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CARDIOVASCULAR > 13/14 – Blood Pressure > Flashcards

13/14 – Blood Pressure Flashcards

1
Q

What are some regulatory actions to increase cardiac output?

A

-adrenergic/NE at heart = adrenal release of E
-adrenergic/NE on veins = increase preload

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1
Q

What are some regulatory actions to increase systemic vascular resistance?

A

-adrenergic/NE on arteries = vasoconstriction

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2
Q

Baroreceptors (mechanoreceptors) are located in:

A

-atria
-aorta
-carotid arteries

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3
Q

Baroreceptors detect:

A

-stretch
*send signals vis cranial nerves IX and X to medulla

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4
Q

What happens with increased stretch/rate of baroreceptors?

A

-engages afferents that activate vagal efferents

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5
Q

What happens with decreased stretch/rate of baroreceptors?

A

-disengages same afferent signals
Ex. lifts the break on SNS

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6
Q

Why is maintaining BP so important?

A

-to ensure adequate perfusion with continuous blood flow throughout the body

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7
Q

Baroreceptors set point:

A

-responsive to + or – changes
-species dependent
-animal dependent
-normal fluctuation
*between BP and number of impulses

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8
Q

Normal fluctuation of baroreceptors set point: decrease in pressure examples

A
  • hypovolemia
    -pharmacological
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9
Q

Normal fluctuation of baroreceptors set point: decrease in pressure

A

-decreased pulse pressure
-reduced amount of stretch detected by baroreceptors=decrease in impulses (‘lifts the brake’)
-increase S activity (via medulla)
-decrease PS activity (via medulla)
*increase CO and SVR = increased BP

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10
Q

Normal fluctuation of baroreceptors set point: increase in pressure examples

A

-arousal
-volume overload
-pharmacological

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11
Q

Normal fluctuation of baroreceptors set point: increase in pressure

A

-increase stretch=applies break=increase baroreceptor firing
-decrease S activity (via medulla)
-increase PS activity (via medulla)
*decrease CO and SVR = decrease BP

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12
Q

What happens when there is prolonged hypertension?

A

-sensitivity/set point of baroreceptors changes and will go down (RIGHTWARD SHIFT)
-atrial remodelling (ex. aorta doesn’t stretch as well=don’t relay signals as well) also contributes

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13
Q

What is important when trying to resolve hypertension?

A

-don’t want to just treat the symptom
-want to RESET set point
*if bring BP down long enough and increase exercise=reset set point

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14
Q

Drugs that can be used to treat hypertension:

A

-alpha receptor blocker
-Ca channel blocker
-diuretic

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15
Q

Alpha receptor blocker:

A

-decrease constriction by SNS

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16
Q

Ca channel blocker:

A

-decrease contractility

17
Q

Diuretic:

A

-decrease preload

18
Q

Baroreflex and giving E:

A

-MAP does not change much
-pulse pressure increases DRAMATICALLY
-heart rate increases

19
Q

Baroreflex, E and receptors:

A

-beta-1 at heart: increase HR and SV
-beta-2 in arteries: decreases tone or attenuates alpha-1 mediate effects (decrease SVR)

20
Q

Baroreflex and giving NE:

A

-MAP increases
-pulse pressure increases
-heart rate decreases

21
Q

Baroreflex, NE and receptors:

A

-beta-1 at heart: increase HR and SV
-alpha-1 in arteries: increase tone (increase SVR)
>

22
Q

RAAS vs. baroreceptors:

A

-baroreceptors: seconds to days
-RAAS: days to weeks

23
Q

RAAS activation can increase:

A

-cardiac output (via blood volume)
-systemic vascular resistance (via vasoconstriction)
*increase in MAP

24
Q

RAAS:

A

-regulation of blood volume and SVR
>CO and MAP

25
Q

Where is the primary site of renin release?

A

-juxtaglomerular cells associated with afferent renal artery

26
Q

What stimulates renin release?

A

-decreased MAP
-sympathetic stimulation
-decrease NaCl concentration in distal tubule
*all interdependent (collectively stimulate release)

27
Q

What is released in response to renin?

A
  1. Angiotensinogen coverts it to angiotensin I (AI)
  2. ACE converts AI to AII
28
Q

angiotensin II release results in increased:

A

-vasoconstriction: increased SVR and MAP
-Na and H2O retention: increased CO and MAP
-aldosterone
-ADH
-thirst
-adrenergic signalling

29
Q

Where are some targets for drugs to ‘turning off’ RAAS pathway?

A

-renin inhibitors
-ACE inhibitors
-A II receptor blockers
-aldosterone receptor blockers
-diuretics

30
Q

How is RAAS modulated? (counter-regulatory system)

A

-cardiac distension
-sympathetic stimulation
-A II
*lead to ANP and BNP release from heart

31
Q

ANP and BNP stand for:

A

-ANP: atrial naturietic peptides
-BNP: brain naturietic peptides

32
Q

What happens when ANP and BNP are released from the heart?

A

-increase venodilation
-increase arterial dilation
-increase GFR
-decrease renin release

33
Q

Increase venodilation with ANP and BNP causes:

A

-decreased central venous pressure (CVP)
-decreased preload
-decreased CO
*veins

34
Q

Increased arterial dilation with ANP and BNP causes:

A

-decreased SVR
-decreased MAP
*arteries

35
Q

Increase GFR with ANP and BNP causes:

A

-decrease Na and H2O retention
-decrease CO
-decrease MAP

36
Q

Decreased renin released with ANP and BNP causes:

A

-decreased A II leading to decreased
>vasoconstriction
>Na and H2O retention
>aldosterone
>thirst
>adrenergic signalling

37
Q

What are some of the consequences with blood loss?

A

*hypovolemia
-decreased MAP
-altered blood gas
-decrease blood volume

38
Q

What happens when BP is low?

A

-lead to decreased perfusion to organs=organ failure=death
*mismatch between organ metabolism and perfusion=anaerobic=acidosis

39
Q

What are some ways to compensate for the consequences of blood loss?

A

-baroreflex (decreased MAP)
-chemoreflex (altered blood gas)
-humoral/RAAS (decrease blood volume)

40
Q

What do the compensation methods for blood loss do?

A

-increase cardiac stimulation
-increase SVR
-cardiac output redistribution
-increase blood volume

CARDIOVASCULAR (17 decks)

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