Key points
There are four major disorders of acid-base balance: respiratory acidosis metabolic acidosis respiratory alkalosis metabolic alkalosis These balance disorders are often accompanied by compensatory changes These changes rarely fully compensate for the primary balance disorder In chronic disease, the magnitude of compensation is greater, resulting in better maintenance of pH.
Clinical Tips
When interpreting blood gas results, it is important to refer to the clinical presentation. Control the pH of the blood. The pH of blood is slightly acidic (between 7,35 and 7,45). To maintain normal function, the body maintains the pH of the blood at about 7.4. The body maintains the blood acid-base balance within this narrow range through three mechanisms.
Intracellular and extracellular buffering systems Regulation by the kidneys Regulation by the lungs The most important pH buffering systems include the hemoglobin, carbonate (which is the weak acid formed when CO2 is dissolved) and bicarbonate (its corresponding weak base) buffering systems. The bicarbonate buffer system works well because the concentration of each of its components can be adjusted independently. This buffering system consists of two important components, CO2 and HCO3 -, the lungs regulate the partial pressure of CO2 in the blood (pCO2) by regulating alveolar ventilation and the kidneys regulate the concentration of HCO3 – by regulating the excretion of carbonic acid and the reabsorption of bicarbonate.
The Henderson-Hasselbalch equation allows the blood gas analyzer to measure pH and pCO2 directly. The concentration of HCO3 – can be calculated according to the Henderson-Hasselbalch equation. As can be seen from the formula, pH depends on the ratio of HCO3 – concentration to pCO2 and is not determined by either one alone. pH = pK (6,1) + log HCO 3 -0,03 x pCO2
Here is a simplified form of the formula that clearly shows the relationship between the three values. If you can remember this simplified formula, it will help you to understand the compensatory changes component that is covered later in this unit. pH ~HCO 3 -pCO2
Defining acidemia
When the pH of the blood is 7,45, it is called alkalemia. Acidosis is a process that allows acid to accumulate in the body, but does not necessarily lead to abnormal pH levels As seen in the Henderson-Hasselbalch equation, acidosis can be induced by either a decrease in HCO3 -concentration or an increase in pCO2: pH ~HCO 3 -pCO2. If alkalosis occurs in conjunction with acidosis, the final pH may be equal to, higher than, or lower than normal Alkalosis is a process that allows alkaline substances to accumulate in the body but does not necessarily result in abnormal pH values As seen in the Henderson-Hasselbalch equation, alkalosis can be induced by either an increase in HCO3 – concentration or a decrease in pCO2: pH ~HCO 3 -pCO2
When only one of the two conditions occurs, it can lead to alkalemia If acidosis occurs along with alkalosis, the final pH may be equal to, higher than, or lower than the normal value of alkaline surplus. When acidosis occurs, a negative alkaline surplus indicates the presence of metabolic acidosis. The base residual is the amount of base or acid required to titrate 1 liter of blood to a pH of 7.4 while pCO2 is held at a constant 5.3 kPa.
Why is arterial blood gas measured?
The purpose of measuring arterial blood gases is to.
Determine acid-base balance Determine oxygenation (arterial pO2 can help us understand the efficiency of gas exchange) Diagnose and establish the severity of respiratory failure (pCO2 can help us understand ventilation) Guide treatment, for example, when administering oxygen therapy or noninvasive ventilation to patients with chronic obstructive pulmonary disease (COPD) or when treating patients with diabetic ketoacidosis.
The four major disorders of acid-base balance are: respiratory acidosis metabolic acidosis respiratory alkalosis metabolic alkalosis.
Interpreting arterial blood gas results using a step-by-step approach
The following method will help you interpret arterial blood gas results systematically and accurately (Table 1).
Table 1 Five-step approach to interpreting arterial blood gas results
Step 1
Is there acidemia or alkalemia?
Step 2
Is the primary disorder of acid-base balance respiratory or metabolic?
Step 3
If it is metabolic acidosis, is the anion gap elevated?
Step 4
Is there compensation? If so, is the compensation moderate?
Step 5
What is the alveolar-arterial oxygen gradient? To check the arterial pO2, combine the inhaled oxygen concentration with the arterial pCO2
First, you need to be familiar with the normal values (Table 2). Please note that each hospital may have slightly different values, so you will want to use your own hospital’s normal values.
