Exam 1 (Notes) Flashcards

1
Q

Common Ions in the Human Body

A
Sodium (Na)
Potassium (K)
Calcium (Ca)
Magnesium (Mg)
Hydrogen (H)
Chloride (Cl)
Bicarbonate (HCO3)
Phosphate (PO4)
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2
Q

the structure of a “typical” human cell

A

contains:
cell membrane
cytoplasm
organelles (RER, SER, nucleus, ribosomes, golgi apparatus, mitochondrion, etc…)

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3
Q

membrane proteins have different functions. Examples of membrane proteins are…

A
transport
receptors for signal transduction
enzymatic activity
cell-cell recognition
attachment to the cytoskeleton and extracellular matrix
cell to cell joining
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4
Q

examples of proteins that work inside and outside the cell are

A
structural proteins
enzyme proteins
transport proteins
contractile proteins
communication proteins
defensive proteins
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5
Q

cells with a similar function are grouped together into _____

A

tissues

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6
Q

two or more tissues that combine structurally and functionally form an _____

A

organ

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7
Q

four tissue types in the body

A

epithelial
connective
muscle
nervous

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8
Q

an organs function is determined by the properties of the ____ within it

A

cells

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9
Q

organs are composed of multiple tissue types

A

dense irregular connective tissue that provides structural support
smooth muscle that narrows the trachea during coughing
healing cartilage that provides flexible support, ensures that the trachea remains open sot hat air can pass through
loose connective tissue that supports the epithelium and houses glands that produce mucus
pseudo stratified ciliated columnar epithelia which produces mucus to trap debris and moves trapped debris out of the trachea

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10
Q

steps for homeostasis

A
  1. Stimulus that produces change in the variable
  2. Receptor that detects change
  3. Input where information is sent along afferent pathway to control center
  4. Output where information sent a long efferent pathway to effector
  5. Response of effector feeds back to reduce the effect of stimulus and returns variable to homeostatic level
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11
Q

the hypothalamus acts as a master regulator defining the set points

A
receives info from:
-frontal lobe
-limbic system
-circulating hormones and signals
-neural signals from sensory pathways
sends instructions to:
-pituitary gland (endocrine output)
-brainstem centers (neural: autonomic)
-brainstem centers (neural: somatic)
-spinal cord centers (neural: autonomic)
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12
Q

what systems control homeostasis

A

nervous and endocrine systems

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13
Q

the autonomic nervous system

A

autonomic pathways are part of the motor system
anatomically and functionally different from the somatic nervous system
the two divisions of the ANS each have their own anatomy (each has a unique set of neurons)
effects on organs are not clearly separable
-many organs receive both sympathetic and parasympathetic innervation: usually one “turns up” organ function and the other “turns down” function (antagonistic actions)
-the two systems work together to regulate organ function with the needs of the body as a whole: for most organs it is the balance of sympathetic to parasympathetic drive that determines function

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14
Q

autonomic centers in the CNS

A

the individual centers direct the appropriate sympathetic and parasympathetic response
usually increase activity in one while decreasing activity in the other

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15
Q

how do the somatic and autonomic nervous systems differ?

A
Somatic:
-conscious control
-one neuron
-one neurotransmitter (ACh)
-myelinated axon innervates effector
-innervate skeletal muscle
-only active when stimulated
Autonomic:
-involuntary
-two neurons
-two neurotransmitters (ACh and NE)
-unmyelinated axon innervates effector
-innervates viscera
-always active, modulate activity
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16
Q

autonomic pathways are 2 neuron systems

A

neuron #1=has its cell body in the CNS
-its axon reaches from the CNS to an autonomic ganglion
–preganglionic neuron
neuron #2=has its cell body in an autonomic ganglion
-its axon reaches through the body to a target organ
-it synapses on: smooth muscle, cardiac muscle, or gland cells in the target organ
–postganglionic neuron

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17
Q

the parasympathetic nervous system

A
  • preganglionic neuron has its cell body in brainstem or sacral spinal cord; ganglion near target or in wall of target organ
  • although parasympathetic fibers only originate from cranial and sacral levels, they provide innervation to organs at all levels of the body
  • there is NO parasympathetic innervation of limbs, skin, or blood vessels
    exception: erectile tissue of penis or clitoris
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18
Q

the “craniosacral” system

A

the “rest and digest” system
preganglionic neurons in cranial nerves 3, 7, 9, 10 and from sacral spinal cord levels S2, 3, 4
Functions:
-storage of energy reserves
-slowing of heart rate
-housekeeping functions: emptying of bowel and bladder
-protection functions: narrowing pupil, airways

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19
Q

the “thoracolumbar” system

A

the “fight of flight” system
preganglionic neurons from all thoracic spinal cord levels an dumber levels L1&2
Functions:
-release of energy reserves
-speeding heart rate, increasing strength of contraction
-increasing blood pressure, shunting flow to organs vital to escape
-increasing air flow to lungs
-dilation of pupil

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20
Q

the sympathetic system

A

preganglionic neurons have cell bodies in spinal cord between 1st thoracic and 3rd lumbar level and axons enter sympathetic chain
the sympathetic chains extend the entire length of the vertebral column, from cervical region all the way to the coccyx. The chains are made up of a series of ganglia interconnected by sympathetic axons bundled into nerves. Axons can travel up or down in the chain, or leave the chain to targets. The chains serve as distribution centers for the sympathetic system
ganglion is part of paired paravertebral sympathetic chain or midline pre vertebral plexus along the aorta
postganglionic neurons have cell bodies in sympathetic ganglion, and axons travel via nerves or on walls of blood vessels into organ to synapse on target cells
although sympathetic fibers only originate only from thoracolumbar levels, they provide innervation to organs at all levels of the body, as well as the targets in the limbs and the skin
sympathetic fibers are everywhere in the body

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21
Q

dual innervation

A

this means the individual cells in an organ receive both sympathetic and parasympathetic innervation
most organs receive both

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22
Q

autonomic plexuses

A

the intermingled weblike networks of the sympathetic and parasympathetic axons in the CNS

