14-11-22 – Blood gas analysis Flashcards
Learning outcomes
- to learn a stepwise approach to the application of arterial blood gas results
- Emphasise the importance of clinical context
What is 1Kpa equal to?
What is considered normal pH?
What is the difference between acidosis and acidaemia?
What is the difference between alkalosis and alkalaemia?
How do we convert from H+ concentration to pH?
- 1kPa is equal to 7.5mmHg
- Normal pH is considered 7.35 – 7.45
- Acidosis means a high hydrogen ion concentration in the tissues.
- Acidaemia refers to a high hydrogen ion concentration in the blood and is the most easily measured indication of tissue acidosis
- Alkalosis means a low hydrogen ion concentration in the tissues.
- Alkalaemia refers to a low hydrogen ion concentration in the blood and is the most easily measured indication of tissue alkalosis
- To convert from H+ concentration to pH, we do the subtraction 80 – H+ concentration in nmol/litre to give us the 2 decimal places for pH (e.g 80 – 60nmol/L of H+ = 20, so pH will be 7.20
What is the human body constantly producing?
What are 3 buffers that maintain pH of the body?
How else is pH maintained?
What are 3 cases where acid-base disturbances occur?
- The human body is continually producing acid
- 3 buffers that maintain pH of the body:
1) Proteins
2) Haemoglobin
3) Carbonic acid / bicarbonate
- Blood pH is also maintained by excretion from the lungs or kidneys
- 3 cases where acid-base disturbances occur:
1) There is a problem with ventilation
2) There is a problem with renal function
3) Overwhelming acid or base load the body can’t handle
Where are arterial blood gases (ABGs) taken from?
Why is this?
How can be test the radial artery supply?
When might the radial artery be difficult to feel?
What artery might we use in this case?
Where are ABGs analysed?
- Arterial blood gases (ABGs) are taken from the radial artery
- This is because it is accessible there is also supply from radial and ulnar artery
- We can test this supply by using the Alan’s test (compare both sides) – occlude the arteries and the palm goes white, release the arteries and the palm goes back to pink
- The radial artery may be difficult to feel if the patient is in shock, so in this case, we use the femoral artery
- ABGs are analysed in a blood gas analyser – if there is not one nearby, the sample has to be chilled
What 4 values are we looking at for in ABG analysis?
What are normal ranges for these arterial and venous values?
- 4 values are we looking at for in ABG analysis and their normal ranges:
1) pH
* Arterial – 7.35 – 7.45
* Venous – 7.32 – 7.45
2) pO2
* Arterial – 12 – 13kPa
* Venous - 3.3 – 5.3kPa
3) pCO2
* Arterial – 4.5 – 5.6 kPa
* Venous – 5.4 – 6.6kPa
4) Bicarbonate (std - standard)
* Arterial – 22 – 26 mmol/L
* Venous – 23 – 27 mmol/L
What is standard bicarbonate?
How are actual and standard bicarbonate linked in health?
What does the standard bicarbonate value reflect?
In what patients might this be used?
What falls in metabolic acidaemia?
What can the actual bicarbonate value be affected by?
What is base excess?
When might we use this value?
- Standard bicarbonate is the plasma bicarbonate concentration of blood that has been equilibrated with gas of normal paCO2 (5.3 kPa) and at 37 degrees.
- In health, actual bicarbonate concentration is the same as standard bicarbonate concentration, because pCO2 is normal in both instances.
- In standard bicarbonate, we are removing the influence of pCO2 by putting in the standard concentration of 5.3, so the standard bicarbonate value will only reflect metabolic influence on the acid-base balance
- This is used in patients with type 2 respiratory failure where a high pCO2 is normal for them
- The standard bicarbonate can be used so we can see if there is metabolic influence on potential acid-base disturbances
- In metabolic acidaemia, we expect to see the standard bicarbonate fall
- The actual bicarbonate can be affected by the pCO2 value, as the pCO2 value can differ in illness
- Base excess is a mirror of standard bicarbonate so in metabolic acidaemia, we expect to see the standard bicarbonate fall, so the base excess will become more negative
- The actual bicarbonate value can be used in those that don’t have respiratory problems
What do we have to remember about ABG results?
What 8 places can we gather clues?
- We have to remember that ABG results are a clue to the puzzle, and mean different things in different circumstances
- 8 places we can gather clues:
1) History
2) Examination
3) What are they breathing (what % of oxygen?)
