Arterial blood gases Flashcards
Why do an arterial blood gas?
Acid base balance
Ventilatory status
Write the equation that shows why CO2 is a volatile acid
Why is CO2 not an acid but acts like one?
It acts like one because when CO2 goes up the pH goes down (via the production of H2CO3).
Carbonic acid is the actual acid, in terms of the substance able to donate a H+
Which acid makes up the most produced by the body?
Among all the acids produced in our body, > 90% (in terms of moles) is CO2.
What happens when CO2 elimination is insufficient?
When CO2 elimination is insufficient, retained CO2 will drive the equation to the right, thereby increasing [H+] and decreasing the pH.
What is respiratory acidosis?
CO2 is called a volatile acid, and the build up or “retention” of CO2 is called RESPIRATORY ACIDOSIS.
What are fixed acids?
“Fixed” or non-volatile acids are products from the oxidation of dietary substrates.
Have to be physically eliminated from the body, typically via the kidneys or liver (where lactate is converted to glucose)
If we make so many acids (volatile + fixed) every day, why isn’t our pH low?
Buffers
3 most important buffers in body -
- Bicarbonate
- Proteins circulating in the blood
- Phosphates
What is the pH of our blood?
7.4
How do the kidneys eliminate fixed acid?
How do we detect an abnormal accumulation of fixed acids?
The anion gap
What does the anion gap measure?
Fundamental principle of biochemistry: for electroneutrality, number of cations = number of anions
What ions are included in the anion gap?
Na + K = 144 mEq/L
Cl + bicarb = 128 mEq/L
There are more uncounted anions than uncounted cations. The uncounted anions minus the uncounted cations is called the ANION GAP.
Which of these is the ion gap?
How is the anion gap calculated?
Two equation options, but the second is most commonly used:
- Anion gap = (Na + K) – (Cl + bicarbonate)
- Anion gap = Na – (Cl + bicarbonate)
Normal AG with this equation = 12
K+ concentration so small it’s not always included in calculation.
What are cations?
Cations = Na+ and K+ plus some uncounted cations
What are anions?
Anions = Cl- and bicarbonate plus some uncounted anions
What is the acronym for the main causes of anion gap acidosis?
What are the most common causes?
- Glycols (ethylene and propylene)
- Oxoproline
•L-lactate
- D-lactate
- Methanol
- Aspirin
•Renal failure
•Ketoacidosis
“GOLD MARK”
Why does the anion gap happen?
What are the 2 catagories of metabolic acidosis?
- Addition of acid (anion gap acidosis)
- Loss of bicarbonate (non anion gap acidosis)
Interpret each anion gap result
Both metabolic acidosis -
- Addition of acid (anion gap acidosis)
- Loss of bicarbonate (non anion gap acidosis)
Where can loss of bicarbonate occur?
In kidney’s or in the pancreatic ducts in the gut
What are the 4 ways loss of bicarbonate can occur?
- Renal tubular acidosis (RTA) - all types result in urinary loss of bicarbonate and a hyperchloremic acidosis
- GI losses
- Acetazolamide
- Excessive chloride administration (intravenous fluids with NaCl)
What is the 6 step approach to analysing an ABG?
- Step 1: Examine the pH, PCO2 and HCO3 –. If they are abnormal:
- Step 2: Determine the primary process. Does the patient have an acidaemia or alkalaemia based on the pH? If so, what type is it?
- Step 3: If a metabolic acidosis is present, calculate the anion gap
- Step 4: Identify the compensatory process
- Step 5: Determine if a mixed acid-base disorder is present
- Step 6: Determine the cause
How would you carry out step 1 - examine the pH, PCO2 and HCO3?
How would you carry out step 2 - determine the primary process?
If an acidosis is present, determine whether it is a:
Respiratory acidosis: high PCO2 (> 5.9 kPa)
Metabolic acidosis: low HCO3- (< 23 mEq/L)
If an alkalosis is present, determine whether it is a:
Respiratory alkalosis: low PCO2 (< 4.8 kPa)
Metabolic alkalosis: high HCO3- (> 30 mEq/L)
Define acidosis
an increase in acid (CO2 or fixed)
Define alkalosis
Alkalosis: low of volatile acid or an increase in bicarbonate
Define acidaemia
Acidaemia: a low blood pH (< 7.38) due to an acidosis
Define alkalaemia
Alkalaemia: a high blood pH (> 7.42) due to an alkalosis
How would you carry out step 3 - calculate the anion gap?
Anion Gap = Na+ – (Cl- + HCO3-)
How would you carry out step 4 - Identify the compensatory process?
How would you carry out Step 5: Determine if a mixed acid-base disorder is present?
Clues that a mixed disorder exists:
- The anion gap should be similar in value to the reduction in bicarbonate
- An anion gap is present but the pH is alkalaemic
- Incomplete compensation for any primary process. Reminder, “complete (ie full) compensation” does not result in a normal pH, but it gets close.
What is a mixed disorder?
Mixed disorder: two or more primary acid-base disturbances
A patient with low blood pressure (due to infection and sepsis) produces lactic acid and develops an anion gap acidosis, while the vigorous NaCL fluid administration to increase blood pressure creates a non-anion gap acidosis.
What acid-base disturbance does this patient have?
So there are two types of metabolic acidosis.
Mixed disorder
How would you carry out step 6 - determine the cause?
