Author: Iain A M Hennessey & Alan G JappSpecialization: Biochemistry Publisher:Translator Team: ĐÀ TIEN SON & TRAN HOANG LONG Publication Year:2016Status:Pending approvalAccess:Community

Arterial blood gas interpretation

gas exchange in the lungs: GENERAL

Cells use oxygen (O2) for energy and release carbon dioxide (CO2). The blood stream delivers oxygen to the cells and takes away CO2. This process depends on the oxygen saturation of the blood and the ability of the lungs to separate CO2 from the blood.

The process of gas exchange in the lungs is the process of transferring O2 from the atmosphere into the blood stream (oxidation) and CO2 from the blood stream to the environment (CO2).

Watching: What is Paco2

This process occurs between the air-filled alveoli and the capillaries called capillaries. Thanks to the ultra-thin structure and extremely close exchange (alveolar-capillary exchange membrane), CO2 and O2 can diffuse back and forth. (Figure 1).

Figure 1: Anatomy of the respiratory system.


The results of arterial blood gas analysis help doctors evaluate the efficiency of gas exchange through measurements of partial pressures of O2 and CO2 in arterial blood (PaO2 and PaCO2).

The partial pressure describes the contribution of a gas in a mixture of gases (e.g. air) to the total pressure. When a gas diffuses into a fluid (such as blood), the amount of gas that diffuses more or less depends on this partial pressure.

Notice the following two symbols:

PO2 = partial pressure of oxygen

PaO2 = partial pressure of oxygen in arterial blood

All gases diffuse from an area of ​​high partial pressure to an area of ​​low pressure. In the alveolar–capillary exchange membrane, the air in the alveoli has higher PO2 and lower PCO2 than in capillary blood. Thus, O2 molecules traveling from the alveoli diffuse into the blood and CO2 molecules diffuse back until the partial pressures are equal.

Notes on Gas Pressures At sea level, barometric pressure (the total pressure of gases in the atmosphere) = 101 kPa = 760 mmHg. atmosphere) = 101 kPa or 760 mmHg. O2 makes up 21% of the air, so the partial pressure of O2 is: = 21% of atmospheric pressure = 21 kPa = 160 mmHg CO2 makes up a very small percentage of the air, so the partial pressure of CO2 in inhaled air is negligible.


CO2 diffuses from the blood stream into the alveoli with high efficiency, so CO2 reduction is practically limited by the rate at which CO2 is “discharged” in the alveoli. Therefore, the PaCO2 index (an indicator that reflects the total amount of CO2 in the arterial blood) depends on alveolar ventilation – the total volume of air transported between the alveoli and the ambient air per minute.

Ventilation is controlled by a center of the brain stem called the respiratory center. This region contains specific chemoreceptors sensitive to PaCO2 and is associated with respiratory muscles. When an abnormality occurs, the respiratory center will adjust the respiratory rate and intensity accordingly (Figure 2).

Normally, the lungs can maintain a normal PaCO2 level even in cases of abnormally elevated CO2 production (such as in sepsis). Therefore, when there is increased PaCO2 in the blood (hypercapnia – hypercapnia) almost always points to hypoventilation in the alveoli.


PaCO2 is dependent on ventilation. Ventilation level is adjusted to maintain PaCO2 within tight limits.

Figure 2: Air conditioning mechanism.

Note about hypoxic drive receptors In patients with persistently elevated PaCO2 (chronic hypercapnia), CO2 threshold-specific receptors gradually become desensitized. The body then depends on specific PaO2 receptors to measure the level of ventilation. At that time, low PaO2 becomes the main stimulus for ventilation. This is called hypoxic drive. With that mechanism, in the group of patients dependent on hypoxic receptor-dependent hypoxia, the over-aggressive correction of hypoxia, accompanied by oxygen assisted breathing, can reduce ventilation, leading to a paroxysmal increase of PaCO2. Therefore, patients with chronic hypercapnia should receive controlled oxygen supplementation, combined with careful blood gas monitoring. This indication does not apply to patients with acute hypercapnia.

HEMOGLOBIN’s OXY Saturation (SO2)

Oxidation is more complicated than CO2 reduction. The first thing we notice: PO2 doesn’t actually tell us how much O2 is in the blood. PO2 is just a measure of the amount of free, unbound O2 molecules in the blood – which makes up a very small amount of the total.

