Electrolytes Flashcards
Effect of acidosis on K
Increased H+ concentration causes H+ to shift ICF, then K shifts ECF
Acidosis causes hyperkalemia
Alkalosis causes Hypokalemia
Effect of Insulin tx on electrolyte balance
Insulin causes glucose to enter cells, and draws K and Phos along with it, potentially causes hypokalemia and hypophosphatemia
Effect of acidosis on ionized ca levels
H+ competes with Ca for binding sites on albumin. Therefore:
Acidosis Ionized (unbound) Ca levels increase Alkalosis Ionized Ca levels decrease
What’s the deal with Chloride and pH
Essentially cl is acidic. So when it’s lost or wasted with diuretics, most common cause of metabolic alkalosis
When HCO3 is lost with significant diarrhea we get hyperchloremia and therefore also metabolic acidosis
Potassium need to knows
3.6-5
• important in repolarization of action potential, mediated ICF osmotic pressure
• diffuses out of cell, actively transported into cell, absorbed dietarily, excreted renally
• Hypokalemia caused by low intake, GI loss in V/D, alkalosis/insulin causing intracellular shift. Hyperkalemia caused by excessive intake, acidosis, cellular trauma
• ecg changes, dysrythmias, muscle weakness
Magnesium need to knows
0.7-1.0
• involved in active transport of Na/K, regulates and moderates transport of calcium to muscle proteins
• Gi absorption, fecal and renal excretion
• hypomag cause by poor intake/GI absorption, diuretic wasting, GI loss with diarrhea. Hypermag caused by high intake renal disfunction
• Hypomag causes neuromuscular overstimulation with tetany, hyperflexion, dysrythmias, N/V. Hypermag causes muscle weakness, hypotension
Na need to knows
135-148
• primary ECF lyte, key to depolarization in action potential, role in fluid balance in kidneys
• serum levels regulated in kidneys primarily by aldosterone, ANP, and ADH. Diffuses into cells, actively transported out
• Hyponatremia caused by excessive hypotonic fluid intake, dilution also. Hypernatremia caused by loss of hypotonic ECF like in significant diuresis, diarrhea, insufficient fluid intake
• primarily neurological effects as neurons either swell or shrivel with intra/extracellular fluid shifts. High serum osmo with hyper, and low osmo with hypo
Phosphate need to knows
0.9-1.4
• cell membrane structure, ATP formation
• absorbed in GI competes with ca creating inverse relationship, excreted in kidneys
• hypo caused by poor intake/absorption, GI/renal wasting, shift into cells in alkalosis, with insulin/glucose. Hyper caused by renal dysfunction, cell lysis
• Hypo causes low ATP problems, muscle weakness, dec contract, confusion. Hyper causes hypocalcemia, bc they have inverse relationship
Calcium need to know
- Membrane permeability, skeletal/cardiac muscle contraction, 99% bound in bones and albumin, 1% Ionized and active in cellular function
- GI absorption, parathyroid hormone liberates from bone inc GI abs dec renal excretion. Calcitonin dec absorption, inc renal excretion
- hypo caused by poor absorption, GI renal wasting, PTH dysfunction. Hyper caused by renal dysfunction
- hypo causes increased cell membrane excitability therefore anxiety, agitation, muscle spasms, dec contractility. Hyper causes opposite
Chloride need to know
100-112
• effects serum osmo along with Na, acid base balance
• GI absorb, renal excretion
• hypo caused by excess bicarb, Na low, GI renal wasting. Hyper caused by bicarbonate deficit, Na high, acidosis
• hypo causes alkalosis, low Na, low K, dysrhythmias, neuro excitability similar to low Na as they move together. Hyper causes acidosis, hypernatremia, dysrhythmias, neuro depression
Major causes of metabolic acidosis
- lactic acidosis – associated with inadequate cellular
oxygenation - renal dysfunction and alterations in HCO3 regulation
- loss of HCO3 from diarrhea, or fistula, drainage etc
Major systemic effects of metabolic acidosis
- Broad vasodilation and dec contractility and dec CO with pulm vasoconstriction therefore decreased o2 supply overall
- pH >7.2 calacholamine should compensate
- pH <7.1 life threatening resistance to vasoactive drugs
- oxyhemoglobin right shift
- decreased cellular response to insulin
