arterial blood gases and the control of respiration Flashcards
1
Q
what does arterial blood gas testing allow us to do?
A
- assess acid base balance in blood and ventilatory status in blood
2
Q
what type of acid is CO2? 6
A
- volatile acid
- among all the acids produced in our body, over 90% is carbon dioxide
- when CO2 elimination is sufficient, retained CO2 will drive the equation to the right therefore increasing H+ and decreasing the pH
- the build-up or retention of `CO2 is respiratory acidosis
- CO2 is not an acid and acts like one
- carbonic acid is the actual acid
3
Q
what are fixed acids? 2
A
- 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)
4
Q
if we make so many acids everyday, why isn’t our pH low? 4
A
- buffers!
- bicarbonate
- proteins that circulate in the blood
- phosphates
5
Q
how do we detect an abnormal accumulation of fixed acids? 5
A
- fundamental principle of biochemistry: for electroneutrality, the number of anions= the number of cations
- cations= Na+ and K+ plus some uncounted cations
- anions= Cl- and bicarbonate plus some uncounted anions
- some cations and anions are found in small amounts and thus are not routinely measured or counted with a blood chemistry panel
- there are more uncounted anions than cations, the uncounted anions minus the uncounted cations is called the anion gap
6
Q
how do we measure the anion gap? 2
A
- (Na+ + K+)- (Cl- and bicarbonate)
- Na+ - (Cl + bicarbonate)- the normal AG with this equation is 12
7
Q
what are the main causes of AG acidosis? 8
A
GOLDMARK
- glycols
- oxoproline
- L-lactate
- D-lactate
- methanol
- aspirin
- renal failure
- ketoacidosis
8
Q
what are the 2 categories of metabolic acidosis?
A
- addition of an acid (anion gap acidosis)
- loss of bicarbonate (non anion gap acidosis) if you shift the carbonic anhydrase equation to the right due to loss of bicarbonate, it leaves us with excess proteins
9
Q
how can we lose bicarbonate? 2
A
- kidneys= failure to reabsorb bicarbonate
- gut= high output of stool means more bicarbonate loss
10
Q
what causes non-anion gap metabolic acidosis? 5
A
- loss of bicarbonate
- renal tubular acidosis (RTA) types I-III, all types result in urinary loss of bicarbonate
- GI losses
- acetazolamide= medications preventing bicarbonate reabsorption
- excessive chloride administration (intravenous fluids with NaCl)= body eliminates or stores bicarbonate
11
Q
what is on a ABG test? 6
A
- pH
- pressure of CO2
- pressure of O2
- bicarbonate level
- base excess
- saturation of oxygen
12
Q
how do we interpret ABG tests? 6
A
- examine the pH, PCO2 and HCO3-, if they are abnormal
- determine the primary process, does the patient have acidaemia, alkalemia based on the pH? if so, what type?
- calculate the anion gap if a metabolic acidosis is present
- compensating for acid base disturbances
- evaluate for a mixed disorder
- determine the cause
13
Q
what is acidosis?
A
an increase in acid (CO2 or fixed)
14
Q
what is alkalosis?
A
low of volatile acid or an increase in bicarbonate
15
Q
what is acidemia?
A
a low blood pH (<7.38)
16
Q
what is alkaemia?
A
a high blood pH (>7.42)
17
Q
how do we determine the primary process?
A
- if an acidosis is present is it respiratory (high PCO2) or metabolic (low HCO3-)
- is an alkalosis is present is it respiratory (low pCO2) or metabolic (high HCO3-)
18
Q
what are the primary disturbances and their compensatory responses?
A
- Respiratory acidosis compensatory metabolic alkalosis (to retain bicarbonate)
- Respiratory alkalosis compensatory metabolic acidosis (eliminate bicarbonate)
- Metabolic acidosis compensatory respiratory alkalosis (to eliminate more CO2)
- Metabolic alkalosis compensatory respiratory acidosis (to retain more CO2)
19
Q
what is the speed of the different compensations? 3
A
- metabolic- can take days as kidneys are slow
- respiratory =- quickly as the lungs are fast
- in either case, compensation is never 100%
20
Q
how do we evaluate a mixed disorder? 4
A
- this is when there are two or more primary acid-base disturbances
clues:
-the anion gap should be similar in value to the reduction in bicarbonate - an anion gap is present but the pH is alkalotic
-incomplete compensation for any primary process
21
Q
what is a metabolic alkalosis caused by? 2
A
vomiting
increased aldosterone
22
Q
what is respiratory acidosis caused by? 3
A
- increased dead space
- weakness
- depression of respiratory centre
23
Q
what is respiratory alkalosis caused by? 2
A
- hyperventilation due to pain or injury
- pregnancy
24
Q
what do the 2 medulla respiratory groups control?
A
- dorsal respiratory group controls quiet breathing, and triggers inspiratory impulse
- ventral respiratory group triggers inspiratory and expiratory impulses during exercise or other times of active exhaustion
25
what is the innervation of the inspiratory muscles? 4
- diaphragm= phrenic nerves, C3-C5
- external intercostal muscles= thoracic nerves, T1-11
- sternocleidomastoid= XI cranial nerve
- scalene muscles= C3-8
26
what is the innervation of the exhalation muscles? 2
- abdominal wall= T5-12
| - internal intercostal muscles= T1-12
27
what does the rhythm generator in the medulla control?
| what can modulate this? 3
- basic autonomic pattern of breathing via a group of neurons
- emotional inputs from the cerebral cortex
- lung receptors
- chemosensors
28
what are the different mechano- and irritant receptors in the lungs? 3
- C-fibre nociceptors: sensitive to a variety of inhaled or locally produced chemical mediators
- mechanically sensitive receptors: cause cough due to aspiration of foreign particles
- lungs stretch receptors: help terminate inspiration and initiate exhalation when the luges are inadequately inflated
29
what do central chemosensors detect? 3
- concentration of H+ in the CSF
- this reflects the concentration of H+ in the blood
- very sensitive
30
what do peripheral chemosensors do? 4
- carotid body: bundle of cells outside the bifurcation of the carotid arteries
- aortic body: bundle of cells within the aortic arch
- carotid and aortic bodies are back up for each other, but normally the carotid arteries do the bulk of peripheral sensing
- both respond to PaO2 and PaCO2, carotid also detect pH
31
explain chemosensors and the PCO2 and ventilatory response? 3
- 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 changed in the PaCO2, and the VE can be increased a great deal
- Opioids blunt this sensitivity; opioid ingestion is one of the most common causes of acute hypercarbic respiratory failure
32
explain peripheral chemosensors and the PO2 and ventilatory response? 3
- 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
- Compared to PaCO2, the body is much less sensitive to changes in PaO2
33
what can cause respiratory depression? 4
- opioids/narcotics
- alcohol
- anaesthesia
- cerebral diseases
34
what can respiratory depression lead to? 3
- - Hypoxaemia hypoxia
- Hypercarbia
- Acute respiratory acidosis
35
what is base excess? 5
- another way to measure the presence of a metabolic disturbance
- the dose of an acid that would be needed to return to the blood to normal H (7.4)
- normal blood=0
- increased in metabolic alkalosis
- decreased in metabolic acidosis
