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Respiratory Acidosis Hyperventilation

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 Acidosis

Respiratory Acidosis

Practice Essentials Respiratory acidosis is an acid-base balance disturbance due to alveolar hypoventilation. Production of carbon dioxide occurs rapidly and failure of ventilation promptly increases the partial pressure of arterial carbon dioxide (PaCO2). [1] The normal reference range for PaCO2 is 35-45 mm Hg. Alveolar hypoventilation leads to an increased PaCO2 (ie, hypercapnia). The increase in PaCO2, in turn, decreases the bicarbonate (HCO3–)/PaCO2 ratio, thereby decreasing the pH. Hypercapnia and respiratory acidosis ensue when impairment in ventilation occurs and the removal of carbon dioxide by the respiratory system is less than the production of carbon dioxide in the tissues. Lung diseases that cause abnormalities in alveolar gas exchange do not typically result in alveolar hypoventilation. Often these diseases stimulate ventilation and hypocapnia due to reflex receptors and hypoxia. Hypercapnia typically occurs late in the disease process with severe pulmonary disease or when respiratory muscles fatigue. (See also Pediatric Respiratory Acidosis, Metabolic Acidosis, and Pediatric Metabolic Acidosis.) Acute vs chronic respiratory acidosis Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (ie, >45 mm Hg) with an accompanying acidemia (ie, pH < 7.35). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal or near-normal pH secondary to renal compensation and an elevated serum bicarbonate levels (ie, >30 mEq/L). Acute respiratory acidosis is present when an abrupt failure of ventilation occurs. This failure in ventilation may result from depression of the central respiratory center by one or another of the foll 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 >>

Hyperventilation | Pathology | Britannica.com

Hyperventilation | Pathology | Britannica.com

Hyperventilation, sustained abnormal increase in breathing . During hyperventilation the rate of removal of carbon dioxide from the blood is increased. As the partial pressure of carbon dioxide in the blood decreases, respiratory alkalosis , characterized by decreased acidity or increased alkalinity of the blood, ensues. In turn, alkalosis causes constriction of the small blood vessels that supply the brain. Reduced blood supply to the brain can cause a variety of symptoms, including light-headedness and tingling of the fingertips. Severe hyperventilation can cause transient loss of consciousness . The alveoli and capillaries in the lungs exchange oxygen for carbon dioxide. Imbalances in the exchange of these gases can lead to dangerous respiratory disorders, such as respiratory acidosis or hyperventilation. In addition, accumulation of fluid in the alveolar spaces can interfere with gas exchange, causing symptoms such as shortness of breath. Anxiety is the most common cause of hyperventilation. Panic disorder, a severe episodic form of anxiety, usually causes hyperventilation with resultant symptoms. Treatment of recurrent hyperventilation begins with a complete explanation by the patient of the condition and the symptoms it causes. Some people benefit from psychotherapy and medications to deal with the underlying anxiety. 3 references found in Britannica articles Corrections? Updates? Help us improve this article! Contact our editors with your feedback. Error when sending the email. Try again later. We welcome suggested improvements to any of our articles. You can make it easier for us to review and, hopefully, publish your contribution by keeping a few points in mind. Encyclopdia Britannica articles are written in a neutral objective tone for a general audience. You 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 >>

