Cardiovascular Physiology Flashcards
1
Q
Why do we have a cardiovascular system?
A
- To provide oxygen and nutrients and remove wastes like carbon dioxide from cells
- Rapid system
- Provides a steep concentration gradient within the vicinity of every cell: important b/c in multicellular organisms as diffusion is too slow
2
Q
Hemodynamics
A
The study of blood flow relates Ohm’s law to fluid flow
3
Q
Relationship between blood flow, blood pressure, and resistance to blood flow
A
F=deltaP/R
4
Q
How does blood flow?
A
From high pressure to low pressure
5
Q
Hydrostatic Pressure
A
Blood hydrostatic pressure is the pressure that the volume of blood within our circulatory system exerts on the walls of the blood vessels that contain it
6
Q
Do we Use Absolute Pressure or the Difference Between Pressures?
A
The pressure differences
-the pressure difference must be greater than the sum of all resistances to create flow
7
Q
What Determines Resistance to Blood Flow?
A
Viscosity = friction between molecules of flowing fluid
Length + diameter = determines amount of contact between moving blood and stationary wall of vessel
8
Q
Puiseuille’s Equation
A
R=8nl/pir^4 R= resistance to blood flow n= viscosity of blood l= and length of vessel r = radius of vessel
9
Q
Functions of the Cardiovascular System
A
- To deliver oxygen and nutrients and remove waste products of metabolism
- Fast chemical signaling to cells by circulating hormones or neurotransmitters
- Thermoregulation
- Mediation of inflammatory and host defense responses against invading microorganisms
10
Q
The Heart
A
The pump
11
Q
Blood Vessels
A
The pipes
12
Q
Blood
A
The fluid to be moved
13
Q
Arterioles
A
Small branching vessels with high resistance
14
Q
Capillaries
A
Transport blood between small arteries and venules; exchange of materials
15
Q
Arteries
A
Move blood away from the heart
16
Q
Veins
A
Move blood towards the heart
17
Q
What type of pressure does this closed circulatory system generate?
A
It generates greater pressures
18
Q
Anatomy of the heart
A
2 atria
2 ventricles
Septa
19
Q
Atria
A
Thin-walled
Low-pressure chambers
Receive blood returning to the heart
20
Q
Ventricles
A
Forward propulsion of blood
21
Q
Interatrial Septum
A
Separates left and right atria
22
Q
Interventricular Septum
A
Separates left and right ventricles
23
Q
Pulmonary Circulation
A
- Blood to and from the gas exchange surfaces of the lungs
- Blood entering lungs=poorly oxygenated blood
- Oxygen diffuses from lung tissue to blood
- Blood leaving lungs=oxygenated
24
Q
Heart Functions as Dual-Path How?
A
- Left side pumps highly oxygenated blood to the systemic system
- Right side pumps poorly oxygenated blood to the pulmonary circuit
25
Systemic Circulation
- Blood to and from the rest of the body
- Blood entering tissues=oxygenated blood
- oxygen diffuses from blood to body tissues
- blood leaving tissues=poorly oxygenated
26
Why are they Called Serial Circuits
Because these steps happen in sequence
27
Series Flow
Found in the cardiovascular system
| -Pulmonary and circulatory circuits
28
Parallel Flow
Occurs in most organs
- each organ is supplied by a different artery
- independently regulate flow to different organs
29
Distribution of Blood Flow at Rest and During Exercise
The cardiovascular system must ensure adequate perfusion of capillaries supply the organs at rest, during exercise, or emergency situation
30
Pericardium
Fibrous sac surrounding the heart and roots of great vessels
31
Functions of the Pericardium
- Stabilization of the heart in the thoracic cavity
- Protection of the heart from mechanical trauma, infection
- Secretes pericardial fluid to reduce friction
- Limits over fillings of the chamber, prevents sudden distension
32
3 Layers of the Pericardium
1. fibrous pericardium
Serous pericardium
-2. parietal
-3. visceral (epicardium)
33
Pericardial Cavity
Pericardial fluid decreases friction
| Separates the parietal pericardium and the visceral pericardium
34
Fibrous Pericardium
Provides protection for the heart and stabilizes the heart in the thoracic cavity by attaching to structures in the chest
35
Parietal Pericardium
Lies underneath the fibrous pericardium and is attached to it
36
Visceral Pericardium
The innermost layer of the pericardial sac
| Called the epicardium when it comes into contact with the heart muscle
37
Serous Layer
A layer composed of cells that secrete a fluid
38
Pericarditis
Inflammation of the pericardium
39
Cardiac Tamponade
Compression of the heart chambers due to excessive accumulation of pericardial fluid
decreases ventricular filling
40
Why is the left ventricle thicker than the right ventricle?