Metabolic Acidosis
- Anion gap metabolic acidosis: GOLD MARK
- Non-anion gap metabolic acidosis: renal tubular acidosis (RTA), GI loss
Metabolic Alkalosis
-Vomiting; increased aldosterone (some medications, ‘contraction alkalosis’)
Respiratory Acidosis (Retention of CO2)
-Increased dead space (emphysema); weakness; depression of respiratory centre
Respiratory Alkalosis
-Hyperventilation due to pain or anxiety; pregnancy
What is the role of pons in respiratory control?
Pons (with 2 nuclei) not essential for respiration but exerts fine control over medullary neurons
What is the respiratory centre?
Pons and medulla
Dorsal Respiratory Group: control quiet breathing, trigger inspiratory impulses
Ventral Respiratory Group: trigger inspiratory and expiratory impulses during exercise or other times of active exhalation
Complete the diagram on the respiratory centre
What does the respiratory centre control?
The respiratory centre controls inspiratory and exhalation efforts
How does the respiratory centre innervate inspiration?
Efferent nerves -> inspiratory muscles
- Diaphragm(s): phrenic nerves, C3-C5
- External intercostal muscles: thoracic nerves T1-T11
- Sternocleidomastoid: XI cranial nerve
- Scalene muscles: C3-C8
How does the respiratory centre innervate expiration?
Efferent nerves -> muscles of exhalation
- Abdominal wall: T5-T12
- Internal intercostal muscles: T1-T12
Which inputs alter the outputs of the respiratory centre?
Inputs from various sources can modify or modulate this rhythm:
- Emotional inputs from the cerebral cortex
- Lung receptors
- Chemosensors (central and peripheral)
What is the role of the rhythm generator?
Rhythm generator in the medulla controls the basic, automatic pattern of breathing via a group of neurons concentrated in the Pre-Botzinger complex.
Where on this diagram is the group of nerves controlled by the rhythm generator?
Rhythm generator in the medulla controls the basic, automatic pattern of breathing via a group of neurons concentrated in the Pre-Botzinger complex.
What are the 3 Mechano- and irritant receptors in the lungs?
- C-fiber nociceptors: sensitive to a variety of inhaled or locally produced chemical mediators (egs. bradykinin, nicotine, methacholine, histamine, etc)
- Mechanically sensitive receptors (sometimes called “cough receptors”): cause cough due to aspiration of foreign particles
- Lung stretch receptors: help terminate inspiration and initiate exhalation when the lungs are adequately inflated
Where do the neuronal projections from Mechano- and irritant receptors cells in the lungs travel to?
The neuronal projections from cells with these receptors travel along vagal nerve afferent fibres to the respiratory centre.
Where are central chemoreceptors located?
On medulla oblongata
How do central chemoreceptors work?
Detect [H+] in the CSF
[H+] in the CSF reflects blood [H+], PaCO2 and CSF CO2 but these are NOT directly sensed by central chemoreceptors
Which chemoreceptors are very sensitive?
Central chemoreceptors
Complete the diagram on peripheral chemoreceptors
Where are peripheral chemoreceptors located?
- Carotid body: bundle of cells outside the bifurcation of carotid arteries
- Aortic body: bundle of cells within aortic arch
How do peripheral chemoreceptors work?
- Carotid and aortic bodies are back up for each other, but normally the carotid bodies do bulk of peripheral sensing
- Both respond to PaO2 (hypoxaemia) and PaCO2. Carotid bodies also detect pH.
What happens when Paco2 builds up?
The body (via increased output from the respiratory centre) increases ventilation if PaCO2 builds up in the blood.
The body is very sensitive to even small changes in the PaCO2, and the VE can be increased a great deal.
What is the effect of opioids?
Opioids blunt sensitivity to PaCO2; opioid ingestion is one of the most common causes of acute hypercarbic respiratory failure.
What happens when there is a drop in Pa02?
Normally: an increase in ventilation occurs (only) when PaO2 drops significantly
However: sensitivity to PaO2 is altered by PaCO2: more sensitive to hypoxaemia in setting of hypercarbia
Does the body respond more sensativley to increase in PaCO2 or decrease in PaO2?
PaCO2
This is due to the dual role of CO2 as a by-product of respiration and as an acid; the body is highly engineered to keep the blood pH constant
What are the causes of respiratory depression?
- Opioids / narcotics (heroin, legal prescription narcotics)
- Alcohol
- Anaesthesia and other sedatives
- Cerebral diseases: ex. cerebral vascular accident
What are the ABG results in respiratory depression?
Respiratory depression leads to:
Hypoxaemic hypoxia
Hypercarbia
Acute respiratory acidosis
What causes loss of a robust respiratory drive?
The respiratory centre becomes less sensitive to chronic elevations in the PaCO2, and respiratory responses become blunted.
“CO2-insensitivity” usually arises from chronic CO2 retention.
What are the ABG results in loss of robust respiratory drive?
This will result in:
- Chronic respiratory acidosis
- Metabolic compensation
- Hypoxaemia due to hypoventilation*
What is the definition of hypoventilation?
Hypoventilation is not defined by VE below a set threshold, but rather is defined as ventilation which is insufficient to maintain a normal PaCO2 and acid base status.
What is base excess?
Base excess is another way to measure the presence of a metabolic disturbance. Historically used term, so you should be aware of it, but clinically not often used nowadays.
How is base excess calculated?
- Base excess = the dose of an acid that would be needed to return blood to normal pH (7.40) under standard conditions (37C and a PCO2 of 5.3 kPa). The base excess is normal blood is about 0. The base excess is increased in a metabolic alkalosis. The base excess is decreased in a metabolic acidosis.
- Somewhat confusingly, a metabolic acidosis is described as a negative base excess rather than a base deficit.
