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  1. 1. Physiology ReviewA work in Progress
  2. 2. National Boards Part I Physiology section Neurophysiology (23%) Membrane potentials, action potentials, synpatictransmission Motor function Sensory function Autonomic function Higher cortical function Special senses
  3. 3. National Boards Part I Physiology (cont) Muscle physiology (14%) Cardiac muscle Skeletal muscle Smooth muscle Cardiovascular physiology (17%) Cardiac mechanisms Eletrophysiology of the heart Hemodynamics Regulation of circulation Circulation in organs Lymphatics Hematology and immunity
  4. 4. National Boards Part I Physiology (cont) Respiratory physiology (10%) Mechanics of breathing Ventilation, lung volumes and capacities Regulation of respiration O2 and CO2 transportation Gaseous Exchange Body Fluids and Renal physiology (11%) Regulation of body fluids Glomerular filtration Tubular exchange Acid-base balance
  5. 5. National Boards Part I Physiology (cont) Gastrointestinal physiology (10%) Ingestion Digestion Absorption Regulation of GI function Reproductive physiology (4%) Endocrinology (8%) Secretion of hormones Action of hormones Regulation Exercise and Stress Physiology (3%)
  6. 6. Weapons in neurophysiologistsarmory Recording Individual neurons Gross potentials Brain scans Stimulation Lesions Natural lesions Experimental lesions
  7. 7. Neurophysiology Membrane potential Electrical potential across the membrane Inside more negative than outside High concentration of Na+ outside cell High concentration of K+ inside cell PO4= SO4= Protein Anions trapped in the cellcreate negative internal enviiornment
  8. 8. Membrane physiology Passive ion movement across the cellmembrane Concentration gradient High to low Electrical gradient Opposite charges attract, like repel Membrane permeability Action potential Pulselike change in membrane permeability to Na+, K+,(Ca++)
  9. 9. Membrane physiology In excitable tissue an action potential is apulse like D in membrane permeability In muscle permeability changes for: Na+" at onset of depolarization, during repolarization Ca++" at onset of depolarization, during repolarization K+" at onset of depolarization, during repolarization
  10. 10. Passive ion movement acrosscell If ion channels are open, an ion willseek its Nerst equilibrium potential concentration gradient favoring ionmovement in one direction is offset byelectrical gradient
  11. 11. Resting membrane potential (Er) During the Er in cardiac muscle, fast Na+and slow Ca++/Na+ are closed, K+channels are open. Therefore K+ ions are free to move, andwhen they reach their Nerst equilibriumpotential, a stable Er is maintained
  12. 12. Na+/K+ ATPase (pump) The Na+/K+ pump which is energydependent operates to pump Na+ out &K+ into the cardiac cell at a ratio of 3:2 therefore as pumping occurs, there is net lossof one + charge from the interior each cycle,helping the interior of the cell remain negative the protein pump utilizes energy from ATP
  13. 13. Ca++ exchange protein In the cardiac cell membrane is a proteinthat exchanges Ca++ from the interior inreturn for Na+ that is allowed to enter thecell. The function of this exchange protein istied to the Na+/K+ pump if the Na+/K+ pump is inhibited, function ofthis exchange protein is reduced & moreCa++ is allowed to accumulate in the cardiaccell contractile strength.
  14. 14. Action potential Pulselike change in membranepermeability to Na+, K+, (Ca++) Controlled by gates Voltage dependent Ligand dependent Depolarization Increased membrane permeability to Na+ (Ca++) Na+ influx Repolarization Increased membrane permeability to K+ K+ efflux
  15. 15. Refractory Period Absolute During the Action Potential (AP), cell isrefractory to further stimulation (cannot berestimulated) Relative Toward the end of the AP or just afterrepolarization a stronger than normal stimulus(supranormal) is required to excite cell
  16. 16. All-or-None Principle Action potentials are an all or nonephenomenon Stimulation above threshold may cause anincreased number of action potentials but willnot cause a greater action potential
  17. 17. Propagation Action potentials propagate (move along)as a result of local currents produced atthe point of depolarization along themembrane compared to the adjacent areathat is still polarized Current flow in biologic tissue is in thedirection of positive ion movement or oppositethe direction of negative ion movement
  18. 18. Conduction velocity Proportional to the diameter of the fiber Without myelin 1 micron diameter = 1 meter/sec With myelin Accelerates rate of axonal transmission 6X andconserves energy by limiting depolarization toNodes of Ranvier Saltatory conduction-AP jumps internode to internode 1micron diameter = 6 meter/sec
  19. 19. Synapes Specialized junctions for transmission ofimpulses from one nerve to another Electrical signal causes release of chemicalsubstances (neurotransmitters) that diffuseacross the synapse Slows neural transmission Amount of neurotransmitter (NT) releaseproportional to Ca++ influx
  20. 20. Neurotransmitters Acetylcholine Catacholamines Norepinephrine Epinephrine Serotonin Dopamine Glutamate Gamma-amino butyric acid (GABA) Certain amino acids Variety of peptides
  21. 21. Neurons May release more than one substanceupon stimulation Neurotransmitter like norepinephrine Neuromodulator like neuropeptide Y (NPY)
  22. 22. Postsynaptic Cell Response Varies with the NT Excitatory NT causes a excitatorypostsynaptic potential (EPSP) Increased membrane permeability to Na+ and/orCa++ influx Inhibitory NT causes an inhibitorypostsynaptic potential (IPSP) Increased membrane permeability to Cl- influx orK+ efflux Response of Postsynpatic Cell reflectsintegration of all input
  23. 23. Response of Postsynaptic Cell Stimulation causing an AP S EPSPS IPSPthreshold Stimulation leading to facilitation S EPSPS IPSPthreshold Inhibition S EPSPS IPSP
  24. 24. Somatic Sensory System Nerve fiber types (Type I, II, III, IV) based on fiberdiameter (Type I largest, Type IV smallest) Ia - Annulospiral (1o) endings of muscle spindles Ib - From golgi tendon organs II Flower spray (2o) endings of muscle spindles High disrimination touch ( Meissners) Pressure III Nociception, temperature, some touch (crude) IV- nociception and temperature (unmyelinated) crudetouch and pressure
  25. 25. Transduction Stimulus is changed into electrical signal Different types of stimuli mechanical deformation chemical change in temperature electromagnetic
  26. 26. Sensory systems All sensory systems mediate 4 attributesof a stimulus no matter what type ofsensation modality location intensity timing
  27. 27. Receptor Potential Membrane potential of the receptor A change in the receptor potential isassociated with opening of ion (Na+)channels Above threshold as the receptor potentialbecomes less negative the frequency ofAP into the CNS increases
  28. 28. Labeled Line Principle Different modalities of sensation dependon the termination point in the CNS type of sensation felt when a nerve fiber isstimulated (e.g. pain, touch, sight, sound) isdetermined by termination point in CNS labeled line principle refers to the specificity ofnerve fibers transmitting only one modality ofsensation Capable of change, e.g. visual cortex in blindpeople active when they are reading Braille
  29. 29. Adaptation Slow-provide continuous information(tonic)-relatively non adapting-respond tosustained stimulus joint capsul muscle spindle Merkels discs punctate receptive fields Ruffini end organs (corpusles) activated by stretching the skin
  30. 30. Adaptation Rapid (Fast) or phasic react strongly when a change is takingplace respond to vibration hair receptors 30-40 Hz Pacinian corpuscles 250 Hz Meissners corpuscles- 30-40 Hz (Hz represents optimum stimulus rate)
  31. 31. Sensory innervation of Spinaljoints Tremendous amount of innervation withcervical joints the most heavily innervated Four types of sensory receptors Type I, II, III, IV
  32. 32. Types of joint mechanoreceptors Type I- outer layer of capsule- lowthreshold, slowly adapts, dynamic, toniceffects on LMN Type II- deeper layer of capsule- lowthreshold, monitors joint movement,rapidly adapts, phasic effects on LMN Type III- high threshold, slowly adapts,joint version of GTO Type IV- nociceptors, very high threshold,inactive in normal joint, active withswelling, narrowing of joint.
  33. 33. Stereognosis The ability to perceive form through touch tests the ability of dorsal column-mediallemniscal system to transmit sensations fromthe hand also tests ability of cognitive processes in thebrain where integration occurs The ability to recognize objects placed inthe hand on the basis of touch alone isone of the most important complexfunctions of the somatosensory system.
  34. 34. Receptors in skin Most objects that we handle are largerthan the receptive field of any receptor inthe hand These objects stimulate a largepopulation of sensory nerve fibers each of which scans a small portion of theobject Deconstruction occurs at the periphery By analyzing which fibers have beenstimulated the brain reconstructs thepattern
  35. 35. Mechanoreceptors in the Skin Rapidly adapting cutaneous Meissners corpuscles in glabrous (non hairy)skin- (more superficial) signals edges Hair follicle receptors in hairy skin Pacinian corpuscles in subcutaneous tissue(deeper)
  36. 36. Mechanoreceptors in the Skin Slowly adapting cutaneous Merkels discs have punctate receptive fields(superficial) senses curvature of an objects surface Ruffini end organs activated by stretching theskin (deep) even at some distance away from receptor
  37. 37. Mechanoreceptors in Glabrous(non hairy) SkinRapidadaptationSuperficial DeepSmall field Large fieldSlowadaptationMeissnersCorpusclePacinianCorpuscleMerkelsDiscRuffiniEnd Organ
  38. 38. Somatic Sensory Cortex Receives projections from the thalamus Somatotopic organization (homunculus) Each central neuron has a receptive field size of cortical representation varies indifferent areas of skin based on density of receptors lateral inhibition improves two pointdiscrimination
  39. 39. Somatosensory Cortex Two major pathways Dorsal column-medial lemniscal system Most aspects of touch, proprioception Anterolateral system Sensations of pain (nociception) and temperature Sexual sensations, tickle and itch Crude touch and pressure Conduction velocity 1/3 that of dorsal columns
  40. 40. Somatosensory Cortex (SSC) Inputs to SSC are organized intocolumns by submodality cortical neurons defined by receptive field modality most nerve cells are responsive to onlyone modality e.g. superficial tactile, deeppressure, temperature, nociception some columns activated by rapidly adaptingMessiners, others by slowly adapting Merkels,still others by Paccinian corp.
