Transcript Slide 1
Angiotensinogen (prohormone produced by liver)
Angiotensin I
ACE (angiotensin-converting enzyme in lungs)
Angiotensin II
20-1
Renin (kidney enzyme released by low BP)
very potent vasoconstrictor
Aldosterone ( BP)
promotes Na+ and water retention by kidneys
increases blood volume and pressure
Atrial natriuretic factor ( BP)
generalized vasodilation
ADH ( BP)
Antidiuretic hormone (water retention)
Epinephrine and norepinephrine effects
most blood vessels
binds to -adrenergic receptors, vasoconstriction
skeletal and cardiac muscle blood vessels
binds to -adrenergic receptors, vasodilation
20-2
ACE inhibitors block the conversion of Angiotensin I to
Angiotensin II
(coughing?) (less effective in some people)
Diuretics decrease total blood volume (K sparing or not)
Beta-blockers (or alpha blockers) block the beta
adrenergic receptors
Angiotensin II receptor blockers – ARBS (esp diabetics)
Calcium channel blocker - Cause vasodilation
Nitroglycerin! for emergencies?
Localized vasoconstriction
Arterioles - most control over peripheral resistance
20-4
pressure downstream drops, pressure upstream rises
enables routing blood to different organs as needed
located on proximal side of capillary beds
most numerous
more muscular by diameter
20-5
Arterioles shift blood flow with changing priorities
During exercise
20-6
perfusion of lungs, myocardium and skeletal muscles
perfusion of kidneys and digestive tract
Only occurs across capillary walls between blood
and surrounding tissues
3 routes across endothelial cells
intercellular clefts
fenestrations
through cytoplasm
Mechanisms involved
20-7
diffusion, transcytosis, filtration and reabsorption
Most important mechanism
Lipid soluble substances
Insoluble substances
20-8
steroid hormones, O2 and CO2 diffuse easily
glucose and electrolytes must pass through channels,
fenestrations or intercellular clefts
Large particles - proteins, held back
Pinocytosis - transport vesicles across cell - exocytosis
Important for fatty acids, albumin and some hormones
(insulin)
20-9
Opposing forces
blood (hydrostatic) pressure drives fluid out of capillary
high on arterial end of capillary, low on venous end
colloid osmotic pressure (COP) draws fluid into capillary
results from plasma proteins (albumin)- more in blood
oncotic pressure = net COP (blood COP - tissue COP)
20-10
Hydrostatic pressure is defined as a physical force
exerted against a surface by a liquid. (BP is an
example)
20-11
Capillary filtration at arterial end
Capillary reabsorption at venous end
Variations by location (glomeruli vs. alveolus)
Capillary filtration ( capillary BP or permeability)
poor venous return
congestive heart failure - pulmonary edema
insufficient muscular activity
Capillary reabsorption
20-12
kidney failure (water retention, hypertension)
histamine makes capillaries more permeable
hypoproteinemia (oncotic pressure blood albumin)
cirrhosis, famine, burns, kidney disease
Obstructed lymphatic drainage
Tissue necrosis
Pulmonary edema
headaches, nausea, seizures and coma
Circulatory shock
20-13
suffocation
Cerebral edema
oxygen delivery and waste removal impaired
excess fluid in tissue spaces causes low blood
volume and low BP
Pressure gradient
7-13 mm Hg venous pressure towards heart
venules (12-18 mm Hg) to central venous pressure (~5 mm Hg)
Gravity drains blood from head and neck
Skeletal muscle pump in the limbs
Thoracic pump
inhalation - thoracic cavity expands (pressure )
abdominal pressure , forcing blood upward
central venous pressure fluctuates
2mmHg- inhalation, 6mmHg-exhalation
blood flows faster with inhalation
20-14
Cardiac suction of expanding atrial space
By the time the blood
makes it through the
capillary bed, blood
pressure has dropped to
almost zero.
Blood returns to the heart
through the veins largely
by the action of your
muscles in concert with
the valves in your veins.
Exercise venous return in many ways
heart beats faster, harder
vessels of skeletal muscles, lungs and heart dilate flow
respiratory rate action of thoracic pump
skeletal muscle pump
Venous pooling occurs with inactivity
venous pressure not enough force blood upward
with prolonged standing, cardiac output may be low
enough to cause dizziness or syncope
prevented by tensing leg muscles, activate skeletal m. pump
20-16
jet pilots wear pressure suits
Any state where cardiac output is insufficient
to meet metabolic needs
Cardiogenic shock - inadequate pumping of heart
(MI)
Hypovolemic shock (a form of low venous return shock)
Septic shock
bacterial toxins trigger vasodilation and ↑ capillary
permeability
Anaphylactic shock
20-17
loss of blood volume: trauma, burns, dehydration
severe immune reaction to antigen, histamine release,
generalized vasodilation, ↑ capillary permeability
20-18
Compensated shock – may be manageable
Decompensated shock - bad
20-19
Homeostatic mechanisms bring about recovery
BP triggers baroreflex and production of
angiotensin II, both stimulate vasoconstriction
If person faints and falls to horizontal position,
gravity restores blood flow to brain; quicker if feet
are raised
Life threatening positive feedback loops occur
20-20
cardiac output myocardial ischemia and infarction
cardiac output goes down even more
slow circulation disseminated intravascular coagulation
slow circulation
ischemia and acidosis of brainstem vasomotor tone,
vasodilation caridac output ischemia and acidosis
of brainstem
Total perfusion kept constant
seconds of deprivation causes loss of consciousness
4-5 minutes causes irreversible brain damage
Responds to changes in blood pressure and chemistry
cerebral arteries: dilate as BP , constrict as BP rises
main chemical stimulus: pH
CO2 + H2O H2 CO3 H+ + (HCO3) hypercapnia (CO2 ) in brain, pH , triggers vasodilation
hypocapnia, pH, vasoconstriction
occurs with hyperventilation, may lead to ischemia, dizziness and
sometimes syncope
20-21
TIA’s - transient ischemic attacks
dizziness, loss of vision, weakness, paralysis, headache or
aphasia
lasts from a moment to a few hours, often early warning
of impending stroke
CVA - cerebral vascular accident (stroke)
Two types
brain infarction caused by ischemia
atherosclerosis, thrombosis, ruptured aneurysm
hemorrhagic stroke
effects range from unnoticeable to fatal
blindness, paralysis, loss of sensation, loss of speech common
20-22
recovery depends on CAUSE, surrounding neurons,
collateral circulation, gender
Highly variable flow – OPPOSITE of brain
At rest
During exercise
arterioles constrict, total flow about 1L/min
arterioles dilate in response to epinephrine and
sympathetic nerves
precapillary sphincters dilate due to lactic acid, CO2
blood flow can increase 20 fold
Muscular contraction impedes flow
20-23
isometric contraction causes fatigue faster than isotonic
Low pulmonary blood pressure
flow slower, more time for gas exchange
capillary fluid absorption
oncotic pressure overrides hydrostatic pressure
Unique response to hypoxia
20-24
pulmonary arteries constrict to redirect flow to better
ventilated region
Pulmonary trunk to pulmonary arteries to lungs
Pulmonary veins return to left atrium
20-25
lobar branches for each lobe (3 right, 2 left)
increased O2 and reduced CO2 levels
Basketlike
capillary beds
surround alveoli
Exchange of
gases with air at
alveoli
20-26
Both ventricles
must eject
same amount
of blood.
They should
have the same
stroke volume.
19-27
Both ventricles
must eject
same amount
of blood.
They should
have the same
stroke volume.
19-28