Blood Vessels:

3 major types of blood vessels are arteries, capillaries and veins.

arteries, arterioles, capillaries, venules and veins (order)
vaso vasorum: blood vessels within blood vessels
Walls of blood vessels have 3 distinct layers/ tunics "coverings"
surround a central blood-containing space= vessel lumen
Innermost tunic: tunica intima
contains/composed of endothelium (simple squamous epithelium)
endothelium is continuous with endocardial lining of the heart, and its flat
cells fit closely together, forming a slick surface that minimized friction as
blood moves through the lumen.
basement membrane: internal elastic membrane
Middle tunic: tunica media
circularly arranged smooth muscle cells (effectors) and sheets of elastic
fibers
smooth muscle is regulated by vasomotor nerve fibers of ANS and
chemicals
innervations is only through this layer for vasoconstriction (reduction in
lumen diameter as smooth muscle contracts) or vasodilation ( increase in
lumen diameter as smooth muscle relaxes.
thickest layer in the arteries
Outermost layer: tunica externa/adventitia
composed largely of loosely woven collagen fibers that protect and
reinforce vessel, and anchor it to surrounding structures.
innervated with nerve fibers, lymphatic vessels, elastic fibers.
larger vessels contain smaller vessels called vasa vasorum: nourish more
external tissues of blood vessel wall.
Arteries: carry blood away from the heart (not always oxygenated)
categorized into three groups: elastic arteries, muscular arteries, and
arterioles
2 major properties: elasticity and contractibility (especially middle layer)
expand with ventricular systole and recoil with ventricular diastole.
Allows for even (equalized) pressure and flow
Elastic (conducting) Arteries
thick-walled arteries near the heart
largest in diameter and most elastic (elastin present in all 3 layers)

large lumens make them low-resistance pathways that conduct blood

from heart to medium-sized arteries they are referred to as conducting
arteries.
pressure reservoirs, expanding and recoiling as blood is ejected from the
heart
they have elastic lamina (extra layer of elastic tissue) for extra support
because there is a greater pressure in these vessels.

Muscular (Distributing) Arteries

deliver blood to specific body organs
diameter (1cm) to (0.3mm). medium-sized vessels
have the thickest tunica media of all vessels
contain more smooth muscle and less elastic tissue than elastic arteries
more active in vasoconstriction and vasodilatation and less distensible
Arterioles:
smallest of the arteries, diameter (0.3mm) to (10um)
delivers blood to capillaries
larger arterioles have all three tunics (chiefly smooth muscle with few
elastic fibers scattered)
smaller arterioles lead to capillary beds and are single layer of smooth
muscle cells around endothelial lining
when arterioles constrict, tissues served are largely bypassed
where arterioles dilate, blood flow into local capillaries increases
dramatically
arterial pulse: the alternating expansion and elastic recoil with each
systole of the left ventricle
Capillaries:
smallest blood vessels
only contain tunica intima
one endothelial cell forms the entire circumference of the capillary wall
pericytes: smooth muscle-like cells that stabilize the capillary wall and help
control capillary permeability
allow exchange of nutrients, gases, hormones and waste products between the
blood and tissues/interstitial fluid
connects arterioles to venules
found near every cell in the body
Structurally there are 3 types of capillaries: continuous, fenestrated, sinusoidal
Continuous capillaries:
abundant in skin and muscles

continuous in the sense that their endothelial cells provide uninterrupted

lining
adjacent cells being joined laterally by tight junctions
intercellular clefts: gaps of unjoined membrane; allow passage of fluids
and solutes