The left ventricle develops higher pressure so that it can pump blood around the entire circulatory system
41
Layers of the Heart Wall
Epicardium
Myocardium
Endocardium
42
Epicardium
Covers the outer surface of the heart
Acts as a protective layer
Connective tissues attach it to the myocardium
43
Myocardium
The muscular wall of the heart and lies underneath the epicardium
- contains muscle cells or myocytes which contract and relax as the heartbeats
- contains nerves and blood vessels
44
Endocardium
The innermost layer of the heart wall
- lines heart cavities and the heart valves
- a thin layer of endothelium which is continuous with the endothelium of the attached blood vessels
45
Myocytes
Cardiac heart muscle
- branched (Y) and joined longitudinally which allows for greater connectivity in the heart
- striated, one nucleus per cell, many mitochondria
46
Intercalculated Disks
Interdigitated region of attachment
| -desmosomes and gap junctions
47
Desmosomes
Adhering junctions that hold cells together in tissues subject to considerable stretching
Mechanically couples one heart cell to another
Proteins involved: cadherins, plaques, intermediate filaments
48
Gap Junctions
Communicating junctions
Electrically couple heart cells, allowing ions to move between cells
-important for the spread of action potentials
Protein Involved: Connexion
49
How are Heart Muscles Arranged?
They are arranged spirally around the circumference of the heart
50
Why are Heart Muscles Arranged Spirally?
When the cardiac muscle contracts and shortens, a wringing effect is produced, efficiently pushing blood upwards towards the exit of major arteries
51
Valves
Thin flaps of flexible, endothelium-covered fibrous tissue attached at the base to the valve rings
- leaflets or cusps
- collagen
52
Valve Rings
Cartilage
| Site of attachment for the heart valves
53
How do valves function?
Unidirectional flow of blood through the heart
Open and close passively due to pressure gradients
-forward pressure gradient opens the one-way valve
-backward gradient closes the one-way valve and it cannot open in the opposite direction
54
Atrioventricular Valves
Found between the atria and ventricles
Prevent backflow of blood into atria when the ventricles contract
Tricuspid and Bicuspid
55
Tricuspid Valve
Right AV valve
| Three leaflets
56
Bicuspid Valve
Left AV valve
| Two leaflets
57
AV Valve Apparatus
Chordae tendineae
| Papillary Muscles
58
Chordae tendineae
Tendinous-type tissue
| Extend from the edges of each leaflet to papillary muscle
59
Papillary Muscles
Cone-shaped muscles
Contraction of papillary muscle causes the chordae tendineae to become taut
-THIS HOLDS THE VALVE CLOSED
60
The Function of the AV Valve Apparatus
Prevents the eversion of the AV valves into the atria during contraction of the ventricles
Valves open and close due to pressure gradients, not from contraction and relaxation of the papillary muscles
61
Semilunar (arterial) Valves
Found between the ventricle and the artery which ejects its blood
No valve apparatus
Semilunar valves open due to pressure differences
-pulmonary valve
-aortic valve
62
Pulmonary Valve
Pulmonary trunk, right ventricle
| 3 cusps
63
Aortic Valve
Aorta
Left ventricle
3 Cusps
64
Cardiac Skeleton
Fibrous skeleton of the heart
- dense connective tissue
- includes the heart valve rings and the connective tissue between the heart valves
65
Cardiac Skeleton Function
Physically separates the atria from ventricles
Electrically inactive and blocks the direct spread of electrical impulses from the atria to the ventricles
Provides support for the heart, providing a point of attachment for the valves leaflets and cardiac muscle
66
Coronary Sinus
A collection of veins joined together to form a large vessel that collects blood from the myocardium of the heart
67
Coronary Circulation
The part of the systemic circulatory system and supplies blood to and provides drainage from the tissues of the heart
68
Coronary Arteries
Arteries supplying the heart
| -aortic sinus is a dilation or out-pocketing of the ascending aorta
