Fluid and electrolytes,
acid base balance,
AND
IV fluids
Prof. M K Alam
MS; FRCS
Intended Learning Outcomes- ILOs
At the end of this presentation students will be able to:
 Understand the normal & abnormal fluid and electrolyte
status in the body.
 Describe how the body maintains the homeostasis.
 Identify and manage fluid and electrolyte abnormalities.
 Understand the mechanism of acid base balance.
 Identify and mange acid base disorders
 Describe different IV fluids and its uses.
Fluid and electrolytes
Fluid & electrolytes
management form an
integral part of surgical care
Fluid and electrolytes
• Homeostasis- integrated action of cellular membrane,
specific organs , local and systemic hormones
• Diseases, trauma, surgery & medicationscan adversely affect the equilibrium
Fluid and electrolytes
Total body water (TBW)
• 60% of body weight (range 50-70%)
• Contained primarily in skeletal muscle
• Slightly higher in men
• Declines steadily with age
• Obese has less body water (Fat is devoid of water)
Fluid Compartments
• Intracellular -
40% of body weight
• Extracellular-
20% of body weight
- Interstitium 15%,
- Intravascular or plasma 5%
• Compartments separated by semipermeable
membrane to maintain the composition differences
INTRACELLULAR electrolytes
• Dominant cation- K⁺ (160 mEq/L) , Mg⁺
• Anions- phosphates (HPO₄) and proteins
Extracellular electrolytes
• Dominant cation- Na⁺(140 mEq/L)
• Anions- chloride (Cl⁻), bicarbonate (HCO₃⁻)
Fluid and electrolytes
Electrical neutrality- balance of cations
and anions on either side of the
membrane
Fluid and electrolytes
• Osmotic forces are prime determinant of water
distribution in the body
• Major determinants of osmotic activity in plasma are
Na⁺, glucose & urea
• Normal serum osmolarity 285 mOsm/L
Fluid and electrolytes
• Regulation of fluid volume mainly by kidney
• Osmoreceptors in posterior Pituitary: ADH release promote retention
of free water by distal renal tubules & collecting ducts.
• Renin-angiotensin-aldosterone system: Acting on kidney increases
water &Na⁺ reabsorption, K⁺ & H⁺ excretion by distal renal tubules.
• Baroreceptors in kidney & carotid: Small role
Fluid balance
Normal state: Fluid gain = fluid loss
FLUID GAIN:
Oral intake- 2-3 L/ day (2/3rd fluid+ 1/3rd solid)
Oxidative metabolism of protein & fat- 400-500 ml/ day
Fluid balance
• FLUID LOSS:
Urine 1-1.5 L /day,
Faeces 250 ml/day
Insensible loss from skin & lung- 600-900 ml/day
(loss increases by 10% for each 1°C rise in body temperature)
MAINTENANCE OF FLUID REQUIREMENTS
 100 ml / 1st 10 kg,
 50ml / 2nd 10kg,
 20 ml / subsequent kg body weight
 70-kg man 2500 ml / day = 35 ml / kg
Water & Electrolyte
abnormalities
Fluid volume deficits (isotonic)
• Aetiology: Vomiting, nasogastric output, GI
fistulas, lengthy abdominal surgery (10ml/kg/hr.),
sepsis, inflammation (3rd space loss )
• Acute loss: Hypotension, tachycardia, oliguria,
altered mention
• Chronic loss: Oliguria, loss of skin turgor,
orthostatic hypotension, low urine Na⁺ and
BUN/creatinine ratio >15:1.
Fluid volume deficits (isotonic)
• Hematocrit- elevated 5%-6%/ L volume deficit
• Treatment: Isotonic solutions (RL, NS) to
restore physiologic parameters
(urine >0.5ml/hr., hemodynamic status)
Volume deficits (uncommon types)
• Hypotonic dehydration:
Iatrogenic,
Inadequate resuscitation with hypotonic solutions
• Hypertonic dehydration:
Impaired consciousness or thirst mechanism,
Inability to obtain water
Fluid volume excess
• Excessive parenteral fluid administration (5% Dextrose).
• Failure of adjustments to intake/output.
