Fluid and Electrolytes balance in patients–

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 – 3^rd 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

• · Diarrhoea
• · Vomiting
• · Diuretics

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.