Cardiovascular Flashcards
(179 cards)
1
Q
Primary role of circulatory system
A
the distribution of dissolved gases and other molecules for nutrition, growth and repair, while simultaneously removing cellular wastes
2
Q
3 basic functional parts of circulatory system
A
- heart
- leucocytes and platelets
- vessels
3
Q
Secondary roles of circulatory system
A
- chemical signalling to cells by means of circulating hormones or neurotransmitters
- dissipation of heat by delivering heat from the core to the surface of the body
- mediation of inflammatory and host defence responses against invading microorganisms
4
Q
Transport into circulatory system
A
- Materials entering the body
- materials moved from cell to cell
- materials leaving the body
5
Q
Materials entering the body
A
- Oxygen
- from lungs to all cells
- Nutrients and Water
- from intestinal tract to all cells
6
Q
Materials moved from cell to cell
A
- Wastes
- from: some cells to live
- immune cells, antibodies, clotting proteins
- from: present in blood continuously to: available to any cell that needs them
- Hormones
- from endocrine cells to target cells
- stored nutrients
- from live and adipose tissue to all cells
7
Q
Materials leaving the body
A
- Metabolic wastes
- from all cells to kidneys
- Heat
- from all cells to skin
- Carbon Dioxide
- from all cells to lungs
8
Q
Circuits in the Heart
A
a dual pump driving blood in two serial circuits
- Pulmonary and Systemic
9
Q
Pulmonary Circuit
A
- pumps deoxygenated blood to the lungs
- mainly works through the right side of the heart
10
Q
Systemic Circuit
A
- feeds oxygenated blood throughout the whole body except the lungs
- mainly works through the left side of the heart
11
Q
Vasculatures
A
- arteries, veins, capillaries
- system of vessels
- system of valves in heart and veins ensures that blood flows in one direction
12
Q
Arteries
A
carrying blood away from the heart
13
Q
Veins
A
carrying blood back to the heart
- contains valves
14
Q
Capillaries
A
smallest vessels where transport takes place
15
Q
Circulation in Systemic Circuit
A
- Coronary circuit
- Digestive tract/liver portal system
- Kidney portal system
16
Q
Right Atrium Transport
A
- receives from: Venae Cavae
- sends blood to: Right Ventricle
17
Q
Right Ventricle Transport
A
- receives from: Right Atrium
- sends blood to: Lungs
18
Q
Left Atrium Transport
A
- receives from: Pulmonary veins
- sends blood to: Left Ventricle
19
Q
Left Ventricle Transport
A
- receives from: Left Atrium
- sends blood to: body except lungs
20
Q
Vanae Cavae
A
- receives from: Systemic veins
- send blood to: Right Atrium
21
Q
Pulmonary Trunk (Artery)
A
- receives from: Right Ventricle
- sends blood to: Lungs
22
Q
Pulmonary Vein
A
- receives from: Veins in the Lungs
- sends blood to: Left Atrium
23
Q
Aorta
A
- receives from: Left Ventricle
- Systemic Arteries
24
Q
Aorta
A
- receives from: Left Ventricle
- Systemic Arteries
25
Blood Flow in Cardiovascular System
- liquid and gases flow down pressure gradients from regions of high pressure to regions of low pressure
26
Initial region of high pressure
created by contraction of the heart
27
Pressure as Blood Flows
- pressure is lost
| - due to friction created between blood and vessel walls
28
Sources of Pressure
- pressure of a fluid is the force exerted on container
- pressure measured in mmHg
- pressure exerted by a fluid in a container that is not moving is equal to the hydrostatic pressure
29
Hydrostatic Pressure
- pressure exerted by gravity downward on the floor of the container as well as on other sides
30
Driving Pressure
- pressure change in liquids without volume change
| - walls of fluid filled ventricles contract, increasing pressure of blood within ventricles
31
Blood Pressure
- heart muscles = relaxed
- pressure exerted by blood decreases
- vessels have the ability to constrict or dilate affecting blood pressure
32
Higher Pressure to Lower Pressure
- pressure gradient created through contraction of the ventricles
- flow of blood is directly proportional to the pressure gradient at each end of the tube (not absolute pressure)
33
Poiseuille's Law
- well defined system
- predict the resistance to flow from the geometry of the vessels and the properties of the fluid
F = ΔP * πr^4 / 8ηl
34
Blood Flow
- inversely proportional to both the length of the vessel and viscosity of the liquid
- flow directly proportional to the 4th power of the vessel radius
F = ΔP * πr^4 / 8ηl
35
Resistance
- resistance in inversely proportional to the 4th power of the vessel
- LARGER RADIUS = LESS RESISTANCE
R = 8ηl / πr^4
36
Ideal Size of a Vessel
- shorter length in tube = less resistance and more flow
