Arterial blood gas (ABG analysis) Flashcards
The respiratory system has 2 main components
ventilatory air pump
Gas exchange surface
Effective gas exchange requires
adequate and matching flow of gas and perfusion of respiratory tissues
V/Q matching
Basic respiratory mechanism
Concs of gases are refreshed on a breath-by-breath basis
Narrow diffusion distance between the alveoli and pulmonary caps
the gap is filled by pulmonary interstitial fluid
02 in Co2 out
Physiological shunting (V/Q matching)
“blood passes lungs without contributing to has exchange”
Low V/Q ratio
Ventilation to one lung or area is decreased or absent
That area is still perfused as body hasnt adapted yet = no gas exchange
Oxygenated and non-oxygentaed blood mixes
e.g., obstruction or ashma attack
Physiological deadspace (V/Q mismatch)
High V/Q ratio
Lung is ventilated but not perfused
No deoxygenated blood mixes
e.g., pulmonary emboli
VQ matching
Compensatory mechanisms to ensure that blood flow matches ventilation
hypoxic vasoconstriction-
hypoxic vasoconstriction-when oxygen levels drop in a lung, the arterioles that supply that area will vasoconstrict, reeucing blood flow to the area that is not perfused. If CO remains static, more BF goes to the areas that are ventilated.
Similar but less effective method for areas that aren’t perfused. Bronchoconstriction and reduced surfactant secretion helps divert air to well-perfused alveoli.
Respiratory failure
“localised mismatching of V/Q ratio”
type 1 respiratory failure
pO2 low and pCO2 normal
hypoxaemic
type 2 respiratory failure
global reduction in flow of either air to alveoli or blood to pulmonary caps
pO2 low and pC02 high
hypercapnic
Acid base balance
↑CO2 + H2O ↔︎ H2CO3 ↔︎ HCO3 + ↑H+
Therefore if you increase pCO2 or decrease HCO3- you decrease arterial pH
pH is proportional to 6.1+log x conc of (HCO3-)/ 0.03 x pCO2
What does the body do in response to chornic acidosis?
Liver
- decrease urea production
- increase production of glutamine
Kidney
- increase glutamine dehydrogenase + PEPCK to catalyse the breakdown of glutamine into NH4+ (ammonium) and HCO3- in the proximal tubule
- Ammonium is then released through micturition
What does the body do in response to chronic respiratory alkalosis?
Kidney
- Decreases plasma [HCO3-]
- Increase the number and activity of type-B intercalated cells in the collecting ducts (they secrete HCO3- from the blood into the tubule lumen helping to increase conc in the final urine therefore lowering the blood conc and pH
Metabiolic factors can affect acid/base balance and therefore blood gases (4)
Alkaline tide
kidney failure
ketone bodies
vomiting
Alkaline tide
when bicarbonate is produced in the intestine is not absorbed by the gut. bicarb bypassses the reabsorption mechanisms
e.g., bowel obstruction
kidney failure
reduced excretion of uric acid leading to metabolic acidosis
ketone bodies
in starvation, diabetic ketoacidosis, sepsis or severe exercise can result in greater lactic acid production
vomiting
loss of H+ from vomiting
Kussmaul’s breathing
Breathing patterns can affect acid/base balance
When we have metabolic acidosis due to:
K= Ketones (diabetic ketoacidosis)
U= Uremia
S= Sepsis
S= salicylates (aspirin)
M= menthanol
A= Aldehydes
U
L= lactic acid
breathing pattern changes to kussmaul’s breathing, deep sighing respiration pattern where we increase tidal volume, allowing us to breathe out more CO2
Lungs excrete excess non volatile gases in the form of
CO2
Reflex increase in ventilation rate
- Increase firing of chemoreceptors
- detected peripherally and centrally
- transmitted to the Central Pattern Generator in the brainstem
- Increased and more frequent phrenic and intercostal nerve activity
- more forceful and drequent contraction of diaphragm and intercostals
- increase rate and depth of breathing (increase V rate)
Respiratory compensation for chronic metabolic acidosis
decrease pH
Increased firing of peripheral chemoreceptors
transmitted APs via the glossopharyngeal and vagus nerves to
Central Pattern Generator in Brainstem
Increased more frequent phrenic and intercostal nerve activity
Increased ventilation rate
increased exhalation of CO2
decreased PCO2 and increased pH
Arterial blood gas
take arterial blood sample (usually from radial artery)
send to specific analyser
electrodes for arterial pH, O2 and CO2
gives info on pH, pCO2, Bicarbonate, pO2 and (base excess?)
