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Physiology 210 > Cardiovascular Physiology > Flashcards

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
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2
Q

Hemodynamics

A

The study of blood flow relates Ohm’s law to fluid flow

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3
Q

Relationship between blood flow, blood pressure, and resistance to blood flow

A

F=deltaP/R

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4
Q

How does blood flow?

A

From high pressure to low pressure

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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

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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

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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

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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
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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
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10
Q

The Heart

A

The pump

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11
Q

Blood Vessels

A

The pipes

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12
Q

Blood

A

The fluid to be moved

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13
Q

Arterioles

A

Small branching vessels with high resistance

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14
Q

Capillaries

A

Transport blood between small arteries and venules; exchange of materials

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15
Q

Arteries

A

Move blood away from the heart

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16
Q

Veins

A

Move blood towards the heart

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17
Q

What type of pressure does this closed circulatory system generate?

A

It generates greater pressures

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18
Q

Anatomy of the heart

A

2 atria
2 ventricles
Septa

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19
Q

Atria

A

Thin-walled
Low-pressure chambers
Receive blood returning to the heart

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20
Q

Ventricles

A

Forward propulsion of blood

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21
Q

Interatrial Septum

A

Separates left and right atria

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22
Q

Interventricular Septum

A

Separates left and right ventricles

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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
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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
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25
Q

Systemic Circulation

A
  • 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
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26
Q

Why are they Called Serial Circuits

A

Because these steps happen in sequence

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27
Q

Series Flow

A

Found in the cardiovascular system

-Pulmonary and circulatory circuits

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28
Q

Parallel Flow

A

Occurs in most organs

  • each organ is supplied by a different artery
  • independently regulate flow to different organs
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29
Q

Distribution of Blood Flow at Rest and During Exercise

A

The cardiovascular system must ensure adequate perfusion of capillaries supply the organs at rest, during exercise, or emergency situation

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30
Q

Pericardium

A

Fibrous sac surrounding the heart and roots of great vessels

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31
Q

Functions of the Pericardium

A
  • 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
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32
Q

3 Layers of the Pericardium

A
  1. fibrous pericardium
    Serous pericardium
    -2. parietal
    -3. visceral (epicardium)
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33
Q

Pericardial Cavity

A

Pericardial fluid decreases friction

Separates the parietal pericardium and the visceral pericardium

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34
Q

Fibrous Pericardium

A

Provides protection for the heart and stabilizes the heart in the thoracic cavity by attaching to structures in the chest

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35
Q

Parietal Pericardium

A

Lies underneath the fibrous pericardium and is attached to it

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36
Q

Visceral Pericardium

A

The innermost layer of the pericardial sac

Called the epicardium when it comes into contact with the heart muscle

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37
Q

Serous Layer

A

A layer composed of cells that secrete a fluid

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38
Q

Pericarditis

A

Inflammation of the pericardium

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39
Q

Cardiac Tamponade

A

Compression of the heart chambers due to excessive accumulation of pericardial fluid
decreases ventricular filling

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40
Q

Why is the left ventricle thicker than the right ventricle?

A

The left ventricle develops higher pressure so that it can pump blood around the entire circulatory system

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41
Q

Layers of the Heart Wall

A

Epicardium
Myocardium
Endocardium

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42
Q

Epicardium

A

Covers the outer surface of the heart
Acts as a protective layer
Connective tissues attach it to the myocardium

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43
Q

Myocardium

A

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
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44
Q

Endocardium

A

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
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45
Q

Myocytes

A

Cardiac heart muscle

  • branched (Y) and joined longitudinally which allows for greater connectivity in the heart
  • striated, one nucleus per cell, many mitochondria
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46
Q

Intercalculated Disks

A

Interdigitated region of attachment

-desmosomes and gap junctions

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47
Q

Desmosomes

A

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

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48
Q

Gap Junctions

A

Communicating junctions
Electrically couple heart cells, allowing ions to move between cells
-important for the spread of action potentials
Protein Involved: Connexion

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49
Q

How are Heart Muscles Arranged?

A

They are arranged spirally around the circumference of the heart

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50
Q

Why are Heart Muscles Arranged Spirally?

A

When the cardiac muscle contracts and shortens, a wringing effect is produced, efficiently pushing blood upwards towards the exit of major arteries

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51
Q

Valves

A

Thin flaps of flexible, endothelium-covered fibrous tissue attached at the base to the valve rings

  • leaflets or cusps
  • collagen
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52
Q

Valve Rings

A

Cartilage

Site of attachment for the heart valves

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53
Q

How do valves function?

