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Dee Unglaub Silverthorn, Ph.D.

H

UMAN

P

HYSIOLOGY

H

UMAN

P

HYSIOLOGY

PowerPoint® Lecture Slide Presentation by

Dr. Howard D. Booth, Professor of Biology, Eastern Michigan University

AN INTEGRATED APPROACH

T H I R D E D I T I O N

Chapter 15 Chapter 15

Blood Flow and the Control of Blood Pressure

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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

About this Chapter About this Chapter

How various blood vessels are constructed and role in circulation

Components of "blood pressure", role and measurement

Product exchange at the capillary beds

Lymph vessels, distribution and role in circulation

How blood pressure and circulation are regulated

Key components of cardiovascular disease

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Arteries: blood from heart

Strong & Elastic

Conduct blood to capillaries

Sphincters

Capillaries: exchange with cells

Veins

Return blood to heart

Valves

The Blood Vessels and the Cardiovascular System The Blood Vessels and the Cardiovascular System

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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

The Blood Vessels and the Cardiovascular System The Blood Vessels and the Cardiovascular System

Figure 15-1: Functional model of the cardiovascular system

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Endothelium

Elastic tissues

Rebounds

Evens flow

Smooth muscles

Fibrous tissue

Tough

Resists stretch

Make Up of Blood Vessels: Arteries and Arterioles Make Up of Blood Vessels: Arteries and Arterioles

Figure 15-2: Blood vessels

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Endothelium: one cell thick

Continuous

Fenestrated

Basement membrane

Make Up of Blood Vessels: Capillaries Make Up of Blood Vessels: Capillaries

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Make Up of Blood Vessels: Capillaries Make Up of Blood Vessels: Capillaries

Figure 15-16: Types of capillaries

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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Thinner walls

Larger diameter

Closer to skin

Less muscle

Less elastic

Make Up of Blood Vessels:

Veins and Venules (Contrasted to Arteries) Make Up of Blood Vessels:

Veins and Venules (Contrasted to Arteries)

Figure 15-3: Metarterioles

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Normal body maturation and growth

Endometrium

Endurance training

Abnormal growth to service cancerous tissue

Wound repair and consequences

Failure to regrow in heart tissues after heart attack

Failure to regrow in brain after stroke Angiogenesis: Growth of New Blood Vessels

Angiogenesis: Growth of New Blood Vessels

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Pulsatile: surges in arteries

Elastic rebound evens & maintains pressure

Blood Pressure:

Generated by Ventricular Contraction Blood Pressure:

Generated by Ventricular Contraction

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Blood Pressure:

Generated by Ventricular Contraction Blood Pressure:

Generated by Ventricular Contraction

Figure 15-4: Elastic recoil in the arteries

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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Blood Pressure (BP): Measurements Blood Pressure (BP): Measurements

"Blood pressure"

Systolic over diastolic

About 120/80 mmHg

Sphygmomanometer

"Estimate of pressure"

Korotkoff sounds

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Blood Pressure (BP): Measurements Blood Pressure (BP): Measurements

Figure 15-7: Measurement of arterial blood pressure

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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Pulse pressure = Systolic–Diastolic

Mean arterial pressure (MAP) = Diastolic + 1/3 pulse pressure

More Blood Pressures:

Pulse and Mean Arterial Pressures More Blood Pressures:

Pulse and Mean Arterial Pressures

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More Blood Pressures:

Pulse and Mean Arterial Pressures More Blood Pressures:

Pulse and Mean Arterial Pressures

Figure 15-5: Pressure throughout the systemic circulation

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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Factors Controlling MAP :

The Driving Pressure for Blood Flow Factors Controlling MAP :

The Driving Pressure for Blood Flow

Blood volume

Cardiac output

Resistance

Distribution

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Factors Controlling MAP :

The Driving Pressure for Blood Flow Factors Controlling MAP :

The Driving Pressure for Blood Flow

Figure 15-10: Factors that influence mean arterial pressure

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Slide Source Hypertension Online www.hypertensiononline.org

-Blockers ACE Inhibitors

AT1 Blockers

Direct renin inhibitors

1-Blockers

2-Agonists All CCBs Diuretics Sympatholytics

Vasodilators

-Blockers

Non-DHP CCBs Diuretics

Blood Blood

Pressure

Pressure == CardiacCardiacOutputOutput 

ACE = angiotensin-converting enzyme; AT1 = angiotensin type 1;

CCBs = calcium channel blockers; DHP = dihydropyridine

Antihypertensive Drug Classes: Action Sites Antihypertensive Drug Classes: Action Sites

Total Peripheral Total Peripheral

Resistance Resistance

AntihypertensiveAntihypertensive Drug ClassesDrug Classes

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Slide Source Hypertension Online www.hypertensiononline.org

Classes of Antihypertensive Drugs Classes of Antihypertensive Drugs

• Aldosterone receptor antagonists (blockers)

• Angiotensin II antagonists

• Angiotensin-converting enzyme inhibitors

 -Blockers

 1-Selective – Nonselective

 -Blockers

 -1/-2

 -1 predominant

 /

– Intrinsic sympathomimetic activity

• Calcium channel antagonists – Nondihydropyridine

– Dihydropyridine

• Central 2 agonists

• Direct renin inhibitors

• Direct vasodilators

• Diuretics

– Thiazide-type – Loop-type

– Potassium-sparing

• Ganglionic blockers

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Arteriole Resistance: Control of Local Blood Flow Arteriole Resistance: Control of Local Blood Flow

Myogenic auto regulation

Paracrines:

Hyperemia

Sympathetic nerves – CNS

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Distribution of Blood in the Body Organs Distribution of Blood in the Body Organs

