Respiratory acidosis: Difference between revisions

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==Differential diagnosis of respiratory acidosis==
The differential diagnosis of respiratory acidosis is generated by considering three structures involved in ventilation: the chest cavity (which expands and contracts the lungs), central processes (i.e. those that affect the central respiratory drive center), and the lungs and airways themselves.
== Physiological response ==
== Physiological response ==
===Mechanism===
===Mechanism===

Revision as of 22:12, 2 September 2012

Respiratory acidosis
ICD-10 E87.2
ICD-9 276.2
DiseasesDB 95

Template:Search infobox For patient information page, click here

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Respiratory acidosis is acidosis (abnormal acidity of the blood) due to decreased ventilation of the pulmonary alveoli, leading to elevated arterial carbon dioxide concentration (PaCO2).

Pathophysiology

Respiratory acidosis is a clinical disturbance that is due to alveolar hypoventilation. Production of carbon dioxide occurs rapidly, and failure of ventilation promptly increases the level of PaCO2. Alveolar hypoventilation leads to an increased PaCO2 (ie, hypercapnia). The increase in PaCO2 in turn decreases the HCO3-/PaCO2 and decreases pH. Hypercapnia and respiratory acidosis occur when impairment in ventilation occurs and the removal of CO2 by the lungs is less than the production of CO2 in the tissues.

Classification

Acute respiratory acidosis

  • The PaCO2 is elevated above the upper limit of the reference range (over 6.3 kPa or 47 mm Hg)
  • Accompanied with acidemia (pH <7.35)

Chronic respiratory acidosis

  • The PaCO2 is elevated above the upper limit of the reference range
  • Accompanied 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 mm Hg).

Causes

Acute

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 (eg, myasthenia gravis, amyotrophic lateral sclerosis, Guillain-Barré syndrome, muscular dystrophy), or airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD) exacerbation.

Chronic

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 (ie, Pickwickian syndrome), neuromuscular disorders such as amyotrophic lateral sclerosis, and severe restrictive ventilatory defects as observed in interstitial fibrosis 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.

