Hyperventilation syndrome (HVS) is characterized by excessive breathing that leads to respiratory alkalosis and associated symptoms like dizziness, tingling, and anxiety. It is often triggered by stress and panic attacks. While the exact cause is unknown, abnormal breathing patterns and a low threshold for stress responses are believed to play a role. Diagnosis is based on symptoms and blood gas analysis showing low carbon dioxide levels. Treatment focuses on breathing retraining and stress management.

1. Hyperventilation syndrome

2. • Hyperventilation syndrome (HVS) represents a
relatively common emergency department (ED)
presentation.
• HVS is a condition in which minute ventilation exceeds
metabolic demands, resulting in hemodynamic and
chemical changes that produce characteristic
dysphoric symptoms.
• Many patients with HVS do not manifest low PaCO2
during attacks.

3. • A better term for this syndrome might be
behavioral breathlessness or psychogenic
dyspnea, with hyperventilation seen as a
consequence rather than a cause of the
condition.
• Some patients may be physiologically at risk
for the development of psychogenic
dyspnea.
• Approximately 50% of patients with
panic disorder and 60% of patients with
agoraphobia manifest hyperventilation as a
symptom, whereas only 25% of patients with
HVS manifest panic disorder.

5. • Hyperpnea or hyperpnoea is increased depth of
breathing when required to meet metabolic
demand of body tissues, such as during or
following exercise, or when the body lacks
oxygen (hypoxia), for instance in high altitude or
as a result of anemia.
• Tachypnea differs from hyperpnea in that
tachypnea is rapid shallow breaths, while
hyperpnea is deep breaths.
• In hyperpnoea, the increased breathing rate is
desirable as it meets the metabolic needs of the
body.

6. • In hyperventilation, the rate of ventilation is
inappropriate for the body's needs (except in
respiratory acidosis, when CO2 needs to be
breathed off).
• The resulting decrease in CO2 concentration results
in the typical symptoms of :
light-headedness, tingling in peripheries, visual
disturbances etc.
• In hyperpnoea, there are generally no such
symptoms

8. Pathophysiology
• Patients with HVS tend to breathe by
using the upper thorax rather than the
diaphragm, and this results in chronic
over-inflation of the lungs.
• When stress induces a need to take a
deep breath, the deep breathing is
perceived as dyspnea.
• The sensation of dyspnea creates anxiety,
which encourages more deep breathing,
and a vicious circle is created.

9. Pathophysiology
• Patients with panic disorder have a lower
threshold for the fight-or-flight response.
• In susceptible patients, even minor
stresses can trigger the syndrome, which
then tends to manifest with primarily
psychiatric complaints (eg, fear of death,
impending doom, or claustrophobia).
• It is believed that HVS patients tend to
focus on somatic complaints related to the
physiologic changes produced by
hyperventilation.

10. Etiology
• The cause of HVS is unknown, but some persons
who are affected appear to have an abnormal
respiratory response to stress, sodium, lactate, and
other chemical and emotional triggers, which results
in excess minute ventilation and hypocarbia.
• In most patients, the mechanics of breathing are
disordered in a characteristic way. When stressed,
these patients rely on thoracic breathing rather than
diaphragmatic breathing, resulting in a hyper-
expanded chest and high residual lung volume.
• Because of the high residual volume, they are then
unable to take a normal tidal volume with the next
breath and consequently experience dyspnea.

11. Etiology
• Proprioceptors in the lung and chest wall
signal the brain with a “suffocation alarm”
that triggers release of excitatory
neurotransmitters that are responsible for
many of the symptoms such as
palpitations, tremor, anxiety, and
diaphoresis.
• The incidence of HVS is higher in first-
degree relatives than in the general
population, but no clear genetic factors
have been identified.

12. Epidemiology
• As many as 10% of patients in a general
internal medicine practice are reported to
have HVS as their primary diagnosis.
• The peak incidence is between the ages
of 15 and 55 years, but cases have been
reported in all age groups except infants.
• HVS has a strong female preponderance:
the female-to-male ratio may be as high as

13. Prognosis
• Patients with chronic HVS experience multiple
exacerbations throughout their lives.
• Children who experience acute HVS often continue this
pattern into adulthood.
• Many patients have associated disorders (eg,
agoraphobia) that may dominate the clinical picture.
• Patients who are treated with breathing retraining,
stress reduction therapy, and various medications (eg,
benzodiazepines or selective serotonin reuptake
inhibitors [SSRIs]) experience significant reductions in
the frequency and the severity of exacerbations.
• Death attributable to HVS is extremely rare.