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23
Q

how do axons travel

A

axons often travel on blood vessels to enter organs

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24
Q

autonomic nervous system affect on smooth muscle

A

ANS can increase or decrease the amount of contraction in a bed of smooth muscle

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25
autonomic nervous system affect on cardiac muscle
ANS can increase or decrease the amount of contraction in the wall of the heart, and regulate rate of contraction
26
autonomic nervous system affect on gland cells
ANS can increase or decrease the amount of secretion produced and released from a gland
27
steps for the general neurochemistry of the autonomic system
1. the CNS stimulates an action potential in the preganglionic neuron 2. the preganglionic neuron releases neurotransmitter at a synapse in the autonomic ganglion 3. the neurotransmitter binds to a receptor on the postganglionic neuron 4. binding of the transmitter stimulates an action potential in the postganglionic neuron 5. the postganglionic neuron releases a neurotransmitter on the target cell 6. binding of the transmitter stimulates the target cell target cell=smooth muscle, cardiac muscle, or gland cell
28
neurochemistry of the parasympathetic system
its an acetylcholine-based system both neurons of the parasympathetic system release the neurotransmitter acetylcholine acetylcholine bonds to a receptor for acetylcholine: a "cholinergic" receptor there are slightly different forms of the acetylcholine receptor one type binds to nicotine and the other binds to muscarine
29
nicotinic receptor
in the parasympathetic system binds nicotine in addition to acetylcholine "nicotinic type cholinergic receptor" "nicotinic receptor" for short
30
muscarinic receptor
in the parasympathetic system binds muscarine in addition to acetylcholine "muscarinic type cholinergic receptor" "muscarinic receptor" for short
31
what do the two receptors in the PNS both bind?
they both bind acetylcholine - nicotinic receptors do not bind muscarine - muscarinic receptors do not bind nicotine
32
steps for the neurochemistry of the parasympathetic system
1. the CNS stimulates an action potential in the preganglionic neuron 2. the preganglionic neuron always releases the neurotransmitter acetylcholine at the parasympathetic ganglion 3. acetylcholine binds to a receptor for acetylcholine on the postganglionic neuron "nicotinic type acetylcholine receptor" 4. the postganglionic neuron releases the neurotransmitter acetylcholine on the target cell 5. acetylcholine binds to a receptor for acetylcholine on the postganglionic neuron "muscarinic type acetylcholine receptor"
33
neurochemistry steps in the sympathetic system
1. the CNS stimulates an action potential in the preganglionic neuron 2. the preganglionic neuron always releases the neurotransmitter acetylcholine at the sympathetic ganglion 3. acetylcholine binds to a receptor for acetylcholine on the postganglionic neuron "nicotinic type acetylcholine receptor" 4. the postganglionic neuron releases the neurotransmitters norepinephrine on the target cell 5. norepinephrine binds to a receptor for norepinephrine on the postganglionic neuron "adrenergic receptor"
34
neurochemistry of the sympathetic system
the preganglionic neuron of the sympathetic system release the neurotransmitter acetylcholine; that acetylcholine binds to a nicotinic type cholinergic receptor (just as in the first part of the parasympathetic system) the postganglionic neuron releases norepinephrine onto a norepinephrine receptor norepinephrine is a slightly modified form of the chemical epinephrine; the older nomenclature called these two chemicals noradrenaline and adrenaline the receptor group that binds "adrenaline-like" compounds are still called "adrenergic receptors" adrenergic receptors bind both norepinephrine and epinephrine, but have slightly different affinities (preferences) for the two chemical forms
35
subtypes of adrenergic receptors
4 main subtypes of adrenergic receptors to be aware of (there are more) alpha 1: usually cause contraction of smooth muscle alpha 2: usually found on the varicosities of sympathetic postganglionic neurons; negative feedback to inhibit further norepinephrine release beta 1: found on cardiac muscle cells beta 2: usually cause relaxation of smooth muscle
36
the two ways to activate targets of the sympathetic system
1. activate individual preganglionic neurons through connections in the CNS. this allows for fine control of individual organs 2. activate release of epinephrine from the adrenal gland; this activates adrenergic receptors everywhere the "fight or flight" response includes activation of all sympathetic neurons as well as release of epinephrine into the bloodstream
37
how does the parasympathetic system operate
only by activation of individual preganglionic neurons by the CNS the parasympathetic system does not activate all at once (unless with drugs or toxins) the parasympathetic system works more slowly
38
when is a drug considered an agonist
if it ends to a receptor and stimulates the same response in the cell as binding the transmitter
39
when is a drug considered an antagonist
if it binds to a receptor but does not create a response in the cell; it blocks the action of the transmitter by occupying the binding site
40
what happens when a drug mimics acetylcholine
it will activate both sympathetic and parasympathetic postganglionic neurons also activates skeletal muscle
41
acetylcholinesterase inhibitors
any drug that blocks the breakdown of acetylcholine prolongs activation of ANS stimulation (EX: nerve gases, pesticides) also causes paralysis by prolonging activation and contraction of all skeletal muscles; death due to paralysis of breathing
42
nicotine
a drug that turns on BOTH sympathetic and parasympathetic systems by activating the nicotinic acetylcholine receptor at all ganglionic synapses nicotine also activates skeletal muscle
43
muscarine
a drug found in certain mushrooms; activates ALL muscarinic receptors at target organs (=targets of parasympathetic pathways plus sweat glands) simultaneous effects: tearing and constricted pupil, drooling, sweating, intestinal pains and diarrhea, slow heart rate, difficulty breathing
44
norepinephrine and epinephrine
norepinephrine is a neurotransmitter of the sympathetic nervous system it activates all adrenergic receptors types of adrenergic receptors: alpha 1 (causes smooth muscle to contract), beta 2 (causes smooth muscle to relax), and beta 1 (located on cardiac muscle cells) norepinephrine is a neurotransmitter of the sympathetic nervous system it activates adrenergic receptors the hormone, epinephrine, released from the adrenal gland, also activates these same adrenergic receptors -epinephrine=adrenaline simultaneous effects: -increased heart rate -increased blood pressure -relaxed airways (easier breathing) -dilated pupil -release of energy reserves
45
blood
classified as a connective tissue, but a fluid rather than solid
46
functions of blood
transporting dissolved gases, nutrients, hormones, and metabolic wastes regulating pH and ion composition of interstitial fluids restricting fluid loss at injury sites (clotting reaction) defending the body against toxins and pathogens regulating body temperature by absorbing and redistributing heat
47
composition of blood
blood can be fractionated into 2 main components: | plasma and cell fraction
48
plasma
``` approximately 46-63% of blood volume ~91% of plasma is water ~8% proteins -albumin -globulins (alpha, beta, gamma) -fibrinogen ~1% other -electrolytes -nonprotein nitrogenous substances -nutrients (organic) -respiratory gases -hormones ```
49
the formed elements fraction contains...
red and white blood cells plus cell fragments called platelets 99.0% of cell fraction are red blood cells
50
hemopoiesis
the process of blood cell formation - occurs in the hollow center of bones (as "red marrow") - in fetal life, occurs mainly in liver and spleen - with aging, fat takes over marrow cavity ("yellow marrow")
51
hemocytoblasts
the stem cells that divide to form all types of blood cells; also called pluripotent stem cells
52
red blood cells
erythrocytes carry oxygen to cells in the body erythrocytes account for slightly less than n half the blood volume, and 99.9% of the formed elements
53
hematocrit
measures the percentage of whole blood occupied by formed elements -commonly referred to as the volume of packed red cells
54
erythropoeisis
the formation of new red blood cells REBCs pass through erythroblast and reticulocyte stages, during which time the cell actively produces hemoglobin process speeds up with in the presence of Erythropoietin (EPO=erythropoeisis stimulating hormone; blood doping strategies often involve this hormone) a normal sample of peripheral blood usually does not contain nucleated RBCs: the nucleus and organelles are ejected after producing hemoglobin
55
maturation of RBCs
~5 days to reticulocyte ~7days to mature RBC life spans of RBC ~120 days during maturation it loses the nucleus
56
erythrocyte structure
biconcave disc provides a large surface to volume ratio to maximize rate of gas diffusion through membrane RBCs lack organelles: NO NUCLEUS shape allows RBCs to stack, bend, and flex
57
how do RBCs travel through capillaries
in a single file line
58
hemoglobin
hemoglobin molecules account for 95% of the proteins in RBCs hemoglobin is a globular protein, formed from two pairs of protein subunits -two alpha subunits, 2 beta subunits -each subunit contains one molecule of heme -each heme has an iron (Fe) at its center -the iron reversibly binds an oxygen molecules -one hemoglobin molecule can bind up to 4 oxygen molecules
