FLUIDS AND ELECTROLYTES

A N N A M A R I E J O S I E F I N E C . K A P U LO N G M D
M AY 1 5 , 2 0 2 0
ECF
o Subdivided into plasma, interstitial fluid and lymph, bone and dense
connective tissue water, transcellular (cerebrospinal, pleural,
peritoneal, synovial, and digestive secretions)
o The two most important from these four are the plasma and
interstitial fluids.
o Plasma or intravascular fluid is contained in blood vessels while
interstitial fluid is confined to all tissues except for the formed
elements of blood.
IMPORTANT TERMS
 OsmolaRity - number of osmotically active particles per
LITER of solvent
 Osmolality - number of osmotically active particles per
KILOGRAM and can be estimated using the formula:
 Tonicity - used to compare the osmotic pressure of a
parenteral solution to that of plasma
Anti Diuretic Hormone
 controls plasma Osmolality
Specialized neurons in the supraoptic and paraventricular nuclei of
the hypothalamus detects changes in extracellular osmolality
 When ECF osmolality is increased, cells shrink, ADH is released
from posterior pituitary which increases water reabsorption in renal
collecting tubules.
 When ECF osmolality is decreased, ADH secretion is decreased
thus allowing diuresis
Anti Diuretic Hormone
 Nonosmolar Release of ADH :
 Decrease in wall tension in atria, vena cava, pulmonary arteries
as detected by the carotid baroreceptors results in reflex increase
of ADH secretion.
 Increased stretch of these receptors suppresses ADH secretion
and increases secretion of Atrial Natriuretic Peptide (ANP)
FLUID PHARMACOLOGY
 Crystalloids
 Colloids
CRYSTALLOIDS
 Solutions of electrolytes in water
 Indicated for replacement of free water and electrolytes but also
may be used for volume expansion
 More fluid will be filtered out of the capillary with crystalloids than
colloids, thus patients have a more positive fluid balance
When infused in normovolemic patients, tissue edema may occur
in compliant tissues.
CRYSTALLOIDS
a. Saline Solutions
 0.9% Sodium Chloride
Isotonic
2L infusion leads to increase in ECF volume, dilutional decrease in hematocrit
and albumin, increase in Cl- and K+ concentrations, decrease in plasma HCO3-
May be given in patients with cerebral edema, preexisting Na+ or Cl- total body
depletion
CRYSTALLOIDS
a. Saline Solutions
 Hypertonic Saline: (1.8%, 3%, 7.5%)
Plasma volume expansion: draws water into extracellular compartment
Correction of hypoosmolar hyponatremia
 Treatment of increased intracranial pressure
 Levels greater than 7.5% may cause endothelial damage; 11.7% can be used as a
sclerosant agent administered into central vein
CRYSTALLOIDS
 B. Balanced Crystalloid Solutions
Have a lower overall osmolarity than 0.9% NaCl, lower Na+ concentration,
lower Cl- concentration
Addition of organic anionic buffers (lactate, gluconate, acetate)
Measured osmolality (265 mOsm/kg)
 Large volumes can cause hyperlactatemia, metabolic alkalosis,
hypotonicity, cardiotoxicity due to acetate
CRYSTALLOIDS
C. Dextrose solutions:
Source of free water
 used with care in the postoperative period due to relative SIADH leads to water
retention
less suitable for intravascular volume expansion because water is able to move
between all fluid compartments, very small volume remains in the intravascular
space
Source of metabolic substrate
 may be coadministered with IV insulin to patients with diabetes to reduce risk
of hypoglycemia
COLLOIDS
 Contain macromolecules suspended in electrolyte solutions (isotonic
saline or balanced crystalloid)
Colloids have a higher colloid osmotic pressure reduces interstitial
edema
Potential intravascular plasma volume expansion effect is maximized
Alter blood rheology, improve blood flow by hemodilution, reduce
plasma viscosity and red cell aggregation effects
COLLOIDS
A. Semisynthetic colloids
May be in the form of Gelatin, Hydroethyl starches, Dextrans
Large dose of semisynthetic molecules (40-60 g/L) may produce undesired effects
on immune, coagulation, renal systems
 May cause anaphylactoid reactions, contribute to renal dysfunction, affect
coagulation
COLLOIDS
B. Human Plasma Derivatives
 The human plasma derivatives include human albumin
solutions, plasma protein fractions, fresh frozen plasma,
and immunoglobulin solution.
Acid Base Analysis
A N N A M A R I E J O S I E F I N E C . K A P U LO N G M D
M AY 1 5 , 2 0 2 0
Acid and Bases
ACID
Act as a proton (H + ) donor
Compound that contains hydrogen and reacts with water to form
hydrogen ions.
BASE
Act as a proton acceptor
Compound that produces hydroxide ions in water.
Acid and Bases
Compensatory Mechanism
Physiological responses to changes in [H + ] are characterized by three
phases:
 (1) immediate chemical buffering
 (2) respiratory compensation
 (3) a slower but more effective renal compensatory response that
may nearly normalize arterial pH even if the pathological process
remains present.
