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Hyperventilation can result in: Choose the correct answer: Hyperventilation can result in A) metabolic acidosis B) dehydration C) respiratory alkalosis D) respiratory acidosis


Respiratory Alkalosis: Background, Pathophysiology, Epidemiology


Ranjodh Singh Gill, MD, FACP, CCD Professor of Internal Medicine and Surgery/Endocrinology, Central Virginia VA Health Care System, Virginia Commonwealth University School of Medicine

Ranjodh Singh Gill, MD, FACP, CCD is a member of the following medical societies: American Association of Physicians of Indian Origin, American College of Physicians, Endocrine Society, International Society for Clinical Densitometry, Medical Society of Virginia, North American Sikh Medical and Dental Association, Richmond Academy of Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Zab Mosenifar, MD, FACP, FCCP Geri and Richard Brawerman Chair in Pulmonary and Critical Care Medicine, Professor and Executive Vice Chairman, Department of Medicine, Medical Director, Women’s Guild Lung Institute, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD, FACP, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society

Disclosure: Nothing to disclose.

Additional Contributors

Ryland P Byrd, Jr, MD Professor of Medicine, Division of Pulmonary Disease and Critical Care Medicine, James H Quillen College of Medicine, East Tennessee State University

Ryland P Byrd, Jr, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society

Disclosure: Nothing to disclose.


Gregg T Anders, DO Medical Director, Great Plains Regional Medical Command , Brooke Army Medical Center; Clinical Associate Professor, Department of Internal Medicine, Division of Pulmonary Disease, University of Texas Health Science Center at San Antonio

Disclosure: Nothing to disclose.

Jackie A Hayes, MD, FCCP Clinical Assistant Professor of Medicine, University of Texas Health Science Center at San Antonio; Chief, Pulmonary and Critical Care Medicine, Department of Medicine, Brooke Army Medical Center

Jackie A Hayes is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Oleh Wasyl Hnatiuk, MD Program Director, National Capital Consortium, Pulmonary and Critical Care, Walter Reed Army Medical Center; Associate Professor, Department of Medicine, Uniformed Services University of Health Sciences

Oleh Wasyl Hnatiuk, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

April Lambert-Drwiega, DO Fellow, Department of Pulmonology and Critical Care Medicine, East Tennessee State University

April Lambert-Drwiega is a member of the following medical societies: American College of Physicians, American Medical Association, American Osteopathic Association, and Southern Medical Association

Hyperventilation – an overview | ScienceDirect Topics


Hyperventilation results in reduction in arterial pressure of carbon dioxide (PaCO2), which causes vasoconstriction, thus reducing CBF, cerebral blood volume, and, subsequently, ICP. This effect usually occurs within minutes of initiation of hyperventilation. It must be noted that metabolic autoregulation is not intact in ischemic brain regions, where brain arterioles are maximally dilated. Vasoconstriction is therefore limited to vessels supplying unaffected brain tissue, a feature that could theoretically lead to redistribution of CBF (reverse steal phenomenon). Michenfelder and Milde examining the effect of hypocapnia in a primate model of acute ischemic stroke, found no differences in mortality or level of neurologic function, although they did note a tendency toward smaller infarct volumes.212 The applicability of hyperventilation is limited by the following major factors: (1) cerebral vasoconstriction can result in cerebral ischemia and (2) the induced elevation of CSF pH is compensated by the choroid plexus within hours, in contrast to the much slower compensation of blood pH, which can require several days. This latter finding implies that the effect of hyperventilation lasts for only a few hours, after which cerebral vessels regain their normal diameter. Termination of hyperventilation at this stage results in an increase of PaCO2 in both blood and CSF, which in turn causes cerebral vasodilation, potentially leading to a rebound effect on ICP. In a randomized trial, Muizelaar and associates examined the effects of hyperventilation alone, hyperventilation plus Tham, and normoventilation (control) in 113 patients with severe head injury, who were divided into two subgroups according to the initial motor score.23 These investigators observed a significantly worse outcome at 3 and 6 months after injury in patients with severe motor scores who were treated with hyperventilation alone. They also demonstrated that hyperventilation alone, in contrast to hyperventilation plus Tham, could not sustain CSF alkalinization. A variety of clinical studies on head injury suggested deleterious effects of hyperventilation on cerebral oxygenation213,214 and metabolism. 215

Hyperventilation is a treatment option for short interventions, to counteract sudden ICP elevations. Under these conditions, the risk of rebound is minimal. Hyperventilation is easily induced through an approximate 10% increase in tidal volume, target levels are 30–35 mm Hg arterial PCO2. However, with regard to the large body of evidence indicating possible deleterious effects of hyperventilation on cerebral oxygenation, metabolism and blood flow, and the lack of any beneficial effect on outcome, long-term hyperventilation cannot be recommended in stroke patients.216

Respiratory Alkalosis – an overview

Recognize common causes and symptoms of respiratory alkalosis.

Understand the cause of Brisket disease, and discuss involvement of the Rapoport-Luebering Shunt in this condition (see Chapter 31).

Explain why the bicarbonate buffer equation is shifted to the left in this condition, and recognize why the plasma [HCO3] should not be used (alone) to evaluate the overall acid-base state.

Discuss why the expresssion (CO2 ln = CO2 Out) applies not only to normal animals, but also to animals with compensated respiratory acid-base disorders.

Outline the renal compensatory mechanisms in this acid-base disorder, and explain why hyperchloremia develops. Also discuss how this change alone is considered acidifying, and thus compensatory (see Chapter 92).

Compare alterations in K+ balance associated with this condition to those in matabolic alkalosis (see Chapter 89).

Explain why a mixed acid-base disturbance would be expected in a patient whose Pco2 and [HCO3] were moving in opposite directions (see Table 87-1).

Table 91-1. Common Causes of Respiratory Alkalosis

Direct stimulation of the CNS respiratory center
   Pain, anxiety and fear
CNS disease
   Traumatic brain injury
   Sepsis (gram-negative, particularly)
   Inflammatory cytokines
   Lesions of the brain stem
Hypermetabolic states
Liver failure
Pharmacologic and hormonal stimulation
   Salicylates (aspirin)
   Progestins (pregnancy)
Reflex hypoxemic stimulation of the respiratory center
Cyanotic heart disease
Decreased inspired O2 tension
High altitude (Brisket disease)
CO, CN, and methemoglobin
Pulmonary disease
Pulmonary edema
Pulmonary thromboembolism
Ventilation-perfusion inequality
Excessive mechanical ventilation

The pathophysiology of hyperventilation syndrome

Hyperventilation is defined as breathing in excess of the metabolic needs of the body, eliminating more carbon dioxide than is produced, and, consequently, resulting in respiratory alkalosis and an elevated blood pH. The traditional definition of hyperventilation syndrome describes “a syndrome, characterized by a variety of somatic symptoms induced by physiologically inappropriate hyperventilation and usually reproduced by voluntary hyperventilation”. The spectrum of symptoms ascribed to hyperventilation syndrome is extremely broad, aspecific and varying. They stem from virtually every tract, and can be caused by physiological mechanisms such as low Pa,CO2, or the increased sympathetic adrenergic tone. Psychological mechanisms also contribute to the symptomatology, or even generate some of the symptoms. Taking the traditional definition of hyperventilation syndrome as a starting point, there should be three elements to the diagnostic criterion: 1) the patient should hyperventilate and have low Pa,CO2, 2) somatic diseases causing hyperventilation should have been excluded, and 3) the patient should have a number of complaints which are, or have been, related to the hypocapnia. Recent studies have questioned the tight relationship between hypocapnia and complaints. However, the latter can be maintained and/or elicited when situations in the absence of hypocapnia in which the first hyperventilation and hypocapnia was present recur. Thus, the main approach to diagnosis is the detection of signs of (possible) dysregulation of breathing leading to hypocapnia. The therapeutic approach to hyperventilation syndrome has several stages and/or degrees of intervention: psychological counselling, physiotherapy and relaxation, and finally drug therapy. Depending on the severity of the problem, one or more therapeutic strategies can be chosen.

What Is It, Treatment & Prevention


What is alkalosis?

Your body is continuously working to maintain the blood’s acid-base (alkali) balance. Alkalosis occurs when there’s too much alkali and not enough acid. Chemical changes in the acid-base balance can reflect changes in metabolism or breathing.

What is respiratory alkalosis?

This condition occurs when your blood doesn’t have enough carbon dioxide (hypocapnia). Your body releases carbon dioxide when you exhale. When you breathe faster, the lower carbon dioxide level in your blood can lead to respiratory alkalosis.

Respiratory alkalosis is usually caused by over-breathing (called hyperventilation) that occurs when you breathe very deeply or rapidly.

Causes of hyperventilation include:

  • Anxiety or panic.
  • Fever.
  • Pregnancy (this is normal).
  • Pain.
  • Tumor.
  • Trauma.
  • Severe anemia.
  • Liver disease.
  • Overdose of certain medicines, such as salicylates or progesterone.
  • Any lung disease that leads to shortness of breath can also cause respiratory alkalosis (such as pulmonary embolism and asthma).
  • Neurologic conditions such as stroke.

Symptoms and Causes

Who is at risk for respiratory alkalosis?

People who experience intense bouts of stress, anxiety, panic or anger are at higher risk for respiratory alkalosis. These conditions can lead to rapid, uncontrolled breathing (hyperventilation).

People on breathing machines (mechanical ventilation) are also at risk. The machines deliver a fixed breath volume for each breath, which can lead to hyperventilation when patients breathe faster. As a critically ill person’s medical needs change, they may need higher or lower levels of breathing assistance. Ongoing monitoring helps healthcare providers determine when to adjust ventilator settings.

What are the symptoms of respiratory alkalosis?

The symptoms can affect any organ system in the body. You may experience:

  • Breathlessness.
  • Dizziness.
  • Numbness and /or tingling in your fingertips, toes and lips.
  • Irritability.
  • Nausea.
  • Muscle spasms or twitching.
  • Fatigue.
  • Dizziness/lightheadedness.
  • Fainting (syncope).
  • Chest discomfort.
  • Shortness of breath.
  • Tremors.
  • Confusion.

