Respiratory alkalosis: Difference between revisions
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| [[Respiratory alkalosis resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']] | | [[Respiratory alkalosis resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']] | ||
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{{CMG}}; {{AE}} [[Priyamvada Singh|Priyamvada Singh, M.D.]] [mailto:psingh13579@gmail.com]{{MSI}} | {{CMG}}; {{AE}} [[Priyamvada Singh|Priyamvada Singh, M.D.]] [mailto:psingh13579@gmail.com]{{MSI}} | ||
==Overview== | ==Overview== | ||
'''Respiratory alkalosis''' is an acid-base disorder, primarily a decrease in partial pressure of carbon dioxide in arterial blood i.e.PaCo2 [normal PaCo2 is 40 mm Hg on average with range between 35-45mm Hg] with or without compensatory decrease in serum bicarbonate [HCO3-] and pH being alkaline (normal pH of blood is 7.35-7.45). Respiratory alkalosis results from increased [[alveoli|alveolar]] respiration ([[hyperventilation]]) leading to decrease in blood [[carbon dioxide]] concentration measured as PaCO2. This leads to decreased hydrogen ion [H+] and [[bicarbonate]] [HCO3-] concentrations. Decreased [H+] leads to increase in pH leading to alkalosis. | '''Respiratory alkalosis''' is an acid-base disorder, primarily a decrease in partial pressure of carbon dioxide in arterial blood i.e.PaCo2 [normal PaCo2 is 40 mm Hg on average with range between 35-45mm Hg] with or without compensatory decrease in serum bicarbonate [HCO3-] and pH being alkaline (normal pH of blood is 7.35-7.45). Respiratory alkalosis in almost all cases results from increased [[alveoli|alveolar]] respiration ([[hyperventilation]]) leading to decrease in blood [[carbon dioxide]] concentration measured as PaCO2. This leads to decreased hydrogen ion [H+] and [[bicarbonate]] [HCO3-] concentrations. Decreased [H+] leads to increase in pH leading to alkalosis. | ||
==Pathophysiology== | ==Pathophysiology== | ||
production of CO2 in body tissues(from oxidation of fat, carbohydrate and carbon skeleton of amino acids in normal metabolic process produces carbon dioxide and water) and elimination of CO2 through lungs are in equilibrium under normal physiology. Most of tissue CO2 is brought to lungs as plasma venous bicarbonate ions. | production of CO2 in body tissues(from oxidation of fat, carbohydrate and carbon skeleton of amino acids in normal metabolic process produces carbon dioxide and water) and elimination of CO2 through lungs are in equilibrium under normal physiology. Most of tissue CO2 is brought to lungs as plasma venous bicarbonate ions. | ||
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====Chronic compensatory stage==== | ====Chronic compensatory stage==== | ||
* Renal mediated | * Renal mediated | ||
* Starts after 24-36 hours | * Starts after 24-36 hours and renal compensation for sustained hypocapnia is complete in 36-72 hours | ||
* For every PaCO2 decrease of 10 mm Hg, serum bicarbonate decreases by 5mEq/L | * For every PaCO2 decrease of 10 mm Hg, serum bicarbonate decreases by 5mEq/L | ||
* Change in pH is unpredictable | * Change in pH is unpredictable | ||
Revision as of 20:04, 16 February 2018
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Resident Survival Guide |
| Respiratory alkalosis | |
| ICD-10 | E87.3 |
|---|---|
| ICD-9 | 276.3 |
| DiseasesDB | 406 |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Priyamvada Singh, M.D. [2]Madhu Sigdel M.B.B.S.[3]
Overview
Respiratory alkalosis is an acid-base disorder, primarily a decrease in partial pressure of carbon dioxide in arterial blood i.e.PaCo2 [normal PaCo2 is 40 mm Hg on average with range between 35-45mm Hg] with or without compensatory decrease in serum bicarbonate [HCO3-] and pH being alkaline (normal pH of blood is 7.35-7.45). Respiratory alkalosis in almost all cases results from increased alveolar respiration (hyperventilation) leading to decrease in blood carbon dioxide concentration measured as PaCO2. This leads to decreased hydrogen ion [H+] and bicarbonate [HCO3-] concentrations. Decreased [H+] leads to increase in pH leading to alkalosis.
