Based on its duration, RA can be classified acute if the condition occurs very rapidly [7], or chronic if RA is long-lasting due to other prolonged physiological conditions. The signs and symptoms of RA depend on its duration, severity, and the underlying disease responsible for the occurrence of the RA episode itself, and many of them mimic the presentation of other disorders.

The low levels of CO2 in the blood can cause cerebral vasoconstriction and thus a reduced blood flow in the brain, which when coupled with hypoxemia might lead to neurological symptoms such as mental confusion or syncope [2]. The neurological symptoms, together with painful tingling of hands and feet, numbness and sweating, can also be caused by voluntary hyperventilation [8].

Low blood carbon dioxide levels might cause two important signs frequently used to diagnose RA. The first is a temporary or chronic sensation of tingling, pricking, tickling or burning all over the skin, a condition known as paraesthesia, which in RA appears to have a peripheral manifestation (peripheral paraesthesia). The second is a disrupted calcium balance, one of the direct consequences of high blood carbon dioxide levels, a condition called hypocalcaemia which leads to involuntary muscles contractions (tetany) and fainting. In chronic states, hypocalcemia is coupled with hyperphosphatemia and renal PTH-resistance [9].

• Pulmonary Disorder

  It is the most frequently occurring acid-base imbalance in hospitalized patients, with the elderly at increased risk because of high incidence of pulmonary disorders and alterations in neurological status. [scribd.com]

  This is the most common acid-base abnormality, associated with many cardiac and pulmonary disorders as one of their early or intermediate clinical findings. [symptoma.com]

  Many cardiac and pulmonary disorders can manifest with respiratory alkalosis as an early or intermediate finding. When respiratory alkalosis is present, the cause may be a minor, non–life-threatening disorder. [emedicine.com]

• Carpopedal Spasm

  # Hyperventilation syndrome related to anxiety can cause alkalosis severe enough to cause carpopedal spasm. # A mild fairly well compensated respiratory alkalosis is the usual finding in pregnancy. # Any condition which decreases pulmonary compliance [ld99.com]

  Signs include hyperpnea or tachypnea and carpopedal spasms. Diagnosis is clinical and with ABG and serum electrolyte measurements. Treatment is directed at the cause. [msdmanuals.com]

  Signs include hyperpnea or tachypnea and carpopedal spasms. Diagnosis is clinical and with arterial blood gas (ABG) and serum electrolyte measurements. Treatment is directed at the cause. [merckmanuals.com]

  spasm Shift 02 dissociation curve to the left (Alkalosis) (Increased affinity of Hb for O2) Correction Treat underlying cause Re-breather mask References and Links Acid-Base: ABG analysis – Anion Gap – SID – NAGMA Metabolic acidosis: Overview – evaluation [lifeinthefastlane.com]

• Muscle Twitch

  Other symptoms of respiratory alkalosis may encompass: agitation seizures dizziness light headedness tingling, numbness irregular heart beats muscle twitching, spasms, weakness Severe respiratory alkalosis can cause your muscle to spasm to such an extent [healthblurbs.com]

  Complications Cardiac arrhythmias Seizures Signs and Symptoms Cardinal Sign: Deep Rapid Breathing (40+ bpm) CNS and neuromuscular disturbances: lightheadedness, agitation, circumoral and peripheral paresthesias, carpopedal spasms, twitching and muscle [nurseslabs.com]

  Symptoms of alkalosis can include any of the following: Confusion (can progress to stupor or coma) Hand tremor Lightheadedness Muscle twitching Nausea, vomiting Numbness or tingling in the face, hands, or feet Prolonged muscle spasms (tetany) The health [nlm.nih.gov]

  D) Irritability, muscle twitching and cramping, seizures." A Choose the compensatory mechanism for respiratory acidosis. [studystack.com]

  Muscle twitching, spasms, and weakness may be noted. Seizures, irregular heart beats, and tetany (muscle spasms so severe that the muscle locks in a rigid position) can result from severe respiratory alkalosis. [medical-dictionary.thefreedictionary.com]

• Chvostek Sign

  Positive Chvostek’s sign Nausea and vomiting Muscle twitching Assessment CIRCULATION May report: History/presence of anemia Palpitations May exhibit: Hypotension Tachycardia, irregular pulse/dysrhythmias EGO INTEGRITY May exhibit: Extreme anxiety (most [nurseslabs.com]

  sign Trousseau's sign Clinical Manifestations, continued Tinnitus Sensation of chest tightness Palpitations Seizures and loss of consciousness ABGs Show pH > 7.45 PaCO2 < 35mmHg Chronic hyperventilation Environmental Calm, quiet, low stimulation Reduce [quizlet.com]

