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103-theme 4 > arterial blood gases and the control of respiration > Flashcards

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
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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
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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)
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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
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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
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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

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7
Q

what are the main causes of AG acidosis? 8

A

GOLDMARK

  • glycols
  • oxoproline
  • L-lactate
  • D-lactate
  • methanol
  • aspirin
  • renal failure
  • ketoacidosis
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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
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9
Q

how can we lose bicarbonate? 2

A
  • kidneys= failure to reabsorb bicarbonate

- gut= high output of stool means more bicarbonate loss

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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
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11
Q

what is on a ABG test? 6

A
  • pH
  • pressure of CO2
  • pressure of O2
  • bicarbonate level
  • base excess
  • saturation of oxygen
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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
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13
Q

what is acidosis?

A

an increase in acid (CO2 or fixed)

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14
Q

what is alkalosis?

A

low of volatile acid or an increase in bicarbonate

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15
Q

what is acidemia?

A

a low blood pH (<7.38)

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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
Q

what is the innervation of the inspiratory muscles? 4

A
  • diaphragm= phrenic nerves, C3-C5
  • external intercostal muscles= thoracic nerves, T1-11
  • sternocleidomastoid= XI cranial nerve
  • scalene muscles= C3-8
26
Q

what is the innervation of the exhalation muscles? 2

A
  • abdominal wall= T5-12

- internal intercostal muscles= T1-12

27
Q

what does the rhythm generator in the medulla control?

what can modulate this? 3

A
  • basic autonomic pattern of breathing via a group of neurons
  • emotional inputs from the cerebral cortex
  • lung receptors
  • chemosensors
28
Q

what are the different mechano- and irritant receptors in the lungs? 3

A
  • 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
Q

what do central chemosensors detect? 3

A
  • concentration of H+ in the CSF
  • this reflects the concentration of H+ in the blood
  • very sensitive
30
Q

what do peripheral chemosensors do? 4

A
  • 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
Q

explain chemosensors and the PCO2 and ventilatory response? 3

A
  • 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
Q

explain peripheral chemosensors and the PO2 and ventilatory response? 3

A
  • 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
Q

what can cause respiratory depression? 4

A
  • opioids/narcotics
  • alcohol
  • anaesthesia
  • cerebral diseases
34
Q

what can respiratory depression lead to? 3

A
    • Hypoxaemia hypoxia
  • Hypercarbia
  • Acute respiratory acidosis
35
Q

what is base excess? 5

A
  • 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

103-theme 4 (19 decks)

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