Acid bas balance


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basic hydrogen ion homeostasis, acid base disturbances and management.

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Acid bas balance

  1. 1. The power of hydrogen
  2. 2. 1. Why not in mmol, mEq, or mg?2. Does the letter p of pH mean partial pressure as with pCo2 and pO2?3. Why in acidosis when H+ increases, the pH decreases ?
  3. 3. H+ is kept at a very low level compared with other ions. In a liter of pure water at 25 o C the number of moles of H+ is about 0.0000001, this is written as 1 x 10-7. The superscript -7 is the power, the exponent or the logarithm. The pH (or the power of hydrogen) is the negative logarithm of H+ concentration .40 nmol/L = 0.0000004 mol/L = 10-7.4 the pH is 7.4
  4. 4. Major body constituent.Physical properties will affect homeostasis.Water ionizes spontaneously into hydrogen and hydroxyl ions.Neutral water _ • H+ = OH = 10 -7 • pH is 7Alkaline if pH > 7Acidic if pH <7
  5. 5. A single highly reactive positive charge.
  6. 6. Protein structure- function. Ionic and hydrogen bonding will determine the final morphology.
  7. 7. pH influences:1. Function of all enzymes.2. Normal electrolyte distribution.3. Myocardial performance (contractility).4. Hemoglobin function.
  8. 8. 1 Metabolic lactate, phosphate, sulphate, acetoacetate or b-hydroxy-butyrateacids Non-volatile. Must be metabolized and excreted in urine. 40-80 mmol/day H+ load.1 Respiratory Carbonic acidacids Volatile, very efficient lung excretion CO2 + H2O ⇄ H2CO3 ⇄ H+ + HCO−3 15,000 mmol/day H+ load.
  9. 9. H + homeostasis is essential for life. NormalpH 7.35-7.45 Compatible with life 6.8-8Three systems for hydrogen homeostasis :  Chemical buffering (immediate).  Respiratory compensation (hours).  Renal compensation (2-4 days).
  10. 10. Simple chemical neutralization.The first line of defense.A weak acid and its associate base.1. Bicarbonate-carbonic acid system2. Plasma proteins3. Hemoglobin
  11. 11. CO2 + H2O ⇄ H2CO3 ⇄ H+ + HCO−3
  12. 12. CO2 + H2O ⇄ H2CO3 ⇄ H+ + HCO−3
  13. 13.  The respiratory system forms the single most important organ + system involved in the control of H concentration. PaCO2 is inversely proportional to alveolar ventilation. Small changes in ventilation can have a profound effect on pH. Ventilation is controlled by pH of CSF.
  14. 14. PCT Reabsorption of bicarbonate . CA- regulated.DCT Addition of new bicarbonate Excretion of H+ Aldosterone- regulated
  15. 15. The normal acid-base status pH 7.35-7.45 Bicarbonate (HCO3-) 22-26 mmol/L PCO2 35-34 mmHg An acid–base disturbance disrupts at least two of these three variables.
  16. 16. The base excess-deficit is the amount or base thatmust be added to blood or removed from it to returnpH to 7.4 and to return the paCo2 to 40 mmHg at fulloxygen saturation and 37o C.Positive values indicate metabolic alkalosis.Negative values indicate metabolic acidosis.
  17. 17.  It is the difference between major measured cations and major measured anions. Anion gap = [Na+] – ([Cl-] + [ HCO3-]) Normal range 12±3 mEq/L (plasma proteins represent 11mEq/L).Unmeasured cations include K+, Ca++, & Mg++. Unmeasured anions include PP, phosphates, sulphates and organic acids. Increased AG in metabolic acidosis reflects an increase in the organic acids.
  18. 18. Increase in Anion Gap / Decrease in bicarbonate < 0.4 Hyperchloraemic normal anion gap acidosis 0.4 - Consider combined high AG & normal AG 0.8 acidosis BUT note that the ratio is often <1 in acidosis associated with renal failure 1 to 2 Usual for uncomplicated high-AG acidosis Lactic acidosis: average value 1.6 DKA more likely to have a ratio closer to 1 due to urine ketone loss (esp if patient not dehydrated) >2 Suggests a pre-existing elevated HCO3 level so consider: a concurrent metabolic alkalosis, or a pre-existing compensated respiratory acidosis
  19. 19. Acids are corrosivesto their containers!
  20. 20. The respiratory system is unable to remove sufficientCO2 from the body →high PCO2 levels (hypercapnia).The following reaction becomes displaced to the rightby the increased PCO2: CO2 + H2O ⇄ H2CO3 ⇄ H+ + HCO−3The consequence of this defect is an increased [H+](i.e. acidosis – reduced pH), and an increased [HCO−3].
