1
Advanced Patho Hesi
1. Acid base analysis-patho
a) Pathophysiologic changes in the concentration of hydrogen ion or base in the
blood leads to acid-base imbalances.
i) Acidemia- pH of the arterial blood <7.35
ii) Acidosis- a systemic increase in hydrogen ion concentration or a loss of
base.
iii) Alkalemia- pH of arterial blood >7.45
iv) Alkalosis- a systemic decrease in hydrogen ion concentration or an
excess of base.
v) Metabolic, respiratory, or mixed etiologies.
b) Normal
i) pH: 7.35-7.45
ii) HCO3: 22-26
iii) CO2: 35-45
c) Abnormal/imbalances
i) Metabolic acidosis: ↓ pH, ↓ HCO3
ii) Metabolic alkalosis: ↑ pH, ↑ HCO3
iii) Respiratory acidosis: ↓ pH, ↑ CO2
iv) Respiratory alkalosis: ↑ pH, ↓ CO2
v) ROME = respiratory opposite, metabolic equal
d) Metabolic acidosis: ↓ pH, ↓ HCO3
i) The concentration of non-carbonic acids increases or bicarbonate (base)
is lost from the extracellular fluid or cannot be regenerated by the kidney.
This can occur quickly, as in from poor perfusion or hypoxemia, or more
slowly, as in renal failure (failure to excrete acid), starvation states, or
diabetic ketoacidosis (excess production of keto acids from lack of insulin).
ii) The buffer systems compensate for the excess acid and attempt to
maintain the arterial pH within a normal range. Hydrogen ions will move to
the intracellular space, and potassium will move to the extracellular space
to maintain an ionic balance. Buffering by bicarbonate lowers the serum
value of hydrogen ions and increases the pH. The respiratory system
compensates for a metabolic acidosis as the reduced pH stimulates
hyperventilation, lowering the PaCO2 and the amount of H2CO3
circulating in the blood. The kidneys excrete the excess acid as NH4+ and
titratable acid (H2PO4-). When acidosis is severe, buffers become
depleted and cannot compensate for the increasing H+ load and the pH
continues to decrease. The ratio of bicarbonate to carbonic acid
decreases to less than 20:1.
iii) In states of metabolic acidosis, potassium is redistributed from the
intracellular to the extracellular space, and is reabsorbed at the apical
membrane of the renal collecting tubule. There is also an increase in the
levels of ionized calcium because acidosis decreases the amount of
calcium bound to albumin.
iv) The evaluation of the anion gap can be helpful when used cautiously to
distinguish different types of metabolic acidosis. Normally, the
concentrations of cations and anions in the plasma are equivalent. Some
, 2
anions, such as protein, sulfates, phosphates, and organic acids, however,
are not measured in the common laboratory evaluations of the blood.
Therefore the normal anion gap represents these unmeasured negative
ions (sulfate, phosphate, lactate, keto acids, albumin). A convenient
measure of the anion gap is the difference between the sum of Na+ and
K+ concentrations and the sum of HCO3- and Cl- concentrations, or about
10-12 mEq/L.
v) In metabolic acidosis a normal anion gap is characteristic of conditions
related to bicarbonate loss with retention of chloride to maintain an ionic
balance. This is called hyperchloremic metabolic acidosis and it occurs
with renal failure or prolonged diarrhea with bicarbonate loss. An elevated
anion gap is characteristic of acidosis associated with accumulation of
anions other than chloride
vi)
vii) Causes of metabolic acidosis
Increased non-carbonic acids (elevated anion gap)
(a) Increased H+ load -- overproduction of acid
(i) Ketoacidosis (e.g., DM, alcoholic ketoacidosis,
starvation)
(ii) Lactic acidosis (e.g., shock)
(iii) Ingestions (e.g., ammonium chloride, ethylene
glycol, methanol, salicylates, paraldehyde)
, 3
(b) Decreased H+ excretion
(i) Advanced renal failure
(ii) Distal renal tubule acidosis
Bicarbonate loss (normal anion gap)
(c) Diarrhea
(i) Ureterosigmoidoscopy/
(ii) Early renal failure
(d) Proximal renal tubule acidosis
e) Metabolic alkalosis: ↑ pH, ↑ HCO3
i) Occurs when bicarbonate concentration is increased, usually caused by
excessive loss of metabolic acids. There is an increase in the 20:1 ratio of
HCO3- and H2CO3. Conditions that can result in metabolic alkalosis are
hydrogen and chloride depletion (i.e., prolonged vomiting, gastric
suctioning), excessive bicarbonate intake, hyperaldosteronism with
hypokalemia, and diuretic therapy.
ii) Respiratory compensation for metabolic alkalosis occurs when the
elevated pH inhibits the respiratory center. The rate and depth of
ventilation are decreased, causing retention of carbon dioxide. The ratio of
HCO3- concentration to H2CO3 concentration is reduced toward normal.
