P A O 5600 Lecture 9 Acid Base Balance (2hrs) Dave

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P A O 5600 Lecture 9 Acid Base Balance (2hrs) Dave

  1. 1. ACID BASE BALANCE I D PAO 5600 Clinical Laboratory Medicine I C With Special Thanks To: Pamela Jaffey MD
  2. 2. OBJECTIVES Identify the sources of H in the body (volatile H+ 1. and nonvolatile acids) 2. D Describe the bicarbonat b ff system and it ib th bi b te t buffer t d its clinical utility in terms of acid base balance 3. Id tif i di ti Identify indications for a arterial blood gas, and f an t i l bl d d the normal values of pH HCO3-, pCO2, pO2 and H, O2 saturation in an arte erial blood gas 4. Define the relationship b between pH and H+ Dave Kotun, NSU O Orlando, PA Program 2
  3. 3. OBJECTIVES Describe t e normal physiologic roles p ayed by esc be the o a phys o og c o es played 5 5. the lungs (the quot;respiratory componentquot;) and kidney (the quot;metabolic componentquot;) in acid-base balance Define the relationship between pH and the 6. serum K+ concentration i terms of acid base i n in f id b balance Describe the regulation of th ventilatory rate b D ib th l ti f the til t t by 7. the central chemorecep ptors in the medulla and the peripheral receptors in the carotid bodies and s aortic arch Dave Kotun, NSU O Orlando, PA Program 3
  4. 4. Introduction It is necessary for the body t maintain the blood pH to • within a very narrow range: 77.35-7.45. A deviation would alter enzy function as well as yme create significant cardiovasc cular disturbance. Dave Kotun, NSU O Orlando, PA Program 4
  5. 5. Introduction This is a difficult task for the bod dy: Metabolic processes produce 15 - 20mol of H+ in the body daily, but th body b t the b d iis capable of f ti ning with plasma llevels bl f functioni ith l l between 36- 44 nmol/L; deviations from these levels ultimately s can cause death The body maintains this pH balance with buffer systems as well as concerted actions of the lungs and kidneys. The main buffer system utilized by th body is the bicarbonate buffer he system. Dave Kotun, NSU O Orlando, PA Program 5
  6. 6. SOURCES OF H+ IN THE BODY E VOLATILE ACIDS Derived from CO2: CO2 di l dissolves iin H2O forms carbonic acid fo bi id dissociates into bicarbonate and H+ e CO2 + H2O H2CO3 H 3- + H+ = THE HCO BICARBONATE BUFFER S SYSTEM Respiration allows H+ to be removed by the Lungs as CO2 e Dave Kotun, NSU O Orlando, PA Program 6
  7. 7. SOURCES OF H+ IN THE BODY E NONVOLATILE ACIDS Derived from Sources othe than CO2: er Metabolic products of su ulfur and phosphorus containing compounds p Lactic acid Keto acids (acetoacetate and beta hydroxybutyrate) e Excreted by the Kidneys Dave Kotun, NSU O Orlando, PA Program 7
  8. 8. BICARBONATE BUFFER S SYSTEM BUFFER = a weak acid (protonate and “conjugate” base ed) (unprotonated ) that minimize chan nges in H upon addition of H+ acid or base BICARBONATE BUFFER: H2CO3 H+ + HCO3- - ( acid) ( conjugate base ) Dave Kotun, NSU O Orlando, PA Program 8
  9. 9. UNIQUENESS OF BICARB BONATE BUFFER SYSTEM THE BICARBONATE BUFFER SYSTEM IS UNIQUE: It has a huge buffering capacity because it communicates with y air (it is an open system) This is in contrast to other buffe of the body which operate in ers a c osed syste closed system ACID BASE LOCATION Hb : HHb Hb Hb- in erythrocytes Proteins: Hprotein Proteins- intracellular Phosphate buffer: H2PO4- HPO H 42- intracellular Dave Kotun, NSU O Orlando, PA Program 9
