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UT Arlington NURS 5315 - Acid Base Disorders Transcript

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1 N5315 Advanced Pathophysiology Acid Base Disorders Laboratory Evaluation of Acid Base Imbalances The serum CO2 is typically included in a BMP or a CMP. It is an indirect measurement of the anion HCO3. An elevation reflects an alkalotic state and a decrease would reflect an acidotic state. Normal lab value for the adult and elderly is between 23-30 mEq/L or mmol/L Arterial Blood Gases have multiple components. The pH is the measure of the body alkalinity and acidity. The value is inversely proportional to the concentration of hydrogen ions in the blood. A low pH would indicate an acidic state and a high hydrogen ion concentration. A high pH would indicate an alkalotic state and a low hydrogen ion concentration. A normal value is between 7.35-7.45. When evaluating a pH, it is best to consider 7.4 normal. If the pH is < 7.4, the individual is acidotic, and if it is > 7.4, the individual is alkalotic. The PaCO2 measures the partial pressure of arterial CO2 in the blood (dissolved in the blood) and reflects ventilation. The higher the CO2 the faster the respirations are and vice versa. It has an inverse relationship with pH. The higher the pH, the lower the CO2 and the opposite is true. Levels of CO2 can rise to a point where the lungs can no longer compensate which can suppress brain function and cause a coma. The PCO2 reflects the lungs’ role in acid base balance. A normal value is between 35-45. HCO3 is a direct measurement of the amount of bicarbonate in the blood. It reflects the metabolic component of acid base balances, specifically the kidney. It is directly related to pH. As the bicarbonate rises, the pH will rise. The opposite is also true. The normal range is 21-28 mEq/L. The PaO2 is a measure of the partial pressure of arterial O2, which is the amount of oxygen content that is dissolved in the arterial blood. The normal range is 80-100mmHg and this has to be adjusted for age in the elderly. The O2 sat measures the percentage of hemoglobin that is saturated with oxygen. At normal values, cells have enough oxygen to function normally. Normal range is from 92%-100% The Base Excess/Deficit is a value which is calculated from the pH, PCO2, and the hematocrit. It represents the amount of anions available for buffering. A negative base excess represents a metabolic acidosis. A positive base excess represents a metabolic alkalosis or compensation for a respiratory acidosis. The normal ranges is -2 through +2 The A-a Gradient measures the differences between the alveolar (A) to arterial (a) O2. It is a calculated value which indicates the difference between alveolar and arterial O2 content. The normal value is < 10mmHg. The normal range increases 1mmHg for every decade a person has lived. For an individual who is 80 years old, the normal gradient could be as high as 18. An elevated value would indicate that there is an issue with O2 diffusing across the alveolar membrane. This can happen in such disease states as: pulmonary edema, pulmonary fibrosis, and ARDS.2 Acid Base Disorders Metabolic Acidosis is a pathological process which results in the reduction of the serum bicarbonate concentration and a low arterial pH. This results from either an excess of H- ions or deficiency of HCO3. There are three pathological mechanisms that cause metabolic acidosis: increased acid production, loss of bicarbonate, or diminished renal excretion of hydrogen. Increased acid production occurs during lactic acidosis, keto acidosis or from the ingestion of acids. Lactic acidosis results from an alteration in the cellular function secondary to hypoxia that leads to the byproduct of lactate. It is a reflection of poor tissue perfusion. It can be caused by poor perfusion or by some medications such as some of the medications used to treat AIDS. If the lactic acidosis is due to poor organ perfusion, fluid resuscitation will often resolve the acidosis. Ketoacidosis results from an alteration in cellular function which prevents the cell from using glucose as energy. The cell begins to break down fat for energy and the byproduct is ketones. The ingestion of methanol, ethylene glycol, propylene glycol, diethylene glycol, and aspirin can all cause a metabolic acidosis. Bicarbonate loss can occur from severe diarrhea or from Type 2 renal tubular acidosis. In this condition, the proximal renal tubule is impaired and cannot reabsorb bicarbonate. Diminished renal acid excretion occurs in the setting of chronic kidney disease and type 1 renal tubular acidosis. The western diet produces a daily nonvolatile metabolic acid load of approximately 50-100meq/daily that must be excreted by the kidneys. The acid base balance is maintained by excreting hydrogen ions in the urine. In CKD, the reduction in the glomerular filtration rate results in decreased acid excretion. In distal (type 1) renal tubular acidosis, a distal tubular dysfunction leads to an accumulation of hydrogen ions. Pathological consequences of acidemia include decreased myocardial contractility, decreased cardiac output and catecholamine resistant hypotension (decreased binding of norepinephrine to its receptors), and hyperkalemia. The first step in the evaluation of a metabolic acidosis is to review the anion gap. This helps to narrow down the possible differentials. A high anion gap acidosis is most likely caused by lactic acidosis, ketoacidosis, or acute and chronic renal failure. A normal anion gap acidosis (hyperchloremic acidosis) is most commonly caused by GI losses from diarrhea, large volumes of saline administration, and medications such as NSAIDs, ACE inhibitors, and trimethoprim. Metabolic Alkalosis results from an excess of HCO3- or deficiency of H-. It is characterized by a pH > 7.4 and bicarbonate > 28. A process that causes a rise in serum bicarbonate and a process which prevents the renal excretion of serum bicarbonate must both occur in order for a metabolic alkalosis to occur. Metabolic alkalosis is usually accompanied by a hypokalemia and its associated symptoms, cardiac arrhythmias from hypokalemia, hypocalcemia and its associated symptoms, hypoventilation and an elevated pCO2. The two most common causes are from gastric stomach content losses or diuretic use. Vomiting results in the loss of hydrochloric acid. In normal physiology the gastric parietal cells produce hydrogen ions and bicarbonate. H+ and Cl- are released into the stomach and HCO3- is released into the blood. H+ then travels into


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