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Lecture 1 Spinal Cord Reflexes

Motor Functions are split into 2 ways o Descending systems systems from above brain stem called Upper Motor neuron systems Basal Ganglia, cerebellum, motor cortex and brainstem centers o The Lower motor neuron systems the motor neurons in the ventral horn of the spinal cord Form synapses at the neuromuscular junction and release AcH, thereby causing muscle contraction These are the Piano Keys in order to get the Tune e.g. movement.. you must play the Piano keys activate these motor neurons Also called the Final common pathway A Skeleton muscle cannot be inhibited- only the level of contraction can change based on the concentration of acetylcholine o To relax a muscle, you must inhibit the motor neuron. Many different things can cause motor neuron excitation. All of these things go to the spinal cord, which will then play the keys on the piano o Nociceptor Sensory Receptors in skin o Skeletal muscle sensory receptors o Receptors in tendons Spinal cord is arranged by levels o Cerivcal spinal cord = hands/arms and chest, etc. Spinal Cord has 2 colors o Gray matter these are neurons in the center bowtie of the spinal cord Dorsal Horn sensory input Intermediate Regions Interneurons Fingers on the keys of the piano Ventral Horn The Motor Neurons reside here o White Matter These are the axons traveling up and down the spinal cord. White due to some myelination Antero - Lateral pain input Ventral lateral motor function/ standing Dorsal - touch/sensory input

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Dorso-lateral descending motor control

2 Major enlargements of the bowtie o Cervical spinal cord o Lumbar Spinal cord o This is because this is where the most motor and sensory information is needed hands and legs Spinal cord is suspended in CSF Cerebral spinal cord 2 roots to the spinal cord o Ventral Root o Dorsal root Contains the dorsal root ganglion cell body for sensory o These Roots combine to make up the peripheral nerve which contains both motor and sensory axons Some are myelinated, some arent. Types of nerve fibers in peripheral nerves o Somatic neurons Muscle Spindles Axon 1A tells spinal cord about length and movement of the muscle. This is parallel to the muscle fibers Golgi Tendons provide info about muscle tension Sits in series with the muscle fibers Free nerve endings measure potential pain.. as well as temperature and crude touch o Motor Neurons Alpha Motor neuron this is the main one it synapses at the neuromuscular junction (NMJ) Gamma Motor Neuron innervates a sensory receptor this is critical to the functioning of the Alpha motor neuron Reflexes a sterotyped motor responses elicited by a defined sensory stimulus o Can be overridden if you think hard enough Reflex Classifications o Autonomic or somatic o Where the reflex is integrated cranial or spinal cord o When the reflex develop - learned or born with it? o The Number of neurons in the reflex loop Skeletal Muscle Sensory Receptor initiated reflex Muscle Stretch Reflex patellar stretch reflex o Muscle Spindle the sensory apparatus. Intrafusal Muscle Fiber

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This is in parallel with the muscle fibers. It detects how long the muscle is, and how its changing o Afferent Sensory neuron inputs on the monosynaptic nerve junction o Motor neuron causes contraction (more Ach) for the quadriceps muscle and relaxation (less Ach) for the hamstring muscle Monosynaptic excitatory reflex Polysynaptic inhibitory reflex o Ipsilateral (same side) and negative feedback. No afterdischarge no sustained contraction Alpha Gamma Co-activation occurs in the stretch reflex o Alpha Motor Neuron actually causes the contraction o Gamma motor neuron it targets the intrafusal muscle fiber and innervates its contractile material to contract. This is important because it keeps the muscle spinal taut so that the length of the muscle can be reported Nociceptor Reflex ex. Ball of the foot crossed extensor/flexor withdrawal reflex o Lift foot when stepped on something sharp.. and kept it up.. also balanced the rest of body o Polysynaptic pathway that is a protective reflex o First, free endings detect pain and transmit to the spinal cor dand contract the quadriceps (flexors) on the foot with pain. o It does the opposite on the other foot. o Afterdischarge is active you dont stop withdrawing your leg and put it back down. Golgi Tendon Reflex (Deep tendon reflex) o The Golgi tendon organ is in series with the muscle It encodes info about tension o 1B Afferent axon o It detects information about muscle contraction o It prevents overstretching of the muscles tendon by causing some inhibition of the muscle that was being contracted, and contracts the antagonist muscles. o Opposite of the myotatic reflex (stretch reflex)

