Acute & Critical Care Medicine Flashcards
(35 cards)
what commonly used fluids are crystalloids and which colloids?
Crystalloids: D5W, NS, LR, Plasmalyte
Colloids: albumin
hyponatremia (lab value and s/s)
- technically < 135
- usually don’t see symptoms until < 120
symptoms can be mild (HA, confusion), or severe (seizures)
types of hyponatremia and treatment
- hypervolemic: too much volume (can be dt cirrhosis, HF, or renal failure) - diurese (can consider conivaptan or tolvaptan but those are $$$)
- isovolemic: likely SIADH - diurese (can consider demecycline off label, or conivaptan or tolvaptan but those are $$$)
- hypovolemic: low volume (can be dt overdiuresing, adrenal insuffiency and salt wasting syndromes) - stop inciting factor, if <120 and/or severe s/s, can do hypertonic saline
all of these are technically hypotonic i think
always try to limit correction to a rate of < 12 mEq/24hrs
tolvaptan (drug class, monitoring)
- selective AVP antagonist (arginine vasopressin receptor antag)
- should be started in a hospital due to rapid Na increase, monitor closely
- do NOT use for more than 30 days dt hepatotox
hypernatremia
- Na > 145
- usually associated with water deficiency
hypokalemia lab values and causes
- K < 3.5 mEq/L
- for every 1 mEq/L drop in K concentration represents a total body deficit of 100-400
- causes; metabolic alkalosis, overdiuresis, meds (amphotericin, insulin)
treatment resistant hypoK
can try giving Mg because it helps with K reuptake
if both hypoMg and hypoK present, correct Mg first
potassium infusion notes
general recommendation for peripheral admin of potasisum is a rate <10 mEq/hr and a [ ] < 10mEq/100 mL
can go a bit higher than these if a patient is severely severely hypoK
if given undiluted or via IV push, can be fatal
hypomagnesemia (labs, causes and treatment)
- Mg <1.3
- causes: chronic alcohol use, diuretics, amphotericin B
- treat Mg < 1 with IV replacement - s/s may include seizures and arrhytmias
- Mg < 1.5 can be replenished with PO
hypophosphatemia common causes
- CKD IS THE MOST COMMON CAUSE
- phosphate binding drugs (calcium salts, sevelemar)
- chronic alcohol intake
- hyperparathyroidism
hypophosphatemia labs and treatment
- if <1mg - severe and very likely symptomatic (muscle weakness and resp failure); treat with IV phos at 0.08 - 0.16 mmol/kg in 100mL NS or D5W over 6 hrs
- if less severe, can treat orally, full replacement often takes at least a week
often pt has concurrent hypoMg and hypoK that needs to be treated
what does an incentive spirometer do
helps facilitate lung expansion for deep breathing (useful if pt has atelectasis)
IVIG off label uses
- multiple sclerosis
- myasthenia graivs
- Guillain-Barre syndrome
IVIG adminstration ntoes and ADR
- slow infusion rate if pt has renal or CV disease
- can cause renal dysfunction esp if the formulation is stabilized with sucrose
- pt can develop infusion reaction, if they do, slow or stop infusion
- thrombosis can occur even in pts wtih no risk factors
- do NOT shake or freeze
what does the APACHE II score do
calculate risk of ICU mortality
dopamine dosing
- low: 1-4 mcg/kg/min (primarily dopamine action)
- medium: 5-10 mcg/kg/min (primarily beta-1 agonist)
- high: 10-20 mcg/kg/min (primarily alpha 1 agonist)
can pressors admin lead to extravasation?
unfortunately yes, treat with phentolamine (alpha 1 blocker)
general pressor ADR
- arrhythmias and tachycardia (esp dopamine and epi)
- necorsis
- phenylephrine can cause brady cardia
- epi can cause high blood sugar
general pressor administration rules
- do NOT use if soln is discoulred or if there is a precipitate
- admin via central line
epinephrine dosing
- 1:10,000 ratio strength (0.1mg/mL) for IV push
- 1:1000 ratio strength (1mg/mL) for IM inj or compounding
what vasopressor acts on what
dopamine had its own card
epinephrine, norepi, phenylephrine, vasopressin
- epinephrine: alpha1, beta1, beta2
- norepinephrine: alpha 1 (with slight beta1)
- phenylephrine: alpha 1
- vasopressin: vasopressin (aka arginine vasopressin AVP and antidiuretic hormone ADH) - does NOT have inotropic or chronotropic effects
nitroglycerin
effect, CI, other notes
- at low dose is a venous dilator, at high dose is an arterial dilator
- do NOT give if SBP < 90 or pt on PDE-5 inhibitor
- pt can develop tachyphylaxis, so efficacy is limited to the first 24-48 hrs of continuous administration
- needs to be stored in a non-PVC container (glass)
Nitroprusside
effect, adr, storage
- 50/50 arterial and venous vasodilator
- produces cyanide (use at lowest dose possible for shortest amount of time, can counter with hydroxocobalamin)
- adr: cyanide toxicity, increased intracranial pressure
- requires light protection and is clear (if it is blue, it has been degraded to cyanide, don’t use)
what inotropes are used in the ICU, what are their MOA
inotropes increase CO -> increases perfusion
dobutamine may turn pink dt oxidation, that’s fine
- dobutamine: beta-1 agonist (minor beta2 and alpha1 agonist) - increases HR and force of contraction -> increased CO
- milrinone: PDE-3 - produces significant vasodilation -> increased CO