69
Cardiac Veins
Collect poorly oxygenated blood and empty it into the coronary sinus, which returns blood to the right atrium
70
Systole (Contraction)
Myocardial blood flow almost ceases and the right and left ventricle are contracting
71
Diastole (Relaxation)
Myocardial blood flow peaks as the ventricles are not contracting
72
Coronary Artery Disease
Caused by atherosclerosis of the coronary arteries supplying blood to the heart tissues
73
Atherosclerosis
Arteries supplying blood to the heart become hardened and narrow due to plaque in the arterial walls
74
Plaque
Fat, cholesterol, calcium, and other substances in the blood
75
Angina
Chest pain or discomfort
| Blood flow to the heart muscle is reduced
76
Myocardial Infarction
Heart attack
| Blood supply to the heart is completely blocked; muscle dies
77
Cardiac Syncytium
When myocytes communicate with each other
| -set of cells that act together; the heart resembles a single, enormous muscle cell
78
Functional Syncytium
If one cell is excited, the excitation spreads over both ventricles (or atria)
-atrial syncytium and a ventricular syncytium
All or nothing property
79
Cardiac Muscle
Action potentials lead to contraction of heart muscles
Two types of myocytes:
-contractile cells
-conducting cells
80
Automaticity
The heart contracts or beats rhythmically as a result of action potentials that it generates itself
81
Contractile Cells
Mechanical work of pumping, propelling blood
Generates pressure to move blood
do not initiate action potentials
82
Conducting Cells
Initiates and conducts the action potentials responsible for contraction of the contractile myocytes
Part of the conducting system of the heart
-are in electrical contact with each other and the cardiac contractile cells through the gap junctions
83
Components of the Conducting System
```
Sinoatrial node
Internodal pathways
Atrioventricular node
Bundle of His
Bundle branches; left and right
Purkinje fibres
```
84
Cardiac Skeleton and Conduction
Non-conducting, no action potentials travel across it
Physically separates the atria from the ventricles, stimuli cannot cross from the atria to the ventricles through the cardiac skeleton
85
Sinoatrial Node
Cardiac Pacemaker
Initiates action potentials
-sets heart rate
The cardiac skeleton isolate the atrial and ventricular myocardium
86
Internodal Pathways
The stimulus passed to contractile cells of both atria and to the AV node
87
Atrioventricular Node
100 msc delay
delay ensures atria depolarize and contract before the ventricles
Contraction of the ventricles would close the AV valves, preventing blood flow from the atria into the ventricles
Allows the ventricles time to fill completely before they contract
88
Excitation of the Ventricles
AV node and Bundle of His are the only electrical connection between atria and ventricles
Left and right branches travel along the interventricular septum and make contact with Purkinje fibres
89
Purkinje Fibres
Large number, diffuse distribution, fast conduction velocity
Left and right ventricular myocytes depolarize and contract nearly simultaneously
90
Pathway of Excitation
SA node - Internodal pathways - AV node - Bundle of His - Right and left branches - Purkinje fibres - Ventricular myocardium
91
Wolff-Parkinson-White Syndrome
There is an extra connection in the heart called an accessory pathway
-the accessory pathway is an abnormal piece of muscle that connects directly between the atria and ventricles
-electrical signals bypass the AV node and move from the atria to the ventricles faster than usual
-transmits electrical impulses abnormally from the ventricles back to the atria
Rapid heart rate or arrhythmias
92
Fast Action Potentials
Found in:
Atrial myocardium
Ventricular myocardium
Bundle of His, Bundle Branches, Purkinje fibres
93
Slow Action Potentials
Found in:
Sinoatrial node
Atrioventricular node
94
The Cardiac Action Potential
Phases of the cardiac action potential are associated with changes in the permeability of the cell membrane mainly to Na+, K+, and Ca2+ ions