Fenestrated capillaries:
endothelial cells are riddled with oval pores, or fenestrations; pores are
covered with membrane but still more permeable
found wherever capillary absorption or filtration occurs: small intestine
and endocrine organs and glomerular capillaries in kidneys.
Sinusoids:
highly modified, leaky capillaries found only in the liver, bone marrow,
spleen, and adrenal medulla.
have large, irregularly shaped lumens and are usually fenestrated.
endothelial lining has fewer tight junctions and larger intercellular clefts
than ordinary capillaries
allow large molecules and even blood cells to pass between blood and
surrounding tissues
in the liver endothelium is discontinuous and lined with hepatic
macrophages (Kupffer cells), which remove and destroy and bacteria.
very torturous (bend a lot), lead to very slow sluggish blood flow, allowing
time for its clean up or modified
Capillary Beds:
interweaving networks that function along with capillaries
microcirculation: flow of blood from an arteriole to a venule
consists of two types of vessels:
1. a vascular shunt: capillaries between arterioles and venules;
called metarteriole ( vessel structurally intermediate between an
arteriole and a capillary; continuous with thoroughfare
channels
(intermediate between a capillary and a venule)
which joins with
postcapillary venule that drains the bed.

to

2. true capillaries: actual exchange vessels; extensions of vascular

shunts
increase surface are for exchange (10-100 per/bed depending on
type of tissue)
precapillary sphincter: smooth muscle valve that surrounds the
root of each capillary at the metarteriole and acts as a valve
regulate blood flow into the capillary

Veins: carry blood toward the heart

Venules:
formed when capillaries unite; combine into the thoroughfare channel that
becomes a venule
post-capillary venules: smallest venules consist entirely of endothelium
around which pericytes congregate (gather into crowds)
fluid and WBC move easily from bloodstream through the walls
only tunica intima and externa are seen in post-capillary venules (scanty
tunica media)
Veins:
venules join to form veins
also have 3 tunics but their walls are thinner and lumens larger than
arteries (usually collapsed and lumens appear slit like)
contain a lot less elastic tissue and smooth muscle (more CT than muscle,
but still remain distensible)
venae cavae returns blood directly to the heart-tunica externa is further
thickened by longitudinal bands of smooth muscle
can accommodate large blood volume due to large lumen and thin walls
sometimes called capacitance vessels and blood reservoirs because up to
65% of blood supply is found in the veins at any time
contain Venous valves (infoldings of tunica intima) to help prevent
backflow
venous valves are most abundant in veins of the limbs where upward flow
of blood is opposed by gravity thus blood pressure pushing blood up to the
extremities needs to be greater than that of gravity
venous sinuses:
veins with only endothelium and no smooth muscle or CT layers
supported by structures around them (coronary sinus & dural sinus)
vascular anastomoses: most organs receive blood from more than one arterial branch
arterial anastomoses: arteries that supply the same territory that merge; provide alternate
pathways called collateral channels, for blood to reach a body region.
artery to artery: arterial anastomosis
artery to vein (arterioles to venues): arteriovenous anastomosis
vein to vein: venous anastomosis (most common)
Skeletal muscle pump: combination of skeletal muscle contractions (milking) and valves
(stop backflow) aid in venous return
Respiratory Pump: during inspiration the diaphragm moves downward causing decrease
in pressure in the chest cavity and increase pressure in abdominal cavity (squeezes/moves
blood from abdominal veins to the thoracic veins)

Blood Flow: volume of blood flowing through a vessel, an organ, or the entire circulation
in a given period (ml/min).
may vary (different pressures) widely through individual organs of the system,
within a given period of time
due to gradient set up by the entering blood (always moves from higher to lower
pressure)
under resting condition it is equal to cardiac output
Blood Pressure (Systemic arterial blood pressure)
pressure exerted by the blood onto the walls of the blood vessels
measure in millimeters of mercury; this pressure causes blood flow
Resistance: opposition to flow and is a measure of the amount of friction blood
encounters as it passes through the vessels.
most friction is encountered in the peripheral (systemic) circulation; thus usually
referred to as peripheral resistance.
three important sources of resistance: blood viscosity, vessel length, and vessel
diameter.
1) Blood viscosity (constant): internal resistance to flow that exists in all fluids
thickness or stickiness of a fluid
the greater the viscosity, the less easily molecules slide past one another and more
difficult it is to get and keep the fluid moving
2) Total blood vessel length (constant): the relationship between total blood vessel
length and resistance is straightforward: the longer the vessel, the greater the resistance.
3) Blood vessel diameter (frequent changes):
Blood flow is proportional to the difference in blood pressure, and inversely proportional
to the resistance. Therefore, increase in lumen size leads to increase in blood flow and
decrease in resistance.
Systemic Blood Pressure:
Systolic arterial BP: When blood flows from left ventricle into aorta, the aortic pressure
is at its highest (120 mmHg) which will push the blood all the way back to right ventricle.

