Respiratory alkalosis treatment is done at affordable cost in India

Respiratory alkalosis treatment is done at affordable- Interstitial lung disease
cost in India- Asthma
Introduction- Emphysema
Background- Chronic bronchitis
Respiratory alkalosis is a clinical disturbance due toMiscellaneous
alveolar hyperventilation. Alveolar hyperventilation leads- Sepsis
to a decreased partial pressure of arterial carbon- Hepatic failure
dioxide (PaCO2), or partial pressure of carbon dioxide- Mechanical ventilation
(PCO2). In turn, the decrease in PCO2 increases the- Heat exhaustion
ratio of bicarbonate concentration to PCO2 and- Recovery phase of metabolic acidosis
increases the pH level. The decrease in PCO2- Congestive heart failure
(hypocapnia) develops when a strong respiratoryDifferential Diagnoses
stimulus causes the lungs to remove more carbonAsthma
dioxide than is produced metabolically in the tissues.Pneumonia, Bacterial
Respiratory alkalosis can be acute or chronic. In acuteAtrial Fibrillation
respiratory alkalosis, the PCO2 level is below the lowerPneumonia, Community-Acquired
limit of normal and the serum pH is alkalemic. In chronicAtrial Flutter
respiratory alkalosis, the PCO2 level is below the lowerPneumonia, Viral
limit of normal, but the pH level is normal or nearAtrial Tachycardia
normal.Pneumothorax
Respiratory alkalosis is the most common acid-baseHead Trauma
abnormality observed in patients who are critically ill. It isPregnancy Diagnosis
associated with numerous illnesses and is a commonHeatstroke
finding in patients on mechanical ventilation. ManyPulmonary Edema, Cardiogenic
cardiac and pulmonary disorders can manifestHyperthyroidism
respiratory alkalosis as an early or intermediate finding.Pulmonary Edema, High-Altitude
When respiratory alkalosis is present, the cause mayMeningitis
be minor; however, more serious disease processesPulmonary Embolism
should also be considered in the differential diagnosis.Metabolic Acidosis
PathophysiologyPulmonary Fibrosis, Idiopathic
Breathing is the body’s way of providing adequateMetabolic Alkalosis
amounts of oxygen for metabolism and for removingSepsis, Bacterial
carbon dioxide produced by the tissues. By sensing theMyocardial Infarction
body’s partial pressure of oxygen (PO2) andToxicity, Salicylate
PCO2, the respiratory system adjusts pulmonaryPanic Disorder
ventilation so that oxygen uptake and carbon dioxideToxicity, Theophylline
elimination at the lungs is equal to that used andOther Problems to Be Considered
produced by the tissues. PO2 is not as closely- Hyperthyroidism: Hyperthyroidism increases ventilation
regulated because adequate hemoglobin saturationchemoreflexes, thereby causing hyperventilation.
can be achieved over a wide range of PO2 levels.These return to normal with treatment of the
Oxygen is dependent on pressure gradients whereas,hyperthyroidism.
carbon dioxide diffuses much easier through an- Pregnancy: Progesterone levels are increased during
aqueous environment, making carbon dioxide regulationpregnancy. Progesterone causes stimulation of the
more complex. The PCO2 must be maintained at arespiratory center, which can lead to respiratory
level that ensures hydrogen ion concentrations remainalkalosis.
in the narrow limits required for optimal protein function.- Congestive heart failure: Patients with congestive
Metabolism generates a large quantity of volatile acidheart failure (and other low cardiac-output states)
(carbon dioxide) and nonvolatile acid. The metabolismhyperventilate at rest, during exercise, and during sleep.
of fats and carbohydrates leads to the formation of aOwing to pulmonary congestion, pulmonary vascular
large amount of carbon dioxide.1 The carbon dioxideand interstitial receptors are stimulated. Additionally, the
combines with water to form carbonic acid. The lungslow cardiac-output state and hypotension stimulate
excrete the volatile fraction through ventilation, and acidbreathing via the arterial baroreceptors.
accumulation does not occur. Significant alterations- Chronic/severe liver disease: Several mechanisms
in ventilation can affect the elimination of carbonhave been hypothesized to explain the hyperventilation
dioxide and lead to a respiratory acid-base disorder.associated with liver disease. Increased levels of
PCO2 is normally maintained in the range of 37-43 mmprogesterone, ammonia, vasoactive intestinal peptide,
Hg. Chemoreceptors in the brain (centraland glutamine can stimulate respiration. Patients with
chemoreceptors) and in the carotid bodies (peripheralsevere disease or portal hypertension may have small
chemoreceptors) sense hydrogen concentrations andpulmonary arteriovenous anastomoses in the lungs or
influence ventilation to adjust the PCO2, PO2, and pH.portal-pulmonary shunts, which result in hypoxemia.
