Theme 4: Lecture 5 - Arterial blood gases, control of respiration and respiratory adaptation Flashcards
Reasons to do an ABG
- To get the acid-base balance of the blood
- To get the ventilatory status
How does CO2 act like an acid even though it isn’t one
It acts like one because when CO2 goes up the pH goes down (via the production of H2CO3).
What is the acid that CO2 turns into
- Carbonic acid
- H2CO3
Respiratory acidosis
A build up or retention of CO2 (the only way to eliminate CO2 from the body is by breathing)
What happens when CO2 elimination insufficient
Retained CO2 will drive the equation to the right, thereby increasing [H+] and decreasing the pH.
Equation for how CO2 makes acid
CO2 + H2O combine reversibly to make H2CO3 dissociates reversibly to make HCO3- + H+
Is CO2 a fixed or volatile acid
Volatile acid
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 in our body every day, why isn’t our pH low
Buffers
What are the 3 most important buffers in our body
- carbonic acid bicarbonate buffer system
- phosphate buffer system (can accept or give off 3 protons)
- protein buffer system (proteins that circulate in the blood and have a histamine residue can combine with or eliminate a proton)
The anion gap
- How we detect an abnormal accumulation of fixed acids
- There are more uncounted anions than uncounted cations. The uncounted anions minus the uncounted cations is called the ANION GAP.
What are the 2 equations for measuring the anion gap
Anion gap = (Na + K) - (Cl + bicarbonate)
Anion gap = Na - (Cl + bicarbonate)
The second equation is more commonly used
What is a normal anion gap with this equation: Anion gap = Na - (Cl + bicarbonate)
12mEq/L
What are the main causes for anion gap acidosis
-Glycols (ethylene and propylene)
-Oxoproline
-L-lactate
-D-lactate
-Methanol
-Aspirin
-Renal failure
-Ketoacidosis
“GOLD MARK”
What causes the anion gap to increase
- An increase in fixed acids
- The conjugate base of fixed acids are extra anions (negative ions), and when present will increase the anion gap.
- Overall, anions will still equal overall number of cations in the blood
What are the 2 categories of metabolic acidosis
- Addition of acid (anion gap acidosis)
- Loss of bicarbonate (non anion gap acidosis)
How are fixed acids eliminated by the kidneys
- CO2 diffuses into the cells of the late distal and collecting tubes
- The combination of CO2 with H2O produces HCO3- and H+
- H+ is actively pumped out of the cell into the tubular lumen (where urine is formed)
- Cl- diffuses after it so that there is electroneutrality
Causes of non anion gap acidosis aka loss of bicarbonate
- Renal tubular acidosis (RTA) (Types I-III: year 2 material, All types result in urinary loss of bicarbonate and a hyperchloremic acidosis)
- GI losses
- Acetazolamide
- Excessive chloride administration (intravenous fluids with NaCl)
How to interpret 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? - Respiratory or metabolic
- 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
Acidosis
an increase in acid (CO2 or fixed)
Alkalosis
low of volatile acid or an increase in bicarbonate
Acidaemia
a low blood pH (< 7.38) due to an acidosis
Alkalaemia
a high blood pH (> 7.42) due to an alkalosis
Markers of respiratory acidosis
- Low pH
- High PCO2
Markers of metabolic acidosis
- Low pH
- Low HCO3-
Markers of respiratory alkalosis
- High pH
- Low PCO2
Markers of metabolic alkalosis
- High pH
- High HCO3-
What would a normal pH mean in an ABG
- There’s no abnormality
- There’s a mixed acid base disorder
What is the compensatory response if the primary disturbance is respiratory acidosis
Compensatory metabolic alkalosis (ie retain HCO3-)
What is the compensatory response if the primary disturbance is respiratory alkalosis
Compensatory metabolic acidosis (ie eliminate HCO3-)
What is the compensatory response if the primary disturbance is metabolic acidosis
Compensatory respiratory alkalosis (ie eliminate more CO2)
What is the compensatory response if the primary disturbance is metabolic alkalosis
Compensatory respiratory acidosis (ie retain more CO2)
Which is quicker, respiratory or metabolic compensation
Respiratory compensation, metabolic compensation can take days
Clues that a mixed disorder exist
- 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 are the main causes for metabolic acidosis
- Anion gap metabolic acidosis - GOLDMARK
- Non anion gap metabolic acidosis - Renal tubular acidosis (RTA), GI losses ect
What are the main causes for metabolic alkalosis
- Vomiting
