Respiratory alkalosis

	WikiDoc Resources for Respiratory alkalosis
Articles
Most recent articles on Respiratory alkalosis Most cited articles on Respiratory alkalosis Review articles on Respiratory alkalosis Articles on Respiratory alkalosis in N Eng J Med, Lancet, BMJ
Media
Powerpoint slides on Respiratory alkalosis Images of Respiratory alkalosis Photos of Respiratory alkalosis Podcasts & MP3s on Respiratory alkalosis Videos on Respiratory alkalosis
Evidence Based Medicine
Cochrane Collaboration on Respiratory alkalosis Bandolier on Respiratory alkalosis TRIP on Respiratory alkalosis
Clinical Trials
Ongoing Trials on Respiratory alkalosis at Clinical Trials.gov Trial results on Respiratory alkalosis Clinical Trials on Respiratory alkalosis at Google
Guidelines / Policies / Govt
US National Guidelines Clearinghouse on Respiratory alkalosis NICE Guidance on Respiratory alkalosis NHS PRODIGY Guidance FDA on Respiratory alkalosis CDC on Respiratory alkalosis
Books
Books on Respiratory alkalosis
News
Respiratory alkalosis in the news Be alerted to news on Respiratory alkalosis News trends on Respiratory alkalosis
Commentary
Blogs on Respiratory alkalosis
Definitions
Definitions of Respiratory alkalosis
Patient Resources / Community
Patient resources on Respiratory alkalosis Discussion groups on Respiratory alkalosis Patient Handouts on Respiratory alkalosis Directions to Hospitals Treating Respiratory alkalosis Risk calculators and risk factors for Respiratory alkalosis
Healthcare Provider Resources
Symptoms of Respiratory alkalosis Causes & Risk Factors for Respiratory alkalosis Diagnostic studies for Respiratory alkalosis Treatment of Respiratory alkalosis
Continuing Medical Education (CME)
CME Programs on Respiratory alkalosis
International
Respiratory alkalosis en Espanol Respiratory alkalosis en Francais
Business
Respiratory alkalosis in the Marketplace Patents on Respiratory alkalosis
Experimental / Informatics
List of terms related to Respiratory alkalosis

	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: Madhu Sigdel M.B.B.S.[2] Priyamvada Singh, M.D. [3]

Overview

Acid-base status of an organism is determined by the extracellular fluid (ECF) hydrogen ion concentration [H+] since pH is equal to minus log of [H+] i.e. pH = -log[H+]. Normal pH of human blood is 7.40 (7.35-7.45). Acidosis raises ECF [H+] thereby lowering pH whereas alkalosis lowers ECF [H+] thereby raising pH of the ECF.

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(4.7-6.0kPa)] with or without compensatory decrease in serum bicarbonate [HCO3-] (normal bicarbonate is 22-30mEq/L in arterial blood gas analysis) and pH being alkaline (normal pH of blood is 7.35-7.45).

Pathophysiology

Production of CO2 in body tissues by intracellular metabolic process(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. CO2 in body tissues from normal metabolic process enters blood in the tissues because its local partial pressure in tissues is greater than the partial pressure in blood flowing through the tissues due to property of gases to diffuse from high pressure to low pressure. Flowing blood transports the CO2 to the lungs, where it diffuses into the alveoli and then to the atmosphere by pulmonary ventilation. The reversible combination of CO2 with water in the red blood cells under the influence of carbonic anhydrase enzyme forms carbonic acid(H2CO3) which dissociates into hydrogen and bicarbonate ions (H+ and HCO3−). HCO3− diffuse from the red blood cells into the plasma, while chloride ions diffuse into the red blood cells to take their place (chloride shift). Hence, most of tissue CO2 is brought to lungs as plasma venous bicarbonate ions that accounts for about 70 percent of the CO2 transported from the tissues to the lungs. Remaining CO2 is transported as carbaminohemoglobin (23%) and as dissolved CO2 in fluids of blood(7%).Hall, John (2016). Guyton and Hall textbook of medical physiology. Philadelphia, PA: Elsevier. ISBN 9781455770052.

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.

Compensation in respiratory alkalosis

compensation for respiratory alkalosis is mostly mediated through plasma buffers and proteins (eg. hemoglobin in RBC, plasma proteins) in acute stage and by kidneys in chronic compensatory stage.

