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Flow Equation
change in pressure over resistance
Pressure
Force exerted by blood
If radius of bv is decreased(vasoconstriction)
resistance is increased
Flow is
Directly related to change in pressure
Resistance is
indirectly related to flow
While pressure is different
flow is constant
Systemic has a higher change in pressure, but,
flow is equal in both systemic and pulmonary circuits
Systemic change in pressure
is created than pulmonary change in pressure
Systemic circuit resistance is greater than pulmonary but why?
resistance is not equal
Factors affecting resistance to flow
*length of vessel, vasoconstriction/vasodilation,
Higher viscosity means
higher resistance
Viscosity
thickness of blood, thicker the viscosity, the lower the flow
Vasoconstriction
decreased radius and higher resistance
Vasodilation
higher radius and lower resistance
What is different between the two circuits?
length of blood vessels
TPR
combined resistance of all bvs in the systemic circuit
Microcirculation bus
arterioles, capillaries, venues
Capillaries
site of exchange, low velocity, blood moves slower
Components of bv walls
smooth muscle, fibrous CT(collagen), Elastic CT(elastin), varies by type of vessel
Elastic arteries
large diameter and lower resistance, walls contain elastin and fibrous tissue, high pressure, closer to heart, thick elastic walls, low compliance, storage site for pressure, expand as blood enters during systole, recoil during diastole
Muscular arteries
small, little elastin and have smooth muscle, smooth muscle regulates vasoconstriction and dilation, further from heart
Low compliance
doesn’t expand easily, small increase causes large increase in pressure
High compliance
expand easily, large increase needed to produce large increase in pressure
Measuring bp w a compressed artery
turbulent flow produced Korotkoff sound
Pressure at first Korotkoff sound is
systolic bp
Measuring bp w uncompressed artery
no sound bc laminar flow, pressure when sound disappears, shows diastolic bp
Pulse pressure
systolic minus diastolic
Where does the body spend most time?
diastole
How is bp shown?
systolic over diastolic
What bv has the highest resistance?
arterioles
Capillaries
have the greatest cross-sectional area, have slowest velocity of blood flow
Continuous capillaries have
intercellular clefts, small water soluble molecules move thru
Fenestrated capillaries have
pores or fenestrations, proteins can move thru, rapid met
Discontinuous capillaries
large gaps, sinusoids are spaces lined with endothelium, proteins can pass
Diffusion w caps
lipid soluble solutes diffuse thru plasma membrane
Metarterioles
between caps and arterioles, directly connect arterioles to venules
Precapillary sphincters
rings of smooth muscle that surround caps on arteriole end, metabolites(o2) cause relaxation
Movement across cap walls
exchange bw blood and cells, normal distribution of ECF
Diffusion
most common mechanism for exchange across cap walls
Lipophilic
across membrane, easy
Lipophobic
thru channels
Transcytosis
exchangeable proteins, endo and exocytosis
Mediated transport
BBB
Filtration
movement out of capillary into interstitial space
Absorption
movement into capillary from interstitial space
Edema
collection of fluid outside capillary, tells you where problem is, fluid out of blood in interstitial space but not reabsorbing it
Hydrostatic
force due to fluid, PUSHING
Osmotic pressure(oncotic - proteins)
osmotic force exerted on water by non permeable solutes, PULLING
Pcap
capillary hydrostatic pressure, capillary bp: favors filtration
Pif
interstitial hydrostatic pressure: favors reabsorption
Ncap
capillary osmotic pressure: favors reabsorption
Nif
interstitial fluid oncotic osmotic pressure: favors filtration
Net Filtration pressure
filtration pressure - absorption pressure
Factors affecting filtration and absorption
standing, injury, liver disease, kidney disease, heart disease
Standing
gravity increases hydrostatic pressure in lower extremities
Injuries
caps damaged they leak proteins and fluid, histamine increases permeability to proteins(they are large), affects Nit and swelling happens
Liver Disease
decreases plasma proteins
Kidney Disease
increases bv and bp, decreases plasma proteins, consequence is edema
Heart Disease
L failure - pulmonary edema
R failure - systemic edema
affecting Pcap edema around ankles(R) or lungs(L)
Determinants of MAP
heart rate, stroke volume, TPR
Regulation of MAP
neural(faster) and hormonal(slower)
MAP is
directly related to heart rate, stroke volume, and TPR
MAP
driving force for blood flow
Hypotension
MAP is less than normal, inadequate blood flow to tissues
Hypertension
MAP is greater than normal, stressor for heart and blood(over perfusing tissues)
Short term MAP regulation
neural control, regulates CO and TPR, involves heart and bus
Long term MAP regulation
regulates bvs, involves kidneys, hormonal control
Sensory receptors of neural control of MAP
baroreceptors(detects change in bp, aorta and carotid), pressure receptors, sometimes called stretch receptors
integration center of neural control of MAP
cardio centers in brainstem, medulla oblongata
Neural control of MAP effectors
heart, arterioles, and veins
Neural control center input
Neural control output
sympathetic(heart and bvs) and parasympathetic(heart nodes)
Baroreceptor reflex - hemorrhage
low bp=low MAP, increased SYM activity, decreased PS activity, greater resistance, less blood flow due to vasoconstriction, quick fix
Vasopressin
vasoconstrictor, kidney reabsorption of water
Angiotensin II
vasoconstrictor, stimulates thirst, stimulates release of aldosterone
Epinephrine
adrenergic receptors, acts on heart, increased SYM activity
Arrhythmia
irregular heart beat
Inspiration
decreased pressure in thoracic cavity, increased PS activity and heart rate
Expiration
increased pressure in thoracic cavity, increased PS activity, decreased heart rate
Chemoreceptors
respond to increases in CO2 levels in blood, regulate them
Thermoregulation
increased body temp, decreases SYM activity to skin, takes precedence over baroreceptor reflex, possible decreased TPR and MAP
Blood is what
55% plasma, 45% cellular components
What are some cellular components?
RBCs, WBCs, Platelets, proteins
Hematocrit
% of RBCs to rest of blood
Secondary polycythemia
hypoxia, decreased O2, kidneys release EPO to increase RBCs
Polycythemia vera
kidneys release EPO and RBCs
Relative polycythemia
malfunction of bone marrow, dehydration
Plasma is
mostly water, nutrient, wastes, gases, and electrolytes
Albumins
osmotic oncotic pressure, pulling force
Globulins
lipid transport, clot formation, and immunity
Fibrinogen
clot formation
Erythrocytes
RBCs, biconcave disk shape, no nucleus or organelles
Spectrin net
flexible membrane that allows RBCs to fit into capillaries
Erythrocyte function
transport O2 and CO2
Hemoglobin
iron and polypeptide chains
Heme
iron containing group that binds to O2 and CO
Globin
4 chains of polypeptides, binds to CO2
Carbonic Anhydrase equation
CO2+H2O←→H2CO3←→H+HCO3
Carbon Dioxide←→carbonic acid←→bicarbonate
How long to erythrocytes live?
120 days
Erythrocytes made in
red bone marrow through process of erythropoiesis