  10. 10. INTERRELATIONSHIP OF CO OMPONENTS OF THE BICARBONATE BUFFER THE HENDERSON- HASSELBA ALCH EQUATION: In general, the Henderson-Hasselbalch eq ation gene al Hende son H equation describes the equilibrium bet tween pH, a weak acid, and conjugate weak base (it is useful in the preparation of buffers) We will apply the Henderson- pp y -Hasselbalch equation q to the bicarbonate buffer syst tem after defining some terms: Dave Kotun, NSU O Orlando, PA Program 10
  11. 11. H&H Henderson-Hasselbalch equation Consider the ionization of a weak acid HA which has some pKa. It is often convenient to be able to relate the pH of a solution of a n weak acid to the pKa of the acid and the extent of ionization. The reaction would be n HA (reversible arrows) H+ + A- The acid dissociation constant (Ka) for this reaction would be given by the equation e This equation can be rearranged to isolate the hydrogen ion concentration on the left, because, remember, we want an equation relating the pH of the solution to the pKa and the extent of ionization of t weak acid. The rearranged form of the equation is the By definition, log 1/ [H+] = pH , and log 1/Ka = pKa , so that by taking t log of the equation above, we get the equation the This is the well-known Henderson-Hasselbalch equation that is often used to perform the calculations required in preparation of buffers d for use in the laboratory, or other applications. Notice several interesting facts about this equation. First, if the pH = pKa, the log of the ratio of dissociate acid and associated acid will be zero, so the concentrations of the two species will be the same. In other words, when the pH equals the pKa, the acid w be half dissociated. will Second, notice that as the pH increases or decreases by one unit relative to the pKa, the ratio of the dissociate form to the associated form of the acid changes by factors of 10 That is if the pH of a solution is 6 and the pKa is 7, the ratio of [ A ]/[ HA] will be 0.1, will if 10. is, 7 A-]/[ 01 the pH were 5, the ratio would be 0.01 and if the pH were 7, the ratio wo ould be 1. Also, note that if the pH is below the pKa, the ratio will be < 1, while if th pH is above the pKa, the ratio will be >1. In short, there is he a lot of information in the Henderson-Hasselbalch equation. You would be wise to study this equation to understand its various e ramifications. Dave Kotun, NSU O Orlando, PA Program 11
  12. 12. DEFINITIONS RELATED TO H HENDERSON HASSELBALCH EQUATION Q DEFINITIONS -log H+ = pH and H+ a inversely proportional are As H+ increases, pH decreases As H + decreases, pH increases -log Ka = pKa Ka = the dissociation constant of a weak acid n BICARBONATE BUFFER SSYSTEM EQUILIBRIUM AS DEFINED BY HENDERSON-HASSELBALCH EQUATION: EQUATION pKa + log HCO3- conjugate base/ pH = g H2CO3conjugate acid Dave Kotun, NSU O Orlando, PA Program 12
  13. 13. Henderson Hasselbach Two equivalent forms o the equation are of and Here, pKa is − log10(K where Ka is the Ka) acid dissociation consta ant, that is: for the reaction: Dave Kotun, NSU O Orlando, PA Program 13
  14. 14. CALCULATION OF NML pH W WITH THE HENDERSON-HASSELBALCH EQUATION Q Definitions: pKa of bicarbonate buffer = 6.1 Solubility coefficient of CO2 in water = 0. 03 pCO2 = the partial pressure of CO2 in an arterial blood gas e Normal = 40 mm Hg Carbonic acid (H2CO3) = (0 ) (pCO2) = (0.03) (40) ( (0.03) (p ( )( ) Normal value of HCO3- in an arterial blood gas = 24 mEq/L pH = 6.1 + log 24 meq/ L (0.03) (0 03) (40 mm Hg) pH = 6.1 + log 20 = 6.1 + 1.3 = 7.4 ( normal pH) Dave Kotun, NSU O Orlando, PA Program 14
