Acid-base

disorders
lab 3
Presented by:
Mirna Ahmed
Egyptian Russian university
Metabolic alkalosis
a. Chloride responsive
“Depletion of chloride”:

1. gastric loss (vomiting, nasogastric suction)

When HCl is lost through vomiting or nasogastric suction, pancreatic secretions are not
stimulated and a net gain of bicarbonate into the systemic circulation occurs, generating a
metabolic alkalosis. Volume depletion maintains alkalosis.
In this case, the hypokalemia is secondary to the alkalosis itself and to renal loss of
potassium ions from the stimulation of aldosterone secretion.

2. Renal response to hypercapnia:

Cl loss at renal tubules as HCO3 is generated leading to Cl depletion;
compensatory metabolic alkalosis to primary respiratory acidosis
b. chloride unresponsive:
1. Hyperaldosteronism, corticosteroids ,Cushing's syndrome
RAAS stimulation s a result of renal hypoperfsion
2. Hypokalemia :

Shift of hydrogen ions into the intracellular space mainly

develops with hypokalemia. As the extracellular potassium
concentration decreases, potassium ions move out of the
cells. To maintain neutrality, hydrogen ions move into the
intracellular space.
Pure hypokalemia (ie, severe potassium ion depletion) causes
mild metabolic alkalosis
Chloride responsive/ Unresponsive:
Diuretics (loop diuretics and thiazide)
.They enhance sodium chloride excretion in the distal convoluted
tubule and the thick ascending loop, respectively. These agents cause
metabolic alkalosis by chloride depletion and by increased delivery of
sodium ions to the collecting duct, which enhances potassium ion and
hydrogen ion secretion.

. Loss of bicarbonate-poor, chloride-rich extracellular fluid, as

observed with thiazide diuretic or loop diuretic therapy, leads to
contraction of extracellular fluid volume. Because the original
bicarbonate mass is now dissolved in a smaller volume of fluid, an
increase in bicarbonate concentration occurs. This increase in
bicarbonate causes, at most, a 2- to 4-mEq/L rise in bicarbonate
concentration.
. Volume depletion also stimulates aldosterone secretion, which enhances
sodium ion reabsorption in the collecting duct and increases hydrogen ion and
potassium secretion in this segment.

. Urine chloride is low after discontinuation of diuretic therapy, while it is high

during active diuretic use.

. Diuretics (loop and thiazide): by multiple mechanisms eg: Secondary

hyperaldosteronism due to volume depletion, Cl depletion, or contraction
alkalosis; may be Cl-unresponsive because of concomitant K depletion
 Others
xss alkali administration:
Administration of sodium bicarbonate in amounts that exceed the capacity of
the kidneys to excrete this excess bicarbonate may cause metabolic alkalosis.
This capacity is reduced when a reduction in filtered bicarbonate occurs, as
observed in renal failure, or when enhanced tubular reabsorption of bicarbonate
occurs.
Mixed Acid-Base disorders
● More than one acid-base imbalance can occur at the same time.
● This is called a mixed acid-base disorder or a complex acid-base disturbance.
● Mixed disorders happen when a patient has a condition that causes one type of
imbalance then a second type of imbalance occurs.

Example:
A patient with an alcohol abuse disorder may develop ketoacidosis due to alcohol
misuse and metabolic alkalosis due to vomiting with loss of stomach acid. The
ketoacidosis increases the acidity of body fluids at the same time the loss of stomach
acid decreases acidity.
Mixed Acid-Base disorders
● Mixed acid-base disturbances may result in misleading test
results that seem normal.
● Health care providers must carefully review laboratory test results
to determine whether a single or mixed acid-base
imbalance is present.