In fact, most of the oxygen molecules in the blood are bound to the hemoglobin protein (Hb; Figure 3). Therefore, the amount of oxygen in the blood depends on two factors:

Hb concentration: This metric represents the amount of oxygen the blood has enough load to carry.

Saturation of Hb with O2 (SO2): This is the percentage of available binding points of Hb that has been attached to an O2 molecule, in other words the oxygen load being used. (Figure 4).


SO2 = O2 saturation in any blood sample. SaO2 = O2 saturation in arterial blood.

Note about pulse oximeter (which We still call it a SpO2 meter SaO2 can be measured with a finger clip or the patient’s earlobe. In most cases, the meter provides complete information about the oxygen status, but when the saturation readings are below 75%, the meter will measure less accurately. When peripheral circulation is reduced, meter-provided measurements will be unreliable. The SpO2 meter also does not measure PaCO2, therefore, should not be used as a substitute for arterial blood gas results in hypoventilation patients.


PO2 does not reflect the amount of oxygen present in the blood. The new SaO2 and Hb concentrations reflect the amount of oxygen present in the arterial blood.

Figure 3: Correlation between free oxygen and hemoglobin bound oxygen in the blood.

Figure 4: Oxygen saturation with hemoglobin.


Now we are clear: the amount of oxygen in the blood depends on the concentration of Hb and SO2. So what does PO2 mean?

PO2 can be understood as a factor promoting the O2 molecule to bind Hb. Or in short: PO2 decides SO2. The oxyhemoglobin dissociation curve (Figure 5) shows that for each PO2 there is a corresponding SO2 value.

In general, the higher the PO2, the higher the SO2, but this arc is not a linear line. The blue segment of the graph is seen as an area of ​​”green grass plains”, where above this threshold, changes in PO2 have only a slight effect on SO2. In contrast, in the “red slope” region, even a small change in PO2 will have a large effect on SO2.

Remember: with a “normal” PaO of about 100mmHg, Hb will be near maximum saturation (above 95%). That means that the blood has used up its oxygen load and that even an increase in PaO2 does not increase the amount of O2 in the arteries.


PO2 is not the amount of O2 in the blood, but is the driving force behind the oxygen saturation of Hb.

Figure 5: The arc shows the dissociation of oxyhemoglobin. The curve shows the relationship between PO2 and the ratio of hemoglobin to oxygen saturation. Note for the sigma graph: almost flat when PO2 is above 80mmHg but PO2 falls below 60mmHg, the graph is sloped. 2,3-DPG: 2,3-diphosphoglycerate.


When Hb is close to reaching the maximum O2 saturation, increasing PO2 does not change the amount of O2 in the blood.

Alveolar ventilation and PaO2

We understand how PaO2 affects SaO2. But what factors determine PaO2?

The three main factors that affect PaO2 are:

Alveolar ventilation

Correlation between ventilation and perfusion (V˙/Q˙ )

Inspiratory Oxygen Concentration (FiO2)

Alveolar ventilation

O2 diffuses very quickly from the alveoli into the blood stream – so the higher the alveolar PO2, the higher the PaO2.

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Unlike atmospheric gases, alveolar gases contain a significant amount of CO2 (Figure 6). More CO2 means lower PO2 (remember: the partial pressure of a gas reflects that gas’s ratio to total volume).

Alveolar hyperventilation allows for more ‘discharge’ of CO2, resulting in higher alveolar PO2. And if ventilation is reduced, on the contrary, CO2 will accumulate when O2 is consumed, leading to a decrease in alveolar PO2.

While hyperventilation can only raise alveolar PO2 slightly (raising it close to the PO2 level of inhaled air), alveolar PO2 and even PaO2 can drop indefinitely if ventilation is ineffective. .

Figure 6: Composition of inhaled and exhaled air in breathing phases.


Both gas exchange processes are dependent on alveolar ventilation: inadequate ventilation will cause a decrease in PaO2 and an increase in PaCO2.

Ventilation/perfusion mismatch and shunt phenomenon

Blood flow through the lungs does not always reach well-ventilated alveoli and not all ventilated alveoli are perfused. This condition is called ventilation/perfusion mismatch (V˙ /Q˙ ).

Imagine there is an area of ​​the lung where the alveoli are poorly ventilated (eg, due to atelectasis or consolidation). Blood through these alveoli returns to the arterial circulation with less O2 and higher than normal CO2. This phenomenon is called shunt1 (Figure 7). It can be understood as the phenomenon of an unoxygenated amount of blood passing through the lungs.