  15. 15. CONCLUSION Henderson-Hasselbalch equa ation allows abnormalities in the pH to be understood on the ba of changes in the ratio of asis bicarbonate to the pCO2 pH = HCO3- ::pCO2 The lungs and kidney continuuously work to adjust pCO2 and bicarbonate to maintain a norm pH mal Dave Kotun, NSU O Orlando, PA Program 15
  16. 16. OF ACID- BASE BALANCE pCO2 = the RESPIRATORY COMPONENT Y because: It depends upon the Rate of Respiration p p p HCO3- = the METABOLIC C COMPONENT because: It’s plasma concentration is m maintained by the kidney, and is affected by amount of nonvolatile acids made Dave Kotun, NSU O Orlando, PA Program 16
  17. 17. REGULATION OF VENTIL LATORY RATE IN THE LUNGS CENTRAL CHEMORECEPTORS IN THE MEDULLA: Are sensitive to pCO2 a pH and ∴ Increase in pCO2 ( and decrease in pH ) Increase in Venntilatory Rate RECEPTORS IN CAROT BODIES AND IN TID AORTIC ARCH: Are Sen nsitive to arterial pO2 (the partial pressure of oxyggen) When pO2 < 60 m mmHg, Ventilatory Rate Increases - the “ hy ypoxic drive” takes over control of ventilatio on Dave Kotun, NSU O Orlando, PA Program 17
  18. 18. Significance of Hypoxic Drive in COPD These patients have em mphysema or chronic bronchitis and chronically havve: Increased pCO2 and decreased pO2 d When they have exacer rbation of their illness with further decrea in pO2, their hypoxic ase drive takes over Excessive O2 administraation (e g pure O2) during (e.g. exacerbation of COPD c could inhibit the hypoxic drive of respiration and cause significant pCO2 p d g p retention and death Dave Kotun, NSU O Orlando, PA Program 18
  19. 19. Regulation of Acid-Base Balance by the Kidney BICARBONATE REABSORP PTION Occurs in the proximal a distal renal tubule and H+ EXCRETION Occurs in the distal rena tubule al Removes nonvolatile ac (waste products of cids ( p metabolism) Sulfuric and phosphoric acids generated from protein c metabolism t b li Ketoacids generated fro fatty acid metabolism om (acetoacetate; beta hyd beta-hyd droxybutyrate; acetone) Accumulation of these ketoacids leads to a serious disorder in diabetics: diabetic ketoacid dosis (further discussion in a ( future lecture) Dave Kotun, NSU O Orlando, PA Program 19
  20. 20. EFFECT OF pH ON PLASM K+ MA CONCENTRATION As pH increases ( serum H+ decreases) (ALKALOSIS) H+ shifts from the intraccellular extracellular compartments, and K + shifts from the extraacellular intracellular compartments HYPO OKALEMIA As H decreases ( serum H+ iincreases) (ACIDOSIS) A pH d ) H + shifts from the extraacellular intracellular compartments, compartments and K + shifts from the intrac cellular extracellular compartments HYPE p ERKALEMIA Dave Kotun, NSU O Orlando, PA Program 20
  21. 21. ARTERIAL BLOOD GAS: NORMAL VALUES AND INDICA ATIONS NORMAL VALUES pH = 7.35- 7.45 pCO2 = 35 – 45 mm Hg (the partial pressure exerted by b CO2) HCO3-= 22- 26mEq/L (c calculated by a machine from the Henderson-Hasselbalch E ti ) Hd H lb l h Equation) pO2 = 80- 100 mmHg (the partial pressure exerted by O2 ) O2 Saturation = 95- 100 (the percentage of 0% hemoglobin saturated w O2) with Dave Kotun, NSU O Orlando, PA Program 21
  22. 22. ARTERIAL BLOOD GAS: N NORMAL VALUES AND INDICATIONS Measurements of abo are MORE ove ACCURATE from ARTERIAL BLOOD t than VENOUS BLOOD Because pH and pC 2 vary depending on site CO that venous blood w obtained from was (bicarbonate will als vary because it is so related to the pH an pCO2). nd Values of pH and pC 2 from arterial blood CO drawn from differen parts of body are same. nt Dave Kotun, NSU O Orlando, PA Program 22
