PROFESSOR DEPT OF OBSTETRICS AND GYNAECOLOGY, UNIVERSITY COLLEGE HOSPITAL, IBADAN Fluid in which cells are insulated in the body function optimally in a narrow limit of pH Normal plasma pH is 7.35-7.45 at 37ºC Slight deviation from this normal can lead to death of the cell. At pH of 7.00 or below, death occurs from acidotic coma while at pH of 7.8 or above, death occurs from tetany Most enzymatic reactions also must take place in certain pH ranges including drug actions. Arterial blood gas values are usually given as pH,pO2, pCO2, [HCO3¯], base excess/deficit and % oxygen saturation Less frequently venous and mixed venous blood gases are measured Mixed venous blood samples are obtained from right atrium , usually through a pulmonary catheter Measurement Arterial blood Mixed blood pH 7.4(7.37-7.44) 7.36 pO2 80-100mmhg 35-40mmhg pCO2 35-40mmhg 41-51mmhg O2 saturation >95% 60-80% [HCO3¯] 22-26mEq/L 22-26mEq/L Base def/excess -2 to +2 -2 to +2
Decrease in base [HCO3¯] is termed base
deficit, increase in base is termed base excess Blood gas machines measure pH, pCO2 and pO2 but [HCO3¯] and base differences are calculated using H/H equation. Henderson-Hasselbalch Equation: pH = 6.1 + log 10 (HCO3-) / (0.03 x pCO2) Henderson Equation: (H+) = 24 x pCO2 / (HCO3-) The Henderson equation is easier to use, but only applies when pH is between 7.2 and 7.6. For this equation, one must calculate [H+] from pH [H+] = 40 mEq/L when pH is 7.4. The [H+] increases 10 mEq/L for a 0.1 unit drop in pH. A change in pCO2 up or down 10mmhg is associated with increase or decrease in pH of 0.08 units. ACIDOSIS(pH<7.37) ALKALOSIS( pH >7.37) Abnormalities in the respiratory and metabolic/renal systems are the major causes of acid-base disturbances An abnormal pCO2 will alter the pH as well as any metabolic disturbance altering [HCO3¯] Any primary disturbance in acid-base homeostasis will evoke a normal compensatory response. A primary metabolic disorder leads to a respiratory compensation and a primary respiratory disorder leads to an acute metabolic compensation due to the buffering capacity of body fluids A more chronic compensation (1-2 days), will require alteration in renal function A- B dist Primary abn Second Resp MA [HCO3¯] pCO2 MALK [HCO3¯] pCO2 RA pCO2 [HCO3¯] RALK pCO2 [HCO3¯] MA= metabolic acidosis, MALK= metabolic alkalosis, RA= Respiratory acidosis, RALK= Respiratory alkalosis Metabolic acidosis is a disorder with low plasma [HCO3-] caused by a net gain of H+ or loss of HCO3- If unopposed, it will result in acidemia. A net gain of H+ is illustrated as follows: CO2 + H2O H2CO3 H+ + HCO3- [H+] = 24 PCO2 / [HCO3-] A rise in [H+] results in a decrease in pH The ↑[H+] drives conversion of HCO3- to H2CO3 and the conversion of H2CO3 to CO2 Thus there is an increase in [H+] and a decrease in pH In chronic metabolic acidosis, acidemia triggers respiratory compensation The ↓ pCO2 drives the conversion of H2CO3 to CO2, and the conversion of H+ and HCO3- to H2CO3 This will result in a ↓ in [H+] and an ↑ in pH towards normal Respiratory compensation begins within the first hour and is complete by 12 to 24 hours However, even with maximum respiratory compensation acidemia persists Metabolic acidosis can be anion gap or a nonanion gap acidosis Anion gap acidosis is caused by decrease in [HCO3¯] by an increase in an unmeasured acid ion either from endogenous or exogenous ingestion (normochloremic) Nonanion gap acidosis (AG 8-12mEq/L). This is due to decrease in [HCO3¯] balance by an increase in chloride (hyperchloremic acidosis) methanol ingestion uremia diabetic ketoacidosis/starvation or ethanol ketoacidosis paraldehyde ingestion iron toxicity (rare) lactic acidosis ethylene glycol rhabdomyolysis salicylates poisoning Fistulae, diarrhoea, starvation Metabolic alkalosis is a disorder with high plasma [HCO3-] caused by a net gain of HCO3- or loss of H+ If unopposed, it will result in alkalemia. A net loss of H+ is illustrated as follows: CO2 + H2O H2CO3 H+ + HCO3- [H+] = 24 PCO2 / [HCO3-] A ↓ in [H+] results in an ↑ in pH The reduced [H+] drives conversion of H2CO3 to HCO3-. Thus [HCO3-] is increased. A net gain of HCO3- is illustrated as follows: CO2 + H2O H2CO3 H+ + HCO3- [H+] = 24 pCO2 / [HCO3-] There is an increase in [HCO3-] The ↑ [HCO3-] drives the consumption of H+, thus ↓ [H+] and ↑ pH With a gain of HCO3- or a loss of H+, [H+] is reduced, [HCO3-] is ↑ed, and pH is ↑ed Alkalemia then triggers respiratory compensation With respiratory compensation, ↓ed alveolar ventilation results in a ↓ in CO2 elimination and an ↑ in pCO2 The ↑ed pCO2 drives the conversion of CO2 to H2CO3 and the dissociation of H2CO3 into H+ and HCO3- This results in an ↑ in [HCO3-], an ↑ in [H+] and a ↓ in pH towards normal Alkalemia also triggers ↑ed glycolysis and lactic acid production This also helps ↑ [H+] and ↓ pH towards normal Respiratory compensation begins within the first hour and is complete by 12 to 24 