Please enable JavaScript.
Coggle requires JavaScript to display documents.
Blood gasses and acid base balance - Coggle Diagram
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
Breathing out CO2 drives the H+ ions in the blood to be formed into H2O molecules
Can also occur via the kidneys
Slower
They excrete H+ ions and regenerate HCO3-
Alkalosis
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
Lightheadedness, confusion, syncope, fits
Fall in ionised calcium
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 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
Not enough blood for the kidneys to filter
Due to potassium deficiency
Due to mineralocorticoid excess
Saline responsive causes
Gastrointestinal - vomiting, gastric damage
Urinary - Diuretics (especially in CCF), nephrotic damage
saline unresponsive causes
Assessed with hypertension - primary hyperaldosteronism, cushing's syndrome
Not assessed with hypertension - severe K+ depletion, Bartter's syndrome
Compensatory responses
Buffering
Release of H+ ions from buffers
Hypoventilation
Usually incomplete
Renal bicarbonate excretion increased
Effects
Often asymptomatic
Potassium depletion
Biochemistry
Low H+
Low bicarbonate
Compensation may decrease pCO2
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
Myasthenia, thoracic trauma, pneumothorax
Pulmonary disease
Restrictive
Extensive fibrosis
Obstructive
Chronic bronchitis, severe asthma
Impaired perfusion
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
Anxiety
Coma
Headaches
Extenson plantars
Myoclonus
Cardiovascular issues
Systemic vasodilation
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
Metabolic acidosis
Causes
Increase in H+ generation
Ketoacidosis
Lactic acidosis
Poisoning
Decreases in H+ excretion
Renal failure
Renal tubular acidosis (Types 1 and 4)
Decreases in buffering capacity
Loss of bicarb buffer
Gastrointestinal - diarrhoea, pancreatic fistula
Renal - renal tubular acidosis type 2
Compensatory responses
Buffering
Leads to further fall in bicarbonate
Hyperventilation
H+ stimulates chemoreceptors
Kussmaul - deep sighing
Lower PCO2 which lowers H+
Limit to how far PCO2 can fall
Increased renal H+ excretion
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
Negative inotropic effect (heart function)
Oxygen delivery to tissues
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
Nervous system
Impaired consciousness - little correlation with H+
Potassium homeostasis
Redistribution of H+ cells in exchange for K+
Plasma K+ will rise while intracellular and total body K+ will fall
Bone
In chronic acidosis there is buffering by bone phosphate leading to decalcification of bones
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
pO2 is stable for 60 mins at 0 degrees
H+, pCO2 and bicarb are stable for up to 30 mins at 22 degrees
If there are any air bubbles in the sample that's an issue
You can end up measuring air rather than blood