  23. 23. ARTERIAL BLOOD GAS: N NORMAL VALUES AND INDICATIONS The value of bicarbon nate from peripheral venous blood Is approximated fro the total CO2 or CO2 om content And is a a few mEq lower than the total CO2 The total CO2 is a a bit higher because it also has dissolved pCO2 CO2 content = dissolv p CO2 + HCO3- ved Dave Kotun, NSU O Orlando, PA Program 23
  24. 24. ARTERIAL BLOOD GAS: C CRITICAL VALUES Tell me, what is a cr me ritical value? pH < 7.25; > 77.55 pCO2 < 20; > 660 HCO3- < 15; > 40 pO2 < 40 O2 saturation < 75% Dave Kotun, NSU O Orlando, PA Program 24
  25. 25. INDICATIONS FOR ARTE ERIAL BLOOD GAS Monitor patients on ve entilators 1. Monitor critically ill non nventilator patients 2. 2 Establish preoperative baseline e 3. parameters Regulate electrolyte th herapy 4. Monitor O2 flow rates 5. 5 Diagnosis and treatme of significant ent 6. metabolic disorders Dave Kotun, NSU O Orlando, PA Program 25
  26. 26. ACID BASE BALANCE II D- PATHO OLOGIC PROCESSES
  27. 27. BJECTIVES Define and contrast the terms acidosis and t 1. alkalosis Describe clinical sce enarios giving rise to the 2. following acid base disorders: Metabolic acidosis; mettabolic alkalosis; respiratory acidosis; respiratory alkalosis Describe the pattern of laboratory values ns 3. 3 for the acid base dis sorders above Dave Kotun, NSU O Orlando, PA Program 27
  28. 28. BJECTIVES 4. Describe how the an nion gap calculation (g (high vs. normal anion gap) helps to g p) p characterize the etioology of metabolic acidosis 5. Identify mechanisms of respiratory and metabolic compensa ation for acid base disorders 6. 6 Utilizing electrolyte and arterial blood gas data as well as clinic history diagnose the cal acid base acid-base disorders above Dave Kotun, NSU O Orlando, PA Program 28
  29. 29. EFINITIONS Acidosis: A process associate with a DECREASE in pH ed and an INCREASE in H+ concentration pH < 7.35 Alkalosis: A process associate with an INCREASE in pH ed and a DECREASE in H+ concentration n pH > 7.45 7 45 Dave Kotun, NSU O Orlando, PA Program 29
  30. 30. DEFINI ITIONS Metabolic id i M t b li acidosis: Decrease in plasma HCO3- a Metabolic alkalosis: Increase in plasma HCO3- Respiratory acidosis: : Increase in pCO2 Respiratory alkalosis s: Decrease in pCO2 Dave Kotun, NSU O Orlando, PA Program 30
  31. 31. Metabolic Acid-Ba Disorders ase They Are Called Metabolic Because the Primary Problem Involves Nonvolatile Acid ds Not CO2, HCO3-, and Renal Function Dave Kotun, NSU O Orlando, PA Program 31
  32. 32. etabolic Acidosis There is decreased b b h d d bicarbonate due to: d Increased accumulalation of nonvolatile acids of loss of HCO3- f m kidney or f f from from GI tract Classified as HIGH A ANION GAP or NORMAL ANION GAP metabol acidosis olic ANION GAP = unme easured anions in the extracellular fluid co ompartment Lactate, citrate, pyr , , py y yruvate, phosphate, sulfate ,p p , Dave Kotun, NSU O Orlando, PA Program 32
  33. 33. ETABOLIC ACIDOSIS S CALCULATION OF ANIO GAP = ON Na+ - ( HCO3- + Cl- ) Normal Anion Gap = 8 – 14 High Anion Gap Metaboliic Acidosis has anion gap > 14 Dave Kotun, NSU O Orlando, PA Program 33
  34. 34. METABOLIC ACID DOSIS H+ from nonvolatile acids (ex ketoacids; lactic acid) x. x combines with bicarbonate (H 3- )and pulls bicarbonate HCO buffer equilibrium toward carb bonic acid (H2CO3) and away from bicarbonate: CO2 + H2O H2CO3 HCO3-+ H+ A decrease in bicarbonate (wwithout an increase in chloride) results in increased anion gap p Dave Kotun, NSU O Orlando, PA Program 34
  35. 35. ETABOLIC ACIDOSIS S HIGH ANION GAP ME ETABOLIC ACIDOSIS Caused by: y Increased nonvolatile acids Increased Endogeno Acid Production ous Lactic acid, Beta- h hydroxybutyrate, Acetoacetate and other organic aacids Toxins Salicylate; methano ethylene glycol; ethanol nol; Decreased Renal Ex xcretion of Acids Renal failure ( ino organic acids ) Dave Kotun, NSU O Orlando, PA Program 35