  21. 21. Alveolar CNS depression Head trauma- drugshypoventilation NMT Residual NMB Muscles Myopathy- MG Chest wall Flail chest- Kyphoscoliosis Pleura Effusion – pneumothorax Airway Upper Laryngeal spasm obstruction Lower Severe bronchospasm Parenchymal Pneumonia- ARDS- aspiration lung disease pneumonitis- interstitial lung disease ……CO2 MH- thyroid storm- prolonged seizure- CHOoverproduction overload in TPN
  22. 22. 1 CNS depression up to coma2 Direct myocardial depression3 Possible hyperkalemia (transcellular)4 Vasculature Systemic VD Hypotension-Respiratory bounding pulseHigh CO2 Cerebral VD ↑ICP Pulmonary VC PHT CNS Depression Narcosis Autonomic Sympasthetic Apprehension stimulation Sweating Tachycardia
  23. 23. 1 Measures to ↑ ETT & Mechanical ventilation alveolar Bronchodilators. ventilation Brain stem stimulants (dopram). Reversal of narcotics (naloxone). Reversal of NDMB.2 Measures to ↓CO2 Dantrolene- NMB- antithyroid drugs- ↓ CHO intake. production when↑N.B. Sodium Is rarely needed unless severe acidosis and bicarbonate associated with CVS collapse. Transient ↑in PCO2 (carbicarb, tromethamine: THAM). Patients with base When they develop acute respiratory failure the line chronic aim of therapy is to return PCO2 to their base line respiratory as normalizing PCO2 to 40 → metabolic alkalosis acidosis require Oxygen therapy must be carefully titrated (hypoxic attention. respiratory drive, normalizing PO2 can→ severe hypoventilation).
  24. 24.  Inappropriate alveolar ventilation relative to CO2 production The following reaction becomes displaced to the left by the decreased PCO2: CO2 + H2O ⇄ H2CO3 ⇄ H+ + HCO−3 The consequence of this defect is a decreased [H+] (i.e. alkalosis – high pH), and a decreased [HCO−3]. Kidneys will excrete increased amounts of HCO3 The renal response has a slow onset and the maximal response takes 2 to 3 days .
  25. 25. 1 Hypoxia Pulmonary Embolism ↑altitude Pneumonia Asthma Pulmonary edema (all types) ↓ Pulmonary compliance.2 Neurologic Stroke encephalitis IC tumors3 Psychiatric Hysterical pain anxiety4 Sepsis and fever Gram negative septicemia5 Pregnancy 50%↑MV- PCO2 around 30mmHg- bicarbonate↓-pH 7.446 Liver disease A respiratory alkalosis is the commonest acid- base disorder found in patients with chronic liver disease7 Intoxication Salicylates toxicity8 Iatrogenic Ventilator induced (common)
  26. 26. 1 Hb ODC →Lt2 Electrolytes K↓ ECG changes-arrhythmias Ileus weakness Ca↓ (ionized) NM irritability CVS depression3 Myocardium Contractile ↓ Contractility element4 Respiratory Vasculature Cerebral Ischemia ↓ CO2 Systemic SVR↑ Coronary Spasm Placenta Perfusion ↓ Pulmonary PVR↓
  27. 27. 1 Correction of the cause The number one priority is correction of any co-existing hypoxemia Administration of oxygen in sufficient concentrations and sufficient amounts is essential.2 Anxiolytics (lorazepam-midazolam)3 CO2-enriched air (bag and mask rebreathing of CO2) is not recommended
  28. 28. Low pH + Decrease in plasma bicarbonate.Compensation: Respiratory The low pH will stimulate the chemoreceptors→ hyperventilation (Kaussmaul’s respiration) CO2 + H2O ⇄ H2CO3 ⇄ H+ + HCO−3 The respiratory compensation for MA →Lowering PCO2→ moving the equation to the left and thus further ↓ HCO−3 Renal -↑ H+ excretion -↑ reabsorption of all filtered HCO−3 - Generation of new HCO−3
  29. 29. 1 Ketoacidosis DM Strong acid Starvation gain Alcoholism High fat diet →consumption of Lactic acidosis Shock Hypoxia HCO−3 Liver failure (N liver: lactate→ G) Renal failure Kidney failure to excrete H+ (High anion gap MA) Intoxication Salicylates Methanol Propylene glycol (organic solvent) Cyanide Paraldehyde2 GIT Severe diarrhea/fistulae: (pancreatic, biliary, HCO − 3 loss intestinal, ileostomy, uretro-segmoidostomy) /ingestion of large amount of anion exchange Normal anion gap resins MA Renal PCT RTA-CA inhibitors (hyperchloraemic) DCT Hypoaldosteronism- spironolactone Iatrogenic Rapid ECF expansion with bicarbonate free fluid e.g. Nacl TPN (Cl) Mineral acid administration
