You are on page 1of 14

Acid-Base (pH


  3] Acid-base balance or imbalance in extra-cellular fluid (ECF).  2] Carbon dioxide (CO2) elimination through respiration. .Arterial Blood Gases Arterial blood gas analysis provides information on the following:   1] Oxygenation of blood through gas exchange in the lungs.

1 kPa (36 – 46 mmHg) Base deficit ±2.35-7.8 – 6.5 Plasma HCO3- 22 – 26 mmol/L O2 saturation 95 – 100% .Arterial blood gas (ABG) and acid-base values (normal ranges) H+ 35-45 nmol/L pH 7.3 kPa (80 – 100 mmHg) PCO2 4.45 PO2 (breathing room air) 10.6 – 13.

• Deviations from normal acid-base status are divided into 4 general categories.Abnormal CO2 removal in lungs (‘respiratory’ acidosis or alkalosis) . depending on the source and direction of the abnormal change in hydrogen concentration. and usually co-exist.Abnormalities in the regulation of bicarbonate and other buffers in blood (‘metabolic’ acidosis or alkalosis) both may. . Causes of acid-base disturbance: . [H+].

alarming lower blood pH • Alkalosis  is caused by the increase in the ratio of [HCO3-]: [H2CO3] of blood above 20:1.• Acidosis  occurs in the fall in the ratio of [HCO3-]: [H2C03] of blood below 20:1. results in rise in blood pH .

other lung diseases. • PaCO2 and [H+] rise • A chronically raised PaCO2 is compensated by renal retention of bicarbonate. depression of respiratory center by drugs or disease. COPD (type II respiratory failure).1. • CAUSES: include ventilatory failure. nerve or muscle disorders that reduce respiratory muscle ability or (transiently) even the simple act of holding one’s breath. .Respiratory acidosis • Hypercapnic acidosis • Caused by excess retention of C02 arising from hypoventilation • As less-than-normal amount of C02 are lost through the lungs increase in CO2 generated more H+ from this source. and the [H+] returns toward normal.

• Compensation for Respiratory acidosis.and add new .1. because impaired respiration is the problem in the first place  The kidneys are most important in compensating for respiratory acidosis. [CO2] is elevated.  The chemical buffers (immediately take up additional H+) × Respiratory mechanism. Conserved all filtered HC03.Respiratory acidosis • In uncompensated state. whereas [HCO3-] is normal. So the normal ratio [HCO3-]: [H2C03] (20:1) and pH is reduced.usually cannot respond with compensatory increased ventilation.

• Consequently. as a result of hyperventilation. Also a result of physiologic mechanism at high altitude) . • CAUSES: fever. too much C02 is blown off. C02 or H+ in body fluids. • Pulmonary ventilation increased out of proportion to the rate of C02 production. anxiety. aspirin poisoning (all excessively stimulate ventilation without regard to status of oxygen. less [H+] is formed this source.Respiratory alkalosis • The primary defect in respiratory alkalosis is excessive loss of C02 from the body.2.

Therefore. the increase pH reflects a reduction in [CO2]. whereas [HC03-] remains normal. the kidneys . anxiety) can overdrive ventilation. hyperventilation does not continue completely unabated. these 2 are normally potent stimuli for driving ventilation –’put brakes’ on the extent to which some non-respiratory factors (fever.plasma [CO2] AND [H+] fall below normal.Respiratory alkalosis • In uncompensated respiratory alkalosis. • Compensatory mechanism.  if the situation continues for a few days.2.  The chemical buffers systems (liberate H+ to diminish severity of alkalosis)  Respiratory mechanism.

-rich fluids from the body of from an accumulation of noncarbonic acid (where plasma HCO3. .Metabolic acidosis • Also known as non-respiratory acidosis encompasses all type of acidosis besides that caused by excess C02 in body fluid. • In uncompensated used up in buffering additional H+). metabolic acidosis is always characterized by reduction in plasma [HCO3-] whereas [C02] remains normal. The problem may arise from excessive loss of HCO3.3.

excess lactic acid is produced. increase plasma [H+] • Strenuous exercise.causes • Severe diarrhoea. . raising plasma [H+] • Uremic acidosis.3.for buffering normal acid load.HCO3-rich digestive juice is lost from the body rather than reabsorbed.Metabolic available to buffer H+. Also. the kidneys cannot rid the body of even normal H+ generated from noncarbonic acid formed by ongoing metabolic processes. so H+ starts to accumulate in body fluids. leading to more H+ in body fluids.when muscle resort to anaerobic glycolysis during strenuous exercise. the kidneys cannot conserve an adequate amount of HCO3. Less HC03.In severe renal failure (uraemia).abnormal fat metabolism resulting from inability of cells to preferentially use glucose because of inadequate insulin action– which leads to formation of excess keto acids. • Diabetes mellitus.

complete compensation is not possible because renal mechanism is not available for pH regulation.3. .Metabolic acidosis • Compensation for metabolic acidosis.  The buffers take up extra H+  The lungs blow off additional H+ -generating CO2  The kidneys excrete more H+ and conserve more • These compensatory measures restore the ratio to normal by HC03reducing [C02] to 75% of normal and by raising [HCO3-] halfway back toward normal (up from 50% to 75% of normal value) • When kidney disease is the cause.

which in uncompensated state.4. • CAUSES: Vomiting. is not accompanied by a change in [C02]. Ingestion if alkaline drugs . • This acid-base disturbance is associated with an increase in [HC03-].Metabolic alkalosis • A reduction in plasma [H+] caused by relative deficiency of noncarbonic acids.

Metabolic alkalosis • In metabolic urine .4. chemical buffer systems immediately liberate H+ • Ventilation is reduced so that extra H+generating C02 is retained in body fluids. the kidneys conserve H+ and excrete excess HC03. • If condition persists for several days.