Table 2: Normal Arterial Blood Gas Values
Arterial pCO2
4, 5-6, 0 kPa
Arterial pO2
11, 0-13, 0 kPa
HCO3 –
22, 0-28, 0 mmol/l
Base residual
-2, 0 to +2, 0
Anion gap
8, 0-16, 0 mmol/l
Chloride ion
98, 0-107, 0 mmol/l
Step 1: Is there acidemia or alkalemia?
Check the pH value, if pH.
7, 45, then the patient has alkalemia
If pH is normal, look for pCO2 and HCO3 – concentrations. If one or both are abnormal, the patient may have a mixed acid-base balance disorder.
Step 2: Is the primary acid-base balance disorder respiratory or metabolic?
Look for pH, pCO2, and HCO3 – concentrations.
If pH 7, 45, then alkalosis is causing alkalemia and: if pCO2 is decreased, then primary respiratory alkalosis is present if HCO3 concentration is increased, then primary metabolic alkalosis is present.
Example 1
Orthopedics asks you to look at a 60-year-old female patient who had a right hip replacement two weeks ago. She presents with respiratory distress. Her arterial blood gas results are as follows.
pH: 7, 48pO2: 8, 0 kPa pCO2: 3, 2 kPa HCO3 -: 25 mmol/l.
What type of acid-base balance disorder does she have?
Step 1: The patient has alkalemia.
Step 2: Her pCO2 is reduced, which determines that this is primary respiratory alkalosis.
This patient has primary respiratory alkalosis. The differential diagnosis should include pulmonary embolism and hospital-acquired pneumonia.
Example 2
You see an 18-year-old male patient in the emergency department. The patient has been vomiting for 24 hours and is feeling unwell. His arterial blood gas results are as follows.
Na+: 138 mmol/lK+: 3, 0 mmol/l urea nitrogen: 7, 8 mmol/l creatinine: 130 µmol/lpH: 7, 49pO2: 12, 7 kPa pCO2: 5, 0 kPa HCO3 -: 31 mmol/l.
Step 1: The patient has alkalemia.
Step 2: His HCO3 – concentration is elevated, indicating the presence of primary metabolic alkalosis.
The patient lost hydrogen ions from the gastrointestinal tract during vomiting, resulting in primary metabolic alkalosis. The patient also has hypokalemia, which may also be associated with metabolic alkalosis.
Step 3: If it is metabolic acidosis, is the anion gap elevated?
Determining the type of acidosis helps to narrow down the potential etiology.
What is the anion gap?
In the body, there is an equal number of cations and anions. Blood tests can measure most of the cations, but only a small number of anions. Therefore, the difference between the measured anions and cations is the amount of unmeasured anions (e.g., plasma albumin) when each is added together.
Since Na+ is the primary measured cation and Cl- and HCO3 – are the primary measured anions, the formula for calculating the anion gap is
Anion gap = Na+ – (Cl- + HCO3 -)
The normal value of the anion gap is 8-16 mmol/l.
Some hospitals include K+ in the calculation of the anion gap. Thus.
Anion gap = (Na+ + K+) – (Cl- + HCO3 -)
If K+ is included in the calculation, the normal value of the anion gap is 12-20 mmol/l.
The main causes of high anion gap acidosis (>16 mmol/l) are given in Table 3.
Table 3 Main etiologies of high anion gap acidosis (>16 mmol/l)
Increased endogenous acid products
Ketoacidosis (e.g., with alcohol, starvation, or diabetes) Lactic acidosis Type A: impaired oxygenation of tissues When perfusion is inadequate (e.g., in shock), tissues undergo hypoxic metabolism, resulting in increased lactate production Type B: unimpaired oxygenation of tissues: e.g., in liver failure, lactate metabolism is reduced. Increased exogenous acidity
Methanol Ethylene glycol (antifreeze) Aspirin
Decreased ability of the body to excrete acid
Chronic renal failure
The main etiology of normal anion gap acidosis (8-16 mmol/l) is generally associated with an increase in plasma Cl- as shown in Table 4.
Table 4 Main etiologies of normal anion gap acidosis (8-16 mmol/l)
Loss of bicarbonate
Transgastrointestinal: diarrhea ileostomy pancreatic fistula, biliary fistula, enterocutaneous fistula Transrenal: type 2 (proximal) tubular acidosis Carbonic anhydrase inhibitor administration
Decreased renal capacity to excrete acid
Type 1 (distal) renal tubular acidosis Type 4 renal tubular acidosis (aldosteronism)
In patients with low albumin, how to correct the anion gap
In the anion gap (8-16 mmol/l), 11 mmol/l is often composed of albumin. Therefore, a decrease in albumin concentration can lower the basal value of the anion gap.
