Fluids/Electrolytes Flashcards Preview

Emergency Medicine 2 > Fluids/Electrolytes > Flashcards

Flashcards in Fluids/Electrolytes Deck (57)
Loading flashcards...
1
Q

Percentage of the body that is fat, protein, and water

A

protein = 18%

Fat = 16%

Water = 60%

2
Q

distribution of body water

A
3
Q

Solute

A

substance dissolved in another substance, known as a solvent. The concentration of a solute in a solution is a measure of how much of that solute is dissolved in the solvent

4
Q

osmosis

A
  • water flows across the membrane to equalize the concentrations
  • Osmosis is the spontaneous net movement of solvent molecules through a semi-permeable membrane into a region of higher solute concentration,
5
Q

osmolarity

A
  • the total number of moles of solutes per liter of solution
  • Salts (mainly Na, Cl)
  • Urea nitrogen (BUN)
  • Glucose
  • Others (small contribution)
  • Whereas osmolality (with an “ℓ”) is a measure of the osmoles (Osm) of solute per kilogram of solvent (osmol/kg or Osm/kg), osmolarity (with an “r”) is defined as the number of osmoles of solute per liter (L) of solution (osmol/L or Osm/L
6
Q

estimated serum osmolarity

A
  • normal ≈ 290 mOsm/L
  • This version is essentially identical as it just includes conversion factors to convert mg/dl to mmol/l
7
Q

tonicity

A
  • the total number of moles of solutes per liter of solution that can exert an osmotic force across a cell membrane
  • tonicity - ability of an extracellular solution to make water move in or out of a cell
  • What is it going to do to the water across the membrane? (draw the fluid or push the fluid)
  • The number of osms will affect where the water goes
8
Q

Types of IV fluids

A
9
Q

crystalloid vs colloid

A
  • Crystalloid solutions—IV fluids containing varying concentrations of electrolytes.
  • Colloid solutions—IV fluids containing large proteins and molecules that tend to stay within the vascular space (blood vessels).
10
Q

hypotonic solution

A
  • D5W & 1/2NS (0.45%)
  • Designed to treat intracellular dehydration - more water less solutes
  • Example: hypernatremia or DKA
  • more solutes inside the cell so it is going to pull water into the cell - rehydrating the cell
  • A carbohydrate solution that uses glucose as the solute dissolved in sterile water.
  • Packed as an isotonic solution but becomes hypotonic once in the body because the glucose is metabolized rapidly by the body’s cells
11
Q

Isotonic solution

A
  • NS (0.9%), Lactated Ringer and Plasmalyte
  • Used to replace extrcellular fluid volume - balanced water and solutes
  • Examples: blood loss, surgery, dehydration
12
Q

Hypertonic solution

A
  • 3% Saline, D10W, D5Win ½ NS
  • Designed to replace extracellular solutes - draws water out of the cell - more solutes less water
  • Example: hyponatremia
  • cells are bloated and this high solute solution will draw water out of the cells
  • Na+ outside of the cell # decreased so fluid shifts to the inside of the cells - bloating them
13
Q

IV fluids that remain in the blood vessels/plasma space

A
  • Colloids are often based on crystalloid solutions, thus containing water and electrolytes, but have the added component of a colloidal substance that does not freely diffuse across a semipermeable membrane
14
Q

colloids

A
  • Albumin- Replace low blood protien, shifts fluid into blood vessels to treat shock after trauma, burns, surgery
  • Dextran- glucose polysaccharide - adjunctive treatment of shock or impending shock due to hemorrhage, burns, surgery or other trauma
  • FFP- replaces plasma coags after trauma or to reverse anticoagulation
  • PRBCs- Red blood cells that have been separated. Used to treat anemia that is symptomatic or HGB less than 7-8 (6).
  • Cant give FFP really if they are on NOACs, but can give if they are on warfarin
15
Q

Medical decision-making on fluids

A
  • Is your patient stable?
  • What are you replacing?
    • Blood
    • Metabolic losses (sweating, breathing)
    • GI losses (vomiting, diarrhea)
    • “Third-spacing” (interstitial edema, ascites, burns)
    • Losses from diuretics, renal disorders, etc.
  • How much do they need?
  • Generic for unstable pt: 1-2L
  • If you give 2L and theyre not getting better, you need to go down a different road
16
Q

how to assess volume status

A
  • Vital signs:
    • HR
    • BP
    • Orthostatics
  • Exam:
    • JVD
    • Skin turgor
    • Mental status
  • US:
    • B lines/IVC
  • Labs:
    • Electrolytes
    • CBC - Increased HCT
17
Q

severity of dehydration based on % of body weight lost

A
18
Q

how fast to run the fluids

A
  • Considerations:
    • Patient in shock
    • Dehydrated but stable patient
    • Patient with CHF or renal failure who may be volume overloaded
    • Maintenance fluids
    • Neuro damage
  • CHF or renal failure – you have someone whos septic but they have CHF and you don’t want to make one condition worse by treating the other condition
19
Q