  36. 36. ETABOLIC ACIDOS SIS HIGH ANION GAP META TABOLIC ACIDOSIS Lactic acidosis as a cau of high anion gap metabolic use acidosis Serum Lactic Acid Increeases In Conditions With Impaired Ti I i d Tissue P f sion Perfusi Shock and Hypotensioon Severe Septicemia p Hypoxia Severe congestive heart failure Severe anemia Anaerobic conditions fav glycolysis for energy vor increased lactate produc ction from pyruvate Dave Kotun, NSU O Orlando, PA Program 36
  37. 37. ETABOLIC ACIDOS SIS High anion gap metabolic a acidosis Keto acidosis as a cause of high anion gap metabolic fg gp acidosis States of insulin deficie ency cause an increase in ketoacids Decreased Insulin increased break down of fat i increased acetyl CoA increased ketones (also called ketoacids – acet ll d k t id etoacetate; b t t t t beta hydroxybutyrate) ketones in blood and urine ke Diabetes: patients have a la of insulin ack Starvation: inadequate carbbohydrate ingestion decreased insulin Alcoholism: same mechanis as starvation ketosis sm Dave Kotun, NSU O Orlando, PA Program 37
  38. 38. ETABOLIC ACIDOS SIS High anion gap meta abolic acidosis Exogenous toxins a a cause of high anion as gap metabolic acido i t b li idosis Substances Ingested By Alcoholics With d Poor Cash Flow: Methanol (wood alc cohol) Ethylene glycol (ant tifreeze) Salicylates (aspirin) Dave Kotun, NSU O Orlando, PA Program 38
  39. 39. ETABOLIC ACIDOSIS S Normal anion gap metabolic acidosis Causes Loss of bicarbonate from GI tract or Kidney - e anion gap is not inc creased, because there is increased reabsorpt tion of chloride anion to maintain electroneuutrality Dave Kotun, NSU O Orlando, PA Program 39
  40. 40. METABOLIC ACID DOSIS GastroIntestinal Loss of Bicarbonate Rich Fluids Diarrhea is the most comm cause of normal mon anion gap metabolic acidosis i t b li id i Pancreatic, Biliary, or Intest tinal Drainage Renal Loss of bicarbonate- loss of bicarbonate in bicarbonate urine due to renal tubular dis sease Renal Tubular Acidosis (RTA) e.g. caused by chronic renal in nfection ( pyelonephritis ); chronic obstruction from kidney stones y Dave Kotun, NSU O Orlando, PA Program 40
  41. 41. METABOLIC ACIDOSI IS NORMAL ANION GAP METAABOLIC ACIDOSIS LABS ASSOCIATED WITH M METABOLIC ACIDOSIS DECREASED plasma HCO3- leads to DECREASED plasma pH HYPERCHLOREMIA occur with NORMAL ANION GAP rs METABOLIC ACIDOSIS: The kidney reabsorbs increased Cl- to balance the loss of anion (bicarbonate) (bi b t ) ACIDOSIS CAUSES HYPER RKALEMIA Acidosis increased serum H+ concentration H+ shifts into m the cells K+ moves out of the cells into the serum f hyperkalemia This is a compensatory mech hanism for dealing with acidosis Dave Kotun, NSU O Orlando, PA Program 41
  42. 42. METABOLIC ALKALO OSIS Caused by loss of H+ It is called Metabolic becau primary disorder involves a loss of use nonvolatile acid (HCL) or seecretion of H+ by kidney There is increased bicarbon nate: loss of H+ drives bicarbonate buffer equilibrium toward in ncreased production of bicarbonate: CO2 + H20 H2CO3 HCO3- +H+ (reaction pulled toward direction of bicarbo onate)) Dave Kotun, NSU O Orlando, PA Program 42
  43. 43. METABOLIC ALKALOSIS CAUSES LOSS OF H+ GASTRIC LOSS of HC CL Vomiting Nasogastric Suction RENAL LOSS of H+ H Some diuretics Increased Aldosterone (Conn’s Syndrome); e Increased Cortisol (Cu ushing’s Syndrome) There is increased Na+ reabsorption coupled with + increased H+ and K+ secretion Dave Kotun, NSU O Orlando, PA Program 43
