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43 Cards in this Set
- Front
- Back
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How is absorption altered in critical care pts?
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-unpredictable
-gastric emptying, gastric motility can change -interactions with enteral feeding/ gastric tubes -GI injury/ disease (trauma, ulcers) USE IV ROUTE if possible |
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How is distribution altered in critical care pts?
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-relates to fluid/hydration status (Vd changes)
-dec albumin (dec protein binding-phenytoin) -inc acute phase proteins (a1-acid glycoprotein- lidocaine) |
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How is metabolism altered in critical care pts?
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-don't adjust, however may be dec.
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How is renal elimination altered in critical care pts?
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-dysfxn common (shock, sepsis, nephrotoxic drugs, HD, CVVH)
-burns/trauma will inc renal elim |
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What is the MOA of succinylcholine? What is the dose, onset, and duration of succinylcholine? How is it eliminated?
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MOA: binds and activates Ach receptors-> sustained depolarization (depolarizing)
Dose: 1.5mg/kg IV onset: 1min duration: 3-5min elim: rapidly hydrolyzed by serum pseudocholinesterase |
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When is succinylcholine used?
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-Rapid sequence intubation (RSI)
-acute short procedure -placement of endotracheal tube |
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What are the ADRs of succinylcholine?
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-apnea
-muscle fasciculations- deep, aching muscle pain (CI in burn, trauma, upper motor neuron disease pts) -hyperkalemia -inc intracranial pressure -inc intraocular pressure |
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How do nondepolarizing NMBA's work?
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-competitively block the action of Ach
-can be reversed (neostigmine, edrophonium) |
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What is the onset, duration, elim, and ADRs of pancuronium?
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Onset: slow
Duration: long (90-100min) Elim: R(45-70%) H (10-15%) ADR: vagolytic;> tachycardia |
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What is the onset, duration, elim, and ADRs of vercuronium?
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Onset: slow/ intermed
Duration: intermed (35-45min) Elim: R(15-50%) H(35-50%) B(30-50%) ADR: none listed |
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What is the onset, duration, elim, and ADRs of rocuronium?
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Onset: rapid
Duration: intermed (30min) Elim: R(33%) B(<75%) ADR: vagolytic at high dose |
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What is the onset, duration, elim, and ADRs of atracurium?
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Onset: intermed
Duration: intermed (25-35min) Elim: Hoffman ADR: histamine release-> sz |
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What is the onset, duration, elim, and ADRs of cistracurium?
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Onset: intermed
Duration: intermed (45-60min) Elim: Hoffman ADR: none listed |
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Why are nondepolarizing NMBAs used?
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-mechanical ventilation
-muscle relaxation in operative settings -RSI if CI to succinylcholine -Manage inc ICP (however prevents neurologic exam) -treat muscle spasms in refractory conditions (tetanus, drug overdose, sz; caution if sz) -dec oxygen consumption (controversial) |
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What are the adverse effects of non-depolarizing NMBAs?
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-pts feel pain/anxiety, but unable to communicate
-prolonged paralysis (prolonged recovery, acute quadriplegic myopathy syndrome, drug holidays dec incidence) -corticosteroids, NSAIDs -immobility (need eye drops, etc) |
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What should be monitored on sustained NMBAs
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-peripheral nerve stimulation of ulnar nerve (toxicity endpt)
-dose adjust to 1-2 twitches |
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What is stress related mucosal disease/ bleeding (SRMD/ SRMB)?
What is the pathophysiology? |
-superficial lesions commonly involving the mucosal layer of the stomach following major physiologic stress
-hypotension, dec cardiac outpt, vasoconstriction, free radicals, reperfusion injury, proinflammatory cytokines -> ischemia of gastric mucosa -> dec HCO3 secretion, dec mucosal blood flow, H+ back diffusion, dec GI motility |
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What is the difference in the clinical presentation of SRMD and PUD?
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-SRMD: multiple lesions, superficial, located prox. stomach, perforation rare, BLD from superficial capillaries, bleeding late in course, more congestion, bleeding than NSAID lesions
-PUD: few lesions, deep, located duodenal bulb, perforation common, BLD from one vessel |
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What are the 3 main risk factors for SRMB?
What are other risk factors? |
- mechanical ventilation/ respiratory failure
-recent hx of GIB/ ulcer -coagulopathy Others: sepsis, mult organ failure, hepatic failure, renal insufficiency, ICU stay>1wk, hypotension/shock, organ transplant, mult trauma/ neurotrauma, major surgery, occult bleeding>6days; drugs (anticoagulants, glucocorticoids, ulcerogenic drugs?) |
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What pH do we maintain to reduce SRMD/ SRMB?
What may this lead to? |
-3.5-4.0
-nosocomial pneumonia and aspiration |
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How does sucralfate work?
What are the ADRs? |
-forms protective barrier
-potential antibacterial properties -does not inc gastric pH ADRs: clogging of tubes, drug interactions, bezoar formation (globs together and causes obstruction) |
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Why are H2RAs used for SRMD?
