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ICOM-Cardio > Cardio-physio-cardiac output-slivkoff > Flashcards

Cardio-physio-cardiac output-slivkoff Flashcards

1
Q

What 3 determinants of stroke volume?

A

afterload, preload, and contractility

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2
Q

Stroke volume X HR =

A

cardiac output

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3
Q

Afterload has a positive/negative affect on stroke volume?

A

negative

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4
Q

Preload and contractility have what kind of effect on stroke volume?

A

positive, as either increase, stroke volume increases

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5
Q

What is preload?

A

filling pressure

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6
Q

What is afterload?

A

arterial pressure opposing ejection

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7
Q

As more venous return enters the heart, the cardiac output increases. This process describes increased preload or afterload?

A

Preload

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8
Q

The more blood you give the heart, the more/less it is going to pump out

A

more

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9
Q

There is an ideal length that maximizes the overlap between actin and myosin and maximizes generated.

A

tension

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10
Q

What are some ways to change the number of crossbridges being made in the sarcomere?

A
  1. alter preload (either more or less)
  2. more Ca2+
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11
Q

According to the Frank-Starling Mechanism diagram, as stroke volume increases, ventricular end diastolic volume .

A

inceases, but it can platuea and decrease if there is too much of either

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12
Q

What 4 main factors can change preload?

A
  1. increase in blood volume (increase preload)
  2. venoconstriction (increase preload)
  3. skeletal muscle pump (increase preload)
  4. nitroprusside (venodilation) -decrease preload
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13
Q

How does inspiration and expiration change preload?

A

inspiration increases preload

expiration decreases preload

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14
Q

What are the main funcitons of ACE inhibitors and angiotensin II receptor blockers?

A

the decrease overall blood volume which in turn decreases BP

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15
Q

What kind of effect does tricuspid and mitral valve stenosis have on stroke volume?

A

decreases stroke volume by decreasing preload and ventricular outflow

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16
Q

What kind of effect does aortic stenosis have on preload or stroke volume?

A

Aortic stenosis would increase diastolic ventricular pressure and lead to decreased ventricular filling, leading to decreased preload and stroke volume

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17
Q

What kind of effect does atrial tachycardia have on stroke volume?

A

It would lead to a fib and decreased ventricular filling time, which would not leave enough time to fill up ventricle

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18
Q

Changing from an upright to supine position does what to preload?

A

It increases preload as there is less blood pooling in lower parts of body

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19
Q

What term describes the arterial pressure right after the aortic valve (pressure through all the major arteries)?

A

afterload

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20
Q

High BP is an increase/decrease in afterload (arterial pressure opposing ejection)?

A

increase

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21
Q

Increasing total peripheral resistance (TPR) would have what effect on afterload?

A

Increase afterload and BP

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22
Q

How does decrease of systemic vascular resistance affect afterload and stroke volume?

A

It woud decrease afterload and therefore increase SV

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23
Q

What effect does hydralazine, ACE inhibitiors, angiotensin II receptor blockers, have on SV and afterload?

A

They are all vasodilators, would decrease BP, which would decrease afterload and increase SV

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24
Q

Exercise causes an increase/decrease in vascular resistance?

A

decrease in vascular resistence, which would increase stroke volume and decrease afterload

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25
Q

Decreased pulmonary resistance caused by phosphodiesterase inhibitors (vasodilator) would have what effect on the right ventricle?

A

Decrease afterload and increase SV to right ventricle

26
Q

What does increased systemic and or peripheral vascular resistance (chronic HTN and vasopressors) and aortic valve stenosis do to afterload and SV?

A

Increase afterload and decrease SV

27
Q

What is another way to describe wall stress?

A

afterload

28
Q

Wall stress increases/decreases with increased ventricular pressure (HTN) and increase ventricular radius (dilated cardiomyopathy)?

A

increases

29
Q

Wall stress increases/decreases with increased ventricular thickness (hypertrophy)?

A

decreases (more myocytes taking on stress, reduces the stress felt by each myocyte)

30
Q

dP/dt (pressure/time) could be a measure of what?

A

contractility (steeper line means more contractility)

31
Q

How to calculation ejection fraction?

