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Is Hyperventilation Acidosis Or Alkalosis?

Acid-base Balance

Acid-base Balance

Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find the Arterial Blood Gases article more useful, or one of our other health articles. Disorders of acid-base balance can lead to severe complications in many disease states.[1]Arterial blood pH is normally closely regulated to between 7.35 and 7.45. Maintaining the pH within these limits is achieved by bicarbonate, other buffers, the lungs and the kidneys. Primary changes in bicarbonate are metabolic and primary changes in carbon dioxide are respiratory. In the absence of any significant respiratory disease or hyperventilation, the primary cause is much more likely to be metabolic. However, central hypoventilation (eg, caused by CNS disturbance such as stroke, head injury or brain tumour) causes respiratory acidosis. In general, the kidneys compensate for respiratory causes and the lungs compensate for metabolic causes. Therefore, hyperventilation may be a cause of respiratory alkalosis or a compensatory mechanism for metabolic acidosis. Deep sighing respiration (Kussmaul breathing) is a common feature of acidosis (hyperventilation in an attempt to remove carbon dioxide) but may take some hours to appear. Investigations Analysis of arterial blood gases provides: pH: determines whether there is an overall acidosis or alkalosis. Venous pH is in practice as reliable as arterial pH. Carbon dioxide partial pressure (PaCO2): if raised with acidosis then the acidosis is respiratory. If decreased with alkalosis then the alkalosis is respiratory. Otherwise any change is compensatory. Standard bicarbonate (SBCe): analysis of blood gases provides a bicarbonate level whic Continue reading >>

Respiratory Alkalosis, Hypocapnia

Respiratory Alkalosis, Hypocapnia

Relative hyperventilation tending to make blood more alkaline: increased pH, decreased hydrogen ion concentrations Can be physiological: pregnancy and high altitude Pathological associated with relative hyperventilation Often no specific manifestations. Hyperventilation may be apparent. If pathological, treat underlying condition (eg, asthma or cardiac failure). In ventilated patients, consider decreasing ventilation. Treat ABC: airway, breathing, circulation. In symptomatic psychogenic hyperventilation: use rebreathing (paper bag). In conscious patients acute respiratory alkalosis can cause neurologic symptoms: dizziness, confusion, syncope, seizures, paresthesias (particularly perioral). Symptoms and signs may be related to underlying conditions such as ischemic or pleuritic chest pain and unrelated to the change in pH. Patients with psychogenic hyperventilation may have symptoms and signs related to severe anxiety. Arterial blood gas: pH > 7.45, pCO2 < 35 mmHg, Bicarbonate > 24 mmol/L, standard base-excess < 0 mmol/L. Check blood gas results for compensation or second disorder. Metabolic compensation will never be complete (pH < 7.40), and will take hours. Therefore, early respiratory alkalosis may appear uncompensated. Compensation: Metabolic side compensates for respiratory acidosis by decreasing renal chloride excretion, leading to decreased strong-ion difference and decreased bicarbonate. Measured by bicarbonate or standard base excess (SBE). In acute respiratory alkalosis : Expected SBE = 0 mmol/L, Expected bicarbonate mmol/L = 24+ 0.2 x (PCO2 - 40) For both bicarbonate and base-excess this estimate is about +/- 2 mmol/L. Underlying change will be renal chloride excretion leading to decreased strong-ion difference. In chronic respiratory alkalosis there is adap Continue reading >>

Respiratory Alkalosis

Respiratory Alkalosis

Author: Ryland P Byrd, Jr, MD; Chief Editor: Zab Mosenifar, MD, FACP, FCCP more... 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, nonlife-threatening disorder. However, more serious disease processes should also be considered in the differential diagnosis. Breathing or alveolar ventilation is the bodys way of providing adequate amounts of oxygen for metabolism while removing carbon dioxide produced in the tissues. By sensing the bodys partial pressure of arterial oxygen (PaO2) and PaCO2, the respiratory system adjusts pulmonary ventilation so that oxygen uptake and carbon dioxide elim Continue reading >>

