What is the ventilator rate in metabolic acidosis?

Respiratory Alkalosis

Respiratory alkalosis is a disturbance in acid and base balance due to alveolar hyperventilation. Alveolar hyperventilation leads to a decreased partial pressure of arterial carbon dioxide (PaCO₂). In turn, the decrease in PaCO₂ increases the ratio of bicarbonate concentration to PaCO₂ and, thereby, increases the pH level; thus the descriptive term respiratory alkalosis. The decrease in PaCO₂ (hypocapnia) develops when a strong respiratory stimulus causes the respiratory system to remove more carbon dioxide than is produced metabolically in the tissues. [1, 2]

Respiratory alkalosis can be acute or chronic. In acute respiratory alkalosis, the PaCO₂ level is below the lower limit of normal and the serum pH is alkalemic. In chronic respiratory alkalosis, the PaCO₂ level is below the lower limit of normal, but the pH level is relatively normal or near normal due to compensatory mechanisms.

Respiratory alkalosis is the most common acid-base abnormality observed in patients who are critically ill. It is associated with numerous illnesses and is a common finding in patients on mechanical ventilation. Many cardiac and pulmonary disorders can manifest with respiratory alkalosis as an early or intermediate finding. When respiratory alkalosis is present, the cause may be a minor, non–life-threatening disorder. However, more serious disease processes should also be considered in the differential diagnosis.

Signs and symptoms of respiratory alkalosis

The hyperventilation syndrome can mimic many conditions that are more serious. Symptoms may include paresthesia, circumoral numbness, chest pain or tightness, dyspnea, and tetany. [11]

Acute onset of hypocapnia can cause cerebral vasoconstriction. An acute decrease in PaCO2 reduces cerebral blood flow and can cause neurologic symptoms, including dizziness, mental confusion, syncope, and seizures. Hypoxemia need not be present for the patient to experience these symptoms. [5]

Respiratory alkalosis may impair vitamin D metabolism, which may lead to vitamin D deficiency and cause symptoms such as fibromyalgia. [14]

Workup in respiratory alkalosis

Alkalemia is documented by the presence of an increased pH level (>7.45) on arterial blood gas determinations. The presence of a decreased PaCO2 level (< 35 mm Hg) indicates a respiratory etiology of the alkalemia.

The following laboratory studies may be helpful:

Serum chemistries
Complete blood count (CBC)
Liver function test
Cultures of blood, sputum, urine, and other sites
Thyroid testing
Beta-human chorionic hormone levels
Drug screens and theophylline and salicylate levels

These include the following:

Chest radiography — Should be performed to help rule out pulmonary disease as a cause of hypocapnia and respiratory alkalosis

Computerized tomography (CT) scanning of the chest — May be performed if chest radiography findings are inconclusive or a pulmonary disorder is strongly considered as a differential diagnosis

Ventilation perfusion scanning — Can be considered in patients who are unable to undergo an intravenous contrast injection associated with CT scanning to assess the patient for pulmonary embolism

Brain magnetic resonance imaging (MRI) — Can be considered if a central cause of hyperventilation and respiratory alkalosis is suggested and the initial brain CT scan findings are negative or inconclusive

Management of respiratory alkalosis

The treatment of respiratory alkalosis is primarily directed at correcting the underlying disorder. Respiratory alkalosis itself is rarely life threatening. Therefore, emergent treatment is usually not indicated unless the pH level is greater than 7.5. Because respiratory alkalosis usually occurs in response to some stimulus, treatment is usually unsuccessful unless the stimulus is controlled. If the PaCO2 is corrected rapidly in patients with chronic respiratory alkalosis, metabolic acidosis may develop due to the renal compensatory drop in serum bicarbonate.

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Pathophysiology

Breathing or alveolar ventilation is the body’s method of providing adequate amounts of oxygen for metabolism while removing carbon dioxide produced in the tissues. By sensing the body’s partial pressure of arterial oxygen (PaO₂) and partial pressure of arterial carbon dioxide (PaCO₂), the respiratory system adjusts pulmonary ventilation so that oxygen uptake and carbon dioxide elimination at the lungs are balanced with the amount used and produced by the tissues.

The PaCO₂ must be maintained at a level that ensures that hydrogen ion concentrations remain in the narrow limits required for optimal protein and enzymatic function. PaO₂ is not as closely regulated as the PaCO2. Adequate hemoglobin saturation can be achieved over a wide range of PaO₂ levels. The movement of oxygen from the alveoli to the vascular system is dependent on pressure gradients. On the other hand, carbon dioxide diffuses much easier through an aqueous environment.