4) Urea and Electrolytes
5) Haemoglobin
6) Glucose
7) Arterial blood gases
8) CXR
What are the 4 steps in the assessment of ABGs?
- 4 steps in the assessment of ABGs:
1) Assess pO2 and oxygenation
2) Assess pH (academia or alkalaemia?)
3) Determine the primary problem (think about the patient)
4) Is compensation occurring?
What do we do when assessing pO2 and oxygenation?
What equipment can be used?
How does it work?
- When assessing pO2 and oxygenation, we are checking for signs of hypoxia
- We can check for signs of central cyanosis (blue discolouration of visible mucosal membranes)
- We can use a pulse oximeter to give continuous assessment of pO2
- It works by shining red light through capillary beds, with different levels of oxygenation in blood leading to the blood being different colours
- The pO2 can be determined by how much light is absorbed, which will differ depending on the colour of the blood
What is the difference between type 1 and type 2 respiratory failure?
- Type 1 respiratory failure occurs when the respiratory system cannot adequately provide oxygen to the body, leading to hypoxemia.
- Type 2 respiratory failure occurs when the respiratory system is unable to sufficiently remove carbon dioxide from the body, leading to hypercapnia
How can oxygen levels that are too high affect COPD?
What factors re responsible for respiratory drive in normal people and those with COPD?
How does oxygen therapy affect this?
What is the V/Q ratio like in COPD?
How does oxygen therapy affect this?
What can all of these factors lead to in COPD?
- In some individuals, the effect of oxygen on COPD is to cause increased carbon dioxide retention
- PCO2 is responsible for respiratory drive, so with increased PCO2, respiration rate increases
- Those with chronically high PCO2, such as type 2 respiratory failure patients, have their PCO2 respiratory drive suppressed
- To make up for this, the body utilises hypoxic drive, which is a form of respiratory drive in which the body uses oxygen chemoreceptors instead of carbon dioxide receptors to regulate the respiratory cycle
- During oxygen therapy, we suppress this hypoxic drive, making things worse
- Lung diseases like COPD or asthma can impair airflow with little effect on pulmonary blood flow, resulting in low ventilation and nearly normal perfusion (decreased V/Q)
- In COPD, oxygen therapy will lead to an increased ventilation-perfusion mismatch, as increased oxygen leads to decreased hypoxic pulmonary vasoconstriction
- This will cause ventilation to lung units with higher V/Q mismatch to be higher, leading to increased alveolar dead space ventilation and decreased overall ventilation
- These factors lead to CO2 retention and an Increased risk of hypercapnic respiratory failure in acute exacerbations of COPD
What are 8 potential effects of high oxygen levels?
- 8 potential effects of high oxygen levels:
1) Increased mortality survivors of cardiac arrest
2) Increased mortality intensive care patients
3) Increased mortality in acute severe asthma
4) Generation of free radicals
* Free radicals damage contributes to the aetiology of many chronic health problems such as cardiovascular and inflammatory disease, cataract, and cancer.
5) Lung toxicity
* Collapse of alveoli due to atelectasis – atelectasis is partial collapse or incomplete inflation of the lung.
* Nitrogen is important in keeping the alveoli open, so giving increased oxygen will lead to decreased Nitrogen, which can lead to atelectasis
* Irritating to mucous membranes
6) Ocular toxicity
7) Myocardial damage
8) Neuro damage
What are the British Thoracic Society guidelines on giving oxygen?
What is SO2?
What SO2 target should we be aiming for?
What 2 conditions can therapeutic high inspired concentration of oxygen be used for?
- British Thoracic Society guidelines on giving oxygen:
- Oxygen is a treatment for hypoxia not dyspnoea alone.
- In an unstable medical emergency give high concentration of oxygen then titrate to target once stable
- Oxygen saturation (SO2) is the fraction of oxygen-saturated haemoglobin relative to total haemoglobin in the blood
- SO2 targets:
- 94-96% (normally)
- 88-92% (type 2 respiratory failure)
- 2 conditions therapeutic high inspired concentration of oxygen can be used for:
1) Pneumothorax
* Can decrease the size of pneumothorax
* If we put a high concentration of air into the alveoli, nitrogen from the air in the pleural cavity will move back into the alveoli (high to low concentration)
2) Carbon monoxide poisoning
* Will make Hb release CO
What is the Alveolar – arterial (A-a) gradient?
What is a typical value for this?
What can a high value indicate?
What is the oxygen cascade?
