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Transcript of Blood Vessels Chapter 19. Blood Vessels: Overview Structure of blood vessel wall Tunica externa –...
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Blood Vessels
Chapter 19
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Blood Vessels: Overview Structure of blood vessel wall
Tunica externa – outer covering mostly collagen Tunica media – elastin & encircling smooth muscle Tunica interna – endothelium
Lumen – the channel Vasa Vasorum – in large vessels, supplies blood to the outer layers
of the vessel wall
Figure 19.1b
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Types of Blood Vessels Arteries – carry cardiac outflow.
Thicker walled & more muscular. Repeated bifurcation (divisions): elastic arteries muscular arteries
arterioles then to: Capillaries – wall has single cell thickness. Repeated anastomosis
(merging) yield: Venules which then anastomose to form: Veins – thin wall, less muscle, more expansible, large lumen, carry
venous return to heart
Figure 19.1b
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Arteries: Types
Elastic arteries – expand & contract passively to accommodate blood volume. Smoothes out pulsatile flow
Muscular arteries – distribution arteries. Deliver blood to organs. Less elastic / more muscle (vasoconstriction)
Arterioles – smallest; endothelium & a single layer of smooth muscle – regulate flow to capillary beds
Figure 19.1b
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Capillaries: Types Continuous: Endothelium with
occasional intercellular clefts
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Capillaries: Types Fenestrated: Endothelial cells full of pores.
Very permeable. Absorption / filtration
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Capillaries: Types Sinusoids: large irregular lumen,
fenestrations & intercellular clefts. Allow movement of large molecules / plasma between circulatory system & extracellular space
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Capillary Beds True capillaries are exchange vessels Precapillary sphincter: smooth muscle that controls blood
flow between metarteriole & true capillary Vascular Shunt: arteriole metarteriole venule
Pericytes: spaced along capillaries to anchor & stabilizeFigure 19.4a,b
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Veins
Venules: small caliber, porous; allow fluid & WBC movement out of circulation
Veins: capacitance vessels which hold 65% of blood supply. Pressure is low.
Venous valves: one way valves that inhibit retrograde flow
Small amount of smooth muscle or elastin Venous sinuses – thin walled flattened veins supported
by surrounding tissue (coronary sinuses, dural sinuses)
Figure 19.1b
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Anastomoses
Anastomoses: collaterals, bypasses & shuntsArterialArteriovenousVenous
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Physiology of Circulation
Introduction to hemodynamics: Blood flow (F)
Blood pressure (BP) &
Resistance (R)
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Blood flow
Blood flow = volume of blood flowing through a structure; ml/min Total blood flow = Cardiac Output Individual structure blood flow varies
example: skin (hot vs. cold); gut (digestion)
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Blood pressure
Blood pressure: force of blood against vessel walls (i.e. 120 mmHg systolic) Pressure gradient keeps blood moving
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ARTERIAL BLOOD PRESSURE Systolic pressure
Pressure peak after ventricular systole. Ave = 120 mm Hg.
Diastolic Pressure Pressure drop during
ventricular diastole. Ave = 80 mm Hg.
BP = 120/80 mm Hg
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Resistance
Resistance: opposition to flow; friction of blood moving through vessels Blood viscosity = blood’s internal resistance to flow Laminar flow: blood at the wall moves slower than
blood in center
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Resistance
Blood vessel length: increased length = increased resistance
Blood vessel diameter: decreased diameter = increased resistance
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Resistance
Resistance varies inversely to the radius4
(i.e. 1/r4)
Doubling the radius: Decreases resistance to R/16
Halving the radius Increases resistance to 16R
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Relationships: Flow, Pressure & Resistance F = P
R P = Phigh - Plow
Increased P yields: Increased Flow
Decreased P yields: Decreased Flow
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Relationships: Flow, Pressure & Resistance F = P
R Increased R yields:
Decreased Flow
Decreased R yields: Increased Flow
Resistance has a greater influence than change in Pressure on Flow
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Systemic Blood Pressure
Systemic BP Arterial BP: depends upon distensibility of the
great vessels & the volume of blood pumped into them (pulsatile)
Ventricular contraction blood flow to aorta aortic stretch pressure:
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Systemic Blood Pressure
Systolic Pressure: peak pressure with aortic filling increases to ~120 mmHg.
Blood run off begins & flows down the pressure gradient into the systemic circulation.
Diastolic pressure: lowest pressure. As aorta recoils, pressure decreases to ~80 mmHg.
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Systemic Blood Pressure
Pulse pressure - Difference between systolic & diastolic pressures. Felt as a pulse during systole.
