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Describe The Respiratory Response To Metabolic Acidosis

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 >>

Intro To Arterial Blood Gases, Part 2

Intro To Arterial Blood Gases, Part 2

Arterial Blood Gas Analysis, Part 2 Introduction Acute vs. Chronic Respiratory Disturbances Primary Metabolic Disturbances Anion Gap Mixed Disorders Compensatory Mechanisms Steps in ABG Analysis, Part II Summary Compensatory Mechanisms Compensation refers to the body's natural mechanisms of counteracting a primary acid-base disorder in an attempt to maintain homeostasis. As you learned in Acute vs. Chronic Respiratory Disturbances, the kidneys can compensate for chronic respiratory disorders by either holding on to or dumping bicarbonate. With Chronic respiratory acidosis: Chronic respiratory alkalosis: the kidneys hold on to bicarbonate the kidneys dump bicarbonate With primary metabolic disturbances, the respiratory system compensates for the acid-base disorder. The lungs can either blow off excess acid (via CO2) to compensate for metabolic acidosis, or to a lesser extent, hold on to acid (via CO2) to compensate for metabolic alkalosis. With Metabolic acidosis: Metabolic alkalosis: ventilation increases to blow off CO2 ventilation decreases to hold on to CO2 The body's response to metabolic acidosis is predictable. With metabolic acidosis, respiration will increase to blow off CO2, thereby decreasing the amount of acid in the blood. Recall that with metabolic acidosis, central chemoreceptors are triggered by the low pH and increase the drive to breathe. For now, it is only important to learn (qualitatively) that there is a predictable compensatory response to metabolic acidosis. Later, during your 3rd or 4th year rotations, you might learn how to (quantitatively) determine if the compensatory response to metabolic acidosis is appropriate by using the Winter's Formula. The body's response to metabolic alkalosis is not as complete. This is because we would need to hypov 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 >>

Acid Base Disorders

Acid Base Disorders

Acid base disorders 1. What is normal pH? Normal Values pH = 7.38 - 7.42 [H+] = 40 nM/L for a pH of 7.4 PaCO2 = 40 mm Hg [HCO3] = 24 meq/L 2. What is the definition for acid base disorder? Acid base disorder is considered present when there is abnormality in HCO3 or PaCO2 or pH. 3. What does acidosis or alkalosis refer to? Acidosis and alkalosis refer to in-vivo derangement's and not to any change in pH. 4. What does acidemia or alkalemia refer to? Acidemia (pH < 7.38) and Alkalemia (pH >7.42) refer to derangement's of blood pH. 5. Which organs are key players in maintaining acid base balance? Kidney, Respiratory system and Central nervous system play a key roles in maintaining the acid base status. 6. What are the primary acid base disorders? Primary acid base disorders Metabolic acidosis Metabolic alkalosis Respiratory acidosis Respiratory alkalosis 7. When would you consider metabolic acidosis? Metabolic acidosis: loss of [HCO3] 0r addition of [H+] 8. When would you consider metabolic alkalosis? Metabolic alkalosis: loss of [H+] or addition of [HCO3] 9. When would you consider respiratory acidosis? Respiratory acidosis: increase in pCO2 10. When would you consider respiratory alkalosis? Respiratory alkalosis : decrease in pCO2 11. What are the required lab values and historical information you need to assess acid base disorders? Recquired lab values/information Arterial blood gases: pH, PaCO2,calculated bicarb Electrolytes: Na, K, Cl, HCO3 BUN, Glucose, Creatinine Clinical history 12. What are anions? List the anions? Anions Chloride Bicarbonate(Total CO2) Proteins Organic acids Phosphates Sulfates 13. What are cations? List the cations? Cations Sodium Potassium Calcium Magnesium 14. What is anion gap? Anion gap (AG) Electrochemical balance: the total anions are the Continue reading >>