If a patient has a low albumin concentration, it will instead behave as a normal anion gap when there is a disturbance in acid-base balance, which usually leads to an elevated anion gap.
For every 10 g/l decrease in albumin concentration, the anion gap decreases by 2 or 5 mmol/l.
Example 3
A 61-year-old male with alcoholic liver disease is admitted with “upper gastrointestinal bleeding”. His blood pressure is 90/40 mm Hg.
His arterial blood gas results were as follows.
Albumin: 20 g/l (n = 40 g/l) Na+: 135 mmol/l K+: 3, 5 mmol/l Cl-: 100 mmol/l pH: 7, 30 pCO2: 3, 3 kPa HCO3 -: 20 mmol/l Lactate concentration: 5 IU/l.
What is his anion gap? What type of acid-base balance disorder does he have?
First calculate the anion gap: Na+ – (HCO3 – + Cl-) = 135 – (100 + 20) = 15 mmol/l. The result obtained is within the normal value of 8-16 mmol/l.
The anion gap was then corrected for the reduced albumin concentration.
Anion gap = 15 mmol/l Albumin concentration decreased by 20 g/l For every 10 g/l decrease in albumin concentration, the anion gap decreased by 2,5 mmol/l
Therefore, the patient’s anion gap decreased by a total of 5 mmol/l The corrected anion gap value is 15 + 5 = 20 mmol/l.
Thus, it is clear that the patient has a high anion gap metabolic acidosis. Given the presence of hyperlactatemia and hypotension, the acidosis is likely secondary to type A lactic acidosis (see Table 3).
Case 4
A 20-year-old male feels unwell, complains of thirst, and consumes large amounts of fluid. His arterial blood gas results are as follows.
Glucose: 30 mmol/l pH: 7, 32 pO2: 11, 5 Pa pCO2: 3, 0 kPa HCO3 -:18 mmol/l Na+: 148 mmol/l K+: 3, 5 mmol/l Cl-: 100 mmol/l.
Which acid-base balance disorder is present in this patient?
Step 1: The patient has acidemia.
Step 2: A decrease in his HCO3 – concentration would indicate the presence of primary metabolic acidosis.
Step 3: Anion gap = (Na+ – (Cl- + HCO3 -) 148 – 118 = 30 mmol/l. The anion gap is elevated.
This patient has a high anion gap metabolic acidosis, most likely caused by diabetic ketoacidosis.
Case 5
A 44-year-old male with ulcerative colitis has had severe diarrhea for two days. His arterial blood gas results were as follows.
Creatinine: 200 µmol/l Urea nitrogen: 17 mmol/l pH: 7, 31 pO2 : 12, 5 kPa pCO2: 4, 0 kPa HCO3 -:16 mmol/l Na+: 136 mmol/l K+: 3, 1 mmol/l Cl-: 121
mmol/l.
Which acid-base balance disorder is present in this patient?
Step 1: The patient has acidemia.
Step 2: His HCO3 – concentration is reduced, which would indicate the presence of primary metabolic acidosis.
Step 3: Anion gap = (Na+ – (Cl- + HCO3 -) 136 – 121 = 15 mmol/l. This result is normal.
This patient has a normal anion gap metabolic acidosis, most likely caused by the loss of HCO3 – due to severe diarrhea.
Step 4: Is there compensation?
Compensation refers to a series of responses that the body makes to correct a disturbance in acid-base balance. Normal compensatory pathways include
The buffering system, which includes hemoglobin, plasma proteins, bicarbonate, and phosphate. This response can occur within minutes Respiratory response, which can occur within minutes to hours
Renal response, which can take up to a week. Why is it so important to identify compensation?
Identifying compensation can help you distinguish between primary acid-base balance disorders and secondary arterial blood gas changes. For example, when a patient has metabolic acidosis, he may be hyperventilating with the sole purpose of lowering
pCO2 to compensate for the metabolic acidosis, thus producing a partially compensated metabolic acidosis that should not be mistaken for primary metabolic acidosis and primary respiratory alkalosis.
