Lecture 3 - Potassium and Magnesium

symptoms of hypokalemia

mild: usually asymptomatic

moderate: muscle cramping, weakness, malaise, myalgias

severe: ECG changes, arrhythmias, cramping, impaired muscle contraction

causes of hypokalemia

poor dietary intake, excessive loss (renal, diarrhea)

potassium shift into intracellular compartment

drug induced

what might cause potassium to shift into the intracellular compartment

metabolic acidosis

insulin

B2 receptor agonists (epinephrine, salmeterol)

how do diuretics cause hypokalemia

inhibit sodium reabsorption in distal tubule and collecting ducts → increase sodium in distal tubule → increase potassium excretion → hypokalemia

vascular fluid volume contraction → stimulates aldosterone secretion → increased potassium renal secretion

how does insulin cause hypokalemia

increased potassium transport into liver/muscle/adipose → hypokalemia

(balanced with glucagon to regulate K levels)

how do decongestants (pseudoephedrine), caffeine, B2 agonists cause hypokalemia

promote intracellular shift to potassium

goals of therapy for hypokalemia (+ all electrolyte) management

prevent/treat serious life threatening complications

normalize serum potassium concentration

identify/correct the underlying cause of hypokalemia

prevent overcorrection of the serum potassium concentration

treatment for mild hypokalemia (K 3.5-4.0 mmol/L)

no pharmacological treatment recommended, encourage increased dietary intake of K rich foods

treatment of moderate hypokalemia (K 3.0-3.4 mmol/L)

initiate potassium supplementation

asymptomatic patients: oral therapy

symptomatic patients/pts intolerant to oral: IV

treatment of severe hypokalemia (K <3.0 mmol/L)

IV potassium

should always be treated

what are the 4 types of potassium salts

chloride, gluconate, phosphate, bicarbonate

when would potassium chloride the preferred salt

primary salt form used, most effective treatment for most common causes

when would potassium phosphate be the preferred salt

patient is both hypokalemic and hypophosphatemic

when would potassium bicarbonate be the preferred salt

potassium depletion occurs in the setting of metabolic acidosis

what is the salt form of IV potassium

potassium chloride

when is IV potassium chloride used

severe hypokalemia (K <2.5 mmol/L)

patient signs (ECG changes, muscle spasms)

unable to tolerate oral therapy

what is the vehicle for IV potassium chloride

saline containing solutions (0.45-0.9% NaCl)

why are dextrose containing solutions not used for IV potassium chloride

Dextrose solutions stimulate insulin secretion → can cause an intracellular shift of potassium → make things worse

symptoms of hyperkalemia

mild: usually asymptomatic

moderate: cardiac arrhythmias

severe: cardiac arrhythmias, weakness, respiratory failure, ascending paralysis

what ECG changes are seen with hyperkalemia

peaking of T wave

PR prolongation

los of P wave

prolonged QRS complex

merged QRT&T wave (sine wave)

what are causes of hyperkalemia

• increased K intake (e.g. from overcorrection of hypo)

• decreased renal K excretion (renal failure, endocrine disorders)

• redistribution of K into extracellular space (metabolic acidosis, DM, CKD, B blockers)

• tubular unresponsiveness to aldosterone

• medications (dose dependent)

treatment of hyperkalemia in asymptomatic patients (K < 6.0 mmol/L)

dietary changes (reduce intake)

drug therapy changes (NSAIDs, ACEi, ARBs increase K)

furosemide (increases urine K excretion)

close follow-up

treatment of moderate-severe hyperkalemia (K 6.0-6.9 // >7.0 mmol/L)

immediate treatment → calcium IV (gloconate/chloride 1g)

decrease extracellular K concentration → promote intracellular movement (insulin, B agonist, sodium bicarbonate)

enhance removal (furosemide, cation exchange resin e.g. kayexalate, hemodialysis

important functions of magnesium

cofactor for many biochemical reactions especially systems dependent on adenosine triphosphate, mitochondrial function, protein synthesis, cell membrane function, parathyroid hormone secretion, glucose metabolism

symptoms of hypomagnesemia

cardiac: heart palpatations, arrhythmias, prolongs QRS, sudden cardiac death

neuromuscular: tetany, twiching, generalized convulsions, Chvostek/Trousseau sign

what are causes of hypomagnesemia

GI: reduced intake, alcoholism, reduced absorption (celiac), increased loss (vomiting/diarrhea)

renal: glomerulonephritis, pyelonephritis, drug induced nephrotoxicity (aminoglycosides, cyclosporine, cisplatin)

medications: PPI (reduce absorption), diuretics/excessive laxatives (increase elimination)

treatment of asymptomatic and serum Mg > 0.5 mmol/L hypomagnesemia

oral supplementation (oxide, hydroxide, chloride, citrate, gluconate)

multiple daily doses are required

most common SE: diarrhea

treatment of symptomatic hypomagnesemia and serum Mg < 0.5 mmol/L

IV magnesium sulfate

what are symptoms of hypermagnesemia

usually asymptomatic

lethargy, confusion, muscle weakness, dysrhythmia

what are causes of hypermagnesemia

GFR decline (moderate-severe CKD)

drug-induced: antacids/laxatives contain magnesium, lithium

other medical conditions: hypothyroidism, Addison disease, viral hepatitis

treatment of hypermagnesemia

reduce intake (stop/reduce antacids/laxatives)

enhance elimination → furosemide 40mg IV, forced diuretics (loop diuretic + 0.45% NaCl = increases urine volume)

antagonise the physiological effect → calcium IV

where is 99% of calcium stored

in the bones

What is the role of phosphate (PO4 3-)

metabolism and bone function

what is the role of bicarbonate (HCO3-)

regulating pH