Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

282 Cards in this Set

  • Front
  • Back
PNS: General Org of ANS Pathway
2 consequtive motor neurons
applies to both symp/parasympathetic NS's
-part of PNS not under voluntary control
-Divisions: sympathetic & parasympathetic NS
sympathetic NS:
associated anatomically w/ thoracic & lumbar regions of spinal cord; thoraco-lumbar
parasympathetic NS:
associated anatomically w/ cranial & sacral regions of brain & nerves ofspinal cord (cranio-sacral)
Structure of Sympathetic NS
sympathetic chain ganglia: -found from cervical to lumbar region on both sides of sp cord
-ganglia on one side interconnected
-ganglia connected to spinal nerves on spinal cord
-1st visceral efferent neuron's cell body found in lateral horn of gray matter
axon of neuron comes out of spinal cord to symp ganglion & can do 1 of 3 things:
1. axon synapses w/ 2nd visceral efferent neuron in ganglion @ entry level
2.axon enters symp chain, goes up chain, & synapses w/ 2nd visceral efferent neuron @ this higher level
3.axon enters symp chain, goes down chain, & synapses w/ 2nd visceral efferent neuron @ this lower level
in all 3 cases, after synapse:
2nd visceral efferent neuron sends its axon through the autonomic nerve to an effector
ANS: generalizations
-1st visceral efferent axon is relatively short in length & carries AP to symp ganglion
-2nd visceral efferent axon is relatively long in length & carries AP to visceral effector
Structure of Parasympathetic Pathway:
1.cranial region
2.sacral region
cranial region:
1.1st visc eff axon passes over some CRANIAL nerve (III,VII,IX,X) & extends to a parasymp ganglion near a visceral effector (very close to organ receiving stim)
2.1st visc axon synapses w/ 2nd visc eff neuron in parasymp ganglion
3.2nd visc eff axon innervates a visceral effector
sacral region:
1.1st visc eff axon emerges from L region sp cord & passes over PELVIC nerve to parasymp ganglion near visc effector
2.1st visc axon synapses w/ 2nd visc eff neuron in a parasymp ganglion
3.2nd visc eff axon extends to & innervates visc effector
parasymp pathway generalizations:
1st visc axon is long in length & 2nd vis eff axon is short in length
General Autonomic Principles
1.autonomic reflexes tend to restore homeostasis very quickly
2.dual autonomic innervation
3.single autonomic innervation
4.autonomic NT, specific & nonspecific to system
5.autonomic antagonism & dominance
dual autonomic innervation:
effector receives both parasymp & symp innervation
single autonomic innervation
effector receives either/or parasymp/symp innervation
autonomic NT
1.acetylcholine (Ach)
2.norepinephrine (NE)
cholinergic neuron if release Ach
1.all preganglionic neurons (both para/symp)
2.all parasymp postganglionic neurons
3.some symp postganglionic neurons
(entire parasymp NS releases Ach)
adrenergic neuron if release NE
-includes: most symp postganglionic neurons
autonomic antagonism & dominance:
applies to dual innervation
-NT of highest concentration produces effect (picture)
NS: Senses
1.Sensory unit
Senses: Sensory Unit
3 elements:
2.neural pathway
3.interpretation center
-detects stimulation & changes to NS language
-special cell or part of sensory neuron
neural pathway:
path AP takes from receptor to brain
interpretation center:
-in cerebral cortex
-interprets sensation/final analysis of out/input
Senses: Receptors
detect stimuli from internal or external environment
Receptors: Specificity
specific to 1 kind of stimulus
-variation related to excessive stimulation that changes sensation to pain:
1.mechanoreceptors: respond to excess stretch
2.temp receptors: hot=burning sensation -> excess heat=pain
Receptors: Fxn
respond to specific stimulus -> produce generator potentials (local depolarizations) -> summate & produce AP