A

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

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54
Q

Atrioventricular Valves

A

Found between the atria and ventricles
Prevent backflow of blood into atria when the ventricles contract
Tricuspid and Bicuspid

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55
Q

Tricuspid Valve

A

Right AV valve

Three leaflets

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56
Q

Bicuspid Valve

A

Left AV valve

Two leaflets

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57
Q

AV Valve Apparatus

A

Chordae tendineae

Papillary Muscles

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58
Q

Chordae tendineae

A

Tendinous-type tissue

Extend from the edges of each leaflet to papillary muscle

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59
Q

Papillary Muscles

A

Cone-shaped muscles
Contraction of papillary muscle causes the chordae tendineae to become taut
-THIS HOLDS THE VALVE CLOSED

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60
Q

The Function of the AV Valve Apparatus

A

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

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61
Q

Semilunar (arterial) Valves

A

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

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62
Q

Pulmonary Valve

A

Pulmonary trunk, right ventricle

3 cusps

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63
Q

Aortic Valve

A

Aorta
Left ventricle
3 Cusps

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64
Q

Cardiac Skeleton

A

Fibrous skeleton of the heart

  • dense connective tissue
  • includes the heart valve rings and the connective tissue between the heart valves
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65
Q

Cardiac Skeleton Function

A

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

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66
Q

Coronary Sinus

A

A collection of veins joined together to form a large vessel that collects blood from the myocardium of the heart

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67
Q

Coronary Circulation

A

The part of the systemic circulatory system and supplies blood to and provides drainage from the tissues of the heart

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68
Q

Coronary Arteries

A

Arteries supplying the heart

-aortic sinus is a dilation or out-pocketing of the ascending aorta

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69
Q

Cardiac Veins

A

Collect poorly oxygenated blood and empty it into the coronary sinus, which returns blood to the right atrium

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70
Q

Systole (Contraction)

A

Myocardial blood flow almost ceases and the right and left ventricle are contracting

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71
Q

Diastole (Relaxation)

A

Myocardial blood flow peaks as the ventricles are not contracting

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72
Q

Coronary Artery Disease

A

Caused by atherosclerosis of the coronary arteries supplying blood to the heart tissues

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73
Q

Atherosclerosis

A

Arteries supplying blood to the heart become hardened and narrow due to plaque in the arterial walls

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74
Q

Plaque

A

Fat, cholesterol, calcium, and other substances in the blood

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75
Q

Angina

A

Chest pain or discomfort

Blood flow to the heart muscle is reduced

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76
Q

Myocardial Infarction

A

Heart attack

Blood supply to the heart is completely blocked; muscle dies

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77
Q

Cardiac Syncytium

A

When myocytes communicate with each other

-set of cells that act together; the heart resembles a single, enormous muscle cell

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78
Q

Functional Syncytium

A

If one cell is excited, the excitation spreads over both ventricles (or atria)
-atrial syncytium and a ventricular syncytium
All or nothing property

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79
Q

Cardiac Muscle

A

Action potentials lead to contraction of heart muscles
Two types of myocytes:
-contractile cells
-conducting cells

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80
Q

Automaticity

A

The heart contracts or beats rhythmically as a result of action potentials that it generates itself

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81
Q

Contractile Cells

A

Mechanical work of pumping, propelling blood
Generates pressure to move blood
do not initiate action potentials

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82
Q

Conducting Cells

A

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

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83
Q

Components of the Conducting System

A 
Sinoatrial node
Internodal pathways
Atrioventricular node
Bundle of His
Bundle branches; left and right
Purkinje fibres
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84
Q

Cardiac Skeleton and Conduction

A

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

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85
Q

Sinoatrial Node

A

Cardiac Pacemaker
Initiates action potentials
-sets heart rate
The cardiac skeleton isolate the atrial and ventricular myocardium

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86
Q

Internodal Pathways

A

The stimulus passed to contractile cells of both atria and to the AV node

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87
Q

Atrioventricular Node

A

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

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88
Q

Excitation of the Ventricles

A

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

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89
Q

Purkinje Fibres

A

Large number, diffuse distribution, fast conduction velocity
Left and right ventricular myocytes depolarize and contract nearly simultaneously

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90
Q

Pathway of Excitation

A

SA node - Internodal pathways - AV node - Bundle of His - Right and left branches - Purkinje fibres - Ventricular myocardium

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91
Q

Wolff-Parkinson-White Syndrome

A

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

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92
Q

Fast Action Potentials

A

Found in:
Atrial myocardium
Ventricular myocardium
Bundle of His, Bundle Branches, Purkinje fibres