• Elderly, cardiac and renal disease patients at risk
• Peripheral edema, pulmonary edema, weight
gain, elevated CVP (normal 5-12mm Hg)
• Treatment: Fluid restriction, loop diuretics
Sodium homeostasis
• Normal serum level:132-144 mEq/ L
• Daily dietary intake: 100-250 mEq (6-15 g/day)
• Excreted through urine, stool and sweat
• Daily urinary excretion: 50-90 mEq/ day
• Renal regulation: reduced loss to 1 mEq/day or
exceed 5000 mEq/day
Hyponatremia
• Hypervolemic: Renal failure-↓water loss,
CCF, Cirrhosis, COPD- ↓CO → ↑water absorption.
• Normovolemic: Urinary Na⁺ loss in Syndrome of
inappropriate secretion of ADH (SIADH) -head injury, stroke,
carcinoma lung
• Hypovolemic: Hypotonic solutions infusion,
Loss of Na⁺ in renal disease- urinary Na⁺ ↑20mEq/L
Hyponatremia
• Symptoms: Na⁺ ˂120 mEq/L
Lethargy, confusion, seizures, anorexia, vomiting, coma
• TSD (total Na⁺ deficit)= 0.6 x wt. in kg x(140- actual Na⁺ level)
Deficit correction 0.5 mEq/L/ hr.
Rapid correction leads to myelin sheath damage
• Treatment: Severe symptoms- rapid correction to 120 mEq/ L, then slowly.
Hypervolemic- fluid restriction, loop diuretics
SIADH- fluid restriction + loop diuretic + vasopressin 2 antagonist
Hypovolemic- normal saline
Hypernatremia
• Aetiology:
- Excess salt intake or reduced salt loss
- Reduced water intake or excess water loss
• Types:
- Hypernatremia with volume depletion most common,
- Hypernatremia with volume excess or normal volume
• Pathophysiology:
- Net Na⁺ gain (hyperosmolar state) leads to water shift from
intracellular to extracellular space (intracellular dehydration)
- Hyperosmolar state leads to thirst & ADH release
Hypernatremia
• ADH abnormalities -
cause massive water loss
• Abnormalities of synthesis - central diabetes insipidus
• Abnormalities of action-
nephrogenic diabetes insipidus
• Central diabetes insipidus- head injury
• Nephrogenic diabetes insipidus- side effect of lithium, interstitial
nephritis, obstructive uropathy
Hypernatremia
• Symptoms:
usually starts at > 160 mEq/L .
Symptomatic at a lower level if rise in Na⁺ level is rapid
• Mainly CNS related- restless, irritable, fever, seizures.
• Treatment: Isotonic saline to correct hypovolemia followed by D5 W
infusion to correct water deficit
• Water deficit= normal BW x normal Na⁺ level/ current Na⁺ level
Potassium homeostasis
• Principal intracellular (155 mEq/L) cation
• Mostly located in skeletal muscle
• Normal serum level 3.5- 5 mEq/L
• Concentration gradient maintained by-
membrane bound Na⁺-K⁺ ATPase pump.
Potassium homeostasis
• Daily K⁺ intake: 1-1.5 mEq/kg body weight
• 90% excreted through kidney
• Internal regulating factors:
Insulin, aldosterone, catecholamines and
acid-base balance
Hyperkalemia
• Serum K⁺ > 5.5 mEq/ L
• Aetiology: Renal failure, adrenal insufficiency,
metabolic acidosis, hemolysis, rhabdomyolysis,
seizures, sever GI bleeding, medications (NSAID),
excessive K⁺ administration
Hyperkalemia
• Pseudohyperkalemia: Thrombocytosis,
leukocytosis, excessive agitation of specimen,
prolonged tourniquet or excessive fist clenching
during blood drawing
• Myocardial toxicity ( K⁺> 6 mEq)- peaked T wave,
prolonged PR interval, complete heart block,
paresthesia, flaccid paralysis
Hyperkalemia
• Treatment:
• 10% Ca-gluconate 10-20 ml- cardioprotective, effective in 1-5 min.
• 10 units insulin in 50 ml + 50% Dextrose- effective in 15-45 min.
