1. Blood Flow and the Control of Blood Pressure
Chapter 15
Blood Flow and the Control of Blood Pressure

2. 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

3. The Blood Vessels and the Cardiovascular System
Arteries: blood from heart
Strong & Elastic
Conduct blood to capillaries
Sphincters
Capillaries: exchange with cells
Veins
Return blood to heart
Valves

4. The Blood Vessels and the Cardiovascular System
Figure 15-1: Functional model of the cardiovascular system

5. Make Up of Blood Vessels: Arteries and Arterioles
Endothelium
Elastic tissues
Rebounds
Evens flow
Smooth muscles
Fibrous tissue
Tough
Resists stretch
Figure 15-2: Blood vessels

6. Make Up of Blood Vessels: Veins and Venules (Contrasted to Arteries)
Thinner walls
Larger diameter
Closer to skin
Less muscle
Less elastic
Figure 15-3: Metarterioles

7. Angiogenesis: Growth of New Blood Vessels
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

8. Blood Pressure: Generated by Ventricular Contraction
Pulsatile: surges in arteries
Elastic rebound evens & maintains pressure

9. Blood Pressure: Generated by Ventricular Contraction
Figure 15-4: Elastic recoil in the arteries

10. Blood Pressure (BP): Measurements
Systolic over diastolic
About 120/80 mmHg
Sphygmomanometer
"Estimate of pressure"
Korotkoff sounds

11. Blood Pressure (BP): Measurements
Figure 15-7: Measurement of arterial blood pressure

12. More Blood Pressures: Pulse and Mean Arterial Pressures
Pulse pressure = Systolic–Diastolic
Mean arterial pressure (MAP) = Diastolic + 1/3 pulse pressure

13. More Blood Pressures: Pulse and Mean Arterial Pressures
Figure 15-5: Pressure throughout the systemic circulation

14. Factors Controlling MAP : The Driving Pressure for Blood Flow
Blood volume
Cardiac output
Resistance
Distribution

15. Factors Controlling MAP : The Driving Pressure for Blood Flow
Figure 15-10: Factors that influence mean arterial pressure

16. Antihypertensive Drug Classes: Action Sites
Cardiac Output 
Blood
Pressure
Total Peripheral
Resistance =
-Blockers
Non-DHP
CCBs
Diuretics
-Blockers
ACE Inhibitors
AT1 Blockers
Direct renin inhibitors
1-Blockers
2-Agonists
All CCBs
Diuretics
Sympatholytics
Vasodilators
Antihypertensive Drug Classes
Antihypertensive Drug Classes: Action Sites
β-Blockers decrease blood pressure primarily by reducing cardiac output. They also decrease renal renin output and, thereby, angiotensin II-mediated vasoconstriction. Angiotensin-converting enzyme inhibitors, angiotensin type-1 blockers, direct renin inhibitors, 1-blockers, 2-agonists, sympatholytics, and vasodilators decrease blood pressure by reducing total peripheral resistance through various mechanisms. Calcium channel blockers can either affect total peripheral resistance (dihydropyridines) or can reduce both cardiac output and total peripheral resistance (nondihydropyridines). Diuretics initially reduce cardiac output by decreasing intravascular fluid volume; with continued therapy, however, they also reduce total peripheral resistance via vasodilation.
ACE = angiotensin-converting enzyme; AT1 = angiotensin type 1;
CCBs = calcium channel blockers; DHP = dihydropyridine 16

17. 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
Classes of Antihypertensive Drugs
There are currently 11 classes and more than 200 different drugs or combinations of drugs approved by the United States Food and Drug Administration to treat hypertension. This slide outlines the different classes of antihypertensive drugs and highlights the major pharmacological differences among drugs within each class when there is important heterogeneity within the class. On average, most antihypertensive drugs decrease systolic and diastolic blood pressures by about 10 mm Hg and 5 mm Hg, respectively, when administered as monotherapy. 17

18. Distribution of Blood in the Body Organs
Responds to metabolic need
Precapillary sphincters
Local & CNS regulators
Huge variations (example: skeletal m 20-85%)

19. Distribution of Blood in the Body Organs
Figure 15-13: Distribution of blood in the body at rest

20. Capillary Blood Flow: Greatest Total Cross Sectional Area
Lowest Velocity
Hydrostatic pressure drops
Figure 15-17: The velocity of flow depends on the total cross-sectional area

21. 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

22. Capillary Exchange: Hydrostatic Pressure Declines
High on arterial side – bulk flow out
Low on venous side – bulk flow in
Fenestrations &/or leaky joints speed exchange
Figure 15-18a: Fluid exchange at the capillary

23. Net Out Flow Into ECF Net filtration – net absorption = net out flow
About 2 L/day collected by lymph vessels
Figure 15-18b: Fluid exchange at the capillary

24. 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

25. Lymphatic System: Structure and Roles (overview)
Figure 15-19: The lymphatic system

26. 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

27. Figure 20.2a

28. Lymphatic System: Overview
Figure 20.1a

29. Lymphatic Vessels
A one-way system in which lymph flows toward the heart
Lymph vessels include:
Microscopic, permeable, blind-ended capillaries
Lymphatic collecting vessels
Trunks and ducts

30. 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

31. 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

32. 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

33. 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

34. 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.

42. Regulation of Blood Pressure
Figure 15-22: The baroreceptor reflex: the response to increased blood pressure

47. Cardiovascular Diseases: #1 killer
Risk Factors:
Smoking
Obesity
Diabetes
Genes
Diseases:
Hypertension
Stroke
"Heart Attack"

48. Mechanism of Atherosclerosis
LDL build up
Plaque
 Flow
Rupture
Clot
Blocked flow
Tissue death

49. How Atherosclerosis Develops
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.

50. Mechanism of Atherosclerosis
Figure 15-24: The development of atherosclerotic plaques

51. Mechanism of Atherosclerosis
Figure 15-24: The development of atherosclerotic plaques

52. Summary 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

53. Summary
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