  Tinnitus Blurred vision Syncope Peripheral Nervous System Symptoms Circumoral /limb paresthesias Cramps Tremor CNS Signs Ataxia Chvostek’s sign Tremor Encephalopathy Coma Seizure manifestations PNS Signs Myoclonus Tetany I have written about these issues [leonchaitow.com]

  ’s sign, tetany, seizures Heightened sensitivity to environmental noise and activity Muscle weakness, unsteady gait PAIN/DISCOMFORT May report: Muscle spasms/cramps, epigastric pain, precordial pain (tightness) RESPIRATION May report: Dyspnea History [scribd.com]

• Muscle Cramp

  Metabolic alkalosis is usually accompanied with hypokalemia, causing, e.g., muscular weakness, myalgia, and muscle cramps (owing to disturbed function of the skeletal muscles), and muscle spasms (from disturbed function of smooth muscles). [courses.lumenlearning.com]

• Circumoral Paresthesia

  Acute respiratory alkalosis causes light-headedness, confusion, peripheral and circumoral paresthesias, cramps, and syncope. Mechanism is thought to be change in cerebral blood flow and pH. [msdmanuals.com]

• Paresthesia

  The chronic form is asymptomatic, but the acute form causes light-headedness, confusion, paresthesias, cramps, and syncope. Signs include hyperpnea or tachypnea and carpopedal spasms. [msdmanuals.com]

  Complications Cardiac arrhythmias Seizures Signs and Symptoms Cardinal Sign: Deep Rapid Breathing (40+ bpm) CNS and neuromuscular disturbances: lightheadedness, agitation, circumoral and peripheral paresthesias, carpopedal spasms, twitching and muscle [nurseslabs.com]

  […] altitudes and with acute anxiety. think of the things that would cause a person to breathe very rapidly and cause large losses of carbon dioxide. symptoms are: ph elevated above 7.45 and pco2 below 35mmhg rapid, deep breathing hyper ventilation agitation paresthesias [allnurses.com]

• Dizziness

  Two months later, he presented at the emergency department with severe weakness, headache, dizziness, dyspnea, anorexia, and confusional state. Arterial blood gas analysis showed mixed respiratory alkalosis with high anion gap metabolic acidosis. [ncbi.nlm.nih.gov]

  The symptoms may include: Dizziness Lightheadedness Numbness of the hands and feet Breathlessness Confusion Chest discomfort Your health care provider will perform a physical exam. [nlm.nih.gov]

  […] cause a person to breathe very rapidly and cause large losses of carbon dioxide. symptoms are: ph elevated above 7.45 and pco2 below 35mmhg rapid, deep breathing hyper ventilation agitation paresthesias seizures confusion hypo kalemia lightheadedness dizziness [allnurses.com]

  Symptoms The symptoms may include: Dizziness Lightheadedness Numbness of the hands and feet Breathlessness Confusion Chest discomfort Exams and Tests Your health care provider will perform a physical exam. [mountsinai.org]

The diagnosis of RA is heavily based on laboratories studies. Arterial blood gas determination can be performed to measure PaCO2 level and detect alkalemia in the blood. Serum chemistries, instead, can be carried out to measure small changes in electrolyte balances, such as minor reductions in the levels of sodium, potassium and phosphate. These changes might be the consequences of an hepatic failure, which can be identified by performing a liver function test. A complete blood cell count and cultures of blood, urine and sputum can reveal episodes of sepsis, while thyroid testing, drug screens and beta-human chorionic gonadotropin (hCG) measurement can rule out hyperthyroidism, drug abuse and pregnancy respectively as causes of hyperventilation.

Imaging studies are also useful to diagnose RA. Chest radiography and CT scanning can be used to detect a pulmonary disease. Alternatively, the cases of pulmonary embolism might be found by coupling CT with ventilation perfusion scanning. Brain magnetic resonance imaging, instead, is much more effective than CT to reveal nervous system complications, especially brain lesions, tumors, traumas or cerebrovascular difficulties.

• Hypocapnia

  KEYWORDS: Healthy volunteers; Hypercapnia; Hypocapnia; Microcirculation; Venous–arterial difference in CO2 [ncbi.nlm.nih.gov]

  Respiratory alkalosis, also called primary hypocapnia, is characterized by low pCO 2 and high pH (> 7.40). Primary hypocapnia reflects pulmonary hyperventilation. [link.springer.com]

• Chloride Increased

  Serum chloride: Increased. Serum calcium: Decreased. Urine pH: Increased, greater than 7.0. Screening tests as indicated to determine underlying cause, e.g.: CBC: May reveal severe anemia (decreasing oxygen-carrying capacity). [nurseslabs.com]

  Serum chloride: Increased. Serum calcium: Decreased. Urine pH: Increased, greater than 7.0. Screening tests as indicated to determine un derlying cause, e.g.: CBC: May reveal severe anemia (decreasing oxygen-carrying capacity). [scribd.com]