When should I see a healthcare provider for alkalosis?

Uncontrolled breathing often needs immediate medical care in a hospital. The treatment for respiratory alkalosis depends on the underlying cause and it needs to be determined by a medical professional. If breathing is under control but you have other alkalosis symptoms, it’s important to get a timely evaluation.

If you suffer from hyperventilation caused by panic or anxiety, the symptoms of respiratory alkalosis can be frightening. This often causes faster breathing, making things worse.

Management and Treatment

How is respiratory alkalosis treated?

Treatment for respiratory alkalosis depends on the underlying cause to reduce hyperventilation. Treating the condition is a matter of raising carbon dioxide levels in the blood.


How can I prevent respiratory alkalosis due to hyperventilation?

Learning how to cope with stress, anxiety, panic and anger can help you avoid hyperventilation.

The following treatments may help you cope:

  • Therapy.
  • Relaxation techniques.
  • Lifestyle changes.
  • Medications.

You may be able to avoid stress-related respiratory alkalosis by:

  • Taking antidepressants for anxiety or medications that reduce the intensity of panic attacks.
  • Building a support system of trusted individuals who can help you regain control of rapid breathing before it progresses to hyperventilating.

Living With

What can I do when I feel like I’m losing control of my breathing?

Steps you can take include:

  • Practice breathing techniques, like pushing air in and out through pursed lips.
  • Using relaxation methods, including meditation, which calm your body and mind.
  • Breathing into a paper bag.

A note from Cleveland Clinic

Respiratory alkalosis occurs when hyperventilation makes it hard for the lungs to get rid of excess carbon dioxide. It can also happen in people who need mechanical ventilation. The condition is not life-threatening. Nor does it have lingering effects on your health. But it’s important to seek medical care for respiratory alkalosis because it’s often a sign of another medical condition. Some people need treatment with supplemental oxygen. Addressing what’s causing you to hyperventilate lowers your risk of future episodes.

An introduction to acid-base balance in health and disease

Normal cell metabolism depends on the maintenance of blood pH
within very narrow limits (7.35-7.45).

Even relatively mild
excursions outside this normal pH range can have deleterious
effects, including reduced oxygen delivery to tissues, electrolyte
disturbances and changes in heart muscle contractility; survival is
rare if blood pH falls below 6.8 or rises above 7.8.

The problem
for the body is that normal metabolism is associated with
continuous production of hydrogen ions (H+) and carbon dioxide
(CO2), both of which tend to reduce pH. The mechanism
which overcomes this problem and serves to maintain normal blood pH
(i. e. preserve acid-base homeostasis) is a complex synergy of
action involving chemical buffers in blood, the red cells
(erythrocytes), which circulate in blood, and the function of three
organs: lungs, kidneys and brain.

Before explaining how these five
elements contribute to the overall maintenance of blood pH, it
would be helpful to quickly review some basic concepts.

What is an acid, what is a base and what is pH? 

An acid is a substance which releases
hydrogen ions (H+) on dissociation in solution.

For example: Hydrochloric acid (HCl) dissociates to hydrogen
ions and chloride ions

HCl  H+ + Cl

Carbonic acid (H2CO3) dissociates to
hydrogen ions and bicarbonate ions

H2CO3 H+ +

We distinguish between strong acids like hydrochloric acid and
weak acids like carbonic acid. The difference is that strong acids
dissociate more than weak acids. Consequently the hydrogen ion
concentration of a strong acid is much higher than that of a weak

A base is a substance which in solution accepts
hydrogen ions.

For example, the base bicarbonate (HCO3)
accepts hydrogen ions to form carbonic acid:

HCO3 + H+

pH is a scale of 0-14 of acidity and alkalinity. Pure water has
a pH of 7 and is neutral (neither acidic nor alkaline). pH above 7
is alkaline and below 7 acidic. Thus the pH of blood (7.35-7.45) is
slightly alkaline although in clinical medicine the term alkalosis
is, perhaps confusingly, reserved for blood pH greater than 7.45
and the term acidosis is reserved for blood pH less than 7.35.

pH is a measure of hydrogen ion concentration (H+).
The two are related according to the following

pH = – log10

where [H+] is the concentration of hydrogen ions in
moles per liter (mol/L)

From this equation

pH 7. 4 = H+ concentration of 40 nmol/L

pH 7.0 = H+ concentration of 100 nmol/L

pH 6.0 = H+ concentration of 1000 nmol/L

It is clear that:

  • the two parameters change inversely; as hydrogen ion
    concentration increases, pH falls
  • due to the logarithmic relationship, a large change in
    hydrogen ion concentration is actually a small change in pH.
    For example, doubling the hydrogen ion concentration causes pH
    to fall by just 0.3

What is a buffer? – the bicarbonate buffer system 

Buffers are chemicals in solution which minimize the
change in pH which occurs when acids are added by ‘mopping up’
hydrogen ions. A buffer is a solution of a weak acid and its
conjugate base. In blood, the principle buffer system is the weak
acid, carbonic acid (H2CO3) and its conjugate
base, bicarbonate (HCO3). To explain how
this system minimizes changes in pH, suppose we add a strong acid,
e. g. HCl, to the bicarbonate buffer:

The acid will dissociate, releasing hydrogen ions:

H+ + Cl

The bicarbonate buffer then ‘absorbs’ the hydrogen ions, forming
carbonic acid in the process:

HCO3 + H+
H2CO3 (carbonic acid)

The important point is that because the hydrogen ions from HCl
have been incorporated into the weak carbonic acid, which does not
dissociate as easily, the total number of hydrogen ions in solution
and therefore the pH do not change as much as would have occurred
in the absence of the buffer.

Although a buffer greatly minimizes
pH change, it does not eliminate it because even a weak acid (like
carbonic acid) dissociates to some extent. The pH of a buffer
solution is a function of the relative concentrations of the weak
acid and its conjugate base.

pH = 6.1 + log ([HCO3] /

Where [HCO3] = concentration of

3] = concentration of carbonic acid

This relationship, known as the Henderson-Hasselbalch equation,
shows that pH is governed by the ratio of base
(HCO3) concentration to acid
(H2CO3) concentration.  

As hydrogen ions are added to the bicarbonate buffer:

H+ +

bicarbonate (base) is consumed (concentration decreases) and
carbonic acid is produced (concentration increases). If hydrogen
ions continue to be added, all bicarbonate would eventually be
consumed (converted to carbonic acid) and there would be no
buffering effect – pH would then fall sharply if more acid were

However, if carbonic acid could be continuously removed from
the system and bicarbonate constantly regenerated, then the
buffering capacity and therefore pH could be maintained despite
continued addition of hydrogen ions. 

As will become clear with more detail of the physiology of
acid-base balance, that is, in effect, what happens in the body. In
essence, the lungs ensure removal of carbonic acid (as carbon
dioxide) and the kidneys ensure continuous regeneration of

This role of the lungs is dependent on a singular
characteristic of the bicarbonate buffering system and that is the
ability of carbonic acid to be converted to carbon dioxide and

The following equation outlines the relationship of all
elements of the bicarbonate buffering system as it operates in the

H+ +
H2O + CO2

It is important to note that the reactions are reversible.
Direction is dependent on the relative concentration of each
element. So that, for example, a rise in carbon dioxide
concentration forces reaction to the left with increased formation
of carbonic acid and ultimately hydrogen ions.

This explains the
acidic potential of carbon dioxide and brings us to the important
contribution that the lungs and red cells make to overall acid-base

Lung function, transport of CO

2 and acid-base

A constant amount of CO2 in blood, essential for normal
acid-base balance, reflects a balance between that produced as a
result of tissue cell metabolism and that excreted by the lungs in
expired air.

By varying the rate at which carbon dioxide is
excreted, the lungs regulate the carbon dioxide content of blood.
The sequence of events from carbon dioxide production in the
tissues to elimination in expired air is described in Fig. 1.
Carbon dioxide diffuses out of tissue cells to surrounding
capillary blood (Fig. 1a). A small proportion dissolves in blood
plasma and is transported to the lungs unchanged.

But most diffuses
into red cells where it combines with water to form carbonic acid.
The acid dissociates with production of hydrogen ions and
bicarbonate. Hydrogen ions combine with deoxygenated hemoglobin
(hemoglobin is acting as a buffer here), preventing a dangerous
fall in cellular pH, and bicarbonate diffuses along a concentration
gradient from red cell to plasma.

Thus most of the carbon dioxide
produced in the tissues is transported to the lungs as bicarbonate
in blood plasma. 

Fig. 1a. CO2 produced in tissues
converted to bicarbonate for transport to lungs.

  • O2 oxygen
  • CO2 carbon dioxide
  • H2CO3 carbonic
  • HCO3 bicarbonate

Fig. 1b. At the lungs bicarbonate converted
back to CO2 and eliminated by the lungs.

At the alveoli in the lungs the process is reversed (Fig. 1b).
Hydrogen ions are displaced from hemoglobin as it takes up oxygen
from inspired air. The hydrogen ions are now buffered by
bicarbonate which diffuses from plasma back into red cell, and
carbonic acid is formed. As the concentration of this rises, it is
converted to water and carbon dioxide. Finally, carbon dioxide
diffuses down a concentration gradient from red cell to alveoli for
excretion in expired air.

Respiratory chemoreceptors in the brain stem respond to changes
in the concentration of carbon dioxide in blood, causing increased
ventilation (breathing) if carbon dioxide concentration rises and
decreased ventilation if carbon dioxide falls.

Kidneys and acid-base balance 

Normal cellular metabolism results in continuous
production of hydrogen ions. We have seen that by combining with
these hydrogen ions, the bicarbonate buffer in blood minimizes
their effect. However, buffering is only useful in the short term,
and ultimately hydrogen ions have to be removed from the body.
Furthermore, it is important that the bicarbonate that is used to
buffer hydrogen ions is continuously replaced.