Opening and closing of ion channels alters the permeability
95
Concentrations of Ions in the heart
[K+]in>[K+]out
[Ca2+]out>[Ca2+]in
[Na+]out>[Na+]in
96
Pacemaker Potential
Slow depolarization to threshold
| Regular spontaneous generation of action potentials
97
Stages of Slow Action Potential
1. Pacemaker potential
- K+ channels = progressive reductive in potassium permeability
- F-type cells = funny
- T-type cells = transient
2. Depolarization
- L-type channels = long-lasting
3. Repolarization
- K+ channels = potassium leaves cell
98
Summary of Slow Action Potential
Depolarization phase is slow due to slow movement of Ca2+
Pacemaker potential due to changes in movement of ions
AV node pacemaker current rises to threshold more slowly
99
Electrocardiograms
Graphic recording of electrical events
Electrical activity of the heart detected on the surface of the body
Voltage gradients in the heart may be as much as 100 mV, translated to charges of up to 1 mV on the skin surface
Used to diagnose heart problems
100
P-wave
Spread of depolarization across atria
-atria contract 25 msec after start of P-wave
First wave on ECG
101
QRS Complex
Spread of depolarization across ventricles
-atria repolarize simultaneously
When the ventricles are depolarizing, the atria are repolarizing
102
T-Wave
Ventricular repolarization
103
Normal ECG
P-wave always followed by QRS complex and T-wave
104
Partial AV Node Block
Every 2nd P-wave is not followed by a QRS complex
105
Complete AV Node Block
No synchrony between atrial and ventricular electrical activities
Ventricles driven by slower bundle of His
106
Cardiac Myocyte
Muscle cell of the heart
107
Intercalated Disk
Where the membranes of two adjacent myocytes are extensively intertwined; desmosomes and gap junction
108
Sarcolemma
Plasma or cell membrane of a muscle cell
109
Sarcoplasmic Reticulum
A special type of smooth endoplasmic reticulum which stores and pumps calcium ions
110
Cardiac Myocyte Structure
Contains myofibrils
Striated
T-tubules = invaginations of sarcolemma; transmit depolarization of membrane into interior of muscle cell
111
Excitation-Contraction Coupling in Cardiac Muscle
Calcium ions regulate the contraction of cardiac muscle
- calcium binds to ryanodine receptors, releasing calcium from the sarcoplasmic reticulum
- calcium dependent calcium release
112
Activation of Cross-Bridge Cycling by Calcium
```
Troponin = contains binding sites for calcium and tropomyosin, and regulates access to myosin-binding sites on actin
Tropomyosin = partially cover the myosin-binding sites on actin at rest, preventing cross-bridges from making contact with actin
```
113
Steps in Cardiac contraction
1. Excitation spreads along the sarcolemma
2. Excitation also spreads to the interior of the cell by T-tubules
3. During plateau phase of action potential, permeability of the cell to calcium increases
4. Calcium enters through L-type Ca2+ channels in sarcolemma and T-tubules
5. Calcium causes the release of calcium from sarcoplasmic reticulum through calcium-release channels
6. Elevation of cytosolic calcium
7. Calcium binds to troponin which unblocks active sites between actin and myosin
8. Cross-bridge cycling and contraction of myofibrils
114
Excitation-contraction coupling in skeletal muscles
Physical coupling between DHP receptor and ryanodine receptor
115
Excitation-contraction coupling in cardiac muscle
L-type Ca2+ channel
-voltage-gate Ca2+ channel
Calcium-dependent calcium release
116
ECC in Cardiac Muscle - Relaxation Steps
1. Influx of calcium stops as L-type Ca2+ channels close
2. SR is no longer stimulated to release calcium
3. SR takes up cytosolic calcium by Ca2+-ATPase
4. Calcium removed from cell by Na+-Ca2+ exchanger
5. Reduced calcium binding to troponin
6. Sites for interaction between myosin and actin are blocked
7. Relaxation of myofibrils
117
Refractory Period
```
Period of time in which a new action potential cannot be initiated
Absolute Refractory Period
-250 msec
-no response to another stimulus
-inactivation of Na+ channels
Prevents tetanus