Lecture 2: Sensory & Motor Pathways Principles of sensory system organization

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o Specific sensory receptor types are sensitive to certain modalities (like pain, light, etc.) o Labeled lines a pathway codes for a particular modality o Sensory info is processed by the opposite side of the brain o Sensory pathways synapse in the thalamus on their way to the cortex Dermatome map (topographic organization) Sensory input at different levels of spinal cord is mapped out across the body o Not precise for touch, pressure, vibration o Accurate for pain and temperature The body is mapped to the somatosensory cortex o The cortical area is proportional to sensory sensitivity o Homunculus a representative body that is made proportionate to the brains cortex. Sensory Pathway o 1st Order Neurons Sensory, cell bodies in the PNS in the dorsal root ganglia and synapse in the dorsal horn o 2nd order neurons CNS neurons in the spinal cord or medulla rd o 3 Order Neurons Located in the contralateral (opposite side) of the brain in the thalamus o All Ascending systems cross before the thalamus. The thalamic projections to the cortex are the same side. Mechanosensory system Dorsal Column medial lemniscal System o Receptors in the skin touch pressure vibration, proprioception (limb location) o 1st Order neurons branch and synapse in the dorsal horn, but also send information to the brain via the ipsilateral dorsal column white matter. Axons are organized such that the lower body is medially organized, and upper body is lateral in the white matter somatotopical organization st o 1 order neuron terminates on the 2nd order neuron in the dorsal column nuclei in the medulla One nucleus for upper limb, one for lower nd o 2 order medullary neurons project to the contralateral side of the thalamus through a fiber called Medial Lemniscus

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o 3rd order neurons are in the thalamus. These project to the cortex. This is also somatotopically organized.

Pain Pathway Spinothalamic/anterolateral pathway o 1st Order sensory receptors free nerve endings detect pain Different receptors from mechanosensory system Bodies are located in the dorsal root ganglia o 2nd order neurons are located in the dorsal horn. The axons from 2nd order neuron crosses the midline and travels in the anterolateral white matter These axons form the spinothalamic tract 2nd order axons synapse on the neurons at many different levels, ipsilaterally and contralatterally (for example, the foot withdraw reflex acts on both sides) Some axons go direct to the thalamus contralaterally rd 3 order neuron is in the thalamus and goes to the cortex o Mechanosensory (right) vs pain (left) pathways: Mechanosensory & Pain pathways from the face via Cranial nerve V Trigeminal nerve Referred pain o The somatosensory cortex is missing representations for things such as the heart, lungs, etc. all visceral organs o Visceral organs refer pain to specific sections of skin o This probably because the organ also synapses on the same neuron in the spinal cord Phantom Limb Pain o When someone loses a limb, central pathways can still be active in the absence of stimuli o People can still feel the missing limb and feel lots of pain

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o Difficult to treat destroying parts of pathway dont relieve pain

Sensory Deficits after Spinal cord injury Spinal Hemisectiondestruction half of the spinal cord o Spinal reflexes below the lesion still work

Topic 3 CNS Motor

Interneurons are fingers on the piano that cause the keys (motor neurons) to play The descending systems access these keys to cause tunes to be played o Upper Motor Neurons There are 2 types of pathways : Direct & Indirect Direct Pathways Called Lateral Pathways o Cortispinal tract/pathway Originates from the cerebellar motor cortex These go through the pyramidal system to the medulla Crosses via pyramidal dissection while going through the pyramidal tract Synapses in the spinal cord and interneurons there. o Rubiospinal pathway Originates from the red nucleus (Midbrain) Synapse in the spinal cord and interneurons o Both Pathways are still crossed o They travel in the lateral white matter on dorsal side

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The Spinal cord is somatotropically organized o distal muscles are lateral and vice versa o Lateral muscles synapse on lateral nuclei Lesions of the motor cortex cause issues with fine motor control but not all movements. Lesions of the spinal cord causes inability to do individual movements of limbs.. limb moves in only one direction. o Pitcher on a mound, but cant pitch the ball