Under this feedback regulator is how the PCO2 isThis stimulates the peripheral chemoreceptors and
maintained within its narrow normal range. When theseleads to hyperventilation.
receptors sense an increase in hydrogen ions,- Salicylate overdose: Initially, a respiratory alkalosis
breathing is increased to “blow off” carbonoccurs, which is followed by a metabolic acidosis that
dioxide and subsequently reduce the amount ofinduces secondary hyperventilation.
hydrogen ions. Various disease processes may cause- Fever and sepsis: Fever and sepsis may manifest as
stimulation of ventilation with subsequenthyperventilation, even before hypotension develops.
hyperventilation. If hyperventilation is persistent, it leadsThe exact mechanism is not known but is thought to
to hypocapnia.be due to carotid body or hypothalamic stimulation by
Hyperventilation refers to an increase in the rate ofthe increased temperature.
alveolar ventilation that is disproportionate to the rate- Pain: Hyperventilation may be due to stimulation of
of metabolic carbon dioxide production, leading to anthe peripheral and central chemoreceptors, as well as
arterial PCO2 below the normal range. Two wordsthe behavioral control system.
often used synonymously with hyperventilation are- Hyperventilation syndrome: This is also known as
tachypnea, an increase in respiratory frequency, andpsychogenic hyperventilation, and it is due to stress
hyperpnea, an increase in the minute volume ofand anxiety, both of which act on the behavioral
ventilation. These should not be used to describerespiratory control system. The hyperventilation
hyperventilation because they are distinct entities andceases during sleep, when the behavioral control
neither results from nor means a change in PaCO2.system is inactive and only the metabolic system is
Hyperventilation is often associated with dyspnea, butcontrolling breathing. The diagnosis of hyperventilation
not all patients who are hyperventilating complain ofsyndrome should be a diagnosis of exclusion. Rule out
shortness of breath. Conversely, patients with dyspneaall organic medical conditions, including pulmonary
need not be hyperventilating.embolism, cardiac ischemia, and hyperthyroidism,
Acute hypocapnia causes a reduction of serum levelsbefore establishing a diagnosis of hyperventilation
of potassium and phosphate secondary to increasedsyndrome.
intracellular shifts of these ions. A reduction in freeWorkup
serum calcium also occurs. Calcium reduction isLaboratory Studies
secondary to increased binding of calcium to serum- Arterial blood gas determinations
albumin. Many of the symptoms present in persons- Alkalemia is documented by the presence of an
with respiratory alkalosis are related to theincreased pH level (>7.44) on arterial blood gas
hypocalcemia. Hyponatremia and hypochloremia maydeterminations.
also be present.- The presence of a decreased PCO2 level (<36
Acute hyperventilation with hypocapnia causes a small,mm Hg) indicates a respiratory etiology of the
early reduction in serum bicarbonate levels resultingalkalemia.
from cellular uptake of bicarbonate. Acutely, plasma pHSerum chemistries
and bicarbonate concentration vary proportionately- Acute respiratory alkalosis causes small changes in
with the PCO2 along a range of 15-40 mm Hg. Theelectrolyte balances. Minor intracellular shifts of sodium,
relationship of PCO2 to arterial hydrogen andpotassium, and phosphate levels occur. A minor
bicarbonate is 0.7 mmol/L per mm Hg and 0.2 mmol/Lreduction in free calcium occurs due to an increased
per mm Hg, respectively. After 2-6 hours, respiratoryprotein-bound fraction.
alkalosis is renally compensated by a decrease in- Compensation for respiratory alkalosis is by
bicarbonate reabsorption. The kidneys respond moreincreased renal excretion of bicarbonate. In acute
to the decreased PCO2 rather than the increased pH.respiratory acidosis, the bicarbonate concentration level
Kidney compensation may take several days anddecreases by 2 mEq/L for each decrease of 10 mm
requires normal kidney function and intravascularHg in the PaCO2 level. In chronic respiratory acidosis,
volume status. The expected change in serumthe bicarbonate concentration level decreases by 5
bicarbonate concentration can be estimated asmEq/L for each decrease of 10 mm Hg in the PaCO2
follows:level. Plasma bicarbonate levels rarely drop below 12
- Acutemm Hg secondary to compensation for primary
- Bicarbonate (HCO3 -) falls 2 mEq/L for eachrespiratory alkalosis.