In patients with a single disorder of acid-base balance, a normal pH (7,35-7,45) can eventually be achieved, if the disorder is not severe, by complete compensation. Despite a normal pH
abnormalities in HCO3 – and pCO2 may also prompt you to consider a mixed acid-base disorder.
You may find it difficult to tell if an acid-base abnormality is mixed or a single compensatory disorder. However, it is useful to remember the expected degree of compensation for a primary balance disorder.
If a parameter changes beyond the expected degree of compensation, it is likely to be a mixed acid-base balance disorder (see Table 5). The compensatory response to metabolic acid-base balance disorders is more difficult to predict than to respiratory acid-base balance disorders.
Table 5, Summary: Compensatory reactions
Disorders of acid-base balance
Initial chemical alterations
Compensatory response
Degree of compensation
Respiratory acidosis
pCO2
HCO3 –
In acute respiratory acidosis, for every 1.3 kPa increase in pCO2, based on 5.3 kPa.
HCO3 – increase in concentration by 1.0 mmol/l decrease in pH by 0.07
In chronic respiratory acidosis, for every 1.3 kPa increase in pCO2 on a 5.3 kPa basis.
HCO3 – concentration increases by 3,5 mmol/l pH decreases by 0,03
Respiratory alkalosis
pCO2HCO3 –
In acute respiratory alkalosis, based on 5.3 kPa, for every 1.3 kPa decrease in pCO2: decrease in HCO3 – concentration by 2.0 mmol/l pH increase by 0.08
In chronic respiratory alkalosis, for every 1.3 kPa decrease in pCO2 on a 5.3 kPa basis: 5.0 mmol/l decrease in HCO3 concentration and 0.03 increase in pH
Metabolic acidosis
HCO3 -pCO2
Metabolic alkalosis
HCO3 -pCO2
The direction of the compensatory reaction is always the same as the direction of the initial chemical change. This is because the basis of the compensatory reaction is the maintenance of the ratio of HCO3 -concentration to pCO2. Remember the relationship between the three in the Henderson-Hasselbalch formula: pH ~ HCO3 -/pCO2.
In chronic diseases, the magnitude of compensation will be greater, resulting in better maintenance of pH.
Metabolic compensation can occur in primary respiratory acid-base disorders, and familiarity with these expected change values can help you diagnose mixed acid-base disorders.
Metabolic compensation
Metabolic compensation takes place over several days. It is divided into two steps.
Cellular buffering, which occurs within minutes to hours. This results in only a mild increase in plasma bicarbonate (HCO3 -) and renal compensation, which occurs within 3 to 5 days.
Thus, acute and chronic disturbances of acid-base balance can occur with different compensatory responses.
In respiratory acidosis, renal excretion of carbonic acid and reabsorption of bicarbonate are increased. In respiratory alkalosis, the kidneys compensate by reducing bicarbonate reabsorption and ammonia excretion. Respiratory compensation
Respiratory compensation takes several hours. Respiratory compensation in metabolic acid-base balance disorders can take up to 12 to 24 hours. This compensatory response begins one hour after the onset of the acid-base disorder and ends after 12 to 24 hours.
The compensatory response begins one hour after the onset of the acid-base disorder and terminates after 12 to 24 hours.
In metabolic acidosis, stimulation of central and peripheral chemoreceptors that control respiration can lead to an increase in alveolar ventilation. This in turn leads to compensatory respiratory alkalosis. Metabolic alkalosis is difficult to compensate for by reducing ventilation. Moreover, hypoventilation can also reduce oxygenation. Therefore, the respiratory system rarely maintains pCO2 above 7.5 kPa. If pCO 2 exceeds this value, a mixed acid-base balance disorder is present, i.e., metabolic alkalosis combined with respiratory acidosis, rather than compensatory metabolic alkalosis.
Mixed acid-base disorders
Mixed acid-base balance disorders are those in which more than one primary acid-base balance disorder is present at the same time. This is common in hospitalized patients. Knowledge of the mechanism and degree of compensation can help you identify these disorders. Please note that respiratory alkalosis and respiratory acidosis cannot coexist.