The following are from the methods of determination and

interpretation of mixed acid-base disorders :
1. Assessment of compensation
2. Calculation of the excess gap in case of AG metabolic
acidosis
Case 1:
A 64-year-old female patient is admitted to ICU following lung volume reduction surgery for
bullous emphysematous lung disease. She is an ex-smoker with a 40-pack-year history and a
background history of hypertension. She was extubated post-procedure, before ICU
admission but still on opiates following surgery. Her medications include amlodipine,
furosemide, and bronchodilators. The following blood gas analysis was done on day 2
postoperative.

pH 7.4
PCO2 64 mmHg
PO2 57 mmHg
Bicarbonate 39 mEq/L
 Interpret the previous ABG report

Step 1: Identify the primary acid-base disorder

• pH = 7.4 ……………….…….. Normal

• PaCO2 = 64 mmHg ……..…. Respiratory Acidosis

• HCO3- = 39

• Acute or chronic …………….Based on history it’s Chronic

Chronic Respiratory Acidosis

Step 2: Assess for compensation

• Expected increase in HCO3=0.35xΔPaCO2=0.35x(64-40 =8.4

• (Calculated HCO3) =8.4+24=32.4 mEq

• The measured HCO3− differs (increases) by more than 2 mEq/L from

calculated value.

• i.e., compensation isn’t appropriate and there is a second A-B disorder

present, which might be Metabolic Alkalosis as HCO3 is increased than
expected.
Mixed acid-base disorders can lead to abnormal or normal pH, this a
case of normal pH
So, If we assume the primary disorder is metabolic alkalosis,

then there is secondary respiratory acidosis.

Step 2: Assess for compensation
• The increase in measured PCO2 = 64-40= 24 mmHg

• Expected increase in PCO2 =(0.9*HCO3)+15 =50.1 (Calculated PCO2)

• The measured PaCO2 differs by more than 4 mmHg from the calculated value.
• i.e., compensation isn’t appropriate and there is a second A-B disorder present,
which might be Respiratory Acidosis as PCO2 is elevated than expected.
Case 2:
You are asked to review a 44-year-old male known epileptic following a prolonged
generalized tonic-clonic convulsion. He is intubated and ventilated.
Arterial blood gas analysis is as follows:

Test Value

pH 7.15

pCO2 35 mmHg

pO2 105 mmHg

HCO3- 10.3 mmol/l

 Interpret the previous ABG report
Step 1: Identify the primary acid-base disorder

• pH = 7.15 ………………..Acidosis
• PaCO2 = 35 mmHg ……Normal but at the lower limit, Metabolic Acidosis is
suspected
• HCO3- = 10.3
Step 2: Assess for compensation

• Expected decrease in PCO2 =(1.5xHCO3)+8 = 23.45 (Calculated PCO2)

• The measured PaCO2 differs (decreases) by more than 4 mmHg from
calculated value.
• i.e.,compensation isn’t appropriate and there is a second A-B disorder present, which
might be Respiratory Acidosis as PaCO2 is elevated than expected.
Case 3:
The following data are from the arterial blood gas analysis of a 71-year-old male with
necrotizing fasciitis:

Parameter Patient Value

pH 7.43
PCO2 23 mmHg
Bicarbonate 15 mmol/L
Lactate 23.0 mmol/L
Sodium 147 mmol/L
Potassium 6.7 mmol/L
Chloride 95 mmol/L
 List the acid-base abnormalities

Step 1: Identify the primary acid-base disorder

• pH = 7.43 …………….. Normal but at higher limit,

Alkalosis is suspected

• PaCO2 = 23 mmHg…..Respiratory Alkalosis

• HCO3- = 15

• Acute or chronic ……..Based on history it’s acute

Acute Respiratory Alkalosis

Step 2: Assess for compensation
• Expected decrease in HCO 3= 0.2x Δ PaCO2 = 0.2x(40-
23)=3.4 (Calculated HCO3)
• Expected HCO3=24-3.4=20.6
• The measured HCO3− differs (decreases) by more than 2
mEq/L from calculated value.

