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Acid-Base Balance Interactive Tutorial

Acid-Base Balance Interactive Tutorial

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Acid-Base Balance Interactive Tutorial

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  1. Acid-Base Balance Interactive Tutorial Emily Phillips MSN 621 Spring 2009 E-mail: All images imported from Microsoft Clipart & Yahoo Image gallery

  2. How to navigate this tutorial: • To advance to the next slide click on the box • To return to the previous slide click on the box • To return to the Main Menu: click the box • Hover over underlined text for a definition/explanation • To return to the last slide viewed click on the button • Click the for additional information

  3. Objectives: • Define acid base balance/imbalance • Explain the pathophysiology of organs involved in acid base balance/imbalance • Identify normal/abnormal and compensated/uncompensated lab values • Explain symptoms related to acid base imbalances and compensated vs. uncompensated • Appropriate interventions and expected outcomes

  4. Main Menu: Acid-Base Pretest The Buffer Systems Acid-Base Review test Metabolic Distubances Respiratory Disturbances Acid-Base Compensation Diagnostic Lab Values ABG Interpretation & Case Studies

  5. Acid-Base Pretest: • What is the normal range for arterial blood pH? 7.38 – 7.46 7.40 – 7.52 7.35 – 7.45

  6. Acid-Base Pretest: • What 2 extracellular substances work together to regulate pH? Sodium bicarbonate & carbonic acid Carbonic acid & bicarbonate Acetic acid & carbonic acid

  7. Acid-Base Pretest: • Characterize an acid & a base based on the choices below. Acids release hydrogen (H+) ions & bases accept H+ ions. Acids accept H+ ions & bases release H+ ions Both acids & bases can release & accept H+ ions

  8. Acid-Base Pretest: • Buffering is a normal body mechanism that occurs rapidly in response to acid-base disturbances in order to prevent changes in what? HCO3- H2CO3 H+

  9. Acid-Base Pretest: • What are the two systems in the body that work to regulate pH in acid-base balance & which one works fastest? The Respiratory & Renal systems Renal The Respiratory & Renal systems Respiratory The Renal & GI systems Renal

  10. Acid-Base Balance: • Homeostasis of bodily fluids at a normal arterial blood pH • pH is regulated by extracellular carbonic acid (H2CO3) and bicarbonate (HCO3-) • Acids are molecules that release hydrogen ions (H+) • A base is a molecule that accepts or combines with H+ ions

  11. Acids and Bases can be strong or weak: • A strong acid or base is one that dissociates completely in a solution - HCl, NaOH, and H2SO4 • A weak acid or base is one that dissociates partially in a solution -H2CO3, C3H6O3, and CH2O

  12. The Body and pH: Protein Buffer system • Homeostasis of pH is controlled through extracellular & intracellular buffering systems • Respiratory: eliminate CO2 • Renal: conserve HCO3- and eliminate H+ions • Electrolytes: composition of extracellular (ECF) & intracellular fluids (ICF) - ECF is maintained at 7.40 HCO3- Buffer system K+ - H+ Exchange

  13. Quick Review: Click the Boxes An Acid is: A Base is: A donator of H+ ions An acceptor of H+ w/ pH <7.0 ions w/ pH >7.0 Regulated by EC Controlled by EC H2CO3 & HCO3- & IC buffer systems Eliminates CO2 Conserves HCO3- Eliminates H+ ions pH is: pH is: Respiratory System: Renal System:

  14. Respiratory Control Mechanisms: • Works within minutes to control pH; maximal in 12-24 hours • Only about 50-75% effective in returning pH to normal • Excess CO2 & H+ in the blood act directly on respiratory centers in the brain • CO2 readily crosses blood-brain barrier reacting w/ H2O to form H2CO3 • H2CO3 splits into H+ & HCO3- & the H+ stimulates an increase or decrease in respirations

  15. Renal Control Mechanisms: • Don’t work as fast as the respiratory system; function for days to restore pH to, or close to, normal • Regulate pH through excreting acidic or alkaline urine; excreting excess H+ & regenerating or reabsorbing HCO3- • Excreting acidic urine decreases acid in the EC fluid & excreting alkaline urine removes base H+ elimination & HCO3- conservation