Now, with a hyperventilation response, we can push more air out into the remaining ‘good alveoli’. This response allows the alveoli to release more CO2, so blood flow through these alveoli removes more CO2. The lower CO2 concentration in non-shunt blood compensates for the high CO2 concentration in the shunt blood stream, thereby maintaining PaCO2.

But oxidation is NOT like that. The blood flowing through the ‘good alveoli’ is no longer able to carry any more O2 because the Hb in the blood is maximally saturated (even with hyperventilation) (recall the “green plains”, Figure 5). Failure to compensate leads to a decrease in PaO2.


Ventilation/perfusion mismatch causes oxygen-poor blood to return to the arterial circulation, thereby reducing PaO2 and SaO2.

As long as total alveolar ventilation is maintained, this disproportion does NOT cause a compensatory increase in PaCO2.

1The term is also applied to describe vascular/alveolar bridges (anatomical shunts).

Figure 7: Effect of shunt on oxygen and carbon dioxide concentrations.

FiO2 and oxidation

The percentage of oxygen delivered (FiO2) represents the percentage of oxygen in the inhaled air. In room air, FiO2 is 21%, but can be increased by supportive oxygen therapy.

Low PaO2 can be a consequence of ventilation/perfusion mismatch or inadequate ventilation, and in either case, increasing FiO2 improves PaO2. Specific FiO2 requirements vary widely, depending on the severity of the oxidative stress, thereby helping the physician select the appropriate oxygen delivery device (Figure 8). When the cause is poor ventilation, it must be remembered that increasing FiO2 will not improve an elevated PaCO2.

Assisted oxygenation complicates blood gas results, as it can be difficult to determine whether a high PaO2 is consistent with FiO2. So, is there any oxidation reduction? A simple rule that is easy to apply, is that if normal, the difference between FiO2 and PaO2 is not more than 75mmHg. However, there is usually an error rate of FiO2, if in doubt, repeat blood gas testing in open air (no oxygen support) should be indicated.

Oxygen delivery devices Nasal frame (glasses): FiO2 2 nonspecific: rate dependent (1–6 L/min) and alveolar ventilation. Normal mask breathing: FiO2 30–50% at 6–10 L/min but inaccurate. May cause CO2 retention at rates below 5L/min, so do not use when providing lower FiO2. Fixed efficiency mask (high flow rate): FiO2 24–60%. Fixed, predictable oxygen supply. Ideal for controlled solution, low concentration precision oxygen therapy. Mask with reserve pocket: FiO2 60–80%. Higher FiO2 levels can be achieved with a tight-fitting mask. Short-term application in respiratory emergency. Intubation: FiO2 21–100%. Used in critically ill patients with a very high O2 requirement, especially patients with respiratory failure. Patients must be sedated, respiratory muscle relaxants and mechanical ventilation.

Figure 8 Oxygen delivery devices.

disorders in gas exchange

Tissue oxygen deficiency, blood oxygen deficiency, and oxygen depletion

Corresponding English terms: hypoxia, hypoxaemia and impaired oxygenation.

Tissue hypoxia is a state in which tissue is not supplied with adequate oxygen for aerobic metabolism 1 (Figure 9). This may be the result of hypoxia in the blood (discussed next) or tissue ischemia or infarction. This condition is often accompanied by lactic acid metabolism as the cells adapt by anaerobic metabolism.

Hypoxaemia is a state in which there is a decrease in the amount of oxygen present in the arterial blood. This may be the result of hypoxia (discussed below), low hemoglobin (anemia) or a decreased affinity of hemoglobin for oxygen (seen in CO poisoning).

Impaired oxygenation is a state of hypoxia due to impaired transport of oxygen from the lungs to the blood. Determined when PaO2 is low (less than 80mmHg).

It is important to note that there is a difference between: oxidative stress (a consequence of hypoxia) and inadequate oxygenation.

(consequence of tissue hypoxia). Let’s consider the same patient with PaO2 = 64mmHg. This patient is hypoxic, suggesting pulmonary disease. However, the patient’s PaO2 will often lead to a SaO2 reading above 90%. As long as hemoglobin and cardiac output are normal, the tissue is adequately oxygenated.

Figure 9: Causes of tissue hypoxia.

respiratory impairment TYPE 1

Type 12 respiratory failure is defined as low PaO2 with normal or decreased PaCO2. These parameters suggest a defect in the oxygenation process even though ventilation is good. It is often caused by a ventilation/perfusion mismatch and is the result of multiple causes (Box 1.3.1). PaCO2 is usually low due to compensatory hyperventilation.

