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The mechanisms by which the body keeps the plasma [H+] constant
Homeostasis of pH is tightly controlled Extracellular fluid = 7.4 Blood = 7.35 7.45 < 6.8 or > 8.0 death occurs Acidosis (acidemia) below 7.35 Alkalosis (alkalemia) above 7.45
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Buffering
H++ HCO3-H2CO3 CO2+H2O H+ is buffered Bicarbonate is consumed To stop the backward reaction which will lead to production of H+ ions, CO2 must be expelled To generate base from the backward reaction H+ must be excreted
Respiratory mechanisms
Hyperventilation H2CO3 H2O + CO2 Carbon dioxide diffuses through the CNS to the respiratory centre and stimulates hyperventilation Hypoventilation less than normal PCO2 results in hypoventilation
Metabolic/Renal mechanisms
Plasma pH: 7.35-7.45 corresponding to [H+] of 43-36 nmol/L (7.4) av Arterial PCO2 : 4.8-5.8 kPa (5.3) av Plasma [bicarbonate]: 21-28 mmol/L (25) av Anion gap: 13-18 mmol/L (15.5) av
What is an ABG?
The Components
pH / PaCO2 / PaO2 / HCO3 / O2sat / BE pH - 7.35 - 7.45 PaCO2 - 35-45 mmHg (4.8-5.8 Kpa) PaO2 - 80-100 mmHg (> 11 mmol/L) HCO3 - 21-27 O2sat - 95-100% Base Excess - +/-2 mEq/L
Desired Ranges
Aids in establishing a diagnosis Helps guide treatment plan Aids in ventilator management Improvement in acid/base management allows for optimal function of medications Acid/base status may alter electrolyte levels critical to patient status/care
Definitions
Standard bicarbonate: The concentration of bicarbonate in plasma of a blood specimen that has, following collection, been equilibrated with O2 and CO2 mixtures at 37C. Conditions: fully oxygenated and PCO2 5.3 kPa or 40 mm Hg
Definitions
Base excess: The amount of strong acid that would be required to titrate one litre of fully oxygenated blood to a pH of 7.4 ([H+]= 40 nm/L) at 37C under conditions where PCO2 is 5.3 kPa or 40 mm Hg
S=solubility coefficient of CO2= 0.23 mmol/J if PCO2 is expressed in kPa and 0.03 mmol/J if PCO2 is expressed in mmHg
Anion gap
Based on the electroneutrality of plasma [total cations] = [total anions] ([Na+] + [K+] +[Ca+]) = ([Cl-]+[HCO3-]+ [pyruvate]+[acetoacetate]+[lactate]+[urate] +[citrate] )
Causes of metabolic acidosis and increased anion gap (increased production of fixed or organic acids)
Lactic acid (shock, infection, hypoxia) Urate (renal failure) Ketones (diabetes mellitus, alcohol) Drugs and toxins (salicylates, biguanides, ethylene glycol, methanol)
Causes of metabolic acidosis and normal anion gap (loss of HCO-3 or ingestion of H+ ions)
Look at the plasma pH Is there acidaemia or alkalaemia? Find the primary cause (parameters with a change consistent with or supporting the change in pH) Find the secondary or compensatory changes (parameters with a change not consistent with or opposing the change in pH)
pH >7.45 PCO2
AG
HCO3
PCO2
AG
HCO3
PCO2
AG
HCO3
pH >7.45
Acute respiratory alkalosis Chronic respiratory alkalosis
Metabolic alkalosis
Mixed alkalosis
Metabolic Acidosis
Processes: Increased acids (endogenous/ exogenous) Increased H+ Decreased excretion of H+ Bicarbonate depletion / loss
Inadequate production of ammonia by the kidney e.g. chronic renal failure Inability to maintain the blood-urine H+ concentration gradient (pH 7.4 : 6) DRTA, Oliguria /Anuria: e.g. acute renal failure
Proximal renal tubular acidosis (PRTA; failure to generate or reclaim bicarbonate) e.g. Fanconi syndrome, carbonate dehydratase inhibitors; e.g. acetazolamide)
Respiratory acidosis
Processes involved: Mechanical blockage of airway Respiratory depression. Structures involved: Brain, meninges, nerves, respiratory muscles, lung tissue
Metabolic alkalosis
NaHCO3 infusions Ingestion of alkali e.g. NaHCO3, MgO, CaCO3 Milk-alkali syndrome (treatment of peptic ulcer).
Respiratory alkalosis
Salicylate toxicity
Initially there is stimulation of the respiratory centre low PCO2, low HCO-3, and respiratory alkalosis Salicylates alter peripheral metabolism production of various organic acids e.g. lactic acid metabolic acidosis with anion gap
Salicylate toxicity
Adults: Mixed respiratory alkalosis and metabolic acidosis Children: Metabolic acidosis