diastolic pressure: when the aortic pressure is lowest (70-80mmHg)

medial arterial pressure(MAP)- the pressure that propels the blood to the tissues.
diastolic pressure plus 1/3 of the pulse pressure; since diastole is longer than systole.
pulse pressure: difference between the systolic and diastolic pressures is called pulse
pressure.
Factors affecting blood pressure: cardiac output, peripheral resistance, and blood
volume
cardiac output: amount of blood ejected by the left ventricle into the aorta each minute.
the principle determinant of blood pressure: CO=SV X HR
if CO increases (by SV or HR) it will lead to an increase in blood pressure
peripheral resistance: impedance of blood flow by vessel wall (arterioles)
function of the arterioles is to also control peripheral resistance and, in turn, blood
pressure by changing diameter (vasoconstriction/ vasodilation)
blood volume (5 liters): Usually constant, but may decrease with hemorrhage, extreme
dehydration, increase in salts, fluid retention, increase in fluid loss
Regulation of Blood Pressure
Any increase in heart rate and force of contraction increases blood pressure and vice
versa
Nervous system controls: short term controls
maintains systemic blood pressure, and alters distribution of blood to specific
body parts for specific functions and alterations
sympathetic response: reflex arcs- pressure R/C-> afferent fibers-> vasomotor
center of the medulla-> vasomotor fibers to vascular smooth muscle
vasomotor center: neural center that oversees changes in the diameter of blood
vessels
- sympathetic system only; nuclei in the medulla which function to control the
diameter of BVs (especially arterioles)
- it is continually sending (steady rate) impulses to vessels, keeping them in
moderate vasoconstriction, especially arterioles (called vasotone or vasomotor tone)
Cardiovascular center= vasomotor center + cardiac centers (cac + cic)
increase in impulses increases constriction and decreases in impulses causes
decrease in vasoconstriction/vasodilation
vessels will be as dilated as possible (their natural state) with no sympathetic
impulses going to them
vasomotor fibers: efferent fibers (sympathetic) to smooth muscle of arterioles;
release norepinephrine for vasoconstriction.

baroreceptor-initiated reflexes: neural receptor located in the carotid sinuses

(dilations in the internal carotid arteries, which provide the major blood supply to
the brain), in the aortic arch, and in the walls of nearly every large artery of the
neck and thorax (elastic arteries).
a)- increase BP stimulates both pressure and stretch of baroreceptors, which send
a rapid stream of impulses to vasomotor center to inhibit it's activity, allowing for
vasodilaton of vessels (arterioles and veins) causing a drop in BP
b- they will also:
- stimulate the Cardiac Inhibitory Center (CIC) (parasympathetic)
- inhibit the Cardiac Acceleratory Center (CAC) (sympathetic)
- which will lead to decrease in cardiac output to help decrease BP. This is usually for
short term control only
Chemoreceptor-initiated Reflexes:
located in carotid and aortic bodies
sensitive to arterial oxygen, CO2 and pH falls (increase in H+ level): decrease
O2 (hypoxia), or an increase in H+ and/or CO2 concentration (hypercapnia)
these bodies will send impulses to vasomotor center (increase sympathetic)
this stimulation will enhance vasoconstriction to increase blood pressure
(causing quicker venous return)
very important in regulating respiratory rate and depth; more important for
respiratory rate than BP
higher brain center: cerebral cortex and hypothalamus
cortex:
intense anger: from cortex to VMC causes an increase sympathetic
stimulation (which leads to vasoconstriction and increases in BP)
emotionally upset: depression (long term); from cortex to VMC decreases
sympathetic stimulation (which leads to vasodilation and decreased BP,
may cause fainting)
hypothalamus: causes redistribution of blood flow, due to exercise, body
temperature and fight or flight response.