59
life span of erythrocytes
approximately 1% of RBC are replaced per day replaced at a rate of approximately 3 million new blood cells entering the circulation per second old or damaged RBC are removed from circulation by spleen before they hemolyze (rupture) components of hemoglobin are individually recycled -heme is stripped of iron and converted to biliverdin (greenish), then bilirubin (yellowish), which is processed by the liver -globin protein fraction is broken down to amino acids, which are used to build other proteins -iron is recycled by being stored in phagocytes, or transported through the blood stream bound to transferrin (free iron is toxic)
60
jaundice
of the bilirubin formed in RBC breakdown, approximately 85% is removed from the blood and processed by the liver failure of the liver to "keep up" with RBC breakdown or blockage of the bile ducts leads to a buildup of bilirubin in the blood. The bilirubin then diffuses out of the blood into tissues all over the body, giving the tissues a yellow color, readily apparent in the sclera of the eyes and the skin
61
anemia
a decrease in the oxygen-carrying capacity of blood symptoms: lethargy, weakness, muscle fatigue, low energy some types of anemia: ion deficiency, hemorrhagic, anaplastic
62
iron deficiency anemia
hemoglobin is not functional without the iron
63
hemorrhagic anemia
from hemorrhage, or severe blood loss; fewer RBC
64
anaplastic anemia
bone marrow fails to produce enough RBC (radiation, immunologic diseases)
65
sickle cell anemia
caused by a mutation of the amino sequence of the beta chain of hemoglobin without sufficient oxygen bound to it, hemoglobin molecules cluster into rods and force the cell into a stiffened, cubed shape. these cells get stuck in capillaries, obstructing blood flow to the tissues, which causes pain and potentially damage to the organs
66
leukocytes
white blood cells - lifespan varies by cell types; may be hours to years - defend the body against pathogens - some are capable of phagocytosis - remove toxins, wastes, and abnormal or damaged cells - are capable of amoeboid movement and positive chemotaxis
67
diapedesis
white blood cells leaving the blood stream in response to chemical signals by squeezing through the vessel wall
68
granulocytes
WBCs named according to staining properties of cytoplasm granules - neutrophil - eosinophil - basophil
69
neutrophil
multilobed nucleus, pale red and blue cytoplasmic granules | 50-70% total WBC population (phagocytic, very mobile, 1st response to injury)
70
eosinophil
bilobed nucleus, red cytoplasmic granules | phagocytes attracted to foreign compounds that have reacted with antibodies
71
basophil
bilobed nucleus, purplish-black cytoplasmic granules | migrate to damaged tissue and release histamine and heparin
72
agranulocytes
lack cytoplasmic granules - lymphocyte - monocyte
73
lymphocyte
large spherical nucleus, thin rim of pale blue cytoplasm
74
monocyte
kidney-shaped nucleus, abundant pale blue cytoplasm
75
complete blood count
CBC one of the most common clinical test performed simple blood test measuring most parameters of blood -hematocrit and hemoglobin concentrations -platelet count -white blood cell count includes counts of relative numbers of each of the types of white blood cell, providing valuable information relative to the type of infection EX: high neutrophil counts indicative of bacterial infections EX: high eosinophil counts indicative of allergy or parasitic infections
76
RBC stem cell
hematopoietic stem cell (hemocytoblast) | *divides into myeloid stem cell and lymphoid stem cell which further divide into granular (M) and agranular (L) WBCS
77
leukemia
leukemia is cancer of the white blood cell lines myeloid and lymphoid types immature and abnormal cells enter circulation, invade tissues -highly active cells, high energy requirements -may take over bone marrow, replacing normal cells --loss of normal RBC results in anemia --loss of WBC results in infection --loss of platelet formation results in clotting problems
78
myeloid leukemia
abnormal granulocytes or other cells of marrow
79
lymphoid leukemia
abnormal lymphocytes
80
platelets
pieces of megakaryocytes flattened discs; membrane bound sacs of chemicals circulate for 9-12 days before being removed by phagocytes
81
steps in blood clotting
1. Vascular spasm: smooth muscle contracts, causing vasoconstriction - reduces diameter of the vessel 2. Platelet plug formation: injury to lining of vessel exposes collagen fibers; platelets adhere - platelets release chemicals that make nearby platelets sticky; platelet plug forms - a positive-feedback loop causing platelet aggregation to block the hole in the vessel wall 3. coagulation: fibrin forms a mesh that traps red blood cells and platelets, forming the clot - enlargement of clot 4. formation of blood clot: the clotting cascade - clotting can be initiated from damage within the vessel (intrinsic pathway) or around the vessel (extrinsic pathway) - eventually, an enzyme called thrombin is activated, which converts soluble fibrinogen molecules in the blood to insoluble, loose fibrin threads - the clot is a gel formed from a network of fibrin threads which trap blood cells and platelets 5. clot retraction: fibrin threads pull in on vessel wall, helping to plug the area and stopping blood loss
82
blood clotting coagulation phase
coagulation is a complicated cascade of biochemical events requires calcium and many blood proteins important to note that the liver is the source of many of these clotting factors
83
dissolution of clot
eventual dissolution of clot: fibrinolysis -an inactive plasma enzyme called plasminogen is incorporated into the clot -chemicals in the clot (thrombin, tissue plasminogen activator=tPA) convert plasminogen to plasmin -plasmin digests fibrin threads and inactivates clotting mechanism NOTE: a genetically engineered version of tPA is used to treat heart attacks and strokes caused by blood clots
84
excessive clotting
blood clots may form in the bloodstream in the absence of any injury a thrombus and embolus may form there are many anti-clotting drugs available (heparin, coumadin, tPA, aspirin)
85
thrombus
an attached blood clot formed by platelets adhering to the blood vessel wall, often at sites of arterial disease
86
embolus
a piece of a thrombus may detach and travel in the bloodstream which may block blood vessels
87
blood surface proteins
A B Rh
88
AB blood
AB antigens no antibodies universal recipient (A, B, AB, O)
89
B blood
B antigen Anti-A antibody receive blood from B, O
90
A blood
A antigen anti-B antibody can receive from A, O
91
O blood
no antigens anti A and anti B antibodies universal donor
92
pressure gradient
blood moves from area of high to area of low pressure
93
cardiovascular circulation pattern
the heart creates a pressure gradient to move blood blood vessels are the rubes that carry blood between heart, lungs, and tissue beds gasses, nutrients, and wastes are exchanged between tissues and blood in capillary beds everywhere the lungs only job is to exchange gas between blood and outside air
94
systemic circuit
blood passes to and from most organs of the body through this circuit arteries carry blood away from the heart veins carry blood toward the heart -in the systemic circuit, arteries carry blood that has high levels of oxygen and low levels of carbon dioxide; systemic veins returning from organs carry blood depleted in oxygen, with high CO2 content --systemic veins leading into the superior and inferior venue cave --aorta and its branches-the systemic arteries
95
pulmonary circuit
blood passes to and from the lungs through this circuit arteries carry blood away from the heart veins carry blood toward the heart -in the pulmonary circuit, pulmonary arteries carry blood to the lungs and still needs to be oxygenated, and is therefore oxygen-poor, CO2 rich -pulmonary veins return freshly oxygenated blood to the left side of the heart --pulmonary artery (trunk) and its branches carry blood from heart into lungs --pulmonary veins carry blood from lungs back to heart
96
right side of heart
deoxygenated blood the right side pump collects oxygen-depleted, carbon-dioxide rich blood from the body through 2 venue cavae, and pumps it to the lungs through the pulmonary arteries
97
left side of the heart
oxygenated blood the left side pump collects newly oxygenated blood from the lungs through pulmonary veins, and pumps it out to the body through the aorta
98
blood vessel anatomy
blood vessels are made up of: endothelium connective tissue smooth muscle
99
blood vessel endothelium
a simple squamous epithelium layer with junctions (tight and desmosomes) that allow communications with neighboring cells
100
blood vessel connective tissue
located between layers and on the outside of organs contains variable numbers of collagen, elastic and elastic fibers nerves can travel in the connective tissue layers of an organ
101
blood vessel smooth muscle
does not have visible striations in its cytoplasm contains actin and myosin and contracts in the presence of calcium contraction=vessel diameter narrows (vasoconstriction) relaxation=vessel diameter increases (vasodilation)
102
two important factors regulating the diameter of cessels
sympathetic nerves innervate blood vessels, but are seldom seen in images as they are diffusely spread out within the muscle layer these nerves release the transmitter norepinephrine, causing smooth muscle to contract and the vessel to constrict, and are thus important for controlling blood vessel diameter and regulating blood flow chemicals produced by cells surrounding the vessel or within the vessel wall also regulate smooth muscle contraction an vessel diameter