If the patient is on O2 support (high FiO2), the arterial blood gas PaO2 may NOT be below the normal range, but will be low at a level inconsistent with the supply gas FiO2.

The severity of type 1 respiratory failure was assessed based on the level of hypoxemia, and ultimately, the occurrence of tissue hypoxia (Table 1.3.1). We recall the image of the arc of the oxygen dissociation graph. Reducing PaO2 to 60mmHg has little effect on SaO2 and is compensable. But beyond this threshold, we will hit a “red slope”, that is, if we reduce PaO2 further, it will drastically reduce SaO2, significantly reduce the amount of O2 in the blood.

Initial treatment in type 1 respiratory failure is aimed at achieving satisfactory PaO2 and SaO2 levels with supportive oxygen, while attempting to manage the underlying cause. In many cases, an SpO2 (pulse oximetry) meter can be used for continuous patient monitoring, as an alternative to repeated blood gas administration.

2Here, the author uses the term Impairment instead of Failure, because respiratory failure is diagnosed only when the PaO2 is below 60mmHg. In our country, there are places where the word “breathing failure” is used.

Box 1.3.1 :Common causes of respiratory failure* Pneumonia Acute asthma Pulmonary infarction Acute respiratory distress syndrome (ARDS) Pneumothorax Alveolar cystitis Pulmonary edema Obstructive pulmonary disease chronic (COPD) * The usual mechanism is ventilation/perfusion mismatch; however, under certain conditions (such as alveolar inflammatory response), the degree of diffusion of gases across the alveolar capillary membrane is impaired.

Table 1.3.1 Assessment of severity of type 1 respiratory failure Mild Moderate Severe PaO2 (kPa) 8–10.6 5.3–7.9 2 (mmHg) 60–79 40–59 2 (%) 90–94 75–89 2 High enough to maintain PaO2 Lactic acid metabolism (sign of tissue hypoxia) ) Organ dysfunction (drowsiness, confusion, renal failure, severe hemodynamic disturbance, coma)

respiratory impairment TYPE 2

Type 2 respiratory failure is defined as a state of high PaCO2 (hyperCO2), due to inadequate alveolar ventilation. Because oxygenation is also dependent on ventilation, the PaO2 is usually low, or normal, due to assisted oxygenation. It should be noted that any cause of type 1 respiratory failure can lead to type 2 respiratory failure if the failure is sudden (Box 1.3.2).

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Acute elevation of PaCO2 leads to acid retention in the blood (see Chapter 1.4), which is dangerous and must be reversed. Chronic hypercapnia is accompanied by an increase in bicarbonate (HCO3-) – a buffer that maintains acid-base balance. However, patients with type 2, when there is a sharp decrease in ventilation, also spike in PaCO2 (a chronic exacerbation), leading to acid accumulation and low blood pH (Table 1.3.2; Box 1.3.3).

Supplemental oxygen improves hypoxia but not hypercapnia, and therefore, treatment of type 2 respiratory failure should include measures to improve ventilation (eg, reducing airway obstruction). breathing, assisted ventilation, and sedation antagonists). It is the abuse of oxygen-supported oxygen in this type 2 patient that further reduces ventilation by violating the body’s hypoxic receptor-dependent mechanism (p. 7).

Since the SpO2 meter does not provide information on PaCO2, it should not be used in patients with type 2 respiratory failure.

Table 1.3.2 Different blood gases in patients with type 2 respiratory failure PaCO2 HCO3 pH Acute ↑ → ↓ Chronic ↑ ↑ → ​​Chronic exacerbation ↑ ↑ ↓

Box 1.3.2 Common causes of respiratory failure type 2 COPD* Opiate/benzodiazepine poisoning Exhaustion Airway foreign body Movable rib array Neuromuscular disorders Gout Scoliosis Sleep apnea (OSA) * COPD causes produce both respiratory failure 1 and 2 (with flare).

Box 1.3.3 Clinical signs of hypercapnia Confusion Lethargy Flapping tremor Pulse Warm extremities Headache


Hyperventilation lowers PaCO2 (hypoCO2) and increases pH respectively (see Chapter 1.4). In chronic cases, hyperventilation is accompanied by an increase in HCO3, a buffer that regulates blood pH. Breathing rate and breathing intensity also increased markedly. Severe reduction in PaCO2 can lead to itching around the mouth, extremities, dizziness, and fainting.