Adrenal Medulla Hormones - effects are long-lived due to slow degradation (1-3) min
during periods of stress adrenal gland releases norepinephrine and epinephrine to
the blood- both hormones enhance sympathetic fight or flight response.
Target: Vasomotor Center- Effect: increase activity, increase vasoconstriction, increase resistance, increase
BP
Norepinephrine- has vasoconstrictive action
Epinephrine- increases cardiac output and promotes generalized vasoconstriction
(except in skeletal and cardiac muscle, where it causes vasodilation)
Heart= B1 receptors; arterioles, veins= alpha receptors
Target: Blood vessels (arterioles and vein (alpha r/c))
- Effects: both increase vasoconstriction
Target: CAC (epinephrine)
- Effects: in. HR and strength of contraction -> in. CO -> in. BP
Atrial Natriuretic Peptide
atria produces atrial natriuretic peptide (ANP)- due to overstretching and
increased blood volume- causes blood volume and BP to decline
Prods the kidneys to excrete more sodium and water from the body- causing
blood volume to drop
Target: Kidneys (afferent arterioles going into the glomerulus's -> in. GFR)
Effects: generalized vasodilatation-> in. filtration-> in. urine production -> dec.
blood volume -> dec. BP
Target: Hypothalamus (posterior pituitary)
Effects: dec. antidiuretic hormone secretion -> in. urine prod. -> dec. BV -> dec.
BP
Target: adrenal cortex
- Effects: dec. aldosterone release (reabsorbs Na+ at kidneys) -> dec. BV -> dec.
BP
Target: Kidneys
Effects: 1) dec. Na+ reabsorption by the collecting ducts (H2O into the urine out
of the body -> where Na+ goes H2O follows) -> dec. BV -> dec. BP
2) dec. renin (small protein enzyme released by kidneys) -> dec. BV ->
dec. BP
Target: Vessels

Effects: in. vasodilatation -> dec. resistance -> dec. BP

Antidiuretic Hormone (ADH; vasopressin)- produced by the hypothalamus and
released from the posterior pituitary gland
Target: Kidneys
Effects: in. conservation of water (by in. permeability of collecting ducts) -> in.
BV -> in. BP
Target: Arterioles (throughout the body)
Effect: in. ADH release, dec. urine production and output -> in BV -> in. BP
Endothelium-Derived Factors: chemicals released from the endothelium
Endothelin and PDGF (prostaglandin-derived factor)
Target: smooth muscle within the vessel wall
Effect: in. vasoconstriction -> in. resistance -> in. BP
Nitrous oxide (called EDRF- endothelium derived relaxin G factor)
Target: smooth muscle within the vessel wall
Effects: in. vasodilatation -> dec. resistance -> dec. BP
Alcohol
Target: hypothalamus and posterior pituitary
Effect: dec. ADH release -> in. urine production/output -> dec. BV -> dec. BP
Target: Vasomotor center
Effects: dec. sympathetic stimulation -> in. vasodilatation -> dec. resistance ->
dec. BP
Target: Vessels
Effects: in. vasodilatation -> dec. resistance -> dec. BP
Aldosterone:
released as a result of in. K+;
angiotensin II and III;
and with a dec. Na+ blood levels;
inhibited by ANP
Target: kidneys (afferent arterioles going into the glomerulus - dec. GFR)
Effects: in. vasoconstriction -> dec. filtration -> dec. urine production -> in. BV
-> in. BP
Target: hypothalamus (posterior pituitary)
Effects: in. antidiuretic hormone secretion -> dec. urine production -> in. BV ->
in. BP
Target: kidneys
Effects: 1) in. Na+ reabsorption via the collecting ducts (dec. Na+ into the urine
-> out o the body, -> in. BV -> in. BP