 Acid and Bases
BODY BUFFERS
Bicarbonate (H 2 CO 3 /HCO 3 − )
Hemoglobin (HbH/ Hb − )
Other intracellular proteins (PrH/Pr − ), phosphates (H 2 PO 4 − /HPO
4 2− ), and ammonia (NH 3 /NH 4 + )
The effectiveness of these buffers in the various fluid compartments is
related to their concentration.
Bicarbonate is the most important buffer in the extracellular fluid
compartment.
Acid and Bases
Henderson–Hasselbalch equation
 Acid and Bases
Metabolic Alkalosis
characterized by hyperbicarbonatemia (>27 mEq/L) and usually by an
alkalemic pH (>7.45)
factors that generate metabolic alkalosis include vomiting and diuretic
administration
 associated with hypokalemia, ionized hypocalcemia, secondary
ventricular arrhythmias, increased digoxin toxicity, and compensatory
hypoventilation (hypercarbia), although compensation rarely results in
PaCO2 above 55 mmHg
Acid and Bases
Metabolic Alkalosis Treatment
Etiologic therapy
Expansion of intravascular volume or the administration of potassium.
Infusion of 0.9% saline will dose-dependently increase serum [Cl−] and decrease
serum [HCO3−]
Nonetiologic therapy
Acetazolamide (a carbonic anhydrase inhibitor that causes renal bicarbonate wasting)
Dialysis against a high-chloride/low bicarbonate dialysate
Infusion of [H+] in the form of ammonium chloride, arginine hydrochloride, or 0.1 N
hydrochloric acid (100 mmol/L).
Acid and Bases
Metabolic Acidosis
Characterized by hypobicarbonatemia (<21 mEq/L) and usually by an acidemic pH
<7.35), can be innocuous or reflect a life-threatening emergency
Occurs when there is buffering by bicarbonate of endogenous or exogenous acid
loads or as a consequence of abnormal external loss of bicarbonate.
 Calculation of the anion gap [AG = [Na+] - ([Cl-] + [HCO3-])] distinguishes between
two types of metabolic acidosis
 Normal Anion Gap (<13 meq/L)
 High Anion Gap (>13 meq/L)
Acid and Bases
Acid and Bases
Metabolic Acidosis
The anesthetic risk associated with metabolic acidosis is proportional
to the severity of the underlying process that produces the metabolic
acidosis.
Patient with hyperchloremic metabolic acidosis may be relatively
healthy, those with lactic acidosis, ketoacidosis, uremia, or toxic
ingestions will be chronically or acutely ill.
Preoperative assessment should emphasize volume status and renal
function.
 Acid and Bases
Metabolic Acidosis Treatment
The treatment of metabolic acidosis consists of treatment of the
primary pathophysiologic process, for ex: hypoperfusion or hypoxia,
and if pH is severely decreased, administration of NaHCO3-.
 Hyperventilation, although an important compensatory response to
metabolic acidosis, is not a definitive therapy for metabolic acidosis.
Acid and Bases
Respiratory Alkalosis
Characterized by hypocarbia (PaCO2 =35 mmHg) and usually by an
alkalemic pH (>7.45), results from an increase in minute alveolar
ventilation (VA), that is greater than that required to excrete
metabolic CO2.
May produce hypokalemia, hypocalcemia, cardiac dysrhythmias,
bronchoconstriction, and hypotension, and may potentiate the
toxicity of digoxin.
Acid and Bases
Respiratory Alkalosis
In addition, both brain pH and cerebral blood flow are tightly
regulated and respond rapidly to changes in PaCO2
Doubling VA reduces PaCO2 to 20 mmHg and halves cerebral blood
flow; conversely, halving minute ventilation doubles PaCO2 and
doubles cerebral blood flow.
Acid and Bases
Respiratory Alkalosis Treatment
Often not required
The most important steps are recognition and treatment of the
underlying cause. For instance, correction of hypoxemia or
effective management of sepsis should result in resolution of the
associated increases in respiratory drive.
Acid and Bases
Respiratory Acidosis
Characterized by hypercarbia (paco2 >45 mmhg) and by a low ph
(<7.35).
Occurs because of a decrease in VA (alveolar ventilation) , an
increase in production of carbon dioxide (VCO2) or both.
 Respiratory acidosis may be either acute, without compensation
by renal [HCO3−] retention, or chronic, with [HCO3−] retention,
offsetting the decrease in pH.
Acid and Bases
Respiratory Acidosis
 Patients with chronic hypercarbia due to intrinsic pulmonary
disease require careful preoperative evaluation.
 Administration of narcotics and sedatives, even in small doses,
may cause hazardous ventilatory depression.
Acid and Bases
Respiratory Acidosis Treatment
Acute respiratory acidosis
 May require mechanical ventilation unless a simple etiologic factor (i.e., narcotic
overdosage or residual muscular blockade) can be treated quickly.
 Bicarbonate administration is never indicated unless severe metabolic acidosis is also
present or unless mechanical ventilation is ineffective in reducing acute hypercarbia.
Chronic respiratory acidosis
 Rarely managed with ventilation but rather with efforts to improve pulmonary function.
 In patients requiring mechanical ventilation for acute respiratory failure, ventilation with
a lung-protective strategy may result in hypercapnia.
Acid and Bases
TY 