P H and acid-base status PDF

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Warning: TT: undefined function: 32 Warning: TT: undefined function: 32pH & acid-base statusThursday 31st January 2019 Week 18Learning objectives:o Define ‘pH’, ‘acidosis’; ‘alkalosis’o Understand the importance of maintaining acid-base balance andhow the body regulates this balance.o Be abl...

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pH & acidacid-base base status Thursday 31st January 2019

Week 18

Learning objectives: o Define ‘pH’, ‘acidosis’; ‘alkalosis’ o Understand the importance of maintaining acid-base balance and how the body regulates this balance. o Be able to go give examples of metabolic and respiratory acidosis/alkalosis relating to clinical data.

pH: The acidity or alkalinity of an aqueous solution pH = -Log10 [H+] → pH is essentially the concentration of H+ ions. In aqueous solutions pH = -Log10 [H3O+] pH 1 (acidic – high concentration of H+ ions) pH 7 (neutral) pH 154 (alkaline – low concentration of H+ ions) A logarithm is the inverse of an exponential – 24 = 16 ⟺ Log2 (16) = 4 Log10 (100) = 2 Logarithms are used to generate straight line graphs from large numbers.

Acid-base homeostasis: The balance between acids and bases The human body is very sensitive to pH, so strong mechanisms exist to maintain it around pH 7.4 ±0.05 • Outside the acceptable range of pH: Proteins are denatured and digested Enzymes do not function Haemoglobins oxygen carrying capacity affected Biochemical reactions are influenced by the pH of their environment.

Metabolic origin of acidity: H+ ions are principally derived from amino acid oxidation – • Incomplete oxidation of energy substrates: Glucose → lactic acid Triglycerides → keto acids • Oxidative metabolism produces CO2

Buffering of blood pH:

pKa is the acid dissociation constant, Ka. When pH = pKa, the acid is 50% protonated, 50% deprotonated.

Calculating pH: Henderson-Hasselbalch equation –

An increase in HCO3- increases pH; an increase in PaCO2 decreases pH.

2 routes of excretion: Renal and respiratory

pH regulation – buffers:

pH regulation – respiratory compensation: Respiratory compensation – acts within minutes/hours (changes in lung volume exhalation – minute volume).

pH regulation – renal compensation: Takes hours/days (changes in blood HCO 3- and H+ concentrations, altering bicarbonate reabsorption into the blood; H+ excretion).

pH regulation – compensation: H+ levels kept to normal levels (pH 7.35-7.45) by altering levels of bicarbonate or PaCO2. Partial compensation of pH occurs when H+ are greater than or less than compensation can manage → change in pH.

Arterial blood gas:

Measurement

Reference range

PaCO2

4.7-6.0 kPa (35 – 45 mmHg)

Serum HCO3-

22-26 mmol/L

pH

7.35-7.45

Acid-base disorders:

Respiratory acidosis: Decreased ventilation (hypoventilation) Leads to increased blood CO2 concentration and decreased pH. Accumulation of CO2 as not expired rapidly enough. Can be acute or chronic – in chronic conditions, HCO3- will be elevated as part of renal compensation. • Can be life-threatening in serious cases.

• • • •

Causes – Anything that decreases ventilation, e.g. • Obstruction of airways • Depression of CNS • Pulmonary disease → COPD COPD – Obstructive lung disease, characterised by chronically poor air flow due to breakdown of lung tissue. Symptoms include shortness of breath, persistent cough; sputum production. COPD is a common cause of respiratory acidosis.

Respiratory alkalosis: ▪ ▪ ▪ ▪

Increased ventilation (hyperventilation) Decreased PaCO2 and increased pH Acute respiratory alkalosis has normal HCO3-. Chronic respiratory alkalosis has decreased HCO3- due to renal compensation.

Causes – • Hypoxia-mediated hyperventilation • Intra-cranial pressure • Drugs, e.g. caffeine; salicylic acid (aspirin) • Pneumonia • Rarely life-threatening in its own right Aspirin – Is a salicylate drug, originally discovered in the bark of willow trees, now made synthetically as an anti-inflammatory medicine to reduce pain and fever. However, overdose causes hyperventilation.

Metabolic acidosis: o o o o o o

The most frequent acid-base imbalance Occurs when the body produces too much acid (i.e. increased production of H+). Or inability of the kidney to reabsorb HCO3-. Respiratory compensation causes hyperventilation to reduce PaCO2. ‘Increased anion gap’ and ‘normal anion gap’. Can lead to coma and death.

Anion gap – The difference between cations (+ve charged ions) and anions (-ve charged ions) is helpful in distinguishing between causes of metabolic acidosis. • A normal gap is 8 – 16 mmol/L +

+

-

-

(Na + K ) - (Cl + HCO ) 3

• High anion gap caused by – Glycols (ethylene glycol, propylene glycol) Oxoproline (pyroglutamic acid, the toxic metabolite of excessive acetaminophen or paracetamol) L-Lactate (standard lactic acid seen in lactic acidosis) D-Lactate (exogenous lactic acid produced by gut bacteria) Methanol (this is inclusive of alcohols in general) Aspirin (salicylic acid) Renal failure (uremic acidosis) Ketones (diabetic, alcoholic; starvation ketosis)

Lactic acidosis: • • • • •

Caused by a build-up of lactate in the blood. Usually occurs when cells receive too little oxygen (hypoxia). Cells metabolise glucose anaerobically; leads to a build-up of lactate. Caused by exercise; can also can be a side effect of drugs (e.g. metformin). Can have genetic causes.

Metabolic alkalosis: ▪ pH is elevated above the normal range. ▪ Alkalosis is caused by a decrease in H+ or an increase in HCO3-.

▪ Compensated for by hypoventilation to increase PaCO2. Causes – • Severe vomiting • Diuretics • Hyperaldosteronism • Retention of bicarbonate Pyloric stenosis – Narrowing of the opening between the stomach and the small intestine. This causes an obstruction, so ingested food is vomited back up instead . Usually occurs in infants (2 – 6 weeks old). Causes metabolic alkalosis due to loss of gastric acid (HCl)....