15. Carpopedal spasm occurs when acute hypocarbia causes
reduced ionized calcium and phosphate levels, resulting in
involuntary contraction of the feet or (more commonly) the
hands .

16. Cardiac symptoms
• The chest pain associated with HVS usually has atypical
features, but on occasion, it may closely resemble
typical angina.
• It tends to last hours rather than minutes, and is often
relieved rather than provoked by exercise. It is usually
unrelieved by nitroglycerin.
• The diagnosis of HVS should be considered in young
patients without cardiac risk factors who present with
chest pain, particularly if the pain is associated with
paresthesias and carpo-pedal spasm.
• ECG abnormalities may include prolonged QT interval,
ST depression or elevation, and T-wave inversion.

17. Cardiac symptoms
• In patients with subcritical coronary artery
stenosis, the vasospasm induced by hypocarbia
may be sufficient to provoke myocardial injury.
• The incidence of HVS is high among patients
with mitral valve prolapse (MVP), and the chest
pain associated with MVP may be due to
hyperventilation.
• Prinzmetal angina (ie, coronary artery
vasospasm) is triggered by HVS, but the chest
pain associated with this syndrome normally
would be expected to respond to nitrates or
calcium channel blockers.

18. Central nervous system symptoms
• Central nervous system (CNS) symptoms occur because
hypocapnia causes reduced cerebral blood flow
(CBF).CBF decreases by 2% for every 1 mm Hg decrease
in PaCO2.
• Symptoms of dizziness, weakness, confusion, and
agitation are common . Patients may experience visual
hallucinations, syncope or seizure .
• Paresthesias occur more commonly in the upper
extremity and are usually bilateral. Perioral numbness is
very common.
Gastrointestinal symptoms
• (eg, bloating, belching, flatus, or epigastric pressure)
may result from aerophagia.

19. Metabolic changes
• Acute metabolic changes result from intracellular shifts and
increased protein binding of various electrolytes during
respiratory alkalosis.
• Acute secondary hypocalcemia can result in carpopedal
spasm, muscle twitching, a prolonged QT interval, and
positive Chvostek and Trousseau signs.
• Hypokalemia tends to be less pronounced than
hypocalcemia but can produce generalized weakness.
• Acute secondary hypophosphatemia is common and may
contribute to paresthesias and generalized weakness.

20. Chvostek’s sign is twitching of facial muscles in response to
tapping over the area of the facial nerve
Trousseau’s sign is carpopedal spasm that results from
ischemia, such as that induced by pressure applied to the upper
arm from an inflated sphygmomanometer cuff .

21. • Chvostek’s sign is neither sensitive nor specific
for hypocalcemia, since it is absent in about one
third of patients with hypocalcemia and is present
in approximately 10% of persons with normal
calcium levels.
• Trousseau’s sign is more sensitive and
specific; it is present in 94% of patients with
hypo-calcemia and in only 1% of persons with
normal calcium levels.

22. Differential Diagnoses :
• Asthma
• Atrial Fibrillation
• Myocardial Infarction
• Diabetic Ketoacidosis
• Metabolic Acidosis
• Nasopharyngeal Stenosis
• Pneumothorax, Pneumomediastinum
• Pulmonary Embolism
• Respiratory Distress Syndrome, Adult
• Carbon monoxide poisoning
• Panic Disorders

23. Approach Considerations
• Upon a first attack of acute HVS, the diagnosis depends
on recognizing the typical constellation of signs and
symptoms and ruling out the serious conditions that can
cause the presenting symptoms.
• Acute coronary syndrome (ACS) and pulmonary
embolism (PE) are the 2 most common serious entities
that may present similarly to HVS.
• Clinical assessment is sufficient to rule these out.
• A standard workup for atypical chest pain, including
pulse oximetry, chest radiography, and ECG, may still be
warranted depending on the clinical picture.

24. Approach Considerations
• Patients with a history of HVS who have undergone an
appropriate workup at some earlier time may not need
any further laboratory evaluation in the setting of a
recurrence. Recognition of the typical constellation of
dyspnea, agitation, dizziness, atypical chest pain,
tachypnea and hyperpnea, paresthesias, and
carpopedal spasm in a young, otherwise healthy patient
with an adequate prior evaluation is sufficient to make
the diagnosis.
• A low pulse oximetry reading in a patient who is
hyperventilating should never be attributed to HVS. The
patient should always be evaluated for other causes of
hyperventilation.

