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Acidosis And Alkalosis Pdf

American Thoracic Society - Interpretation Of Arterial Blood Gases (abgs)

American Thoracic Society - Interpretation Of Arterial Blood Gases (abgs)

Interpretation of Arterial Blood Gases (ABGs) Chief, Section of Pulmonary, Critical Care & Sleep Medicine Bridgeport Hospital-Yale New Haven Health Assistant Clinical Professor, Yale University School of Medicine (Section of Pulmonary & Critical Care Medicine) Interpreting an arterial blood gas (ABG) is a crucial skill for physicians, nurses, respiratory therapists, and other health care personnel. ABG interpretation is especially important in critically ill patients. The following six-step process helps ensure a complete interpretation of every ABG. In addition, you will find tables that list commonly encountered acid-base disorders. Many methods exist to guide the interpretation of the ABG. This discussion does not include some methods, such as analysis of base excess or Stewarts strong ion difference. A summary of these techniques can be found in some of the suggested articles. It is unclear whether these alternate methods offer clinically important advantages over the presented approach, which is based on the anion gap. Step 1: Assess the internal consistency of the values using the Henderseon-Hasselbach equation: If the pH and the [H+] are inconsistent, the ABG is probably not valid. Step 2: Is there alkalemia or acidemia present? Remember: an acidosis or alkalosis may be present even if the pH is in the normal range (7.35 7.45) You will need to check the PaCO2, HCO3- and anion gap Step 3: Is the disturbance respiratory or metabolic? What is the relationship between the direction of change in the pH and the direction of change in the PaCO2? In primary respiratory disorders, the pH and PaCO2 change in opposite directions; in metabolic disorders the pH and PaCO2 change in the same direction. Decrease in [HCO3-] = 5( PaCO2/10) to 7( PaCO2/10) If the observed compensa 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 >>

66: Acidosis And Alkalosis

66: Acidosis And Alkalosis

Systemic arterial pH is maintained between 7.35 and 7.45 by extracellular and intracellular chemical buffering together with respiratory and renal regulatory mechanisms. The control of arterial CO2 tension (Paco2) by the central nervous system (CNS) and respiratory system and the control of plasma bicarbonate by the kidneys stabilize the arterial pH by excretion or retention of acid or alkali. The metabolic and respiratory components that regulate systemic pH are described by the Henderson-Hasselbalch equation: Under most circumstances, CO2 production and excretion are matched, and the usual steady-state Paco2 is maintained at 40 mmHg. Underexcretion of CO2 produces hypercapnia, and overexcretion causes hypocapnia. Nevertheless, production and excretion are again matched at a new steady-state Paco2. Therefore, the Paco2 is regulated primarily by neural respiratory factors and is not subject to regulation by the rate of CO2 production. Hypercapnia is usually the result of hypoventilation rather than of increased CO2 production. Increases or decreases in Paco2 represent derangements of neural respiratory control or are due to compensatory changes in response to a primary alteration in the plasma [HCO3−]. The most common clinical disturbances are simple acid-base disorders; i.e., metabolic acidosis or alkalosis or respiratory acidosis or alkalosis. Primary respiratory disturbances (primary changes in Paco2) invoke compensatory metabolic responses (secondary changes in [HCO3−]), and primary metabolic disturbances elicit predictable compensatory respiratory responses (secondary changes in Paco2). Physiologic compensation can be predicted from the relationships displayed in Table 66-1. In general, with one exception, compensatory responses return the pH toward, but not to Continue reading >>

Payperview: Acid-base And Electrolyte Abnormalities During Renal Support For Acute Kidney Injury: Recognition And Management - Karger Publishers

Payperview: Acid-base And Electrolyte Abnormalities During Renal Support For Acute Kidney Injury: Recognition And Management - Karger Publishers

