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CVT Apex > ANS Reflexes > Flashcards

ANS Reflexes Flashcards

1
Q

The reflexes

A

“3 B’s in the CV…Ouch”

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2
Q

baroreceptor reflex is a (-/+) feedback loop

A

negative

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3
Q

What does the baroceptor reflex cause?

A

bradycardia + hypoTN

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4
Q

What will cause the baroreceptor reflex?
What surgeries especially?

A

mechanical stimulation in the carotid sinus & transverse aortic arch

carotid endarterectomy/stenting
mediastinoscopy

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5
Q

The first line defense against arterial BP changes

A

baroreceptor reflex

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6
Q

The setpoint for baroreceptors can increase or decrease. How long does this take?

A

1-3 days

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7
Q

Why does the baroreceptor function exist?

A
  • keeps arterial BP around a set point
  • preserve CO during hemorrhage/shock
  • maintain BP from supine to standing

(first line defense against arterial BP changes)

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8
Q

CV reflexes are reflex loops between…

A

CV and CNS systems

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9
Q

The 2 mechanisms that control blood volume and BP

A

neural & hormonal

neural: short term (secs-min)
ANS

hormonal: long term (mins-days)
RAAS

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10
Q

ANS reflex receptors

A

mechanoreceptors
(pressure & stretch)

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11
Q

hormonal reflex receptors
(3)

A

RAAS
vasopressin
natriuretic peptides

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12
Q

the baroreceptor reflex is a (low/high) pressure arterial reflex

A

high

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13
Q

How does the baroreceptor reflex respond to increased & decreased BP?

A

(high pressure ART baroreceptor reflex)

increased BP = decreases HR, contractility, SVR

decreased BP = increases HR, contractility, SVR

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14
Q

Why are chronic HTN patients not tolerant of hypoTN?

A

they have a higher BP setpoint, so their BP autoregulates at a higher MAP range

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15
Q

t/f
the baroreceptor reflex can control BP long term

A

true

baroreceptor mechanisms exist on a continuum w/ substantial overlap

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16
Q

another name for baroreceptor reflex

A

carotid sinus reflex

hence manipulating the carotid bifurcation during carotid endarterectomy can cause bradycardia

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17
Q

triggering the baroreceptor reflex during mediastinoscopy

A

pressure from the scope on the transverse aortic arch can cause bradycardia

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18
Q

Negative
vs.
Positive

feedback loop

A

negative: the stimulus/disturbance & response oppose each other

positive: the stimulus/disturbance & response reinforce each other

positive feedback loops are less common

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19
Q

Baroreceptor reflex in action

A
  1. increased MAP stretches baroreceptors (transv. A arch & carotid A bifurcation), altering the rate of AP generation
  2. afferent pathways send APs to the control centers (A.Arch → Vagus nerve; Carotid → carotid sinus n./hering’s →CN IX/glossphryng)
  3. afferent info @ NTS in the medulla (control center)
  4. efferent (via SNS & vagus) → heart & vascular
  5. slows HR & dilates (decreases SVR)
  6. decreased MAP
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20
Q

where are baroreceptors located?

A

transverse aortic arch
&
bifurcation of carotid arteries (carotid sinus)

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21
Q

Where do baroreceptors in the transverse aortic arch & bifurcation of carotid arteries send their afferent signals?

A

“Transverse To Ten”

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22
Q

The glosspharyngeal & vagus nerves are (afferent/efferent) pathways for the baroreceptor reflex

A

afferent

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23
Q
A
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24
Q

Which common drugs can diminish the baroreceptor reflex?

A

Labetalol
Sevo
(decrease BP AND HR)

Prop (usually but not always)

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25
Q

Drugs with which effects will preserve the BRR?

A

those that:
↓HR + ↑BP (norepi)
or
↑HR + ↓BP (hydralazine, thiopental)

cannot decrease both

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26
Q

Preservation of the BRR means that HR will ___ when the BP ___

A

HR adjusts as needed when BP changes

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27
Q

What shows the the BRR is impaired?

A

a BP change does NOT produce the expected compensatory change in HR!

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28
Q

What agents/classes will impair the BRR?

A
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29
Q

how do the VAs affect the BRR?

A
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30
Q

How do induction agents affect BRR?

A
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31
Q

Which vasodilators preserve the BRR?

A

hydralazine
NTG
nipride

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32
Q

how does hydralazine preserve the BRR?

A

potent vasodilation drops SVR
BUT
BRR produces an increase in HR

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33
Q

How do beta blockers affect the BRR?

A
  • may impair it
  • depends on extent of beta blockade (may produce compenastory ↑HR if hypoTN)
  • Labetalol also antagonizes A1 = risk of ortho hypoTN
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34
Q

How does NE affect HR?

35
Q

These catecholamines increase HR regardless of dose

A

NOT norepi

36
Q

T/F:
Phenylephrine is a catecholamine

37
Q

T/F:
Phenylephrine preserves the BRR

A

True
increases BP but bradycardia is common

38
Q

How do antihypertensives affect the BRR?

(not including B-blkrs)

A

CCBs and PDEs impair it

ACEI alone will not, but if used with another arterial dilator OR hypovolemia, it reduces CV response to increased BP

39
Q

The Bezold Jarisch reflex will cause (3)

A
  1. bradycardia
  2. hypoTN
  3. coronary artery dilation
40
Q

When does the Bezold-Jarisch reflex occur?

