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DEFINITIONS acidemia/alkalemia acidosis/alkalosis an abnormal pH
a process that if uncompensated would lead to an abnormal pH
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HENDESON-HASSELBACH H+ = 24 pCO2 HCO3 H+ = 24 lungs kidney H+ = 24 40
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HENDERSON-HASSELBACH
H+ of 40nmol = pH of 7.4 for each 0.1 increase in pH multiply normal H+ x 0.8 for each 0.1 decrease in pH multiply normal H+ x 1.25
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EXPECTED COMPENSATION
metabolic acidosis - 1 HCO3/ 1 pCO2 metabolic alkalosis - variable resp. acidosis acute 1 HCO3 / 10 pCO2 chronic 3-4 HCO3 / 10 pCO2 resp. alkalosis acute 2-3 HCO3 / 10 pCO2 chronic 5 HCO3 / 10 pCO2
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ACID-BASE COMPENSATION
METABOLIC CHANGES RESPIRATORY CHANGES ALKALOSES DECREASE pCO2 INCREASE HCO3 pH 7.4 DECREASE HCO3 INCREASE p CO2 ACIDOSES
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THE ANION GAP [Na] - (Cl + HCO3) Anion gap albumin HCO3 Na Cl
![THE ANION GAP [Na] - (Cl + HCO3) Anion gap albumin HCO3 Na Cl](http://slideplayer.com./slide/716739/2/images/6/THE+ANION+GAP+%5BNa%5D+-+%28Cl+%2B+HCO3%29+Anion+gap+albumin+HCO3+Na+Cl.jpg "THE ANION GAP [Na] - (Cl + HCO3) Anion gap albumin HCO3 Na Cl")
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ANION GAP METABOLIC ACIDOSIS
ketoacidosis lactic acidosis uremic acidosis intoxications ASA methanol ethylene glycol paraldehyde
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ASSESSMENT OF ACID-BASE DISTURBANCES
Arterial pH Hx & Px < 7.35 Acidemia > 7.45 Alkalemia Check pH High HCO3 Metabolic Alkalosis Check pCO2 and HCO3 High pCO2 Respiratory Acidosis Low pCO2 Respiratory Alkalosis Low HCO3 Metabolic Acidosis Expected compensation ACUTE CHRONIC 10 Pco2 :1 HCO3 10 Pco2 :3 HCO3 10 Pco2 :2 HCO3 10 Pco2 :5 HCO3 1 HCO3: 1 pCO2 1 HCO3: 0.5 pCO2 May be increased due to increased negative charge of proteins Check Anion Gap Na-(Cl+HCO3) =12-16 >16 COPD Drugs-CNS/Resp Depressants Drugs High Altitude ASA Pregnancy Sepsis Normotensive Hypertensive Ketoacidosis Lactic Acidosis Renal Failure Intoxications ASA Methanol Ethylene Glycol HCO3 Loss R.T.A. Diarrhea Possible Diagnoses Urine Cl > 10 Diuretics Conn’s Cushing’s Renal Artery Stenosis < 10 Vomiting Post-hypercapneia
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ANION GAP - METABOLIC ACIDOSIS
H+ gaining acidoses the H+ is buffered by HCO3- so this is consumption of bicarbonate and a fall in plasma HCO3 This process converts strong acids to weak acids H2So4 + NaHCO3 NaHSO4 + H2CO3
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ANION GAP METABOLIC ACIDOSES
The consumption of bicarbonate by combining with a cation is electrically neutral and thus the Cl concentration stays normal as the bicarbonate falls and thus the anion gap [Na-(Cl+HCO3)] increases
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NON-ANION GAP METABOLIC ACIDOSIS
renal tubular acidosis diarrhea hyperailementation
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ASSESSMENT OF ACID-BASE DISTURBANCES
Arterial pH Hx & Px < 7.35 Acidemia > 7.45 Alkalemia Check pH High HCO3 Metabolic Alkalosis Check pCO2 and HCO3 High pCO2 Respiratory Acidosis Low pCO2 Respiratory Alkalosis Low HCO3 Metabolic Acidosis Expected compensation ACUTE CHRONIC 10 Pco2 :1 HCO3 10 Pco2 :3 HCO3 10 Pco2 :2 HCO3 10 Pco2 :5 HCO3 1 HCO3: 1 pCO2 1 HCO3: 0.5 pCO2 May be increased due to increased negative charge of proteins Check Anion Gap Na-(Cl+HCO3) =12-16 >16 COPD Drugs-CNS/Resp Depressants Drugs High Altitude ASA Pregnancy Sepsis Normotensive Hypertensive Ketoacidosis Lactic Acidosis Renal Failure Intoxication's ASA Methanol Ethylene Glycol HCO3 Loss R.T.A. Diarrhea Possible Diagnoses Urine Cl > 10 Diuretics Conn’s Cushing’s Renal Artery Stenosis < 10 Vomiting Post-hypercapneia
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NON-ANION GAP MATABOLIC ACIDOSES
These are HCO3 losing type metabolic acidoses The loss of HCO3 by the lower GI tract or the kidneys results in the need for increased Cl reabsorption to maintain electroneutrality Thus as HCO3 falls, Cl increases and the anion gap [Na-(Cl+HCO3)] stays normal
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RENAL TUBULAR ACIDOSIS
Renal loss of HCO3 PCT a decrease in the tubular maximum for HCO3 reabsorption DCT a failure to be able to secrete H+
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BICARBONATE RECLAMATION (PCT)
URINE NaHCO3 CO2 + H2O CA CA H2CO3 Na H2CO3 HCO3 H+ HCO3 CA = Carbonic Anhydrase pCO2 + H2O
