Respiratory alkalosis
<figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline><figure-inline> </figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline></figure-inline> |
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 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
Compensation in respiratory alkalosis
Acute compensatory stage
- Starts within minutes to hours
- Mediated through the plasma buffer
- For every pCO2 decrease of 10, serum bicarbonate decreases by 2
- Change in pH is unpredictable
Chronic compensatory stage
- Renal mediated
- Starts within 1-3 days
- For every pCO2 decrease of 10, serum bicarbonate decreases by 5
- Change in pH is unpredictable
Classification
There are two types of respiratory alkalosis: chronic and acute.
Acute respiratory alkalosis
- 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
- 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.