The document discusses regional circulations, focusing on coronary, cerebral, and cutaneous circulation. It provides details on the anatomy, blood supply, regulation, and clinical implications of each circulation. For coronary circulation, it describes the blood vessels that supply the heart muscle and how blood flow is regulated to meet myocardial oxygen demands. For cerebral circulation, it outlines the unique anatomical features of the brain's blood supply and factors that control blood flow. For cutaneous circulation, it explains the role of arteriovenous anastomoses and arterioles in regulating heat transfer and sympathetic nervous system control of cutaneous blood flow.
4. Coronary blood vessels
Heart receives blood supply from two coronary
arteries
– Left coronary artery
Anterior descending branch
Circumflex branch
– Right coronary artery
Dominance
– Right in 50%
– Left in 20%
– Equal in 30%
5. Coronary circulation
4% of Cardiac Output
high resting blood flow of 70-80 ml/min/100g
– At maximal cardiac work: 300-400 ml/min/100 g
Has a high capillary density (3000-5000 mm2, about
one capillary per myocyte)
large surface area
short diffusion distances (≤9µm)
6. Coronary blood flow
Coronary blood flow occurs
during diastole
Why
– During systole, contraction of
heart musculature squeezes
the coronary vessels
– This effect is more in deeper
layers (subendocardial vessels)
than superficial layers
(epicardial vessels)
– This effect is maximal in the
left ventricle
7.
8. Coronary circulation
myocardial blood flow is characterized by
almost complete oxygen extraction (70-80%)
from the blood across the coronary capillaries
therefore, blood flow must increase to increase
oxygen delivery to the heart
myocardial oxygen delivery is FLOW LIMITED
aortic pressure provides driving force for
coronary blood flow
10. Metabolic (Functional) Hyperemia
primary determinant of coronary blood flow is
myocardial oxygen consumption
– which is dependent on metabolic activity
myocardial oxygen consumption is influenced by
– cardiac pressure development
– wall tension
– heart rate
– cardiac output
– inotropic state
– Afterload
– preload
11.
12. Mechanism
The exact means by which increased oxygen
consumption causes coronary circulation not known
Possible mechanism
– Hypoxia -> vasodilator substances to be released from
cardiac muscle cells
– Adenosine is the main vasodilator substance
– adenosine produced in myocytes from the metabolism of
ATP
– stimulates nitric oxide release from endothelium
– nitric oxide is a potent vasodilator
13. Other factors
K+ ions
H+ ions
CO2
Bradykinin
Prostaglandins
Lactate
14. Reactive hyperemia
brief occlusion of coronary vessel is followed by
a transient increase in coronary blood flow
occlusion results in the accumulation of
vasodilator metabolites in the interstitium
magnitude and duration of extra flow
dependent on the duration of the occlusion
15.
16. Autoregulation
blood flow is relatively constant at perfusion
pressures from 60 mmHg → 150 mmHg
metabolic and myogenic mechanisms involved
curve resets upward at elevated O2 such as
during exercise
autoregulatory capacity is important in
maintaining coronary flow when vessels are
partially obstructed
DR. RAJNEE
18. Neural control
sympathetic vasoconstrictor fibers - tonic
activity
– direct effect of SNS stimulation is vasoconstriction
via α1-adrenergic receptors
– net effect of sympathetic stimulation of the heart is
to increase coronary blood flow due to increase in
the production of metabolic vasodilators with
increased oxygen consumption
DR. RAJNEE
19. Neural control
parasympathetic cholinergic fibers
– → direct effect to vasodilate coronary resistance
vessels via endothelial release of NO
– net effect of parasympathetic stimulation of the
heart may actually be reduced coronary blood flow
resulting from decreased heart rate and oxygen
consumption
DR. RAJNEE
20. When the systemic BP falls
The overall effect of increase in noradrenergic
discharge is increased coronary blood flow due
to
– Metabolic changes
– On the contrary cutaneous, renal and splanchnic
vessels are constricted
– Protecting the heart
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22. Clinical conditions
CAD (Coronary artery disease)
– Coronary artery disease (CAD) (or atherosclerotic
heart disease) is the end result of the accumulation