Respiratory Alkalosisclinical Presentation

Respiratory Alkalosisclinical Presentation

Respiratory AlkalosisClinical Presentation Author: Ryland P Byrd, Jr, MD; Chief Editor: Zab Mosenifar, MD, FACP, FCCP more... Clinical manifestations of respiratory alkalosis depend on its duration, its severity, and the underlying disease process. Note the following: The hyperventilation syndrome can mimic many conditions that are more serious. Symptoms may include paresthesias, circumoral numbness, chest pain or tightness, dyspnea, and tetany. [ 8 ] Acute onset of hypocapnia can cause cerebral vasoconstriction. An acute decrease in PaCO2 reduces cerebral blood flow and can cause neurologic symptoms, including dizziness, mental confusion, syncope, and seizures. Hypoxemia need not be present for the patient to experience these symptoms. [ 3 ] The first cases of spontaneous hyperventilation with dizziness and tingling leading to tetany were described in 1922 in patients with cholecystitis, abdominal distention, and hysteria. [ 9 ] Haldane and Poulton described painful tingling in the hands and feet, numbness and sweating of the hands, and cerebral symptoms following voluntary hyperventilation. [ 10 ] Physical examination findings in patients with respiratory alkalosis are nonspecific and are typically related to the underlying illness or cause of the respiratory alkalosis. Note the following: 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 as obvious. Positive Chvostek and Trousseau signs may be elicited. [ 2 ] Patients with underlying pulmonary disease may have signs suggestive of pulmonary disease, such as crackles, wheezes, Continue reading >>

Evaluation Of Respiratory Alkalosis

Evaluation Of Respiratory Alkalosis

Respiratory alkalosis is a systemic acid-base disorder characterized by a primary reduction in arterial partial pressure of carbon dioxide (PaCO2), which produces an elevation in pH, and consequent decrease in bicarbonate (HCO3-) concentration, as buffering mechanisms. [1] Arbus GS, Herbert LA, Levesque PR, et al. Characterization and clinical application of the "significance band" for acute respiratory alkalosis. N Engl J Med. 1969;280:117-123. It may occur as a simple primary disorder, a sole respiratory abnormality in which a decrease in PaCO2 results from excess alveolar CO2 excretion relative to CO2 production. Respiratory alkalosis may also occur as compensation for an underlying process, such as metabolic acidosis, or as a separate component of a mixed acid-base disorder, in which case the PaCO2, HCO3-, and pH are determined by the combined effects of the underlying acid-base disorders. [2] Foster GT, Varizi ND, Sassoon CS. Respiratory alkalosis. Respir Care. 2001;46:384-391. Respiratory alkalosis can be classified into three categories: 1) as a component of disease processes, 2) accidentally induced, and 3) deliberately induced (therapeutic). [3] Laffey JG, Kavanagh BP. Hypocapnia. N Engl J Med. 2002;347:43-53. Accidental respiratory alkalosis develops as a consequence of inappropriate settings of mechanical ventilation, or associated with extracorporeal membrane oxygenation. [3] Laffey JG, Kavanagh BP. Hypocapnia. N Engl J Med. 2002;347:43-53. Therapeutic respiratory alkalosis or hypocapnia has been applied to temporarily treat intracranial hypertension or neonatal pulmonary artery hypertension. [4] Allen CH, Ward JD. An evidence-based approach to management of increased intracranial pressure. Crit Care Clin. 1998;14:485-495. [5] Walsh-Sukys MC, Tyson JE, Wrig Continue reading >>

Central Lactic Acidosis, Hyperventilation, And Respiratory Alkalosis: Leadingclinical Features In A 3-year-old Boy With Malignant Meningeal Melanoma.

Central Lactic Acidosis, Hyperventilation, And Respiratory Alkalosis: Leadingclinical Features In A 3-year-old Boy With Malignant Meningeal Melanoma.