You should consider mixed disorders of acid-base balance when
A compensatory response is present, but there is an under- or over-compensation of pCO2 and HCO3 – concentrations that are abnormal and change in opposite directions (one increases and the other decreases). In disorders of single acid-base balance, the direction of the compensatory response and the direction of the initial abnormal change are always the same pH is normal, but the pCO2 or HCO3 – concentration is abnormal. In a single acid-base balance disorder, the compensatory response rarely returns pH to normal, and if the compensated pH returns to normal, a mixed acid-base balance disorder is considered.
Empirically.
When pCO2 is elevated and HCO3 – concentration is decreased, respiratory acidosis and metabolic acidosis coexist When pCO2 is decreased and HCO3 –
concentration increases, respiratory alkalosis and metabolic alkalosis coexist.
Example 6
A 30-year-old female patient with a history of depression has taken an overdose of benzodiazepines. Her arterial blood gas results are as follows: pH: 7,3 pO2: 11 kPa pCO2: 8 kPa HCO3 -: 25 mmol/l.
Which acid-base balance disorder does she suffer from?
Step 1: The patient has acidemia.
Step 2: The patient’s pCO2 is elevated, thus determining that this is primary respiratory acidosis.
Step 4: The patient’s HCO3 – concentration is normal, indicating that there is no substitution. This is because the patient had a rapid onset and metabolic compensation takes several days.
The patient has acute respiratory acidosis due to an overdose of benzodiazepines, which depresses the respiratory center.
Case 7
A 78-year-old male patient with severe chronic obstructive pulmonary disease (COPD) has the following arterial blood gas results.
pH: 7, 34 pO2: 9, 0 kPa pCO2: 7, 9 kPa HCO3 -: 32 mmol/l.
Which acid-base balance disorder does he suffer from?
Step 1: The patient has acidemia.
Step 2: His pCO2 and HCO3 – concentrations are both elevated.
This is part of.
a. chronic respiratory acidosis with moderate metabolic compensation?
b. Metabolic alkalosis combined with respiratory compensation?
c. Mixed respiratory acidosis and metabolic alkalosis?
Step 4.
a. pCO2 is higher than normal by 2,6 kPa. the direction of compensatory change is always the same as the direction of the initial change. In chronic respiratory acidosis, the expected compensatory changes are: for every 7.0 mmol/l increase in HCO3 -, the pH decreases by 0.06 (i.e. pH is 7.34 and HCO3 – concentration is 32 mmol/l).
b. Since the respiratory system rarely maintains pCO2 above 7.5 kPa and the patient’s pH was below 7.35, his history is not consistent with primary metabolic alkalosis.
c. The pH in this case is acidic and the metabolic compensation is consistent with a change in pCO2.
This suggests that the patient has chronic respiratory acidosis secondary to severe COPD.
Case 8
A 20-year-old male with progressive muscular dystrophy admitted with a “urinary tract infection” has a temperature of 39º C. The patient is febrile, his peripheral vessels are dilated, and his blood pressure is 90/60 mm Hg. He has been catheterized since 1 hour ago and has urinated 5 ml. His arterial blood gas results are as follows.
pH: 7, 28 pO2: 10, 8 kPa pCO2: 6, 0 kPa HCO3 -: 18 mmol/l Na+: 146 mmol/l K+: 4, 5 mmol/l Cl-: 101 mmol/l.
Which acid-base balance disorder does the patient have?
Step 1: The patient has acidemia.
Step 2: His pCO2 is elevated and his HCO3 – concentration is decreased.
Step 3: His anion gap is elevated (146 – 101 + 18) = 27 mmol/l.
Step 4: In case of metabolic acidosis, pCO2 should decrease. In case of respiratory acidosis, the HCO3 concentration should be increased. Thus, it is evident that he has a mixed acid-base balance disorder. It is certain that he suffers from a combination of high anion gap metabolic acidosis, most likely caused by infectious shock, and respiratory acidosis, caused by progressive muscular dystrophy.
Step 5: What is the alveolar-arterial oxygen gradient (A-a gradient)?
The A-a gradient is the difference between the calculated alveolar pO2 and the arterial pO2 measurement. Arterial pO2 is a function of gas exchange and the fraction of O2 concentration in the inhaled air (FiO2). Thus, its normal value is not constant.
By calculating the A-a gradient, you can determine if a given arterial oxygen measurement is normal for a patient with the following conditions.
Altitude Inhaled oxygen concentration Respiratory rate.
This provides a way to assess gas exchange and can be done at the bedside.