I have read the Karger Terms and Conditions and agree. Acute kidney injury (AKI) is associated with electrolyte and acid-base disturbances such as hyperkalemia, metabolic acidosis, hypocalcemia and hyperphosphatemia. The initiation of dialysis in AKI can efficiently treat these complications. The choice of dialysis modality can be made based on their operational characteristics to tailor the therapy according to the clinical scenario. Each dialysis modality can also trigger significant electrolyte and acid-base disorders, such as hypokalemia, hypophosphatemia and metabolic alkalosis, which may direct changes in fluid delivery and composition. Continuous techniques may be particularly useful in these situations as they allow more time for correction and to maintain balance. This review provides an overview of the electrolyte and acid-base disturbances occurring in AKI and after the initiation of dialysis and discusses therapeutic options in this setting. Claure-Del Granado RME, Soroko S, Chertow GM, Himmelfarb J, Ikizler AT, Paganini EP, Mehta RL: Assessment of metabolic acidosis in critically ill patients with acute kidney injury (AKI). J Am Soc Nephrol 2010;21:55A. Cooper DJ, Walley KR, Wiggs BR, Russell JA: Bicarbonate does not improve hemodynamics in critically ill patients who have lactic acidosis. A prospective, controlled clinical study. Ann Intern Med 1990;112:492498. Rocktaschel J, Morimatsu H, Uchino S, Ronco C, Bellomo R: Impact of continuous veno-venous hemofiltration on acid-base balance. Int J Artif Organs 2003;26:1925. Uchino S, Bellomo R, Ronco C: Intermittent versus continuous renal replacement therapy in the icu: Impact on electrolyte and acid-base balance. Intensive Care Med 2001;27:10371043. Kierdorf HP, Leue C, Arns S: Lactate- or bicarbonate-buffer Continue reading >>

The Treatment Of Dehydration, Acidosis And Alkalosis

The Treatment Of Dehydration, Acidosis And Alkalosis

THE TREATMENT OF DEHYDRATION, ACIDOSIS AND ALKALOSIS Under various circumstances a syndrome called dehydration develops. The patient shows diminished turgor of the skin, sunken eyes, poor circulation, oliguria and concentration of the blood with respect to red cells and serum proteins. While an inadequate intake of water will produce some of these symptoms, the fully developed picture occurs almost exclusively when, as a result of vomiting, diarrhea, sweating or abnormal diuresis, the body has lost extracellular electrolyte (salts) as well as water. Furthermore, this fully developed picture of dehydration can be produced when extracellular electrolyte is no longer available to the body as a whole because it has been fixed in the inflammatory exudate of a burn. In dehydration the evidences of loss of fluid volume are confined chiefly to extracellular fluids. The central feature is the deficiency of extracellular electrolyte, since dehydration can develop either with or without loss of water from the body as a Continue reading >>

Blood Gas Analysis--insight Into The Acid-base Status Of The Patient

Blood Gas Analysis--insight Into The Acid-base Status Of The Patient

Acid-Base Physiology Buffers H+ A- HCO3- CO2 Buffers H+ A- CO2 Cells Blood Kidney Lungs Fluids, Electrolytes, and Acid-Base Status in Critical Illness Blood Gas Analysis--Insight into the Acid-Base status of the Patient The blood gas consists of pH-negative log of the Hydrogen ion concentration: -log[H+]. (also, pH=pK+log [HCO3]/ 0.03 x pCO2). The pH is always a product of two components, respiratory and metabolic, and the metabolic component is judged, calculated, or computed by allowing for the effect of the pCO2, ie, any change in the pH unexplained by the pCO2 indicates a metabolic abnormality. CO +H 0ºº H CO ººHCO + H2 2 2 3 3 - + CO2 and water form carbonic acid or H2CO3, which is in equilibrium with bicarbonate (HCO3-)and hydrogen ions (H+). A change in the concentration of the reactants on either side of the equation affects the subsequent direction of the reaction. For example, an increase in CO2 will result in increased carbonic acid formation (H2CO3) which leads to an increase in both HCO3- and H+ (\pH). Normally, at pH 7.4, a ratio of one part carbonic acid to twenty parts bicarbonate is present in the extracellular fluid [HCO3-/H2CO3]=20. A change in the ratio will affect the pH of the fluid. If both components change (ie, with chronic compensation), the pH may be normal, but the other components will not. pCO -partial pressure of carbon dioxide. Hypoventilation or hyperventilation (ie, minute2 ventilation--tidal volume x respitatory rate--imperfectly matched to physiologic demands) will lead to elevation or depression, respectively, in the pCO2. V/Q (ventilation/perfusion) mismatch does not usually lead to abnormalities in PCO2 because of the linear nature of the CO2 elimination curve (ie, good lung units can make up for bad lung units). Diffus 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 >>

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