Acid-Base Balance PPT only

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Polly
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258115
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Acid-Base Balance PPT only
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2014-01-24 14:48:38
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Acid Base Balance
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Med surg 2014
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Acid-Base Balance
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  1. Alterations in Acid-Base Balance
    • Outline from PPT
    • Lemone Pages 222-237
  2. As hydrogen ion concentration falls the pH rises and the solution becomes more base
    • As the hydrogen ion increases the pH falls and becomes more acid
    • • Normal ratio of acid to base is 20 parts base to 1 part acid, slightly alkaline
    • * The body maintains acid base balance by either saving or excreting acid or base
    • substances.
    • * Acidosis occurs when there is excess acid present, increase in hydrogen ion
    • concentration.
    • * Alkalosis occurs when there is excess base present, decrease in hydrogen ion
    • concentration.
  3. Two types of acids:
    • * 1. Carbonic Acid – volatile respiratory acid, eliminated or retained in the lungs, through
    • either hyperventilation or hypoventilation.
    • * 2. Nonvolatile acids – must be metabolized or excreted from the body in fluid, lactic acid,
    • hydrochloric acid
  4. Buffer
    • * A substance or group of substances that control the hydrogen ion concentration, by
    • absorbing hydrogen ions, or by releasing hydrogen ions.
    • * Respond immediately but have limited capacity to maintain
  5. 2 Major buffer systems: Lungs and Renal Systems:
  6. * Bicarbonate-carbonic acid system, ratio 20/1
    • * Phosphate buffer system, intra cellular
    • * Protein buffers, intracellular and plasma
  7. 1.Lungs
    • * Responds in minutes
    • * Respiratory center in the brain stem
    • * Occurs automatically
    • * Adjusts the depth and frequency of respiration according to the pH of the blood
    • • Hyperventilaiton ?
    • • Hypoventilation ?
  8. 2.Renal System
    • • Slower to respond and may take hours to days correct an imbalance
    • • Excrete H ions, or generate and reabsorb bicarbonate in response to an acid pH
    • • Retain H ions, or generate and excrete bicarbonate in response to an alkaline
    • The kidneys provide a more inclusive corrective response to acid-base balance/disturbances
    • than respiratory, however it is slower…
    • Kidneys:
    • Compensation requires a few hours to several days to begin, but the compensation is more
    • thorough and selective than that of other regulators, ie buffers and respiratory.
    • In acidosis, the ph decreases and excess H ions are secreted with buffers into the urine.
    • In alkalosis, the pH increases and excess bicarb ions move into the kidneys tubules, combine with
    • sodium, and then are excreted in the urine.
    • Selective regulation of bicarbonate occurs in kidneys.
    • 1. The kidneys restore bicarb by excreting hydrogen ions and retaining bicarbonate
    • ions.
    • 2. Excess H ions are excreted in the urine (in the form of phosphoric acid)
    • 3. The alteration of certain amino acids in the renal tubules, results in a diffusion of
    • ammonia. The ammonia combines with excess H ions and is then excreted in
    • urine.
  9. Three major determinants of acid base balance:
    • 1. pH – measure of the hydrogen ion concentration of the blood.
    • • Normal pH: 7.35 –7.45
    • 2. PaCO2 – measures the partial pressure of carbon dioxide in arterial blood,
    • effectiveness of ventilation.
    • • Normal PaCO2: 35 – 45 mmHg
    • 3. HCO3 – indicates the quantity of bicarb in the extracellular fluid. This is a
    • base substance and indicates a metabolic disorder.
    • * Normal 22 – 26 mEq/L
  10. • Base excess, calculated value for buffer base capacity: the amount of acid or base added
    • to blood to obtain a pH of 7.4
    • • Normal -3 - +3
  11. Classifications:
    • 1. Acidosis
    • OR
    • 2. Alkalosis
  12. Determined by the Origin of the problem
    • • Simple or combined
    • • Simple has one cause either respiratory or metabolic
    • • Combined more severe, both respiratory & metabolic are the cause
  13. Alteration States of Acid-Base Balance:
    • 1.Metabolic Alkalosis:
    • • Primary excess of HCO3 in the extracellular fluid secondary to the loss of acid or the
    • addition of HCO3
    • • pH > 7.45
    • • HCO3 > 26 mEq/L
    • • Bicarbonate excess, loss of acid or gain of HCO3
  14. A deficit of carbonic acid and a decrease in H ion concentration that results from accumulation of
    base or from a loss of acid without an equal or comparable loss of base in body fluids.
  15. Major causes of Metabolic Alkalosis:
    • • Hydrogen loss
    • • GI loss, suctioning or vomiting
    • o Leads to an excessive loss of hydrochloric acid
    • • Response to hypokalemia ( low potassium)
    • • kidneys preserve K excrete H ion instead or K moves out of the cells and H ion
    • moves in.