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93
Q

Slow Action Potentials

A

Found in:
Sinoatrial node
Atrioventricular node

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94
Q

The Cardiac Action Potential

A

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

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95
Q

Concentrations of Ions in the heart

A

[K+]in>[K+]out
[Ca2+]out>[Ca2+]in
[Na+]out>[Na+]in

96
Q

Pacemaker Potential

A

Slow depolarization to threshold

Regular spontaneous generation of action potentials

97
Q

Stages of Slow Action Potential

A
  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
Q

Summary of Slow Action Potential

A

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
Q

Electrocardiograms

A

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
Q

P-wave

A

Spread of depolarization across atria
-atria contract 25 msec after start of P-wave
First wave on ECG

101
Q

QRS Complex

A

Spread of depolarization across ventricles
-atria repolarize simultaneously
When the ventricles are depolarizing, the atria are repolarizing

102
Q

T-Wave

A

Ventricular repolarization

103
Q

Normal ECG

A

P-wave always followed by QRS complex and T-wave

104
Q

Partial AV Node Block

A

Every 2nd P-wave is not followed by a QRS complex

105
Q

Complete AV Node Block

A

No synchrony between atrial and ventricular electrical activities
Ventricles driven by slower bundle of His

106
Q

Cardiac Myocyte

A

Muscle cell of the heart

107
Q

Intercalated Disk

A

Where the membranes of two adjacent myocytes are extensively intertwined; desmosomes and gap junction

108
Q

Sarcolemma

A

Plasma or cell membrane of a muscle cell

109
Q

Sarcoplasmic Reticulum

A

A special type of smooth endoplasmic reticulum which stores and pumps calcium ions

110
Q

Cardiac Myocyte Structure

A

Contains myofibrils
Striated
T-tubules = invaginations of sarcolemma; transmit depolarization of membrane into interior of muscle cell

111
Q

Excitation-Contraction Coupling in Cardiac Muscle

A

Calcium ions regulate the contraction of cardiac muscle

  • calcium binds to ryanodine receptors, releasing calcium from the sarcoplasmic reticulum
  • calcium dependent calcium release
112
Q

Activation of Cross-Bridge Cycling by Calcium

A 
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
Q

Steps in Cardiac contraction

A
  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
Q

Excitation-contraction coupling in skeletal muscles

A

Physical coupling between DHP receptor and ryanodine receptor

115
Q

Excitation-contraction coupling in cardiac muscle

A

L-type Ca2+ channel
-voltage-gate Ca2+ channel
Calcium-dependent calcium release

116
Q

ECC in Cardiac Muscle - Relaxation Steps

A
  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
Q

Refractory Period

A 
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
Q

Systole

A

Ventricular contraction and blood ejection

119
Q

Diastole

A

Ventricular relaxation and blood filling

120
Q

Cardiac Cycle

A

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
Q

Isovolumetric Ventricular Contraction (systole)

A

All heart valves closed, blood pressure in the ventricles remains constant

122
Q

Ventricular Ejection (systole)

A

Pressure in ventricles exceeds that in arteries, semilunar valves open and blood ejected into the artery

123
Q

Stroke Volume (systole)

A

Volume of blood ejected from each ventricle during systole

124
Q

Isovolumetric Ventricular Relaxation (diastole)

A

all heart valves closed, blood volume remains constant, pressure drops

125
Q

Ventricular filling (diastole)

A

AV valves open, blood flows into ventricles from atria. Ventricles receive blood passively

126
Q

Atria contraction (diastole)

A

occurs at the end of ventricular filling

127
Q

Cardiac Cycle - Diagram

A

Review this

128
Q

Pressure-volume curve

A

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
Q

End-diastolic Volume (EDV)

A

Amount of blood in each ventricle at the end of ventricular diastole

130
Q

End-systolic Volume (ESV)

A

Amount of blood in each ventricle at the end of ventricular systole

131
Q

Stroke Volume

A

Volume of blood pumped out of each ventricle during systole

132
Q

Stroke Volume Formula

A

SV=EDV-EDS (usually 70-75 mL)

133
Q

Wigger’s Diagram

A

Understand this diagram that shoed the pressure and volume changes for the heart

134
Q

Do the right side or the left side of the hear have lower pressure?

A

The right side has lower pressure than the left ventricle during systole

135
Q

2 Heart Sounds

A

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
Q

How does blood flow normally?

