Respiratory alkalosis

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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: 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
• 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

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

Less Common Symptoms

Less common symptoms of [disease name] include

• [Symptom 1]
• [Symptom 2]
• [Symptom 3]

• 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

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 is present with both increase in respiratory rate and tidal volume
• Cheyne-Stokes type of breathing may be present
• Low blood pressure in mechanically ventilated patients with respiratory alkalosis

Skin

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

• Description (Adapted from Dermatology Atlas)

  Description (Adapted from Dermatology Atlas)

• 

  Description (Adapted from Dermatology Atlas)

HEENT

• HEENT examination of patients with [disease name] is usually normal.

OR

• Abnormalities of the head/hair may include ___
• Evidence of trauma
• Icteric sclera
• Nystagmus
• Extra-ocular movements may be abnormal
• Pupils non-reactive to light / non-reactive to accommodation / non-reactive to neither light nor accommodation
• Ophthalmoscopic exam may be abnormal with findings of ___
• Hearing acuity may be reduced
• Weber test may be abnormal (Note: A positive Weber test is considered a normal finding / A negative Weber test is considered an abnormal finding. To avoid confusion, you may write "abnormal Weber test".)
• Rinne test may be positive (Note: A positive Rinne test is considered a normal finding / A negative Rinne test is considered an abnormal finding. To avoid confusion, you may write "abnormal Rinne test".)
• Exudate from the ear canal
• Tenderness upon palpation of the ear pinnae/tragus (anterior to ear canal)
• Inflamed nares / congested nares
• Purulent exudate from the nares
• Facial tenderness
• Erythematous throat with/without tonsillar swelling, exudates, and/or petechiae

Neck

• Neck examination of patients with [disease name] is usually normal.

OR

• Jugular venous distension
• Carotid bruits may be auscultated unilaterally/bilaterally using the bell/diaphragm of the otoscope
• Lymphadenopathy (describe location, size, tenderness, mobility, and symmetry)
• Thyromegaly / thyroid nodules
• Hepatojugular reflux

Lungs

• Pulmonary examination of patients with [disease name] is usually normal.

OR

• Asymmetric chest expansion / Decreased chest expansion
• Lungs are hypo/hyperresonant
• Fine/coarse crackles upon auscultation of the lung bases/apices unilaterally/bilaterally
• Rhonchi
• Vesicular breath sounds / Distant breath sounds
• Expiratory/inspiratory wheezing with normal / delayed expiratory phase
• Wheezing may be present
• Egophony present/absent
• Bronchophony present/absent
• Normal/reduced tactile fremitus

Heart

• Cardiovascular examination of patients with [disease name] is usually normal.

OR

• Chest tenderness upon palpation
• PMI within 2 cm of the sternum (PMI) / Displaced point of maximal impulse (PMI) suggestive of ____
• Heave / thrill
• Friction rub
• S1
• S2
• S3
• S4
• Gallops
• A high/low grade early/late systolic murmur / diastolic murmur best heard at the base/apex/(specific valve region) may be heard using the bell/diaphgram of the otoscope

Abdomen

Abdominal examination of patients with [disease name] is usually normal.

OR

• Abdominal distention
• Abdominal tenderness in the right/left upper/lower abdominal quadrant
• Rebound tenderness (positive Blumberg sign)
• A palpable abdominal mass in the right/left upper/lower abdominal quadrant
• Guarding may be present
• Hepatomegaly / splenomegaly / hepatosplenomegaly
• Additional findings, such as obturator test, psoas test, McBurney point test, Murphy test

Back

• Back examination of patients with [disease name] is usually normal.

OR

• Point tenderness over __ vertebrae (e.g. L3-L4)
• Sacral edema
• Costovertebral angle tenderness bilaterally/unilaterally
• Buffalo hump

Genitourinary

• Genitourinary examination of patients with [disease name] is usually normal.

OR

• A pelvic/adnexal mass may be palpated
• Inflamed mucosa
• Clear/(color), foul-smelling/odorless penile/vaginal discharge

Neuromuscular

• Neuromuscular examination of patients with [disease name] is usually normal.

OR

• Patient is usually oriented to persons, place, and time
• Altered mental status
• Glasgow coma scale is ___ / 15
• Clonus may be present
• Hyperreflexia / hyporeflexia / areflexia
• Positive (abnormal) Babinski / plantar reflex unilaterally/bilaterally
• Muscle rigidity
• Proximal/distal muscle weakness unilaterally/bilaterally
• ____ (finding) suggestive of cranial nerve ___ (roman numerical) deficit (e.g. Dilated pupils suggestive of CN III deficit)
• Unilateral/bilateral upper/lower extremity weakness
• Unilateral/bilateral sensory loss in the upper/lower extremity
• Positive straight leg raise test
• Abnormal gait (describe gait: e.g. ataxic (cerebellar) gait / steppage gait / waddling gait / choeiform gait / Parkinsonian gait / sensory gait)
• Positive/negative Trendelenburg sign
• Unilateral/bilateral tremor (describe tremor, e.g. at rest, pill-rolling)
• Normal finger-to-nose test / Dysmetria
• Absent/present dysdiadochokinesia (palm tapping test)

Extremities

• Extremities examination of patients with [disease name] is usually normal.

OR

• Clubbing
• Cyanosis
• Pitting/non-pitting edema of the upper/lower extremities
• Muscle atrophy
• Fasciculations in the upper/lower extremity

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

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.
• 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

Treatment

• Respiratory alkalosis is not a life threatening disorder, so treatment is directed at the underlying causes of the disorder.
  • patients with hyperventilation disorder (eg. anxiety, conversion disorder) are benefited from rebreathing mask.
  • High altitude sickness is treated with acetazolamide 250mg 12 hourly, Dexamethasone 4mg 6 hourly, oxygen therapy and descent to lower altitude in severe cases.
  • For critically ill patients on mechanical ventilation with respiratory alkalosis, tidal volume and respiratory rate needs to be decreased with adequate pain control.
  • Sedatives and antidepressants should not be used in cases of respiratory alkalosis.

Related Chapters

• Metabolic alkalosis
• Acid-base imbalance
• Metabolic acidosis
• Respiratory acidosis
• Anion gap
• Hypocalcemia