Psychogenic hyperventilation often occurs in pseudo-disease or dramatic fashion, and patients often complain of severe dyspnea. At that time, it will be difficult for the doctor to distinguish from causes from respiratory disease. Blood gas in this case will give low PaCO2 and normal PaO2.

Hyperventilation also occurs to offset the response to metabolic acidosis (secondary hyperventilation), which is described in Chapter 1.4. Other causes are listed in Table 1.3.3.

Table 1.3.3 Common causes of hyperventilation Primary Psychological stress Hypoxemia Salicylate toxicity Liver cirrhosis Pain, psychological trauma Fever CNS disorders Secondary Metabolic acidosis (any cause)


Four types of abnormal arterial blood gas results in gas exchange disorders are summarized in Table 1.3.4.

Table 1.3.4 Abnormal pattern of arterial blood gas results in gas exchange disorders PaO2 PaCO2 HCO3 Respiratory impairment Type 1 ↓ ↓/→ → Acute Type 2 ↓/→ ↑ → Chronic Type 2* ↓ /→ ↑ ↑ Hyperventilation → ↓ ↓/→ * Chronic exacerbation is defined as ↑ H+ in chronic patient.

Note about: alveolar–arterial blood pressure difference Alveolar–arterial blood pressure gradient (A – a gradient) is the difference between alveolar PO2 (average total alveolar) and arterial blood PO2. This differential pressure indicates whether PaO2 is consistent with the level of alveolar ventilation and is therefore an indicator of the degree of V/Q mismatch. Clinically, the main use of A-a gradient is to detect a slight increase in V/Q disproportion – when PaO2 is still within the normal range (as in pulmonary embolism) and to detect V/Q disproportion in patients with high blood pressure. type 2 respiratory failure (distinguishes simple type 2 from mixed respiratory failure). Calculation of alveolar–arterial gradient is not required in part 2 of the book (clinical case), but if you are interested, you can read the instructions in the Appendix.

acid-base balance: GENERAL

The terms acidity and alkalinity refer to the concentration of free hydrogen ions (H+) in a solution. The concentration of H+ can be expressed directly as nanomol/L or pH (see next page).

Solutions with high H+ concentration (low pH) are acidic and solutions with low H+ concentration (high pH) are basic (alkaline). The neutral point is the point at which a solution changes from alkaline to acidic (pH = 7, H+ = 100 nmol/L).

An acid liberates H+ when dissolved in solution. The acid therefore increases the concentration of H+ in the solution (or in other words, lowers the pH). A base will accept H+ when dissolved in solution, thereby reducing free H+ (in other words: increasing pH). A buffer is a substance that can both accept and release H+ depending on its concentration H+ around. Therefore, the buffer system can resist large changes in the concentration of H+.

Normally, blood has a pH around 7.35–7.45 (H+ = 35–45 nmol/L) and is therefore slightly alkaline. If blood pH is below 7.35, we have acidosis. If it is above the upper limit of 7.45, we have alkaline blood.

Acidosis is any process that lowers blood pH; Alkalosis is any process that increases the pH of the blood.

What is pH? The pH index (short for “power of hydrogen”) is a simple way to show large changes in H+ concentration, which, even though you’ve known about it before, seems to be born to make us feel better. confused! This indicator is a “negative logarithmic” (Figure 10). “Negative” means that the pH will decrease as the concentration of H+ increases (pH 7.1 will be more acidic than pH 7.2). “Logarithmic” means that 1 time change in pH corresponds to 10 times change in H+ concentration (so pH=7 will be 10 times more acidic than a solution with pH=8).

Why is acid-base balance so important?

For efficient cellular metabolism, H+ concentrations must be maintained within very narrow limits. Failure to control pH balance leads to inefficient cellular metabolism, which ultimately leads to death. (Figure 10).

Figure 10 pH/H+ scale .

maintain acid-base balance

Where do H+ ions in the body come from?

The process of breaking down sugars and fats for energy and producing CO2, which circulates in the blood as carbonic acid (see Box on next page).

Protein metabolism also produces hydrochloric acid, sulfuric acid and other metabolic acids.

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Therefore, H+ must be eliminated to maintain normal blood pH.

Where are H+ ions eliminated?