  41. 41. Somatosensory cortex Brodman area 3, 1, 2 (dominate input) 3a-from muscle stretch receptors (spindles) 3b-from cutaneous receptors 2-from deep pressure receptors 1-rapidly adapting cutaneous receptors These 4 areas are extensivelyinterconnected (serialparallelprocessing) Each of the 4 regions contains a completemap of the body surface homonculus
  42. 42. Somatosensory Cortex 3 different types of neurons in BM area 1,2 havecomplex feature detection capabilities Motion sensitive neurons respond well to movement in all directions but not selectivelyto movement in any one direction Direction-sensitive neurons respond much better to movement in one direction than inanother Orientation-sensitive neurons respond best to movement along a specific axis
  43. 43. Other Somatosensory CorticalAreas Posterior parietal cortex (BM 57) BM 5 integrates tactile information frommechanoreceptors in skin with proprioceptiveinputs from underlying musclesjoints BM 7 receives visual, tactile, proprioceptiveinputs intergrates stereognostic and visual information Projects to motor areas of frontal lobe sensory initiationguidance of movement
  44. 44. Secondary SSC (S-II) Secondary somatic sensory cortex (S-II) located in superior bank of the lateral fissure projections from S-1 are required for functionof S-II projects to the insular cortex, which innervatesregions of temporal lobe believed to beimportant in tactile memory
  45. 45. Pain vs. Nociception Nociception-reception of signals in CNS evokedby stimulation of specialized sensory receptors(nociceptors) that provide information abouttissue damage from external or internal sources Activated by mechanical, thermal, chemical Pain-perception of adversive or unpleasantsensation that originates from a specific regionof the body Sensations of pain Pricking, burning, aching stinging soreness
  46. 46. Nociceptors Least differentiated of all sensoryreceptors Can be sensitized by tissue damage hyperalgesia repeated heating axon reflex may cause spread of hyperalgesia inperiphery sensitization of central nociceptor neurons as aresult of sustained activation
  47. 47. Sensitization of Nociceptors Potassium from damaged cells-activation Serotonin from platelets- activation Bradykinin from plasma kininogen-activate Histamine from mast cells-activation Prostaglandinsleukotriens fromarachidonic acid-damaged cells-sensitize Substance P from the 1o afferent-sensitize
  48. 48. Nociceptive pathways Fast A delta fibers glutamate neospinothalamic mechanical, thermal good localization sharp, pricking terminate in VBcomplex of thalamus Slow C fibers substance P paleospinothalamic polymodal/chemical poor localization dull, burning, aching terminate; RF tectal area of mesen. Periaqueductal gray
  49. 49. Nociceptive pathways Spinothalamic-major neo- fast (A delta) paleo- slow (C fibers) Spinoreticular Spinomesencephalic Spinocervical (mostly tactile) Dorsal columns- (mostly tactile)
  50. 50. Pain Control Mechanisms Peripheral Gating theory involves inhibitoryinterneruon in cordimpacting nocicep.projection neurons inhibited by C fibers stimulated by A alpha beta fibers TENS Central Direct electrical + tobrain - analgesia Nociceptive controlpathways descend tocord Endogenous opiods
  51. 51. Muscle Receptors Muscle contain 2 types of sensory receptors muscle spindles respond to stretch located within belly of muscle in parallel with extrafusalfibers (spindles are intrafusal fibers) innervated by 2 types of myelinated afferent fibers group Ia (large diameter) group II (small diameter) innervated by gamma motor neurons that regulate thesensitivity of the spindle golgi tendon organs respond to tension located at junction of muscletendon innervated by group Ib afferent fibers
  52. 52. Muscle Spindles Nuclear chain Most responsive to muscle shortening Nuclear bag- most responsive to muscle lengthening Dynamic vs static bag A typical mammalian muscle spindlecontains one of each type of bag fiberavariable number of chain fibers ( 5)
  53. 53. Muscle Spindles sensory endings primary-usually 1/spindleinclude allbranches of Ia afferent axon innervate all three types much more sensitive to rate of change of lengththan secondary endings secondary-usually 1/spindle from group IIafferent innervate only on chain and static bag information about static length of muscle
  54. 54. Gamma Motor System Innervates intrafusal fibers Controlled by: Reticular formation Mesencephalic area appears to regulate rhythmicgate Vestibular system Lateral vestibulospinal tract facilitates gammamotor neuron antigravity control Cutaneous sensory receptors Over skeletal muscle, sensory afferent activatinggamma motor neurons
  55. 55. Golgi tendon organ (GTO) Sensitive to changes in tension each tendon organ is innervated by single groupIb axon that branchesintertwines amongbraided collagen fascicles. Stretching tendon organ straightens collagenbundles which compresseselongates nerveendings causing them to fire firing rate very sensitive to changes in tension greater response associated with contraction vs.stretch (collagen stiffer than muscle fiber)
  56. 56. CNS control of spindlesensitivity Gamma motor innervation to the spindle causescontraction of the ends of the spindle This allows the spindle to shortenfunction whilethe muscle is contracting Spindle operate over wide range of muscle length This is due to simultaneously activating bothalphagamma motor neurons during musclecontraction. (alpha-gamma coactivation) In slow voluntary movements Ia afferents oftenincrease rate of discharge as muscle is shortening
  57. 57. CNS control of spindle sensitivity In movement the Ia afferents dischargerate is very sensitive to variartions in therate of change of muscle length This information can be used by thenervous system to compensate forirregularities in the trajectory of amovementto detect fatigue of localgroups of muscle fibers
  58. 58. Spindles and GTOs As a muscle contracts against a load: Spindle activity tends to decrease GTO activity tends to increase As a muscle is stretched Spindle activity increases GTO activity will initially decrease
  59. 59. Summary Spindles in conjunction with GTOsprovide the CNS with continuousinformation about the mechanical state ofa muscle For virtually all higher order perceptualprocesses, the brain must correlatesensory input with motor output toaccurately assess the bodies interactionwith its environment
  60. 60. Transmission of signals Spatial summation increasing signal strength transmitted byprogressively greater # of fibers receptor field # of endings diminish as you move from center toperiphery overlap between fibers Temporal summation increasing signal strength by frequency ofIPS
  61. 61. Neuronal Pools Input fibers divide hundreds to thousands of times tosynapse with arborized dendrites stimulatory field Decreases as you move out from center Output fibers impacted by input fibers but not equally Excitation-supra-threshold stimulus Facilitation-sub-threshold stimulus Inhibition-release of inhibitory NT
  62. 62. Neuronal Pools Divergence in the same tract into multiple tracts Convergence from a single source from multiple sources Neuronal circuit causing both excitationand inhibition (e.g. reciprocal inhibition) insertion of inhibitory neuron
  63. 63. Neuronal Pools Prolongation of Signals Synaptic Afterdischarge postsynaptic potential lasts for msec can continue to excite neuron Reverberatory circuit positive feedback within circuit due to collateralfibers which restimulate itself or neighboringneuron in the same circuit subject to facilitation or inhibition
  64. 64. Neuronal Pools Continuous signal output-self excitatory continuous intrinsic neuronal discharge less negative membrane potential leakly membrane to Na+/Ca++ continuous reverberatory signals IPS increased with excitation IPS decreased with inhibition carrier wave type of information transmissionexcitation and inhibition are not the cause ofthe output, they modify output up or down ANS works in this fashion to control HR,vascular tone, gut motility, etc.