2) in. renin ( a small protein enzyme released by the kidneys) -> in.
aldosterone -> in. BV -> in. BP

Target: vessels
Effects: in. vasoconstriction -> in. resistance -> in. BP

renal regulation (kidneys) :

direct: either increase or decrease urine production and release to increase or
decrease BV and BP
indirect: renin-angiotensin mechanism (major regulator)
Juxtaglomerular Apparatus (JGA): is located in the final portion of the
ascending loop of Henle, it helps regulate osmotic renal blood pressure
contains two portions- macula densa and juxtaglomerualar cells
macula densa: cells of distal tubules narrowed, have been modified for chemical
or osmotic sensation ( inc. or dec. of solute concentration of filtrate)
juxtaglomerular cells: smooth muscle cells of the afferent arterioles are
modified, 1) they enlarge, 2) their nuclei becomes round, and 3) they have
cytoplasm granules that produce and store prorenin (renin)
These cells sense blood pressure changes, more significantly if there is a dec. in
BP
With dec. systemic BP, the kidneys release renin which activates angiotensinogen
to angiotensin I (weak vasoconstrictor), which is converted in the lungs to
angiotensin II by angiotensin converting enzyme (powerful vasonstrictor)
also stimulates the adrenal cortex to release aldosterone, causing the kidneys to in.
reabsorption of Na+ and water
Angiotensin:
Target: adrenal cortex
Effect: in. aldosterone release -> (reabsorbs Na+ at the kidneys) -> in. BV -> in.
BP
Target: vasomotor center (VMC)
Effects: in. sympathetic stimulation -> dec. vasodilator/in. vasoconstriction -> in.
resistance -> in. BP
Target: cardiac center
Effect: in. CAC and dec. CIC -> in. CO -> in. BP
Hepatic Portal System:
Runs from digestive tract, pancreas, spleen to the liver.
Substances that have been absorbed will be stored, metabolized, detoxified
after blood has been filtered through the liver, it enters the hepatic vein, exists the
liver, and enters the inferior venae cavae.
small veins of the digestive tract, pancreas, and spleen form the three large veins;
inferior and superior mesenteric veins and the splenic vein. All join to form the
hepatic portal vein.
Fetal Circulation:

fetus receives nutrients and oxygen from and eliminates carbon dioxide and
wasters into maternal blood via placenta (attaches to umbilicus) and umbilical
cord, made up of one vein and two arteries
placenta is formed by embryonic (trophoblasts) and maternal endometrial
tissue; fetal portion of placenta is called "chorion", maternal portion is called
decidua basalis
umbilical cord contains blood vessels that form capillary beds in the placenta.
Waste from fetal blood diffuses out of the capillaries into maternal blood in
lacuna (intervillous space) in the placenta and then into mother's uterine veins.
Nutrients follow opposite flow (maternal arteries -> intervillous space -> fetal
capillaries)
blood passes from fetal circulation to placenta via two umbilical arteries
(deoxygenated blood), which are branches of the internal iliac arteries.
From the placenta there's a single umbilical vein (oxygenated blood) to the liver
of the fetus where it bifurcates.
One branch enters the liver and joins the hepatic portal vein;
the other branch is called the ductus venosus (bypasses the liver) and joins the
IVC.
Blood from the lower extremities (deoxygenated) is mixed with oxygenated blood
from the ductus venosus in the IVC.
Blood flows into right atria and through the foramen ovale (in inter-atrial
septum) into left atria into systemic circulation.
Any blood entering right ventricle is pumped into pulmonary trunk and sent
through arteriosus (a shunt from pulmonary trunk to aorta).
From aorta down to common iliac art. -> internal iliac artery -> umbilical arteries
-> placenta

