UDK  616.152.11                   

ISSN 2466-2992 (Online) (2018) br.1-2, p. 20-24

COBISS.SR-ID 36418569


ACID-BASE BALANCE INTERPRETATION



Natalija Vuković1 , Milan Elenkov2

1Clinic for Anesthesiology and Intensive Care, Clinical Center Niš,

2Department for Anesthesiology and Intensive Care, General hospital Pirot



Summary:


Acid-base analysis is important diagnostic method in the therapeutic approach of many diseases. Accurate and timely diagnosis of acid-base disorders can be lifesaving or produce crucial changes in the disease course. Although technological innovations have brought better quality and a number of new information’s, acid-base interpretation still presents challenge. Physiological acid base method uses carbonic acid-bicarbonate system as basis for interpretation. In this way, changes in par­tial pressure of carbon dioxide produces changes in bicarbonate in the typical order and vice versa. This method implicit two basic metabolic and respiratory disorders.   


Keywords: Acid-base, acidosis, alkalosis



INTRODUCTION


Blood gas analysis can be driven from ca­pillary, peripheral arterial, peripheral and cen­tral venous blood sampling and from pulmo­nary artery. [1] It provides the assessment of acid-base disorders, ventilation and oxygena­tion in patients. [2] Furthermore, the compari­son of acid-base results from different blood samples provides a comprehensive approach to metabolism derangements and hemodyna­mic characteristics. [3,4]. Advanced analyzers measure and calculate the pH, partial pressure of carbon dioxide (PCO2), partial pressure of oxygen (PO2), concentration of bicarbonate (HCO3), base excess (BE), lactate and anion gap (AG). All of the above obliges us to regu­larly revise our knowledge about acid base.

In this review we will revise three basic steps in the interpretation of the acid-base analysis of peripheral arterial blood gas sample. The physiological ranges of acid-base parameters differ between different analyzers but there are average values (Table 1). For the interpretation it is easier to assume that the normal pH is 7.40 and the PaCO2 is 40mmHg.


























Step one

What is the primary abnormality, metabolic or respiratory?


The primary metabolic disorder occurs in these two cases [5]:

a) If the pH and PaCO2 change in the same direction

b) If the pH changes, while the PaCO2 stays normal


In this way, the patient will have metabolic acidosis if the pH and PaCO2 fall, or the pH falls and the PaCO2 is normal (Figure 1).

If the pH and PaCO2 rise, or the pH rises and the PaCO2 is normal, the patient will have metabolic alkalosis (Figure 2).

The primary respiratory disorder is present if the pH and PaC

O2 change in the opposite direction. An increase in PaCO2 is respiratory acidosis, while a decrease in PaCO2 is respira­tory alkalosis.




















Step two

In the situation where the patient has metabo­lic acidosis the anion gap should be calculated.

The anion gap is the assumption that the nega­tively charged anions and positively charged cations in the serum equal electrical neutrality. [6.7] It represents the difference between unmeasured anions and cations. [8] It is calcu­lated on the basis of electrolyte measurements as follows in the equation1.1:

1.1. AG = (Na+ + K+) – (Cl- + HCO3-)

The normal value of AG is 12±3mmol/L. [6] Nowadays, with more accurately measured electrolytes, the normal range of AG has decreased up to 7 ± 4mmol/L. [9]

Metabolic acidosis can be divided into those having an elevated AG and those with a nor­mal AG (10). The high AG acidosis occurs after the addition of acids or decreased excretion of endogenous acids. In those situations hydro­gen ions combine with bicarbonate, decrease it and produce an increase in the AG (Figure 3).

The normal AG acidosis is characterized by the loss of bicarbonate (diarrhea etc.) or addition of chloride (rapid administration of isotonic saline etc.), (Figure 4).











































Step three

Is there a compensation or superimposed se­condary abnormality?

This question should be answered for all the primary disorders. So, if the patient has meta­bolic alkalosis we should follow the explana­tion for compensation in metabolic alkalosis, for the patient with respiratory acidosis, we follow the interpretation for respiratory acido­sis etc.

