Exam 3 Flashcards

1
Q

What are the first 3 components of nutritional assessment?

A
  1. Risk Factors for Malnutrition - These pts need nutrition as EARLY as possible; Can use screening tools to determine risk
    - Under body weight (20% below IBW), involuntary weight loss of > 10% within 6 months, alcohol/substance abuse, protracted nutrient losses
    - ICU: if they are NPO for over 10 days (we use 7 days), gut malfunction, increased metabolic needs (trauma/burn, high dose steroids) and/or mechanical ventilation
  2. History -
    - Dietary: Previous diet, any problems, eating disorders, N/V/D?
    - Medical: Surgical history (need to know if GI tract is still connected and working)
    - Medications: Any that decrease nutrient absorption, alter taste, increase/decrease appetite, cause N/V?
  3. Athropometrics - Look at trends
    - Somatic (muscle) protein status: weight, triceps skin fold, physical appearance, arm muscle circumference
    - Transthyretin (prealbumin): 2-3 day half life, normal serum conc. is 15-40mg/dL****we are especially worried if this is under 10. ***keep in mind ICU patients are in an inflammatory state, so this number may not tell you the whole story
    - C-Reactive Protein (CRP): can help us see why prealbumin is decreasing. If prealbumin decreases as CRP increases, it’s due to inflammation. If prealbumin decreases as CRP is normal, it’s due to malnutrition.
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2
Q

What do the NUTRIC scores mean?

A

NUTRIC - High Risk of malnutrition (6-10, or 5-9 w/o IL-6), Low Risk of malnutrition (0-5 (0-4 w/o IL-6))

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3
Q

What are the last 2 components of nutritional assessment?

A
  1. Classifications of (chronic) Malnutrition -
    - Marasmus (protein-calorie malnutrition): decrease in total intake and/or utilization of food. Pts have cachectic appearance. Experience wasting of skeletal muscle and SQ fat. Treated by providing a well-balanced substrate +/- vit B.
    - Kwashiorkor (protein malnutrition): Adequate caloric intakes, but have relative protein malnutrition. Seen in catabolic trauma patients and burn patients. Present with large belly, diarrhea, decreased muscle mass, failure to gain weight, etc. Treated with carbs followed by high protein
    - Could also be a mix of the two
  2. Nitrogen Balance - Measurement of urinary excretion of nitrogen as urea nitrogen. It gives an indication of how we are using protein stores
    - Nitrogen is released from protein catabolism, is converted to urea, then excreted in the urine. If stress goes up, protein catabolism increases, which increases UUN.
    - Ideal goal is +3 to +5 grams
    - Nitrogen balance = N(in)-N(out)
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4
Q

What is the process of calculating a patient’s nutritional requirements based on height, weight, and clinical situation? (caloric needs, NPC, and protein requirements)

A
  • use NBW if pt’s actual body weight is 130% more than IBW. If it’s under 130% of IBW, use actual weight

Caloric needs:
Total energy expenditure = REE (resting) x stress/activity factor(s)
- TEE = REE x 1.2 (abbreviated Weir equation)
- Most patients will need 25-30kcal/kg/day (use NBW if obese)
- Non-stressed/depleted pts need 20-25kcal/kg/day

Protein needs:
- pts with mod to severe stress (ICU/trauma/surgery/burn): 1.5-2g/kg/day
- floor pts: 1-1.5h/kg/day
- maintenance: 0.8-1g/kg/day
- 1g protein = 4g kcal

NPC: non-protein calories
- Standard distribution is 70% dextrose & 30% fat
- Range is 70-85% dextrose, 15-30% fat
- Adjust due to blood sugars, triglycerides, RQ
- 100/0 can be used during sepsis or bloodstream infections
- 1g dextrose = 3.4 kcal
- 1g lipids = ~10 kcal

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5
Q

What are the indications for parenteral nutrition (PN - 6) and enteral nutrition (EN)?

A

*starting nutrition therapy early decreases ICU length of stay and increases patient outcomes
**all hospitalized patients should be started on some nutrition within 48 hours

Parenteral (IV) -
- anticipated prolonged NPO course (>7 days)
- inability to absorb nutrients via the gut (small bowel or colonic ileus, extensive small bowel resection, malabsorptive state, intractable V/D)
- enterocutaneous fistulas
- inflammatory bowel disease
- hyperemesis gravidum
- bone marrow transplantation

Enteral - if the gut works, use it
- oral consumption inadequate/contraindicated: esophageal obstruction, head and neck surgery, dysphagia, trauma, CVA, dementia
*provides GI stimulation, less risk of bacterial translocation (decreased infectious morbidity/mortality with EN), avoids risks associated with IVs, more physiologic than PN (esp bolus feeds), less stringent protocol, and less $$

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6
Q

What are the various routes and methods for the administration of PN and EN?

A

Parenteral -
- peripheral: dextrose and AA solutions are hypertonic, which are not well tolerated via peripheral vein. Requires large volumes of fluid, which may not be the best choice for HF or AKI/CKD pts. Calories are limited through this route and we can only do it for a short amount of time, so maybe we should not do peripheral access at all and just wait for central line, or don’t do PN at all.
- central: Allows administration of hypertonic solutions & more calories can be delivered. BUT more risk of infection & inserting central line can be risky. Can do central venous catheter (subclavian, internal jugular, or femoral vein), short term percutaneously inserted, or PICC, tunneled or implanted port for long term.
*there are single, double, and triple lumens (want at least 2-3 lumens for med administration)

Enteral -
- Nasogastric (NG)/Orogastric (OG), Nasojejunal (NJ)/Orojejunal (OJ), Gastrostomy (PEG), Jejunostomy; PEG/PEJ
- Administration: bolus (>200mL over 5-10 min, used primarily in pts with gastrostomy), intermittent (>200mL over 20-30 minutes, 4-8 feedings/day), continuous infusion (admin over 12-24 hours/day, need infusion pump, preferred with jejunum), trickle or trophic (slow infusion at 10-30mL/hr)

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7
Q

How do you choose a patient’s PN regimen (protein and carbs)?

