How to Maintain Fluid & Electrolytes balance

Fluid and Electrolytes balance in patients–

fluid balance m
electrolyte balance

Water is –General—

  • · 50% of body weight in women
  • · 60% in men

Water is contained in the body in two major compart­ments :

  • 1. ECF (Extra-cellular fluid) – 25%
  • 2. ICF (Intra-cellular fluid) – 75%

ECF is present in the blood vessels i.e. intravascu­lar compartment and outside the blood vessels in the interstitium i.e. extravascular.

  • a. Intravascular or Plasma water
  • b. Extravascular or Interstitial fluid

The ratio of intravascular to extravascular is 1:3. 

Osmolality —

  • in mosmol/Kg (miliosmol per Kg) is the particle concentration of a fluid.
  • ECF osmolality = ICF osmolality
  • ECF particles are Na+, (1-, HCO-3
  • ICF contains K+, organic phosphate esters (ATP1, cre­atine phosphate, phospholipids). .
  • K + concentration reflects the amount of ICF because the ICF mainly contains potassium and potassium is mainly contained in the ICF.
  • Na+ concentration tells about the ICF.
  • Organic solutes or osmolytes are inositol, betaine, glutamine.
  • Ineffective osmoles like urea do not contribute to water shift but volume of ICF and ECF.
  • Fluid shift between ICF and ECF is determined by star­ling forces, capillary’ hydraulic pressure and colloid osmotic pressure.

Water Balance

Normal plasma osmolality is 275 – 290 mosmol/Kg Water intake = Water excretion — Loss of water occurs from Urine

  • Stool
  • Skin
  • Respiratory tract
  • Maximal urine osmolality is 1200 mosmol/kg. 600 mosmols must be excreted per day. Minimum urine output is 500 ml /day.
  • Water intake by thirst is regulated by osmoreceptors located in anterolateral hypothalamus.
  • Osmotic threshold for thirst is 295 mosmol/kg.
  • water excretion is regulated by AVP (Arginine va­sopressin peptide) also called A (Antidiuretic hor­mone), synthesized in hypothalamus and ‘secreted by the posterior pituitary gland.
  • Baroreceptors in carotid sinus act like osmoreceptors. Osmotic threshold for AVP release is 280 – 290 mosmol/kg.
  • Tonicity depends mainly on Na+ concentration.AVPsecretion is regulated by —
  • · Thirst
  • · Volume
  • · Nausea
  • · Pain
  • · Stress
  • · Hypoglycemia
  • · Pregnancy
  • · Drugs.

Kidney excretes water by —

  • 1. Filtration and delivery of water and electrolytes to nephron.
  • 2. Reabsorption of Na+ and (1- in thick ascending limb of loop of Henle and distal nephron.
  • 3. No reabsorption of water from collecting ducts in absence of AVP (Arginine vasopressin).
  • Sodium balance [Na+ is pumped out by Na+ K+ ATPase pump.]
  • 90% of Na+ is extracellular.
  • Sodium intake – Increased Na+ intake results in in­creased Na renal excretion to maintain Na+ balance.
  • Sodium excretion – Effective circulating volume keeps normal GFR.
  • Decreased effective circulating volume results in de­creased GFR.
  • 2/3 of filtered Na+ is reabsorbed in PCT (proximal convoluted tubule, 1/3 in thick ascending limb of loop of henle, 5% by thiazide sensitive Na+, Cl­  cotrasporter. 
  • Final Na+ reabsorption occurs in collecting ducts.
  • HYPOVOLEMIA occurs due to volume depletion, and salt and water loss. 

Causes of renal loss of sodium and water  :

  • · Diuretics
  • · Diabetes mellitus (excretion of glucose and urea
  • leading to osmotic diuresis)
  • · Hyperalimentation (high protein)
  • · Mannitol
  • · Tubular and interstitial disorders
  • · Acute tubular necrosis.

Causes of obligatory renal Na+ and water loss:

  • When the GFR is <25 ml /min there is obligatory re­nal Na+ loss as in :
  • · Decreased ECF
  • · Hypoaldosteronism (Mineralocorticoid deficiency)
  • · Central diabetes insipidus (CDI)
  • · Nephrogenic diabetes insipidus.

Causes of extra renal loss of sodium and water Extrarenal loss occurs from

  • · GIT
  • · Skin
  • · Respiratory tract
  • · Burns
  • · Pancreatitis – 3rd space accumulation which is sequestration of fluid in space which is neither extracellular nor intracellular
  • · Peritonitis.