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BICARBONATE REGENERATION(DCT)
URINE NaHPO4 CO2 + H2O NaHSO4 CA H2CO3 Na HCO3 H+ HCO3 NH3 NH4+ CA = Carbonic Anhydrase H2SO4 H2PO4
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METABOLIC ALKALOSIS vomiting post-hypercapneic diuretics
Bartter’s syndrome
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ASSESSMENT OF ACID-BASE DISTURBANCES
Arterial pH Hx & Px < 7.35 Acidemia > 7.45 Alkalemia Check pH High HCO3 Metabolic Alkalosis Check pCO2 and HCO3 High pCO2 Respiratory Acidosis Low pCO2 Respiratory Alkalosis Low HCO3 Metabolic Acidosis Expected compensation ACUTE CHRONIC 10 Pco2 :1 HCO3 10 Pco2 :3 HCO3 10 Pco2 :2 HCO3 10 Pco2 :5 HCO3 1 HCO3: 1 pCO2 1 HCO3: 0.5 pCO2 May be increased due to increased negative charge of proteins Check Anion Gap Na-(Cl+HCO3) =12-16 >16 COPD Drugs-CNS/Resp Depressants Drugs High Altitude ASA Pregnancy Sepsis Normotensive Hypertensive Ketoacidosis Lactic Acidosis Renal Failure Intoxications ASA Methanol Ethylene Glycol HCO3 Loss R.T.A. Diarrhea Possible Diagnoses Urine Cl > 10 Diuretics Conn’s Cushing’s Renal Artery Stenosis < 10 Vomiting Post-hypercapneia
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VOMITING Lose NaCl Lose HCl Lose volume
this loss of acid generates the metabolic alkalosis ECF volume contraction also leads to secondary hyperaldosteronism
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VOMITING Renal reaction volume contraction leads to avid Na reabsorption NaCl first with elimination of Cl from urine Na-H exchange but alkalosis means not much H available Na-K exchange but loss of K limits this thus NaHCO3 absorption which perpetuates the alkalosis
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METABOLIC ALKALOSIS-POST HYPERCAPNEIA
The primary problem is respiratory acidosis with the increased pCO2 leading to increased HCO3 to compensate If the pCO2 is suddenly normalized (e.g. by a respirator) the HCO3 is now in excess and there is a metabolic alkalosis. This metabolic alkalosis is called post-hypercapneic metabolic alkalosis
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METABOLIC ALKALOSIS-POST HYPERCAPNEIA
The kidney takes time to get rid of the excess HCO3 and if the patient is volume contracted the kidney may not be able to get rid of the HCO3 because it is avid for Na reabsorption.
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RESPIRATORY ACIDOSIS Alveolar hypoventilation Acute
airway obstruction, drugs, CNS disease 1 mEq/l increase HCO3/10 mmHg pCO2 Chronic (>72 hr.) COPD, CNS disease 3-4 mEq/l increase HCO3/10 mmHg pCO2
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ASSESSMENT OF ACID-BASE DISTURBANCES
Arterial pH Hx & Px < 7.35 Acidemia > 7.45 Alkalemia Check pH High HCO3 Metabolic Alkalosis Check pCO2 and HCO3 High pCO2 Respiratory Acidosis Low pCO2 Respiratory Alkalosis Low HCO3 Metabolic Acidosis Expected compensation ACUTE CHRONIC 10 Pco2 :1 HCO3 10 Pco2 :3 HCO3 10 Pco2 :2 HCO3 10 Pco2 :5 HCO3 1 HCO3: 1 pCO2 1 HCO3: 0.5 pCO2 May be increased due to increased negative charge of proteins Check Anion Gap Na-(Cl+HCO3) =12-16 >16 COPD Drugs-CNS/Resp Depressants Drugs High Altitude ASA Pregnancy Sepsis Normotensive Hypertensive Ketoacidosis Lactic Acidosis Renal Failure Intoxications ASA Methanol Ethylene Glycol HCO3 Loss R.T.A. Diarrhea Possible Diagnoses Urine Cl > 10 Diuretics Conn’s Cushing’s Renal Artery Stenosis < 10 Vomiting Post-hypercapneia
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RESPIRATORY ALKALOSIS
Alveolar Hyperventilation Acute drugs, sepsis, CNS disease 2 mEq/l decrease HCO3/10 mmHg pCO2 Chronic altitude, pregnancy, liver disease, CNS disease 5 mEq/l decrease HCO3/10 mmHg pCO2
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ASSESSMENT OF ACID-BASE DISTURBANCES
Arterial pH Hx & Px < 7.35 Acidemia > 7.45 Alkalemia Check pH High HCO3 Metabolic Alkalosis Check pCO2 and HCO3 High pCO2 Respiratory Acidosis Low pCO2 Respiratory Alkalosis Low HCO3 Metabolic Acidosis Expected compensation ACUTE CHRONIC 10 Pco2 :1 HCO3 10 Pco2 :3 HCO3 10 Pco2 :2 HCO3 10 Pco2 :5 HCO3 1 HCO3: 1 pCO2 1 HCO3: 0.5 pCO2 May be increased due to increased negative charge of proteins Check Anion Gap Na-(Cl+HCO3) =12-16 >16 COPD Drugs-CNS/Resp Depressants Drugs High Altitude ASA Pregnancy Sepsis Normotensive Hypertensive Ketoacidosis Lactic Acidosis Renal Failure Intoxications ASA Methanol Ethylene Glycol HCO3 Loss R.T.A. Diarrhea Possible Diagnoses Urine Cl > 10 Diuretics Conn’s Cushing’s Renal Artery Stenosis < 10 Vomiting Post-hypercapneia
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ACID-BASE
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