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Acid-Base (pH) Imbalance
Prepared by: SYAFIQAH HANI BT ZABLE
Arterial Blood Gases
Arterial blood gas analysis provides information on the following: 1] Oxygenation of blood through gas exchange in the lungs. 2] Carbon dioxide (CO2) elimination through respiration. 3] Acid-base balance or imbalance in extra-cellular fluid (ECF).
Arterial blood gas (ABG) and acid-base values (normal ranges)
H+ 35-45 nmol/L pH 7.35-7.45
PO2 (breathing room air) 10.6 – 13.3 kPa (80 – 100 mmHg)
PCO2 4.8 – 6.1 kPa (36 – 46 mmHg)
Base deficit ±2.5
Plasma HCO3- 22 – 26 mmol/L
O2 saturation 95 – 100%
• Deviations from normal acid-base status are divided into 4 general categories, depending on the source and direction of the abnormal change in hydrogen concentration, [H+].
Causes of acid-base disturbance:- Abnormal CO2 removal in lungs (‘respiratory’ acidosis or alkalosis)- Abnormalities in the regulation of bicarbonate and other buffers in blood (‘metabolic’ acidosis or alkalosis)
both may, and usually co-exist.
• Acidosis occurs in the fall in the ratio of [HCO3-]: [H2C03] of blood below 20:1, alarming lower blood pH• Alkalosis is caused by the increase in the ratio of [HCO3-]: [H2CO3] of blood above 20:1, results in rise in blood pH
1- 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. • PaCO2 and [H+] rise• A chronically raised PaCO2 is compensated by renal retention of bicarbonate, and the [H+] returns toward normal. • CAUSES: include ventilatory failure, COPD (type II respiratory failure), other lung diseases, depression of respiratory center by drugs or disease, nerve or muscle disorders that reduce respiratory muscle ability or (transiently) even the simple act of holding one’s breath.
1- Respiratory acidosis• In uncompensated state, [CO2] is elevated, whereas [HCO3-] is normal. So the normal ratio [HCO3-]: [H2C03] (20:1) and pH is reduced. • Compensation for Respiratory acidosis.
The chemical buffers (immediately take up additional H+)× Respiratory mechanism- usually cannot respond with
compensatory increased ventilation, because impaired respiration is the problem in the first place
The kidneys are most important in compensating for respiratory acidosis. Conserved all filtered HC03- and add new HCO3- to plasma while simultaneously secreting and accordingly, excreting more H+
2- Respiratory alkalosis• The primary defect in respiratory alkalosis is excessive loss of C02 from the body, as a result of hyperventilation.• Pulmonary ventilation increased out of proportion to the rate of C02 production, too much C02 is blown off. • Consequently, less [H+] is formed this source. • CAUSES: fever, anxiety, aspirin poisoning (all excessively stimulate ventilation without regard to status of oxygen, C02 or H+ in body fluids. Also a result of physiologic mechanism at high altitude)
2- Respiratory alkalosis• In uncompensated respiratory alkalosis, the increase pH reflects a reduction in [CO2], whereas [HC03-] remains normal. • Compensatory mechanism.
The chemical buffers systems (liberate H+ to diminish severity of alkalosis)
Respiratory mechanism- plasma [CO2] AND [H+] fall below normal, these 2 are normally potent stimuli for driving ventilation –’put brakes’ on the extent to which some non-respiratory factors (fever, anxiety) can overdrive ventilation. Therefore, hyperventilation does not continue completely unabated.
if the situation continues for a few days, the kidneys compensate by conserving H+ and excreting more HCO3-
3- Metabolic acidosis• Also known as non-respiratory acidosis encompasses all type of acidosis besides that caused by excess C02 in body fluid.• In uncompensated state, metabolic acidosis is always characterized by reduction in plasma [HCO3-] whereas [C02] remains normal. The problem may arise from excessive loss of HCO3- -rich fluids from the body of from an accumulation of noncarbonic acid (where plasma HCO3- is used up in buffering additional H+).
3- Metabolic acidosis- causes• Severe diarrhoea- HCO3-rich digestive juice is lost from the body rather than reabsorbed. Less HC03- is available to buffer H+, leading to more H+ in body fluids.• Diabetes mellitus- 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, increase plasma [H+]• Strenuous exercise- when muscle resort to anaerobic glycolysis during strenuous exercise, excess lactic acid is produced, raising plasma [H+]• Uremic acidosis- In severe renal failure (uraemia), 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. Also, the kidneys cannot conserve an adequate amount of HCO3- for buffering normal acid load.
3- Metabolic acidosis• Compensation for metabolic acidosis.
• These compensatory measures restore the ratio to normal by reducing [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, complete compensation is not possible because renal mechanism is not available for pH regulation.
The buffers take up extra H+The lungs blow off additional H+ -generating CO2The kidneys excrete more H+ and conserve more HC03-
4- Metabolic alkalosis• A reduction in plasma [H+] caused by relative deficiency of noncarbonic acids. • This acid-base disturbance is associated with an increase in [HC03-], which in uncompensated state, is not accompanied by a change in [C02].• CAUSES: Vomiting, Ingestion if alkaline drugs
4- Metabolic alkalosis• In metabolic alkalosis, chemical buffer systems immediately liberate H+• Ventilation is reduced so that extra H+generating C02 is retained in body fluids.• If condition persists for several days, the kidneys conserve H+ and excrete excess HC03- in urine