Cardoivascular Physiology - Lecture 5

Question 1

Cardiac Output

Answer 1

The amount of blood moved per unit of time

CO = hear rate (HR) x stroke volume (SV)

Question 2

Cardiac AV Valves structure

Answer 2

Fibrous skeletal rings that isolate the atrium and ventricles electrically

Question 3

What is the “first heart sound”

Answer 3

AV valves closing

Question 4

What is the “second heart sound”

Answer 4

Closure of the aortic and pulmonary vlaves

Question 5

What are the different types of heart murmurs?

Answer 5

Stenosis = narrowing
Regurgitation = insufficiency - can lead to backflow
Other septal defects

Question 6

Series

Answer 6

Components are connected end-to-end to form only one path for electrons/blood to flow through the circuit
The second component gets whatever electrons/blood is leftover

Question 7

Parallel

Answer 7

Components are connected between the same two sets of electrically common points, creating multiple paths for electrons/blood to flow
Same amount of electrons go to each point

Question 8

The systemic and pulmonary circulations are in what?

Answer 8

Series

So all of the blood going back to the heart will be oxygenated

Question 9

Organs in the systemic circulation are in what?

Answer 9

Parallel

So every organ gets oxygenated blood

Question 10

Flow

Answer 10

Volume per unit time

F = /\P/R

Question 11

Systole

Answer 11

When ventricles are contracting

Question 12

Diastole

Answer 12

When ventricles are relaxed

Question 13

Study up on the Wigger’s diagram

Answer 13

Good job!

Question 14

What would the Wigger’s diagram for the R side look like compared to the L?

Answer 14

Pressure for the R side won’t be as high

This is because the R side doesn’t have to pump the blood as far

Question 15

What would the Cardiac Output be for a ventricle with a rate of 72 bpm, and ejects 70 mL of blood with each beat?

Answer 15

CO = HR x CV
CO = 72 bpm x 0.07 L/beat
CO = 5.0 L/min

Question 16

How do parasympathetics effect HR?

Answer 16

Slow them down

Question 17

How do sympathetics effect HR?

Answer 17

Speed them up

Question 18

How does sympathetic stimulation increase HR?

Answer 18

It increases the Na influx at funny channels, allowing the cells to reach threshold and depolarize faster

Question 19

How does parasympathetic stimulation decrease HR?

Answer 19

Acts on funny channels to decrease Na influx, causing threshold and depolarization to take longer to achieve

Question 20

How do you increase HR?

Answer 20

Increase activity of sympathetics to the heart
Increase plasma epinephrine
Decrease activity of parasympathetics to the heart

Question 21

What are the three factors that influence stroke volume?

Answer 21

Preload
The magnitude of sympathetic input to the ventricles
Afterload

Question 22

Preload

Answer 22

The volume of blood in the ventricles just before contraction (end-diastolic volume)

Question 23

Afterload

Answer 23

The pressure against which the ventricle pumps (Pressure in the aorta)
Increased afterload causes decreased stroke volume because the ventricle has to work harder to get the pressure up

Question 24

What does the Frank-Starling mechanism say?

Answer 24

To increase the heart’s stroke volume, fill it more fully with blood - the stretch of the ventricle will align its actin and myosin in a more optimal pattern of overlap

Question 25

How can you further increase stroke volume

Answer 25

Fill it more fully with blood (Frank-Starling mech.) -AND- Deliver sympathetic signals (this will cause the ventricular cells to also relax more rapidly, allowing more time to refil)

Question 26

What is the mechanism of sympathetic effects of cardiomyocyte contractility

Answer 26

1) Phosphorylate Ca channel - allowing more trigger Ca to enter the cell 2) Ca binds to Ryanodine receptor - PKA phosphorylates ryanodine to keep the channel open longer, releasing even more Ca into the cytoplasm 3 + 4) PKA phosphorylates myofilaments to increase kinetics - myofilaments produce more force due to increased Ca 5) More Ca is sucked up and stored in the SR

Question 27

Effects of autonomics on the SA node

Answer 27

``` Symp = increased HR P-symp = decreased HR ```

Question 28

Effects of autonomics on the ventricular muscle

Answer 28

``` Symp = increased contractility P-symp = no sig effect ```

Question 29

To increase stroke volume, what could you increase?

Answer 29

End-diastolic volume Norepinephrine delivery from symp neurons Epinephrine delivery from the adrenal medulla

Question 30

To increase HR, what could you increase?

Answer 30

Norepinephrine delivery from symp neurons Epinephrine delivery from adrenal medulla Reduce parasympathetic input

Question 31

Can you increase HR without increasing stroke volume, and vice versa?

Answer 31

No - to increase one is to increase the other

Question 32

Ejection fraction

Answer 32

Measurement of contractility Defined as the ratio of the stroke volume minus end systolic volume to the end diastolic volume EF = SV / EDV SV = EDV - ESV

Question 33

Hypertrophic cardiomyopathy

Answer 33

Increase in the heart wall thickness (particularly in the interventricular septum) which interferes with blood ejection Happens with hypertensive patients - because the ventricle has to work harder, it gets bigger, which compensates preload volume Can lead to angina, arrythmias, or sudden cardiac death