Maintenance fluids (adults)

A
  • To replace normal daily losses
    • Urine, sweat, breathing, stool
  • 70-kg adult loses about 2500-3000 mL/day
    • 100-125 mL/hr
20
Q

Maintenance fluids (children)

A
  • 4-2-1 Rule
  • Use the Broselow Tape!
  • Weight and length (M2)
  • Use Broselow tape
  • 15mg kiddo – 50mL/h
  • 4ccfluid per Kg per hour for first 20 kg
21
Q

Rule of thumb in a volume depleted patient

A
  • start with 10-15 mL/kg bolus then reassess
22
Q

Burns are special: Parkland formula

A
23
Q

what about the pH

A
  • Hypoperfusion leads to metabolic acidosis
  • GI tract fluid losses also affect pH:
    • Vomiting: lose H+ (alkalosis)
    • Diarrhea: lose HCO3- (acidosis)
  • Distribution of K+ depends on pH
  • Organ function is affected by abnormal pH
  • Long story short- when the cells don’t get enough O2 they can’t break down glucose completly and puruvate is formed which is converted to lactate.
  • Most cells in the body normally metabolize glucose to form water and carbon dioxide in a two-step process. First, glucose is broken down to pyruvate through glycolysis. Then, mitochondria oxidize the pyruvate into water and carbon dioxide by means of the Krebs cycle and oxidative phosphorylation. This second step requires oxygen. The net result is ATP, the energy carrier used by the cell for metabolic activities and to perform work, such as muscle contraction. When the energy in ATP is used during cell work via ATP hydrolysis, hydrogen ions, (positively charged protons) are released. The mitochondria normally incorporate these free hydrogen nuclei back into ATP, thus preventing buildup of unbound hydrogen cations, and maintaining neutral pH.[citation needed]
  • If oxygen supply is inadequate (hypoxia), the mitochondria are unable to continue ATP synthesis at a rate sufficient to supply the cell with the required ATP. In this situation, glycolysis is increased to provide additional ATP, and the excess pyruvate produced is converted into lactate and released from the cell into the bloodstream, where it accumulates over time. While increased glycolysis helps compensate for less ATP from oxidative phosphorylation, it cannot bind the hydrogen cations that result from ATP hydrolysis. Therefore, hydrogen cation concentration rises and causes acidosis.[7]
  • The excess hydrogen cations produced during lactic acidosis are widely believed to actually derive from production of lactic acid. This is incorrect , as cells do not produce lactic acid; pyruvate is converted directly into lactate, the anionic form of lactic acid.
  • Rule of thumb: restore plasma volume first
  • Mother Nature often takes care of the pH
  • Virtually never need to give H+ in alkalosis
  • Rarely need to give HCO3- in acidosis
24
Q

Causes of non-focal ALOC

A
  • ITS COMA!
  • Infection
    • (e.g. meningitis, encephalitis)
  • Trauma
  • Seizures
  • CVA (stroke)
  • Overdose (tox), opioids
  • Metabolic
    • e.g. hypoglycemia, hyponatremia
  • Alcohol
  • Not infection, trauma, stroke, OD, or alcohol
  • THIS IS A METABOLIC PROBLEM
25
Q

Sodium (Na+)

A
  • Can be too high or too low
  • Can result from
    • too much or too little salt
    • too little or too much water
    • factitious results (lab error, high glucose or lipids)
  • Abnormal Na+ usually presents as
  • Neurologic Symptoms
    • abnormal serum osmolarity
    • brain cells shrink or swell
26
Q

Hormonal control of Na+

A
  • Antidiuretic hormone (ADH) conserves WATER
    • Too much ADH → water intoxication
    • Too little ADH → kidney can’t concentrate urine
  • Aldosterone conserves SODIUM
    • Too much aldosterone → Na retention, K loss
    • Too little aldosterone → Na loss, K retention
  • ADH - No pee - doesn’t make you pee
27
Q

Hyponatremia: some causes

A
  • Water intoxication
  • Syndrome of Inappropriate ADH (SIADH)
    • Remember ADH CONSERVES WATER - holds onto water therefore diluting Na+
  • Diuretics
  • Factitious or “pseudohyponatremia”
  • Fruita
  • The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is defined by the hyponatremia and hypo-osmolality resulting from inappropriate, continued secretion or action of the antidiuretic hormone arginine vasopressin (AVP) despite normal or increased plasma volume, which results in impaired water excretion.
  • type 2 diabetes drugs,seizure drugs, antidepressants, heart and blood pressure drugs, cancer drugs, anesthesia
28
Q