    • • HCO3 retention
    • a. excessive bicarb replacement
    • b. excessive use of antacids (sodium bicarbonate)
    • • Calcium combines with serum proteins: reducing the amt of ionized calcium, causing a
    • hypocalcemia, manifestations similar to those of a low calcium
  16. Other Causes:
    • • Diuretics
    • o Loss of H ions and chloride (acids) due to diuresis; causes a compensatory
    • increase in the amount of bicarbonate in the blood. Too much acid not enough
    • base.
    • • Hyperaldosteroneism
    • o Increase in aldosterone triggers kidneys to reabsorb fluid and sodium, results in
    • a loss of H ions.
    • • Massive transfusion of whole blood
    • o The citrate anticoagulant used for the storage of blood is metabolized to
    • bicarbonate.
  17. Pathophysiology of Metabolic Alkalosis:
    • • K+ moves out of the cell and H+ moves into the cell
    • • Kidney reabsorbs K+ and wastes H +
    • • Lungs respond by decrease in resp rate and depth
  18. Clinical Manifestations of Metabolic Alkalosis:
    • • May be asymptomatic, 7.45 pH
    • • Severe alkalosis = neurologic manifestations confusion, spasms hands and feet,
    • hyperreflexia, similar to hypocalcemia
    • • If pH is > 7.55 it is life threatening, respiratory failure, dysrhythmias, seizure, coma
    • • Shallow slow breathing
    • • Due to lungs trying to hold on to Co2
  19. Others possible manifestations of Metabolic alkalosis:
    • • Drowsiness, dizziness, nervousness, confusion
    • • Tachycardia, possible dysrhythmias
    • • Anorexia, N/V
    • • Tremors, hypertonic muscles, muscle cramps, tetany, tingling of extremities, seizures
    • • Hypoventilation- as lungs try to compensate by retaining CO2
  20. Treatment of Metabolic Alkalosis:
    • • If the cause is hypokalemia and hypovolemia, treat with saline solutions and K+
    • replacements
    • • If the cause is diuretics, treat with oral potassium replacement
    • • Correct u underlying cause
    • Nursing Interventions for Metabolic Alkalosis:
    • • Monitor for S/S of respiratory distress
    • • Monitor Labs-Potassium and calcium levels
    • • Initiate Safety precautions
    • • Prepare to admin meds as ordered
    • • Prepare to admin IV fluids to promote excretion of bicarbonate
    • • Treat underlying cause of alkalosis
  21. Nursing DX of Metabolic Alkalosis:
    • • Impaired gas exchange
    • • Ineffective airway clearance
    • • Risk for injury
  22. 2.Metabolic Acidosis:
    • A total concentration of buffer base that is lower than normal, with a relative increase in the H ion
    • concentration, resulting from the loss of too much base and or too much retention of acid
    • • Excess acid or loss of bicarbonate
    • • Develops during the course of another disease process
    • • Bicarb < 22 mEq/L, pH < 7.35
  23. Pathophysiology of Metabolic Acidosis:
    • • HCO3 is utilized or lost and the end result is an excess in circulating acids
    • • Increased production of acids
    • fasting, starvation, Ketoacidosis
    • drug or poison ingestion
    • lactic acidosis
    • Impaired excretion – renal failure
    • • Loss of intestinal secretions, GI, biliary or pancreatic,
    • • Increased chloride, abnormal renal function, saline infusions, and TPN
    • • NG tube suction, diarreha, fistulas (bicarb loss)
  24. Other causes of metabolic acidosis:
    • * Diabetes mellitus or Ketoacidosis—Due to insufficient insulin which causes and increase of
    • fat metabolism, leading to build up of excess ketones and other acids; the bicarbonate is
    • quickly depleted.
    • * Excessive ingestion of aspirin (acetylsalicylic acid)-- results in an increase in H ions.
    • * A high-- fat diet causes a rapid accumulation of the waste products of fat metabolism, leading
    • to an excess build up of ketones and acids.
    • * An insufficient metabolism of carbohydrates—when the oxygen supply is not sufficient for
    • the metabolism of carbs, lactic acid is produced and lactic acidosis is the result.
    • * Malnutrition—improper metabolism of nutrients causes fat catabolism, leading to an excess
    • build up of ketones and acids.
    • * Renal insufficiency, acute renal injury, or chronic kidney disease—causes increased waste
    • products to be retained instead of excreted. Acids increase and bicarbonate is unable to
    • maintain acid-base balance.
    • * Severe diarrhea—intestinal and pancreatic secretions are normally alkaline; therefore if
    • excessive loss of these base or alkaline secretions leads to acidosis.