These two tasks,
elimination of hydrogen ions and regeneration of bicarbonate, are
accomplished by the kidneys. Renal tubule cells are rich in the
enzyme carbonic anhydrase, which facilitates formation of carbonic
acid from carbon dioxide and water. Carbonic acid dissociates to
bicarbonate and hydrogen ions. The bicarbonate is reabsorbed into
blood and the hydrogen ions pass into the lumen of the tubule and
are eliminated from the body in urine.

This urinary elimination is
dependent on the presence in urine of buffers, principally
phosphate and ammonia ions.


Most acid-base disturbances result from

  • disease or damage to organs (kidney, lungs, brain) whose
    normal function is necessary for acid-base homeostasis,
  • disease which causes abnormally increased production of
    metabolic acids such that homeostatic mechanisms are
  • medical intervention (e.g. mechanical ventilation, some

Arterial blood gases are the blood test used to identify and
monitor acid-base disturbances. Three parameters measured during
blood gas analysis, arterial blood pH (pH), partial pressure of
carbon dioxide in arterial blood (pCO2(a)) and
concentration of bicarbonate (HCO3) are of
crucial importance (see Table I for reference (normal) range).
Results of these three allow classification of acid-base
disturbance to one of four etiological categories: 

  • Respiratory acidosis
  • Respiratory alkalosis
  • Metabolic acidosis
  • Metabolic alkalosis






pCO2 (kPa)







TABLE I. Approximate reference (normal)

To understand how the results of pH, pCO2(a)
and bicarbonate are used to classify acid-base disturbances in this
way, we must return to the Henderson-Hasselbalch equation

pH = 6.1 + log ([HCO3]
/ [H2CO3])

We measure pH and bicarbonate but not carbonic acid
(H2CO3). However, there is a relationship
between pCO2(a) and H2CO3
which allows restatement of the Henderson-Hasselbalch equation in
terms of the three parameters (pH, pCO2(a) and
bicarbonate) measured during blood gas analysis:

pH = 6.1 + log ([HCO3] /
pCO2(a) × 0.23))

By removing all constants from this equation, the relationship
between the three measured parameters can be more simply

pH ∝ [HCO3]

This relationship, crucial for an understanding of all that
follows concerning acid base disturbances, states that arterial
blood pH is proportional to the ratio of bicarbonate concentration
to pCO2(a). It allows the following

  • pH remains normal so long as the ratio
    [HCO3] : pCO2(a)
    remains normal
  • pH increases (i.e. alkalosis occurs) if
    either [HCO3]
    increases or
    pCO2(a) decreases.
  • pH decreases (i.e. acidosis occurs) if either
    [HCO3] decreases
    or pCO2(a)
  • If both
    pCO2(a) and
    [HCO3] are increased by relatively the
    same amount, the ratio and therefore the pH are normal
  • If both pCO2(a)
    and [HCO3] are
    decreased by relatively the same amount, the ratio and
    therefore the pH are normal.

Acid-base disturbances affect primarily either
pCO2(a), in which case it is called a
respiratory disturbance, or
[HCO3], in which case it is called a
non-respiratory or metabolic

  • If the primary disturbance is a raised
    pCO2(a) (which causes acidosis – see
    above), the condition is called respiratory
  • If the primary disturbance is a reduced
    pCO2(a) (which causes alkalosis – see
    above), the condition is called respiratory
  • If the primary disturbance is associated with reduced
    bicarbonate (which results in acidosis – see above), the
    condition is called metabolic
  • If the primary disturbance is associated with raised
    bicarbonate (which results in alkalosis – see above), the
    condition is called metabolic

Causes of acid-base disturbances 

Respiratory acidosis – (raised

reduced pH)

Respiratory acidosis is characterized by increased
pCO2(a) due to inadequate alveolar ventilation
(hypoventilation) and consequent reduced elimination of
CO2 from the blood. Respiratory disease, such as
bronchopneumonia, emphysema, asthma and chronic obstructive airways
disease, may all be associated with hypoventilation sufficient to
cause respiratory acidosis.

Some drugs (e.g. morphine and
barbiturates) can cause respiratory acidosis by depressing the
respiratory center in the brain. Damage or trauma to the chest wall
and the musculature involved in the mechanics of respiration may
reduce ventilation rate. This explains the respiratory acidosis
that can complicate the course of diseases such as poliomyelitis,
Guillain-Barre syndrome and recovery from severe chest trauma.

Respiratory alkalosis – (reduced

pCO2(a), increased pH) 

By contrast, respiratory alkalosis is characterized by decreased
pCO2(a) due to excessive alveolar ventilation
and resulting excessive elimination of CO2 from blood.
Disease in which, due to reduced oxygen in blood (hypoxemia), the
respiratory center is stimulated can result in respiratory

Examples here include severe anemia, pulmonary embolism
and adult respiratory syndrome. Hyperventilation sufficient to
cause respiratory alkalosis can be a feature of anxiety attacks and
response to severe pain. One of the less welcome properties of
salicylate (aspirin) is its stimulatory effect on the respiratory
center. This effect accounts for the respiratory alkalosis that
occurs following salicylate overdose. Finally, overenthusiastic
mechanical ventilation can cause respiratory alkalosis.

Metabolic acidosis – (decreased

3, decreased pH) 

Reduced bicarbonate is always a feature of metabolic
acidosis. This occurs for one of two reasons: increased use of
bicarbonate in buffering an abnormal acid load or increased losses
of bicarbonate from the body. Diabetic ketoacidosis and lactic
acidosis are two conditions characterized by overproduction of
metabolic acids and consequent exhaustion of bicarbonate.

In the
first case, abnormally high blood concentrations of keto-acids
(b-hydroxybutyric acid and acetoacetic acid) reflect the severe
metabolic derangements which result from insulin

All cells produce lactic acid if they are deficient of oxygen,
so increased lactic acid production and resulting metabolic
acidosis occur in any condition in which oxygen delivery to the
tissues is severely compromised.

Examples include cardiac arrest
and any condition associated with hypovolemic shock (e.g. massive
fluid loss). The liver plays a major role in removing the small
amount of lactic acid that is produced during normal cell
metabolism, so that lactic acidosis can be a feature of liver

Abnormal loss of bicarbonate from the body can occur during
severe diarrhea. If unchecked, this can lead to metabolic acidosis.
Failure to regenerate bicarbonate and excrete hydrogen ions
explains the metabolic acidosis that occurs in renal

Metabolic alkalosis – (increased

3 , increased pH)  

Bicarbonate is always raised in metabolic alkalosis. Rarely,
excessive administration of bicarbonate or ingestion of bicarbonate
in antacid preparation can cause metabolic alkalosis, but this is
usually transient. Abnormal loss of hydrogen ions from the body can
be the primary problem. Bicarbonate which would otherwise be
consumed in buffering these lost hydrogen ions consequently
accumulates in blood. Gastric juice is acidic and gastric
aspiration or any disease process in which gastric contents are
lost from the body represents a loss of hydrogen ions.

projectile vomiting of gastric juice, for example, explains the
metabolic alkalosis that can occur in patients with pyloric
stenosis. Severe potassium depletion can cause metabolic alkalosis
due to the reciprocal relationship between hydrogen and potassium

Compensation – a consequence of acid-base

It is vital for life that pH does not waiver too far from normal,
and the body will always attempt to return an abnormal pH towards
normal when acid-base balance is disturbed. Compensation is the
name given to this life-preserving process. To understand
compensation, it is important to recall that pH is governed by the
ratio [HCO3] : pCO2(a).
So long as the ratio is normal, pH will be normal. 

Consider the patient with metabolic acidosis whose pH is low
because bicarbonate [HCO3] is low. To
compensate for the low [HCO3] and restore
the all-important ratio towards normal the patient must lower his
pCO2(a). Chemoreceptors in the respiratory
center of the brain respond to a rising hydrogen ion concentration
(low pH), causing increased ventilation (hyperventilation) and
thereby increased elimination of carbon dioxide; the
pCO2(a) falls and the ratio
[HCO3] : pCO2(a) returns
towards normal.

Compensation for metabolic alkalosis in which
[HCO3] is high, by contrast, involves
depression of respiration and thereby retention of carbon dioxide
so that the pCO2(a) rises to match the increase
in [HCO3]. However, depression of
respiration has the unwelcome side effect of threatening adequate
oxygenation of tissues. For this reason respiratory compensation of
metabolic alkalosis is limited.

Primary disturbances of pCO2(a) (respiratory
acidosis and alkalosis) are compensated for by renal adjustments of
hydrogen ion excretion which result in changes in
[HCO3] that compensate appropriately for
primary change in pCO2(a). Thus the renal
compensation for respiratory acidosis (raised
pCO2(a)) involves increased reabsorption of
bicarbonate, and renal compensation for respiratory alkalosis
(reduced pCO2(a)) involves reduced bicarbonate

The concept of acid-base balance during compensation
is conveyed visually in Fig. 2. Table II summarizes the blood gas
results that characterize all four acid-base disturbances before
and after compensation.

Fig. 2. The “acid-base balance” : compensation
restores normal pH






in pCO2 





in pCO2





in bicarb.





in bicarb.








of repiratory







of brain



Renal failure





– clinical


























but limited



in metabolic


Initial blood

gas results



























Blood gas

results after






but closer

to normal







but closer

to normal








but closer to









sation in



Blood gas

results after




pH normal





pH normal





pH normal







sation in



friendly version of table, pdf.

TABLE II. Blood gas results in disturbances of
acid-base balance

Respiratory compensation for a primary metabolic disturbance
occurs much more quickly than metabolic (renal) compensation for a
primary respiratory disturbance. In the second case, compensation
occurs over days rather than hours.

If compensation results in
return of pH to normal then the patient is said to be fully
. But in many cases the compensation returns pH
towards normal without actually achieving normality; in such cases
the patient is said to be partially compensated.

reasons described above, metabolic alkalosis is very rarely fully

Mixed acid-base disturbances 

It might be assumed from the above discussion that
all patients with acid-base disturbance suffer from only one of the
four categories of acid-base balance. This may well be the case,
but in particular circumstances patients can present with more than
one disturbance.

