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AP2 > Lecture 1-28 (Loops) > Flashcards

Lecture 1-28 (Loops) Flashcards

Cardiac (Loops)

1
Q

What are mixed vasodilators? How do they work? Examples

A

They dilate the arteries, decreasing RVR, and veins, decreasing systemic filling pressure.

Sodium Nitroprusside
Nipride

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2
Q

Sodium Nitroprusside & Nipride are both ________ and they will fall apart in ______

A

Nitric oxide donors

sunlight

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3
Q

In mixed vasodilators, the more prominent effect is seen in the ________

A

systemic filling pressure

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4
Q

Nitroglycerin is a __________ and has more effects on the _______ than the __________

A

Venous dilator

veins

arteries

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5
Q

What effects does nitroglycerin have on the heart? What pathology is this useful in?

A

Reduces preload
-reduces metabolic demand

MI

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6
Q

T/F: We can give nitroglycerin for a big MI

A

F

big MI probably wiped out preload. Nitroglycerin will reduce reload even further.

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7
Q

ACE inhibitors work more specifically on the _______ which ______ afterload

A

arteries

decrease

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8
Q

Which vasodilator works ONLY on the arteries? What is its MOA?

A

hydralazine

unknown

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9
Q

What type of vasoconstrictor is phenylephrine? What does it mainly work on? How does this effect the heart?

A

Mixed vasoconstrictor

Bigger effect on the veins = increased preload

increases afterload

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10
Q

After an MI, the ______ kicks in by doing what?

A

Nervous system

Increasing sympathetic activity & venous tone (systemic filling pressure)

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11
Q

Describe cardiac output and R atrial pressure in an MI

A
  1. CO drops without any compensatory mechanisms.
  2. Max increase sympathetic activity (heart) & increased venous tone/catecholamines (Psf) to increase CO back to 5
  3. Fluid retention increases (Psf) –> catecholamines decreases –> decrease in sympathetic activity (heart) –> R Atrial pressure increases –> CO stays at 5
  4. Fluid retention increases even more (Psf) –> catecholamines decrease –> sympathetic activity returns to normal (heart) –> R atrial pressure increases even more –> CO stays at 5
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12
Q

After an MI, why do we need sympathetic stimulation to return back to normal or catehcolamines to decrease?

A

Predisposes to arrhythmias

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13
Q

What will R atrial pressure be after an MI, when compensatory effects have returned sympathetic activity to normal?

A

8 mmHg

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14
Q

What happens when we stand up?

A

CNS tightens blood vessels to prevent passing out

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15
Q

During heart failure, SVR _______, Psf _______, volume expansion ________, venous compliance _____

A

increases
Increases
increases
decreases

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16
Q

Increasing SVR has what effect on RVR?

A

Decreases the slope, making it more difficult for blood to return to the heart

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17
Q

Whats the difference between preload & afterload?

A

Preload: pressure to fill heart

afterload: pressure heart has to pump against outside of aortic valve

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18
Q

What happens when afterload is increased?

A

Its harder to pump blood out the heart

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19
Q

Where is preload?

A

Pressure at the end of phase 1
-Pressure where EDV is

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20
Q

Where is afterload?

A

Pressure at the end of phase 2
-Pressure where diastolic pressure is & where aortic valve opens (right before it opens)

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21
Q

How does increasing preload affect the cardiac cycle/curve?

A

Increase preload –> Increase EDV (filling volume) –> Increase SV –> Increase SBP

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22
Q

How does decreasing preload affect the cardiac cycle/curve?

A

decrease preload –> decrease EDV (filling volume) –> decrease SV –> decrease SBP

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23
Q

How does increasing afterload affect the cardiac cycle/curve?

A

Increase afterload –> increase time in phase 2 to get to higher diastolic pressure/afterload –> decrease time in phase 3 (ejection) –> aortic valve closes early at higher pressure –> increased SBP –> decrease SV –> increase ESV –> increase HR

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24
Q

When it’s harder for the heart to pump, we worry about ________

A

remodeling/hypertropy

25
Q

With increased afterload and sick patients, we may want to consider ______ the BP if tolerable

26
Q

How does decreasing afterload affect the cardiac cycle/curve?

A

Decrease afterload –> decrease time in phase 2 to get to lower diastolic pressure/afterload –> increase time in phase 3 (ejection) –> aortic valve closes later at lower pressure –> decrease SBP –> increase SV –> decrease ESV –> decrease HR

27
Q

Increasing afterload ________ the metabolic demands of the heart, and decreasing afterload ________ the metabolic demands of the heart

A

Increases

Decreases

28
Q

How does increasing contractility affect the cardiac cycle/curve?

A

Increase contractility –> increase time in phase 3 –> increase SBP –> Increase SV –> aortic valve closes later at higher pressure –> decrease ESV

29
Q

How does decreasing contractility affect the cardiac cycle/curve?

