that acts a vasocontrcitor.
INC SVR
Dec CPL
INC MAP
Vasopressin...
Released from the post pit as a vasoconstrictor.
What are the 2 opposing mechanisms in microcirculation?
Intrinsic Vs Extrinsic
*Intrinsic tries to match perfusion to metabolic activity and AR bloo flow.
*Extrinsic, under neural and hormonal control, attemps to maintain systemic pressure at the expense of regional areas.
The majority of transcap exchange is due to this mechanism?
Rapid or slow?
Diffusion.
Rapid.
3 factors of permiabiliy
*inversely proportional to size of substance.
*directly proportional to lipd solubility of substance.
*How tightly endothelial cells are packed together.
What is the effect of histamine on perm?
Histamine inc perm by acting on endo. cells.
Rate of ultrafiltration is determined by?
*The perm of cap wall to water.

*The balance b/t hydrostatic and colloid osmotic pressure.
2 components of cap ultrfiltration coefficient?
1.Cap surface area.

2.Perm of water
Besides cap coef, what are the other two factors of the Starling equation? Which is most important?
*Pc=hydrostatic cap pressure
*COP=colloid osm press of plams.

*Pc is most important.
Filtration occurs when...
Pc>COPp
Reabsorbtion occurs when
Pc<COPp
Increased venous pressure will have what effect on filtration and reabsorbtion?
Increasd filtration and less reabsorbtion due to the decreased pressure drop along cap bed.
What is the effect of Inc arteriolar dilation on filtration and reabsorbtion?
Increased filtration and less reabsorbtion.
What is the effect of dehydration or arteriolar constriction on filtration and reabsorbtion?
Decrease in filtration and an increase in reabsorbtion.
How much RBC oxygen extraction reserve is there in cardiac circulation?
Almost zero!
What is the ratio between CO, VO, and coronary Q?
1:1:1 ratio exist b/t these components in order to prevent ishemia b/c there is estienally no reserve in cardiac circ.
T/F
L ventricular output determines oxygen demand?
True.
What are the 4 specific determinates of heart work and oxygen demand?
1.PL - inc PL, inc SV
2.AL - oxygen demand is directly related to AL, however, SV is indirectly related.
3.CTY
4.HR
What are the 4 specific determinates of heart work and oxygen demand?
1.PL - inc PL, inc SV
2.AL - oxygen demand is directly related to AL, however, SV is indirectly related.
3.CTY
4.HR
Two determinants of coronary flow?
1.Pressure diastolic
2.Diastolic duration - 80% of coronary blood flow occurs in diastole.
*If tachy, limited coronary Q.
T/F intrinsic regulation is the major regulator of coronary resistance and flow?
TRUE. Intrinsic metabolic control is the mafor mechanism along with excellent AR.
*Key metabolites are adenosine, CO2, and H+.
*Myogenic control is present as well.
T/F intrinsic regulation is the major regulator of coronary resistance and flow?
TRUE. Intrinsic metabolic control is the mafor mechanism along with excellent AR.
*Key metabolites are adenosine, CO2, and H+.
*Myogenic control is present as well.
T/F
The brain has extensive lymphatics to protect against edema?
False, this is why ICP must be tightly regulated.
3 volumes important to remain constant in cerebral circ.
1.CSF
2.ISF
3.BV
3 volumes important to remain constant in cerebral circ.
1.CSF
2.ISF
3.BV
What is the numerical value of ICP?
10 mmHg
While the brain exhibits good AR(similar to heart), what additional factor can put the brain at risk for reduced blood flow?
Gravity
Newton
Metabloic and myogenic control are major factors, what are two main dilators of cerebral blood vessels?
CO2 and H+ are potent vasodilators.
*Inc CO2 and dec pH lead to vasodilation.
4 common conditions that increase ICP?
1.Excessive cap filtration due to damage induced inc in perm - concussion
2.Blockage of CSF aquaduct and villi - tumor/mengititis
3.Hemorrage
4.Tumors
T/F
Increases in venous pressure are significant at the brain level?
False, given the brains position above the heart, inc in VP is rarely sig.
T/F
Active regions in the brain can steal blood away from inactive portions of the brain.
True, this shunting of blood assists the brain increasing blood flow in times of stress.
T/F
Pulmonary circulation is a High P, Low R, High Q, and High CPL circuit.
FALSE!
LOW P, Low R, High Q, High CPL.
*must be low pressure to ensure no excess filtration and edema.
T/F
Myogenic and metabolic control is critical in pulm circ?
FALSE,
active control is limited so lungs can receive inc flow w/o inc Pressure.
T/F
There is abundant lymphatics in the lungs to safeguard against edema.
True.
Along with little net capo filtration, lymph system limits the possibilty for pulm edema.
Where in the lungs would pulm edema furst be noticable?
What can this b ea sign of?
First appears in the lung bases as a sign of LHF.
T/F
Pulm SM cells lack strecth activated ion channels?
True, allows inc flow w/o inc in pressure.
What are the effects on pulm vascular SM when oxygen levels decrease?
Unlike other tissues where a dec in oxygen causes vasodilation, in the lungs, lack of oxygen causes vasoconstriction. This helps shunt blood to areas of active oxygen transfer.
5 factors of artetial BP
HR
CPL
SV
SVR
BV
What is the most important MAP reflex?
Where are they located?
Carotid-Aortic baroreflex = arterial BR