For example, consider the patient with a chronic
lung disease such as emphysema who has a long-standing partially
compensated respiratory acidosis. If this patient were also a
diabetic who had not taken his normal insulin dose and as a result
was in a state of diabetic ketoacidosis, blood gas results would
reflect the combined effect of both respiratory acidosis and
metabolic acidosis.

Such mixed acid-base disturbances are not
infrequent and may be difficult to unravel on the basis of arterial
blood gas results alone.


The maintenance of normal blood pH involves several organ systems
and depends on circulatory integrity. It is not surprising then
that disturbance of acid-base balance can complicate the course of
widely diverse diseases as well as trauma to many parts of the
body. The body has considerable power to preserve blood pH, and
disturbances usually imply either severe chronic disease or acute
critical illness.

The results of arterial blood gas analysis can
identify acid–base disturbance and provide valuable information as
to its cause.   

Some suggested further

  • Thomson WST, Adams JF, Cowan RA. Clinical acid-base
    balance. Oxford: Oxford Medical Publications 1997 
  • Harrison RA. Acid-base balance. Respir Care Clin N. America
    1995; 1,1: 7-21
  • Woodrow P. Arterial blood gas analysis. Nursing Standard
    2004; 18,21: 45-52
  • Sirker AA, Rhodes A, Gounds RM, Bennet ED. Acid-base
    physiology: the ‘traditional’ and the ‘modern’ approach.
    Anaesthesia 2002; 57: 348-56   

Evaluation of respiratory alkalosis – Differential diagnosis of symptoms

Respiratory alkalosis is a systemic acid-base disorder characterized by a primary reduction in arterial partial pressure of carbon dioxide (PaCO₂), which produces an elevation in pH above 7.45, and consequent decrease in bicarbonate (HCO₃-) concentration, as buffering mechanisms.[1]Arbus GS, Herbert LA, Levesque PR, et al. Characterization and clinical application of the “significance band” for acute respiratory alkalosis. N Engl J Med. 1969 Jan 16;280(3):117-23.
It may occur as a simple primary disorder, a sole respiratory abnormality in which a decrease in PaCO₂ results from excess alveolar CO₂ excretion relative to CO₂ production. Respiratory alkalosis may also occur as compensation for an underlying process, such as metabolic acidosis, or as a separate component of a mixed acid-base disorder, in which case the PaCO₂, HCO₃-, and pH are determined by the combined effects of the underlying acid-base disorders.[2]Foster GT, Varizi ND, Sassoon CS. Respiratory alkalosis. Respir Care. 2001 Apr;46(4):384-91.

Respiratory alkalosis can be classified into three categories:

  1. as a component of disease processes

  2. accidentally induced

  3. deliberately induced (therapeutic).[3]Laffey JG, Kavanagh BP. Hypocapnia. N Engl J Med. 2002 Jul 4;347(1):43-53.

Accidental respiratory alkalosis develops as a consequence of inappropriate settings of mechanical ventilation, or associated with extracorporeal membrane oxygenation.[3]Laffey JG, Kavanagh BP. Hypocapnia. N Engl J Med. 2002 Jul 4;347(1):43-53.
Therapeutic respiratory alkalosis or hypocapnia has been applied to temporarily treat intracranial hypertension or neonatal pulmonary artery hypertension.[4]Allen CH, Ward JD. An evidence-based approach to management of increased intracranial pressure. Crit Care Clin. 1998 Jul;14(3):485-95.
[5]Walsh-Sukys MC, Tyson JE, Wright LL, et al. Persistent pulmonary hypertension of the newborn in the era before nitric oxide: practice variation and outcomes. Pediatrics. 2000 Jan;105(1 Pt 1):14-20.


Respiratory alkalosis is common. Two large studies of inpatients from the US evaluating arterial blood samples showed a respiratory alkalosis prevalence of 22.5% to 44.7%.[6]Hodgkin JE, Soeprono FF, Chan DM. Incidence of metabolic alkalemia in hospitalized patients. Crit Care Med. 1980 Dec;8(12):725-8.
[7]Mazzara JT, Ayres SM, Grace WJ. Extreme hypocapnia in the critically ill patient. Am J Med. 1974 Apr;56(4):450-6.
Because arterial blood was withdrawn at various times in the patients’ hospital course, these figures probably represent instances of respiratory alkalosis from disparate categories. In an Italian study, arterial blood samples obtained from 110 consecutive patients at the time of hospital admission demonstrated respiratory alkalosis in 24%.[8]Palange P, Carlone S, Galassetti P, et al. Incidence of acid-base and electrolyte disturbances in a general hospital: a study of 110 consecutive admissions. Recenti Prog Med. 1990 Dec;81(12):788-91.

The occurrence of accidentally induced respiratory alkalosis may be inferred from a retrospective study of intubated patients with burns (146 people) who received mechanical ventilation for aeromedical transport. The frequency of respiratory alkalosis was 19%, in which 39% of patients received volume-assist control and 17% of patients on intermittent mandatory ventilation experienced hypocapnia.[9]Barillo DJ, Dickerson EE, Cioffi WG, et al. Pressure-controlled ventilation for the long-range aeromedical transport of patients with burns. J Burn Care Rehabil. 1997 May-Jun;18(3):200-5.
[10]Hooper RG, Browning M. Acid-base changes and ventilator mode during maintenance ventilation. Crit Care Med. 1985 Jan;13(1):44-5.
In volume-assist control (or volume control), patients may receive either controlled or assisted breaths. When the patient triggers the ventilator, a breath of identical duration and magnitude is delivered from the machine. In intermittent mandatory ventilation, machine breaths are interposed among the patient’s spontaneous breaths. Yet another study reported that the majority of patients undergoing cardiopulmonary bypass (86 people) were hypocapnic during the rewarming phase, and that this disorder persisted in many until the time of ICU arrival.[11]Millar SM, Alston RP, Andrews PJ, et al. Cerebral hypoperfusion in immediate postoperative period following coronary artery bypass grafting, heart valve, and abdominal aortic surgery. Br J Anesth. 2001 Aug;87(2):229-36.

The study did not report the actual frequency of hypocapnia.[11]Millar SM, Alston RP, Andrews PJ, et al. Cerebral hypoperfusion in immediate postoperative period following coronary artery bypass grafting, heart valve, and abdominal aortic surgery. Br J Anesth. 2001 Aug;87(2):229-36.


Therapeutic respiratory alkalosis or hypocapnia has traditionally been applied to temporarily treat intracranial hypertension.[4]Allen CH, Ward JD. An evidence-based approach to management of increased intracranial pressure. Crit Care Clin. 1998 Jul;14(3):485-95.
However, the benefit of therapeutic hypocapnia remains unproven and it should be limited to life-threatening elevated intracranial pressure.[12]Curley G, Kavanagh BP, Laffey JG. Hypocapnia and the injured brain: more harm than benefit. Crit Care Med. 2010 May;38(5):1348-59.
[13]Badjatia N, Carney N, Crocco TJ, et al; Brain Trauma Foundation; BTF Center for Guidelines Management. Guidelines for prehospital management of traumatic brain injury 2nd edition. Prehosp Emerg Care. 2008;12(suppl 1):S1-S52.
Its application in either elevated intracranial pressure or neonatal pulmonary hypertension has not been shown to improve survival, and therefore its use should be carefully limited.[3]Laffey JG, Kavanagh BP. Hypocapnia. N Engl J Med. 2002 Jul 4;347(1):43-53.
[5]Walsh-Sukys MC, Tyson JE, Wright LL, et al. Persistent pulmonary hypertension of the newborn in the era before nitric oxide: practice variation and outcomes. Pediatrics. 2000 Jan;105(1 Pt 1):14-20.
[14]Rusnak M, Janciak I, Majdan M, et al. Severe traumatic brain injury in Austria VI: effects of guideline-based management. Wien Klin Wochenschr. 2007 Feb;119(1-2):64-71.
With the availability of nitric oxide and other vasodilators, therapeutic hypocapnia application in neonatal pulmonary hypertension will be expected to decline.[15]Latini G, Del Vecchio A, De Felice C, et al. Persistent pulmonary hypertension of the newborn: therapeutical approach. Mini Rev Med Chem. 2008 Dec;8(14):1507-13.
[16]Kelly LE, Ohlsson A, Shah PS. Sildenafil for pulmonary hypertension in neonates. Cochrane Database Syst Rev. 2017 Aug 4;(8):CD005494.



In respiratory alkalosis, initial suppression of the respiratory center and reduction in plasma bicarbonate concentration attenuate the rise in pH. Excess CO₂ excretion (alveolar hyperventilation) and the resulting low arterial PaCO₂ (hypocapnia) inhibits the respiratory centre through a negative feedback loop. The systemic effect of the initial reduction in PaCO₂ can be described by the modified Henderson-Hasselbalch equation as follows:

The decrease in PaCO₂ reduces the PaCO₂/HCO₃- ratio, hence reducing the H+ concentration, which results in alkalemia. The decrease in PCO₂ also leads to a reduced rate of H+ secretion and increased rate of bicarbonate excretion by the renal tubules as an intracellular buffering mechanism. 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+. Alkalemia inhibits carbonic anhydrase activity, resulting in reduced H+ secretion into the renal tubule.[17]Jacobson HR. Effects of CO2 and acetazolamide on bicarbonate and fluid transport in rabbit proximal tubules. Am J Physiol. 1981 Jan;240(1):F54-62.
HCO₃- reabsorption is dependent on combining with H+ to form carbonic acid, which later dissociates into H₂O and CO₂. Owing to the reduced H+ concentration in the renal tubule, there is inadequate H+ concentration to react with the filtered HCO₃-. HCO₃- reabsorption decreases, resulting in reduced plasma HCO₃- concentration and attenuation of pH.

The physicochemical (Stewart or strong ion difference) approach to acid-base analysis similarly shows that acute hyperventilation and fall in PaCO₂ slowly lead to hyperchloremic renal compensation. The hyperchloremia is related to excretion of filtered sodium and potassium with bicarbonate as hydrogen secretion decreases in proximal and distal tubules. As the plasma strong ion difference decreases, the plasma bicarbonate concentration decreases, resulting in the return of serum pH towards normal. Both the traditional and the Stewart approaches illustrate that renal compensation is caused by a change in the ratio of PaCO₂ to bicarbonate (see above modified Henderson-Hasselbalch equation).[18]Seifter JL. Integration of acid-base and electrolyte disorders. N Engl J Med. 2014 Nov 6;371(19):1821-31.

