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    Metabolic Acidosis
    Clinical Manifestations
    • hyperkalemia: shift of acid to ICF and K+ to the ECF
    • anorexia, nausea, and vomiting
    • warm, flushed skin
    • cardiac dysrhythmias & CNS dysfunction
    • headache, diarrhea, tremors


    Metabolic Alkalosis
    Clinical Manifestations
    • cardia dysrhythmias; seizures; confusion; muscle twitching, agitation
    • >pH;>HC03; normal PaCo2 or elevated if compensation occurs


    Respiratory Acidosis
    Clinical Manifestations
    • > PaCo2; HCO3 is normal or > with renal compensation
    • vasodilatation; cardiac dysrhythmias, tachycardia, somnolence, decreased ventilation


    Respiratory Alkalosis
    Clinical Manifestations
    • > pH; < PaC02; HCO3 normal or low due to compensation
    • nausea, vomiting, tingling of fingers
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Etiology and Clinical Manifestations ::

Metabolic Acidosis

    Etiology: Loss of base: such as in cases of severe diarrhea
    or
    Gain of metabolic acids: Anaerobic metabolism; Drug overdose (e.g.salicylates); Renal failure; Diabetic ketoacidosis

    Manifestations: headache and lethargy are early symptoms; warm flushed skin; seizures; mental confusion; muscle twitching; agitation; coma (severe acidosis); anorexia, nausea, vomiting and diarrhea; deep and rapid respirations (Kussmaul respirations); hyperkalemia (shift of acid to the ICF and K+ to the ECF); cardiac dysrhythmias.
    Decreased blood pH; decreased HCO3; normal PaCO2 or decreased if compensation is occurring.

    (The "nursing interventions" button on the homepage will lead the user to these nursing interventions listed under each problem. It would be nice to have a pull-down menu under "nursing interventions" for metabolic acidosis, metabolic alkalosis, respiratory acidosis, and respiratory alkalosis) on the homepage).

    Nursing Interventions: Assess the clinical symptoms, health history, and lab results. Identify the underlying cause to intervene appropriately. When there is sever acidosis (pH < 7.1), sodium bicarbonate is necessary to bring the pH to a safe level. Correct the sodium and water deficits, as well.

Metabolic Alkalosis

    Etiology: Loss of metabolic acids: such as in cases of prolonged vomiting or gastrointestinal suctioning. Hyperaldosteronism can cause sodium retention and loss of hydrogen ions and potassium.
    or
    Gain of Base: an increased intake of bicarbonate. Diuretics (e.g. furosemide) can cause sodium, potassium, and chloride excretion more than bicarbonate excretion.

    Manifestations: general weakness, muscle cramps, hyperactive reflexes, tetany (due to a decrease in calcium); shallow and slow respirations; confusion and seizures may occur in severe situations. Increased blood pH; increased HCO3; normal PaCO2 or elevated if compensation is occurring.

    Nursing Interventions: Assess the clinical symptoms, health history, and lab results. Identify the underlying cause to intervene appropriately. If potassium levels are decreased administer potassium as ordered per physician. If acid-base disturbance is due to hypochloremic alkalosis with volume depletion, administer a sodium chloride IV solution. If the condition is caused by hyperaldosteronism, administer potassium.

Respiratory Acidosis

    Etiology: Carbon dioxide is retained when ventilation is depressed; therefore, leading to acidosis and hypercapnia (excess PaCO2).

    Clinical Manifestations: restlessness, apprehension and then lethargy are initial signs; muscle twitching, tremors, seizures, and coma can ensue; rapid respirations initially and then decreased due to adaptation; vasodilation due to acidosis (CO2 is a vasodilator), therefore the skin might be pink, unless there is hypoxemia; tachycardia.
    Decreased blood pH; Increased PaCO2; Normal HCO3 or elevated if compensation is occurring.

    Nursing Interventions: Assess the clinical symptoms, health history, and lab results. Identify the underlying cause to intervene appropriately. Restore alveolar ventilation (this will remove excess CO2), and if spontaneous ventilation is compromised (e.g. due to drug overdose or neuromuscular disorders) provide mechanical ventilation. Monitor the pH, PaCO2, PaO2, and HCO3 very closely. A rapid decline of the PaCO2 can lead to respiratory alkalosis with seizures and death. Check for hypoxemia and hypercapnia when administering oxygen. Oxygen can work as a respiratory depressant when the person's respiratory center is no longer stimulated by a low pH and elevated PaCO2. Renal buffering generally corrects an uncomplicated chronic respiratory acidosis.


Respiratory Alkalosis

Etiology: occurs when there is alveolar hyperventilation and a decrease in PaCO2 (hypocapnia). Hypoxemia (caused by pulmonary disease, high altitudes, or congestive heart failure), hypermetabolic conditions (fever or anemia), gram-negative sepsis, hysteria, or cirrhosis of the liver can stimulate hyperventilation.

Clinical Manifestations: confusion, dizziness, paresthesias (tingling of extremities), seizures and coma; tachypnea (deep and rapid respirations) causes respiratory alkalosis. Nausea and vomiting might be present. Increased blood pH; Decreased PaCO2; Normal HCO3 or decreased if compensation is occurring.

Nursing Interventions: Assess the clinical symptoms, health history, and lab results. Identify the underlying cause to intervene appropriately. Correct the hypoxemia and reverse the hypermetabolic states if present. Correct symptoms from hysterical hyperventilation by rebreathing from a paper bag (increases PaCO2).



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