Raad Dowais, MD

Fluid Balance
General Concepts
 Fluid Balance = Intake - Output
- Ideally should be ZERO

 Sensible losses
 Urination
 Defecation
 Sweating
 Wound drainage

 Insensible losses
 skin or lungs
Body water
 Full-term baby ~80%
 1 year child ~65%
 Lean Adult Male ~60%
 Adult female ~50-55%
 Elderly ~45%
Fluid Compartments
 In M 7o kg, 60% of body weight is water (42L)
 Intracellular
 40% of BW (28 L)
 Extracellular
 20% of BW (14 L)
 INTERSTITIAL 15% (10.5 L)
 INTRAVASCULAR 5% (3.5 L)
 Lymph
 CSF
 Synovial fluid
 pleural, pericardial, and peritoneal fluid
 Aqueous humor …
Main forces behind any molecular movement
between body compartments:

1- Osmotic pressure
created by the dissolved electrolytes in body
fluids

2- Hydrostatic pressure
created by the water in body fluids
Volume disturbances
Volume deficit Volume excess
General Weight loss Weight gain (first sign )
decreased skin turgor
Sunken eyes Peripheral edema
Dry mucus membranes
Thirst
Irritability
Cardiac Tachycardia Increased CVP
Hypotension Distended neck veins
Collapsed neck veins Murmur
Renal Oliguria
Azotemia
GI Ileus Bowel edema
Pulmonary Pulmonary edema
Dehydration
 Caused by:
 Excessive fluid loss
 Decreased fluid intake
 Third space fluid shifting
 IV Therapy
 Crystalloids
 Colloids
Serum osmolality =
(2 x Na) + (glucose/18) + (BUN/2.8)
= 290 to 310 (plasma expanders)
 draw interstitial fluid into the
 Isotonic bloodstream)
D5W, 0.9% NaCl or Lactated
 Albumin
Ringers
 Hypotonic  Dextran
0.45% NaCl  HES (Hydroxyethyl starch)
 Hypertonic  Gelofusin
D5/0.9% NaCl, D5/0.45% NaCl
Distribution of fluids
 Intravascular volume increment after 1 L of :

DW5% 83 ml

½ NS (0.45% NaCl) 167 ml

NS (0.9% NaCl) 250 ml

Hypertonic saline (3% NaCl) 500 ml

Daily requirements for adults
(maintenance)

 Fluid:
0-10 kg  100 ml/kg
10-20 kg  50 ml/kg
>20 kg  20 ml/kg
Or 35-50 ml/kg lean weight
Or to maintain urine output 0.5-1 ml/h

 Na+ 1-2 mEq/kg

 K+ 0.5-1 mEq/kg
Intraoperative 3rd space replacement
 Small incisions (e.g., inguinal hernia repair) 1-3
mL/kg/hour
 Medium-sized incisions (e.g.,sigmoidectomy)
3-7 mL/kg/hour
 Larger incisions (e.g., pancreaticoduodenectomy)
9-11 ml/kg/hour
Postoperative fluid management
 Aims to maintain an adequate urine output (0.5 to 1.0
mL/kg/hour)
 Sequestration continues for 12 hours post-op
 GI losses that exceed 250 mL/day should be replaced with
an equal volume of crystalloid
 Mobilization of 3rd-space fluid begins 2-3 days post-op
 gastric losses should be replaced with NS or 1/2 NS + KCl
 pancreatic, biliary, small and large intestine losses should
be replaced with Lactated Ringer’s
Electrolytes
Sodium-Potassium Pump
 Uses ATP to Pumps 3
 Sodium (abundant
Na+ out and 2 K+ in
outside cells) tries to get
into cells
 Prevents cell swelling
and creates an
 Potassium (abundant electrical charge
inside cells) tries to get allowing
out of cells neuromuscular
impulse transmission
Sodium
 Major extracellular cation