Respiratory alkalosis can manifest as acute or chronic. Acute respiratory alkalosis occurs from the onset of hypocapnia for up to 6 hours.[1]Arbus GS, Herbert LA, Levesque PR, et al. Characterization and clinical application of the “significance band” for acute respiratory alkalosis. N Engl J Med. 1969 Jan 16;280(3):117-23.
Chronic respiratory alkalosis with renal compensatory mechanisms begins 6 hours after the onset of hypocapnia and becomes complete within 2 to 5 days.[1]Arbus GS, Herbert LA, Levesque PR, et al. Characterization and clinical application of the “significance band” for acute respiratory alkalosis. N Engl J Med. 1969 Jan 16;280(3):117-23.
[19]Santra G, Paul R, Das S, et al. Hyperventilation of pregnancy presenting with flaccid quadriparesis due to hypokalaemia secondary to respiratory alkalosis. J Assoc Physicians India. 2014;62:536-538
[20]Berend K, de Vries AP, Gans RO. Physiological approach to assessment of acid-base disturbances. N Engl J Med. 2014 Oct 9;371(15):1434-45.
In acute respiratory alkalosis, the relationship between the decrease in serum HCO₃- and the decrease in PaCO₂ can be expressed as:

where the decrease in HCO₃- is from a normal value of 24 mEq/L and the decrease in PaCO₂ is from a normal value of 40 mmHg. For instance, an acute decrease in PaCO₂ of 20 mmHg will result in serum HCO₃- of approximately 22 mEq/L : that is, a decrease of 2 mEq/L (0.1 x 20) from the normal value of serum HCO₃- of 24 mEq/L. Notable deviation of serum HCO₃- concentration from the predicted value suggests acid-base disorder other than isolated acute respiratory alkalosis.

In chronic respiratory alkalosis, serum HCO₃- is further reduced owing to suppression of renal tubular H+ secretion and HCO₃- reabsorption. Thus, the magnitude of the decrease in H+ concentration is attenuated to a greater extent than in the acute stage. In chronic respiratory alkalosis, the relation between the decrease in serum HCO₃- and the decrease in PaCO₂ can be expressed as:[21]Gennari FJ, Goldstein MB, Schwartz WB. The nature of the renal adaptation to chronic hypocapnia. J Clin Invest. 1972 Jul;51(7):1722-30.

[22]Krapf R, Beeler I, Hertner D, et al. Chronic respiratory alkalosis: the effect of sustained hyperventilation on renal regulation of acid-base equilibrium. N Engl J Med. 1991 May 16;324(20):1394-401.

In this instance, a persistent decrease in PaCO₂ of 20 mmHg will decrease serum HCO₃- by 8 mEq/L from its normal value of 24 mEq/L, resulting in serum HCO₃- of 16 mEq/L. In patients with isolated chronic respiratory alkalosis, serum HCO₃- rarely decreases below 12 to 14 mEq/L.[20]Berend K, de Vries AP, Gans RO. Physiological approach to assessment of acid-base disturbances. N Engl J Med. 2014 Oct 9;371(15):1434-45.

Respiratory alkalosis leads to increased serum lactate by mildly increasing lactate production and by decreasing lactate clearance.[23]Eldridge F, Salzer J. Effect of respiratory alkalosis on blood lactate and pyruvate in humans. J Appl Physiol. 1967 Mar;22(3):461-8.
[24]Druml W, Grimm G, Laggner AN, et al. Lactic acid kinetics in respiratory acidosis. Crit Care Med. 1991 Sep;19(9):1120-4.
Interestingly, in one small study, induced respiratory alkalosis in trained athletes by voluntary hyperventilation has been shown to attenuate performance decline as measured by peak and mean power output in repeated sprinting. This is thought to be due to retardation of the acidosis caused by exercise-induced lactic acidosis.[25]Sakamoto A, Naito H, Chow CM. Hyperventilation as a strategy for improved repeated sprint performance. J Strength Cond Res. 2014 Apr;28(4):1119-26.

Respiratory alkalosis also alters electrolyte homeostasis, separate from its renal compensatory mechanisms.


  • Initially, hyperkalemia occurs owing to hyperventilation-induced augmentation of alpha-adrenergic activity. Afterwards, hypokalemia ensues owing to transcellular shift, decreased renal reabsorption, and bicarbonaturia. Bicarbonaturia increases renal potassium excretion.[26]Krapf R, Caduff P, Wagdi P, et al. Plasma potassium response to acute respiratory alkalosis. Kidney Int. 1995 Jan;47(1):217-24.
    [27]Sanchez MG, Finlayson DC. Dynamics of serum potassium change during acute respiratory alkalosis. Can Anaesth Soc J. 1978 Nov;25(6):495-8.
    Hypokalemia is usually mild but can be severe in pregnant women due to high circulating progesterone levels causing hyperventilation and respiratory alkalosis. One case report described a patient with respiratory alkalosis-induced hypokalemia leading to flaccid paralysis.[19]Santra G, Paul R, Das S, et al. Hyperventilation of pregnancy presenting with flaccid quadriparesis due to hypokalaemia secondary to respiratory alkalosis. J Assoc Physicians India. 2014;62:536-538


  • In the acute phase, hypophosphatemia may be related to increased cellular uptake.[28]Brautbar N, Leibovici H, Massry SG. On the mechanism of hypophosphatemia during acute hyperventilation: evidence for increased muscle glycolysis. Miner Electrolyte Metab. 1983 Jan-Feb;9(1):45-50.
    [29]Hoppe A, Metler M, Berndt TJ. Effect of respiratory alkalosis on renal phosphate excretion. Am J Physiol. 1982 Nov;243(5):F471-5.
    Conversely, the chronic phase is associated with hyperphosphatemia together with hypocalcemia due to parathyroid hormone resistance.[30]Krapf R, Jaeger P, Hulter HN. Chronic respiratory alkalosis induces renal PTH-resistance, hyperphosphatemia, and hypocalcemia in humans. Kidney Int. 1992 Sep;42(3):727-34.

Bronchoconstriction is a prominent manifestation of physiologic changes in the lung.[31]Jamison JP, Glover PJ, Wallace WF. Comparison of the effects of inhaled ipratropium bromide and salbutamol on the bronchoconstrictor response to hypocapnic hyperventilation in normal subjects. Thorax. 1987 Oct;42(10):809-14.

[32]Rodriguez-Roisin R. Gas exchange abnormalities in asthma. Lung. 1990;168(Suppl):599-605.
[33]Bayindir O, Akpinar B, Ozbek U, et al. The hazardous effects of alveolar hypocapnia on lung mechanics during weaning from cardiopulmonary bypass. Perfusion. 2000 Jan;15(1):27-31.
Effects on the pulmonary artery, and pH-related changes in respiratory alkalosis, can induce pulmonary arterial vasodilation, which is used commonly to treat neonatal persistent pulmonary hypertension.[5]Walsh-Sukys MC, Tyson JE, Wright LL, et al. Persistent pulmonary hypertension of the newborn in the era before nitric oxide: practice variation and outcomes. Pediatrics. 2000 Jan;105(1 Pt 1):14-20.
[34]Fike CD, Hansen TN. The effect of alkalosis on hypoxia-induced vasoconstriction in lungs of newborn rabbits. Pediatr Res. 1989 Apr;25(4):383-8.
Tachycardia is also consistent with physiologic changes inherent in respiratory alkalosis and is related to increased sympathetic activity and to hypokalemia.[26]Krapf R, Caduff P, Wagdi P, et al. Plasma potassium response to acute respiratory alkalosis. Kidney Int. 1995 Jan;47(1):217-24.
[35]Samuelsson RG, Nagy G. Effects of respiratory alkalosis and acidosis on myocardial excitation. Acta Physiol Scand. 1976 Jun;97(2):158-65.
Chest pain may occur through coronary vasospasm or decreased myocardial oxygen delivery owing to increased O₂ affinity to hemoglobin.[36]Neill WA, Hattenhauer M. Impairment of myocardial O2 supply due to hyperventilation. Circulation. 1975 Nov;52(5):854-8.

Data also suggest that respiratory alkalosis significantly decreased in vivo microcirculatory flow as measured by reflectance confocal microscopy during states of sustained hypocapnia (PaCO₂ 20.9 ± 2.9). This was seen without concomitant decrease in cardiac output.[37]Morel J, Gergelé L, Dominé A, et al. The venous-arterial difference in CO2 should be interpreted with caution in case of respiratory alkalosis in healthy volunteers. J Clin Monit Comput. 2017 Aug;31(4):701-707.
Ventricular and atrial arrhythmias have also been reported in acute and chronic respiratory alkalosis.[38]Wildenthal K, Fuller DS, Shapiro W. Paroxysmal atrial arrhythmias induced by hyperventilation. Am J Cardiol. 1968 Mar;21(3):436-41.
[39]Hisano K, Matsuguchi T, Ootsubo H, et al. Hyperventilation-induced variant angina with ventricular tachycardia. Am Heart J. 1984 Aug;108(2):423-5.
[40]Brown EB Jr, Miller F. Ventricular fibrillation following a rapid fall in alveolar carbon dioxide concentration. Am J Physiol.1952 Apr;169(1):56-60.

Gastrointestinal and hepatic symptoms are seen in acute (but not in chronic) respiratory alkalosis. Acute respiratory alkalosis produces nausea, vomiting, and increased GI motility.[41]Bharucha AE, Camilleri M, Ford MJ, et al. Hyperventilation alters colonic motor and sensory function: effects and mechanisms in humans. Gastroenterology. 1996 Aug;111(2):368-77.
The mechanism for increased colonic tone is dependent on the presence of hypocapnia (and not eucapnic hyperventilation), which seems to have a direct effect on colonic smooth muscle.[42]Ford MJ, Camelleri MJ, Hanson RB, et al. Hyperventilation, central autonomic control, and colonic tone in humans. Gut. 1995 Oct;37(4):499-504.