  16. Mechanisms of Acid-Base Balance: • The ratio of HCO3- base to the volatile H2CO3 determines pH • Concentrations of volatile H2CO3 are regulated by changing the rate & depth of respiration • Plasma concentration of HCO3- is regulated by the kidneys via 2 processes: reabsorption of filtered HCO3- & generation of new HCO3-, or elimination of H+ buffered by tubular systems to maintain a luminal pH of at least 4.5 Phosphate Buffer system Ammonia Buffer system

  17. Acid-Base Balance Review test: • The kidneys regulate pH by excreting HCO3- and retaining or regenerating H+ TRUE FALSE

  18. Acid-Base Review test: • H2CO3 splits into HCO3- & H+ & it is the H+ that stimulates either an increase or decrease in the rate & depth of respirations. TRUE FALSE

  19. Acid-Base Review test: • Plasma concentration of HCO3- is controlled by the kidneys through reabsorption/regeneration of HCO3-, or elimination of buffered H+ via the tubular systems. TRUE FALSE

  20. Acid-Base Review test: • The ratio of H+ to HCO3- determines pH. TRUE FALSE

  21. Acid-Base Review test: • Secreted H+ couples with filtered HCO3- & CO2 & H2O result. TRUE FALSE

  22. Metabolic Disturbances: • Alkalosis: elevated HCO3- (>26 mEq/L) • Causes include: Cl- depletion (vomiting, prolonged nasogastric suctioning), Cushing’s syndrome, K+ deficiency, massive blood transfusions, ingestion of antacids, etc. • Acidosis: decreased HCO3- (<22 mEq/L) • Causes include: DKA, shock, sepsis, renal failure, diarrhea, salicylates (aspirin), etc. • Compensation is respiratory-related

  23. Metabolic Alkalosis: • Caused by an increase in pH (>7.45) related to an excess in plasma HCO3- • Caused by a loss of H+ ions, net gain in HCO3- , or loss of Cl- ions in excess of HCO3- • Most HCO3- comes from CO2 produced during metabolic processes, reabsorption of filtered HCO3-, or generation of new HCO3- by the kidneys • Proximal tubule reabsorbs 99.9% of filtered HCO3-; excess is excreted in urine

  24. Metabolic Alkalosis Manifestations: • Signs & symptoms (s/sx) of volume depletion or hypokalemia • Compensatory hypoventilation, hypoxemia & respiratory acidosis • Neurological s/sx may include mental confusion, hyperactive reflexes, tetany and carpopedal spasm • Severe alkalosis (>7.55) causes respiratory failure, dysrhthmias, seizures & coma

  25. Treatment of Metabolic Alkalosis: • Correct the cause of the imbalance • May include KCl supplementation for K+/Cl- deficits • Fluid replacement with 0.9 normal saline or 0.45 normal saline for s/sx of volume depletion • Intubation & mechanical ventilation may be required in the presence of respiratory failure

  26. Metabolic Acidosis: • Primary deficit in base HCO3- (<22 mEq/L) and pH (<7.35) • Caused by 1 of 4 mechanisms • Increase in nonvolatile metabolic acids, decreased acid secretion by kidneys, excessive loss of HCO3-, or an increase in Cl- • Metabolic acids increase w/ an accumulation of lactic acid, overproduction of ketoacids, or drug/chemical anion ingestion

  27. Metabolic Acidosis Manifestations: • Hyperventialtion (to reduce CO2 levels), & dyspnea • Complaints of weakness, fatigue, general malaise, or a dull headache • Pt’s may also have anorexia, N/V, & abdominal pain • If the acidosis progresses, stupor, coma & LOC may decline • Skin is often warm & flush related to sympathetic stimulation

  28. Treatment of Metabolic Acidosis: • Treat the condition that first caused the imbalance • NaHCO3 infusion for HCO3- <22mEq/L • Restoration of fluids and treatment of electrolyte imbalances • Administration of supplemental O2 or mechanical ventilation should the respiratory system begin to fail