Final Physio Lab 24 Flashcards | Quizlet

Final Physio Lab 24 Flashcards | Quizlet

For normal breathing did the pH stay within the normal range? What happens to the pH level during hyperventilation? Alkalosis ( reduces amount of CO2 inside the body) What happens to the pH level during hyperventilation with normal breathing? During rebreathing what happens to the pH level? acidosis ( breathing in CO2 back in that you are originally breathing out) What happens to the pH when you increase or decrease the pCO2 of the blood? If the pCO2 is decreased the pH increases ( breathing off CO2 increases pH due to less CO2 in the body) What happens to the urine concentration if there is an increased pH? There will be more HCO3- in the urine due to it the pH levels being so basic ( too basic) What happens to the urine concentration if there is a decreased pH? There will more H+ in the urine because the pH is too acidic How would you describe the values you obtained during the respiratory repose to normal metabolism? Everything is normal ( ie pH and CO2 levels) What happens during respiratory response to increased metabolism? the heart rate increases and the need for O2 increases but you aren't bringing in enough so the pH decreases since you have more CO2 in the body How would you expect the respiratory system to respond in order to compensate to increased metabolism? Increase your breathing and hyperventilate to blow off more CO2 enabling the body to get to normal pH range. What happens with the pH when the metabolic rate decreases? How would you expect the respiratory system to respond in order to compensate decreases metabolism? Decrease your breathing and hypoventilate to increase CO2 in the body which will get the pH level to normal ranges a term used to denote hydrogen ion concentration in body fluids a substance that releases H+ in a solution a substance tha Continue reading >>

Respiratory Acidosis

Respiratory Acidosis

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 .) 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 following: Central nervous system disease or drug-induced r Continue reading >>

Respiratory Compensation

Respiratory Compensation

Publisher Summary This chapter elaborates the bicarbonate buffer system and respiratory compensation. The plasma pH is defined as –log [H+], and when [H+] increases, the pH decreases. The condition of high plasma pH is called alkalosis and low plasma pH is acidosis. The body has three lines of defense against departures from normal plasma pH—the chemical buffers, the respiratory system, and the renal system. The chemical buffers passively resist changes in pH by absorbing excess H+ when pH falls or by releasing H+ ions when pH rises. Chemical buffers include proteins, phosphate, and bicarbonate buffers. All of these equilibrate with a single [H+], and so the buffer systems are linked. This is the isohydric principle, and because of this link, adjustment of the bicarbonate buffer system controls all buffer systems. The bicarbonate buffer system has two components that include plasma [CO2] and [HCO3−]. The respiratory system controls plasma pH by adjusting the [CO2]. The equilibrium between dissolved CO2 and H2CO3 is accelerated by carbonic anhydrase. Respiratory alkalosis results from hyperventilation as the primary disturbance. Hyperventilation also forms the respiratory compensation of metabolic acidosis. It is found that complete compensation of pH disturbances requires the kidney to change plasma [HCO3−]. Increased Carbon Dioxide: Respiratory Acidosis Respiratory acidosis may result from a primary respiratory disorder or it can be a physiologic respiratory compensation for a metabolic alkalosis. An increase in HCO3− of 1 mEq/L should result in an increase in PCO2 of 0.7 mm Hg in both dogs and cats.1,3 Pathologic respiratory acidosis results from an imbalance in CO2 production via metabolism and excretion via the lung. Common causes include large airway obst Continue reading >>

Metabolic Alkalosis: Respiratory Compensation

Metabolic Alkalosis: Respiratory Compensation

Definition Metabolic alkalosis is a very common primary acid–base disturbance associated with increased plasma HCO3. Increased extracellular HCO3 is due to net loss of H+ and/or addition of HCO3. The most common cause of metabolic alkalosis is gastrointestinal acid loss because of vomiting or nasogastric suctioning; the resulting hypovolemia leads to secretion of renin and aldosterone and enhanced absorption of HCO3.Diuretics are another common cause of metabolic alkalosis. Thiazides (e.g., hydrochlorothiazide) and loop diuretics (e.g., furosemide) induce a net loss of chloride and free water, without altering bicarbonate excretion, and can cause a volume “contraction” alkalosis. When metabolic alkalosis is persistent, it usually reflects an inability of the kidney to excrete HCO3. Rare inherited renal causes of metabolic alkalosis exist (e.g., Bartter syndrome). A typical respiratory response to all types of metabolic alkalosis is hypoventilation leading to a pH correction towards normal. Increases in arterial blood pH depress respiratory centers. The resulting alveolar hypoventilation tends to elevate PaCO2 and restore arterial pH toward normal. The pulmonary response to metabolic alkalosis is generally less predictable than the response to metabolic acidosis. Hypoxemia, as a result of progressive hypoventilation, eventually activates oxygen-sensitive chemoreceptors; the latter stimulates ventilation and limits the compensatory pulmonary response. Consequently, PaCO2 usually does not rise above 55 mm Hg in response to metabolic alkalosis. As a general rule, PaCO2 can be expected to increase 0.25–1 mm Hg for each 1 mEq/L increase in [HCO3–]. Subspecialty Keyword history See Also: Sources PubMed Continue reading >>

