Cardiovascular Flashcards
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
Q
Blood Flow in Cardiovascular System
A
- liquid and gases flow down pressure gradients from regions of high pressure to regions of low pressure
26
Q
Initial region of high pressure
A
created by contraction of the heart
27
Q
Pressure as Blood Flows
A
- pressure is lost
- due to friction created between blood and vessel walls
28
Q
Sources of Pressure
A
- 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
Q
Hydrostatic Pressure
A
- pressure exerted by gravity downward on the floor of the container as well as on other sides
30
Q
Driving Pressure
A
- pressure change in liquids without volume change
- walls of fluid filled ventricles contract, increasing pressure of blood within ventricles
31
Q
Blood Pressure
A
- heart muscles = relaxed
- pressure exerted by blood decreases
- vessels have the ability to constrict or dilate affecting blood pressure
32
Q
Higher Pressure to Lower Pressure
A
- 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
Q
Poiseuille’s Law
A
- 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
Q
Blood Flow
A
- 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
Q
Resistance
A
- resistance in inversely proportional to the 4th power of the vessel
- LARGER RADIUS = LESS RESISTANCE
R = 8ηl / πr^4
36
Q
Ideal Size of a Vessel
A
- shorter length in tube = less resistance and more flow
- larger radius tube = less resistance and more flow
37
Q
Velocity
A
- 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
Q
The Heart
A
- 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
Q
Pericardium
A
- 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
Q
Atrioventricular Valves (AV)
A
- 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
Q
Semilunar Valves
A
- 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
Q
Ventricular Contraction
A
- AV valves stay closed to prevent blood flow backward into the atria
- Semilunar valves open
43
Q
Ventricular Relaxation
A
- AV valves open
- semilunar valves close to prevent blood that has entered the arteries from flowing back into the ventricles
44
Q
Cardiac Conduction System
A
- SA node
- AV node
- auto rhythmic cells
- group with most rapid pacemaker activityset heart rate
45
Q
SA Node
A
- pacemaker
- the group of cells where cardiac action potentials originate
- spreads through autorhythmic cells
46
Q
AV Node and Purkinje fibres
A
- slower pacemaker activity over ridden by that of the SA node
47
Q
Atrial Conduction
A
- atrial muscle has 4 special conducting bundles
- Backman’s bundle
- Anterior Pathway
- Middle Pathway
- Posterior Pathway
- relatively slow (80-100 ms)
48
Q
Backman’s Bundle
A
- conducts action potentials from the SA pacemaker into the left atrium causing contraction
49
Q
Anterior, Middle, Posterior Internodal Pathways
A
- conduct the action potential from the SA node to the AV node, depolarizing right atrial muscle along the way
50
Q
Ventricular Conduction
A
- 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
Q
Process of Ventricular Conduction
A
- depolarization proceeds through the septum to the apex
- spreads up the wall of the ventricles from apex to base
52
Q
Ventricular Muscles
A
- have spiral arrangement that ensures blood is squeezed upwards from the apex of the heart
53
Q
Complete Conduction Block
A
- 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
Q
Electrocardiogram (ECG, EKG)
A
- 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
Q
Einthoven’s Triangle
A
- 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
Q
ECG Electrical Activity
A
- 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
Q
ECG Properties
A
- 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
58
Q
Conducting System of the Heart
A
- SA Node
- Internodal Pathways
- AV Node
- Bundle of HIS
- Bundle Branches
- Purkinje fibres
59
Q
End Diastolic Volume
A
- the maximal volume in the ventricle, after ventricular filing
- 70 kg man at rest ~135ml
60
Q
End-Systolic Volume
A
- 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
Q
Stroke Volume
A
- 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
Q
Cardiac Output
A
- 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
Q
Cardiac Output Calculation
A
- total blood flow
- CO = Heart Rate + Stroke Volume
64
Q
Cardiac Output Modifications
A
- adjusting heart rate
- modulating stroke volume
65
Q
Adjusting Heart Rate
A
- parasympathetic
- sympathetic
- blocking HCN channels
- opening K+ channels
- blocking T-type channels
66
Q
Modulating Stroke Volume