Respiratory mechanism

The lungs are responsible for removing CO2. PaCO2 – partial pressure of carbon dioxide in the blood depends on pulmonary ventilation. If the process of CO2 production changes, when necessary, the body will adjust respiration to increase / decrease CO2 emissions, in order to maintain PaCO2 within normal limits. Most of the acid produced in the body is in the form of CO2, so the lungs are responsible for excreting most of the endogenous acid.

Renal mechanism (metabolic mechanism)

The kidneys excrete metabolic acids. The kidneys excrete H+ in the urine and reabsorb HCO3-. HCO3- is a base (thus accepting H+ ions), so it is possible to reduce the concentration of H+ in the blood. The kidneys can regulate H+ and HCO3- secretion in response to changes in metabolic acid production. However, the kidneys not only regulate acid-base balance; The kidneys must also maintain stable concentrations of the major electrolytes (Na+ and K+) and strive to maintain electroneutrality (that is, the balance between the total number of negative and positive electrons in the body). The need to perform these tasks sometimes conflicts with the task of maintaining pH – either leading to acid-base disturbances, or making adjustments difficult.


Only one chemical reaction The following reaction is critical to understanding acid-base balance: H2O + CO2 ↔ H2CO3 ↔ H+ + HCO3 – First, the equation shows: CO2 enters the blood to become an acid. The more CO2 added to the blood, the more H2CO3 acid is formed, which will dissociate to produce H+. Second, this equation suggests that blood pH depends not only on the amount of CO2 or HCO3, but also on the ratio of CO2:HCO3. Therefore, a change in CO2 alone will not change the pH unless there is also a change in HCO3 to ensure the ratio (and vice versa). Since CO2 is controlled by respiration and HCO3 is excreted by the kidneys, this ratio explains how compensatory processes control blood pH.

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Renal Equilibrium Reactions There are two main equilibrium reactions that affect acid-base regulation: The sodium ion (Na+) is retained by exchange for a K+ ion or an H+ ion. When K+ is lacking, H+ must be compensated (and vice versa). Therefore, more H+ ions are excreted through Na+ exchange. Cl− and HCO3− are the main negatively charged ions (anions) that can be balanced with positively charged ions (cations, mainly Na+ and K+). When a large amount of Cl- is lost, more HCO3- is retained; when and when HCO 3- is consumed a lot (by the kidneys or through the digestive tract), more Cl- will be retained. Thus, in general, K+ and H+ tend to increase and decrease in the same direction, while an initial change in Cl- or HCO3- will result in the remaining ion changing in the opposite direction.


Acidosis is any process that lowers blood pH. If the acidosis is caused by an increase in PaCO2, it is called a respiratory acidosis; If acidosis is due to any other cause, there is a decrease in HCO3, it is called metabolic acidosis.

Alkalization is any process that increases blood pH. If alkalosis is caused by a decrease in PaCO2, it is called respiratory alkalosis; If for any other reason, there is an increase in HCO3, it is called metabolic alkalosis.

PaCO2 increase = Respiratory acidosis

Decreased PaCO2 = Respiratory Alkalosis

Increased HCO3 = Metabolic Alkalinity

Decreased HCO3 = Metabolic acidosis

The kidneys and respiratory system work together to maintain blood pH within normal limits. If one of the two systems is overloaded, altering blood pH, the other will automatically adjust to limit fluctuations (for example, if the kidneys do not excrete metabolic acids, the lungs will increase Ventilate to release more CO2). We call it compensation.

The disorder of acid-base balance can therefore be seen as two counterweights of the microscopic balance – which we consider below:

Normal acid-base balance

When the acid-base balance is perfectly normal, there is no acidosis or alkalosis; It’s like a small pound, but neither side has to carry a single weight. (Figure 11).

Uncompensated acid-base disorder

When acidosis or alkalosis occurs, the “weights” are out of balance, leading to acidosis or alkalosis, respectively. In Figure 12, there is a primary respiratory acidosis with no counterbalanced metabolism.

Figure 11: Normal acid-base balance

Figure 12: Decompensated respiratory acidosis


As we have described, a respiratory or metabolic disorder is often compensated for by adjusting other organ systems to correct the original disturbance. An important point is: the compensatory respiratory responses are more rapid – from a few minutes to a few hours, while the metabolic responses usually take several days.

Figures 13 and 14 illustrate two lung patterns that respond to primary metabolic acidosis by increasing alveolar ventilation to increase CO2 emissions (compensatory respiratory alkalosis). In Figure 13, acidosis persists despite compensating (partially compensatory); and in Figure 14, blood pH has returned to the normal range (fully compensated).

