Critical Care Flashcards

1
Q

When 1 L of NS is given, how much will stay in the intravascular space?

A

250mL

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2
Q

Crystalloids Versus Colloids

A

Crystalloids: contain various concentrations of electrolytes or dextrose that pass between semi-permeable membranes, mostly staying in extravascular or interstitial space
-Benefits: less costly, less adverse reactions
-Ex: 5% Dextrose (D5W), 0.9% NaCl (NS), Lactated Ringer’s (LR), Plasma-Lyte A

Colloids: LARGE molecules (typically protein or starch) dispersed in solution that remain in INTERVASCULAR space and increase oncotic pressure
-Ex. albumin, hydroxyethyl starch, dextran
-Hydroxyethyl starch: BBW for mortality, renal injury, and coagulopathy

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3
Q

When would you give certain types of crystalloids or colloids?

A

Crystalloids: usually first line for fluid replacement
-NS or LR: often in shock states for volume resuscitation

-Hypertonic saline: can be used in stroke or enchepalitis combined with hyponatremia when brain is susceptible to having higher Na+ concentrations that could shift fluid from periphery into brain

-D5W: when “free water” is needed INTRACELLULARLY –> does NOT go into intravascular (DO NOT use for fluid resuscitation)

Colloids: if pt is actively bleeding or Hgb <7

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4
Q

Hyponatremia is Na < _______, but usually isn’t symptomatic until Na <_______.

Hypernatremia is Na > ______.

What are s/sx of hyponatremia? Severe s/sx?

A

<135; <120; >145

Hyponatremia: HA, confusion, lethargy, gait disturbances
-Typically from cerebral edema and increased intracranial pressure
-Severe s/sx: seizures, coma, respiratory distress

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5
Q

Which electrolyte can cause risk of osmotic demylination syndrome (ODS) or central pontine myelinolysis (paralysis, seizures, death) if replaced too quickly? What is the max rate that this electrolyte should be corrected?

A

Na+ - correct no more rapidly than 12 mEq/L/24 hours

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6
Q

Causes and Treatment of Hyponatremia

A

Hypervolemic: fluid overload (ex. cirrhosis, HF, renal failure) –> diuretics with fluid restriction preferred TX
-Arginine vasopressin (AVP) receptor antagonists (conivaptan, tolvaptan)

Hypovolemic: diuretics, self-wasting syndromes, adrenal insufficiency, blood loss, or N/V –> correct underlying cause
-Severe: hypertonic 3% NaCl IV

Isovolemic: syndrome of inappropriate antidiuretic hormone (SIADH) –> diuresis w/ fluid restriction, D/C drugs contributing to SIADH, demeclocyline, AVP receptor antagonists

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7
Q

Conivaptan:
-Brand
-MOA
-ROA
-AVEs
-CIs
-Monitoring

A

Brand: Vaprisol

MOA: dual arginine vasopressin antagonist (vasopressin 1A and 2)

ROA: injection

AVEs: orthostatic hypotension, fever, hypokalemia, injection site rxns (>60%)

CIs: hypovolemic hyponatremia, anuria, concurrent usage w/ strong CYP3A4 inhibitor

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8
Q

Tolvaptan:
-Brand
-MOA
-ROA
-AVEs
-CIs

A

Brand: Samsca

MOA: selective arginine vasopressin antagonist (vasopressin 2 = V2)

ROA: PO (tablet)

AVEs: THIRST, DRY MOUTH, NAUSEA, POLYURIA, weakness, hyperglycemia, hypernatremia
-Avoid usage >30 days and in liver disease/cirrhosis (HEPATOTOXICITY)

CIs: hypovolemic hyponatremia, anuria, concurrent usage w/ strong CYP3A4 inhibitor, inability to sense or respond to thirst, urgency to raise Na+

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9
Q

Hypernatremia: Causes and Treatment

A

Hypovolemic: dehydration, N/V -> fluids

Hypervolemic: intake of hypertonic fluids –> diuresis

Isovolemic: diabetes insipidus (DI) which decreases antidiuretic hormone (ADH) –> desmopressin

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10
Q

Potassium:
Hyperkalemia is often from ________ and is defined as K+ > ______mEq/L.

Hypokalemia, which is a more common experience in hospitalized pts, is defined as K+ <____mEq/L. A drop of 1 mEq/L below this value represents a total body deficit of ___-___mEq.