Receptors: Types
-receive stimuli from outside body
-pick up sensations from skin, eye, ear, nasal cavity & tongue
Exteroreceptors: Cutaneous/Skin receptors
located in dermis/tongue
-respond to light touch
-detect deep pressure
-detect temperature
-detect pain
Cutaneous/Skin receptors: light touch
ruffinis corpuscles, meiseners corpuscles, Krause's end bulbs, Merkels Discs
Cutaneous/Skin receptors: deep pressure
pacinian corpuscles in subcutaneous tissue & CT around joints
Cutaneous/Skin receptors: temperature
free nerve endings
-both heat (skin temp increase 30-45 degC; 45deg kills tissue & sense pain)
& cold (skin temp decrease 40-10 degC
Cutaneous/Skin receptors: pain
free nerve endings throughout entire body generally, except in the brain
Exteroreceptors: Types of pain
1.somatic pain
2.visceral pain
3.referred pain
somatic pain:
1.superficial: comes from skin only
2.deep: arises from skeletal musc & tendons
visceral pain:
from internal organs
referred pain:
pain originates in muscle tendon or body organ; pain perceived as coming from superficial area of skin
1.deep somatic
3.never superficial somatic
referred pain ex:
angina & appendicitis
1.brain: where sensations interpreted
2.interneuron @ sp cord: sends AP to brain
3.sensory neuron: sends AP to interneuron
-brain familiar w/ pain originating from Larm & unfamiliar w/ pain from heart, so interprets pain coming from Larm b/c it can't seperate them (pic)
muscles, joints & tendons, muscle spindles, golgi tendon organs
deep body organs
1.stretch receptors
4.temperature receptors
Interoreceptors: stretch receptors
respond when organ stretches
Interoreceptors: baroreceptors
respond to change in pressure
-bv's & heart
-RA, aorta, sup/inf vena cavae, carotid sinus
Interoreceptors: chemoreceptors
respond to change in chemical composition of ECF
-aorta, carotid artery, medulla oblongata
Interoreceptors: temperature receptors
monitor temperature of blood
Special Senses:
1.Gustatory Sense (taste)
2.Olfaction (smell)
4.Auditory & Equilibrium Senses
Gustatory Sense (Taste)
1.Taste Cells
3.interpretation center
Gustatory Sense: Taste cells
-located in taste buds, found in taste papillae on tongue
-5 kinds: sweet,sour,bitter,salty, umami (meat protein)
-universely distributed, not localized
Gustatory Sense: taste route
sensation->saliva->surface tongue->b/w papillae->stimulate/enter specific taste bud
Gustatory Sense: Innervation
-facial nerve supplies taste buds on anterior 2/3 tongue
-glossopharyngeal nerve supplies taste buds on posterior 1/3 tongue
Gustatory Sense: interpretation center
found in frontal lobe of cerebrum
Olfaction (smell)
1.receptors& pathway
2.interpretation center
Olfaction: receptors
olfactory cells found in high epithelium of nasal cavity
-respond to water or lipid soluble substances & volatilize
olfaction route:
olfactory cells send AP -> olfactory bulb->olfactory tract/nerve->frontal lobe
Olfaction: interpretation center
found @ frontal lobe of cerebrum
1.structure of the eye
2.physiology of vision
Vision: Structure of the Eye:
1.layers of tissues
2.cavities & humors
4.Lacrimal Apparatus
Layers of Tissues:
3.choroid coat
outer layer; white of the eye; WFCT/collagenousCT;providing for skeletal element
front of sclera; clear tissue; covers iris
choroid coat:
middle layer; highly vascularized=good blood supply; dark pigmented;
1.posterior choroid
2.anterior choroid
posterior choroid:
supports retina & provides nutrition to retina
anterior choroid:
specialized into 2 structures:
1.ciliary body
anterior choroid: ciliary body
-internally: ciliary muscles, smooth musc, involuntary
-in front of ciliary musc: ciliary processes- extensions off main ciliary body; attached to zonular fibers around lens ...