1. Eur J Pediatr. 2008 Apr;167(4):483-5. Epub 2007 May 30. Central lactic acidosis, hyperventilation, and respiratory alkalosis: leadingclinical features in a 3-year-old boy with malignant meningeal melanoma. Blher S(1), Schulz M, Bierbach U, Meixensberger J, Trbs RB, Hirsch W, SchoberR, Kiess W, Siekmeyer W. (1)Hospital for Children and Adolescents, University of Leipzig, Oststrasse 21-25, 04317, Leipzig, Germany. [email protected] Meningeal tumors are extremely rare in children and are diagnostically as well astherapeutically challenging. Among the least common types of malignancies inchildhood is malignant melanoma, counting for less than 1% of pediatric tumors.Due to the rarity and the wide spectrum of appearance, initial clinical features may be misleading. A 3-year-old boy was referred to our hospital with symptoms ofhyperventilation, dyspnoea, tachycardia, respiratory alkalosis, inarticulatespeech, and fatigue. Measurement of pH in cerebrospinal fluid (CSF) yieldedcentral lactic acidosis despite alkalosis in peripheral blood. Diagnostic imagingprocedures as well as histology and immunohistochemistry revealed the diagnosisof a malignant meningeal melanoma. We hypothesize that central lactate productionof the tumor nests might have induced central acidification, thus inducinghyperventilation by stimulation of central chemoreceptors. This case is a modelexample of the key role of central pH as an inducer/suppressor of ventilation in humans and illustrates the critical importance of central pH for regulating both ventilation and acid-base homeostasis. Thus, pH of CSF should be measuredwhenever a malignant brain tumor is suspected. Continue reading >>

Respiratory Alkalosis

Respiratory Alkalosis

Respiratory alkalosis is a consequence of the rate of excretion of carbon dioxide exceeding the rate of production, leading to a decrease in PCO2. Larry R. Engelking, in Textbook of Veterinary Physiological Chemistry (Third Edition) , 2015 Steady state blood CO2 levels remain relatively constant in compensated respiratory acidosis and alkalosis (i.e., CO2 in=CO2 out). Uncompensated respiratory alkalosis is associated with an increased blood pH, and a modestly decreased HCO3 concentration. Renal compensation for respiratory alkalosis involves a decrease in HCO3 reabsorption. The blood pH may be within the normal range in some mixed acid-base disorders. A mixed acid-base disturbance is indicated when the Pco2 and blood HCO3 concentration are moving in opposite directions. Mixed acid-base distrubances can be additive, or subtractive. The bicarbonate buffer equation is shifted to the left in metabolic acidosis and respiratory alkalosis. Respiratory alkalosis can be due to either direct or reflex hypoxemic stimulation of the respiratory center, to pulmonary disease, or to excessive mechanical ventilation. Horacio J. Adrogu, Nicolaos E. Madias, in Comprehensive Clinical Nephrology (Fourth Edition) , 2010 Respiratory alkalosis is the acid-base disturbance initiated by a reduction in CO2 tension of body fluids. The secondary decrease in plasma HCO3 concentration observed in acute and chronic hypocapnia is an integral part of the respiratory alkalosis. Whole-body CO2 stores are decreased and Paco2 is less than 35mmHg (4.7kP) in patients with simple respiratory alkalosis who are at rest and at sea level. An element of respiratory alkalosis may still occur with higher levels of Paco2 in patients with metabolic alkalosis, in whom a normal Paco2 is inappropriately low for this prim Continue reading >>

Respiratory Alkalosis

Respiratory Alkalosis

Respiratory alkalosis is a medical condition in which increased respiration elevates the blood pH beyond the normal range (7.35–7.45) with a concurrent reduction in arterial levels of carbon dioxide.[1][3] This condition is one of the four basic categories of disruption of acid–base homeostasis.[medical citation needed] Signs and symptoms[edit] Signs and symptoms of respiratory alkalosis are as follows:[4] Palpitation Tetany Convulsion Sweating Causes[edit] Respiratory alkalosis may be produced as a result of the following causes: Stress[1] Pulmonary disorder[2] Thermal insult[5] High altitude areas[6] Salicylate poisoning (aspirin overdose) [6] Fever[1] Hyperventilation (due to heart disorder or other, including improper mechanical ventilation)[1][7] Vocal cord paralysis (compensation for loss of vocal volume results in over-breathing/breathlessness).[8] Liver disease[6] Mechanism[edit] Carbonic-acid The mechanism of respiratory alkalosis generally occurs when some stimulus makes a person hyperventilate. The increased breathing produces increased alveolar respiration, expelling CO2 from the circulation. This alters the dynamic chemical equilibrium of carbon dioxide in the circulatory system. Circulating hydrogen ions and bicarbonate are shifted through the carbonic acid (H2CO3) intermediate to make more CO2 via the enzyme carbonic anhydrase according to the following reaction: This causes decreased circulating hydrogen ion concentration, and increased pH (alkalosis).[9][10] Diagnosis[edit] The diagnosis of respiratory alkalosis is done via test that measure the oxygen and carbon dioxide levels (in the blood), chest x-ray and a pulmonary function test of the individual.[1] The Davenport diagram allows clinicians or investigators to outline blood bicarbonate concentr Continue reading >>