```
118
Systole
Ventricular contraction and blood ejection
119
Diastole
Ventricular relaxation and blood filling
120
Cardiac Cycle
The cardiac cycle length is the period of time from the beginning of one heartbeat to the beginning of the next
- each heartbeat involves one ventricular systole and one ventricular diastole
- the heart spends most of its time is diastole
121
Isovolumetric Ventricular Contraction (systole)
All heart valves closed, blood pressure in the ventricles remains constant
122
Ventricular Ejection (systole)
Pressure in ventricles exceeds that in arteries, semilunar valves open and blood ejected into the artery
123
Stroke Volume (systole)
Volume of blood ejected from each ventricle during systole
124
Isovolumetric Ventricular Relaxation (diastole)
all heart valves closed, blood volume remains constant, pressure drops
125
Ventricular filling (diastole)
AV valves open, blood flows into ventricles from atria. Ventricles receive blood passively
126
Atria contraction (diastole)
occurs at the end of ventricular filling
127
Cardiac Cycle - Diagram
Review this
128
Pressure-volume curve
Pressure is generated when the muscles of the heart chamber contract as well as when a chamber fills with blood
Blood always flows from a region of higher pressure to a region of lower pressure
Valves open and close in a response to a pressure gradient
129
End-diastolic Volume (EDV)
Amount of blood in each ventricle at the end of ventricular diastole
130
End-systolic Volume (ESV)
Amount of blood in each ventricle at the end of ventricular systole
131
Stroke Volume
Volume of blood pumped out of each ventricle during systole
132
Stroke Volume Formula
SV=EDV-EDS (usually 70-75 mL)
133
Wigger's Diagram
Understand this diagram that shoed the pressure and volume changes for the heart
134
Do the right side or the left side of the hear have lower pressure?
The right side has lower pressure than the left ventricle during systole
135
2 Heart Sounds
Lub = closure of AV valves - onset of systole
Dub = closure of semilunar valves - onset of diastole
The sounds result from vibrations caused by the passive closing of the valves
136
How does blood flow normally?
Laminar flow and makes no sound
| -characterized by smooth concentric layers of blood moving in parallel down the length of a blood vessel
137
Abnormal Blood Flow
May be turbulent
- makes sounds = murmer
- stenosis
- insufficiency
138
Stenosis
Blood flows rapidly through a narrowed valve; leaflets do not open completely
139
Insufficient Valve
Blood flows backward through leaky valve; leaflets do not close completely
140
Sympathetic Innervation of the Heart
The entire heart, including the atria, ventricles, SA node, AV node
141
Parasympathetic Innervation of the Heart
Atria, SA node, AV node
142
Parasympathetic Stimulation of the SA Node
rate of depolarization decreases; heart rate decreases
143
Sympathetic Stimulation of the SA Node
rate of depolarization increases; heart rate increases
144
Parasympathetic Stimulation of the AV Node
Conduction decreases; increased AV node delay
145
Sympathetic Stimulation of the AV Node
Conduction increases; decreased AV node delay
146
Parasympathetic Stimulation of the Atrial Muscle
Decreased contractility
147
Sympathetic Stimulation of the Atrial Muscle
Increased contractility
148
Parasympathetic Stimulation of the Ventricular Muscle
No significant innervation; no effect
149
Sympathetic Stimulation of the Ventricular Muscle
Increased contractility
150
Cardiac Output (CO)
The amount of blood pumped by each ventricle in one minute
151
Cardiac Output Formula
CO = HR (heart rate) * SV (stroke volume)
152
Factors Affecting Cardiac Output
Heart rate
| Stroke Volume
153
How do we alter heart rate?
Modifying the activity of the SA node
154
How do we alter stroke volume?
Altered by varying the strength of the contraction of the ventricular myocardium
- increased contraction = increased stroke volume
- decreased contraction = decreased stroke volume
155
Does the ventricles completely empty out after each contraction?