Paediatric Acid-base Disorders: A Case-based Review Of Procedures And Pitfalls

Paediatric Acid-base Disorders: A Case-based Review Of Procedures And Pitfalls

Paediatric acid-base disorders: A case-based review of procedures and pitfalls J Bryan Carmody , MD and Victoria F Norwood , MD Department of Pediatrics, Division of Pediatric Nephrology, University of Virginia, Charlottesville, Virginia, USA Correspondence: Dr J Bryan Carmody, Department of Pediatrics, Division of Pediatric Neprhology, University of Virginia, PO Box 800386, Charlottesville, Virginia 22903, USA. Telephone 434-924-2096, e-mail [email protected] , [email protected] Copyright 2013 Pulsus Group Inc. All rights reserved Acid-base disorders occur frequently in paediatric patients. Despite the perception that their analysis is complex and difficult, a straightforward set of rules is sufficient to interpret even the most complex disorders provided certain pitfalls are avoided. Using a case-based approach, the present article reviews the fundamental concepts of acid-base analysis and highlights common mistakes and oversights. Specific topics include the proper identification of the primary disorder; distinguishing compensatory changes from additional primary disorders; use of the albumin-corrected anion gap to generate a differential diagnosis for patients with metabolic acidosis; screening for mixed disorders with the delta-delta formula; recognizing the limits of compensation; use of the anion gap to identify hidden acidosis; and the importance of using information from the history and physical examination to identify the specific cause of a patients acid-base disturbance. Keywords: Acid-base equilibrium, Acid-base imbalances, Acidosis, Alkolosis, Blood Les troubles de lquilibre acido-basique sont frquents chez les patients dge pdiatrique. Mme si on les croit difficiles et complexes analyser, des rgles simples suffsent pour interprter mme les Continue reading >>

Disorders Of Acid-base Balance

Disorders Of Acid-base Balance

Module 10: Fluid, Electrolyte, and Acid-Base Balance By the end of this section, you will be able to: Identify the three blood variables considered when making a diagnosis of acidosis or alkalosis Identify the source of compensation for blood pH problems of a respiratory origin Identify the source of compensation for blood pH problems of a metabolic/renal origin Normal arterial blood pH is restricted to a very narrow range of 7.35 to 7.45. A person who has a blood pH below 7.35 is considered to be in acidosis (actually, physiological acidosis, because blood is not truly acidic until its pH drops below 7), and a continuous blood pH below 7.0 can be fatal. Acidosis has several symptoms, including headache and confusion, and the individual can become lethargic and easily fatigued. A person who has a blood pH above 7.45 is considered to be in alkalosis, and a pH above 7.8 is fatal. Some symptoms of alkalosis include cognitive impairment (which can progress to unconsciousness), tingling or numbness in the extremities, muscle twitching and spasm, and nausea and vomiting. Both acidosis and alkalosis can be caused by either metabolic or respiratory disorders. As discussed earlier in this chapter, the concentration of carbonic acid in the blood is dependent on the level of CO2 in the body and the amount of CO2 gas exhaled through the lungs. Thus, the respiratory contribution to acid-base balance is usually discussed in terms of CO2 (rather than of carbonic acid). Remember that a molecule of carbonic acid is lost for every molecule of CO2 exhaled, and a molecule of carbonic acid is formed for every molecule of CO2 retained. Figure 1. Symptoms of acidosis affect several organ systems. Both acidosis and alkalosis can be diagnosed using a blood test. Metabolic Acidosis: Primary Bic Continue reading >>

Respiratory Regulation Of Acid Base Balance

Respiratory Regulation Of Acid Base Balance

The acid base balance is vital for normal bodily functions. When this equilibrium is disrupted, it can lead to severe symptoms such as arrhythmias and seizures. Therefore, this balance is tightly regulated. In this article, we will look at the buffering system, responses of the respiratory and urinary systems and relevant clinical conditions. Blood has the ability to be insensitive to small changes in pH, which is a characteristic known as “buffering”. This is due to the basal levels of bicarbonate and hydrogen ions in blood. The chemical reaction is given by: This reaction can be used to control pH, as will be discussed in the next section. For example, in metabolically active tissues, there is an increase in hydrogen ions. These can then react with bicarbonate in the red blood cells to form carbon dioxide which can then be exhaled by the lungs. The compensatory systems of the body rely on this equation. This will be discussed in more detail later. Henderson-Hassalbalch Equation The Henderson-Hassalbalch equation relates the pH to the ratio between the concentration of bicarbonate and the partial pressure of carbon dioxide. It is given by: This shows that the ratio between bicarbonate production and partial pressure of carbon dioxide drive the pH levels of the blood. By increasing bicarbonate levels, the pH will rise and turn more alkaline, and by increasing the partial pressure of carbon dioxide the pH of blood will fall and turn acidic. The usual range of blood pH is from 7.35 to 7.45. When pH levels drop below 7.35, it is said to be acidotic, and when pH levels rise above 7.45 it is said to be alkalotic. How is Balance Restored? When blood pH deviates from the normal range, there are two body systems which are activated to restore equilibrium. The respiratory sy Continue reading >>

