Arterial Blood Gas (ABG) Flashcards
Indications for ABG
New hypoxia
Suspected pH change
Acute unwell patient
Interpretation:
Step 1 - pH:
- What can you learn from looking at this?
- What is the normal pH range?
Step 2 - PaCO2:
- What does it mean if this matches the pH?
Step 3 - HCO3-:
- What does it mean if this matches the pH?
If there is acidosis/alkalosis
7.35-7.45
It is a respiratory problem - either resp acidosis/alkalosis
It is a metabolic problem - either met acidosis/alkalosis
Interpretation:
Step 4 - PaO2:
- Under what value is classed as hypoxaemia in room air?
- FiO2 is the fraction of inspired oxygen. If they are on normal air, it would be 0.21. If on oxygen therapy, how many kPa below the FIO2 should the PaO2 be expected to be?
Step 5 - Compensation:
- What 2 parameters change to try and compensate for it?
- What is meant by partial and complete compensation?
Step 6 - Base excess:
- What parameter does base excess match?
Step 7 - Anion gap:
- What formula is used to calculate this? - think about cations (+ve’s) and anions (-ve’s)
- Why type of metabolic imbalance is it used to work out a cause for?
<8kPa
10 kPa below
====
PaCO2 and HCO3-
Partial - pH still abnormal
Complete - pH normal
Matches HCO3- but takes into account other bases
(Na + K) - (Cl +HCO3)
Metabolic acidosis - it estimates unmeasurable plasma anions
Minimising the pain of ABGs:
What can be done as an alternative?
When is the only time ABG’s can be done with anaesthetic?
VBG’s
Emergencies or if the patient is unconscious
VBG’s:
What 2 parameters are accurate on this?
What can also be measured in a VBG for sepsis or DKA?
How many kPa can you subtract from
pH
HCO3- (1 mmol/L higher than arterial)
(THIS makes sense as there is gas exchange at tissues so O2 and CO2 will not reflect what has happened in the lungs)
Lactate
You can roughly estimate the arterial PaCO2 by subtracting 0.7 kPa from the venous PvCO2.
Definitions:
What is resp failure?
What parameter dictates there is resp failure?
What is hypoxia?
What is hypoxaemia?
There are 4 types of hypoxia. Define each one?:
- Cytotoxic
- Anaemic
- Hypoxic hypoxia
- Stagnant
Low arterial O2 levels
Inadequate gas exchange resulting in hypoxia
PaO2 <8kPa - it is further subdivided by PaCO2
Inadequate tissue oxygenation
Being toxic to cells e.g. cyanide
Fewer Hb available to bind to oxygen
Ventilation problems
Shock - blood not moving
Types 1 Resp failure:
What are the following parameters like:
- PaO2
- PaCO2
Why can PaCO2 also be low?
Due to hyperventilation as compensation
Low PaO2 <8kPa
Normal PaCO2
Types 1 Resp failure:
It is caused mainly by V/Q mismatch.
- V can be due to alveolar collapse or congestion. Give examples of pathology that could cause this? - 4
- V can also be due to airway obstruction. Give examples of pathology that could cause this? - 3
- Would the V/Q ratio increase/decrease if V is affected?
- Q is affected by 1 thing, what is it?
- Would the V/Q ratio increase/decrease if Q is affected?
Type 1 resp failure could also be caused by lowered O2 uptake. What 2 things could cause this?
Why does R-L cardiac shunt cause type 1 resp failure?
V/Q ratio decreases - V gets smaller (numerator)
Alveolar collaspe or congestion:
- Pulmonary oedema
- Pneumonia
- Atelectasis (e.g. pneumothorax)
- ARDS
Airway obstruction:
- Asthma
- COPD
- Foreign body
PE
Hypoventilation or low FiO2 (high altitude)
================
A right-to-left shunt results in decreased blood flow through the pulmonary system, leading to decreased blood oxygen levels (hypoxemia).
Type 2 Resp failure:
It is defined as hypoxaemia and hypercapnia.
Above what kPa is it classed as hypercapnia?
What is the cause knowing it involves hypercapnia?
Why can pulmonary disease such as asthma, COPD and pneumonia cause this?
What drug may reduce respiratory drive?
What else could reduce respiratory drive? - 2
What does chronic retainer mean in COPD?
BASICALLY, ANYTHING THAT STOPS YOU FROM GETTING AIR IN
PaCO2 >6kPa
Due to failing respiratory efforts - muscles become tired
Sedative drugs - opioids
CNS tumour
Trauma
Long term respiratory acidosis which has been metabolically compensated leading to normal pH
Clinical features of acute hypoxia?
Clinical features of long term hypoxia:
- Hypoxia causes activation of erythropoiesis mediated by increased erythropoietin (EPO) production. What does this lead to?