of atheromatous plaques within the walls of the
coronary arteries that supply the myocardium
– Is the leading cause of death worldwide
WHO Data
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24. Clinical conditions
CAD causes
– Angina pectoris, commonly
known as angina
is severe chest pain due to
ischemia (a lack of blood and
hence oxygen supply) of the
heart muscle, generally due to
obstruction of the coronary
arteries
– Myocardial infarction (MI)
commonly known as a heart
attack
is the interruption of blood
supply to part of the heart,
causing some heart cells to die
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26. General Characteristics
brain least tolerant of organs to ischemia
-↓blood flow for 5 seconds →loss of
consciousness
-↓blood flow for a few minutes →irreversible
damage
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27. Anatomical details
Two internal carotids
Two vertebral arteries
– Basilar artery
Circle of Willis
No crossing over from R to L (because of equal
pressure)
Occlusion of vessel produces ischaemia and
infarction
DR. RAJNEE
28. General Characteristics
Rest: blood flow
– of 50-60 ml/min/100 g (750 ml/min)
(in contrast Coronary: 70-80 ml/min/100g; 250ml/min)
15% of cardiac output
– (in contrast Coronary: 4% of CO)
Exercise: blood flow of 750 ml/min
greatest flow goes to grey matter (100
ml/min/100 g)
35% O2 extraction at rest
DR. RAJNEE
29. Notable Anatomic Characteristics
circulation is enclosed in a rigid skull →
constant volume
brain tissue is incompressible
brain “floats” in a water bath of cerebrospinal
fluid
high capillary density (3000 - 4000/mm2)
→large surface area, short diffusion distances
blood-brain barrier - tight junctions between
endothelial cells →prevents circulating
vasoactive substances from affecting cerebral
blood flow
DR. RAJNEE
31. Normal Flow
Constant cerebral blood flow is maintained
under varying conditions
Factors affecting the total cerebral blood flow
– Arterial pressure at brain level
– Venous pressure at brain level
– The intracranial pressure
– The viscosity of blood
– The degree of active contraction/dilatation of
cerebral arterioles
This is controlled by local vasodilator metabolites
DR. RAJNEE
32. Role of intracranial pressure
Since the brain is enclosed within the skull the volume
of blood, brain and CSF should remain constant
(Monro-Kellie hypothesis)
ICP is normally 0-10 mmHg
Whenever ICP increases, cerebral vessels are
compressed
Change in venous pressure cause a similar change in
ICP
Rise in venous pressure decreases CBF by
compressing the vessels thereby decreasing perfusion
pressure
DR. RAJNEE
33. Autoregulation
pronounced autoregulatory capacity from 50 -
170 mmHg
both myogenic and metabolic mechanisms
involved
sympathetic nervous system activity can shift
the curve to the right
DR. RAJNEE
37. Arterial pH (acidosis)
– has little effect
– H+ does not cross the BBB
Arterial PO2 (normal, 80-100 mmHg)
– diffuses easily from blood to cerebral ECF
– hypoxia (PO2<40-50 mmHg) →dilatation
– PO2 > 100 mmHg →little effect
– dilatation adenosine mediated (?)
DR. RAJNEE
38. Neural control
Sympathetic nervous system
– rich innervation from superior cervical ganglion
– maximum sympathetic nervous system activity
causes only small vasoconstrictor response
– baroreceptor reflexes have little influence on
cerebral blood flow
– ↑sympathetic nervous system activity may prevent
hyperperfusion during acute ↑ in MAP
DR. RAJNEE
39. Neural control
Parasympathetic nervous system
– innervation via facial and superficial petrosal nerves
– stimulation of nerves cause vasodilatation (ACh stimulates
NO release)
– cut nerves → no effect
– physiological importance is unknown
Other
– ↑nerve activity → ↑NO release → local vasodilatation
– Perivascular neurons also contain 5HT (serotonin) a
powerful vasoconstrictor - may cause vasospasm
eg. in migraine
DR. RAJNEE
40. Metabolic
Potassium
– ↑K+ (i.e., seizures, hypoxia) → vasodilatation
– ↑K+ → stimulation of Na+/K+ATPase → hyperpolarize membrane
– stable concentration in autoregulatory range
Adenosine
– ↑ interstitial adenosine concentration with hypoxia, ischemia, ↓ perfusion
pressure, ↑metabolic activity, ↓supply/demand
– vasodilatation occurs
Nitric Oxide
– NO synthase active under basal conditions
– tonic vasodilator effect
– glial-derived (astrocytes) - NOS stimulated by NE, bradykinin, glutamate
→ Role?