Peripheral and CNS effects of hypocapnia occur at a threshold of PaCO₂ <20 mmHg.[43]Rafferty GF, Saisch GN, Gardner WN. Relation of hypocapnic symptoms to rate of fall of end-tidal PCO2 in normal subjects. Respir Med. 1992 Jul;86(4):335-40.
Symptoms include vertigo, dizziness, anxiety, euphoria, clumsiness, forgetfulness, hallucinations, and seizure.[44]Perkin GD, Joseph R. Neurological manifestations of the hyperventilation syndrome. J R Soc Med. 1986 Aug;79(8):448-50.

Unilateral somatic symptoms have also been reported, including partial seizures, migraines, or stroke-like symptoms. CNS symptoms are initiated by changes in pH (rather than changes in PaCO₂), which reduce cerebral blood flow, causing cerebral ischemia that ultimately accounts for neurologic symptoms.[45]Gardner WN. The pathophysiology of hyperventilation disorders. Chest. 1996 Feb;109(2):516-34.
Peripheral manifestations include tetany and paresthesias. These neurologic manifestations are mediated by hyperventilation-induced increased neural excitability caused by hypocalcemia and, possibly, hypophosphatemia.[45]Gardner WN. The pathophysiology of hyperventilation disorders. Chest. 1996 Feb;109(2):516-34.
[46]Macefield G, Burke D. Paraesthesiae and tetany induced by voluntary hyperventilation: increased excitability of human cutaneous and motor axons. Brain. 1991 Feb;114 ( Pt 1B):527-40.
[47]Edmondson JW, Brashear RE, Li TK. Tetany: quantitative interrelationships between calcium and alkalosis. Am J Physiol. 1975 Apr;228(4):1082-6.

In determining whether a second primary acid-base process coexists with respiratory alkalosis, the pH is a key factor, because compensatory mechanisms do not restore the pH entirely. Significant deviations of HCO₃- concentration predicted in acute, or in chronic, respiratory alkalosis indicate a second primary acid-base process. Note that serum HCO₃- rarely decreases below 12 to 14 mEq/L in isolated chronic respiratory alkalosis and values below this suggest an independent component of metabolic acidosis.[48]Kaehny WD. Respiratory acid-base disorders. Med Clin North Am. 1983 Jul;67(4):915-28.
If hypocapnia occurs with acidemia, a primary respiratory alkalosis is present, if the degree of hypocapnia is greater than would be expected in response to the coexisting metabolic acidosis.

90,000 Hyperventilation is … What is Hyperventilation?

Hyperventilation (from ancient Greek ὑπέρ – above, above + lat. ventilatio ventilation ) – intensive breathing that exceeds the body’s oxygen demand. Distinguish between hyperventilation as a symptom of the disease and hyperventilation in diving (controlled and uncontrolled). There are also special breathing techniques based on hyperventilation.

Physiology of hyperventilation

Breathing carries out gas exchange between the external environment and alveolar air, the composition of which under normal conditions varies in a narrow range.With hyperventilation, the oxygen content rises slightly (by 40-50% of the initial), but with further hyperventilation (about a minute or more), the content of CO 2 in the alveoli decreases significantly, as a result of which the level of carbon dioxide in the blood falls below normal (this condition is called hypocapnia). Hypocapnia in the lungs with deep breathing shifts the pH to the alkaline side, which changes the activity of enzymes and vitamins. This change in the activity of metabolic regulators disrupts the normal course of metabolic processes and leads to cell death.To maintain the constancy of CO 2 in the lungs, the following defense mechanisms have emerged in the process of evolution:

  • spasms of the bronchi and blood vessels;
  • increase in the production of cholesterol in the liver as a biological insulator that thickens cell membranes in the lungs and blood vessels;
  • decrease in blood pressure (hypotension), reducing the excretion of CO 2 from the body.

But spasms of the bronchi and blood vessels reduce the flow of oxygen to the cells of the brain, heart, kidneys and other organs.A decrease in CO 2 in the blood increases the bond between oxygen and hemoglobin and makes it difficult for oxygen to enter the cells (the Verigo-Bohr effect). A decrease in oxygen supply to tissues causes oxygen starvation of tissues – hypoxia. Hypoxia, in turn, leads first to loss of consciousness, and then to the death of brain tissue.

Hyperventilation in diving

Controlled hyperventilation

Effective use of your lungs is paramount in diving.To increase the supply of oxygen before a dive, controlled hyperventilation is used – the diver makes several deep and quick breaths (in no case allowing hypoxia) and dives while inhaling. Excessive hyperventilation before diving can lead to loss of consciousness at shallow depths (and thus become uncontrollable).

Uncontrolled hyperventilation

Uncontrolled hyperventilation can occur as a result of any physical activity and leads to unwanted brain hypoxia.So, it can be when running, cycling, but it is especially dangerous with intensive swimming, since in the latter case, loss of consciousness will lead to drowning.

Prevention of loss of consciousness with hyperventilation

For most healthy people, the first signs of hypoxia are light-headedness or unconsciousness, anxiety, lack of bodily sensations, which due to inexperience may be noticed too late. But with the timely detection of symptoms, it is enough to stop swimming on the surface of the water, roll over onto your back and hold your breath while inhaling until carbon dioxide accumulates in the blood and brain tissues.

Hyperventilation as a breathing technique

The use of breathing techniques based on hyperventilation allows one to enter an altered state of consciousness. However, such techniques are intended for occasional use [1] .

Hyperventilation as a symptom of the disease

Occurs with tachypnea (rapid shallow breathing) without a decrease in tidal volume, with an increase in the minute volume of respiration and alveolar ventilation.Distinguish between chronic (hyperventilation syndrome) and temporary hyperventilation. There are various causes of hyperventilation, in particular neurological and mental disorders [2] . In most cases, the cause is nervous tension. The attack can last for hours, but the usual duration of a hyperventilating attack is 20-30 minutes. One way to interrupt such an attack (and sometimes prevent it) is to breathe in a paper bag to replace the exhaled carbon dioxide [3] .

See also



90,000 Hyperventilation / Helpful Hints / Spearfishing Portal

Hyperventilation is intensive pulmonary ventilation designed to increase the time the diver is underwater. A person breathes air, but atmospheric air is not the gas medium in which gas exchange takes place in the body. Higher mammals have developed such features of the respiratory system that they create their own gaseous environment, which is distinguished by its composition from atmospheric air.This environment is alveolar air.

The constancy of the composition of the alveolar air is explained by the fact that under normal conditions no more than 1/6 of the volume of air in the lungs is exchanged with each inhalation and exhalation.

The drop in the partial pressure of oxygen in the alveolar air is below 38 mm. Hg (5%) quickly leads to acute oxygen starvation of the brain, an increase in the partial pressure of oxygen up to 1.5 ata during many hours of breathing causes inflammation in the lungs, and an increase in the partial pressure of oxygen more than 3 ata leads to the occurrence of oxygen convulsions.An increase in the partial pressure of carbon dioxide in the alveolar air above 64 mm. rt. Art. quickly leads to carbon dioxide poisoning, and a sharp drop below 15 mm. rt. Art. – to stop breathing. A decrease in the partial pressure of carbon dioxide in the alveolar air occurs as a result of hyperventilation i.e. enhanced ventilation of the lungs.

In underwater sports, hyperventilation of the lungs is carried out by diving (before and immediately after diving), when breathing in an aqualung with increased breathing resistance, and with prolonged artificial respiration from mouth to mouth and from mouth to nose.An increase in the time of hyperventilation to 1-2 minutes leads to dizziness, and its further increase to loss of consciousness.

It should be added that all the data presented above are based on testing volunteers in EXCELLENT physical condition – and therefore can in no way serve as a starting point. There is a method for determining the individual maximum possible hyperventilation time, which is used in the French Navy:

Sit in a chair, take a stopwatch in your hands and relax for a couple of minutes.Then, starting the stopwatch, start breathing as deeply and as often as possible. Listen to yourself and, having caught the moment of slight dizziness, euphoria and creepy feet and hands, timed this time. Stop hyperventilating immediately !!! Keep in mind that its continuation can lead to fainting, which only a perfectly healthy organism can cope with without any problems (alas … such a minority). Based on this, I would advise to carry out experiments with hyperventilation of long duration immediately in the intensive care unit of the nearest emergency room.

Let’s go back to the experiment. You got the time usually within one minute. (If your result is greater, then this does not mean your superpowers !!! – it only means your deteriorated ability to feel your body !!!) Dividing the resulting time by 3 you have the maximum permissible hyperventilation time for you personally !!! For safety reasons, never exceed it !!!

It is known from practice that underwater swimmers and divers quite often deal with hyperventilation of the lungs.However, not all of them are aware of the dangers that lie in wait for theoretically untrained and inexperienced swimmers. In an adult at rest, pulmonary ventilation is 5 – 6 l / min. When swimming, running and other types of physical activity, the minute volume of respiration increases to 80 liters or more.

If pulmonary ventilation exceeds the body’s requirements, hyperventilation occurs. According to S. Miles (1971), hyperventilation occurs if the minute volume of respiration in a person at rest exceeds 22.5 liters.It is necessary to distinguish between short-term voluntary hyperventilation of the lungs, produced before diving, and prolonged, involuntary, which, as a rule, is accompanied by dizziness, loss of consciousness and sometimes ends in death from respiratory arrest.

Voluntary hyperventilation of the lungs is done before diving in order to stay underwater longer. This hyperventilation is performed by increasing and deepening breathing.

Before diving into the water, the diver can take 4-6 (and sometimes more) deep and quick breaths and exhalations without dizziness.If it occurs, you should hold your breath for 20-30 s, wait for the dizziness to stop, exhale, then take a deep breath again, that is, make a supply of air, and only after that dive. The appearance of dizziness is a sign of the onset of hypoxia (oxygen starvation of the brain)!

Involuntary hyperventilation may occur in swimmers in response to breathing with some additional resistance. This additional resistance is created by the breathing tube, which is included in the No. 1 diving equipment set.With such additional breathing resistance, adolescents, as well as people suffering from neurasthenia, and adult novice divers are especially susceptible to hyperventilation.