| - larger radius tube = less resistance and more flow
37
Velocity
- depends on flow rate and cross-sectional area
- how fast blood flows past a certain point
v = Q/A
- equal flow rate = velocity is more rapid in narrow sections of vessel
38
The Heart
- located in the centre of the thoracic cavity
- apex angles slightly downward to the left of the body
- encased in a tough membranous sac (Pericardium)
- composed mostly of myocardium covered by thin inner and outer layers of epithelium and connective tissue
39
Pericardium
- double walled sac filled with a thin layer of clear pericardial fluid
- lubricates the external surface of the heart as it beats within the sac
40
Atrioventricular Valves (AV)
- allow flow from the atria into the ventricles
- attached to a papillary muscle in each ventricle by chord tendineae (tendon)
- these muscles only supply stability to valves, don't open them
- RA -> RV: TRICUSPID valve
- 3 flaps
- RST: Right Side Triscupid
- La -> LV: BICUSPID (mitral)
41
Semilunar Valves
- one way valves that exist between the ventricle and outflow artery
- both have 3 cup-like leaflets
- LV -> Aorta ( AORTIC VALVE)
- RV -> Pulmonary artery: PULMONARY VALVE
- these valves do not need connective tendons due to shape of them
42
Ventricular Contraction
- AV valves stay closed to prevent blood flow backward into the atria
- Semilunar valves open
43
Ventricular Relaxation
- AV valves open
| - semilunar valves close to prevent blood that has entered the arteries from flowing back into the ventricles
44
Cardiac Conduction System
- SA node
- AV node
- auto rhythmic cells
- group with most rapid pacemaker activityset heart rate
45
SA Node
- pacemaker
- the group of cells where cardiac action potentials originate
- spreads through autorhythmic cells
46
AV Node and Purkinje fibres
- slower pacemaker activity over ridden by that of the SA node
47
Atrial Conduction
- atrial muscle has 4 special conducting bundles
1. Backman's bundle
2. Anterior Pathway
3. Middle Pathway
4. Posterior Pathway
- relatively slow (80-100 ms)
48
Backman's Bundle
- conducts action potentials from the SA pacemaker into the left atrium causing contraction
49
Anterior, Middle, Posterior Internodal Pathways
- conduct the action potential from the SA node to the AV node, depolarizing right atrial muscle along the way
50
Ventricular Conduction
- layer of connective tissue prevents conduction directly from atria to ventricle
- conduction slows down through the AV node to allow blood from atria to empty in to ventricles
51
Process of Ventricular Conduction
- depolarization proceeds through the septum to the apex
| - spreads up the wall of the ventricles from apex to base
52
Ventricular Muscles
- have spiral arrangement that ensures blood is squeezed upwards from the apex of the heart
53
Complete Conduction Block
- when electrical activity can't be transferred from the atria to ventricles
- caused by damage in conduction pathways
ex) block at bundle of His results in complete dissociation between atria and ventricles
- SA node continues as pacemaker for atria, but electrical activity doesn't make it to ventricles so purkinje fibres take over as pacemaker
- requires artificial pacemaker
54
Electrocardiogram (ECG, EKG)
- electrodes on skin's surface can record electrical activity of the heart
- possible because salt-solutions (NaCl-based ECF) are good conductors of electricity
- show the summed electrical activity generated by all the cells of the heart
55
Einthoven's Triangle
- hypothetical triangle created around the heart when electrodes placed on both arms and left leg
- three "leads" (pairs of electrodes)
- ECG recorded one lead at a time, where one electrode acts as a positive electrode
56
ECG Electrical Activity
- moving towards positive electrode of the lead then an upward deflection is recorded
- moving away from positive electrode is downward deflection
- moving perpendicular to axis of electrodes causes no deflection
57
ECG Properties
- Waves: appear as deflections above or below the baseline
- Segments: the sections of baseline between two waves
- Intervals: combo of waves and segments
- P wave: atrial depolarization
- P-R Segment: conduction through AV node and AV bundle
- QRS Complex: ventricular depolarization
- T Wave: ventricular repolarization
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Conducting System of the Heart
1. SA Node
2. Internodal Pathways
3. AV Node
4. Bundle of HIS
5. Bundle Branches
6. Purkinje fibres
59
End Diastolic Volume
- the maximal volume in the ventricle, after ventricular filing
- 70 kg man at rest ~135ml
60
End-Systolic Volume
