Exam 1 (Notes) Flashcards
Common Ions in the Human Body
Sodium (Na) Potassium (K) Calcium (Ca) Magnesium (Mg) Hydrogen (H) Chloride (Cl) Bicarbonate (HCO3) Phosphate (PO4)
the structure of a “typical” human cell
contains:
cell membrane
cytoplasm
organelles (RER, SER, nucleus, ribosomes, golgi apparatus, mitochondrion, etc…)
membrane proteins have different functions. Examples of membrane proteins are…
transport receptors for signal transduction enzymatic activity cell-cell recognition attachment to the cytoskeleton and extracellular matrix cell to cell joining
examples of proteins that work inside and outside the cell are
structural proteins enzyme proteins transport proteins contractile proteins communication proteins defensive proteins
cells with a similar function are grouped together into _____
tissues
two or more tissues that combine structurally and functionally form an _____
organ
four tissue types in the body
epithelial
connective
muscle
nervous
an organs function is determined by the properties of the ____ within it
cells
organs are composed of multiple tissue types
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
steps for homeostasis
- Stimulus that produces change in the variable
- Receptor that detects change
- Input where information is sent along afferent pathway to control center
- Output where information sent a long efferent pathway to effector
- Response of effector feeds back to reduce the effect of stimulus and returns variable to homeostatic level
the hypothalamus acts as a master regulator defining the set points
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)
what systems control homeostasis
nervous and endocrine systems
the autonomic nervous system
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
autonomic centers in the CNS
the individual centers direct the appropriate sympathetic and parasympathetic response
usually increase activity in one while decreasing activity in the other
how do the somatic and autonomic nervous systems differ?
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
autonomic pathways are 2 neuron systems
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
the parasympathetic nervous system
- 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
the “craniosacral” system
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
the “thoracolumbar” system
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
the sympathetic system
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
dual innervation
this means the individual cells in an organ receive both sympathetic and parasympathetic innervation
most organs receive both
autonomic plexuses
the intermingled weblike networks of the sympathetic and parasympathetic axons in the CNS
how do axons travel
axons often travel on blood vessels to enter organs
autonomic nervous system affect on smooth muscle
ANS can increase or decrease the amount of contraction in a bed of smooth muscle
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
autonomic nervous system affect on gland cells
ANS can increase or decrease the amount of secretion produced and released from a gland
steps for the general neurochemistry of the autonomic system
- the CNS stimulates an action potential in the preganglionic neuron
- the preganglionic neuron releases neurotransmitter at a synapse in the autonomic ganglion
- the neurotransmitter binds to a receptor on the postganglionic neuron
- binding of the transmitter stimulates an action potential in the postganglionic neuron
- the postganglionic neuron releases a neurotransmitter on the target cell
- binding of the transmitter stimulates the target cell
target cell=smooth muscle, cardiac muscle, or gland cell
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
nicotinic receptor
in the parasympathetic system
binds nicotine in addition to acetylcholine
“nicotinic type cholinergic receptor”
“nicotinic receptor” for short
muscarinic receptor
in the parasympathetic system
binds muscarine in addition to acetylcholine
“muscarinic type cholinergic receptor”
“muscarinic receptor” for short
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
steps for the neurochemistry of the parasympathetic system
- the CNS stimulates an action potential in the preganglionic neuron
- the preganglionic neuron always releases the neurotransmitter acetylcholine at the parasympathetic ganglion
- acetylcholine binds to a receptor for acetylcholine on the postganglionic neuron “nicotinic type acetylcholine receptor”
- the postganglionic neuron releases the neurotransmitter acetylcholine on the target cell
- acetylcholine binds to a receptor for acetylcholine on the postganglionic neuron “muscarinic type acetylcholine receptor”
neurochemistry steps in the sympathetic system
- the CNS stimulates an action potential in the preganglionic neuron
- the preganglionic neuron always releases the neurotransmitter acetylcholine at the sympathetic ganglion
- acetylcholine binds to a receptor for acetylcholine on the postganglionic neuron “nicotinic type acetylcholine receptor”
- the postganglionic neuron releases the neurotransmitters norepinephrine on the target cell
- norepinephrine binds to a receptor for norepinephrine on the postganglionic neuron “adrenergic receptor”
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
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
the two ways to activate targets of the sympathetic system
- activate individual preganglionic neurons through connections in the CNS. this allows for fine control of individual organs
- 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
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
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
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
what happens when a drug mimics acetylcholine
it will activate both sympathetic and parasympathetic postganglionic neurons
also activates skeletal muscle
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
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
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
