Respiratory alkalosis

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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: Madhu Sigdel M.B.B.S.[2] Priyamvada Singh, M.D. [3], Eiman Ghaffarpasand, M.D. [4]


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 means 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).


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−) ions. 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%).

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

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


There are two types of respiratory alkalosis: chronic and acute.

Acute respiratory alkalosis

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

Less Common Risk Factors


Tissue hypoxia (hypoxemia)

Stimulation of chest receptors

Stimulators of central respiratory drive

Systemic diseases

Special considerations

Differential Diagnosis

Abbreviations: ABG (arterial blood gas); ACE (angiotensin converting enzyme); BMI (body mass index); CBC (complete blood count); CSF (cerebrospinal fluid); CXR (chest X-ray); DOE (dyspnea on exercise); ECG (electrocardiogram); FEF (forced expiratory flow rate); FEV1 (forced expiratory volume); FVC (forced vital capacity); JVD (jugular vein distention); MCV (mean corpuscular volume); Plt (platelet); RV (residual volume); SIADH (syndrome of inappropriate antidiuretic hormone); TSH (thyroid stimulating hormone); Vt (tidal volume); WBC (white blood cell);

Organ system Diseases Clinical manifestations Diagnosis Other features
Symptoms Physical exam
Loss of consciousness Agitation Weight loss Fever Chest pain Cough Orthopnea DOE Cyanosis Clubbing JVD Peripheral edema Auscultation CBC ABG Imaging Spirometry Gold standard
Acute Dyspnea Respiratory system Chest and Pleura,

Lower airway

Asthma attack[3] - + - - +/- + - - + - - - Wheeze Eosinophil Respiratory alkalosis Normal FEV1, PEF Physical exam and


Chest pain
COPD exacerbation[4] - + - + + + + - + +/- +/- +/- Wheeze, Rhonchi, and Crackles WBC, ↑RBC Respiratory alkalosis Hyperexpansion FEV1/FVC Clinical assessment Acute exacerbations of chronic bronchitis (AECB)
Pneumonia[5] - - - + + + - - - - - - Wheeze, Rhonchi, and Crackles WBC, neutrophilia Respiratory alkalosis Lobar consolidation Normal Chest X-ray and CT Scan productive cough
Pneumothorax[6] - - - - + - - - - - +/- - Diminished breath sounds Normal O2, ↑CO2 Radiolucency without lung marking Vt CXR and Chest CT scan Tracheal deviation
Pulmonary embolism[7] - - - - + - - +/- - - - - Normal Normal Respiratory alkalosis Normal Normal Pulmonary CT angiography Pleuritic chest pain
Rib fractures (flail chest)[8] - + - - + - - - - - - - Normal Normal Respiratory alkalosis Fracture marks Normal Chest X-ray Pneumothorax
Cardiovascular system Acute myocardial ischemia[9] +/- + - +/- + - + + - - - - Normal Normal Respiratory alkalosis Normal Normal Cardiac troponin I Nausea and vomiting, Positive pertinent risk factors, such as hypertension, diabetes, and smoking
Acute heart failure[10] +/- + - - +/- + +/- + + - + + S3 Normal Respiratory alkalosis Cardiothoracic ratio Vt B-type natriuretic peptide (BNP) and N-terminal proBNP (NT-proBNP) Excessive sweating, high blood pressure
Tachyarrhythmia[9] +/- + - - +/- - - - - - - - High pulse rate Normal Respiratory alkalosis Normal Normal ECG Palpitation
Pulmonary edema[11] +/- + - + + + + + + + + + Basal crackle Normal Respiratory alkalosis Bat wing pattern, air bronchograms Vt, ↑RV Cardiac Catheterization Tachypnea
Central nervous system Encephalitis[12] + + - + - - - - - - - - Normal WBC, neutrophilia Respiratory alkalosis Normal Normal CSF PCR Confusion
Traumatic brain injury[13] + +/- - - - - - - - - - - Normal Normal Respiratory alkalosis Intracerebral hemorrhage Normal Brain CT scan Lucid interval
Toxic/Metabolic Salicylate poisoning[14] + - - - - - - - + - - - Normal Normal Metabolic acidosis, Respiratory alkalosis Normal Normal Blood test Vomiting, Tinnitus, Confusion, Hyperthermia
Systemic Pregnancy[15] - - - - +/- - - - - - - + Normal WBC, RBC Respiratory alkalosis Normal Vt, ↑RV βhCG Missed period, Hyperemesis
Sepsis[16] +/- - - + - - - - - - - - Normal WBC, neutrophilia Respiratory alkalosis Normal Normal SIRS criteria Chills, Confusion
Organ system Diseases Clinical manifestations Diagnosis Other features
Symptoms Physical exam
Loss of consciousness Agitation Weight loss Fever Chest pain Cough Orthopnea DOE Cyanosis Clubbing JVD Peripheral edema Auscultation CBC ABG Imaging Spirometry Gold standard
Chronic Dyspnea Respiratory system Chest and Pleura,