Indirect (Extrapyramidal) pathways Brainstem/ventromedial Pathways o Reticular Nuclei Posture & Walking o Superior Colliculus vision & Vestibular nuclei balance Tectospinal tract visual system Vestibulospinal tract vestibular system o These innervate more of the proximal muscles o Arise from Circuits originating in cortex, brainstem, cerebellum o Synapse on neurons in the brainstem o Brainstem neurons project into the spinal cord o Really important in the maintenance of posture and coordinated head/eye movements Motor deficits after spinal cord injury- spinal hemisection o Flaccid paralysis on the ipsilateral side o Spastic Paralysis reflexes are still present, but no input from the brain o Clonus tap on the patellar tendon, and itll keep going up and down instead of just doing it once. Descending input is needed to stop the oscillation. Brown sequard Syndrome- Sensory & motor deficits following a hemisection

Topic 4 Cerebral cortex and function

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3 types of cells in the CNS o Neurons o Glia (10x the amount of neurons) Astrocytes Oligodendrocytes myelin in the CNS Microglia phagocytes. Immune system of brain o Ependymal cells line the Ventricles Choroid plexus modified ependymal cells that produce CSF CSF fills ventricles & subarachnoid space o Produced 500 ml/ day. 150 ml in total. Turns over 3-4x / day. o 2 foramens that let the CSF into the subarachnoid space o Hydrocephalus the inability to absorb/drain CSF A shunt is used to drain csf to the abdomen o CSF is chemically regulated Important in chemosensory function More acidic than blood Due to the blood brain barrier Meninges o Dura Mater 2 Sinuss are created by folds of the dura mater and these drain the CSF from the brain. Subdural space contains venous system o Arachnoid Mater Subarachanoid space is between the arachnoid & Pia mater The CSF resides here. Contains arterial system Arachnoid granulations arachnoid mater poking through the dura mater and drains csf into the venous sinus o Pia mater Subdural bleeding o pushes the brain from the outside Subarachnoid bleeding o Bleeds into the brain and balloons inside the brain Blood Brain Barrier o Capillaries are one cell thick o Astrocyte feet combine together to form the blood brain barrier o Tight junctions restrict diffusional passage of large molecules Prevents transport of everything not small, lipid soluble or gas o Other molecules cross the barrier through many specific membrane transporters Cerebral Cortex o Frontal cortex motor and function

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Personality and emotion Orbital frontal cortex addictive behaviors o Parietal Cortex sensory functions & integration Contralateral neglect syndrome if right side is damaged, you cant process some things from the left visual field Occipital lobe primary visual cortex o The brain processes the image upside down versus the visual field and location of the brain o The outer part of the cortex does more with macular (main part of field) while inner parts do binocular parts Temporal Lobe Audition learning, memory, facial recognition, language o If temporal lobe is damaged AGNOSIAS Difficult recognizing, identifying and naming categories of objects Right cortex unable to recognize faces Separation of complex functions between cerebral hemispheres o There is a lateralization (left/right) o Wada Procedure disproved that left/right handedness indicated which hemisphere of the brain was dominant Injection of a fast acting barbiturate into the left/right carotid artery so that the hemisphere goes to sleep Language repeating a spoken word o Wernickes area processes the sound from the auditory cortex, and passes it through the angular gyrus (yellow) to brocas area. o Brocas area has to do with the motor function for speech and projects to the motor cortex Repeating a written word o Visual Cortex Angular Gyrus wernickes area brocas area motor cortex Corpus Callosum connects the two hemispheres - ~200 million axons o Cutting the corpus callosum helps severe epileptic o Its very difficult to figure out what the deficit of cutting the corpus callosum was o Sterognosis Experiment Objects is held in the left hand (right hemisphere) Object held in left hand cant be named Object held in right hand can be named The effects of stroke o Aphasia change in expression or comprehension