A
- normally as force of contraction increases, stroke volume increases
67
Q
Two Factors that Determine Force Generated by Cardiac Muscle
A
- Contractility of the heart
2. Length of the muscle fibres at beginning of contraction
68
Q
Contractility of the Heart
A
- intrinsic ability of cardiac muscle fibres to contract at any given fibre length
- a function of Ca2+ entering and interacting with contractile filaments
69
Q
Contractility
A
- controlled by nervous and endocrine system
- increased by catecholamines
- increases as amount of Ca2+ available increases
70
Q
Ionotropic Agent
A
any chemical that affects contractility
71
Q
Iontropic Effect
A
- the influence of an iontropic agent
- positive inotropic effect
- chemicals increasing contractility - negative inotropic effect
- decreasing contractility
72
Q
Catecholamine’s Effect on Contractility
A
- Norepinephrine and Epinephrine
- released from the sympathetic neuron or adrenal medulla
- cause a postive inotropic effect REGARDLESS of EDV
73
Q
Sympathetic Modulation of Contraction (SV)
A
- phosphorylation of Ca2+ channels increases calcium conductance during AP’s
- phosphorylation of RyR enhances sensitivity to Ca2+, increasing release of Ca2+ from SR
- increases rate of myosin ATPase
- phosphorylation of SERCA (PLN) increases speed of Ca2+ re-uptake which increases Ca2+ storage
74
Q
Increasing Sarcomere Length
A
- increases force of contraction (SV)
- skeletal length tension relationship explained by degree of overlap between thick and thin filaments
75
Q
Raising Sarcomere Length:
A
- increases Ca2+ sensitivity of myofilaments
- stretched sarcomere = decreased diameter, which reduce distance Ca2+ needs to diffuse
- puts additional tension on stretch-activated Ca2+ channels, increasing Ca2+ entry from extracellular space and increasing Ca2+ induced Ca2+ release increasing tension
76
Q
Frank-Starling Law
A
- 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
Q
Preload
A
- the degree of myocardial stretch prior to contraction
78
Q
Venous Return
A
- blood returning from veins to heart
79
Q
Factors Affecting Venous Return
A
- Skeletal Pump
- Respiratory Pump
- Sympathetic contraction of veins
80
Q
Skeletal Pump
A
- 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
Q
Respiratory Pump
A
- 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
Q
Sympathetic Constriction of Veins
A
- decreases their volume squeezing blood back towards that heart
83
Q
Afterload
A
- 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
Q
Echocardiography
A
- ultrasound for heart
- to look at size of chambers and sound of heart
85
Q
Ejection Fraction
A
- the percentage of EDV ejected from the heart (SV)
EF = SV/EDV
86
Q
Vessels
A
- 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
Q
Endothelial cells
A
- 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
Q
Artery Materials
A
- endothelium (least)
- elastic tissue (2nd most)
- smooth muscle (most)
- fibrous tissue
89
Q
Arteriole Materials
A
- endothelium (least)
2. smooth muscle (most)
90
Q
Capilliary Materials
A
only endothelium
91
Q
Venule Materials
A
- endothelium (least)
2. fibrous tissue
92
Q
Vein Materials
A
- endothelium (least)
- elastic tissue (2nd most)
- smooth muscle (most)
- fibrous tissue
93
Q
Vascular Smooth Muscle
A
- 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
Q
Arteries
A
- walls that are both stiff and springy (pressure reservoir)
- thick Smooth muscle layer and large amounts of elastic and fibrous connective tissue
95
Q
Arterioles
A
- branch off from arteries
- mainly contain vascular smooth muscle
96
Q
Microcirculation
A
- made up of arterioles, capillaries, and venues
97
Q
Metarterioles
A
- cut across the microcirculation
- act as a capillary bypass vessels
98
Q
Capillaries
A
- 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
Q
Interendothelial Cells
A
- aid in the transport of small solutes and water
100
Q
Fenestrations
A
- membrane lines conduits running through them to allow the transport
101
Q
Pericytes
A
- determine how leaky a capillary is
- more pericytes: less leaky
- thought to control blood vessels (contract them)
102
Q
Continuous Capillary
A
- most common
- thicker endothelial cells that do not contain fenestrations
- only allow passage of water and small ion through tight junctions
103
Q
Fenestrated Capillary
A
- thin endothelial cell that are perforated with fenestrations
- fenestrations often have a thin diaphragm
- small molecule passage
104
Q
Discontinuous Capillary
A
- lack a basal membrane
