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| ==Differential diagnosis of respiratory acidosis== | | ==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. | | 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 ==
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| ===Mechanism===
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| Metabolism rapidly generates a large quantity of volatile acid (CO<sub>2</sub>) and [[nonvolatile acid]]. The metabolism of fats and carbohydrates leads to the formation of a large amount of CO<sub>2</sub>. The CO<sub>2</sub> combines with H<sub>2</sub>O to form carbonic acid (H<sub>2</sub>CO<sub>3</sub>). The lungs excrete the volatile fraction through ventilation, and acid accumulation does not occur. A significant alteration in ventilation that affects elimination of CO<sub>2</sub> can cause a respiratory acid-base disorder. The ''Pa''CO<sub>2</sub> is maintained within a range of 39-41 mm Hg in normal states.
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| 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 ''Pa''CO<sub>2</sub>, PaO<sub>2</sub>, 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 ''Pa''CO<sub>2</sub>.
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| In acute respiratory acidosis, compensation occurs in 2 steps.
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| * The initial response is cellular buffering that occurs over minutes to hours. Cellular buffering elevates plasma bicarbonate (HCO<sub>3</sub><sup>-</sup>) only slightly, approximately 1 mEq/L for each 10-mm Hg increase in ''Pa''CO<sub>2</sub>.
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| * 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.
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| ===Estimated changes===
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| In renal compensation, plasma bicarbonate rises 3.5 mEq/L for each increase of 10 mm Hg in ''Pa''CO<sub>2</sub>. The expected change in serum bicarbonate concentration in respiratory acidosis can be estimated as follows:
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| * Acute respiratory acidosis: HCO<sub>3</sub><sup>-</sup> increases 1 mEq/L for each 10-mm Hg rise in ''Pa''CO<sub>2</sub>.
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| * Chronic respiratory acidosis: HCO<sub>3</sub><sup>-</sup> rises 3.5 mEq/L for each 10-mm Hg rise in ''Pa''CO<sub>2</sub>.
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| The expected change in pH with respiratory acidosis can be estimated with the following equations:
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| * Acute respiratory acidosis: Change in pH = 0.008 X (40 - ''Pa''CO<sub>2</sub>)
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| * Chronic respiratory acidosis: Change in pH = 0.003 X (40 - ''Pa''CO<sub>2</sub>)
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| 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]].
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| ==References== | | ==References== |
| {{reflist|2}} | | {{reflist|2}} |
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
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Ear Nose Throat
|
No underlying causes
|
Endocrine
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No underlying causes
|
Environmental
|
No underlying causes
|
Gastroenterologic
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Necrotizing enterocolitis
|
Genetic
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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
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No underlying causes
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Iatrogenic
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No underlying causes
|
Infectious Disease
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Clostridium tetani, Poliomyelitis
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Musculoskeletal / Ortho
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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
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Neurologic
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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
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Nutritional / Metabolic
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Subacute necrotising encephalomyelopathy
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Obstetric/Gynecologic
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No underlying causes
|
Oncologic
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No underlying causes
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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
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Psychiatric
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No underlying causes
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Pulmonary
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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
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Renal / Electrolyte
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No underlying causes
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Rheum / Immune / Allergy
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Myasthenia gravis, Polymyositis, Guillain-Barre syndrome
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Sexual
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No underlying causes
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Trauma
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Flail chest, Cervical spine injury, Pneumothorax
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Urologic
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No underlying causes
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Dental
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No underlying causes
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Miscellaneous
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Asphyxiation, Reduced level of consciousness, Congenital failure of autonomic control, Shallow Breathing
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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.
References
Template:WikiDoc Sources