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TopDrawer
Kay's Top Drawer Lecture Barry
| Question | Answer |
|---|---|
| Propofol's MOA | Stimulation of GABA, highly lipid soluble therefore quick onset and short duration. |
| True or Flase. Propofol is indicated for induction, sedation, outpatient anesthesia, but significant N/V effects. | False. Propofol is indicated for induction, sedation, outpatient anesthesia, and has antiemetic qualities. |
| Since Propofol contains soybean oil, glycerol and egg lecithin, it should not be given to anyone with what allergy? | Egg allergy. |
| How can we reduce Propofol's significant pain/burning on injection? | Give with Lidocaine, give slowly into large vein. |
| Since Propofol can support bacterial growth, we should always use sterile technique and throw it away (blank) hours after opening. | Six. |
| Why does Propofol decrease HR and BP? | It decreases SVR and CO. |
| We should not use Propofol for patients with these cardiac conditions: | CV collapse, hypovolemia, or labile BP. |
| The amount of respiratory depression caused by Propofol depends on... | The dose of Propofol we gave. |
| Propofol decreases ICP(intracranial pressure) by decreasing what other factor? | CBF(cerebral blood flow). |
| Propofol is a common induction drug. What is the induction dose? | 1.5-2mg/kg for IV induction. |
| Propofol is often used as a continuous infusion for sedation. What is our dose for sedation? | 50-200mcq/kg/min IV infusion for sedation. |
| Propofol has a quick onset. How quick? | Less than one minute. |
| What is Propofol's duration? | < 10 minutes. |
| Simply, how is Propofol metabolized? | Hepatic, with renal excretion. |
| Ketamine is a dissociative anesthetic. What is its MOA? | Interacts with NMDA receptors, opiod receptors, monoaminergic receptors, muscarinic and voltage-sensitive calcium receptors; causes direct stimulation of the CNS to inhibit norepinephrine re-uptake into post ganglionic nerve endings to stimulate the SNS. |
| What are the four indications for using Ketamine? | general anesthesia, CV collapse, sedation for mentally challenged. |
| Ketamine is a derivative of what commonly abused street hallucinogenic? | Phencyclidine(PCP). |
| How does Ketamine compare to Phencyclidine(PCP)? | It is 1/10th as potent, but both cause hallucinations. |
| How do we pre-treat potential hallucinations from Ketamine? | We give it with a Benzo(Versed). |
| True or false: Ketamine is an excellent drug for induction but does not have any analgesic effects. | False. Ketamine causes profound analgesia. |
| True or false: Ketamine has an active metabolite, Norketamine that is 2 x as potent as Ketamine. | False: Norketamine is an active metabolite but is 1/3rd-1/5th as potent as Ketamine. |
| True or false: Ketamine's effects on the cardiovascular system include causing an increase in BP, HR, CO, PAP, CVP, and CI. | True. |
| Ketamine crosses the blood-brain barrier. How does it increase ICP? | It is a cerebral dilator. |
| Ketamine does not depress respirations, maintains upper airway reflexes, and is a bronchodilator. What is a big negative thing that it does to your airway? | Causes increased oral secretions. |
| Ketamine is often chosen for induction in children or uncooperative patients because in addition to the IV route, it can be given IM or PR. What are the induction doses for each? | For induction: 1-2mg/kg IV, 4-10mg/kg IM, 8mg/kg PR. |
| What is Ketamine's onset? | Onset: 30 sec IV, 3-4 min IM. |
| What is Ketamine's duration? | Duration: 5-10 mins IV, 15-25 mins IM |
| True or false: Ketamine is primarily metabolized via the kidneys. | False. Primary organ of Ketamine metabolism is the liver. |
| Thiopental(Pentothal)'s MOA is to activate (blank) and depress (blank). | GABA, RAS. |
