Respiratory acidosis pathophysiology

Respiratory acidosis Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Respiratory acidosis from other Diseases
Epidemiology and Demographics
Screening
Natural History, Complications and Prognosis
Diagnosis
History and Symptoms
Physical Examination
Laboratory Findings
Chest X Ray
CT
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Surgery
Primary Prevention
Secondary Prevention
Future or Investigational Therapies
Case Studies
Case #1
Respiratory acidosis pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Respiratory acidosis pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Respiratory acidosis pathophysiology
CDC on Respiratory acidosis pathophysiology
Respiratory acidosis pathophysiology in the news
Blogs on Respiratory acidosis pathophysiology
Directions to Hospitals Treating Respiratory acidosis
Risk calculators and risk factors for Respiratory acidosis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Associate Editor(s)-in-Chief: Vamsikrishna Gunnam M.B.B.S [2]

Overview

Respiratory acidosis is an result of imbalance between acid-base due to alveolar hypoventilation.The normal range is 35-45 mm Hg for PaCO₂.Increase in the production of carbon dioxide due to  failure of ventilation results in sudden increase of the partial pressure of arterial carbon dioxide (PaCO₂) above the normal range. Alveolar hypoventilation is one of the cause to increased PaCO₂ which is is called hypercapnia.Hypercapnia and respiration acidosis occur while impairment in air flow happens and the elimination of carbon dioxide by the respiratory system is much less than the production of carbon dioxide in the tissues.Respiratory acidosis encountered in the emergency department and inpatient patients, as well as in intensive care units and postoperative patients.

Pathophysiology

Metabolism

• Metabolism in the body tissues rapidly generates a big quantity of volatile acids which are like eg carbon dioxide and nonvolatile acid.
• The metabolism of fats and carbohydrates ends up in the formation of a huge quantity of carbon dioxide.
• The carbon dioxide combines with water to form carbonic acid (H2 CO3). The lungs excrete the unstable fraction via ventilation, and generally acid accumulation does not occur.
• A considerable alteration in ventilation that affects elimination of carbon dioxide can cause a respiratory acid-base disease. The partial arterial pressure of carbon dioxide (PaCO2) is normally maintained in between 35-45 mm Hg.

Alveolar ventilation

• Alveolar air flow is under the control of the central breathing centers, which can be placed in the pons and the medulla.
• ventilation is prompted and controlled by using chemoreceptors for PaCO2, partial pressure of arterial oxygen (PaO2), and pH placed inside the brainstem, as well as by means of neural impulses from lung-stretch receptors and impulses from the cerebral cortex.
• Failure of air flow quickly results in an increase within the PaCO2.

Physiologic compensation

Acute cellular compensatory stage

• In acute respiratory acidosis, the body’s compensation happens in two steps.
• The preliminary reaction is cellular buffering that takes place within minutes to hours.
• Cellular buffering results in elevation of plasma bicarbonate values, but only slightly (approximately 1 mEq/L for every 10-mm Hg increase in PaCO2).

Chronic renal compensatory stage

• The second step occurs because of the renal compensation that occurs within 3-5 days.
• With renal compensation, renal excretion of carbonic acid is elevated, and bicarbonate reabsorption is accelerated.

• The predicted alternate in serum bicarbonate concentration in respiratory acidosis can be estimated as follows:
  • Acute respiration acidosis – Bicarbonate increases via 1 mEq/L for each 10-mm Hg upward push in % 2.the extreme exchange in bicarbonate is, therefore, pretty modest and is generated via the blood, extracellular fluid, and cellular buffering machine.
  • chronic respiratory acidosis – Bicarbonate will increase by means of 3.5 mEq/L for every 10-mm Hg upward push in % 2. The more change in bicarbonate in chronic respiratory acidosis is accomplished by means of the kidneys. The reaction starts soon after the onset of respiration acidosis however calls for three-five days to turn out to be whole.
  • The change in pH in respiratory acidosis can be estimated with the following equations:
    • Acute respiratory acidosis – Change in pH = 0.008 × (40 – PaCO ₂)
    • Chronic respiratory acidosis – Change in pH = 0.003 × (40 – PaCO ₂)

Electrolytes

• Respiratory acidosis does no longer have a outstanding effect on serum electrolyte levels.
• Some small results arise in calcium and potassium levels.
• Acidosis decreases binding of calcium to albumin and has a tendency to increase serum ionized calcium levels.
• Similarly, acidemia causes an extracellular shift of potassium.
• Respiratory acidosis, but, rarely causes clinically significant hyperkalemia.