- the minimal amount of blood in the ventricles, blood left after ventricular contraction
- ~65ml
- provides safety margin, a more forceful contraction of the heart will because a larger stroke volume resulting in a decrease in ESV
- need additional blood in ventricles to compensate for changes in contractility
61
Stroke Volume
- amount of blood ejected during a single ventricular contraction
- ~70ml
- SV = EDV - ESV
- can increase to as high as 100ml
- modulated by the autonomic NS, venous return and certain drugs
62
Cardiac Output
- flow of blood delivered from one ventricle in a given time period
- CO's of pulmonary and systematic circuit are usually identical
- if offset, blood pools in the circuit with the weaker side of heart
- can raise to 30-35 L/min during exercise
63
Cardiac Output Calculation
- total blood flow
| - CO = Heart Rate + Stroke Volume
64
Cardiac Output Modifications
- adjusting heart rate
| - modulating stroke volume
65
Adjusting Heart Rate
- parasympathetic
- sympathetic
- blocking HCN channels
- opening K+ channels
- blocking T-type channels
66
Modulating Stroke Volume
- normally as force of contraction increases, stroke volume increases
67
Two Factors that Determine Force Generated by Cardiac Muscle
1. Contractility of the heart
| 2. Length of the muscle fibres at beginning of contraction
68
Contractility of the Heart
- intrinsic ability of cardiac muscle fibres to contract at any given fibre length
- a function of Ca2+ entering and interacting with contractile filaments
69
Contractility
- controlled by nervous and endocrine system
- increased by catecholamines
- increases as amount of Ca2+ available increases
70
Ionotropic Agent
any chemical that affects contractility
71
Iontropic Effect
- the influence of an iontropic agent
- positive inotropic effect
- chemicals increasing contractility
- negative inotropic effect
- decreasing contractility
72
Catecholamine's Effect on Contractility
- Norepinephrine and Epinephrine
- released from the sympathetic neuron or adrenal medulla
- cause a postive inotropic effect REGARDLESS of EDV
73
Sympathetic Modulation of Contraction (SV)
1. phosphorylation of Ca2+ channels increases calcium conductance during AP's
2. phosphorylation of RyR enhances sensitivity to Ca2+, increasing release of Ca2+ from SR
3. increases rate of myosin ATPase
4. phosphorylation of SERCA (PLN) increases speed of Ca2+ re-uptake which increases Ca2+ storage
74
Increasing Sarcomere Length
- increases force of contraction (SV)
| - skeletal length tension relationship explained by degree of overlap between thick and thin filaments
75
Raising Sarcomere Length:
1. increases Ca2+ sensitivity of myofilaments
- stretched sarcomere = decreased diameter, which reduce distance Ca2+ needs to diffuse
2. puts additional tension on stretch-activated Ca2+ channels, increasing Ca2+ entry from extracellular space and increasing Ca2+ induced Ca2+ release increasing tension
76
Frank-Starling Law
- the amount of force developed by the cardiac muscle of a ventricle depends on the initial stretch of the ventricle walls
- caused by ventricular filing
- amount of force indicated by SV
- preload
- SV increases with increasing EDV
77
Preload
- the degree of myocardial stretch prior to contraction
78
Venous Return
- blood returning from veins to heart
79
Factors Affecting Venous Return
1. Skeletal Pump
2. Respiratory Pump
3. Sympathetic contraction of veins
80
Skeletal Pump
- skeletal muscle activity compresses veins in the extremities pushing blood back to the heart
- increased muscle activity of the extremities can increase venous return
81
Respiratory Pump
- during inspiration the chest expands and diaphragm moves down creating a sub atmospheric pressure in the thoracic cavity, this draws blood into the vena cava that exists within this cavity
- also during inspiration veins in the abdomen are compressed also forcing blood back to the heart
82
Sympathetic Constriction of Veins
- decreases their volume squeezing blood back towards that heart
83
Afterload
- the end load against which the heart contracts to eject blood
- primarily determined by the pressure in the outflow artery prior to contraction (aorta or pulmonary artery)
- can be increase in pathological situations
- increased arterial blood pressure, decrease aortic compliance
- clinically arterial blood pressure an indirect indicator of afterload
84
Echocardiography
- ultrasound for heart
| - to look at size of chambers and sound of heart
85
Ejection Fraction
- the percentage of EDV ejected from the heart (SV)
EF = SV/EDV
86
Vessels
- aorta>arteries>arterioles>capillaries>venules>veins>vena cava
