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CPR Exam 1 > Regulation Of BP > Flashcards

Regulation Of BP Flashcards

1
Q

What are the three major systems that regulate BP?

A 
Baroreceptor reflex (rapid) 
Endocrinologically via renin-angiotensin-aldosterone system (slower) 
Some input form ADH and ANP (slower)
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2
Q

Describe the reflex arc for baroreceptors

A

Baroreceptors - TRP channels sense changes in stretch of the arterial walls
Afferents - alter firing rate of afferent neurons
Coordination occurs in NTS - vasomotor center in medulla
Efferents: Both the SNS and PNS (vagus); travel into cerebral cortex and hypothalamus
Effect/outcomes - changes in MAP by altering CO and TPR

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3
Q

Where are the detectors for BP located?

A 
Carotid sinus (CN IX and sinus nerve of Hering) 
Aortic sinus (vagus and aortic N) 
Leading to nucleus tractus solitarius (NTS)
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4
Q

Describe the detectors for sensing changes in BP

A

Mechanoreceptors respond to changes in arterial pressure to return to normal and act within seconds
Chemoreceptors are also present and respond to PO2, PCO2 and pH

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5
Q

If there is decreased pressure and decreased stretch what will the firing rate of the afferents be?

A

Decreased firing rate in order to increase pressure

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6
Q

If there is an increase in pressure with an increase in stretch what will the firing rate of afferents be?

A

Increased firing rate with a goal to decrease pressure

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7
Q

Afferents are most responsive to what?

A

The rate of change in pressure rather than just the magnitude of change

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8
Q

What is the difference between the aortic and carotid sinus?

A

Aortic has higher threshold for activation, continues to respond above saturation, less sensitive to rate, less effected by decreases

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9
Q

What acts as the control center for the baroreceptor reflex?

A

Brain/brainstem regions including the nucleus of tractus solitarius (NTS), dorsal motor nucleus of the vagus and nucleus ambiguus, and rostral ventrolateral medulla

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10
Q

What activates the SNS?

A

Decreased pressure and decreased baroreceptor firing rate

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11
Q

What does the SNS influence?

A

Heart muscle (atria and ventricles), SA node directly, vessels, also to adrenal gland via splanchnic Ns

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12
Q

What are the effects of the SNS on the CVS?

A

Constriction of arterioles and veins (alpha receptors)
Increases HR and contractility (B1 receptors)
Fluid retention by kidney due to afferent arteriole constriction and renin secretion

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13
Q

What is the PNS activated by?

A

Increased pressure and increased baroreceptor firing rate

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14
Q

What influence does the PNS have on the CVS?

A 
Decreases HR (vagus N signal to SA node, muscarinic receptors) 
Little direct influence on vasculature (indirect vasodilation on blood vessels (e.g. stimulate NO release))
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15
Q

Describe orthostatic hypotension

A

Lying supine and rising to standing position causes lightheadedness and dizziness upon standing which can result in syncope
Normal movement helps move blood back to the heart but when lying down blood pools in the legs, venous return and CO decrease, MAP decreases
Activates baroreceptor response

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16
Q

Venous pooling can also occur in what?

A

Edema

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17
Q

Baroreceptor reflex occurs within seconds and does what?

A

Attenuates somewhat with time

18
Q

What hormonal responses occur to regulate vascular and body fluid dynamic changes?

A

RAAS system
ADH (vasopressin)
ANP

19
Q

How do the baroreceptors adapt?

A

Able to adjust set point to different conditions

Ex. HTN resets baroreceptors to regulate pressure at a higher set point

20
Q

What is renin?

A

An enzyme secreted by juxtaglomerular cells in walls of renal afferent arterioles into the bloodstream in response to low BP and in response to sympathetic stimulation

21
Q

What stimulates renin secretion?

A

B1 adrenergic receptor activation

Decrease of NaCl at the macula densa

22
Q

Renin causes the conversion of angiotensinogen into what?

A

Angiotensin I (inactive) in the blood

23
Q

What is angiotensin I converted to?

A 
Angiotensin II (active) in the lungs (and kidneys) to begin the compensation mechanism 
Sympathetic stimulation also increases secretion
24
Q

What are the actions of angiotensin II?

A

Causes secretion of aldosterone from the adrenal cortex
Leads to Na and H2O retention by the kidneys
Also stimulates secretion of aDH which reduces urine production (fluid retention)

25
Q

What effect does angiotensin II have on arterioles?

A

Causes global vasoconstriction of arterioles by binding to specific receptors (AT1 receptors)
Increases TPR and BP

26
Q

Describe ADH (vasopressin)

A

Short half life (16-24 mins)

Acts on V1 receptors (smooth muscle) and V2 receptors (collecting ducts)

27
Q

ADH is secreted in response to what?

A

Angiotensin II, atrial receptors in presence of low preload, increased osmolality of blood, SNS activation

28
Q

What is the action of ADH?

A

Increase TPR and water retention

29
Q

What are the three forms of natriuretic peptides?

A

Atrial (ANP)
Brain (BNP)
C-type (CNP)

30
Q

What causes increased secretion of ANP?

A

Excessive preload of atria and ventricles

31
Q

What are the effects of ANP secretion?

A 
Arteriolar dilation (decreases TPR)
Increased fluid loss (decreases preload)
Inhibits renin (decreases both TPR and preload)
32
Q

What does ANP protect against?

A

Overdilation or overstretching of cardiac chambers

33
Q

What can cause decreased blood volume?

A

Hemorrhage, dehydration, loss of body fluids

34
Q

What does decreased blood volume cause?

A

Decreased venous return, preload, SV, CO and MAP

35
Q

What is the compensatory response for hemorrhage?

A

Carotid sinus nerve firing rate decreases
HR, contractility, CO and TPR increases
Unstressed volume decreased
Secretion of epinephrine, ADH, renin, angiotensin II and aldosterone increase

36
Q

What are unmodifiable causes of HTN?

A

Increasing age and family history

37
Q

What are modifiable causes for HTN?

A

Obesity, physical inactivity, elevated salt consumption

38
Q

How much salt intake is recommended by the American Heart Association?

A

No more than 2300 mg/d but ideal is to limit to 1500mg/d

39
Q

What are the results of chronic HTN and salt intake?

A

Increased Na concentration and osmolarity
Water retention
Increased SNS activity, CO and increased TPR

40
Q

What is the compensation that occurs during heart failure?

A

Poor ventricular function, reduced CO and SV
Hormonal imbalances
-neurohormonal responses (SNS and RAAS activation)
-Natriuretic peptides (ANP/BNP)

41
Q

What is the response to exercise?

A

Increased sympathetic output (B1 receptors) and decreased parasympathetic output
Increased HR/contractility
Increased venous return
Selective arteriolar vasoconstriction due to alpha 1 receptor activation (overall slight increase in MAP)

42
Q

What are the effects of alpha-1 receptor activation that occur during exercise?

A

Constriction to skin, splanchnic regions, kidney and inactive muscle
Vasodilation at active muscle and coronary circulation due to release of lactate, K ions, adenosine (active hyperemia)
Pulse pressure increases, SBP increases, DBP doesnt change much
TPR deceases

CPR Exam 1 (14 decks)

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