all together, ciliary muscles + ciliary processes =
suspensory ligament, which attaches ciliary body to lens
anterior choroid: iris
color part of choroid; opening @ center = pupil; fxn: control amount of light that enters eye by changing the diameter of pupil w/ 2 structures:
1.dilator pupillae
2.sphincter pupillae
dilator pupillae:
intrinsic muscles that increase pupil opening
sphincter pupillae:
intrinsic muscles that decrease pupil opening
both dilator/sphincter pupillae:
smooth muscle, involuntary
inner most layer; sensative to light; lies adjacent to vitreous humor; 6 layers
6 layers of Retina:
1.photoreceptor neurons
2.bipolar neurons
3.ganglion neurons
4.macula lutea
5. fovea centralis
6.optic disc
Retina: photoreceptor neurons
-rods or cones
-directly a/g choroid coat
-last row of cells affected by light
photoreceptor neurons respond to light rays:
initiate AP->rods/cones connect to bipolar layer
Retina: bipolar neurons
take AP from rods/cones to ganglion neuron
Retina: ganglion neuron
-next to vitreous humor
-inner-most neurons of retina
-very long axons; converge to one point: optic disc, forming optic nerve
Retina: macula lutea
"yellow spot"
-posterior center of retina directly behind pupil
-depression @ center: fovea centralis
Retina: fovea centralis
contains about 3million cones in fovea & about 100million rods outside fovea
Retina: optic disc
"blind spot"
-convergence of ganglion neurons
-beginning of optic nerve
-@ this point of retina, cant see an image b/c no rods/cones present @ disc
Structure of the Eye: Cavities & Humors
1.posterior cavity
2.anterior cavity
3.formation & circulation of aqueous humor
Posterior Cavity:
-borders: lens to retina
-contains gel: vitreous humor
vitreous humor:
helps to maintain intraocular pressure in the eye/keep eye from collapsing
Anterior Cavity:
-borders: lens to cornea
-made of 2 chambers:
1.anterior chamber: cornea to iris
2.posterior chamber: iris to lens
Formation & Circulation of Aqueous Humor:
1.blood plama filtered thru capillaries in ciliary processes to chamb of ant cavity, causes pressure & flows
3.thru pupil
4.into ant chamb of ant cavity; now must be drained out of eye thru
5.canal of schlemm, into
6.small veins in sclera
*as aqueous humor moves through the eyes,
it leaves nutrients for cornea/lens & carries wastes to veins for disposal
problem if flow interrupted:
-pressure >25mmHg (norm=20-25mmMercury)
-lack of drainage: block @ canal of schlemm OR
-too much production: accumulates aqueous humor @ ant cavity
-->pressure expressed backward on retina & damages rods/cones & person has potential to become blind
-folds of skin (upper/lower eyelid)
-affected by 2 skeletal muscles:
1.palpebrae superioris: raises upper eyelid
2.orbicularis oculi:closes both eyelids, invol
Eyelid: 3 elements
1.Palpebral Fissure
Palpebral Fissure:
space b/w upper and lower eyelids
mucous memb
1.palpebral conj: covers inner surface of both eyelids
2.ocular conj:covers anterior sclera, but not cornea; continuous w/ 1.
fusion of eyelids
1.lateral canthus: fusion on side of eye
2.medial canthus: next to nose
little red bump @ medial canthus; land mark for eye doctors
Lacrimal Apparatus:
1.Lacrimal Glands
2.Lacrimal canals
3.Nasolacrimal Duct
Lacrimal Apparatus: Lacrimal Glands
-found @ sup-lat region of orbit
-produce/release tears
-tears flow over eye surface->medial canthus, where you find 2 lac canals
Lacrimal Apparatus: Lacrimal Canals
-1 above & 1 below caruncle
-drains tears off surface of eye
-fxn: keeps conjunctiva moist
-sends tears to lacrimal sac
Lacrimal Apparatus: Nasolacrimal Duct
-receives tears from lacrimal sac
-sends tears to nasal cavity
-sends small amount, but constant flow
Lacrimal Apparatus: Tears
1.derive from blood plasma, so nearly same chem comp w/ far less pr
2.keep conjunctiva moist/lubricated so eyeballs can close over them cleanly
3.contains lysozyme that destroys any bacteria coming into eye
4.if dont kill bac, eye infxn: conjunctivitis/"pink eye": inflammation of sclera
Vision: physiology of vision
2.image focusing
3.stimulation of retina
4.cone stimulation
1.image focus
2.rods & cones rxn
3.transmission of APs
4.visual interpretation center
rods&cones rxn-
react to light->photochemical rxns; initite APs
transmission of APs-
thru optic nerve->thru pathways to final destination->cerebral cortex in occipital lobe
visual interpretation center-
in occipital lobes; final interpretation occurs here
image focusing:
1.far vision
2.near vision
far vision:
-image >20ft away from eye
-light rays coming to eye @ parallel orientation
-choroid coat in norm anatomical position (tension exerted on suspensory ligament)
-tension makes lens somewhat flattened->low curvature
-image focused on the retina
near vision:
-object <20ft away from eye
-light rays come in eye divergent from point where image located
-ciliary muscles contract & ciliary body moved forward
-tension reduced on susp lig
-lens has elastic prop, so w/ less tension, becomes > convex->higher curvature
-image focused on retina
1.emmetropia: normal eye
2.accomodation: some abnormality assoc w/ eye
nearsightedness; can see near
->common cause:ant/post dimensions of eye too long
-refractive power of cornea/lens too strong (focus light rays short of retina in vitreous humor & image blurred)
farsightedness; can see far