  65. 65. Rhythmical Signal Output Almost all result from reverberating circuits excitatory signals can increases amplitude frequency of rhythmic output inhibitory signals can decrease amplitude frequency of rhythmic output examples include the dorsal respiratorycenter in medulla and its effect on phrenicnerve activity to the diaphragm
  66. 66. Stability of Neuronal Circuits Almost every part of the brain connects withevery other part directly or indirectly Problem of over-excitation (epileptic seizure) Problem controlled by: inhibitory circuits fatigue of synapses decreasing resting membrane potential long-term changes by down regulation of receptors
  67. 67. Special Senses Vision Audition Chemical senses Taste Smell
  68. 68. Refraction Light rays are bent refractive index = ratio of light in a vacuum tothe velocity in that substance velocity of light in vacuum=300,000 km/sec Light year 9.46 X 1012 km Refractive indices of various media air = 1 cornea = 1.38 aqueous humor = 1.33 lens = 1.4 vitrous humor = 1.34
  69. 69. Refraction of light by the eye Refractive power of 59 D (cornealens) Diopter = 1 meter/ focal length central point 17 mm in front of retina inverted image- brain makes the flip lens strength can vary from 20- 34 D Parasympathetic + increases lens strength Greater refractive power needed to readtext
  70. 70. Errors of Refraction Emmetropia- normal vision; ciliary musclerelaxed in distant vision Hyperopia-farsighted- focal pt behind retina globe short or lens weak ; convex lens to correct Myopia-nearsighted- focal pt in front ofretina globe long or lens strong; concave lens to correct Astigmatism- irregularly shaped cornea (more common) lens (less common)
  71. 71. Visual Acuity Snellen eye chart ratio of what that person can seecompared to a person with normal vision 20/20 is normal 20/40 less visual acuity What the subject sees at 20 feet, thenormal person could see at 40 feet. 20/10 better than normal visual acuity What the subject sees at 20 feet, thenormal person could see at 10 feet
  72. 72. Visual acuity The fovea centralis is the area ofgreatest visual acuity it is less than .5 mm in diameter ( 2 deg ofvisual field) outside fovea visual acuity decreases tomore than 10 fold near periphery point sources of light two m apart onretina can be distinguished as twoseparate points
  73. 73. Fovea and acute visual acuity Central fovea-area of greatest acuity composed almost entirely of long slendercones aids in detection of detail blood vessels, ganglionic cells, innernuclearplexiform layers are displacedlaterally allows light to pass relatively unimpeded toreceptors
  74. 74. Depth Perception Relative size the closer the object, the larger it appears learned from previous experience Moving parallax As the head moves, objects closer moveacross the visual field at a greater rate Stereopsis- binocular vision eyes separated by 2 inches- slightdifference in position of visual image onboth retinas, closer objects are morelaterally placed
  75. 75. Accomodation Increasing lens strength from 20 -34 D Parasympathetic + causes contraction ofciliary muscle allowing relaxation ofsuspensory ligaments attached radiallyaround lens, which becomes more convex,increasing refractive power Associated with close vision (e.g. reading) Presbyopia- loss of elasticity of lens w/ age decreases accomodation
  76. 76. Formation of Aqueous Humor Secreted by ciliary body (epithelium) 2-3 ul/min flows into anterior chamber and drained byCanal of Schlemm (vein) intraocular pressure- 12-20 mmHg. Glaucoma- increased intraocular P. compression of optic N.-can lead to blindness treatment; drugssurgery
  77. 77. Photoreceptors RodsCones Light breaks down rhodopsin (rods) andcone pigments (cones) rhodopsin Na+ conductance photoreceptors hyperpolarize release less NT (glutamate) whenstimulated by light
  78. 78. Bipolar Cells Connect photoreceptors to eitherganglionic cells or amacrine cells passive spread of summated postsynapticpotentials (No AP) Two types ON- hyperpolarized by NT glutamate OFF- depolarized by NT glutamate
  79. 79. Ganglionic Cells Can be of the ON or OFF variety ON bipolar + ON ganglionic OFF bipolar + OFF ganglionic Generate AP carried by optic nerve Three subtypes X (P) cells Y (M) cells W cells
  80. 80. X vs Y Ganglionic cellsCell type X(P) Y(M)Input Bipolar AmacrineReceptive field Small LargeConduction vel. Slow FastResponse Slow adaptation Fast adaptationProjects to Parvocellular ofLGNMagnocellularof LGNFunction color vision BW movment
  81. 81. W Ganglionic Cells smallest, slowest CV many lack center-surround antagonisticfields they act as light intensity detectors some respond to large field motion they can be direction sensitive Broad receptive fields
  82. 82. Horozontal Cells Non spiking inhibitory interneurons Make complex synaptic connections withphotorecetorsbipolar cells Hyperpolarized when light stimulates inputphotoreceptors When they depolarize they inhibitphotoreceptors Center-surround antagonism
  83. 83. Amacrine Cells Receive input from bipolar cells Project to ganglionic cells Several types releasing different NT GABA, dopamine Transform sustained ON or OFF totransient depolarizationAP in ganglioniccells
  84. 84. Center-Surround Fields Receptive fields of bipolargang. C. two concentric regions Center field mediated by all photoreceptors synapsingdirectly onto the bipolar cell Surround field mediated by photoreceptors which gainaccess to bipolar cells via horozontal c. If center is on, surround is off
  85. 85. Receptive field size In fovea- ratio can be as low as 1 cone to1 bipolar cell to 1 ganglionic cell In peripheral retina- hundreds of rods cansupply a single bipolar cellmany bipolarcells connected to 1 ganglionic cell
  86. 86. Dark Adaptation In sustained darkness reform light sensitivepigments (RhodopsinCone Pigments) of retinal sensitivity 10,000 fold cone adaptation-100 fold Adapt first within 10 minutes rod adaptation-100 fold Adapts slower but longer than cones (50 minutes) dilation of pupil neural adaptation
  87. 87. Cones 3 populations of cones with differentpigments-each having a different peakabsorption l Blue sensitive (445 nm) Green sensitive (535 nm) Red sensitive (570 nm)
  88. 88. Visual Pathway Optic N to Optic Chiasm Optic Chiasm to Optic Tract Optic Tract to Lateral Geniculate Lateral Geniculate to 10 Visual Cortex geniculocalcarine radiation
  89. 89. Additional Visual Pathways From Optic Tracts to: Suprachiasmatic Nucleus biologic clock function Pretectal Nuclei reflex movement of eyes- focus on objects of importance Superior Colliculus rapid directional movement of both eyes
  90. 90. Primary Visual Cortex Brodman area 17 (V1)-2x neuronaldensity Simple Cells-responds to bar of light/dark abovebelow layer IV Complex Cells-motion dependent but sameorientation sensitivity as simple cells Color blobs-rich in cytochrome oxidase incenter of each occular dominace band starting point of cortical color processing Vertical Columns-input into layer IV Hypercolumn-functional unit, block through allcortical layers about 1mm2
  91. 91. Visual Association Cortex Visual analysis proceeds along manypaths in parallel form color motion depth
  92. 92. Control of Pupillary Diameter Para + causes size of pupil (miosis) Symp + causes size of pupil (mydriasis) Pupillary light reflex optic nerve to pretectal nuclei to Edinger-Westphal to ciliary ganglion to pupillarysphincter to cause constriction (Para)
  93. 93. Function of extraoccular muscles Medial rectus of one eye works with thelateral rectus of the other eye as a yokedpair to produce lateral eye movements Medial rectus adducts the eye Lateral rectus abducts the eye
  94. 94. Raising/lowering/torsioningElevateDepressTorsionAbducted AdductedEye EyeSuperior rectus Inferior obliqueInferior rectus Superior obliqueSuperior obliqueInferior obliqueSuperior rectusInferior rectus
  95. 95. Innervation of extraoccularmuscles Extraoccular muscles controlled by CN III,IV, and VI CN VI controls the lateral rectus only CN IV controls the superior oblique only CN III controls the rest
  96. 96. Sound Units of Sound is the decibel (dB) I (measured sound) Decibel = 1/10 log -------------------------- I (standard sound) Reference Pressure for standard sound .02 X 10-2 dynes/cm2
  97. 97. Sound Energy is proportional to the square ofpressure A 10 fold increase in sound energy = 1 bel One dB represents an actual increase insound E of about 1.26 X Ears can barely detect a change of 1 dB
  98. 98. Different Levels of Sound 20 dB- whisper 60 dB- normal conversation 100 dB- symphony 130 dB- threshold of discomfort 160 dB- threshold of pain
  99. 99. Frequencies of Audible Sound In a young adult 20-20,000 Hz (decreases with age) Greatest acuity 1000-4000 Hz
  100. 100. Tympanic Membrane Ossicles Impedance matching-between soundwaves in airsound vibrations generatedin the cochlear fluid 50-75% perfect for sound freq.300-3000Hz Ossicular system reduces amplitude by 1/4 increases pressure against oval window 22X increased force (1.3) decreased area from TM to oval window (17)
  101. 101. Ossicular system (cont.) Non functional ossicles or ossicles absent decrease in loudness about 15-20 dB medium voice now sounds like a whisper attenuation of sound by contraction of Stapedius muscle-pulls stapes outward Tensor tympani-pull malleous inward
  102. 102. Attenuation of sound CNS reflex causes contraction of stapediusand tensor tympani muscles activated by loud sound and also by speech latency of about 40-80 msec creation of rigid ossicular system whichreduces ossicular conduction most effective at frequencies of1000 Hz. Protects cochlea from very loud noises,masks low freq sounds in loud environment
  103. 103. Cochlea System of 3 coiled tubes Scala vestibuli Scala media Scala tympani
  104. 104. Scala Vestibuli Seperated from the scala media byReissners membrane Associated with the oval window filled with perilymph (similar to CSF)
  105. 105. Scala Media Separated from scala tympani by basilarmembrane Filled with endolymph secreted by striavascularis which actively transports K+ Top of hair cells bathed by endolymph
  106. 106. Endocochlear potential Scala media filled with endolymph (K+) baths the tops of hair cells Scala tympani filled with perilymph(CSF) baths the bottoms of hair cells electrical potential of +80 mv existsbetween endolymph and perilymph dueto active transport of K+ into endolymph sensitizes hair cells inside of hair cells (-70 mv vs -150 mv)
  107. 107. Scala Tympani Associated with the round window Filled with perilymph baths lower bodies of hair cells
  108. 108. Function of Cochlea Change mechanical vibrations in fluid intoaction potentials in the VIII CN Sound vibrations created in the fluid causemovement of the basilar membrane Increased displacement increased neuronal firing resulting an increasein sound intensity some hair cells only activated at high intensity
  109. 109. Place Principle Different sound frequencies displacedifferent areas of the basilar membrane natural resonant frequency hair cells near oval window (base) short and thick respond best to higher frequencies (4500Hz) hair cells near helicotrema (apex) long and slender respond best to lower frequencies (200 Hz)
  110. 110. Central Auditory Pathway Organ of Corti to ventraldorsalcochlear nuclei in upper medulla Cochlear N to superior olivary N (mostfibers pass contralateral, some stayipsilateral) Superior olivary N to N of laterallemniscus to inferior colliculus via laterallemniscus Inferior colliculus to medial geniculate N Medial geniculate to primary auditorycortex
