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Pain nu600

pain nu600 exam4

QuestionAnswer
pain is defined as what? unpleasant sensory and emotional experience with actual or potential tissue damage.
nociception tissue injury, inflammatory mediator
nociception aka windup, carried to dorsal horn of spinal cord
nociception output neurons from dorsal horn cross into the anterior lateral quadrant and ascend spinal cord
nociception impulse travels via the A-alpha and delta fibber in spinothalmic tract
alpha and delta fibers enter thalmus- termination the primary somatosensory cortex
opoids effect on nociception receptors affect mu delta and kappa, affect transmission by opening Na Ca and K channels
Opening of Na Ca and K decrease the firing of action potential for pain transmission, thus its blocked
consequence of pain aka nociception prolong recovery, immune response interference, increase adrenergic and catecholamine response, increase SNS tone, aberrant vitals, increase O2 demand, resp complication, hypovent decrease cough
opioids reduce adrenoctorcotropic hormone, stress hormone, reduce cortisol, cardiac friendly, fluid dynamic stability
frontload pre-emptive, “prophylactic”
opioid inhibits adenylate cyclase; hyper polarization of neuron which suppress neural discharge
opioids presynamptically blocking release of dopamine, norepi and substance P
opoid receptors mu 1 and mu2
Mu1 supra spinal, euphoria, meiosis, nausea and vomiting, urine retention, puritus
Mu2 resp depression, brady, illeus,
delta receptor mediator of mu, physical dependence receptor
kappa spinal analgesia, sedation, miosis (pupil constriction)
sigma hypertonia, dysphoria
fentanyl rapid onset, ideal anesthesia adjunct, acute pain, 100 times more potent than MSO4, 100mcg=10mg of morphine T1/2 200min
fentanyl untoward effect resp depression within 5-15min after admin, chest wall rigid, bradycardia, somnolence, nausea
fentanyl pharmacokinetics onset immediate; duration 30min, volume distribution 4L per kilo, half life 219min,
first pass effect in liver , metabolized to INACTIVE metabolites (renal and hepatic patients, elderly: accumulation)
fentanyl cleared in urine 75% 10% unchanged in urine. continuous infusion or repeated bolus accumulated (asians very sensitive)
fentanyl pharmacodynamics affect mostly Mu, less activation of kappa and delta, specific effect with each receptor.
fentanyl dosage supplied in 50mcg/ml. Low dose fentanyl 1-3mcg/kg titrate to affect.
moderate dose fentanyl 3-10mcg/kg blunt response to laryngoscopy and sudden changes in surgical stim,
large dose fentanyl 50-150mcg/kg cardiac anesthesia does NOT depress myocardium, induce histamine and contributes to stable hemodynamics
fentanyl pharmacodynamics mu1 and ; resp dep, sedation, dysmotility, prolactin and GH release, brady, euphoria
mu receptor location cerebral cortex, thalmus, hypothalmus, midbrain, pos, medulla, dorsal horn, gut, peripheral tissue
kappa receptors analgesia, not as effective as mu or delta. NO resp dep, Dysphoria (ketamine)
Pain in elderly individual, generalize need less drug. decreased hepatic=less protein=increase half life, more body fat, decreased renal. benzo not a good idea.
fentanyl administration PO lollipop, IV, Intrathecal, epidural, transdermal patch
multimodal analgesia opoids used with NSAIDS, cox2 inhibitor, tylenol, shown to be opioid sparing; reduce adverse/side effect
equianalgesia 10mg morphine IV equal to dilaudid 1.5mg/IV (equivelancy chart)
sufentanyl and fentanyl su is 10X more potent than fent. su is 25mcg/kg/hr others are mcg/kg/min. su is highly protein bound. hangs around.