| Thiopental(Pentothal) is a commonly used induction drug in what setting? | Obstetrics. |
| For what three conditions is Thiopental(Pentathol) contraindicated? | (AIP)Acute intermittent porphyria, variegate porphyria and (SA)status asthmaticus. |
| Thiopental(Pentothal) is contraindicated in the patient with AIP(acute intermittent porphyria. What is this disease? | the 2nd most common porphyria, AIP is a rare congenital metabolic disorder affecting the production of heme, the oxygen-binding prosthetic group of hemoglobin. It is characterized by a deficiency of the enzyme porphobilinogen deaminase. |
| True or false: Thiopental(Pentothal) causes a higher incidence of N/V. | True. |
| Does Thiopental(Pentothal) release histamine? | Yes. |
| What is the induction dose for Thiopental(Pentothal)? | 3-5 mg/kg Adults. 5-6 mg/kg Children. |
| Thiopental(Pentothal) has a quick onset. How quick? | 30-60 seconds. |
| What is the duration of Thiopental(Pentothal)? | 5-30 minutes. |
| Simply, how is Thiopental(Pentothal) metabolized? | Hepatic/renal. |
| Etomidate(Amidate) causes induction by mimicing the inhibitory action of GABA and... | Depressing RAS. |
| For what patient population is Etomidate(Amidate) particularly indicated? | Patients with volume depletion and/or impaired CV function. |
| Etomidate(Amidate) is dissolved in propylene glycol causing what SE? | Pain on injection. |
| True or false: Etomidate(Amidate) is an antiemetic? | False. It causes N/V. |
| Long-term use of Etomidate(Amidate) can cause what SE? | Adrenocortical suppression. |
| Myoclonic movements brought on by Etomidate(Amidate) can be lessened by pre-treating with what drugs? | Opioids/benzos. |
| Etomidate(Amidate) decreases CBF(cerebral blood flow), ICP(intracranial pressure), and CMR(blank). | Cerebral metabolic rate. |
| What is the induction dose of Etomidate(Amidate)? | 0.2-0.6 mg/kg IV. |
| What is onset time for Etomidate(Amidate)? | 30-60 sec |
| Etomidate's duration? | 3-5 minutes. |
| True or False: Metabolism of Etomidate(Amidate) consists of plasma esterase/hepatic mircosomal enzymes cause rapid breakdown to active metabolites with renal excretion. | False. plasma esterase/hepatic mircosomal enzymes cause rapid breakdown to INACTIVE metabolites with renal excretion. |
| List the three aminosteroid nondepolarizing muscle relaxants. | Rocuronium, Vecuronium, Pancuronium. |
| List the three benzolisoquinoline nondepolarizing muscle relaxants. | Mivacurium, Atracurium, Cisatracurium |
| What are the two types of nondepolarizing muscle relaxants? | Aminosteroid and benzolisoquinoline. |
| True or false: Nondepolarizing muscle relaxant's MOA is: competes with Acetylcholine(Ach) for binding to nicotinic receptor alpha subunits to cause muscle relaxation, competitive antagonist of Ach. | True. |
| At physiologic pH, are the aminosteroid nondepolarizing muscle relaxants ionized or unionized? What does this mean? | Ionized, low lipid solubility. |
| True or false: due to their low lipid solubility, aminosteroid nondepolarizing muscle relaxants do not cross the blood-brain barrier. | True. |
| True or false: aminosteroid nondepolarizing muscle relaxants have a high histamine release and a low volume of distribution. | False. They have a LOW histamine release and a low volume of distribution. |
| Rocuronium(Zemuron) is a nondepolarizing aminosteroid muscle relaxant of intermediate duration. Why would this drug be given before Sux? | To prevent fasiculation. |
| What are the intubating doses of Rocuronium(Zemuron)? | 0.6mg/kg, 1.2mg/kg for RSI. |
| What is the defasiculating dose of Rocuronium(Zemuron) when it is given prior to Sux? | 5mg. |
| What are the onset and duration times for Rocuronium(Zemuron)? | Onset: 1-2 min (dose dependent); duration: abt 30 minute. |
