Hyperventilation syndrome
BY
AHMAD YOUNES
PROFESSOR OF THORACIC MEDICINE
Mansoura faculty of medicine
Hyperventilation syndrome
• Hyperventilation syndrome (HVS) represents a relatively
common emergency department (ED) presentation that
is readily recognized by most clinicians.
• The underlying patho-physiology has not been clearly
elucidated.
• HVS is a condition in which minute ventilation exceeds
metabolic demands, resulting in hemodynamic and
chemical changes that produce characteristic dysphoric
symptoms.
• Inducing a drop in PaCO2 through voluntary
hyperventilation reproduces these symptoms.
• Many patients with HVS do not manifest low
PaCO2 during attacks.
Hyperventilation syndrome
• 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.
• Symptoms of HVS and panic disorder overlap
considerably, though the 2 conditions remain distinct.
• 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.
The Diagnostic and Statistical Manual of Mental Disorders,
Fourth Edition, classifies the anxiety disorders into the
following categories:
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Anxiety due to a general medical condition
Substance-induced anxiety disorder
Generalized anxiety disorder
Panic disorder
Acute stress disorder
Posttraumatic stress disorder (PTSD)
Adjustment disorder with anxious features
Obsessive-compulsive disorder (OCD)
Social phobia
Specific phobia and agoraphobia
Hyperpnea or hyperventilation
• 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.
• 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 .
Panic Disorder
• Panic disorder is characterized by the
spontaneous and unexpected occurrence of
panic attacks, the frequency of which can vary
from several attacks per day to only a few attacks
per year.
• Panic attacks can occur in other anxiety
disorders but occur without discernible
predictable precipitant in panic disorder
• To make the diagnosis of panic disorder, panic
attacks cannot directly or physiologically result
from substance use, medical conditions, or
another psychiatric disorders
Panic attacks are a period of intense fear in which 4 of 13
defined symptoms develop abruptly and peak rapidly less
than 10 minutes from symptom onset.
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Palpitations
Sweating
Trembling or shaking
Sense of shortness of breath or smothering
Feeling of choking
Chest pain or discomfort
Nausea or abdominal distress
Feeling dizzy, unsteady, light-headed, or faint
Derealization or depersonalization (feeling detached from oneself)
Fear of losing control or going crazy
Fear of dying
Numbness or tingling sensations
Chills or hot flashes
Collectively, phobic disorders (social phobia, specific
phobia, and agoraphobia) are the most common forms of
psychiatric illness, surpassing the rates of mood disorders
and substance abuse
• Agoraphobia is defined as anxiety toward places or
situations in which escape may be difficult or
embarrassing
• Most cases of agoraphobia develop as a complication of
panic disorders.
• A person previously experiences a panic attack in a
specific situation or environment and this triggers a
vicious circle.
• They begin to worry so much about having a panic
attack again that they feel the symptoms of panic attack
returning when they are in a similar situation or
environment. This then causes the person to avoid that
particular situation or environment.
Conversion disorder, factitious disorder,
and malingering
• Conversion disorder, factitious disorder,
and malingering have one major characteristic
in common: they represent conditions that are
not ‘real’.
• Properly diagnosing your patient with one of
these psychiatric ailments will allow you to
create appropriate plans of care for your
patients .
1. Conversion Disorder: is a psychiatric condition
that results in a neurological complaint or symptom,
without any underlying neurological cause.
• Patient’s may experience seizures (i.e. ‘pseudoseizures’), weakness, non-responsiveness, numbness,
and even vision loss.
• The symptoms are not intentional, yet upon further
investigation no biological explanation for the
symptoms can be found.
• The name “conversion disorder” formerly known as
"hysteria", comes from Sigmund Freud who stated that
stress can cause a psychiatric ailment to ‘convert’ to a
medical problem.
• It is thought that symptoms arise in response to
stressful situations affecting a patient's mental health.