DR. RAJNEE
41. Central Nervous System Ischemic
Response
When the blood flow to the brain has been sufficiently
interrupted to cause ischemia of the vasomotor center
these vasomotor neurons become strongly excited
causing massive vasoconstriction as a means of
raising the blood pressure to levels as high as the
heart can pump against
This response can raise the blood pressure to levels as
high as 270 mm Hg for as long as 10 minutes
DR. RAJNEE
42. Central Nervous System Ischemic
Response
This response is a last ditch stand to preserve the
blood flow to vital brain centers
it does not become activated until blood pressure has
fallen to at least 60 mm Hg, and it is most effective in
the range of 15 to 20 mm Hg
If the cerebral circulation is not reestablished within 3
to 10 minutes, the neurons of the vasomotor center
cease to function
↑sympathetic nervous system vasoconstrictor activity
to systemic resistance vessels →↑TPR → ↑MAP → ↑∆P
→ ↑cerebral blood flow
DR. RAJNEE
43. Cushing’s Reflex
The Cushing reflex is a special type of CNS reflex resulting from
an increase in intracranial pressure
space-occupying lesion (i.e., tumor, hemorrhage) will ↑ICP
forces brainstem down into the foramen magnum
brainstem becomes compressed → ischemia
↑sympathetic nervous system vasomotor drive to systemic
resistance vessels → vasoconstriction →↑TPR →↑MAP →↑∆P →
↑cerebral blood flow
baroreceptor-mediated reflex bradycardia
Main features: hypertension, bradycardia, respiratory
depression
The Cushing reflex is usually seen in the terminal stages of
acute head injury
DR. RAJNEE
47. Stroke
rapidly developing loss of brain function due to
disturbance in the blood supply to the brain,
caused by a blocked or burst blood vessel
This can be due to ischemia caused by
thrombosis or embolism
or due to a hemorrhage
DR. RAJNEE
50. CUTANEOUS CIRCULATION
primary role is regulation of internal
temperature
protection against the environment
blood pressure control
6% of the CO at rest (10-20 ml/min/100g)→
↓50% to retain heat, ↑7-fold to lose heat
DR. RAJNEE
52. Arteriovenous anastomoses
coiled, thick-walled vessels
direct connections between dermal arterioles and veins
provide low resistance shunt pathways → feed dermal venous
plexus
little basal tone (myogenic)
little metabolic control - no autoregulation or reactive
hyperemia
sympathetic nervous system vasoconstrictor innervation has
almost exclusive control
→tonic activity
located in “acral skin”: areas of high SA/vol. - fingers, toes,
palms, soles, lips, nose, ears
passive vasodilation due to ↓sympathetic nervous system
activity
DR. RAJNEE
53. Arterioles
located in non-acral skin - limbs, trunk, scalp
high density of α-adrenergic receptors
lack of β2-adrenergic receptors
sympathetic nervous system vasoconstrictor
innervation - little activity at normal core temperature
sympathetic nervous system cholinergic (vasodilator)
innervation is prominent to sweat glands →
BRADYKININ
bradykinin mediates “active” vasodilation
arterioles exhibit autoregulation, reactive hyperemia
and basal tone (myogenic)
DR. RAJNEE
54. Venous Plexus
contains greatest cutaneous blood volume -
acts as a reservoir
important for heat transfer
sympathetic nervous system vasoconstrictor
innervation
DR. RAJNEE
55. Control of Cutaneous Blood Flow
Sympathetic Nervous System
– to conserve heat SNS activity increases causing
vasoconstriction and reducing heat transfer to the
environment
– to lose heat SNS activity is reduced causing
vasodilation and enhanced heat transfer to the
environment
DR. RAJNEE
56. Local Skin Reflexes
local warming will produce local vasodilation
and sweating
local cooling will produce local vasoconstriction
due to increased affinity of α2-adrenergic
receptors for norepinephrine
intensity controlled by central brain
temperature centers
cutting spinal cord results in extremely poor
temperature regulation
DR. RAJNEE
58. Cold-Induced Vasodilation
– when temperature falls, smooth muscle becomes
paralyzed and vasodilatation occurs
Physical compression (e.g. sitting)
– ischemia →accumulation of metabolites →
stimulates nociceptors → pain → shift weight
– → reactive hyperemia (substance P/CGRP?)