->common cause:ant/post dimensions of eye too short
-refractive power of cornea/lens too weak (focus light rays behind retina & image blurred)
curvature of cornea/lens is imperfect & person sees parts of image in focus & parts blurred
affect the lens;
-lens made up of protein: crystaline
-as age, protein denatured & lens that is usually clear is now opaque ->defracts light rays (rather than refracting them)
near point of eye moves farther away from eye surface w/ age
-greatest change occurring 45-50yo
-lens becomes less elastic w/ age & can no longer accomodate to near objects as did previously
Stimulation of Retina:
Rhodopsin Cycle;
1.rods contain rhodopsin or 11-cis-rhodopsin
2.light ray shines on
3.11-cis-retinal changes to trans-retinal + opsin
4.trans-retinal seperates from opsin
5.w.o light, trans-retinal changes back to 11-cis-retinal & but back together w/ opsin thru chemical rxn
composed of opsin (protein) & 11-cis-retinal (derived from vit A)
all in all,
-light breaks down rhodopsin
-dark areas put rhodopsin back together
APs started:
in rods when broken down into trans-retinal
Cone Stimulation:
3 types of cones & primary colors:
1.Erythrolabe: red cone
2.Cyanolabe: blue cone
3.Chlorolabe: green cone
-blue light stimulates cyanolabes->stimulates APs
-green light stimulates chlorolabes->stimulates APs
-both sent to occipital lobes
most common colorblindness:
red/green (minor blue/yellow)
Auditory & Equilibrium Senses:
auditory vestibular apparatus:
1.external ear
2.middle ear
3.inner ear
external ear:
2.ear lobe
3.external auditory meatus
*tympanic membrane=border b/w outer/middle ear
-elastic cartilage +skin
-directs sound waves to external auditory canal
ear lobe-
-adipose tissue, CT, skin
-purely cosmetic; no hearin fxn
external auditory meatus-
-tube extends from pinna->middle ear
-opening covered by eardrum/tympanic membrane
middle ear:
hollow space in temporal bone;
1.ear ossicles
ear ossicles-
3; smallest bones in head;
-fxnal bones that articulate w/ each other:
1.malleus-articulates w/ tympanium
3.stapes-articulates w/ membrane oval window
1.external auditory meatus
2.oval & round windows
3.mastoid sinuses (cells)
4.eustachian tube
oval & round windows-
covered by membranes
mastoid sinuses-
spaces in mastoid process
eustachian tube-
auditory tube; connects middle ear to mouth
Inner ear:
housed in petrous process in temporal bone;
-bony & membranous labyrinths
bony -> membranous labyrinths
1.semicircular canals 3 ->semicircular ducts
2.vestibule->utricle & saccule
3.cochlea->cochlear duct/scala media
Inner Ear fluids:
1.perilymph: fluid b/w bony & memnranous structures
2.endolymph: found inside membranous structures
-they dont mix
membranous labyrinth-
1.semicircular canals
5.cochlear duct
membranous labyrinth: semicircular ducts
-all arranged 90deg to one another
-named for direction they point: superior/lateral/posterior
-connect to ampullae found @ base of ducts ... only 5 b/c superior/posterior share
membranous labyrinth: ampulla
1.crista ampullaris
ampulla-crista ampullaris
cluster of neurons w/ hairlike ext off surface making contact w/ cupula
gelatin like/strong gel tht contacts hairlike endings starting APs
-movement of endolymph causes cupula to move AP
function of semicircular ducts & ampulla
provide us w/ a sense of angular acceleration or rotation
rotation pattern:
head rotates->endolymph moves->cupula moves->stimulates crista neurons->send AP over vestibular branch XIIIcranial nerve-> to brain & body receives angular sense
*impt in balance & posture
membranous labyrinth: utricle
-located in sup region of vestibule
-connected to saccule in vestibule
-all 5 ampullae connect to utricle
2.otolithic membrane
cluster of sensory neurons w/ hairlike ext off surface
utricle-otolithic membrane
above macula; gel like; in contact w/ hairlike ext's
made of calcium carbonate called otoconia, statconia, otoliths
-lie on top of otolithic mem & weight it down/keep in place
utricle: fxn
1.proprioceptor for the head (tells what position head in) us a sense of linear acceleration in the horizontal plane
3.endolymph in utricle->head moves endolymph->stimualtes macula->sense of location
membranous labyrinth: saccule
-similar to utricle
-connected to ut. by ductus reuniens connecting to cochlear duct
-fxn:provide for vertical plane linear acceleration
*also passes over vestibular branch XIIIcranial nerve->brain
membranous labyrinth: cochlear duct
scala media;
1.triangular in xsection
2.extends to cochlea in form of spiral
3.forms compartments inside cochlea
4.cochlear duct is shorter than cochlea, so connection @ tip b/w scala vestibuli & tympani: heligotrema
5.organ of corti
compartments inside cochlea:
1.scala vestibuli: perilymph
2.cochlear duct: endolymph
3.scala tympani: perilymph
organ of corti:
-inside cochlear duct
-rests on basilar memb b/w scala media & tympani
-cluster of sensory neurons w/ hairlike ext in contact w/ tectorial membrane
organ of corti fxn:
-detect sound waves in the inner ear
-place theory of sound detection
place theory of sound detection:
sound waves cause vib in perilymph of s.vestibuli->transferred to vestibular memb->to endolymph of>vib's now occur in basilar memb->causes organ of corti to vib & hairlike ext contact tectorial memb stimulating organ of corti neurons...