2. Factitious Disorder (Munchausen Syndrome )
• Factitious Disorder (a Somatoform Disorder): is a
condition where patients intentionally fake disease, or
intentionally cause disease in order to play the ‘patient
role’.
• The main distinction between this and conversion
disorder is the intentional nature of factitious disorder.
• Often referred to a factitious disorder is characterized
by patients frequently feigning illness to obtain
attention, sympathy, or other emotional feedback.
• They achieve this goal through exaggerating symptoms,
deliberately faking symptoms, or even intentionally
creating real symptoms.
Münchausen syndrome by proxy
• Münchausen syndrome by proxy (MSbP or MBP)
is a term that is used to describe a behavior pattern
in which a caregiver deliberately exaggerates,
fabricates, and/or induces physical, psychological,
behavioral, and/or mental health problems in those
who are in their care.
• With deception at its core, this behavior is an
elusive, potentially lethal, and frequently
misunderstood form of child abuse or medical
neglect that has been difficult to define, detect and
confirm.
3. Malingering
• Malingering is the intentional faking or creating of
illness in order to obtain secondary gain (e.g. workers
compensation, disability payments, avoiding work or jail
time, pain medication, etc.).
• Malingering is NOT a psychiatric illness; this is the first
major distinction from the other two disorders.
• Malingering is an intentional abuse of the medical
system to obtain personal benefit.
• Malingerers abuse the system to obtain secondary gain
while patients with factitious disorder attempt only to
obtain emotional, or primary gain. In simpler terms, the
end goal of a malingerer usually involves monetary
value, while the goals of patients with factitious disorder
have no such value
QUICK REVIEW
• Conversion Disorder: Unintentional,
due to emotional stressors, no ‘gain’
to the patient
• Factitious Disorder (Munchausen):
Intentional, primary or ‘emotional’
gain
• Malingering: Intentional, secondary
and often monetary gain.
Pathophysiology of HVS
• Acute HVS accounts for only 1% of cases but is more
easily diagnosed.
• Chronic HVS can present with a myriad of respiratory,
cardiac, neurologic, or gastrointestinal (GI) symptoms
without any clinically apparent over-breathing by the
patient.
• Because of the subtlety of hyperventilation, many
patients with chronic HVS are admitted and undergo
extensive and expensive testing in an attempt to
discover organic causes of their complaints.
• Certain stressors provoke an exaggerated respiratory
response, including emotional distress, sodium lactate,
caffeine, isoproterenol, cholecystokinin, and Co2 .
Pathophysiology
• Patients with HVS were shown to be more likely to have
had overprotective parents when they were children. A
sudden stressful situation later in life can then incite the
first episode of HVS.
• Infusion of lactate provokes symptoms of panic in 80%
of patients with panic disorder but in only 10% of
controls. Approximately one half of the lactate
responders develop acute hyperventilation as part of the
panic reaction.
• Lactate levels are higher and remain elevated longer in
patients with panic disorder than in controls, suggesting
that abnormal metabolism of lactate is involved in the
pathogenesis,
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.
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.
• Initiating stimuli and abnormal stress responses may be
identical but are expressed differently in each group.
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.
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.
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-tomale ratio may be as high as 7:1.
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.
Prognosis
• A leftward shift in the oxyhemoglobin dissociation curve
and vasospasm related to low PaCO2 could cause
myocardial ischemia in patients with coronary artery
disease (CAD) and hyperventilation syndrome.
• Certain patients are disabled psychologically by their
symptoms, and many patients carry false diagnoses.
• Patients with HVS often undergo unnecessary testing
and suffer from the complications of these interventions
(eg, angiography, thrombolytics, or nasal reconstruction).
• Withholding such therapy may be difficult in a patient
with crushing chest pain and dyspnea. the chronicity of
the condition often causes different physicians to repeat
these unnecessary investigations.
Patient Education
• Patients should receive :
1- Clear explanation of the underlying pathophysiology and
2- should be instructed in the technique of
deflation of the upper chest followed by controlled
diaphragmatic breathing.