- all contain inner layer of thin endothelial cells and can be wrapped in a combination of elastic tissue, smooth muscle or firbrous tissue
87
Endothelial cells
- inner layer of all vessels
- thought to only be a passive barrier
- important in secreting paracrines (substances that signal changes in near by cells) regulation of blood pressure, blood vessel growth, absorption of materials
88
Artery Materials
1. endothelium (least)
2. elastic tissue (2nd most)
3. smooth muscle (most)
4. fibrous tissue
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Arteriole Materials
1. endothelium (least)
| 2. smooth muscle (most)
90
Capilliary Materials
only endothelium
91
Venule Materials
1. endothelium (least)
| 2. fibrous tissue
92
Vein Materials
1. endothelium (least)
2. elastic tissue (2nd most)
3. smooth muscle (most)
4. fibrous tissue
93
Vascular Smooth Muscle
- amount of smooth muscle varies
- there is a state of partial contraction at all times (tone)
- can be influenced by a variety of substances including neurotransmitters, hormones, paracrines
- these substances bind receptors ultimately resulting in an increase in cytosolic Ca2+ causing contraction
94
Arteries
- walls that are both stiff and springy (pressure reservoir)
| - thick Smooth muscle layer and large amounts of elastic and fibrous connective tissue
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Arterioles
- branch off from arteries
| - mainly contain vascular smooth muscle
96
Microcirculation
- made up of arterioles, capillaries, and venues
97
Metarterioles
- cut across the microcirculation
| - act as a capillary bypass vessels
98
Capillaries
- smallest vessels in CV system
- where majority of exchange between blood and interstitial space occue
- single layer of endothelial layer surrounded by a basal lamina (extracellular matrix)
- gases can passively diffuse across
- linked by interendothelial junctions
- some cells contain fenestrations
- often surrounded by pericytes (BBB)
99
Interendothelial Cells
- aid in the transport of small solutes and water
100
Fenestrations
- membrane lines conduits running through them to allow the transport
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Pericytes
- determine how leaky a capillary is
- more pericytes: less leaky
- thought to control blood vessels (contract them)
102
Continuous Capillary
- most common
- thicker endothelial cells that do not contain fenestrations
- only allow passage of water and small ion through tight junctions
103
Fenestrated Capillary
- thin endothelial cell that are perforated with fenestrations
- fenestrations often have a thin diaphragm
- small molecule passage
104
Discontinuous Capillary
- lack a basal membrane
- have large open fenestrations and gaps between endothelial cells
ex) liver and spleen
105
Methods of Transport in Capillaries
1. Transcellular Transport
2. Paracellular Transport
3. Transcytosis
106
Transcellular Transport
- diffusion accrocs the endothelial cell membrane
| - gases, small lipid soluble molecules, water (aquaporin channels)
107
Paracellular Transport
- diffusion through interendothelial junctions, pores, and fenestrations (water, small water soluble and small polar molecules)
108
Transcytosis
- the combination of endocytosis, vesicular transport, and exocytosis that transport macromolecules across endothelial cells
109
Venules
- in-between veins and capillaries
110
Veins
- more numerous and have a larger volume, thinner walls and more elastic tissue compared to arteries
- venous circulation = volume reservoir of the circulatory system
111
Angiogenesis
- formation of new blood vessels
- adult microcirculation is constant
- exceptions: vessel growth during wound healing, endurance training, inflammation, tumor growth, endometrium during menstrual cycle
- angiogenic growth factors (mitogens-pro mitotic) activate receptors on endothelial cells
112
Angiogenesis Process
- activated endothelial cells produce proteases that degrade basal lamina so it can move away from parent cell
- endothelial cells proliferate into the surrounding matrix and form sprouts towards the angiogenic stimulus in tandem
- sprouts form loops to become a full-fledged vessel lumen as cells migrate to site of angiogenesis
113
Angiogenesis Promoters
- Vascular Endothelial growth factors (VEGF)
- Fibroblast growth factors (FGFs)
- Angioprotein 1 (ANGPT1)
114
Angiogenesis Inhibitors
- Endostatin
- Angiostatin
- Angioprotein 2 (ANGPT2)
115
Angiogenesis in Tumors
- angiogenesis is a necessary part of the process of progression of cancer from all, localize neoplasms to larger, growing, and potentially metastatic tumors
- understanding of this may provide treatment options for other CV diseases
