Water, electrolytes and acid-base balance

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12 Water, electrolytes and acid-base balance

Questions

Question 1

1. Why do conditions that cause retention of sodium, such as cardiac failure, result in low serum sodium?
2. What is meant by ‘free water’?

Question 2

Why is there a difference in the pattern of oedema in nephrotic syndrome and cardiac oedema? How is it related to the interstitial spaces and all that? I am confused.

Question 3

Why is there a difference in the clinical presentation of oedema due to renal failure and oedema due to cardiac failure, and how is this related to the loose nature of the interstitial tissue in the periorbital area? The answer given was that it is because, in cardiac failure, there is orthopnoea and the most dependent portion in this case is the legs, which is why the oedema occurs there. You also mentioned that in renal failure there is no orthopnoea and the patient doesn’t have to sit up, hence the difference. This does not seem to take into account right ventricular heart failure (RVF), where there is no question of orthopnoea. Pedal oedema is found in right ventricular failure. Is the answer not that, in congestive heart failure (CHF) there is pump failure (and the heart cannot pump blood against gravity) hence oedema in the dependent areas, whereas in renal failure there is no pump failure and the heart does not lose its capacity to pump blood against gravity. The oedema in this case develops in those tissues that have a loose interstitium, one such site being the periorbital area of the face. This is the reason for the difference in clinical presentation.

Question 4

What treatment is recommended for recurrent attacks of generalized swelling, with angio-oedema, in a middle-aged female patient?

Question 5

Is an osmotic diuresis, due to hyperglycaemia for instance, a cause of both hyponatraemia and hypernatraemia. Please explain how this can be the case.

Question 6

What is the mechanism of β2-agonists (albuterol) in correcting hyperkalaemia in emergency? How does it cause a shift of potassium?

Question 7

Why do we give sodium lactate along with sodium bicarbonate in acidotic patients? How does sodium lactate then act?

Question 8

How does hypochloraemia alone cause a metabolic alkalosis?

Question 9

I have read the part concerning acid-base imbalances and I would like to ask about two things:

1. Why is there a higher concentration of anions (18) on measuring the anion gap while there is a high concentration of immeasurable anions? I would have expected a higher concentration of cations because most of them are measurable.
2. Could you explain to me in more details how NaCO3 loss or HCl retention could lead to normal anion gap acidosis?

Question 10

What is the exact formula for calculating the serum anion gap?

Question 11

What is the role of IV saline in the management of a cirrhotic patient with a serum sodium of 120mmol/L?

Question 12

Why do we give calcium gluconate to a patient with severe hyperkalaemia?

Question 13

Can you explain the respiratory alkalosis and metabolic acidosis in salicylate poisoning?

Question 14

In an elderly patient with oedema due to heart failure, which is the best diuretic to start treatment with? Some books recommend thiazides whereas others use loop diuretics.

Answers

Answer 1

1. One explanation is the non-osmotic release of antidiuretic hormone (ADH), due to arterial underfilling causing the retention of water and a dilutional hyponatraemia. A second explanation is that reduced delivery of chloride to the diluting segment of the ascending loop of Henle because of avid reabsorption of sodium and chloride in the proximal tubule. This results in a reduced ability to generate ‘free water’ and produce a dilute urine so hyponatraemia occurs due to water excess.
2. The term ‘free water’ is a concept that is used to describe the movement of water independent of sodium.

Answer 2

In all conditions associated with oedema there is increased extracellular volume associated with renal sodium chloride retention.

The oedema in all conditions is usually in the ankles in all patients but this depends on body position. Patients with the nephrotic syndrome are not usually breathless and so lie flat and the oedema occurs in the face. The reverse is true for cardiac failure.

Answer 3

We are obviously going to disagree. Can we give you an example? In nephrotic syndrome, patients have periorbital oedema in the morning because of lying flat; in heart failure, the patient cannot lie flat because of orthopnoea. As oedema progresses, all spaces are eventually filled with fluid.

