Myocardial Perfusion (Coronary Arteries), Etc

Front 1

Describe the anatomy of Coronary Circulation

Back 1

Left coronary artery--> Provides blood to left ventricle - 50% of total flow. Includes the circumflex artery. Left Anterior Descendens - 50% of total flow. Posterior descending artery comes off the circumflex artery in 40% of the pop.

Right coronary artery--> supplies blood to the SA node, AV node, and RBB. Posterior descending artery comes off of it in 60% of the population.

Front 2

Describe the capillary density of coronary arteries.

Back 2

Very high capillary density.

Front 3

Capillary density of an organ directly correllates with it's

Back 3

metabolic activity.

Heart is VERY metabolically active, VERY dense capillaries.

However, the heart only gets 5% of blood flow!!!

Front 4

Coronary blood flow serves one function, which is?

Back 4

To supply nutrients and clear wastes.

Front 5

The maxiumum level of blood flow to the heart is..

Back 5

HIGH 400 mL/min!!!

Why? In case the heart is working overtime...coronary arteries can vasodilation, greatly increasing O2 supply if needed.

Front 6

Cardiac O2 Extraction = ____% at rest.

Back 6

65-70% at rest!!

Heart is never really at rest!!!

Front 7

Cardiac O2 Extraction is measured by

Back 7

A-V O2 Difference

(CaO2 - CvO2)....of coronary arteries and veins.

Basal AV O2 Difference of heart is 65-70%

Front 8

What drives the level of vasodilation of the coronary arteries?

Back 8

O2 Consumption (VO2) by the heart.

VO2 = Q * (CaO2 - CvO2) (just thought I'd throw that in :)).
(Fick's Law. )

Front 9

Basal blood flow to the heart is

Back 9

HIGH (5%)

Why? because the heart is never at rest. It constantly needs O2.

(Hearts BASAL O2 Extraction Rate is 65-70%!!!)

Front 10

The only way to increase O2 Delivery to the stressed heart is to

Back 10

Vasodilate the coronary arteries to increase blood flow.

Front 11

CAD

Back 11

prevents coronary artery vasodilation.

Leads to heart ischemia.

Front 12

Ischemia causes a rapid decrease in

Back 12

Ischemia causes a rapid decreased in myocardial contractility.

And chest pain...from anaerobic respiration of the heart.

Front 13

Occlude a coronary artery for 5 secs, get an immediate drop in _______.

Back 13

Occlude a coronary arter for 5 secs, get an immediate drop in contractility.

Front 14

Occlude a coronary artery for longer than 5 secs, what happens?

Back 14

Immediate drop in contractility (very rapid).
Ventricle becomes akinetic.
BP will plummet.

Front 15

When you occlude an artery and then let it go, there is a temporary rebound of increased flow that is equal in magnitude to the amount of decreased flow. This is called.

Back 15

Reactive Hyperemia.

Front 16

As you move from the epicardium to the endocardium, coronary blood flow will only occur during...

Back 16

Diastole

Due to an increased Tm, caused by increased Po (tissue pressure) with contraction.

Front 17

True or False

Coronary BF throughout the heart wall is the same.

Back 17

FALSE

There is a marked drop in BF as you move from the eipcardium to the endocardium due to an increased Tm with contraction.

Front 18

The magnitude of tissue pressure (Po) in the endocardium at least equals.....?

Back 18

The magnitude of tissue pressure in the endocardium at least equals SBP.

(the pressure with contraction.)

Front 19

Explain to me what happens to Coronary BF Relative to Aortic BF During the Cardiac Cycle?

Back 19

ISOVOLUMETRIC CONTRACTION *Ventricle muscle squeezes on blood, but no contraction. This increases tissue pressure (Po) and decreases Tm, decreasing coronary BF.
*Coronary BF decreases BEFORE aortic BP increases due to isovolumetric contraction.

RAPID EJECTION: Coronary BF has a rapid DROP. Aortic BP rapidly increases.