MSO4 gold standard, phase 2 glucuronidation gives active metabolite: M6G M3G. M6G is 25% as powerful of MSO4 at Mu M3G is 1/20 (5%)
Elimination half life of MSO4 T1/2 beta 114min parent, active metabolite M6G 173min
Sufentanyl 10X more potent than fentanyl, high dose cardiac and spinal procedures, faster induction, emergence, ideal for continuous, mcg/kg/HR,
sufenta analgesia d/c sufenta 40 min before expected wake-up, continue to run propofol 150mcg/kg/min. long analgesia after wakeup. sufenta 25mcg/kg/HR
Remifentanyl rapid onset, infusion only (bolus=apnea), hydrolysis of ester linkage, broken down by plasma cholinesterase. renal/hepatic disease no affect. 40mcg/ml
Pseudo-cholinerstrase deficiency does not affect remi.
Remi follow up drug need a protein bound analgesia, follow up. this drug does not have long lasting analgesia. 40mcg/ml
hydromorphone AKA dilaudid intermediate, semi-synthetic opioid treat moderate to severe pain. onset 5 min, duration 4-5 hours. no active metabolite good for renal pts.
meperidine aka Demerol from phenylpiperdine, active metabolite Normaperedine: can cause seizures, not recommended for sickle cell, CNS disorders, renal failure, or children. Histamine release local and immediate.
Demerol AKA meperidine should not be given with MAO inhibitors, cause resp dep, hypoten and worse like circulatory collapse
Mu 2 for opioids cause sedation, resp dep, apnea. due to cotrical and brainstem receptor.
Narcan aka naloxone supplied in 400mcg/10ml , 40 mcg/ml give 20 mcg for 0.5ml keep Mu1 get rid of mu2 resp depression. Big dose equal flash pulmonary edema.
narcotic untoward effect GI PONV, decrease gastric motility, constipation, fecal impaction, bowel obstruction, Biliary spasm
PONV higher patient satisfaction indicator than post op Pain. subjective wave like sensation in throat or epigastrum. stimulation of serotonin, histamine, dopamine. chemo receptor trigger zone.
CN3 cranial nerve 3 myosis oculomotor
partial agonist/antagonist Nalbuphine aka nubane. Strong kappa agonist and mu antagonist. Kappa gives analgesia with less risk of resp depression.
partial agonist mixed with narcan called subaxone (4:1) no narcotic, NSAID Toradol and spinal .
subaxone aka buprenorphine partial agonist can cause resp dep, if given to narcotic pts can cause withdrawal. used for opioid addiction pts.
narcan aka naloxone antagonist, does not last as long as opioid 64min half life, rapid admin= withdrawal, seizure, dysrhythmia, intense pain. flash pulm edema, mechanism unknown
narcan for heroin OD rapid reversal
narcan for anesthesia 400mcg or 0.4mg/ml diluded in 10ml to give 40mcg/ml. give 20mcg or 0.5ml every 5 min until desired effect. antagonize mu 2 responsible for resp depression and sedation.
dexmedetomidine aka precedex selective alpha 2 adrenergic agonist, NOT a narcotic. dextro isomer of medetomidine. precedex is 10X more selective for alpha 2 receptors than clonidine. refractory hypotension, NO amnesia, needs Benzo supplement
dexmedetomidine aka precedex produces sedation, analgesia, mild resp depression, can be used in MAC case with natural airway, general anesthesia, loading dose 0.5mcg/kg followed by infusion 5 to 10mcg/kg/HR.
dexmedtomidine aka precedex Antagonist atipamezole. Precedex has no amnestic effect, effectively treats emergence delirium in children.
clonidine is prototypical Alpha 2 agonist. inhibits catecholamine release, renin release with subsequent vasodilation.
NON opioid analgesic NSAID, cox 2 celebrex. protective Cox 1gastric mucosal, renal and platelets; cox 1 up regulated to inflammation . BAD GFR no toradol.
cox2 non protective to tissue, mediates pain, inflammation, fever. end in ~coxib. MI and CVA may be increased with chronic user.
cyclooxygenase (cox) catalyze synthesis of prostoglandin from arachidonic acid. prostoglandins mediate renal perfusion, platelet aggeration, inflam response. NSAID block cox.
NSAID suppression of proaglandins and thromboxanes stomach prostoglandin E2 and I2, kidney prostoglandin E2, platelets thromboxane A2 and prostoglandin I2. these inhibitions = adverse effect of NSAID.