organ of corti neurons next to oval window:
detect high pitch sounds
organ of corti neurons next to helicotrema:
detech low pitch sounds
neurons send AP->
over auditory branch of XIIIcranial nerve to brain, where sound waves interpreted
tranmission & detection of sound in ear:
sound waves directed to ext aud meatus by pinna->cause mvmt in tympanium->transferred to malleus, incus, stapes, round window memb->transferred to perilymph in s.vestibuli->transfers to endolymp
transferrred to basilar memb w/ organ of corti->causes stimulation in organ corti->stimluates APs to XIIIcranial nerve->brain & interpretted
mvmt of basilar memb or perilymph in s.tympani:
in contact w/ round window mem->middle ear & at this point sound waves are eliminated (would hear echos if didnt stop)
Circulatory System: Components
1.fluids: blood, lymph
2.vessels: pathways for flow of fluids; BV, lymphV
3.heart: muscular pump
Circulatory System: Subdivisions
1.Cardiovascular system: heart, BVs, blood
2.Lymphvascular system: lymph nodes, lymphVs, lymph
Cardiovascular System:
2.heart structure
heart: location
mediastinum: space b/w lungs, sternum, vertebral column
heart: base
top of atria
heart: apex
inferior end, tip of left ventricle only
-tip of LV is found in the 5th intercostal space (b/w 5/6ribs) 2/3 left of midline
heart structure:
2.pericardial sac
4.cardiac cycle
heart structure: wall
-3 layers of tissue
1.endocardium:endothelium, single layer from inner layer bv's
2.myocardium: cardiac muscle; greatest bulk of heart
3.epicardium: visceral pericardium; serous memb
heart structure: pericardial sac
-surrounds heart
-pericardial space/cavity just under sac containing pericardial fluid
pericardial sac comp:
1.outer layer:connective tissue memb
2.inner layer: serous memb contacts pericardial cavity
3.pericardial cav contains pericardial fluid
4.function of fluid is to reduce friction b/w heart & other structures
heart structure: chambers
1.upper chambers
2.lower chambers
upper chambers
-L&R atria
-thin walled w/ small amt pumping
R atrium
-connected to superior and inferior vena cavae
-Ratrio-ventricular orifice connects RA to RV
-tricuspid valve in orifice
L atrium
-connects to 4 pulmonary veins at base of L atrio-ventricular orifice opening into L ventricle
-bicuspid/mitral valve
lower chambers
-L&R ventricles
-thick walled & do most of pumping action
-interventricular septum b/w
R ventricle
-connects to pulmonary trunk sending blood to lungs
L ventricle
-connected to aorta or aortic arch sending blood to every part of body except lungs
papillary muscle
ext of ventricular wall; connected to chordae tendinae, which are connected to tricuspid/bicuspid valve
heart structure: cardiac cycle
mechanical action of heart during a single heart beat
1.diastasis & diastole
2.atrial systole
3.atrial diastole
4.ventricular systole
5.ventricular diastole
systole vs diastole:
1.systole:contraction of vent
2.diastole:relaxation of vent
heart is at complete relaxation b/w cycles
ventricles relaxing
atrial systole:
-both atria contract at same time together
-prior to this blood filled heart to 70% of its capacity
-remaining 30% to be reached by atria systole
atrial diastole:
atria relaxing
ventricular systole:
-ventricles contract, blood flows from LV to aorta and from RV to pulmonary trunk
-papillary muscles contract to ensure bicuspid,tri valves stay closed
ventricular diastole:
vent's relax->reduces pressure in vent's->creates tendency for blood to flow back into vent's, but prevented when semilunar valves (in aorta&pulmonary trunk) close to prevent backflow
heart structure: heart sounds
-sounds made during cardiac cycle
heart sounds: normal
systolic sound:
1st; long duration; low pitch; caused by contraction of ventricles->atrioventricular valves closing
diastolic sound
2nd; short duration; high pitch; louder; caused by relaxation of ventricles->semilunar valves closing
abnormal heart sounds:
murmurs; due to malfxning heart valves; hear extra sound
2.valvular insufficiency
portions of valves fuse&dont open to their full extent; blood coming thru smaller opening @ faster rate ->causes abnormal sound
stenosis occurs:
largely in bicuspid/aortic semilunar valve & somewhat in tricuspid/pulmonary trunk semilunar valves