You can also use it to calculate the efficiency of oxygen diffusion from the alveolar to the arterial circulation. Alveolar pO2 is always higher than arterial pO2. For a normal person, the A-a gradient is between 2 and 4 kPa. An increase in this gradient means that gas exchange is inadequate and is abnormal when it exceeds 4 kPa.
Calculating the A-a gradient
When air is breathed at sea level, the partial pressure of inhaled oxygen is 21 kPa. Upon entering the airway, the partial pressure of inhaled oxygen (i.e., PiO2) drops to 20 kPa due to water vapor saturation of the upper airway. upon reaching the alveoli, the alveolar cells take up O2 and replace it with CO2, which further reduces alveolar pO2 to 13 to 14 kPa.
The ratio of pCO2 production to pO2 consumption is determined by the respiratory quotient. The ratio is estimated to be 0, 8. Thus, alveolar pO2 is equal to the difference between PiO2 and alveolar pCO2. The value of pCO2 is increased slightly by dividing by the respiratory quotient.
Alveolar pO2
= inspiratory pO2 – alveolar pCO2 / 0,8
= inspiratory pO2 – alveolar pCO2 x 1, 2
Since alveolar pCO2 is approximately equal to arterial pCO2, it follows that
Alveolar pO2 = Inspiratory pO2 – Arterial pCO2 x 1, 2.
Because the A-a gradient is the difference between the calculated alveolar pO2 and the measured arterial pO2, the alveolar pO2 is subtracted from the calculated arterial pO2 to give the A-a gradient as follows
Alveolar pO2 = PiO2 – Arterial pCO2 x 1, 2
A-a gradient = alveolar pO2 – arterial pO2
PiO2 = effective inhalation pO2.
Example 9
A 21-year-old female patient with known anxiety disorder presents to the emergency department with “shortness of breath”. Her chest x-ray is normal and her respiratory rate is 20 breaths/min. Without oxygen, her arterial blood gas results are as follows.
pH: 7, 46 pO2: 10, 4 kPa pCO2: 3, 7 kPa HCO3 -: 25 mmol/l.
Are the patient’s current symptoms caused by a panic attack or is there another more serious etiology?
Calculated alveolar pO2
= PiO2 – 1,2 x pCO2
= 20 – (1, 2 x 3, 7)
= 20 – 4, 44
= 15, 56 kPa
A-a gradient = 15, 56 – 10, 4 = 5, 16 kPa (n = 2-4 kPa).
The A-a gradient is elevated. This indicates that the patient has inadequate gas exchange and that oxygen is not diffusing efficiently from the alveoli to the arterial circulation. This means that the measured arterial blood oxygen value is too low relative to the patient’s respiratory rate. You should suspect that the patient has a pulmonary embolism.
Four common causes of disorders of acid-base balance
Respiratory acidosis
Respiratory acidosis is a clinical condition caused by inadequate alveolar ventilation (i.e., respiratory failure). Respiratory failure can lead to a rapid increase in arterial pCO2. The main causes are listed in Table 6.
Table 6, Major etiologies of respiratory acidosis
Inhibition of the respiratory center
Drugs, such as opioids and benzodiazepines Central nervous system pathology after oxygen therapy in patients with chronic hypercapnia
Respiratory muscle weakness due to neuromuscular disorders
Motor neuron disease bilateral diaphragmatic paralysis, as seen in patients with poliomyelitis Guillain-Barré syndrome Myasthenia gravis multiple sclerosis
chest wall or thoracic abnormalities
obesity hypoventilation syndrome kyphosis kyphoscoliosis scleroderma
Diseases affecting gas exchange
chronic obstructive pulmonary disease (COPD) pneumonia severe asthma acute pulmonary edema
Airway obstruction
obstructive sleep apnea
Respiratory alkalosis
Respiratory alkalosis is a clinical condition caused by alveolar hyperventilation. Respiratory alkalosis can be acute or chronic in onset. The main etiologies are listed in Table 7.
Table 7, Major etiologies of respiratory alkalosis
Increased excitability of the central nervous system
Pain and anxiety Hyperventilation Cerebrovascular accident Meningitis Encephalitis Tumor Cranio-cerebral trauma
Hypoxemia or tissue hypoxia
Hypertension Severe anemia Ventilation/perfusion abnormalities
Lung disease
Asthma pulmonary embolism pneumonia pulmonary edema interstitial lung disease pneumothorax
Drugs (respiratory stimulants)
Salicylates Aminophylline Progesterone
Metabolic acidosis
Metabolic acidosis is a clinical disease characterized by a relative increase in the total amount of acid in the body. The presence of metabolic acidosis signals the presence of other underlying disease in the organism, which you should take into account.