Answer 4

This sounds like idiopathic oedema of women. It might respond to diuretics. Antidiuretic hormone (ADH) acts on vasopressin (V2) receptors located on principal cells. ADH promotes water reabsorption in the collecting ducts and this might be a factor in the cause of the oedema. V2 receptor antagonists are now available.

Further reading

Hays RM (2006) Vasopressin antagonists – progress and promise. New England Journal of Medicine355: 2146–2148.

Answer 5

Hypernatraemia is due to loss of Na+ and water with the osmotic diuresis. This causes dehydration and hypernatraemia. Hyponatraemia occurs because antidiuretic hormone (ADH) stimulates thirst; excess water compared to sodium is drunk, and hyponatraemia occurs.

Answer 6

β2-adrenergic receptors increase the activity of the sodium-potassium ATPase pump in the cell membrane. This is followed by the excretion of excess potassium in the urine.

Answer 7

Sodium lactate intravenous infusion is obsolete for the treatment of metabolic acidosis. It carries the risk of lactic acidosis and should not be used.

Answer 8

If chloride is lost either through the kidney or via the stomach, there is a preferential absorption of bicarbonate in the distal tubule. This leads to metabolic alkalosis.

Answer 9

1. Normally there is an anion gap of approximately 12mmol/L. Albumin normally makes up the largest portion of these unmeasured anions.
2. The loss of bicarbonate, e.g. from the gastrointestinal tract, is initially compensated but eventually the increased loss of bicarbonate leads to hydrogen ion excess; that is, acidosis (Fig. 12.1).
image

Fig. 12.1 The Flenley acid-base nomogram. This was derived from a large number of observations in patients with ‘pure’ respiratory or metabolic disturbances. The bands show the 95% confidence limits representing the individual varieties of acid-base disturbance. The central white box shows the approximate limits of arterial pH and Pco2 in normal individuals.

Answer 10

Anion gap is calculated using serum concentrations as:

image

The normal value is 6–12mmol/L.

Answer 11

The initial management is with water restriction as the hyponatraemia is dilutional. IV saline therapy depends on:

• the rapidity of the development of hyponatraemia
• whether the patient is symptomatic.

In most patients with liver disease, the onset is slow and the patient is consequently asymptomatic; Hypertonic saline 3% should only be given to patients with neurological symptoms and signs and must be given extremely slowly so that the change in serum sodium should not exceed 15mmol over 48 hours.

Answer 12

Calcium ions protect the cell membrane from the effects of hyperkalaemia although they don’t alter the potassium concentration. The correction of this acute hyperkalaemia is shown in Box 12.1.

Box 12.1 Correction of severe hyperkalaemia

1 Immediate

Attach ECG monitor and IV access Protect myocardium

• 10mL of 10% calcium gluconate IV over 5min
• Effect is temporary but dose can be repeated after 15min

Drive K+ into cells

• Insulin 10 units + 50mL of 50% glucose IV over 10–15min followed by regular checks of blood glucose and plasma K+
• Repeat as necessary
• and/or correction of severe acidosis (pH < 6.9): infuse NaHCO3 (1.26%)
• and/or salbutamol 0.5mg in 100mL of 5% glucose over 15min (rarely used)

2 Later

Deplete body K+ (to decrease plasma K+ over the next 24h):

• Polystyrene sulphonate resins:

• 15g orally up to three times daily with laxatives
• 30g rectally followed 3–6 hours later by an enema

• Haemodialysis or peritoneal dialysis if the above fails

Answer 13

Initially, there is stimulation of the respiratory centre with hyperventilation leading to respiratory alkalosis. Metabolic acidosis ensues because of compensatory mechanisms including the renal excretion of bicarbonate and potassium as well as the accumulation of lactate, pyruvate and ketone bodies.

Answer 14

Bendroflumethiazide is a cheap, effective agent that, if given early in the day, causes a diuresis that does not interfere with sleep. Chlortalidone, another thiazide, has a longer action and can be given on alternate days. It is useful if a patient has prostatic symptoms as it produces a slower diuresis. Loop diuretics, e.g. furosemide and bumetanide, act within 1 hour of administration and would be used as first line in a severe acute situation, e.g. pulmonary oedema.

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