ABGs, control of respiration and respiratory adaption Flashcards by Rebecca Webster

what is arterial blood gas testing

Main reason for it is to assess acid base balance and ventilatory status

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how is CO2 a volatile acid

Reacts with water to produce carbonic acid
>90% (in terms of moles) of acid in body is C02
Retention of CO2 is respiratory acidosis
Retained CO2 will drive equation to the right (higher proton and lower pH)

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What are fixed acids

Fixed or non volatile acids are products from oxidation of dietary substrates
Have to be physically eliminated from the body via kidneys or liver (lactate converted to glucose)

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what do buffers do in the body

Buffers prevent pH dropping too low when we make acids everyday (blood pH is higher than pure water)

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what buffers are in the body

Bicarbonate
Blood proteins
Phosphates

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how do we detect abnormal accumulation of fixed acids

Electroneutrality, same number of cations and anions
Cations = Na and K, some uncounted ions
Anions= Cl and bicarbonate, some uncounted

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what are uncounted ions

Some cations and anions are found in small amounts, are not routinely measured or counted in blood chemistry panel
Na+K=144mEq/l
Cl+Bicarb=128mEq/l

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what is an anion gap

More uncounted anions than cations (uncounted anions – cations= anion gap)
AG=(Na+K)-(Cl+bicarb)
Or no K as minimal
Normal gap is 12

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what are the main causes of AG acidosis

Glycols (ethylene and propylene)
Oxoproline
L-lactate Common
D-lactate
Methanol 
Aspirin 
Renal Failure Common
Ketoacidosis Common
GOLD MARK

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What 2 categories of metabolic acidosis

Addition of acid (AG acidosis)

Loss of bicarbonate (non-anion gap acidosis) aka hypercholraemic

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how is bicarbonate lost in metabolic acidosis

Loss of bicarb in kidneys or gut
Kidneys unable to remove acid from blood (decreased reabsorption or production)
Pancreas secretes bicarb to balance out gut pH (loss by diahorrea)

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what are types/causes of metabolic acidosis

Renal tubular acidosis
Type I-III
All types result in urinary loss of bicarb and hyperchloremic acidosis
Gi losses
Acetazolamide
Excessive chloride administration (intravenous fluids with NaCl)

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how are Acid base disorders evaluated via ABG testing

pH
PCO2
PO2
HCO3
BEecf base excess
sO2* oxygen saturation

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how can an ABG be interpreted

Examine PH, PCO2 and HCO3, if abnormal then
Determine the primary process, acidaemia or alkalaemia based on pH
If metabolic acidosis calculate anion gap
Identify the compensatory process
Determine if a mixed acid-base disorder is present
Determine the cause

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what is acidosis and alkalosis

acidosis- increase in acid (CO2 or fixed)

alkalosis- low volatile acid or an increase in bicarb

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what is acidaemia and alkalaemia

acidaemia - low blood pH

alkalaemia - high blood pH

how can the primary process be determined

If acidosis present 
respiratory acidosis - high PCO2
Metabolic acidosis - low HCO3
If alkalosis present 
Respiratory alkalosis low PCO2
metabolic alkalosis high HCO3

How can the compensatory process identified

Primary disturbance – compensatory response
Resp acidosis – comp metabolic alkalosis (ie retain HCO3)
Resp alkalosis – comp metabolic acidosis (ie eliminate HCO3)
Metabolic acidosis – comp resp alkalosis (ie eliminate more CO2)
MetaboLic alkalosis – compensatory resp acidosis (ie retain more CO2)

how can compensation vary

Metabolic – kidneys slow (hours to days)
Lungs- respiratory fast (seconds)
Neither case is compensation 100%
Full compensation reaching 7.35-7.45

how can a mixed disorder be evaluated

Anion gap similar in value to the reduction in bicarb
Anion gap is present but pH is alkalaemic
Incomplete compensation for any primary process

