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H+ homeostasis

The mechanisms by which the body keeps the plasma [H+] constant

The Body and pH

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

Three Major Mechanisms

Buffering Expulsion or retention of CO2 Generation / reclamation of HCO3 /excretion of H+

Body buffers (I)

Extracellular HCO3 /H2CO3 2-/H PO HPO4 2 4 Plasma proteins

Body buffers (II)

Intracellular HCO3 /H2CO3 2-/H PO HPO4 2 4 Proteins & Amino-acids


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

Excretion of H+ Bicarbonate generation Bicarbonate reabsorption / reclamation

The proton pump

The proton pump

The proton pump excretes H+ and generates bicarbonate

Parameters used in assessing acid-base balance

Plasma pH Arterial PCO2 Plasma [bicarbonate]

Anion gap (AG)

Parameters used in assessing acidbase balance: Reference ranges

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

Why Order an ABG?

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

Parameters used in assessing acid-base balance

Others: Actual bicarbonate Standard bicarbonate Base excess PO2

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

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

pH / Henderson-Hasselbalch Equation using the dynamics of the bicarbonate buffer

pH = pK + 1ogl0 [HCO3-] [H2CO3] pH = 6.10 + 1ogl0 [HCO3 -] S.PCO2 pH = ~ [base] [acid ]

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] )

([Na+] + [K+]) -([Cl-]+[HCO3-]) = Anion Gap (AG).

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)

Proximal renal tubular acidosis Diarrhoea Drugs (acetazolamide) Addisons disease

Pancreatic fistulae Ammonium chloride ingestion

Key to solving acid-base problems:

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)

Simple acid-base disturbances

pH< 7.35 PCO2 AG HCO3

pH >7.45 PCO2



Simple acid-base disturbances

pH< 7.35
Acute respiratory acidosis Chronic respiratory acidosis Metabolic acidosis Mixed acidosis







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

Mechanisms of acid-base disturbances: Metabolic acidosis

Addition of hydrogen ions to body fluids in excess of the excretory capacity (Processes that add hydrogen ions to body fluids faster than the body can excrete) (here , there is Starvation ketosis nothing wrong with Diabetic ketoacidosis the kidneys) Lactic acidosis Ingestion of substances that are acidic or yield acidic metabolites e.g. NH4Cl, methanol, paraldehyde, salicylates

Mechanisms of acid-base disturbances: Metabolic acidosis

Failure to excrete hydrogen ions at the normal rate (here , there is something wrong
with the kidneys)

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

Mechanisms of acid-base disturbances: Metabolic acidosis

Loss of bicarbonate from the body From the GIT e.g. severe diarrhoea, fistulous drainage, uretero-sigmoidostomy

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

Mechanisms of acid-base disturbances: Respiratory acidosis

Increased alveolar PCO2 leading to increased arterial PCO2 Lung disease e.g. chronic airways obstruction, respiratory distress syndrome Weakness of respiratory muscles e.g. poliomyelitis CNS disease e.g. encephalitis, meningitis Drug overdose e.g. hypnotics, anaesthetics

Metabolic alkalosis

Processes involved: Loss of H+ Gain of base

Mechanisms of acid-base disturbances: Metabolic alkalosis

Metabolic Alkalosis Loss of hydrogen ions from the body Loss of H+ in vomit Diuretics (potassium non-sparing diuretics) Na+ , K + increased excretion of H+ ([H+]) Mineralocorticoid excess Na+ , K + increased excretion of H+ [H+] Glucocorticoid excess Na+ , K + increased excretion of H+ [H+] K+ depletion if severe increased excretion of H+ [H+]

Mechanisms of acid-base disturbances: Metabolic alkalosis

Addition of base to body fluids in excess of the excretory capacity

NaHCO3 infusions Ingestion of alkali e.g. NaHCO3, MgO, CaCO3 Milk-alkali syndrome (treatment of peptic ulcer).

Respiratory alkalosis

Loss of carbon dioxide

Mechanisms of acid-base disturbances: Respiratory alkalosis

Respiratory alkalosis Lowered alveolar PCO2 Voluntary overbreathing, hysteria Artificial ventilation Drug overdose e.g. salicylate poisoning sometimes

Salicylate toxicity: blood [salicylate]> 30mg dL

Usually: Accidental in children Deliberate in young adults In the treatment of: Rheumatoid arthritis Dermatosis

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

Salicylate toxicity: other features

Sweating Vomiting Dehydration A metabolic alkalosis can occur as a result of vomiting

Salicylate toxicity: useful laboratory measurements

Total body K+ : () Plasma total CO2 : () Plasma [urea]: ()

Salicylate toxicity: Management

Initially and in case of spasm of pyloric sphincter: Gastric lavage After significant absorption of salicylate: Forced alkaline diuresis