"Bicuspid stenosis" "aortic stenosis"
valvular insufficiency:
incompetence; portion of heart valve lost due to disease & valves dont close completely -> leak/regurgitation
back flow of blood:
aorta->LV, pulmonary trunk->RV, or LV->LA, RV->RA
Structure & Fxn of Cardiac Musc Cells: Histology
1.cross striations: b/c of sarcomeres- actin, myosin, myofilaments
2.1 nucleus/cell
3.cytoplasm banches
4.intercalated discs where 2 cardiac musc cells connect & gap jxns present here allowing for AP to move quickly from one cell to another
Structure & Fxn of Cardiac Musc Cells: Functional Syncytium
1 stimulus causes the entire structure of heart to react
Structure & Fxn of Cardiac Musc Cells: All or None Law
a stimulus =/> threshold stimuluates a heartbeat & stimulus < threshold leads to no rxn
-applies to entire heart, not indiv cells
Structure & Fxn of Cardiac Musc Cells: AP
.3 sec in heart (much slower than .002sec in sk.musc)
-RP @ 95mV, crosses threshold, AP to +25mV --> 120mV total voltage
phases of AP:
1.depolarization: Na entry
2.plateau phase: Kexit/Ca entry
3.repolarization: K exit
*absolute refractory period long & relative refractory period short
absolute RP:
.25sec; no other stim can stimulate AP during this time; heart cannot be summated/tetanized
relative RP:
.05sec following absolute; strong stim can cause 2nd heart beat; tetanized->attack
electrical activity of heart as relates to cardiac cycle:
1.sino-atrial node (SA node)
2.Atrio-ventricular node (AV node)
3.ventricular conducting system
SA node:
1.located @ wall of RA near where sup vena cava enters
2.automatically depolarizes & sends AP to
3.Atrial conducting pathway
automatically depolarizes-
normal adult @ rest, SA node fires off 70-80 APs/min->governing HR
atrial conducting pathway-
nerve fiberlike braches; found in both L&RA; fxn:send APs to atrial myocardium & cause atrial systole
AV node:
located at base of RA b/w RA & RV; receives AP from atrial conducting pathway
AV node fxns:
1.delays AP for fraction of a sec allowing time for completion of atrial diastole
2.transmisson of AP to ventricular conducting system
ventricular conducting system:
1.AV bundle:bundle of his; nervelike structure in interventricular septum; spilts in 2:
2.L&R bundle branches in septum
3.purkinje fibers: nervelike fibers found in all regions of both ventricles
perkinje fibers fxn:
get AP to all regions of ventricles quickly & simultaneously
all electrical activity assoc w/ 1 heartbeat
EKG: basis
ap from heart->tranferred to body fluids->conduct electrical act thruout whole body up to skin->attach electrodes to ankles, wrists, areas over chest, electrical signals detected by electrodes
EKG: pattern
1. p wave
2. qrs complex
3. t wave
4. 2 intervals
p wave:
represents atrial depolarization, resulting in atrial systole
qrs complex:
ventricular dep, resulting in ventricular systole
t wave:
ventricular rep, resulting in ventricular diastole
2 intervals:
1.P-R interval: time it takes for single AP to move from SA->AV node
2.Q-T interval: all electrical act of ventricles (dep & rep)
EKG: value
diagnostic tool in that it allows us to det HR & if any abnorm conduction of AP thru the heart
normal HR
70-80 bpm
any condition that alters normal heart rhythm
1.alterations in SA node act
2.Ectopic Foci
alterations in SA node act:
-HR of 60bpm/less
1.trained athletes
2.untrained myxedema
bradycardia: trained athlete
heart musculature builds up and they contain large SV; need higher HR, so undergo bradycardia during sleep
bradycardia: untrained myxedema
hypothyroidism; abnormally slow HR; result of excess use of beta blockers (drug)
HR =/> 100bpm; results from normal exercise, hypotension: BP too low, so inc HR to compensate pumping blood to body, severe anxiety/stress, excess use nicotine
Ectopic Foci
creation of abnormal pacemakers that become governing body of HR over pacemaker SA node
Ectopic Foci: most common cause
localized ischemia:lack of blood supply to regions of heart; also results from excess use of nicotine, caffeine
Ectopic Foci: Effects
1.single EF, PVC
2.single EF, Flutter
3.multiple EFs
single EF, PVC
pre-ventricular contraction; initiate AP->stimulates 1 HB out of order (typically caused by caffeine, not seriuos)
single EF, Flutter
