The body has the remarkable ability to maintain plasma pH within the narrow range of 7.35 7.45. It does so by means of chemical buffering mechanisms by the kidneys and the lungs. Although single acid-base (e.g., metabolic acidosis) imbalances do occur, mixed acidbase imbalances are more common (e.g., metabolic acidosis/respiratory acidosis as occurs with cardiac arrest). METABOLIC ACIDOSIS (PRIMARY BASE BICARBONATE [HCO3] DEFICIENT) Metabolic acidosis (primary base bicarbonate [HCO3] deficiency) reflects an excess of acid (hydrogen) and a deficit of base (bicarbonate) resulting from acid overproduction, loss of intestinal bicarbonate, inadequate conservation of bicarbonate, and excretion of acid, or anaerobic metabolism. Metabolic acidosis is characterized by normal or high anion gap situations. If the primary problem is direct loss of bicarbonate, gain of chloride, or decreased ammonia production, the anion gap is within normal limits. If the primary problem is the accumulation of organic anions (such as ketones or lactic acid), the condition is known as high anion gap acidosis. Compensatory mechanisms to correct this imbalance include an increase in respirations to blow off excess CO2, an increase in ammonia formation, and acid excretion (H+) by the kidneys, with retention of bicarbonate and sodium. High anion gap acidosis occurs in diabetic ketoacidosis; severe malnutrition or starvation, alcoholic lactic acidosis; renal failure; high-fat, low-carbohydrate diets/lipid administration; poisoning, e.g., salicylate intoxication (after initial stage); paraldehyde intoxication; and drug therapy, e.g., acetazolamide (Diamox), NH4Cl. Normal anion gap acidosis is associated with loss of bicarbonate form the body, as may occur in renal tubular acidosis, hyperalimentation, vomiting/diarrhea, smallbowel/pancreatic fistulas, and ileostomy and use of IV sodium chloride in presence of preexisting kidney dysfunction, acidifying drugs (e.g., ammonium chloride). CARE SETTING This condition does not occur in isolation but rather is a complication of a broader problem that may require inpatient care in a medical-surgical or subacute unit. RELATED CONCERNS

fatigue. decreased mental function . muscle weakness CIRCULATION May exhibit: Hypotension. nausea/vomiting May exhibit: Poor skin turgor.Plans of care specific to predisposing factors Fluid and electrolyte imbalances Renal dialysis Respiratory acidosis (primary carbonic acid excess) Respiratory alkalosis (primary carbonic acid deficit) Patient Assessment Database (Dependent on Underlying Cause) ACTIVITY/REST May report: Lethargy. skin. irregular (dysrhythmias) Jaundiced sclera. dry mucous membranes NEUROSENSORY May report: Headache. wide pulse pressure Pulse may be weak. mucous membranes (liver failure) ELIMINATION May report: Diarrhea May exhibit: Dark/concentrated urine FOOD/FLUID May report: Anorexia. drowsiness.

Bicarbonate (HCO3): Decreased. cholestyramine (Questran) Discharge plan DRG projected mean length of inpatient stay depends on underlying cause May require change in therapies for underlying disease process/condition Refer to section at end of plan for postdischarge considerations DIAGNOSTIC STUDIES Arterial pH: Decreased. delirium. depression. confusion..g. coma Decreased deep-tendon reflexes. Kussmaul s respirations (deep. e.. . signs of sepsis TEACHING/LEARNING History of alcohol abuse Use of carbonic anhydrase inhibitors or anion-exchange resins. rapid breathing) SAFETY May report: Transfusion of blood/blood products Exposure to hepatitis virus May exhibit: Fever.g. less than 7. stupor. e. muscle weakness RESPIRATION May report: Dyspnea on exertion May exhibit: Hyperventilation.35. lethargy.May exhibit: Changes in sensorium. less than 22 mEq/L.

Plan in place to meet needs after discharge Because no current nursing diagnosis speaks clearly to metabolic imbalances.. Plasma lactic acid: Elevated in lactic acidosis. Achieve homeostasis. e. . Urine pH: Decreased. the following interventions are presented in a general format for inclusion in the primary plan of care.PaCO2: Less than 35 mm Hg. 2. tall T wave. and treatment needs understood. Serum chloride: Increased.g. less than 4. 3. Condition. Serum glucose: May be decreased or increased depending on etiology. Free of complications. DISCHARGE GOALS 1. renal tubular acidosis). Prevent/minimize complications. 2. Serum ketones: Increased in DM. ECG: Cardiac dysrhythmias (bradycardia) and pattern changes associated with hyperkalemia. Anion gap: Higher than 14 mEq/L (high anion gap) or range of 10 14 mEq/L (normal anion gap). alcohol intoxication.5 (in absence of renal disease). 3. Provide information about condition/prognosis and treatment needs as appropriate. Serum potassium: Increased (except in diarrhea. NURSING PRIORITIES 1. prognosis. starvation. Base excess: Negative. 4. Physiological balance restored.

swallowing antifreeze. Summary of important aspects of Chapter 5 : Metabolic Acidosis y Metabolic acidosis is an abnormal primary process causing an increase in fixed acids in the blood. peripheral venoconstriction and pulmonary vasoconstriction. A more clinically useful classification is to divide metabolic acidosis into 2 groups: High anion gap acidosis and Normal anion gap acidosis. peripheral arteriolar vasodilatation. a metabolic panel and a complete blood count. confusion and lethargy. Metabolic acidosis treatments include finding the underlying issues causing the acidosis and potentially prescribing sodium bicarbonate (baking soda) to balance the blood's acidity level. Such compensation rarely if ever returns the pH to normal. Better security of drugs may prevent accidental ingestion (eg of salicylates) by young children. direct myocardial depression. sympathetic stimulation. The peripheral chemoreceptors sense the acidaemia and stimulate the respiratory centre. . Most adult ICUs are familiar with some usually teenage or young adult patients who are admitted multiple times with acute DKA due to poor compliance with insulin administration. The most visible symptoms are rapid breathing. A particular example would be the prevention of episodes of diabetic ketoacidosis in insulindependent diabetic patients. The anion gap & the delta ratio may be useful aids in assessment of metabolic acidosis. Different causes of acidosis have some different specific management principles. The decrease in bicarbonate level occurs either because of a gain of fixed acid or a loss of base.Prevention of the primary disease or better management may be an option in some cases. If you feel you may be suffering from metabolic acidosis. The most important aspect of management involves correction of the primary disorder if possible. Important metabolic effects include hyperventilation. Some of these problems may respond to better diabetic education and counselling. There are many possible metabolic acidosis symptoms. seek the advice of your primary care physician who can run tests such as an arterial blood gas. y y y y y y Metabolic Acidosis y Metabolic acidosis occurs when the acid base in the bloodstream becomes unbalanced. decreased arrhythmia threshold. Metabolic acidosis can be caused by underlying factors such as kidney failure. diabetic ketoacidosis. too much aspirin consumption and shock as well as the overall health of the patient. The resulting hyperventilation causes a compensatory decrease in arterial pCO2 which partly returns the arterial pH towards normal. Buffering causes the plasma bicarbonate to fall to a level lower than expected and tends to cause an acidaemia.

Eating a balanced diet of low-fat Consult your doctor on recommendations for a healthy diet and exercise program and keep your life as stress-free as http://www. Read more: Best Way . fruits and vegetables along with consuming one to three liters of water per day will go a long way toward preventing metabolic acidosis.Acidosis Prevention | eHow.Metabolic acidosis prevention focuses on keeping your body in the best overall health possible.html#ixzz0vYD3vrV4 .ehow.

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