Acid base disordersDr. Mohamed Elbahnasawy

Ass. lecturer of emergency medicineTanta university

The following six-step process helps ensure a complete interpretation of every ABG. In addition, you will find tables that list commonly encountered acid-base disorders.

Many methods exist to guide the interpretation of the ABG. This discussion does not include some methods, such as analysis of base excess or Stewart’s strong ion difference. A summary of these techniques can be found in some of the suggested articles. It is unclear whether these alternate methods offer clinically important advantages over the presented approach, which is based on the “anion gap.”

INTRODUCTION

7.35-7.45 pH80-100 mmHg PaO235-45 mmHg PaCO2

95-100% O2 saturation22-26 mEq/L HCO3 Or - 2+ BASE excess

Normal values

pH pH is a - ve logarithmic scale of the concentration of hydrogen ions in a

solution. It is inversely proportional to the concentration of hydrogen ions. When a solution becomes more acidic the concentration of hydrogen ions

increases and the pH falls. Normally the body’s pH is closely controlled at between 7.35 – 7.45. This is

achieved through buffering and excretion of acids. Buffers include plasma proteins and bicarbonate (extracellular) and proteins,

phosphate and haemoglobin (intracellularly). Hydrogen ions are excreted via the kidney and carbon dioxide is excreted via

the lungs. Changes in ventilation are the primary way in which the concentration of H+

ions is regulated. Ventilation is controlled of the concentration of CO2 in the blood.

If the buffers and excretion mechanisms are overwhelmed and acid is continually produced, the he pH falls. This creates a metabolic acidosis.

If the ability to excrete CO2 is compromised this creates a respiratory acidosis. Note that a normal pH doesn’t rule out respiratory or metabolic pathology. This

why you must always look at all the values other than pH as there may be a compensated or mixed disorder

Components o ABG

Partial pressure (PP) Partial pressure is a way of assessing the number of

molecules of a particular gas in a mixture of gases. It is the amount of pressure a particular gas contributes to the total pressure. For example, we normally breathe air which at sea level has a pressure of 100kPa, oxygen contributes 21% of 100kPa, which corresponds to a partial pressure of 21kPa.

When used in blood gases, Henry’s law is used to ascertain the partial pressures of gases in the blood. This law states that when a gas is dissolved in a liquid the partial pressure (i.e. concentration of gas) within the liquid is the same as in the gas in contact with the liquid. Therefore you can measure the partial pressure of gases in the blood.

PaO2 is the partial pressure of oxygen in arterial blood PaCO2 is the partial pressure of carbon dioxide in

arterial blood.NB Kpa = 7.6 x mmHG.

Base excess (BE)• This is the amount of strong base which would need to be added or subtracted from a substance in order to return the pH to normal (7.40).• A value outside of the normal range (-2 to +2 mEq/L) suggests a metabolic cause for the acidosis or alkalosis.• In terms of basic interpretation• A base excess more than +2 mEq/L indicates a metabolic alkalosis.• A base excess less than -2 mEq/L indicates a metabolic acidosis.

Bicarbonate (HCO3)• Bicarbonate is produced by the kidneys and acts as a buffer to maintain a normal pH. The normal range for bicarbonate is 22 – 26mmol/l.• If there are additional acids in the blood the level of bicarbonate will fall as ions are used to buffer these acids. If there is a chronic acidosis additional bicarbonate is produced by the kidneys to keep the pH in range.• It is for this reason that a raised bicarbonate may be seen in chronic type 2 respiratory failure where the pH remains normal despite a raised CO2.

pH is closely controlled in the human body and there are various mechanisms to maintain it at a constant value. It is important to note that the body will never overcompensate as the drivers for compensation cease as the pH returns to normal. In essence compensation for an acidosis will not cause an alkalosis or visa versa.

Compensation

• If a metabolic acidosis develops the change is sensed by chemoreceptors centrally in the medulla oblongata and peripherally in the carotid bodies.

• The body responds by increasing depth and rate of respiration therefore increasing the excretion of CO2 to try to keep the pH constant.

o The classic example of this is ‘Kussmaul breathing’ the deep sighing pattern of respiration seen in severe acidosis including diabetic ketoacidosis. Here you will see a low pH and a low pCO2 which would be described as a metabolic acidosis with partial respiratory compensation (partial as a normal pH has not been reached).