103
blood vessel layers
3 layers tunica intima tunica media tunica externa
104
tunica intima
innermost layer of the blood vessel - lined by the endothelium - supported by connective tissue (collagen)
105
tunica media
middle layer | -smooth muscle with various amounts of elastic fibers
106
tunica externa
outer layer | -connective tissue
107
how do arteries and veins walls differ
arteries have stronger, thicker walls than the vein of the same size; arteries generally contain more smooth muscle an often more elastic fibers
108
categories vessels by size
blood vessels closest to the heart have the largest diameter | ratio of tissues in wall changes with size of vessel
109
vessels can be categorized by function
``` capacitance vessels elastic arteries muscular arteries resistance vessels exchange vessels ```
110
capacitance vessels
because veins have little muscle and few elastic fibers in their wall, they have little ability to resist stretch, and often hold much of the circulating blood
111
elastic arteries
the target arteries closest to the heart contain a lot of elastic fibers, and swell with blood each time the heart pumps
112
muscular arteries
smaller diameter arteries distributing to organs
113
resistance vessels
arterials are small diameter with a few layers of smooth muscle; contraction or relaxation of that muscle creates great changes in diameter, and thus great changes in resistance to blood flow
114
exchange vessels
capillaries are the only vessels where materials move through the vessel wall
115
distribution of blood
30-35% of blood volume contained in heart, arteries and capillaries 60-65% of blood in the venous system
116
venous valves
valves that veins have to prevent blood from flowing backward formed from foldings of tunica intimate skeletal muscle activity around deep veins compresses veins and pushes blood toward heart: the "muscular pump"
117
what happens when the venous values don't work properly and there is back flow of blood
back-pressure in veins and venous valve failure creates dissension in the vein walls valve failure may be due to genetic factors or to locally high venous pressure
118
anatomy of capillaries
a capillary is little more than a tube of endothelial cells supported by a basal lamina the thin wall allows exchange of materials between the bloodstream and the cells in the organ capillaries are thus called the exchange vessels
119
how substances pass through a capillary wall
through the epithelial cell membrane -diffusion (passive) -pinocytosis (active) though tiny pores (fenestrations) in the epithelial cell membranes (size filter) through spaces between epithelial cells (bulk flow)
120
3 types of capillaries
continuous capillaries | fenestrated capillariesssnusoidal capillaries
121
continuous capillaries
have complete endothelial lining-cells tightly bound to one another are found in all tissues except epithelia and cartilage permit diffusion of water, small solute, and lipid-soluble materials block RBC and plasma proteins specialized continuous capillaries are found in the CNS and create the "blood- brain barrier"
122
fenestrated capillaries
``` have small pores in endothelial lining permit rapid exchange of water and larger solutes between plasma and interstitial fluid found in areas requiring more exchange -choroid plexus -endocrine organs -kidneys -intestinal tract ```
123
sinusoidal capillaries
have large gaps between adjacent endothelial cells permit free exchange of water and large plasma proteins between blood and interstitial fluid found in: liver, spleen, bone marrow, endocrine organs -phagocytic cells monitor blood at sinusoids
124
pre-capillary sphincters
regulates blood flow through capillary beds - arterioles often have areas of extra muscle in their wall as they branch into a capillary network; these sphincters contract to decrease blood flow into a capillary bed - a sphincter acts as a valve
125
T/F: arteries and veins generally parallel one another and share the same names
T
126
systemic arteries
the single vessel leaving the left side of the heart is the aorta the aorta includes: -the aortic arch -the thoracic cavity (in the thoracic cavity) -the abdominal aorta (below the diaphragm)
127
systemic veins
blood returns to the right side of the heart through two large unpaired veins above the diaphragm, blood returns through the superior vena cava below the diaphragm, blood returns thought he inferior vena cava
128
general functional patterns of the pulmonary and systemic circulation
in any one cycle, a drop of blood passes to one capillary bed and then back to the heart peripheral artery and vein distribution is the same on the right and left, except near the heart
129
anatomy of the heart
the heart lies in the thoracic cavity in a central area called the mediastinum, between the two lungs. it is positioned just to the left of midline, posterior to the sternum and ribs 2-4 the idea base is located superiorly and is attached by large blood vessels the pointed apex lies inferiorly, and rests on the diaphragm
130
what is the heart enclosed in
the heart is enclosed in a fibrous sac called the pericardial sac - the outer part of the sac is dense connective tissue, and is strong and does not stretch - the lining of the sac is a moist membrane comprising the pericardial cavity
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what is located within the fibrous sac
within the fibrous sac, the heart is surrounded by the pericardial cavity the pericardial cavity is formed from a single sheet of moist ("serous") membrane enclosing a collapsed space the heart has pushed into this membrane, which adheres to the heart surface as the visceral pericardium. The outer layer of the membrane is the parietal pericardium the heart is not IN the cavity, but is surrounded by it on all sides there is no space in the cavity, but there is a thin layer of fluid that allows the visceral and parietal pericardial layers to slide against one another without friction as the heart fills and empties
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problems within the pericardial cavity can create life-threatening conditions
infection, inflammation, or fluid accumulation within the pericardial cavity leads to compression of the heart this prevents the heart from adequately filling with blood, and effects its ability to pump
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how many chambers does the heart have?
``` 4 total chambers right side pump=2 chambers -right atrium -right ventricle left side pump -left atrium -left ventricle on each side, a valve separates the atrium from the ventricle: atrioventricular valves (AV valves) ```
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surface anatomy of the heart
atria are thin-walled, and each has an expandable outer flap called the auricle, most visible form the anterior view the apex is the most inferior part of the left ventricle; the base is the superior end where the great vessels attach grooves (sulci) separate the atria from ventricles coronary arteries and veins travel in the surface grooves before entering the heart wall
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coronary arteries
first branches from the aorta carry oxygenated blood to the heart tissue coronary arteries lie in grooves in the heart surface cushioned by small amounts of fat 4 main coronary arteries: -right coronary artery -left coronary artery -circumflex artery -left anterior descending (LAD) artery
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right coronary artery
supplies the right atrium, both ventricles, SA and AV nodes, and posterior wall with blood
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left coronary artery
immediately splits into the circumflex artery and the left anterior descending (LAD) artery
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circumflex artery
supplies the left atrium, septum, and posterior wall with blood
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left anterior descending (LAD) artery
aka anterior inter ventricular artery | supplies both ventricles anteriorly
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coronary veins
accompany the arteries collecting blood from he heart wall and returning it to the right atrium
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heart layers
3 total layers endocardium myocardium epicardium
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endocardium
innermost; endothelium supported by connective tissue
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myocardium
middle layer; cardiac muscle
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epicardium
outer layer; connective tissue with fat, coronary vessels, and visceral pericardium
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which heart wall is thicker than the other
the left ventricle wall is thicker than the right - the right ventricle is a low pressure pump - the left ventricle is a high pressure pump
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what nerves innervate the heart and cause an increase in heart activity
sympathetic stimulators increase heart activity - NE released from sympathetic axons - Epi from the bloodstream (adrenal hormone) - both work on the same "beta-adrenergic" type receptor
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what nerve innervates the heart and causes a decrease in heart activity