| Vecuronium(Norcuron)is an intermediate NMB, no histamine release, no effect on BP, HR, Cardiac stability. It may precipitate if given with what drug? | Thiopental. |
| What is the dose of Vecuronium(Norcuron)? | 0.08-0.12 mg/kg IV. |
| Pancuronium(Pavulon) is a long acting NMB without histamine release. What causes its mild increase of HR and subsequent increase in BP? | Antimuscarinic stimulation. |
| Due to its antimuscarinic stimulation, Pancuronium(Pavulon) should not be used in patients with IHSS(idiopathic hypertrophic subaortic stenosis). What is another term for this condition? | Hypertrophic obstructive cardiomyopathy. |
| What is the dose of Pancuronium(Pavulon)? | 0.08-0.12 mg/kg. |
| What are the onset, peak, and duration times for Pancuronium(Pavulon) | Onset: 2-3 min; duration: 60-100 min. |
| How are the benzolisoquinolines metabolized? | Hofmann Elimination, ester hydrolysis, plasma cholinesterase metabolism. |
| Most benzolisoquinolines cause changes in HR and BP because they release... | Histamine. |
| Mivacurium(Mivacron), a short acting benzolisoquinoline NMB causes histamine release and bronchoconstriction. It is metabolized by plasma(pseudo)cholinesterase just like what depolarizing muscle relaxant? | Succinylcholine. |
| Mivacurium(Mivacron) is given in divided doses to minimize histamine release. What will the total dose be? | 0.15-0.25 mg/kg . |
| What are onset and duration times for Mivacurium(Mivacron)? | Onset: 2 minutes; duration: 20-30 min. |
| Atracurium(Tracrium) is an intermediate acting NMB, Hofmann elimination/ester hydrolysis, small histamine release, minimal BP changes or reflex tachycardia. Its primary metabolite is Laudanosine, which can cause what? | Seizure activity(rare). |
| What is the dose of Atracurium(Tracrium)? | 0.3-0.6mg/kg IV. |
| What are the onset and duration times for Atracurium(Tracrium)? | Onset: 2-3 min; duration: 20-35 min. 95% recovery in 60-70 min |
| Cisatracurium(Nimbex) is an intermediate/long acting benzolisoquinoline NMB that undergoes Hoffman elimination. What makes it a good choice for longer cases, cardiac and renal? | No changes in BP/HR, no histamine release(unlike many other benzolisoquinolines) |
| What is the dose of Cisatracurium(Nimbex)? | 0.15-0.2mg/kg IV. |
| What are the onset and duration times for Cisatracuriium(Nimbex)? | Onset: 2-3 min; peaks 3-5 mins duration: 40-70 min.20-35 min to begin recovery: up to 93 min for 90% return. |
| True or false: Succinylcholine(Anectine or SCH) is the only depolarizing NMB in use in America. | True. |
| True or false: Succinylcholine's MOA is that it binds to the alpha subunits of muscarinic cholinergic receptors, this allows sodium/calcium influx and potassium efflux, resulting in depolarization of the muscle. | False. Succinylcholine's MOA is that it binds to the alpha subunits of NICOTINIC cholinergic receptors, this allows sodium/calcium influx and potassium efflux, resulting in depolarization of the muscle. |
| After onset of Succinlycholine, the receptor remains depolarized until... | Succinylcholine diffuses away from it. |
| Succinylcholine mimics the action of what endogenous ligand? | Acetylcholine. |
| Succinylcholine is an Acetylcholine receptor agonist or antagonist? | Agonist. |
| True or false. Major indications for using Succinylcholine are: rapid muscle relaxation, very short cases, OB, RSI, Laryngospasm, full stomachs, bad airways, MH patients. | False. Major indications for using Succinylcholine are: rapid muscle relaxation, very short cases, OB, RSI, Laryngospasm, full stomachs, and bad airways. However Sux CAUSES MH!!! |
| True or false. Succinylcholine is a triggering agent for MH. | True. |