Metabolism generates a large quantity of volatile acid (carbonic acid excreted as carbon dioxide by the lungs) and nonvolatile acid. The metabolism of fats and carbohydrates leads to the formation of a large amount of carbon dioxide, [3] which combines with water to form carbonic acid. The lungs excrete the volatile fraction through ventilation so that acid accumulation does not occur. Significant alterations in ventilation can affect the elimination of carbon dioxide and lead to a respiratory acid-base disorder.

PaCO₂ is normally maintained in the range of 35-45 mm Hg. Chemoreceptors in the brain (central chemoreceptors) and in the carotid bodies (peripheral chemoreceptors) sense hydrogen concentrations and influence ventilation to adjust the PCO₂ and pH. This feedback regulator is how the PaCO₂ is maintained within its narrow normal range. When these receptors sense an increase in hydrogen ions, breathing is increased to “blow off” carbon dioxide and subsequently reduce the amount of hydrogen ions. Various disease processes may cause stimulation of ventilation with subsequent hyperventilation. If hyperventilation is persistent, it leads to hypocapnia.

Hyperventilation refers to an increase in alveolar ventilation that is disproportionate to the rate of metabolic carbon dioxide production, leading to a PaCO₂ level below the normal range, or hypocapnia. Hyperventilation is often associated with dyspnea, but not all patients who are hyperventilating complain of shortness of breath. Conversely, patients with dyspnea need not be hyperventilating.

Acute hypocapnia causes a reduction of serum levels of potassium and phosphate secondary to increased intracellular shifts of these ions. A reduction in free serum calcium also occurs. Calcium reduction is secondary to increased binding of calcium to serum albumin due to the change in pH. Many of the symptoms present in persons with respiratory alkalosis are related to hypocalcemia. [4] Hyponatremia and hypochloremia may also be present.

Acute hyperventilation with hypocapnia causes a small, early reduction in serum bicarbonate levels resulting from cellular shift of bicarbonate. Acutely, plasma pH and bicarbonate concentration vary proportionately with the PaCO₂ along a range of 15-40 mm Hg. The relationship of PaCO₂ to arterial hydrogen and bicarbonate is 0.7 mmol/L per mm Hg and 0.2 mmol/L per mm Hg, respectively. [5] After 2-6 hours, renal compensation begins via a decrease in bicarbonate reabsorption. The kidneys respond more to the decreased PaCO₂ rather than the increased pH. Complete kidney compensation may take several days and requires normal kidney function and intravascular volume status. [5] The expected change in serum bicarbonate concentration can be estimated as follows:

Acute — Bicarbonate (HCO₃ — ) falls 2 mEq/L for each decrease of 10 mm Hg in the PCO₂; that is, ΔHCO₃ = 0.2(ΔPCO₂); maximum compensation: HCO₃ — = 12-20 mEq/L

Chronic — Bicarbonate (HCO₃ — ) falls 5 mEq/L for each decrease of 10 mm Hg in the PCO₂; that is, ΔHCO₃ = 0.5(ΔPCO₂); maximum compensation: HCO₃ — = 12-20 mEq/L

Note that a plasma bicarbonate concentration of less than 12 mmol/L is unusual in pure respiratory alkalosis alone and should prompt the consideration of a metabolic acidosis as well (ie, the presence of a mixed acid-base disorder). [4]

The expected change in pH with respiratory alkalosis can be estimated with the following equations:

Acute respiratory alkalosis: Change in pH = 0.008 X (40 – PCO₂)
Chronic respiratory alkalosis: Change in pH = 0.017 X (40 – PCO₂)

A study by Morel et al suggested that when respiratory alkalosis is present, caution be used in the employment of venous-arterial difference in CO₂ (ΔCO₂) as an indicator of the adequacy of tissue perfusion (as has been proposed for shock states). Using healthy volunteers in whom either hypocapnia or hypercapnia was induced, the investigators found a significant increase in ΔCO₂ in the hypocapnic subjects, who also had a significant decrease in skin microcirculatory blood flow. [6]

Respiratory acidosis

Respiratory acidosis is a state in which decreased ventilation (hypoventilation) increases the concentration of carbon dioxide in the blood and decreases the blood’s pH (a condition generally called acidosis).