DR. RAJNEE
59. Hormones
– epinephrine → constriction
– angiotensin II → constriction
– vasopressin → constriction
Role in Blood Pressure Control
– Hypotension → ↑sympathetic nervous system →AVA,
arteriole and venous constriction
– → ↑TPR and mobilization of blood to support venous
pressure
– During exercise enhanced blood flow to the cutaneous
circulation is necessary for
– dissipating heat → reduces venous return to the heart →
arterial pressure falls
DR. RAJNEE
60. White reaction
When a pointed object is drawn across the skin
Stroke lines becomes pale
Called white reaction
Due to mechanical stimulus initiating
precapillary sphincter contraction
DR. RAJNEE
61. Triple response
When the skin is stroked more strongly
Triple response
– 1. Red reaction
Capillary dilatation
– 2. Wheal (swelling)
Increased capillary permeability
– 3. Flare (redness spreading out from injury)
Arteriolar dilatation
Due to axon reflex
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62. Axon reflex
A response in which impulses initiated in
sensory nerves by the injury are relayed
antidromically down other branches of the
sensory nerve fibres
Skin
Arteriole
DR. RAJNEE
65. enormous range of blood flow in skeletal
muscle: 3.0 ml/min/100 g at rest (20% of CO)
exercise: 100 ml/min/100g (80-85% of CO)
resistance vessels have high resting tone
(myogenic)
DR. RAJNEE
66. Regulation of Skeletal Muscle Blood
Flow
Neural
– neural control dominates at rest
– tonic sympathetic nervous system vasoconstrictor
activity (1 Hz) - α1-adrenergic receptor mediated
– an increase in sympathetic nervous system activity
(4-5 Hz) can decrease flow by 70%
– vasodilatation at rest is passive due to withdrawal
of sympathetic nervous system activity
– sympathetic-cholinergic fibers are anatomically
present - physiological role is uncertain
DR. RAJNEE
68. Hormonal
– circulating epinephrine vasodilates at low
concentration (β2-adrenergic receptor),
– constricts at high concentration (α1/α2-adrenergic
receptors)
– vasopressin → constricts
– angiotensin II → constricts
DR. RAJNEE
69. Metabolism (functional hyperemia)
with increased activity there is an increase in
the production of vasodilator metabolites
vasodilator metabolites are dominant during
exercise although sympathetic nervous system
activity to the working muscle is also enhanced
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71. Physical Factors
cyclical contraction and relaxation of active
skeletal muscle vessels
vessels are compressed during the contraction
phase → blood flow becomes intermittent
muscle perfusion is enhanced by the muscle
pump
during activity muscle pump lowers the venous
pressure which increases the pressure gradient
driving flow
DR. RAJNEE
73. Autoregulation
– blood flow is relatively constant from 60 → 120
mmHg (mainly myogenic)
Reactive Hyperemia
– brief occlusion of blood flow is followed by a
transient increase in flow
74. Role of Skeletal Muscle Circulation in Blood
Pressure Control
– large mass of tissue: 40 - 45% of body weight
– major site of resistance vessels
– Peripheral resistance regulated by controlling
muscle resistance
– resistance influenced by
tonic vasoconstrictor activity
metabolic vasodilators
regulation by reflex mechanisms (baroreceptors,
cardiopulmonary receptors, etc.)
76. blood flow 25% of resting CO - can increase by
30 -100% after a meal
blood flow is closely coupled to absorption of
water, electrolytes and nutrients
Series/parallel configuration: the venous
drainage from the capillary bed of the
gastrointestinal tract, spleen and pancreas
flows into the portal vein, which provides most
of the blood flow to the hepatic circulation
77.
78. the hepatic artery provides the remainder of
the blood flow into the liver
high compliance venous system (25
ml/mmHg/kg) → acts as a reservoir (especially
the liver)
contains 20% of the blood volume at rest
DR. RAJNEE
79. Neural
Sympathetic nervous system
– innervation of arterioles, precapillary sphincters and
venous capacitance vessels
– little or no basal sympathetic nervous system tone
– ↑sympathetic nervous system activity → strong
vaso- and venoconstriction →
– redistributes BF, and increases functional circulating
blood volume (“mobilization”)
80. Parasympathetic nervous system
no innervation of blood vessels
↑activity → ↑motility, ↑metabolism→
functional hyperemia due to local vasodilator
metabolites (NO?)
DR. RAJNEE
83. Autoregulation
– poorly developed → metabolic mechanism
dominates
Autoregulatory escape
– ↑sympathetic nervous system activity → transient ↓
in BF
– after 2 -4 minutes blood flow returns towards
normal due to accumulation of metabolites
(adenosine) and vasodilation of arterioles
– veins remain constricted
DR. RAJNEE
84. Role in Blood Pressure Control
Hypotension
– vasoconstriction due to ↑sympathetic nervous
system, AII and VP→ ↑TPR
– venoconstriction →displaces blood centrally →
↑CVP → ↑SV
87. Renal circulation
At rest 25% CO, 1.2-1.3 l/min
Pressure drop across the glomerulus is only 1-3 mmHg
Further drop at the efferent arteriole
Regulation
– Norepinephrine, Angiotensin II - vasoconstriction
– Dopamine – vasodilatation
– Sympathetic activity (alpha receptor) – vasoconstriction
– Stimulation of renal nerves - increases renin secretion
Autoregulation is present
– Myogenic effect, NO may be involved
Renal cortex high blood flow poor O2 extraction but in medulla
low blood flow but high O2 extraction