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128 Cards in this Set
- Front
- Back
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What substances are least likely to penetrate lipid bilayers |
Ions - Na+, K-, Cl- Large water soluble molecules and ions do not diffuse through the lipid bilayer and therefore generally must use channels to enter and exit cells and cross the blood brain and placental barriers. |
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Endocytosis vs Exocytosis |
Endocytosis -molecules transported into the cell Exocytosis - Molecules transported out of the cell (neurotransmitters) Proteins reabsorbed from the proximal tubule of the kidney by pinocytosis. |
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Name 5 second messengers |
Cyclic adenosine monophosphate (cAMP) cyclic guanosine monophosphate (cGMP) calcium calmodulin inositol triphosphate (IP3) Second Messenger action is tissue-specific. |
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Why does insulin treat hyperkalemia |
insulin stimulates the Na+-K- pump. Insulin, by stimulating the Na+K- pump drives K+ into cells. Insulin also opens glucose channels, which permits the transfer of glucose into fat and skeletal muscles.
Glucose is given just to prevent hypoglycemia |
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Why does Beta-2 adrenergic receptor agonists cause hypokalemia |
stimulate the Na+-K+ pump. Beta adrenergic receptor agonists drive potassium into cells stimulating Na-K pump. Ritodrine and Terbutaline promote hypokalemia. |
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Extracellular vs Intracellular levels for Na, K, Ca Mg, Cl, PO4, and HCO3 |
Na Extra- 145 and Intra 10 K Extra 4 and Intra 140 Ca2 Extra 2.0 and Intra <1.0 Mg2 Extra 2 and Intra 50 PO4 Extra 2 and Intra 75 HCO3 Extra 24 and Intra 10. PIMP -Potassium IN Magnesium and Phos In the cell. |
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Resting Membrane Potential with Hyperkalemia and Hypokalemia |
Hyperkalemia - cell will depolarize - resting membrane potential decrease -60 Hypokalemia - cell will hyper polarize - resting membrane will increase to -80 |
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In the Neuron, voltage-gated sodium channels are found principally where |
in the axon and are concentrated in the nodes of ranvier. |
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Name three examples of how Na channels can become an inactivated state |
cardioplegia depolarization by succs Local anesthetics block |
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Hypocalcemia va Hypercalcemia how do they effect the release of neurotransmitter at the nerve terminals |
Hypocalcemia associated with decrease of neurotransmitter released Hypercalcemia associated with increase of neurotransmitter released Ca and Mg are antagonistic - High Mg = Low Ca High Ca = Low Mg |
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What all does acetylcholinesterase degrade |
local anesthetics, Neostigmine, Edrophonium, remifentanil, and esmolol. |
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Phase 1 block vs Phase II block |
Phase 2 - competitive inhibition, FADE, post-tetantic facilitation, antagonized by anticholinesterases, no fasiculations. Phase 1 -decreased in single twitch, response to high frequency remained, no fade, muscle fasciculation precede block, potentiated by anti cholinesterase ... SUCC metabolized by plasma cholinesterase WORKS ON SKELETAL MUSCLE. Phase II block can be mimic by SUCC if large dose given. |
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ED 95 of Succ, Roc, Vec, Cis, Panc |
Suc and Roc = 0.3 Vec, Cis, Panc= 0.05 ALL NDMR can be eliminated renal if not other routes available. |
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Elimination of NDMR Biliary, Renal, Metabolism |
Renal - Panc Biliary - Vec and Roc Metabolism - Succ, Cis (hoffman elimination) |
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which muscle relaxants produce histamine release |
Sch, Mivacurium, atracurium, d-tubo, metocurarine. |
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Which MR cause Tachycardia & HTN |
Panc. |
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Adverse effects of Succ's (1-6) |
1. release of K+ from cells = 0.5 meq/L in normal patients and 5-10meq/l in burn,trauma,or head-inury 2.myalgia (muscle pains)- 24-48 hrs after 3.dysrhythmias 4.AV conduction block 5.increase intraocular pressure 5-15 6. MH |
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Adverse effects of Succ's (7-11) |
7. increased ICP [myotonic contraction of eye] 8.prolonged resp paralysis 9.myoglobinuria 10. fasciculations 11.increased intragastric pressure |
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which conditions proliferate SUCC at the extra junctional postsynaptic cholinergic nicotinic receptors? and What is the Major Concern? |
Major Concern= Hyperkalemia 1. Thermal trauma (burns) 2.spinal cord transection (paraplegia) 3.skeletal muscle trauma 4.upper motor neuron injury (Head injury, CVA, parkinsons dx) 5.prolonged immobility. |
