NEET MBBS UG PG BSC Nursing Notes

🟣 Acid-base balance - Fluid and electrolyte balance

The normal pH of arterial blood is 7.35–7.45. Normally hydrogen (H⁺) ions are buffered by two main systems:

▪️Proteins including haemoglobin comprise a fixed buffering system.
▪️Bicarbonate is a very important buffer, as it has both a gaseous and an aqueous phase:

CO2 ↔️ CO2 + H2O ↔️ H2CO3 ↔️ H⁺ + HCO3⁻

This means that bicarbonate buffering is a very powerful way of maintaining the body’s pH through both rapid and slow compensation:
▪️Rapid compensation takes place at the lungs, where CO2 can be blown off in response to acidosis. This reduces the amount of H2CO3 (carbonic acid) in the blood as shown by the equation and so acutely compensates for acidosis. Conversely, if pCO2 concentrations rise, e.g. in hypoventilation, then acidosis can result (respiratory acidosis).
▪️In long-term abnormalities of pH balance, this mechanism is inadequate because the body’s stores of bicarbonate become depleted. The kidney is able to compensate for this, by increasing its reabsorption of bicarbonate in the proximal tubule.

The arterial blood gas is used to assess acid–base status. The pH is first examined to see if the patient is acidotic or alkalotic. The pCO2 and bicarbonate are then examined to identify the cause of any acid–base disturbance and any compensation that may have occurred. Most arterial blood gas machines also provide the base excess. This is a calculated figure, which provides an estimate of the metabolic component of the acid–base balance. The base excess is defined as the amount of H+ ions that would be required to return the pH of the blood to 7.35, if the pCO2 were adjusted to normal. A normal base excess is –2 to +2. A more negative base excess signifies a metabolic acidosis (hydrogen ions need to be removed) and a more positive base excess signifies a metabolic alkalosis (hydrogen ions need to be added). The pO2 is examined separately to determine if there is respiratory failure.

▫️ There are four main patterns:

🔸 Acidosis with high pCO2 defines a respiratory acidosis. If this is acute, there is no compensation (i.e. the bicarbonate levels are normal). In chronic respiratory acidosis renal reabsorption of bicarbonate will reduce the acidosis (partial metabolic compensation) or return the pH to a normal level (complete metabolic compensation). Causes include respiratory failure.

🔸 Acidosis with low bicarbonate and negative base excess defines a metabolic acidosis. If the patient is able the respiration will increase to reduce carbon dioxide and hence return the pH to normal (partial or complete respiratory compensation). Causes of metabolic acidosis include salicylate poisoning, lactic acidosis or diabetic ketoacidosis. Alternatively failure to excrete acid or increased loss of HCO3− , such as renal tubular disease and diarrhoea. Hyperkalaemia may occur as an important complication particularly if there is also acute renal failure.

🔸 Alkalosis with a low carbon dioxide defines respiratory alkalosis. This may result from any cause of hyperventilation including stroke, subarachnoid haemorrhage, meningitis, pyrexia, hyperthryoidism, pregnancy or anxiety. It is generally an acute condition and so little compensation occurs.

🔸 Alkalosis with a high bicarbonate and a positive base excess defines metabolic alkalosis. It is rare and may be caused by loss of acid from the gastrointestinal tract (e.g. vomiting) or from the kidney (e.g. Cushing or Conn’s syndrome). Hypokalaemia may occur.

🔺 Fluid regimens
These should consist of maintenance fluids (which covers normal urinary, stool and insensible losses) and replacement fluids for additional losses and to correct any pre-existing dehydration. Fluid regimens must also take into account that patients of differing weight have different fluid and electrolyte requirements (see Table 1.4). Potassium is added to intravenous fluids in patients who are not being fed, although this should be done with care. Both hypokalaemia and hyper-kalaemia are potentially life-threatening and serum potassium must be checked daily in patients who are given potassium replacement. Patients with acute or chronic renal failure should not have potassium added routinely to fluid replacement (although hypokalaemia should of course be treated). Rapid administration of potassium is dangerous, so even in hypokalaemia no more than 10 mmol/h is recommended (except in severe hypokalaemia within an intensive care setting) and the potassium must be uniformly mixed in the bag.

A typical daily maintenance regime for a 70 kg man with normal cardiac and renal function consists of 8 hourly bags of:
➔ 1 L of 0.9% saline with 20 mmol KCl added,
➔ 1 L of 5% dextrose with 20 mmol KCl added and
➔ 1 L of 5% dextrose with 20 mmol KCl added.

In general, dextrosaline is not suitable for maintenance, as it provides insufficient sodium and tends to cause hyponatraemia. Postoperative patients are also more prone to hyponatraemia due to mild SIADH, so may require proportionally more sodium, e.g. 2 L of 0.9% saline to 1 L of 5% dextrose. Replacement fluids generally need to be 0.9% saline, as losses tend to have a high sodium concentration, e.g. drain fluid, blood, vomitus and diarrhoea.

Fluids should not be prescribed without taking into account the patient’s current fluid balance, continued losses and underlying coexistent diseases. It should also be remembered that intravenous fluids do not provide any significant nutrition.

🟢 Intravenous fluids - Fluid and electrolyte balance

Intravenous fluids may be necessary for rapid fluid replacement, e.g. in a shocked patient, or for maintenance in patients who are unable to eat and drink or who are unable to maintain adequate intake in the face of large losses, e.g. due to diarrhoea. When prescribing intravenous fluids certain points should be remembered:

➖ Are intravenous fluids the best form of fluid replacement? If possible, oral fluids are preferable or if swal-low is impaired consider nasogastric administration, which has the advantage of allowing nasogastric feed to be given to provide nutrition.