Acute compensatory stage

Starts within minutes to hours and mediated by body's non-bicarbonate buffers (hemoglobin, intracellular proteins and phosphates, plasma proteins) and it consists of cellular uptake of HCO3- and buffered by intracellular phosphates and proteins^[1]
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 process where reduction in PaCO2 leads to decreased renal tubular H+ secretion. Within the renal tubular cells, CO2, under the influence of carbonic anhydrase enzyme, combines with H2O to form carbonic acid (H2CO3), which then dissociates into HCO3- and H+. Alkalosis inhibits carbonic anhydrase activity, resulting in reduced H+ secretion into the renal tubule. As a result, there is not enough H+ in the renal tubular fluid to react with all the filtered HCO3− from glomerular capillaries of the kidneys. Therefore, the HCO3− that cannot react with H+ is not reabsorbed and is excreted in the urine. This causes a decrease in urinary net acid excretion(mostly ammonium ions NH4+) and due to increased bicarbonate excretion, body's bicarbonate stores is reduced.
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
pH in chronic compensation is near normal

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.

Risk Factors

Common Risk Factors

Common risk factors in the development of respiratory alkalosis include:
- Old age
- Mechanical ventilation
- Lung diseases
- Liver diseases
- Infection
- High altitude
- Anxiety disorder
- CNS infections

Less Common Risk Factors

Less common risk factors in the development of respiratory alkalosis include:
- Drugs
- Poisoning

Causes^[2]

Tissue hypoxia (hypoxemia)

Pneumonia
Aspiration of foreign body, food or vomitus
Pulmonary embolism
Bronchospasm/laryngospasm (eg. in asthma)
Drowning
Anemia
High altitude
Cyanotic heart disease
Circulatory failure or hypotension

Stimulation of chest receptors

Pneumonia
Asthma
Pneumothorax/hemothorax
Flail chest
Cardiac failure
Pulmonary edema (non-cardiogenic)
Adult/infant respiratory distress syndrome
Interstitial lung disease

Stimulators of central respiratory drive

Pain
Anxiety
Fever
High altitude
Anemia
Drugs like doxapram and large doses of aspirin (stimulate the respiratory center), Gallium nitrate, cocaine, catecholamines
CNS causes, including stroke, subarachnoid haemorrhage, meningitis, encephalitis, CNS tumor
Caffeine overdose and coffee abuse, methylxanthines (eg. theophyllin, aminophyllin)
Progesterone

Systemic diseases

Sepsis
Liver failure
Hyperthyroidism
Pregnancy
Iatrogenically during mechanical ventilation of patients
Carbon monoxide poisoning
Recovery from metabolic acidosis
Heat exposure

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.
Respiratory alkalosis is the most common acid base abnormality in critically ill patients.

History and Symptoms

Symptoms of respiratory alkalosis depends upon duration of disease and underlying diseases. Symptoms of acute respiratory alkalosis are related to 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.

History

Patients with respiratory alkalosis may have a positive history of:

Anxiety disorders or primary neurologic diseases
Lung or liver diseases
Critical illness with mechanical ventilation

Common Symptoms

Common symptoms of acute respiratory alkalosis 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:
- 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.

Physical Examination

Physical examination findings of patients with respiratory alkalosis is related to the underlying causes.

Appearance of the Patient

Patients with acute respiratory alkalosis usually appear anxious in primary hyperventilation syndrome, OR are ill appearing in mechanically ventilation whereas are comfortable in chronic respiratory alkalosis.

Vital Signs

High-grade / low-grade fever
Tachycardia may be present
Tachypnea or hyperpnea is present with both increase in respiratory rate and tidal volume
Cheyne-Stokes type of breathing may be seen in upper pontine lesion or heart failure
Low blood pressure in mechanically ventilated patients with respiratory alkalosis

Skin

Cyanosis is present in hypoxic patient
Jaundice may be present in liver disease

HEENT

HEENT examination of patients with respiratory alkalosis is usually normal.

Neck

Neck examination of patients with respiratory alkalosis is usually normal

Lungs

Lungs are hyporesonant in hemothorax/hyperresonant in pneumothorax
Fine/coarse crackles upon auscultation of the lung suggest interstitial lung disease/pneumonia as a cause of respiratory alkalosis

Heart

Cardiovascular examination of patients with respiratory alkalosis is usually normal except in patients with coronary artery disease

Abdomen

Hepatomegaly and right upper quadrant tenderness may be seen in cirrhosis

Back

Back examination of patients with respiratory alkalosis is usually normal.

Genitourinary

Genitourinary examination of patients with respiratory alkalosis is usually normal

Neuromuscular

Focal neurologic signs and depressed level of consciousness is seen in respiratory alkalosis of neurologic cause

Extremities

Extremities examination of patients with respiratory alkalosis show positive Trousseau signs in acute hypocapnia as a result of tetany.

Approach to acid-base disorders

Check pH on ABG

pH<7.35=Acidosis

pH>7.45=Alkalosis

Check PaCO2

PaCO2 > 45mm Hg = Respiratory acidosis Primary cause: hypoventilation

PaCO2 Normal or < 35mm Hg = Metabolic acidosis