Acid-Base

Balance
Compensation refers to the body processes that occur to counterbalance an acid-base disturbance. When compensation has occurred, the pH will be
within normal limits.
Metabolic acidosis A total concentration of buffer base that is lower than normal, with a relative increase in the hydrogen ion concentration. This
results from loss of buffer bases or retention of too many acids without sufficient bases, and occurs in conditions such as renal failure and diabetic
ketoacidosis, from the production of lactic acid, and from the ingestion of toxins, such as acetylsalicylic acid (aspirin).
Metabolic alkalosis A deficit or loss of hydrogen ions or acids or an excess of base (bicarbonate) that results from the accumulation of base or from
a loss of acid without a comparable loss of base in the body fluids. This occurs in conditions resulting in hypovolemia, the loss of gastric fluid,
excessive bicarbonate intake, the massive transfusion of whole blood, and hyperaldosteronism.
Respiratory acidosis A total concentration of buffer base that is lower than normal, with a relative increase in hydrogen ion concentration; thus a
greater number of hydrogen ions is circulating in the blood than the buffer system can absorb. This is caused by primary defects in the function of the
lungs or by changes in normal respiratory patterns as a result of secondary problems. Any condition that causes an obstruction of the airway or
depresses respiratory status can cause respiratory acidosis.
Respiratory alkalosis A deficit of carbonic acid or a decrease in hydrogen ion concentration that results from the accumulation of base or from a
loss of acid without a comparable loss of base in the body fluids. This occurs in conditions that cause overstimulation of the respiratory system.

Respiratory acidosis: (carbonic acid excess) occurs when a person hypoventilates which leads to a buildup of CO2, resulting in a
buildup of carbonic acid in the blood
i. Cause: COPD, barbiturate or sedative OD, chest wall abnormality, severe pneumonia, atelectasis, respiratory muscle
weakness, and mechanical hypoventilation
ii. Pathophysiology: CO2 retention from hypoventilation
iii. Compensatory mechanism: HCO3- retention by kidney and secretion of H+ into the urine
iv. Clinical manifestations: drowsiness, confusion, dizziness, HA, coma, decreased blood pressure, ventricular
fibrillation (related to Hyperkalemia from compensation), warm flushed skin, seizures, and hypoventilation with
hypoxia
Respiratory alkalosis: (carbonic acid deficit) occurs with hyperventilation and the primary cause is hypoxemia from acute pulmonary
disorders.
v. Cause: hyperventilation (hypoxemia, pulmonary emboli, anxiety, fear, pain, exercise, fever), stimulated respiratory
center (septicemia, encephalitis, brain injury, salicylate poisoning), and mechanical hyperventilation
vi. Pathophysiology: increased CO2 excretion from hyperventilation
vii. Compensatory mechanism: HCO3- excretion by the kidneys. Compensated respiratory alkalosis is rare.
viii. Clinical manifestations: dizziness, light-headedness, confusion, HA, tachycardia, dysrhythmias (related to
hypokalemia from compensation), nausea, vomiting, epigastric pain, tetani, numbness, tingling of extremities,
hyperreflexia, seizures, and hyperventilation
Metabolic acidosis (base bicarbonate deficit) occurs when an acid other than carbonic acid accumulates in the body or when
bicarbonate is lost from body fluids
ix. Cause: diabetic ketoacidosis, lactic acidosis, starvation, severe diarrhea, renal tubular acidosis, renal failure, GI
fistulas, and shock
x. Pathophysiology: gain of fixed acid and inability to excrete acid or loss of bicarbonate.
xi. Compensatory mechanism: CO2 excretion by lungs. Patients often develop kussmaul respirations (deep, rapid
breathing) while the kidneys attempt to excrete additional acid.
xii. Clinical manifestations: drowsiness, confusion, dizziness, HA, coma, decreased blood pressure, dysrhythmias
(related to Hyperkalemia from compensation), warm flushed skin, nausea, vomiting, diarrhea, abdominal pain, and
deep, rapid respirations
Metabolic alkalosis: (base bicarbonate excess) occurs when a loss of acid or a gain in bicarbonate occurs
xiii. Cause: severe vomiting, excess gastric suctioning, diuretic therapy, K+ deficit, excess NaHCO3 intake, and excessive
mineral corticoids
xiv. Pathophysiology: loss of strong acid or gain of base
xv. Compensatory mechanisms: CO2 retention by the lungs, The compensatory mechanism to correct metabolic
alkalosis is limited. There is a decreased respiratory rate to increase the plasma level of CO2, but once the plasma
CO2 reaches normal levels it causes stimulation of chemoreceptors and results in ventilation.
xvi. Clinical manifestations: dizziness, light-headedness, confusion, HA, tachycardia, dysrhythmias (related to
hypokalemia from compensation), nausea, vomiting, anorexia, tetany, tremors, tingling of fingers and toes, muscle
cramps, hypertonic muscles, seizures, and hypoventilation
In both respiratory and metabolic acidosis the CNS is depressed acidosis is a downer
In both respiratory and metabolic alkalosis the CNS is irritated alkalosis is an upper