Metabolic Acidosis

Metabolic Acidosis

Metabolic acidosis is a condition that occurs when the body produces excessive quantities of acid or when the kidneys are not removing enough acid from the body. If unchecked, metabolic acidosis leads to acidemia, i.e., blood pH is low (less than 7.35) due to increased production of hydrogen ions by the body or the inability of the body to form bicarbonate (HCO3−) in the kidney. Its causes are diverse, and its consequences can be serious, including coma and death. Together with respiratory acidosis, it is one of the two general causes of acidemia. Terminology : Acidosis refers to a process that causes a low pH in blood and tissues. Acidemia refers specifically to a low pH in the blood. In most cases, acidosis occurs first for reasons explained below. Free hydrogen ions then diffuse into the blood, lowering the pH. Arterial blood gas analysis detects acidemia (pH lower than 7.35). When acidemia is present, acidosis is presumed. Signs and symptoms[edit] Symptoms are not specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite and weight gain, muscle weakness, bone pain, and joint pain. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Overcompensation via respiratory alkalosis to form an alkalemia does not occur. Extreme acidemia leads to neurological and cardia Continue reading >>

Response To Disturbances

Response To Disturbances

The body tries to minimize pH changes and responds to acid-base disturbances with body buffers, compensatory responses by the lungs and kidney (to metabolic and respiratory disturbances, respectively) and by the kidney correcting metabolic disturbances. Body buffers: There are intracellular and extracellular buffers for primary respiratory and metabolic acid-base disturbances. Intracellular buffers include hemoglobin in erythrocytes and phosphates in all cells. Extracellular buffers are carbonate (HCO3–) and non-carbonate (e.g. protein, bone) buffers. These immediately buffer the rise or fall in H+. Compensation: This involves responses by the respiratory tract and kidney to primary metabolic and respiratory acid-base disturbances, respectively. Compensation opposes the primary disturbance, although the laboratory changes in the compensatory response parallel those in the primary response. This concept is illustrated in the summary below. Respiratory compensation for a primary metabolic disturbance: Alterations in alveolar ventilation occurs in response to primary metabolic acid-base disturbances. This begins within minutes to hours of an acute primary metabolic disturbance. Note that complete compensation via this mechanism may take up to 24 hours. Renal compensation for a primary respiratory disturbance: Here, the kidney alters excretion of acid (which influences bases as well) in response to primary respiratory disturbances. This begins within hours of an acute respiratory disturbance, but take several days (3-5 days) to take full effect. Correction of acid-base changes: Correction of a primary respiratory acid-base abnormality usually requires medical or surgical intervention of the primary problem causing the acid-base disturbance, e.g. surgical relief of a colla Continue reading >>

Respiratory Compensation

Respiratory Compensation

Metabolic Acidosis Respiratory compensation for metabolic disorders is quite fast (within minutes) and reaches maximal values within 24 hours. A decrease in Pco2 of 1 to 1.5 mm Hg should be observed for each mEq/L decrease of in metabolic acidosis.27 A simple rule for deciding whether the fall in Pco2 is appropriate for the degree of metabolic acidosis is that the Pco2 should be equal to the last two digits of the pH. For example, compensation is adequate if the Pco2 decreases to 28 when the pH is 7.28. Alternatively, the Pco2 can be predicted by adding 15 to the observed (down to a value of 12). Although reduction in Pco2 plays an important role in correcting any metabolic acidosis, evidence suggests that it may in some respects be counterproductive because it inhibits renal acid excretion. Fetoplacental Elimination of Metabolic Acid Load Fetal respiratory and renal compensation in response to changes in fetal pH is limited by the level of maturity and the surrounding maternal environment. However, although the placentomaternal unit performs most compensatory functions,3 the fetal kidneys have some, although limited, ability to contribute to the maintenance of fetal acid–base balance. The most frequent cause of fetal metabolic acidosis is fetal hypoxemia owing to abnormalities of uteroplacental function or blood flow (or both). Primary maternal hypoxemia or maternal metabolic acidosis secondary to maternal diabetes mellitus, sepsis, or renal tubular abnormalities is an unusual cause of fetal metabolic acidosis. Pregnant women, at least in late gestation, maintain a somewhat more alkaline plasma environment compared with that of nonpregnant control participants. This pattern of acid–base regulation in pregnant women is present during both resting and after maximal e 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 >>

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