  44. 44. METABOLIC ALKALOSIS Labs L b associated with metabolic alkalosis i t d ithh t b li lk l i Increased bicarbonate leads to increased pH Hypokalemia occurs as part of a s compensatory mech hanism Decreased plasma H+ H+ shift from the cells into the serum K+ shifts from the serum into the cells h h ll hypokalemia kl Dave Kotun, NSU O Orlando, PA Program 44
  45. 45. COMPENSATION FOR ME ETABOLIC ACID-BASE DISORDERS Respiratory compenssation occurs for metabolic acid-base d disorders To assess compensa ation, remember that pH = HCO3- pCO2 Henderson-Hasselbal equation shows the lch relationship between pH, bicarbonate, and pCO2 as indicated ab bove Dave Kotun, NSU O Orlando, PA Program 45
  46. 46. COMPENSATION FOR META ABOLIC ACID-BASE ISORDERS Respiratory compensa p y p ation occurs for metabolic acid-base di disorders METABOLIC ACIDOSIS (pH <7.35; H+ S: (p ; concentration is high) A primary decrease in bicarbonate results in a n decrease in pH; to br ring the pH up toward normal, the pCO2 nee to be decreased eds This i Thi is accomplished b increasing li h d by i i ventilatory rate to blow off CO2 w Labs: L b A decrease in b th HCO3- and pCO2 d i both d CO Dave Kotun, NSU O Orlando, PA Program 46
  47. 47. COMPENSATION FOR META ABOLIC ACID-BASE ISORDERS METABOLIC ALKAL LOSIS: pH > 7.45; H+ conc centration is low Remember that pH = bicarbonate pCO2 A primary increase in bicarbonate results in an i increased pH; to b i the pH down d H to bring th H d toward normal, the pCO2 needs to be raised This is accomplishe by decreasing ed ventilatory rate to r retain more CO2 Labs: an increase in both HCO3- and pCO2 Dave Kotun, NSU O Orlando, PA Program 47
  48. 48. RESPIRATORY ACID B BASE DISORDERS They are called res spiratory because the primary problem involves pCO2 m and pulmonary function Dave Kotun, NSU O Orlando, PA Program 48
  49. 49. ESPIRATORY ACID DOSIS Defect: Retention of CO2 resulting from O hypoventilation Causes Chronic Obstructive Pulmonary Disease e (COPD) emphysem chronic bronchitis (to ma; be di b discussed)d) Neuromuscular Disorders Causing Weakness of Respiratory Musc cles Spinal cord injury; amyotrophic lateral sclerosis ; (ALS); multiple sclerosis ( MS) Guillian- Barre Syn ndrome Dave Kotun, NSU O Orlando, PA Program 49
  50. 50. RESPIRATORY AC CIDOSIS Defect: Retention of CO2 resulting from f hypoventilation Causes Respiratory Center Depression General anesthesia; sedative and narcotic drugs; CNS brainstem pathology (tumor; trauma; stroke) Lung Conditions Obesity- Obesity Hypovent tilation Syndrome (Pickwickian Syndrome) Flail chest from multiple rib fractures Kyphoscoliosis Dave Kotun, NSU O Orlando, PA Program 50
  51. 51. RESPIRATORY AC CIDOSIS Defect: Retention of CO2 resulting from O hypoventilation CHRONIC OBSTRUCTIVE LUNG DISEASE AS A CAUSE OF RESPIRATORY ACIDOSIS Smoking Plays An Impo ortant Role in the Pathogenesis of these disorders Dave Kotun, NSU O Orlando, PA Program 51
  52. 52. RESPIRATORY ACID DOSIS (cont.) ( ) Defect: Retention of CO2 result ting from hypoventilation EMPHYSEMA: Destruction of air spaces and loss of elasticity ( due to increased s protease activity associated with ssmoking ) results in difficulty exhaling CO2 CHRONIC O C C O C BRONCHITIS: S Criteria for diagnosis- Persistent C Cough and Sputum Production for at least 3 Months in 2 Consecu utive Years Chronic Irritation from Cigarette Smok and Microbiologic Infections ke Excessive Mucous Production in S Small and Large Airways Obstruction Dave Kotun, NSU O Orlando, PA Program 52