IV Therapy

Acid-Base Balance
Many patients need maintenance IV fluid therapy when they cannon take oral fluids while other patients need corrective or
replacement therapy for losses.
Hypotonic solutions: provide more water than electrolytes therefore diluting the ECF. Maintenance fluids are generally
hypotonic because normal daily losses are hypotonic. These fluids have the potential to cause cellular swelling so patients need to
be monitored closely for changes in mental status as this may indicate cerebral edema.
xvii. 5% Dextrose in water: (technically isotonic, but physiologically hypotonic) provides 50 g/L of glucose, provides
free water necessary for renal excretion of solutes, used to replaced water losses, treats hypernatremia, provides 170
cal/L and does not provide electrolytes.
xviii. 0.45% NS: hypotonic, provides free water in addition to Na and Cl, used to replaced hypotonic fluid losses, used as
maintenance fluid although it does not replace daily losses of other electrolytes, and provides no calories.
Isotonic solutions: expands only the ECF with no net loss from the ICF. This type of fluid replacement is idea for a patient with
an ECF volume deficit. Excessive administration of isotonic saline should be avoided because it can result in elevated sodium and
chloride levels. Isotonic saline can be used when a patient is experiencing both fluid and sodium losses or with vascular fluid
replacement in hypervolemic shock.
xix. 5% Dextrose in water
xx. 0.9% NS: isotonic, used to expand intravascular volume and replace extracellular fluid losses, only solution that can
be administered with blood products, contains Na and CL in excess of plasma levels, does not provide free water,
calories, or other electrolytes, and may cause intravascular overload or hyperchloremic acidosis
xxi. 5% Dextrose in 0.225% NS: provides Na, Cl, and free water, used to replace hypotonic losses and treat
hypernatremia, and provides 170 cal/L
xxii. Ringers solution: similar in composition to plasma except that is has excess CL, no Mg, and no HCO3, does not
provide free water or calories, used to expand the intravascular volume, and replace extracellular fluid losses.
xxiii. Lactated Ringers solution: similar in composition to normal plasma except does not contain Mg, contains, Na, K,
Cl, Ca, and lactate (precursor to bicarb), used to treat losses from burns and lower GI, may be used to treat mild
metabolic acidosis but should not be used to treat lactic acidosis, and does not provide free water or calories
Hypertonic solutions: inititially raises the osmolality of ECF and expands it. This draws water out of the cells into the EFC.
These solutions are used to treat hypovolemia and hyponatremia. These solutions require close monitoring of blood pressure, lung
sounds, and serum Na levels because of the risk for intravascular fluid volume excess. The primary use of these solutions is for
provisional calories with parenteral nutrition. You can administer 10% dextrose or less through a peripheral line, but any
concentration higher needs to given through a central line.
xxiv. 10% Dextrose in water: provides free water only, no electrolytes, and provides 340 cal/L
xxv. 3.0% NS: used to treat symptomatic hyponatremia and must be administered slowly and with extreme caution
because it may cause dangerous intravascular volume overload and pulmonary edema
xxvi. 5% Dextrose in 0.45% NS: same as 0.45% NS, but provides 170 cal/L
xxvii. 5% Dextrose in 0.9% NS: same as 0.9% NS, but provides 170 cal/L
- IV additives can be added to these solutions for specific electrolyte imbalances. KCl, CaCl, MgSO4, and HCO3- are common
additives in basic IV solutions.
- Plasma Expanders: these stay in the vascular space and increase the osmotic pressure.
Include colloids (protein solutions such as plasma, albumin, and commercial plasmas), dextran, and hetastarch (Hespan). These
additions help to increase vascular fluid.

Acid-Base Balance