116
Blood Pressure (Systemic Circuit)
- ventricular contraction creates the force necessary to propel blood through CV system
- aorta and large arteries sustain driving pressure during ventricular diastole
117
Ventricular Contraction Process
1. ventricle contracts
2. semilunar valve opens. blood ejected from ventricles flows into arteries
3. aorta and arteries expand and store pressure in elastic walls
118
Ventricular Relaxation Process
1. isovolumic ventricular relaxation
2. semilunar valve shuts, preventing flow back into ventricle
3. elastic recoil of arteries sends blood forward into rest of circulatory system
119
Blood Pressure
- pressure highest in the aorta and decreases throughout circuit
- aortic pressure highest during ventricular contraction (systole)
- aortic pressure lowest during ventricular relaxation (diastole)
120
Pulse Pressure
- difference between systolic and diastolic pressure
- > systolic pressure - diastolic pressure
- only exists on the arterial/areriole side of circuit
121
Mean Arterial Blood Pressure
- reflects the driving pressure for blood flow
- not simply the average of systolic and diastolic pressure (100mg) because equal amounts of times are not spent in systole and diastole
- balance between blood flow into and out of arteries
122
Mean Arterial Blood Pressure Equation
= diastolic pressure + 1/3 (pulse pressure)
123
Hypotension
- represents when blood pressure falls too low
| - because driving force for blood flow to be inadequate to overcome the opposition by gravity
124
Hypertension
- represents when the blood pressure is chronically elevated
- high pressure on vessel walls cause them to weaken or rupture and leak
- cerebral hemorrhage (stroke) of vessel in brain
- believed to be due to increased peripheral resistance without cardiac output change
125
Sphygmomanometer
- estimates blood pressure
- cuff goes on Brachial Artery
- closes off artery, pressure above 120 mm Hg
- slowly releases so Korotkoff sounds are heard
- fully released, artery no longer compressed
126
Mean Arterial Pressure and CO
- mean arterial pressure proportional to cardiac output x peripheral resistance
- if cardiac output increase and peripheral does not change -> increase in volume in arteries and increase in arterial pressure
127
Factors Influencing Mean Arterial Blood Pressure
- blood volume
- cardiac output
- resistance of system to blood flow
- relative distribution of blood between arterial and venous blood vessels
128
Volume Reservoir of CV
- Veins
129
Pressure Reservoir of CV
- arteries
130
Increases in Blood Volume
- affects blood pressure
- small changes in blood volume occur from ingestion of food and liquids
- primarily resolved by kidneys
131
Decreases in Blood Volume
- requires an integrated response from the kidneys, cardiovascular system (increase sympathetic output) and ingestion of fluid
132
Resistance in Arterioles
- contributes to >60% of total resistance to flow in cardiovascular system
- influenced by:
- alter in vascular smooth muscle (changing radius)
1. Local control
2. Sympathetic reflexes
3. Hormones
133
Local Control
1. Myogenic Autoregulation
| 2. Paracrines alter Vascular Smooth Muscle
134
Myogenic Autoregulation
- some vascular smooth muscle can regulate its own state of contraction
- increase in blood pressure leads to vascular smooth muscle in wall of arteriole to stretch and then contract (vasoconstriction)
- stretch activated channels
135
Paracrines Alter Vascular Smooth Muscle
- local blood flow allows individual tissues regulate their own blood supplies
- paracrines can act on nearby arterial vessels to relax it
- metabolism related: decrease O2, increase CO2, NO, H+, lactate, adenosine
- paracrines can also increase blood to an area with damage
- non-metabolism: kinins, histamine (inflammation), serotonin
136
Sympathetic Control
- primarily sympathetic neurons innervate arterioles and tonically control arteriolar diameter through activation and deactivation of alpha1 adrenergic receptors
- increase norepinephrine: constricts vessel
- decrease norepinephrine: dilates vessel
- secondary method releases epinephrine
137
Sympathetic Control with Release of Epinephrine
- release from adrenal medulla in response to sympathetic activation
- has a low affinity for alpha receptors that cause vasoconstriction
- has high affinity for beta2 adrenergic receptors that lead to vasodilation
138
Vasoconstriction
- caused by norepinephrine binding to alpha1 receptor
| - more found in GI tract than in muscle
139
Vasodilation
- caused by epinephrine binding to beta2 receptor
| - more found in muscle than in GI tract
140
Flow is Proportional to...