A

Parenteral -
protein:
- want to choose most concentrated product (ex. Travasol 10%)
carbs:
- final dextrose conc. of over 10% in adults and 12.5% in peds shouldn’t be infused into peripheral vein (irritation); usually we do D5W
- max carbohydrate utilization: 4-5mg/kg/min

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8
Q

How do you choose a patient’s PN regimen (fat)?

A

Parenteral -
fat:
- IV fat emulsion provides concentrated source of calories
- check for allergies (glycerin & egg) with intralipid
- do not exceed 60% of caloric intake as lipid
- lipid rate for adults generally 1-1.5g/kg/day (max of 2.5g/kg/day if tolerating)
*propofol is a 10% lipid solution (1.1 kcal/mL)
- can only hang IV fat emulsion by itself for 12 hours due to stability (if in 3-in-1, can do 24 hours)

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9
Q

How do you choose a patient’s EN regimen (formula)? What should we not supplement with impact peptide? What types of proteins and fats are best for absorption?

A

Impact 1.5 - (immune modulating - arginine, glutamine, omega-3s, antioxidants) inc. protein content
- target pt population: major elective surgery, trauma, burn, head or neck cancer, mechanically ventilated
- use with caution in severe sepsis pts
*since this already have glutamine, DO NOT supplement glutamine

jevity - standard

glucerna - low carb (diabetic patients)

nepro - kidney patients (less volume)

  • partially digested proteins are better for absorption, medium chain fatty acids better for absorption, glucose polymers usually used for tube feeding
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10
Q

What is clinimix and how does the pt’s renal function impact if we give Clinimix vs. Clinimix E?

A

Clinimix = standard TPN w/o lipid +/- electrolytes

CrCl < 50 = no electrolytes
CrCl ≥ 50 = with electrolytes

*most pts get 83.3mL/hr
**this is usually a short term thing until we can get a custom TPN

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11
Q

What does SMOFlipid contain and how is that different from Intralipid?

A

Intralipid:
Soybean oil 10% (linoleic acid (omega-6))
Glycerin 2.25%
Egg yolk phospholipid 1.2%
Water for injection
- Intralipid contains glycerin and egg (allergies)

SMOFlipid: better combo of fat
S - Soybean oil 30%(omega-6)
M - Medium chain triglycerides (longer chains are harder to break down)
O - Olive oil (omega 9)
F - Fish oil (omega 3)

  • SMOF shows improved liver function & lower increase in TG levels from baseline compared to intralipid.
  • Less pro-inflammatory, less neg impact on liver function, reduced risk of infection, and decreased length of stay compared to non-omega-3 PN
  • SMOFlipid is superior to intralipid!!!
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12
Q

What electrolytes are we worried about in renal disease? What precipitation do we try to avoid? What should we put in TPNs to avoid deficiencies? Can we put iron in the TPN? What trace elements should we add in liver dysfunction and renal disease?

A
  • Caution in renal disease: potassium, phosphate, magnesium
  • Want to avoid calcium + phosphorous precipitation (Ca x Phos > 150)
  • Can add multivitamins
  • Must put trace elements in TPN or else they will become deficient (zinc, copper, chromium, selenium, manganese, iron)
  • Do not put iron in a TPN, if giving iron, do it in a separate bag

In liver dysfunction: d/c trace elements, supplement only zinc and selenium

In renal disease (CKD/ESRD on HD): use selenium and chromium w/ caution.

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13
Q

What are the normal daily ranges for calcium, magnesium, phosphorus (mMol -> mEq conversion), sodium, potassium, and chloride/acetate? What’s the balancing equation?

A

calcium: 10-20 mEq (given as calcium gluconate)
magnesium: 8-24 mEq
phosphorus: 15-45 mMol (or 0.3mMol/kg to start); 1mMol of Phos = 1.4mEq Phos
*do not put in bag if renal failure
sodium: 1-2 mEq/kg (or 1/2 NS = 77mEq/L)
potassium: 0.5-1mEq/kg to start (up to 2 mEq/kg)
chloride: (acid) PRN for 2/3 acid-base balance
acetate: (base) PRN for 1/3 acid-base balance

positives (Na+ and K+) - negatives (phos) = remaining to balance
- then do 2/3 as chloride, 1/3 acetate

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14
Q

How do we determine the rate of initiation and discontinuation of PN?

A

Start at 25% of goal and achieve the final rate within 24 hours (titrate). Max rate of infusion is 200mL/hr

Initiation:
- check blood glucose q4-6 hours before each increase the rate
- if BG is >200, contiue same rate x4 hours and recheck, if repeat BG is >200, consider treating

Cessation: Titrate down
- Decrease rate by q2hrs until rate is <50mL/hr, then d/c

Can do PN cycling (infusion over 12-18 hours per day). There’s no specific guidelines for this, but generally cut back during first and last hour of infusion

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15
Q

How do we initiate enteral tube feeding?

A
  1. initiate at full strength at 25mL/hr
  2. advance 25mL/hr q4-6hr as tolerated up to goal rate
    - check residuals q4-6hr
    - don’t dilute formula
    *can do cyclic over 8-20hrs/day to increase independence for the patient
    **if we can’t achieve >50-60% goal calories in the first week, we should consider PN
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16
Q

How do you design a protocol for monitoring a patient receiving PN or EN?