  53. 53. ESPIRATORY ACIDOSIS Defect: Retention of CO2 resulting from f hypoventilation Neuromuscular disorders as a cause of respiratory s acidosis AMYLIOTROPHIC LAT TERAL SCLEROSIS (ALS)- “Lou (ALS) Lou Gherig’s Disease” Progressive Degenera g g ation of Motor Neurons in the Brain and Spinal Cord pr rogressive weakness and wasting of muscles needed for R Respiration and Movement Death typically i D th t i ll in 3 yeears Dave Kotun, NSU O Orlando, PA Program 53
  54. 54. RESPIRATORY AC CIDOSIS Defect: Retention of CO2 re esulting from hypoventilation Neuromuscular disorders as a cause of respiratory acidosis Multiple sclerosis (MS) One of the more comm CNS Diseases mon Usually characterize by Chronic Remitting and Relapsing ed Course Pathology -Multiple ar reas of Myelin Loss in the CNS white matter Gillian - Barre Syndrom me Acute or Subacute illness with motor impairment, sometimes requiring aassisted ventilation Causes- preceding up respiratory or gastrointestinal pper infection Immunizations Dave Kotun, NSU O Orlando, PA Program 54
  55. 55. ESPIRATORY ALKALO OSIS Defect: Depletion f D f t D l ti of CO2 R lti f Resulting from hyperventilation Causes C Stimulation of the brains stem respiratory center Emotional states: excitement; anxiety Fever Pregnancy Salicylates and Sepsis: Both of these may cause a mixed respiratory alkalosis and metabolic acidosis d Dave Kotun, NSU O Orlando, PA Program 55
  56. 56. RESPIRATORY AL LKALOSIS Defect: Depletion of CO2 Resulting from O hyperventilation Causes (cont ) (cont.) Cardiac disease Congestive Heart Failure Pulmonary Edema (rapid breathing) Severe congestive hea failure results in g art hypoperfusion lactic acidosis metabolic c acidosis Mechanical over ventila ation Dave Kotun, NSU O Orlando, PA Program 56
  57. 57. ABS IN RESPIRATORY A ACID BASE ACID-BASE DISORDERS Respiratory acidosis s pH decreases; pCO2 increases O Hyperkalemia (H+ go into cells; K + goes into oes the plasma) Respiratory alkalosis pH increases; pCO2 decreases Hypokalemia (H + go into the plasma; K + oes goes iinto th cells) t the ll ) Dave Kotun, NSU O Orlando, PA Program 57
  58. 58. OMPENSATION FOR RESSPIRATORY CID BASE CID-BASE DISORDERS Metabolic compensation occurs for respiratory acid – base disorders When assessing compe ensation, remember that pH is determined by the ratio of bicarbonate to pCO2 Respiratory acidosis (p < 7.35; high H+) p y (pH g A primary increase in p 2 (from excessive CO2 pCO retention) results in a de ecrease in pH To bring the pH up towa normal, the kidney ard compensates by reabso orbing MORE bicarbonate Dave Kotun, NSU O Orlando, PA Program 58
  59. 59. OMPENSATION FOR RESSPIRATORY CID BASE CID-BASE DISORDERS Metabolic M t b li compensation occurs f respiratory acid – ti for it id base disorders When Wh assessing compe ti remember th t pH iis i ensation, b that H determined by the ratio of bicarbonate to pCO2 on Respiratory alkalosis (pH > 7.45; low H+) H 7 45; A primary decrease in pCO2 (from hyperventilation) results in a increase in pH To bring the pH down t toward normal, the kidney compensates by reabso orbing LESS bicarbonate Dave Kotun, NSU O Orlando, PA Program 59
  60. 60. CALCULATION OF COMPE ENSATION FACTOR Purpose: 1. To determine if the c compensatory change in pCO2 is appropriate f the prim change iin HCO3- to i for h imary h maintain a HCO3-/ pCO2 ratio compatible with normal O pH (and if compensato change in bicarbonate is ory appropriate for primary change in pCO2) y 2. 2 To determine if it is a “ simple metabolic OR simple” respiratory acid-base disorder, or a mixed acid – base disorder Dave Kotun, NSU O Orlando, PA Program 60