A

Decrease contractility –> decrease time in phase 3 –> decrease SBP –> decrease SV –> aortic valve closes earlier at lower pressure –> increase ESV

30
Q

What type of medication can we use to treat decreased contractility in a heart failure pt after remodeling? Why?

A

Afterload reducer such as ACE inhibitor or hydralazine

Increase phase 3 –> increase SV –> decrease ESV

decreases the metabolic demands of the heart allowing for a decreased HR

31
Q

What does the area underneath the cardiac cycle curve represent?

A

passive tension to fill the heart

32
Q

What happens to passive tension in HR?

A

increase dt blood volume retention

This volume for passive filling is needed in these pts for a normal CO

33
Q

How does Aortic valve stenosis affect the cardiac cycle/curve?

A

Increase afterload/diastolic pressure –> increase time in phase 2 to get to higher pressure to open aortic valve –> decrease time in phase 3 (ejection) –> aortic valve closes early at much higher pressure –> increase SBP –> decrease SV –> increase ESV –> increase HR –> increase preload –> increase EDV

34
Q

What is a hallmark symptom in aortic valve stenosis?

A

Narrowed PP

34
Q

In aortic stenosis, the pressure in the L vent has to greatly _________ to open the aortic valve

35
Q

With aortic stensis, the pressure in the aorta is ________ the ventricle

A

much lower than in

36
Q

With aortic stensis, R atria pressure is expected to ______-

37
Q

Mitral valve stenosis is a ______ problem with the ________ ventricle

A

Filling

Left

38
Q

How does Mitral valve stenosis affect the cardiac cycle/curve?

A

Mitral valve stenosis –> Decrease EDV –> decrease SV –> decrease CO –> increase HR

39
Q

How does the heart compensate for mitral valve stenosis? Where are these changes seen at?

A

Increase preload
increase Psf
Increase atrial pressure
increase blood volume

These increases in pressure & volume are seen in front of the L atria (pulmonary circuit/lungs)

40
Q

Does L atria pressure increase during Mitral valve stenosis?

41
Q

What does severe Mitral valve stenosis require? Why?

A

Mitral valve replair/replacement to prevent pulm HTN

A continued/prolonged high increase in pressure/volume in the pulmonary circuit –> pulmonary HTN –> pulomary edema –> impaired gas exchange

Compensatory effects of mitral valve stenosis to increase CO causes this

42
Q

What pathology can severe mitral valve stenosis lead to?

A

pulmonary HTN –> pulmonary edema

43
Q

What is the pathology of aortic valve insufficiency?

A

Regurgitation

Retrograde blood movement when the aorta valve is closed & pressure in aorta is higher than L vent.

44
Q

In aortic valve insufficiency, during what phases is there the most amount of backflow? Why?

A

End of phase 4
phase 1 (esp. early part)

This is where the aorta pressure is highest & L vent pressure is lowest

45
Q

When L vent volume is increasing while the aorta is closed, what does this mean?

A

Aortic insufficiency/regurgitation

46
Q

In aortic valve insufficiency/regurgitation what is the relevance of phase 1 in the cardiac cycle/curve?

A

The L ventricle is fillinf from 2 places at once:

-L atria during diastole
-Aorta from retrograde backflow

47
Q

How does Aortic valve insufficiency/regurgitation affect the cardiac cycle/curve?

A

Aortic valve insufficiency/regurgitation –> Increase EDV –> Decrease DBP –> Increase SV –> Increase SBP

48
Q

What results from Aortic valve insufficiency/regurgitation?

A

L vent dilation dt increased EDV –> increased problems w/ aortic valve & problem w/ mitral valve dt increase L vent volume

49
Q

In Aortic valve insufficiency/regurgitation, the PP ______

50
Q

In Aortic valve insufficiency/regurgitation, during what phases are there retrograde backflow from aorta only? Both aorta and atria?

A

Phase 4

Phase 1

51
Q

T/F: Aortic & mitral valve regurgitation have isovolumetric phases

A

F

The volumes are changing in phases 2 & 4

52
Q

Why is the SV so large in Aortic valve insufficiency/regurgitation?

A

To make up for all the extra volume dt backflow & atria filling

53
Q

What is the pathology of Mitral Regurgitation?

A

Blood is moving from L vent retrograde into L atria dt leaky valve

54
Q

In Mitral Regurgitation, when is blood more likely to move retrograde into the L atria? What phases are these? What happens to ventricular volume?

A

When L vent pressure is higher than L atria pressure

Phase 2
Phase 3
Phase 4

Decreasing

55
Q

In Mitral Regurgitation, what is happening during systole?

A

Systole is phase 3. The mitral valve is closed –> blood is leaking back into the L atria from the L vent. –> volume in L vent decreasing –> decrease in SBP

56
Q

How does Mitral valve regurgitation affect the cardiac cycle/curve?

A

Mitral valve regurgitation –> increase EDV –> increased preload –> decreased SV –> decreased SBP –> decreased ESV

57
Q

In Mitral valve regurgitation the preload is _________

AP2 (13 decks)

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