Assessment of Acid-Base Balance Flashcards
what pH range and [H+] does the body need to be within
pH - 7.35-7.45
[H+] - 35-45nmol/l
what processes produce acid in the body
cellular respiration (CO2 and water which make carbonic acid)
metabolic processes (ketones, lactate etc.)
what things help to remove acid from the body
buffers
lungs
kidney
what things help to remove acid from the body
buffers
lungs
kidneys
hypoventilation will cause
resp. acidosis
hyperventilation will cause
resp. alkalosis
what changes in H+ and HCO would result in metabolic acidosis and what would cause these changes
high H+ (overproduction or impaired secretion)
low HCO3- (unusual losses)
what changes in H+ and HCO would result in metabolic alkalosis and what would cause these changes
low H+ (projectile vomiting)
high HCO3- (unusual ingestion e.g. IV sodium bicarb treatment)
how does the body compensate in respiratory acidosis
increased retention of HCO3- by kidneys
how does the body compensate in respiratory acidosis
increased retention of HCO3- by kidneys
this is a slow process
how does the body compensate in respiratory alkalosis
decreased retention of HCO3- by the kidneys
this is a small and usually marginal process
how does the body compensate in metabolic acidosis
increased resp. rate to decrease CO2
increased retention of HCO3 by kidneys
how does the body compensate in metabolic alkalosis
decreased resp. rate to increase CO2
decreased retention of HCO3 by kidneys
this is usually minimal
what is deep fast breathing called and when does it occur
kusmal breathing
when resp. rate increases to compensate for metabolic acidosis
what practical things should be considered before does ABGs
would a venous sample do?
consider usual local anaesthetic
consider appropriate site (usually radial, likely femoral in arrest)
analyse ASAP
how long is an ABG sample stable
10 minutes
60 minutes on ice
what are the six steps for interpreting blood gases
- is the patient adequately oxygenated (does this suggest a respiratory cause?)
- what is their pH (acidosis or alkalosis)
- is there CO2 disturbance (resp?)
- is there HCO3 disturbance (metabolic?)
- what is the primary disturbance (usually this will match the underlying cause/symptoms and direction of change)
- is there compensation (does the timing of clinical picture fit - e.g. very acute can’t have metabolic compensation)
- if it doesn’t make sense (did you sample wrong? ask for help)
what is base excess
the amount of H+ per litre of blood required to return [H+] to the reference range at a reference range pCO2
when will a base excess be positive or negative
positive - metabolic alkalosis
negative - metabolic acidosis
what is the standard bicarb
what the bicarbonate would be if pCo2 were reference range
what will the standard bicarb be in
purely resp disorder
purely metabolic disorder
mixed resp-met disorder
ref. range standard bicarb
approx equivalent to acutal bicarb
significant difference with actual bicarb
if someone has low CO2 and low bicarb but high H what do they have
high pH = acidosis
low bicarb = metabolic
low CO2 would cause alkalosis and HCO3 compensation wouldn’t cause acidosis
so metabolic acidosis with respiratory compensation
what is the anion gap
difference between most abundant cations and anions
[Na+] - [Cl-] - [HCO3 -]
what causes of metabolic acidosis would you expect the anion gap to be normal
severe diarrhoea
high interstinal fistula output
renal tubular acidosis
what causes of metabolic acidosis would you expect the anion gap to be high
diabetic ketoacidosis
lactic acidosis
aspirin overdose
alcohol poisoning
renal failure
chronic metabolic acidosis can have what effect on bone
buffering by bone
leading to decalcification
which compensatory mechanisms are usually marginal (i.e. you wouldn’t expect them to cause alkalosis from acidosis or vice versa)
metabolic compensation for respiratory alkalosis
respiratory and metabolic compensation for metabolic alkalosis
the alkalosis ones - you are unlikely to get acidotic as a result of compensation to alkalosis
causes of acute respiratory acidosis
airway obstruction
cardio-pulmonary arrest
COPD exacerbation
pneumonia
opiate toxicity
guillain-barre syndrome
myasthenia gravis
causes of chronic respiratory acidosis
COPD
obstructive obesity
pulmonary fibrosis
MND
myopathy
effects of respiratory acidosis on body
hypercapnia causing:
shortness of breath
neurological symptoms - anxiety, coma, headaches
cardiovascular - systemic vasodilation
causes of acute respiratory alkalosis
asthma, COPD exacerbation,PE
pain
panic attack
iatrogenic (e.g. overventilation when under GA)
altitude sickness
innappropriate stimulation of respiratory centre in brain stem (head injury etc.)
chronic cause of respiratory alkalosis
pregnancy
but physiological and compensated by mild metabolic acidosis
effects of respiratory alkalosis
acute hypocapnia - lightheadedness, confusion, syncope, fits, paraesthesia
cardiovascular - increased heart rate, vasoconstriction, angina in those with CVD
causes of metabolic alkalosis
loss of H+
- vomiting
- hypokalaemia (e.g. secondary to loop diuretic)
- primary hyperaldosteronism
gain of HCO3-
- sodium bicarbonate infusion (common cause in CKD)