1-Cardiovascular Physiology

Front 1

Define:
Preload
Afterload

Back 1

Preload = The degree of stretching experience by the V msks during Vdiastole (after atrial contraction). Proportional to EDV; affects ability to produce tension.
Afterload = The pressure that a chamber of the heart must generate in order to eject blood. big AL = longer isovolm contraction = shorter ventricular ejection = larger ESV = small SV

Front 2

During diastole, a small change in ventricular pressure will have a large effect on what?

Back 2

In diastole, a small change in ventricular pressure will have a large effect on ventricular volume (small increase in Ped = large increase in Ved)

Front 3

What determines the pressure of a ventricle during diastole? When is this not true?

Back 3

During diastole the pressure of a ventricle is determined by the venous pressure, except when there is stenosis.
Pvein = PRELOAD = major determinant of Ved

Front 4

What does the body do in response to a decrease in cardiac compliance? What effect (long & short) does this have?

Back 4

if cardiac compliance falls then the body will increase venous pressure to ensure that the heart still fills (ie an increase in venous P = increase in Ved). This rise in venous pressure will cause congestion and eventually remodeling of the ventricles.

Front 5

What 6 factors affect venous return?

Back 5

1. blood volume
2. compliance of veins (controlled by sympathetics)
3. Axial muscle activity
4. venous contractions and valves
5. gravity
6. negative thoracic pressure

Front 6

with regards to cardiac ouput, two factors are kept relatively fixed while a third factor is varied (to determine CO). What are these factors?

Back 6

P aorta and Pveins are kept relatively fixed, Total Periph Resistance varies and in doing so determines CO.

Front 7

When/why are some pt's given diuretics? Why do you need to be careful when diuresing these pts?

Back 7

If the renin-angio-aldost system detects a fall in Bp (d/t less compliant vent) it can respond by increasing the blood volume, which in turn increase the ED pressure. This is often treated with diuretics but you must be careful not to drop venous pressure too low b/c elevated venous pressures are required to fill the less compliant ventricles.

Front 8

How does compliance affect P-V relationships?

Back 8

High compliance (in arteries): need a BIG change in P to affect Volume
Low compliance (in veins): need a little change in P = BIG change in Volume

Front 9

What keeps blood moving when the heart is in diastole?

Back 9

The stored pressure energy that's in the walls of the arteries.

Front 10

Resistance is inversely proportional to ________ and directly proportional to ______. (xtics of b.vessels)
Therefore a small change in _____ will cause a big change in ________.

Back 10

Resistance inversely P to radius^4
directly proportional to length.
A small change in diameter will cause a big change in resistance

Front 11

What affect does increasing radius have on resistance and flow?

Back 11

Increasing radius will decrease resistance and increase flow by the same factor.

Front 12

What happens to flow,resistance and pressure as you add b.vessels in parallel?

Back 12

As you add pipes in parallel the total flow increases, the resistance falls, and the pressure difference across the pipes doesn't change too much.
E.g add 3 pipes = 3Q, R/3

Front 13

What causes local control of TPR? ie what triggers dilation, constriction and both?

Back 13

dilation: adenosine, CO2, low pH
constriction: high O2, high pH
Temp: both

Front 14

What two mechanisms provide upstream, intrinsic regulation of arterioles?

Back 14

1. Myogenic dilation: low Bp = dilation (increases radius, less resistance, more flow and more pressure)
2. Sheer stress response: blood flowing past causes release of NO = vasodilation

Front 15

For a fixed CO, if TPR falls, what will happen to Part?

Back 15

A drop in TPR means that several collateral vessels have opened and thus blood will flow too quickly from A --> V. The heart must compensate by increasing CO to shift blood back into the arteries (until it does so, there is a transient drop in Part!)

Front 16

What are the 3 intrinsic responses to a drop in TPR? (ie how does body compensate?)