Respiratory compensation

•In response to a respiratory acidosis, for example in CO2 retention secondary to COPD,

the kidneys will start to retain more HCO3 in order to correct the pH.

•Here you would see a low normal pH with a high CO2 and high bicarbonate.

•This process takes place over days.•It is important to ensure that the compensation

that you see is appropriate, i.e. as you would expect. If not then you should start to think about

mixed acid base disorders.

Metabolic compensation

6 – STEP APPRAOCH

Step 1: Assess the internal consistency of the values using the Henderseon-Hasselbach equation:

[H+] = 24 x (PaCO2/HCO3) PH = 6.1 X (HCO3/.003XPaCO2)

If the pH and the [H+] are inconsistent, the

ABG is probably not valid.

Step 1

Ph Approximate [H+](mmol/L)

7.00 100

7.05 89

7.10 79

7.15 71

7.20 63

7.25 56

7.30 50

7.35 45

7.40 40

7.45 35

7.50 32

7.55 28

7.60 25

7.65 22

Is there alkalemia or acidemia present?pH < 7.35 acidemiapH > 7.45 alkalemia

This is usually the primary disorder Remember: an acidosis or alkalosis may be

present even if the pH is in the normal range (7.35 – 7.45)

You will need to check the PaCO2, HCO3- and anion gap

Step 2

Is the disturbance respiratory or metabolic  ?What is the relationship between the direction of change in the pH and the

direction of change in the PaCO2 ?In primary respiratory disorders, the pH and PaCO2 change in opposite directions ;

in metabolic disorders the pH and PaCO2 change in the same direction

Step 3

Acidosis Respiratory pH ↓  PaCO2  ↑

Acidosis Metabolic& pH ↓ PaCO2  ↓

Alkalosis Respiratory pH ↑ PaCO2  ↓

Alkalosis Metabolic pH ↑ PaCO2   ↑

Is there appropriate compensation for the primary disturbance?

Usually, compensation does not return the pH to normal (7.35 – 7.45).

Step 4

Disorder Expected compensation Correction factor

Metabolic acidosis PaCO2 = (1.5 x [HCO3-]) +8 ±2

Acute respiratory acidosis

Increase  in  [HCO3-]= ∆ PaCO2/10

±3

Chronic respiratory acidosis (3-5 days)

Increase  in  [HCO3-]= 3.5(∆ PaCO2/10)

 

Metabolic alkalosis Increase in PaCO2 = 40 + 0.6(∆HCO3-)

 

Acute respiratory alkalosis

Decrease in  [HCO3-]= 2(∆ PaCO2/10)

 

Chronic respiratory alkalosis

Decrease in  [HCO3-] = 5(∆ PaCO2/10) to 7(∆ PaCO2/10)

Calculate the anion gap (if a metabolic acidosis exists) :

AG= [Na+]-( [Cl-] + [HCO3-] )=12 ± 2

Step 5

A normal anion gap is approximately 12 meq/L. In patients with hypoalbuminemia, the normal anion

gap is lower than 12 meq/L; the “normal” anion gap in patients with hypoalbuminemia is about 2.5 meq/L lower for each 1 gm/dL decrease in the plasma albumin concentration (for example, a patient with a plasma albumin of 2.0 gm/dL would be approximately 7 meq/L.)

Corrected anion gap = AG + 2.5(4-albumin) If the anion gap is elevated, consider calculating the

osmolal gap in compatible clinical situations.◦ Elevation in AG is not explained by an obvious case (DKA, lactic

acidosis, renal failure◦ Toxic ingestion is suspected

OSM gap =  measured OSM – (2[Na+] - glucose/18 – BUN/2.8◦ The OSM gap should be < 10

If an increased anion gap is present, assess the relationship between the increase in the anion gap and the decrease in [HCO3-].Assess the ratio of the change in the anion gap

(∆AG ) to the change in [HCO3-] (∆[HCO3-]): ∆AG/∆[HCO3-]This ratio should be between 1.0 and 2.0 if an uncomplicated anion gap metabolic acidosis is present.If this ratio falls outside of this range, then another metabolic disorder is present:If ∆AG/∆[HCO3-] < 1.0, then a concurrent non-anion gap metabolic acidosis is likely to be present.If ∆AG/∆[HCO3-] > 2.0, then a concurrent metabolic alkalosis is likely to be present