The treatment of respiratory alkalosis depends on the underlying disease which has caused the increase in blood carbon dioxide levels, and should mainly be directed at counterbalancing the effects of this disorder. After controlling the external stimulus responsible for the episode of hyperventilation, three simple strategies can be followed to immediately decrease the carbon dioxide levels, especially in the cases of panic or anxiety. The first is to breathe into a paper bag, which allows the patient to breath the CO2 rich air that has previously been exhaled into the bag itself. The levels of carbon dioxide should decrease after a few acts of breathing, getting the situation back to normal and under control. The second simple strategy is to get reassurance by a loved one or by the healthcare staff, a psychological approach which helps the patient calm down and reduce the respiratory rate. The third strategy, instead, would be to limit oxygen intake into the lungs, something that can be achieved for example by breathing through one single nostril.
The use of sedatives and antidepressants can be useful as well, if the cause of the hyperventilation status is a chronic psychological disorder whose effects on respiration can only be put temporarily under control by following the simple strategies seen above. Beta-adrenergic blockers, instead, can be used in hyperadrenergic states that lead to hyperventilation syndrome [10].

The prognosis of RA varies very much from case to case, and depends on the nature and severity of the underlying disease. Particular care must be taken in chronic states, where subsequent complications can be much more serious due to the longer effects of RA on the body systems affected.

The primary cause of RA is alveolar hyperventilation. This can be related to different conditions, such as psychophysical stresses (anxiety, pain and fear), noxious drugs (analeptics, propanidid, salicylic acid), and pulmonary stimuli (embolism, pneumonia, asthma or edema). If hyperventilation becomes persistent, it might lead to a decrease of PaCO2 in the lungs, a state known hypocapnia. Other possible causes of RA can be pregnancy, sepsis or especially liver failure [3].

Since respiratory alkalosis comes as side effect of other underlying pathological conditions, it is very difficult to indicate precise epidemiological data. It is particularly frequent in critically ill patients, whose morality/morbidity depends on the nature of the associated disease rather than respiratory alkalosis itself.

As previously said, the increased breathing caused by the respiratory stimulus results in an increased alveolar respiration and thus a net loss of CO2. This loss is the direct consequence of the altered chemical balance of CO2 circulating through the blood vessels system, which, in the attempt of maintaining its dynamic equilibrium, follows the principle of Le Chatelier: “If a dynamic equilibrium is disturbed by a change in the conditions, the position of equilibrium moves to counteract the change itself.” In other words, the system disturbed by external factors tends to readjust itself by counteracting the change with a shift in concentration, temperature, volume, or pressure. In this case, the dynamic equilibrium is represented by the following chemical formula: CO2 + H2O → H2CO3 → HCO3- + H+

Bearing in mind the equilibrium represented by this formula helps understand the dynamic behind RA. The decrease of CO2 is neutralized by a shift of the balance towards the reagents, which means a higher quantity of carbon dioxide at the expanse of the hydrogen ions, whose concentration turns out to be reduced accordingly. Since the metabolism does not manage to make up for this loss, especially when this is pronounced and abrupt, the levels of pH in the blood decrease. The CO2 in excess is then released as gaseous CO2, expelled through the respiratory tracts leading to the mouth and nostrils. It has to be noted that just a fraction of the CO2 produced by the body is eliminated in this manner, while a great part of it combines with water to form carbon acid (H2CO3). The majority of carbon dioxide comes from the metabolism of fats and carbohydrates [4].

Maintaining the PaCO2 balance is thus paramount for the body, and this can be achieved through a feedback system between the lungs and the chemoreceptors of hydrogen ion concentration in the brain (central chemoreceptors) and in the carotid bodies (peripheral chemoreceptors). When this system reads an increase in hydrogen ion concentrations, it induces an increase in breathing to blow off the carbon dioxide in excess. The state of reduced quantity of carbon dioxide in the blood is called hypocapnia. This in turn can affect the plasma concentration of many other ions, such as calcium, potassium and phosphate. For example, in the presence of the decreased carbon dioxide concentrations previously indicted, calcium tends to excessively bind to serum albumin, the globular protein produced by the liver to maintain the proper oncotic pressure, as consequence of the subsequent increase of pH. This condition is known as hypocalcemia, and is responsible for the majority of the symptoms observed in the RA cases [5].

If the lungs experience too many difficulties and are no longer capable of compensating bicarbonate deficiency, the kidneys get into action to try to restore the previous levels [6], as they control the retention and the excretion of this ion in the body. The renal compensation starts only after 2 to 6 hours from the beginning of RA episode, and its completion might take several days under normal conditions of kidney functions and intravascular volume status [2].