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o Brocas Area unable to speak but can understand language Motor or expressive aphasia o Wernickes Area unable to comprehend spoken or visual info Sensory or receptive aphasia Brain Death o Patient came in a coma and its not medically induced o Greatly reduced cerebral circulation o No response to painful stimuli other than spinal reflexes o Brainstem must be dead as well Midbrain eyes, relays auditory and visual info, descending control of skeletal muscles No pupillary light reflexes Pons coordinates respiration, maintenance of upright posture, vestibular system induced eye movement No eye movements with vestibular stimulation Medulla blood pressure, heart rate, respiration, standing Apnea w/ co2 level over 60 mmhg (very high)

Topic 5: Endocrine Thyroid & Glucose stuff Hormone chemical messenger secreted by a cell that is transported to a distant target where the hormone exerts its effects in low conc. Mechanisms all work via 2nd messenger systems o Hormones work by binding to ligand gated receptors and then: o Alter membrane potentials/regular transport/cause exocytosis Classes of hormones o Peptides derived from amino acids. Ex. Insulin, TRH, TSH o Amines derives from tyrosine. Ex. E, NE, thyroid hormones o Steroids Derived from cholesterol. Ex. Cortisol, aldosterone Thyroid hormones they are always required o Required for normal maturation of the nervous system o Required for normal bodily growth o Required for normal alertness and reflexes o Major determinate of the rate at which the body produces heat o Facilitates the activity of the sympathetic nervous system by stimulating the synthesis of Beta receptors for E & NE Thyroid Hormone release can be controlled via hormones, neurotransmitters or ion/nutrient changes Release of T3/T4 (thyroid hormones) o The Hypothalamus releases TRH (thyrotropin-releasing hormone) that goes to the anterior pituitary via portal capillaries o The TRH binds to the a G protein phospholipase C, IP3 DAG receptor in the anterior pituitary. Ip3 calcium release

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o The anterior pituitary releases TSH thyroid stimulating hormone o The TSH binds to a follicular cell in the thyroid to a G protein coupled Adenylyl cyclase, cAMP second messenger pathway This is a complex pathway TSH pathway o Enhances the transport of iodine into the follicular cell o Iodination of tyrosine residues that is sitting in a long peptide chains waiting. This is why the hormones can be stored everything is stored on the thyro-globulin peptide chain in the colloid o The protein can then be endocytosed to an endosome in the follicular cell that chops up the thyroglobulin into T3 & T4 o TSH exerts a growth factor effect and causes hyperplasia of the follicular cells as well. T3 & T4 then bind to thyroxin binding protein which carries the hormones through the blood stream. o T4 = Thyroxin. 4 iodines o T3 = more biologically active. 3 iodines. o T3 is involved in negative feedback to regulate the levels of TRH & TSH Hypothyroidism 2 ways it can happen o Follicular cells are making too little T3/T4. Because of this, TSH & TRH are very high. This causes hyperplasia (TSH) Goiter Hashimotos disease an autoimmune disorder o Secondary hypothyroidism too little T3/T4 due to too little TRH/TSH. No goiter because too little TSH Hyperthyroidism o Tumor Too much T3/T4 and low TRH/TSH no goiter o Graves Disease due to TSI thyroid stimulating immunoglobin is a TSH receptor antibody that stimulates TSH receptor Causes goiter because of TSH like effects Autoimmune disease o Secondary hyperthyroidism too much TSH/TRH goiter o Hyperthyroidism affects B receptors and causes increased contractility in the heart

Glucose Stuff Increase in Plasma concentration of glucose causes the stimulation of beta islet cells in the pancreas. >100 mg/dL is the threshold o Glucose level rises in the B Cell o ATP Production will increase due to the glucose increase Closes a potassium ATP Channel