  111. 111. Primary Auditory Cortex Located in superior gyrus of temporal lobe tonotopic organization high frequency sounds posterior low frequency sounds anterior
  112. 112. Air vs. Bone conduction Air conduction pathway involves externalear canal, middle ear, and inner ear Bone conduction pathway involves directstimulation of cochlea via vibration of theskull (cochlea is imbedded in temporalbone) reduced hearing may involve: ossicles (air conduction loss) cochlea or associated neural pathway(sensory neural loss)
  113. 113. Sound Localization Horizontal direction from which soundoriginates from determined by twoprincipal mechanisms Time lag between ears functions best at frequencies3000 Hz. Involves medial superior olivary nucleus neurons that are time lag specific Difference in intensities of sounds in both ears involves lateral superior olivary nucleus
  114. 114. Exteroceptive chemosenses Taste Works together with smell Categories (Primary tastes) sweet salt sour bitter (lowest threshold-protective mechanism) Olfaction (Smell) Primary odors (100-1000)
  115. 115. Taste receptors May have preference for stimuli influenced by past history recent past adaptation long standing memory conditioning-association
  116. 116. Primary sensations of taste Sour taste- caused by acids (hydrogen ion concentration) Salty taste- caused by ionized salts (primarily the [Na+]) Sweet taste- most are organic chemicals (e.g. sugars, estersglycols, alcohols, aldehydes, ketones, amides,amino acids)inorganic salts of PbBe Bitter- no one class of compounds but: long chain organic compounds with N alkaloids (quinine,strychnine,caffeine, nicotine)
  117. 117. Taste Taste sensations are generated by: complex transactions among chemical andreceptors in taste buds subsequent activities occuring along the tastepathways There is much sensory processing,centrifugal control, convergence,globalintegration among related systemscontributing to gustatory experiences
  118. 118. Taste Buds Taste neuroepithelium - taste buds intongue, pharynx,larynx. Aggregated in relation to 3 kinds of papillae fungiform-blunt pegs 1-5 buds /top foliate-submerged pegs in serous fluid with1000s of taste buds on side circumvallate-stout central stalks in serous filledmoats with taste buds on sides in fluid 40-50 modified epithelial cells grouped inbarrel shaped aggregate beneath a smallpore which opens onto epithelial surface
  119. 119. Innervation of Taste Buds each taste nerve arborizesinnervatesseveral buds (convergence in 1st order) receptor cells activate nerve endings whichsynapse to base of receptor cell Individual cells in each bud differentiate,functiondegenerate on a weekly basis taste nerves: continually remodel synapses on newlygenerated receptor cells provides trophic influences essential forregeneration of receptorsbuds
  120. 120. Adaptation of taste Rapid-within minutes taste buds account for about 1/2 ofadaptation the rest of adaptation occurs higher inCNS
  121. 121. CNS pathway-taste Anterior 2/3 of tongue lingual N. to chorda tympani to facial (VII CN) Posterior 1/3 of tongue IX CN (Petrosal ganglion) base of tongue and palate X CN All of the above terminate in nucleustractus solitarius (NTS)
  122. 122. CNS pathway (taste cont) From the NTS to VPM of thalamus viacentral tegmental tract (ipsilateral) which isjust behind the medial lemniscus. From the thalmus to lower tip of the post-centralgyrus in parietal cortexadajacentopercular insular area in sylvian fissure
  123. 123. Olfactory Membrane Superior part of nostril Olfactory cells bipolar nerve cells 100 million in olfactory epithelium 6-12 olfactory hairs/cell project in mucus react to odors and stimulate cells
  124. 124. Cells in Olfactory Membrane Olfactory cells- bipolar nerve cells which project hairs inmucus in nasal cavity stimulated by odorants connect to olfactory bulb via cribiform plate Cells which make up Bowmans glands secrete mucus Sustentacular cells supporting cells
  125. 125. Characteristics of Odorants Volatile slightly water soluble- for mucus slightly lipid soluble for membrane of cilia Threshold for smells Very low
  126. 126. Primary sensations of smell Anywhere from 100 to 1000 based ondifferent receptor proteins odor blindness has been described for atleast 50 different substances may involve lack of a specific receptor protein
  127. 127. Receptor Resting membrane potential when notactivated = -55 mv 1 impulse/ 20 sec to 2-3 impulses/ sec When activated membrane pot. = -30 mv 20 impulses/ sec
  128. 128. Glomerulus in Olfactory Bulb several thousand/bulb Connections between olfactory cells andcells of the olfactory tract receive axons from olfactory cells (25,000) receive dendrites from: large mitral cells (25) smaller tufted cells (60)
  129. 129. Cells in Olfactory bulb Mitral Cells- (continually active) send axons into CNS via olfactory tract Tufted Cells- (continually active) send axons into CNS via olfactory tract Granule Cells inhibitory cell which can decrease neuraltraffic in olfactory tracts receive input from centrifugal nerve fibers
  130. 130. CNS pathways Very old- medial olfactory area feeds into hypothalamusprimitive areas oflimbic system (from medial pathway) basic olfactory reflexes Less old- lateral olfactory area prepyriformpyriform cortex -only sensorypathway to cortex that doesnt relay viathalamus (from lateral pathway) learned control/adversion Newer- passes through the thalamus toorbitofrontal cortex (from lateral pathway) - conscious analysis of odor
  131. 131. Medial and Lateral pathways 2nd order neurons form the olfactory tract project to the following 1o olfactorypaleocortical areas Anterior olfactory nucleus Modulates information processing in olfactorybulbs Amygdala and olfactory tubercle Important in emotional, endocrine, and visceralresponses of odors Pyriform and periamygdaloid cortex Olfactory perception Rostral entorhinal cortex Olfactory memories
  132. 132. Homeostasis Concept whereby body states areregulated toward a steady state Proposed by Walter Cannon in 1932 At the same time Cannon introducednegative feedback regulation an important part of this feedback regulationis mediated by the ANS through thehypothalamus
  133. 133. Autonomic Nervous System Controls visceral functions functions to maintain a dynamic internalenvironment, necessary for properfunction of cells, tissues, organs, under awide variety of conditionsdemands
  134. 134. Autonomic Nervous System Viscerallargely involuntary motorsystem Three major divisions Sympathetic Fightflightfright emergency situations where there is a sudden D ininternal or external environment Parasympathetic Rest and Digest Enteric neuronal network in the walls of GI tract
  135. 135. ANS Primarily an effector system Controls smooth muscle heart muscle exocrine glands Two neuron system Preganglionic fiber cell body in CNS Postganglionic fiber cell body outside CNS
  136. 136. Sympathetic Nervous System Pre-ganglionic cells intermediolateral horn cells C8 to L2 or L3 release primarily acetylcholine also releases some neuropeptides (eg. LHRH) Post-ganglionic cells Paravertebral or Prevertebral ganglia most fibers release norepinephrine also can release neuropeptides (eg. NPY)
  137. 137. Mass SNS discharge Increase in arterial pressure decreased blood flow to inactiveorgans/tissues increase rate of cellular metabolism increased blood glucose metabolism increased glycolysis in livermuscle increased muscle strength increased mental activity increased rate of blood coagulation
  138. 138. Normal Sympathetic Tone 1/2 to 2 Impulses/Sec Creates enough constriction in bloodvessels to limit flow Most SNS terminals releasenorepinephrine release of norepinephrine depends onfunctional terminals which depend on nervegrowth factor
  139. 139. Parasympathetic NervousSystem Preganglionic neurons located in several cranial nerve nuclei inbrainstem Edinger-Westphal nucleus (III) superior salivatory nucleus (VII) inferior salivatory nucleus (IX) dorsal motor (X) (secretomotor) nucleus ambiguus (X) (visceromotor) intermediolateral regions of S2,3,4 release acetylcholine
  140. 140. Parasympathetic NervousSystem Postganglionic cells cranial ganglia ciliary ganglion pterygopalatine submandibular ganglia otic ganglia other ganglia located near or in the walls ofvisceral organs in thoracic, abdominal, pelvic cavities release acetylcholine
  141. 141. Parasympathetic nervoussystem The vagus nerves innervate the heart,lungs, bronchi, liver, pancreas,all the GItract from the esophagus to the splenicflexure of the colon The remainder of the colonrectum,urinary bladder, reproductive organs areinnervated by sacral preganglionic nervesvia pelvic nerves to postganglionicneurons in pelvic ganglia
  142. 142. Enteric Nervous System Located in wall of GI tract (100 millionneurons) Activity modulated by ANS
  143. 143. Enteric Nervous system Preganglionic Parasympathetic project toenteric ganglia of stomach, colon, rectumvia vaguspelvic splanchnic nerves increase motility and tone relax sphincters stimulate secretion
  144. 144. Enteric Nervous System Myenteric Plexus (Auerbachs) between longitudenalcircular muscle layer controls gut motility can coordinate peristalsis in intestinal tract that hasbeen removed from the body excitatory motor neurons release Achsub P inhibitory motor neurons release Dynorphin vasoactive intestinal peptide
  145. 145. Enteric Nervous System Submucosal Plexus Regulates: ionwater transport across the intestinalepithelium glandular secretion communicates with myenteric plexus releases neuropeptides well organized neural networks
  146. 146. Visceral afferent fibers Accompany visceral motor fibers inautonomic nerves supply information that originates insensory receptors in viscera never reach level of consciousness responsible for afferent limb ofviscerovisceral and viscerosomaticreflexes important for homeostatic control andadjustment to external stimuli
  147. 147. Visceral afferents Many of these neurons may release anexcitatory neurotransmitter such asglutamate Contain many neuropeptides can include nociceptors visceral pain distension of hollow viscus
  148. 148. Neuropeptides (visceralafferent) Angiotension II Arginine-vasopressin bombesin calcitonin gene-related peptide cholecystokinin galamin substance P enkephalin somatostatin vasoactive intestinal peptide
  149. 149. Autonomic Reflexes Cardiovascular baroreceptor Bainbridge reflex GI autonomic reflexes smell of food elicits parasympathetic releaseof digestive juices from secretory cells of GItract fecal matter in rectum elicits strong peristalticcontractions to empty the bowel
  150. 150. Intracellular Effects SNS-postganglionic fibers Norepinephrine binds to a alpha or betareceptor which effects a G protein Gs proteins + adenyl cyclase which raisescAMP which in turn + protein kinase activitywhich increases membrane permeability to Na+ Ca++ Parasympathetic-postganglionic fibers Acetylcholine binds to a muscarinicreceptor which also effects a G protein Gi proteins - adenyl cyclase and has theopposite effect of Gs
  151. 151. Effects of Stimulation Eye:S dilates pupilsP- constricts pupil, contracts ciliarymuscleincreases lensstrength Glands:in general stimulated by P but S + willconcentrate secretion by decreasing bloodflow. Sweat glands are exclusivelyinnervated by cholinergic S GI tract:S -, P + (mediated by enteric) Heart: S +, P - Bld vessels:S constriction, P largely absent
  152. 152. Effects of Stimulation Airway smooth muscle: S dilation Pconstriction Ducts: S dilation P constriction Immune System: S inhibits, P ??
