Arterial Blood Pressure Regulation Flashcards

1
Q

Enumerate aims of ABP regulation

A
  1. Keep ABP in an adequate value prevent excessive rise or fall.
  2. To dec minute-to-minute fluctuations of ABP
  3. To readjust ABP whenever it is disturbed.
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2
Q

Compare short and long term regulation of ABP

A

Short: involve nervous mechanisms & rapid acting hormones. Very rapid (few seconds to one minute), does not last long and does not reach full correction of ABP. Affect capacity
Long: renal mecganisms by pressure diuresis and pressure naturesis occur by action of hormones on salt and water excretion affrct volume. Slow onset within days or weeks, prolonged action (months to years). It can reach full correction of ABP.

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3
Q

Define intermediate term regulation

A

Vascular mechanisms, starts after some minutes continues to hours or days. Involve both volume (capillary fluid shift) and capacity (stress and antistress relaxation)

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4
Q

Mention the range of sensitivity of each type of receptor

A

Baroreceptors, 60-200 mmHg for carotid but 80-200 for aortic
Chemoreceptors, below 80 mmHg
CNS ischemic reflex (VMC itself is the receptor), below 50 mmHg

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5
Q

The only receptors acting normally all the time are ….

A

Arterial baroreceptors

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6
Q

Classify baroreceptors

A

A. Arterial baroreceptors: carotid sinus & aortic arch baroreceptors
B. Cardiopulmonary baroreceptors: atrial (A & B), ventricular, pulmonary receptors

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7
Q

Arterial baroreceptors are located in ….

A

Adventitia of carotid sinus & aortic arch

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8
Q

Define buffer nerves

A

Sinus nerve branch from glossopharyngeal from carotid sinus
Aortic nerve branch from vagus from aortic arch
To VMC & CIC

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9
Q

Mention stimuli for arterial baroreceptors

A

MAP

Pulse pressure

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10
Q

GR: At any MAP, baroreceptor reflex is enhanced at high rather than low PP

A

Because they are easily adapted

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11
Q

Describe function of arterial baroreceptor

A

Short term regulation only. Their primary response is to regulate ABP adequately to prevent excessive rise in ABP & minimize fluctuations to nearly third. Also responsible for vagal tone & HR maintenance.

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12
Q

Describe function of arterial baro in normal ABP

A

Their discharge leads to:
Stimulated depressor area & dec vasomotor tone, thus dec TPR
Stimulated CIC, thus decrease HR by inc vagal tone

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13
Q

Nmention role of baroreceptors in inc ABP

A

Baroreceptor reflex is enhanced leading to more inhibition if VM tone & more decrease in HR

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14
Q

Nmention role of baroreceptors in excessive inc ABP

A

Besides maximal activation of baroreceptor reflex, the hypothalamic symoathetic dilator center is stimulated leading to active VD of skeletal muscle BV by cholinergic symp
May inhibit respiratory center (adrenaline apnea)

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15
Q

Nmention role of baroreceptors in dec ABP

A

Less baroreceptor discharge leading to stimulation of pressor area and inc VM tone lesding to inc TPR, inhibition of CIC leading to inc HR

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16
Q

Describe effect of hemorrhage on baroreceptors

A

SBP dec due to dec SV & DBP is inc due to inc HR. Dec in PP keeps baroreceptors less stimulated leadsing maintainance if VC & normalization of ABP. Carotid sinus baroreceptors have the major role since they respond to inc and dec if ABP, while aortic only sense inc.

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17
Q

Postural changes mainly stimulate ……

A

Carotid sinus baroreceptors

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18
Q

Describe effect of baroreceptor reflex on veins

A

When ABP falls, this leads to inc symp NA discharge, leading to venoconstriction, dec capatictance of veins, inc VR , inc COP & inc ABP.

19
Q

Describe effect of baroreceptors on contractility

A

Normal baroreceptor discharge leads to dec sympathetic discharge, and little stimulation of cardiac contractility
Inc b.d. leads to cessation of s.d. & no stimulation if cardiac contractility
Dec b.d. leads to more activity of s.d. & an inc in cardiac contractility, SV & COP.

20
Q

Baroreceptors have …. Effect on respiration

A

Inhibitory

21
Q

What happens to baroreceptors in case of HTN

A

They are reset & cannot correct the high ABP but help maintain the new level and decrease fluctuations from the new hyoertensive level

22
Q

Describe carotid sinus syndrome

A

The baroreceptors are hypersensitive & respond to pressure on the neck resulting in inhibition of VMC & stimulation of vasodilator sympathetic center leading to dec ABP & loss of conscienceness. It is the correct response to a wring stimulus.