PP = 120 - 80 = 40 mm Hg
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Systemic Blood Pressure
Pulse pressure = systolic - diastolic
Mean Arterial Pressure = average pressure throughout the cycle MAP = diastolic + pulse pressure
3 MAP = ~90 mmHg
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Capillary BP
Capillary BP ~40 mmHg at the start of the capillary bed ~20 mmHg at the end
Higher pressure would destroy capillaries Capillary permeability is high enough that
exchange process occurs at low pressure
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Venous BP / Venous Return
Venous BP (non pulsatile)
Respiratory pump: pressure changes in the thorax & abdomen b/c of breathing
Muscular pump: skeletal muscle activity
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Maintaining BP Maintaining BP: CO = P
R
P = CO x R
Alteration of BP depends on CO & R
CO = HR x SV; a function of venous return; under neural & hormonal influences
P = (HR x SV) x R
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Neural Effectors of CO
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Resistance: Short Term Control
Short term control by neural & chemical factors Alters blood distribution Maintains MAP by changes in vessel diameter
Operate via baroreceptors & chemoreceptors
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Short Term: Neural Control
Vasomotor center (medulla): exerts vasomotor tone via vasomotor fibers that innervate smooth muscle of vessels
SNS activity generalized vasoconstriction
Input from baroreceptors & chemoreceptors to vasomotor center modifies vasomotor output
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Short Term: Neural Control
Baroreceptors: Carotid sinuses (monitor blood flow to brain) Aortic (monitor blood flow to periphery)
Detect changes in MAP Chemoreceptors: detect [O2], [CO2] & pH
(carotid & aortic bodies)
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MAINTAINING BLOOD PRESSURE
Short Term Mechanisms: Chemical Epinephrine and Norepinephrine -
Enhances the sympathetic nervous system. Epi increases cardiac output; NE is a vasoconstrictor.
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MAINTAINING BLOOD PRESSURE
Short Term Mechanisms: Chemical Atrial Natriuretic Peptide (ANP) -
Antagonist of aldosterone. Causes excretion of Na+ and H2O from body
Reduces blood volume and blood pressure
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MAINTAINING BLOOD PRESSURE
Short Term Mechanisms: Chemical Antidiuretic Hormone (ADH) -
Released at high amounts when MAP drops to low levels; it acts as a vasoconstrictor (its other name is vasopressin).
It also conserves water, but this is not an important short-term mechanism.
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MAINTAINING BLOOD PRESSURE
Short Term Mechanisms: Chemical Angiotensin II - A potent
vasoconstrictor produced within the blood.
ACE
Angiotensinogen
Angiotensin I
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MAINTAINING BLOOD PRESSURE
Short Term Mechanisms: Chemical Nitric Oxide (NO) -
Promotes vasodilation, lowering MAP.Secreted by endothelial cells in
response to high flow rate
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MAINTAINING BLOOD PRESSURE
Short Term Mechanisms: Chemical Inflammatory chemicals - Histamine
and other chemicals released during inflammation are vasodilators.
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MAINTAINING BLOOD PRESSUREShort Term Mechanisms: Chemical Alcohol -
Antagonist of ADH (lowers blood volume and blood pressure)
Promotes vasodilation (thereby reducing resistance and blood pressure).
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Long term control: Renal
Direct renal Increased renal flow & BP increased filtrate from kidney which
results in decreases in volume & in pressure Decreased renal flow & BP decreased filtrate; conservation of
volume & increases in BP Indirect renal
Decreased BP results in renin release Angiotensin II (vasoconstrictor) which stimulates: Aldosterone & ADH release which conserve Na & water
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MAINTAINING BLOOD PRESSURE
Long Term
Mechanisms:
Renal
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Alterations in BP
Hypotension (low BP): systolic <100 mmHg Hypertension (high BP) systolic >140/90
Primary HTN – no specific cause; lifestyle & heredity Secondary HTN – identifiable cause; increased renin,
arteriosclerosis, endocrine disorders
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Alterations in BP
Autoregulation; local changes in blood flow Intrinsic: modifying diameter of local arterioles Metabolic: endothelial response (NO, etc) Myogenic: smooth muscle responds to increased
stretch with increased tone
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Blood Flow Through Capillaries
Fluid exchange: Hydrostatic pressure vs. colloid osmotic pressure
Hydrostatic Pressure pushes fluid out down pressure gradient (HPc) Interstitial Hydrostatic Pressure (HPif) pushes fluid into capillaries Colloid Osmotic Pressure: large molecules pull H2O toward themselves.
Interstitial (OPif) & Capillary (OPc)
NFP = (HPc – HPif) – (OPc – OPif)
Figure 19.16
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Net Filtration Pressure of Capillaries
Net Filtration Pressure of capillaries NFP = (HPc – HPif) – (OPc – OPif)
NFP at arterial end of capillary bed = 10 mmHg Hydrostatic
NFP at venous end of capillary bed = -8 mmHg Oncotic
Figure 19.16
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Circulatory Shock Circulatory Shock: marked decrease in
blood flow Symptoms: increased HR, thready pulse,
marked vasoconstriction; Marked fall in BP is a late symptom
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Circulatory Shock: Causes
Hypovolemic: inadequate volume (hemorrhage, dehydration, burns)
Vascular: normal volume but global vasodilation Anaphylaxis: allergies (histamine) Neurogenic: failure of autonomic nervous system Septic: bacteria (bacterial toxins are vasodilators)
Cardiogenic pump failure