Acute and Critical Care Flashcards
What are the difference between crystalloids and colloids?What are 4 crystalloids? What are 3 colloids?
Crystalloids: infused into vasculature but then they can go into the interstitial space, cheaper and safer than colloids
- 5% dextrose
- 0.9% NaCl
- lactated ringers
- multiple electrolyte injection (Plasma-Lyte A)
Colloids: stays in the vasculature, has side effects
- Albumin 5%, 25%
- Dextran
- Hydroxyethyl starch
What is the definition of hyponatremia and risk of hyponatremia? What steps do we take to assess hyponatremia and how do we treat?
Hyponatremia = Na < 135 mEq/L
- with Na ≤ 120, symptoms may be seizures, lethargy, confusion, coma, respiratory arrest
- Assess serum osmolality
Isotonic:
2. Assess volume status
Hypovolemic - give sodium containing solutions
Hypervolemic - give diuretics, fluid restriction, or AVP receptor antagonists
Isovolemic - give diuretics, fluid restriction, demeclocycline ( if SIADH), AVP receptor antagonists
When correcting, want to correct by less than 12 mEq/L day
What are the arginine vasopressin receptor antagonist? When are they used, what risks do they have, what side effects, and what are notes for initiation?
Conivaptan - injection
Tolvaptan (Samsca) - oral
- used for isovolemic (SIADH) and hypervolemic hyponatremia
- Risks: osmotic demyelination syndrome, hepatotoxicity
- Side effects: thirst, nausea, dry mouth, polyuria
- must start/restart in the hospital, monitor Na
What is the definition of hypernatremia? How do we assess how do we treat?
Hypernatremia = Na > 145 mEq/L
- associated with water deficit and hypertonicity
Hypovolemic: fluids
Hypervolemic: diuretics
Isovolemic: desmopressin
- frequently due to diabetes insipidus
Potassium replacement - how much total body deficit is seen if a drop of 1 mEq/L in K+? What is the max infusion rate of K+ given through a peripheral line?
Magnesium replacement - when to replace IV?
Phosphorus replacement - when to replace IV?
Potassium:
- Drop of 1mEq/L in K (below 3.5) represents a total body deficit of 100-400 mEq
- Potassium replacement protocol to determine amount of K+ to replace with
- Peripheral line maximum infusion rate of ≤10mEq/hr and max concentration of 10mEq/100mL (can be fatal if undiluted or via IV push)
- Identify underlying cause
Magnesium:
- Mg < 1 mEq/L with life threatening symptoms -> replace IV
- Necessary for potassium uptake
- Replacement regimen should continue for 5 days to replace body stores
Phosphorus:
- PO4 < 1mg/dL -> replace IV
- Full replacement takes 1 week or longer
intravenous immunoglobulin - what is it used for? What are the 2 boxed warnings? What are some side effects? What is a dosing and storage consideration? Does IVIG impact vaccinations?
Used for:
- immunodeficiency conditions
- Off label: multiple sclerosis, myasthenia gravis, Guillain-Barre
Boxed warnings
- acute renal dysfunction
- thrombosis
Side effects
- headache, nausea, diarrhea
- injection site reaction, infusion reaction
- renal failure or blood dyscrasias (rare)
- fever
Dosing: use a slower infusion rate in renal and CV disease patients
Storage: do not freeze or shake
IVIG impairs a patient’s response to vaccines
What does the APACHE II score tell you?
APACHE II - Acute Physiologic Assessment and Chronic Health Evaluation II
Helps estimate the risk of ICU mortality. The higher the score, the higher your likelihood of dying before you get out of the ICU
What are the receptor targets of these vasopressors: dopamine, epinephrine, norepinephrine, phenylephrine, vasopressin, angiotensin II
dopamine - dose-dependent receptor effects; D1 -> beta-1 -> alpha-1
epinephrine and norepinephrine - mixed alpha-1 and beta-1 agonist
Phenylephrine - pure alpha-1 agonist
vasopressin - vasopressin agonist
angiotensin II - vasoconstriction, aldosterone release
What doses or dopamine would cause what receptor activity?
Low (renal) dose: 1-4 mcg/kg/min
- dopamine-1 agonist
- see renal vasoconstrition/improved renal perfusion
Medium dose: 5-10mcg/kg/min
- beta-1 agonist
- heart rate increase (positive inotropic effect)
High dose: 10-20mcg/kg/min
- alpha-1 agonist
- vasopressor effect
What is the difference in IV push and IM epinephrine concentration?
IV push - 0.1mg/mL (1:10,000 ratio strength)
IM injection - 1mg/mL (1:1000 ratio strength)
What should we treat vasopressor extravasation with?
Phentolamine - alpha-1 blocker
Vasopressors are all vesicants, so they would all be administered through a central line
nitroglycerin vs. nitroprusside - When do we use? Selectivity (venous vs. arterial)? Boxed warnings/contraindications? Side effects? What is important about nitroprusside metabolism?
nitroglycerin:
- Use: active myocardial ischemia or uncontrolled HTN
- Selectivity: low dose -> venous, high dose -> arterial
- Contraindications: SBP < 90mmHg, use with PDE5-i
- Side effects: causes tachyphylaxis in 24-48hrs (resistance), headache, tachycardia
Nitroprusside:
- Use: better BP effect, should not be used in active myocardial ischemia due to “coronary steal” where it can divert blood away from the disease coronary arteries
- Selectivity: mixed
- Boxed warning: metabolism produces cyanide, excessive hypotension, must be diluted
- Side effects: headache, tachycardia, thiocyanate/cyanide toxicity
- Metabolism causes thiocyanate and cyanide formation, which can cause toxicity if renal or hepatic insufficiency; can co-administer with hydroxocobalamin to reduce/treat the toxicity
What are the MOAs of these inotropes: dobutamine, milrinone
Inotropes increase the contractility of the heart
dobutamine: beta-1 agonist
milrinone - phosphodiesterase-3 inhibitor (produces inotropic effects with significant vasodilation)
What are the 4 types of shock? What are common causes and treatment?