Pentothal induction used in TIVA, no nuero interference
sodium thiopental keystone of barbiturate induction, barbituric acid, lacks cns activity. structure change in carbon 2 and 5 will alter function.
substitution of methyl radical on carbon 5 pro epileptic, methohexitol or brevitol are examples of oxybarbiturates. burns on injection
thiobarbiturates sulfure to carb 2 sodium ppentothal, or thiopental. increase lipid solubility, onset, increase hynotic shorten duration
pentobarbitol aka nembuitol used in physician assisted suicide in OR. PO or IV cause server N and V
Barbiturates interact with inhibitory GABA. increases Cl channel opening, create state of hyper polarization inhibiting action potential. hypnosis, unconsciousness with bolus, lipophyllic, and re-distributes fast from brain.
Redistribution of barbituates cause cessation of effect not metabolism. use lean body mass to calculate dose
application of barbituates decrease ICP, reduce CMRO2, ICP=CPP-MAP, control seizure, induction of anesthesia, sedation occaionall. NO analgesia, Keep airway reflexes
barbiturates protect from focal ischemic but less golbal prevention, ie after cardiac arrest. DO NOT cause muscle relaxation. Methohexitol can cause involuntary muscle movement
barbiturates contraindicated porphyria vampire disease. not to be used with etomidate or barbs
barbitruates extravasation admin procane 1% and heat to relieve pain
intra arterial injection of barbitrates bad thing, give heparin to prevent clots. alpha adrenergic blocking to vasopastic area
etomidate carboxylated imidazole containing compound, initial water soluble after injection ring forms, lipid soluble. burns myocolinc 0.3mg increases GABA affinity. myoclonis is reduced by giving opioids or benzo. R + predominant
pharmacokenetics of etomidate lipid soluble, 99% non ionized at physiologic pH. but highly protein bound. can cross brain blood but stored in muscle. initial wake up due to re-distrib but full recovery from metablism of hydrolysis
Etomidate Good stable cardiovas profile, no stored in fat ie lower cumulative effect. dose 0.3mg/kg
etomidate aka amidate the bad adrenalcontrcal function reduces up to 5-24hrs, as soon as 30min. prevents cholesterol conversion to cortisol via hydroxylase inhibition. no good for spesis, replace steroids.
physiological response to etomidate acute hypovolemeic patient= profound hypotension. no histamine relase no altering of renal/hepatic flow, arterial injection=no worries
etomidate and CNS vasoconstrictor, decrease cereberal blood flow, 35%ICP, decrease CMRO2 45%. focal epilepsy increase beta waves. can terminate status epilepticus.
Ketamine best used at extreme ages. Kappa receptor. Gabba should be used. “mono anesthetic” agent. profound amnesia, profound analgesia like fentanyl. immobility. safe for cardiac due to sympathetic outflow.
Ketamine dose 2mg/kg IV onset one min. 4mg/kg IM onset 5 min. retrograde amnesia
ketamine structure cyclo-hexanone ring, two optical isomere S- and D+ the S- more intense analgesia and less emergence rx at sigma opoid receptor. phencycladine chemically similar to PCP or Angel dust
Ketamine solubility lipid soluble, not protein bound, cross Blood brain. brain 5times greater than plasma concern.
ketamine initial awakening due to re distribution. cataleptic state. dissociative state: thalamus dissociated from cortex and limbic.eyes are open. corneal and reflexes intact. nystagmic presentation precursor to PONV
ketamine and etomidate can have hypertonus involuntary movement
pharmacodynamics of Ketamine inhibits glutamate at NMDA site (amnestic property) binds to nicotinic and muscarnic cholinergic receptors. and opioid receptor as well. also interacts with Na and Ca voltage dependend ion channels. increase HR and BP sympathetic tone
metabolism of ketamine first de methylation with P450 to yield nor-ketamine (active metabolite) 1/4 of potency of ketamine. Nor-ketamine participate in mu agonist. then conjugated into water soluble compound and excreted in urine.
ketamine in CNS increases cerebral blood flow, not significant increase ICP with vented patient, non vented can increase ICP. no increase of CMRO2, may have neuroprotective role as NMDA implicated with cerebral ischemic.