A

profound hypovolemia

slows HR to allow filling time

41
Q

T/F:
The Bezold-Jarisch reflex is a cardio-inhibitory reflex

42
Q

the five and dime reflex

A

oculocardiac

afferent: trigmeninal CN V
efferent: Vagus CN X

43
Q

Bainbridge reflex function

A

prevents damming or sludging or blood in veins, artia and pulmonary circulation

44
Q

How does persistent hypoxemia trigger reflexes?

A

causes SNS activation:
increased HR & inotropy to increase the CO

45
Q

Persistent hypoxemia triggers SNS activation. Its effects are part of the ____ reflex.

A

chemoreceptor

46
Q

Bainbridge reflex

A

tachycardia due to increased venous return

LOW pressure cardiopulm baroreceptor reflex

47
Q

The bainbridge reflex sensor

A

low pressure stretch receptors firing more frequently during atrial filling

bainbridge: tachycardia during increased venous return

48
Q

Low pressure baroreceptors

A

volume detectors found in atria and lung vasculature

49
Q

Bainbridge reflex
start to finish

A
  1. stimulus: increased blood vol
  2. sensor: low pressure stretch receptors in atria increase their firing
  3. afferent: Vagus to NTS
  4. control center: NTS + its projections to medulla’s CV centers
  5. efferent: PNS and SNS to SA node
  6. effector & response: SA node changes HR
50
Q

Can you saturate the bainbridge reflex? What happens?

A

yes

those with lower baseline HR experience greatest increase in HR

51
Q

T/F:
Tachycardia cause by the Bainbridge reflex has significant effects on contractility and stroke volume.

A

False
insignificant

52
Q

counterbalances the baroreceptor reflex

A

bainbridge

53
Q

The biphasic effect of venous return & blood volume on heart rate

A
  • volume loading AND depletion cause graded increases in heart rate
  • volume loading: bainbridge reflex prevails
  • volume depletion: high pressure baroreceptor reflex dominates
54
Q

When is heart rate change from the bainbridge reflex minimal?

A

when the effective circulating volume is normal

55
Q

cardiac congestion leads to…

56
Q

Bezold-Jarisch Reflex (BJR)

A
  • cardiorespiratory reponse to IV Veratrum alkaloids
  • bradycardia, hypoTN apnea
  • classic triad: bradycardia, hypoTN, dilated coronaries
57
Q

triggers the BJR

A
  • noxious ventricular stimuli (MI, low venous return, thrombolysis)
  • veratrum alkaloids
  • nicotine
  • capsaicin
  • histamine
  • serotonin
  • snake/insect venoms
58
Q

the BJR is a cardio-inhibitory reflex that may play a prominent role in…

A

cardioprotective reflexes in response to noxious stimuli

59
Q

BJR
Feedback Loop

A

Dromotropic: effect on the conduction speed of electrical impulses

60
Q

your pt becomes bradycardic and hypotensive after their spinal/epidural. which reflex is this?

61
Q

Procedures likely to elicit BJR

A
  • spinal/epidural
  • shoulder shurgery w/ regional in sitting position
62
Q

These cardiac conditions make the BJR less pronounced

A

hypertrophy & AFIB

63
Q

Bainbridge vs BJR
(preload)

64
Q

these reflexes tend to override the baroreceptor reflex

A

bainbridge and BJR

65
Q

Bainbridge vs BJR
overall

66
Q

What do chemoreceptor typically control?

A

ventilation

some facets include CV responses

67
Q

T/F:
the strongest drive/stimulus at peripheral chemoreceptors is hypercarbia

A

FALSE
hypoxia

68
Q

hypoxia’s
feedback loop

A
  • ilicits afferents from carotid & aortic bodies via Hering nerve (of CN 9) & vagus, respectively → NTS
  • effector reponses: increase RR, Vt, MV
  • CV responses depend on acuity
  • acute: activate PNS (↓HR & ionotropy)
  • persistent: activate SNS (↑HR & ionotropy & CO)
69
Q

How much volatile is needed to blunt the chemoreceptor response?

A

subanesthetic concentrations!
<0.1 MAC

nitrous will attentuate it as well in a dose dependent fashion

70
Q

How do opioids affect the chemoreceptor response?

A

dose dependent attenuation

71
Q

Vasovagal reflex triggers

“vasovagal syncope” “neurocardiogenic syncope”

A
  • stress (blood draws, seeing blood, acute pain)
  • peritoneal stretch/distention (esp rapid insufflation)
72
Q

What makes you more likely to faint from the vasovagal reflex?

A
  • warm room
  • volume loss
  • upon standing
73
Q

Why can you faint from the vasovagal reflex?

A

transiet drop in perfusion pressure to the brain

74
Q

Vasovagal reflex

Feedback loop

A
  1. vagal afferents → higher CNS (hypothalamus)
  2. acts thru ANS nuclei to massively stimulate the PNS & abolish SNS
  3. massive vasodilation but NO baroreceptor activation
  4. ↓HR + ↓SV = ↓CO
  5. the sudden drop in SVR & CO profoundly decrease MAP
  6. global cerebral ischemia (dizziness or fainting)
75
Q

vasovagal reflex

At what point does a drop in CBF cause LOC?

A

if CBF is decreased for ~10 secs

(only a few seconds = dizzy or feeling faint)

77
Q

vasovagal reflex

after regaining consciouness, oliguria can occur due to ….

A

high plasma levels of vasopression (ADH)

78
Q

vasovagal reflex

How serious can rapid insufflation be?

A

a profound vasovagal reaction can cause acute CV collapse and cardiac arrest

79
Q

Oculocardiac reflex
stimuli/triggers

80
Q

Oculocardiac reflex
feedback loop

83
Q

How to treat Oculocardiac reflex

CVT Apex (11 decks)

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