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** Tachypnea or hyperpnea,  
** 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. Alkalosis also increases protein-bound fraction of calcium reducing free calcium.
** 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. Alkalosis also increases protein-bound fraction of calcium reducing free calcium.
** Respiratory patterns in respiratory alkalosis my be regular with increased rate and tidal volume OR Cheyne-Stokes type


==Related Chapters==
==Related Chapters==

Revision as of 21:21, 16 February 2018

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Resident
Survival
Guide
Respiratory alkalosis
ICD-10 E87.3
ICD-9 276.3
DiseasesDB 406

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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

Systemic diseases

Special considerations

Symptoms

  • Symptoms of acute respiratory alkalosis are related to the decrease blood carbon dioxide levels (PaCO2) that leads to reduced cerebral blood flow resulting from vasoconstriction of cerebral vessels. Most of the symptoms arise when PaCO2 falls below 30 mm Hg and include:
    • Light-headedness, syncope
    • Confusion,
    • Seizures,
    • Peripheral and circumoral paresthesias, and cramps.
    • Chest pain and shortness of breath are seen in patients hyperventilating due to pain or anxiety.
    • Chronic respiratory alkalosis is generally well tolerated without apparent clinical symptoms
  • 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. Alkalosis also increases protein-bound fraction of calcium reducing free calcium.
    • Respiratory patterns in respiratory alkalosis my be regular with increased rate and tidal volume OR Cheyne-Stokes type

Related Chapters

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