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Acute Care > Compensatory Mechanisms > Flashcards

Compensatory Mechanisms Flashcards

1
Q

Explain homeostasis

A

It is an automatic, self-regulating process that is essential to maintain optimal biochemical function. It is only a ST response and can only compensate for minor insults from normal homeostatic range.

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2
Q

What does perfusion do?

A

Provides oxygen and nutrients to cells to maintain cell function. It also removed metabolic waste.

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3
Q

What is perfusion reliant upon?

A

Good blood flow i.e. pressure and volume, and a good reserve of 02

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4
Q

What is MAP and what helps maintain MAP?

A

Mean arterial pressure - it is the driving pressure for perfusing organs; vasoconstriction helps maintain MAP.

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5
Q

What is pulse pressure? what is important about it?

A

it is the different between systolic and diastolic BP, what is important is whether it is widening or narrowing.

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6
Q

What system maintains homeostasis?

A

the neuro-endocrine system

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7
Q

What is the calculation for BP

A

BP= CO x SVR (xHR)

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8
Q

What does SVR stand for?

A

systemic vascular resistance of arterial system

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9
Q

what is the calculation for cardiac output?

A

CO = SV x HR

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10
Q

What is stroke volume?

A

the volume of blood pumping from the left ventricle in mls

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11
Q

What does blood pressure regulation address?

A

ST occurences; moving from sitting to standing or life-threatening events ie haemorrhage.

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12
Q

What is the primary system that regulates BP

A

sympathetic nervous system (SNS) I.E. the neural response (autonomic NS)

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13
Q

what is the back-up response for BP regulation?

A

RAAS - renin-angiotensin-aldosteone system i.e. the humoral response

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14
Q

what is the main compensation of BP?

A

vasoconstriction

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15
Q

what effect would this have?

A

in order to maintain systolic BP, it would raise diastolic BP, this therefore means that diastolic BP is a direct representation of how vasoconstricted the body is

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16
Q

what compensatory mechanism will indicate direct decompensation?

A

SV will decrease, and if it is less than 25-30mls then there is a low volume of blood in the system.

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17
Q

What is the primary response when we begin to decompensate i.e. decrease in BP.

A

Neural-baroreceptor reflexes

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18
Q

What is process of the neural-baroreceptor reflexes?

A
  1. a decrease in SV = reduced stretch in vessel wall
  2. baroreceptors respond to this reduced stretch
  3. Signal is sent to vasometer centre and cardiac centre i.e. cardiovascular system in the brain stem
  4. This stimulates the ANS ( SNS )
19
Q

What is the effect of the NB reflexes?

A

stimulation of arteriolar vasoconstriction and tachy

20
Q

why does someone become tachy after a drop in SV?

A

due to the NB reflexes - so that to increase the amount of 02 reaching cells i.e. to increase perfusion and to compensate the drop in BP

21
Q

what are the main indications of decompensation?

A

Diastolic and systolic drop after an increase in diastolic, also the pulse will rise with systolic then will keep rising above it.

22
Q

What two hormones act as neurotransmitters in SNS?

A

Noradrenaline and adrenaline

23
Q

what receptors do the SNS hormones act at?

A

adrenergic receptors

24
Q

where is noradrenaline realised from? and what stimulates it?

A

released from sympathetic nerve endings and from stimulation of adrenal medulla

25
Q

what receptors does noradrenaline work on specifically?

A

alpha receptors

26
Q

what affect does noradrenaline have on alpha 1 receptors?

A
  1. vasoconstiction ie increase in BP
  2. Dilatation of pupils
  3. increased closures of bladdr internal sphincter
27
Q

what affect does noradrenaline have on alpha 2 receptors?

A

inhibition of noradrenaline release (-ve feedback system)

2. inhibition of insulin release

28
Q

where is adrenaline released rfrom?

A

adrenal medulla

29
Q

what receptors does adrenaline work on?

A

beta receptors, predomintely beta 1

30
Q

what affect does adrenaline have on beta 1 receptors?

A
  1. increase in myocardial contractility

2. increase in HR

31
Q

Where are the beta 1 receptors?

A

in the heart

32
Q

where are the beta 2 receptors?

A

in the lungs

33
Q

what affect does adrenaline have onbeta 2 receptors?

A
  1. vasodilation
  2. bronchodilation
  3. increased release of glucagon and stored glycogen
34
Q

what is an adrenergic agonist?

A

a drug that stimulates a response from the adrenergic receptor

35
Q

what is an adrenergic antagonist?

A

a drug that inhibits the function of adrenergic receptors

36
Q

what receptors are stimulated as part of the ‘stress response’?

A

all receptors

37
Q

give an example of a beta 2 adrenergic agonist?

A

salbutamol

38
Q

give an example of a beta 1 antagonist? and what does it do?

A

all beta blockers, and they slow HR

39
Q

summary of 4 effects of SNS on body and what positive effect does it have on homeostasis?

A
  1. increase HR
  2. increase SV ie contractility of heart
  3. vasoconstriction of arterioles ie increase in BP
  4. increase in peripheral resistance ie SVR

and overall it increase perfusion to cells

40
Q

what initiates the RAAS? and what is stimulated?

A

Low/poor renal perfusion initiates RAAS - it stimulates juxtaglomerular cells around kidney nephrons

41
Q

what is the step by step process of RAAS?

A

low BP = renin (kidney) + angiontensinogen (liver) = angiotensin 1 + angiotensin-converting enzyme = angiotensin 2

42
Q

what cause renin to be released from kidneys?

A

low BP / low perfusion of kindeys

43
Q

what effect does angiotensin 2 have?

A
  1. stimulates SNS
  2. increased thirst : acts directly on distant convo-tuble to release Na+ into system and water follows
  3. stimulates adrenal to release aldosterone
  4. sends signal to putuitary glands and activates ADH secretion
  5. vasoconstriction
44
Q

what affect do ACE inhibitors have on RAAS?

A

prevent the conversion of angiontensin 1 to angiotensin 2 ie reduces BP

Acute Care (2 decks)

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