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If you use a nerve muscle stimulator on the right wrist and the pt has right sided hemiplegia- what will happen to the twitch |
The twitch on the right will be greater than the left - b/c nicotinic receptors are up-regulated on the right. |
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Malignant Hyperthermia most common first sign |
increase in end title CO2 Other signs include trismus, whole body rigidity, initial signs of tachy/tachypnea from sympathetic nervous system secondary to hyper metabolism and hypercarbia. temperature increase 1-2degrees every 5 minutes |
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MH is a mutation of what receptor |
RyR1- in sarcoplasmic reticulum of skeletal muscle. - leads to sustained contractions + increased metabolism. |
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What is Treatment for MH |
Dantrolene 2.5 mg/kg up to 10 to 20 acts on SR to decrease the release of calcium to contractile proteins
each vial is 20mg with 3g of mannitol = mix with sterile water 50ml. |
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Drugs that increase blocks |
Abx (neomycin, strepto, polymyxin, tetracycline, Local anesthetics, volatile agents, low K+, High Mg, Resp Acid, hypothermia, Age, Obesity, lithium, diuretics, CA Channel |
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Drugs that decrease blocks |
Anticonvulsants thermal burn, 10 days manifests, peaks 40, declines 60 2 nondepolarizers given in sequence |
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Peripheral Nerve Stimulator Single twitch and TOF how many hz double burst suppressions Tetany |
TOF = 2hz every 0.5seconds DBS = two short bursts 50 hz tetanic simulation separated by 750 ms. Tetany = 50hz 5 seconds. |
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Receptor blockade correlation with percent of receptors occupied 95%, 90%, 75-80%, 70%, 50% |
95% - diaphragm movement 90% - abdominal relaxation (1 twitch present) 75-80%- Tidal volume returns to normal (5ml/kg)(single twitch strong, but not a good indicator) 70%- VC at least 20ml/kg 50% - passes inspiratory pressure test- sustained bite, head lift, hand grip. good indicator |
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Noreepi and epi release percentages from adrenal medulla |
80% epi and 20% nore epi unless pheo then opposite. |
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What enzymes metabolism catecholamines in the body |
MAO - concentrated in mitochondria of presynaptic nerve terminals COMT - found in blood, liver, and kidneys. |
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What is the end product of epi and nore epi |
Nore epi and Epi Vanillylmandelic acid (VMA) - in the urine. Dopamine - homovanillic acid (HVA) |
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Duchennes muscular dystrophy |
X-Linked recessive disorder (males exclusively)
concerns: cardiac arrest myocardial dysfunction, SUCC hyperkalemia (AVOID SUCC), delayed gastric emptying, retention of pulmonary secretions, and MH |
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Myasthenia gravis (MG) |
characterized by weakness and easy fatigability of skeletal muscles. - caused by autoimmune destruction of nicotinic acetylcholine receptors at NMJ. most common is ocular |
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MG treatment
Big risk for MG patients with surgery |
Tx: Anticholinesterases which lead to cholinergic crisis = SLUDBM
Risk - postoperative resp failure. |
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Lambert Eaton Syndrome |
Characterized by skeletal muscle weakness - usually lower extremities. usually seen with cancer Activity will help strength in LES |
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Dose of Succ for IV and IM for laryngospasm How to prevent bradycardia with SUCC |
Laryngospasm = 0.1-0.5 mg/kg IV and 4-6 mg/kg IM Brady - give atropine prior to induction. |
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MR distribute primarily to what body compartment? what law do they follow? |
Extracellular fluid compartment. Law of Mass action - Le Chateliers principle. |
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Hoffman elimination is dependent on two factors and what does hoffman elimination eliminate |
Temperature and PH (will increase with Alk/High temp and decrease with Acid/low temp) eliminates CIS |
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MG patients and NDMR and DMR Eaton Lambert and NDMR and DMR |
NDMR = increased sensitivity to NDMR DMR = Can be either sensitive or resistant. Eaton Lambert - Sensitive to both NDMR and DMR |
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What Abx is the most potent at prolonging NDMR |
#1Polymixins (rarely used bc nephrotoxicity) Aminoglycosides - (neomycin, strepto, and kanamycin) |
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If the patient is reversed with an anti cholinesterase agent at the end of the case and SUCC is given to break a laryngospasm will the block be prolonged or shorten |
Prolonged. |
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Echothiophate does what to SUCC |
prolongs because it inhibits plasma cholinesterase. |