What are the ADRs? |
-flexible dosage forms (IV, po/enteral)
-ADRs: minimal, colonization/pneumonia, drug interactions, tachyphylaxis, thrombocytopenia (rare) |
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Why are PPIs used for SRMD?
What are the ADRs? |
-profound acid suppression
-no tachyphylaxis ADRs: pneumonia, inc risk of C.diff, cost, formulation/admin issues (enteric coated, limited data for IV use) |
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How is enteral feeding used for SRMD?
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-controversal, may offer some protection
-may be used as primary prophylaxis, but not best idea |
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When should PPI/H2RA be d/c for prophylaxis?
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-probably when moved from ICU
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What is agitation?
What causes agitation? |
-state of anxiety accompanied by motor restlessness
-sx of underlying disorder |
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What is delirium?
What triggers delirium? |
-temporary state of mental confusion
-sepsis, hypoglycemia, hyponatremia, other endocrine disorders, altered sleep/wake cycle, metastatic diseases of brain, head injury, CNS infections, drugs (sedative, analgesics) |
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What are the consequences of pain?
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-agitation
-inc sympathetic nervous system activation, raises catecholamine levels -inc oxygen consumption -hypermetabolic response -long term emotional and social consequences (PTSD) |
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How can oversedation be problematic?
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-inc time on mechanical ventilation
-inc ICU and hospital length of stay -obscure neurological function testing |
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How is sedation assessed?
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-subjective -no gold std
-Ramsey scoring system (6pt) -Riker Sedation-Agitation scale (7 item, 7pts) -Richmond Sedation-Agitation scale (10pt) -Objective -Bispectral index (100pts=awake) |
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How is delirium assessed?
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-ICDSC: high sensitivity, mod specificity (8 item, 0-8; 8=delirium)
-CAM-ICU: high sensitivity and specificity, high inter-rater reliability |
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What is the MOA of BZDs?
Why are they used in critcal care pts? What are the adverse effects? |
-bind and inh GABA
-anxiolytic, hypnosis, antegrade amnesia -ADR: respiratory depression, CV effects (hypotension, tachycardia), withdrawal, potential association w/ delirium (lorazepam) |
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What are some advantages and disadvantages of diazepam for sedation?
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A: fast onset, minimal CV effects, easy to taper since long t1/2
D: long t1/2, CYP 2C19 met, causes phlebitis |
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What are some advantages and disadvantages of lorazepam for sedation?
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A: flexible dosage (IV, po, IM), predictable sedation length, few drug interactions
D: prolonged in liver disease/ end stage renal failure, delayed onset, association with development of delirium, IV formulation contains propylene glycol |
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The IV formulation of lorazepam contains what solvent? What may this cause? How is it monitored?
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-propylene glycol
-lactic acidosis, nephrotoxicity at high dose or prolonged infusion -measure osmol gap osm gap=measured osm-(2Na)+(BUN/2.8)+ (glu/18) >10=toxicity |
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What are some advantages and disadvantages of midazolam for sedation?
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A:rapid onset, works well for procedural sedation,
D: unpredictable t1/2 (prolonged in renal disease), CYP 3A4 interactions, only used for short-term use |
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What is flumazenil? What are some possible adverse effects of this drug?
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-BZD antagonist
-ADR: precipitate BZD withdrawal, sz |
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What are some advantages and disadvantages of propofol for sedation?
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A: rapid onset and offset, provides antegrade amnesia, highly titratable (no changes with renal/hepatic damage), may reduce ICP
D: emulsion can cause hypertriglyceridemia (check 48 hr and periodically), req dedicated IV catheter, inc risk of infection (change bag q12h), apnea, hypotension, bradycardia, pancreatitis, sz/ neuroexcitatory syndrome, propofol infusion syndrome (acidosis, rhabdomyolysis, hypotension, arrhythmias), EDTA causes electrolyte abnormalities, withdrawal |
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What should be monitored with propofol infusion?
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-triglycerides
-CK -LFTs -metabolic acidosis -bradycardia -hypotension |
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What are the advantages and disadvantages of dexmedetomidine?
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A: analgesic effect, no respiratory depression, less delirium
D: significant CV effects (bradycardia, hypotension-esp if volume depleted), impairment of elim in hepatic dysfunction |
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What are the advantages and disadvantages of haloperidol in delirium/ pyschosis?
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A: mild sedation w/o analgesia or amnesia, minimal changes in HR, BP, ventilation, long t1/2, IV/PO
D: prolongation of QT interval (measure daily), dec sz threshold, possible EPS, NMS (altered consciousness, tachycardia, diaphoresis, muscle rigidity, granulocytosis, anxiety, tachypnea, hyperthermia, inc CPK, hyperglycemia) |
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What atypical antipyschotics are used for delirium? What are some advantages and disadvantages of using atypicals over haloperidol for delirium?
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-risperidone (Risperdaol)
-olanzapine (Zyprexa) -quetiapine (Seroquel) -Abilify and Geodon used, not studied A: less QT prolongation, fewer EPS D: limited data, tapering up, olanza (NMS, hypotension), higher mortality in 1 study |
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What addition sedation guideline protocols are used?
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daily interruption of sedative infusion (dec mechanical ventilation and length of ICU stay)
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