hours. Chloride–responsive (urine Cl < 10 mEq/L): vomiting, NG drainage, diuretics, post– hypercapneic, cystic fibrosis, villous adenoma, congenital chloride diarrhea. Chloride–resistant (urine Cl > 10mEq/L): hypokalemia, primary aldosteronism, secondary aldosteronism (CHF, cirrhosis & ascites), Cushing’s syndrome, Steroid administration Miscellaneous: poorly resorbed anion (high dose carbenicillin, refeeding alkalosis, administration of alkali (e.g. overshoot from treatment of acidosis, massive transfusions with citrate anticoagulant, milk alkali). Respiratory acidosis is a disorder with high pCO2 caused by reduced CO2 elimination (or hypoventilation). There is a compensatory rise in plasma[HCO3]. If unopposed, it will result in acidaemia. Respiratory acidosis is illustrated as follows: CO2 + H2O H2CO3 H+ + HCO3- [H+] = 24 PCO2 / [HCO3-] In acute respiratory acidosis, ↑pCO2 drives → CO2 to H2CO3, and H2CO3 → ↑ HCO3- and ↑ H+, and ↓PH In chronic respiratory acidosis, ↑ PCO2 triggers renal compensation There is an ↑ H+ excretion into the urine and ↑ generation of new HCO3- in the blood by the kidney The resultant effects are:↑ [HCO3-], ↓H+], and ↑pH towards normal Renal compensation begins within 24 hours and is complete in 5 days Despite compensation, the pH remains in the lower range of normal. Treat by increasing ventilation- intubate and place on ventilator, increase ventilator rate. If sedation was given, reverse with Nalaxone Respiratory center inhibition (sedatives, opiates, O2 in CO2 retainer) Neuromuscular disorder (Guillain–Barré, myasthenia gravis, hypokalemia) Chest wall disorder (rib fractures, pulmonary oedema, severe pnuemonia) Airway obstruction (acute- asthma, chronic- COPD) Acute and chronic lung disease Respiratory alkalosis is a disorder with ↓ pCO2 cause by ↑CO2 elimination (hyperventilation). If unopposed, it will result in alkalemia Respiratory alkalosis is illustrated as follows: CO2 + H2O H2CO3 H+ + HCO3- [H+] = 24 PCO2 / [HCO3-] In acute respiratory alkalosis, ↓ pCO2 drives the conversion of H2CO3 to CO2, and the association of HCO3- and H+ to form H2CO3 The result is a ↓ in [HCO3-], a ↓ in [H+] and an ↑ in pH In chronic respiratory alkalosis, the low pCO2 triggers renal compensation There is a ↓ in secretion of H+ into the urine and ↓ in generation HCO3- by the kidney The resultant is a ↓ in [HCO3-], an ↑ in [H+] and a ↓ in pH towards normal Renal compensation begins within hours and is complete in 3 days. pH often can be restored to normal CNS disorders, anxiety, hyperventilation syndrome, head injury, CVA, Tumors Hypoxia Pulmonary receptor stimulation (asthma, pneumonia, pulmonary edema, PE), anxiety, drugs (early salicylate toxicity, theophylline) liver failure Sepsis Fever Pulmonary embolus, CCF Pregnancy This occurs in seriously ill patients where two or more different primary acid-base disorders occur simultaneously The net effect may be additive eg metabolic/respiratory acidosis resulting in extreme alteration; or opposite eg metabolic acidosis/ respiratory alkalosis, they will nullify each other’s effect Identify primary disturbance as acidosis or alkalosis (pH <7.37 or > 7.44) Identify the primary disturbance as metabolic or respiratory eg if the blood gas is acidotic, and if pCO2 is >40mmhg and [HCO3¯]>24mEq/L, then the problem is respiratory acidosis Identify which component is altered in the same direction as the pH Checking the degree of compensation and calculating the anion gap ) ANION GAP (AG) = [Na+] – ([Cl-] + [HCO3-]) = 10 2 mEq/L (8-12 mEq/L There are anions and cations that are easily measured, i.e. Na+, Cl- and HCO3- Normally [Na+] is in excess of the sum of [Cl-] and [HCO3-]. This is due to the presence of unmeasured anions Unmeasured anions include inorganic anions (SO42- and PO42-), and organic anions (lactate, - hydroxybutyrate and salicylate), and anionic proteins In certain types of metabolic acidosis, the unmeasured anions are ↑ed in concentration, thus resulting in an ↑ed in the anion gap Suppose that metabolic acidosis is due to the net gain in H+A-, were A- is some unmeasured anion Then HCO3- combines with H+ to form H2CO3; H2CO3 is converted to CO2, and CO2 is lost by alveolar ventilation The net result is that HCO3- is replaced by A- Plasma [HCO3-] falls as [A-] increases Since, [Na+] and [Cl-] remain constant, the anion gap increases Normal range of AG 8-12mEq/L Obtained from highly vascularized places eg heel Commonly used for paediatric patients( arterial blood are difficult and more traumatic to obtain in them). pH Same as arterial or lower (7.35-7.40) pCO2 Same as arterial or higher 40-45 pO2 Lower than arterial 45-60 O2 Saturation >70% is acceptable Blood gases can give an idea of level of oxgenation Usually given as pO2, % O2 saturation Oxygen saturation depends on pH, 2,3-DPG, temperature. A shift to the right means acidosis, fever (reduced O2) while to the left means alkalosis eg in hypothermia, banked blood