ketamine and cardiovascular negative inotropic, compensated by sympathetic nervous system stimulation; Elevates catecholamines. can be blunted with benzo, anesthtic agent or beta blocker.
ketamine and digoxin and epinephrine may reverse digitalis induces dysrhythmia. but predispose myocardium to dysrhythmia when local anesthetic containing epi are injected.
pulmonary effect of ketamine upper reflex intact. induce salivary and bronchial secretion. (pre glycopyrolate), bronchodialtor (can be given for asthma attack) elevates pulm vascular resistance and increase right vent workload
hematologic effect of ketamine reversible inhibition of platelet aggregation like aspirin.
ketamine may enhance muscle relaxation due to interference Ca ion binding.
Ketamine enhance acetylcholine effect by inhibiting plasma cholinesterase
ketamine and aminophylline lower seizure and dysrhythmia threshold.
Propofol non barbiturate sedative hypnotic anesthetic agent. in 10% soybean oil and purified egg lecithin emulsion
propofol and PONV 10mg for rescue PONV
propofol mechanism of action exerts effect on GABA, increase in Cl transmembreane hyper polarization of post synaptic cell results in neuron inhibition
Hepatic metabolism of propofol extensive and rapid. results ineffective water soluble metabolite.
propofol administration 2mg/kg render patient unconscious 30seconds. metabolic clearance exceeds hepatic blood flow postulated to be pulmonary
propofol in lungs 2,6 diisopropyl-1,4
propofol does cross into fetal circulation but appears to be rapidly cleared in the neonate
propofol drug of choice rapid induction/emergence. outpatient surgery, TIVA. PEDS need larger amount due to volume of distribution and elevated clearance. found in colostrum upto 8 hours after given to mom
propofol and geriatric need less 25 to 50% less. smaller central volume, reduced Clarence. hypotension, NOT used on hypotensive decreased CO , volume depleted or shock patents.
propofol infusion after bolus titrate to effect. colonoscopy 25-100mcg/kg/min. for TIVA 100-300mcg/kg/min.
Propofol infusion syndrome green urine. tachycardia, met acidosis, myocardial dysfunction, rhabdomylosis, treat with DC of propofol, check labs met acidosis, serum lactate, rhabdo, renal function
propofol PONV direct depressant of medulla. 10mg dose, sub therapeutic dose to treat PONV
propofol and CNS anticonvulsant via Cl inhibition. decrease cerebral blood flow, decrease ICP and CMRO2.
Propofol and cardiovascular system volume resuscitation prior to induction for patients at risk. baroreceptors are depressed. bradycardia and a-systole have been reported post induction. SNS attenuation and Parasymp dominance
propofol and thiopental propofol greater decrease in MAP CO and SVR. relaxation of vascular smooth muscle inhibition of SNS; has negative inotropic effect by decrease Ca intracellular. disaster in hyovolemic or LV dysfunction pts
propofol and respiration blunt hypoxia and hypercarbia, supplement with oxygen. dose dependent of depression of ventilation. hypoxic vasoconstriction remain intact
propofol and infection supports bacterial growth. aseptic techniques used, wipe down ports and rubber stopper, discard after 6 hours of opening. tubing every 12 hours. follow departmental guidelines.
Muscarinic antagonist acts on M2-M4, prevents Ach from producing its effects
M2 receptor mediated by Ach, negative chronotropic/ionotropic extracellular to intracellular. Gprotein-inhibits C-Amp-Ca channel blocked-increased K conduction.
Example of M2 atropine
Atropine brady treatment, binds to M2, SB JB AVB. Dose 0.4-1mg IV onset 1 min Duratino 30-60min.
Alternative to Atropine Glycopyrolate, less tachy response in cardiac pts.
Beta Blocker used to treat Symptomatic non sustained VT. Sustained monomorphic VT. Polymorphic VT.