| Succinylcholine can cause what electrolyte abnormality? | Hyperkalemia. |
| Dibucaine is a local anesthetic that will inhibit normal plasma cholinesterase activity by about... | 80%. |
| What is a normal Dibucaine number? | 80. |
| What does an abmormal Dibucaine number(below 60) indicate? | Atypical plasma cholinesterase. Patient will have a prolonged block from Succinylcholine or any other drug that is mainly metabolized by pseudocholinesterase. |
| If pt's Dibucaine number is 40-60, what does she have? | Heterozygous atypical enzyme. |
| A patient with heterozygous atypical enzyme(Dibucaine number 40-60) will experience what kind of reaction to Succinylcholine? | A prolonged block of 20-40 minutes. |
| If a pt's Dibucaine number is below 20, what does she have? | Homozygous atypical enzyme. |
| What does the Dibucaine number indicate? | The % of inhibition of pseudocholinesterase activity. |
| What is a phase II block? | Inhibition of nerve impulse transmission across the myoneural junction unaccompanied by depolarization of the motor end plate. |
| What causes pain after patients receive Succinylcholine? | Pain is caused by muscle fasiculations. |
| What three pressures does Succinylcholine increase? | Intraocular pressure, intragastric pressure, intracranial pressure. |
| Why can it be difficult to open your patient's jaw after administering Succinylcholine? | Sux can cause masseter muscle rigidity leading to insufficient relaxation of jaws. |
| Does Succinylcholine release a lot of histamine? | No, it causes minimal histamine release. |
| Why does Succinylcholine cause a decrease in HR? | Muscarinic stimulation. |
| Children have a higher risk of Succinylcholine-induced hyperkalemia. What can cause Succinylcholine-induced cardiac arrest in children? | Undiagnosed myopathies. |
| True or false: use Succinylcholine with caution in burns. | True. |
| Succinylcholine should be used with caution in any condition that causes an increase in... | Potassium. |
| After Succinylcholine diffuses away from the neuromuscular junction, it is hydrolyzed in the plasma and liver by... | Plasma cholenesterase, aka pseudocholinesterase. |
| What is the weak active metabolite of Succinylcholine called? | Succinylmonocholine. |
| Low levels of pseudocholinesterase will do what to your Succinylcholine block? | Prolong it. |
| What is the IV dose of Succinylcholine? | 1-1.5 mg/kg IV. |
| To prevent excessive muscle fasiculations, what do we often pretreat with before administering Succinylcholine? | 5mg of Rocuronium(Zemuron). |
| Onset/duration of Succinylcholine? | Onset: 30-60 seconds IV; 2-5 mins IM duration: very short, 4-6 min IV. 10-30 minutes IM. |
| What is the dose of Succinylcholine for laryringospasm? | 20mg IV. |
| Reversal agents are also called... | Cholinesterase inhibitors. |
| How do cholinesterase inhibitors work to reverse neuromuscular blockade? | By inhibiting the enzyme that breaks down Ach, they iindirectly increase the amount of Ach to compete for the receptor sites (nicotinic) as the NMB dissociates and diffuses away from the NMJ to restore nueromuscular funtion. |
| Cholinesterase inhibitors allow additional acetylcholine to be available to compete for binding sites at the nicotinic receptors(NMJ). However increased levels will also lead to unwanted... | Muscarinic stimulation. |
| Too-high levels of Ach will affect receptors in the CV, Resp, and GI systems. What are its effects? | Bradycardia, bronchospasm, and N/V. |
| What do we give to prevent cholinesterase inhibitor-induced over-stimulation of the muscarinic receptors by too much Ach? | An anticholinergic. |
| Anticholinergics have the greatest affinity for which receptors, nicotinic or muscarinic? | Muscarinic. |