  153. 153. Fate of released NT Acetylcholine (P) rapidly hydrolysed byaetylcholinesterase Norepinephrine uptake by the nerve terminals degraded by MAO, COMT carried away by blood
  154. 154. Precursors for NT Tyrosine is the precursor for Dopamine,NorepinephrineEpinephrine Choline is the precursor for Acetylcholine
  155. 155. Receptors Adrenergic Alpha Beta Acetylcholine receptors Nicotinic found at synapes between prepost ganglionicfibers (both SP) Muscarinic found at effector organs
  156. 156. Receptors Receptor populations are dynamic Up-regulate increased # of receptors Increased sensitivity to neurotransmitter Down-regulate decreased # of receptors Decreased sensitivity to neurotransmitter Denervation supersensitivity Cut nerves and increased # of receptors causingincreased sensitivity to the same amount of NT
  157. 157. Higher control of ANS Many neuronal areas in the brain stemreticular substance and along thecourse of the tractus solitarius of themedulla, pons,mesencephalon aswell as in many special nuclei(hypothalamus) control differentautonomic functions. ANS activated, regulated by centers in: spinal cord, brain stem, hypothalamus,higher centers (e.g. limbic system cerebral cortex)
  158. 158. Neural immunoregulation Nerve fibers project into every organ involved in monitoring both internal external environment controls output of endocrineexocrineglands essential components of homeostaticmechanisms to maintain viability of organism local monitoringmodulation of hostdefenseCNS coordinates host defenseactivity
  159. 159. Central Autonomic Regulation Major relay cell groups in brain regulateafferentefferent information convergence of autonomic informationonto discrete brain nuclei autonomic function is modulated by Dsin preganglionic SNS or Para toneand/or Ds in neuroendocrine (NE)effectors
  160. 160. Central Autonomic Regulation different components of central autonomicregulation are reciprocally innervated parallel pathways carry autonomic info toother structures multiple chemical substances mediatetransduction of neuronal infomation
  161. 161. Important Central AutonomicAreas Nucleus Tractus Solitarius Parabrachial Nucleus Locus Coeruleus Amygdala Cerebral Cortex Hypothalamus Circumventricular Organs (fenestratedcaps)
  162. 162. Control of Complex Movements Involve Cerebral Cortex Basal Ganglia Cerebellum Thalamus Brain Stem Spinal Cord
  163. 163. Motor Cortex Primary motor cortex somatotopic arrangement greater than 1/2 controls handsspeech + of neuron stimulate movements insteadof contracting a single muscle Premotor area anterior to lateral portions of primary motorcortex below supplemental area projects to 10 motor cortex and basalganglia
  164. 164. Motor Cortex (cont.) Supplemental motor area superior to premotor area lying mainly in thelongitudnal fissure functions in concert with premotor area toprovide: attitudinal movements fixation movements positional movements of headeyes background for finer motor control of arms/hands
  165. 165. The reticular nuclei Pontine reticular nuclei transmit excitatory signals via the pontine(medial) reticulospinal tract stimulate the axial trunkextensor musclesthat support the body against gravity receive stimulation from vestibular nuclei deep nuclei of the cerebellum high degree of natural excitability
  166. 166. The Reticular Nuclei (cont.) Medullary reticular nuclei transmit inhibitory signals to the sameantigravity muscles via the medullary(lateral) reticulospinal tract receive strong input from the cortex, rednucleus, and other motor pathways counterbalance excitatory signals from thepontine reticular nuclei allows tone to be increased or decreaseddepending on function needing to beperformed
  167. 167. Role of brain stem in controllingmotor function Control of respiration Control of cardiovascular system Control of GI function Control of many stereotyped movements Control of equilibrium Control of eye movement
  168. 168. Primary Motor Cortex Vertical Columnar Arrangement functions as an integrative processing system + 50-100 pyramidal cells to achieve musclecontraction Pyramidal cells (two types of output signals) dynamic signal excessively excited at the onset of contraction to initiatemuscle contraction static signal fire at slower rate to maintain contraction
  169. 169. Initiation of voluntary movement Plan and Program Begins in somatosensory association areas Execution Motor cortex outputs To the cord - skeletal muscle To the spinocerebellum Feedback from the periphery To the spinocerebellum
  170. 170. Postural Reflexes Impossible to separate postural adjustmentsfrom voluntary movement maintain body in up-right balanced position provide constant adjustments necessary tomaintain stable postural background forvoluntary movement adjustments include static reflexes(sustained contraction)dynamic short termphasic reflexes (transient movements)
  171. 171. Postural Control (cont) A major factor is variation of in thresholdof spinal stretch reflexes caused by changes in excitability of motorneuronschanges in rate of discharge inthe gamma efferent neurons to musclespindles
  172. 172. Postural Reflexes Three types of postural reflexes vestibular reflexes tonic neck reflexes righting reflexes
  173. 173. Vestibular function Vestibular apparatus-organ that detectssensations of equilibrium Consists of semicircular canalsutricle saccule embedded in the petrous portion oftemporal bone provides information about position andmovement of head in space helps maintain body balance and helpscoordinate movements
  174. 174. Vestibular apparatus Utricle and Saccule Macula is the sensory area covered with a gelatinous layer in which manysmall calcium carbonate crystals are imbedded hair cells in macula project cilia into gelatinouslayer directional sensitivity of hair cells to causedepolarization or hyperpolarization detect orientation of head w/ respect to gravity detect linear acceleration
  175. 175. Vestibular apparatus (cont) Semicircular canals Crista ampularis in swelling (ampulla) Cupula loose gelatinous tissue mass on top of crista stimulated as head begins to rotate 3 pairs of canals bilaterally at 90o to oneanother. (anterior, horizontal, posterior) Each set lie in the same plane right anterior - left posterior right and left horizontal left anterior - right posterior
  176. 176. Semicircular Canals Filled with endolymph As head begins to rotate, fluid lags behindand bend cupula generates a receptor potential which altersthe firing rate in VIII CN which projects tothe vestibular nuclei detects rotational acceleration deceleration
  177. 177. Semicircular Canals Stimulation of semicircular canals on siderotation is into. (e.g. Right or clockwiserotation will stimulate right canal) Stimulation of semicircular canals isassociated with increased extensor tone Stimulation of semicircular canals isassociated with nystagmus
  178. 178. Semicircular Canals Connections with vestibular nucleus viaCN VIII Vestibular nuclei makes connectionswith CN associated with occularmovements (III,IV, VI) and cerebellum Can stimulate nystagmus slow component-(tracking)can be initiatedby semicircular canals fast component- (jump ahead to new focalspot) initiated by brain stem nuclei
  179. 179. Semicircular Canals Thought to have a predictive function toprevent malequilibrium Anticipitory corrections works in close concert with cerebellumespecially the flocculonodular lobe
  180. 180. Other Factors - Equilibrium Neck proprioceptors-providesinformation about the orientation of thehead with the rest of the body projects to vestibular apparatus cerebellum cervical joints proprioceptors can overridesignals from the vestibular apparatus prevent a feeling of malequilibrium Proprioceptive and Exteroceptiveinformation from other parts of the body Visual signals
  181. 181. Posture Represents overall position of the body limbs relative to one anothertheirorientation in space Postural adjustments are necessary for allmotor tasksneed to be integrated withvoluntary movement
  182. 182. VestibularNeck Reflexes Have opposing actions on limb muscles Most pronounced when the spinal circuitsare released from cortical inhibition Vestibular reflexes evoked by changes inposition of the head Neck reflexes are triggered by tilting orturning the neck
  183. 183. Postural Adjustments Functions support headbody against gravity maintain center of the bodys mass aligned balanced over base of support on the ground stabilize supporting parts of the body whileothers are being moved Major mechanisms anticipatory (feed forward)-predict disturbances modified by experience; improves with practice compensatory (feedback) evoked by sensory events following loss of balance
  184. 184. Postural adjustments Induced by body sway Extremely rapid (like simple stretch reflex) Relatively stereotyped spatiotemporalorganization (like ssr) appropriately scaled to achieve goal ofstable posture (unlike ssr) refined continuously by practice (likeskilled voluntary movements)
  185. 185. Postural mechanisms Sensory input from: cutaneous receptors from the skin (espfeet) proprioceptors from jointsmuscles short latency (70-100 ms) vestibular signals (head motion) longer latency (2x proprioceptor latency) visual signals longer latency (2x proprioceptor latency)
  186. 186. Postural Mechanisms (cont) In sway, contraction of muscles to maintainbalance occur in distal to proximalsequence forward sway Gastrohampara backward sway Tibquadabd responses that stabilize posture arefacilitated responses that destabilize posture inhibited
  187. 187. Effect of tonic neck reflexes onlimb muscles Extension of neck + extensors ofarms/legs Flexion of neck + flexors of arms/legs Rotation or lateral bending + extensors ipsilateral + flexors contralateral
  188. 188. Basal Ganglia Input nuclei Caudate Putamen caudate + putamen = striatum Nucleus accumbens Output nuclei Globus Pallidus-external segment Subthalamic nucleus Substantia nigra Ventral tegmental area