 Attracts fluid and helps preserve fluid volume

 Combines with chloride and bicarbonate to help

regulate acid-base balance
 Normal range 135 - 145 mEq/L
Hyponatremia
 < 135 mEq/L
 May be classified as:
- Hypovolemic (diuretics, vomiting, …)
- Hypervolemic (HF, RF, LF, …)
- Isovolemic
• Pseudohyponatremia with very high serum glucose or
lipids.
Hyponatremia
 Primarily neurologic symptoms
 Headache, Nausea/Vomiting,
altered mental status, stupor,
seizures, coma
 Hypovolemia - poor skin turgor, tachycardia, decreased BP,
orthostatic hypotension
 Hypervolemia - edema, hypertension, weight gain, bounding
tachycardia
Management of hypoNa+
 MILD CASE  SEVERE CASE
 hyper/isovolemic:  Infuse hypertonic
Restrict fluid intake NaCl solution
(3%NaCl) slowly
 Hypovolemic:  Furosemide to remove
increased Na+ intake excess fluid
(IV or oral)  Monitor in ICU
 Treat the underlying
cause
Hypernatremia
 Less common than hyponatremia
 Thirst is the body’s main defense
 fluid shifts from intra to extracellular space
 May be caused by water deficit or over-intake of
Na+
 may result from diabetes insipidus
Manifestations of hyperNa+
 Think S-A-L-T
 Skin flushed
 Agitation
 Low grade fever
 Thirst
 Mainly neurological symptoms
 Signs of associated hypo or hypervolemia
Management of hyperNa+
 Correct underlying  Monitor for s/s of
problem (if known) cerebral edema

 Gradual hypotonic  Monitor serum Na+ level

fluid replacement (to every few hours
avoid brain edema)
 Seizure precautions
Potassium
 Major intracellular cation
 Hypo or hyperK+ can lead to serious neuromuscular
and cardiac problems
 Normal levels = 3.5 – 5.5 mEq/L
 Most ingested K+ is excreted by the kidneys
(~90%)
 Increased K+  Aldosterone secretion , Na+
reabsorption and K+ excretion
Hypokalemia
 Serum K+ < 3.5 mEq/L
 caused by
- GI losses (vomiting, diarrhea, ileostomy, …)
- non-K+ sparing diuretics (thiazide, furosemide)
- insufficient intake (IV fluids without K+…)
Manifestations of hypoK+
 Skeletal muscle:
- weakness

 Cardiac muscles:
- ECG changes (flattening and inversion of T wave, Q-T
prolongation, visible U wave, ST depression, Torsades de
points, ventricular tachycardia)
- Digitalis toxicity
- Orthostatic hypotension

 Smooth muscles:
- constipation, ileus
Treatment of hypoK+
 Increase dietary K+
 Oral KCl supplements
 IV K+ replacement
 Change to K+-sparing diuretic (spironolactone)
 Monitor ECG changes
 Treat underlying causes
IV K+ Replacement
 Mix well when
adding to an IV
solution bag
 Rates usually 10-20
mEq/hr, not to
exceed 40 mEq/h NEVER GIVE K+
 “40 in 400 over 4 h” IV PUSH
“40 in 500 over 2 h”
Hyperkalemia
 > 5.5 mEq/L
 Causes:
- Renal failure
- Increased intake (?) (food rich in K+ or salt substitute + renal
impairment)

- Blood transfusion
- Drugs (K+ sparing diuretics, ACEI, …)
- Extensive trauma, hemolysis, rhabdomyolysis,
reperfusion injury…
Manifestations of hyperK+
 Muscle weakness (especially legs)
 ECG changes (tented T wave with narrow base,
prolonged P-R, loss of P wave, shortened QT interval,
ST-segment depression, heart block, cardiac arrest)
 Hypotension
 Nausea, abdominal cramps, diarrhea
Management of hyperK+
 Emergency
 Mild
 10% calcium gluconate
 Loop diuretics IV over 2-3 min. to protect the heart
(Lasix)
 Sodium bicarbonate
 Dietary restriction to shift K+ from extra to intracellular space

 Moderate  IV Glucose + insulin

to shift K+ to intracelluar
 chelating agents
 Salbutamol nebulizer
Calcium polystyrene sulfonate
(e.g. Sorbisterit, Ca-  Chelating agents
Resonium)
Sodium polystyrene sulfonate  Hemodialysis
(e.g. Kayexalate, Anti-Kalium-
NA)  Monitoring in ICU
Magnesium
 Helps produce ATP
 Role in protein synthesis & carbohydrate
metabolism
 Helps cardiovascular system function
(vasodilation)
 Regulates muscle contractions
Hypomagnesemia
 < 1.5 mEq/L, <0.75 mmol/L
(mmol vs mEq ** )
 Causes:
- poor dietary intake
- poor GI absorption
- Chronic alcoholism
- excessive GI/urinary losses (diuretics, stoma, diarrhea…)
- Prolonged IV fluids without Mg++
Manifestations of hypoMg++
 CNS
CVS
 Altered LOC
Tachycardia
 Confusion
HTN
 Hallucinations
ECG changes

