MET-ACIDOSIS

8/8/2019 MET-ACIDOSIS

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METABOLIC ACIDOSIS

The body has the remarkable ability to maintain plasma pH within the narrow range of

7.357.45. 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 acid-

base 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 gapsituations. 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, small-

bowel/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


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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, fatigue; muscle weakness

CIRCULATION

May exhibit: Hypotension, wide pulse pressure

Pulse may be weak, irregular (dysrhythmias)

Jaundiced sclera, skin, mucous membranes (liver failure)

ELIMINATION

May report: Diarrhea

May exhibit: Dark/concentrated urine

FOOD/FLUID

May report: Anorexia, nausea/vomiting

May exhibit: Poor skin turgor, dry mucous membranes

NEUROSENSORY

May report: Headache, drowsiness, decreased mental function


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May exhibit: Changes in sensorium, e.g., stupor, confusion, lethargy, depression, delirium,

coma

Decreased deep-tendon reflexes, muscle weakness

RESPIRATION

May report: Dyspnea on exertion

May exhibit: Hyperventilation, Kussmauls respirations (deep, rapid breathing)

SAFETY

May report: Transfusion of blood/blood products

Exposure to hepatitis virus

May exhibit: Fever, signs of sepsis

TEACHING/LEARNING

History of alcohol abuse

Use of carbonic anhydrase inhibitors or anion-exchange resins, e.g., 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, less than 7.35.

Bicarbonate (HCO3): Decreased, less than 22 mEq/L.


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PaCO2: Less than 35 mm Hg.

Base excess: Negative.

Anion gap: Higher than 14 mEq/L (high anion gap) or range of 1014 mEq/L (normal anion

gap).

Serum potassium: Increased (except in diarrhea, renal tubular acidosis).

Serum chloride: Increased.

Serum glucose: May be decreased or increased depending on etiology.

Serum ketones: Increased in DM, starvation, alcohol intoxication.

Plasma lactic acid: Elevated in lactic acidosis.

Urine pH: Decreased, less than 4.5 (in absence of renal disease).

ECG: Cardiac dysrhythmias (bradycardia) and pattern changes associated with

hyperkalemia, e.g., tall T wave.

NURSING PRIORITIES

1. Achieve homeostasis.

2. Prevent/minimize complications.

3. Provide information about condition/prognosis and treatment needs as appropriate.

DISCHARGE GOALS

1. Physiological balance restored.

2. Free of complications.

3. Condition, prognosis, and treatment needs understood.4. Plan in place to meet needs after discharge

Because no current nursing diagnosis speaks clearly to metabolic imbalances, the following

interventions are presented in a general format for inclusion in the primary plan of care.


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Prevention of the primary disease or better management may be an option in some cases.

A particular example would be the prevention of episodes of diabetic ketoacidosis in insulin-

dependent diabetic patients. 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. Some of these problems may respond to better diabetic education and

counselling.Better security of drugs may prevent accidental ingestion (eg of salicylates) by young children.

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. Buffering causes the plasma bicarbonate to fall to a level lower than expected and

tends to cause an acidaemia.

y The decrease in bicarbonate level occurs either because of a gain of fixed acid or a loss of

base.

y A more clinically useful classification is to divide metabolic acidosis into 2 groups: High

anion gap acidosis and Normal anion gap acidosis.

y Important metabolic effects include hyperventilation, sympathetic stimulation, decreased

arrhythmia threshold, direct myocardial depression, peripheral arteriolar vasodilatation,

peripheral venoconstriction and pulmonary vasoconstriction.

y The peripheral chemoreceptors sense the acidaemia and stimulate the respiratory centre.

The resulting hyperventilation causes a compensatory decrease in arterial pCO2 which

partly returns the arterial pH towards normal. Such compensation rarely if ever returns the

pH to normal.

y The most important aspect of management involves correction of the primary disorder if

possible. Different causes of acidosis have some different specific management principles.

y The anion gap & the delta ratio may be useful aids in assessment of metabolic acidosis.

Metabolic Acidosis

y Metabolic acidosis occurs when the acid base in the bloodstream becomes unbalanced.

Metabolic acidosis can be caused by underlying factors such as kidney failure, diabetic

ketoacidosis, swallowing antifreeze, too much aspirin consumption and shock as well as the

overall health of the patient.

There are many possible metabolic acidosis symptoms. The most visible symptoms arerapid breathing, confusion and lethargy. If you feel you may be suffering from metabolic

acidosis, seek the advice of your primary care physician who can run tests such as an

arterial blood gas, a metabolic panel and a complete blood count.

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.


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Metabolic acidosis prevention focuses on keeping your body in the best overall health

possible. Consult your doctor on recommendations for a healthy diet and exercise program

and keep your life as stress-free as possible. Eating a balanced diet of low-fat meats, fruits

and vegetables along with consuming one to three liters of water per day will go a long way

toward preventing metabolic acidosis.

Read more: Best Way - Acidosis Prevention |

eHow.com http://www.ehow.com/way_5829169_acidosis-prevention.html#ixzz0vYD3vrV4

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MET-ACIDOSIS