Hyperventilation

Hyperventilation

Not to be confused with hypoventilation or Hyperventilation syndrome. Hyperventilation (a.k.a. overbreathing) occurs when the rate or tidal volume of breathing eliminates more carbon dioxide than the body can produce.[1][2][3] This lowers the concentration of carbon dioxide dissolved in the blood leading to hypocapnia. The body normally attempts to compensate for this homeostatically but if this fails or is overridden the blood pH will rise, leading to respiratory alkalosis. The symptoms of respiratory alkalosis include: dizziness, tingling in the lips, hands or feet, headache, weakness, fainting and seizures. In extreme cases it may cause carpopedal spasms, a flapping and contraction of the hands and feet.[3][4] Factors that may induce or sustain[2] hyperventilation include: physiological stress, anxiety, high altitude, head injury, stroke, respiratory disorders such as asthma, pneumonia or hyperventilation syndrome,[5] cardiovascular problems such as pulmonary embolisms, anemia, an incorrectly calibrated medical respirator[1][3] and adverse reactions to certain drugs. Hyperventilation can also be induced intentionally to achieve an altered state of consciousness such as in the choking game, or in an attempt to extend a breath-hold dive. [edit] See also[edit] List of terms of lung size and activity Control of respiration Choking game a game which may involve hyperventilation in order to induce temporary syncope and euphoria Respiratory alkalosis Shallow water blackout, the role of hyperventilation in some drowning incidents Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

Respiratory acidosis can arise from a break in any one of these links. For example, it can be caused from depression of the respiratory center through drugs or metabolic disease, or from limitations in chest wall expansion due to neuromuscular disorders or trauma (Table 90-1). It can also arise from pulmonary disease, card iog en ic pu lmon a ryedema, a spira tion of a foreign body or vomitus, pneumothorax and pleural space disease, or through mechanical hypoventilation. Unless there is a superimposed or secondary metabolic acidosis, the plasma anion gap will usually be normal in respiratory acidosis. Introduction Respiratory acidosis is characterized by an increased arterial blood PCO2 and H+ ion concentration. The major cause of respiratory acidosis is alveolar hypoventilation. The expected physiologic response is an increased PHCO3. The increase in concentration of bicarbonate ions (HCO3) in plasma (PHCO3) is tiny in patients with acute respiratory acidosis, but is much larger in patients with chronic respiratory acidosis. Respiratory alkalosis is caused by hyperventilation and is characterized by a low arterial blood PCO2 and H+ ion concentration. The expected physiologic response is a decrease in PHCO3. As in respiratory acidosis, this response is modest in patients with acute respiratory alkalosis and much larger in patients with chronic respiratory alkalosis. Although respiratory acid-base disorders are detected by measurement of PCO2 and pH in arterial blood and may reveal the presence of a serious underlying disease process that affected ventilation, it is important to recognize the effect of changes in capillary blood PCO2 in the different organs on the binding of H+ ions to intracellular proteins, which may change their charge, shape, and possibly their funct 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 >>

Hyperventilation And Blood Acid-base Balance In Hypercapnia Exposed Red Drum(sciaenops Ocellatus).

Hyperventilation And Blood Acid-base Balance In Hypercapnia Exposed Red Drum(sciaenops Ocellatus).

1. J Comp Physiol B. 2016 May;186(4):447-60. doi: 10.1007/s00360-016-0971-7. Epub2016 Feb 27. Hyperventilation and blood acid-base balance in hypercapnia exposed red drum(Sciaenops ocellatus). (1)Marine Science Institute, The University of Texas at Austin, Port Aransas, TX, 78373-5015, USA. [email protected] (2)Marine Science Institute, The University of Texas at Austin, Port Aransas, TX, 78373-5015, USA. Hyperventilation is a common response in fish exposed to elevated water CO2. Itis believed to lessen the respiratory acidosis associated with hypercapnia bylowering arterial PCO2, but the contribution of hyperventilation to bloodacid-base compensation has yet to be quantified. Hyperventilation may alsoincrease the flux of irons across the gill epithelium and the cost ofosmoregulation, owing to the osmo-respiratory compromise. Therefore, hypercapnia exposed fish may increase standard metabolic rate (SMR) leaving less energy forphysiological functions such as foraging, migration, growth and reproduction.Here we show that gill ventilation, blood PCO2 and total blood [CO2] increased inred drum (Sciaenops ocellatus) exposed to 1000 and 5000 atm water CO2, and that blood PCO2 and total blood [CO2] decrease in fish during hypoxia inducedhyperventilation. Based on these results we estimate the ventilatorycontributions to total acid-base compensation in 1000 and 5000 atm water CO2. Wefind that S. ocellatus only utilize a portion of its ventilatory capacity toreduce the acid-base disturbance in 1000 atm water CO2. SMR was unaffected byboth salinity and hypercapnia exposure indicating that the cost of osmoregulationis small relative to SMR, and that the lack of increased ventilation in 1000 atmwater CO2 despite the capacity to do so is not due to an energetic tradeoffbetween ac Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