➖ Which intravenous fluid should be given? Ideally this should be the one that matches any fluid and electrolyte deficit or losses most closely. For example, blood loss should be replaced with a blood transfusion and salt and water loss (e.g. vomiting, diarrhoea) with normal saline. Additional potassium replacement is often needed in bowel obstruction, but may be dangerous in renal failure.

➖ In calculating the volume required for maintenance check if is there increased insensible loss, e.g. due to sweating in pyrexial patients, or are there other fluids being administered which need to be taken into account? For example, some patients are on intravenous drugs or intravenous nutritional supplements (total parenteral nutrition).

➖ Patients at risk of cardiac failure (elderly, cardiac disease, liver or renal impairment) require special caution as they are more prone to develop fluid overload.

There is no universally applicable fluid regimen. The choice of fluid given and the rate of administration depend on the patient, any continued losses and all patients must have continued assessment of their fluid balance using fluid balance charts, observations and clinical examination as well as monitoring of serum electrolytes by serial blood tests.

🔺 Fluid preparations
Intravenous fluid has to be isotonic to lysis of red blood cells. The administration of water alone would lead to water moving across cell membranes by osmosis, such that the cells would swell up and burst. Giving hypertonic fluid is equally dangerous, as it causes water to move out of cells.

➖ Most intravenous fluids used are crystalloids (saline, dextrose, combined dextrose/saline, Hartmann’s solution). It should be remembered that dextrose is rapidly metabolised by the liver; hence giving dextrose solution is the equivalent of giving water to the extra-cellular fluid compartment. If insufficient sodium is given in conjunction, or the kidneys do not excrete the free water, hyponatraemia results. This is a common problem, often because of inappropriate use of dextrose or dextrosaline and because stress from trauma or surgery as well as diseases such as cardiac failure promote antidiuretic hormone (ADH) release. This leads to a mild form of syndrome of inappropriate antidiuretic hormone (SIADH;) where there is water retention by the kidneys with resulting hyponatraemia.

➖ Colloids (albumin, dextran or gelatin-based fluids) contain high-molecular-weight components that tend to be retained in the intravascular compartment. This increases the colloid osmotic pressure (oncotic pressure) of the circulation and draws fluid back into the vascular compartment from the extracellular space. A smaller volume of colloid compared to crystalloid is needed to have the same haemodynamic effect. Theoretically they are of benefit for rapid expansion of the intravascular compartment; however, they have anti-coagulant, antiplatelet and fibrinolytic effects, which may be undesirable. There has been no consistent demonstrable benefit of using colloid over crystalloid in most circumstances. In addition, the use of albumin solution in hypoalbuminaemic patients (which seems logical) has been associated with increased pulmonary oedema, possibly due to rapid haemodynamic changes or capillary leakage of albumin.

🔵 Hypokalaemia - Fluid and electrolyte balance

A serum potassium level of

🔵 Hyperkalaemia - Fluid and electrolyte balance

A serum potassium level of >5.5 mmol/L is defined as hyperkalaemia. Hyperkalaemia of >6.0 mmol/L can cause cardiac arrhythmias and sudden death without warning.

🔺Incidence
This is a common problem, affecting as many as 1 in 10 inpatients.

🔺Pathophysiology
Hyperkalaemia lowers the resting potential, shortens the cardiac action potential and speeds up repolarisation, therefore predisposing to cardiac arrhythmias. The rapidity of onset of hyperkalaemia often influences the risk of cardiac arrhythmias, such that patients with a chronically high potassium level are asymptomatic at much greater levels.

🔺Clinical features
Hyperkalaemia is almost always asymptomatic and only diagnosed on blood testing. There may be a history of conditions that predispose to hyperkalaemia and it is important to take a careful drug history. Foods high in potassium include bananas, citrus fruits, tomatoes and salt substitutes. The first indication of hyperkalaemia may be a cardiac arrhythmia or sudden cardiac arrest. Uncommonly there may be reduced tendon reflexes and muscle power.

🔺Investigations
U&Es, calcium, magnesium to look for evidence of renal impairment and any associated abnormality in sodium, calcium and magnesium. Low calcium can increase the risk of arrhythmia. An arterial blood gas to look for acidosis may be indicated and diabetics should have their glucose checked.

An ECG should be performed immediately in all cases. Abnormalities occur in the following order: tall, tented T-waves, small P-wave and a widened, abnormal QRS complex. Patients may develop bradycardia or complete heart block, and if left untreated may die from ventricular standstill or fibrillation. Continuous ECG monitoring should occur until the hyperkalaemia is treated and ECG abnormalities resolve.

🔺Management
Ideally hyperkalaemia should be prevented in at-risk patients by regular monitoring of serum levels and care with medication and intravenous supplements. Once hyper-kalaemia is diagnosed, withdraw any potassium supplements or causative drugs.

If the hyperkalaemia is mild (7 mmol/L, it is a medical emergency:

➖ Calcium gluconate is given intravenously. The calcium provides some immediate cardio-protection by reducing myocardial excitability, even in a patient with normal serum calcium levels. It can be repeated after a few minutes if the abnormalities on ECG persist.

➖ Until treatment of the underlying cause can take place, a glucose and insulin infusion promotes intracellular K+ uptake. Salbutamol nebulisers have a similar effect through β receptor stimulation. These can be repeated whilst the underlying cause is addressed, but have only a temporary effect.

➖ Diuretics, e.g. loop diuretics can be used to increase renal excretion. Oral ion-exchange resins or enemas may be used to increase gastrointestinal elimination of potassium. Oral resins can cause severe constipation, so these should be given with laxatives and are not a long-term solution.

➖ Any acidosis should be corrected.

➖ Refer to a renal physician or intensive care unit for haemofiltration or haemodialysis if the hyperkalaemia is refractory to treatment or if there is severe renal failure.