Go though steps O, A, B, C
Step O
Normal pO2= 13.3 kPa
- <10 suggests respiratory problem
- >10 but pH is normal suggets a metabolic problem
If the patient is breathing artificial oxygen concentrations then it should
Where pO2 is less than 10 we should look at:
- Normal/ low (type 1 RF) caused by V/Q mismatch
- High, then (type II RF) due to conditions that reduce our tidal volume
Normal ranges for ABG
O2- 13.3 kPa (<10 resp problem // >10 but pH normal is metabolic problem)
pH- 7.35-7.45
CO2- <4.7 is alkalitic >6.00 is acidic
HCO3- <20mM is acidotic >28 is alkolitic
Step A
Acidosis or alkalosis? (look at pH)
normally under a very tight control of 7.35-7.45
- <7.35 = too acidic = acidosis
- >7.45 = to
- o basic = alkalosis
NB- type 1 RF or mixed/ base disorder may be balancing each other out for a patient to have a normal pH. e.g., patient with ketoacidosis who is vomiting.
Step B
Buffers (CO2/HCO3-)
Acidotic blood- look at CO2
- CO2 high - resp failure - resp failure
- CO2 normal/ low - bicarb low - metabolic acidosis
Alkalotic blood
- CO2 too low- resp. alkalosis - breathing too much- blow off too much CO2
- Bicarb levels too high - metabolic alkalosis
Step C- Chronic/ compensated
Identify how acute the acid/base disturbance is by whether the body has started its compensatory mechanisms yet
Resp. acidosis- Bicarb level – body tries to produce more bicarb
Met. acidosis- PCO2 level –Falls as we start to breathe more
Resp. alkalosis- Bicarb level –Falls to balance poeple breathing too much
Met. Alkalosis- PCO2 –risen to compensate for too much bicarb
Base excess
useful in conjunction with [HC03-] to confirm any component of an acid-base disorder
“the amount of strong acid that has to be added to fully oxygenate blood held at body temperature and normal PCO2 to return ut to a pH of 7.40”
negative value indicates a base deficit
-2 t0 +2 is normal range
+2 is metabolic alkalosis
-2 is metabolic acidosis
Example 1
Patient is brought into casualty department semi-conscious. Patient was found at home with an empty bottle of sleeping pills nearby.
pH 7.16 (low 7.16< 7.35)
PCO2 10.7 (high 10>6)
Bic 28 (normal)
pO2 5.3 (low 5.3< 10)
Base excess -0.4 (normal)
Step O- O2 low
Step A- acidosis
Step B- high CO2 + low O2 (resp. acidosis)
Step C- bicarb is normal (acute resp.acidosis)
Presentation fits with clinical history – reduced consciousness causes a reduction in tidal volume
Alternatively:
Example 2
Patient suffers catastrophic stroke and following the event was seen to be irregular and inadequate. Patient was intubated and ventilated with an inspired oxygen concentration of 40%.
pH 7.63 High
pCO2 low
Bic 20 mmol.L-1 normal
pO2 35.3 high
base excess normal
O- high
A- alkalosis
B- CO2 low Bic low? (respiratory alkalosis)
C- Bicarb starting to get low- beginings of compensation?
Patient is being overventilated. Setting on ventilator needs to be changed.
Alternatively it is someone who is hyperventilating.
Example 3
Patient with abdominal pain due to a duodenal ulcer has been admitted to the medical ward with persistent vomiting. He was also taking large quantities of sodium bicarbonate to ease the pain.
pH- 7.54 High
pCO2- 6.7 High
Bic- 33 mmol high
pO2- 11.1 High
Base excess- 17.6 (large amounts of acid had to be added - excess bicarb)
O- high
A- high- alkalosis
B- CO2 high Bic high (metabolic alkalosis)
C- starting to see a degree of compensation as CO2 Is starting to rise
Patient has been vomiting too much acid out- not enough left to balance base
Example 4-
A 52-year-old man was admitted unconscious to casualty. He was a known diabetic on daily insulin. One week ago he had developed a chest infection. He stayed at home and because he stopped eating he stopped his insulin. Over the preceding days he had become increasingly drowsy and in the morning of admission he was unrousable.
pH 7.19
PCO2: 4.0
bic: 11.1
pO2; 13.3
Base excess; 15.3
O; normal
A; acidic
B; low + base excess suggesting too much acid most likley metabolic
C; CO2 is starting to fall - most likley respiratory response to acidosis- KUSSMAUL breathing
Started to have ketoacidosis. Could be a septic patient with lactic acidosis.