A

Hyperkalemia: from CKD often; K+ > 5-5.5 mEq/L

Hypokalemia: <3.5mEq/L; 100-400 mEq (in other words, for every 10mEq given, K+ will increase by 0.1mEq/L)

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11
Q

hich electrolyte is typically diluted prior to being given IV? What is the concern of higher concentrations?

A

Potassium - higher concentrations particularly in peripheral lines can be painful to the pt and low or high levels of K+ can cause cardiac arrhythmias (typically no more than 10mEq/hr or 10mEq/100mL in concentration).

In severe scenarios, a central line can be used that higher concentrations can be given.

In general, PO potassium should be given first prior to IV.

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12
Q

If supplementing potassium, but not increasing, what electrolyte may need to be replaced as it necessary for potassium uptake?

A

Magnesium

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13
Q

Treatment and causes of hypokalemia

A

Causes: metabolic acidosis, overdiuresis, medications (insulin, amphotericin, diuretics)

When feasible, give PO potassium first - if NOT IV (potassium chloride premixed IV preferred)

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14
Q

Hypomaganesemia:
-Mg <___mEq/L
-Causes
-Treatment

A

Mg <1.3 mEq/L

Causes: alcohol use, diuretics, amphotericin B, vomiting/diarrhea

Treatment:
-If life-threatening (seizures, arrhythmias) and Mg <1mEq/L: IV mangesium sulfate

-If Mg <1.5mEq/L, but >1mEq/L: magnesium oxide PO

-Treatment should continue for 5 days to fully replace body’s stores

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15
Q

Phosphorus:
-Hyperphosphatemia is often due to __________.

-Hypophosphatemia: symptoms, causes, treatment

A

Hyperphosphatemia: caused by CKD

Hypophosphatemia:
-Caused by phosphate-binding drugs (calcium salts, sevelamer), chronic alcohol intake, hyperparathyroidism

-Treatment: when PO4 <1mg/dL typically give 0.08-0.16 mmol/kg in 500mL of NS or D5W over 6 hours; less severe: PO

-Treatment should last one week or longer to fully replace body’s stores

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16
Q

Intravenous immunoglobulin:
-Brands
-MOA
-ROA, administration notes
-TX
-AVEs
-CIs

A

Brands: Gammagard, Gamunex-C, Octagam, Privigen

MOA: immunoglobulin (IgG) from plasma of at least 1,000 or more (FDA minimum, but typically 3,000-10,000) donors to replace antibodies

ROA: IV - do NOT freeze, SHAKE, or heat

TX: immunodeficient patients
-Off-label: MS, myasthenia gravis, Guillain-Barre syndrome

AVEs: INFUSION RXNS (flushing, chest tightness, fever, chills, hypotension - SLOW/STOP infusion if needed), HA, nausea, diarrhea
-Rare: blood dyscrasias, renal failure (usually occurs within 7 days and more likely w/ products stabilized w/ sucrose)
-IMPAIRS RESPONSE TO VACCINES: NEED TO SPACE BETWEEN

CIs: IgA deficiency (use product with lowest IgA)

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17
Q

What is the APACHE II Test?

A

The Acute Psychologic Asessement and Chronic Health Evaluation II - ICU mortality risk assessment

18
Q

What medications in the ICU are typically given through an central line?

A
  1. Vasopressors
  2. Vasodilators
  3. Inotropes

Often given as continuous infusion

Central line allows medications to be given into heart where maximum blood flow is. Blood dilutes concentratations, and medications can be given at higher concentrations.

19
Q

Vasopressors: drugs, MOA

A

Drugs/MOA: cause peripheral vasoconstriction that increase systemic vascular resistance (SVR), increasing BP
-Phenylephrine: alpha1 agonist
-Norepinephrine: alpha 1 agonist > beta-1 agonist (DOC usually)
-Epinephrine: alpha-1, beta-1, and beta-2 agonist (not used as much since not selective)
-Vasopressin: vasopressin receptor agonist (constriction only, no inotropic or chronotropic effects)

Dopamine: dose-dependent receptor activity
-Low doses (1-4 mcg/kg/min): dopamine-1 agonist (improves renal function)
-Medium doses (5-10 mcg/kg/min): beta-1 agonist (positive inotropic effects beneficial in HF)
-High doses (10-20 mcg/kg/min): alpha-1 agonist (vasopressor)

20
Q

Vasopressors (ex. dopamine, EPI, norepinephrine, phenylephrine, vasopressin):
-AVEs
-Warnings/BBW
-Monitoring