DIASTOLE:
*Coronary BF has a LARGE increase due to REACTIVE HYPEREMIA.
*(The reactive hyperemia will be larger in the L. ventricle than the right b/c the L. ventricle exerted more SBP on the tissue than the right.)
*Aortic BP decreases back to diastolic. DBP is the pressure head for coronary blood flow.

Front 20

What is the pressure head for flow to the coronary arteries?

Why?

Back 20

DIASTOLIC BLOOD PRESSURE

Contraction (SBP) increases tissue pressure when decreases the Tm of the coronary arteries, decreasing flow. Therefore max flow is determined by DBP.

Front 21

After rapid ejection, why does the left ventricle have a larger increase in coronary blood flow than the right?

Back 21

Reactive Hyperemia will increase flow in proportion to the magnitude to the decreased flow. The left ventricle decreases flow more (it's contraction is stronger.).

Front 22

The subendothelium is particularly vulnerable to conditions that may hinder vasodilation such as...

Back 22

atherosclerosis.

Front 23

Four Factors that influence myocardial O2 Consumption (VO2)

Back 23

1) Heart Rate
2) Contractility
3) Afterload (Pressure Work)
4) Preload (Volume Work)

(The first three are metabolically costly).

VO2 = CO * (CaO2 - CvO2)
--all of the above affect cardiac output

Front 24

Myocardial O2 consumption has a ______ effect on Cornary BF.

Autonomic NS has a _____ effect on coronary blood flow.

Back 24

Myocardial O2 consumption has a direct effect on Cornary BF.

Autonomic NS has a indirect effect on coronary blood flow.

Front 25

________ influences coronary blood flow more than anything else.

Back 25

myocardial VO2.

Front 26

The fact that CA BF is directly related to myocardial VO2 is an example of

Back 26

Active Hyperemia.

Front 27

How does the SNS regulate Coronary BF?

Back 27

Indirectly via Active Hyperemia.

*Stimulation of the left stellate ganglion by the SNS causes alpha mediated vasoconstricton of CA's. You have a inital drop in flow. THIS IS TEMPORARY.

* WHY???, SNS stimulation also causes increased HR and contractility. This increased metabolic activity and VO2, causing ACTIVE HYPEREMIA, and increases coronary BF.

*(Increased VO2 of heart overrides alpha mediated vasoconstriction)....even in a fibrillating heart!!!!!!

Front 28

Does the PNS have a direct effect on Coronary BF?

Back 28

NO.

May have a mild indirect effect via decreased HR, contractility, and decreased VO2....causing less CA vasodilation.

Front 29

Maximum O2 Extraction of the Heart happens when?

Back 29

WHEN THE HEART IS AT REST!!!!

65-70%

This means when the heart is working hard...it can't extract more O2 from the blood...it may even extract less.
So the only way the heart can get more O2 when working hard is TO VASODILATE coronary arteries to INCREASE FLOW.

Front 30

What three Factors Control Coronary Blood Flow?

Back 30

A) MECHANICAL (TISSUE PRESSURE FROM CONTRACTION)
---->Increased tissue pressure (Po) from contraction will reduce the transmural pressure gradient (Tm = Po-Pi). This will compress the vessel
-----> Therefore, as you move from the epicardium to the endocardium, coronary BF will only occur during DIASTOLE, due to decreased Tm.

B) METABOLIC
----> Changes in O2 consumption (VO2), via changes in [HR, CONTRACTILITY, AFTERLOAD, PRELOAD]
---> HR, contractility, and afterload cause and increased metabolic demand
-----> Changes in preload just increase CO
-----> VO2 = CO * (CaO2 - CvO2)

C) NEURAL
------> SNS stimulations indirectly vasodilates via Active Hyperemia (Increase HR and contractility, VO2).
-------> PNS stimulation indirectly decreases BF by decreasing HR, contractility and VO2.

Front 31

Two Types of Collateral Blood Flow

Back 31

1) Small arteriole to small arteriole

2) Capillary to capillary (not present in humans).