A

Laminar flow and makes no sound

-characterized by smooth concentric layers of blood moving in parallel down the length of a blood vessel

137
Q

Abnormal Blood Flow

A

May be turbulent

  • makes sounds = murmer
  • stenosis
  • insufficiency
138
Q

Stenosis

A

Blood flows rapidly through a narrowed valve; leaflets do not open completely

139
Q

Insufficient Valve

A

Blood flows backward through leaky valve; leaflets do not close completely

140
Q

Sympathetic Innervation of the Heart

A

The entire heart, including the atria, ventricles, SA node, AV node

141
Q

Parasympathetic Innervation of the Heart

A

Atria, SA node, AV node

142
Q

Parasympathetic Stimulation of the SA Node

A

rate of depolarization decreases; heart rate decreases

143
Q

Sympathetic Stimulation of the SA Node

A

rate of depolarization increases; heart rate increases

144
Q

Parasympathetic Stimulation of the AV Node

A

Conduction decreases; increased AV node delay

145
Q

Sympathetic Stimulation of the AV Node

A

Conduction increases; decreased AV node delay

146
Q

Parasympathetic Stimulation of the Atrial Muscle

A

Decreased contractility

147
Q

Sympathetic Stimulation of the Atrial Muscle

A

Increased contractility

148
Q

Parasympathetic Stimulation of the Ventricular Muscle

A

No significant innervation; no effect

149
Q

Sympathetic Stimulation of the Ventricular Muscle

A

Increased contractility

150
Q

Cardiac Output (CO)

A

The amount of blood pumped by each ventricle in one minute

151
Q

Cardiac Output Formula

A

CO = HR (heart rate) * SV (stroke volume)

152
Q

Factors Affecting Cardiac Output

A

Heart rate

Stroke Volume

153
Q

How do we alter heart rate?

A

Modifying the activity of the SA node

154
Q

How do we alter stroke volume?

A

Altered by varying the strength of the contraction of the ventricular myocardium

  • increased contraction = increased stroke volume
  • decreased contraction = decreased stroke volume
155
Q

Does the ventricles completely empty out after each contraction?

A

No

156
Q

Factors Affecting Heart Rate

A

Increased sympathetic activity
-increase heart rate
Increased parasympathetic activity
-decreased heart rate

157
Q

Effect of the Sympathetic System on Heart Rate

A

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
Q

Effect of the Parasympathetic System on Heart Rate

A

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
Q

Sympathetic Stimulation on Pacemaker Potential

A

Pacemaker potential rises more quickly to threshold, or takes less time to reach threshold, increasing the heart rate

160
Q

Parasympathetic Stimulation on Pacemaker Potential

A

Pacemaker potential rises more slowly to threshold, or takes more time, decreasing heart rate

161
Q

3 Factors Affecting Stroke Volume

A

End-diastolic volume (EDV; preload)
Contractility of the ventricles
Afterload

162
Q

Preload

A

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
Q

EDV

A

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
Q

Sympathetic Stimulation of Venous Smooth Muscle

A

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
Q

Frank-Starling Mechanism

A

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
Q

Mechanism of the Length-tension Relationship

A

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
Q

Contractility

A

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
Q

Sympathetic Stimulation and Contractility

A

The stroke volume is greater at any given EDV during sympathetic stimulation
More rapid contraction and more rapid relaxation
Ventricles ejecting more blood

169
Q

Ejection Fraction

A

EF = SV/EDV

170
Q

Mechanism of Sympathetic Effect on Contractility

A

Acts through a G protein coupled mechanism

171
Q

Afterload

A

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
Q

Endothelium

A

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
Q

Pressures in the Systemic and Pulmonary Circuits

A

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
Q

Arteries

A

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
Q

Elastic Arteries

A

Many elastic fibres, few smooth muscle cells

Expand and recoil in response to pressure changes

176
Q

Muscular Arteries

A

Many smooth muscle cells, few elastic fibres

Distributes blood

177
Q

Arterioles

A

1-2 layers of smooth muscle cells

Resistance vessels

178
Q

Vasoconstriction

A

Contraction of arterial smooth muscle decreases the diameter of the artery
-decreased blood flow to organs

179
Q

Vasodilation

A

Relaxation of arterial smooth muscle increases the diameter of the artery
-increased blood flow to organs

180
Q

Functions of Arterioles

A

Regulate blood flow to organs
-capillary beds
Determine MAP
-resistance

181
Q

Resistance in Arterioles

A

High resistance vessels due to their small size

  • causes drop in mean arterial pressure (MAP)
  • altering arteriolar diameter alters resistance and flow
182
Q

Intrinsic or Basal Tone

A

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
Q

Extrinsic Factors

A

Factors external to the organ or tissue; who body needs (MAP); nerves and hormones

184
Q

Intrinsic Factors

A

Local controls; organs and tissees alter their own arteriolar resistances independent of nerves or hormones