 Neuromuscular
 Muscle weakness GI
Dysphagia
 Leg/foot cramps
Anorexia
 Tetany
Nausea/vomiting
 Chvostek’s & Trousseau’s signs
Treatment of hypoMg++
 Mild
 Dietary supplements
 Severe
 IV magnesium sulfate infusion pump
 Monitor ECG and symptoms
Hypermagnesemia
 > 2.5 mEq/L, >1.25 mmol/L
 Not common
 Causes :
- Renal dysfunction (most common cause)
- Iatrogenic
- Addison’s disease, Adrenocortical insufficiency,
Untreated DKA
Manifestations of hyperMg++
 Decreased neuromuscular activity
 Respiratory failure
 Generalized weakness
 nausea/vomiting
Treatment
 IV fluids (if renal function is normal)
 Loop diuretics (get rid of Mg++)
 Calcium gluconate
 Mechanical ventilation for respiratory depression
 Hemodialysis
Calcium
 99% in bones, 1% in serum and soft tissue (measured by
serum Ca++)
 Normal serum level:
8.5 - 10.5 mg/dl (4.2 - 5.2 mEq/L or 2.1 - 2.6 mmol/L).
 ~50% ionized (1.1 – 1.3 mmol/L)
 Role in contraction of all types of muscles
 Participates in blood clotting

Levels regulated and affected by:

PTH, vit-D, calcitonin, serum Albumin
Hypocalcemia
 Causes:
- Inadequate intake
- Malabsorption
- Hypoalbuminemia (low total but normal ionized)
- Acute pancreatitis
- thyroid or parathyroid surgery
- loop diuretics
- Blood transfusion (citrate)
- hypomagnesemia*
Manifestations of hypoCa++
 Neuromuscular
 Anxiety, confusion, irritability, hyperreflexia,
muscle twitching, paresthesias (peri-oral,
fingers, toes), tetany, convultions, Chvostek’s
sign, Trousseau sign
 Diarrhea
 Diminished response to digoxin
 ECG changes

https://www.youtube.com/watch?v=ZY_DMrbKpl4
https://www.youtube.com/watch?v=S2BS0XqFcY0
Treatment of hypoCa++
 Calcium gluconate IV
 Oral calcium and vitamin D
 Monitor ECG and for convulsions if necessary
Hypercalcemia
Main causes:
 Cancer (Mets, tumors producing PTH like peptides)
commonest cause in hospitalized pt

 Hyperparathyroidism
commonest cause in general

 Prolonged immobilization
 Addissonian crisis
Manifestations of hyperCa++
 Fatigue, confusion, lethargy, coma
 Muscle weakness, hyporeflexia
 Hypertension
 Bradycardia  cardiac arrest
 Anorexia, nausea/vomiting
 Peptic ulcer
 ileus, constipation
 Polyuria*, renal calculi, renal failure
Treatment
 treat underlying cause (CA, PTH, …)
 Adequate hydration with IV fluids
 Loop diuretics (to kick out Ca++)
 Corticosteroids
Phosphorus
 The primary anion in the intracellular fluid
 Crucial to cell membrane integrity, muscle function,
neurologic function and metabolism of carbs, fats and
protein
 Functions in ATP formation, phagocytosis, platelet
function and formation of bones and teeth

 Normal range 1 - 1.5 mmol/L

Hypophosphatemia
 Can cause acute respiratory failure and need for MV

 Causes:
- respiratory alkalosis (hyperventilation)
- Excessive insulin release, and refeeding syndrome
- Malabsorption
- Diuretics
- Hyperparathyroidism
- Extensive burns
manifestations of hypoPhos
 Musculoskeletal  Cardiac
 muscle weakness  hypotension
 respiratory muscle  decreased cardiac
failure output

 CNS
 confusion, anxiety,
seizures, coma
Treatment
 MILD/MODERATE  SEVERE
 Dietary modifications  IV replacement using