1. Pressure Gradient
| 2. Resistance to Flow
141
Distribution of Blood to Tissues
- selectively alter blood flow to organs is important in cardiovascular regulation (local/reflex)
- at rest amount of blood flow depends on # and size of arteries feeding the organ
- regional varieties occur because arterioles are arranged parallel
142
Flow in Arterioles
- arranged in parallel so they receive blood at same time
- total blood flow of arterioles = CO
- flow for each arteriole depends on resistance
- if an arteriole constricts resistance increases and blood flow decreases
- blood is diverted away from high resistance arterioles and towards low resistance arterioles
143
Regulation of Cardiovascular Function
CNS!
| - coordinates reflex control of blood pressure and the distribution of blood to tissues
144
Main Integrating Centre for Cardiovascular Centre
Medullary cardiovascular control center (CVCC)
145
CVCC
- maintains a sufficient mean arterial pressure to ensure adequate blood flow to the brain and heart
- receives input from sensory receptors and other brain regions
- has ability to specifically alter function in a few organs or tissues
- integrates sensory info and initiates appropriate response
146
Baroreceptor Reflex
- the primary reflex pathway for homeostatic control of mean arterial blood pressure
- tonically active stretch sensitive mechanoreceptors
- situated on the aorta and on the carotid artery
- senses stretch when there is an increase of blood pressure and increases their firing rate
147
Baroreceptor Reflex Process
1. arteriole constricts > increase resistance > increased total peripheral resistance
2. > increase
TPR x CO > increase MAP
3. increase MAP > baroreceptors fire > baroreceptor reflex
4. baroreceptor reflex > decrease CO, increase TPR x decrease CO = MAP restored
148
Orthostatic Hypotension
- triggers baroreceptor
- when you get out of bed
- CO falls from 5L/min to 3 L/min
- baroreceptors act fast, within 2 heartbeat MAP is increased
149
Peripheral Chemoreceptors
- located on the aortic arch and carotid artery
- sense alterations in blood-gas concentrations [O2] [CO2] and changes in blood pH
- send info back to CVCC, which results in change in autonomic output to return blood gas levels to normal
- peripheral chemoreceptor activation change ventilation within the respiratory system
150
Hypothalamus
- capable of altering cardiovascular function in response to emotional stress
ex) seeing blood may make one faint (vasovagal syncope)
- results in a large increase in parasymp output (decrease CO)
- reduction in symp output (large decrease in peripheral resistance) (fall in blood pressure fails to activate normal baroreceptor response)
- parasympathetic decrease in HR
151
Bulk Flow
- the mass movement of fluid as the result of hydrostatic or osmotic pressure gradients
- play out capillary filtration and absorption
152
Filtration
- if bulk flow is resulting in the movement of fluid out of the capillaries
153
Hydrostatic Pressure
- the pressure I'm the blood vessels drives fluid out of the capillaries through pores and leaky cell junctions (filtration)
- PUSHES FLUID OUT
154
```
Colloid Osmotic Pressure
Oncotic Pressure (π)
```
- the pressure that draws fluid into the capillaries is the pressure created by the plasma proteins in the blood
- DRAWS FLUID BACK IN
155
Capillary Filtration and Absorption
- π steady in capillary, exceeds interstitial space π (zero)
- PH in vessels decreases as blood travels through capillaries due resistance and exceeds interstitial PH (zero)
- at the arterial end PH exceeds π causing net filtration
- at the venous end π exceeds PH and there is absorption
- overall: net filtration resulting in loss of 3L of fluid/day
156
Lymphatic Vessels
- assist CV system with returning fluid and proteins lost through the capillaries
- similar to capillaries
- has a singel endothelial layer
- contain large inter endothelial junctions (one-way valve)
- nodes distributed that contain immune cells
157
Initial Lymphatic Segment
- interstitial hydrostatic pressure is higher than inside the lymphatic causing the microvalves to open and fluid to flow in
- when they fill up with fluid, the hydrostatic pressure exceeds interstitial so micro valves close and secondary valves open
158
Collecting Lymphatics
- contain smooth muscle that actively propel fluid and one way valves to prevent back flow, skeletal muscle assists as well