300bpm; HBs coordinated, but pumping action inefficient: heart not allowed to fill to full volume, so not pumping otuput normally
multiple EFs
multiple pacemakers indpt of one another & coordination of HBs lost; muscle has no pumping action @ all
atria fibrillation:
atria dont contract in coordination; ventricles contract irregularly, but ventricular contraction capable of sustaining life; inefficient pump all together
ventricular fibrillation:
coronary thrombosis (blood clot)occurring in coronary artery, leads to local ischemia, resulting in:
vent. fibrillation results in:
1.myocardial infarction: death of cardiac ventricular musc
2.multiple EF: prevents vent from contracting in norm manner-> no pumping action in vent & if severe enough, >6min, leads to death due to lack of blood supply to brain
interference of AP conduction thru heart:
damage to AV node, bundle of his, or L/R bundle branches compromise AP conduction
1.heart block
2.myocardial infarction
heart block:
atria beat @ faster rate than ventricles due to improper/blocked input of AP to vent
myocardial infarction:
necrosis of ventricular myocardium & replaced w/ scar tissue -> conduction of AP slower than norm
Cardiac Physiology:
1.Cardiac Output
Cardiac Output
volume of blood pumped out of the heart each min
Cardiac Output: determining factors
1.SV-volume blood ejected w/ systole (avg 72ml/min)
2.HR- avg 75bpm
3.CO=SV*HR- avg 5.4 L/min @ rest & can inc as high as 30 L/min during exercise due to inc SV & inc HR
Cardiac Output: factors controlling change of CO
1.intrinsic autoregulation/starlings law of the heart
2.nervous reflex control of CO
intrinsic autoregulation/starlings law of the heart
the greater the vol blood entering during diastole, the greater the bol blood pumped out during systole
intrinsic autoregulation mechanisms:
1.venous return:vol of blood returning to RA from sup/inf vena cava each min
increased venous return->
greater stretchon vetnricular myocardium-> muscle responds to stretch w/ myocardium inc force of conraction -> inc SV -> inc CO (start w/ > coming in, end w/ > going out)
nervous reflex control of CO
1.parasymp innervation
2.vagal tone
3.symp innervation
4.mechanisms of action
parasymp innervation:
L&R vagus nerves (2) innervate the heart & use Ach as NT
-Rvagus nerve supplies SA node
-Lvagus nerve supplies AV node
-both send FEW fibers to ventricular myocardium
vagal tone:
continual, low level vagal input to heart; few APs come to this region & this keeps heart at norm rate of act/slows it
symp innervation:
T1-T6 spinal nerves (6) innervate the heart & release NE as NT; all supply SA node, AV node, & vent myocardium
mechanisms of action:
1.alterations of HR
2.alterations of contractile forces of heart
alterations of HR
-inc parasymp input largely & dec act of SA node->dec HR-> dec CO
-inc symp input & inc SA node act-> inc HR-> inc CO
alterations of contractile forces of heart
-inc symp stimulation-> inc force of contrxn to vent myocardium-> inc SV-> inc CO (strong effect)
-inc parasymp stimulation-> slight dec force of contrxn to vent myocardium-> slight dec SV-> slight dec CO
pathological conditions altering CO:
1.prob w/ heart valves leading to valvular insufficiency: blood flows backward a/g norm flow -> dec SV-> dec CO
2.stenosis: in bicuspid valve; dec SV-> dec CO
3.anemia: lack of O2 carrying capacity in blood; tissues in body dont receive adequate blood supply-> inc HR-> inc CO
Cardiac Physiology: BVs
3 layers make up BV wall:
1.Tunica Adventitia/Externa: outer layer, CT
2.Tunica Media: middle layer, smooth musc
3.Tunica Interna/Intima: innermost layer, in contact w/ blood, made of endothelium tissue->very smooth tissue preventing blood clotting inside BV
BV: types
1.elastic arteries
2.muscular arteries
elastic arteries:
contain elastic CT in them @ walls; begin @ aorta, branches to include brachiocephalicA, subclavians, common carotids, common iliac A; do not collapse
muscular arteries:
no elastic CT; ext/int carotids, brachials, subscapulars, radial/ulnar A, ext/int iliacs, femoral, deep femoralA; do not collapse
arteries subdivide into smaller arteries: arterioles
smaller diameter; tunica media decreased
connect arterioles to venules w/o forming capillaries
-no tunica externa or media