Back 16

1. The Pveins goes up from blood shifting A --> V
2. The increased Pveins = higher preload = higher Ved = bigger SV / CO
3. Low Part = low afterload = bigger SV and CO

** These changes can only compensate so much!! P art will still be at least a little low!!

Front 17

What happens when you eat a big meal? What are the intrinsic and extrinsic responses of the body? (2 intrinsic/innate and 3 extrinsic)

Back 17

TPR falls b/c splanchnic bed opens up!
Intrinsic:
-P veins rises = preload goes up = Ved bigger
- Part falls = lower afterload = lower Ves

Extrinsice: Symp activation
- increase in TPR
- decrease in venous compliance = raises P veins
- increased HR (also d/t loss of psymp), shifts ESPVR leftward

Front 18

When you exersize, you get the same hemodynamic effects as when you eat, except what?

Back 18

Increased motor neuron activity causes stimulates the symp system and resets the baroreceptors to higher threshold

Front 19

What is the formula to calculate MAP?

MAP - P veins =

Back 19

MAP = 2/3Dbp + 1/3Sbp

MAP - Pveins = CO x TPR = HR x SV x TPR

Front 20

What are the 3 cardiac determinants of MAP?

Back 20

1. HR: when high CO goes up and so does MAP
2. Ved: high when heart has high compliance and this increases SV/CO thus raising MAP
3. Ves: is ESPVR shifts Left, Ves falls and CO/SV go up, raising MAP

Front 21

What are the 2 vascular determinants of MAP

Back 21

1. TPR: both the # and the size of the arterioles. When TRP is high MAP is high.
2. P veins: when the compliance of the veins falls, their pressure rises and this increases CO/SV = higher MAP

Front 22

What are the 4 short term sources of MAP control?

Back 22

1. Baroreceptors - when stimulated they activate the symps = Increased HR, [Ca], Bvolume, and TPR. Decreased Venous compliance, ejection time, parasymp activity. If chronic stimulation, the Breceptors will think high Bp is normal and raise their threshold
2. Stretch receptors - in veins and atria. If Bvolume goes up, symps get activated to transfer blood from V --> A
3. Metabolites - if the MAP goes up, the tissue get better perfused, [metabolites] go down, vessels contract and TPR goes up
4. Myogenic response: increased MAP causes constriction of the Resist arteries, causing an increase in TPR.
** 3 & 4 can contribute to hypertension!

Front 23

Why is the blood supply to the kidneys comparable to a portal system?

Back 23

B/c blood goes from afferent arteriole, to the glomerulus capillaries, to the efferent arteriole, to the peritubular capillaries (loop of Henle comes off this) to the vein.

Front 24

how/where is pressure controlled in the nephron?

Back 24

the efferent arteriole can constrict/dilate to adjust the amount of pressure in the peritubular capillaries, where the hydrostatic pressure is usually low and the oncotic pressure is high.

Front 25

What regulates pressure in the aff & eff arterioles of the nephron? (3)

Back 25

1. myogenic response
2. JGM aparaturs
3. Angiotensinogen II and sympathetics

Front 26

How do the beta receptors of the heart respond to chronic stimulation by the sympathetic system?

Back 26

They phosphorylate B1 receptors and this inactivates them . Protective mechanism but interferes with regulation of CO.

Front 27

What are 4 causes of L ventricular failure?

Back 27

1. CAD leading to an MI
2. Valvular heart disease (mitral)
3. Chronic HTN
4. Diseased heart muscle (e.g. myocarditis)

Front 28

What's the difference between stable and unstable angina?

Back 28

Stable - atherosclerosis causing ischemic pain that is relieved with rest.
Unstable - when pain occurs even at rest (clot gets superimposed on plaque)

Front 29

What type of disfunction is caused by cardiac hypertrophy? What causes this condition? How does the body respond?
What are the 3 main symptoms/treatment?

Back 29

Diastolic dysfunction w/o afterload demand.
Genetic defect in proteins, collagen, etc, such that cardiac muscles can't generate enought force. Body responds by stimulating hypertrphy. This lowers Ved (low complnc & chamber size) and obstructs blood ejection.
-angina; effort induced syncope; SOB d/t poor diastolic compliance of L vent.
Give B-blockers, and Ca-chnl blockers.