parasympathetic stimulators decrease heart activity - ACh released from parasympathetic axons - ACh works on "muscarinic-type ACh" receptors
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two sets of valves located in the heart
atrioventricular valves | semilunar valves
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atrioventricular valves
between atria and ventricles right AV valve has 3 flaps: tricuspid left AV valve has 2 flaps: bicuspid also called mitral valve
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semilunar valves
between ventricles and their exit pipe leaving right ventricle: pulmonary leaving left ventricle: aortic
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what determines whether valves are open or closed
pressure gradients
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blood flow through the right side pump
blood enters the right atrium from he superior and inferior venue cavae venous blood returning from the heart wall empties directly into the right atrium blood passes through the open tricuspid valve to enter the right ventricle blood leaves the right ventricle through the pulmonary valve to enter the pulmonary trunk the pulmonary trunk branches into right an left pulmonary arteries carrying blood to the lungs
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the left side pump
blood returns from the lungs to the left atrium through the 2 right and 2 left pulmonary veins blood passes through the open bicuspid valve to enter the left ventricle blood leaves the left ventricle through the aortic valve to enter the aorta the aorta gives off right and left coronary arteries before ascending to the aortic arch
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anatomy of the AV valves
AV valves have fibrous flaps anchored by string-like chordae tenineae to muscular pegs protruding from the ventricle wall-papillary muscles
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anatomy of the semilunar valves
a semilunar valve has 3 fibrous flaps attached to the wall of the vessel (aorta or pulmonary trunk); no muscles or chordae tendinae are involved with these passive valves
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heart valves mechanism
when a valve closes, its cusps (flaps) nest together to fill the space
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valve disease/illness
valves can be damaged by disease or illness, leading to stiffness of the valve tissue and failure to open fully or close completely
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lub
the first heart sound occurs when the atrioventricular valves close normal sound produced by turbulence as AV valves close and blood pushes against them
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dub
the second heart sound occurs when the semilunar valves close normal sound produced by turbulence as semilunar valves close and blood pushes against them
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heart murmur
abnormal sounds produced by regurgitation through faulty valves or by damaged valve flaps
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what are the two types of cardiac muscle cells
``` contractile cells (99%) pacemaker cells (<1%) ```
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contractile cells
99% cardiac muscle cells which contract to push blood the cells of the myocardium
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pacemaker cells
<1% of the conducting system specialized cardiac muscle cells; do not contract initiate and distribute the action potentials that stimulate contraction "auto rhythmic"-allow the heart to beat on its own rhythm is adjustable: the cardiovascular center of the medulla controls sympathetic and parasympathetic nerves to the heart which act on pacemaker cells to adjust the heart rate to the needs of the body pacemaker cells are specialized cardiac muscle cells not neurons they are buried in the heart wall, so not visible at the gross level
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steps of the conducting system of the heart
1. at the sinoatrial (SA) node a cluster of cells in the wall of the right atrium next to the superior vena cava usually sets the rate of heart contraction begins atrial contraction, then passes signal to the AV node 2. at the Atrioventricular (AV) node a cluster of cells at the junction between the atria and ventricles receives electrical signal from SA node, slows impulse before passing it on to Bundle of His 3. Bundle of His an bundle branches fibers carrying impulse down septum between right an left ventricles 4. Purkinje Fibers (subendocardial network cells) distribute throughout myocardium, from base upward into ventricles
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pacemaker cells of the conducting system of the heart
pacemaker slowly depolarize to threshold, then fire an action potential the rate of spontaneous depolarization determines the heart rate SA node generates 80-100 action potentials per minute -fastest rate of firing, so drives all the other cells of conducting system at this rate AV node generates 40-60 action potentials per minute
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bradycardia
abnormally slow heart rate (<60 bpm)
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tachycardia
abnormally fast heart rate (>100 bpm)
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ectopic pacemaker
abnormal cells in chamber wall generate high rate of action potentials bypass conducting system: affected area of ventricle doesn't wait for signals through the regular pathway results in disruption of ventricular contractions; ventricle may not contract bottom-to-top, so poor blood ejection
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pacemaker device
a pacemaker device may be implanted to regulate abnormal heart activity
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pumping blood
a mechanical event initiated by electrical events normally, the SA node generates an action potential, and passes the signal down the conductive system Purkinje fibers distribute the stimulus to the contractile cells, which make up most of the ventricle wall
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characteristics of contractile cardiac muscle cells
small size single, central nucleus branching interconnections between cells -intercalated discs
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intercalated discs contain ___ types of cell-cell junctions. What are they
2 gap junctions desmosomes
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gap junctions
connect cytoplasm of one cell directly into cytoplasm of another allowing for ion flow and "electrical coupling"
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desmosomes
physically tie cells together
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the action potential of a single contractile cardiac muscle cell
1. Depolarization is due to Na+ influx through fast voltage-gated Na+ channels. a positive feedback cycle rapidly opens many Na+ channels, reversing the membrane potential. Channel inactivation ends this phase 2. Plateau phase is due to Ca2+ influx through slow Ca2+ channels. This keeps the cell depolarized because most K+ channels are closed 3. Depolarization is due to Ca2+ channels inactivating and K+ channels opening. This allows K+ efflux, which brings the membrane potential back to its resting voltage * the resting membrane potential of contractile cells is stable (unlike that of the conductive cells like those of the SA node)
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the role of calcium ions in cardiac contractions
contraction of a cardiac muscle cell is produced by an increase in calcium ion cardiac muscle tissue is very sensitive to extracellular Ca2+ concentrations Calcium channel blockers are a group of powerful medications for heart patients
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steps of cardiac contractions and the role of calcium
1. action potential enters from adjacent cell 2. voltage-gated Ca2+ channels open. Ca2+ enters cell 3. Ca2+ induces Ca2+ release through ryanodine receptor-channels (RyR) 4. local release causes Ca2+ spark 5. Summed Ca2+ sparks create a Ca2+ signal 6. Ca2+ ions bind to troponin to initiate contraction. Actin-Myosin cross bridges form 7. Relaxation occurs when Ca2+ unbinds from troponin 8. Ca2+ is pumped back into the sarcoplasmic reticulum for storage 9. Ca2+ is exchanged with Na+ 10. Na+ gradient is maintained by the Na+-K+ ATPase
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comparing action potentials of skeletal and cardiac muscle
in skeletal muscle, the action potential is brief relative to the contraction. A second action potential soon after the first increases cytoplasmic calcium levels and increased the strength of contraction in cardiac muscle, the action potential lasts as long as the contraction. One contraction is over and calcium is sequestered before another can begin, preventing summation of contraction and tetany. This ensures time for the heart to fill between contractions
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electrocardiogram
ECG or EKG a recording of electrical events in the heart, representing ALL the action potentials from ALL the cardiac cells-conducting and contractile
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P wave
atria depolarize
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QRS complex
ventricles depolarize
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T wave
ventricles repolarize
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features of an ECG