Determining this underlying pathology is crucial to the adoption of an appropriate treatment plan.
Metabolic acidosis is divided into two categories.
Increased anion gap type normal anion gap type.
Metabolic alkalosis
Metabolic alkalosis is a relatively common clinical condition characterized by hypercapnia. The main etiologies are shown in Table 8.
Table 8, Major etiologies of metabolic alkalosis
Hydrogen ion loss
Transgastrointestinal: vomiting nasogastric tube aspiration Transrenal: primary adrenocorticotropism, e.g., secondary to Crohn’s disease or Cushing’s disease Medullary collaterals or thiazide diuretics after hypercapnia
transfer of hydrogen ions into the cells
Hypokalemia
Concentrated alkalosis
Diuretics
Please note that
The HCO3 – concentration in the body is normal when the total amount of extracellular bicarbonate is relatively constant, and the decrease in extracellular fluid volume results in an increase in plasma HCO3 – concentration A 65-year-old male patient with kyphosis who has been suffering from kyphosis for many years presents to your clinic with complaints of intermittent exertional shortness of breath. The patient’s lung fields are clear and his arterial blood gas results are as follows: pH: 7, 35pO2: 7, 5 kPapCO2: 7, 9 kPaHCO3 -: 33 mmol/l.
Which type of acid-base balance disorder is present in the patient?
a.Acute respiratory acidosis
b, chronic respiratory acidosis
c, mixed acute respiratory acidosis and metabolic alkalosis
Acute respiratory acidosis
The patient is in chronic respiratory acidosis.
Chronic respiratory acidosis
Step 1: The patient’s pH is normal.
Step 2: The patient’s pCO2 is elevated, thus determining that this is respiratory acidosis.
Step 4: The patient’s HCO3 – concentration is elevated. This is because his pH is below 7,4, which is acidic and indicates a compensatory response. This compensatory response is consistent with chronic respiratory acidosis and not acute respiratory acidosis.
Keep in mind that with chronic disease, the compensations are greater, allowing for better pH maintenance. In the case of acute respiratory acidosis, the pH would be 7, 26 and the HCO3 – concentration would be 28 mmol/l.
Thus, this patient has chronic respiratory acidosis.
Mixed acute respiratory acidosis and metabolic alkalosis
This patient has chronic respiratory acidosis.
You see a 20-year-old female patient in the emergency department who has acute severe asthma. Her speech is intermittent and she is unable to finish a complete sentence. The ED has given oxygen bag mask oxygen with an oxygen flow rate of 15 l/min. Her arterial blood gas results are as follows: pH: 7, 47pO2: 11, 2kPapCO2: 3, 7 kPaHCO3 -: 25 mmol/l.
Which type of acid-base balance disorder does the patient have?
aAcute respiratory alkalosis
b chronic respiratory alkalosis
cCompensated metabolic acidosis
aAcute respiratory alkalosis
Step 1: This patient has alkalosis.
Step 2: Her pCO2 decreases, thus determining that this is respiratory alkalosis.
Step 4: Her HCO3 – concentration is normal, indicating that there is no compensatory. This is consistent with her acute medical history. Thus, the patient has acute respiratory alkalosis.
b Chronic respiratory alkalosis
The patient has acute respiratory alkalosis.
cCompensated metabolic acidosis
The patient had acute respiratory alkalosis.
The patient was treated with continuous nebulized inhalation and intravenous aminophylline, but after 30 minutes, the patient was still not improving. The patient’s arterial blood gas was rechecked with an oxygen bag mask and the results were as follows: pH:7, 32pO2: 8, 8 kPapCO2: 6, 2 kPaHCO3 -: 25 mmol/l.
Which type of acid-base balance disorder does the patient have now?
aAcute respiratory acidosis
bChronic respiratory acidosis
cAcute metabolic acidosis
a , acute respiratory acidosis
Step 1: This patient has acidemia.
Step 2: Her pCO2 is elevated, thus determining that this is respiratory acidosis.
Step 4: Her HCO3 – concentration is normal, indicating that there is no substitution. From this, the patient has acute respiratory acidosis.