Torsade de Pointes similar to polymorphic VT except for prolonged QT. treated with Mg
examples of SVT/VT Afib, Aflutter, VT, Polymor VT, tdp
beta blocker second generation lopressor aka metoprolol ie B1 selective (kinda). Esmolol also B1 selective
Lopressor AKA metoprolol B1 selective, metabolized in liver, half life 3-4 hours, treats SVT and ST. Decrease HR, conduction of atria to AV node
SVT is above the AV node
WPW wolf parkinson white, renetry svt. retrograde wide QRS, antegrade narrow QRS
Lopressor treats the following Aflutter 150-250, Afib greater than 250, Atrial Tach greater than 150, ST greater than 100, WPW short PR and Delta waves
Lopressor Dose 5mg IV over 5 min, max of 15mg, 1mg under anesthesia to start. dose dependent on B2. high doses effect islet of pancreas and bronchial smooth muscle.
Beta blocker high doses can cause hypo/hyperglycemia. delay recovery from hypoglycemia (glycogenolysis). increased insulin from Beta cell on pancreas cause hypoglycemia most often. response blunted by Beta blocker ie tachy
Esmolol beta1, half life 8-9min plasma esterase, Dose 0.5mgkg over 1 min. Infusion 50mcg/kg over 4 min. (50mcg=0.5mg) max of 300mcg/kg/min. bolus of 10-100mg or 0.5mcg/kg. Usual dose 10mg.
Beta blocker overdose Glucagone 5-10mg over 1 min. infusion of 1-10mg/hr. Anticholenergic. Isoproterinol or epi at 2-20mcg/min.
Sodium channel blocker example Lidocaine associated with blocking Na and some K channel in cardiac cell.
Action potential diagram stage4. -90mv resting potential. stage0 rapid sodium In. stage1 K and Cl out. stage2 Ca in K out Ca slow cause plateau. stage3 K out. stage4 resting potential.
Lidocaine class 1B fast Na channel blocker. shorten effective refractory, little effect on SA and AV node and accessary pathway.
Lidocaine used to treat Sustained VT, polymorphic VT, abnormal EF, Tdp with prolonged QTI. Dose: 1-1.5mg/kg repeat 0.5-075mg/kg over 5-10min. max of 3mg/kg.
Amiodarone aka cordarone class3 prolongs stage3-K out and Ca kept in. also inhibits Na channels class1 and Ca channels class 4. increases effect refractory, decrease slope of diastolic depolarization of SA and AV node.
amiodarone composition and effects benzofuran derivative, contains iodine may convert T4 to T3. thyroxine to triiodothyronine. may be pulmonary toxic. dyspnea cough or hypoxia. use low O2 or else ARDS
amiodarone dose alive 150mg/100ml over 10min. followed by infusion of 1mg/min for 6 hours. and then 0.5mg/min for 18hours. max daily dose 2.2g
amiodarone dose dead 300mg IV push for VF when shock and vasopressin has failed. with 20-30ml of ns or D5.
amiodarone vs procanimide use amio instead has less cardiac depressive effects.
adenosine mechanism of action acts on receptor bed of AV node. activates adenylate cyclase and decreases action potential. open K causing hyperpolarization, depresses SA and AV node
adenosine dose and use SVT and re-entry. Dose 60-120mcg/kg/min. 6mg then 12mg then 12. half life 1 to 6 seconds. used for SVT and WPW. may cause Afib have cardioversion ready.
wpw conduction is through bundle of kent
vasopressin aka ADH aka AVP argenine vasopressin 40u IV or IO one time dose, pre or post first dose of epi. post defib. half life 10-20min. vasoconstriction cause used in cardiac patients causes ischemia.
Magnesium unknown mechanism of action for anti-arrhythmia. effects Na K and Ca channels. depress automaticity and conduction through AV node, bundle of His and across accessory pathways.
Magnesium uses and dose torsades des pointes, hypomag with MI. Dose 1-2g IV over 1-2min upto 5-10g.
Ca channel blocker uses antianginal, anti-arrhythmic, anti HTN. Nifedipine HTN, Nicardipine HTN, Verapimil arrhythmia. block phase2
Ca channel blocker phase 2 blocked so what? prolongs phase 2 negative chronotropic effect. should be used for atrial not vent dysrythmia ie vent foci dependent on inward flux of Ca.
Calcium antagonist ie blocker for arrhythmias verapamil and diltiazem: reduce chronotropic ionotropic and dromotropic. slow SA node and conduction of AV nice.
