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Respiratory alkalosis treatment is done at affordable cost in India

Respiratory alkalosis treatment is done at affordable cost in India

Introduction

Background

Respiratory alkalosis is a clinical disturbance due to alveolar hyperventilation. Alveolar hyperventilation leads to a decreased partial pressure of arterial carbon dioxide (PaCO2), or partial pressure of carbon dioxide (PCO2). In turn, the decrease in PCO2 increases the ratio of bicarbonate concentration to PCO2 and increases the pH level. The decrease in PCO2 (hypocapnia) develops when a strong respiratory stimulus causes the lungs to remove more carbon dioxide than is produced metabolically in the tissues. Respiratory alkalosis can be acute or chronic. In acute respiratory alkalosis, the PCO2 level is below the lower limit of normal and the serum pH is alkalemic. In chronic respiratory alkalosis, the PCO2 level is below the lower limit of normal, but the pH level is normal or near normal.

Respiratory alkalosis is the most common acid-base abnormality observed in patients who are critically ill. It is associated with numerous illnesses and is a common finding in patients on mechanical ventilation. Many cardiac and pulmonary disorders can manifest respiratory alkalosis as an early or intermediate finding. When respiratory alkalosis is present, the cause may be minor; however, more serious disease processes should also be considered in the differential diagnosis.

Pathophysiology

Breathing is the body’s way of providing adequate amounts of oxygen for metabolism and for removing carbon dioxide produced by the tissues. By sensing the body’s partial pressure of oxygen (PO2) and PCO2, the respiratory system adjusts pulmonary ventilation so that oxygen uptake and carbon dioxide elimination at the lungs is equal to that used and produced by the tissues. PO2 is not as closely regulated because adequate hemoglobin saturation can be achieved over a wide range of PO2 levels. Oxygen is dependent on pressure gradients whereas, carbon dioxide diffuses much easier through an aqueous environment, making carbon dioxide regulation more complex. The PCO2 must be maintained at a level that ensures hydrogen ion concentrations remain in the narrow limits required for optimal protein function.

Metabolism generates a large quantity of volatile acid (carbon dioxide) and nonvolatile acid. The metabolism of fats and carbohydrates leads to the formation of a large amount of carbon dioxide.1 The carbon dioxide combines with water to form carbonic acid. The lungs excrete the volatile fraction through ventilation, and acid accumulation does not occur. Significant alterations in ventilation can affect the elimination of carbon dioxide and lead to a respiratory acid-base disorder.

PCO2 is normally maintained in the range of 37-43 mm Hg. Chemoreceptors in the brain (central chemoreceptors) and in the carotid bodies (peripheral chemoreceptors) sense hydrogen concentrations and influence ventilation to adjust the PCO2, PO2, and pH. Under this feedback regulator is how the PCO2 is maintained within its narrow normal range. When these receptors sense an increase in hydrogen ions, breathing is increased to “blow off” carbon dioxide and subsequently reduce the amount of hydrogen ions. Various disease processes may cause stimulation of ventilation with subsequent hyperventilation. If hyperventilation is persistent, it leads to hypocapnia.

Hyperventilation refers to an increase in the rate of alveolar ventilation that is disproportionate to the rate of metabolic carbon dioxide production, leading to an arterial PCO2 below the normal range. Two words often used synonymously with hyperventilation are tachypnea, an increase in respiratory frequency, and hyperpnea, an increase in the minute volume of ventilation. These should not be used to describe hyperventilation because they are distinct entities and neither results from nor means a change in PaCO2. Hyperventilation is often associated with dyspnea, but not all patients who are hyperventilating complain of shortness of breath. Conversely, patients with dyspnea need not be hyperventilating.

Acute hypocapnia causes a reduction of serum levels of potassium and phosphate secondary to increased intracellular shifts of these ions. A reduction in free serum calcium also occurs. Calcium reduction is secondary to increased binding of calcium to serum albumin. Many of the symptoms present in persons with respiratory alkalosis are related to the hypocalcemia. Hyponatremia and hypochloremia may also be present.