decrease of 10 mm Hg in the PCO2Complete blood cell count
- That is, ?HCO3 = 0.2(?PCO2)- An elevation of the WBC count may indicate early
- Maximum compensation: HCO3 - = 12-20 mEq/Lsepsis as a possible etiology of respiratory alkalosis.
Chronic- A reduced hematocrit value may indicate severe
- Bicarbonate (HCO3 -) falls 5 mEq/L for eachanemia as the potential cause of respiratory alkalosis.
decrease of 10 mm Hg in the PCO2Liver function test: Findings may be abnormal if hepatic
- That is, ?HCO3 = 0.5(?PCO2)failure is the etiology of the respiratory alkalosis.
- Maximum compensation: HCO3 - = 12-20 mEq/LCultures of blood, sputum, urine, and other sites: These
Note that a plasma bicarbonate concentration of lessshould be considered, depending on information
than 12 mmol/L is unusual in pure respiratory alkalosisobtained from the history and physical examination and
alone.if sepsis or bacteremia are thought to be the cause
The expected change in pH with respiratory alkalosisof the respiratory alkalosis.
can be estimated with the following equations:Imaging Studies
- Acute respiratory alkalosis: Change in pH = 0.008 X- Chest radiography
(40 – PCO2)- Perform chest radiography to help rule out pulmonary
- Chronic respiratory alkalosis: Change in pH = 0.017 Xdisease as a cause of hypocapnia and respiratory
(40 – PCO2)alkalosis.
Frequency- Potential etiologies that may be confirmed based on
United Stateschest radiography findings include pneumonia,
The frequency of respiratory alkalosis variespulmonary edema, aspiration pneumonitis,
depending on the etiology. It is the most commonpneumothorax, and interstitial lung disease.
acid-base abnormality observed in critically ill patients.CT scanning
Mortality/Morbidity- CT scanning of the chest may be performed if chest
Morbidity and mortality of patients with respiratoryradiography findings are inconclusive or a pulmonary
alkalosis depend on the nature of the underlying causedisorder is strongly considered as a differential
of the respiratory alkalosis and associated conditions.diagnosis. CT scanning is more sensitive for helping
Clinicaldetect disease, and findings may reveal abnormalities
Historynot seen on the chest radiograph.
Clinical manifestations of respiratory alkalosis depend- Consider spiral CT angiography of the chest if
on its duration, its severity, and the underlying diseasepulmonary embolism is suggested.
process.- Consider CT scanning of the brain if a central cause
- The hyperventilation syndrome can mimic manyof hyperventilation and respiratory alkalosis is
conditions that are more serious. Symptoms maysuggested. Specific etiologies that may be diagnosed
include paresthesias, circumoral numbness, chest painbased on brain CT scan findings include
or tightness, dyspnea, and tetany.cerebrovascular accident, CNS tumor, and CNS
- Acute onset of hypocapnia can cause cerebraltrauma.
vasoconstriction. Therefore, an acute decrease inVentilation perfusion scanning: Consider this scan in
PCO2 reduces cerebral blood flow and can causepatients who are unable to have intravenous contrast
neurologic symptoms, including dizziness, mentalto assess for pulmonary embolism.
confusion, syncope, and seizures.Brain MRI
- The first cases of spontaneous hyperventilation with- If a central cause of hyperventilation and respiratory
dizziness and tingling leading to tetany were describedalkalosis is suggested and the initial brain CT scan
in 1922 by Goldman in patients with cholecystitis,findings are negative or inconclusive, an MRI of the
abdominal distention, and hysteria.2brain can be considered.
- Haldane and Poulton described painful tingling in the- MRIs may reveal abnormalities not seen on CT
hands and feet, numbness and sweating of the hands,scans. Possible etiologies based on MRIs include
and cerebral symptoms following voluntarycerebrovascular accident, CNS tumor, and CNS
hyperventilation.3trauma.