No
156
Factors Affecting Heart Rate
Increased sympathetic activity
-increase heart rate
Increased parasympathetic activity
-decreased heart rate
157
Effect of the Sympathetic System on Heart Rate
Increases the slope of the pacemaker potential (faster depolarization)
- increases HR
- increases F-type (allows Na+ to enter cell) and T-type (allows Ca2+ to enter cell) channel permeability
158
Effect of the Parasympathetic System on Heart Rate
Decreases the slope of the pacemaker potential (slower depolarization)
- decreases HR
- decreases F-type channel permeability (reduced Na+ in cell)
- hyperpolarizes cells (increases K+ permeability)
159
Sympathetic Stimulation on Pacemaker Potential
Pacemaker potential rises more quickly to threshold, or takes less time to reach threshold, increasing the heart rate
160
Parasympathetic Stimulation on Pacemaker Potential
Pacemaker potential rises more slowly to threshold, or takes more time, decreasing heart rate
161
3 Factors Affecting Stroke Volume
End-diastolic volume (EDV; preload)
Contractility of the ventricles
Afterload
162
Preload
Tension of load on myocardium before it begins to contract or amount of filling of ventricles at the end of diastole
-the ventricles will contract more forcefully when they have been stretched prior to contraction
163
EDV
The volume of blood in the ventricles at the end of ventricular diastole or the volume of blood in the ventricles after the ventricles have completed filling
164
Sympathetic Stimulation of Venous Smooth Muscle
Increases the return of blood to the heart through vasoconstriction, increasing filling of the ventricles
-sympathetic stimulation only, parasympathetic does no innervate venous muscle
165
Frank-Starling Mechanism
The relationship between EDV and SV
Main determinant of cardiac muscle fibre (sarcomeres) length is degree of diastolic filling: preload
Increase filling - increase EDV - increase cardiac fibre length - greater force during contraction and greater SV
166
Mechanism of the Length-tension Relationship
When the ventricle is filled more fully with blood, there is an increased force of contraction and a greater stroke volume
-stretches the heart = increases the sarcomere length
167
Contractility
The strength of contraction at any given EDV
| A change in the contractility of the ventricles will alter the volume of blood pumped by the ventricles during systole
168
Sympathetic Stimulation and Contractility
The stroke volume is greater at any given EDV during sympathetic stimulation
More rapid contraction and more rapid relaxation
Ventricles ejecting more blood
169
Ejection Fraction
EF = SV/EDV
170
Mechanism of Sympathetic Effect on Contractility
Acts through a G protein coupled mechanism
171
Afterload
Tension (arterial pressure) against which the ventricles contract
-often called the load
As afterload increases, SV decreases
Any factor that restricts blood flow through arterial system will increase afterload
172
Endothelium
Smooth, single-celled layer of endothelial cells
Endothelium of vessels is continuous with endocardium of the heart
Physical lining that blood cells do not normally adhere to
173
Pressures in the Systemic and Pulmonary Circuits
Pressures in the systemic and pulmonary circuits generated from ventricular contraction decrease as the blood moves further along the circuit
Pulmonary vascular resistance is much lower the systemic total resistance
174
Arteries
Smooth muscle, elastic fibres, connective tissues
Muscular walls allow arteries to contract and change diameters
Elasticity permits passive changes in vessel diameter in response to changes in blood pressure
175
Elastic Arteries
Many elastic fibres, few smooth muscle cells
| Expand and recoil in response to pressure changes
176
Muscular Arteries
Many smooth muscle cells, few elastic fibres
| Distributes blood
177
Arterioles
1-2 layers of smooth muscle cells
| Resistance vessels
178
Vasoconstriction
Contraction of arterial smooth muscle decreases the diameter of the artery
-decreased blood flow to organs
179
Vasodilation
Relaxation of arterial smooth muscle increases the diameter of the artery
-increased blood flow to organs
180
Functions of Arterioles
Regulate blood flow to organs
-capillary beds
Determine MAP
-resistance
181
Resistance in Arterioles
High resistance vessels due to their small size
- causes drop in mean arterial pressure (MAP)
- altering arteriolar diameter alters resistance and flow
182
Intrinsic or Basal Tone
Arteriolar smooth muscle is partially contracted in the absence of external factors
-other factors can increase or decrease the state of contraction to cause vasoconstriction or vasodilation
183