- Increased aldosterone
- (some medications, ‘contraction alkalosis’ - increase in pH as a result of fluid losses)
What are the main causes of respiratory acidosis (retention of CO2)
- Increased dead space (emphysema)
- weakness
- depression of respiratory centre
What are the main causes of respiratory alkalosis
- Hyperventilation due to pain of anxiety
- Pregnancy
What makes up the respiratory centre
The pons and medulla
Where are the pons and medulla located
- In the hindbrain
- The pons is superior to the medulla
What makes up the pons (pontine respiratory group
- Pneumotaxic center
- Apneustic center
What makes up the medulla
- Ventral respiratory group
- Dorsal respiratory group
What does the dorsal respiratory group control
control quiet breathing, trigger inspiratory impulses
What does the ventral respiratory group control
trigger inspiratory and expiratory impulses during exercise or other times of active exhalation
What does the pons do
not essential for respiration but exerts fine control over medullary neurons
What does the respiratory centre do
controls inspiratory and exhalation efforts
What are the inspiratory muscles
- Diaphragm
- External intercostal muscles
- Sternocleidomastoid
- Scalene muscles
What are efferent nerves
These are motor neurons carrying neural impulses away from the central nervous system and toward muscles to cause movement. Efferent neurons send signals from the brain to the muscles, glands, and organs of the body in response to sensory input
Which nerves innervate the diaphragm
Phrenic nerves, originate from C3,4,5
Which nerves innervate the external intercostal muscles
Thoracic nerves, originate from T1-T11
Which nerve innervates the sternocleidomastoid
XI cranial nerve
Which nerves innervate the scalene muscles
C3-8
What are the muscles of expiration
- Abdominal wall
- Internal intercostal muscles
What is the innervation of the abdominal wall
T5-12
What is the innervation of the internal intercostal muscles
T1-T12
Pre-Botzinger complex
- Rhythm generator in the medulla
- controls the basic, automatic pattern of breathing
- Makes breathing smooth so that you don’t normally notice it
What inputs can modify the breathing rhythm
- Emotional inputs from the cerebral cortex
- Lung receptors
- Chemosensors (central and peripheral)
C-fiber noniceptors
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
How does information about stimuli in the lungs reach the brain
The neuronal projections from cells with these receptors travel along vagal nerve afferent fibres to the respiratory centre.
Central chemoreceptors (chemosensors)
- 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
- Are very sensitive
Where are the peripheral chemoreceptors (chemosensors)
In the carotid body and aortic body
What is the carotid body
Bundle of chemoreceptor cells outside the bifurcation of the carotid arteries
What is aortic body
Bundle of chemoreceptor cells within the aortic arch
What do the peripheral chemoreceptors detect
- Both aortic and carotid bodies respond to PaO2 (hypoxaemia) and PaCO2.
- Carotid bodies also detect pH.
The effect of opioids on peripheral chemoreceptors
- Opioids the blunt the sensitivity of chemoreceptors to PCO2
- Opioid ingestion is one of the most common causes of acute hypercarbic respiratory failure.
The peripheral chemoreceptors and ventilatory response to PCO2
- 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 ventilation can be increased a great deal.
The peripheral receptors and ventilatory response to PO2
- 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
- Main point: compared to PaCO2 the body is much less sensitive to changes in PaO2
- 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
Causes of respiratory depression
- Opioids / narcotics (heroin, legal prescription narcotics)
- Alcohol
- Anaesthesia and other sedatives
- Cerebral diseases: ex. cerebral vascular accident (aka a stroke)
What does respiratory depression lead to
- Hypoxaemic hypoxia
- Hypercarbia
- Acute respiratory acidosis
What is a loss of robust respiratory drive
- The respiratory centre becomes less sensitive to chronic elevations in the PaCO2, and respiratory responses become blunted
- Occurs in patients with COPD
What will a loss of robust respiratory drive lead to
- Chronic respiratory acidosis
- Metabolic compensation
- Hypoxaemia due to hypoventilation
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.
- Base excess = the dose of an acid that would be needed to return bloodto 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.