Metabolic acidosis

Respiratory compensation for metabolic acido­sis is hyperventilation with reduction of PaCO2. [10]. The expected PaCO2 for each patient is calculated from equation 1.2. [11] In this equation, the concentration of bicarbonate that is used is from the patient’s acid-base re­sult.


1.2.  Expected PaCO2= (1.5 x HCO3-) + 8 (± 2)


If the PaCO2 from the analysis is the same as the expected one, the patient has compensated metabolic acidosis. If the measured PaCO2 exceeds the expected one, then the patient has metabolic acidosis as the first derangement and the respiratory acidosis as the second one. If the measured PaCO2 is lower than the expected one, then the patient has primary metabolic acidosis with secondary respiratory alkalosis.


Metabolic alkalosis

The expected PaCO2 in patients that have metabolic alkalosis as primary disorder is calcula­ted from the equation 1.2. [12] Again, like in the previous case, the concentration of bicarbonate is the one we have from the patient’s blood gas analysis.


1.3.  Expected PaCO2= (0.7 x HCO3-) +20 (± 2)


In the situation where the PaCO2 from the analysis is the same as the expected one, the patient has compensated metabolic alkalosis. If the measured PaCO2 exceeds the expected one, there is no compensation and metabolic alkalosis occurs as the first disorder and the respiratory acidosis as the second one. If the measured PaCO2 is lower than the expected one, then the patient has primary metabolic alkalosis with secondary respiratory alkalosis.


Respiratory acidosis

Compensation for raised PaCO2 in respiratory acidosis is the increased reabsorption of HCO3- in the kidney proximal tubules. [5] The re­lationship is analyzed by calculating ∆ pH/∆PaCO2. The results of ∆pH/∆PaCO2 or (7.40-measured pH) / (40-measured PaCO2) are then compared to given:

● ∆pH/∆PaCO2

If the result is > 0.008 then there is associated metabolic acidosis

If the result is between 0.003-0.008 that is compensated respiratory acidosis

If the result is < 0.003 there is associated metabolic alkalosis


If the result of ∆pH/∆PaCO2 is 0.003-0.008 the patient has partially compensated respiratory acidosis. If the calculation is greater than 0.008 then there is respiratory acidosis with se­condary metabolic acidosis. In the situation where ∆pH/∆PaCO2 is less than 0.003 the pa­tient has respiratory acidosis with associated metabolic alkalosis.


Respiratory alkalosis

Compensation in respiratory alkalosis is de­creased reabsorption of HCO3- in the kidney with decreased concentration in plasma HCO3-. As in the case of respiratory acidosis, this compensation is slow and needs time to reach its full realization. The respiratory disorder will be partially compensated during the time of compensation. The calculation of the ∆ pH/∆PaCO2 is again accomplished with nor­mal values of pH of 7.40 and PaCO2 of 40mmHg and the results are compared to those given:

∆pH/∆PaCO2

If the result is > 0.008 then there is associated metabolic alkalosis

If the result is between 0.002-0.008 that is compensated respiratory alkalosis

If the result is < 0.002 there is associated metabolic acidosis


If the ∆pH/∆PaCO2 result is between 0.002-0.008 the patient has partially compensated respiratory alkalosis. If the calculation is greater than 0.008 then there is respiratory alkalosis with secondary metabolic alkalosis. In the situation where ∆pH/∆PaCO2 is less than 0.002 the patient has respiratory alkalosis with associated metabolic acidosis.



CONCLUSION


This was just one way of interpreting results of the acid-base analysis. For complete compre­hensive interpretation clinical anamnesis and examination with history of illness are of utmost importance. New elements of acid-base

analysis like Lactate, Alb and electrolytes are additional parameters which can be analyzed. All of the previous enhance diagnostic process and better treatment plan of diseases.



REFERENCES


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9. Winter D, Pearson R, Gabow A, Schultz L, Lepoff B. The fall of the serum anion gap. Arch Intern Med 1990; 150: 311-3. doi:10.1001/archinte.1990.00390140057012.

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Korespondencija/Correspondence


Natalija VUKOVIĆ, MD, PhD

Clinical Centre Niš

Clinic for Anesthesiology and Intensive Care

Bulevar Zorana Djindjića 48, Niš

e-mail: massha.vukovic@gmail.com


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