A

AVEs: arrhythmias, tachycardia (especially dopamine and EPI), bradycardia (phenylephrine), necrosis (gangrene), hyperglycemia (EPI), tachyphylaxis, peripheral and gut ischemia

Warnings: extreme caution w/ MAOIs, prolonged hypertension (especially dopamine, EPI, and norepinephrine)

BBW:
-Dopamine and norepinephrine: extravasation
-All others are vesicants when administered IV
-Treat extravasation with phentolamine (alpha-1 blocker - majority of vasopressors are alpha-1 agonists), alternatively nitroglycerin ointment can be used if unavailable

Monitoring: CONTINUOUS BP, HR, MAP, ECG, urine output, infusion site for extravasation

21
Q

Epinephrine IV push dose should be at ____mg/mL. Epinephrine IM injection or compounding IV products dose should be at____mg/mL

A

IV push: 0.1mg/mL

IM injection/compounded IV: 1mg/mL

22
Q

Vasodilators:
-Drugs
-MOA
-TX
-AVEs
-CIs
-Administration considerations

A

Drugs: nitroglycerin, nitroprusside

MOA:
-Nitroglycerin: at low doses, venous vasodilator; at high doses, aterial vasodilator
-Nitrprusside: mixed vasodilator (equal between arterial and venous)

TX: MI (nitroglycerin only), uncontrolled HTN

AVEs: HA, tachycardia, increased intracranial pressure
-Nitroglycein: tachyphylaxis within 24-48 hours
-Nitroprusside: BBW of cyanide toxicity (excessive hypotension especially in renal or hepatic impairement); “coronary steal” from greater effect on BP and causing blood to be diverted away from coronary arteries

CIs: nitroglycerin used with PDE5 inhibitors (hypotensive crisis) or riociguat or SBP <90mmHg

Administration:
-Nitroglycerin: requires non-PVC containers (ex. glass or polyolefrin): permeates PVC

-Nitroprusside: requires light protectionl use only clear solution (blue indicates degradation to cynanide)

23
Q

Treatment for cyanide poisoning from nitroprusside

A

Sodium thiosulfate and sodium nitrate (Nithiodote)

-Hydroxocobalamin can be used to reduce risk of thiocyanate toxicity

24
Q

Inotropes:
-Drugs
-MOA
-TX/When to use
-AVEs
-Monitoring

A

Drugs: dobutamine, milrinone

MOA: “inodilators” - intropes that increase contraction + vasodilation
-Dobutamine: beta-1 agonist with WEAK beta-2 and alpha-1 agonist
-Milrinione: phoesphodiesterase-3 (PDE-3) inhibitor - selective to cardiac and vascular tissue

TX: use only when BP is adequate to produce vasodilation and when contraction of heart needed (ex. MI)

AVEs:
-Dobutamine: hyper/hypotension, ventricular arrhythmias, tachycardia, angina
-Milrinone: ventricular arrhythmias, hypotension

Monitoring: continuous BP and ECG, HR, central venous pressure (CVP), MAP, urine output, LFTs, renal function (milrinone)
-Dobutamine may turn slightly pink from oxidation, but potency is NOT lost

25
Q

Shock: define, labs, severe s/sx

A

Shock: characterized by hypoperfusion often in setting of hypotension (SBP <90mmHg or MAP <70mmHg)

Labs:
-Systemic vascular resistance (SVR): high in most types of shock to try to increase BP, except in distributive shock where cytokines and inflammatory mediators decrease SVR

-Temperature: >38.3C or <36C

-HR > 90bpm

-RR >20 bpm or PaCo2 </= 32mmHg

-WBC > 12x10^3 or <4x10^3 cells/mm3

Severe s/sx: increase lactate >1mmol/min, altered mental status, organ dysfunction (decreased SBP, lactate, SCr increased by >0.5mg/dL, low urine output, hypoexemia)

26
Q

TX of obstructive, cardiogenic, and hypovolemic shock

A

Obstructive: treat underlying cause (PE, cardiac tamponade)
-Fluids and vasopressors may be given, thrombolytics for PE

Cardiogenic (ADHF):
-Volume overloaded: loop diuretics, vasodilators
-Hypoperfusion: concern of decreasing kidney function –> inotropes, vasopressors (AVOID: vasodilators)
-Both: careful combination and monitoring

Hypovolemic: from trauma/dehydration or GI bleeds
-First line: crystalloids (NS typically at 30mL/kg about 2L or LR - does NOT have enough K+ to drastically change K), do NOT use D5W (does not go IV)
-Active bleed or Hgb <7: colloids