Common Causes

Causes by Organ System

Cardiovascular No underlying causes
Chemical / poisoning Agrocide, Agronexit, Aparasin, Aphtiria, Ben-Hex, Benhexol, Benzene hexachloride, Bexol, Chloresene, Cone shell poisoning, HCH-gamma, Hexachlorocyclohexane (gamma), Lindane, Poison hemlock, Tetrodotoxin, Tick paralysis
Dermatologic No underlying causes
Drug Side Effect Acetylcarbromal, Alfentanil, Alprazolam, Amylobarbitone, Barbitone, Bromazepam, Brotizolam, Butabarbital, Butalbital, Butobarbitone, Camazepam, Chlordiazepoxide, Cinolazepam, Clobazam, Clonazepam, Clorazepate, Clotiazepam, Cloxazolam, Cyclobarbital, Demethyldiazepam, Diazepam, Doxefazepam, Drug overdose, Estazolam, Ethyl loflazepate, Etizolam, Etomidate, Fentanyl, Flurazepam, Fluridrazepam, Fospropofol, General anaesthesia, Halazepam, Haloxazolam, Hexobarbital, Ketazolam, Loprazolam, Lorazepam, Lormetazepam, Medazepam, Mephobarbital, Methohexital, Mexazolam, Midazolam, Nitrazepam, Oxazepam, Oxazolam, Pentobarbital, Pethidine, Phenobarbital, Pinazepam, Prazepam, Primidone, Promethazine, Propofol, Quazepam, Remifentanil, Secobarbital, Sufentanil, Tapentadol, Temazepam, Tetrazepam, Thiamylal, Thiopentone, Tofisopam, Triazolam
Ear Nose Throat No underlying causes
Endocrine No underlying causes
Environmental No underlying causes
Gastroenterologic Necrotizing enterocolitis
Genetic Athabaskan brain stem dysgenesis, Edstrom myopathy, Jeune thoracic dystrophy syndrome, Muscular dystrophy, Nemaline myopathy, Perry syndrome, Pitt-Hopkins syndrome, Ullrich congenital muscular dystrophy, X-linked myotubular myopathy, Stuve-Wiedemann syndrome
Hematologic No underlying causes
Iatrogenic No underlying causes
Infectious Disease Clostridium tetani, Poliomyelitis
Musculoskeletal / Ortho Cervical spine injury, Congenital diaphragmatic hernia, Congenital fiber-type disproportion myopathy, Diaphragm paralysis, Idiopathic spinal scoliosis, Rib fracture, Severe kyphoscoliosis, Stuve-Wiedemann syndrome, Muscular dystrophy, Nemaline myopathy, Ullrich congenital muscular dystrophy, X-linked myotubular myopathy, Neuromuscular diseases, Myasthenia gravis, Polymyositis
Neurologic Amyotrophic lateral sclerosis, Brain death, Brown-Vialetto-van Laere syndrome, Central sleep apnea, CNS depression, Congenital failure of autonomic control, Guillain-Barre syndrome, Motor neuron disease, Neuromuscular diseases, Raised intracranial pressure, Subacute necrotising encephalomyelopathy, X-linked infantile spinal muscular atrophy, Athabaskan brain stem dysgenesis, Diaphragm paralysis
Nutritional / Metabolic Subacute necrotising encephalomyelopathy
Obstetric/Gynecologic No underlying causes
Oncologic No underlying causes
Opthalmologic No underlying causes
Overdose / Toxicity Acetylcarbromal, Alfentanil, Alprazolam, Amylobarbitone, Barbitone, Bromazepam, Brotizolam, Butabarbital, Butalbital, Butobarbitone, Camazepam, Chlordiazepoxide, Cinolazepam, Clobazam, Clonazepam, Clorazepate, Clotiazepam, Cloxazolam, Cyclobarbital, Demethyldiazepam, Diazepam, Doxefazepam, Drug overdose, Estazolam, Ethyl loflazepate, Etizolam, Etomidate, Fentanyl, Flurazepam, Fluridrazepam, Fospropofol, General anaesthesia, Halazepam, Haloxazolam, Hexobarbital, Ketazolam, Loprazolam, Lorazepam, Lormetazepam, Medazepam, Mephobarbital, Methohexital, Mexazolam, Midazolam, Nitrazepam, Oxazepam, Oxazolam, Pentobarbital, Pethidine, Phenobarbital, Pinazepam, Prazepam, Primidone, Promethazine, Propofol, Quazepam, Remifentanil, Secobarbital, Sufentanil, Tapentadol, Temazepam, Tetrazepam, Thiamylal, Thiopentone, Tofisopam, Triazolam, Oxygen
Psychiatric No underlying causes
Pulmonary Chronic bronchitis, Chronic obstructive pulmonary disease, Emphysema, Foreign body in respiratory tract, Hyaline membrane disease, Obesity hypoventilation syndrome, Obstructive sleep apnea, Pickwickian syndrome, Pneumothorax, Pulmonary hypoplasia, Respiratory depression, Respiratory distress syndrome, Severe asthma, Shallow Breathing , Snoring, Stuve-Wiedemann syndrome, Tracheal stenosis
Renal / Electrolyte No underlying causes
Rheum / Immune / Allergy Myasthenia gravis, Polymyositis, Guillain-Barre syndrome
Sexual No underlying causes
Trauma Flail chest, Cervical spine injury, Pneumothorax
Urologic No underlying causes
Dental No underlying causes
Miscellaneous Asphyxiation, Reduced level of consciousness, Congenital failure of autonomic control, Shallow Breathing

Causes in Alphabetical Order


Differential diagnosis of respiratory acidosis

The differential diagnosis of respiratory acidosis is generated by considering three structures involved in ventilation: the chest cavity (which expands and contracts the lungs), central processes (i.e. those that affect the central respiratory drive center), and the lungs and airways themselves.

Physiological response

Mechanism

Metabolism rapidly generates a large quantity of volatile acid (CO2) 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 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 39-41 mm Hg in normal states.

Alveolar ventilation is under the control of the central respiratory centers, which are 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 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.

Estimated changes

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 = 0.008 X (40 - PaCO2)
  • Chronic respiratory acidosis: Change in pH = 0.003 X (40 - PaCO2)

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.

References


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