A
  • monitor ionized calcium (don’t want to mess with albumin)

Parenteral -
- Baseline: CMP, Mg, Phos, Ca; Hepatic function panel, prealbumin/CRP, and PT/INR
- q4-6h: finger sticks for glucose, residuals, distention, vomiting, aspiration
- Daily: vitals, I/Os, CMP, electrolytes (ICU setting)
- Twice weekly: prealbumin/CRP (1/2 life 2-3 days)
- Weekly: triglycerides, RQ

Enteral -
- GI: q4-6h check gastric residuals & emesis, check stools daily, bloating/distention, bronchial/tracheal aspirate
- Metabolic: I/Os, bowel movements, weight (2-3x/week), electrolytes, glucose, BUN/SCr daily if unstable, Mg/Phos/Ca/triglycerides/LFTs weekly, albumin/prealbumin/CRP/nitrogen balance weekly
- Mechanical: feeding tube placement, feeding tube patency

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17
Q

How do you calculate a patient’s nitrogen balance? What factors may affect nitrogen loss?

A

Non-urinary sources of nitrogen loss can include: sweat, feces, respirations, GI fistula, would drainage, skin exfoliation, burns (accounts for 10-15% of nitrogen excretion, the other 85-90% is excreted in urine)

Nitrogen balance = (N in) - (N out)

N in = [24 hour protein intake (g)]/6.25
N out = 24hr UUN(g) + factor(3-5g, usually use 4g)

*goal is +3 to +5, so if the nitrogen balance is low, we need to add protein to the nutrition.

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18
Q

What are the results of indirect calorimetry? What adjustments may need to be made to the patient’s nutrition regimen?

A

Indirect calorimetry is more specific for critically ill patients, since it looks at what is actually happening in their body.

We use the abbreviated Weir equation: TEE = REE x 1.2

For all energy production, oxygen is consumed and carbon dioxide is produced. We can look at the respiratory quotient to get an idea of if we are over or underfeeding the patient.
- RQ > 1 = over-feeding (lipogenesis)
- RQ <1 = under-feeding (starting to use protein for calories)
- The goal RQ is 0.85-0.95!!! (monitor once weekly)

Based on the RQ, we know whether or not to give more or less food.

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19
Q

What are the potential gastrointestinal, metabolic, and mechanical complications associated with PN?

A

PN -
- Mechanical (catheter-related): clotting of line, displacement
- Infectious: catheter-related sepsis, solution contamination, bacterial translocation (bacteria that relocates from other sites in GI due to not having gastric acid from enteral feeding)
- Metabolic: electrolyte imbalances, fluid imbalances, hyper and hypoglycemia, liver function abnormalities

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20
Q

What are the potential gastrointestinal, metabolic, and mechanical complications associated with EN?

A

EN -
- GI: High gastric residuals (only hold if >500mL), aspiration (elevate head of bed 30-45º, do post-pyloric, do continuous infusion), N/V or decreased motility, abdominal distention, diarrhea, constipation
*can give prokinetics to help with N/V, aspiration
*evaluate meds (diarrhea: hyperosmolar meds, sorbitol, antibiotics)

  • Metabolic: hyper/hypoglycemia (check meds & insulin regimen), overhydration/dehydration, electrolyte imbalance (hyponatremia most common)
  • Mechanical: clogging of feeding tube, tube malposition, rhinitis, sinusitis
  • Medication-related: clogged feeding tubes, drug-tube feed interactions
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21
Q

Which drugs (antibiotics (4), anti-retrovirals (3), other (4)) have drug/tube feed interactions? How should we administer these meds?

A

Antibiotics: fluroquinolones, intraconazole solution, tetracyclines, penicillin V
Antiretrovirals: didanosine, dolutegravir, indinavir
Other: levothyroxine, phenytoin, theophylline, warfarin

Administration:
- Hold tube feed
- 1 hour later, give medication
- wait 2 hours, resume tube feed

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22
Q

What are the doses of these prokinetic drugs: metoclopramide, erythromycin, naloxone, methylnaltrexone

A

metoclopramide: 10mg IV/PO/feeding tube QID; PRN for N/V

erythromycin: base is 250-500mg PO/feeding tube TID or 3mg/kg IV Q8hr

naloxone: 8mg via feeding tube QID

methylnaltrexoneL weight based dosing IV x1

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23
Q

What are the signs and symptoms of refeeding syndrome and essential fatty acid deficiency? What are strategies that we can do to prevent these disorders from occuring?

A

Refeeding syndrome: Fluid, micronutrient, electrolyte, vitamin imbalances. Usually occurs w/in first few days of feeding a starved patient. This is potentially life threatening!!
- Hypophosphatemia, hypomagnesemia, hypokalema
- Replace the electrolytes as early as we can to avoid this (before initiating feeds). Then start low and titrate up. also give thiamine.
- limit fluid to 800mL/day, less than 150g/day of carbs
- only give 50% of calorie needs

Essential fatty acid deficiency: Giving continuous infusion of dextrose inhibits movement of fatty acid, which can lead to EFAD. Usually happens around 10-14 days on fat-free PN regimen
- Dry scaly skin, brittle hair, lack of luster
- Give twice weekly fat emulsion (500mL 10% or 250mL 20%)

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24
Q

What are the strategies for delivering medications via feeding tubes and managing medication-related complications with EN?

A
  • Liquid meds are preferred whenever possible
  • Crush the tablet into a fine powder (or empty capsule contents) and mix in water, but do not crush sustained-release or enteric coated formulations
  • Administer each medication separately
  • Ensure adequate flushing with water between each med
  • Dilute hypertonic medications or those irritating to the gastric mucosa in at least 30mL of water before administrating

Unclogging tube: 1 sodium bicarb tab, 1 pancreatic enzyme cap, & 10mL of warm sterile water
- Clamp this in the tube for 15-30 mins, then flush when complete

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25
Q

What is important to note with EN for these special populations: Acute renal failure, hepatic failure, pulmonary failure, acute pancreatitis, burn

A

Acute renal failure: CRRT will need increased protein, HD will need less, prealbumin may be falsely high due to accumulation

Hepatic failure: standard enteral formulations usually good

Pulmonary failure: these pts can’t get a lot of volume, so we need to use calorically dense formulations (ex. impact peptide), refeeding is really bad in these pts (monitor phosphate carefully)

Acute pancreatitis: increased protein requirements, yes you can still use enteral feeding, PN does not affect pancreatic secretion and function

Burn: high protein and calorie requirements, start feeding early

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26
Q

What is are the MOA, adverse effects (5), indications (1), contraindications (3) of the depolarizing neuromuscular blocking agents?