27
Q

Vasodilatory / Distributive Shock: Treatment

A

Typically from septic shock (infection) or anaphylaxis

-Within 1 hour: broad spectrum antibiotics

-30mL/kg of crystalloid (NS or LR) for hypotension –> albumin if a lot of crystalloid needed

-Within 6 hours: vasopressors if MAP <65mmHg (may be higher in hx of HTN or atherosclerosis) OR give soon if need to optimize organ perfussion –> DOC is norepinephrine (vasopressin can be addedm, dopamine in bradycardia, phenylephrine in resistant hypotension or EPI)

28
Q

General TX of pain in ICU

A

IV opioids (morphine, hydromorphone, fentanyl) - first line for analgesia

Pain scale should be used to assess

29
Q

Agitation TX in ICU

A

Non-BZDs are preferred which may contribute as well to delirium and have improved ICU outcomes/LOS

-BZD options typically used: midazolam (short acting, caution w/ active metabolite in renal dysfunction that may prolong action), lorazepam –> can be important for use in alcohol/BZD withdrawl or seizures

-Dexmedotmidine (Precedex): alpha-2 agonist (can decrease BP) that can be used in intubated AND non-intubated pts

-Propofol (Diprivan): oil-in-water emulsion (milk appearance) that is recommended ONLY in intubation, can cause hypertriglycedimeia from oil

-Evaluated with RASS Score: +4 = very combative, 0 = alert and calm, and -5 = unarousable

30
Q

Delirium in ICU TX

A

No medications recommended for prophylaxis, but controlling pt’s environment and mobilization are recommended
-Providng sedation with NON-BZDs can help prevent

TX: quetiapine (mildly sedating, little risk for movement disorders) preferred, haloperidol has less evidence but common in practice

31
Q

Dexedetomidine:
-Brand
-MOA
-AVEs
-Warnings
-Administration considerations

A

Brand: Precedex

MOA: alpha-2 receptor agonist

AVEs: hypo/hypertension, bradycardia, dry mouth, nausea, constipation

Warnings: caution in hepatic impairment, DM, heart block, bradycardia, sevre ventricular dysfunction, hypovolemia, or chronic HTN

Administration considerations:
-does NOT require refrigeration
-Duartion of infusion should NOT exceed 24 hours per FDA labeling
-Use for intubated and non-intubated pts (less respiratory depression)

32
Q

Propofol:
-Brand
-MOA
-AVEs
-CIs
-Administration/preparation considerations

A

Brand: Diprivan

MOA: short-acting general anesthetic

AVEs: hypotension, apnea, hypertriglyceridemia, green urine/hair/nails beds, propofol-related infusion syndrome (PRIS), myoclonus, pancreatitis, pain on injection (particularly peripheral vein), QT prolongation

CIs: hypersensitivity to egg or soy

Considerations:
-Shake well before use - do not use if separation occurs
-Use strict aseptic technique due to bacterial growth potential; discard vial and tubing within 12 hours after usage
-Do not use filter <5 microns for administration
-Does NOT require refrigeration

33
Q

Etomidate:
-Brand
-MOA
-TX
-Warning
-Monitoring

A

Brand: Amidate

MOA: ultra-short acting nonbarbiturate hypnotic

TX: induction agent for intubation

Warning: inhibits 11-B-hydroxylase which can lead to decreased cortisol production for up to 24 hours

Monitoring: s/sx of adrenal insufficiency (hypotension, hyperkalemia), respiratory status, BP, HR< infusion site, sedation scale

34
Q

Ketamine
-Brand
-MOA
-Usage in ICU
-Warnings
-Monitoring

A

Brand: Ketalar

MOA: NMDA receptor antagonist

TX: inducation agent of intubation
-Off-label: continuous sedation, pain

Warning: emergence reactions (vivid dreams, hallucinations, delirium), cerbrospinal fluid (CSF) pressure elevation, respiratory depression/apnea, dependence/tolerance

Monitoring: BP, HR, respiratory status, emergence reactions, sedation scale’

-Pretreatment with BZDs can decrease incidence of emergence reactions by about 50%

35
Q

Stress Ulcers
-Why do stress ulcers occur, and who is at additional risk?
-Prophylaxis options

A

Stress ulcers occur during critical illness when the body diverts blood flow to body’s major organs and less flows to the gut resulting in breakdown of gastric mucosal defense mechanisms (prostaglandin synthesis, bicarbonate production, and cell turnover)
-Ex. mechanical ventilation >48 hours, coagulopathy, major burns, sepsis, traumatic brain injury, acute renal failure, high dose systemic steroids

Prophylaxis Options: H2RAs or PPIs
-H2RAs: can cause thrombocyoptenia (cimetidine), mental status changes (especially elderly or in renal impairment), dose adjustment in renal impairment

-PPIs: risk of GI infections (particularly C. diff), fractures, and nosocomial pnuemonia

36
Q

Anesthetics are commonly used in ICU. What is the main concern?

