Below is a summary of the chapter content. The topic is described in detail in the Oxford Handbook of Critical Care (see below).

Acid-Base Balance (ABB)

Acidemia	Normal pH of the blood	Alkalemia
pH < 7,35	pH 7,35 - 7,45	pH > 7,45

Bicarbonate buffer

The most predominant buffer in plasma. 

The lungs and kidneys are the organs involved in regulating bicarbonate buffer. 

Disturbances in the respiratory component tend to be compensated by the metabolic component and vice versa. A change in the same direction (respiratory and metabolic acidosis are present) is called a combined ABB disorder. This condition is severe because compensatory mechanisms are exhausted.

The pace of compensation and response to changes varies between the lungs and kidneys.
The lungs can adapt to changes in buffer balance within seconds-minutes, the kidneys rather than hours to days. 

With full compensation, blood pH should be normal (7.35-7.45), although severe acid-base disturbances may be present. The Boston Rules could be used to precisely calculate the degrees of compensation.

Classification of ABB disorders

Respiratory ABB disorder

Respiratory alkalosis	Normal value	Respiratory acidosis
pCO2 < 4,6 kPa	pCO2 4,6 - 6,0 kPa	pCO2 > 6,0 kPa

1kPa = 7,5 mmHg (torr)

Metabolic ABB disorder

Metabolic acidosis	Normal value	Metabolic alkalosis
HCO3 < 22 mmol/l	HCO3 22 - 26 mmol/l	HCO3 > 26 mmol/l
BE < -2 mmol/l	BE -2 - 2 mmol/l	BE > 2 mmol/l

Base base (BB), Base excess (BE)
BB or BE differ between the current and normal values of all buffering systems (bicarbonate, phosphate, and negative charges on albumin).

To assess the metabolic component alone, BE is preferable to HCO3 concentration because BE is calculated to the normal pCO2 value of 5 kPa, not the current value.
So, BB/BE instead of HCO3 is more specific for evaluating metabolic disorders.  

Respiratory disorders ABB

Respiratory acidosis

pH < 7.35, pCO2 > 6 kPa, (HCO3- > 26 mmol/l suggest compensation)

Impaired elimination of CO2 from the body

• Hypoventilation, Asphyxia
• Depression of the respiratory centre (Intoxication, Meningitis, Spinal cord tumours)
• Airway obstruction
• Lung injury/disease (PE, ARDS, Pneumonia, Smoke inhalation)
• Chest Injury (Trauma, PNO, Fluidothorax)
• Musculoskeletal and neuromuscular disorders (Myasthenia gravis, Spinal cord injury,...)

Increased CO2 production

• Fever, convulsions

Therapy

• Initial ABCDE approach 
• Oxygen administration alone will not improve respiratory acidosis caused by hypoventilation
• Ventilatory support, consciousness checks
• In intoxications, antidotes (e.g. opioids - naloxone) can be given 
• Often, ventilatory support required (NIV/IPPV)
• Supportive treatment for convulsions, temperature (cooling, antipyretics)

Respiratory alkalosis

pH > 7.45, pCO2 < 4.6 kPa, (HCO3- < 22 mmol/l suggest compensation)

Increased elimination of CO2 from the body

• Hyperventilation 
• Stimulation of the respiratory centre (anxiety, pain, fever)
• Stimulant intoxication (cocaine, methamphetamine,...)
• Pulmonary causes (PE, pneumonia, bronchial asthma attack)
• Septic patient with tachypnea
• Hepatic failure
• Heart failure
• Poorly adjusted IPPV

Therapy

• Initial ABCDE approach
• Calming the patient, breathing exercise, sedation
• Treat the underlying cause: anxiolytics, antipyretics, analgesics
• In severe alkalosis, watch for ionogram disturbances: Hypophosphatemia, hypokalemia, hypomagnesemia

Metabolic disorders ABB

Metabolic acidosis

pH < 7.35, HCO3 < 22 mmol/l, (pCO2 < 4.6 kPa suggest compensation)

Anion gap

Metabolic acidosis (MAc) is a common ABB disorder in critical patients. 

The Anion Gap (AG) calculation is used to detect the presence of acid anions that are not detectable by conventional laboratory methods.

Normal AG is 12 ± 4 mmol/l.
When AG >16 mmol/l, we evaluate the disorder as High AG Metabolic Acidosis (HAGMA).
AG < 16 mmol/l is graded as Normal AG Metabolic Acidosis (NAGMA).

HAGMA

The most common causes of HAGMA can be summarized using the acronym (CAT MUDPILES)

• CO, CN - cyanide
• Alcoholic ketoacidosis and starvation ketoacidosis
• Toluene
• Metformin, methanol
• Uremia
• DKA
• Paracetamol, propylene glycol
• Iron - Iron, isoniazid
• Lactate acidosis
• Ethylene glycol
• Salicylates

NAGMA

• Excess chloride (use of excessive amounts of saline solution)
• Diuretics Acetazolamide, Addison's disease
• GIT causes - diarrhea/vomiting, fistulas (pancreatic, ureteral, biliary, small bowel, ileostomy)
• Renal tubular acidosis

Therapy

• ABCDE approach
• Treatment of individual causes is beyond the scope of this chapter, but diagnosis of the specific cause is the key to successful treatment. 
• Only in critical situations of pH < 7.1, along with renal failure or peri-resuscitation, do we use bicarbonate replacement in MAc therapy; it is necessary to identify the underlying cause and initiate therapy.

Metabolic alkalosis

pH > 7.45, HCO3- > 26, (pCO2 > 6 suggest compensation)
elevation of pCO2 stimulates the respiratory centre, MAlk compensation is limited by this mechanism

• Acid loss from GIT
• Vomiting, suctioning, repeated gastric lavage,...
• Some diuretics (thiazides or loop diuretics)
• Ingestion of alkaline substances
• During iatrogenic intervention (dialysis - citrate)

Relationship between ABB disorders and kalaemia

Blood pH affects the levels of kalaemia. 

In severe acidosis (pH<7.2), there is a large amount of H+ ions in the plasma; this excess is pumped into the cells by exchangers and channels and displaces the most dominant intracellular cation into the blood plasma: K+. Therefore, hyperkalemia in severe acidosis is an expected finding. 

Recommended reading for this chapter: