2
receptors)
Vascular volume depends on
Intake of fluids (thirst)
Output of fluids (urine, sweat, etc)
Distribution of fluids (Starlings law)
Myocardial contractility (MC proportional to sympathetic
tone [
1
receptors])
Characteristics of some adrenoceptors
(sympathetic nerves)
2
1
2
Smooth
muscle
Arteries/
veins
constrict constrict/
dilate
dilate
Skeletal
muscle
dilate
Heart
Rate
(increase)
Force of
contraction
increase
Tissues
and effects
receptors
Beat-to-Beat Modulation of Blood
Pressure
Controlled by baroreceptor reflex arch
Baroreceptors located in aortic arch
Increased stretching due to higher aortic arch
pressure increased vagal nerve activity
decreased heart rate decreased cardiac
output decreased blood pressure
Fast acting
Autonomic Regulation of Blood Pressure
Coordinates and integrates all
regulators of cardiovascular function
Can regulate both cardiac output and
blood vessel size via sympathetic
and parasympathetic innervation of
cardiovascular end-organs (heart,
vasculature, kidneys, adrenal glands,
etc)
Autonomic Regulation of the Heart
Heart Rate
Parasympathetic input via vagus nerve
causes decrease in HR (dominates)
Sympathetic input to sino-atrial node
causes increase in HR (usually minor)
Heart contractility
Increased by sympathetic activity
causing release of epinephrine,
norepinephrine from adrenal gland
II. Background to Arrhythmia -
Rhythm of the Heart
Human heart is four-
chambered
Chambers need to contract
sequentially (atria, then
ventricles) and in
synchronicity
Also need relaxation
between contractions to
allow refilling of chambers
Above controlled
electrically (Purkinje fibers
allow rapid, organized
spread of activation)
Regulation of Heart Rate
Primarily accomplished by sinoatrial node (SA)
Located on right atrium
Receives autonomic input
When stimulated, SA signals atrial contractile fibers
atria depolarization and contraction (primes
ventricles with blood)
Depolarization picked up by atrioventricular
node (AV node) depolarizes ventricles
blood discharged to pulmonary artery and
dorsal aorta eventually rest of body
Sequential Discharge of SA and AV nodes
III. Background to Congestive Heart Failure
Maintenance of Normal Heart Function
Normal cardiac output needed to adequately perfuse
peripheral organs
Provide O
2
, nutrients, etc
Remove CO
2
, metabolic wastes, etc
Maintain fluid flow from capillaries into interstitium and back
into venous system if flow reduced or pressure increased in
venous system build up of interstitial fluid = edema
Because CO is a function of
Heart Rate determined by pacemaker cells in the sinoatrial
node
Stroke volume determined by fill rate and contractile force
Atrial/ventricular/valvular coordination
Any negative change on above can lead to inadequate
perfusion and development of the syndrome of heart failure
IV. Background to Reduced Vascular Blood
Flow: Blood Vessel Anatomy and Function
Arterial blood vessels
Smooth muscle (slow, steady contraction)
elastic tissue (stretch on systole, recoil on diastole)
Contain about 10% of blood volume
Arterioles have sphincters which regulate 70% of blood pressure
Venous blood vessels
Highly distensible, some contractility
Contain over 50% of blood volume
Capillaries
Tiny but contain greatest cross-sectional area to allow high exchange
rate
Contain precapillary sphincters to regulate blood flow
5% of blood volume
All vasculature under ANS and humeral control
Quantification of Total Peripheral Resistance
TPR = _L _ for sum of all blood vessels
r
4
(Poiseuilles equation)
Where r = radius of blood vessel
L = length of blood vessel
= viscosity of blood (function of
hematocrit) hematocrit =
Therefore: change in blood vessel radius has
greatest effect on TPR
Note: 70% of TPR produced/controlled by
arterioles target of drug treatment
Relationship between blood flow
and radius of a blood vessel
0.5
0.063
Relationship between blood pressure,
velocity and total area of vasculature
Humeral Regulation of Blood Pressure:
Renin-Angiotensin-Aldosterone System
Renin: secreted by the kidney in response to reduced blood pressure
or blood volume
Angiotensin: Renin converts Angiotensinogen Angiotensin I
Angiotensin Converting-Enzyme (ACE): converts Angiotensin I
Angiotensin II in lung
Angiotensin II:
Actions:
Intense vasoconstriction increase TPR
Causes release of Aldosterone from adrenal gland promotes Na+ and
water reabsorption in kidney cause increased blood volume.
Regulatory negative feedback on the release of Renin.
CNS: Stimulate thirst in hypothalamus, stimulate sympathetic outflow.
- All above designed to bring arterial blood pressure
back up to normal set-point
Autonomic regulation
of the vasculature
Increased sympathetic activity
reduction in blood vessel opening
(caliber) increase in vascular
resistance etc. etc increase
blood pressure
Stop talking now and
let them go!
Im outta
here!