A

Stroke volume/ end diastolive volume

32
Q

What do catecholamines and positive inotropes (digoxin) do to heart contractility?

A

increases contractility

33
Q

What does loss of myocardium, B-blockers, non-dihydropyridin Ca2+ channel blockers, and dilated cardiomyopathy do to contractility?

A

Decreases contractility

34
Q

What effect does decreased extracellular Na+ (due to decreased Na+/Ca2+ exchanger activity) have on contractility?

A

Increases contractility as there is more Ca2+ left in the heart

35
Q

What effect does digitalis have on contractility?

A

It inhibits the Na+/K+ pump, which decreases the intracellular Na+, which decreases activity of the Na+/Ca2+ exchanger, leading to increase Ca2+ in the heart and increased contractility

36
Q

What is the effect of thyroid hormones on contractility?

A

Increases contractility (by making more B1 adrenergic receptors)

37
Q

What effec do B1-receptor blockers have on contractility?

A

decreases contractility

38
Q

What effect does hypoxia have on contractility?

A

Decreases it

39
Q

What do narcotic overdose, hypercapnia (increased CO2), hyperkalemia, and acidosis have in common as concerning contractility?

A

they decrease contractility

40
Q

What effect does increase venous tone have on preload?

A

contraciton of venous vessels enhances venous return and preload

41
Q

As blood moves through the heart, increased arterial constriction would lead to increased/decreased peripheral resistance, which would increase/decrease stoke volume?

A

increased peripheral resistance; decreased stroke volume

42
Q

Arterial vasodilation/ vasoconstriction leads to increased SV and CO?

A

vasodilation (less pressure for the heart to fight against)

43
Q

Venous vasodilation/venoconstriction leads to decreased SV and CO?

A

vasodilation (as there is less oompf of the blood entering the heart)

44
Q

More blood volume (venous return) and increased venous tone (activated by SNS) does what to preload?

A

Increases preload

45
Q

What does an increase ventricular radius and ventriclar pressure do to afterload according to LaPlace’s law (wall stress = increased afterload)?

A

increases afterload, decreasing SV and CO

46
Q

According to LaPlace’s law, how does increased ventricular thickness affect wall stress, and therefore afterload?

A

Ventricular thickness decreases wall stress (shared load by more myocytes) and decreases afterload

47
Q

What is the product of CO and systemic vascular resistance?

A

Blood pressure

48
Q

What do SNS a1 receptors, angiotensin II, endothelin, and O2 have in common?

A

They decrease arteriolar diameter, vasoconstriction

49
Q

What do B2 receptors, NO, adenosisn, decreased pH, and prostaglandins have in common?

A

They increase arteriolar diameter, leading to vasodilation

50
Q

What is the pressure that is measured when the heart has stopped?

A

Mean circulatory filling pressure or mean systemic pressure

51
Q

Cardiac output will always match .

A

venous return

52
Q

Given the same contractility, if you increase volume into the system (IV), what happens to the mean circulatory filling pressure (when heart is stopped)?

A

The mean circulatory filling pressure will increase, which will result in an increase in CO or venous return?

53
Q

which way does the vascular funtion curve shift with increased blood volume?

A

It shifts the curve up

54
Q

which way does the vascular funtion curve shift with decreased blood volume?

A

It shifts the curve down

55
Q

If we increase contractility, what type of effect will occur with the cardiac function curve?

A

The curves shifts upward

56
Q

If we decrease contractility, what type of effect will occur with the cardiac function curve?

A

The curve shifts down.

57
Q

What happens to the curves during increased total peripheral resistance (TPR or vasoconstriction)?

A

The cardiac funtion curve and vascular function curve shift down but the pivot point stays the same.

58
Q

What happens to the curves during decreased total peripheral resistance (TPR or vasodilation)?

A

They both increase but the pivot point stays the same.

59
Q

Review diagram

A
60
Q

What happens to the pressure volume loop with excercise?

A

SV increases, EDV increases, contractility increases, decrease in afterload. ( We have not added more blood but squeezed out the blood in the veins with the skeletal muscle pumps).

61
Q

Review diagram

A

ICOM-Cardio (32 decks)

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