Electrolyte Disturbances Flashcards
Potassium
- where in cell
- importance
- how excreted
- mostly intracellular
- ratio intra/extracellular essential for cell membrane potential
- mostly excreted by kidneys
Hyperkalemia
- value
- Greater than 5.1/5.5 mEq/L
- > 7 can lead to hemodynamic and neuro consequences
- > 8.5 can lead to respiratory paralysis or cardiac arrest, can be fatal
Hyperkalemia
- causes
- Lab/human error (if break RBC can leak K+ out)
- Renal failure and acidosis (Cell will bring excess H+ into cell, push K+ out. Total body K+ has not changed but shift has occurred)
- Cell death (burn, tumor lysis syndrome)
- Drugs, toxins, medications
• K+ supplements
• Non-selective BB (propranolol)
• Succinylcholine (paralytic used in Em medicine)
• Digoxin
• K-sparing diuretics (spironolactone)
• ACEi
• Pentamidine and trimethoprim - ACEi and trimethoprim were most common drug causes in recent study
- Reduced kidney function was common cause in recent study
Hyperkalemia
- EKG findings
- Peaked T wave
- Widened QRS
- Loss of P wave
- Sine wave
- V-fib/asystole
Hyperkalemia
- Treatment
- Treat once confirmed not a lab error, true hyperkalemia and >6.5 or EKG changes
- Figure out the CAUSE don’t just treat the imbalance
Then
1. Membrane antagonism
2. Intracellular shift of K+
3. Eliminate K+ from body
Hyperkalemia
- Membrane antagonism (tx)
• Calcium, stabilizes heart
• Dr. Hunt uses when Hyperkalemic and EKG changes
• Options
- Calcium chloride (3X ca content as ca gluconate, give through central line)
- Calcium gluconate (better if only have peripheral line but less bang for buck)
Hyperkalemia
- intracellular shift of K (tx)
- IV insulin (co-transporter forces K back into cells)
- Albuterol/Salbutamol
- IV sodium bicarb (only if in acidosis)
Hyperkalemia
- Eliminate K from the body (tx)
- Kayexalate (binds in bowel, comes out in stool). Risk of colonic necrosis
- Furosemide (risk of hypokalemia). Dr. Hunts first option, let nephrologist order kayexalate
- Dialysis: if reduced kidney function, not a rapid solution
Hyperkalemia
- mnemonic
C BIG K Di • Calcium • Bicarb, beta agonist • Insulin • Glucose • Kayexelate, Lasix • Dialysis
Pseudohyperkalemia
- D/t collection and storage of specimen
- Pt clenched fist when sample was taken, difficulty collecting sample
- Cooling of sample or deterioration dt length of storage
- Thrombocytosis
- Severe leukocytosis can cause psuedohypokalemia
Hypokalemia
- value
Serum K+ <3.5 mEq/L, severe is <2.5
Hypokalemia
- first steps
- Assess muscle weakness, increased respiratory muscle use
- EKG changes? Medical emergency
- ABG usually helpful
Hypokalemia
- causes
**Think diuretics and diarrhea
- Drugs (thiazides, furosemide), Toluene in huffers
- GI loss (v/d)
- Hormones (high aldosterone or cortisol)
- Bicarb: metabolic alkalosis (H+ out of cell, K+ in)
- Renal tubular defects
- Mg deficiency
- Decreased intake
- Increased loss
• Renal (CHF, nephrotic syndrome, dehydration)
• Renal tubular defects
• GI losses (v/d/laxatives)
• Drugs (diuretics, ampho B, mannitol, aminoglycosides)
- Transcellular shifts
• Alkalosis (vomiting, diuretics)
• Insulin
• Beta agonists
Hypokalemia
- clinical presentation
- CV: arrhythmia, EKG change
- Skeletal muscle: weakness (MC presentation in ER), cramps, tetany, paralysis (K<2)
- Smooth muscle: constipation, urinary retention
- Metabolic alkalosis
Hypokalemia
- EKG changes
- PR prolongation
- T wave flatten/inversion
- ST depression
- U waves
- Long QT interval (T&U fuse together)
Hypokalemia
- Tx
- PO replacement preferred
- IV also an option
- Goals: K between 4 and 4.5 mEq/L
- Might have to increase Mg too (>1.0)
- 1 mEq drop in serum level = 100-200 mEq loss in total body store
- Options
KCL PO, KCL IV, K-phos, K-bicarb, K-citrate
Hypokalemia
- when is IV indicated
- Dysrhythmias
- Prominent sx
- Unable to tolerate PO
- Likely if K<2.5
- Give slowly, preferably via central line
Sodium
- where in body
- how does it move around
- two major hormones related to Na levels
- Extracellular cation, closely related to total body water
- Moves into cells depending on osmolality
- Moved out of cell by Na/K ATPase
- Renin: released with low intravascular volume: triggers Na reabsorption and K secretion in distal nephron via aldosterone
- ADH: released when there is high serum osmolality. Enhances renal water reabsorption. Also triggered by angiotensin, catecholamines, opiates, caffeine, stress, hypoglycemia, hypoxia
Hyponatremia
- serum level
<135 mmol/L
- Must ensure true hyponatremia by adjusting for glucose
- For every 100 above 100 glucose, add 1.6 mmol sodium
Hyponatremia
- first steps
Quickly eval:
- neuro symptoms
- what is the pt’s volume status
Hyponatremia
- Three types
- hypervolemic
- Euvolemic
- Hypovolemic
Hyponatremia
- hypervolemic
- Decreased effective circulating volume, fluid elsewhere (edema): CHF, hepatic cirrhosis, nephrotic syndrome
- ADH is stimulated = water retention
- CHF, cirrhosis, nephrotic syndrome
- Pt will look “wet”
Hyponatremia
- euvolemic
• Inappropriate ADH (SIADH, etc.)
- SIADH, psychogenic polydipsia, beer potomania, adrenal insufficiency, MDMA, hypothyroid
- SIADH causes: tumor, infection, trauma, pulm dz, drugs (diuretics and chemo)
• Pt not wet or dry
Hyponatremia
- hypovolemic
- ADH secretion stimulated by volume depletion: Renal loss, GI loss, excessive sweating, 3rd spacing
- Pt will look dry
Hyponatremia
- clinical presentation
- when <125 mmol/L
• Lethargy, confusion, agitation • n/v • weakness • focal neuro deficits • Seizures (increased risk when <120) • Altered LOC *pts with chronic hyponatremia may tolerate lower levsl without sx than acute onset