Respiratory acidosis is a medical emergency in which decreased ventilation (hypoventilation) increases the concentration of carbon dioxide in the blood and decreases the blood's pH (a condition generally called acidosis). Carbon dioxide is produced continuously as the body's cells respire, and this CO2 will accumulate rapidly if the lungs do not adequately expel it through alveolar ventilation. Alveolar hypoventilation thus leads to an increased PaCO2 (a condition called hypercapnia). The increase in PaCO2 in turn decreases the HCO3−/PaCO2 ratio and decreases pH. Terminology[edit] Acidosis refers to disorders that lower cell/tissue pH to < 7.35. Acidemia refers to an arterial pH < 7.36.[1] Types of respiratory acidosis[edit] Respiratory acidosis can be acute or chronic. In acute respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range (over 6.3 kPa or 45 mm Hg) with an accompanying acidemia (pH <7.36). In chronic respiratory acidosis, the PaCO2 is elevated above the upper limit of the reference range, with a normal blood pH (7.35 to 7.45) or near-normal pH secondary to renal compensation and an elevated serum bicarbonate (HCO3− >30 mm Hg). Causes[edit] Acute[edit] Acute respiratory acidosis occurs when an abrupt failure of ventilation occurs. This failure in ventilation may be caused by depression of the central respiratory center by cerebral disease or drugs, inability to ventilate adequately due to neuromuscular disease (e.g., myasthenia gravis, amyotrophic lateral sclerosis, Guillain–Barré syndrome, muscular dystrophy), or airway obstruction related to asthma or chronic obstructive pulmonary disease (COPD) exacerbation. Chronic[edit] Chronic respiratory acidosis may be secondary to many disorders, including COPD. Hypoventilation Continue reading >>

Respiratory Alkalosis | Definition Of Respiratory Alkalosis By Medical Dictionary

Respiratory Alkalosis | Definition Of Respiratory Alkalosis By Medical Dictionary

Respiratory alkalosis | definition of respiratory alkalosis by Medical dictionary Related to respiratory alkalosis: metabolic alkalosis , respiratory acidosis Respiratory alkalosis is a condition where the amount of carbon dioxide found in the blood drops to a level below normal range. This condition produces a shift in the body's pH balance and causes the body's system to become more alkaline (basic). This condition is brought on by rapid, deep breathing called hyperventilation. Respiratory alkalosis is an alkali imbalance in the body caused by a lower-than-normal level of carbon dioxide in the blood. In the lungs, oxygen from inhaled air is exchanged for carbon dioxide from the blood. This process takes place between the alveoli (tiny air pockets in the lungs) and the blood vessels that connect to them. When a person hyperventilates, this exchange of oxygen for carbon dioxide is speeded up, and the person exhales too much carbon dioxide. This lowered level of carbon dioxide causes the pH of the blood to increase, leading to alkalosis. The primary cause of respiratory alkalosis is hyperventilation. This rapid, deep breathing can be caused by conditions related to the lungs like pneumonia , lung disease, or asthma . More commonly, hyperventilation is associated with anxiety , fever, drug overdose, carbon monoxide poisoning, or serious infections. Tumors or swelling in the brain or nervous system can also cause this type of respiration. Other stresses to the body, including pregnancy , liver failure, high elevations, or metabolic acidosis can also trigger hyperventilation leading to respiratory alkalosis. Hyperventilation, the primary cause of respiratory alkalosis, is also the primary symptom. This symptom is accompanied by dizziness , light headedness, agitation, and Continue reading >>

