Acid-Base Balance

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Polly
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Acid-Base Balance
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2014-01-24 14:47:34
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Acid Base Balance
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2014 Adv Med Surg
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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, loss of H ions = alkalosis
    • • HCO3 > 26 mEq/L, increase in base = alkalosis
    • • 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. It rarely occurs
    • as a primary disorder, but rather after a hospitalization, hypokalemia, or treatment with a bicarbonate
    • solution.
  15. Major causes of Metabolic Alkalosis:
    • • Hydrogen loss
    • • GI loss, gastric 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
    • • Excess bicarbonate administration
    • • Possibly due to overzealous attempt to correct acidosis
    • • Excessive administration or use of 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 base and not enough acid.
    • • 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.
  16. 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
  17. Clinical Manifestations of Metabolic Alkalosis:
    • pH greater than 7.45
    • • May be asymptomatic, or be similar to s/s of hypocalcemia—
    • • Numbness and tingling around mouth, fingers, toes, dizziness, trousseaus sign,
    • muscle spasms
    • • 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
    • • Metabolic Alkalosis excites the CNS
    • • Shallow slow breathing- decreased respirations
    • • Due to lungs trying to hold on to Co2
    • • Can lead to respiratory failure with:
    • • Hypoxemia, lungs not taking in enough Oxygen
    • • Respiratory acidosis; due to Lungs retaining too much CO2
    • • Monitor electrolyes for imbalance:
    • • Potassium –Hypokalemia
    • • Hypocalcemia: as pH increases, Ca++ binding occurs and serum Ca++ levels
    • decrease
    • • Hyponatremia and hypochloremia
    • • Urine chloride tell you if client is chloride responsive or chloride resistant
    • • BE increases
    • Others possible manifestations of Metabolic alkalosis:
    • • Drowsiness, dizziness, nervousness, confusion: decreased LOC
    • • Hypotension
    • • Tremors, hyper reflexia, hypertonic muscles, muscle cramps, tetany, tingling of
    • extremities, seizures
    • • Hypoventilation , leads to respiratory failure-as lungs compensate by retaining CO2
  18. Compensation manifestation of Metabolic Alkalosis:
    • • Lungs: attempt to retain Co2, by slowing breathing
    • • Kidneys conserve H ions and excrete HCO3
    • • PaCO2 increases with compensation
    • • Urine pH greater than 6
  19. Treatment of Metabolic Alkalosis:
    • • Goal is to treat underlying problem
    • • If the cause is hypokalemia and hypovolemia, treat with saline solutions and K+
    • Replacements
    • o Admin potassium chloride and chloride solution as ordered:
    • o K= balance allows kidneys to more effectively conserve H ions
    • o Chloride promotes renal excretion of bicarbonate
    • • If the cause is diuretics, treat with oral potassium replacement as ordered
    • • In severe cases: acidifying solution, such as hydrochloric acod or ammonium chloride
    • may be ordered
    • • Restore Fluid balance
  20. Nursing Interventions for Metabolic Alkalosis:
    • • Monitor for S/S of respiratory distress- *Monitor rate and depth of Respirations!
    • • Assess LOC
    • • Assess VS
    • • Monitor I&O
    • • Monitor ABGs
    • o Note-remember to apply firm pressure to ABG puncture site for 2-5 minutes
    • • Monitor Labs-Potassium/hypokalemia and calcium levels and other electrolytes
    • • Initiate Safety precautions
    • • Prepare to admin meds as ordered
    • o Zantac or Pepcid may be ordered to reduce secretion of H ions and loss from GI
    • drainage
    • • Prepare to admin IV fluids to promote excretion of bicarbonate
    • o Normal saline IV fluids
    • o Potassium if hypokalemia
    • Treat underlying cause of alkalosis
    • • Initiate safety precautions to protect pt from injury
    • • Monitor ECG for any conduction abnormalities
  21. Educate client:
    • • Take antacids correctly and prevent excess dosing, teach risks
    • • Teach pt s/s to report to their healthcare provider, especially those at risk-elderly
    • • Teach s/s of hypokalemia to report to healthcare providers
    • • Use of supplements such as potassium only as ordered, diet, other problems that may cause
    • hypokalemia: loop diuretics, decreased aldosterone production
    • • Contact health provider if uncontrolled or extended vomiting or diarrhea
  22. Nursing DX of Metabolic Alkalosis:
    • • Priority Nursing DX is: Impaired gas exchange
    • • Ineffective airway clearance
    • • Fluid Volume Deficit
    • • Metabolic alkalosis pts often have accompanying FVD
    • • Risk for injury- due to decreased LOC-confusion, Hypotension, seizures
  23. Metabolic Alkalosis SNAP Shot:
  24. 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.
