Fluid Balance in Physiology Quiz

Hypovolaemia

• Defined as the loss of sodium and water resulting in extracellular fluid (ECF) loss.
• Common causes include blood loss, internal fluid loss, diuretics, sweating, and vomiting.
• Clinical signs include low jugular venous pressure (JVP) and low urine output.
• Laboratory tests often reveal high albumin, urea levels, and hematocrit.
• Physiological responses involve baroreceptors triggering ADH release and activation of RAAS, leading to water retention and sodium reabsorption.
• Treatment typically includes administration of 0.9% NaCl and 5% glucose, along with fluid and salt restriction.

Hypervolaemia

• Characterized by the gain of sodium and water, which increases extracellular fluid volume.
• Common causes include excessive isotonic intravenous fluids and sodium retention due to congestive heart failure (CHF) and primary hyperaldosteronism.
• Clinical signs consist of high JVP, peripheral and pulmonary edema, shortness of breath (SOB), and ascites.
• Physiological responses include atrial distension releasing ANP, which promotes natriuresis and diuresis, leading to vasodilation.
• Management often involves diuretics and fluid and salt restrictions.

Impaired Sodium Transport: Hypokalaemia

• Defined as the loss of potassium resulting in extracellular fluid loss, specifically levels below 5mmol/L.
• Causes include redistribution (e.g., alkalosis), diuretics, Conn’s syndrome, and gastrointestinal fluid loss.
• Clinical manifestations include skeletal muscle weakness, polyuria, cardiac arrhythmias, and ECG changes such as decreased T wave height.
• Physiological impact includes hyperpolarization and increased excitability of cells.
• Treatment focuses on reversing the cause, with options like oral or IV KCl and amiloride.

Impaired Sodium Transport: Hyperkalaemia

• Characterized by the gain of potassium leading to elevated levels in extracellular fluid.
• Causes involve lysed cells, acidosis, lack of insulin, beta-blocker effects, and renal retention due to reduced glomerular filtration rate (GFR).
• Clinical signs include skeletal muscle paralysis, significant ECG changes (peaked T waves, prolonged QRS), and potential cardiac arrest.
• Physiological effects result in depolarization and reduced cellular excitability.
• Treatment includes stabilizing membrane potential with calcium salts, shifting potassium into cells (insulin and glucose, beta-agonists), and methods to remove potassium (diuretics, resin in the gut, dialysis).

Impaired Water Transport: Hyponatraemia

• Defined as sodium loss resulting in low osmolality in extracellular fluid.
• Urine dilution failure leads to concentrated urine, occurring under different ECF volume conditions.
• Common causes include chronic kidney disease (CKD), loop or thiazide diuretics, and excessive ADH.
• Clinical symptoms may include headache, nausea, vomiting, seizures, and cognitive impairments.
• Treatment approaches vary based on ECF status, generally involving fluid restriction or careful sodium replacement.

Impaired Water Transport: Hypernatraemia

• Characterized by sodium gain leading to high osmolality.
• Causes include chronic renal failure, high fluid losses, and diabetes insipidus.
• Clinical signs can include confusion, muscle weakness, and complications from central bleeding or cerebral shrinkage.
• Treatment typically involves the administration of hypotonic solutions to correct fluid imbalance.