• 100 mEq of sodium bicarbonate - if metabolic acidosis
• K⁺exchange resin 50-100 gm enema- slow action
• Hemodialysis
Hypokalemia
• K⁺ ˂ 3.5 mEq/L
• Aetiology: Vomiting, diarrhea, GI fistula, diuretics
• Metabolic alkalosis often coexists (↓ renal conservation)
• Weakness, flattening of T wave,
arrhythmias in patients on digoxin
• Treatment: IV K⁺ for severe cases
Oral K⁺ 60-80 mEq/ day for milder cases
Calcium Homeostasis
• 99% body Ca⁺- in bone,
not readily exchangeable
• Homeostasis- exchange between bone and ECF, renal excretion, and
intestinal absorption
• Homeostasis mainly controlled by PTH
• Plasma calcium: 10 mg/dl.
• ECF Ca⁺: Ionized, Non-ionized, Protein-bound
Calcium Homeostasis
• Low ionized Ca⁺ → ↑ PTH and ↑ 1,25-dihydroxyvitamin D3
Both stimulate bone absorption by increasing osteoclastic activity
• Increased ionized ca → ↓ PTH and ↓1,25-dihydroxyvitamin
D3, which decreases bone absorption
• Intestinal absorption- primarily on 1,25-dihydroxy vitamin D3,
• Renal excretion:
PTH and vitamin D increases distal tubular
reabsorption of calcium. Calcitonin inhibits calcium reabsorption
• Alkalosis ↑ ca excretion, acidosis ↓excretion
Hypercalcemia
• Aetiology: Hyperparathyroidism, malignancy, thiazide,
acute adrenal insufficiency, prolonged immobilization
• Clinical features:
CNS: Muscle fatigue, weakness, personality disorders,
psychoses, confusion, depression, and coma
CVS: Hypertension, shortening of QT interval
GIT: Nausea, vomiting, and abdominal pain
Renal: Nephrocalcinosis → chronic renal failure, Nephrolithiasis
Treatment of Hypercalcemia
• Promote diuresis by infusion of normal saline
• Add KCl 20-30 mEq / L of intravenous fluid
• Furosemide to enhance calcium excretion
• Treat the underlying cause:
-Primary HPT: Surgery
-Bone metastasis: Bisphosphonates,
calcitonin, steroids
Hypocalcaemia
• Aetiology
-Thyroid or parathyroid surgery
-Acute pancreatitis
-Pancreatic and small bowel fistulae
-Vitamin D deficiency: Malabsorption, lack of exposure to sunlight
-Renal failure →Vit. D₃ deficiency→ ↓ intestinal absorption
• Clinical features: (ca < 8 mg/dL)
Muscle cramps, perioral tingling, paresthesia, laryngeal stridor, tetany, seizures,
and psychotic behavior, hyperactive deep tendon reflexes.
Treatment of Hypocalcaemia
• IV calcium
(calcium gluconate or calcium chloride)
50 mg/minute (2.5 mEq/minute)
• Oral calcium ( citrate, carbonate)
• Vitamin D₃ (Calcitriol)- increases intestinal absorption
Magnesium
• Total body content : 2,000 mEq- 50% in bone, the remaining
in the intracellular space.
• < 1% of total in the extracellular space (1.4 to 2 mEq/L or 1.7
to 2.3 mg/dL).
• Daily intake: 25 mEq
• Excretion primarily by the kidneys
• Excretion increased by hypermagnesemia, hypercalcemia,
metabolic acidosis, and phosphate depletion.
Excretion decreased by metabolic alkalosis.
Hypermagnesemia
• Aetiology: chronic or acute renal failure, Mg-containing
antacids/ laxatives intake , severe burns, crush injuries,
rhabdomyolysis, severe metabolic acidosis, extracellular
volume depletion
• Clinical features:
Depressed neuromuscular function.
Loss of deep tendon reflexes, paralysis , coma. Hypotension or
even cardiac arrest can occur if levels exceed 18 mg/dL.
Treatment of Hypermagnesemia
• Calcium- 5 to 10 mEq, slow i.v
(antagonizes the effects of magnesium)
• Volume expansion
• Correction of acid-base disturbances
• Loop diuretics
• Hemodialysis
• Avoid Mg- containing medications
Hypomagnesemia
• Aetiology: Malnutrition, steatorrhea, increased GI losses ,
prolonged IV fluid replacement without Mg, loop diuretics,
aminoglycosides, insulin for DKA, diuretic phase of acute renal
failure
• Clinical features: Similar to hypocalcemia
Muscle
fasciculations, weakness, tetany, carpopedal spasm, nausea,
vomiting, and personality changes. Hypokalemia by renal K
wasting.
