Transportation: The acid transport mechanism in the blood are

1. By the binding of acids to plasma proteins, such as albumin, or

2. By binding to the bicarbonate buffer system. A buffer has the property of resisting changes in pH. Bicarbonate ions can bind to excess hydrogen ions in the blood to form carbonic acid, which can then dissociate into the water and carbon dioxide.

Elimination: The liver can metabolize certain acids, such as lactic acid and ketone bodies, and convert them into less acidic compounds that can be excreted from the body. The other organs responsible for acid elimination from the body are

1. Lungs; CO2 expiration

2. Kidneys; 1. bicarbonate absorption in the PCT, 2. H+ secretion in the DCT (aldosterone mediated), and 3. NH4+ secretion in the collecting duct.

Acidemia ---> Hyperkalemia  (pH 0.1  -->  K 0.6)

Alkalemia ---> Hypokalemia

The ABG value represents in the order; pH/PaCO2/PaO2/HCO3/O2Sat

Phosphate is absorbed in the PCT, blocked by a high level of PTH, resulting in phosphate acting as a buffer in the renal tubules (distal).

ABG reading steps; Example (1) pH; 7.35/PaCO2; 38/HCO3; 20

1. Determine acedemia or alkalemia. Here pH is below 7.4, hence Acidemia

2. Determine which process (acidosis or alkalosis) is in the same direction as the pH disorder (acidemia or alkalemia). Here metabolic acidosis (bicarbonate below 24) is in the direction of the pH disorder (acidemia). The diagnosis is Metabolic Acidosis.

3. Look for compensation. Here metabolic acidosis. Use winter's formula. The required PaCO2 is 38. The diagnosis is Metabolic acidosis compensated with Respiratory alkalosis.

Remember,  

1. Compensation does not return the pH to normal, 

2. Patients never "overcompensate", 

3. Compensation for metabolic alkalosis is relatively poor, and 

4. By predicting the normal compensatory response to primary acid-base disorders, the mixed disorder can be identified  (if a given patient is not compensating as predicted, a second or third abnormality must be present).

Example (2): pH; 7.35/PaCo2; 30/HCO3; 10

1. Determine (pH) acidemia or alkalemia; Here Acidemia

2. Determine the process (acidosis or alkalosis) in the same direction with the pH; Metabolic; Here, Metabolic Acidosis. 

3. Look for compensation; The required PaCO2 is 23, but here it is 30. Therefore a second disorder is present. PaCO2 is higher than predicted; hence the second disorder here is Respiratory acidosis.  The diagnosis is "Metabolic acidosis + Respiratory acidosis". 

Example (3); pH; 7.32/PaCO2; 28/HCO3; 14, Na+; 140, Cl-; 116

Answer: Normal Gap Metabolic Acidosis 

Example (4); pH; 7.28/PaCO2; 24/HCO3; 12, Na+; 128, Cl-; 94

Answer: Elevated Metabolic Acidosis

Example (5); A diabetic patient with acute dyspnoea; pH; 7.47/PaCO2; 20/HCO3; 14, Na+; 135, Cl-; 14

Answer: Respiratory alkalosis + Normal Gap Metabolic Acidosis

Example (6); A female patient is brought in an unconscious state; pH; 7.09/PaCO2; 34/HCO3; 10, Na+; 135, Cl-; 112, Albumin; 2.

Answer: Elevated Gap Metabolic Acidosis + Respiratory Acidosis

The Delta ratio interpretations are as follows

1. Lower than expected; HAGMA + NAGMA

2. Within expected range; HAGMA alone

3. Higher than expected; HAGMA + Metabolic alkalosis

Explanation; 

Example (7); 75-year-old woman with Acute diarrhoeal disease. pH; 7.29/PaCO2; 30/HCO3; 14. Na+: 128, Cl-: 94

Answer:  HAGMA + NAGMA (as the Delta ratio is less than one, 0.8)

Example (8); 35-yrs-old with Type 1 DM came with vomiting and abdominal pain. pH; 7.27/PaCO2; 27/HCO3; 12. Na+; 140, Cl-; 98

Answer; Here Delta ratio is 1.5. Even though the clinical picture is of ketoacidosis, but delta ratio is not falling in 0.8 - 1.2, hence suspect a concurrent metabolic alkalosis. 