Complications
• The complications encountered in patients with
this syndrome are related mainly to the
invasive procedures and investigations (eg,
angiography) that are used in the workup of
HVS .
• Complications may also occur as a result of
symptoms produced indirectly by
hyperventilation (eg, injuries sustained in a fall
during a syncopale episode attributable to
hyperventilation).
Screening for OSA prior to surgery
• Pulse oximetry as a single metric of sleep apnea lacks the
sensitivity and specificity of PSG and multi-channel home
sleep testing .
• If the goal is only to cipher out those with an AHI of 15 or
20 or more, pulse oximetry can be considered.
• Centers for Medicare and Medicaid Services, 2009
reported that the final decision supporting equally
effective testing utilizing PSG and home sleep tests, as
measured by outcomes and patient compliance
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• While patients with mild OSA may not require preoperative
PAP therapy, patients with moderate and severe OSA who
have been on PAP therapy should continue treatment in the
preoperative period .
• Patients who have been noncompliant with instructions for
CPAP use prior to surgery and are in need of CPAP postsurgery, pose the highest risk of potential complications .
Acute hyperventilation
• Patients often present dramatically, with
agitation, hyperpnea and tachypnea, dyspnea,
wheezing, chest pain , dizziness, palpitations,
tetanic cramps (eg, carpopedal spasm),
paresthesias, generalized weakness, and
Syncope. The patient often complains of a
sense of suffocation.
• An emotionally stressful precipitating event can
often be identified.
• Wheezing may be heard because of bronchospasm from hypo-carbia.
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 .
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.
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.
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
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may result from aerophagia.
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.
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 .
• 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 hypocalcemia and in only 1% of persons with normal
calcium levels.
Chronic hyperventilation
• The diagnosis of chronic HVS is much more difficult than
that of acute HVS because hyperventilation is usually not
clinically apparent. Often, these patients have already
undergone extensive medical investigations and have been
assigned several misleading diagnoses.
• Two thirds of patients with chronic HVS have a persistently
slightly low PaCO2 with compensatory renal excretion of
bicarbonate, resulting in a near-normal pH level.
• These patients tend to have more prominent CNS
symptoms than patients who maintain normal PaCO2 during
attacks.
• Usually present with dyspnea and chest pain.
• Frequent sighing respirations (2-3 breaths/min) and
frequent yawning are noted.
Chronic hyperventilation
• The respiratory alkalosis can be maintained with
occasional deep sighing respirations, which are observed
often in patients with chronic HVS.
• When faced with an additional stress that provokes
hyperventilation, the physiologic acid-base reserve is
less, and these patients become symptomatic more
readily than patients without HVS.
• Dry mouth occurs with mouth breathing and anxiety.
• Many of these patients suffer from obsessive-compulsive
disorders, experience sexual and marital difficulties, and
have poor adaptations to stress.
• Chronic HVS may have symptoms that mimic those of
virtually any serious organic disorder, but they usually
have atypical features of these diseases.
Differential Diagnoses :
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Asthma
Atrial Fibrillation
Myocardial Infarction
Diabetic Ketoacidosis
Metabolic Acidosis
Nasopharyngeal Stenosis
Pneumothorax, Pneumomediastinum
Pulmonary Embolism
Respiratory Distress Syndrome, Adult
Carbon monoxide poisoning
Panic Disorders
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. More
specific testing is sometimes warranted.
• A standard workup for atypical chest pain, including
pulse oximetry, chest radiography, and ECG, may still
be warranted depending on the clinical picture.
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.
Approach Considerations
• A normal pulse oximetry reading is not helpful,
because a severe defect in gas exchange can
easily be masked by hyperventilation.
• A fraction of patients with chronic PE will have
compensated chronic hyperventilation that may
mimic primary chronic hyperventilation.
• 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.
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.