| Because anticholinergics have the greatest affinity for muscarinic receptors, they are also called... | Antimuscarinics. |
| What are the three reasons to give a cholinesterase inhibitor? | 1. NMB reversal 2. diagnose and treat myasthenia gravis 3. treat central anticholinergic syndrome |
| Main goal of reversal is to maximize nicotinic transmission and minimize... | Muscarinic side effects. |
| Cholinesterase inhibitors can cause SLUD. What does that stand for? | Salivation, lacramation, urination, salivation. |
| What can too much cholinesterase inhibitors do to the airway? | Cause bronchial secretions, bronchospasm/constriction. |
| How do cholinesterase inhibitors slow HR? | They cause slow conduction velocity of the cardiac impulse through the AV node. |
| Physostigmine crosses the BBB, which causes what? | CNS excitement. |
| True or false: excessive doses of cholinesterase inhibitor might potentiate NMB. | True. |
| Neostigmine(Prostimine) inhibits hydrolysis of Ach by acetylcholinesterase. For each 1mg that we give, how much glycopyrolate should we mix in the same syringe? | 0.2 mg. |
| Neostigmine(Prostimine) is rapid and effective for reversing profound NMB. What organ metabolizes it? | The liver. |
| What is the dose of Neostigmine(Prostimine)? | 0.04-0.08mg/kg. |
| What is the max dose of Neostigmine(Prostimine)? | 5mg. |
| The onset of Neostigmine(Prostimine) is | 1-20 minutes. |
| What is the duration of Neostigmine(Prostimine)? | 1-2 hours |
| Which anticholinergic do you give with Neostigmine(Prostimine)? | Glycopyrolate. |
| Endrophonium(Tensilon, Enlon) is used to reverse short acting NMB. What antocholinergic is it given with? | Atropine. |
| How does Endrophonium(Tensilon, Enlon) work? | Decreases Acetylcholinesterase at sites of cholinergic transmission. |
| What is Enlon Plus? | A mixture of edrophonium and atropine together in the same vial. |
| What is the dose of Endrophonium(Tensilon, Enlon) with Atropine? | 0.25-1 mg/kg IV with atropine 0.014 mg per 1 mg of edrophonium. |
| Onset/duration of Endrophonium(Tensilon, Enlon)? | Onset: 1-2 min; duration: 5-20 minutes. |
| Pyridostigmine(Reginol) is used to reverse NMB. How does it work? | Inhibits the breakdown of acetylcholine by acetylcholinesterase. |
| What is the dose of Pyridostigmine(Reginol) with Atropine? | Dose: 10-20 mg IV with atropine 0.6-1.2 mg IV. |
| Why is Physostigmine(Antilirium) not used very often for reversal? | It easily crosses blood-brain barrier, exacerbates Parkinsonian symptoms. |
| We don't normally use the cholinesterase inhibitor Physostigmine(Antilirium) for reversal. What is it indicated for? | It is used to treat central anticholinergic syndrome (Atropine toxicity). |
| Dose/onset/duration of Physostigmine(Antilirium)? | Dose: 0.01-0.03 mg/kg IV; onset: 3-5 min; duration; 30min-5hrs. |
| You can have full TOF with how much receptors still blocked? | 75%. |
| Which muscles are more resistant to block: facial muscles (orbicularis oculi), or those innervated by the ulnar nerve (adductor pollicis muscle)? | Adductor Pollicis muscle. |
| What are five factors that can delay or inhibit antagonism of blockade(reversal)? | 1. Hypothermia 2. profound block 3. respiratory acidosis 4. certain antibiotics 5. hypokalemia/hypomagnesium |
| Atropine is a competitive Ach antagonist. Where does it act? | At central and peripheral muscarinic receptors. |
| What are the three indications for giving Atropine? | Reversal, decreasing secretions, brady arrythmias. |
| True or false: Atropine crosses the blood-brain barrier, is contraindicated in narrow-angle glaucoma, decreases intestinal motility, and causes miosis. | False. Atropine crosses the blood-brain barrier, is contraindicated in narrow-angle glaucoma, decreases intestinal motility, and causes mydriasis. |