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
blood
classified as a connective tissue, but a fluid rather than solid
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
composition of blood
blood can be fractionated into 2 main components:
plasma and cell fraction
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
the formed elements fraction contains…
red and white blood cells plus cell fragments called platelets
99.0% of cell fraction are red blood cells
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”)
hemocytoblasts
the stem cells that divide to form all types of blood cells; also called pluripotent stem cells
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
hematocrit
measures the percentage of whole blood occupied by formed elements
-commonly referred to as the volume of packed red cells
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
maturation of RBCs
~5 days to reticulocyte
~7days to mature RBC
life spans of RBC ~120 days
during maturation it loses the nucleus
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
how do RBCs travel through capillaries
in a single file line
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
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)
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
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
iron deficiency anemia
hemoglobin is not functional without the iron
hemorrhagic anemia
from hemorrhage, or severe blood loss; fewer RBC
anaplastic anemia
bone marrow fails to produce enough RBC (radiation, immunologic diseases)
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
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
diapedesis
white blood cells leaving the blood stream in response to chemical signals by squeezing through the vessel wall
granulocytes
WBCs named according to staining properties of cytoplasm granules
- neutrophil
- eosinophil
- basophil
neutrophil
multilobed nucleus, pale red and blue cytoplasmic granules
50-70% total WBC population (phagocytic, very mobile, 1st response to injury)
eosinophil
bilobed nucleus, red cytoplasmic granules
phagocytes attracted to foreign compounds that have reacted with antibodies
basophil
bilobed nucleus, purplish-black cytoplasmic granules
migrate to damaged tissue and release histamine and heparin
agranulocytes
lack cytoplasmic granules
- lymphocyte
- monocyte
lymphocyte
large spherical nucleus, thin rim of pale blue cytoplasm
monocyte
kidney-shaped nucleus, abundant pale blue cytoplasm
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
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
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
myeloid leukemia
abnormal granulocytes or other cells of marrow
lymphoid leukemia
abnormal lymphocytes
platelets
pieces of megakaryocytes
flattened discs; membrane bound sacs of chemicals
circulate for 9-12 days before being removed by phagocytes
steps in blood clotting
- Vascular spasm: smooth muscle contracts, causing vasoconstriction
- reduces diameter of the vessel - 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 - coagulation: fibrin forms a mesh that traps red blood cells and platelets, forming the clot
- enlargement of clot - 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 - clot retraction: fibrin threads pull in on vessel wall, helping to plug the area and stopping blood loss
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
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
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)
thrombus
an attached blood clot formed by platelets adhering to the blood vessel wall, often at sites of arterial disease
embolus
a piece of a thrombus may detach and travel in the bloodstream which may block blood vessels
blood surface proteins
A
B
Rh
AB blood
AB antigens
no antibodies
universal recipient (A, B, AB, O)
B blood
B antigen
Anti-A antibody
receive blood from B, O
A blood
A antigen
anti-B antibody
can receive from A, O
O blood
no antigens
anti A and anti B antibodies
universal donor
pressure gradient
blood moves from area of high to area of low pressure
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
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
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
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
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
blood vessel anatomy
blood vessels are made up of:
endothelium
connective tissue
smooth muscle
blood vessel endothelium
a simple squamous epithelium layer with junctions (tight and desmosomes) that allow communications with neighboring cells
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
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)
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
blood vessel layers
3 layers
tunica intima
tunica media
tunica externa
tunica intima
innermost layer of the blood vessel
- lined by the endothelium
- supported by connective tissue (collagen)
tunica media
middle layer
-smooth muscle with various amounts of elastic fibers
tunica externa
outer layer
-connective tissue
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
categories vessels by size
blood vessels closest to the heart have the largest diameter
ratio of tissues in wall changes with size of vessel
vessels can be categorized by function
capacitance vessels elastic arteries muscular arteries resistance vessels exchange vessels
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
elastic arteries
the target arteries closest to the heart contain a lot of elastic fibers, and swell with blood each time the heart pumps
muscular arteries
smaller diameter arteries distributing to organs
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
exchange vessels
capillaries are the only vessels where materials move through the vessel wall
distribution of blood
30-35% of blood volume contained in heart, arteries and capillaries
60-65% of blood in the venous system
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”
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