Hypovolemic - low volume
- causes: trauma, GI bleed
- treatment: fluid
Distributive - blood vessels are leaky
- causes: anaphylaxis, sepsis
- treatment: fluid, vasopressors (norepinephrine is DOC for septic shock)
Cardiogenic - heart damages
- causes: acute decompensated heart failure
- treatment: inotropes, diuretics, vasopressors
Obstructive - something blocking the blood flow
- causes: massive pulmonary embolism
- treatment: correct cause
What are the 3 principles for treating shock?
- Fill the tank - optimize preload with IV crystalloid bolus (PRN)
- Squeeze the pipes - peripheral vasoconstrictor (alpha-1 agonist) to increase SVR
- Kick the pump - beta-1 agonist to improve myocardial contractility and cardiac output
What is the formula to calculate MAP
MAP = ([2xDBP]+SBP)/3
What are the two common causes of ICU infections
- Mechanical ventilation
- Foley catheters
How do we treat acute decompensated heart failure?
If volume overload is the problem -> loop diuretics, vasodilators (NTG, nitroprusside, nesiritide)
If hypoperfusion is the problem -> inotropes (dobuatmine, milrinone) & consider vasopressor (dopamine, norepinephrine, phenylephrine) if pt becomes hypotensive
**avoid vasodilators as these can decrease BP and worsen hypoperfusion
What is preferred to treat agitation? What scale is used to assess agitation?
Non-benzodiazepines are preferred
- propofol
- dexmedetomidine (can use in both intubated and non-intubated
- BZDs: lorazepam, midazolam
Use validated sedation scales (RASS) and titrate to light sedation
What is preferred to treat delirium?
- Early mobilization and control of patient’s environment
- Quetiapine (atypical antipsychotic) is preferred over haloperidol
- sedation with non-BZDs should help prevent delirium
Drugs for agitation/sedation:
Dexmedetomidine - MOA, side effects, important notes
Propofol - contraindications, side effects, monitoring, important notes
Lorazepam - toxicity
Midazolam - contraindications, important note
Etomidate - use, monitoring
Ketamine - warnings
Dexmedetomidine: alpha-2 agonist
- Side effects: hypo/hypertension, bradycardia
- Notes: does not require refrigeration, should not exceed 24 hours infusion per FDA labeling, can be used for sedation in intubated and non-intubated patients
Propofol:
- Contraindications: hypersensitivity to egg or soy
- Side effects: hypotension, apnea, hypertriglyceridemia, green urine/hair/nail beds, propofol-related infusion syndrome (PRIS - can be fatal)
- Monitor: triglycerides
- Notes: potential for bacterial growth, so discard vial and tubing within 12 hours of use; this is an oil-in-water emulsion that provides 1.1kcal/mL
Lorazepam: propylene glycol toxicity can lead to acute renal failure and metabolic acidosis
Midazolam:
- Contraindicated with potent CYP3A4 inhibitors
- Notes: can accumulate in renal impairment since it has an active metabolite
Etomidate:
- used as induction agent for intubation given it’s ultra short half life
- Monitor for s/sx of adrenal insufficiency (hypotension, hypokalemia)
Ketamine
- Warning: emergence reactions (hallucinations/dreams/delirium)
What are risk factors for the development for stress ulcers? What do we use for prevention and what some cautions with those agents?
Stress ulcers result from decreased blood flow to the gut
Mechanical ventilation for over 48 hours
Coagulopathy
Sepsis
Traumatic brain injury
Major burns
Acute renal failure
High dose systemic steroids
Prevention:
- H2RAs: caution for thrombocytopenia and CNS side effects (if renal adjustments not made)
- PPIs: caution for C. diff, osteoporotic fractures, nosocomial pneumonia
What is a rare adverse effect of inhaled anesthetics? Which anesthetic should not be given IV?
Inhaled anesthetics may cause malignant hyperthermia
Do not give bupivacaine epidurals IV
What is the most common local anesthetic? What are two common inhaled anesthetics? What are two common injectable anesthetics?
Local - Lidocaine
Inhaled - Desflurane, sevoflurane
Injectable - Bupivacaine, ropivacaine
Which neuromuscular blocking agents are depolarizing vs non-depolarizing and what is the difference? What do you use to monitor paralysis with these?
Depolarizing - succinylcholine
- activates the acetylcholine receptors and desensitizes them
Non-depolarizing - cisatracurium, rocuronium
- blocks acetylcholine from binding to the receptor
Monitor with “train-of-four” to observe twitches
What medication can be used to reduce secretions when using NMBAs? What medications can enhance the neuromuscular blocking activity of the NMBAs, leading to toxicity?
Glycopyrrolate - anticholinergic that can be used to reduce secretions
Can lead to toxicity: aminoglycosides, polymyxins
What are common side effects for all non-depolarizing NMBAs? What type of metabolism does cisatracurium go through?
Side effects of non-depolarizing NMDAs: flushing, bradycardia, hypotension, tachyphylaxis
cisatracurium metabolized by Hofmann elimination (independent of renal and hepatic function)
What are hemostatic agents used for and what are the 3 examples of systemic hemostatic agents?
Hemostasis means causing bleeding to stop. These systemic hemostatic drugs work by inhibiting fibrinolysis or enhancing coagulation which can be beneficial in select circumstances (Ex. brain hemorrhage)
- aminocaproic acid
- tranexamic acid
- recombinant factor VIIa
(there are many topical thrombolytic agents that are used surgically. they usually have the word “thromb” in it)