Acute hyperventilation with hypocapnia causes a small, early reduction in serum bicarbonate levels resulting from cellular uptake of bicarbonate. Acutely, plasma pH and bicarbonate concentration vary proportionately with the PCO2 along a range of 15-40 mm Hg. The relationship of PCO2 to arterial hydrogen and bicarbonate is 0.7 mmol/L per mm Hg and 0.2 mmol/L per mm Hg, respectively. After 2-6 hours, respiratory alkalosis is renally compensated by a decrease in bicarbonate reabsorption. The kidneys respond more to the decreased PCO2 rather than the increased pH. Kidney compensation may take several days and requires normal kidney function and intravascular volume status. The expected change in serum bicarbonate concentration can be estimated as follows:

Acute Bicarbonate (HCO3 -) falls 2 mEq/L for each decrease of 10 mm Hg in the PCO2 That is, ?HCO3 = 0.2(?PCO2) Maximum compensation: HCO3 - = 12-20 mEq/L Chronic Bicarbonate (HCO3 -) falls 5 mEq/L for each decrease of 10 mm Hg in the PCO2 That is, ?HCO3 = 0.5(?PCO2) Maximum compensation: HCO3 - = 12-20 mEq/L

Note that a plasma bicarbonate concentration of less than 12 mmol/L is unusual in pure respiratory alkalosis alone.

The expected change in pH with respiratory alkalosis can be estimated with the following equations:

Acute respiratory alkalosis: Change in pH = 0.008 X (40 – PCO2) Chronic respiratory alkalosis: Change in pH = 0.017 X (40 – PCO2)

Frequency

United States

The frequency of respiratory alkalosis varies depending on the etiology. It is the most common acid-base abnormality observed in critically ill patients.

Mortality/Morbidity

Morbidity and mortality of patients with respiratory alkalosis depend on the nature of the underlying cause of the respiratory alkalosis and associated conditions.

Clinical

History

Clinical manifestations of respiratory alkalosis depend on its duration, its severity, and the underlying disease process.

The hyperventilation syndrome can mimic many conditions that are more serious. Symptoms may include paresthesias, circumoral numbness, chest pain or tightness, dyspnea, and tetany. Acute onset of hypocapnia can cause cerebral vasoconstriction. Therefore, an acute decrease in PCO2 reduces cerebral blood flow and can cause neurologic symptoms, including dizziness, mental confusion, syncope, and seizures. The first cases of spontaneous hyperventilation with dizziness and tingling leading to tetany were described in 1922 by Goldman in patients with cholecystitis, abdominal distention, and hysteria.2 Haldane and Poulton described painful tingling in the hands and feet, numbness and sweating of the hands, and cerebral symptoms following voluntary hyperventilation.3

Physical

Physical examination findings in patients with respiratory alkalosis are usually nonspecific and are related to the underlying illness or cause of the respiratory alkalosis.

Many patients with hyperventilation syndrome appear anxious and are frequently tachycardic. Understandably, tachypnea is a frequent finding. In acute hyperventilation, chest wall movement and breathing rate increase. In patients with chronic hyperventilation, these physical findings may not be obvious. Positive Chvostek and Trousseau signs may be elicited. Patients with underlying pulmonary disease may have signs suggestive of pulmonary disease, such as crackles and rhonchi. Cyanosis may be present if the patient is hypoxic. If the underlying pathology is neurologic, the patient may have focal neurologic signs or a depressed level of consciousness. Cardiovascular effects of hypocapnia in healthy and alert patients are minimal, but in patients who are anesthetized, critically ill, or receiving mechanical ventilation, the effects can be more significant. Cardiac output and systemic blood pressure may fall as a result of the effects of sedation and positive-pressure ventilation on venous return, systemic vascular resistance, and heart rate. Cardiac rhythm disturbances may occur because of increased tissue hypoxia related to the leftward shift of the hemoglobin-oxygen dissociation curve.

Causes

The differential diagnosis of respiratory alkalosis is broad; therefore, a thorough history, physical examination, and laboratory evaluation are helpful in limiting the differential and arriving at the diagnosis.

