ABG Flashcards
The main chemical equation that is a principle of ABGs
H+ + HCO3- H2CO3 H2O + CO2
How extra acid can be eliminated from the body? (3)
• Bicarbonate is used as a buffer, plasma proteins can also hold on to the acid (may be given
when necessary)
- Hyperventilation (rapid compensation)
- Kidney working -> production of HCO3 (slow: hours/days compensation)
Causes of respiratory acidosis
- airway obstruction (foreign body, epiglottis),
- respiratory depression (heroin, opioids)
- impaired alveolar filling (full of pus - infection)
- MSK (muscular dystrophy)
What happens to HCO3- in acute respiratory acidosis
•It takes long time to compensate with HCO3-;
therefore in acute resp acidosis we will have normal
HCO3 and BE (as it has not compensated yet)
•As kidney compensate by conserving HCO3, HCO3 would increase and BE too (but takes time)
Potential causes of metabolic acidosis
- increase in H+ formation (DKA, lactic acidosis)
- increase in exogenous H+ (extra acid from somewhere else: methanol, ethanol, drugs)
- decrease in H+ excretion (cannot excrete H+: renal failure)
- decrease in HCO3- (renal loss, gut loss)
What’s metabolic acidosis?
Excess of acid or decrease in HCO3-
What happens in metabolic acidosis with respiratory compensation?
Compensation:
increased RR -> hyperventilation (decreased CO2 but
still not alkalotic) => Metabolic acidosis with resp compensation
What’s respiratory alkalosis?
Low CO2 due to increase ventilation
Causes of respiratory alkalosis (3 categories)
A. Central: hysteria, hyperventilation, head injury, stroke (breathing centres may be affected)
B. Lungs/hypoxia: PE, pulmonary oedema, fibrosis (needs to breath harder to maintain fairly normal sats)
C. Drugs: salicylate (aspirin, pain relieving meds)
How body compensates for respiratory alkalosis?
Compensation: excretion of HCO3 via kidneys to
normalise acidosis (but takes time)
What’s metabolic alkalosis?
excess of H+ loss or excess of extra base
Causes of metabolic alkalosis (3 categories)
A. Acid loss: (prolonged vomiting, gastric aspiration, hypokalaemia -> acid into cells so potassium can get out to normalise)
B. Renal loss (hypokalaemia, hypochloraemia)
C. Gaining base (iatrogenic, milk-alkali syndrome *rare now as we use PPI to reduce indigestion; in the past milk was used)
How does body compensate for metabolic alkalosis?
slow breathing down (to retain more CO2)-> so we
can correct alkalosis (by adding some H+ from CO2
increase)
What may be suggestive of possible chronic respiratory failure?
Chronic: was going on for some time -> Bicarb is conserved due to body trying to compensate for acidosis
What’s the aim of normal stats and what’s the aim of stats for COPD?
- normal sats: >94%
- COPD person: 88 - 92% (aim for no more than 92%)
What’s type 2 respiratory failure?
high CO2 and low O2
What may be seen on ABGs in a person who lost/has decreased hypoxic drive?
high bicarbonate and BE -> as this is a compensation for high CO2
*Small group of COPD (15-20%) - not everybody
*Rare, but happens in severe and chronic asthma
How much of O2 would nasal mask deliver?
Nasal mask would deliver 24% - 28% (1L -2L)
Reserviour mask
- another name
- use
- concentration of O2 used
Benefits of venturi mask use? What does it allow us to do?
- To make sure that a patient gets right amount of O2 -> venturi system
- Venturi allows to alter speed of oxygen that is delivered -> so we can make sure we can alter the concentration of O2 that we want
What are normal ranges for ABGs?
How quick respiratory compensation is?
Respiratory compensation may occur rapidly -> as we either decrease or increase the amount of alveolar ventilation:
- Increased ventilation: blowing off more CO2 -> pH will increase (more alkaline)
- Decreased ventilation: retaining CO2 -> pH will decrease (more acidic)
How quick metabolic compensation is?
Metabolic compensation occurs slowly (few days) as kidney must either reduce HCO3 production (to decrease pH -> to be more acidic) or increase HCO3
production (to increase pH -> more alkali)
What’s seen in type 1 respiratory failure?
low O2 and normal CO2
Neurological effects of hypercapnia
- headache
- papilloedema
- extensor plantar responses
- myoclonus
- anxiety
- confusion
- impaired GCS
Signs (3) of hypoxemia
- cyanosis
- drowsiness
- breathlessness
Picture of metabolic acidosis
low pH, low HCO3, low BE
What’s the purpose of the anion gap?
- is used to determine presence of unmeasured ions
- It allows us to see if metabolic acidosis is due to increased acid production vs decreased acid excretion or loss of HCO3-
What’s normal anion gap?
Normal anion gap: 4 - 12 mmol/L
The formula of calculation of anion gap
Anion gap = Na+ - (Cl- + HCO3-)
What does increased anion gap mean?
Increased anion gap -> increased acid production or acid ingestion (diabetic ketoacidosis, lactic acidosis, aspirin overdose -> ingestion of acid)
What does decreased anion gap mean?
Decreased anion gap -> decreased acid excretion or loss of HCO3 (GI loss of HCO3 -> diarrhoea,
ileostomy; retaining H+ -> renal tubular acidosis; Addison’s disease)
Picture of metabolic alkalosis
increased pH, increased HCO3, increased BE
Mixed respiratory and metabolic acidosis
- picture
- causes
Picture: increased CO2, decreased HCO3, decreased pH
Causes: cardiac arrest, multi-organ failure
Mixex respiratory and metabolic alkalosis
- picture
- causes
Picture: low CO2, high HCO3, high pH
Cause: liver cirrhosis with diuretic use, hyperemesis gravidarum, excessive ventilation in COPD
What ABG picture may indicate salicylate overdose?
(salicylate and its metabolites are acidic) -> metabolic acidosis + gemeration of ammonia -> stimulation of respiratory centre -> hyperventilation -> low CO2
What may high anion gap be suggestive of?
Anion gap would pick metabolic
acidosis -> high anion gap in Aspirin OD
What may cause inaccurate pulse oximetry readings?
