Control of CV System Flashcards
Minute to minute control of CV
Local control
VD substances, by products of tissue metabolism - act on small vessels
NO, PGEs
Neurohormonal Control
ANS: peripheral R that respond to changes in BP, volume, gas tension
Includes BRR, Bainbridge, coronary chemoR
Consequences of Bainbridge Reflex
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
Aldosterone
Decreased Na excretion, more water retained
Angiotensin II
VC, increased aldosterone production - decreased Na excretion, more water retention to raise BP
ANP
released from atrial myocytes in response to dissension
Increase Na excretion with accompanying increase in water loss
Endogenous antagonist to AGT
Ventricular Mechanoreceptors
ventricular endocardium – discharge parallel with changes in ventricular pressure (BEZOLD-JARISCH REFLEX)
decrease HR and peripheral VD, resulting in bradycardia and hypotension
Coronary ChemoR/BJR
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
Effect of coronary chemoR
bradycardia, increased minute ventilation, coronary artery vasodilation
controlled by NTS in medulla
SNS control of CV System
T1-L2 Spinal Cord Segments
Pre ganglionic sympathetic nerve cell bodies: bulbospinal tract
–Descending inhibitory pathways – serotoninergic
–Descending excitatory pathways - adrenergic
Location of Preganglionic Neurons for SNS CV Control
o Pre-ganglionic nerves to ventral roots of spinal cord (bulbospinal tract) to paravertebral ganglia just outside of vertebral column
Location of Postganglionic Neurons for SNS CV Control
o Post-ganglionic neurons in cranial, middle, and caudal (stellate) cervical ganglion – release NE which binds to adrenoreceptors on cardiac cell membrane
PNS: Fiber Arrangement
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
Nicotinic ACh R
Opens Na, K channels - excitatory
Cholinergic R
Gq or Gi
decrease in phase 4 slope, hyperpolarization of membrane K channel activation
PSNS: Vagus N
- 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
SNS Role
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
Arterial Baroreceptors
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
Which CN is assoc with the carotid sinus?
CN IX
Which CN assoc with aortic arch?
CN X
Set Points of Arterial Baroreceptors
- 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)
Role of the Atria
Basically atria senses how much vol, tell brain whether need to + or - water
Atrial A R: HR
Atrial B R: changes in atrial volume
Increased atrial volume…
activates A, B MR –> CN X –> medulla
Can increase HR (Bainbridge reflex) or decrease HR (BRR, activation of atrial depressor C fibers)
ANP
produced in atrial CaM IRT atrial distention, increases Na excretion in kidney (increased H2O loss)
BNP
produced in ventricular CaM depends on increased ventricular filling pressures, myocardial stretch
Ventricular MechanoR/BJR
(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
Carotid and Aortic Bodies = ChemoR
- 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
ANS: Efferent Output
**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
Control of HR
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
Immediate/Short Term regulation of NP
- ANS: HR, vessel tone/capacity
- Vascular BR/Stretch reflexes: HR, vessel tone/capacity
- Cardiac stretch R
- ChemoR
- Humoral responses: epi, NE
- Local factors
Local factors to Impact BP
PaO2 (lower O2 = vasodilation, increased O2 = VC), local metabolites, increased production of CO2, lactate, H, myogenic autoregulation = adjust vessel tone to changes in BP
Intermediate Control of BP
Transcapillary Fluid Shifts via Starling’s
Hormonal responses - renin, AGT
Long Term Control of BP
o Oral fluid consumption: regulates net fluid intake
o Renal control system: ADH, aldosterone, ANP: regulates total body water, renal fluid output
What is the most important system for short term determinants of ABP?
Central, peripheral barorecepots
Consequences of Failure to Restore BP
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
Autoregulation
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
ADH/VP
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
Active Dilation of BV
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
Triggers for Active Dilation
o Myogenic mechanism = <30s ischemia
o Metabolic mechanism = >30s ischemia
Local factors that cause VC
Stretch
Endothelian (ETa R)
TXA2
Local Facts that Cause VD
Histamine
NO, PGI2, EDHF
CO2, lactate, adenosine, K
Under resting conditions…
only 1/3-1/2 capillaries being perfused
Capillary BF affected by:
perfusion pressure, blood flow rate, tissue metabolic rate, O2 tension, plasma viscosity
As BF viscosity increases…
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