Respiratory Alkalosis

Respiratory Alkalosis

What is respiratory alkalosis? Respiratory alkalosis occurs when the levels of carbon dioxide and oxygen in the blood are not balanced. Your body needs oxygen to function properly. When you inhale, you introduce oxygen into the lungs. When you exhale, you release carbon dioxide, which is a waste product. Normally, the respiratory system keeps these two gases in balance. Respiratory alkalosis occurs when you breathe too fast or too deep and carbon dioxide levels drop too low. This causes the pH of the blood to rise and become too alkaline. When the blood becomes too acidic, respiratory acidosis occurs. Hyperventilation is typically the underlying cause of respiratory alkalosis. Hyperventilation is also known as overbreathing. Someone who is hyperventilating breathes very deeply or rapidly. Causes of hyperventilation Panic attacks and anxiety are the most common causes of hyperventilation. However, they’re not the only possible causes. Others include: pain drug use fever infection If you’re experiencing hyperventilation (especially for the first time), don’t assume you know the cause. Make an appointment with your doctor. Overbreathing is a sign that respiratory alkalosis is likely to develop. However, low carbon dioxide levels in the blood also have a number of physical effects, including: dizziness bloating feeling lightheaded numbness or muscle spasms in the hands and feet discomfort in the chest area confusion dry mouth tingling in the arms feeling short of breath The treatment for respiratory alkalosis depends on the underlying cause. Panic and anxiety-related causes Treating the condition is a matter of raising carbon dioxide levels in the blood. The following strategies and tips are useful for respiratory alkalosis caused by overbreathing due to panic and anx Continue reading >>

Respiratory Alkalosis

Respiratory Alkalosis

Respiratory Alkalosis = a primary acid-base disorder in which arterial pCO2 falls to a level lower than expected. If there is a co-existing metabolic acidosis, then the expected pCO2 used for comparison is not 40mmHg but a calculated value which adjusts for the amount of change in arterial pCO2 which occurs due to respiratory compensation. hyperventilation (ie increased alveolar ventilation) is the mechanism responsible for the lowered arterial pCO2 in ALL cases of respiratory alkalosis. this low arterial pCO2 will be sensed by the central and peripheral chemoreceptors and the hyperventilation will be inhibited unless the patients ventilation is controlled. Central Causes (direct action via respiratory centre) Other supra-tentorial causes (pain, fear, stress, voluntary) Various drugs (eg analeptics, propanidid, salicylate intoxication) Various endogenous compounds (eg progesterone during pregnancy, cytokines during sepsis, toxins in patients with chronic liver disease) Pulmonary Causes (act via intrapulmonary receptors) Hypoxiaemia (act via peripheral chemoreceptors) this is different to the situation with a metabolic alkalosis where maintenance of the disorder requires an abnormality to maintain it as well as the problem which initiated it. increased neuromuscular irritability (eg paraesthesias such as circumoral tingling & numbness; carpopedal spasm) decreased intracranial pressure (secondary to cerebral vasoconstriction) inhibition of respiratory drive via the central & peripheral chemoreceptors cerebral blood flow (CBF) decreases quite markedly with hypocapnia cerebral vasoconstriction (causing decreased cerebral blood flow) shift of the haemoglobin oxygen dissociation curve to the left (impairing peripheral oxygen unloading) Compensation in an ACUTE Respiratory Al Continue reading >>