| What is the dose of Atropine? | dose: 0.01 mg/kg in combo with Edrophonium. |
| Onset/duration of Atropine? | Onset: less than 1 min; duration: 2-4 hours. |
| How does Atropine leave the body? | Hepatic/renal elimination. |
| Glycopyrolate is a synthetic muscarinic, acting as a competitive Ach antagonist. Where does it act? | On the peripheral muscarinic receptors. |
| What is Glycopyrolate used in combination with for reversal? | Neostigmine. |
| Why is Glycopyrolate unlikely to cause CNS toxicity? | It does not cross the blood-brain barrier. |
| What is the dose of Glycopyrolate? | 0.2 mg per 1 mg Neostigmine. |
| Onset/duration of Glycopyrolate? | Onset: 1-2 min; duration: 3-7 min |
| Glycopyrolate is eliminated the same way as Atropine, which is how? | Hepatic/renal. |
| Scopolamine is a competitive antagonist of acetylcholine at muscarinic receptors, what else does it antagonize? | Serotonin and histamine. |
| How do we use Scopolamine? | To decrease secretions, as an antiemetic, and for motion sickness/vertigo. |
| What is the dose of Scopolamine? | Dose: 0.2-0.6 mg IM/IV before surgery; patch. |
| How does Ephedrine act? | DIRECT stimulation of alpha-1, beta-1 and some beta-2, INDIRECT endogenous release of norepinephrine. Adrenergic agonist, sympathomimetic amine. |
| What are the four factors Ephedrine will increase? | BP, HR, CO and contractility. |
| What makes Ephedrine the vasopressor of choice in OB? | It increases maternal BP, but has very little effect on uterine blood flow. |
| True or false: Ephedrine has an antiemetic effect, and is a bronchodilator. | True. |
| Tachyphylaxix is a rapid decrease in the response to a drug after repeated doses over a short period of time. What pressor does this occur in? | Ephedrine. |
| Careful when using Ephedrine in CAD. What conditions is it contraindicated for? | MAO inhibitors, IHSS, pheochromocytoma, closed angle glaucoma. |
| What is the dose of Ephedrine? | Titrated to effect. |
| How is Ephedrine mixed? | Mix 1 vial (50 mg) in 9 cc of NS to make a 5 mg/cc concentration, also premixed syringes. |
| Onset/duration of Ephedrine? | Onset: almost immediate; duration: 3-10 min. |
| How do you give Ephedrine for antiemetic effect? | 25 mg with Vistaril 25 mg in one syringe (1cc) IM about 20 min before the end of surgery. |
| How does Phenylephrine(Neosynephrine) work? | Directly stimulates the alpha-1 receptors, minimal stimulation of beta-1 and alpha-2 at high doses. |
| What are the indications for giving Phenylephrine(Neosynephrine)? | Treat hypotension, decrease CO in patients with ischemic heart disease, treat symptoms in tetralogy Fallot. |
| What are the effects of administerine Phenylephrine(Neosynephrine)? | Vasoconstriction, increase BP, reflex decrease in HR, increase coronary blood flow. |
| How do you mix Phenylephrine(Neosynephrine)? | Mix 0.1 cc(10 mg/cc vial) in 10 cc NS. |
| What is the dose of Phenylephrine(Neosynephrein)? | 50-100 mcg titration. |
| How does Hydralazine(Apresoline) work to bring down BP? | Direct vasodilation of vascular smooth muscle, decrease precapillary arteriolar resistance, VASODILATOR. |
| What are the indications for Hydralazine(Apresoline)? | Decrease SVR by relaxing arterioles, decrease PVR and BP, increase HR and CO. |
| How is Hydralazine(Apresoline) used in pregnancy? | Used after Labetalol in pregnancy with PIH(pregnancy-induced hypertension) to decrease BP while increasing uterine blood flow. |
| What is the dose of Hydralazine(Apresoline)? | 2.5-5 mg boluses every 15 min. |
| What is the max dose of Hydralazine(Apresoline)? | 20-40 mg. |
| Onset/duration of Hydralazine(Apresoline)? | Onset: 10-15 min; duration: 2-6 hours. |
| What is Labetolol(Trandate)? | Nonselective Beta-1 and Beta-2 with alpha-1 antagonist, primarily considered a BETA BLOCKER. |