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
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)
3 types of capillaries
continuous capillaries
fenestrated capillariesssnusoidal capillaries
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”
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
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
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
T/F: arteries and veins generally parallel one another and share the same names
T
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)
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
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
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
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
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
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
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)
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
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
right coronary artery
supplies the right atrium, both ventricles, SA and AV nodes, and posterior wall with blood
left coronary artery
immediately splits into the circumflex artery and the left anterior descending (LAD) artery
circumflex artery
supplies the left atrium, septum, and posterior wall with blood
left anterior descending (LAD) artery
aka anterior inter ventricular artery
supplies both ventricles anteriorly
coronary veins
accompany the arteries collecting blood from he heart wall and returning it to the right atrium
heart layers
3 total layers
endocardium
myocardium
epicardium
endocardium
innermost; endothelium supported by connective tissue
myocardium
middle layer; cardiac muscle
epicardium
outer layer; connective tissue with fat, coronary vessels, and visceral pericardium
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
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
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
two sets of valves located in the heart
atrioventricular valves
semilunar valves
atrioventricular valves
between atria and ventricles
right AV valve has 3 flaps: tricuspid
left AV valve has 2 flaps: bicuspid also called mitral valve
semilunar valves
between ventricles and their exit pipe
leaving right ventricle: pulmonary
leaving left ventricle: aortic
what determines whether valves are open or closed
pressure gradients
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
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
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
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
heart valves mechanism
when a valve closes, its cusps (flaps) nest together to fill the space
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
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
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
heart murmur
abnormal sounds produced by regurgitation through faulty valves or by damaged valve flaps
what are the two types of cardiac muscle cells
contractile cells (99%) pacemaker cells (<1%)
contractile cells
99%
cardiac muscle cells which contract to push blood
the cells of the myocardium
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
steps of the conducting system of the heart
- 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 - 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 - Bundle of His an bundle branches
fibers carrying impulse down septum between right an left ventricles - Purkinje Fibers (subendocardial network cells)
distribute throughout myocardium, from base upward into ventricles
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
bradycardia
abnormally slow heart rate (<60 bpm)
tachycardia
abnormally fast heart rate (>100 bpm)
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
pacemaker device
a pacemaker device may be implanted to regulate abnormal heart activity
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
characteristics of contractile cardiac muscle cells
small size
single, central nucleus
branching interconnections between cells
-intercalated discs
intercalated discs contain ___ types of cell-cell junctions. What are they
2
gap junctions
desmosomes
gap junctions
connect cytoplasm of one cell directly into cytoplasm of another allowing for ion flow and “electrical coupling”
desmosomes
physically tie cells together
the action potential of a single contractile cardiac muscle cell
- 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
- Plateau phase is due to Ca2+ influx through slow Ca2+ channels. This keeps the cell depolarized because most K+ channels are closed
- 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)
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
steps of cardiac contractions and the role of calcium
- action potential enters from adjacent cell
- voltage-gated Ca2+ channels open. Ca2+ enters cell
- Ca2+ induces Ca2+ release through ryanodine receptor-channels (RyR)
- local release causes Ca2+ spark
- Summed Ca2+ sparks create a Ca2+ signal
- Ca2+ ions bind to troponin to initiate contraction. Actin-Myosin cross bridges form
- Relaxation occurs when Ca2+ unbinds from troponin
- Ca2+ is pumped back into the sarcoplasmic reticulum for storage
- Ca2+ is exchanged with Na+
- Na+ gradient is maintained by the Na+-K+ ATPase
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
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
P wave
atria depolarize
QRS complex
ventricles depolarize
T wave
ventricles repolarize
features of an ECG
- atrial depolarization, initiated by the SA node, causes the P wave
- with atrial depolarization complete, the impulse is delayed at the AV node
- ventricular depolarization begins at the apex, causing the QRS complex. Atrial repolarization occurs
- ventricular depolarization is complete
- ventricular repolarization begins at apex, causing the T wave
- ventricular depolarization is complete
defibrillator
shocks the heart back into a normal rhythm
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
what makes blood move?
