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Boards: Cardiovascular > Control of CV System > Flashcards

Control of CV System Flashcards

1
Q

Minute to minute control of CV

A

Local control

VD substances, by products of tissue metabolism - act on small vessels

NO, PGEs

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2
Q

Neurohormonal Control

A

ANS: peripheral R that respond to changes in BP, volume, gas tension

Includes BRR, Bainbridge, coronary chemoR

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3
Q

Consequences of Bainbridge Reflex

A

Atrial B R - respond to changes in atrial volume: decreased HR with increased volume (IVF bolus)

Decrease SNS to renal arterioles = VD, decreased release of ADH from hypothalamus, release of ANP/BNP from atrial myocytes to increase Na excretion

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4
Q

Aldosterone

A

Decreased Na excretion, more water retained

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5
Q

Angiotensin II

A

VC, increased aldosterone production - decreased Na excretion, more water retention to raise BP

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6
Q

ANP

A

released from atrial myocytes in response to dissension

Increase Na excretion with accompanying increase in water loss

Endogenous antagonist to AGT

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7
Q

Ventricular Mechanoreceptors

A

ventricular endocardium – discharge parallel with changes in ventricular pressure (BEZOLD-JARISCH REFLEX)

decrease HR and peripheral VD, resulting in bradycardia and hypotension

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8
Q

Coronary ChemoR/BJR

A

Carotid and aortic arch contain specialized chemoreceptors

Set point is pH below 7.40, CO2 above 40mmHg, Oxygen below 80mmHg

Increase minute ventilation, restore arterial pH, CO2 and O2 to normal

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9
Q

Effect of coronary chemoR

A

bradycardia, increased minute ventilation, coronary artery vasodilation

controlled by NTS in medulla

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10
Q

SNS control of CV System

A

T1-L2 Spinal Cord Segments

Pre ganglionic sympathetic nerve cell bodies: bulbospinal tract
–Descending inhibitory pathways – serotoninergic
–Descending excitatory pathways - adrenergic

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11
Q

Location of Preganglionic Neurons for SNS CV Control

A

o Pre-ganglionic nerves to ventral roots of spinal cord (bulbospinal tract) to paravertebral ganglia just outside of vertebral column

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12
Q

Location of Postganglionic Neurons for SNS CV Control

A

o Post-ganglionic neurons in cranial, middle, and caudal (stellate) cervical ganglion – release NE which binds to adrenoreceptors on cardiac cell membrane

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13
Q

PNS: Fiber Arrangement

A

Long pre-ganglionic nerve fibers in CNS

Cervical spinal cord: III, IX, X; S2-S3

ACh: neurotransmitter pre, post
Short post-ganglionic fibers in ganglion located in target organ

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14
Q

Nicotinic ACh R

A

Opens Na, K channels - excitatory

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15
Q

Cholinergic R

A

Gq or Gi

decrease in phase 4 slope, hyperpolarization of membrane K channel activation

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16
Q

PSNS: Vagus N

A
  • R vagus: slows depolarization of SA node
  • L vagus: slows depolarization of AV node

Cardiac response to vagal N discharge transient, both nodes rich in AChE = beat by beat effect on the heart

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17
Q

SNS Role

A

fibers originate from intermediolateral columns of upper thoracic SC, synapse in middle/stellate ganglia, form complex nerve plexus mixed with PNS fibers
* NT = NE
* Slower onset, longer duration than ACh

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18
Q

Arterial Baroreceptors

A

Stretch receptors (mechanoreceptors) – carotid sinus/aortic arch

Respond to increased ABP via increased sensory nerve firing –> CN IX/X –> nucleus tractus solitaries within CNS

Decrease ABP via inhibition of SNS to decrease HR

19
Q

Which CN is assoc with the carotid sinus?

A

CN IX

20
Q

Which CN assoc with aortic arch?

A

CN X

21
Q

Set Points of Arterial Baroreceptors

A
  • Inactive at ABP <60mm Hg
  • Maximum firing at 180mm Hg
  • Set point ~100mm Hg
  • BR = short-term control only: most ax drugs interfere with BR responsiveness (esp inhalants)
22
Q

Role of the Atria

A

Basically atria senses how much vol, tell brain whether need to + or - water

Atrial A R: HR
Atrial B R: changes in atrial volume

23
Q

Increased atrial volume…

A

activates A, B MR –> CN X –> medulla

Can increase HR (Bainbridge reflex) or decrease HR (BRR, activation of atrial depressor C fibers)

24
Q

ANP

A

produced in atrial CaM IRT atrial distention, increases Na excretion in kidney (increased H2O loss)

25
Q

BNP

A

produced in ventricular CaM depends on increased ventricular filling pressures, myocardial stretch