- Why does it cause pulmonary HTN?
- What does this pulmonary HTN lead to in the heart?
SOB Restlessness Agitation Confusion Central cyanosis
Polycythaemia
Chronic hypoxia also can trigger inflammation and damage to the blood vessels. This can lead to scarring, which narrows and stiffens the blood vessels and increases the blood pressure even more.
Cor pulmonale
Clinical features of hypercapnia:
On the brain - 4 - why do these things happen?
What effect does it have on peripheral blood arteries, vasoconstriction or vasodilation?
How does the above then affect the HR?
What type of pulse will they have?
What sign may be seen on examination that suggests CO2 retention?
How does it affect the eyes?
Headache
Confusion
Drowsiness
Coma
{ Due to low brain pH }
Peripheral vasodilation
Tachycardia - it has to compensate for less preload
Bounding pulse - look up
Tremor/flap
Papilloedema
Management:
Type 1 resp failure:
Oxygen is given. What is the percentage range of the oxygen that is given?
When is assisted ventilation needed?
24-60%
PaO2 < 8kPa despite 60% O2
Management:
Type 2 resp failure:
Why should oxygen therapy be controlled?
What percentage of oxygen should it be started at?
After how long should the ABG be redone?
Respiratory centres are probably insensitive to CO2 and respiration is driven by hypoxia.
24%
20 minutes
Resp Acidosis:
What type of respiratory failure causes this?
What should be done for those with hypercapnia that is not improving?
Type 2 resp failure
ITU for ventilatory support
Resp alkalosis:
What causes this?
Hyperventilation
Metabolic acidosis - Anion gap:
What does the anion gap estimate?
What formula is used to calculate this? - think about cations (+ve’s) and anions (-ve’s)
The normal range if +ve. What does this mean?
Estimates the unmeasured ions (e.g. sulfates, proteins, ketoacids)
(Na + K) - (Cl +HCO3)
It means there are usually more +ve (cations) than -ve (anions) which are measurable. There shouldn’t be a gap so we know there have to be other anions making up for that gap.
Metabolic acidosis - Anion gap:
Raised anion gap acidosis:
- Why does the gap increase?
Causes:
Excess production of acids:
- What DM complication would cause this?
- What else may cause build up acids? - think sepsis
Ingestion of acids:
- What 3 things can you ingest?
Inability to clear acids:
- What will decrease your ability to clear acids?
Loss of bicarbonate:
- How can bicarb be lost?
- What is an iatrogenic cause of bicarb loss?
- What is a renal cause of bicarb loss?
HCO3- falls to compensate for acidosis and unmeasured anions associated with acid accumulate to make up for lose of HCO3-.
This is due to increased production, or reduced excretion of fixed/organic acids.
DKA
Lactic acidosis (poorly perfused tissues e.g. shock, infection, tissue ischaemia) ==== Salicylates Ethylene glycol Methanol - alcohol
Alcohol diminishes hepatic gluconeogenesis and leads to decreased insulin secretion, increased lipolysis, impaired fatty acid oxidation, and subsequent ketogenesis, causing an elevated anion gap metabolic acidosis.
Diarrhoea
High output stoma
Renal tubular necrosis - allows more bicarb to be lost as unable to reabsorb and maintain acid-base balance
Renal failure - produces urate
Metabolic acidosis - Anion gap:
Normal anion gap acidosis:
- What compensates for the loss of HCO3- making the gap normal?
Causes:
- Why does renal tubular acidosis cause this?
- What is a GI cause?
- Why does the drug acetazolamide cause this?
- Why does Addisons disease cause it?
- Why does saline excess cause this?
Chloride - look at formula
Sometimes called hyperchloremic acidosis
====
Excretion of hydrogen ions or reabsorption of filtered bicarbonate is impaired, leading to a chronic metabolic acidosis with a normal anion gap.
Diarrhoea
Inhibits the reabsorption of bicarbonate
The metabolic acidosis is due to insufficiency of aldosterone, which decreases acid secretion in the kidney.
Rapid isotonic saline infusion predictably results in hyperchloraemic acidosis. The acidosis is due to a reduction in the strong anion gap by an excessive rise in plasma chloride as well as excessive renal bicarbonate elimination.
Metabolic alkalosis:
2 mechanisms of how this happens?
Raised HCO3-
Loss of H+
Metabolic alkalosis:
H+ loss:
- GI - 1
- Why do loop and thiazide diuretics cause H+ loss?
HCO3- gain:
- What drug may someone take excessively? - think GI
Vomiting
They cause hypokalaemia:
- Due to a low extracellular potassium concentration, potassium shifts out of the cells.
- In order to maintain electrical neutrality, hydrogen shifts into the cells, raising blood pH.
Antacids
