diabetestalk.net

What Is Respiratory Alkalosis And Acidosis?

Acidosis And Alkolosis

Acidosis And Alkolosis

The normal pH value for the body fluids is between pH 7.35 and 7.45. When the pH value of body fluids is below 7.35, the condition is called acidosis, and when the pH is above 7.45, it is called alkalosis. Metabolism produces acidic products that lower the pH of the body fluids. For example, carbon dioxide is a by-product of metabolism, and carbon dioxide combines with water to form carbonic acid. Also, lactic acid is a product of anaerobic metabolism, protein metabolism produces phosphoric and sulfuric acids, and lipid metabolism produces fatty acids. These acidic substances must continuously be eliminated from the body to maintain pH homeostasis. Rapid elimination of acidic products of metabolism results in alkalosis, and the failure to eliminate acidic products of metabolism results in acidosis. The major effect of acidosis is depression of the central nervous system. When the pH of the blood falls below 7.35, the central nervous system malfunctions, and the individual becomes disoriented and possibly comatose as the condition worsens. A major effect of alkalosis is hyperexcitability of the nervous system. Peripheral nerves are affected first, resulting in spontaneous nervous stimulation of muscles. Spasms and tetanic contractions and possibly extreme nervousness or convulsions result. Severe alkalosis can cause death as a result of tetany of the respiratory muscles. Although buffers in the body fluids help resist changes in the pH of body fluids, the respiratory system and the kidneys regulate the pH of the body fluids. Malfunctions of either the respiratory system or the kidneys can result in acidosis or alkalosis. Acidosis and alkalosis are categorized by the cause of the condition. Respiratory acidosis or respiratory alkalosis results from abnormalities of the r Continue reading >>

Acid Base Disorders

Acid Base Disorders

Arterial blood gas analysis is used to determine the adequacy of oxygenation and ventilation, assess respiratory function and determine the acid–base balance. These data provide information regarding potential primary and compensatory processes that affect the body’s acid–base buffering system. Interpret the ABGs in a stepwise manner: Determine the adequacy of oxygenation (PaO2) Normal range: 80–100 mmHg (10.6–13.3 kPa) Determine pH status Normal pH range: 7.35–7.45 (H+ 35–45 nmol/L) pH <7.35: Acidosis is an abnormal process that increases the serum hydrogen ion concentration, lowers the pH and results in acidaemia. pH >7.45: Alkalosis is an abnormal process that decreases the hydrogen ion concentration and results in alkalaemia. Determine the respiratory component (PaCO2) Primary respiratory acidosis (hypoventilation) if pH <7.35 and HCO3– normal. Normal range: PaCO2 35–45 mmHg (4.7–6.0 kPa) PaCO2 >45 mmHg (> 6.0 kPa): Respiratory compensation for metabolic alkalosis if pH >7.45 and HCO3– (increased). PaCO2 <35 mmHg (4.7 kPa): Primary respiratory alkalosis (hyperventilation) if pH >7.45 and HCO3– normal. Respiratory compensation for metabolic acidosis if pH <7.35 and HCO3– (decreased). Determine the metabolic component (HCO3–) Normal HCO3– range 22–26 mmol/L HCO3 <22 mmol/L: Primary metabolic acidosis if pH <7.35. Renal compensation for respiratory alkalosis if pH >7.45. HCO3 >26 mmol/L: Primary metabolic alkalosis if pH >7.45. Renal compensation for respiratory acidosis if pH <7.35. Additional definitions Osmolar Gap Use: Screening test for detecting abnormal low MW solutes (e.g. ethanol, methanol & ethylene glycol [Reference]) An elevated osmolar gap (>10) provides indirect evidence for the presence of an abnormal solute which is prese 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 >>

Effect Of Respiratory Acidosis And Respiratory Alkalosis On Renal Transport Enzymes.

Effect Of Respiratory Acidosis And Respiratory Alkalosis On Renal Transport Enzymes.