Front 32

Arteriole to arteriole collateral blood flow will maintain tissue perfusion if an occusion occurs where?

Back 32

UPSTREAM

Occlusions downstream will decrease perfusion. (no capillary to capillary connections).

Front 33

Arteriole to arteriole collateral BF is helpful in the heart by preventing what?

Back 33

TRANSMURAL INFACTS.

Front 34

Three Things that Determine How much a tissue infarcts:

Back 34

1) Degree of collateral flow.
2) Amt of tissue supplied by the occluded vessel
3) Duration of ischemia

The most determining factor is the amount of collateral blood flow.

Front 35

What factor is the most influential in determining the degree of tissue infact during an MI?

Back 35

The degree of collateral BF.

(inversely related).

Front 36

What is the only way to increase collateral blood flow to the heart??

Back 36

CHRONICALLY REDUCED BLOOD FLOW to the heart.

Which is dangerous.

Front 37

T/F

Exercise can increase collateral BF to the heart and help prevent transmural MI's.

Back 37

FALSE.

Front 38

Anatomy of the brain vasculature

Back 38

Internal Carotid Artery and Basilar Arteries perfuse the Circle of Willis.

Front 39

The capillary density of the brain is...

Back 39

HIGH

3000-4000 mm^3!!!!

Brain is VERY metabolically active.

Front 40

Characteristics of the Blood Brain Barrier

Back 40

TIGHT capillary junctions.

Water soluble things CANNOT cross. (w/o active transport).

Only lipid soluble things can passively diffuse across.

Front 41

Function of cerebral blood flow

Back 41

Deliver nutrients and rid wastes.

Front 42

In the brain, TOTAL/ combined blood volume, brain tissue, and CSF are

Back 42

CONSTANT

to prevent increased ICP due to SKULL

Front 43

In the brain

TOTAL Blood Flow is ________.

REGIONAL Blood Flow is __________.

Back 43

In the brain

TOTAL Blood Flow is CONSTANT.

REGIONAL Blood Flow is VARIABLE.

(The variations in regional BF depend on the activity of the brain. Brain uses different area for different activities.).

Front 44

Different regions of the brain will have variations in blood flow depending on _______.

This is an example of ________.

Back 44

Different regions of the brain will have variations in blood flow depending on the activity/ region of the brain being used.

This is an example of Active Hyperemia.

Front 45

Explain how arterial CO2 effects cerebral BF.

Back 45

CO2 dissociates into H+ and HCO3- via carbonic anhydrase. The H+ (acidosis) will affect cerebral vasculature.

* INCREASED PCO2:
---> Vasodilation. (increased ICP!!)
--->Hyperventilate the patient to decrease ICP.

* DECREASED PCO2:
---> Cerebral Vasoconstriction (Decreased ICP)
----> Decrease RR to increase BF.

Front 46

The ultimate regulator of cerebral vasculature with changes in pCO2 is..

Back 46

H+

Front 47

The neural control of Cerebral Blood Flow....

Back 47

IS NONEXISTENT.

Brain can only regulate CBF via changes in MAP.

Front 48

The brain can only regulate Cerebral Blood Flow via

Back 48

Changes in MAP. (Pressure Head)

Front 49

What is the pressure head for cerebral blood flow?

Back 49

MAP

Front 50

Pts with chronic HTN will experience what if you BP is maintained at 120/80?

Back 50

Decreased cerebral blood flow.

(Frank starling curve has shifted to the right. )

MAY SEE CUSHING'S RESPONSE

Front 51

Cushing Response

Back 51

Pronounced activation of the SNS in response to CEREBRAL ISCHEMIA

VERY STRONG

*POTENT increase in MAP via alpha mediated vasoconstriciton

*BRADYCARDIA :
----> HTN stimulates baroreceptor afferents, which stimulate NTS
----->NTS stimulates NA and DMV to cause bradycardia. (BARORECEPTOR REFLEX)