1. atrial depolarization, initiated by the SA node, causes the P wave 2. with atrial depolarization complete, the impulse is delayed at the AV node 3. ventricular depolarization begins at the apex, causing the QRS complex. Atrial repolarization occurs 4. ventricular depolarization is complete 5. ventricular repolarization begins at apex, causing the T wave 6. ventricular depolarization is complete
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defibrillator
shocks the heart back into a normal rhythm
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the cardiac cycle
one cycle=from the start of one heart beat to the start of the next heartbeat two phases: -systole (contraction) -diastole (relaxation) begins with initiation of action potential at SA node -produces action potentials in cardiac muscle cells (contractile cardiac cells) of Atria --both atria begin contracting=atrial systole -signal is transmitted through conduction system both ventricles contract, apex to base, pushing out blood=ventricular systole -atria begin relaxing=atrial diastole ventricles relax, heart refills=ventricular diastole
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what makes blood move?
a pressure gradient -blood moves from area of high pressure to area of low pressure open valve
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blood pressure
the pressure exerted by blood onto the wall of the container directly related to volume of blood inside places feeling blood pressure: heart chambers, blood vessels (including capillaries)
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comparing the left and right pressures
right pressure is much lower than left pressure
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cardiac output
the volume of blood pumped by the left ventricle in one minute =number of beats/minute X volume with each beat =heart rate X stroke volume CO=HR X SV
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end-diastolic volume
EDV | the amount of blood in the left ventricle just before contraction
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end-systolic volume
ESV the amount of blood left in the left ventricle after contraction (it doesn't all get pumped)
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stroke volume
SV the amount pumped out of the left ventricle during systole SV=EDV-ESV
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factors that affect cardiac output
cardiac output can be adjusted with changes to one or more variable - heart rate (speeding up or slowing down) - end diastolic volume (how much blood fills ventricle between beats) - end systolic volume (how much ventricle pumps out each beat)
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control of heart rate
autonomic innervation is the primary factor affecting HR - cardiovascular center of medulla oblongata in the brainstem drives the autonomic nervous system: one part of this, the cardiac center, regulates heart activity - -cardioacceleratory center - -cardioinhibitory center
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cardioacceleratory center
controls sympathetic neurons, causes them to release more norepinephrine at SA node (increases heart rate); NE binds to Beta-1 adrenergic receptors on SA node cells
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cardioinhibitory center
controls parasympathetic neurons of vagus nerve, leading to acetylcholine release at SA node (slows heart rate); ACh binds to muscarinic receptors on SA node cells
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autonomic innervation of the heart
note that parasympathetic fibers innervate the SA and AV nodes with the transmitter ACh sympathetic fibers innervate both nodes, atrial muscle an ventricular muscle with the transmitter NE drug target: circulating epinephrine mimics this sympathetic nervous system effect
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how is heart rate controlled?
autonomic axons adjust heart rate by slowing down or speeding up the rate of spontaneous depolarization of pacemaker cells chronotropic drugs are used to alter heart rate
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control of stroke volume
two main factors influence the EDV factors that cause more blood to return to heart result in larger fill volume (the EDV) filling time: duration of ventricular diastole longer fill time results in larger fill volume related to heart rate venous return: rate of blood flow during ventricular diastole -vasoconstriction is a critical factor affecting venous return
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the sympathetic nervous system innervates blood vessels and controls vessel diameters
sympathetic fibers are always "talking" to the smooth muscle in the walls of blood vessels...this is called sympathetic "tone". this continuous rate of action potential firing leads to continuous release of transmitter and sustained low level of contraction of the smooth muscle, and thus partial vasoconstriction of the vessel increased sympathetic activity increases the degree of constriction to reduce blood flow=vasoconstriction decreased sympathetic activity decreases the degree of constriction, dilating the vessel to increase blood flow=vasodilation sympathetic transmitter: norepinephrine receptor type: alpha-type adrenergic receptors usually, vasodilation of blood vessels occurs because local chemicals in active tissues trigger the smooth muscle cells to relax, increasing blood flow and providing more oxygen and nutrients to the tissue
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how does vasoconstriction increase venous return
vasoconstriction mobilizes blood in the capacitance vessels | more blood flow through lungs and arterial circulation distributing to organs
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three main factors influence the end systolic volume
factors that cause more blood to be pumped from ventricle affect volume left in ventricle after systole (the EDV) preload contractility afterload
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preload
ventricular stretching during diastole
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contractility
force produced during contraction, at a given preload
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afterload
tension the ventricle needs to produce to open the aortic valve and eject blood
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preload affects stroke volume
preload is the degree of ventricular stretching during diastole directly proportional to EDV: more blood in ventricle=more stretch stretch affects the ability of muscle cells to produce tension
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contractility affects stroke volume
how hard the ventricle contracts is affected by factors that adjust calcium levels in the muscle cells sympathetic nervous system activity affects contraction strength -stimulation of the sympathetic nerves causes release of norepinephrine on the heart cells, leading the ventricles to contract with more force, and pump out more blood (increasing volume and thus decreasing ESV) hormones from the bloodstream (epinephrine, norepinephrine, thyroid hormone) affect contraction strength
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two ways that heart function is controlled clinically
beta blockers | calcium channel blockers
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beta blockers
contractile cells have beta-1 adrenergic receptors to respond to epinephrine and norepinephrine acts on the heart at receptors for NE or Epi blocks sympathetic receptors, so inhibits sympathetic activity used to: -decrease contractility to ease workload on a weak heart (reduces oxygen needs) -decrease heart rate-decreases CO (and therefore BP) to treat hypertension also used to treat arrhythmias
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calcium channel blockers
decrease calcium entry or release in contractile cells; less calcium=less actin/myosin interaction=less tension act on ventricle wall contractile cells and on smooth muscle cells in blood vessel walls blocks calcium channels to decrease amounts of intracellular calcium available for actin/myosin used to: -decrease contractility in ventricle to decrease SV and CO, and therefore BP -decrease contraction in smooth muscle of blood vessels, leading to vasodilation and decrease in BP and afterload
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afterload affects stroke volume
afterload is the aortic pressure that must be overcome in order for the ventricle to eject blood any factor that restricts arterial blood flow increases peripheral resistance, and affects the heart as after load (valve stenosis, high blood pressure, atherosclerosis, etc...) as afterload increases, stroke volume decreases, and therefore ESV increases
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ejection fraction
an important clinical measure of heart function the percentage of EDV pumped out in one beat (one stroke) -a weak heart pumps out less blood
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ejection fraction number 50-75%
heart's pumping ability is normal | heart's pumping ability is low
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ejection fraction number 36-49%
heart's pumping ability is below normal
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35% and below
heart's pumping ability is low
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main factors affecting cardiac output
