Wednesday, February 4, 2015

Macronutrients: cations

Potassium seems to be the main alkaline ion inside cells followed by magnesium - either way, magnesium is key to controlling both. Sodium and Calcium are extracellular, outside cells, and can be controlled by hydration and diuretics and Mag mur.

Dogs and cats draw only Mag mur, which controls 3 of the 4 cations (the 4th, sodium, is regulated by fluids), so that's all we need to know about Cations.

From here:


Potassium is the most abundant intracellular cation (positively charged ion) in the body. The intracellular concentration is around 20 times greater than in the extracellular fluid, resulting in a large concentration gradient. This maintains the excitability of nerve and muscle cells.
Hyperkalaemia results in progressive conduction problems, which if left untreated can result in cardiac arrest and death. Patients often present with weakness, which progresses to flaccid paralysis or deep tendon reflexes, and cardiac arrest.

Hypokalaemia can cause ventricular tachycardia, and can be caused by pH changes. Hypokalaemia can also be due to increased loss of potassium through renal excretion, which may be caused by diabetes insipidus, hypercalcaemia, hyperaldosteronism, excessive fluid replacement therapy and diarrhoea.

Many patients who are potassium deficient are also deficient in magnesium. Magnesium is important for potassium uptake and for the maintenance of intracellular potassium levels, particularly in the myocardium.


Magnesium is the second most abundant intracellular cation. The interaction with magnesium and the enzyme sodium–potassium ATPase (which acts to pump potassium into cells in exchange for sodium) plays a crucial part in regulating cellular concentration gradients.

Hypermagnesaemia is rare in patients without significantly impaired renal function; magnesium is mainly excreted by the kidneys, which have the capacity to secrete large quantities. Elevated serum magnesium levels can be seen following extensive soft-tissue injury or necrosis (e.g. trauma, burns or following cardiac arrest) as magnesium is mobilised from within cells.

Hypermagneasaemia may lead to nausea, lethargy and weakness, which can lead to respiratory failure, paralysis and coma. Treatment of hypermagnesaemia is based on the patient’s fluid and kidney function. Patients with hypovolaemia and normal renal function can be treated with aggressive intravenous hydration therapy, which will rebalance serum ion concentrations.Magnesium acts as a calcium channel blocker, and at high concentrations this can give rise to electrical conduction abnormalities and require intravenous calcium administration.

Hypomagnesaemia can occur in chronic or acute asthma. It can be due to conditions that affect absorption from the gastrointestinal tract, such as diarrhoea. Signs and symptoms of hypomagnesaemia include neuromuscular manifestations such as tetany (involuntary contraction of muscles), tremors, seizures, delirium and psychosis.


Sodium is the main extracellular cation in the body and has significant effects on serum osmolality. Together with potassium it has a large role in controlling membrane potentials in the myocardium, and therefore a significant role in governing cardiac action potentials. However, unlike potassium, fluctuations in serum sodium levels rarely cause significant cardiac problems until severe variation from normal physiological values has occurred.

Symptoms of sodium deviations are rarely cardiac specific and usually include nausea, vomiting, weakness and confusion, which can result in seizures or coma if left untreated. Excess total body water in relation to sodium is often seen in patients with severe cardiac failure, whereby compensatory mechanisms for sodium regulation are compromised (resulting in hypervolaemic hyponatraemia). Patients should be placed on fluid restriction and treated with a diuretic, which will reduce water levels and gradually correct serum sodium levels.


Calcium has a significant effect on cells in the myocardium, affecting conduction, intracellular signalling and contraction of muscle fibres. In particular, calcium levels can alter the duration of the plateau phase of the myocardial action potential and affect heart conduction.

Hypercalcaemia affects smooth muscle fibres, causing muscle weakness. Hypercalcaemia can be managed initially with aggressive fluid administration, such as sodium chloride 0.9% to encourage renal excretion and [homeopathic] diuretics. If unsuccessful, intravenous bisphosphonates can be used to slow the rate of bone turnover and reduce serum calcium levels, which is commonly undertaken in those with concomitant malignancy.

Symptoms of hypocalcaemia include cramps and tetany and require rapid intravenous treatment with intravenous calcium. Patients  should also be given intravenous magnesium to aid correction.

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