A

Succinylcholine -
- MOA: binds and activates Ach receptors, resulting in a sustained depolarizing of neuromuscular junction, so the muscle contraction can’t occur (paralytic)
- pretty quick onset at ~1min, duration quick ~3-5mins
- used for rapid sequence intubation (RSI), NOT used for a sustained neuromuscular blockade
- AEs: APNEA (be ready to intubate), muscle fasciculations (deep muscle pain), hyperkalemia, prolonged apnea, intracranial pressure elevation
- CIs: major burns, crash injury, upper motor neuron disease (all due to hyperkalemia)

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27
Q

What is are the MOA, adverse effects (3), indications (7), drug interactions (2) of the nondepolarizing neuromuscular blocking agents? What are the 2 classes + class specific AEs of NDNMBAs?

A
  • MOA: competetively block the action of Ach (do NOT activate receptors, so they don’t cause initial fasciculations)
    *reversal is possible using acetylcholinesterase inhibitors (pyridostigmine, neostigmine) and sugammadex; these aren’t generally used in the ICU
  • Indications: immediate/sustained paralysis, mechanical ventilation (esp. if acute lung injury or acute respiratory distress syndrome (ARDS)), operative settings (for muscle relaxation), RSI (if contraindicated to succinylcholine), manage increased intracranial pressure (severe posturing, difficulties in mechanical ventilation, and refractory ICP), therapeutic hypothermia (body temp 32-34ºC post cardiac arrest), decreased oxygen consumption, etc.
  • AEs: paralysis of respiratory muscles/apnea, inadequate pain and sedation (NMBAs don’t provide analgesic, sedative, or anxiolytic effect), prolonged paralysis/muscle weakness (ICUAW)
  • Drug interactions: corticosteroids and NMBAs

Two Classes:
1. Aminosteroidal: pancuronium (slow onset, renal elim), vecuronium (slow/intermediate onset, 50-50 elim), rocuronium (rapid onset, hepatic elim)
- AEs: pancuronium = vagolytic; rocuronium = vagolytic at high dose
2. Benzylisoquinolinium: atracurium (intermediate onset), cisatracurium (intermediate onset)
- AEs: atracurium = dose dependent histamine release

28
Q

What should we monitor in patients on neuromuscular blockers?

A

*monitoring is challenging and associated with significant variability in response
**goal = lowest dose possible, minimization of ADRs

test toxicity endpoint through peripheral nerve stimulation: nerve stimulated 4 times
- number of twitches are recorded (4/4 = <75% suppression, 1/4 = 90% suppression)
- we usually dose to 1-2 twitches (do not titrate to 0/4)

29
Q

What are the differences between agitation, pain, and delirium?

A

agitation: apprehension, increased motor activity, autonomic arousal; may be manifested by fearful withdrawal; it’s a state of anxiety accompanied by motor restlessness

pain: more than 50% of ICU patients experience pain & it’s associated with physiologic/psychological consequences

delirium: acute cerebral dysfunction with a change or fluctuation in baseline mental status, inattention, and either disorganized thinking or altered level of consciousness
- cardinal features include disturbed level of consciousness and either a change in cognition (memory/disorientation/language) or development of a perceptual disturbance (hallucination/delusion)

30
Q

What do we use to assess pain if the patient cannot self-report?

A

Behavior pain scale (BPS)

Critical Care Pain Observation Tool (CPOT)

these look at facial expressions & body movements

31
Q

What are the common indications for the use of pharmacologic sedation and treatment of delirium in critically ill patients?

A

sedation - the act of calming, especially by the administration of a sedative drug
- use as adjuncts for anxiety and agitation, can supplement sedatives with non-pharm efforts
- many pts on mechanical ventilators will need some pharmacologic sedation
- should be started after providing adequate analgesia and treating reversible physiological causes and should NOT be used as a method of restraint, coercion, etc.
*over sedation is problematic. It can increase time on mechanical vent & increase ICU/hospital length of stay.

32
Q

What are the methods used to assess the degree of and/or adequacy of sedation?

A

Goal = adequate sedation, but not over sedation. LESS IS BEST. Want pt to be calm and arousable (follow simple commands)
- we can have daily sedation interruption to help w/ this

assessment scales:
- Richmond-Agitation-Sedation Scale (RASS)
- Sedation-Agitation Scale (SAS)
- Bispectral Index (BIS) - not recommended, it’s not standard and results may vary; uses EEG

33
Q

What are the different pharmacologic properties of sedatives and antipsychotic agents (haloperidol, risperidone, olanzapine, quetiapine)?

A

benzodiazepines - (lorazepam, midazolam (IV), (diazepam))
- MOA: bind/activate GABA receptor, which hyperpolarizes cells to make them resistant to excitation
- cause anxiolysis, antegrade amnesia, anticonvulsant
- elderly are more sensitive
- AEs: respiratory depression, some CV effects (minimal), withdrawal possible (taper when d/c), delayed emergence from sedation, potential association with delirium

propofol -
- MOA: binds on multiple receptors to cause CNS depression
- very titratable. rapid onset and offset
- can be used as anesthetic at higher doses
- the upper limit (80mcg/kg/min) is important for propofol infusion syndrome
- AEs: apnea, hypotension, bradycardia, hypertriglyceridemia, pain upon infusion, elevation of pancreatic enzymes, Propofol Infusion Syndrome (acidosis, bradycardia, lipidema)!!!, withdrawal if ≥7 days of therapy

dexmedetomidine -
- MOA: selective α2 agonist. In CNS, this inhibits noradrenalin release. In peripheral receptors, causes bradycardia and hypotenstive effects.
- does not cause respiratory depression, least incidence of delirium (can be used in non-ventilated pt)
- even when pt is sedated, the pt can be woken up & follow simple commands
- do not use if deep sedation is required
- AEs: CVs effects such as transient increase in BP w/ rapid administration, bradycardia/hypotension
- dose: 0.2-0.7mcg/kg/hr (no loading dose)
*FYI, we use this different than the package insert recommends

antipsychotic agents -
- Haloperidol: antagonized dopamine mediated neurotransmission; see some sedative effects, minimal hemodynamic effects, can be used IV and PO; no evidence that haloperidol reduces duration of delirium; potential torsades de points!!!! also decreases seizure threshold, possible EPS and Neuroleptic Malignant Syndrome (NMS)
- Atypical antipsychotics: safety advantages over haloperidol; not doses as aggressively as haloperidol; less EPS, but still risk for Torsades de Points