Extrinsic Factors
Factors external to the organ or tissue; who body needs (MAP); nerves and hormones
184
Intrinsic Factors
Local controls; organs and tissees alter their own arteriolar resistances independent of nerves or hormones
185
Extrinsic Controls: Nerves
Sympathetic innervation
- NE causes vasoconstriction
- sympathetic tone can be increased or decreased
- regulating MAP by influencing arteriolar resistance throughout the body
- noncholingeric and nonadrenergic nerves cause vasodilation
186
Extrinsic Controls: Hormones
Epinephrine from adrenal medulla causes vasoconstriction or vasodilation
187
Local Controls: Active Hyperemia
Local control which acts to increase blood flow when the metabolic activity of an organ or tissue increases
Hyperemia = excess of blood flow in the vessels supplying an organ or tissue
188
Local Controls: Flow Autoregulation
Changes in arterial blood pressure alters blood flow to an organ
-changes in the concentration of local chemicals
Arterioles change their resistance to maintain constant blood flow in the presence of a pressure change
Constant metabolic activity
No nerves or hormones involved
May also be mediated by the myogenic response
-direct response of arteriolar smooth muscle to stretch
189
Reactive Hyperemia
Form of flow autoregulation
Occurs at constant metabolic rate
Occurs due to changes in the concentrations of local chemicals
Occlusion of blood flow = greatly decreases oxygen levels and increases metabolites = arterioles dilate = blood flow greatly increases once occlusion is removed
190
Capillaries
One endothelial cell thick
-no smooth muscle or elastic tissue
Exchange of material fluid between blood and interstitial fluid
Intercellular clefts = narrow water-filled space at the junctions between cells
191
Types of Capillaries
Continuous
Fenestrated
Sinusoidal
192
Continuous Capillaries
Endothelial cells form an uninterrupted tube, surrounded by complete basement membrane
Exchange of water, small solutes, lipid-soluble material, no exchange of blood and plasma proteins
Most tissues
tight junctions = low permeability
193
Pericytes
Lie external to the endothelium; may help stabilize the walls of blood vessels and help regulate blood flow through capillaries
194
Fenestrated Capillaries
```
Contains fenestrae (pores) that penetrate the endothelial lining
Surrounded by complete basement membrane
Rapid exchange of water and solutes
Endocrine organs, choroid plexus, GI tract, kidneys
```
195
Sinusoid Capillaries
```
Discontinuous capillaries; flattened and irregularly shaped capillaries
-large fenestrae and gaps between cells
-basement membrane thin or absent
Free exchange of water and solutes
Live, bone marrow, spleen
```
196
Microcirculation
The circulation of blood through the smallest vessels in the body
- precapillary spincter
- metarteriole
197
Precapillary Sphincter
```
At entrance to a capillary
Ring of smooth muscle
Alters blood flow
No innervation
-respond to local factors
```
198
Metarteriole
Connects arterioles to venules
Contains smooth muscle cells
Change diameter to regulate flow
199
Diffusion
Movement of substance down its concentration gradient
- short distance to travel across a capillary
- moves down concentration gradient
200
Trancytosis
Use of vesicles to cross endothelial cells
| -fused vesicle channel = endocytic and exocytic vesicles form a water-filled channel across the cell
201
Bulk Flow
Movement of protein-free plasma across the capillary wall
| -distribution of extracellular fluid volume
202
Filtration
Movement of protein-free plasma from capillary to interstitial fluid
203
Reabsorption
Movement of protein-free plasma from interstitial fluid to capillary
204
Bulk Flow: Hydrostatic Pressure
Pressure that drive fluid movement in and out of the capillary
- capillary hydrostatic = pressure exerted on the inside of capillary walls by blood which favours fluid movement out of the capillary
- interstitial fluid hydrostatic pressure = fluid pressure exerted on the outside of the capillary walls by interstitial fluid which favours fluid movement into capillary (NEGLIGIBLE)
205
Bulk Flow: Colloid Osmotic Pressures
Pressures that drive fluid movement (bulk flow) into and out of the capillary
- blood colloid osmotic pressure = osmotic pressure due to non-permeating plasma proteins inside of the capillaries which favours fluid movement into the capillaries
- interstitial fluid colloid osmotic pressure = small amount of plasma proteins may leak out of capillaries into interstitial space which favours fluid movement out of capillaries (NEGLIGIBLE)
206
Bulk Flow: Net Exchange Pressures
When net filtration pressure is positive = favours filtration