159
Edema
- an abnormal accumulation of fluid in the interstitial space
- occurs because:
1. inadequate lymph drainage
2. a disruption in normal balance between capillary filtration and absorption (filtration>absorption)
i) increased capillary hydrostatic pressure (heart failure)
ii) decease in plasma protein concentration (malnutrition, liver failure)
iii) increase in interstitial proteins (excessive leakage of proteins out of capillaries)
160
Cross Sectional Area of Blood Flow
- with each branching of a vessel, the two new branches always have a higher total cross sectional area than the parent vessel
- single capillaries = small csa
- ALL capillaries together = large csa
161
Velocity of Blood Flow
- rate of blood flow through capillaries plays a role in the efficiency of exchange between the blood and the interstitial fluid
- slow velocity ensures adequate gas and nutrient exchange at the capillaries
162
Velocity of Blood Equation
= Flow rate / c.s. area
163
Cardiovascular Disease
- disorders of the heart and blood vessels
| - heart attacks, strokes
164
Uncontrolled Risk Factors of CVD
- age, sex, family history of early CVD, genetic
165
Controlled Risk Factors of CVD
- cigarette smoking, obesity, sedentary lifestyle and untreated hypertension
- combination of both; diabetes, hyperlipidemia
166
Atherosclerosis
- inflammatory process leading to hardening or narrow of arteries
167
Lipoproteins
1. High-density lipoprotein-cholesterol complexes
| 2. Low-density lipoprotein-cholesterol complexes
168
High-Density Lipoprotein Cholesterol Complexes (HDL-C)
- high levels associated with lower risk of heart attack
| - H = healthy
169
Low-Density Lipoprotein Cholesterol Complexes (LDL-C)
- "bad" cholesterol, elevated levels associated with coronary heart disease
- necessary for cholesterol transport in to cells, LDL-C's proteins are digested to amino acids and the freed cholesterol is used to make cell membranes and steroid hormones
170
Cholesterol
- not readily soluble in aqueous solutions
| - joins with lipoproteins
171
Development of Atherosclerotic Plaques
1. LDL-C accumulates btwn endothelium and connective tissue and is oxidized
2. macrophage ingest cholesterol and become foam cells
3. smooth muscle cells begin to divide and take up cholesterol
4. lipid core accumulates beneath endothelium
5. fibrous scar tissue forms to wall of lipid core
6. smooth muscle cells divide and contribute to thickening intimacy
7. calcifications are deposited within the plaque
8. macrophages may release enzymes that dissolve collagen and convert plaque from stable to unstable
9. platelets that are exposed to collagen activate and initiate a blood clot
172
Myocardial Infarction
- heart attack
- happens if a clot blocks blood flow to heart muscle
- lack of O2 leads to ATP supply declining, the contractile cells are unable to remove Ca2+ from cytosol
- high intracellular [Ca2+] closes gap junctions in damaged cells, electrically isolating them
- large damaged region can because irregular heart beat (arrhythmia)
173
Hypertension
- failure of homeostasis
- doubles risk for CVD for each 20/10 mmHg increase in blood pressure above the baseline value of 115/75
- 90% of hypertensive patients have primary hypertension with no definitive cause besides genetics
- possibly lack of nitric oxide production
- remaining 5-10% of hypertension cases is usually secondary to an underlying condition
174
Effects of Hypertension
- adaption of the baroreceptors to higher pressure with a down regulation of their activity
- a risk factor for atherosclerosis
- hypertension increases afterload
- increased force the heart must overcome causes myocardial contractile cells to undergo hypertrophy
- eventually heart begins to fail
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Hypertension Treatments
- Ca2+ channel blockers (L-type)
- diuretics
- beta blockers
- ACE inhibitors and angiotensin receptor blockers
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L-Type Channel Treatment
- relax vascular smooth muscle and/or decrease CO (HR and force of contraction)
177
Diuretics
- increase urination removing excess fluid to decrease blood volume
178
Beta Blockers
- block B1 adrenergic receptors decreasing CO
179
ACE Inhibitors and Angiotensin Receptor Blockers
- prevent vasoconstrictions from renin-angiotensin aldosterone axis