Respiratory compensation is not very efficient, however, and chronic or
severe metabolic alkalosis requires therapeutic intervention.
iii)
iv) Hypochloremic metabolic alkalosis occurs when acid loss is caused by
vomiting or gastric suctioning with depletion of ECF sodium, chloride, and
potassium. Renal compensation is not very effective because the volume
depletion and loss of electrolytes stimulate a paradoxical response by the
kidneys. The kidneys increase bicarbonate reabsorption to maintain an
anionic balance because the ECF chloride concentration is decreased.
, 4
The resulting excretion of H+ and reabsorption of bicarbonate prevent
correction of the alkalosis (Fig. 3.18). The kidneys also increase sodium
reabsorption. When potassium concentration is depleted, hydrogen ion
moves to the intracellular space and is excreted to maintain an
electrochemical balance.
v) With alkalemia, hydrogen ions are redistributed from the intracellular to the
extracellular space and potassium moves to the intracellular space to
preserve electroneutrality. With hyperaldosteronism, the excess
aldosterone causes sodium retention and loss of hydrogen and potassium
ions. Mild volume expansion ensues, and bicarbonate is retained along
with the sodium, thereby causing alkalosis. Diuretics, such as thiazides,
ethacrynic acid, and furosemide, produce mild alkalosis by enhancing
sodium, potassium, and chloride excretion more than bicarbonate
excretion.
f) Respiratory acidosis: ↓ pH, ↑ CO2
i) Respiratory disorders of acid-base balance are caused by increases or
decreases of alveolar ventilation in relation to the metabolic production of
carbon dioxide. Respiratory acidosis occurs when there is alveolar
hypoventilation. Carbon dioxide is retained, increasing [H+] (as H2CO3),
thus decreasing the ratio of HCO3- to PCO2, and producing acidosis.
Carbon dioxide excess in the blood is called hypercapnia. The common
causes include depression of the respiratory center (brainstem trauma,
oversedation), paralysis of the respiratory muscles, disorders of the chest
wall (kyphoscoliosis, pickwickian syndrome, flail chest), and disorders of
the lung parenchyma (e.g., pneumonitis, pulmonary edema, and chronic
obstructive lung disease).
ii) Respiratory acidosis may be acute or chronic. Airway obstruction is the
most common cause of acute respiratory acidosis. Acute compensation
for respiratory acidosis is not effective because the renal buffer
mechanism takes time to function. Further, the protein buffers provide
marginal compensation, and HCO3- is not a good buffer for CO2. Acute
Advanced Patho Hesi
1. Acid base analysis-patho
a) Pathophysiologic changes in the concentration of hydrogen ion or base in the
blood leads to acid-base imbalances.
i) Acidemia- pH of the arterial blood <7.35
ii) Acidosis- a systemic increase in hydrogen ion concentration or a loss of
base.
iii) Alkalemia- pH of arterial blood >7.45
iv) Alkalosis- a systemic decrease in hydrogen ion concentration or an
excess of base.
v) Metabolic, respiratory, or mixed etiologies.
b) Normal
i) pH: 7.35-7.45
ii) HCO3: 22-26
iii) CO2: 35-45
c) Abnormal/imbalances
i) Metabolic acidosis: ↓ pH, ↓ HCO3
ii) Metabolic alkalosis: ↑ pH, ↑ HCO3
iii) Respiratory acidosis: ↓ pH, ↑ CO2
iv) Respiratory alkalosis: ↑ pH, ↓ CO2
v) ROME = respiratory opposite, metabolic equal
d) Metabolic acidosis: ↓ pH, ↓ HCO3
i) The concentration of non-carbonic acids increases or bicarbonate (base)
is lost from the extracellular fluid or cannot be regenerated by the kidney.
This can occur quickly, as in from poor perfusion or hypoxemia, or more
slowly, as in renal failure (failure to excrete acid), starvation states, or
diabetic ketoacidosis (excess production of keto acids from lack of insulin).
ii) The buffer systems compensate for the excess acid and attempt to
maintain the arterial pH within a normal range. Hydrogen ions will move to
the intracellular space, and potassium will move to the extracellular space
to maintain an ionic balance. Buffering by bicarbonate lowers the serum
value of hydrogen ions and increases the pH. The respiratory system
compensates for a metabolic acidosis as the reduced pH stimulates
hyperventilation, lowering the PaCO2 and the amount of H2CO3
circulating in the blood. The kidneys excrete the excess acid as NH4+ and
titratable acid (H2PO4-). When acidosis is severe, buffers become
depleted and cannot compensate for the increasing H+ load and the pH
continues to decrease. The ratio of bicarbonate to carbonic acid
decreases to less than 20:1.
iii) In states of metabolic acidosis, potassium is redistributed from the
intracellular to the extracellular space, and is reabsorbed at the apical
membrane of the renal collecting tubule. There is also an increase in the
levels of ionized calcium because acidosis decreases the amount of
calcium bound to albumin.
iv) The evaluation of the anion gap can be helpful when used cautiously to
distinguish different types of metabolic acidosis. Normally, the
concentrations of cations and anions in the plasma are equivalent. Some
, 2
anions, such as protein, sulfates, phosphates, and organic acids, however,
are not measured in the common laboratory evaluations of the blood.