34
Q

What is a rational treatment algorithm for the sedation and delirium of critically ill adult patients?

A

2 subsets of delirium: hyperactive (agitation/motor restlessness, delusions more common), hypoactive (calm/lethargy, confusion/sedation more common)
*take out risk factors of benzos/blood transfusions, recognize other risks/triggers (hx of HTN, psychoactive drugs, environment, sepsis, endocrine disorders, brain diseases)
**assess delirium

Nonpharm:
- early mobilization
- optimize sleep, hearing, and vision
- improve cognition

Pharm: not used for prevention and not recommended for routine treatment
- short term antipsychotics may be used [haloperidol, atypical antipsychotics (risperidone/olanzapine/quetiapine)] for delirium associated with significant stress; be cautious of QT interval
- dexmedetomidine is recommended were agitation is preventing weaning of the vent/extubation

35
Q

What are some summarizing points of the PAD guidelines (

A

Provide adequate analgesia and treat reversible physiological causes (active and preemptive analgesia, sleep promotion, mobility)

Try to reduce sedation when you can. The sedation goal and endpoint should be established and regularly defined.

Regular assessment and response to therapy should be systemically documented.

Less is more, go as light as we can. The goal is for the patient to be calm and arousable & able to follow simple commands

Measures that encourage light sedation, patient assessment, and close titration of sedation may be beneficial.

36
Q

What is the idea of analgesia-first sedation? Which is DOC in pt with delirium+agitation, which benzo should be used for short term vs. long term, when is propofol preferred? When do we need to taper off? What is the role of the pharmacist in the management of sedation and delirium

A

“Analgesia-first sedation” is recommended
- pain is often primary source of agitation
- not a universal recommendation

  • Dexmedotodime is drug of choice in pt with delirium and agitation; But don’t use dexmed if patient is really hypotensive
  • Propofol is preferred vs. benzodiazepines
  • Benzos can still play a role (ex. anxiety, seizures, withdrawal)
  • Midazolam may be used for very rapid sedation and procedural sedation (short term only 24-48hrs max), but Lorazepam is used more commonly for prolonged sedation
  • Propofol may be preferred sedative when rapid awakening is desired and in neurotrauma; also preferred over benzos & probs dexmed in cardiac surgery

Prolonged sedation (5-7 days) will need to be tapered off gradually (esp with BZDs or propofol)

Pharmacists should be involved in agent selection/patient monitoring & establishing institutional guidelines

37
Q

What are the risk factors, signs/symptoms, and goals of therapy for acute liver injury and cirrhosis? What do we use to assess in cirrhosis

A

Acute:
- AST & ALT (0-50 IU/L) elevated with acute liver injury
- Alk phos (30-120 IU/L) elevated w/ biliary tract injury from acute liver injury (gallstone)
- Bilirubin (0-1.4mg/dL) elevated in acute injury (gallstone) and chronic liver disease
- Signs/Symptoms: abdominal pain, jaundice, N/V/D
- Goal: reverse toxic effects & prevent long term damage

Chronic: Cirrhosis is irreversible fibrosis of liver
- Albumin (3.6-5g/dL) decreased in chronic liver disease
- INR (0.9-1.1) increased w/ chronic liver disease
- Platelets (150-450k) decreased with chronic liver disease
- Signs/symptoms: fatigue, weight loss, ascites, jaundice (due to inc. bili), hepato/splenomegaly, encephalopathy
- Complications: Ascites, esophageal varices, hepatic encephalopathy, spontaneous bacterial peritonitis, thrombocytopenia, hyponatremia, hepatorenal syndrome (rare)
Assess liver function: Child Pugh score, MELD score to assess 3-month mortality risk & is used in transplant prioritization

38
Q

What are the 3 types of DILI? Which 5 meds are the most common to cause DILI?

A

Direct Hepatotoxicity - Caused when agent given in high doses (APAP)

Idiosyncratic Hepatotoxicity - Caused due to metabolic or immunologic reaction (antibiotics)

Indirect Hepatotoxicity - Indirect action of agent on liver or immune system (antineoplastic agents, glucocorticoids, monoclonal antibodies, protein kinase inhibitors)

*Amov-clav, isoniazid, nitrofurantoin, TMZ-SMZ, and minocycline are the 5 meds with highest risk of causing DILI

39
Q

How do we formate a treatment plan (doses, side effects, interactions, monitoring, education) for a pt with acute livery injury (APAP DILI) so that we minimize complications and prevent worsening liver injury?

A

Caused when high doses (over 8g) of APAP is taken. Results in toxic levels of NAPQI, which causes direct heptatoxicity.

Goal of therapy: Reverse toxic metabolite (NAPQI) through use of NAC +/- activated charcoal

NAC: Give if indicated by Rumack-Matthew Nomogram (hours post ingestion & APAP plasma concentration)
- PO: 140mg/kg PO loading dose followed by 70 mg/kg Q4H x 72H
- IV: 1st dose is 150mg/kg infused over 1 hour, then 50mg/kg infused over 4 hours, third dose is 100mg/kg infused over 10 hours

Monitor: liver enzymes q12-24hrs and signs/symptoms

40
Q

For a cirrhosis pt, how do we make a treatment plan (dosing, side effects, interactions, monitoring, education) for ascites? What drug class should we avoid with ascites pts?