PhysicalProcedures
Physical examination findings in patients with- Perform a lumbar puncture if the history and physical
respiratory alkalosis are usually nonspecific and areexamination findings are suggestive of a CNS
related to the underlying illness or cause of theinfectious process. Perform cytologic analysis in
respiratory alkalosis.patients suggested to have meningeal metastasis.
- Many patients with hyperventilation syndrome appearTreatment
anxious and are frequently tachycardic.Medical Care
Understandably, tachypnea is a frequent finding.Treatment of respiratory alkalosis is primarily directed
- In acute hyperventilation, chest wall movement andat correcting the underlying disorder.
breathing rate increase. In patients with chronic- Respiratory alkalosis itself is rarely life threatening.
hyperventilation, these physical findings may not beTherefore, emergent treatment is usually not indicated
obvious.unless the pH level is greater than 7.5. Because
- Positive Chvostek and Trousseau signs may berespiratory alkalosis usually occurs in response to
elicited.some stimulus, treatment is usually unsuccessful unless
- Patients with underlying pulmonary disease may havethe stimulus is controlled.
signs suggestive of pulmonary disease, such as- If the PCO2 is corrected rapidly in patients with
crackles and rhonchi. Cyanosis may be present if thechronic respiratory alkalosis, metabolic acidosis may
patient is hypoxic.develop due to the renal compensatory drop in serum
- If the underlying pathology is neurologic, the patientbicarbonate.
may have focal neurologic signs or a depressed level- The tidal volume and respiratory rate may be
of consciousness.decreased in mechanically ventilated patients who
- Cardiovascular effects of hypocapnia in healthy andhave respiratory alkalosis. Inadequate sedation and
alert patients are minimal, but in patients who arepain control may be the etiology of respiratory
anesthetized, critically ill, or receiving mechanicalalkalosis in patients breathing over the set ventilator
ventilation, the effects can be more significant. Cardiacrate.
output and systemic blood pressure may fall as a- In hyperventilation syndrome, patients benefit from
result of the effects of sedation and positive-pressurereassurance, rebreathing into a paper bag during acute
ventilation on venous return, systemic vascularepisodes, and treatment for underlying psychological
resistance, and heart rate.stress. Sedatives and/or antidepressants should be
- Cardiac rhythm disturbances may occur because ofreserved for patients who have not responded to
increased tissue hypoxia related to the leftward shiftconservative treatment. Beta-adrenergic blockers may
of the hemoglobin-oxygen dissociation curve.help control the manifestations of the hyperadrenergic
Causesstate that can lead to hyperventilation syndrome in
The differential diagnosis of respiratory alkalosis issome patients.
broad; therefore, a thorough history, physical- In patients presenting with hyperventilation, a stepwise
examination, and laboratory evaluation are helpful inapproach should be used to rule out potentially
limiting the differential and arriving at the diagnosis.life-threatening, organic causes first.
- Central nervous systemConsultations
- PainBased on the findings from the history, physical
- Hyperventilation syndromeexamination, laboratory studies, and imaging modalities,
- Anxietythe necessity for assistance from consultants such as
- Psychosispulmonologists, neurologists, or nephrologists can be
- Feverdetermined.
- Cerebrovascular accidentFollow-up
- MeningitisPrognosis
- Encephalitis- The prognosis of respiratory alkalosis is variable and
- Tumordepends on the underlying cause and the severity of
- Traumathe underlying illness.
HypoxiaPatient Education
- High altitude- Patients with hyperventilation syndrome as the
- Severe anemiaetiology of their respiratory alkalosis may particularly
- Right-to-left shuntsbenefit from patient education. The underlying
Drugspathophysiology should be explained in simple terms,
- Progesteroneand patients should be instructed in breathing
- Methylxanthinestechniques that may be used to relieve the
- Salicylateshyperventilation. Reassurance is key for these patients.
- CatecholaminesMiscellaneous
- NicotineMedicolegal Pitfalls
Endocrine- The most important factor in managing respiratory
- Pregnancyalkalosis is to recognize that it may be associated with
- Hyperthyroidismserious medical disorders. Many of these conditions
Pulmonarymay be life threatening if not diagnosed early. If the
- Pneumothorax/hemothoraxcause of respiratory alkalosis cannot be readily
- Pneumoniadetermined, a list of differential diagnoses should be
- Pulmonary edemadeveloped and all serious medical conditions should be
- Pulmonary embolismexcluded.
- Aspiration