(11)

Question 1

she said she’s not going to test us on this stuff - but would probably be a good idea to take a quick look at it

Question 2

1-4. Cardiac output is controlled by what four things?

Answer 2

1. heart rate
2. myocardial contractility
3. preload
4. afterload

(cardiac function and vascular function are intertwined)

Question 3

(regulation of the heart - SNS)

1. what areas of the heart have sympathetic innervation?
2. predominant receptor type?

Answer 3

1. sinus node, atrial tissue, AV node (widespread in both atria and ventricles)
2. Beta1 (for sympathetic nervous system)

Question 4

(sympathetic effects)

1. increase or decrease contractilty? how?
2. affect on releaxation? how?
3. affect on heart rate?

Answer 4

1. increase; increase Ca entry, increase Ca release from SR - does by increasing catecholamines (NE or epinephrine)

(she then talked a little about what happens when catecholamine does its thing - look a diagram)

2. enhances releaxation; decreases Ca affinity of Tn complex; increases Ca uptake by SR
3. increases

Question 5

(Sympathetic Effects)

(sinus node rate)

1. hyperpolarization –> activation of If –> Na (and K) move in
2. leads to what? also speeds what?
3. affect on AV node?

Answer 5

2. faster phase 4 depolarization; subsidiary pacemakers
3. faster conduction through AV node (also shorter refractory period - so it can conduct more impulses)

Question 6

(Regulation of the Heart - PNS)

1. what areas of the heart have parasympathetic innervation?

Answer 6

1. sinus node, AV node, atrial tissue

Question 7

(Parasympathetic Effects)

1. affect on sinus node rate? how?
2. affect on Av nodal conduction? refractory period?
3. contractility? how?

Answer 7

1. decreases; Ach-activated K channels (so more positive leaving, so will take longer to depolarize to point of threshold)

(will reduce phase 4)

2. slowed AV nodal conduction; longer
3. decreases (but with little clinical effect); inhibit NE release from SNS nerves

Question 8

(Physiologic Control of HEart Rate)

1. mediated by what?
2. releated to changes in slope of what in what?
3. What normally predominates? flucuations of vagal tone –> ?
4. breathing will speed up as you breath in a little bit
5. Resting HR related to what three things?

Answer 8

1. ANS
2. phase 4 depolarization in sinus node cells
3. vagal influence (parasympathetic); sinus arrhythmia
5. species size, metabolic rate, and autonomic balance

Question 9

(Sinus Arrhythmia)

1. also called normal or respiratory sinus arrhythmia
2. related to flucuations in what?
3. is it a good thing?
4. “heart rate variability”

(people with disease have less variabliity)

(its good cause it indicates that you don’t have constant sympathetic drive all of the time)

Answer 9

2. vagal tone (often associated with respiration)
3. yepp

Question 10

(Clinical assessment of contractility)

1. not very practical
2. need to measure what?
3. can also obtain by volume infusion
4. lots of overlap

Answer 10

2. LV end-diastolic P

Question 11

(Clincial assessment of contractiliy)

1. during what phase in ventrcular pressure rising really fast?

i don’t really understand this…

watch at 35:00 4/19 8AM

i think it bascialy shows that the steeper the line is the more contractiilty there is

don’t typically measure this - cause you need to put cathether in left ventricle

kind of impractical

Answer 11

1. contraction (both valves are closed)

Question 12

(Clinical Assessment of Contractility)

EDV = end diastolic volume

ESV = end systolic volume

EF is often reported

is this a pure indication of contractility? no - while this is decent because it is influenced by loading condictions (esp afterload)

Question 13

(Clinical Assessment of Contractility)

(Ejection phase indices - afterload dependent)

(Fractional Shortening)

1. the % change from what to what?
2. obtained by what?
3. is another index of the extent of what?

Answer 13

1. diastolic to systolic LV diameter
2. echocardiography
3. LV fiber shortening

Question 14

take a look at this… goes with slide before i think

she keeps talking about the fact that ejection phase indices are effected by afterload - which is a negative - so know that

Question 15

(Pressure - Volume Loops)

1. Relating LV pressure to volume is one what of assessing what two thigs?

she then talked about graph for awhile

at point D mitral valve is opened

at point a we are filled and pressure starts coming up

at point b aortic valve opens

at point c aortic valve closes because relaxation has started

Answer 15

1. Starling effect and contractility of LV

Question 16

(Pressure - volume loops)

1. this is the effect of what?
2. increased contractilty gives you larger or smaller end systolic volume?

(positive inotropic effect)

Answer 16

1. increased contractilty
2. lower (able to get more blood out)

Question 17

(Pressure - Volume loops)

1. this is the effect of what?
2. do we get to smaller than original volume?

Answer 17

1. increased preload
2. no

Question 18

(Pressure - Volume Loops)

1. this is the effect of what?

makes it less easy to eject blood

2. what happens to end systolic volume?

Answer 18

1. increased afterload
2. it gets bigger

(has a bit of a negative effect on hearts ability to eject blood)

Question 19

heart would be big

degree of shortening - kind of a weeny difference

notice that filling pressure is even higher - reduced compliance of ventricular wall

maximum pressure isn’t all that great

Answer 19

this is how radiograph would look

size between diastolic and systolic wouldn’t be too different