- have large open fenestrations and gaps between endothelial cells
ex) liver and spleen
105
Q
Methods of Transport in Capillaries
A
- Transcellular Transport
- Paracellular Transport
- Transcytosis
106
Q
Transcellular Transport
A
- diffusion accrocs the endothelial cell membrane
- gases, small lipid soluble molecules, water (aquaporin channels)
107
Q
Paracellular Transport
A
- diffusion through interendothelial junctions, pores, and fenestrations (water, small water soluble and small polar molecules)
108
Q
Transcytosis
A
- the combination of endocytosis, vesicular transport, and exocytosis that transport macromolecules across endothelial cells
109
Q
Venules
A
- in-between veins and capillaries
110
Q
Veins
A
- 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
Q
Angiogenesis
A
- 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
Q
Angiogenesis Process
A
- 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
Q
Angiogenesis Promoters
A
- Vascular Endothelial growth factors (VEGF)
- Fibroblast growth factors (FGFs)
- Angioprotein 1 (ANGPT1)
114
Q
Angiogenesis Inhibitors
A
- Endostatin
- Angiostatin
- Angioprotein 2 (ANGPT2)
115
Q
Angiogenesis in Tumors
A
- 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
Q
Blood Pressure (Systemic Circuit)
A
- ventricular contraction creates the force necessary to propel blood through CV system
- aorta and large arteries sustain driving pressure during ventricular diastole
117
Q
Ventricular Contraction Process
A
- ventricle contracts
- semilunar valve opens. blood ejected from ventricles flows into arteries
- aorta and arteries expand and store pressure in elastic walls
118
Q
Ventricular Relaxation Process
A
- isovolumic ventricular relaxation
- semilunar valve shuts, preventing flow back into ventricle
- elastic recoil of arteries sends blood forward into rest of circulatory system
119
Q
Blood Pressure
A
- pressure highest in the aorta and decreases throughout circuit
- aortic pressure highest during ventricular contraction (systole)
- aortic pressure lowest during ventricular relaxation (diastole)
120
Q
Pulse Pressure
A
- difference between systolic and diastolic pressure
- > systolic pressure - diastolic pressure
- only exists on the arterial/areriole side of circuit
121
Q
Mean Arterial Blood Pressure
A
- 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
Q
Mean Arterial Blood Pressure Equation
A
= diastolic pressure + 1/3 (pulse pressure)
123
Q
Hypotension
A
- represents when blood pressure falls too low
- because driving force for blood flow to be inadequate to overcome the opposition by gravity
124
Q
Hypertension
A
- 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
Q
Sphygmomanometer
A
- 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
Q
Mean Arterial Pressure and CO
A
- 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
Q
Factors Influencing Mean Arterial Blood Pressure
A
- blood volume
- cardiac output
- resistance of system to blood flow
- relative distribution of blood between arterial and venous blood vessels
128
Q
Volume Reservoir of CV
A
- Veins
129
Q
Pressure Reservoir of CV
A
- arteries
130
Q
Increases in Blood Volume
A
- affects blood pressure
- small changes in blood volume occur from ingestion of food and liquids
- primarily resolved by kidneys
131
Q
Decreases in Blood Volume
A
- requires an integrated response from the kidneys, cardiovascular system (increase sympathetic output) and ingestion of fluid
132
Q
Resistance in Arterioles
A
- 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
Q
Local Control
A
- Myogenic Autoregulation
2. Paracrines alter Vascular Smooth Muscle
134
Q
Myogenic Autoregulation
A
- 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
Q
Paracrines Alter Vascular Smooth Muscle
A
- 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
Q
Sympathetic Control
A
- 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
Q
Sympathetic Control with Release of Epinephrine
A
- 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
Q
Vasoconstriction
A
- caused by norepinephrine binding to alpha1 receptor
- more found in GI tract than in muscle
139
Q
Vasodilation
A
- caused by epinephrine binding to beta2 receptor
- more found in muscle than in GI tract
140
Q
Flow is Proportional to…
A
- Pressure Gradient
2. Resistance to Flow
141
Q
Distribution of Blood to Tissues
A
- 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
Q
Flow in Arterioles
A
- 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
Q
Regulation of Cardiovascular Function
A
CNS!