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o Membrane potential will depolarize o Causes a voltage gated calcium to open calcium influx Calcium induced calcium release o Calcium causes release of insulin vesicles Increase levels of insulin o Causes glucose uptake in muscles and fat cells o Causes glucose release to stop in the liver and causes uptake Increase in synthesis of glucagon and triglycerides Insulin Receptor tyrosine kinase receptor o Causes insertion of GLUT4 transporters in the cell. o Brain, kidney and intestines arent insulin dependent they use GLUT1 transporters instead Glucose tolerance test a way to test for diabetes o Can differentiate between non diabetic and type 1 & 2 o Oral Test Fast overnight & glucose is measured in the blood Drink a known Conc. Of glucose Normal person sugar spikes and drop rapidly Diabetic sugar spikes and goes down really slowly Type 2 the insulin will still be made so youll see it affect the curve, but you wont see it with type 1 Type 1 Diabetes Insulin Hyposecretion insulin dependent o 10% of diabetics o Autoimmune disease o Glucosuria the kidneys cant reabsorb all glucose so its excreted it. Osmotic diuresis loss of lots of water due to glucose Polyuria excessive urination Polydipsia excessive thirst o Body will break down glycogen and fats for energy polyphagia o Diabetic ketoacidosis build up of ketones from fat break down will cause acidity in the blood and can lead to coma Insulin Shock hypoglycemia o Insulin excess o Causes the body to take up too much glucose and reduces the glucose available in the blood for the brain to use Type 2 Diabetes o Caused by genetics and being overweight o Insulin resistance defect in the B cells ab ility to secrete insulin Gestational diabetes 4% of pregnancies o Women can become diabetics due to insulin resistance o Insulin resistance is connected to levels of progesterone and cortisol

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o May be due to peptide hormone hPL (human placental lactogen) o Problems go away after delivery Topic 6: Cardiac Output and excitation coupling in vascular smooth muscle

Mean arterial pressure we cannot change this directly; it is changed by cardiac output and stroke volume and peripheral resistance Main features of the CV system o Heart is a double pump and each side is equal volumes o Arterial system is high pressure, venous is low pressure o Right atrium Right ventricle lungs left atrium Left Ventricle aorta (body) Coordination of the heart beat o SA Node (pacemaker) AV Node (delays contractions of ventricles from atria) bundle of his purkinje fibers o ECG analysis P wave = atrial depolarization Q wave = depolarization through bundle of his RS Wave = ventricular r depolarization T Wave = ventricular repolarization o ECG Pathology PR interval lengthening indicates 1st degree AV conduction block QRS loss after P waves indicate 2nd degree AV block Lengthening of QT interval indicates congenital defects in voltage gated Na+ or K+ channels. A Singularly most important function of the CV system is to ensure continuous system is to ensure adequate blood flow through capillaries Poiselles law o P = F * R Delta P = pressure gradient along the tube F = flow of fluid R = resistance to fluid flow Mean Arterial Pressure (MAP) cardiac version of poiselles law o MAP = CO * R MAP = Mean pressure in aorta mean pressure at right atrium CO = cardiac output - liters/min CO = Heart Rate * Stroke Volume

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R = peripheral resistance (TPR or SVR) SA Node Cell o Able to be autorhythmic o As the membrane repolarizes, an HCN non-specific cation channel opens This helps to depolarize the action potential o Nodal cells lack voltage gated Na+ channels. They use calcium channels instead. Heart Rate Control o SA Node cells are pacemaker cells 100 bpm o Av node cells are at lower rate 40-60 bpm o Unregulated heart rate 100 bpm o Decreasing heart rate Increase parasympathetic activity. Muscarinic receptor causes K+ channel to open and hyperpolarize the potential. Because of this, it takes longer for the pacemaker potential to fire. (chronotropic effect) Dromotropic (conduction) effect does the same o Increasing the heart rate E & NE increase sympathetic activity via B receptors Mechanical events in the cardiac cycle o Systole Period of Contraction o Diastole period of relaxation The heart has isovolumetric contraction and relaxation of the ventricles Stroke volume = end diastolic volume end systolic

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Pressure Volume Loop for the left ventricle Should be able to determine if stroke volume changed and whether it was due to frank-starling or due to change in contractility Regulating stroke volume o Frank Starling law o Increasing Contracility Frank-starling law o Increasing sarcomere length of muscle fibers can increase stroke volume Increase EDV Increase SV o Tension can be increased rapidly as the sarcomere length. Skeletal muscle cant increase as much Cardiac Function curve is the same as the frank starling curve, just different axes o Increase in blood volume or venous pressure, you will increase EDV thereby stroke volume/ cardiac output Role of the veins o Holds 60% of the blood of the body o Increasing sympathetic nerve activity causes venoconstriction. This causes more venous return to the heart venous pressure venous return atrial pressure EDV Stroke Volume Cardiac Output