Post-Partum
Umbilical arteries become medial umbilical ligaments
Umbilical veins become round ligament of the liver
placenta delivered by mother as afterbirth
ductus venosus becomes ligamentum venosus (fibrous cord in liver)
forament ovale closes and becomes fossa ovalis
ductus arteriosus closes, atrophies, and becomes ligamentum arterosum
Cerebral System:
total cerebral blood flow is very constant despite broad range of arterial pressure.
Interference can lead to fainting or stroke
aorta -> brachicephalic artery -> right common carotid artery -> bifurcates into
right external and internal carotid artery and those in turn become right anterior
and middle cerebral arteries.
On the left side the common carotid artery branches directly from the aorta, then
follows the same branching pattern. These vessels supply middle and anterior
brain bilaterally.

right and left subclavian arteries will branch into right and left vertebral arteries
respectfully. They will unite at the base of the brain and become the basilar artery,
which, in turn, bifurcates and become left and right posterior cerebral arteries
the Circle of Willis: posterior communicating arteries connect posterior cerebral
arteries to middle cerebral arteries. Anterior communicating arteries connect both
the anterior cerebral arteries to complete the circle. Encircling the pituitary gland,
it allows an alternative route in case of an occlusion of the internal carotid or
vertebral arteries.

Normal BP
systolic between 110-140
diastolic between 75-80
hypotension- low blood pressure
systolic less than 100 mm Hg
orthostatic hypotension (malfunctioning carotid sinus reflex): light headedness,
slight disorientation, dizziness with postural changes. When standing up
hypertension- high blood pressure
140/90 mm Hg is baseline
160/95 mm Hg is dangerous
primary hypertension (essential hypertension)
- seen in 85-90% of affected people.
- cannot be attributed to any particular organic cause
secondary hypertension
- seen in 10-15% of affected people
- due to identifiable cause, such as atherosclerosis, kidney disease or adrenal
cortex, and hypersecretion
- it can ulimately damage the brain, heart and kidneys.
- common in overweight and obese people due to an increase in vessel length,
loads to an increase peripheral resistance
Primary Hypertension
Causative theories:
smooth muscle cells retain Na+ and water and swell; this decreases lumen
diameter resulting in an increase in peripheral resistance and BP
early kidney disease, undetectable clinically resulting in a slight decrease in the
rate of fluid excretion. This increases volume and BP
minor arterisclerotic changes decrease the sensitivity of baroreceptors; theydon't
respond normally to unusual fluctuations of pressure
emotional stress- through the vasomotor center of the medulla impulses are sent
out causing vasoconstriction of arterioles; increase in PR and BP

in some individuals, essential hypertension can progress to malignant

hypertension, with death resulting within 2 years without treatment

Secondary (nonessential) hypertension

hypertension that develops as a consequence of a disease state already present in
the cardiovascular nervous, endocrine, or excretory systems
Cardiovascular Hypertension: arteriosclerosis, decrease in elasticity of vessels,
inability to distend. In. PR and BP
Renal Hypertension: kidney disease that dec. GFR, thus increasing renin,
increaseing vasoconstriction -> in. PR and BP; or, renin causes increase of
angiotensin II, increasing aldosterone, thus increasing volume and BP
Endocrine: pheochromocytoma is a benign tumor of the adrenal medulla gland.
The tumor releases epinephrine and norepinephrine. In. E, NE causes in. HR and
in in force of contraction -> in. BP
Neurogenic Hypertension: due to nervous system damage or malfunction such as
cerebral ischemia, cerebral hemorrhage, tumor or never injury that would prevent
autonomic reflexes from working, increase sympathetic output -> in. PR and CO
-> in. BP
Effects of hypertension
1) Heart: myocardium is being asked to pump against an in. BP; there are greater oxygen
and nutritional demands by the myocardium
left ventricle hypertrophies (in. mass)
coronary blood supply increase at a slower rate than the muscle mass
the result is decrease in Oxygen supply to myocardium
hypoxia -> ischemia -> angina pectoris -> cardiac arrhythmias, dec. pump
efficiency and in. chance of cardiac failure
increase coronary artery pressure may increase atherosclerosis -> in. PR and dec.
oxygen to myocardium
2) vessels of brain, heart and lung
in. BP may weaken walls
in. rate of sclerosis
in. possibility of rupture such as stroke and hemorrhage
3) Kidney: in. possibility of sclerosis and glomerular changes which in turn increase
chances of failure
Shock or Hypotension (Circular shock)
dec. output or reduced blood volume causing a general hypoxia (dec. O2 and
nutrients); loss of blood leads to increased histamine release. S/S- pale, clammy
skin, cyanosis (ears & fingers), feeble rapid pulse, shallow rapid breathing, dec.
body temp, mental confusion or unconsciousness.
mild shock: vasoconstriction and water retention will compensate

