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Acid-Base Balance

Acid-Base Balance. Keseimbangan asam basa:. Homeostasis cairan tubuh tergtg pada pH darah arterial normal pH diatur oleh carbonic acid (H 2 CO 3 ) and bicarbonate (HCO 3 - ) ekstraseluler Asam mrpkan molekul yang melepaskan dlm btk ion H + Basa, mrpkn molekul yg menerima ion H +.

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Acid-Base Balance

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  1. Acid-Base Balance

  2. Keseimbangan asam basa: • Homeostasis cairan tubuh tergtg pada pH darah arterial normal • pH diatur oleh carbonic acid (H2CO3) and bicarbonate (HCO3-) ekstraseluler • Asam mrpkan molekul yang melepaskan dlm btk ion H+ • Basa, mrpkn molekul yg menerima ion H+

  3. Asam kuat atau basa kuat : senyawa yg dpt terdisosiasi sempurna dalam larutan/air: - HCl, NaOH, and H2SO4 • Asam lemah/basa lemah: terdisosiasi parsial : H2CO3, C3H6O3, and CH2O

  4. Regulasi 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

  5. Mekanisme kontrol respirasi: • Bekerja cepat dalam beberapa menit utk kontrol pH, maksimal 12-24 jam • Hanya efektif 50-75% • Kelebihan CO2 dan H dalam darah akan lsg memberi sinyal ke pusat respirasi otak • CO2 melewati barier darah-otak bereaksi dgn H2O membentuk H2CO3 • H2CO3 dihidrolisis menjadi H+ & HCO3- , H akan menstimulasi peningkatan atau penurunan respirasi

  6. Mekanisme kontrol oleh ginjal : • Tidak bekerja secepat sist respirasi, bisa selama beberapa hari utk mengembalikan pH atau mendekati normal • Mengatur pH melalui ekskresi asam atau alkalin urin; mengekskresikan kelebihan H dan membentuk atau mereabsorpsi HCO3- • Menurunkan keasaman urin dengan ekskresi asam ke EC dan menurunkan kebasaan urin dengan ekskresi basa H+ elimination & HCO3- conservation

  7. 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

  8. 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

  9. 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

  10. 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

  11. 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

  12. 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

  13. 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

  14. 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

  15. 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

  16. 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

  17. 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

  18. 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

  19. 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.

  20. 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

  21. 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

  22. 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

  23. 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

  24. 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

  25. 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

  26. 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

  27. Normal Arterial Blood Gas (ABG) • Arterial pH: 7.35 – 7.45 • HCO3-: 22 – 26 mEq/L • PaCO2: 35 – 45 mmHg • TCO2: 23 – 27 mmol/L • PaO2: 80 – 100 mmHg • SaO2: 95% or greater (pulse ox) • Base Excess: -2 to +2 • Anion Gap: 7 – 14

  28. Acid-Base pH and HCO3- • Arterial pH of ECF is 7.40 • Acidemia: blood pH < 7.35 (increase in H+) • Alkalemia: blood pH >7.45 (decrease in H+) If HCO3- levels are the primary disturbance, the problem is metabolic

  29. Acidosis: loss of nonvolatile acid & gain of HCO3- • Alkalosis: excess H+ (kidneys unable to excrete) & HCO3- loss exceeds capacity of kidneys to regenerate

  30. Acid-Base PCO2, TCO2 & PO2 • If PCO2 is the primary disturbance, the problem is respiratory; it’s a reflection of alveolar ventilation (lungs) • PCO2 increase: hypoventilation present • PCO2 decrease: hyperventilation present • TCO2 refers to total CO2 content in the blood, including CO2 present in HCO3- • >70% of CO2 in the blood is in the form of HCO3- • PO2 also important in assessing respiratory function

  31. Base Excess or Deficit: • Measures the level of all buffering systems in the body – hemoglobin, protein, phosphate & HCO3- • The amount of fixed acid or base that must be added to a blood sample to reach a pH of 7.40 • It’s a measurement of HCO3- excess or deficit

  32. Anion Gap: • The difference between plasma concentration of Na+ & the sum of measured anions (Cl- & HCO3-) • Representative of the concentration of unmeasured anions (phosphates, sulfates, organic acids & proteins) • Anion gap of urine can also be measured via the cations Na+ & K+, & the anion Cl- to give an estimate of NH4+ excretion

  33. Anion Gap • The anion gap is increased in conditions such as lactic acidosis, and that result from elevated levels of metabolic acids (metabolic acidosis) • A low anion gap occurs in conditions that cause a fall in unmeasured anions (primarily albumin) OR a rise in unmeasured cations • A rise in unmeasured cations is seen in hyperkalemia, hypercalcemia, hyper-magnesemia, lithium intoxication or multiple myeloma

  34. Sodium Chloride-Bicarbonate Exchange System and pH: • The reabsorption of Na+ by the kidneys requires an accompanying anion - 2 major anions in ECF are Cl- and HCO3- • One way the kidneys regulate pH of ECF is by conserving or eliminating HCO3- ions in which a shuffle of anions is often necessary • Cl- is the most abundant in the ECF & can substitute for HCO3- when such a shift is needed.

  35. Acid-Base w/o Compensation:

  36. Interpretation Practice: Resp. Acidosis • pH: 7.31 Right! • PaCO2: 48 Try Again • HCO3-: 24 Try Again • pH: 7.47 Try Again • PaCO2 : 45 Right! • HCO3- : 33 Try Again Resp. Alkalosis Metabolic Acidosis Resp. Alkalosis Metabolic Alkalosis Metabolic Acidosis Back to Key

  37. Interpretation Practice: • pH: 7.20 Try Again • PaCO2: 36 Try Again • HCO3-: 14 Right! • pH: 7.50 Try Again • PaCO2 : 29 Right! • HCO3- -: 22 Try Again Metabolic Alkalosis Resp. Acidosis Metabolic Acidosis Metabolic Alkalosis Resp. Alkalosis Resp. Acidosis Back to Key

  38. Acid-Base Fully Compensated:

  39. Interpretation Practice: Compensated Resp. Alkalosis • pH: 7.36 Try Again • PaCO2: 56 Try Again • HCO3-: 31.4 Right! • pH: 7.43 Right! • PaCO2 : 32 Try Again • HCO3: 21 Try Again Compensated Metabolic Acidosis Compensated Resp. Acidosis Compensated Resp. Alkalosis Compensated Metabolic Alkalosis Compensated Metabolic Acidosis Back to Key

  40. Acid-Base Partially Compensated:

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