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Name 4 anticholinergic drugs and best and worse at secretions, sedations, and HR. |
Atropine Worse Secretions, Best HR Glyco- Least sedation Scop- Best secretions, Best Sedation, Least HR Ipratropium - Bronchodilator. Large dose atropine can interfere with sweating |
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How is anticholinergic syndrome treated |
Physostigmine IV 15-60mcg/kg IV (very fast acting and metabolized) |
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What test checks for pseudocholinesterase activity |
Dibucaine test normal is 80% reduction Heterozygote - 40-60% - one atypical gene Homozygous atypical plasma cholinesterase = 20%. - prolong SUCC by 6-8 hours |
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How do anti cholinesterase or cholinesterase inhibitors work |
Edrophonium, neostigmine, pyridostigmine and phyostigmine (tertiary amine) These agents compete with acetylcholine for sites on acetylcholinesterase, thereby preventing acetylcholine attachment to and breakdown by this enzyme. |
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Difference in binding between edrophonium and Neostigmine |
Edro = electrostatically and forms hydrogen bond Neo = binds covalently- and forms inactive complex. |
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Recovery from Muscle relaxants comparing diaphragm, laryngeal and orbicularis oculi muscle to the thumb |
Respond to and recovery from muscle relaxants sooner than the thumb First Flaccid and First Firm. |
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What percent of receptors are blocked if you have a full train of four |
70% may be still blocked |
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Best indicator that muscle relaxant has been reversed |
Tongue depressor test. hold in teeth for 5 seconds.
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What is released for all sympathetic postganglioninc nerves? What is the one exception |
Nore epi released from all sympathetic except in sweat glands release acetycholine. |
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Cfibers are responsible for what Afibers? A-Beta/a-alpha fibers? |
C-fibers - throbbing pain and temperature A-Delta - sharp, prickling pain, and temperature A-Beta and A-Alpha - proprioception and motor |
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Sympathetic outflow whats its called? Where are the cardioaccelerator fibers located? Sympathetic outflow located? |
Thoracolumbar outflow Cardio T1-T4 Sympathetic T1-L2/L3 |
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What are signs of horners syndrome |
Happens when stellate ganglion blocked Ipsilateral mitosis (pupil constriction), ptosis (Drooping eyelid), enophthalmous (lazy eye), flushing, anhydrosis( can't sweat), stuffiness, increased skin temp |
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Alpha 2 Pre vs Post synaptic |
Alpha 2 Pre = synthesis and release of noreepi is decreased and cause decrease in b/p etc.... Alpha 2 Post = early transient HTN - stimulates noreepi. |
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Synthesis of Noreepi and termination |
Synthesis = Tyrosine to Dopa to Dopamine to NE to Epi. Termination (3) =Diffusion first step, but mainly by reuptake (80%), also by metabolism (MAO). |
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How does ephedrine work and whats contraindicated with it |
Ephedrine - indirect acting sympathomimetics - displacing NE from sympathetic nerve terminals (also has some direct acting) avoided with MAO inhibitor, Meperidine= can cause HTN crisis. |
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Beta 2 responses cause what to glucose and K |
Beta 2 promotes Hyperglycemia, Hypokalemia Ex Ritodrine (yutopar) - causes tachy, hyperglycemia, and hypokalemia. |
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When is Renin Released |
Decreased renal BP, or increase sympathetic nervous system, and CI Renin released from Juxtaglomerular cells |
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What stimulates aldosterone release |
Angiotensin II and high serum Potassium less potent reasons - low Na and ACTH |
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Name the three indirecting agents for NE |
Ephedrine, Metarminol, and Mephentermine |
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Agent and Receptors stimulated Isoproterenol, Dobutamine, Terbutaline, Ritodrine, Noreepi, Dopamine |
Iso = Beta1 and Beta2 Dobutamine - Beta 1 and min Alpha 1 Terbutaline and Ritodrine - Beta 2 and min Beta 1 NE = Everything except Beta 2 Dopamine = Alpha1,2 and Beta 1, min beta 2 |
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Phenoxybenzamine Phentolamine |
Long acting - non selective alpha adrenergic antagonist treat bp with pheo. Phentolamine - non-sleective alpha-adrenergic antagonist |
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Yohimbine Prazosin |
Yohimbine = only alpha2 selective adrenergic antagonist = treat impotence and orthostatic hypotension Prazosin = alpha 1 selective antagonist - Fast acting |
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Propranolol