Pulse CO-oximeters
• Pulse Co-oximetry measures absorption at
several wavelengths to distinguish the
percentage of oxygenated Hemoglobin
compared to the total amount of hemoglobin
(Hb), including carboxyhemoglobin (carboxyHb), Methemoglobin (met-Hb), oxyhemoglobin
(oxy-Hb), and reduced Hb.
• When a patient presents with carbon monoxide
poisoning (CO), the pulse CO-oximeter will
detect the levels of each hemoglobin and will
report the oxyhemoglobin saturation as
markedly reduced ,
Pulse CO-oximeters
• Traditionally, this measurement is made from arterial
blood processed in a blood gas analyzer with a COoximeter.
• More recently, pulse CO-oximeters have made it
possible to estimate carboxyhemoglobin with noninvasive technology similar to a Pulse oximeter.
• In contrast, the use of a standard pulse oximeter is not
effective in the diagnosis of CO poisoning as
patients suffering from carbon monoxide
poisoning may have a normal oxygen saturation
reading on a pulse oximeter .
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.
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.
Rebreathing into a paper bag
1- Have the hyperventilating person
breathe slowly into a paper bag
that's held closely around his or
her mouth and nose.
2- The person should breathe like
this for five to seven minutes.
3-Talk to the individual the entire
time. Try to distract him or her and
make the person feel comfortable
and safe.
4- If symptoms fail to improve or
the person loses consciousness,
take him or her to the emergency
room.
Approach Considerations
• Patients should be referred to a consultant
psychiatrist, psychologist with expertise in
managing HVS.
• Some physiotherapists and respiratory
therapists have extensive experience in
retraining patients in proper breathing
techniques and should be consulted.
Breathing Techniques
• Rebreathing into a paper bag is no longer a
recommended technique, because significant hypoxia
and death have been reported.
• Paper bag rebreathing is often unsuccessful in
reversing the symptoms of HVS, because patients have
difficulty complying with the technique. 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.
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.
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.
Why is calm breathing important?
• ¨ Our breathing changes when we are feeling
anxious. We tend to take short , quick, shallow
breaths, or even hyperventilate; this is called
“overbreathing”.
• ¨ It is a good idea to learn techniques for
managing “overbreathing”, because this type of
breathing can actually make you feel even more
anxious (e.g., due to a racing heart, dizziness, or
headaches)!
• ¨ Calm breathing is a great portable tool that you
can use whenever you are feeling anxious.
However, it does require some practice.
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.
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.
Helpful Hints
• Make sure that you aren’t hyperventitating; it is
important to pause for a few seconds after each breath.
• Try to breathe from your diaphragm or abdomen.
• Your shoulders and chest area should be fairly relaxed
and still. If this is challenging at first, it can be helpful to
first try this exercise by lying down on the floor with one
hand on your heart, the other hand on your abdomen.
Watch the hand on your abdomen rise as you fill your
lungs with air, expanding your chest. (The hand over
your heart should barely move, if at all.)
Pharmacologic Therapy
• Several medications, including benzodiazepines and
selective serotonin reuptake inhibitors (SSRIs), have
been employed to reduce the frequency and severity of
episodes of hyperventilation.
• These agents require prolonged use and are best
managed by a consultant on an ongoing outpatient
basis rather than through sporadic prescriptions after
an ED visit.
• Use of benzodiazepines for stress relief and for
resetting the trigger for hyperventilation is effective, but
again, patients may require prolonged treatment.
Pharmacologic Therapy
• Benzodiazepines are useful in the treatment of
hyperventilation resulting from anxiety and panic
attacks.
• By binding to specific receptor sites, these agents
appear to potentiate the effects of gamma-aminobutyric
acid (GABA) and to facilitate inhibitory GABA
neurotransmission and the actions of other inhibitory
transmitters.
• Alprazolam (xanax) is indicated for treatment of anxiety
and management of 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.
Pharmacologic Therapy
• 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.