Central nervous system Pain Hyperventilation syndrome Anxiety Psychosis Fever Cerebrovascular accident Meningitis Encephalitis Tumor Trauma Hypoxia High altitude Severe anemia Right-to-left shunts Drugs Progesterone Methylxanthines Salicylates Catecholamines Nicotine Endocrine Pregnancy Hyperthyroidism Pulmonary Pneumothorax/hemothorax Pneumonia Pulmonary edema Pulmonary embolism Aspiration Interstitial lung disease Asthma Emphysema Chronic bronchitis Miscellaneous Sepsis Hepatic failure Mechanical ventilation Heat exhaustion Recovery phase of metabolic acidosis Congestive heart failure

Differential Diagnoses

Asthma

Pneumonia, Bacterial

Atrial Fibrillation

Pneumonia, Community-Acquired

Atrial Flutter

Pneumonia, Viral

Atrial Tachycardia

Pneumothorax

Head Trauma

Pregnancy Diagnosis

Heatstroke

Pulmonary Edema, Cardiogenic

Hyperthyroidism

Pulmonary Edema, High-Altitude

Meningitis

Pulmonary Embolism

Metabolic Acidosis

Pulmonary Fibrosis, Idiopathic

Metabolic Alkalosis

Sepsis, Bacterial

Myocardial Infarction

Toxicity, Salicylate

Panic Disorder

Toxicity, Theophylline

Other Problems to Be Considered

Hyperthyroidism: Hyperthyroidism increases ventilation chemoreflexes, thereby causing hyperventilation. These return to normal with treatment of the hyperthyroidism. Pregnancy: Progesterone levels are increased during pregnancy. Progesterone causes stimulation of the respiratory center, which can lead to respiratory alkalosis. Congestive heart failure: Patients with congestive heart failure (and other low cardiac-output states) hyperventilate at rest, during exercise, and during sleep. Owing to pulmonary congestion, pulmonary vascular and interstitial receptors are stimulated. Additionally, the low cardiac-output state and hypotension stimulate breathing via the arterial baroreceptors. Chronic/severe liver disease: Several mechanisms have been hypothesized to explain the hyperventilation associated with liver disease. Increased levels of progesterone, ammonia, vasoactive intestinal peptide, and glutamine can stimulate respiration. Patients with severe disease or portal hypertension may have small pulmonary arteriovenous anastomoses in the lungs or portal-pulmonary shunts, which result in hypoxemia. This stimulates the peripheral chemoreceptors and leads to hyperventilation. Salicylate overdose: Initially, a respiratory alkalosis occurs, which is followed by a metabolic acidosis that induces secondary hyperventilation. Fever and sepsis: Fever and sepsis may manifest as hyperventilation, even before hypotension develops. The exact mechanism is not known but is thought to be due to carotid body or hypothalamic stimulation by the increased temperature. Pain: Hyperventilation may be due to stimulation of the peripheral and central chemoreceptors, as well as the behavioral control system. Hyperventilation syndrome: This is also known as psychogenic hyperventilation, and it is due to stress and anxiety, both of which act on the behavioral respiratory control system. The hyperventilation ceases during sleep, when the behavioral control system is inactive and only the metabolic system is controlling breathing. The diagnosis of hyperventilation syndrome should be a diagnosis of exclusion. Rule out all organic medical conditions, including pulmonary embolism, cardiac ischemia, and hyperthyroidism, before establishing a diagnosis of hyperventilation syndrome.

Workup

Laboratory Studies

Arterial blood gas determinations Alkalemia is documented by the presence of an increased pH level (>7.44) on arterial blood gas determinations. The presence of a decreased PCO2 level (<36 mm Hg) indicates a respiratory etiology of the alkalemia. Serum chemistries Acute respiratory alkalosis causes small changes in electrolyte balances. Minor intracellular shifts of sodium, potassium, and phosphate levels occur. A minor reduction in free calcium occurs due to an increased protein-bound fraction. Compensation for respiratory alkalosis is by increased renal excretion of bicarbonate. In acute respiratory acidosis, the bicarbonate concentration level decreases by 2 mEq/L for each decrease of 10 mm Hg in the PaCO2 level. In chronic respiratory acidosis, the bicarbonate concentration level decreases by 5 mEq/L for each decrease of 10 mm Hg in the PaCO2 level. Plasma bicarbonate levels rarely drop below 12 mm Hg secondary to compensation for primary respiratory alkalosis. Complete blood cell count An elevation of the WBC count may indicate early sepsis as a possible etiology of respiratory alkalosis. A reduced hematocrit value may indicate severe anemia as the potential cause of respiratory alkalosis. Liver function test: Findings may be abnormal if hepatic failure is the etiology of the respiratory alkalosis. Cultures of blood, sputum, urine, and other sites: These should be considered, depending on information obtained from the history and physical examination and if sepsis or bacteremia are thought to be the cause of the respiratory alkalosis.

