Ch 15: Ch 15: Blood Flow and the Control Blood Flow and the Control

of Blood Pressure of Blood Pressure

1. Blood pressure (BP) and Regulation

2. Exchange at capillaries

3. Lymphatic system

4. Cardio-vascular diseases

Keypoints

Fig 15-2

Angiogenesis Growth of new blood vessels – occurs

during– Normal body maturation and growth– Monthly re-growth of functional endometrium– Wound healing– Endurance training– Cancer growth

Clinical implications: Promote or inhibit angiogenesis with relevant cytokines

Pressure created by ventricular contraction is driving force for blood flow

Pulsatile blood flow in arteries Elastic arteries expand and recoil for continuous blood flow

Pulse wave disappears past arterioles

Blood PressureBlood PressureFig 15-4

Blood Pressure (BP) Measurements

Ventricular pressure difficult to measure measure arterial BP

BP highest in the arteries – falls continuously throughout systemic circulation

Read as “Systolic over diastolic”– normal value 120 / 80 mm Hg

2003: New range for blood pressure readings between 120/80 and 139/89 “Prehypertension”

Diastolic pressure in ventricle: ? mm Hg

Auscultation of brachial artery with stethoscope in cubital fossa

Based on effects of

laminar flow vs.

turbulent flow

BP Estimated by SphygmomanometryBP Estimated by Sphygmomanometry

Principles ofPrinciples of SphygmomanometrySphygmomanometryCuff inflated until brachial artery compressed

and blood flow stopped kind of kind of sound?sound?

Compare to Fig 15-7

turbulent flow

Slowly release pressure in cuff:

Pressures at which . . . . . . sound (= blood flow) first heard:

. . . sound disappeared:

CDAnimation

Cardiovascular System: Measuring Blood Pressure

Mean Arterial Pressure

Sometimes useful to have single value for driving pressure: Mean Arterial Pressure

MAP = Diastolic P + 1/3 Pulse PressureMAP = Diastolic P + 1/3 Pulse Pressure (for 60 -80 bpm)

MAP for 120/80 = ?

MAP closer to diastolic pressure – why?

MAP influenced byMAP influenced by Cardiac output

Peripheral resistance (role of arterioles see Ch14) most common cause of hypertension

Total blood volume

Blood distributionFigs 15-8 & 10Figs 15-8 & 10

BP too low:BP too low:

Driving force for blood flow unable to overcome gravity

O2 supply to brain

Symptoms?

ShockShock= generalized circulatory failure

Hypovolemic shock volume loss (dehydration, blood loss, burns)

Distributive shock loss of vascular tone (anaphylactic, septic, toxic)

Cardiogenic shock pump failure

Dissociative shock inability of RBC to deliver O2 (CO poisoning)

Cell damage due to inadequate perfusionSigns and symptoms?Management ?

BP too high:BP too high:

Weakening of arterial walls lead to Weakening of arterial walls lead to AneurysmsAneurysms Risk of rupture & Risk of rupture & hemorrhagehemorrhage

Cerebral hemorrhageCerebral hemorrhage

Rupture of major artery Rupture of major artery

Exchange at the CapillariesExchange at the Capillaries Capillaries are anatomically designed for

exchange

Capillary blood flow: Greatest total cross sectional area Velocity ?

Most cells within ____ µm of capillary – why?

Direct correlation between # of caps and metabolic needs of tissue

Three types of exchange of molecules across the barrier

Fig 15-16

Methods of Capillary Exchange1. Paracellular diffusion

2. Transendothelial transport (transcytosis) – some diffusion

3. Bulk flow: mass movement of H2O and dissolved solutes as result of hydrostatic or osmotic pressure

Filtration – flow direction out of caps Absorption – flow direction into caps

Two Forces Regulate Capillary Bulk Flow

Hydrostatic P: lateral component of fluid flow

Osmotic P: due to solute difference (main solute difference due to?)

Mostly: Net filtration at arterial end Net re-absorption at venous end

Fig 15-18Fig 15-18

cap = 25 mmHg

= Pcap + cap

Fig 15-18

Fluid Exchange

Close functional association with three other systems

1.

2.

3.

3) Lymphatic System3) Lymphatic System

Lymphatic System Functions

Return filtered fluid & proteins to circulatory system (anatomical design!) – Fig 15-18

Transfer fat from small intestine to circulatory system

Trap and deal with pathogens

EdemaEdemaDue to disruption of capillary exchangeDue to disruption of capillary exchange

2 major causes:

1. Blockage of lymph drainage – Cancer & fibrotic growth– Pathogens

2. Capillary filtration > absorption– Venous pressure due to right / left

heart failure– Plasma protein concentration due to

liver failure or severe malnutrition (Kwashiorkor)

Right or Left Heart Failure?

Alveolar Flooding

SwedenSweden

Kroniskt invalidiserande lymfödem (2,1 liter) i höger arm sedan 8 år.

Kwashiorkor

Reflex control:Reflex control: Baroreceptor Reflex Baroreceptor Reflex = 1= 1o o

homeostatic control for BP homeostatic control for BP

Baroreceptors = stretch Baroreceptors = stretch sensitive ______receptors sensitive ______receptors in in aorta and carotid arteryaorta and carotid artery

Medullary CVCC integrates Medullary CVCC integrates neural neural controlcontrol

Regulation of Blood PressureRegulation of Blood Pressure

CDAnimation

Cardiovascular System: Blood Pressure Regulation Fig 15-22

Additional Control of BPAdditional Control of BP Arterial chemoreceptors activated by

O2

Cerebral cortex– emotional responses such as blushing &

fainting vasovagal response

Integration with Kidney function

Orthostatic hypotension normally triggers Baroreceptor reflex

Account for ~ 1/2 of deaths in US – most common: CAD or CHDCAD or CHD

Uncontrollable & controllable risk factors

Gender, age, genetics

Cigarette smoking, obesity, high BP, high cholesterol, DM

Cardiovascular Disease (CVD)Cardiovascular Disease (CVD)

Cigarette Smoking: Nicotinic cholinergic receptors stimulate Nicotinic cholinergic receptors stimulate

sympathetic neurons at ?sympathetic neurons at ?

Vasoconstriction & BP Vasoconstriction & BP

Risk for atherosclerosis Risk for atherosclerosis

Carbon monoxide Carbon monoxide (myocardium extracts most of (myocardium extracts most of OO22 brought to it under resting conditions) brought to it under resting conditions)

AtherosclerosisAtherosclerosisChanges in artery walls start with Changes in artery walls start with

lipid deposits lipid deposits

Macrophage ingests LDL-cholesterol Macrophage ingests LDL-cholesterol

Fatty streaks just under endothelial lining of Fatty streaks just under endothelial lining of larger arterieslarger arteries

MacrophageMacrophageparacrines attract smooth muscle paracrines attract smooth muscle cellscells

Smooth muscle cells proliferateSmooth muscle cells proliferate stable plaques vs. vulnerable plaquesstable plaques vs. vulnerable plaques

Cerebral and coronary thrombi and emboli Cerebral and coronary thrombi and emboli ? ?

Fig 15-24Fig 15-24

Role of Elevated Cholesterol in Role of Elevated Cholesterol in Development of AtherosclerosisDevelopment of Atherosclerosis

Lipids insoluble in plasma lipoproteins

Chylomicron to muscle & adipose cells, VLDL to adipose cells

2 main types of cholesterol carriers: HDL to liver vs. LDL to body cells

the endthe end

Essential HypertensionEssential Hypertension