Am J Physiol. 1994 Sep;267(3 Pt 2):F390-9. Effect of respiratory acidosis and respiratory alkalosis on renal transport enzymes. Department of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock 79430. We studied the effect of respiratory acidosis and respiratory alkalosis on acid-base composition and on microdissected renal adenosinetriphosphatase (ATPase) enzymes. Rats were subjected to hypercapnia or hypocapnia of 6, 24, and 72 h duration. After 6 h of hypercapnia, collecting tubule (CT) ATPases were not changed. At 24 h, plasma bicarbonate was 35 +/- 1 meq/l (P < 0.01) and CT H-ATPase and H-K-ATPase activities were 90% greater than controls (P < 0.01). By 72 h, plasma bicarbonate was 37 +/- 1 meq/l (P < 0.005 vs. control) and CT enzyme activity had increased even more, averaging approximately 130% of control (P < 0.05). Significant increases in enzyme activities were also observed in the proximal convoluted tubule and medullary thick ascending limb. Plasma aldosterone was three to four times that of control at all three time periods. In hormone-replete adrenalectomized rats, acid-base parameters and ATPase activities were the same as those seen in adrenal intact animals. After 6 h of hypocapnia, plasma bicarbonate was not significantly changed, but H-ATPase and Na-K-ATPase activities were decreased by 35% along the entire nephron (P < 0.05). H-K-ATPase activity in CT also decreased by 35%. At 24 h, plasma bicarbonate was 20.5 +/- 0.5 meq/l (P < 0.05 vs. control) and CT H-ATPase and H-K-ATPase activities were 60% less than control (P < 0.01). By 72 h, plasma bicarbonate was 18.5 +/- 0.5 meq/l (P < 0.05); however, only CT H-ATPase activity continued to fall, averaging 75% less than control (P < 0.005). Hypocapnia had no effect on plasma aldosteron Continue reading >>

Causes Of Respiratory Acidosis And Alkalosis - Deranged Physiology

Causes Of Respiratory Acidosis And Alkalosis - Deranged Physiology

Causes of Respiratory Acidosis and Alkalosis Respiratory acidosis and alkalosis are featured in virtually every paper, and being able to identify a respiratory acid-base disturbance is a vital skill for the CICM fellowship candidate. The SAQs will frequently require the application of the usual rules of compensation to reveal a hidden acid-base disorder, eg. "this patient has a low CO2 but it is not low enough". Questions which involve respiratory acid-base disturbances are too numerous to list. Some representative examples include the following: Question 12.3 from the second paper of 2014 Question 3.4 from the first paper of 2013 Question 3.5 from the first paper of 2013 Question 8.3 from the first paper of 2012 Question 9.1 from the first paper of 2011 Question 7.2 from the first paper of 2009 Several CICM fellowship questions revolve around the core question, "what possible causes for this respiratory acid-base disturbance can you think of ?" The causes can be split into aetiological categories, as below: Causes of Respiratory Acidosis and Alkalosis Rebreathing of CO2-containing expired gas Insufflation of CO2 into body cavity (eg for laparoscopic surgery) CO2 increases by 3mmg for every minute of apnoea central respiratory depression eg. by drugs or post-ictally neuromuscular disorders resulting in weakness lung or chest wall defects resulting in restriction The pH change in response to a chronic respiratory acid-base disturbance 0: An acute change in PaCO2 will not change the Standard Base Excess. 4: In chronic disorders, the expected change in SBE will be 0.4 times the change in PaCO2 ... i.e. expected SBE = 0.4 (40 - PaCO2) 1: In compensation for metabolic acidosis, the compensatory change in PaCO2 will be proportional to the SBE. ..i.e. expected CO2 = 40 + (1.0 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 >>

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 >>

Respiratory Alkalosis

Respiratory Alkalosis

Background 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. Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

What is respiratory acidosis? Respiratory acidosis is a condition that occurs when the lungs can’t remove enough of the carbon dioxide (CO2) produced by the body. Excess CO2 causes the pH of blood and other bodily fluids to decrease, making them too acidic. Normally, the body is able to balance the ions that control acidity. This balance is measured on a pH scale from 0 to 14. Acidosis occurs when the pH of the blood falls below 7.35 (normal blood pH is between 7.35 and 7.45). Respiratory acidosis is typically caused by an underlying disease or condition. This is also called respiratory failure or ventilatory failure. Normally, the lungs take in oxygen and exhale CO2. Oxygen passes from the lungs into the blood. CO2 passes from the blood into the lungs. However, sometimes the lungs can’t remove enough CO2. This may be due to a decrease in respiratory rate or decrease in air movement due to an underlying condition such as: There are two forms of respiratory acidosis: acute and chronic. Acute respiratory acidosis occurs quickly. It’s a medical emergency. Left untreated, symptoms will get progressively worse. It can become life-threatening. Chronic respiratory acidosis develops over time. It doesn’t cause symptoms. Instead, the body adapts to the increased acidity. For example, the kidneys produce more bicarbonate to help maintain balance. Chronic respiratory acidosis may not cause symptoms. Developing another illness may cause chronic respiratory acidosis to worsen and become acute respiratory acidosis. Initial signs of acute respiratory acidosis include: headache anxiety blurred vision restlessness confusion Without treatment, other symptoms may occur. These include: sleepiness or fatigue lethargy delirium or confusion shortness of breath coma The chronic form of Continue reading >>