A

Ascites - fluid accumulation in peritoneal space due to compensatory mechanisms from portal HTN & hypoalbuminemia
- s/sx: abdominal distension, abdominal pain, shortness of breath, nausea

Goal of therapy: minimize ascitic fluid & symptoms, reduce need for paracentesis, limit side effects, prevent subsequent complications
**AVOID NSAIDS!!!!

Non-pharm:
- Sodium restriction (<2g/day)
- Assess for liver transplant

1st line:
- Aldosterone antagonist (spironolactone) + loop diuretic (furosemide) in 100/40 ratio
- Side effects for spironolactone: AKI, inc. potassium, gynecomastia); Furosemide: AKI, decreased potassium

2nd line:
- Paracentesis (if >5L removed, administer 25% albumin, 6-8g per liter removed)
- TIPS procedure

Monitoring: s/sx of ascites, SCr, K+

41
Q

For a cirrhosis pt, how do we make a treatment plan (dosing, side effects, interactions, monitoring, education) for esophageal varices?

A

EV - portal HTN causes hepatic/splanchnic vasodilation, which results in decreases perfusion, so compensatory varices (small offshoots) form. If the varices bleed, that can be very severe.

Risk factors for variceal bleeding: larger varices size, cirrhosis severity, red color markings noted on endoscopy, active alcohol use

Variceal Bleeding Prophylaxis:
- Non-selective beta blockers (nadolol, propranolol, carvedilol) or EVL recommended (as monotherapy)
- Non-selective beta blocks antagonize beta1 to decrease HR and CO & antagonize beta2, which causes splanchic vasoconstriction; Use in window of moderate disease
- Side effects for beta blockers: drowsiness or insomnia, bradycardia, hypotension

Monitoring:
- HR (<60bpm), BP (SBP >90), s/sx of VH

Variceal Bleeding: *no PPIs
- S/Sx: pos. endoscopy, throwing up blood, dark blood in stool, fatigue, light headed/dizzy, hypotension
- Treat with blood transfusion
- Octreotide (vasoconstrictor)
- Antibiotics for prophylaxis (3rd gen cephalosporin: ceftriaxone) until hemorrhage resolution (max 7 days)
- Then do EVL (gold standard for EV bleeding, do w/in 12h)
- After EVL, do secondary prophylaxis (EVL q1-4weeks, NSBB indefinitely (nadolol, propranolol)
*no Vitamin K

Monitoring:
- Octreotide: N/V, HTN, bradycardia, hyperglycemia
- Ceftriaxone: Diarrhea; monitor s/sx of infection, ** don’t need to monitor SCr

42
Q

For a cirrhosis pt, how do we make a treatment plan (dosing, side effects, interactions, monitoring, education) for hepatic encephalopathy?

A

Hepatic encephalopathy - ammonia accumulates & is shunted into circulation. This hyperammonemia then results in neuronal dysfunction which leads to hepatic encephalopathy
- s/sx: delirium, convulsions, coma, hoomy/irritable temper, asterixis

Treatment:

1st line:
- Lactulose titrated to target at least 3 BMs daily

Secondary prophylaxis: lactulose (after any occurrence of HE)

Reccurent: rifaximin 550mg BID

Side effects:
Lactulose: aspiration, dehydration, hypernatremia

Monitor:
- BMs
- Mental status

43
Q

For a cirrhosis pt, how do we make a treatment plan (dosing, side effects, interactions, monitoring, education) for spontaneous bacterial peritonitis (SBP)?

A

SBP - due to translocation of bacteria from the gut that cross the intestinal barrier
- S/sx: fever, abdominal pain/tenderness, leukocytosis, encephalopathy, some asymptomatic

Diagnose by culture of paracentesis fluid. If PMNs > 250, they have SBP. PMNs = WBC from fluid x % neutrophils.

Treatment:
- 3rd gen cephalosporin (ceftriaxone): 5-7 day duration
- Albumin: Day 1 is 1.5g/kg x1 (w/in 6 hours of SMP diagnosis), Day 3 is 1g/kg x1

Side effects/monitoring:
- Cephalosporins: diarrhea; monitor s/sx of infection, don’t need to monitor SCr

Secondary prophylaxis: indefinitely
- Bactrim PO daily (preferred)
- Ciprofloxacin 500mg PO daily

Side effects/monitoring:
- Bactrim: AKI, agranulocytosis, hyperkalemia, hyponatremia, SJS; monitor Scr, electrolytes, CBC
- Ciprofloxacin: resistance, musculoskeletal side effects, QTc prolongation, rash, AMS; moniotr mental status, CBC, renal function

44
Q

What is the role of these processes in maintaining normal acid-bace balance? (buffering systems, bicarb reasborption, H+ excretion, ventilatory regulation, hepatic regulation)

A

Buffering systems - bicarbonate is our most important buffer
- bicarb buffer: rapid onset and intermediate capacity. We have a lot of bicarb (most available); when acid is added, bicarb is going to become carbonic acid, then will disassociate to CO2 and H2O, then we blow off the CO2. Now the body needs new HCO2-.
- phosphate buffer: intermediate onset and capacity. We have some phosphate in intracellular spaces & in bone, but we don’t want to have to use this.
- proteins: rapid onset, limited capacity. Not really going to use this unless we don’t have anything else.

Bicarbonate reabsorption and H+ excretion (renal regulation) -
- Bicarb reabsorption: 85-90% of bicarb is reabsorbed by proximal tubule.
- H+ excretion (aka bicarb generation): takes place in distal tubule. Either happens due to ammonium excretion (common) or titratable activity (less, limited by phosphate). This comprisees ~50% of net acid excretion

Ventilatory regulation - rapid onset and HUGE capacity. Chemoreceptors sense that we have too much CO2, then they increase rate and depth of ventilation so we can breath it off

Hepatic regulation - Proteins are oxidated in the liver, which generates ammonium and bicarb. The ammonia is eliminated via urea synthesis. Decreased urea synthesis can cause metabolic alkalosis, so it is thought that the liver can regulate urea synthesis depending on pH of blood. (probably minimal effect though)

45
Q

What effect do carbonic anhydrase inhibitors have on our bicarb concentrations?