26
Q

Ventricular MechanoR/BJR

A

(ventricular endocardium) discharge in parallel with changes in ventricular pressure to regulate SBP, myocardial work

Ventricular distention stimulates powerful depressor reflexes = decreased HR, decreased SVR = bradycardia, hypotension

ventricular non-myelinated C fibers initiated by impulses from ventricular distention or injection of certain chemicals (capsaicin, serotonin) into coronary arteries

27
Q

Carotid and Aortic Bodies = ChemoR

A
  • Receive highest BF/gram of tissue of any organ in body
  • Sensitive to changes in PaO2, PaCO2, pH, temp, help to regulate resp function IRT decreased pH, PaO2, increased PaCO2
  • Increased afferent activity from chemoR: increase Vmin (minute ventilation) = restore blood pH, PaCO2, PaO2

Hypoxia, hypercarbia, non-resp acidosis (ischemia): bradycardia, decreased SVR, vasodilation of coronary arteries

28
Q

ANS: Efferent Output

A

**Nucleus tracus solitarius (NTS) in medulla = relay station **
 Hypothalamus links somatic/ANS responses: initiates adrenergic constriction of resistance, capacitance vessels; cholinergic dilation of SkM, CaM during fight/flight

29
Q

Control of HR

A

o ANS (SNS, PNS) both innervate SA node –> fibers can modify intrinsic HR
o ANS fibers also influence conduction velocity of APs through heart

autonomic influences on initial rate of depol of AP +/- influences on conduction characteristics of gap junctions btw cardiac cells

30
Q

Immediate/Short Term regulation of NP

A
  1. ANS: HR, vessel tone/capacity
  2. Vascular BR/Stretch reflexes: HR, vessel tone/capacity
  3. Cardiac stretch R
  4. ChemoR
  5. Humoral responses: epi, NE
  6. Local factors
31
Q

Local factors to Impact BP

A

PaO2 (lower O2 = vasodilation, increased O2 = VC), local metabolites, increased production of CO2, lactate, H, myogenic autoregulation = adjust vessel tone to changes in BP

32
Q

Intermediate Control of BP

A

Transcapillary Fluid Shifts via Starling’s
Hormonal responses - renin, AGT

33
Q

Long Term Control of BP

A

o Oral fluid consumption: regulates net fluid intake
o Renal control system: ADH, aldosterone, ANP: regulates total body water, renal fluid output

34
Q

What is the most important system for short term determinants of ABP?

A

Central, peripheral barorecepots

35
Q

Consequences of Failure to Restore BP

A

capillary hydrostatic pressure decreases = movement of fluid from interstitial spaces to capillaries to increase IV vol, can restore up to 50% IV vol within hrs

36
Q

Autoregulation

A

automatic adjustment of BF through tissue regardless of MAP driving blood through tissues
 Unconscious adjustment of arterial/arteriolar SmM tone to maintain constant BF through tissue across wide range of pressures (~MAP 60-160 mmHg)

MOA: adaptive metabolic, myogenic, neurogenic FB mechanisms

Outside this interval, tissue/organ blood flow substantially altered: may result in decreased/nonuniform perfusion parameters
* Becomes pressure-dependent = under or over perfused

37
Q

ADH/VP

A

produced in hypothalamus, transported to posterior pituitary via nerve axons
* ADH: collecting duct of kidney - H2O conservation, increase plasma vol
* Vasopressin (ADH) = VC via activation of V1a R on blood vessels (Gq), influential redistribution of systemic blood flow, esp mesenteric vessels

38
Q

Active Dilation of BV

A

vascular tone < non-neurogenic basal level
* Result of pressure-sensitive mechanism (myogenic component), metabolic mechanism (influenced by O2 tension)
o Both mechanisms linked to release of local VD mediators = reactive hyperemia

39
Q

Triggers for Active Dilation

A

o Myogenic mechanism = <30s ischemia
o Metabolic mechanism = >30s ischemia

40
Q

Local factors that cause VC

A

Stretch
Endothelian (ETa R)
TXA2

41
Q

Local Facts that Cause VD

A

Histamine
NO, PGI2, EDHF
CO2, lactate, adenosine, K

42
Q

Under resting conditions…

A

only 1/3-1/2 capillaries being perfused

43
Q

Capillary BF affected by:

A

perfusion pressure, blood flow rate, tissue metabolic rate, O2 tension, plasma viscosity

44
Q

As BF viscosity increases…

A

As viscosity increases, vascular hindrance decreases = improved tissue perfusion
o Resistance to flow = viscosity x vascular hindrance

Shape/diameter of vessels not fixed: altered IRT changes in viscosity - represented by changes in vascular hindrance

Boards: Cardiovascular (11 decks)

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