Figure 15-13: Distribution of blood in the body at rest

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Lowest Velocity

Hydrostatic

pressure drops

Capillary Blood Flow:

Greatest Total Cross Sectional Area Capillary Blood Flow:

Greatest Total Cross Sectional Area

Figure 15-17: The velocity of flow depends on the total cross- sectional area

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Capillary Exchange:

Colloidal Osmotic Pressure is Constant Capillary Exchange:

Colloidal Osmotic Pressure is Constant

Proteins stay in capillary

Water, oxygen, glucose – move out

CO2, N wastes, water – move in

Bulk flow out on arterial side, in on venous side

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High on arterial side – bulk flow out

Low on venous side – bulk flow in

Fenestrations &/or leaky joints speed exchange

Capillary Exchange: Hydrostatic Pressure Declines Capillary Exchange: Hydrostatic Pressure Declines

Figure 15-18a: Fluid exchange at the capillary

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Net filtration – net absorption = net out flow

About 2 L/day collected by lymph vessels Net Out Flow Into ECF

Net Out Flow Into ECF

Figure 15-18b: Fluid exchange at the capillary

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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Lymphatic System: Structure and Roles (overview) Lymphatic System: Structure and Roles (overview)

Lymphatic structures

Capillaries with valves

Lymph vessels

Lymph nodes & organs

Immune defense: lymphocytes

Transport of fats

Collects excess ECF

Returns to plasma

Edema

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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Lymphatic System: Structure and Roles (overview) Lymphatic System: Structure and Roles (overview)

Figure 15-19: The lymphatic system

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Lymphatic System: Overview Lymphatic System: Overview

Consists of two semi-independent parts

A meandering network of lymphatic vessels

Lymphoid tissues and organs scattered throughout the body

Returns interstitial fluid and leaked plasma proteins back to the blood

Lymph – interstitial fluid once it has entered lymphatic vessels

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Figure 20.2a

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Lymphatic System: Overview Lymphatic System: Overview

Figure 20.1a

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Lymphatic Capillaries Lymphatic Capillaries

Similar to blood capillaries, with modifications

Remarkably permeable

Loosely joined endothelial minivalves

Withstand interstitial pressure and remain open

The minivalves function as one-way gates that:

Allow interstitial fluid to enter lymph capillaries

Do not allow lymph to escape from the capillaries

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Lymphatic Capillaries Lymphatic Capillaries

During inflammation, lymph capillaries can absorb:

Cell debris

Pathogens

Cancer cells

Cells in the lymph nodes:

Cleanse and “examine” this debris

Lacteals – specialized lymph capillaries present in intestinal mucosa

Absorb digested fat and deliver chyle to the blood

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Lymphatic Trunks Lymphatic Trunks

Lymph is delivered into one of two large trunks

Right lymphatic duct – drains the right upper arm and the right side of the head and thorax

Thoracic duct – arises from the cisterna chyli and drains the rest of the body

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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Lymph Transport Lymph Transport

The lymphatic system lacks an organ that acts as a pump

Vessels are low-pressure conduits

Uses the same methods as veins to propel lymph

Pulsations of nearby arteries

Contractions of smooth muscle in the walls of the lymphatics

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Regulation of Blood Pressure and Heart Rate Regulation of Blood Pressure and Heart Rate

Medullary cardiac control center (Brainstem)

Cardioacceleratory Center

Cardioinhibitory Center

Baroreceptor reflex

Carotid

Aortic

Kidney: blood volume

Hypothalamus & Cortex: stress, blushing, etc.

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Regulation of Blood Pressure Regulation of Blood Pressure

Figure 15-22: The baroreceptor reflex: the response to increased blood pressure

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Risk Factors:

Smoking

Obesity

Diabetes

Genes

Diseases:

Hypertension

Stroke

"Heart Attack"

Cardiovascular Diseases: #1 killer Cardiovascular Diseases: #1 killer

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LDL build up

Plaque

 Flow

Rupture

Clot

Blocked flow

Tissue death

Mechanism of Atherosclerosis Mechanism of Atherosclerosis

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We now understand that atherosclerosis is a chronic inflammation of arteries, which develops over decades in response to the biologic effects of risk factors.

Atherogenesis begins as a qualitative change to intact endothelial cells; when subjected to oxidative, hemodynamic, or biochemical stimuli (from smoking, hypertension, or

dyslipidemia) and inflammatory factors, they change their permeability to promote the entry and retention of blood-borne monocytes and cholesterol-containing LDL particles.

Inflammation and biochemical modifications ensue, causing endothelial and smooth-

muscle cells to proliferate, produce extracellular matrix molecules, and form a fibrous cap over the developing atheromatous plaque.

Plaques lead to clinical symptoms by producing flow-limiting stenoses (causing stable angina) or by provoking thrombi that interrupt blood flow on either a temporary basis (causing unstable angina) or a permanent one (causing myocardial infarction).

Physical disruption (rupture) of the plaque exposes procoagulant material within the core of the plaque to coagulation proteins and platelets, triggering clotting.

How Atherosclerosis Develops

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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Blood vessels, anatomy & role in circulation

Measuring blood pressures, MAP & pulse pressure

Role of resistance in BP and distribution of blood

Autoregulation, baroreceptros, medullary cardiac control center and CNS regulation of blood pressure & distribution

Summary Summary

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Hydrostatic & colloidal osmotic pressures direct bulk flow in capillary exchange by diffusion, fenestrations & leaky joints

Role of lymphatic system to return excess ECF to plasma

Atherosclerosis common to several cardiovascular diseases

Summary Summary

References

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