Carbon dioxide is produced continuously as the body’s cells respire, and this CO₂ will accumulate rapidly if the lungs do not adequately expel it through alveolar ventilation. Alveolar hypoventilation thus leads to an increased PaCO₂ (a condition called hypercapnia). The increase in PaCO₂ in turn decreases the HCO₃ − /PaCO₂ ratio and decreases pH.

Types [ edit ]

Respiratory acidosis can be acute or chronic.

• In acute respiratory acidosis, the PaCO₂ is elevated above the upper limit of the reference range (over 6.3 kPa or 45 mm Hg) with an accompanying acidemia (pH <7.36).
• In chronic respiratory acidosis, the PaCO₂ is elevated above the upper limit of the reference range, with a normal blood pH (7.35 to 7.45) or near-normal pH secondary to renal compensation and an elevated serum bicarbonate (HCO₃ − >30 mEq/L).

Causes [ edit ]

Acute [ edit ]

Acute respiratory acidosis occurs when an abrupt failure of ventilation occurs. This failure in ventilation may be caused by depression of the central respiratory center by cerebral disease or drugs, inability to ventilate adequately due to neuromuscular disease (e.g., myasthenia gravis, amyotrophic lateral sclerosis, Guillain–Barré syndrome, muscular dystrophy), or airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD) exacerbation.

Chronic [ edit ]

Chronic respiratory acidosis may be secondary to many disorders, including COPD. Hypoventilation in COPD involves multiple mechanisms, including decreased responsiveness to hypoxia and hypercapnia, increased ventilation-perfusion mismatch leading to increased dead space ventilation, and decreased diaphragm function secondary to fatigue and hyperinflation.

Chronic respiratory acidosis also may be secondary to obesity hypoventilation syndrome (i.e., Pickwickian syndrome), neuromuscular disorders such as amyotrophic lateral sclerosis, and severe restrictive ventilatory defects as observed in interstitial lung disease and thoracic deformities.

Lung diseases that primarily cause abnormality in alveolar gas exchange usually do not cause hypoventilation but tend to cause stimulation of ventilation and hypocapnia secondary to hypoxia. Hypercapnia only occurs if severe disease or respiratory muscle fatigue occurs.

Physiological response [ edit ]

Mechanism [ edit ]

Metabolism rapidly generates a large quantity of volatile acid (H₂CO₃) and nonvolatile acid. The metabolism of fats and carbohydrates leads to the formation of a large amount of CO₂. The CO₂ combines with H₂O to form carbonic acid (H₂CO₃). The lungs normally excrete the volatile fraction through ventilation, and acid accumulation does not occur. A significant alteration in ventilation that affects elimination of CO₂ can cause a respiratory acid-base disorder. The PaCO₂ is maintained within a range of 35–45 mm Hg in normal states.

Alveolar ventilation is under the control of the respiratory center, which is located in the pons and the medulla. Ventilation is influenced and regulated by chemoreceptors for PaCO₂, PaO₂, and pH located in the brainstem, and in the aortic and carotid bodies as well as by neural impulses from lung stretch receptors and impulses from the cerebral cortex. Failure of ventilation quickly increases the PaCO₂.

In acute respiratory acidosis, compensation occurs in 2 steps.

• The initial response is cellular buffering (plasma protein buffers) that occurs over minutes to hours. Cellular buffering elevates plasma bicarbonate (HCO₃ − ) only slightly, approximately 1 mEq/L for each 10-mm Hg increase in PaCO₂.
• The second step is renal compensation that occurs over 3–5 days. With renal compensation, renal excretion of carbonic acid is increased and bicarbonate reabsorption is increased. For instance, PEPCK is upregulated in renal proximal tubule brush border cells, in order to secrete more NH₃ and thus to produce more HCO₃ − . [1]

Estimated changes [ edit ]

In renal compensation, plasma bicarbonate rises 3.5 mEq/L for each increase of 10 mm Hg in PaCO₂. The expected change in serum bicarbonate concentration in respiratory acidosis can be estimated as follows:

• Acute respiratory acidosis: HCO₃ − increases 1 mEq/L for each 10 mm Hg rise in PaCO₂.
• Chronic respiratory acidosis: HCO₃ − rises 3.5 mEq/L for each 10 mm Hg rise in PaCO₂.