1. heart rate control factors - autonomic nervous system (sympathetic and parasympathetic) - circulating hormones 2. stroke volume control factors - EDV: end diastolic volume - -filling time - -rate of venous return - ESV: end systolic volume - -preload (stretch on ventricle wall) - -contractility (calcium availability within muscle cell) - -afterload (downstream resistance)
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regulating blood flow
organs must receive a steady supply of oxygen and nutrients in order to survive. maintaining a steady flow of blood the organs is the job of the cardiovascular system both the heart and the blood vessels are capable of change in order to adjust the flow of blood there are only 5 liters of blood in the body, and it is constantly being redistributed between different organ system
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flow is a function of ___and ___
pressure and resistance
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blood flow to tissues
=difference in blood pressure between heart and capillaries/(divided by) peripheral resistance blood flows from a region of high pressure to one of lower pressure; the greater the pressure difference driving the movement, the greater the flow the heart generates pressure to overcome resistance; the greater the peripheral resistance, the lower the flow
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what produces the pressure in the cardiovascular system?
the heart | blood flows from an area of high pressure to an area of low pressure
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arterial blood pressure
usually refers specifically to arterial pressure
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venous pressure
pressure in the venous system
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capillary hydrostatic pressure
pressure within the capillary beds
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systolic pressure
the peak arterial pressure during ventricular systole
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diastolic pressure
the minimum arterial pressure during diastole
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systolic pressure in elastic arteries
during systole, the heart forces blood into the vessels and exerts great pressure on the vessel walls
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diastolic pressure in elastic arteries
during diastole, the heart is not pushing blood, but the recoil of the walls of the elastic arteries continues to push blood and exert pressure
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pulse pressure
the difference between systolic pressure and diastolic pressure pulse pressure creates the "throbbing" feeling in an artery; not present in capillaries and veins
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blood pressure is recorded in two ways
1. systolic/diastolic pressure typically 120/80 | 2. mean arterial pressure (MAP) =diastolic pressure+1/3 pulse pressure; typically 93
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hypertension
abnormally high blood pressure (greater than 140/90)
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hypotension
abnormally low blood pressure (less than 90/60)
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pulse pressure creates a throbbing sensation in the artery
pulse points! arteries large enough to have pulse pressure arteries close enough to skin surface to palpate
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where does resistance come from
1. vascular resistance 2. viscosity 3. turbulence
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vascular resistance
due to friction between blood and the vessel wall | dependent on vessel length (constant) and diameter (adjustable)
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viscosity
resistance caused by molecules and suspended materials in a liquid (cells, proteins, etc...) blood is about 4 times more viscous than water
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turbulence
swirling action within vessel that disturbs smooth flow
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factors that increase total blood flow
an increase in cardiac output causes a steeper pressure gradient less resistance, which is caused by vasodilation, reduction in vessel length, or decrease in blood viscosity
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factors that decrease total blood flow
a decrease in cardiac output causes a smaller pressure gradient greater resistance which is caused by vasoconstriction, increase in vessel length, or increase in blood viscosity
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changing vessel diameter on the venous side of the circuit influences___, which alters cardiac output
preload
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capillary dynamics
exchange of materials at capillaries is vital to homeostasis capillaries and their beds are OPTIMIZED for exchange a continuous capillary, the most common capillary in the body, has a wall one squamous cell thick. exchange occurs across this wall
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capillary beds are optimized for exchange of materials
the power in numbers although one capillary has the smallest diameter of any vessel, there are so many of them that the TOTAL cross-sectional area is higher at the capillary level than at any other point of the circulation
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how do you optimize exchange in the capillary beds
the high cross-sectional area of the capillary circulation creates a drop in pressure at that point of the circulation, and a decrease in flow velocity these two features-low pressure and slow flow-optimize exchange in the capillary beds
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3 forces at work moving materials across capillary walls
diffusion filtration reabsorption
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diffusion
``` the movement of ions or molecules along a concentration gradient form high concentration to low concentration diffusion routes for important substances: passive movement, so ongoing lipids and lipid soluble materials such as O2 and CO2 diffuse through endothelial plasma membranes some ions (Na, K, Ca, Cl) diffuse through ion channels in plasma membranes water, ions, and small molecules such as glucose diffuse between adjacent endothelial cells or through fenestrated capillaries large, water-soluble compounds like plasma proteins and blood cells are too big to pass through continuous or fenestrated capillaries and can only get across the big, leaky sinusoidal capillaries ```
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filtration
water and small solutes squeezed out of the capillary into the interstitial fluid driven by blood pressure (capillary hydrostatic pressure)
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reabsorption:
water drawn back into the capillary from the interstitial fluid pulled by osmotic pressure exerted by large plasma proteins trapped in blood
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how does the filtration force change across a capillary bed?
capillary hydrostatic pressure (CHP) at arterial end 35 mmHg capillary hydrostatic pressure at venous end is 18 mmHg filtration pressure declines as blood moves across capillary bed
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how dies the reabsorptive force change across a capillary bed?
plasma proteins are trapped in blood, so exert a constant force along the bed this force is called the colloid osmotic pressure (COP)
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net filtration pressure
NFP is the difference between net hydrostatic pressure and net osmotic pressure (how much is pushed out minus how much is drawn back in)
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forces in capillary exchange
net filtration pressure changes along the length of the capillary -at arterial end of capillary, fluid moves out of capillary, into interstitial fluid -at venous end of capillary, fluid moves into capillary,out of interstitial fluid -these movements are not equal normally capillaries filter more than they reabsorb
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edema
the accumulation of interstitial fluid due to abnormal leakage from capillaries - local edema is part of the normal inflammatory process (injury, bite) - systemic (bodywide) edema affects the cardiovascular system
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recovery of interstitial fluid
lymphatic vessels return interstitial fluid to the bloodstream -a separate set of vessels; do not carry blood -one way drainage system, not a "lymphatic circuit" interstitial fluid collected into lymphatic vessels is called lymph lymphatic fluid is drained through a series of lymphatic vessels and returned to the blood stream close to the heart lymph nodes interspersed along the lymphatic channels serve as filters to remove pathogens before the lymph is returned to the blood stream
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cardiovascular regulation
goal is to maintain tissue perfusion (blood flow through the tissues -deliver O2 and nutrients to tissues and organs -remove CO2 and wastes from tissues flow is affected by -cardiac output -blood pressure -peripheral resistance cardiovascular regulation changes blood flow to a specific area different organs have different metabolic needs at different times
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3 factors influence cardiac output and blood pressure