what is a mixed disorder

Mixed disorder- two or more primary acid-base disturbances

how is the cause determined

Metabolic acidosis (anion gap GOLD MARK, non AG – renal tubular acidosis, GI loss)
Metabolic alkalosis (vomiting, increased aldosterone (some medications – contraction alkalosis))
Respiratory acidosis (increased dead space (emphysema, weakness, depression of respiratory centre)
Respiratory alkalosis (hyperventilation due to pain or anxiety, pregnancy)

what are pons

Part of the brainstem (with 2 nuclei) not essential for respiration but exert fine control over medullary neurons

what makes up the respiratory centre

Dorsal respiratory group control quiet breathing, trigger inspiratory muscles
Ventral respiratory group trigger and inspiratory and expiratory impulses during exercise or other times of active exhalation

what are the inspiratory muscles and their innervations

``` Efferent nerves -> inspiratory muscles Diaphragm(s): phrenic nerves, C3-5 External intercostal muscles: thoracic nerves T1-T11 Sternocleidomastoid: XI cranial nerve Scalene muscles: C3-8 ```

what are the exhalatory muscles and their innervations

Efferent nerves-> muscles of exhalation Abdominal Wall: T5-T12 Internal intercostal muscles: T1-T12

how do inputs alter the outputs of the RC

can modify or modulate this rhythm (emotional inputs from cerebral cortex, lung receptors, chemosensors – central and peripheral)

what does the rhythm generator do

Rhythm generator in the medulla controls basic autonomic pattern of breathing via a group of neurons concentrated in the Pre-Botzinger complex

what are the mechano and irritant receptors in the lungs

1 C-fiber nociceptors: sensitive to a variety of inhaled or locally produced chemical mediators 2 mechanically sensitive receptors (aka cough receptors) cause a cough due to aspiration of foreign particles 3 Lung stretch receptors help terminate inspiration and initiate exhalation when lungs adequately inflated The neuronal projections from cells with these receptors travel along vagal nerve afferent fibres to RC

what are chemosensors

Detect H+ in the CSF, very sensitive (increase ventilation is too high) Reflect blood H+, PO2 and CSF CO2 but not directly sensed by central chemoreceptors

what are peripheral chemosensors

Carotid body: bundle of cells outside the bifurcation of the carotid arteries Aortic Arch: bundle of cells in aortic arch Back up each other, normally carotid body does bulk of sensing Both respond to PaO2 (hypoxaemia) and PaCO2, carotid bodies also detect pH

how does PCO2 affect ventilatory response

Body (via inc output from RC) increases ventilation if PaC02 builds up in blood Body sensitive to small changes in PaCO2 and VE can increase a great deal

what do opioids do to ventilatory

Opioids blunt sensitivity, opioid ingestion one of most common causes of acute hypercarbic respiratory failure

what does P02 do to ventilatory response

Normally an increase in ventilation occurs (only) when PaO2 drops significantly Sensitivity to PaO2 is altered by PaCO2, more sensitive to hypoxaemia in hypercarbia (body less sensitive to PaO2 changes) Due to role of CO2 as a by product of respiration and as an acid, body highly engineered to keep blood pH constant

what causes respiratory depression

``` Opioids/ narcotics Alcohol Anasthesia and other sedatives Cerebral diseases eg stroke Leads to Hypoxaemic hypoxia Hypercarbia Acute respiratory acidosis ```

how does loss of robust respiratory drive affect ventilatory response

Poor ventilation, lots of dead spaces eg COPD RC becomes less sensitive to chronic elevations in PaCO2 and resp response is blunted Results in Chronic respiratory acidosis Metabolic compensation Hypoxaemia due to hypoventilation

how are blood gases done in clinical practice

same as AGB interpretation +Consider PaO2 Results written pH/PaCO2/PaO2/Bicarb Interpret compensation/primary disturbance/oxygenation

what is base excess

Another way to measure presence of metabolic disturbance | Dose of acid to return blood to normal pH