The expected change in pH with respiratory acidosis can be estimated with the following equations:

• Acute respiratory acidosis: Change in pH = 0.08 X ((40 − PaCO₂)/10)
• Chronic respiratory acidosis: Change in pH = 0.03 X ((40 − PaCO₂)/10)

Respiratory acidosis does not have a great effect on electrolyte levels. Some small effects occur on calcium and potassium levels. Acidosis decreases binding of calcium to albumin and tends to increase serum ionized calcium levels. In addition, acidemia causes an extracellular shift of potassium, but respiratory acidosis rarely causes clinically significant hyperkalemia.

Diagnosis [ edit ]

Diagnoses can be done by doing an ABG (Arterial Blood Gas) laboratory study, with a pH 45 mmHg in an acute setting. Patients with COPD and other Chronic respiratory diseases will sometimes display higher numbers of PaCO2 with HCO3- >30 and normal pH.

Terminology [ edit ]

• Acidosis refers to disorders that lower cell/tissue pH to < 7.35.
• Acidemia refers to an arterial pH < 7.36. [2]

See also [ edit ]

References [ edit ]

1. ^ Boron, Walter F. (2005). Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. p. 858. ISBN1-4160-2328-3 .
2. ^
3. Yee AH, Rabinstein AA (February 2010). «Neurologic presentations of acid-base imbalance, electrolyte abnormalities, and endocrine emergencies». Neurol Clin. 28 (1): 1–16. doi:10.1016/j.ncl.2009.09.002. PMID19932372.

Arterial Blood Gases

Arterial Blood Gases [ edit | edit source ]

Blood Gas Analyser

Arterial blood gases (ABG’s) is a blood test that is used to give an indication of ventilation, gas exchange, and acid-base status and is taken from an arterial blood supply [1] . The arterial blood gas test is one of the most common tests performed on patients in intensive care units. At other levels of care, pulse oximetry plus transcutaneous carbon dioxide measurement is a less invasive alternative method of obtaining similar information. [2]

To perform this test, blood is collected from a specific artery, usually the wrist’s radial artery. This blood sample allows an accurate determination of the amount of oxygen that passes from the lungs to the blood. This test is the one most commonly performed to diagnose cases of respiratory failure [3] .
Arterial blood gas test results can show if:

• Lungs are getting enough oxygen.
• Lungs are removing enough carbon dioxide.
• Kidneys are working properly. [2]

Uses [ edit | edit source ]

ABGs are very useful for detecting conditions that cause respiratory failure. Including: Lung Failure; Acute respiratory distress syndrome (ARDS); Sepsis; Diabetic ketoacidosis (DKA); Cystic fibrosis; Pneumonia; Emphysema; Hypovolemic shock; Acute heart failure; Cardiac arrest; Kidney Failure; Septic Shock; Trauma; Chronic vomiting; Uncontrolled diabetes; Asthma ; Chronic Obstructive Pulmonary Disease (COPD); Hemorrhage; Drug Overdose; Metabolic Disease; Chemical Poisoning; To check if lung condition treatments are working. [4]

Measurements [ edit | edit source ]

The key components of an ABG are:

1. pH — This measures the balance of acids and bases in the blood.
2. Partial pressure of oxygen (PaO2) — This measures the pressure of oxygen dissolved in the blood.
3. Partial pressure of carbon dioxide (PaCO2) — This measures the amount of carbon dioxide in the blood and how well carbon dioxide can move out of the lungs.
4. Bicarbonate (HCO3) — This is calculated using the measured values of pH and PaCO2 to determine the amount of the primary compound made from carbon dioxide (CO2.)
5. Oxygen saturation (O2 Sat) — This measures how much hemoglobin in the blood is carrying oxygen.
6. Oxygen content (O2CT) — This measures the amount of oxygen in the blood.
7. Hemoglobin — This measures the amount of hemoglobin in the blood.

Normative Values [ edit | edit source ]

According to the National Institute of Health, typical normal values are:

• pH: 7.35-7.45
• Partial pressure of oxygen (PaO2): 75 to 100 mmHg
• Partial pressure of carbon dioxide (PaCO2): 35-45 mmHg
• Bicarbonate (HCO3): 22-26 mEq/L
• Oxygen saturation (O2 Sat): 94-100% [4]

Interpretation of ABGs [ edit | edit source ]

1. Look at the pH
   • Increased = Alkalosis
   • Decreased = Acidosis
2. Look at the PaCO2
   • Increased = Respiratory Acidosis
   • Decreased = Respiratory Alkalosis
3. Look at the HCO3
   • Increased = Metabolic Alkalosis
   • Decreased = Metabolic Acidosis
4. Identify if there is a compensation
   • Full compensation if the pH is within the normal range
   • Partial compensation if either the PaCO2 or HCO3 value is wavering to compensate for the primary acid-base disturbance; but, the pH is still not within the normal physiologic range.
5. Look at the O2

The results should always be read and compared in reference to the patient’s previous ABG (if available) as you will then be able to assess a trend and make a more accurate assessment on whether you should treat or if your treatment has been successful or not.