Respiratory Acidosis/alkalosis

Respiratory Acidosis/alkalosis

In an attempt ot compensate, the kidneys retain bicarbonate and excrete excess H+ ions into the urine Initially the hyperventilation and respiratory stimulation caause abnormal rapid respirations(tachypnea); in an attempt to compensate, the kidneys excrete excess circulation bicarbonate into the urine. The total concentration of buffer base is lower than normal, with a relative increase in hydrogen ion concentration; thus a greater number of hydrogen ions is circulating in the blood than can be absorbed by the buffer system. A deficit of carbonic acid and a decrease in hydrogen ion concentration that results from the accumulation of base or from a loss of acid without a comparable loss of base in the body fluids. 1.Monitor for signs of respiratory distress. 2.Provide emotional support and reassurance to the client. 3.Encourage appropriate breathing patterns. 4.Assist with breathing techniques and breathing aids as prescribed. a.Encourage voluntary holding of the breath if appropriate b.Provide use of a rebreathing mask as prescribed c.Provide carbon dioxide breaths as prescribed (rebreathing into a paper bag) 5.Provide cautious care with ventilator clients so that they are not forced to take breaths too deeply or rapidly. 6.Monitor electrolyte values, particularly potassium and calcium levels. 8.Prepare to administer calcium gluconate for tetany as prescribed. 1.Monitor for signs of respiratory distress. Continue reading >>

Metabolic Acidosis And Hyperventilation Induced By Acetazolamide In Patients With Central Nervous System Pathology

Metabolic Acidosis And Hyperventilation Induced By Acetazolamide In Patients With Central Nervous System Pathology

ACETAZOLAMIDE, a carbonic anhydrase inhibitor, is used in patients with meningeal inflammation, mild intracranial hypertension, and basal skull fractures to decrease the formation of cerebrospinal fluid (CSF). It causes mild metabolic acidosis by inhibiting the reabsorption of bicarbonate (HCO−3) ions from renal tubules. This effect has been used successfully in the treatment of patients with chronic respiratory acidosis with superimposed metabolic alkalosis 1 and central sleep apnea syndrome. 2 Life-threatening metabolic acidosis during acetazolamide therapy has been observed only in patients with renal impairment or 3 diabetes 4 and in elderly patients. 5 Severe metabolic acidosis, associated with acetazolamide, in the absence of other predisposing factors has not been reported in patients with central nervous system disease. We report three cases of severe metabolic acidosis and hyperventilation during acetazolamide therapy in normal doses in adult patients without renal impairment. A 35-yr-old man with a head injury underwent craniotomy for evacuation of a traumatic left temporal extradural hematoma. Postoperatively, the patient underwent mechanical ventilation to maintain a partial pressure of arterial carbon dioxide (Paco2) of 30–35 mmHg. On the third postoperative day, 250 mg acetazolamide administered every 8 h through a nasogastric tube was started to treat a CSF leak from the operative wound. A T-piece trial of weaning was started on the fourth postoperative day. On the fifth postoperative day, patient respiratory rate increased to 40–44 breaths/min. Arterial blood gas analysis showed metabolic acidosis resulting in compensatory hypocapnia and a normal pH (table 1). The patient was sedated and underwent artificial ventilation for the next 6 days. Attempt 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 >>

Ph Control: Respiratory Acidosis

Ph Control: Respiratory Acidosis

Normally, the kidneys and lungs maintain a pH between 7.35 - 7.45 in extracellular fluid. Respiratory acidosis occurs when the lungs cannot eliminate enough carbon dioxide from the body’s tissues. The typical reason is hypoventilation, or a low respiratory rate, causing the plasma pH to fall below 7.35 due to excessive carbon dioxide in the blood. When this occurs, certain chemoreceptors in the body are stimulated to increase the respiratory rate. The kidneys also help by secreting more hydrogen ions (acid) into the tubular fluid and generating more bicarbonate (base) to help stabilize the pH. Respiratory acidosis can cause many physiological problems, particularly in the nervous and cardiovascular systems which are sensitive to pH fluctuations. Continue reading >>

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