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Propranolol - avoid with asthma (more selective for beta 2 then beta 1) Esmolol - metabolized by red blood cell ester, used for intraoperative HTN and SVT, help with tachy on intubation. (beta 1 and beta2) |
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Labetalol ratio IV beta to alpha |
Labetalol - good for htn emergencies treats alpha 1, beta 1 and beta 2. decrease HR, myocardial contractility, and SVR 7:1 beta to alpha ratio (stronger beta). |
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Side effects of Beta Blockers |
Hyperkalemia, Hypoglycemia, Bronchoconstricition, CV effects
Withdrawal hypersensitivity - due to up regulation of beta blockers |
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Treatment of excess beta blockers |
Atropine, Dobutamine, Ca Cl, Glucagon, and pacemaker DONT USE DOPAMINE |
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Pheo should you alpha or beta block first |
Alpha then Beta !! |
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Down vs Up Regulation |
Down occurs with chronic exposure to agonist ( less receptors) Up regulation occurs with chronic exposure to antagonist. (more receptors) |
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Parasympathetic outflow whats its other name? What arises from it? and where does each cranial nerve correlate too |
Craniosacral outflow Cranial Nerves III, VII, IX, X and S2-S4 CN III ( midbrain), VII (Pons), IX & X (Medulla) |
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Cromolyn sodium |
Prophylactic treatment with cromolyn sodium prevents histamine release and bronchoconstriction. |
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Insulin receptors contain an active tyrosine kinase domain... what is the function of kinase? |
kinases catalyze the addition of a phosphate group to a substrate. |
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What higher center regulates the sympathetic nervous system |
hypothalamus |
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Brainstem auditory evoked potential BAEP |
auditory clicks look at cranial nerve 8 |
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Visual Evoked Potentials VEP |
surgeries near optic nerve. monitor integrity of cranial nerve II |
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VEP SSEP and BAEP list in order of most resistant to least resistant to anesthetics |
VEP most sensitive to anesthetics BAEP least sensitive to anesthetics SSEP in the middle= dose related depression |
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Pathway for Fast-Sharp Pain Whats the major neurotransmitter |
A Delta Fibers enter dorsal horn and terminate in rexed's lamina I and V. Anterolateral pathway Major neurotransmitter is Glutamate binds to AMPA and NMDA, binds postsynaptic. |
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Pathway for Slow-Chronic Pain Whats the major neurotransmitter |
C Fibers Primarily Lamina II and Lamina III. Anterolateral pathway Major Neurotransmitter is Substance P, binds to NK-1 (neurokinin 1) binds postsynaptic |
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Which lamina is the substantia gelatinosa |
Lamina II ..... some say lamina II and III |
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Dermatome Landmarks C4, T4, T8, T10, L4-L5, S2-S5 |
C4= Clavicle T4= Nipples T8 = Xiphoid T10 = Umbilicus L4-L5 = Tibia S2-S5= Perineum |
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Morphine Hydrophilic opioid Neuraxial anesthesia |
Intrathecal = onset is slow and prolonged. rostral spread of morphine in CSF cause late resp depression. Epidural = Onset is slow and prolonged.Uptake is faster when epidural compared to intrathecal so resp depression occurs within 2 hours. |
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Fentanyl Neuraxial anesthesia Lipophilic opioid (Alfentanil, Sufentanil) |
Intrathecal = diffusion is fast out of the CSF. Rapid onset and quick duration. Early depression occurs bc of significant systemic uptake. Minimal Rostral spread Epidural = Same as Intrathecal |
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Spinal Analgesia |
when transmission of pain impulses through the substantia gelatinosa (Lamina II) is suppressed. Mu-2 is dominate receptors, but all can involved. Act in the periventricular/periaqueductal gray. Neuraxial anesthesia blocks pain signals. |
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Supraspinal Analgesia |
Occur when opioids act at brain sites including the limbic, hypothalamus, and thalamus. Supraspinal is dominated by Mu1, but also kappa, and delta. Only receptor not used is M2 IV opioids "I feel pain, but don't care" |
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What modulates pain? What neurons act as the gate keeper for pain? |
the dorsolateral tract modulates pain Gate keeper is Enkephalin |
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MU1 vs MU 2 |
Mu-1= Spinal and Supraspinal, Decreased HR, Euphoria, Pruritus, Urinary retention, low abuse Mu-2 = Spinal Analgesia, Resp Depression, Physical Dependence, Constipation. |
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Kappa and Delta |