  189. 189. Basal Ganglia Consist of 4 principal nuclei the striatum (caudateputamen) the globus pallidus (internalexternal) the substantia nigra subthalamic nucleus
  190. 190. Basal Ganglia Do not have direct input or outputconnections with the spinal cord Motor functions of the basal ganglia aremediated by the motor areas of thecortex Disorders have three characteristictypes of motor disturbances tremorother involuntary movements changes in posturemuscle tone povertyslowness of movement
  191. 191. Two major circuits of BG Caudate circuit large input into caudate from theassociation areas of the brain caudate nucleus plays a major role incognitive control of motor activity cognitive control of motor activity Putamen circuit subconcious execution of learned patternsof movement
  192. 192. Cerebellum-little brain By weight 10% of total brain Contains1/2 of all neurons in brain Highly regular structure motor systems are mapped here Complete destruction produces nosensory impairmentno loss in musclestrength Plays a crucial indirect role in movement posture by adjusting the output of themajor descending motor systems
  193. 193. Functional Divisions Vestibulocerebellum (floculonodular lobe) input-vestibular N: output-vestibular N. fxn-governs eye movementbody equilibrium Spinocerebellum (vermis intermediate) input-peripheryspinal cord: output-cortex fxn-major role in movement, influencing mediallateraldescending motor systems Cerebrocerebellum (lateral zone) input-pontine N. output-premotor cortex fxn-planninginitiation of movementextramotorprediction mental rehersal of complex motor actions conscious assessment of movement errors Higher cognitive function-executive functions
  194. 194. Cerebellum Cerebellar cortex three pairs of deep nuclei from which mostof output originates from. fastigial Interposed (globoseemboliform) dentate connected to brain stem by 3 sets ofpeduncles superior which contains most efferent project. Middle Inferior- most afferent from spinal cord
  195. 195. Major features of cerebellum fxn receives info about plans for movementfrom brain structures concerned withprogrammingexecution of movement cerebellum receives information aboutmotor performance from peripheralfeedback during course of movement compares central info w/ actual motor response projects to descending motor systems viacortex
  196. 196. Higher Cortical function Cerebral Cortex About 100 billion neurons contained in a thin layer2-5 mm thick covering all convolutions of thecerebrum Three major cell types Granular, pyramidal, fusiform Typically 6 layers (superficial to deep) molecular, external granular, external pyramidal, internalgranular, internal pyramidal, mutiform All areas of cerebral cortex make extensive afferent efferent connections with the thalamus
  197. 197. The Cerebral Cortex Layer I -Molecular Layer mostly axons Layer II-External Granule Layer granule (stellate) cells Layer III-External Pyramidal layer primary pyramidal cells
  198. 198. Cerebral Cortex Layer IV-Internal Granule Layer main granular cell layer Layer V- internal pyramidal layer dominated by giant pyramidal cells Layer VI- multiform layer all types of cells-pyramidal, stellate, fusiform
  199. 199. Cerebral Cortex Three major cell types Pyramidal cells souce of corticospinal projections major efferent cell Granule cells short axons- function as interneurons (intra cortical processing) excitatory neurons release 1o glutamate inhibitory neurons release 1o GABA Fusiform cells least numerous of the three gives rise to output fibers from cortex
  200. 200. Cerebral Cortex Most output leave cortex via V VI spinal cord tracts originate from layer V thalamic connections from layer V Most incoming sensory signals terminatein layer IV Most intracortical association functions -layers I, II, III large # of neurons in II, III- short horozontalconnections with adjacent cortical areas
  201. 201. Cerebral Cortex All areas of the cerebral cortex haveextensive afferent and efferentconnections with deeper structures ofbrain. (eg. Basal ganglia, thalamusetc.) Thalamic connections (afferent andefferent) are extremely important andextensive Cortical neurons (esp. in associationareas) can change their function asfunctional demand changes
  202. 202. Concept of a DominantHemisphere General interpretative functions ofWernickesangular gyrus as well asspeechmotor control are more welldeveloped in one cerebral [email protected] 95% of population- left hemisphere If dominate hemisphere sustains damageearly in life, non dominate hemisphere candevelop those capabilities of speech language comprehension (Plasticity)
  203. 203. Lingustic Dominance Handedness Dominant Hemisphere Left or mixed handed Left- 70% Right- 15% Both- 15% Right handed Left- 96% Right- 4% Both- 0%
  204. 204. Right brain, left brain The two hemispheres are specializedfor different functions dominant (usually left) language based intellectual functions interpretative functions of symbolism,understanding spoken, written words analytical functions- math speech non dominant (usually right) music non verbal visual experiences (e.g. bodylanguage) spatial relations
  205. 205. Allocortex Made up of archicortexpaleocortex 10% of human cerebral cortex Includes the hippocampal formation whichis folded into temporal lobeonly viewedafter dissection hippocampus dentate gyrus subiculum
  206. 206. Hippocampal formation Three parts Hippocampus- 3 layers (I, V, VI) Dentate gyrus- 3 layers (I, IV, VI) Subiculum Receives 10 input from the entorhinalcortex of the parahippocampal gyrusthrough: perforantalveolar pathway
  207. 207. Hippocampal formation Plays an important role in declarativememory Declarative- making declarative statements ofmemory Episodic-daily episodes of life Semantic-factual information
  208. 208. Memory Memories are caused by groups ofneurons that fire together in the samepattern each time they are activated. The links between individual neurons,which bind them into a single memory,are formed through a process calledlong-term potentiation. (LTP)
  209. 209. Classification of Memory (cont) Memory can also be classified as: Declarative-memory of details of anintegrated thought memory of: surroundings, timerelationships causemeaning of theexperience Reflexive (Skill)- associated with motoractivities e.g. hitting a tennis ball which includecomplicated motor performance
  210. 210. Role of Hippocampus inMemory The hippocampus may store long termmemory for weeksgradually transfer itto specific regions of cerebral cortex The hippocampus has 3 major synapticpathways each capable of long-termpotentiation which is thought to play a rolein the storage process
  211. 211. Storage of Memory Long term memory is represented inmutiple regions throughout the nervoussystem Is associated with structural changes insynapes increase in # of both transmitter vesicles release sites for neurotransmitter increase in # of presynaptic terminals changes in structures of dendritic spines increased number of synaptic connections
  212. 212. Memory (cont) The memory capability that is sparedfollowing bilateral lesions of temporal lobetypically involves learned tasks that havetwo things in common tasks tend to be reflexive, not reflective involve habits, motor, or perceptual skills do not require conscious awareness orcomplex cognitive processes. (e.g.comparisonevaluation
  213. 213. Memory Environment alters human behavior bylearningmemory Learning process by which we acquire knowledgeabout the world Memory process by which knowledge is encoded,storedretrieved
  214. 214. Neural Basis of Memory Memory has stagescontinuallychanging long term memory- plastic changes physical changes coding memory arelocalized in multiple regions of the brain reflexivedeclarative memory mayinvolve different neuronal circuits
  215. 215. Higher Cortical Function Primary areas Visual- occipital pole (BM 17) Auditory-superior gyrus of temporal lobe (BM41) Primary motor cortex-pre central gyrus (BM 4) Primary somatosensory cortex- post centralgyrus (BM 3,1,2) Secondary and Association areas Large percentage of human brain
  216. 216. Association Areas Integrate or associate info. from diversesources Large % of human cortex High level in the hierarchy Lesions here have subtle and unpredictablequality
  217. 217. Association Areas Prefrontal Executive functions Judgment Planning for the future holdingorganizing events from memory for prospectiveaction Processing emotion-learning to control emotion (actingunselfishly) Parieto-occipito-temporal Spatial relationships Recognizing complex form prosopagnosia Limbic Motivation, behavioral drives, emotion
  218. 218. Heart muscle AtrialVentricular striated enlongated grouped in irregularanatamosing columns 1-2 centrally located nuclei Specialized excitatoryconductivemuscle fibers (SA node, AV node, Purkinjefibers) contract weakly few fibrils
  219. 219. Syncytial nature of cardiacmuscle Syncytium = many acting as one Due to presence of intercalated discs low resistance pathways connecting cardiaccells end to end presence of gap junctions
  220. 220. SA node Normal pacemaker of the heart Self excitatory nature less negative Er leaky membrane to Na+/CA++ only slow Ca++/Na+ channels operational spontaneously depolarizes at fastest rate overdrive suppression-inhibits other cells automaticity contracts feebly Stretch on the SA node will increase Ca++and/or Na+ permeability which will increaseheart rate
  221. 221. AV node Delays the wave of depolarization fromentering the ventricle allows the atria to contract slightly ahead ofthe ventricles (.1 sec delay) Slow conduction velocity due to smallerdiameter fibers In absence of SA node, AV node may actas pacemaker but at a slower rate
  222. 222. Cardiac Cycle Systole isovolumic contraction ejection Diastole isovolumic relaxation rapid inflow- 70-75% diastasis atrial systole- 25-30%
  223. 223. Cardiac cycle:Pressure changesOver timeLeft ventricularVolume changesEKG