According to S. Miles (1971), those who master a new technique always have a feeling of anxiety, which may be accompanied by involuntary hyperventilation, sometimes leading to fainting. A. A. Askerov and V. I. Kronshtadsky-Karev (1971) found that in adolescents, when breathing with a small additional resistance, hyperventilation occurs in 40% of cases, and in adults – novice sportsmen-divers – in 25, 9% of cases.According to the research of J.S. Halden and J.G. Priestley (1937), even neurasthenia is accompanied by shallow breathing. Therefore, persons suffering from it, when swimming in set No. 1, should be especially careful.

Thus, snorkeling is not such a harmless activity and requires careful attention from both the divers and the coaches. In the literature on underwater sports, there are descriptions of the deaths of submariners who swam in set No. 1.Moreover, the authors consider the only cause of unhappiness to be a prolonged holding of breath when diving to a depth and the loss of consciousness associated with it from hypoxia, based on the fact that the dead were found at the bottom of the reservoir with a breathing tube clamped in their teeth.

However, there are cases that cannot be explained in this way. For example, in 1973 in Gelendzhik Bay, boy K. (age 15) swam in set No. 1 on the surface of the water. He looked at the inhabitants of the seabed. The depth of the bay in this place barely reached 1.5 m.By chance, the parents noticed that the son was in one place for a very long time, about 20 minutes, without moving. When they approached him, it turned out that he was already dead. In this case, the only cause of death could be only hyperventilation, which led to severe hypoxia and respiratory arrest.

JS Halden and JG Priestley (1937) give an example of how English dentists have successfully used pulmonary hyperventilation in their practice. They asked the patient to hyperventilate, there was a short-term loss of consciousness, and the extraction of teeth was carried out without pain. If a swimmer is found lying at the bottom of the reservoir, this does not mean that he lost consciousness during a prolonged breath-holding at depth.So, in 1971 in Alushta, sportsman-submariner 3., born in 1949, who sailed in set No. 1, was discovered 300 m from the coast at a depth of Yum. The breathing tube was clamped in his teeth, his hands pressed tightly to his chest. (By the way, the last two signs are characteristic of oxygen starvation of the brain.) After removing from the water, signs of the suction action of the mask (hemorrhages in the sclera and bleeding from the nose), as well as symptoms of ear barotrauma (bleeding from the ears), were revealed. a diving athlete, even a beginner, when diving to a depth equalizes the pressure in the mask space with the outer one.In this case, it is enough to make a slight exhalation with the nose under the mask. The presence of signs of ear crimping and barotrauma in an experienced submariner confirms that he went to the bottom, already being in an unconscious state. This means that the loss of consciousness occurred on the surface as a result of hyperventilation and subsequent hypoxia.

Pre-dive hyperventilation is done to increase the body’s oxygen stores, which allows the diver to stay underwater for longer periods.For example, V.I. Tyurin cites data that hyperventilation with air lengthens the time of arbitrary holding of breath relative to the initial value by 1.5 times, breathing with oxygen by 2.5 times, hyperventilation with oxygen by 3 times. It is important that hyperventilation with oxygen excludes loss of consciousness in a diver even with involuntary breath holding.

During hyperventilation, oxygen reserves in the body increase due to the following factors: an increase in its content in arterial blood by 2 -% ‘, a very significant increase in the partial pressure of oxygen in the alveolar air – by 40-50% against the initial; increase in oxygen tension in blood plasma.It should be borne in mind that tissue respiration is provided precisely by oxygen physically dissolved in the tissues. At rest, the blood plasma contains 0.3 ml of oxygen per 100 ml of blood, and when breathing pure oxygen – up to 22 ml (S.V. Anichkov, 1954). Oxygen dissolved in blood plasma is in almost complete equilibrium with alveolar air and determines the supply of oxygen to erythrocytes (AM Charny, 1961). Therefore, the higher the partial pressure of oxygen in the alveolar air, the more oxygen enters the blood plasma and interstitial fluid.Consequently, during hyperventilation, a sufficiently large supply of oxygen is created in the body, which makes it possible to significantly increase the time of arbitrary breath holding and the duration of the diver’s stay under water.

The indicated positive effect of voluntary hyperventilation is manifested only when it is performed correctly. If voluntary or involuntary hyperventilation is delayed, then a number of dysfunctions of some organs and organ systems appear in the body, which can lead not only to loss of consciousness, but also to respiratory arrest and death.

With prolonged hyperventilation, simultaneously with an increase in the oxygen content in the body, carbon dioxide is “washed out” from the lungs and its tension in the blood decreases – hypocapnia. Normally, the carbon dioxide content in the alveolar air remains at a constant level.

Carbon dioxide is the end product of metabolic processes in the body. It is a physiological irritant of the respiratory center and a regulator of the tone of blood vessels. A certain amount of carbon dioxide must be constantly present in the blood.The carbon dioxide content in arterial blood under normal conditions is 41 mm Hg. Art., in the venous – 43-45 mm Hg. Art. and in the alveolar air – about 40 mm Hg. Art. After hyperventilation, the partial pressure of carbon dioxide in the alveolar air decreases to 12-16 mm Hg. Art.

In response to the “flushing” of carbon dioxide from the lungs and blood, there is a reflex vasoconstriction of the cerebral vessels. This prevents excess removal of carbon dioxide from the brain tissue. Through constricted blood vessels, the flow of blood to the brain decreases sharply, and the supply of oxygen to the latter decreases, which leads to hypoxia even in the presence of an increased amount of oxygen in arterial blood after hyperventilation.

In the experiments of S. Schwartz and R. Breslau (1968), hyperventilation with oxygen at a pressure of 4 ata (0.4 MPa) did not lead to oxygen seizures due to a sharp spasm of cerebral vessels and a decrease in oxygen delivery to the brain. Although without hyperventilation under such oxygen pressure, oxygen cramps usually occur after 5-15 minutes. Breathing pure oxygen under high pressure without hyperventilation also leads to vasoconstriction in the brain, but not to the same extent as as a result of hypocapnia.The state of oxygen starvation of the brain during hyperventilation is aggravated by the development of hypoxic collapse. In this case, there is a decrease in vascular tone, expansion of blood vessels and capillaries and, consequently, the deposition and decrease in the volume of circulating blood, which, in turn, causes a drop in arterial blood pressure and increased hypoxia.

In addition to the narrowing of the cerebral vessels, the “flushing” of carbon dioxide from the lungs during hyperventilation leads to a change in the acid-base balance in the body towards alkalization.Gas alkalosis occurs, as the amount of acids in the body decreases. Alkalinization of blood and brain tissue leads to the fact that the affinity of hemoglobin for oxygen increases, the dissociation of oxy-hemoglobin worsens, that is, the elimination of oxygen from hemoglobin occurs with great difficulty. And even if there is a sufficient amount of oxygen in the blood, hemoglobin holds it firmly and makes it difficult to move to the brain tissues. This phenomenon was discovered by the Russian scientist B.F. Verigo in 1892, 10 years later it was confirmed by the students of X.Bohr in Copenhagen and as a result is called the Verigo-Bohr effect.

Further studies of the issue have shown that the affinity of hemoglobin for oxygen also increases with strong acidification of blood and brain tissues, for example, in a state of clinical death. Gas alkalosis with hyperventilation further enhances cerebral hypoxia and worsens the human condition. Hypoxia during hyperventilation with air is the root cause of all pathological disorders in the body. But this is only the initial reason.Further events are the result of the developed hypoxia. Hypoxia of the brain and respiratory center with prolonged hyperventilation with air can lead to respiratory arrest and a tragic outcome.

During hyperventilation with oxygen under atmospheric pressure, hypoxia does not occur, although the “washing out” of carbon dioxide and vasoconstriction of the cerebral vessels occurs in the same way as during hyperventilation with air. But consciousness is not lost at the same time. The high partial pressure of oxygen in this case ensures the course of metabolic processes in the brain.This confirms that hypoxia is ultimately the cause of loss of consciousness and respiratory arrest during hyperventilation with air.

Prevention of loss of consciousness during hyperventilation

When swimming in set No. 1, it is important to know the symptoms of the onset of oxygen starvation in the brain and the ability to prevent serious consequences that can occur during hyperventilation. When hypoxia of the brain occurs during hyperventilation, precursors of loss of consciousness appear, which are called aura (from lat.aura – a breath of breeze). This means that the initial symptoms of hypoxia are so weak that they are difficult to catch. True, on land they are more noticeable. These are dizziness, ringing in the ears, a state of mild stunning, a feeling of creeping in the limbs, paresthesia, and later – a painful feeling of lightheadedness, tremors of the limbs, impaired coordination of movements. During swimming with a breathing tube, the aura manifests itself only as a feeling of incomprehensible awkwardness, slight stunning and anxiety, which turns into a feeling of fear, and immediately before loss of consciousness – fear of death, which drives the swimmer to the shore.At the same time, the swimming speed increases, and the tragic outcome is accelerated. Meanwhile, if a feeling of awkwardness and anxiety arises, it is enough to stop swimming, turn on your back and hold your breath while inhaling as much as possible. There will be an accumulation of carbon dioxide in the blood and brain tissues, and good health will be restored.

“Sportsman Submariner” magazine

Artificial ventilation of the lungs at night in people with nervous, muscle or chest diseases who have persistent breathing problems

Review question

We reviewed the evidence for the effect of night-time ventilation in people with chronic (i.e.e. constant) difficulty breathing spontaneously due to diseases of the nerves, muscles or chest.


Weakness of the respiratory muscles or changes in respiratory control are major complications of nerve or muscle and chest disease. These problems can lead to hypoventilation, a condition in which not enough air gets into the lungs. Subsequently, people may need devices to help them breathe (mechanical ventilation).Artificial lung ventilation is widely used in people with nervous and muscular diseases or chest deformities, as a result of which chronic hypoventilation develops. We wanted to find out whether artificial ventilation at night actually improves survival and reduces symptoms of hypoventilation in this group and to compare different types of ventilation.