Ca channel blocker side effects hypoten, decrease CO negative ionotropic. AVOID in limited cardiac reserves, WPW, dig tox, sick sinus syndrome.
Verapamil dose 2.5-5mg repeat 30min. atrial tachy treated. 10min duration 2-4 hours. max 20mg. hepatic elimination. T1/2 3-7 hours.
Cardizem dose 5-20mg IV (0.25mg/kg) or 20-25mg over 15min. onset 20min duration 2-3hrs. hepatic elimination. used in feocromocitoma adrenal tumor surgery.
verapamil conduction and precautions greatest anti-arrhythmic effect, depress AV prolong refractory period, does not alter intraventricular BUT depresses amp and velocitty of depolarization. NOT to be used with WPW AFIB, avoid in CHF.
Side effect of verapimil and nifidipine can cause dig toxicity, increase it by 30%, AV blocks, myocardial depression. hemodnamic reversed with calcium infusion NOT electrophysiologic.
Clinical uses for peripheral vasodilators Treatment of hypertension Produce controlled hypotension Increased LV stroke volume with regurgitant lesion.
Clinical uses for Nitro vasodilators Useful in symptomatic patients with left ventricular dysfunction. Decrease preload Decrease effects of peripheral vasoconstrictors.
Direct vasodilators sodium nitroprusside, nitroglycerin, hydralazine. all three produce nitric oxide.
nipride aka sodium nitroprusside produces arterial and venous relaxation
Nitro relaxes venous more than arterial
hydralazine relaxes arterial
nitric oxide aka NO affects cardiovascular tone, via gas pulmonary vascular relaxation. negative inotrpoic and chrono. bronchodiation VQ mismatch mediator.
NO and Platelets inhibits aggregation activated platelet guanylate cyclase decreases intracelluar Ca.
NO and Nervous system is relases in response of N-MDA receptor. involved in antinociception and modulation of anesthetic effects.
NO when inhaled pulmonary vasodilatioin, NOT systemic. During bypass pulmonary hypertension can cause endothelial destruction NO at 20ppm used to treat. Preop assessment of reversible pulm HTN establish need for cardiac or lung transplant.
Nipride aka sodium nitroprusside uses emergency HTN, controlled hypoten, acute pulm Edema. onset in seconds, duration 1-2min. decrease preload and afterload decrease filling pressure. LV volume decreased ie decrease myocardial O2 consumption
Nipride dose and toxicity Infusion 0.5mcg/kg/min titrate up to 10mcg/kg/min. Boluses of 1-2mcg blunt response to intubation. Mixed in D5 in water light sensative. can cause cyanide toxcity.
Nipride or SNP or sodium nitropursside metabolism takes electron from Fe of oxyhemoglobin makes unstable SNP radical and Fe+3 Methemoglobin. decomposes to 5 cyanide ions.
treatment and symptoms of cyanide toxicity tachyphylaxis, metabolic acid, mixed venous O2=Discontinue the gtt. give O2. treat acidosis with Sodium Nitrite3% 4-6mg/kg over 3-5min. it binds to cyanide ions.
another treatment for cyanide Sodium thiosulfate 150mg/kg over 15min can be given every 2 hours, converts cyanide to thiocynate.
NItroglycerine uses angina pectoris and ischemia. reduce BP, venodialtion increase venous capacitance ie decrease preload. lower cardiac filling, less O2 consumption and requirement.
nitro dose and steal can cause coranary steal in heart, and robinhood in brain. Dose 0.3mg sublingual up to 3 tab. reliefe 1-3 min lasts 30 min. IV is 1-2min onset up to 10min duration.
Nitro uses treat CHF, deliberate hypotension, relax smooth muscle of biliary tract and relief of narcotic induced biliary spasm. Dose: 5-10mcg/min coranary steal and cereberal robinhood
nitro mixed in 50mg in 250D5W
Hydralazine arterial relaxation, treat HTN, Dose 5-20mg Tachy as a result of decrease in BP. onset 15min. duration 2-4hours. Infusion 0.25-1.5mcg/kg/min
Created by: Rooz