DEFINITIONS

acidemia/alkalemia
an abnormal pH

acidosis/alkalosis
a process that if uncompensated would lead to an abnormal pH

HENDESON-HASSELBACH
H+ = 24 pCO2 HCO3 lungs kidney 40 24

H+ = 24

H+ = 24

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

EXPECTED COMPENSATION
metabolic acidosis - 1 HCO3/ 1 pCO2 metabolic alkalosis - variable resp. acidosis
acute chronic acute chronic 1 HCO3 / 10 pCO2 3-4 HCO3 / 10 pCO2 2-3 HCO3 / 10 pCO2 5 HCO3 / 10 pCO2

resp. alkalosis

ACID-BASE COMPENSATION
METABOLIC CHANGES ALKALOSES INCREASE HCO3 DECREASE pCO2 RESPIRATORY CHANGES

pH 7.4
DECREASE HCO3 INCREASE p CO2

ACIDOSES

THE ANION GAP

[Na] - (Cl + HCO3)
albumin HCO3 Na Anion gap

Cl

ANION GAP METABOLIC ACIDOSIS

ketoacidosis lactic acidosis uremic acidosis intoxications
ASA methanol ethylene glycol paraldehyde

ASSESSMENT OF ACID-BASE DISTURBANCES

Hx & Px
Check pH

Arterial pH
< 7.35 Acidemia > 7.45 Alkalemia
High HCO3 Metabolic Alkalosis Low pCO2 Respiratory Alkalosis

Check pCO2 High pCO2 Low HCO3 and HCO3 Metabolic Acidosis Respiratory Acidosis Expected compensation ACUTE CHRONIC Check Anion Gap Na-(Cl+HCO3) Possible Diagnoses

1 HCO3: 1 pCO2 1 HCO3: 1 pCO2

10 Pco2 :1 HCO3 10 Pco2 :3 HCO3

1 HCO3: 0.5 pCO2 1 HCO3: 0.5 pCO2 May be increased due to increased negative charge of proteins

10 Pco2 :2 HCO3 10 Pco2 :5 HCO3

COPD Drugs-CNS/Resp Depressants Drugs Normotensive Hypertensive Ketoacidosis High Altitude HCO3 Loss Lactic Acidosis ASA R.T.A. Renal Failure Pregnancy Diarrhea Urine Cl Intoxications Sepsis ASA Methanol > 10 Conns Ethylene Glycol < 10 Diuretics Cushings Vomiting Renal Artery Stenosis Post-hypercapneia

=12-16

>16

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

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

NON-ANION GAP METABOLIC ACIDOSIS

renal tubular acidosis diarrhea hyperailementation

ASSESSMENT OF ACID-BASE DISTURBANCES

Hx & Px
Check pH

Arterial pH
< 7.35 Acidemia > 7.45 Alkalemia
High HCO3 Metabolic Alkalosis Low pCO2 Respiratory Alkalosis

Check pCO2 High pCO2 Low HCO3 and HCO3 Metabolic Acidosis Respiratory Acidosis Expected compensation ACUTE CHRONIC Check Anion Gap Na-(Cl+HCO3) Possible Diagnoses

1 HCO3: 1 pCO2 1 HCO3: 1 pCO2

10 Pco2 :1 HCO3 10 Pco2 :3 HCO3

1 HCO3: 0.5 pCO2 1 HCO3: 0.5 pCO2 May be increased due to increased negative charge of proteins

10 Pco2 :2 HCO3 10 Pco2 :5 HCO3

COPD Drugs-CNS/Resp Depressants Drugs Normotensive Hypertensive Ketoacidosis High Altitude HCO3 Loss Lactic Acidosis ASA R.T.A. Renal Failure Pregnancy Diarrhea Urine Cl Intoxication's Sepsis ASA Methanol > 10 Conns Ethylene Glycol < 10 Diuretics Cushings Vomiting Renal Artery Stenosis Post-hypercapneia

=12-16

>16

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

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+

BICARBONATE RECLAMATION (PCT)

CO2 + H2O
CA H2CO3 HCO3 H+ CA

URINE NaHCO3

Na
HCO3

H2CO3

CA = Carbonic Anhydrase

pCO2 + H2O

BICARBONATE REGENERATION(DCT)
CO2 + H2O
CA H2CO3 HCO3 H+ NH4+

URINE

NaHPO4 NaHSO4

Na
HCO3

NH3 CA = Carbonic Anhydrase

H2PO4

H2SO4

METABOLIC ALKALOSIS
vomiting post-hypercapneic diuretics Bartters syndrome

ASSESSMENT OF ACID-BASE DISTURBANCES

Hx & Px
Check pH

Arterial pH
< 7.35 Acidemia > 7.45 Alkalemia
High HCO3 Metabolic Alkalosis Low pCO2 Respiratory Alkalosis