Pseudohyponatremia

A
  • Due to very high concentrations of glucose, lipids, or proteins in plasma
    • Water is drawn osmotically out of cells and into the plasma
    • Increased volume of water in the plasma “dilutes” the Na+ level
  • Each 100 mg/dL glucose elevation decreases the measured Na+ by about 1.6-1.8 mEq/L
  • Treatment: manage the underlying cause (eg, treat the glucose)
29
Q

treatment of hyponatremia

A
  • Consider both the volume status and the serum osmolarity
  • What does our “hazing” patient have?
    • Excess volume
    • Excess water relative to sodium
    • Low serum osmolarity / tonicity
30
Q

Hypervolemic hyponatremia

A
  • Cause: excess water
  • Symptoms(cerebral edema): confusion, headache, vomiting, seizures, coma, death
31
Q

hypervolemic hyponatremia: rx

A
  • If stable, restrict water intake and wait
  • If seizing/coma, must correct sodium faster using hypertonic saline
32
Q

hypovolemic hyponatremia

A
  • Hyponatremia with decreased extracellular fluid (eg, diuretics; diarrhea):
  • Rx: volume replacement (usually NS)
33
Q

Too rapid correction of low Na+

A
  • Too-rapid correction of low Na+ (by giving sodium) may cause shrinkage of brain cells, leading to brain damage (central pontine myelinolysis)
  • Don’t want water to exit the cells too quickly and cause permanent damage
34
Q

abnormal sodium

A
  • In general, it’s best to correct it no faster than it occurred
  • In chronic patients, try to correct Na+ at a rate of no more than 0.5 mEq/hour
35
Q

causes of hypernatremia

A
  • Too little water
    • No access/ unable to drink
    • Defective thirst (elderly)
    • Losses from fever, sweating, hyperventilation
    • No ADH (antidiuretic hormone)
  • Too much salt
    • Rare: mostly children (accidental ingestion)
    • Iatrogenic (hypertonic fluids or drugs)
36
Q

Hypernatremia - sx

A
  • Generally when Na+ >155-160 or Osm >350
  • Irritability, restlessness
  • Seizures
  • Coma
  • Permanent neurological damage
37
Q

oral rehydration fluids

A
38
Q

sodium - key points

A
  • Major solute in ECF
  • Affects plasma volume, osmolarity
  • The brain is the main victim of abnormal Na+
  • Correct abnormal Na+ no faster than it developed
39
Q

hyperkalemia - causes

A
  • Too much K+ going in to the body
    • Overdose, iatrogenic, lethal injection, some drugs
  • Too little K+ excreted
    • Renal failure; K-sparing diuretics
  • Shift of K+ from INTRAcellular to EXTRAcellular fluid (acidosis)
  • Cell destruction (eg, crush injury, burns, rhabdo)
  • False elevation due to hemolysis in blood tube
40
Q

potassium

A
  • It’s all about the heart
    • Slowed conduction
    • Cardiac arrest
  • Does not have a significant effect on plasma volume or osmolarity
  • EKG changes:
    • 5.5 mEq/L: Peaked T-waves (repolarization abnormalities)
    • >6.5 mEq/L: P wave flattens, PR prolongation (paralysis of atria)
    • >7.0 mEq/L: QRS prolongation, ventricular arrhythmias
    • > 9.0 mEq/L: Cardiac arrest 2/2 asystole, V fib or PEA
41
Q

treatment of hyperkalemia

A
  1. Protect the cardiac conduction system
  2. Shift K+ from the ECF into cells
  3. Remove excess K+ from the body
42
Q

protect the heart

A
  • Calcium counteracts the effects of hyperK+ on the heart conduction system — give
    • 1 amp of 10% Calcium Chloride, or
    • 2-3 amps of 10% Calcium Gluconate
  • Repeat if needed to narrow the QRS interval
  • Calcium chloride when youre coding!! 2-3x more powerful than gluconate
  • Any other time, give calcium gluconate
43
Q

move K from ECF into cells

A
  • IV insulin (regular) 10 U + 50mL D50W
  • Na bicarbonate 44 mEq IV
  • High-dose (20 mg) nebulized albuterol
  • If you already have a ton of sugar on board, you don’t need to give dextrose
44
Q