-single layer of endoth cells only
-derived from aterioles or metarterioles
-allows for exchange of materials b/w blood & body fluids
capillary divisions:
1.continuous: no openings in walls; most common
2.fenestrated: opening in walls/pores; found in kidneys
3.sinusoids: very large pores; found in spleen & liver
formed by fusion of capillaries; walls not as thick, but similar to arterioles; diameter larger than arterioles
formed by fusion of venules; wall thickness less & diameter larger than artery; vein walls collapsable due to much less smooth musc in vein wall than artery wall
vein: blood reservoir
in normal conditions, veins hold up to 59% of total blood volume; larger veins have internal valves-found in arms, legs, inf vena cava
BV fxns: arteries & arterioles
transport blood (usually oxygenated, but not always) FROM heart; EXCEPT pulmonary trunk & arteries carry deoxygenated blood from heart
BV fxns: elastic arteries
1.provide pulse wave: blood enters aorta under press->aorta expands during systole->elastic elements retract aorta to norm pos w/ following diastole causing HB
pulse path:
starts in aorta, then transported to all elastic & muscular arteries, to radial artery for you to det pulse/HR
BV fxns: arterioles
diameter changes easily w/autonomic stimulation -> major BP regulators in body
BV fxns: capillaries
exchange of substance b/w blood plasma & tissue fluids
BV fxns: venules & veins
carry blood (usually deoxygenated) TO heart; EXCEPT pulmonary veins carry oxygenated blood to heart
BV fxns: large veins
arms & legs; contain valves that help prevent backflow of blood in veins
1.muscular pump
muscular pump:
1.musc contrxns "squeeze" vein & cause blood to move
2.musc relaxation removes compression/press off vein & cause blood to flow backward->valves close & prevent regurgitation maintaing blood flow toward heart
BV: general plan circulation
LA->LV->aorta->coronary sys OR systemic sys->arteries->arterioles->capillaries->venules->veins->vena cava (sup or inf)->RA->RV->pulmonary trunk of pulmonary sys->arteries->arterioles->capillaries->venules->veins->LA
blood flow systems:
start & come back to LA; flow thru 3 systems:
1.coronary sys: supplies heart
2.systemic sys: supplies all parts of body except heart & lungs
3.pulmonary sys: supplies lungs
BV: blood pressures in systemic circulation
goes to every part of body BUT lungs/heart;
1.systolic pressure
2.diastolic pressure
3.pulse pressure
4.mean arteriol pressure
systolic pressure:
pressure exerted on aorta & arteries during vetnricular systole
-@ rest 120 mmHg
diastolic pressure:
pressure exerted on aorta & arteries during ventricular diastole
-@ rest 80 mmHg
pulse pressure:
difference b/w SP & DP
-@ rest 120-80= 40 mmHg
-faint pulse lower 40 mmHg ->heart not beating as strong
mean arterial pressure (MAP)
BP; average of SP & DP 120+80=200/2 = 100 mmHg in aorta
1.driving force of blood thru BVs
2.force that causes fluid exchng in blood capillaries move further away from heart, MAP dec b/c BVs cause resistance to blood flow-> pressure dec
*by time reaches arterioles, 55% of resistance has occurred
BV: regulation of MAP
1.MAP=CO*PR (peripheral resistance: resistance to flow in BVs) relationships: inc CO-> inc MAP & inc PR-> inc MAP
main factors determining PR
1.viscosity of blood: thickness; high viscosity->high PR-> high BP; low viscosity-> low PR-> low BP
2.diameter of arterioles: very impt b/c arterioles major BP regulators
diameter of arterioles:
1.control center: vasomotor center in MO; sends out symp impulses to smooth musc arterioles
2.vasomotor tone
vasomotor tone:
continual output; few in #; maintain arteriole smooth musc partially contracted state
vasomotor deviations: output from VM center->vasoconstriction-> inc PR
2.dec output from VM center->vasdilation->dec PR
regulatory mechanisms related to PR
1.vasomotor baroreflex
2.vasomotor chemoreflex
vasomotor baroreflex:
change in pressure causing reflex;
found in aortic arch & carotid sinus;
-aortic receptors connected to VM center by vagus nerve
-carotid receptors connected to VM center by glossopharyngeal nerve
vasomotor chemoreflex:
change in O2/CO2 press in arterial blood, pH;
found in aortic arch (vagus nerve concxn)& int carotid A (glossop. concxn)