Imaging Studies

Chest radiography Perform chest radiography to help rule out pulmonary disease as a cause of hypocapnia and respiratory alkalosis. Potential etiologies that may be confirmed based on chest radiography findings include pneumonia, pulmonary edema, aspiration pneumonitis, pneumothorax, and interstitial lung disease. CT scanning CT scanning of the chest may be performed if chest radiography findings are inconclusive or a pulmonary disorder is strongly considered as a differential diagnosis. CT scanning is more sensitive for helping detect disease, and findings may reveal abnormalities not seen on the chest radiograph. Consider spiral CT angiography of the chest if pulmonary embolism is suggested. Consider CT scanning of the brain if a central cause of hyperventilation and respiratory alkalosis is suggested. Specific etiologies that may be diagnosed based on brain CT scan findings include cerebrovascular accident, CNS tumor, and CNS trauma. Ventilation perfusion scanning: Consider this scan in patients who are unable to have intravenous contrast to assess for pulmonary embolism. Brain MRI If a central cause of hyperventilation and respiratory alkalosis is suggested and the initial brain CT scan findings are negative or inconclusive, an MRI of the brain can be considered. MRIs may reveal abnormalities not seen on CT scans. Possible etiologies based on MRIs include cerebrovascular accident, CNS tumor, and CNS trauma.

Procedures

Perform a lumbar puncture if the history and physical examination findings are suggestive of a CNS infectious process. Perform cytologic analysis in patients suggested to have meningeal metastasis.

Treatment

Medical Care

Treatment of respiratory alkalosis is primarily directed at correcting the underlying disorder.

Respiratory alkalosis itself is rarely life threatening. Therefore, emergent treatment is usually not indicated unless the pH level is greater than 7.5. Because respiratory alkalosis usually occurs in response to some stimulus, treatment is usually unsuccessful unless the stimulus is controlled. If the PCO2 is corrected rapidly in patients with chronic respiratory alkalosis, metabolic acidosis may develop due to the renal compensatory drop in serum bicarbonate. The tidal volume and respiratory rate may be decreased in mechanically ventilated patients who have respiratory alkalosis. Inadequate sedation and pain control may be the etiology of respiratory alkalosis in patients breathing over the set ventilator rate. In hyperventilation syndrome, patients benefit from reassurance, rebreathing into a paper bag during acute episodes, and treatment for underlying psychological stress. Sedatives and/or antidepressants should be reserved for patients who have not responded to conservative treatment. Beta-adrenergic blockers may help control the manifestations of the hyperadrenergic state that can lead to hyperventilation syndrome in some patients. In patients presenting with hyperventilation, a stepwise approach should be used to rule out potentially life-threatening, organic causes first.

Consultations

Based on the findings from the history, physical examination, laboratory studies, and imaging modalities, the necessity for assistance from consultants such as pulmonologists, neurologists, or nephrologists can be determined.

Follow-up

Prognosis

The prognosis of respiratory alkalosis is variable and depends on the underlying cause and the severity of the underlying illness.

Patient Education

Patients with hyperventilation syndrome as the etiology of their respiratory alkalosis may particularly benefit from patient education. The underlying pathophysiology should be explained in simple terms, and patients should be instructed in breathing techniques that may be used to relieve the hyperventilation. Reassurance is key for these patients.

Miscellaneous

Medicolegal Pitfalls

The most important factor in managing respiratory alkalosis is to recognize that it may be associated with serious medical disorders. Many of these conditions may be life threatening if not diagnosed early. If the cause of respiratory alkalosis cannot be readily determined, a list of differential diagnoses should be developed and all serious medical conditions should be excluded.

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