Lytes acid and base Flashcards
All lytes are measured in
mEq/L
Sodium level
135-145
K+ level
3.5-5.0
Ca2+ level
4.5-5.5
Phosphate level
2.5-4.5
Mg level
1.5-2.5
Sodium function
90% of ECF cations Regulates osmotic forces and H20 balance For muscle and nerves with K and Ca Helps with pH through sodium bicarb and sodium phosphate Particaptes in cell reactions
Hypernatremia
> 145
From extra sodium or too little water
It causes intracellular dehydration and movement of water to ECF which may cause hypervolemia
Hypernatremia etiology
1. Excessive water loss from Diabetes insipidus Fever Resp infections (tachypnea) Diarrhea (osmotic) 2. Too little water 3. Too much sodium too much Nabicarb Saltwater near drowning Over secretion of aldosterone
ADH
Vasopressin
Increases solute free water reabsorption
Constricts arteries
Released from hypertonicity
Clinical manifestations
- Thirst and signs of high ADH (polydipsia, oliguria, anuria)
- Intracellular dehydration
- H20 out of cells (headache, agitation, restlesness, decreased reflexes, seizures)
- Decreased vascular volume - tachy, weak and thready pulse, low BP
Hyponatremia
<135
Vomiting, diarrhea (inflammatory) GI suctioning, burns, sweating, lack of salt intake
Some diuretics
Hormone imbalances (low aldosterone high ADH)
Too much water
Kidney failure
Hypeglycemia as it draws water into ECF, lowering serum Na
Clinical manifestations of hyponatermia
Cramps, weakness, headache, depression, apprehension, impending doom, personality changes, lethargy, stupor, coma (from nerves not being able to depolarize)
GI - anorexia, nausea, vomting, cramps, diarrhea
Increased ICF causing pitting edema and hypotension
Potassium function
Maintaining RMP
Predominant ICF cation
Regulation of K+
Kidneys via diffusion, distal tubular cells determines whether it will be secreted into urine or reabsorbed into distal tubules
K+ and diuretics
increase flow rate of K+ through distal tubules increasing K+ secretion
There are K+ sparing diuretics which can counter this
K+ and pH
H+ accumulate in ICF and kick K+ out of cell
decreased ICF decreases secretion of K+ by distal tubular cells creating a state of hyper K
Hyper K causes
> 5.5 mEq/L
From increased K+
or a shift out of cells from
Trauma, burns, crush injuries, acidosis, insulin deficiency, hypoxia
Also decreased renal excretion from renal failure, aldosterone deficit, K+ sparing diuretics, ACE inhibtors, Angiotensin II receptor blockers
Hyper K clinical manifestation
GI -nausea, vomiting, cramps, diarrhea Muscles -paraesthesia -muscle weakness Cardiovascular -arrythmias, cardiac arrest Oligura Acidosis
Hypo K
<3.5 from
- Inadeqaute intake
- Renal loss (non K+ sparing, cushings, aldosteronism, steroids)
- Vomiting, diarrhea, GI suction, draining GI fistula
- Transcompartmental shift from ventolin, alkalosis, insulin