  224. 224. Ventricular Volumes End Diastolic Volume-(EDV) volume in ventricles at the end of filling End Systolic Volume- (ESV) volume in ventricles at the end of ejection Stroke volume (EDV-ESV) volume ejected by ventricles Ejection fraction % of EDV ejected (SV/EDV X 100%) normal 50-60%
  225. 225. Terms Preload-stretch on the wall prior tocontraction (proportional to the EDV) Afterload-the changing resistance(impedance) that the heart has to pumpagainst as blood is ejected. i.e. Changingaortic BP during ejection of blood from theleft ventricle
  226. 226. Atrial Pressure Waves A wave associated with atrial contraction C wave associated with ventricular contraction bulging of AV valves and tugging on atrial muscle V wave associated with atrial filling
  227. 227. Function of Valves Open with a forward pressure gradient e.g. when LV pressurethe aortic pressurethe aortic valve is open Close with a backward pressure gradient e.g. when aortic pressureLV pressure theaortic valve is closed
  228. 228. Heart Valves AV valves MitralTricupid Thinfilmy Chorda tendineae act as check lines to preventprolapse papillary muscles-increase tension on chorda t. Semilunar valves AorticPulmonic stronger construction
  229. 229. Law of Laplace Wall tension = (pressure)(radius)/2 At a given operating pressure as ventricularradius , developed wall tension . tension force of ventricular contraction two ventricles operating at the same pressure butwith different chamber radii the larger chamber will have to generate more walltension, consuming more energyoxygen This law explains how capillaries canwithstand high intravascular pressurebecause of a small radius, minimizesdeveloped wall tension
  230. 230. Control of Heart Pumping Intrinsic properties of cardiac muscle cells Frank-Starling Law of the Heart Within physiologic limits the heart will pumpall the blood that returns to it without allowingexcessive damming of blood in veins heterometrichomeometric autoregulation direct stretch on the SA node
  231. 231. Mechanism of Frank-Starling Increased venous return causes increasedstretch of cardiac muscle fibers. (Intrinsiceffects) increased cross-bridge formation increased calcium influx both increases force of contraction increased stretch on SA node increases heart rate
  232. 232. Heterometric autoregulation Within limits as cardiac fibers arestretched the force of contraction isincreased more cross bridge formation as actin overlapis removed more Ca++ influx into cell associated with theincreased stretch
  233. 233. Homeometric autoregulation Ability to increase strength ofcontraction independent of a lengthchange Flow induced Pressure induced Rate induced
  234. 234. Extrinsic Influences on heart Autonomic nervous system Hormonal influences Ionic influences Temperature influences
  235. 235. Control of Heart by ANS Sympathetic innervation- + heart rate + strength of contraction + conduction velocity Parasympathetic innervation - heart rate - strength of contraction - conduction velocity
  236. 236. Interaction of ANS SNS effects and Parasympathetic effectsblocked using propranolol (beta blocker) atropine (muscarinic blocker) respectively. HR will increase Strength of contraction decreases From the previous results it can be concludedthat under resting conditions: Parasympathetic NS exerts a dominate inhibitoryinfluence on heart rate Sympathetic NS exerts a dominate stimulatoryinfluence on strength of contraction
  237. 237. Cardioacclerator reflex Stretch on right atrial wall + stretchreceptors which in turn send signals tomedulla oblongata + SNS outflow to heart AKA Bainbridge reflex Helps prevents damning of blood in the heart central veins
  238. 238. Major Hormonal Influences Thyroid hormones + inotropic + chronotropic also causes an increase in CO by BMR
  239. 239. Ionic influences Effect of elevated [K+]ECF dilation and flaccidity of cardiac muscle atconcentrations 2-3 X normal (8-12 meq/l) decreases resting membrane potential Effect of elevated [Ca++] ECF spastic contraction
  240. 240. Effect of body temperature Elevated body temperature HR increases about 10 beats for every degreeF elevation in body temperature Contractile strength will increase temporarilybut prolonged fever can decrease contractilestrength due to exhaustion of metabolicsystems Decreased body temperature decreased HR and strength
  241. 241. Terminology Chronotropic (+ increases) (- decreases) Anything that affects heart rate Dromotropic Anything that affects conduction velocity Inotropic Anything that affects strength of contraction eg. Caffeine would be a + chronotropic agent(increases heart rate)
  242. 242. EKG Measures potential difference across thesurface of the myocardium with respect totime lead-pair of electrodes axis of lead-line connecting leads transition line-line perpendicular to axis oflead
  243. 243. Rate Paper speed- 25 mm/sec 1 mm = .04 sec. Normal rate ranges usually between 60-80bps Greater than 100 = tachycardia Less than 50 = bradycardia
  244. 244. Electrocardiography P wave-atrial depolarization QRS complex-ventricular depolarization T wave-ventricular repolarization
  245. 245. Leads A pair of recording electrodes + electrode is active - electrode is reference The direction of the deflection (+ or -) isbased on what the active electrodesees relative to the reference electrode Routine EKG consists of 12 leads 6 frontal plane leads 6 chest leads (horizontal)
  246. 246. Type of DeflectionWave ofDepolarizationWave ofRepolarizationMovingtoward + elect.deflection deflectionMovingtoward - elect. deflection deflection
  247. 247. Hypertrophy Hypertrophy of one ventricle relative to theother can be associated with anything thatcreates an abnormally high work load onthat chamber. e.g. Systemic hypertension increasing workload on the left ventricle prolonged QRS complex ( .12 sec) axis deviation to the side of problem increased voltage of QRS in V leads
  248. 248. Blood flow to myocardium The myocardium is supplied by thecoronary arteriestheir branches. Cells near the endocardium may be ableto receive some O2 from chamber blood The heart muscle at a resting heart ratetakes the maximum oxygen out of theperfusing coronary flow (70% extraction) Any demand must be met by coronaryflow
  249. 249. Circulation The main function of the systemiccirculation is to deliver adequateoxygen, nutrients to the systemictissues and remove carbon dioxide other waste products from the systemictissues The systemic circulation is also servesas a conduit for transport of hormones,and other substances and allows thesesubstances to potentially act at adistant site from their production
  250. 250. Functional Parts systemic arteries designed to carry blood under highpressure out to the tissue beds arteriolespre capillary sphincters act as control valves to regulate local flow capillaries- one cell layer thick exchange between tissue (cells)blood venules collect blood from capillaries systemic veins return blood to heart
  251. 251. Basic theory of circulatoryfunction Blood flow is proportional to metabolicdemand Cardiac output controlled by local tissueflow Arterial pressure control is independent oflocal flow or cardiac output
  252. 252. Hemodynamics Flow Pressure gradient Resistance Ohms Law V = IR (Analogous to D P = QR)
  253. 253. Flow (Q) The volume of blood that passes a certainpoint per unit time (eg. ml/min) Q = velocity X cross sectional area At a given flow, the velocity is inverselyproportional to the total cross sectional area Q = D P / R Flow is directly proportional to D P andinversely proportional to resistance (R)
  254. 254. Pressure gradient Driving force of blood difference in pressure between two points proportional to flow (Q) At a given Q the greater the drop in P in asegment or compartment the greater theresistance to flow.
  255. 255. Resistance R= 8hl/p r4 h = viscosity, l = length of vessel, r = radius Parallel circuit 1/RT= 1/R1+ 1/R2 + 1/R3 + 1/RN RTsmallest individual R Series circuit RT = R1 + R2 + R3 + RN RT = sum of individual Rs The systemic circulation ispredominantly a parallel circuit
  256. 256. Advantages of Parallel Circuitry Independence of local flow control increase/decrease flow to tissuesindependently Minimizes total peripheral resistance(TPR) Oxygen rich blood supply to every tissue
  257. 257. Viscosity Internal friction of a fluid associated withthe intermolecular attraction Blood is a suspension with a viscosity of 3 most of viscosity due to RBCs Plasma has a viscosity of 1.5 Water is the standard with a viscosity of 1 With blood, viscosity 1/ velocity
  258. 258. Viscosity considerations atmicrocirculation velocity decreases which increasesviscosity due to elements in blood sticking together cells can get stuck at constriction pointsmomentarily which increases apparentviscosity fibrinogen increases flexibility of RBCs in small vessels cells line up whichdecreases viscosity and offsets the aboveto some degree (Fahaeus-Lindquist)
  259. 259. Hematocrit % of packed cell volume (10 RBCs) Normal range 38%-45%
  260. 260. Laminar vs. Turbulent Flow Streamline silent most efficient normal Cross mixing vibrational noise least efficient frequently associatedwith vessel disease(bruit)
  261. 261. Reynolds number Probability statement for turbulent flow The greater the R#, the greater theprobability for turbulence R# = v D r/h v = velocity, D = tube diameter, r = density,h = viscosity If R#2000 flow is usually laminar If R#3000 flow is usually turbulent
  262. 262. Doppler Ultrasonic Flow-meter Ultrasound to determine velocity of flow Doppler frequency shift function of thevelocity of flow RBCs moving toward transmitter, compresssound waves, frequency of returning waves Broad vs. narrow frequency bands Broad band is associated with turbulent flow narrow band is associated laminar flow
  263. 263. Distensibility Vs. Compliance Distensibility is the ability of a vessel tostretch (distend) Compliance is the ability of a vessel tostretch and hold volume
  264. 264. Distensibility Vs. Compliance Distensibility = D Vol/D Pressure X Ini. Vol Compliance = D Vol/D Pressure Compliance = Distensibility X Initial Vol.