*They are located in the carotid bodies and the aortic arch.
How are the caroid-aortic BR activated?
Stretching of the arterial wall generates impulses in the nerve endings of the sensory fibers.
Describe the pathway of stimuli/response given an inc in MAP on carotid-aortic BR.
INC MAP
INC BR
DEC symp activity (dec beta-1)
INC Parasym (inc muscarinic)
DEC CO
DEC MAP
T/F
The most imp physiologic funx of the arterial BR is to rapidly moderate flucuations in BP.
True
Cardio-pulm BR are low pressure reflexes that mainly adjust?
BV, sensed by distension of thoracic vein and atria.
Where are the cardio-pilm BR located?
Located at the junx of VC and RA, and junx of Pulm Vein and LA.
When do cardio-pulm BR fire?
What exactly are they monitoring?
The receptors fire during atrial diastole in proportion to stretch on thoracic veins and atria.
Measuring CVP as a funx of venous BV, CPL, and CO.
Pathway of events after cardio-pulm BR detect dec in CVP.
Dec in CP BR
INC in symp (NE) tone (HR, SVR, PL, CTY)
Dec in parasym
Dec CPL
INC CVP
T/F
Arterial BR trump Cardio-pulm BR.
True, which is important in HF patients.
Why is it important that the arterial anf cardio-pulm BRs work together?
B/C CP BRs can pick up changes in the venous side that the arterial BR may miss.
How can capillary fnx assit in a hemorrage patient?
Hemorrage will dec arterial pressure, therefor reduce filtration and inc reabsorbtion thru caps. This can lead to an "injection" of 1.5 L of fluid to help maintain CO and MAP.
What are the 2 secondary arterial pressure reflexes?
1.Peripheral ChemoRecpetors in carotid bodies and aorta.
2.Central CR in brain
What are CR sensing?
Why is the metabolic rate of CR cells important?
CR sense arterial gasses(PO2 and PCO2) and pH.
CR cells have the highet metabolic rate of any cells in the body, which make them sensitive to any changes.
T/F
Central CR exhibit a one-way reflex.
TRUE, they sense diff b/t CSF and ISF.
T/F
Central CR exhibit a one-way reflex.
TRUE, they sense diff b/t CSF and ISF.
What are the normal values for PO2, PCO2, and pH?
PO2= 95 mmHg

PCO2= 40 mmHg

pH= 7.4
Sympathetic are stimulated by central CR by?
Hypoxemia, acidemia, or Hypercapnia.
*one exception is that severe changes to oxygen and pH can directly depress myocardial and vas. SM.
Hallmarks of Cerebral Ischemic Reflex.
Extremely high HR (200) with a normal BP, in response to hemorrhagic shock.
Hallmarks of Cushing reflex?
Elevated MAP, with norm/low HR.
In response to elevated ICP (MVC).
Both Cerebral Ischemic reflex and Cushing reflex are intiated by which receptors?
Central CR.
Both Cerebral Ischemic reflex and Cushing reflex are intiated by which receptors?
Central CR.