Check pCO2 High pCO2 Low HCO3 and HCO3 Metabolic Acidosis Respiratory Acidosis Expected compensation ACUTE CHRONIC Check Anion Gap Na-(Cl+HCO3) Possible Diagnoses

1 HCO3: 1 pCO2 1 HCO3: 1 pCO2

10 Pco2 :1 HCO3 10 Pco2 :3 HCO3

1 HCO3: 0.5 pCO2 1 HCO3: 0.5 pCO2 May be increased due to increased negative charge of proteins

10 Pco2 :2 HCO3 10 Pco2 :5 HCO3

COPD Drugs-CNS/Resp Depressants Drugs Normotensive Hypertensive Ketoacidosis High Altitude HCO3 Loss Lactic Acidosis ASA R.T.A. Renal Failure Pregnancy Diarrhea Urine Cl Intoxications Sepsis ASA Methanol > 10 Conns Ethylene Glycol < 10 Diuretics Cushings Vomiting Renal Artery Stenosis Post-hypercapneia

=12-16

>16

VOMITING
Lose NaCl Lose HCl Lose volume this loss of acid generates the metabolic alkalosis ECF volume contraction also leads to secondary hyperaldosteronism

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

METABOLIC ALKALOSISPOST 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

METABOLIC ALKALOSISPOST 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.

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

ASSESSMENT OF ACID-BASE DISTURBANCES

Hx & Px
Check pH

Arterial pH
< 7.35 Acidemia > 7.45 Alkalemia
High HCO3 Metabolic Alkalosis Low pCO2 Respiratory Alkalosis

Check pCO2 High pCO2 Low HCO3 and HCO3 Metabolic Acidosis Respiratory Acidosis Expected compensation ACUTE CHRONIC Check Anion Gap Na-(Cl+HCO3) Possible Diagnoses

1 HCO3: 1 pCO2 1 HCO3: 1 pCO2

10 Pco2 :1 HCO3 10 Pco2 :3 HCO3

1 HCO3: 0.5 pCO2 1 HCO3: 0.5 pCO2 May be increased due to increased negative charge of proteins

10 Pco2 :2 HCO3 10 Pco2 :5 HCO3

COPD Drugs-CNS/Resp Depressants Drugs Normotensive Hypertensive Ketoacidosis High Altitude HCO3 Loss Lactic Acidosis ASA R.T.A. Renal Failure Pregnancy Diarrhea Urine Cl Intoxications Sepsis ASA Methanol > 10 Conns Ethylene Glycol < 10 Diuretics Cushings Vomiting Renal Artery Stenosis Post-hypercapneia

=12-16

>16

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

ASSESSMENT OF ACID-BASE DISTURBANCES

Hx & Px
Check pH

Arterial pH
< 7.35 Acidemia > 7.45 Alkalemia
High HCO3 Metabolic Alkalosis Low pCO2 Respiratory Alkalosis

Check pCO2 High pCO2 Low HCO3 and HCO3 Metabolic Acidosis Respiratory Acidosis Expected compensation ACUTE CHRONIC Check Anion Gap Na-(Cl+HCO3) Possible Diagnoses

1 HCO3: 1 pCO2 1 HCO3: 1 pCO2

10 Pco2 :1 HCO3 10 Pco2 :3 HCO3

1 HCO3: 0.5 pCO2 1 HCO3: 0.5 pCO2 May be increased due to increased negative charge of proteins

10 Pco2 :2 HCO3 10 Pco2 :5 HCO3

COPD Drugs-CNS/Resp Depressants Drugs Normotensive Hypertensive Ketoacidosis High Altitude HCO3 Loss Lactic Acidosis ASA R.T.A. Renal Failure Pregnancy Diarrhea Urine Cl Intoxications Sepsis ASA Methanol > 10 Conns Ethylene Glycol < 10 Diuretics Cushings Vomiting Renal Artery Stenosis Post-hypercapneia

=12-16

>16

ACID-BASE
Disorder Metabolic Acidosis Metabolic Alkalosis Respiratory Acidosis Respiratory Alkalosis Serum pH Serum pCO2
Serum HCO3