  25. 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.
  26. 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.
  27. 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
    • The acidotic states depresses cell membrane excitability = depressed CNS. Severe decrease in pH
    • below 7.0 can cause depressed myocardial contractility = decreased cardiac output
    • • Excess acid or loss of bicarbonate
    • • Develops during the course of another disease process
    • • Bicarb is less than 22 mEq/L, pH is Less than 7.35
  28. Pathophysiology of Metabolic Acidosis:
    • • HCO3 is utilized or lost and the end result is an excess of circulating acids
    • • Increased production of acids, for example:
    • • 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, diarrhea, fistulas (bicarb loss)
    • • Rarely happens alone, usually accompanied by other problems or during the course of
    • another disease, such as:
    • • Chronic diarrhea, GI Fistula, GI Suctioning
    • • Leads to excess loss of bicarbonate which is excreted by the pancrease and
    • secreted into the small intestine
    • • Starvation, malnutrition, DM
    • • Both oxygen and glucose are necessary for normal cell
    • production
    • • Starvation or DM cause a lack of insulin to move into cells, the body begins to break
    • down fatty acid=Ketones=DKA
    • • Renal failure, results in impaired excretion of metabolic acids
    • • Acute lactic acidosis, a result of tissue hypoxia due to shock or cardiac arrest
    • • Metabolism shifts to anaerobic by the cells = production of lactate and H ions,
    • forming lactic acid
    • • Diabetic Ketoacidosis (DKA), lack of insulin=fat metabolism results= excess ketones
    • • Hyperthyroidism, Trauma, Shock, Severe infection, or Fever
  29. Causes of metabolic acidosis:
    • Basic mechanism that cause metabolic acidosis are:
    • 1. Accumulation of metabolic acids: thru excess production of acids or impaired
    • elimination by the kidney.
    • 2. Excess loss of bicarbonate
    • 3. An increase in chloride levelss
    • * 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.
  30. 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.
  31. Interventions 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 increased potassium level:
    • o Normal functioning Kidneys retain potassium when trying to rid body of H ions
    • o Note: 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.)
    • • Monitor labs for increse in calcium level
    • • Monitor for decrease in magnesium level
    • * 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.
  32. Manifestations of Metabolic Acidosis:
    • PH less than 7.35, HCO3 Less than 22
    • Affects many body systems
    • • GI: Anorexia, N/V, diarrhea, Abd pain
    • • Altered LOC, confusion,
    • • Weakness, fatigue, general malaise, Headache
    • • Skin is often warm and flushed
    • • Muscle twitching
    • • Drowsiness/lethargy, can progress to stupor then coma (CNS Depression)
    • • Dysrhythmias
    • • pH below 7.0 can lead to depressed myocardial contractility then cardiac arrest
    • • Kussmaul’s resp , rapid and deep respirations
    • • Hypotension, peripheral vasodilatation
    • • Hyperkalemia possible, resulting in ECG changes related to hyperkalemia
    • • BE decreases and AG calculation increases
  33. Compensations Manifestations:
    • • Lungs- Respirations increase and deepen to blow off excess CO2
    • • Kidneys- Retain HCO3
    • • Urine pH less than 6
    • • PaCO2 decreases when compensation is occurring
  34. Medications:
    • • Bicarbonate PO or IV route:
    • o Sodium Bicarbonate- most common
    • o Other alkalizing solution: lactate, citrate, acetate
    • Monitor pt carefully during med admin:
    • Too rapid correction of acidosis may lead to alkalosis
    • Also, hypokalemia, also hypernatremia and hyperosmolality: leading to fluid overload
  35. Collaborative care of Metabolic Acidosis:
    • • Goal is to correct underlying problem/disorder and correct acid-base balance
    • • Monitor: ABG’s,
    • • Labs-Serum Electrolytes: K=, Calcium
    • • Monitor EC: may show s/s of Acidotic state and/or hyperkalemia
    • • Diabetic Ketoacidosis, tx insulin, monitor blood glucose
    • • Renal Function study may be ordered
    • • Alcoholic, saline solutions
    • • Provide hydration to restore water, nutrients, and electrolytes
    • • May have order to admin IV solution with sodium bicarbonate to correct acidotic state
    • • Monitor I & O, and daily weights
    • • Monitor Vital signs—especially rate and depth of respirations and bradycardia
    • • Asscess LOC
    • • Assess GI
    • • Initiate satety precautions to protect pt from injury
    • • AS a last resort, Mechanical ventilation may be used only if all other interventions are
    • ineffective
  36. Educate patient on Metabolic Acidosis:
    • • Seek health care if prolonged Diarrhea is present
    • • Teach diabetic pt the importance of preventing DKA, starvation, alcoholism
    • o Diet, medication management
    • o What to do if DKA does occur:
    • • Teach to monitor for early signs of acidosis and seek medical attention:
    • o flu like symptoms: malaise, fatigue, n/v, anorexia, abd pain)
    • • Teach underlying cause of acid –base imbalance: Renal, DM, etc.