| What is Labetolol(Trandate) indicated for? | Acute and chronic HTN in pregnant patients, treat increases in BP and HR from stimulation (intubation). |
| What drug has a faster onset: Hydralazine or Labetolol? | Labetolol. |
| How does Labetolol(Trandate) affect the plasma renin system? | It decreases it. |
| How does Labetolol-induced BP reduction affect CO and PVR? | It decreases them. |
| Does Labetolol(Trandate) cause rebound HTN? | No. |
| What is the dose of Labetolol(Trandate)? | 5-10 mg titrated boluses IV. |
| What is the max dose of Labetolol(Trandate)? | 300 mg. |
| Onset/duration of Labetolol(Trandate)? | Onset: 1-2 min; duration: 2-3 hours. |
| How does Esmolol(Breviblock) decrease the force and rate of contractions? | It is a selective beta-1 antagonist. |
| What are the indications for Esmolol(Breviblock)? | Treatment of perioperative tachycardia, HTN, acute MI; good for decreasing HR during intubation/extubation. |
| Esmolol(Breviblock) has a very short duration of action. What does it do in the body? | Decrease HR, CO and some decrease in BP, no rebound effects. |
| When is Esmolol(Breviblock) contraindicated? | Brady, heart block, cardiogenic shock and heart failure. |
| Onset/duration of Esmolol(Breviblock)? | Onset: rapid; duration; 30 min. |
| How is Esmolol(Breviblock) dosed? | Dose: 10 mg boluses, .5-1 mg/kg bolus then 10-300 mcg/kg/min infusion for hypotensive technique. |
| How does Esmolol(Breviblock) leave the body? | Metabolized rapidly by esterases in the cytosol of red blood cells, rapid redistribution, urinary excretion. |
| Propanolol(Inderal) is a Beta-1 and Beta-2 antagonist. What is it indicated for? | HTN, angina, IHSS (idiopathic hypertrophic subaortic stenosis), pheochromocytoma, acute MI. |
| What does Propanolol(Inderal) do? | Decrease BP due to decrease in myocardial contractility, HR, CO therefore a decrease in myocardial oxygen demand; bronchospasm, AV block and bradycardia, withdrawal syndrome (can get upregulation of Beta receptors, increase in BP, HR and chest pain. |
| What is the dose of Propanolol(Inderal)? | 0.5 mg every 3-5 min, titrate to desired effect. |
| What is the max dose of Propanolol(Inderal)? | 0.15 mg/kg. |
| Onset/duration of Propanolol(Inderal)? | Onset: < 2 min; duration: < 10 min. |
| Reglan(Metoclopramide) is an antiemetic. How does it work? | Gastrointestinal prokinetic, benzamide, D2 dopamine antagonist in CTZ (centrally), blocks dopamine in the GI tract (peripherally). |
| How does Reglan(Metoclopramide) work as an antiemetic? | Blocks dopamine receptors and also blocks serotonin receptors in the CTZ of the CNS (in higher doses). |
| Reglan(Metoclopramide) enhances response to Ach of tissues in upper GI tract, what does this cause? | Enhanced motility and accelerated gastric emptying. |
| Reglan(Metoclopramide) increases lower esophageal sphincter tone, what does this cause? | Speeds gastric emptying and lowers gastric volume. |
| Indications for Reglan(Metoclopramide)? | Preop for aspiration prophalaxis (GERD or Diabetic), antiemetic effect (blocks dopamine receptors). |
| What are some side effects of Reglan(Metoclopramide)? | Causes sedation, restlessness and extrapyramidal symptoms from dopamine antagonism, hypotension. |
| What are contraindications for Reglan(Metoclopramide)? | Bowel obstructions, parkinsons, elderly, epilepsy, pheochromocytoma. |
| Dose for Reglan(Metoclopramide)? | 10-20 mg IV in preop. |
| Onset/duration for Reglan(Metoclopramide)? | Duration: 1-2 hours; onset: 1-3 min. |
| Pepcid(Famotadine) is an H2 receptor antagonist. Where does it act? | Competitive inhibition of histamine at H2 receptors of the gastric parietal cells. |