Research characteristics

This review includes 10 clinical trials involving 173 people with persistent, stable hypoventilation.Three clinical trials included only participants with motor neuron diseases, three other trials all participants had chest deformity only, and there was one clinical trial that included only participants with Duchenne muscular dystrophy. The remaining three clinical trials had mixed populations.

Clinical trials have compared mechanical ventilation with standard care (five trials), compared different ventilation methods (four trials), or both (one trial).

Key results and quality of evidence

We have found that artificial ventilation at night can alleviate the symptoms of chronic hypoventilation and prolong survival. However, the quality of the studies was very low. The benefits of long-term mechanical ventilation should be confirmed in further clinical trials.

Evidence is current to June 2014.

What is chronic hyperventilation?

Chronic hyperventilation is the physical act of constantly breathing in more air than the body needs.This is also known as excessive breathing. Hyperventilation syndrome (HVS) is a persistent condition that results from a lack of regulation of breathing after one episode of hyperventilation. There is no single known cause of HVS, although secondary psychological or physiological conditions can contribute to the development of acute and chronic cases of HVS. Treatment of chronic HVS often requires retraining of breathing and referral to a specialist, such as a therapist or psychiatrist.

Normal breathing contributes to the balance of oxygen and carbon dioxide levels in the blood. Rapid, shallow breathing associated with hyperventilation lowers blood carbon dioxide levels, leading to respiratory acidosis and restriction of blood vessels. When blood vessels are constricted, oxygenated blood is prevented from entering the brain, which impairs the functioning of the nervous and circulatory systems. Restoring the balance of oxygen and carbon dioxide levels in the bloodstream is essential for the proper regulation of numerous body systems.

Most cases of hyperventilation are caused by anxiety caused by a stressful or traumatic event or situation. Secondary physical conditions such as infection, heart attack, and asthma can cause a person to breathe shallowly, contributing to irregular breathing. Psychological disorders such as agoraphobia can contribute to symptoms of chronic hyperventilation. People with chronic hyperventilation syndrome will exhibit recurrent symptoms that establish a pattern of occurrence – this is the chronic 90 130 aspect of the problem.In severe cases of chronic hyperventilation, an individual may develop neurological disorders such as changes in vision or impaired mental functioning.

Traditional treatment for hyperventilation involves restoring carbon dioxide to the bloodstream. This can be achieved by inhaling a small paper bag. The paper bag can be effective in the short term as an intervention tool, but it can cause too much carbon dioxide to be reintroduced into the bloodstream if used for too long.When properly exercised, promoting deep, slow breathing in the abdomen will accomplish the same goal as a paper bag.

Medical attention should be sought when there are episodes of hyperventilation, as other diagnoses may carry the same symptoms. People in the midst of an episode may experience chest constriction or pain, lightheadedness, or numbness of the face or limbs. Treatment for episodes of hyperventilation depends on the severity of the episode and the resolution of secondary or underlying conditions. To alleviate immediate symptoms, treatment may include medication, trained breathing, chest compression to restore normal breathing, or, in severe cases, sedation.Options for relieving symptoms of chronic hyperventilation may include breathing retraining, relaxation exercises, and talking therapy.


Hyperventilation of the lungs, its symptoms of manifestation

Often stress leads to the fact that a person begins to breathe very deeply or shallowly. This is a temporary phenomenon that can pass quickly enough on its own or with the help of special techniques. However, the symptoms of lung disease sometimes appear in this way too.In this case, the diagnosis can only be made by first examining the patient.

Hyperventilation of the lungs and its manifestations

An attack of hyperventilation occurs as a result of increased ventilation of the lungs, which appears with increased frequency and increased breathing. At the same time, a large amount of carbon dioxide is released from the lungs, which leads to a decrease in it in the blood (hypocapnia). The acidity of the blood decreases, and it becomes more alkaline. Oxygen ceases to enter the tissues, which causes oxygen starvation (or hypoxia).

Pulmonary hyperventilation is temporary and chronic.

The causes of temporary hyperventilation are most often stress, fear, an attack of a panic attack, various neuroses. Adrenaline (“stress hormone”), which is released into the bloodstream, causes increased breathing. A similar condition appears with a lack of oxygen (high in the mountains), as well as due to the intake of certain medications that stimulate the respiratory center in the brain (the drug “Cititon”, all kinds of psychostimulants such as caffeine), with infectious diseases, high fever, bleeding, and so on.The duration of an attack usually ranges from half an hour to several hours (rarely).

Chronic hyperventilation of the lungs is a consequence of a disease accompanied by organic damage to the brain (trauma, tumor). It can be provoked by a heart attack with ischemia, arterial hypertension, and lung disease. With toxicosis in pregnant women, as well as in patients with renal failure, when various toxic substances accumulate in the blood, an attack of hyperventilation also occurs quite often.

Predisposing factors for the development of an attack are various diseases of the brain and nervous system, as well as the age factor – most often, hyperventilation of the lungs occurs in childhood (up to 12 years), with hormonal maturation in adolescents and in the elderly.

Signs of hyperventilation

Hyperventilation syndrome is accompanied by frequent shallow or, on the contrary, deep breathing, increasing anxiety, fear, dry mouth, palpitations, visual impairment, paresthesias (“goose bumps” on the skin, pain in the fingertips).With a prolonged and intense attack, there is a decrease in normal mental performance, disorientation, dizziness, and often fainting. Shifts in the biochemical blood test that occur during attacks of hyperventilation sometimes affect certain nerve structures, exciting them, which can lead to seizures.

With a significant decrease in the concentration of carbon dioxide in the blood, a decrease in blood pressure, narrowing of the lumen of blood vessels in the brain and redistribution of blood flow are likely.These factors impair the blood supply to the brain and heart.

Doctor’s help

During a visit to a medical facility, a doctor will be able to conduct a thorough examination, evaluate how a person breathes. If it is found that the breathing rate is not high enough, the doctor can show you how to breathe correctly.

If hyperventilation of the lungs is suspected, the following tests are carried out: electrocardiogram, chest x-ray, blood test for carbon dioxide and oxygen content, computed tomography of the chest, analysis of ventilation and blood supply to the lungs.

New device allows you to sober up just by breathing

Scientists have developed a new way to remove alcohol from the body. It is very simple: you just need to … breathe very deeply. And not to lose consciousness at the same time will help a new device that supplies the body with carbon dioxide.

The development is described in a scientific article published in Scientific Reports by a group led by Joseph Fisher of the University of Toronto.

The joke that “no blood was found in your alcohol” is not so funny.A lot of deaths happen due to the fact that drinkers inadvertently cross the line beyond which the concentration of alcohol in the blood becomes simply dangerous.

However, there is no way to remove the poison from the blood right on the spot. 90% of alcohol is excreted through the liver, and the only way to urgently help her in this matter is hemodialysis. However, this procedure can only be performed in a hospital.

Researchers have now tried a very simple method: hyperventilating the lungs. To put it simply, a person who has gone overboard needs to breathe deeply and often.In this case, alcohol is intensively removed from the blood.

“But you can’t just hyperventilate, because after a couple of minutes you will feel dizzy and pass out,” Fischer warns.

The fact is that during hyperventilation, too much carbon dioxide is removed from the blood. Meanwhile, a certain level of this substance is necessary for us for the normal functioning of the respiratory system.

To recoup this loss, the authors propose a simple approach.They designed an apparatus that included a carbon dioxide cylinder, a mask, and some other equally simple components. The whole structure turned out to be the size of a briefcase.

“This is a very simple, low-tech device that can be made anywhere in the world: no electronics, computers, or filters are required,” Fischer notes. “It’s almost impossible to explain why we didn’t try it [using it] decades ago.”

Five healthy adult male volunteers participated in the experiment.They drank enough to raise their blood alcohol concentration to 0.1% (moderate intoxication stage). The participants then breathed deeply and quickly, filling up the lack of carbon dioxide with the new apparatus.

Experiments have confirmed that in this way alcohol is excreted from the body at least three times faster than exclusively through the liver. And the new device allows a person not to lose consciousness from a lack of carbon dioxide in the blood.

Nevertheless, this does not mean that you should take a can of carbon dioxide with you to a party.After all, an excess of carbon dioxide in the inhaled air can lead to a deterioration in health and even loss of consciousness! It is necessary to monitor the CO level 2 (for which a special device is needed).

In addition, the new approach still needs to be thoroughly tested by third-party experts before it can be approved for mainstream use.

By the way, earlier Vesti.Ru talked about how alcoholic rats helped scientists find salvation for the liver.We also wrote about a unique case when it turned out that a woman’s bladder produces alcohol on its own.

90,000 Fast and deep breathing helps to remove alcohol from the body

Canadian scientists have shown for the first time that the rate of elimination of alcohol from the body can be increased by three times with hyperventilation. They also presented a device that will help keep enough carbon dioxide in the body during hyperventilation so that the patient does not lose consciousness.The research is published in Scientific Reports.

According to the World Health Organization, about 3 million people die every year from alcohol abuse. The ethanol contained in alcoholic beverages affects the body’s performance, for example, impaired brain function, blood circulation and even nail growth. And if a certain level of ethanol is exceeded, organs can be damaged, which, in turn, can lead to death. The prevalence and danger of alcohol forces scientists to look for new ways to save people from intoxication.

Typically 90% of alcohol is removed from the body by the liver, which works at a constant rate. Since the pace and volume of its work cannot be increased, other means must be used to protect against intoxication. Canadian scientists have found that the rate of elimination of alcohol from the body can be increased through hyperventilation – fast and deep breathing. This allows alcohol to be flushed out of the body three times faster than if only the liver were involved. “But you can’t just hyperventilate, because after a couple of minutes you will feel dizzy and pass out,” said Joseph Fisher, one of the researchers in the Department of Anesthesiology at the University of Toronto.This is due to the fact that during hyperventilation, carbon dioxide is also excreted from the body along with alcohol, which leads to such symptoms.

Canadian scientists have developed a device that allows a patient to get rid of alcohol by hyperventilating, while simultaneously returning the amount of carbon dioxide necessary for normal well-being to the body.