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o This changes the pressure volume loop preload increase Contraction of ventricular muscle o Gap junction depolarizes from the action potential. o A voltage gated L type Ca2+ channel in t tubule opens Calcium induced calcium release o Calcium released from SR binds to troponin and allows the actin/myosin to interact and contract the sarcomere o Changes in contractility is all about how the muscle is handling calcium Increasing contractility Increased Contracility Graph o Increasing in developed tension without changing muscle length o B adrenergic receptor activates cAMP and phosphorylates the L type Ca2+ channel so it opens longer Ryanodine receptor (Ca channel in SR) also phosphorylated Ca transporter back into the SR is also phosphorylated o Ejection Fraction (EF) = SV/EDV Normally 50% -75% Contracility = Ejection Fraction Frank-starling property represents changes due to increase in EDV/venous return. Increasing contractility represents intrinsic changes in the muscle performance Another way to alter mean arterial pressure, you can change peripheral resistance o CV variables for resistance to blood flow L = length of CV system (constant) n = viscosity of the blood r = radius of the blood vessel Main thing that alters resistance Smooth Muscles

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o Not striated o Innervated by the autonomic nervous system sympathetic system o Contains actin & myosin, tropomyosin, but NOT troponin Troponin = calcium binding that causes tropomyosin shift o Can develop comparable max tension as striated muscle, but the timing is different. Such as time taken to generate smooth muscle o Smooth muscle can be relaxed by neurotransmitter, unlike skeletal muscle o Smooth muscle lacks a specialized end plate/junction for neurotransmitter release o Contraction of smooth muscle can be initiated by hormones and paracrines, unlike skeletal muscle Ex. E, cortisol, angiotension II, nitric oxide, histamine o Unlike skeletal muscle, smooth muscle can be initiated by mechanical stretch o Actin and myosin are arranged in diagonal bundles and dont have sarcomeres. Cross bridges are much slower o Smooth muscle membrane is more complex. Has voltage gated Ca2+ channel Alpha receptors bind E or NE G protein/phospholipase C / Ip3. IP3 opens Ca channel in SR Smooth Muscle Contraction o Cytosol level of Calcium increases (IP3 of Ca induced Ca) o No Troponin. Ca binds to calmodulin (CaM) o CaM associates with MLCK. MLCK phosphorylates a protein in the light chain in head of myosin o Once myosin is phosphorylated, it binds actin and shortens. o Relaxation is done via lowering calcium conc. o Myosin phosphatase takes off the phosphate from the myosin

Topic 7: Vascular System Most drop in blood pressure covers over the arterioles o They are the primary determinant of blood flow resistance o Determine the relative distribution of blood to body parts This is done by changing radius. Radius flow Control of the arteriolar radius o Local control Myogenic activity. Pressure Stretch

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Causes vasoconstriction Paracrines from metabolism O2 Co2 H+, K+ Osmolarity Causes vasodilation Paracrine signal molecules NO, histamine, adenosine - Vasodilation Endothelin-1 Vasoconstriction o Extrinsic control Nervous - sympathetic input (NE alpha receptor) Causes vasoconstriction Neurons can release NO and cause vasodilation Hormonal Epinephrine o Alpha 1 receptor vasoconstrict o Beta 2 receptor vasodilation o Different vessels have different receptors Angiotensin II vasoconstriction Arginine vasopressin (AVP) vasoconstriction Cortisol vasoconstrict Atrial natriuretic peptide (ANF) vasodilator Local Control autoregulation o Active hyperemia when organs increase activity PO2 Arterioler radius Blood Flow o Flow Autoregulation due to drop in pressure (like bleeding) Arterial pressure blood flow to organ PO2 metabolites Vessel wall stretch Arterioler radius Blood Flow Doesnt have to be only drop in Pressure, also works for increase in pressure Autoregulation of Glomerular filtration rate(GFR) in kidney is an example of flow regulation Capillary exchange and bulk flow o Diffusion, facilitated diffusion and transcytosis Bulk Flow o Mass movement of water and dissolved solutes between and blood and interstitial fluid o Main function is to distribute the extracellular fluid o Result of the balance between hydrostatic (blood pressure) and osmatic pressures (due to conc. Gradients) o Interstitial fluid can be thought of as a reservoir Capillary wall is highly permeable to everything but large proteins o This creates a osmotic pressure o As you pass through a capillary, hydrostatic pressure decreases. This is due to decreasing resistance.