 Oral supplements potassium phosphate or

sodium phosphate
Hyperphosphatemia
Causes:
- Impaired kidney function
- Cell damage, hemolysis, extensive trauma
- Hypoparathyroidism
- Respiratory acidosis
- Increased dietary intake
manifestations
 Arrythmias
 Hyperreflexia
 Muscle weakness
 Oliguria
Management
 Low-phosphorus diet
 Decrease absorption with antacids that bind
phosphorus
 Treat underlying cause of respiratory acidosis or
DKA
 IV saline for severe hyperphosphatemia in patients
with good kidney function
Arterial Blood Gases
 pH 7.35 - 7.45

 PaCO2 35 - 45 mmHg

 HCO3 22-26 mEq/L

 Acidosis: process of increasing H+ concentration
 Alkalosis : process of decreasing H+ concentration

Acidemia
 pH < 7.35
 Caused by accumulation of acids or by a loss of bases

Alkalemia
 pH > 7.45
 Caused by accumulation of bases or by a loss of acids
pH regulatory systems
 Chemical buffers
 Respiratory system
 Kidneys
Chemical Buffers
 Immediate acting
 Combine with offending acid or base to neutralize
harmful effects until another system takes over
Respiratory System
 Lungs regulate blood levels of CO2
 CO2 + H2O = Carbonic acid
 High CO2 = slower breathing (hold on to carbonic
acid and lower pH)
 Low CO2 = faster breathing (blow off carbonic acid
and raise pH)
 Twice as effective as chemical buffers, but effects
are temporary
Kidneys
 Reabsorb or excrete  Adjustments by the
excess acids or bases kidneys take hours to
into urine days to accomplish
 Produce bicarbonate  Bicarbonate levels and
pH levels increase or
decrease together
Acid-Base Imbalances
 Respiratory Acidosis

 Respiratory Alkalosis

 Metabolic Acidosis

 Metabolic Alkalosis
Respiratory Acidosis
 Hypoventilation
 CO2 increases, pH decreases

 Causes:
- depression of respiratory center
- lung diseases (atelectasis, pneumonia, …)
- Airway obstruction
- Post op abdominal surgery
- Inappropriate Mechanical ventilation settings
- Deep sedation

Treatment involves correcting the underlying cause

ABG Results
 Uncompensated  Compensated
 pH < 7.35  pH Normal

 PaCO2 >45  PaCO2 >45

 HCO3 Normal  HCO3 > 26

Respiratory Alkalosis
 Causes:
- Hyperventilation caused by pain or anxiety…
- Bronchial asthma
- salicylate poisoning
- use of nicotine or aminophylline
- hypermetabolic states or acute hypoxia (overstimulates
the respiratory center)

- Wash out of CO2 === increase in pH

ABG Results
 Uncompensated  Compensated
 pH > 7.45  pH Normal

 PaCO2 < 35  PaCO2 < 35

 HCO3 Normal  HCO3 < 22

Metabolic Acidosis
High anion gap metabolic acidosis

 Ketoacidosis (DKA, alcoholism, starvation…)

 Lactic acidosis (shock, heart failure, pulmonary disease, hepatic disease,
seizures, strenuous exercise)
 Acidic toxin (salicylate overdose, methanol, ethylene glycol…)
 Renal failure

Normal anion gap metabolic acidosis

 Renal tubular acidosis

 Loss of HCO3- (diarrhia, ileostomy, high-output
enterocutaneous fistula,…)
 Anion Gap = [Na+] - ([Cl−] + [HCO − ])
 Example: 136 – (102 + 24) = 10
 Normally < 12-14

 High anion gap means there is an acid that is

causing the metabolic acidosis (lactic, ketone, salicylate,…)
ABG Results
 Uncompensated  Compensated
 pH < 7.35  pH Normal

 PaCO2 Normal  PaCO2 < 35

 HCO3 < 22  HCO3 < 22

Metabolic Alkalosis
 Commonly associated with hypokalemia
hypochloremia and hypocalcemia
 Causes:
- Excessive vomiting
- NG suction
- Cushing’s syndrome
- Conn’s syndrome (hyper aldosteronemia)
ABG Results
 Uncompensated  Compensated
 pH > 7.45  pH Normal

 PaCO2 Normal  PaCO2 > 45

 HCO3 >26  HCO3 > 26