When holding such a blood gas result, how can we recognize which is the primary disorder and which is the compensatory reaction?

The first rule to remember is that overcompensation does not occur. The midpoint of acid-base balance is pH = 7.4 (H+ 40). If the balance shifts towards acidosis (pH 7.4), primary alkalosis should be considered.

The second rule is: the patient is more important than the ABG. When considering a blood gas reading, the clinical picture should always be taken into account. For example, if the patient in the situation in Figure 14 is accompanied by diabetes, with a high level of ketones in the urine, it is clear that metabolic acidosis is the primary process (diabetic ketosis).

Figure 13: Partially compensated metabolic acidosis

Figure 14: Fully compensated metabolic acidosis

Acid-base disorder

When a primary metabolic and primary respiratory disorder occurs at the same time, it is called a mixed acid-base disorder.

If these two processes are in opposition, the result will be similar to that of a compensated acid-base disorder (Figure 14) and minimize the pH fluctuations. A very illustrative example is in salicylate poisoning: primary hyperventilation (respiratory alkalosis) and metabolic acidosis (acidic salicylate) occur independently of each other.

Conversely, if these two processes both cause pH to shift in the same direction (metabolic acidosis and respiratory acidosis; or metabolic alkalosis and respiratory alkalosis), then acidosis, or alkalosis, occurs in the blood. will happen (Figure 15).

Alkaline math

One method that can be used in blood gas analysis is acid-base mapping (Figure 16). By comparing the Paco2 value and the H+/pH value on the chart, most blood gases can be identified. If the point we determine is outside the predefined regions, we consider it a mixed disorder.

Notes on … predicting compensatory responses It is not always easy to distinguish two opposing primary processes in the case of a compensated disorder. A more precise method than previously described involves calculating the predicted compensatory responses for any primary disorder. However, these formulas are often unnecessary and unnecessary in case studies (Section 2).

Figure 15: Mixed acidosis

Figure 16: Alkaline maths


Metabolic Acidosis

Metabolic acidosis is any process that, without increasing PaCO2, lowers blood pH. This condition is recognized on blood gas results when: decreased HCO3 and negative BE (residual alkalinity).

Metabolic acidosis can be caused by accumulation of metabolic acids (overabsorption, increased production or decreased renal excretion) or by excessive loss of bases (HCO3). When overproduction or absorption of acid occurs, the kidneys (if functioning normally) increase H+ excretion and thereby prevent, or at least mitigate, acidosis. When the renal output is not enough to resist the decrease in HCO3, the lungs will increase ventilation to reduce PaCO2, which is a normal response of the body. When this compensatory respiratory response is overloaded, acidosis occurs.

The severity of metabolic acidosis should be assessed based on both the potential process and the resulting acidosis. HCO3 values ​​below 15mmol/L (or BE + > 55) indicate severe acidosis.

The predominant symptom of metabolic acidosis is usually the process of hyperventilation (Kussmaul breathing pattern) to compensate through respiration. Other findings are often nonspecific and related to potential causes. Contaminated blood very severe acidosis (pH

Box 1.5.1 Metabolic acidosis (low HCO3)

There is increased anion gap

Lactic acidosis (hypoxemia, infarction, shock, sepsis) Ketoacidosis (diabetes, fasting, alcohol poisoning) Renal failure (stagnation of sulphate, phosphate, urate) Toxicity (aspirin, methanol, ethylene glycol) Massive rhabdomyolysis

Normal anion gap

Renal tubular acidosis (types 1, 2 and 4) Diarrhea (loss of HCO3 − ) Adrenal insufficiency Poisoning by ingestion of ammonium chloride After ureterostomy – sigmoidectomy Drugs (eg: acetazolamide)

Metabolic Acidosis and ANION Gap

Calculating the anion gap (see next page) can help determine the cause of the metabolic acidosis.

Metabolic acidosis with a normal anion gap is usually caused by loss of HCO3- through the kidneys (tubular acidosis) or from the gastrointestinal tract (diarrhea). The kidneys respond to a decrease in HCO3- by retaining Cl-, thereby ensuring charge neutralization. Cl- is one of two anions participating in the anion gap calculation formula, and thanks to that, the anion gap is maintained. Because there is an increase in Cl- ions, metabolic acidosis with a normal anion gap is called “hyperchloremic metab