25. Approach Considerations
•ABG is indicated if any doubt exists as to the
patient’s underlying respiratory status; it may be
helpful when HVS-induced acidosis is suspected,
or when shunting or impaired pulmonary gas
exchange is considered.

26. Approach Considerations
• ABG sampling confirms a compensated
respiratory alkalosis in a majority of cases. The
pH is typically near normal, with a low PaCO2
and a low bicarbonate level.
• ABG sampling is also useful in ruling out
toxicity from carbon monoxide poisoning, which
may present similarly to HVS.
• Toxicology screening is indicated.
• If acute PE is being considered, ELISA D-dimer
assay may be helpful.

27. Approach Considerations
• Imaging studies are not indicated when the
diagnosis of HVS is clear.
• Because PE can present with findings identical
to those of HVS, a first-ever episode of acute
HVS may warrant V/Q scanning or CT
pulmonary angiography to rule out perfusion
defects.
• Chest radiography is indicated for patients who
are at high risk for cardiac or pulmonary
pathology.

28. Approach Considerations
• ECG changes are common and may include the
following:
1- ST depression or elevation
2- Prolonged QT interval
3- T-wave inversion
4- Sinus tachycardia
• Rebreathing into a paper bag is not recommended in
the field. Deaths have occurred in patients with acute
myocardial infarction (MI), pneumothorax, and
pulmonary embolism (PE) who were initially
misdiagnosed with HVS and treated with paper bag
rebreathing.

29. Breathing Techniques
• Rebreathing into a paper bag is no longer a recommended
technique, because significant hypoxia and death have been
reported
• . Moreover, carbon dioxide itself may be a chemical trigger for
anxiety in these patients.
• Simple reassurance and an explanation of how hyperventilation
produces the patient’s symptoms are usually sufficient to
terminate the episode.
• Provoking the symptoms by having the patient voluntarily
hyperventilate for 3-4 minutes often convinces the patient of the
diagnosis.

30. Breathing Techniques
• Most patients with HVS tend to breathe with the upper
thorax and have hyper-inflated lungs throughout the
respiratory cycle. Because residual lung volume is high,
they are unable to achieve full tidal volume and
experience dyspnea.
• Physically compressing the upper thorax and having
patients exhale maximally decreases hyperinflation of
the lungs.
• Instructing patients to breathe abdominally, using the
diaphragm more than the chest wall, often leads to
improvement in subjective dyspnea and eventually
corrects many of the associated symptoms.

31. What is “calm breathing”?
• Calm breathing (sometimes called “diaphragmatic
breathing”) is a technique that helps you slow down
your breathing when feeling stressed or anxious.
• Newborn babies naturally breathe this way, and singers,
wind instrument players, and yoga practitioners use this
type of breathing.
• Diaphragmatic breathing slows the respiratory rate,
gives patients a distracting maneuver to perform when
attacks occur, and provides patients with a sense of
self-control during episodes of hyperventilation.
• This technique has been shown to be very effective in a
high proportion of patients with HVS.

32. How to Do It?
• Calm breathing involves taking smooth,
slow, and regular breaths.
• Sitting upright is usually better than
lying down or slouching, because it can
increase the capacity of your lungs to fill
with air.
• It is best to 'take the weight' off your
shoulders by supporting your arms on
the side-arms of a chair, or on your lap.

33. How to Do It ?
1. Take a slow breath in through the nose, breathing into
your lower belly (for about 4 seconds)
2. Hold your breath for 1 or 2 seconds
3. Exhale slowly through the mouth (for about 4 seconds)
4. Wait a few seconds before taking another breath
• About 6-8 breathing cycles per minute is often helpful to
decrease anxiety, but find your own comfortable
breathing rhythm.
• These cycles regulate the amount of oxygen you take in
so that you do not experience the fainting, tingling, and
giddy sensations that are sometimes associated with
overbreathing.

34. Pharmacologic Therapy
• Benzodiazepines are useful in the treatment of hyperventilation
resulting from anxiety and panic attacks.
• Lorazepam (ativan) is a sedative-hypnotic of the
benzodiazepine class that has a short time to onset of effect
and a relatively long half-life.
• Diazepam (valium) depresses all levels of the CNS (eg, limbic
and reticular formation), possibly by increasing the activity of
GABA. It is considered second-line therapy for seizures.
• Paroxetine (paxil) is the alternative drug of choice for HVS. It is
a potent selective inhibitor of neuronal reuptake of serotonin
and has a weak effect on neuronal reuptake of norepinephrine
and dopamine.