  30. 30. Nausea and vomitingAbdominal painChange in sensoriumTachypneaDecreased musclestrengthDecreased myocardialcontractilityArteriolar dilatationVenoconstrictionPHT
  31. 31. 1 Emergency management of life- E.g. endotracheal intubation, mechanical ventilation, threatening conditions always has CPR and treatment of hyperkalemia. the highest priority. Maintain hyperventilation in ventilated patients Expected PCO2= (1.5 x actual bicarbonate) + 8 mmHg.2 Specific DKA Insulin, IV fluids, K LA (shocked) Oxygen, fluids, blood, vasopressors and inotropes Salicylates Alkalinization of urine by sodium bicarbonate.3 Correction of any respiratory Reversal of NMB. component of acidemia Reversal of narcosis Bronchodilators4 Losses Fluids Replace deficit Electrolytes Replace deficit Sodium Indications if PH < 7.2 bicarbonate Severe hypobicarbonatemia (<4 mEq/L) NOT be given Severe hyperchloremic acidemia on a routine Dosage Empirical: Calculated upon base deficit: basis 1 mEq/kg BDX BW X 30% In practice half the dose is given.5 Refractory MA Hemodialysis
  32. 32. A metabolic alkalosis is a primary acid-base disorder which causes the plasma bicarbonate to rise to a level higher than expected.Compensatory hypoventilationExpected pCO2 = 0.7 [HCO3] + 20 mmHgHypoventilation may be absent: •Pain •Pain with arterial puncture • Hypoxemia
  33. 33. Chloride- Conditions causing Vomiting90% sensitive Urine Cl is low<10 ECF volume depletion. CHPS NG suction Diarrhea mmol/L Diuretics Chloride- Increased H excretion ↑Mineralocorticoid activity,10% resistant in exchange of Na Hypoaldosteronism, Caushing Urine Cl is Severe hypokalemia low>20 mmol/LRare causes Others Large doses of NaHCO3(+renal insufficiency) Massive blood transfusion (citrate in liver→ bicarbonate) Large doses of sodium penicellin Addition of Milk alkali syndrome base to ECF Re-feeding Recovery from metabolic acidosis
  34. 34. 1 Hb ODC →Lt2 Electrolytes K↓ ECG changes-arrhythmias Ileus weakness Ca↓ (ionized) NM irritability CVS depression3 Myocardium Contractile ↓ Contractility element4 Respiratory Vasculature Cerebral Ischemia ↓ CO2 Systemic SVR↑ Coronary Spasm Placenta Perfusion ↓ Pulmonary PVR↓
  35. 35. The cause Cl- Nacl infusion (correction of sensitive ECF& Na depletion) Cl- Aldosterone resistant antagonists(spironolactone) K infusion (correction of K depletion)Temporary ph>7.6 → vit C, Hcl, NH4cl Acetazolamide to ↑renal bicarbonate excretionRefractory Hemodialysis
  36. 36. Hypoxemia is areal danger1. Hypoventilation (respiratory response to metabolic alkalosis)2. Pulmonary microatelectasis (consequent to hypoventilation)3. Increased ventilation-perfusion mismatch (as alkalosis inhibits HPVC)4. Oxygen unloading may be impaired (shift of the ODC to the left).  The body’s major compensatory response to impaired tissue oxygen delivery is to increase COP but this ability is impaired if hypovolemia and decreased myocardial contractility are present. Give oxygen!
  37. 37. Step 1. <7.35—acidosisLook at the pH 7.35-7.45—normal or compensated acidosis >7.45—alkalosisStep 2. PCO2 <35 mm Hg—respiratory alkalosis Look for respiratory component or compensation for metabolic acidosis(volatile acid= CO2) (if so, BD* > −5) PCO2 35-45 mm Hg—normal range PCO2 >45 mm Hg—respiratory acidosis (acute if pH <7.35, chronic if pH in normal range and BE > +5)Step 3. BD >−5 metabolic acidosis Look for a metabolic component BE −5 to +5 normal range(buffer base) BE >5 alkalosis
  38. 38. Put this information together:1 Acidosis CO2 <35 mm Hg ± BD >−5 acute metabolic acidosis2 Normal range pH CO2 <35 BD >−5 acute metabolic acidosis plus compensation3 Acidosis PCO2 >45 mm Hg normal range BE acute respiratory acidosis4 Normal range pH PCO2 >45 mm Hg BE >+5 prolonged respiratory acidosis5 Alkalosis PCO2 >45 mm Hg BE >+5 metabolic alkalosis6 Alkalosis PCO2 <35 mm Hg BDE normal range acute respiratory alkalosis7 If acid-base picture doesn’t conform to any of these, a mixed picture is present.