185
Q

Extrinsic Controls: Nerves

A

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
Q

Extrinsic Controls: Hormones

A

Epinephrine from adrenal medulla causes vasoconstriction or vasodilation

187
Q

Local Controls: Active Hyperemia

A

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
Q

Local Controls: Flow Autoregulation

A

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
Q

Reactive Hyperemia

A

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
Q

Capillaries

A

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
Q

Types of Capillaries

A

Continuous
Fenestrated
Sinusoidal

192
Q

Continuous Capillaries

A

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
Q

Pericytes

A

Lie external to the endothelium; may help stabilize the walls of blood vessels and help regulate blood flow through capillaries

194
Q

Fenestrated Capillaries

A 
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
Q

Sinusoid Capillaries

A 
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
Q

Microcirculation

A

The circulation of blood through the smallest vessels in the body

  • precapillary spincter
  • metarteriole
197
Q

Precapillary Sphincter

A 
At entrance to a capillary
Ring of smooth muscle
Alters blood flow
No innervation
-respond to local factors
198
Q

Metarteriole

A

Connects arterioles to venules
Contains smooth muscle cells
Change diameter to regulate flow

199
Q

Diffusion

A

Movement of substance down its concentration gradient

  • short distance to travel across a capillary
  • moves down concentration gradient
200
Q

Trancytosis

A

Use of vesicles to cross endothelial cells

-fused vesicle channel = endocytic and exocytic vesicles form a water-filled channel across the cell

201
Q

Bulk Flow

A

Movement of protein-free plasma across the capillary wall

-distribution of extracellular fluid volume

202
Q

Filtration

A

Movement of protein-free plasma from capillary to interstitial fluid

203
Q

Reabsorption

A

Movement of protein-free plasma from interstitial fluid to capillary

204
Q

Bulk Flow: Hydrostatic Pressure

A

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
Q

Bulk Flow: Colloid Osmotic Pressures

A

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
Q

Bulk Flow: Net Exchange Pressures

A

When net filtration pressure is positive = favours filtration
When net filtration pressure is negative = favours absorption

207
Q

Net Filtration and Net Reabsorption Along the Capillary

A

Transition point between filtration and reabsorption lies closer to venous end of capillary
-more filtration that absorption

208
Q

Distribution of Blood Volume

A

60% of blood volume is in the venous system

A lot of blood is found in the liver, bone marrow, and skin

209
Q

Veins

A

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
Q

Venous Valves

A

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
Q

Varicose Veins

A

Valves do not function properly when vein walls weaken, stretch
Blood pools and vessels distend

212
Q

Mechanisms for Venous Return

A 
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
213
Q

Venous Return and Frank-Starling Law

A

Increased venous return results in increased stroke volume through the Frank-Starling mechanism

214
Q

Lymphatic System Components

A

Lymphatic capillaries
Lymph vessels
Lymph nodes

215
Q

Lymph Capillaries

A

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
Q

Lymph Vessels

A

Formed from convergence of lymphatic capillaries
One-way valves
Empty into venous system
IF is called lymph once it enters the lymph vessels

217
Q

Lymph Nodes

A

Immune response

218
Q

Mechanism of Lymph Flow

A

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
Q

Arterial Blood Pressure

A

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
Q

Compliance

A

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
Q

Systolic Pressure

A

Maximum blood pressure during ventricular systole

222
Q

Diastolic Pressure

A

Minimum blood pressure at the end of ventricular diastole

223
Q

Systolic/Diastolic Pressure

A

120/80 mmHg

Normal blood pressure

224
Q

Pulse Pressure

A

Systolic - diastolic

225
Q

Hypertension

A

Chronically increased arterial blood pressure

226
Q

Hypotension

A

Abnormally low blood pressure

227
Q

Mean Arterial Pressure

A

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
Q

MAP Formula

A

MAP = CO * TPR

  • TPR=total peripheral resistance
  • can be determined by total arteriolar resistance
229
Q

TPR

A

The combined resistance of all of the systemic vessels

230
Q

Short-Term Regulation of MAP

A

Seconds to hours
Baroreceptors reflexes
Adjusts CO and TPR resistance by ANS

231
Q

Long-Term Regulation of MAP

A

Adjust Blood Volume

Restore normal salt and water balance through mechanisms that regulate urine output and thirst

232
Q

Arterial Baroreceptors

A

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
Q

Baroreceptor Action Potential Frequency

A

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
Q

The Medullary Cardiovascular Center

A

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
Q

Chemoreceptors

A

Respond to O2 and pH levels in blood

  • affect respiration and blood pressure through the cardiovascular center
  • aortic and carotid bodies

Physiology 210 (12 decks)

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