Describe the oxygen cascade.
Why is it important?
- The Alveolar – arterial (A-a) gradient is the difference between PAO2 and PaO2
- It is normally less than 15 mmHg (2kPa), with higher values indicating problems with exchange
- The oxygen cascade looks at how pO2 levels change in different parts of the body
- The PO2 from the airways gets lower and lower till it reaches its lowest at the mitochondria
- The oxygen cascade and alveolar – arterial gradient allows us to see if the drop in PO2 is just part of natural physiology, or if there is a problem with oxygenation
What 4 things do we have to look at when assessing oxygenation?
- 4 things we have to look at when assessing oxygenation:
1) What is the inspired oxygen concentration?
2) How old is the patient?
* A PO2 of 10 in a young person is worrying, but a PO2 of 10 in a 90-year-old may be normal
* This can be because of V/Q mismatch due to losing some elasticity in the lungs (normal blood flow, lower ventilation)
3) What is the atmospheric pressure?
* Higher altitudes have lower atmospheric pressure
* E.g high altitude PO2 of 7kPa seems low, but 7kPa still makes up the same % of atmospheric pressure as seen at sea level (about 21% of atmospheric pressure is PO2)
* This person may be hypoxic, but there is not a problem with oxygenation, as adaptations from the body have likely been put in place
* Hypoxia is a state in which oxygen is not available in sufficient amounts at the tissue level to maintain adequate homeostasis; this can result from inadequate oxygen delivery to the tissues either due to low blood supply or low oxygen content in the blood (hypoxemia)
* Systemically, adaptations to hypoxia include increased ventilation, cardiac output, blood vessel growth, and circulating red blood cell numbers
4) What situation is the patient in?
* A PO2 of 14kPa seems good, but if the patient is being given 60% oxygen just to maintain this PO2, this implies that there is a problem with oxygenation
* This patient is not hypoxic, but does have a problem with oxygenation
Example patient scenario 1
- Example patient scenario 1
- Patient presents with excess sweating and small pin-point pupils
- The respiratory rate is 6
- Due to ventilation, it is expected that PO2 is low and PCO2 is high
- The working prognosis (likely cause) is an opioid overdose
- The ABG results comes back as follows:
1) pH 7.20 – low value, patient has academia
2) pO2 28.7kPa – high value, so can dial back on oxygen or take oxygen off
3) pCO2 11kPa – high value
4) HCO3 - (standard)25mmol/l – normal value - Due to low respiratory rate and high PCO2, we suspect that the primary problem is an acute respiratory problem from the drugs causing respiratory depression
- This has caused acute respiratory acidosis
- To keep the pH the same, the bicarbonate has to go up as the PCO2 goes up (pH in correlation with HCO3/PCO2)
- In this case, compensation has not occurred, as the bicarbonate value has not increased beyond a normal value
- This is to be expected, as metabolic compensation takes days (24-48 hours)
- The kidneys compensate for a respiratory acidosis by tubular cells reabsorbing more HCO3 from the tubular fluid, collecting duct cells secreting more H+ and generating more HCO3, and ammoniagenesis leading to increased formation of the NH3 buffer.
Example patient scenario 2
- Example patient scenario 2
- Patient presents with central cyanosis, so he doesn’t need to be blood gassed
- We will suspect that the PO2 will be low
- He has a history of type 2 respiratory failure
- He has COPD and comes in with an acute exacerbation
- Type 2 respiratory failure occurs when the respiratory system is unable to sufficiently remove carbon dioxide from the body, leading to hypercapnia
- The ABG results comes back as follows:
1) pH 7.32 – acidaemia, but not as severe as previous patient
2) pO2 6kPa – low value
3) pCO2 10.6kPa – high value
4) HCO3(standard)37mmol/l – high value - In this case, it is normal for his PO2 to be low
- The target oxygen saturation (SO2) for those with Type 2 respiratory failure is 88-92%
- Although the PCO2 is similar to the last patient, the pH isn’t nearly as low, but there is still some respiratory acidaemia being caused by an acute COPD exacerbation
- This is because this is a chronic condition, so the kidneys have had time to compensate
- In chronic respiratory acidosis the kidneys compensate by retaining bicarbonate.
- This takes a few days to reach its maximal value, and once this value has been reached, the kidneys can set this at the new normal, which is what has happened in this case
Comparisons of acute and chronic respiratory disorders ABG results
Comparisons of acute and chronic respiratory disorders ABG results