Kappa - Responsible for sedation and Dysphoria. low abuse, diuresis, spinal/supraspinal Delta - Physical dependence, constipation, Resp Depression, and spinal/supraspinal. |
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Remifentanil |
Ultra short acting opioid . Metabolized by non-specific esterases. Mu receptor agonist no delta or kappa. |
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Opioid Antagonists and Side Effects |
Naloxone, Naltrexone (long acting), and Nalmefene. SE Reversal of analgesia, excitement, Tachy, HTN, Dysrhythmias, Pulmonary Edema.... SE can be from SNS from reversal of analgesia. |
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which two diseases are barbiturates absolutely contraindicated |
Status Asthmaticus and porphyria |
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Rank Opioids from most potent to least Alfentanil, Fentanyl, Meperidine, Morphine, Remi, Sufentanil) |
Sufetanil (2000-4000x morphine)(most lipid soluble) Remi (220-470xmorphine) Fentanyl (50-100x morphine) Alfentanil (10x morphine) Morphine Meperidine (1/10th morphine) |
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Rank the following stimuli according to amount of opioid needed breast surgery, intubation, lower abdominal surgery, upper abdominal surgery, skin incision, skin closure |
Intubation> Upper abdominal surgery> breast surgery = lower abdomen surgery = skin incision > skin closure Intubation = MOST and Skin closure = Least |
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what is the most common side effect of administration of spinal |
pruritus other side SE most serious Resp depression (late), urinary retention, n/v, sedation, ileus |
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Cranial Nerves Oh Oh Oh To Touch And Feel A Girls Vagina Ah Heaven 1-6 |
1- Olfactory - Smells 2. Optic - Sees 3. Oculomotor - Move eyes - Adduction of eye, pupil size (Medial rectus) 4. Trochlear - Moves eyes 5. Trigeminal - Chews, Sensory from Face 6. Abducens - Moves eyes, Abduction of eye (lateral rectus) |
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Cranial Nerves Oh Oh Oh To Touch And Feel A Girls Vagina Ah Heaven 7-12 |
7. Facial - Facial muscles, taste anterior 2/3 of tongue 8. Acoustic - Balance and Audition 9. Glossopharyngeal - Taste - Posterior 1/3 of tongue. carotid body and carotid sinus 10. Vagus - All KINDS, HR, larynx and pharynx 11. Accessory - shoulder and hand movements 12. Hypoglossal - moves tongue |
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CSF Circulation Route |
Choroid Plexus Lateral Ventricles Foramina of Munro Third Ventricle Aqueduct of Sylvius Fourth Ventricle Foramine of Lushka and Foramen of Magendie Subarachnoid Space Brain to arachnoid Villi |
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Site of formation of CSF |
Choroid plexus of lateral, third, and 4th ventricle. |
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Site of Reabsorption of CSF
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Arachnoid villi and arachnoid granulations |
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Circle Of Willis whats it do |
permits collateral blood flow in the event of a major vessel becomes occluded Major vessels include right and left internal carotids and the basilar artery(supplied by IJ's) |
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Which vessels in the Circle of Willis are not paired? |
Basilar and anterior communicating arteries arent paired. |
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Circle of Willis and Stump Pressure |
Measures the pressure transmitted through the circle of willis back to the carotid artery. Stump pressure >40 mmhg is consider as good as golden standard of EEG monitoring at predicting ischemia during cross-clamp. |
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Flow through Circle of Willis Very Big Posterior Polyps Invade My Aging Ass |
V- Vertebral B- Basilar P-Posterior Cerebral P-Posterior Communicating I-Internal Carotid M- Middle cerebral A-Anterior communicating A-Anterior Cerebral |
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Which agents increase both cerebral blood flow and cerebral metabolism (2)
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Nitrous Oxide and Ketamine |
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Intravenous anesthetics do what to cerebral blood flow and metabolism |
IV agents decrease both cerebral metabolism and cerebral blood flow |
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Volatile Agents do what to cerebral metabolism and cerebral blood flow |
Cerebral metabolism decrease and cerebral blood flow increases with volatile agents Can be offset with hyperventilation. |
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Arterial Blood supply to the spinal cord how many anterior and posterior arteries? what precent goes with each? |
one anterior spinal artery (75% travels length of cord) two posterior spinal arteries (25%). Also have radicular arteries that enter each side of the cord. |
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Radicular arteries how many? Whats the most important and why? |