Lower airway

Bronchial asthma[3] - + +/- - +/- + - - + + - - Wheeze Eosinophil Respiratory alkalosis, Metabolic acidosis Pulmonary hyperinflation,

Bronchial wall thickening

FEV1/FVC Spirometry before and after bronchodilator Paroxysmal respiratory distress
COPD[4] - - +/- - - + + + + + + +/- Expiratory wheeze RBC Respiratory alkalosis, Metabolic acidosis ↑ Bronchovascular markings, Cardiomegaly FEV1/FVC Physical exam and


Heavy smoking history
Emphysema[17] - - - - - +/- - - + + - - Expiratory wheeze, Hyperinflation Normal Respiratory alkalosis, Metabolic acidosis Flattening of diaphragm, vertical heart FEV1/FVC Physical exam and


Barrel chest
Toxic/Metabolic Metabolic acidosis[18] - - + - - - - - - - - - Normal Normal Metabolic acidosis, Respiratory alkalosis Normal Normal ABG Confusion, Vomiting
Systemic Anxiety[19] + + + - +/- +/- - - - - - - Normal Normal Respiratory alkalosis Normal Normal Psychological interview Sweating, Palpitation

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.


Patients with respiratory alkalosis may have a positive history of:

Common Symptoms

Common symptoms of acute respiratory alkalosis include:

  • Signs include:
    • Carpopedal spasm due to tetany as a result of decreased levels of ionized calcium in the blood (ionized calcium [Ca++] 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



  • HEENT examination of patients with respiratory alkalosis is usually normal.


  • Neck examination of patients with respiratory alkalosis is usually normal




Hepatomegaly and right upper quadrant tenderness may be seen in cirrhosis


  • Back examination of patients with respiratory alkalosis is usually normal.


  • Genitourinary examination of patients with respiratory alkalosis is usually normal


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


Approach to acid-base disorders

Check pH on ABG
Check PaCO2
PaCO2 > 45mm Hg = Respiratory acidosis Primary cause: hypoventilation
PaCO2 Normal or < 35mm Hg = Metabolic acidosis
Check PaCO2
PaCO2 > 45mm Hg = Metabolic alkalosis
PaCO2 < 35mm Hg = Respiratory alkalosis Primary cause: hyperventilation
HCO3- > 29 eg. vomiting
Check HCO3-
Normal or slight decrease = Acute respiratory alkalosis eg. fever, panic attack
Decreased < 24 = Chronic respiratory alkalosis eg. Anemia, CNS causes

Laboratory Findings

  • Arterial blood gas analysis(ABG):
    • It is the diagnostic test of choice for respiratory alkalosis
    • primary respiratory alkalosis has pH> 7.45, PaCO2 <35mm Hg or 4.7kPa while PaO2 is normal(>80mm Hg or 10.7kPa)
  • Serum electrolytes: Decrease in [HCO3-],[Na+], [K+] and ionized [Ca++] are seen in acute hypocapnia due to intracellular shift whereas decreased [HCO3-] and hyperphosphatemia are seen in sustained hypocapnia.[20]
  • Other laboratory test and imaging studies that may be useful in respiratory alkalosis to find out the causes includes:
    • Urine pH and urinalysis
    • CBC: elevated WBC in sepsis
    • Blood/sputum/urine C/S: for sepsis
    • EKG and ECHO: for congestive heart failure
    • Drug screening test
    • Thyroid function test: to rule out hyperthyroidism
    • Liver function test: abnormal in hepatic causes
    • pulmonary function test: to rule out chest infections
    • V/Q scan: to rule out pulmonary embolism
    • Chest X-ray: for chest infection
    • CT scan: for pulmonary embolism
    • MRI brain: to rule out CNS cause of hyperventilation


  • Respiratory alkalosis is not a life threatening disorder, so treatment is directed at the underlying causes of the disorder.

Related Chapters

Template:WikiDoc Sources

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