  29. Quick Metabolic Review: • Metabolic disturbances indicate an excess/deficit in HCO3- (<22mEq/L or >26mEq/L • Reabsorption of filtered HCO3- & generation of new HCO3- occurs in the kidneys • Respiratory system is the compensatory mechanism • ALWAYS treat the primary disturbance

  30. Respiratory Disturbances: • Alkalosis: low PaCO2 (<35 mmHg) • Caused by HYPERventilation of any etiology (hypoxemia, anxiety, PE, pulmonary edema, pregnancy, excessive ventilation w/ mechanical ventilator, etc.) • Acidosis: elevated PaCO2 (>45 mmHg) • Caused by HYPOventilation of any etiology (sleep apnea, oversedation, head trauma, drug overdose, pneumothorax, etc.) • Compensation is metabolic-related

  31. Respiratory Alkalosis: • Characterized by an initial decrease in plasma PaCO2 (<35 mmHg) or hypocapnia • Produces elevation of pH (>7.45) w/ a subsequent decrease in HCO3- (<22 mEq/L) • Caused by hyperventilation or RR in excess of what is necessary to maintain normal PaCO2 levels

  32. Respiratory Alkalosis Manifestations: • S/sx are associated w/ hyperexcitiability of the nervous system & decreases in cerebral blood flow • Increases protein binding of EC Ca+, reducing ionized Ca+ levels causing neuromuscular excitability • Lightheadedness, dizziness, tingling, numbness of fingers & toes, dyspnea, air hunger, palpitations & panic may result

  33. Treatment of Respiratory Alkalosis: • Always treat the underlying/initial cause • Supplemental O2 or mechanical ventilation may be required • Pt’s may require reassurance, rebreathing into a paper bag (for hyperventilation) during symptomatic attacks, & attention/treatment of psychological stresses.

  34. Respiratory Acidosis: • Occurs w/ impairment in alveolar ventilation causing increased PaCO2 (>45 mmHg), or hypercapnia, along w/ decreased pH (<7.35) • Associated w/ rapid rise in arterial PaCO2 w/ minimal increase in HCO3- & large decreases in pH • Causes include decreased respiratory drive, lung disease, or disorders of CW/respiratory muscles

  35. Respiratory Acidosis Manifestations: • Elevated CO2 levels cause cerebral vasodilation resulting in HA, blurred vision, irritability, muscle twitching & psychological disturbances • If acidosis is prolonged & severe, increased CSF pressure & papilledema may result • Impaired LOC, lethargy/coma, paralysis of extremities, warm/flushed skin, weakness & tachycardia may also result

  36. Treatment of Respiratory Acidosis: • Treatment is directed toward improving ventilation; mechanical ventilation may be necessary • Treat the underlying cause • Drug OD, lung disease, chest trauma/injury, weakness of respiratory muscles, airway obstruction, etc. • Eliminate excess CO2

  37. Quick Respiratory Review: • Caused by either low or elevated PaCO2 levels (<35 or >45mmHg) • Watch for HYPOventilation or HYPERventilation; mechanical ventilation may be required • Kidneys will compensate by conserving HCO3- & H+ • REMEMBER to treat the primary disturbance/underlying cause of the imbalance

  38. Compensatory Mechanisms: • Adjust the pH toward a more normal level w/ out correcting the underlying cause • Respiratory compensation by increasing/decreasing ventilation is rapid, but the stimulus is lost as pH returns toward normal • Kidney compensation by conservation of HCO3- & H+ is more efficient, but takes longer to recruit

  39. Metabolic Compensation: • Results in pulmonary compensation beginning rapidly but taking time to become maximal • Compensation for Metabolic Alkalosis: • HYPOventilation (limited by degree of rise in PaCO2) • Compensation for Metabolic Acidosis: • HYPERventilation to decrease PaCO2 Begins in 1-2hrs, maximal in 12-24 hrs

  40. Respiratory Compensation: • Results in renal compensation which takes days to become maximal • Compensation for Respiratory Alkalosis: • Kidneys excrete HCO3- • Compensation for Respiratory Acidosis: • Kidneys excrete more acid • Kidneys increase HCO3- reabsorption