• i.e., compensation isn’t appropriate and there is a second A-B

disorder present, which might be Metabolic Acidosis as
Lactate is highly elevated and HCO3 is decreased than
expected.
Step 3: Calculate Anion gap

Anion gap= Na+ − (Cl- + HCO3-)

= 147 − (95+15)
= 37 > 12 mEq/L
High Anion gap metabolic acidosis
Step 4: Calculate Excess gap

= 37 -12 = 25 mEq/L
Excess gap+ HCO3= 25+15= 40 (>26)
Concurrent metabolic alkalosis is present
 case 4:
A 29-year-old female is admitted to ICU extubated following an emergency Caesarian
section under general anesthesia at 38 weeks gestation for pre-eclampsia and failure to
progress. The following data were taken on admission to ICU:
Comment on this ABG report and explain the abnormalities

Step 1: Identify the primary acid-base disorder

• pH = 7.31 ………..... Acidosis

• PaCO2 = 42 mmHg …. Normal

• HCO3- = 20.5 ……low

Metabolic acidosis
Step 2: Assess for compensation

expected PCO2 = (1.5*HCO3)+8

=(1.5*20.5)+8
=38.75 mm Hg
adequately compensated
Case 5:
The following arterial blood gas was taken from a female hospitalized for recurrent •
urinary tract infections. She was transferred to the ICU because of nosocomial
pneumonia.
 a. Comment on her acid-base status

Step 1: Identify the primary acid-base disorder

• pH = 7.53 ……………….……..Alkalosis

• PaCO2 = 31 mmHg …………. Respiratory Alkalosis

• HCO3- = 25

• Acute or chronic ……………..Based on history it’s acute

• Acute Respiratory Alkalosis

Step 2: Assess for compensation

• Expected decrease in HCO3=0.2xΔPaCO2 = 0.2x(40-31) =1.8 (Calculated HCO3)

• 24-1.8=22.2 mEq

• The measured HCO3− differs by more than 2 mEq/L from calculated value.
• compensation is inappropriate
• Expected concurrent metabolic alkalosis.
b. List two likely causes of the acid-base abnormality

1. Respiratory alkalosis: Hyperventilation due to

pneumonia.

2. Metabolic alkalosis: vomiting or diuretic use.

Case 6:
A 43-year-old man, with no history of previous illnesses is admitted with septic
shock requiring the administration of high-dose vasopressor and
corticosteroids. His blood results after oxygen and support ventilation are as
follows:
b. Describe the acid-base abnormalities

Step 1: Identify the primary acid-base disorder

• pH = 7.64 ……………….……..Alkalosis

• PaCO2 = 28 mmHg …………. Respiratory Alkalosis

• HCO3- = 29

• Acute or chronic ……………..Based on history it’s

acute

Acute Respiratory Alkalosis

Step 2: Assess for compensation

• Expected decrease in HCO3= 0.2x Δ PaCO2= 0.2x(40-28)=

2.4

• (Calculated HCO3)=24-2.4=21.6

• Then the measured HCO3− differs by more than 2 mEq/L

from the calculated value.
• i.e., compensation isn’t appropriate and there is a second
A-B disorder present, which might be Metabolic Alkalosis
as HCO3 is elevated than expected.
b. Enlist other causes that may lead to such acid-base disorders

1. Respiratory alkalosis: Hyperventilation –

spontaneous or by mechanical ventilation.
2. Metabolic alkalosis: Recent use of
corticosteroids
A 70-year-old man was admitted to the hospital because he was unwell for about a
week and was vomiting for the previous 5 days. The patient was hypotensive, and his
skin turgor was poor. He was hyperventilating and was very distressed. Biochemistry
results showed Na+ 127 mEq/L, K+ 3.5 mEq/L, Cl- 79 mEq/L. ABG results were pH 7.54,
pCO2 56 mmHg, HCO-3 33 mEq/L.

1. What is the type and subtype of primary acid base disorder?

2. Is there a secondary acid base disorder? Justify.

3. How would this case be managed?

Thank you