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 Figure 19.1b 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

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 & stabilize Figure 19.4a,b

Veins Figure 19.1b 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)

Anastomoses Anastomoses: collaterals, bypasses & shunts Arterial Arteriovenous Venous

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 14

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: Blood vessel diameter: 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 = rP R rP = Phigh - Plow Increased rP yields: Increased Flow Decreased rP yields: Decreased Flow

Relationships: Flow, Pressure & Resistance F = rP 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 22

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 Higher pressure would destroy capillaries ~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 = rP R rP = CO x R Alteration of BP depends on CO & R CO = HR x SV; a function of venous return; under neural & hormonal influences rP = (HR x SV) x R

Neural Effectors of CO 27

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)

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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. 32

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 When the atria of the heart encounter increased pressure they secrete ANP 33

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. 34

MAINTAINING BLOOD PRESSURE Short Term Mechanisms: Chemical Angiotensin II - A potent vasoconstrictor produced within the blood. Angiotensinogen Also causes aldosterone and ADH release ACE Angiotensin I 35

MAINTAINING BLOOD PRESSURE Short Term Mechanisms: Chemical Nitric Oxide (NO) - Promotes vasodilation, lowering MAP. Secreted by endothelial cells in response to high flow rate 36

MAINTAINING BLOOD PRESSURE Short Term Mechanisms: Chemical Inflammatory chemicals - Histamine and other chemicals released during inflammation are vasodilators. 37

MAINTAINING BLOOD PRESSURE Short Term Mechanisms: Chemical Alcohol - Antagonist of ADH (lowers blood volume and blood pressure) Promotes vasodilation (thereby reducing resistance and blood pressure). 38

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 40

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 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