Lecture 9 – the control of cardiac output Flashcards Preview

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Flashcards in Lecture 9 – the control of cardiac output Deck (43):
1

What is the average cardiac output(CO)? (at rest)

5L/min Cardiac output= heart rate x stroke volume

The average resting heart is 72 bpm 

Average stroke volume is 70 ml per beat

Average cardiac output, at rest, is 72 x 70 = 5L/min

2

CO = ?x?

CO= heart rate x stroke volume

3

What is preload?

- The ‘filling pressure’ of the heart

- Right atrium (central venous) pressure

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4

What is afterload?

- The pressure against which the heart has to pump

- Aortic pressure

5

What is venous return ?

Venous return is the rate of blood flow back to the heart. It normally limits cardiac output

6

LVEDP?

Left ventricular end-diastolic pressure

7

What is a positive inotrope?

something that increases the force of contraction

8

What is a negative inotrope?

something that decreases the force of contraction

9

what is the main determinant of the stroke volume?

Preload

10

What can shift the starling curve upwards?

sympathetic stimulation or positive inotropes

11

positively chronotropic agent function?

increases heart rate

12

negatively chronotropic agent function

decreases heart rate

13

what does a positively lusitropic agent do?

increases the rate of relaxation

14

what does a negatively lusitropic agent do?

decreases the rate of relaxation

15

What happens to skeletal muscle vessels during dynamic exercise?

They get vasodilated

16

What is dynamic exercise?

Running, swimming etc.

17

What is static (isometric) exercise?

weight lifting etc.

18

What is peripheral resistance(TPR)?

The total resistance to flow of blood in the systemic circuit; the quotient produced by dividing the mean arterial pressure by the cardiac minute-volume.

19

What happens to peripheral resistance(TPR) during dynamic exercise?

It decreases massively

20

Why does total peripheral resistance decrease during dynamic exercise?

Metabolic waste products and other signals from exercising muscles causes the arterioles feeding the capillary beds in the working muscles to relax (dilate or open up) in an attempt to increase blood flow to the working muscle. This dilation is generally larger than constriction taking place in capillary beds to other tissues not involved in exercise. The net result is a dilation or opening up of arterioles and reduction in total peripheral resistance.

21

What happens to peripheral resistance(TPR) during static exercise?

It increases significantly

22

What is cardiac output?

Cardiac output is the volume of blood pumped by the heart per minute (mL blood/min). Cardiac output is a function of heart rate and stroke volume. The heart rate is simply the number of heart beats per minute. The stroke volume is the volume of blood, in milliliters (mL), pumped out of the heart with each beat.

23

What is the myocardium?

The myocardium is the muscular wall of the heart, or the heart muscle. It contracts to pump blood out of the heart and then relaxes as the heart refills with returning blood.

24

The heart is a 'premissive' pump, what does that mean ??

Within physiological limits, it only pumps out what comes back into it! 

 

Cardiac Output = Venous Return 

25

The Frank – Starling Relationship ??

The more blood in the ventricle at the end of diastole the bigger the stroke volume 

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26

Explain

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the first thing to remeber is that the left and right circuits of the heart are in series with each other

So if there is a transient increase in RV output there will flow more blood to the capillaries in the lungs 

this means that there will be an increase in the pulmonary veins and thus an increase in the LV

there is an increase in stroke volume and LV output

LV output matches the RV output

 

27

What is the explanation of the Frank-Starling mechanism??

(i) The length-tension relationship 

(ii) Changes in muscle filament Ca sensitivity 

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28

length-tension relationship?

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29

What happens to skeletal ,muscle vessels when you do static exercise?

they get compressed

30

Examples of sympathetic stimulation??

Adrenalin

Noradrenalin

'inotropic' drugs

31

what does syphatetic stimulation do to the starling curve??

what does it represent??

it makes an upward shift in the curve

 

The upward shift in the ‘Starling curve’ represents an increase in the intrinsic force of contraction of the heart - this is called ‘contractilty’ 

 

This is also called the inotropic state of the heart/muscle

A positive inotrope is something that increases the force of contraction*

A negative inotrope is something that decreases force of contraction*

*at the same preload or fibre length 

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32

contractility?

How strongly the heart contracts at a given fiber length

33

Afterload has little affect on the Frank - Starling relationship 

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34

The SA node (pacemaker) action potential ??

as in the neuronal action potentail voltage gated ion channels play a big role but in the cardiac muscle it is Ca and not Na iosn that 

 

as the voltage gets more and more positive more and more Ca channels open

and they are the ones that give the upstroke in the graph

the If channel is turned on when the voltage gets more negative and since it is an Na channel - Na flows in to the cells

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35

what is the primary cardiac pacemaker ??

the sino-atrial (SA) node

 

- it drives the heart rate

36

Why is the pacemaker current also known as the funny current

becuase the Ichannels open when the area gets more negative, and this is unusual 

 

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37

what does symphatetic stimulation(autonomic agonists) do to the pacemaker action potential??

Increases ‘funny current’

faster rate of diastolic

depolarisation

faster heart rate 

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38

what effect does parasympathetic stimulation(autonomic agonists) have on the pacemaker action potential??

decreases ‘funny current’ 

opens KACh channels 

slower rate of diastolic depolarisation 

slower heart rate 

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39

Lusitropy??

Rate of relaxation

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40

What happens to TPR during exercise?

Dynamic exercise - it goes down

Static exercise - it goes up

41

Cardiac output and dynamic exercise ??

Heart rate increases 3-fold 

Cardiac output increases 5-6 fold 

Stroke volume increases 2 fold 

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42

Cardiac output in trained (elite) athletes ??

Heart rate increases 3-fold 

Cardiac output increases 6-7 fold 

Stroke volume increases 2-3 fold 

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43

explain control of cardiac output

When venous return increases End diastolic volume increases. This increases stroke volume which then increases the CO

we can stimulate this with symphetic activity 

 

parasympathetic activity can decrease heart rate and this decreases CO

 

Exercise can have an affect on this

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