auto regulation -causes immediate, localized homeostatic adjustments neural mechanisms -respond quickly to changes at specific sites endocrine mechanisms -slowest, direct long-term changes
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autoregulation
local regulation of blood flow within tissues: adjusted by changing peripheral resistance while cardiac output stays the same; the main effect is to change the diameter of the blood vessel wall local vasodilators increase local blood flow: some are local chemical change sin busy tissues some are chemicals released by inflammation (histamine) elevated local temperature is an additional factor local vasoconstrictors decrease local blood flow: some are local chemical changes in quiet tissues some are chemicals released by damaged tissues
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baroreceptor reflexes
respond to changes in blood pressure
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chemoreceptor reflexes
respond to changes in chemical composition, particularly pH and dissolved gases
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baroreceptor reflex is a neural mechanism
input: sensory feedback from aortic arch and carotid body integration: cardiovascular center of medullar oblongata decides what adjustments need to be made output: 1. alterations in balance of sympathetic and parasympathetic output to heart to adjust cardiac output 2. alteration in sympathetic output to blood vessels
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cardiovascular adaptation
blood, heart, and cardiovascular system work together as a unit allows for both short- and long-term responses to physical and physiological changes
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standing up
in rising from a lying to a standing position, the effect of gravity is to cause blood to accumulate in capacitance veins of the legs and feet -less blood returns to heart (decreased EDV) -stroke volume decreases (SV is a function of EDV) -cardiac output decreases (CO=SV X HR) -blood pressure decreases -decreased blood flow to brain a rapid response by the cardiovascular system raises blood pressure and restores blood flow to brain within a few beats 1. carotid and aortic baroreceptors detect low BP 2. cardiovascular center in medulla of brainstem activates sympathetic branch of ANS, decreases parasympathetic 3. sympathetic nerves to blood vessels cause vasoconstriction in arteries and veins (increasing EDV) 4. sympathetic nerves to heart increase heart rate and force of ventricular contraction, increasing stroke volume and restoring cardiac output and blood pressure
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response to light exercise
driven by metabolic buildup, extensive vasodilation occurs, increasing circulation to active muscles skeletal muscle activity enhances venous return via "muscular pump" venous return increases and increases stretch on ventricular wall -(frank-starling principle): increased stretch increases contractility to increase stroke volume and cardiac output
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response to heavy exercise
induces same changes as light exercise, but also activates sympathetic nervous system -sympathetic stimulation increases heart rate and contractility, increasing cardiac output to about four times resting level selective vasoconstriction restricts blood flow to "nonessential" organs and redirects blood flow to skeletal muscles, lungs, and heart. blood supply to brain is unaffected
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the cardiovascular response to hemorrhaging
entire cardiovascular system adjusts to maintain blood pressure and restore blood volume
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short term elevation of blood pressure (seconds)
carotid and aortic reflexes stimulate cardiovascular center in medulla -increase cardiac output by increasing heart rate and contractility -peripheral vasoconstriction improves venous return (increasing preload, SV, CO) hormonal effects (minutes) -increase cardiac output by increasing heart rate and contractility -increase peripheral vasoconstriction (E, NE, ADH, angiotensin 2)
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long term restoration of blood volume (hours to weeks)
recall of fluids from interstitial spaces aldosterone and ADH promote fluid retention and reabsorption thirst increases to replace fluid volume erythropoietin stimulates red blood cell production to replace RBC loss
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circulatory shock
short-term responses compensate for blood losses of up to 20% of total blood volume failure to restore blood pressure results in circulatory shock -intense vasoconstriction shunts blood away from organs and into bloodstream to maintain blood pressure -prolonged vasoconstriction causes cells in organs to die and organ damage results
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hypertension
``` high blood pressure risk factors: -genetics -gender (males more at risk) -high cholesterol levels -obesity -chronic stress -cigarette smoking -often no known cause strain on the system: -increased work for heart, leading to heart enlargement -greater oxygen demands lead to ischemia -stress on blood vessel walls promotes arteriosclerosis clinical intervention: -lifesyle, diet, and exercise changes -drugs: calcium and channel blockers, diuretics, ACE inhibitors ```
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atherosclerosis
atherosclerosis is an inflammatory disease - narrowing of opening: decreased blood flow to tissues - decreased blood flow: heart works harder to overcome resistance - calcification over time: loss of ability to dilate/constrict
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the model for atherosclerosis
1. high levels of LDLin blood lead to accumulation of LDLin tunica intima 2. chemical reaction of LDLin intimate leads to lymphocyte and monocyte attraction from blood; LDL recognized as foreign 3. chemicals released from lymphocytes and macrophages induce inflammation, causing thickening in wall of artery - plaques contain: lipids, connective tissue, calcium deposits "hardening of arteries"
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coronary artery disease
when atherosclerosis affects coronary arteries, the function of the heart is compromised -decreased coronary blood flow can lead to angina pain and eventually to a heart attack
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symptoms of heart attack
chest discomfort: most heart attacks involve discomfort in the center of the chest that lasts more than a few minutes, or that goes away and comes back. it can feel like uncomfortable pressure, squeezing, fullness, or pain discomfort in other areas of the upper body: symptoms can include pain or discomfort in one or both arms, the back, neck, jaw, or stomach shortness of breath: with or without chest discomfort other signs: may include breaking out in a cold sweat, nausea, or lightheadedness
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a stress test is often used to assess heart problems
patient is asked to walk on a treadmill while heart is being monitored a medical team is present to watch for changes in ECG, shortness of breath, chest pain, or other signs of heart problems
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coronary bypass surgery
a technique to restore blood flow to the heart wall | less invasive options include balloon angiography and/or the insertion of a stent to open the blocked artery
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arrhythmias
atrial fibrillation | ventricular fibrillation
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atrial fibrillation
atria can depolarize at rate of 500 beats per minute without driving ventricle beyond normal limits atrial wall "quivers" blood clots may form near the atrial walls, creating emboli and leading to stroke
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ventricular fibrillation
purkinje cells fire abnormally;muscle overly sensitive to stimulation ventricle wall "quivers" and fails to pump out of heart leads to cardiac arrest
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congestive heart failure
heart cannot pump enough blood to body organs causes: -damage to heart: infection, heart attack, congenital defects -coronary artery disease -heart valve disease or defects leads to backward flow in system as heart pumps inadequately, blood backs up on venous see -edema in tissues, including visible swelling in limbs -back up into lungs interferes with breathing
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alpha blockers
acts on smooth muscle in blood vessel walls blocks sympathetic receptors, so inhibits sympathetic activation and reduces smooth muscle contraction used to: -dilate blood vessels and decreased BP to treat hypertension
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aging changes in blood
decreased hematocrit impacts oxygen delivery changes to clotting factors increase clot likelihood pooling of blood in legs due to venous valve deterioration
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aging changes in blood vessels
arteries become less elastic leading to wall rupture or aneurysm plaque deposits and calcification of vessel walls reduce blood flow and may trigger clot formation leading to stroke
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aging changes within the heart impact cardiac output
changes in nodal and conducting cells reduced elasticity of cardiac (fibrous) skeleton progressive atherosclerosis and valve stiffening replacement of damaged cardiac muscle cells by scar tissue