Respiratory Alkalosis
Respiratory alkalosis is a disturbance in acid and base balance due to alveolar hyperventilation. Alveolar hyperventilation leads to a decreased partial pressure of arterial carbon dioxide (PaCO2). In turn, the decrease in PaCO2 increases the ratio of bicarbonate concentration to PaCO2 and, thereby, increases the pH level, thus the descriptive term of respiratory alkalosis. The decrease in PaCO2 (hypocapnia) develops when a strong respiratory stimulus causes the respiratory system to remove more carbon dioxide than is produced metabolically in the tissues.
Respiratory alkalosis can be acute or chronic. In acute respiratory alkalosis, the PaCO2 level is below the lower limit of normal and the serum pH is alkalemic. In chronic respiratory alkalosis, the PaCO2 level is below the lower limit of normal, but the pH level is relatively 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 with respiratory alkalosis as an early or intermediate finding. When respiratory alkalosis is present, the cause may be a minor, non–life-threatening disorder. However, more serious disease processes should also be considered in the differential diagnosis.
Pathophysiology
Breathing or alveolar ventilation is the body’s way of providing adequate amounts of oxygen for metabolism while removing carbon dioxide produced in the tissues. By sensing the body’s partial pressure of arterial oxygen (PaO2) and PaCO2, the respiratory system adjusts pulmonary ventilation so that oxygen uptake and carbon dioxide elimination at the lungs is balanced to that used and produced by the tissues.
The PaCO2 must be maintained at a level that ensures hydrogen ion concentrations remain in the narrow limits required for optimal protein and enzymatic function. PaO2 is not as closely regulated as the PaCO2. Adequate hemoglobin saturation can be achieved over a wide range of PaO2 levels. The movement of oxygen from the alveoli to the vascular system is dependent on pressure gradients. On the other hand, carbon dioxide diffuses much easier through an aqueous environment.
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. 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.
PaCO2 is normally maintained in the range of 35-45 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 and pH. This feedback regulator is how the PaCO2 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 alveolar ventilation that is disproportionate to the rate of metabolic carbon dioxide production, leading to a PaCO2 level 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. However, these terms should not be used to describe hyperventilation because they are distinct entities and neither necessarily results in 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 due to the change in pH. Many of the symptoms present in persons with respiratory alkalosis are related to hypocalcemia. Hyponatremia and hypochloremia may also be present.
Acute hyperventilation with hypocapnia causes a small, early reduction in serum bicarbonate levels resulting from cellular shift of bicarbonate. Acutely, plasma pH and bicarbonate concentration vary proportionately with the PaCO2 along a range of 15-40 mm Hg. The relationship of PaCO2 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 renal compensation begins by decreasing bicarbonate reabsorption. The kidneys respond more to the decreased PaCO2 rather than the increased pH. Complete kidney compensation may take several days and requires normal kidney function and intravascular volume status.
A study by Morel et al suggested that when respiratory alkalosis is present, caution be used in the employment of venous-arterial difference in CO2(ΔCO2) as an indicator of the adequacy of tissue perfusion (as has been proposed for shock states). Using healthy volunteers in whom either hypocapnia or hypercapnia was induced, the investigators found a significant increase in ΔCO2 in the hypocapnic subjects, who also had a significant decrease in skin microcirculatory blood flow.
Warburg
Dr. Otto Warburg was awarded the Nobel Prize for Medicine in 1931, but his discoveries have been suppressed by the medical establishment so successfully that only alternative medicine researchers ever learn of them, or of him. The Nobel Foundation explained why it awarded Dr. Warburg the Nobel Prize by writing, "For his discovery of the nature and mode of action of the respiratory enzyme, the Nobel Prize has been awarded to him in 1931. This discovery has opened up new ways in the fields of cellular metabolism and cellular respiration. He has shown, among other things, that cancerous cells can live and develop, even in the absence of oxygen".
Dr. Warburg discovered that cancer cells are not fueled by oxygen as normal cells are. The high levels of oxygen that are found in healthy, alkaline bodies are toxic to cancers. He found that cancers get their energy from sugars and a process of fermentation in acidic environments. He proved empirically the relationship between cancers, acidic body pH, and cellular oxygen starvation. His findings demonstrated that cancers are merely a symptom of acidosis, and therefore it is impossible to truly cure any cancer without first curing the underlying acidosis.
Standard cancer care now means almost certainly dying from either the cancer, or more likely, the treatment itself. Cancer deaths usually result from the toxic effects of mainstream cancer treatments. These increase a body's acidity, virtually guaranteeing that cancer symptoms will return elsewhere, even if the initial tumors are destroyed. Thus, the dismal lifetime failure rate of standard cancer medicine is a jaw-dropping 96%. They call it medicine and claim that it is scientifically validated, but it only works 4% of the time. Doing nothing is a more effective treatment for cancers than standard therapies. To manipulate the statistics, any patient who does not die within 5 years is reported to have had a successful treatment. The treatments stimulate the acidic conditions that originally caused the cancers, because they damage the same immune system that is needed to fight cancer cells, and the treatments randomly damage the organs throughout a body. Therefore, cancers tend to spread rapidly following standard treatments.
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