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Plasma osmotic (oncotic) inwards water movement NFP = net filtration pressure = filtration absorption NFP is usually positive more filtration than absorption Excess filtrate is taken up by the lymph system Pc= Hydrostatic pressure (out) Pif= interstitial fluid pressure if osmotic force due to if fluid protein conc. (out of cap) o c osmotic force due to protein conc in blood (into cap.) Pulmonary capillaries capillary exchange processes are identical except there is a small net filtration o Pc is very low and large if Vascular function curve o Measures change in the atrial pressure as cardiac output changes o No cardiac output central venous pressure (7mmhg) only o As cardiac pressure increases, atrial pressure will decrease. o Hypovolemia causes a downward shift while hypervolemia causes an upward shift Flipping the axes of the vascular function curve and plotting cardiac function leads to 2 intersecting curves called the steady state point o Transfusion vascular curve moves to the right, steady state point moves up o Increase in contractility will shift the cardiac curve up and left

o o o o o o o

Lecture 8: Regulation of arterial blood pressure Short Term regulation o Baroreceptors blood pressure receptors in the aorta and in the carotid arteries One is located at the arch of the aorta and the other is in the carotid arteries o Only variables heart rate, stroke volume and resistance

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Fixing high blood pressure o Sympathetic outflow decreases. Less NE & excitation. o Increase parasympathetic signals decrease heart rate o Stroke volume cant change EDV, but you can change contractility by reducing sympathetic outflow Fixing Low Blood Drive o More sympathetics More NE & E, increasing resistance and heart rate and contractility. o Withdraw parasympathetic brake and all activity Long Term Regulation of high blood pressure decrease blood volume o Kidneys will increase urinary loss of water and sodium Lower activity of RAAS renin angiotensin-aldosterone system. Causes more Na+ excretion Renin causes angiotensin II (by ACE enzyme) to go and produce aldosterone Decrease Kidney tubular reabsorption of NA+ o If high Blood Volume is detected first Activity of low pressure baroceptors detect blood volume and tells the medulla AVP (anti diuretic hormone) secretion decreases causes more diuresis Atrial natriuretic peptide (ANP) pathway As plasma volume increases, atrial fibers release ANP It decreases aldosterone Afferent dilation and efferent constriction in kidney arterioles Increase in GFR. Decreases Na+ reabsorption Regulation of aterial blood pressure in shock o Shock = sustained drop in mean arterial blood pressure Septic shock infection Hypovolemic shock o Hemorrhage 10%-20% rapid loss of blood volume o Short term regulation Drop in blood volume drop in EDV Drop in SV Increase heart rate and contractility Increase peripheral resistance baroreceptor reflex Increase Sympathetic system, EDV rise in cardiac output Reflex compensations work towards normalcy Use the RAAS system

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system MAP GFR Renin Release Renin converts angiotensinogen into angiotensin I ACE converts Angiotensin I to angiotensin II Angiotensin II goes to adrenal cortex and releases aldosterone Aldosterone causes na+ and H20 to be retained AVP cases vasoconstriction and aldosterone to be released GFR wont be the same anymore because no auto regulation o Long term response Drop in capillary hydrostatic pressure Increased fluid absorption from interstitial compartment increase in plasma volume restore MAP Increase absorption because of starling forces in the capillary more water leaves from interstitial fluid (reservoir) and enters blood plasma Called autotransfusion redistribution not replacement o Sometime after hemorrhage plasma rises back and beyond original value, but erythrocyte cant regenerate. o Red blood cell replacement can be done via erythropoietin release by the kidney to stimulate more production, but takes days to weeks for replacement. Cardiogenic shock due to congestive heart failure o Lower cardiac output o Consequence of prolonged hypertension diastolic dysfunction Serious hypertrophy and ventricular volume decreases o Systolic dysfunction consequence of damage to ventricular tissue due to decreased coronary blood flow (heart attack) o Coronary arteries provide the heart muscles with blood from the base of the aorta o Left anterior descending branch widowmaker can get blocked left ventricle loses blood Cardiovascular responses to cardiac failure / systolic dysfunction o Decreased CO triggers baroreceptor reflex Increases HR, SV, Contractility, and Resistance Initially beneficial restoring CO & MAP Long term leads to massive expansion of extracellular fluid volume. RAAS Aldosterone AVP H20 retention Causes EDV SV to increase CO o This is bad because heart is damaged o Frank starling curve is significantly lower o Asking the heart to work harder

