Blood gasses and acid base balance

Hydrogen ion homeostasis

Buffering

Haemoglobin 'chloride shift'

CO2 enters red blood cell and reacts with water

This forms carbonic acid (H2CO3)

Carbonic acid then dissociates into H+ and HCO3-

Haemoglobin then uptakes H+ ions acting as a buffer forming HbH

The remaining HCO3- leaves the rbc and Cl- enters to keep the cell electrically neutral

Helps regulate the conc of H+ ions in the blood

Helps Hb release O2 when CO2 levels are high in the blood

Phosphate buffering

Other proteins can be used as buffers

Exchange of intracellular K+ for H+

Intracellular shift of H+ ions and extracellular shift of K+

H+ excretion

Mainly occurs via respiration

Can also occur via the kidneys

Breathing out CO2 drives the H+ ions in the blood to be formed into H2O molecules

Slower

They excrete H+ ions and regenerate HCO3-

Alkalosis

Acidosis

Excess H+

Over 45 nmol/L

Respiratory acidosis

Causes

Co2 retention

Caused by malfunction of excretory mechanisms or its control

CNS depression or disease / neurological disease

Caused by drugs, strokes, spinal cord lesions, motor neuron disease

Defects in respiratory function

Mechanical defects

Pulmonary disease

Myasthenia, thoracic trauma, pneumothorax

Restrictive

Obstructive

Impaired perfusion

Extensive fibrosis

Chronic bronchitis, severe asthma

Massive pulmonary embolism

Compensatory responses

Buffering

Renal hydrogen ion excretion

Bicarbonate regeneration

Effects

Depends on the underlying cause

In the case of hypoxia

Cyanosis, drowsiness, breathlessness, skin looks blue-ish

High CO2 levels cause

Neurological issues

Cardiovascular issues

Systemic vasodilation

Anxiety

Coma

Headaches

Extenson plantars

Myoclonus

Biochemistry

Acute respiratory acidosis

High CO2

High H+ ions

normal / high bicarbonate

Chronic respiratory acidosis

High PCO2

High/normal H+

Because the kidneys have had time to normalize it

High bicarbonate

Acute + chronic respiratory acidosis

High PCO2

High H+

High bicarbonate

deficit of H+ ion

Less than 38 nmol/L

Respiratory alkalosis

Causes

Increased rate pf CO2 excretion

Stimulation of respiratory center

Hyperventilation

stimuli to respiratory center

Cortical - pain, fever

Local - trauma, tumours

Drugs, toxins - salicylate, liver failure

Hypoxemia - R to L shunts, pulmonary disease

Compensatory responses

Buffering

Reduced renal H+ excretion

Reduced amounts of bicarbonate reabsorbed by the kidneys

Effects

Underlying disorder effects

Acute hypocapnia

Cerebral vasoconstriction

Fall in ionised calcium

Lightheadedness, confusion, syncope, fits

Preioral, peripheral paraesthesia

Cardiovascular

Increased heartrate

Biochemistry

Acute respiratory alkalosis

Low PCO2

Low H+

Small decrease in bicarbonate

Chronic respiratory alkalosis

Renal compensation results in only marginally low H+

Further fall in bicarbonate - cannot go lower than 12 nmol/L

Metabolic acidosis

Causes

Increase in H+ generation

Decreases in H+ excretion

Decreases in buffering capacity

Ketoacidosis

Lactic acidosis

Poisoning

Renal failure

Renal tubular acidosis (Types 1 and 4)

Loss of bicarb buffer

Gastrointestinal - diarrhoea, pancreatic fistula

Renal - renal tubular acidosis type 2

Compensatory responses

Buffering

Hyperventilation

Increased renal H+ excretion

Leads to further fall in bicarbonate

H+ stimulates chemoreceptors

Kussmaul - deep sighing

Lower PCO2 which lowers H+

Limit to how far PCO2 can fall

Biochemsitry

High H+ ions

Low bicarbonate

Fall in PCO2

Extracellular K+

Anion gap

+ions - -ions = roughly 15nmol/L

Gap is due to proteins and some small anions

In metabolic acidosis gap is normal in bicarb loss and increased in raised acid production

Effects

Cardiovascular

Oxygen delivery to tissues

Nervous system

Potassium homeostasis

Bone

In chronic acidosis there is buffering by bone phosphate leading to decalcification of bones

Impaired consciousness - little correlation with H+

Negative inotropic effect (heart function)

Right shift of oxyhaemoglobin dissasociation curve , facilitates O2 delivery

Reduced 2.3-DGP results in a left shift of the curve

This takes some hours but leads to reduced O2 delivery

Redistribution of H+ cells in exchange for K+

Plasma K+ will rise while intracellular and total body K+ will fall

metabolic alkalosis

Causes

Excess loss of H+, increased alkali intake

Bicarbonate if filtered by the kidneys

For metabolic alkalosis to occur in this case there must be some issue with renal absorption

Due to extracellular volume contraction

Due to potassium deficiency

Not enough blood for the kidneys to filter

Due to mineralocorticoid excess

Saline responsive causes

saline unresponsive causes

Assessed with hypertension - primary hyperaldosteronism, cushing's syndrome

Not assessed with hypertension - severe K+ depletion, Bartter's syndrome

Gastrointestinal - vomiting, gastric damage

Urinary - Diuretics (especially in CCF), nephrotic damage

Compensatory responses

Buffering

Hypoventilation

Renal bicarbonate excretion increased

Release of H+ ions from buffers

Usually incomplete

Effects

Often asymptomatic

Potassium depletion

Biochemistry

Low H+

Low bicarbonate

Compensation may decrease pCO2

Assessment of acid base status

Clinical assessment

Medical history checked

Examination can give some info but not much

Blood tests are most important

Main test is arterial blood-gas analysis

Practical aspects of assessment

Oxygen levels must be measured ASAP or the sample must be iced to slow the respiration of blood cells maintaining correct pO2 level

If there are any air bubbles in the sample that's an issue

You can end up measuring air rather than blood

pO2 is stable for 60 mins at 0 degrees

H+, pCO2 and bicarb are stable for up to 30 mins at 22 degrees