- coordinates reflex control of blood pressure and the distribution of blood to tissues
144
Q
Main Integrating Centre for Cardiovascular Centre
A
Medullary cardiovascular control center (CVCC)
145
Q
CVCC
A
- 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
Q
Baroreceptor Reflex
A
- 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
Q
Baroreceptor Reflex Process
A
- arteriole constricts > increase resistance > increased total peripheral resistance
- > increase
TPR x CO > increase MAP - increase MAP > baroreceptors fire > baroreceptor reflex
- baroreceptor reflex > decrease CO, increase TPR x decrease CO = MAP restored
148
Q
Orthostatic Hypotension
A
- 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
Q
Peripheral Chemoreceptors
A
- 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
Q
Hypothalamus
A
- 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
Q
Bulk Flow
A
- the mass movement of fluid as the result of hydrostatic or osmotic pressure gradients
- play out capillary filtration and absorption
152
Q
Filtration
A
- if bulk flow is resulting in the movement of fluid out of the capillaries
153
Q
Hydrostatic Pressure
A
- the pressure I’m the blood vessels drives fluid out of the capillaries through pores and leaky cell junctions (filtration)
- PUSHES FLUID OUT
154
Q
Colloid Osmotic Pressure Oncotic Pressure (π)
A
- the pressure that draws fluid into the capillaries is the pressure created by the plasma proteins in the blood
- DRAWS FLUID BACK IN
155
Q
Capillary Filtration and Absorption
A
- 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
Q
Lymphatic Vessels
A
- 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
Q
Initial Lymphatic Segment
A
- 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
Q
Collecting Lymphatics
A
- contain smooth muscle that actively propel fluid and one way valves to prevent back flow, skeletal muscle assists as well
159
Q
Edema
A
- 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
Q
Cross Sectional Area of Blood Flow
A
- 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
Q
Velocity of Blood Flow
A
- 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
Q
Velocity of Blood Equation
A
= Flow rate / c.s. area
163
Q
Cardiovascular Disease
A
- disorders of the heart and blood vessels
- heart attacks, strokes
164
Q
Uncontrolled Risk Factors of CVD
A
- age, sex, family history of early CVD, genetic
165
Q
Controlled Risk Factors of CVD
A
- cigarette smoking, obesity, sedentary lifestyle and untreated hypertension
- combination of both; diabetes, hyperlipidemia
166
Q
Atherosclerosis
A
- inflammatory process leading to hardening or narrow of arteries
167
Q
Lipoproteins
A
- High-density lipoprotein-cholesterol complexes
2. Low-density lipoprotein-cholesterol complexes
168
Q
High-Density Lipoprotein Cholesterol Complexes (HDL-C)
A
- high levels associated with lower risk of heart attack
- H = healthy
169
Q
Low-Density Lipoprotein Cholesterol Complexes (LDL-C)
A
- “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
Q
Cholesterol
A
- not readily soluble in aqueous solutions
- joins with lipoproteins
171
Q
Development of Atherosclerotic Plaques
A
- LDL-C accumulates btwn endothelium and connective tissue and is oxidized
- macrophage ingest cholesterol and become foam cells
- smooth muscle cells begin to divide and take up cholesterol
- lipid core accumulates beneath endothelium
- fibrous scar tissue forms to wall of lipid core
- smooth muscle cells divide and contribute to thickening intimacy
- calcifications are deposited within the plaque
- macrophages may release enzymes that dissolve collagen and convert plaque from stable to unstable
- platelets that are exposed to collagen activate and initiate a blood clot
172
Q
Myocardial Infarction
A
- 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
Q
Hypertension
A
- 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
Q
Effects of Hypertension
A
- 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
175
Q
Hypertension Treatments
A
- Ca2+ channel blockers (L-type)
- diuretics
- beta blockers
- ACE inhibitors and angiotensin receptor blockers
176
Q
L-Type Channel Treatment
A
- relax vascular smooth muscle and/or decrease CO (HR and force of contraction)
177
Q
Diuretics
A
- increase urination removing excess fluid to decrease blood volume
178
Q
Beta Blockers
A
- block B1 adrenergic receptors decreasing CO
179
Q
ACE Inhibitors and Angiotensin Receptor Blockers
A
- prevent vasoconstrictions from renin-angiotensin aldosterone axis