Remove excess K from the body

A
  • Urgent hemodialysis
  • Lasix 40-80mg and NS if urinating
  • Sodium polystyrene sulfonate (Kayexalate™)
    • Ion exchange resin (note: Na+ load)
    • Oral or by enema
    • Slow; uncertain benefit; GI tract ulcerations
45
Q

hypokalemia

A
  • ECG changes
    • Flattened T-waves
    • Prolonged QT interval
    • U-waves
    • Ventricular arrhythmias
  • Intestinal ileus
  • Muscle weakness - paralysis
46
Q

hypokalemia causes

A
  • Loss of body K+ stores
    • Diuretics (except for spironolactone)
    • Volume loss (vomiting, diarrhea)
  • Shift of K+ into the cell
    • Alkalosis (pH ∆ +0.1 ~ K+ ∆ -0.5)
    • Insulin + glucose
    • β-2 adrenergic drugs (eg, albuterol)
47
Q

hypokalemia Rx

A
  • 50 mEq raises serum K+ by ~ 1 mEq/L
  • Oral replacement
    • Not as fast, but safer
  • IV
    • Big vein, give slowly (local pain, vein irritation)
    • Maximum rate 20 mEq/hr (some say up to 40)
48
Q

potassium key points

A
  • Major effects on the heart, not the brain
  • Muscle weakness
  • When potassium levels are low, the cells cannot repolarize and are unable to fire repeatedly, and muscles and nerves may not function normally.
49
Q

calcium

A
  • Important role in
    • Transmission of nerve impulses
    • Contraction of muscles
    • Cardiac electrical conduction
    • Many other important functions
50
Q

where is calcium stored

A
  • Stored in bone (reservoir)
  • Balance controlled by
    • Parathyroid hormone ↑ Ca++
    • Calcitonin ↓ Ca++
    • Vitamin D ↑ Ca++
  • In blood, Ca++ is bound to protein (albumin)
    • Lab measures total vs. ionized (free) levels
51
Q

hypocalcemia

A
  • Lack of parathyroid hormone
    • PT glands accidentally injured/removed during thyroid surgery
  • Chronic renal failure
  • Acute pancreatitis
  • Alkalosis
  • Massive blood transfusions
  • It forms chelated clumps of calcium from the fatty sludge in the pancreas
  • Paresthesias
  • Hyperreflexia, clonus, tetany
  • Prolonged QT interval on ECG → Torsades
  • Treatment: calcium
    • Oral and IV
52
Q

signs of hypocalcemia

A

Inflate cuff 20mmHg above SBP for 3-5min which increases the irritability of the nerves and causes flexion of the wrist and mcp joints. – carpal spasm and adduction of thumb

53
Q

hypercalcemia causes

A
  • Too much PTH (hyperparathyroidism)
  • Cancer with bone metastases
  • Vitamin D overdose
  • Thiazide diuretics
  • Prolonged immobility
  • Many other causes
54
Q

hypercalcemia sx

A
  • Lethargy, confusion, coma
  • Muscle weakness
  • Anorexia and abdominal pain (pancreatitis)
  • Polyuria (loss of kidney concentrating ability) leading to dehydration
55
Q

hypercalcemia rx

A
  • Give IV fluids (0.9%NS)
    • Large amounts often needed to restore ECF volme
  • Increase Ca++ excretion with a LOOP diuretic (eg, furosemide)
  • Drugs to decrease Ca++ release from bone
    • Calcitonin, mithramycin, corticosteroids
56
Q

phosphorus

A
  • Hypo:
    • Sx: muscle dysfunction, weakness, decreased cardiac output, confusion, delirium. Symptoms usually occur with levels less than 2mg/dL
    • Treat underying cause - DKA/diarrhea, antacid therapy, Vit D def.
    • Tx: Oral repletion until level <1mg/dL then give IV
  • Like Calcium - found in teeth and bones - need vit D to metabolize
  • Sxs are nondescript and don’t come on basic chem panels
  • You need to order mag and phos any time youre considering electrolyte issues
  • Hyper:
    • Usually asymtomatic
    • Secondary to laxatives/enemas, renal failure, prolonged exercise
    • Tx: diet/phosphate binders if indicated
  • Like Calcium - found in teeth and bones - need vit D to metabolize
57
Q

Magnesium

A
  • Hypo:
    • Diarrhea, PPI, etoh, dieutetic use
    • Sx occur rapidly due to storage in bones/cells
    • 60-65% ICU pts
    • Tx: replete w oral or IV
  • Ca++ delpletion goes hand in hand - parathyroid
  • 2 percent of hospitalized patients [1]. The incidence rises to as high as 60 to 65 percent in patients in an intensive care setting in which nutrition, diuretics, hypoalbuminemia, and aminoglycosides may play important role
  • Hyper:
    • Sx: decreased ca++, muscle weakness, N/V, cardiac arrest
    • Renal failure
    • Tx: Ca gluconate, lasix, dialysis