Respiratory Alkalosis

Respiratory Alkalosis

Uncompensated Laboratory Results: pH =7.58, pCO2 = 27, HCO3- = 24. a. List the condition - acidosis or alkalosis, metabolic or respiratory, compensated or uncompensated. b. What is the primary cause of the condition? Hyperventilation - excess loss of CO2 gas. c. Explain why the pH is high using the other lab results, using the primary cause, and equilibrium principles. If there is an excess loss of carbon dioxide from the lungs, it is also low in the blood. If carbon dioxide is low, the equilibrium shifts left, as a result the hydrogen ion concentration decrease, which results in the pH increasing. d. State and explain how the compensation will return pH to normal using equilibrium principles. Compensation is for the kidney's to excrete more bicarbonate, which gives a lower bicarbonate in the blood. As a result the equilibrium shifts to the right to compensate for the loss of bicarbonate. As a result, the hydrogen ion concentration then increase, which gives a decrease in the pH more toward normal. e. Explain how the treatment with __?___ will work using equilibrium principles. The treatment according to the Table 2 is to hold breath or breath into a paper bag. What will this do? This will serve to help retain more carbon dioxide in the blood. If the carbon dioxide level is higher in the blood, the equilibrium will shift right to increase the hydrogen ion and decrease the pH. Continue reading >>

5.5 Metabolic Acidosis - Compensation

5.5 Metabolic Acidosis - Compensation

Acid-Base Physiology 5.5.1 Hyperventilation Compensation for a metabolic acidosis is hyperventilation to decrease the arterial pCO2. This hyperventilation was first described by Kussmaul in patients with diabetic ketoacidosis in 1874. The metabolic acidosis is detected by both the peripheral and central chemoreceptors and the respiratory center is stimulated. The initial stimulation of the central chemoreceptors is due to small increases in brain ISF [H+]. The subsequent increase in ventilation causes a fall in arterial pCO2 which inhibits the ventilatory response. Maximal compensation takes 12 to 24 hours The chemoreceptor inhibition acts to limit and delay the full ventilatory response until bicarbonate shifts have stabilised across the blood brain barrier. The increase in ventilation usually starts within minutes and is usually well advanced at 2 hours of onset but maximal compensation may take 12 to 24 hours to develop. This is �maximal� compensation rather than �full� compensation as it does not return the extracellular pH to normal. In situations where a metabolic acidosis develops rapidly and is short-lived there is usually little time for much compensatory ventilatory response to occur. An example is the acute and sometimes severe lactic acidosis due to a prolonged generalised convulsion: this corrects due to rapid hepatic uptake and metabolism of the lactate following cessation of convulsive muscular activity, and hyperventilation due to the acidosis does not occur. The expected pCO2 at maximal compensation can be calculated from a simple formula The arterial pCO2 at maximal compensation has been measured in many patients with a metabolic acidosis. A consistent relationship between bicarbonate level and pCO2 has been found. It can be estimated from the Continue reading >>

Respiratory Alkalosis: Causes And Regulation

Respiratory Alkalosis: Causes And Regulation

Respiratory Alkalosis: Causes and Regulation Watch short & fun videos Start Your Free Trial Today An error occurred trying to load this video. Try refreshing the page, or contact customer support. You must create an account to continue watching Start Your Free Trial To Continue Watching As a member, you'll also get unlimited access to over 70,000 lessons in math, English, science, history, and more. Plus, get practice tests, quizzes, and personalized coaching to help you succeed. Coming up next: The Causes of Chronic Obstructive Pulmonary Disease (COPD) Log in or sign up to add this lesson to a Custom Course. Custom Courses are courses that you create from Study.com lessons. Use them just like other courses to track progress, access quizzes and exams, and share content. Organize and share selected lessons with your class. Make planning easier by creating your own custom course. Create a new course from any lesson page or your dashboard. Click "Add to" located below the video player and follow the prompts to name your course and save your lesson. Click on the "Custom Courses" tab, then click "Create course". Next, go to any lesson page and begin adding lessons. Edit your Custom Course directly from your dashboard. Name your Custom Course and add an optional description or learning objective. Create chapters to group lesson within your course. Remove and reorder chapters and lessons at any time. Share your Custom Course or assign lessons and chapters. Share or assign lessons and chapters by clicking the "Teacher" tab on the lesson or chapter page you want to assign. Students' quiz scores and video views will be trackable in your "Teacher" tab. You can share your Custom Course by copying and pasting the course URL. Only Study.com members will be able to access the entire Continue reading >>