  37. Nursing diagnosis:
    • • Decrease cardiac output
    • • Risk for fluid volume excess:
    • o Due to bicarbonate treatment meds: lead to hypernatremia, hyperosmolality, and fluid
    • excess
    • • Risk for injury: due to altered mental status and brain function/CNS depression
  38. Metabolic Acidosis SNAP Shot:
  39. Etiology: Loss of base: such as in cases of severe diarrhea OR
    • Gain of metabolic acids: Anaerobic metabolism; Drug overdose (e.g.salicylates-aspirin); Renal failure; DM-
    • ketoacidosis
  40. 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.
  41. 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.
  42. 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
  43. Diagnostics of respiratory acidosis:
    • • PaCo2 > 45
    • • pH < 7.35
    • • Electrolytes, bicarb >26
    • • Chest x ray
  44. Clinical Manifestations of Respiratory Acidosis:
    • • Skin is warm/flushed
    • • Tachycardia
    • • Papilledema
    • • Headache
    • • Altered mental status, LOC
    • • Muscle twitching
    • • Rapid/slow onset
  45. Collaborative Care of Respiratory Acidosis:
    • • Pharmacology, antibiotics & bronchdilators
    • • Respiratory support, restore alveolar ventilation
    • • CAUTION, COPD, their hypoxemia stimulates their breathing, ^ O2 decreases their drive
  46. Respiratory Acidosis: SNAP Shot:
  47. Etiology: Carbon dioxide is retained when ventilation is depressed; therefore, leading to acidosis and
    hypercapnia (excess PaCO2).
  48. 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.
  49. 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.
  50. 4.Respiratory alkalosis:
  51. • Bicarb < 24, PaCO2 < 35, pH > 7.45
    • Increase in rate of alveolar ventilation, decrease in carbon dioxide
  52. Causes of respiratory alkalosis:
    • • Respiratory center stimulation, fever
    • • Trauma CNS
    • • Excessive Mechanical ventilation
  53. Collaborative Care of respiratory alkalosis:
    • • ABG’s,Lytes
    • • Anxiety induced, sedatives
    • • Treat hypoxia
  54. Clinical manifestation of respiratory alkalosis:
    • • Dizziness
    • • Diaphoresis
    • • Palpitations
    • • Dyspnea
    • • Anxiety
    • • convulsions
  55. 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
  56. Interpreting ABG’s:
    • Acidosis< pH 7.35 – 7.45 > alkalosis
    • • Alkalosis < PaCO2 35 –45 > acidosis
    • • Acidosis < HCO3 22 – 26 > alkalosis
  57. Each ABG has a first, middle & last name
    • • First – compensated or uncompensated
    • • Middle – metabolic or respiratory
    • • Last – acidosis or alkalosis
  58. Respiratory Alkalosis: Snap Shot
  59. 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.
  60. 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.
  61. 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).
  62. Manifestations Quick Reference :
  63. 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
  64. Metabolic Alkalosis
    • Clinical Manifestations
    • cardia dysrhythmias; seizures; confusion; muscle twitching, agitation
    • >pH;>HC03; normal PaCo2 or elevated if compensation occurs
  65. Respiratory Acidosis
    • Clinical Manifestations
    • > PaCo2; HCO3 is normal or > with renal compensation
    • vasodilatation; cardiac dysrhythmias, tachycardia, somnolence, decreased ventilation
  66. Respiratory Alkalosis
    • Clinical Manifestations
    • > pH; < PaC02; HCO3 normal or low due to compensation
    • nausea, vomiting, tingling of fingers

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