A

These inhibit the activity of carbonic anhydrase, which decreases the entry of CO2 and H2O for reabsorption. This causes bicarb to be excreted in the urine, then metabolic acidosis can occur.

46
Q

What are the adverse consequences that result from acidemia and/or alkalemia? (CV, Metabolic (K+? anaerobic glycolysis?), CNS, other)

A

Acidemia: pH <7.35
- Cardiovascular: decreased cardiac output, impairment of cardiac contractility, increased pulmonary vascular resistance and arrhythmias (it’s harder for heart to pump blood)
- Metabolic: insulin resistance, inhibition of anaerobic glycolysis, hyperkalemia
- CNS: coma or AMS
- Others: decreased respiratory muscle strength, hyperventilation, dyspnea

Alkalemia: pH >7.45
- Cardiovascular: decreased coronary blood flow (not perfusing heart as well), arteriolar constriction, decreased anginal threshold, arrhythmias
- Metabolic: decreased K+, Ca, and Mg, stimulation of anaerobic glycolysis
- CNS: decreased cerebral blood flow, seizures
- Others: decreased respirations

47
Q

How do you calculate and interpret an anion gap and delta gap? When would you calculate this?

A

Anion gap = Na+ - (Cl- + HCO3-)
*Normal anion gap = 3-11 mEq/L

Delta gap = anion gap - normal gap (10)
then add Delta gap + pt’s bicarb
If over ~26, there is a metabolic alkalosis on top of the acidosis

48
Q

How do you calculate and interpret the compensatory response for any given acid-base disorder?

A

[in kidneys] H+ + HCO- <-> H2CO3 <-> [in lungs] CO2 + H20
- The body compensates when one system is out of range in order to maintain normal balance. The ratio of CO2 to bicarb (HCO3-) is really important for the pH of blood.
- Normal PaCO2 = 40
- Normal HCO3 = 24

Check how compensated it is w/ the table

If metabolic acidosis - calculate anion gap/delta gap if needed

49
Q

What is the pathophysiology of metabolic acidosis?

A

decreased bicarb, which is compensated with decreased CO2.

Hyperchloremic (non-anion gap) acidosis - loss of plasma bicarb that is replaced by Cl-.
- GI bicarb loss (diarrhea, pancreatic fistulas/biliary drainage)
- renal bicarb wasting (problem is with the proximal tubule, so they have reduced ability to reabsorb bicarb [caused by various drugs/diseases], eventually renin-angiotensin system is activated, which causes more problems can see hypokalemia with this one)
- impaired renal acid excretion (type I RTA: distal tubule defect, H+ cannot be pumped into tubule lumen, which means we lose bicarb & potassium (K+ is excreted)) (type IV RTA: hypoaldosteronism causes increased H+ retension) (chronic renal failure so we are not able to secrete H+)
- exogenous acid gain (TPN, Acl or Ammonium Cl administration)

Elevated anion gap acidosis: overall, HCO3- losses are replaced with another anion besides Cl-
M - methanol intoxication
U - Uremia
D - Diabetic ketoacidosis
P - poisoning/PEG
I - Intoxication/infection
L - Lactic acidosis (normal is ~1, levels between 5-9 are deadly): caused by shock, drug toxins (ex. alcohol), leukemia, hepatic/renal failure, diabetes mellitus, etc.
E - Ethylene glycol
S - Salicylates/Sepsis: salicylates are acid & but they stimulate respiratory drive, which causes alkalosis (pH may end up looking normal)

50
Q

What are the symptoms of metabolic acidosis? (6)

A
  • Deep, rapid respirations (Kussmaul)
  • Peripheral vasodilation (tachycardia/ventricular arrhythmias, decreases contractility)
  • Hyperkalemia
  • Lethargy/coma
  • N/V
  • Bone demineralization in chronic acidotic states
51
Q

What is the treatment for metabolic acidosis? What are the side effects we need to look out for? (4)

A

Treat underlying cause!

Acute bicarb therapy (consider if pH is <7.10-7.15)
- Indicated in hyperkalemia, pH <7.10 and cardiac arrest after defibrillation, ventilation, meds have been used, and overdoses (to alkalinize the urine so drugs will be excreted)
- Dose (mEq): [0.5L/kg (Ibw)] x (desired bicarb - actual bicarb); Use 12 for desired bicarb, then give 1/3-1/2 of the dose and see how the patient does
- Supplement K+ if needed

Side effects from too much bicarb:
- Overalkalination can reduce cerebral flow and impair oxygen release from Hb (shift to the left occurs, tissues are not getting oxygen)
- Hypernatremia/hyperosmolality
- CSF acidosis (CO2 diffuses into CSF)
- Hypocalcemia

**some pts may need chronic bicarb

52
Q

What is the pathophysiology of metabolic alkalosis?

A

Increased bicarb, so CO2 is increased (less breathing)

3 main causes:
1. Loss of acid from GI tract or urine
2. administration of HCO3- or bicarb precursor
3. Contraction alkalosis - loss of Cl- rich, HCO3- poor fluid
*sometimes impaired renal function results in decreased bicarb excretion
*volume and chloride depletion often contribute (dec. arterial blood volume, dec. ability of kidney to excrete bicarb, inc. capacity of the proximal tubule to reabsorb bicarb)

Contraction alkalosis (saline responsive alkalosis)
- urinary chloride <10-20 mEq/L
3 main causes:
1. Diuretic therapy (MOST COMMON) - furosemide, torsemide, bumetanide, HCTZ: dec. volume stimulates aldosterone, which inc. distal tubular Na+ reabsorption and H+/K+ secretion. H+ in the lumen is associated with bicarb reabsorption (proximal) & bicarb generation (distal). Also hypokalemic and hypochloremic state contributes to inc. bicarb.
2. Vomiting and NG suction: 1L/day lost w/ persistant vomiting
3. Exogenous bicarb administration or blood transfusions: ex. fluids, LRs, TPNs & blood transfusions have citrate that breaks down HCO3-.