a pressure gradient
-blood moves from area of high pressure to area of low pressure
open valve
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)
comparing the left and right pressures
right pressure is much lower than left pressure
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
end-diastolic volume
EDV
the amount of blood in the left ventricle just before contraction
end-systolic volume
ESV
the amount of blood left in the left ventricle after contraction
(it doesn’t all get pumped)
stroke volume
SV
the amount pumped out of the left ventricle during systole
SV=EDV-ESV
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)
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
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
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
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
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
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
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
how does vasoconstriction increase venous return
vasoconstriction mobilizes blood in the capacitance vessels
more blood flow through lungs and arterial circulation distributing to organs
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
preload
ventricular stretching during diastole
contractility
force produced during contraction, at a given preload
afterload
tension the ventricle needs to produce to open the aortic valve and eject blood
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
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
two ways that heart function is controlled clinically
beta blockers
calcium channel blockers
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
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
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
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
ejection fraction number 50-75%
heart’s pumping ability is normal
heart’s pumping ability is low
ejection fraction number 36-49%
heart’s pumping ability is below normal
35% and below
heart’s pumping ability is low
main factors affecting cardiac output
- heart rate control factors
- autonomic nervous system (sympathetic and parasympathetic)
- circulating hormones - 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)
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
flow is a function of ___and ___
pressure and resistance
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
what produces the pressure in the cardiovascular system?
the heart
blood flows from an area of high pressure to an area of low pressure
arterial blood pressure
usually refers specifically to arterial pressure
venous pressure
pressure in the venous system
capillary hydrostatic pressure
pressure within the capillary beds
systolic pressure
the peak arterial pressure during ventricular systole
diastolic pressure
the minimum arterial pressure during diastole
systolic pressure in elastic arteries
during systole, the heart forces blood into the vessels and exerts great pressure on the vessel walls
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
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
blood pressure is recorded in two ways
- systolic/diastolic pressure typically 120/80
2. mean arterial pressure (MAP) =diastolic pressure+1/3 pulse pressure; typically 93
hypertension
abnormally high blood pressure (greater than 140/90)
hypotension
abnormally low blood pressure (less than 90/60)
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
where does resistance come from
- vascular resistance
- viscosity
- turbulence
vascular resistance
due to friction between blood and the vessel wall
dependent on vessel length (constant) and diameter (adjustable)
viscosity
resistance caused by molecules and suspended materials in a liquid (cells, proteins, etc…) blood is about 4 times more viscous than water
turbulence
swirling action within vessel that disturbs smooth flow
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
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
changing vessel diameter on the venous side of the circuit influences___, which alters cardiac output
preload
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
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
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
3 forces at work moving materials across capillary walls
diffusion
filtration
reabsorption
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
filtration
water and small solutes squeezed out of the capillary into the interstitial fluid
driven by blood pressure (capillary hydrostatic pressure)
reabsorption:
water drawn back into the capillary from the interstitial fluid
pulled by osmotic pressure exerted by large plasma proteins trapped in blood
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
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)
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)
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
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
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
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
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
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
baroreceptor reflexes
respond to changes in blood pressure
chemoreceptor reflexes
respond to changes in chemical composition, particularly pH and dissolved gases
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
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
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
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
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
the cardiovascular response to hemorrhaging
entire cardiovascular system adjusts to maintain blood pressure and restore blood volume
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)
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
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
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
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
the model for atherosclerosis
- high levels of LDLin blood lead to accumulation of LDLin tunica intima
- chemical reaction of LDLin intimate leads to lymphocyte and monocyte attraction from blood; LDL recognized as foreign
- chemicals released from lymphocytes and macrophages induce inflammation, causing thickening in wall of artery
- plaques contain: lipids, connective tissue, calcium deposits “hardening of arteries”
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
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
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
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
arrhythmias
atrial fibrillation
ventricular fibrillation
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
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
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
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
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
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
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