  25. Assessment of metabolic acidosis:
    • * Monitor for hyperpnea with kussmaul’s respirations. Respirations are increased as the lungs
    • attempt to rid the body of excess CO2.
  26. Inerventions for Metabolic acidosis:
    • * Monitor for signs of respiratory distress
    • * Assess LOC
    • * Monitor I & O
    • o Provide fluid and electrolyte replacement as prescribed
    • * Prepare to administer meds (buffers) as prescribed: sodium bicarbonate
    • * Initiate safety measures and seizure precautions
    • * Monitor labs for potassium level: as metabolic acidosis resolves, potassium moves back into
    • the cells and the serum potassium level decreases. (When excess H ions are present they are
    • pushed into cells, H ions are pushed out.)
    • * If pt has severe diarrhea, monitor for S/S of Metabolic acidosis.
    • Interventions for metabolic acidosis due to DM or Ketoacidosis:
    • * Give insulin as prescribed to hasten the movement of glucose into the cells, which will
    • decrease the concurrent ketosis.
    • • When glucose is being properly metabolized, the body will stop converting fats to
    • glucose.
    • • Monitor for circulatory collapse caused by Polyuria, due to hyperglycemic state;
    • Osmotic diuresis may lead to extracellular volume deficit.
    • Interventions for kidney disease:
    • • Dialysis may be used to remove proteins and waste products form blood
    • • A diet low in protein and high in calories helps decrease the amount of protein waste
    • products resulting in lower acid levels.
  27. Manifestations of Metabolic Acidosis:
    • • Anorexia
    • • N/V
    • • Abd pain
    • • Weakness
    • • Altered LOC, confusion
    • • Dysrhythmias
    • • Kussmaul’s resp , rapid and deep
  28. Collaborative care of Metabolic Acidosis:
    • • ABG’s, lytes, ECG
    • • Diabetic ketoacidosis, tx insulin
    • • Alcoholic, saline solutions
    • • Correct the underlying disorder, renal disorders
  29. 3. Respiratory Acidosis:
    • • A retention of carbonic acid, increase in CO2 and decreases the pH.
    • • Depressed respiratory center
    • • Cardiac arrest
    • • Structural alterations in thorax/ lungs
    • • Neuromuscular impairment
    • • Mechanical ventilators
  30. Diagnostics of respiratory acidosis:
    • • PaCo2 > 45
    • • pH < 7.35
    • • Electrolytes, bicarb >26
    • • Chest x ray
  31. Clinical Manifestations of Respiratory Acidosis:
    • • Skin is warm/flushed
    • • Tachycardia
    • • Papilledema
    • • Headache
    • • Altered mental status, LOC
    • • Muscle twitching
    • • Rapid/slow onset
  32. Collaborative Care of Respiratory Acidosis:
    • • Pharmacology, antibiotics & bronchdilators
    • • Respiratory support, restore alveolar ventilation
    • • CAUTION, COPD, their hypoxemia stimulates their breathing, ^ O2 decreases their drive
  33. 4.Respiratory alkalosis:
  34. • Bicarb < 24, PaCO2 < 35, pH > 7.45
    • Increase in rate of alveolar ventilation, decrease in carbon dioxide
  35. Causes of respiratory alkalosis:
    • • Respiratory center stimulation, fever
    • • Trauma CNS
    • • Excessive Mechanical ventilation
  36. Collaborative Care of respiratory alkalosis:
    • • ABG’s,Lytes
    • • Anxiety induced, sedatives
    • • Treat hypoxia
  37. Clinical manifestation of respiratory alkalosis:
    • • Dizziness
    • • Diaphoresis
    • • Palpitations
    • • Dyspnea
    • • Anxiety
    • • convulsions
  38. Nursing care of respiratory alkalosis:
    • • Sensory/perception alterations
    • • Altered thought process
    • • Ineffective breathing pattern
    • • Risk for injury
    • • Acidosis, Decreased CO, FVD
    • • Impaired gas exchange
    • • Interpreting ABG’s
    • • Acidosis< pH 7.35 – 7.45 > alkalosis
    • • Alkalosis < PaCO2 35 –45 > acidosis
    • • Acidosis < HCO3 22 – 26 > alkalosis
  39. Interpreting ABG’s:
    • Acidosis< pH 7.35 – 7.45 > alkalosis
    • • Alkalosis < PaCO2 35 –45 > acidosis
    • • Acidosis < HCO3 22 – 26 > alkalosis
  40. Each ABG has a first, middle & last name
    • • First – compensated or uncompensated
    • • Middle – metabolic or respiratory
    • • Last – acidosis or alkalosis

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