Primary Acid-base disturbances [ edit | edit source ]

1. Uncompensated Respiratory Acidosis: This occurs when there is an increase in the PaCO2 level without a resultant alteration (increase) of the HCO3 value. Thus, there will an acidosis due to respiratory failure (inability to remove excess carbondioxide from the blood and the lungs).
2. Partially compensated Respiratory Acidosis: This occurs when there is an increase in the PaCO2 level with a resultant alteration (increase) of the HCO3 value; but, the pH is still not within the normal range. Thus, there will still be acidosis due to respiratory failure (inability to remove excess carbondioxide from the blood and the lungs).
3. Fully compensated Respiratory Acidosis: This occurs when there is an increase in the PaCO2 level with a resultant alteration (increase) of the HCO3 value; thereby, balancing the pH within the normal range. Thus, there will be compensation for the acidosis due to respiratory failure (inability to remove excess carbondioxide from the blood and the lungs) with metabolic alkalosis.
4. Uncompensated Respiratory Alkalosis: This occurs when there is a decrease in the PaCO2 level without a resultant alteration (decrease) of the HCO3 value. Thus, there will be an alkalosis due to respiratory failure (excess carbondioxide exhalation from the lungs and reduced carbondioxide tension in the blood).
5. Partially compensated Respiratory Alkalosis: This occurs when there is a decrease in the PaCO2 level with a resultant alteration (decrease) of the HCO3 value; but, the pH is still not within the normal range. Thus, there will be an alkalosis due to respiratory failure (excess carbondioxide exhalation from the lungs and reduced carbondioxide tension in the blood).
6. Fully compensated Respiratory Alkalosis: This occurs when there is a decrease in the PaCO2 level with a resultant alteration (decrease) of the HCO3 value; thereby, balancing the pH within the normal range. Thus, there will be compensation for the alkalosis due to respiratory failure (excess carbondioxide exhalation from the lungs and reduced carbondioxide tension in the blood) with metabolic acidosis.
7. Uncompensated Metabolic Acidosis: This occurs when there is an decrease in the HCO3 level without a resultant alteration (decrease) of the PaCO2 value. Thus, there will an acidosis due to metabolic failure (inability of the kidney to retain adequate bicarbonate).
8. Partially compensated Metabolic Acidosis: This occurs when there is a decrease in the HCO3 level with a resultant alteration (decrease) of the PaCO2 value; but, the pH is still not within the normal range. Thus, there will still be acidosis due to metabolic failure (inability of the kidney to retain adequate bicarbonate).
9. Fully compensated Metabolic Acidosis: This occurs when there is a decrease in the HCO3 level with a resultant alteration (decrease) of the PaCO2 value; thereby, balancing the pH within the normal range. Thus, there will be compensation for the acidosis due to metabolic failure (inability of the kidney to retain adequate bicarbonate) with respiratory alkalosis.
10. Uncompensated Metabolic Alkalosis: This occurs when there is a increase in the HCO3 level without a resultant alteration (increase) of the PaCO2 value. Thus, there will be an alkalosis due to metabolic failure (inability of the kidney to excrete excess bicarbonate).
11. Partially compensated Metabolic Alkalosis: This occurs when there is an increase in the HCO3 level with a resultant alteration (increase) of the PaCO2 value; but, the pH is still not within the normal range. Thus, there will be an alkalosis due to metabolic failure (inability of the kidney to excrete excess bicarbonate).
12. Fully compensated Metabolic Alkalosis: This occurs when there is an increase in the HCO3 level with a resultant alteration (increase) of the PaCO2 value; thereby, balancing the pH within the normal range. Thus, there will be compensation for the alkalosis due to metabolic failure (inability of the kidney to excrete excess bicarbonate) with respiratory acidosis.
13. Mixed Acid-Base disturbances: This occurs when there is either both metabolic and respiratory acidosis present or metabolic and respiratory alkalosis present at the same time of analysing arterial blood gases

Tutorials [ edit | edit source ]