Treatment of hypomagnesemia
• Mild cases: oral magnesium
• Large deficit: IV Mg-sulfate 50-100 mEq/ day
ACID-BASE BALANCE
ACID-BASE System
• Acid: donate a H⁺ ion – HCl , H2CO3
• Base: accept a H⁺ -HCO3
• Acid-base homeostasis: equilibrium in H+, PCO2, and HCO3• H+ concentration - expressed as pH
• Normal pH - 7.35 to 7.45
• Acidemia - pH < 7.35
• Alkalemia- pH > 7.45
Acid-base disturbance
• Acidosis- respiratory, metabolic.
• Alkalosis- respiratory , metabolic
• Assessment- arterial blood gas analysis (radial artery)
• Normal ABG report:
pH- 7.36- 7.44
H⁺- 44-36 nml/L
HCO₃- 23-28 mmol/L
pCO₂- 36-44 mmHg (4.8-5.9 kPa)
pO₂- 80- 100 mmHg (10.6- 13.3 kPa)
Acid-base disturbance
Compensatory mechanisms:
1. Respiratory compensation- most rapid (minutes)
2. Blood buffers (in hours)
Blood buffers - bicarbonate (65%)- most important, protein 30%
Respiratory system.
Kidneys.
3. Kidney (days)
Metabolic acidosis
• ↓ pH, ↓ bicarbonate concentration.
• Increased production of endogenous acids ( increased anion gap acidosis) shock, severe hemorrhage, liver failure, diabetic ketoacidosis.
• Increased bicarbonate loss (normal anion gap acidosis)- diarrhoea, intestinal
fistula.
• Respiratory compensation- fall in pCO₂ - resp. alkalosis
• Treatment: Fluid resuscitation, base deficit correction by bicarbonate
Metabolic alkalosis
• ↑ pH, ↑ bicarbonate concentration.
•
Respiratory compensation - ↑pCO₂ - resp. acidosis
• Associated with hypokalemia, hypochloraemia.
• Aetiology: Loss of acid as vomitus in gastric outlet obstruction.
• Treatment: Replace fluid, K⁺ and chloride and treatment of
primary cause
Respiratory acidosis
• ↑pCO₂, ↑plasma bicarbonate, ↓pH
• Respiratory depression (head injury, opioids drugs)
• Pulmonary disease (asthma, COPD)
• Metabolic compensation- renal bicarbonate retention.
• Treatment: Ventilatory support.
Respiratory alkalosis
• Result of hyperventilation- pain, hysterical hyperventilation,
CNS disorders, salicylate poisoning, liver failure.
• ↑pH, ↓pCO₂
• May develop tetany- ↓ ionized Ca⁺ due to alkalosis.
• No specific treatment
Types of intravenous fluid
• 5% Dextrose: 5Gm dextrose/ 100 ml, isotonic, not useful in resuscitation.
• 10, 20 & 50 % Dextrose:- Hypertonic , used for diabetics or hypoglycemics.
• Normal saline: 0.9% NaCl, 9Gm NaCl in 1L (Na 154 mmol), pH 5.
• Ringer’s lactate (Hartman’s): < NaCl ( Na 131 mmol) + K⁺, HCO₃, Ca⁺ & Mg⁺, pH 6.5
• NS & RL: For replacing ECF loss. RL closely match ECF and less risk of hyperchloremia.
• Hypertonic saline:
Used for hyponatraemic seizures, cerebral oedema.
• Dextrose Saline: 5% Dextrose with N saline- hypertonic, used with caution.
4.3% Dextrose with 1/5 N saline more safe.
• Colloids:
Albumin (4.5%), gelatin, hydroxyethyl starch [HES], dextran- all stay longer in
intravascular space after resuscitation. Side effects- coagulopathy, pruritus, anaphylactic reaction
Maintenance fluid & electrolyte in 24 hours
Example for an adult in normal condition:
• Normal saline: 500- 1000 ml +
• 5% Dextrose: 2 L- 2.5 L +
• Potassium chloride: 60-80 mmol added to IV fluids.
• Adjust according to intake/output, and serum
electrolytes result.