8 radicular arteries - 1 cervical, two thoracic, one in upper lumbar. The Largest is the Artery of Adamkiewicz - usually enters on left side in lower thoracic region. Major source of blood supply to lower two-thirds of the spinal cord. Possible paraplegia if interrupted. originates between T-8-T12 (75%)usually, some L1-L2 (10%). |
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Coma vs Decorticate Rigidity vs Decerebrate Rigidity |
Coma - damage to RAS Decorticate - damage above cerebellum and brainstem (protect yourself) Decerebrate - damage to brainstem or cerebral lesions. (Don't protect yourself) |
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Intracranial Pressure-Volume curve Whats Normal ICP ? What part of the curve are associated with high ICP? Cushing Triad would be seen at what part of the curve? Focal vs Global ischemia what part of the curve? |
Normal ICP = less than 15 Stage 3 and 4 associated with High ICP Crushing triad seen in stage 3 - Decrease HR, Increase BP, irregular respirations Local ischemia point 3 and global at point 4. |
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Cerebral Steal (luxury perfusion) |
When cerebral vasculature dilates (hypoventilation/Vasodilator) and shunts blood to non-ischemia areas of brain instead of ischemia areas. |
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Inverse Steal (Robin Hood, Reverse Steal) |
patient with ischemic region of brain is hyperventilated and constricts blood vessels and ischemia areas of the brain get extra blood diverted too them. Rob from rich and give to the poor! Ischemia areas are always maximally dilated |
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Skull Anatomy Where is the Sella Turcica? Where is the frontal lobes Temporal Lobes? Brainstem and Cerebellum? |
Sella Turcica, which houses the pituitary gland, is part of the sphenoid bone.(middle cranial fossa) Frontal lobes - anterior cranial fossa Temporal lobes - middle cranial fossa Brainstem and Cerebellum - posterior cranial fossa |
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Withdrawing entrained Air during Craniotomy- whats the correct position? |
Multi-orifice catheter-Positoned high in right atrium 2cm below the SVC- atrial junction.
Single orifice catheter is 3cm above the junction of the SVC-artial junction. |
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When do the fontanelles close Anterior, Posterior, Anterolateral, and posterolateral |
Posterior 2 months Anterolateral - two months Anterior 18 months Posterolateral - two years |
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What is cerebral blood flow in ml/min? in ml/100g/min, % of cardiac output |
Cerebral Blood Flow 750 ml/min 50ml/100g/min 15% of cardiac output |
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Cerebral Perfusion Pressure = what |
MAP- ICP. |
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Three Factors that alter cerebral vascular resistance are? what is the most important determinant of cerebral blood flow |
Changes in PaCo2, PO2, and temperature alter resistance PaCO2 is the single most important with ranges between 20-80. |
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Decrease in cerebral blood flow for each degree of temperature change |
7% decrease in cerebral blood flow/cerebral metabolism for every 1 degree of temperature change. |
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when would expect to see focal ischemia and global ischemia (what ICP) |
focal at 25-55 global 55 |
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what percentage of the brain is blood, brain, and CSF |
brain 80% blood 12% CSF 8% (1st to move out when ICP increases) |
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8 things to do to tx high ICP |
1. mannitol (#2)/ lasix (#3) 2.steroid (#4) 3. hyperventilate (fastest #1) 4.restrict fluids 5.HOB 30 degree 6.potent cerebral vasoconstrictor (prop, etomidate, thiopental) 7.control bp 8.cool patient to 34 degree |
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Mannitol dosing and how does it work |
Mannitol a sugar - can't permeate the cerebral capillary- cause high osmotic pressure and moves fluids Dose 0.25-1 g/kg. no effect on blood glucose. |
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What agents don't you give to a neuro patient |
D5W and Ketamine |
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Where is CSF located |
between pia and arachnoid |
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Most common site of obstruction for CSF |
aqueduct of slyvius |
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autonomic hyperreflexia occurs usually with a lesion at what level? What occurs with autonomic hyperreflexia? Whats most effective anesthesia for these patients? |
T5 to T6 Vasodilation above the lesion and Vasoconstriction below the lesion. = TX the vasoconstriction. Spinal Anesthesia |
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St. John Wart whats you major concern |
CYP450 induced. |
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Where do you place a doppler with VAE |
right atrium - 3rd to 6th intercostal spaces right of the sternum. |