  265. 265. Volume-Pressure relationships A D volume D pressure In systemic arteries a small D volume isassociated with a large D pressure In systemic veins a large D volume isassociated with a small D pressure Veins are about 8 X more distensible and 24X more compliant than systemic arteries Wall tone 1/ compliancedistensibility
  266. 266. Control of Blood Flow (Q) Local blood flow is regulated in proportion tothe metabolic demand in most tissues Short term control involves vasodilatationvasoconstriction of precapillary resist. vessels arterioles, metarterioles, pre-capillary sphincters Long term control involves changes in tissuevascularity formation or dissolution of vessels vascular endothelial growth factorangiogenin
  267. 267. Role of arterioles Arterioles act as an intergrator of multipleinputs Arterioles are richly innervated by SNSvasoconstrictor fibers and have alphareceptors Arterioles are also effected by local factors(e.g.)vasodilators, circulating substances
  268. 268. Local Control of Flow (shortterm) Involves vasoconstriction/vasodilatation ofprecapillary resistance vessels Local vasodilator theory Active tissue release local vasodilator(metabolites) which relax vascular smoothmuscle Oxygen demand theory (older theory) As tissue uses up oxygen, vascular smoothmuscle cannot maintain constriction
  269. 269. Local Vasodilators Adenosine carbon dioxide adenosine phosphate compounds histamine potassium ions hydrogen ions PGEPGI series prostaglandins
  270. 270. Autoregulation The ability to keep blood flow (Q) constantin the face of a changing arterial BP Most tissues show some degree ofautoregulation Q metabolic demand In the kidney both renal Q and glomerularfiltration rate (GFR) are autoregulated
  271. 271. Control of Flow (long term) Changes in tissue vascularity On going day to day reconstruction of the vascularsystem Angiogenesis-production of new microvessels arteriogenesis shear stress caused by enhanced blood flow velocityassociated with partial occlusion Angiogenic factors small peptides-stimulate growth of new vessels VEGF (vascular endothelial growth factor)
  272. 272. Changes in tissue vascularity Stress activated endothelium up-regulatesexpression of monocyte chemoattractantprotein-1 (MCP-1) attraction of monocytes that invade arterioles other adhesion moleculesgrowth factorsparticipate with MCP-1 in an inflammatoryreaction and cell death in potential collateralvessels followed by remodeling development of newenlarged collateralarteriesarterioles
  273. 273. Changes in tissue vacularity(cont.) Hypoxia causes release of VEGF enhanced production of VEGF partly mediatedby adenosine in response to hypoxia VEGF stimulates capillary proliferation and mayalso be involved in development of collateralarterial vessels NPY from SNS is angiogenic hyperactive SNS may compromise collateralblood flow by vasoconstriction
  274. 274. Vasoactive Role of Endothelium Release prostacyclin (PGI2) inhibits platelet aggregation relaxes vascular smooth muscle Releases nitric oxide (NO) whichrelaxes vascular smooth muscle NO release stimulated by: shear stress associated with increased flow acetylcholine binding to endothelium Releases endothelinendothelialderived contracting factor constricts vascular smooth muscle
  275. 275. Microcirculation Capillary is the functional unit of thecirculation bulk of exchange takes place here Vasomotion-intermittent contraction ofmetarterioles and precapillary sphincters functional Vs. non functional flow Mechanisms of exchange diffusion ultrafiltration vesicular transport
  276. 276. Oxygen uptake/utilization = the product of flow (Q) times the arterial-venousoxygen difference O uptake = (Q) (A-V O2 difference) Q=300 ml/min AO2= .2 ml O2/ml VO2= .15 ml O2/min 15 ml O2 = (300 ml/min) (.05 mlO2/ml) Functional or Nutritive flow (Q) is associated withincreased oxygen uptake/utilization
  277. 277. Capillary Exchange Passive Diffusion permeability concentration gradient Ultrafiltration Bulk flow through a filter (capillary wall) Starling Forces Hydrostatic P Colloid Osmotic P Vesicular Transport larger MW non lipid soluble substances
  278. 278. Ultrafiltration Hydrostatic P gradient (high to low) Capillary HP averages 17 mmHg Interstitial HP averages -3 mmHg Colloid Osmotic P (low to high) Capillary COP averages 28 mmHg Interstitial COP averages 9 mmHg Net Filtration P = (CHP-IHP)-(CCOP-ICOP) 1 = 20 - 19
  279. 279. Colloid Osmotic Considerations The colloid osmotic pressure is a functionof the protein concentration Plasma Proteins Albumin (75%) Globulins (25%) Fibrinogen (1%) Calculated Colloid Effect is 19 mmHg Actual Colloid Effect is 28 mmHg Discrepancy is due to the Donnan Effect
  280. 280. Donnan Effect Increases the colloid osmotic effect Large MW plasma proteins (1o albumen)carries negative charges which attract +ions (1o Na+) increasing the osmotic effectby about 50%
  281. 281. Effect of Ultrastructure of CapillaryWall on Colloid Osmotic Pressure Capillary wall can range from tightjunctions (e.g. blood brain barrier) todiscontinuous (e.g. liver capillaries) Glomerular Capillaries in kidney havefiltration slits (fenestrations) Only that protein that cannot crosscapillary wall can exert osmotic pressure
  282. 282. Reflection Coefficient Reflection Coefficient expresses howreadily protein can cross capillary wall ranges between 0 and 1 If RC = 0 All colloid proteins freely cross wall, none arereflected, no colloid effect If RC = 1 All colloid proteins are reflected, none crosscapillary wall,full colloid effect
  283. 283. Lymphatic system Lymph capillaries drain excess fluidfrom interstitial spaces No true lymphatic vessels found insuperficial portions of skin, CNS,endomysium of muscle,bones Thoracic duct drains lower bodyleftside of head, left arm, part of chest Right lymph duct drains right side ofhead, neck, right arm and part of chest
  284. 284. CNS-modified lymphaticfunction No true lymphatic vessels in CNS Perivascular spaces contain CSF communicate with subarachnoid space Plasma filtrateescaped substances inperivascular spaces returned to thevascular system in the CSF via thearachnoid villi which empties into duralvenous sinsus Acts a functional lymphatic system in CNS
  285. 285. Formation of Lymph Excess plasma filtrate-resembles ISFfrom tissue it drains [Protein] 3-5 gm/dl in thoracic duct liver 6 gm/dl intestines 3-4 gm/dl most tissues ISF 2 gm/dl 2/3 of all lymph from liverintestines Any factor that filtration and/or reabsorption will lymph formation
  286. 286. Rate of Lymph Formation/Flow Thoracic duct- 100 ml/hr. Right lymph duct- 20 ml/hr. Total lymph flow- 120 ml/hr (2.9 L/day) Every day a volume of lymph roughlyequal to your entire plasma volume isfiltered
  287. 287. Function of Lymphatics Return lost protein to the vascular system Drain excess plasma filtrate from ISFspace Carry absorbed substances/nutrients(e.g. fat-chlyomicrons) from GI tract Filter lymph (defense function) at lymphnodes lymph nodes-meshwork of sinuses lined withtissue macrophages (phagocytosis)
  288. 288. Arterial blood pressure Arterial blood pressure is created by theinteraction of blood with vascular wall Art BP = volume of blood interacting withthe wall inflow (CO) - outflow (TPR) Art BP = CO X TPR Greater than 1/2 of TPR is at the level ofsystemic arterioles
  289. 289. Systole During systole the left ventricular output(SV) is greater than peripheral runoff Therefore total blood volume rises whichcauses arterial BP to increase to a peak(systolic BP) The arteries are distended during this time
  290. 290. Diastole While the left ventricle is filling, the arteriesnow are recoiling, which serves tomaintain perfusion to the tissue beds Total blood volume in the arterial tree isdecreasing which causes arterial BP to fallto a minimum value (diastolic BP)
  291. 291. Hydralic Filtering Stretch (systole)recoil (diastole) ofthe arterial tree that normally occursduring the cardiac cycle This phenomenon converts anintermittent output by the heart to asteady delivery at the tissue beds saves the heart work As the distensibility of the arterial tree with age, hydralic filtering is reduced,and work load on the heart is increased
  292. 292. Mean Arterial Blood Pressure The mean arterial pressure (MAP) is notthe arithmetical mean between systole diastole determined by calculating the area underthe curve, and dividing it into equal areas MAP= 1/3 Pulse Pressure + DBP(approximation)
  293. 293. Effects of SNS + Most post-ganglionic SNS terminalsrelease norepinephrine. The predominant receptor type is alpha(a)a response is constriction of smoothmuscle Constriction of arterioles reduce blood flowand help raise arterial blood pressure (BP) Constriction of arteries raise arterial BP Constriction of veins increases venous return
  294. 294. SNS (cont) SNS + causes widespread vasoconstrictorcausing blood flow with 3 exceptions Brain arterioles weakly innervated Lungs arterioles weakly innervated Pulmonary BF = C.O. Heart direct vasoconstrictor effects over-ridden by SNSinduced increase in cardiac activity which causesrelease of local vasodilators (adenosine)
  295. 295. Critical Closing Pressure As arterial pressure falls, there is a criticalpressure below which flow ceases due tothe closure of the arterioles. This critical luminal pressure is required tokeep arterioles from closing completely vascular tone is proportional to CCP e.g. SNS + of arterioles CCP
  296. 296. Mean Circulatory Filling Pressure If cardiac output is stopped, arterial pressure willfall and venous pressure will rise MCFP = equilibration pressure where arterial BP= venous BP equilibration pressure may be prevented byclosure of the arterioles (critical closingpressure) responsible for pressure gradient drivingperipheral venous return
  297. 297. VascularCardiac Function Vascular function At a given MCFP as Central VenousPressure , venous return If MCPF = CVP; venous return goes to 0 Cardiac function As central venous pressure increases,cardiac output increases due to bothintrinsicextrinsic effects
  298. 298. Central Venous Pressure The pressure in the central veins (superior inferior vena cava) at the entry into theright atrium. Central venous pressure = right atrialpressure
  299. 299. Vasomotor center Collection of neurons in the medullapons Four major regions pressor center- increase blood pressure depressor center- decrease blood pressure sensory area- mediates baroreceptor reflex cardioinhibitory area- stimulates X CN Sympathetic vasoconstrictor tone due to pressor center input 1/2 to 2 IPS maintains normal arterial blood pressure
  300. 300. Control of Blood Pressure Rapid short term control involves thenervous systems effect on vascularsmooth muscle Long term control is dominated by thekidneys- Renal-body fluid balance
  301. 301. Control of Blood Pressure Concept of Contents vs. Container Contents blood volume Container blood vessels Control of blood pressure is accomplishedby either affecting vascular tone or bloodvolume