23
Q

Compare type A & type B atrial receptors

A

Type A: high pressure, respond to high ABP & cause VD, Bradycardia & dec contractility. May act in pulmonary circulation, to dec ABP & HR, in sudden pulmonary HTN
Type B: low pressure, repond to inc blood volume leading to VD of peripheral arterioles, inc capillary fluid shift (intermediate reg), dec secretion of ADH, VD of afferent arterioles in kidney & inc GFR, inc urine formation & inc ANP (long-term reg)

24
Q

Chemoreceptor discharge leads to secretion of …..

A

Adrenaline

25
Q

Direct effect if chemoreceptor discharge on HR is ….

Why is this effect masked?

A

Bradycradia

Due to increased HR secondary to circularing adrenaline and due to associated increased respiration

26
Q

In Bezold-Jarisch reflex injection of …… leads to ….. This effect may be associated with

A

Veratridine & serotonin
Hypotension & bradycardia
MI

27
Q

CNS ischemic reflex persists for …..

A

5-7 min

28
Q

Detail the Cushing Reflex

A

In case of cranial hemorrhage or brain tumour, ICP increases leading to compression of blood vessels, brain ischemia & dec blood flow to VMC. This leads to strong vasocontrictor tone leading to severe hypertenion (which maintains blood flow to brain) and bradycardia.

29
Q

Explain the bradycardia associated with Cushing reflex

A

Increased rate of arterial baroreceptor discharge & direct stimulation of CIC

30
Q

Rapidly acting hormones act within …..

A

20 min

31
Q

GR: Adrenaline & NA are secreted in case of fall in ABP

A

Decreased barireceptor activity
Increased chemosreceptor activity
Increased activity of CNS ischemic reflex

32
Q

Describe effects of adrenaline

A

Act on alpha & beta receptors
Adranline has more effect on heart compared to NA leads to inc HR & SV thus CO is inc
Hasless effect on ABP, as it cuases VC & VD of skeletal muscle BV leading to little change in TPR, SBP is inc while DBP is slighly dec. little effect of MAP & but PP is augmented

33
Q

Describe effects of noradrenaline

A

Act on alpja receptors only, on heart ot directly inc HR & SV but this effect is counteracted by its effect on ABP. It causes generalizaed VC, leading to inc TPR & ABP, which stimulated baroreceptors dec HR & CO. So net effect is inc TPR & ABP & dec HR & CO.

34
Q

ADH is synthesized by … & stored in ….

A

Hypothalamus

Posterior pituitary

35
Q

How is ADH released?

A

It is released in inc plasma osmotic pressure or stimulation of cardiopulmonary volume receptors when atrial blood volume or pressure is dec

36
Q

Describe action of ADH

A

When released it acts on V2 receptors in distal renal & collecting tubules, leading to water retention dec urine & inc blood volume.
At higher levels ct on V1 receptors in resistance vessels causing VC & inc ABP

37
Q

When is Renin secreted?

A
  1. Renal hypoperfusion: decreased ABP & Renal ischemia
  2. Hyponatremia
  3. Sympathetic discharge to JGA
38
Q

Describe action of renin

A

Activate angiotensiogen (alpha2 globin made by liver) to angiotensin-I (a decapeptide), cleaved by ACE which is flound in vascular endothelium but esp pulmonary vasculature into an octapeotide (angiotensin II) which is the active component of the system.

39
Q

What is the function of angiotensin II

A
  1. Potent VC, leads to inc TPR, SBP & DBP
  2. Stimulate secretion of aldosterone inc Na & water retention by kidneys, inc circulating blood voluem & ABP
  3. Stimulate subfronical areas in brain inc drive to drink water
40
Q

Describe capillary fluid shift

A

When ABP rises, filtration in arterial end is augmented, resbsorption at venous end is dec leading to shift if fluid to tissue and dec blood volume & dec ABP. Opposite occurs with dec ABP, where the whole length can become reabsorptive.

41
Q

Describe stress-relaxation mechanism

A

When ABP inc big vessel open more and more to yielding to the high ABP (stress-relaxation), thus dec ABP toward normal value. But when it dec the vessel closes on the blood leading to inc ABP towards normal value (anti-stress relaxation)

42
Q

Describe rolebof rebal control

A

In inc ABP, GFR inc leading to pressure diuresis & pressure naturesis dc blood volume , VR & COP & ABP
Opposite occurs in decrease

43
Q

Mention role of slowlu acting hormones

A

RAAS & ADH have long-term regulatory effects in addition to rapid effects
Cortisol & aldosterone lead to Na & water retention
Atrial naturetic peptide released from stretching of atria by inc circulating blood volume & pressure, inc diuresis & naturesis dec blood volume & ABP. May have VD, anti-renin, anti-aldosterone, anti-ADH.