Therefore the normal anion gap represents these unmeasured negative
ions (sulfate, phosphate, lactate, keto acids, albumin). A convenient
measure of the anion gap is the difference between the sum of Na+ and
K+ concentrations and the sum of HCO3- and Cl- concentrations, or about
10-12 mEq/L.
v) In metabolic acidosis a normal anion gap is characteristic of conditions
related to bicarbonate loss with retention of chloride to maintain an ionic
balance. This is called hyperchloremic metabolic acidosis and it occurs
with renal failure or prolonged diarrhea with bicarbonate loss. An elevated
anion gap is characteristic of acidosis associated with accumulation of
anions other than chloride
vi)
vii) Causes of metabolic acidosis
Increased non-carbonic acids (elevated anion gap)
(a) Increased H+ load -- overproduction of acid
(i) Ketoacidosis (e.g., DM, alcoholic ketoacidosis,
starvation)
(ii) Lactic acidosis (e.g., shock)
(iii) Ingestions (e.g., ammonium chloride, ethylene
glycol, methanol, salicylates, paraldehyde)
, 3
(b) Decreased H+ excretion
(i) Advanced renal failure
(ii) Distal renal tubule acidosis
Bicarbonate loss (normal anion gap)
(c) Diarrhea
(i) Ureterosigmoidoscopy/
(ii) Early renal failure
(d) Proximal renal tubule acidosis
e) Metabolic alkalosis: ↑ pH, ↑ HCO3
i) Occurs when bicarbonate concentration is increased, usually caused by
excessive loss of metabolic acids. There is an increase in the 20:1 ratio of
HCO3- and H2CO3. Conditions that can result in metabolic alkalosis are
hydrogen and chloride depletion (i.e., prolonged vomiting, gastric
suctioning), excessive bicarbonate intake, hyperaldosteronism with
hypokalemia, and diuretic therapy.
ii) Respiratory compensation for metabolic alkalosis occurs when the
elevated pH inhibits the respiratory center. The rate and depth of
ventilation are decreased, causing retention of carbon dioxide. The ratio of
HCO3- concentration to H2CO3 concentration is reduced toward normal.
Respiratory compensation is not very efficient, however, and chronic or
severe metabolic alkalosis requires therapeutic intervention.
iii)
iv) Hypochloremic metabolic alkalosis occurs when acid loss is caused by
vomiting or gastric suctioning with depletion of ECF sodium, chloride, and
potassium. Renal compensation is not very effective because the volume
depletion and loss of electrolytes stimulate a paradoxical response by the
kidneys. The kidneys increase bicarbonate reabsorption to maintain an
anionic balance because the ECF chloride concentration is decreased.
, 4
The resulting excretion of H+ and reabsorption of bicarbonate prevent
correction of the alkalosis (Fig. 3.18). The kidneys also increase sodium
reabsorption. When potassium concentration is depleted, hydrogen ion
moves to the intracellular space and is excreted to maintain an
electrochemical balance.
v) With alkalemia, hydrogen ions are redistributed from the intracellular to the
extracellular space and potassium moves to the intracellular space to
preserve electroneutrality. With hyperaldosteronism, the excess
aldosterone causes sodium retention and loss of hydrogen and potassium
ions. Mild volume expansion ensues, and bicarbonate is retained along
with the sodium, thereby causing alkalosis. Diuretics, such as thiazides,
ethacrynic acid, and furosemide, produce mild alkalosis by enhancing
sodium, potassium, and chloride excretion more than bicarbonate
excretion.
f) Respiratory acidosis: ↓ pH, ↑ CO2
i) Respiratory disorders of acid-base balance are caused by increases or
decreases of alveolar ventilation in relation to the metabolic production of
carbon dioxide. Respiratory acidosis occurs when there is alveolar
hypoventilation. Carbon dioxide is retained, increasing [H+] (as H2CO3),
thus decreasing the ratio of HCO3- to PCO2, and producing acidosis.
Carbon dioxide excess in the blood is called hypercapnia. The common
causes include depression of the respiratory center (brainstem trauma,
oversedation), paralysis of the respiratory muscles, disorders of the chest
wall (kyphoscoliosis, pickwickian syndrome, flail chest), and disorders of
the lung parenchyma (e.g., pneumonitis, pulmonary edema, and chronic
obstructive lung disease).
ii) Respiratory acidosis may be acute or chronic. Airway obstruction is the
most common cause of acute respiratory acidosis. Acute compensation
for respiratory acidosis is not effective because the renal buffer
mechanism takes time to function. Further, the protein buffers provide
marginal compensation, and HCO3- is not a good buffer for CO2. Acute