| Pepcid competitively inhibits histamine at H2 receptors of the gastric parietal cells. What does this cause in the body? | Inhibits gastric acid secretion and raises gastric pH (effects gastric acid produced after the Pepcid is given). |
| Why aren't the effects of Pepcid(Famotadine) immediate? | Because it only effects gastric acid produced after the Pepcid is given. |
| Pepcid(Famotadine) decreases gastric volume and increases gastric... | pH. |
| Pepcid(Famotadine) is given in preop to decrease risk of aspirational pneumonia, and for what patients? | Pts with GERD, Peptic Ulcer Disease. |
| What are some SE of Pepcid(Famotadine)? | Dizziness and headaches. |
| What is the IV dose of Pepcid(Famotadine)? | Dose: 20 mg IV. |
| Onsed/duration of Pepcid(Famotadine)? | Onset: 1-2 hours; duration: 10-12 hours. |
| Zofran(Odansetron) is a selective 5-HT3 receptor antagonist, blocks the N/V receptors where? | specific 5-HT3 serotonin receptors in the CTZ(chemoreceptor trigger zone). |
| When do we use Zofran(Odansetron)? | Preventive and rescue treatment for N/V, used in chemo. |
| What are some SE of Zofran(Odansetron)? | Can cause headaches, constipation, increase in liver enzymes. |
| Zofran(Odansetron) is free from extrapyramadal effects, sedation or respiratory depression. Why? | Because it has NO effect on dopaminergic, cholinergic or histaminergic receptors. |
| Dose for Zofran(Odansetron)? | 4 mg IV in preop, intraop or postop. |
| Onset/duration for Zofran(Odansetron)? | Onset: 30 min; duration: 4-6 hours. |
| Anzemet(Dolasetron) is a 5-HT3 receptor antagonist. Where does it act? | On the N/V specific receptors in the CTZ(chemoreceptor trigger zone). |
| Anzemet(Dolasetron) is a pretreatment for what condition? | Nausea/vomiting. |
| Headaches are a possible SE of Anzemet(Dolasetron). A breakdown product of this drug can do what to the heart? | Can cause prolonged QT interval and should be used carefully in patients on antiarrhythmics or prolonged QT. |
| Dose of Anzemet(Dolasetron)? | Dose: 12.5 mg preop or intraop. |
| Onset/duration of Anzemet(Dolasetron)? | Onset: 20-30 min; duration: 4-6 hours. |
| Phenergan(Promethazine) is a phenothiazine. How does it work? | Exerts its antiemetic effect by blocking dopamine D2 receptors in CTZ. |
| Phenergan(Promethazine) is a rescue drug for N/V, what else is it sometimes used for? | Anxiety. |
| Phenergan(Promethazine)causes sedation and hypotension, will increase the sedative effects of benzos and opiods. What is its extrapyramidal effect? | Akathisia(restlessness). |
| What is the IV dose of Phenergan(Promethazine) and how is it given? | dose: 12.5-25 mg IV (should be diluted in at least 10 cc of LR and given in top port slowly). |
| Onset/duration of Phenergan(Promethazine)? | Onset: 3-5 min; duration: 4-6 hours. |
| Decadron(Dexamethasone) is a corticosteroid what is its mode of action in regards to N/V? | Found to enhance the effects of other antiemetics, inhibition of prostaglandin synthesis, release endorphins, positive psycho. effects, antiinflammatory. |
| What are some adverse effects of Decadron(Dexamethasone)? | Genital itching (hot feeling), hyperglycemia, adrenal suppression, lightheadedness, increase in liver enzymes. |
| Be careful when using Decadron(Dexamethasone) with this patient population. | Diabetics. |
| Dose/duration of Decadron(Dexamethasone)? | Dose: 4-8 mg IV on induction; duration about 24 hours. |
| What is Vistaril(Hydroxyzine) indicated for? | N/V, pruritus, antianxiety. |
| What are SE of Vistaril(Hydroxyzine)? | Sedation, pain on injection. |
| How is Vistaril(Hydroxyzine) administered? | 25 mg mixed with Ephedrine 25 mg IM 20 minutes before end of surgery (Careful using this mixture in Hypertensives). |
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