  61. 61. CALCULATION OF COMPEN NSATION FACTOR Purpose: A simple acid base disorder is one in which acid-base there is only 1prima acid-base disturbance ary (e.g. metabolic acid dosis) A mixed acid-base d disorder is one in which there are 2 or more acid-base disturbances e occurring at the sam time me If the calculated compe ensation is appropriate, then i th it is a simple disord i l di rder If the compensation is n what is expected, it not may b a mixed disorde be i d di der Dave Kotun, NSU O Orlando, PA Program 61
  62. 62. CALCULATION OF RESPIRA ATORY COMPENSATION FACTOR FOR METABOLIC A ACID-BASE ACID BASE DISORDERS Metabolic id i M t b li acidosis pCO2 should decrease by 1.2 mmHg for each fall in 1.0 mEq/L of HCO3- Metabolic alkalosis pCO2 should increase by 0 4 – 0 7 mmHg for 0.4 0.7 each rise of 1.0 mEq of HCO3- q/L Dave Kotun, NSU O Orlando, PA Program 62
  63. 63. ALCULATION OF COMPENSSATION FACTOR FOR ESPIRATORY ACID BASE D ACID-BASE DISORDERS Respiratory acidosis ACUTE HCO3- rises 1 mEq/L for ea rise of 10 mmHg in p 2 q ach g pCO CHRONIC HCO3- rises 3-4 mEq/L for e each rise of 10 mmHg in Pco2 Respiratory lk l i R i t alkalosis ACUTE HCO3 falls 2-3 mEq/L for each decrease of 10 mmHg in pCO2 23 3- CHRONIC HCO3- falls 5 mEq/L for eac decrease of 10 mmHg in pCO2 ch Dave Kotun, NSU O Orlando, PA Program 63
  64. 64. ONCLUSIONS Metabolic acid – bas disorders se Primary Problem is with Nonvolatile Acids HCO3- N Acids, and Kidney Metabolic acidosis: decrrease in bicarbonate Metabolic alkalosis: incr rease in bicarbonate Compensation is b Adjusti V til t R t and C ti i by Adj sting Ventilatory Rate d pCO2 (occurs over minute hours) es/ Metabolic acidosis: decrrease in pCO2 Metabolic alkalosis: incr rease in pCO2 Dave Kotun, NSU O Orlando, PA Program 64
  65. 65. ONCLUSIONS Summary of labs: Metabolic acidosis pH decreased; HCO3- decreased; ; pCO2 decreased Normal Anion Gap Meta abolic Acidosis: Hyperchloremia Metabolic alkalosis pH increased; HCO3- increased; pCO2 increased Dave Kotun, NSU O Orlando, PA Program 65
  66. 66. ONCLUSIONS Respiratory acid – ba disorders ase Primary Problem is with pCO2 and lungs p Respiratory acidosis: inc crease in pCO2 Respiratory alkalosis: de ecrease in pCO2 Compensation is by Adjussting Reabsorption of HCO3- by the Kidney (occurs ov days) ver Respiratory acidosis: inc crease in bicarbonate Respiratory lk l i de R i t alkalosis: decrease iin bi b t bicarbonate Dave Kotun, NSU O Orlando, PA Program 66
  67. 67. ONCLUSIONS Summary of labs: Respiratory acidosis pH decreased pCO2 increased HCO3- increased Respiratory alkalosis pH increased pCO2 decreased HCO3- decreased Dave Kotun, NSU Orlando, PA Program 67
  68. 68. Conclusions Changes in serum K+ concent tration resulting from changes in pH ACIDOSIS HYPERKALEMIA A ALKALOSIS HYPOKALEMIA A Note – this concept is ve important in diabetes ery Dave Kotun, NSU O Orlando, PA Program 68
  69. 69. ONCLUSIONS Simple id base di orders Si l acid – b dis d One primary problem (re espiratory or metabolic) Mixed acid – base diso orders TWO ( or more ) PRIMA PROBLEMS O o oe ARY O S Examples of Mixed Acid- Base Disorders COPD with shock and L Lactic Acidosis = Respiratory p y Acidosis and Metabolic Acidosis c Pregnancy with excess Vomiting = Respiratory Alkalosis sive and Metabolic Alk l is d M t b li Alkalosis Dave Kotun, NSU O Orlando, PA Program 69
  70. 70. Time for Questions ??????????? Q s Dave Kotun, NSU O Orlando, PA Program 70

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