Front 30

What is responsible fore the decrease in SV in pt's with heart failure?

Back 30

1. Weakness of muscle (d/t MI or genetics)
2. Ineffective contraction of myocytes, d/t fibrotic tissue
3. Dilation of ventricle will increase radius and decrease the pressure in the ventricle.

Front 31

What happens to the diastolic functioning of pt's with heart failure?

Back 31

diastolic impairment (curve shifts upward) b/c fibrotic and hypertrophied tissue is non-compliant, results in a lower Ved.

Front 32

Why do heart failure pt's have reduced exercise tolerance?

Back 32

B/c they are using their cardiac reserve at rest. If they increase their HR this will actually lower their CO b/c of their diastolic/filling failures.

Front 33

What causes vascular remodeling and what is the consequence to the local tissues?

Back 33

Persistent and chronic sympathetic stimulation and AgII activation leads to vconst which a decrease in perfusion to the tissues.

Front 34

Class I : Na chnl blockers & Na/K blockers
Used for what?
Mechanism?
Potential danger?

Back 34

Arrythmias, especially those caused by ischemia (tachy/triggered)
Use-dependance - will bind to the channels in cells that are firing more frequently and inactivate the Na channels = reduced excitability = antiarrhythmic.
** can prolong AP duration and this increases the risk of a re-entry or circus arrythmia.

Front 35

What type of arrythmia are B-blockers used for? How does this arrhythmia develop?

Back 35

For triggered arrhythmias that occur as a result of excessive [Ca]. When the level of [Ca] gets too high you can have spontaneous release, into the cell and the Ca pumped out in xchange for a 3Na (=net +1) leading to cell depol and AP firing and propagation.
Also cause a suppression of symp response.

Front 36

Class III: K+ channel blockers
Used for what?
mechanism?
Danger?

Back 36

Used for A-fib, and other tachycardias.
Prolong cellular repolarization by inactivating the K+ channels, thus slowing the eflux of K+ from the cell. They can prevent circus/re-entry arrhythmias b/c by the time the depol signal arrives back at the originating cell, that cell will still be depolarizing (inexcitable).
Dangerous in that they can promote triggered arrhythmias - the longer the time between AP's the greater the chance that enough spontaneous events will happen to trigger an AP.

Front 37

Class IV: Ca++ channel blockers
Use? why?

Back 37

Primarily for HTN and angina b/c vdilate the resistance arterioles and the heart vessels. Only used for nodal arrythmias b/c they preferentially bind to Ca channels there.

Front 38

What is the difference between flutter and atrial fibrilation?

Back 38

Fibrillation occure where there are migrating, random areas of depolarization in the heart. It is so random and uncoordinated that no pressure is generated and people die.
Flutter - regularly irregular arrhythmia, is a triggered arrhythmia. Ventricular flutter is survivable.

Front 39

What is digitalis used for? What does it do?

Back 39

DIgoxin blocks Na/Ca channels thus causing a build-up of Ca in SER. This promotes relaxation and increases the strength of the contraction. It also slows the HR by increasing vagal tone (reduces the rate of electrical signals through the AV node thus making it useful in supravent tachy!)

Front 40

When would you use adrenergic agonists? Why?

Back 40

These are used when the heart is very weak, ie in emergencies (used to keep person alive) and post cardiac transplant Sx. Will increase strength of contraction

Front 41

Most diuretics work by blocking what 2 things?
What are the physiological effects of this

Back 41

Diuretics block Na+ retention and inhibit aldosterone. This reduces fluid volume = lower mean filling pressure = reduced venous pressure = reduced tissue edema.

Front 42

How do vasodilators increase CO?
What are some examples of these drugs?
CCB effects on ESPVR curve? why?

Back 42

They decrease TPR and this reduces afterload and BP = increase cardiac output.
ACE inhibitors will block the vcon effects of Ang II
CCB: preferentially block Ca entry into vascular smooth muscles = prevent constriction. Also bind to nodal cells and slow their rate of firing. ** will shift the ESPVR curve R b/c some effect on heart myocytes**