Step 6

Disorder pH Primary problem Compensation

Metabolic acidosis ↓ ↓ in HCO3- ↓ in PaCO2

Metabolic alkalosis ↑ ↑ in HCO3- ↑ in PaCO2

Respiratory acidosis ↓ ↑ in PaCO2 ↑ in [HCO3-]

Respiratory alkalosis ↑ ↓ in PaCO2 ↓ in [HCO3-]

Table 1: Characteristics of acid-base disturbances

Airway obstruction- Upper airway obstruction like FB , acute epiglottitis- Lower◦ COPD◦ asthma◦ other obstructive lung disease

CNS depression Sleep disordered breathing  (OSA ) Neuromuscular impairment Ventilatory restriction Increased CO2  production: shivering, rigors, seizures,

malignant hyperthermia, hypermetabolism, increased intake of carbohydrates

Incorrect mechanical ventilation settings

Table 2: Selected etiologies of respiratory acidosis

o CNS stimulation: fever, pain, fear, anxiety, CVA, cerebral edema, brain trauma, brain tumor, CNS infectiono Hypoxemia or hypoxia: lung disease, profound anemia, low FiO2o Stimulation of chest receptors: pulmonary edema, pleural effusion, pneumonia, pneumothorax, pulmonary emboluso Drugs, hormones: salicylates, catecholamines, medroxyprogesterone, progestins

o Pregnancy, liver disease, sepsis, hyperthyroidism

Table 3: Selected etiologies of respiratory alkalosis

o Hypovolemia with Cl- depletiono GI loss of H+

Vomiting, gastric suction, villous adenoma, diarrhea with chloride-rich fluid

o Renal loss H+ Loop and thiazide diuretics, post-hypercapnia

(especially after institution of mechanical ventilation)

o Hypervolemia, Cl- expansiono Renal loss of H+:  edematous states (heart failure,

cirrhosis, nephrotic syndrome), hyperaldosteronism, hypercortisolism, excess ACTH, exogenous steroids, hyperreninemia, severe hypokalemia, renal artery stenosis, bicarbonate administration

Table 4: Selected causes of metabolic alkalosis

Elevated anion gap:◦ Methanol intoxication◦ Uremia◦ Diabetic ketoacidosisa, alcoholic ketoacidosis, starvation

ketoacidosis◦ Paraldehyde toxicity◦ Isoniazid◦ Lactic acidosisa

Type A:  tissue ischemia Type B:  Altered cellular metabolism

◦ Ethanolb or ethylene glycolb intoxication◦ Salicylate intoxication

Rhabdomyolsis

Table 5: Selected etiologies of metabolic acidosis

o

Normal anion gap:

will have increase in [Cl-]o

GI loss of HCO3-

Diarrhea, ileostomy, proximal colostomy, ureteral diversiono

Renal loss of HCO3-

proximal RTA carbonic anhydrase inhibitor (acetazolamide)o Renal tubular disease ATN Chronic renal disease Distal RTA Aldosterone inhibitors or absence NaCl infusion, TPN,

NH4+ administration

Table 6: Selected mixed and complex acid-base disturbances

Disorder Characteristics Selected situationsRespiratory acidosis with metabolic acidosis

↓in pH↓ in HCO3↑ in PaCO2

 

Cardiac arrest Intoxications Multi-organ failure

Respiratory alkalosis with metabolic alkalosis

↑in pH↑ in  HCO3-  ↓ in PaCO2    

Cirrhosis with diuretics Pregnancy with vomiting Over ventilation of COPD

Respiratory acidosis with metabolic alkalosis

pH in normal range↑ in PaCO2,↑ in  HCO3- 

COPD with diuretics, vomiting, NG suction

Severe hypokalemia

Respiratory alkalosis with metabolic acidosis

pH in normal range↓ in PaCO2↓ in HCO3           

Sepsis Salicylate toxicity Renal failure with CHF or

pneumonia Advanced liver disease

Metabolic acidosis with metabolic alkalosis   

pH in normal rangeHCO3- normal   

Uremia or ketoacidosis with vomiting, NG suction, diuretics, etc.