Blood Vessels

Chapter 19

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

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

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

Capillaries: Types Continuous: Endothelium with

occasional intercellular clefts

Capillaries: Types Fenestrated: Endothelial cells full of pores.

Very permeable. Absorption / filtration

Capillaries: Types Sinusoids: large irregular lumen,

fenestrations & intercellular clefts. Allow movement of large molecules / plasma between circulatory system & extracellular space

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

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

Anastomoses

Anastomoses: collaterals, bypasses & shuntsArterialArteriovenousVenous

Physiology of Circulation

Introduction to hemodynamics: Blood flow (F)

Blood pressure (BP) &

Resistance (R)

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)

Blood pressure

Blood pressure: force of blood against vessel walls (i.e. 120 mmHg systolic) Pressure gradient keeps blood moving

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

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

Resistance

Blood vessel length: increased length = increased resistance

Blood vessel diameter: decreased diameter = increased resistance

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

Relationships: Flow, Pressure & Resistance F = P

R P = Phigh - Plow

Increased P yields: Increased Flow

Decreased P yields: Decreased Flow

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

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:

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.

Systemic Blood Pressure

Pulse pressure - Difference between systolic & diastolic pressures. Felt as a pulse during systole.

PP = 120 - 80 = 40 mm Hg

Systemic Blood Pressure

Pulse pressure = systolic - diastolic

Mean Arterial Pressure = average pressure throughout the cycle MAP = diastolic + pulse pressure

3 MAP = ~90 mmHg

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

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

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

Neural Effectors of CO

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

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

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)

MAINTAINING BLOOD PRESSURE

Short Term Mechanisms: Chemical Epinephrine and Norepinephrine -

Enhances the sympathetic nervous system. Epi increases cardiac output; NE is a vasoconstrictor.

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

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.

MAINTAINING BLOOD PRESSURE

Short Term Mechanisms: Chemical Angiotensin II - A potent

vasoconstrictor produced within the blood.

ACE

Angiotensinogen

Angiotensin I

MAINTAINING BLOOD PRESSURE

Short Term Mechanisms: Chemical Nitric Oxide (NO) -

Promotes vasodilation, lowering MAP.Secreted by endothelial cells in

response to high flow rate

MAINTAINING BLOOD PRESSURE

Short Term Mechanisms: Chemical Inflammatory chemicals - Histamine

and other chemicals released during inflammation are vasodilators.

MAINTAINING BLOOD PRESSUREShort Term Mechanisms: Chemical Alcohol -

Antagonist of ADH (lowers blood volume and blood pressure)

Promotes vasodilation (thereby reducing resistance and blood pressure).

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

MAINTAINING BLOOD PRESSURE

Long Term

Mechanisms:

Renal

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

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

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

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

Circulatory Shock Circulatory Shock: marked decrease in

blood flow Symptoms: increased HR, thready pulse,

marked vasoconstriction; Marked fall in BP is a late symptom

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