Respiratory Alkalosis

Respiratory Alkalosis

(Video) Overview of Acid-Base Maps and Compensatory Mechanisms By James L. Lewis, III, MD, Attending Physician, Brookwood Baptist Health and Saint Vincents Ascension Health, Birmingham Respiratory alkalosis is a primary decrease in carbon dioxide partial pressure (Pco2) with or without compensatory decrease in bicarbonate (HCO3); pH may be high or near normal. Cause is an increase in respiratory rate or volume (hyperventilation) or both. Respiratory alkalosis can be acute or chronic. The chronic form is asymptomatic, but the acute form causes light-headedness, confusion, paresthesias, cramps, and syncope. Signs include hyperpnea or tachypnea and carpopedal spasms. Diagnosis is clinical and with ABG and serum electrolyte measurements. Treatment is directed at the cause. (See also Acid-Base Regulation , Acid-Base Disorders , and Hyperventilation Syndrome .) Respiratory alkalosis is a primary decrease in Pco2 (hypocapnia) due to an increase in respiratory rate and/or volume (hyperventilation). Ventilation increase occurs most often as a physiologic response to hypoxia (eg, at high altitude), metabolic acidosis , and increased metabolic demands (eg, fever) and, as such, is present in many serious conditions. In addition, pain and anxiety and some CNS disorders (eg, stroke, seizure [post-ictal]) can increase respirations without a physiologic need. Distinction is based on the degree of metabolic compensation. Excess HCO3 is buffered by extracellular hydrogen ion (H+) within minutes, but more significant compensation occurs over 2 to 3 days as the kidneys decrease H+ excretion. Pseudorespiratory alkalosis is low arterial Pco2 and high pH in mechanically ventilated patients with severe metabolic acidosis due to poor systemic perfusion (eg, cardiogenic shock, during CPR). Pseu Continue reading >>

6.2 Respiratory Alkalosis - Causes

6.2 Respiratory Alkalosis - Causes

Hyperventilation is the mechanism in ALL cases Hyperventilation (ie increased alveolar ventilation) is the mechanism responsible for the lowered arterial pCO2 in ALL cases of respiratory alkalosis. This low arterial pCO2 will be sensed by the central and peripheral chemoreceptors and the hyperventilation will be inhibited unless the patients ventilation is controlled. 1. Central Causes (direct action via respiratory centre) Other 'supra-tentorial' causes (pain, fear, stress, voluntary) Various drugs (eg analeptics, propanidid, salicylate intoxication) Various endogenous compounds (eg progesterone during pregnancy, cytokines during sepsis, toxins in patients with chronic liver disease) 2. Hypoxaemia (act via peripheral chemoreceptors) Respiratory stimulation via peripheral chemoreceptors 3. Pulmonary Causes (act via intrapulmonary receptors) 4. Iatrogenic (act directly on ventilation) Can a decreased CO2 production cause respiratory alkalosis? Hyperventilation is the mechanism in all of the situations in the above list & indeed in all cases. Theoretically, a decreased carbon dioxide production could result in respiratory alkalosis if alveolar ventilation remained fixed. But this would not occur in a normal person because any drop in arterial pCO2 would reflexly cause a decreased ventilation (via chemoreceptor inhibitory input into the respiratory centre). About the only situation where maybe a decrease in CO2 production could be the mechanism of respiratory alkalosis would be in an intubated patient on fixed ventilation during Anaesthesia or in Intensive Care Unit and where the CO2 production was low due to hypothermia and decreased metabolic rate. However, even in such a circumstance, this mechanism is usually referred to as 'excessive controlled ventilation' (which it Continue reading >>

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