Pathophysiology
production of CO2 in body tissues(from oxidation of fat, carbohydrate and carbon skeleton of amino acids in normal metabolic process produces carbon dioxide and water) and elimination of CO2 through lungs are in equilibrium under normal physiology. Most of tissue CO2 is brought to lungs as plasma venous bicarbonate ions.
Compensation in respiratory alkalosis
compensation for respiratory alkalosis is mediated through kidneys.
Acute compensatory stage
- Starts within minutes to hours
- Mediated through the plasma buffer
- For every PaCO2 decrease of 10 mm Hg, serum bicarbonate decreases by 1-2mEq/L
- Change in pH is unpredictable
Chronic compensatory stage
- Renal mediated
- Starts after 24-36 hours and renal compensation for sustained hypocapnia is complete in 36-72 hours
- For every PaCO2 decrease of 10 mm Hg, serum bicarbonate decreases by 5mEq/L
- Change in pH is unpredictable
Classification
There are two types of respiratory alkalosis: chronic and acute.
Acute respiratory alkalosis
- Lasting for less than 24-48 hours
- Increased levels of carbon dioxide are "blown off" by the lungs, which are hyperventilating.
- During acute respiratory alkalosis, the person may lose consciousness where the rate of ventilation will resume to normal.
Chronic respiratory alkalosis
- Lasting for longer than 24-48 hours
- For every 10 mM drop in pCO2 in blood, there is a corresponding 5 mM of bicarbonate ion drop.
- The drop of 5 mM of bicarbonate ion is a compensation effect which reduces the alkalosis effect of the drop in pCO2 in blood. This is termed metabolic compensation.
Causes
Lung and airways
Central respiratory drive
- Pain
- Anxiety
- Fever
- High altitude
- CNS tumor
- Drugs like doxapram and large doses of aspirin (stimulate the respiratory center), Gallium nitrate
- CNS causes, including stroke, subarachnoid haemorrhage, meningitis, encephalitis
- Caffeine overdose and coffee abuse, methylxanthines (eg. theophyllin, aminophyllin)
- Progesterone
Systemic diseases
- Sepsis
- Salicylates
- Liver failure
- Hyperthyroid
- Pregnancy
- Hypotension
- CHF
- Anxiety, hysteria, and stress
- Iatrogenically during mechanical ventilation of patients
Special considerations
- Sepsis or salicylate toxicity are the only single disorders that cause both an elevated anion gap metabolic acidosis and a respiratory alkalosis.
- Ischemia, infection or infarction of the central respiratory centers may result either respiratory acidosis (decreased respiratory drive) or respiratory alkalosis (increased respiratory drive)
- Asthma, and Pneumonia can also present with either repiratory alkalosis or acidosis. Asthma typically presents with a respiratory alkalosis, however as the patient tires, respiratory acidosis may occur.
- Pulmonary embolus can be a life threatening condition and often presents as respiratory alkalosis.
- Progesterone is sometimes used as a respiratory stimulant in obstructive sleep apnea and hypoventilation.
Symptoms
- Symptoms of acute respiratory alkalosis are related to the decrease blood carbon dioxide levels (PaCO2) that leads to reduced cerebral blood flow and include: light-headedness, confusion, seizures, peripheral and circumoral paresthesias, cramps, and syncope. Signs include: tachypnea or hyperpnea, carpopedal spasm due to tetany as a result of decreased levels of ionized calcium in the blood (ionized calcium are driven inside cells in exchange for hydrogen ion [H+] as compensatory mechanism to correct pH) with no fall in total serum calcium level.