Preventing respiratory alkalosis means preventing its cause. If the cause of RA is another major disease, such as an infection or a neuronal disorder, following the relative treatment reserved for these conditions would be the appropriate course of action for the patient. But frequently RA comes as a result of a psychological conditions, such as stress, panic or anxiety. In this case, dealing with RA means to adjust and learn to control the psychological stimulus responsible for the episode of hyperventilation. The patient could organize a plan of action together with a therapist based on daily breathing exercises and the taking of appropriate drugs.

The blood pH in respiratory alkalosis (RA) exceeds the normal range of 7.35-7.45 usually observed in the plasma of healthy individuals. The mechanism responsible for this pathological condition [1] is easy to understand in its essential steps. After an initial respiratory stimulus, which causes alveolar hyperventilation, the partial pressure of carbon dioxide (PaCO2) in the lungs decreases, and this in turn provokes an increase in the ration of bicarbonate to PaCO2, with the subsequent increase of pH levels in the blood. Due to the speed of the process the quantity of CO2 lost is greater that the quantity of CO2 produced by the organic metabolism in the tissues.

Respiratory alkalosis can be an acute or chronic condition. Acute RA is characterized by PaCO2 levels below normal and a basic pH (alkalemic), while the chronic RA is characterized always by PaCO2 levels below normal but with a neutral or almost neutral pH. This is the most common acid-base abnormality [2], associated with many cardiac and pulmonary disorders as one of their early or intermediate clinical findings.

Respiratory alkalosis (RA) is a pathological condition defined by elevated blood pH levels due to increased respiration. After an initial respiratory stimulus, the partial pressure of carbon dioxide (PaCO2)in the lungs decreases, and this in turn provokes an increase in the ration of bicarbonate to PaCO2, with the subsequent increase of pH levels in the blood. The primary cause of RA is alveolar hyperventilation, usually associated with psychophysical stresses (anxiety, pain and fear), noxious drugs (analeptics, propanidid, salicylic acid), and pulmonary stimuli (embolism, pneumonia, asthma or edema).

There are three simple strategies that can be followed to immediately decrease the carbon dioxide levels, especially in the cases of panic or anxiety. The first is to breathe into paper bag, which allows the patient to breath the Co2 rich air previously exhaled into the bag itself. The second simple strategy is to get reassurance by a loved one or by the healthcare staff, a psychological approach which helps the patient calm down and reduce the respiratory rate. The third strategy, instead, would be to limit oxygen intake into the lungs, for example by breathing through one single nostril.

Preventing RA means preventing its cause. When RA is the result of a psychological condition, the patient has to adjust and learn how to control the psychological stimulus responsible for the hyperventilation episode. He/she could organize a plan of action together with a therapist based on daily breathing exercises and the taking of appropriate drugs.

1. Johnson RA. Respiratory alkalosis: a quick reference. Vet Clin North Am Small Anim Pract. May 2008;38(3):427-30, vii.
2. DuBose TD Jr. Acidosis and Alkalosis. In: Kasper DL, Braunwald E, Fauci AS, Hauser Sl, Longo DL, Jameson JL, eds. Harrison's Principles of Internal Medicine. 16th. New York, NY: McGraw-Hill; 2005:270-1.
3. Lee WM, Stravitz RT, Larson AM. Introduction to the revised American Association for the Study of Liver Diseases Position Paper on acute liver failure 2011. Hepatology. Mar 2012;55(3):965-7.
4. Kazmaier S, Weyland A, Buhre W, et al. Effects of respiratory alkalosis and acidosis on myocardial blood flow and metabolism in patients with coronary artery disease. Anesthesiology. Oct 1998;89(4):831-7.
5. Effros RM, Wesson JA. Acid-Base Balance. In: Mason RJ, Broaddus VC, Murray JF, Nadel JA, eds. Murray and Nadel's Textbook of Respiratory Medicine. Vol 1. 4th ed. Philadelphia, PA: Elsevier Saunders; 2005:192-93.
6. Adrogué HJ, Madias NE. Secondary responses to altered acid-base status: the rules of engagement. Journal of the American Society of Nephrology 2010 : JASN21 (6): 920–3.
7. Arbus GS, Herbert LA, Levesque PR, Etsten BE, Schwartz WB. Characterization and clinical application of the "significance band" for acute respiratory alkalosis. The New England journal of medicine 280 1969 (3): 117–23.
8. Haldane JS, Poulton EP. The effects of want of oxygen on respiration. J Physiol. 1908;37:390-407.
9. Krapf R, Jaeger P, Hulter HN. Chronic respiratory alkalosis induces renal PTH-resistance, hyperphosphatemia and hypocalcemia in humans. Kidney International 1992 (42): 727–734.
10. Effros RM, Wesson JA. Acid-Base Balance. In: Mason RJ, Broaddus VC, Murray JF, Nadel JA, eds. Murray and Nadel's Textbook of Respiratory Medicine. Vol 1. 4th ed. Philadelphia, PA: Elsevier Saunders; 2005:192-93.