severe shock: dec. venous return to heart will lead to dec. cardiac output; heart
becomes hypoxic. Hypoxia of other tissues due to prolonged vasoconstriction;
shock cycle is intensified (positive feedback)
hypovolemic shock: Simples form; due to increase of blood; as with
hemorrhaging, severe vomiting, diarrhea, burns. S/S- in. HR, intense
vasoconstriction, diverting blood from reservoirs (skin and veins) to stabilize
blood pressure.

A. Definitions:
Shock is a failure of circulation. Blood pressure decreases so low that circulation
is inadequate to meet the nutritional needs of body cells.
the name given the type of shock is based on the factors that lead to its
development
regardless of cause, the pathophysiology of shock is the same; cycle of dec.
venous return and dec. CO

B. Classification of Shock (Types of shock)

1) Hypovolemic Shock:
loss of whole blood -> bleeding from accident, surgery, etc.
loss of plasma -> burns, vomiting, diarrhea, profuse sweating, increased urine
output, any kind of dehydration
plasma shifts to the interstitial space; dec. blood volume
2) Cardiogenic Shock: results from seriously low cardiac output (heat cannot maintain
mean arterial pressure) following
extensive myocardial infarction
heart failure
prolonged cardiac arrhythmia
3) Neurogenic Shock: alteration in the nervous system's control of vasomotor tone ->
vasodilation -> poor venous return -> dec. CO -> dec. BP caysed by
nervous system injury to medulla
low blood sugar (hypoglycemia)
severe pain
drug abuse
4) Vasogenic Shock: cause does not originate in the nervous system (with other factors
affecting blood vessels) resulting in vasodilation and poor venous return
anaphylactic shock: examples- histamine release causes massive vasodilation,
decrease venous return, decrease cardiac output
C. Pathophysiology of Shock - 3 general stages

1. Compensated Shock
Goal: conserve and mobilize existing body fluids to increase and maintain cardiac
output
- Physiological mechanism include:
- baroreceptor reflex
- sympathetic response
- kidney response
- Progressive Shock
- The cause of the shock is not corrected and the compensation mechanism
can no longer maintain mean arterial pressure and cardiac output.
- body tissues are damaged from low blood perfusion; the intense
sympathetic stimulation -> harmful
- increase stimulation, decrease flow -> ischemia
- decrease oxygen, decrease aerobic respiration, and
increase anaerobic respiration with an increase lactic acid formation and increase
CO2 buildup (low blood volume at lung surface); the increase lactic acid and CO2
causes acidosis
decrease O2 and PH stimulates arterioles to vasodilate; this
increases BP in capillary and fluid shifts to the interstitial space; increase VR and
further decrease CO
- normal compensatory mechanisms fail
- Decompensated or Irreversible Shock
- irreversible death is inevitable
- decrease pH (metabolic acidosis); decrease activity of metabolic
energy producing enzymes
- without ATP, decrease muscle (arteriole) contraction, decrease cardiac
strength, decrease CO and toxic materials released from deteriorating tissues. One of
these is myocardial toxic factor released from ischemic pancreatic cells. These factors
depress cardiac function, decrease CO, decrease cerebral circulation and increase
restlessness, convulsions. Coma and death result