A

With many ROAs, using lidocaine numerous times a day even topically can cause QT prolongation. Lidocaine can also be combined with EPI since EPI can vasoconstrict the area to keep lidocaine working in one area, but some mixups between EPI/lidocaine and just EPI have cause deaths.

Pay attention to ROA with bupivacaine as well - EPIDURAL only, but IV (can be fatal).

37
Q

What medications can enhance neuromuscular blocking agents?

A

AMINOGLYCOSIDES, POLYMYXINS, CCBs, cyclosporine, inhaled anesthetics, lithium, quinidine, vancomycin

38
Q

Neuromuscular Blocking Agents (NMBAs):
-Drugs
-MOA
-Indications
-Administration Considerations
-Reversal agents

A

Drugs/MOA: paralyze skeletal muscle
-Depolarizing: succinylcholine - resembles ACh which binds to receptors and densitizes them
-Non-depolarizing: atracurium, cisatracurium, pancuronium, rocuronium, vecuronium - bind to ACh receptor, blocking actions of endogenous ACh

Indicaitons: intubation, muscle spasms, prevent shivering during therapeutic hypothermia after cardiac arrest
-Succinylcholine: usually for intubation

Administration Considerations:
-ONLY paralzes: pt should receive an agent for sedation and analgesia prior to usage
-ALL lablels have: “WARNING: PARALYZING AGENT” –> careful with medication errors
-Drugs cause pt to be unable to breathe, move, blink, or cough: take care to protect the skin, lubricate eyes, and suction the aiwary to clear secretions

Revesersal agent: neostigmine, sugammadex
-Glycopyrrolate: reduce secretions

39
Q

Compare the different neuromuscular blocking agents, particularly in metabolism and onset/duration of action and class side effects:
-Succinylcholine
-Atracurium
-Cisatracurium
-Pancuronium
-Rocuronium
-Vecuronium

A

Succinylcholine: short acting, fast onset (30-60 seconds)

Non-depolarizing agents: all can cause flushing, bradycardia, hypotension, tachyphylaxis
-Atracurium and Cistracurium (Nimbex): short t1/2, intermediate acting, metabolized by Hofmann elimination (independent of renal and hepatic function)

-Rocuronium: intermediate-acting

-Vecuronium: intermediate-acting, CAN ACCUMULATE in renal or hepatic dysfunction

-Pancuronium: LONG-ACTING, CAN ACCCUMULATE in renal or hepatic dyfunction, increases HR

40
Q

Aminocaproic acid:
-Brand
-MOA
-ROA
-TX
-AVEs

A

Brand: Amicar

MOA: hemostatic agent - inhibit fibrinolysis or enhance coagulation to stop bleeding

ROA: PO, injection

TX: excessive bleeding during cardiac surgery, liver cirrhosis, and urinary fibronolysis –> NOT to use in active clots or given with factor IX, increasing thrombosis risk

AVEs: thrombosis, injection site reactions

41
Q

Tranexamic acid:
-Brand
-MOA
-ROA
-TX
-AVEs
-CI

A

Brand: Cyklokapron, Lysteda

MOA: hemostatic agent - inhibit fibrinolysis or enhance coagulation to stop bleeding

ROA: PO (Lysteda) , injection (Cyklokapron)

TX: bleeding w/ hemophilia or off-label for surgical bleeding and trauma-associated hemorrhage; tablet for menorrhagia (heavy menstrual bleeding)

AVEs: thrombosis, injection site reactions

CI (injection): acquired defective color vision, active intravascular clotting, subarachnoid hemorrhage; PO - concurrent use of hormonal contraceptive or thromboembolic disease hx/current

42
Q

Recombinant Factor VIIa:
-Brand
-ROA
-TX
-BBW

A

Brand: NovoSeven RT, Sevenfact)

ROA: injection

TX: hemophilia and factor VII deficiency; has been used off-label successfully for warfarin-related bleeding events and hemorrhage from trauma

BBW: thrombotic events particularly when used off-label