Saline resistant alkalosis
- urinary chloride >30 mEq/L
- Key difference: no chloride depletion or there is an inability to reabsorb chloride
1. Increased mineralocorticoid activity: Enhances Na-K exchange and H+ secretion. H+ secretion increases bicarb reabsorption
2. Hypokalemia: Increases H+ secretion
3. Renal tubular chloride wasting: Impaired NaCl reabsorption. The volume depletion activates the RAA system, leading to H+ secretion & hypokalemia

53
Q

What are the symptoms of metabolic alkalosis?

A
  • Muscle cramps, weakness, paresthesias
  • Postural dizziness
  • Cellular hypoxia (shift to the left due to alkalosis), mental confusion, coma, seizures
  • Direct myocardial suppression, CV collapse, arrhythmias
54
Q

What is the treatment for metabolic alkalosis?

A

Correct the underlying cause!!
- Rapid correction not necessary, but treatment is still needed

Saline responsive:
- Fluids! NaCl or KCl included: This will expand intravascular volume & replenish Cl-, which allows Na+ to be reabsorbed with Cl-, not exchanged with H+ or reabsorbed with bicarb
*be careful in pts with HF or hepatic/renal failure
*may need to supplement K+
*may need LRs for some patients, but need to be careful since LR gets broken down into bicarb
- Carbonic anhydrase inhibitors: Helpful in patients who can’t tolerate excess fluid or sodium
*need to supplement K+ then
- HCl in either D5W or NS if pt has contraindication to Na replacement, failure of therapies, or confirmed alkalosis (bicarb > 50, pH > 7.55)
- Ammonium chloride
*CNS toxicities, N/V with Ammonium chloride
- H2RAs/PPIs can be used for pts with NG suction or vomiting

Saline resistant:
- Correct hypokalemia w/ potassium-sparing diuretic or KCl supplementation
- Decrease dose of mineralcorticoid or use one with less mineralcorticoid activity
- Add spironolactione
- Correct hyperaldosteronism by giving fluids

55
Q

What is the pathophysiology of respiratory acidosis?

A

Increased CO2, so kidneys increase bicarb
- Almost always due to a failure of excretion of breath

  • Airway obstruction (asthma, foreign body, aspiration)
  • Reduces stimulus for respiration from CNS (drug overdose, sleep apnea, CNS infections, trauma)
  • Failure of heart or lungs (PE, cardiac arrest)
  • Neuromuscular defects affecting nerves or skeletal muscles requires for ventilation (ALS, Guillain-Barre)
  • Mechanical ventilation
56
Q

What are the symptoms of respiratory acidosis? (respiratory, CNS, CV)

A
  • Respiratory: dyspnea/SOB
  • CNS: HA, drowsiness, confusion, coma, seizures
  • CV: tachycardia, arrhythmias, and/or hypotension
57
Q

What is the treatment for respiratory acidosis?

A

Correct the underlying cause!
- Mechanical ventilation or oxygen (use caution with O2 for COPD patient, since O2 will decrease their drive to breathe)
- Avoid rapid correction to prevent alkalemia
- MAY need to use bicarb w/ acute acidosis if pH is <7.15, where patient is at greater risk for arrhythmias

58
Q

What is the pathophysiology of respiratory alkalosis?

A

Decreased CO2, so kidneys decrease bicarb
- Breathing too much

  • Central stimulation of respiratory (anxiety, pain, injury, trauma)
  • Peripheral stimulation of respiration (hypoxemia, hypotension, high altitude, CHF)
  • Mechanical ventilation
  • Pulmonary (pulmonary edema, PE, pneumonia)
  • Salicylate intoxication (remember dual disorder)
59
Q

What are the symptoms of respiratory alkalosis?

A
  • CNS: lightheadedness, confusion, seizures
  • Dec. cerebral blood flow
  • Tetany/muscle cramps
  • N/V
60
Q

What is the treatment for respiratory alkalosis?

A

Treat underlying cause!!
- Ventilation, sedation, paralysis (need to calm them down)

61
Q

How do you develop a supplementation plan based on patient age? (iron and zinc)

A

iron: for premature neonates, 2mg/kg/day is automatically indicated

zinc: not routinely used, unless deficient

62
Q

How do you calculate fluid for a given pediatric patient?

A

Fluids: Holliday-Segar Method
up to 10kg: 100mL/kg
10-20kg: 1000mL + 50mL/kg for every kg greater than 10
20kg+: 1500mL + 20mL/kg for every kg greater than 20

63
Q

What is the caloric density of breast milk? How do pharmacokinetic variables affect drug distribution into breast milk (6)?

A

Breast milk - 20kcal/ounce (20kcal/30mL)

  • A drug with high oral bioavailability is more likely to be absorbed by an infant

Characteristics that increase breastmilk:
- Non-ionized
- Small molecular weight
- Low Vd (concentrated in blood -> milk)
- Little protein binding
- High lipid solubility
- Long t1/2

64
Q

Through breast feeding, which drugs harm the infant directly, and which reduce milk production?

A

Harm the infant directly - immunosuppressants, chemotherapy, radioactive agents

Reduce milk production - ergots, decongestants

65
Q

How much cholecalciferol should breastfed babies get vs formula fed?

A

partially or fully breastfed - 400 IU (10mcg) daily

formula fed: 200-400 IU (10mCg) until receiving 1000mL/formula/day

66
Q

What is automatically indicated in premature neonates?

A

iron supplementation 2mg/kg/day