Elevated gap metabolic acidosis + Metabolic alkalosis 

In this case, HAGMA is due to ketoacidosis, and Metabolic alkalosis is due to vomiting.

Example (9); 48-year-old alcoholic found unconscious in a pool of vomitus. pH; 7.17/ PaCO2; 65/ HCO3; 22, Albumin; 1.6, Na+; 136, Cl-; 98

Answer; The respiratory acidosis is not compensated appropriately, and bicarb is low, meaning additional metabolic acidosis is present. The adjusted (for low albumin) AG is elevated (22). Delta ratio is 5

Respirtory Acidosis + Elevated Gap Metabolic acidosis + Metabolic Alkalosis

This patient has ketoacidosis from alcoholism. intoxication causes central respiratory suppression and metabolic alkalosis from vomiting.  

The first step in any alcohol (Methanol, Ethanol or Glycol) metabolism is the conversion to acetaldehyde by the Alcohol dehydrogenase (ADH) enzyme. This reaction requires the coenzyme NAD+ (nicotinamide adenine dinucleotide) and results in the release of hydrogen ions (H+). And next step is further oxidation by the Aldehyde dehydrogenase enzyme. 

Methanol --> Formaldehyde  --> Formate

Ethanol --> Acetaldehyde --> Acetate

Ethylene glycol --> Glycoaldehyde --> Glycolate

Propylene glycol --> Lactaldehyde --> Lactate

The affinity of ADH to ethanol is higher than that of formaldehyde or glycolaldehyde. So ethanol infusion is given to slow down the formation of formate or glycolate in case of poisoning with methanol or glycol. Formeprazole inhibits alcohol dehydrogenase but is not available widely.  

Serum Osmolar gap: 

It measures the difference between the calculated and measured levels of osmolality in the blood. To calculate the expected osmolality, one can use the following formula:

2 x [Na+] + glucose/18 + BUN/2.8

A normal serum osmolar gap is typically less than 10 mOsm/kg. A high serum osmolar gap (>20) indicates suspected toxic alcohol ingestion. 

Diarrhoea can cause

1. Volume depletion

2. Acid-base disturbance (stool is alkaline)

3. Electrolytes abnormalities

loss of salts of organic acid anions (eg, propionate, lactate, acetate, and butyrate) is the most important cause of metabolic acidosis in patients with diarrhoea. The loss of large quantities of sodium or potassium salts of organic acid anions (which represent potential bicarbonate) is physiologically equivalent (from an acid-base perspective) to losing equal quantities of sodium or potassium bicarbonate. Diarrhea caused by cholera is more commonly associated with high stool concentrations of true bicarbonate. Acute metabolic acidosis should increase distal tubule hydrogen ion secretion and initially reduce urine pH below 5.5. However, if the acidosis persists and becomes chronic, a major increase in urine ammonium excretion will develop. This large increase in urine ammonium will increase the urine pH. 

Example: A code blue is called after a 680-year-woman undergoing TEE prior to elective cardioversion for atrial fibrillation developed dyspnoea and confusion. On exam, she is in respiratory distress and is cyanotic. O2 saturation is 85% (SpO2) with 10-litre oxygen via face mask.  pH 7.45/PaCO2 36/HCO3 24/ PaO2 340/ SaO2 100. 

Answer: [cyanosis is common with met Hb (carboxy Hb sometime has a cherry red appearance)]

Step 1; calculate A-a gradient

PAO2 = FiO2 (Pi-PH2O) - [PaCO2/RQ] = 0.60 (760-47) - [36/0.8] = 383

A-a gradient = PAO2-PaO2 = 383-340 = 43

Step 2: Expected A-a gradient = age/4+4 + 50 (FiO2-0.21) = 41

Step 3: Saturation gap = | SpO2-SaO2 | = | 85%-100% | = 15% , seen in methemoglobinemia

  Courtesy: Tintinalli, Eric Strong MD

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