Metabolic Acidosis Or Respiratory Alkalosis? Evaluation Of A Low Plasmabicarbonate Using The Urine Anion Gap.

Metabolic Acidosis Or Respiratory Alkalosis? Evaluation Of A Low Plasmabicarbonate Using The Urine Anion Gap.

1. Am J Kidney Dis. 2017 Sep;70(3):440-444. doi: 10.1053/j.ajkd.2017.04.017. Epub2017 Jun 7. Metabolic Acidosis or Respiratory Alkalosis? Evaluation of a Low PlasmaBicarbonate Using the Urine Anion Gap. Batlle D(1), Chin-Theodorou J(2), Tucker BM(3). (1)Division of Nephrology & Hypertension, Department of Medicine, The Feinberg School of Medicine, Northwestern University, Chicago, IL. Electronic address: [email protected] (2)Division of Nephrology & Hypertension, Department of Medicine, The Feinberg School of Medicine, Northwestern University, Chicago, IL. (3)Section of Nephrology, Department of Medicine, Yale University School of Medicine, New Haven, CT. Hypobicarbonatemia, or a reduced bicarbonate concentration in plasma, is afinding seen in 3 acid-base disorders: metabolic acidosis, chronic respiratoryalkalosis and mixed metabolic acidosis and chronic respiratory alkalosis.Hypobicarbonatemia due to chronic respiratory alkalosis is often misdiagnosed as a metabolic acidosis and mistreated with the administration of alkali therapy.Proper diagnosis of the cause of hypobicarbonatemia requires integration of thelaboratory values, arterial blood gas, and clinical history. The informationderived from the urinary response to the prevailing acid-base disorder is useful to arrive at the correct diagnosis. We discuss the use of urine anion gap, as asurrogate marker of urine ammonium excretion, in the evaluation of a patient withlow plasma bicarbonate concentration to differentiate between metabolic acidosis and chronic respiratory alkalosis. The interpretation and limitations of urineacid-base indexes at bedside (urine pH, urine bicarbonate, and urine anion gap)to evaluate urine acidification are discussed.Copyright 2017 National Kidney Foundation, Inc. Published by E Continue reading >>

Respiratory Alkalosis

Respiratory Alkalosis

Abstract: 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. Respiratory Alkalosis Respiratory alkalosis results from excessive ventilation (hyperventilation). In respiratory alkalosis, Pco2 falls, leading to an increase in pH (alkalosis). If the alkalosis persists for more than 12 hours, the alkalosis may be partially compensated by decreased renal H+ excretion. During respiratory alkalosis, HCO3− may fall acutely owing to equilibration with depleted CO2. There is a 2 mEq/L decrease in HCO3− per 10 mm Hg decrease Pco2 that is chemical and not part of the renal compensation. Common causes of respiratory alkalosis include hyperventilation from voluntary effort (anxiety) or stimulation of central respiratory centers secondary to meningitis or a fever. 2 Respiratory Alkalosis Respiratory alkalosis is associated with an increase in pH and a decrease in pCO2. a Causes of Respiratory Alkalosis Respiratory alkalosis is due to hyperventilation, whic Continue reading >>

Acid-base Disorders

Acid-base Disorders

Content currently under development Acid-base disorders are a group of conditions characterized by changes in the concentration of hydrogen ions (H+) or bicarbonate (HCO3-), which lead to changes in the arterial blood pH. These conditions can be categorized as acidoses or alkaloses and have a respiratory or metabolic origin, depending on the cause of the imbalance. Diagnosis is made by arterial blood gas (ABG) interpretation. In the setting of metabolic acidosis, calculation of the anion gap is an important resource to narrow down the possible causes and reach a precise diagnosis. Treatment is based on identifying the underlying cause. Continue reading >>

The Effects Of Respiratory Alkalosis And Acidosis On Net Bicarbonate Flux Along The Rat Loop Of Henle In Vivo.