When net filtration pressure is negative = favours absorption
207
Net Filtration and Net Reabsorption Along the Capillary
Transition point between filtration and reabsorption lies closer to venous end of capillary
-more filtration that absorption
208
Distribution of Blood Volume
60% of blood volume is in the venous system
| A lot of blood is found in the liver, bone marrow, and skin
209
Veins
Expand and recoil passively with changes in pressure
High capacitance vessels as can store large amount of blood
Highly distensible at low pressure and have little elastic recoil
Reservoir for blood
210
Venous Valves
Low pressure system
Composed of two leaflets or folds = prevents the backflow of blood into the capillaries
-blood flows in one direction only
Compartmentalize blood
211
Varicose Veins
Valves do not function properly when vein walls weaken, stretch
Blood pools and vessels distend
212
Mechanisms for Venous Return
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Smooth muscle in veins
-innervated by sympathetic neurons
Skeletal muscle pump
-compresses veins
-venous pressure increases, forcing more blood back to the heart
Respiratory pump
-inspiration causes an increase in venous return
-breathe deeper=blood to heart faster
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213
Venous Return and Frank-Starling Law
Increased venous return results in increased stroke volume through the Frank-Starling mechanism
214
Lymphatic System Components
Lymphatic capillaries
Lymph vessels
Lymph nodes
215
Lymph Capillaries
Single layer of endothelial cells
Large water-filled channels permeable to all interstitial fluid components
IF enters lymphatic system through capillaries by bulk flow
Closed end tubes
216
Lymph Vessels
Formed from convergence of lymphatic capillaries
One-way valves
Empty into venous system
IF is called lymph once it enters the lymph vessels
217
Lymph Nodes
Immune response
218
Mechanism of Lymph Flow
Return of fluid from interstitial fluid to blood
Mechanism
-lymphatic vessels have smooth muscle; responsive to stretch
-sympathetic nervous system
-skeletal muscle contractions
-respiratory pump
219
Arterial Blood Pressure
Determined by the volume of blood in the vessels and the compliance of a vessel
Large arteries function as pressure reservoirs due to elastic recoil
-not as compliant as veins
220
Compliance
Ability to distend and increase volume with increasing transmural pressure
The greater the compliance of a vessel, the more easily it can be stretched
221
Systolic Pressure
Maximum blood pressure during ventricular systole
222
Diastolic Pressure
Minimum blood pressure at the end of ventricular diastole
223
Systolic/Diastolic Pressure
120/80 mmHg
| Normal blood pressure
224
Pulse Pressure
Systolic - diastolic
225
Hypertension
Chronically increased arterial blood pressure
226
Hypotension
Abnormally low blood pressure
227
Mean Arterial Pressure
The pressure driving blood into the tissues averaged over the cardiac cycle
-ensures organ perfusion
Pulse pressure decreases as distance from heart increases
-pressure pulses disappear at level of arterioles
-smooth flow at capillaries
MAP decreases as distance from heart increases
The largest drop in pressure occurs across the arterioles (high resistance vessels)
228
MAP Formula
MAP = CO * TPR
* TPR=total peripheral resistance
- can be determined by total arteriolar resistance
229
TPR
The combined resistance of all of the systemic vessels
230
Short-Term Regulation of MAP
Seconds to hours
Baroreceptors reflexes
Adjusts CO and TPR resistance by ANS
231
Long-Term Regulation of MAP
Adjust Blood Volume
| Restore normal salt and water balance through mechanisms that regulate urine output and thirst
232
Arterial Baroreceptors
Carotid sinus and aortic arch baroreceptors
Respond to mean arterial pressure and pulse pressure
Respond to changes in pressure when walls of vessel stretch/relax
-degree of stretching is directly proportional to pressure
233
Baroreceptor Action Potential Frequency
Rate of discharge is proportional to the mean arterial pressure
Increase in MAP increases rate of firing of baroreceptors
Decrease in MAP decreases rate of firing of baroreceptors
Respond to changes in pulse pressure
234
The Medullary Cardiovascular Center
Located in the medulla oblongata
Receives inout from baroreceptors
Alter vagal stimulation (parasympathetic) to the hear and sympathetic innervation to heart, arterioles, and veins
Baroreceptors adapt to sustained changes in arterial pressure
235
Chemoreceptors
Respond to O2 and pH levels in blood
- affect respiration and blood pressure through the cardiovascular center
- aortic and carotid bodies
