Lecture 4 unit 1 Flashcards

1
Q

how does ventricular systole start?

A

when depolarized cardiac muscle fibers in the ventricles begin to contract, causing an increase in pressure within the ventricles and a rapid closing of the AV valves

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2
Q

what is the result of ventricular systole?

A

ejection of blood into circulation

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3
Q

what happens in ventricular diastole?

A

starts when depolarized ventricular muscle reduces contraction to the point that blood is no longer ejected into circulation, causing a rapid closing of the semilunar valves

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4
Q

what is the result of ventricular diastole?

A

passive filling of the ventricles

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5
Q

what is atrial systole?

A
very brief 
(ventricular filling is largely passive)
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6
Q

what happens in atrial diastole?

A

begins when ventricular systole begins

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7
Q

what is CO (cardiac output)?

A

the volume of blood pumped by the ventricles in a given unit of time

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8
Q

was is the formula for Cardiac Output?

A

CO (L/min) = stroke volume (L/beat) x heart rate (beats/min)

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9
Q

what is the stroke volume (SV) at rest?

A

0.07 L/beat

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10
Q

what is the heart rate (HR) at rest?

A

75 beats/min

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11
Q

what is cardiac output at rest?

A

5.25 L/min

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12
Q

what are the determinants of stroke volume (SV)?

A
  1. aortic (or pulmonary artery) blood pressure. AKA the “after load”
  2. end diastolic volume or “preload”
  3. active or passive contractility
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13
Q

the ventricles can’t eject blood into thee aorta or pulmonary artery until what?

A

the pressure in the ventricle exceeds the pressure in the artery

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14
Q

What does an increase in pressure have a major impact on?

A

the work of the heart and on the stroke volume

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15
Q

What kind of pumps are the cardiac chambers?

A

mechanical pumps

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16
Q

what do the cardiac chambers pump?

A

only what is delivered to them

17
Q

what is “preload” slang for?

A

“end-diastolic volume”

18
Q

what does the “preload” or “end-diastolic volume” have a major impact on?

A

stroke volume

19
Q

stroke volume cannot increase unless what?

A

the rate of cardiac filling also increases

20
Q

what is contractility?

A

the strength of cardiac muscle contraction

21
Q

is contractility active or passive?

A

both

22
Q

what is active contractility

A

stimulation of the sympathetic nerves to the heart

23
Q

what is passive contractility

A

the result of changing the length of the cardiac muscle fibers (“Frank-Starling mechanism”)

24
Q

what is the result of the action of norepinephrine or epinephrine?

A
  • increased rate of pacemaker activity

- increased force fo cardiac muscle contraction

25
Q

what happens in active contractility

A

-the AP invades the t-tubules, and calcium is released from the sarcoplasmic reticulum

26
Q

what else does norepinephrine increase?

A

the calcium permeability of the plasma membrane (the sarcolemma) in cardiac muscle, letting in more Ca2+

27
Q

what is the result of active contractility?

A

the number of actin/myosin cross bridge interactions is increased

28
Q

sympathetic nerve endings release norepinephrine which initiates what?

A

a cyclic AMP second messenger system inside cardiac muscle cells in order to increase contractility

29
Q

what does the “Frank-Starling” mechanism refer to?

A

the relationship between the rise in stroke volume and the rise in preload

30
Q

what happens if the preload is increased

A

EVEN IN A HEART WITH NO NERVE SUPPLY, the stroke volume will increase systematically

31
Q

what is the typical cardiac sarcomere length?

A

1.9 micrometers