o RAAS

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o Cardiac function graph much lower due to hypervolemia. More atrial pressure and less cardiac output. Ventricle muscles will start to tear o EDV is too big.. tension needed is too much Peripheral Edema(Swelling of the body) occurs Pulmonary edema fluid build in the lungs o Gas cant really diffuse well through the water Increase in peripheral resistance more work load Heart Failure Treatments o Diuretics causes excretion of water o Increase cardiac contractility - cardiac ionotropic drugs Digitalis (digoxin) poisons the Na/K ATPase pumps Causes increase Ca+ in the cell o Inhibit AVP binding to receptors in kidney and vascular muscles Increases excretion of water o Inhibit the RAAS system ACE inhibitors ACE inhibitors block formation of angiotension II / aldosterone o Vasodilators organic nitrates / nitroglycerin Anaphylaxis an extreme allergic reaction o A type of allergic response classified as immediate hypersensitivity o Rapid onset. Mediated by IgE immunoglobulins, mast cells, and basophils o Immunity stuff Humoral immune response Memory B cells make antibodies Cell mediated responses T cells cytotoxic T cells and helper T cells Helper T cells when activated, make the humoral response much larger and better. Cytotoxic not used. Humoral response recognizes the antigen and makes antigens and the antigens wait for the next time. Mast cell has IgE on its surface and binds to the allergen. Releases histamine and other inflammatory mediators Inflammatory response will divert more fluid away from blood increase vascular permeability Histamine will cause hypotension by binding to smooth vascular muscles Swelling of the tissue around airways (Angio-edema) Bronchiolar smooth muscle contraction Epinephrine (epi-pen) is used to reverse anaphylaxis. Vasoconstriction of the blood via A1 receptor

o o o o

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Bronchodilation via B2 receptor Hypertension o Chronically increased MAP 140/90 + o Major abnormality is increased peripheral resistance o Baroreceptor reflexes reset to a different resting value o Could also be due to kidney dysfunction in a small subset of the population o This will call diastolic dysfunction o Hypertension will increases the chances of having a stroke Treatments for hypertensive disease o Diuretics o B1 adrenergic blocks decrease CO, HR & SV. Decrease CO & MAP o Calcium channel blocks decreases total peripheral resistance, but can increase risk of heart attack (due to calcium channels in the heart) o ACE inhibitors Renal hypertension is best treated with ACE inhibitors Vasovagal syncope : emotional fainting o Happens due to sudden drop in Blood pressure due to vasodilation o Inhibition of smooth muscle & sympathetic innervation o Baroreceptor reflex becomes uncoupled Hyponatremia o Occurred in 1% of new York marathoners in the past o Cause by salt lost in sweat, though runners were hydrated o Overhydration dilutes the plasmas Na+ content and blood flow to kidneys is significantly lower Interstitial Na content remains normal Due to this imbalance, water flows into the interstitial space Swelling of hands, feet, constriction of chest People died due to brain swelling, fainting, coma, death o Treatment hypertonic saline IV

Ecstasy induced hyponatremia article key points Due to genetic variation one can metabolize MDMA slower MDMA forms inhibitor complexes with CYP2D6 an enzyme that is used to breakdown MDMA. This can lead to acute toxicity o CYP2D6 is also affected by other drugs as well MDMA causes a lot of dehydration and fever. Acute Kidney Injury can occur o Dose dependent correlation of proximal tubule damage Hyponatremia o Excessive water intake is associated with MDMA use. People try to hydrate to prevent fever

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o HMMA is a metabolite of MDMA that is a more potent inducer of ADH (antidiuretic hormone (AVP) ) o Serum sodium conc. Drops, causing hyponatremia

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