Vomiting leads to loss of H+ ions resulting in meta­. bolie alkalosis.

.Diarrhoea leads to loss of HCO-3 ions resulting in metabolic acidosis.

Insensible water loss is 500 ml / day.

-Insensible water loss is increased in fever, heat expo­sure, exercise and sweating.

Sweat is hypotonic

. In hyperventilation there is increased water loss. Severe haemorrhage results in volume depletion.

Pathophysiology of Hypovolemia —-

  • There is decreased plasma volume leading to hypoten­sion, decreased venous return, decreased cardiac output, activation of RAS (renin angiotensin system), decreased GFR, decreased sodium excretion, in­creased tubular reabsorption of sodium.
  • Decreased ANP (atrial natriuretic peptide) and in­creased aldosterone and AVP result in increased re­absorption of sodium by collecting ducts.

Clinical features of Hypovolemia

  • There is history of vomiting, diarrhoea, polyuria and diaphoresis.
  • There is fatigue, weakness, muscle cramps, thirst and postural dizziness.
  • There is oliguria, cyanosis, abdominal and chest pain and confusion.
  • There is decreased skin turgor, dry oral mucous mem­brane.

Signs of hypovolaemia —

  • decreased JVP, hypoten­sion, tachycardia, and hypovolemic shock.
  • In hypovolemic shock there is hypotension, tachy­cardia, peripheral vasoconstriction, cyanosis, cold and clammy hands, oliguria and altered mental state.
  • Lab data 
  • BUN (blood urea nitrogen), plasma creatinine are in­creased.
  • GFR (Glomerular filtration rate) is decreased BUN – creatinine ratio is 10 : 1 normally
  • In prerenal azotaemia the urea is elevated greatly and BUN to serum creatinine ratio becomes 20 : 1.
  • Increased urea production is seen in
  • · Hyperalimentation with protein
  • · Glucocorticoid therapy
  • · GI (gastrointestinal) bleeding

Volume depletion and sodium:

  • Volume depletion can lead to hyponatraemia, hypernatraemia or normal sodium level.
  • Hypokalemia is defined as plasma K+ concentration less than 3.5 meq/L .
  • Hyperkalemia is defined as plasma K+ concentra­tion more than 5 meq/L.

Causes of Hypokalemia

Causes of Hyperkalemia

  • · Renal failure
  • · Adrenal insufficiency
  • · Metabolic acidosis.

Causes of Metabolic alkalosis

  • · Diuretics
  • · Vomiting
  • · Nasogastric suction.

Causes of Metabolic acidosis

  • · Renal failure
  • · Tubulointerstitial disorders
  • · Adrenal insufficiency
  • · Diarrhoea
  • · Ketoacidosis
  • · Lactic acidosis.

Treatment of Hypovolaemia Oral fluids —-

  • IV fluids – Normal saline (Isotonic saline) 0.9% NaCI or 154 meq / L Na 3% NaCI or 513 meq / L Na
  • In hyponatremia hypertonic saline is given to raise sodium concentration by 1-2 mmol/hr for first 3-4 hours and not more than 12 mmol/L during first 24 hours. Rapid correction of hyponatremia can result in ODS (Osmotic Demy­elination Syndrome) which is flaccid paralysis, dysarthria, dysphagia.
  • The quantity of sodium required to increase the plasma sodium concentration can be estimated by multiplying the deficit in plasma sodium con­centration by total body water.
  • Total body water is 50-60% of lean body weight in women and men respectively.
  • So to raise the sodium concentration from 110­120 mmol in 70kg man will require (120-110) x 70 x .6 = 420 mmol of sodium.
  • In hypernatremia 0.45% NaCI is given which is 77 meq/L sodium
  • 5% dextrose in water
  • Blood transfusion
  • Albumin infusion
  • Dextran IV
  • For hypokalemia give potassium chloride IV or oral.

Treatment of Hyperkalemia—

  • Stop food substances with high potassium. Calcium gluconate in dose of 10 ml of 10% solu­tion in 2 – 3 minutes.
  • 10 – 20 units of regular insulin with 25 – 50 gm of glucose is given IV. Insulin causes potassium shift into cells and glucose is given to prevent hypoglycaemia.

This is a short description about fluid balance in patient, if you have any question you can put comment in comment box.

Related Posts:
You May Also Like::