The Effects Of Respiratory Alkalosis And Acidosis On Net Bicarbonate Flux Along The Rat Loop Of Henle In Vivo.

Am J Physiol. 1997 Nov;273(5 Pt 2):F698-705. The effects of respiratory alkalosis and acidosis on net bicarbonate flux along the rat loop of Henle in vivo. Department of Medicine, University College London Medical School, United Kingdom. We have studied the effects of acute respiratory alkalosis (ARALK, hyperventilation) and acidosis (ARA, 8% CO2), chronic respiratory acidosis (CRA; 10% CO2 for 7-10 days), and subsequent recovery from CRA breathing air on loop of Henle (LOH) net bicarbonate flux (JHCO3) by in vivo tubule microperfusion in anesthetized rats. In ARALK blood, pH increased to 7.6, and blood bicarbonate concentration ([HCO3-]) decreased from 29 to 22 mM. Fractional urinary bicarbonate excretion (FEHCO3) increased threefold, but LOH JHCO3 was unchanged. In ARA, blood pH fell to 7.2, and blood [HCO3-] rose from 28 to 34 mM; FEHCO3 was reduced to < 0.1%, but LOH JHCO3 was unaltered. In CRA, blood pH fell to 7.2, and blood [HCO3-] increased to > 50 mM, whereas FEHCO3 decreased to < 0.1%. JHCO3 was reduced by approximately 30%. Bicarbonaturia occurred when CRA rats breathed air, yet LOH JHCO3 increased (by 30%) to normal. These results suggest that LOH JHCO3 is affected by the blood-to-tubule lumen [HCO3-] gradient and HCO3- backflux. When the usual perfusing solution at 20 nl/min was made HCO3- free, mean JHCO3 was -34.5 +/- 4.4 pmol/min compared with 210 +/- 28.1 pmol/min plus HCO3-. When a low-NaCl perfusate (to minimize net fluid absorption) containing mannitol and acetazolamide (2 x 10(-4) M, to abolish H(+)-dependent JHCO3) was used, JHCO3 was -112.8 +/- 5.6 pmol/min. Comparable values for JHCO3 at 10 nl/min were -35.9 +/- 5.8 and -72.5 +/- 8.8 pmol/min, respectively. These data indicate significant backflux of HCO3-along the LOH, which depends on the bloo Continue reading >>

Abg: Respiratory Acidosis/metabolic Alkalosis

Abg: Respiratory Acidosis/metabolic Alkalosis

Home / ABA Keyword Categories / A / ABG: Respiratory acidosis/metabolic alkalosis ABG: Respiratory acidosis/metabolic alkalosis A combined respiratory acidosis / metabolic alkalosis will result in elevated PaCO2 and serum bicarbonate. Which process is the primary disorder (e.g. primary respiratory acidosis with metabolic compensation versus primary metabolic alkalosis with respiratory compensation) is dependent on the pH in an acidotic patient, the acidosis is primary (and the alkalosis is compensatory) and vice versa. Compensation behaves in accordance with the following rules: Metabolic Acidosis: As bicarbonate goes from 10 to 5, pCO2 will bottom out at 15. pCO2 = 1.5 x [HCO3-] + 8 (or pCO2 = 1.25 x [HCO3-]) Metabolic Alkalosis: compensation here is less because CO2 is driving force for respiration. pCO2 = 0.7 x [HCO3-] + 21 (or pCO2 = 0.75 x [HCO3-]) Acutely: [HCO3-] = 0.1 x pCO2 or pH = 0.008 x pCO2 Chronically: [HCO3-] = 0.4 x pCO2 or pH = 0.003 x pCO2 Respiratory Alkalosis: Metabolic compensation will automatically be retention of chloride (i.e., hyperchloremic, usually referred to as loss of bicarb although it is the strong ion difference that matters). If you have an anion gap, then youve automatically got a little bit of an acidosis on top of the compensation (because the compensation should be a NON-gap acidotic process. Acutely: [HCO3-] = 0.2 x pCO2 (or pH = 0.008 x pCO2) Chronically: [HCO3-] = 0.4 x pCO2 (or pH = 0.017 x pCO2) 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 >>

More in ketosis