Arterial blood gas (ABG analysis) Flashcards

1
Q

The respiratory system has 2 main components

A

ventilatory air pump

Gas exchange surface

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2
Q

Effective gas exchange requires

A

adequate and matching flow of gas and perfusion of respiratory tissues

V/Q matching

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3
Q

Basic respiratory mechanism

A

Concs of gases are refreshed on a breath-by-breath basis

Narrow diffusion distance between the alveoli and pulmonary caps

the gap is filled by pulmonary interstitial fluid

02 in Co2 out

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4
Q

Physiological shunting (V/Q matching)

A

“blood passes lungs without contributing to has exchange”

Low V/Q ratio

Ventilation to one lung or area is decreased or absent

That area is still perfused as body hasnt adapted yet = no gas exchange

Oxygenated and non-oxygentaed blood mixes

e.g., obstruction or ashma attack

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5
Q

Physiological deadspace (V/Q mismatch)

A

High V/Q ratio

Lung is ventilated but not perfused

No deoxygenated blood mixes

e.g., pulmonary emboli

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6
Q

VQ matching

A

Compensatory mechanisms to ensure that blood flow matches ventilation

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7
Q

hypoxic vasoconstriction-

A

hypoxic vasoconstriction-when oxygen levels drop in a lung, the arterioles that supply that area will vasoconstrict, reeucing blood flow to the area that is not perfused. If CO remains static, more BF goes to the areas that are ventilated.

Similar but less effective method for areas that aren’t perfused. Bronchoconstriction and reduced surfactant secretion helps divert air to well-perfused alveoli.

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8
Q

Respiratory failure

A

“localised mismatching of V/Q ratio”

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9
Q

type 1 respiratory failure

A

pO2 low and pCO2 normal

hypoxaemic

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10
Q

type 2 respiratory failure

A

global reduction in flow of either air to alveoli or blood to pulmonary caps

pO2 low and pC02 high

hypercapnic

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11
Q

Acid base balance

A

↑CO2 + H2O ↔︎ H2CO3 ↔︎ HCO3 + ↑H+

Therefore if you increase pCO2 or decrease HCO3- you decrease arterial pH

pH is proportional to 6.1+log x conc of (HCO3-)/ 0.03 x pCO2

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12
Q

What does the body do in response to chornic acidosis?

A

Liver

  • decrease urea production
  • increase production of glutamine

Kidney

  • increase glutamine dehydrogenase + PEPCK to catalyse the breakdown of glutamine into NH4+ (ammonium) and HCO3- in the proximal tubule
  • Ammonium is then released through micturition
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13
Q

What does the body do in response to chronic respiratory alkalosis?

A

Kidney

  • Decreases plasma [HCO3-]
  • Increase the number and activity of type-B intercalated cells in the collecting ducts (they secrete HCO3- from the blood into the tubule lumen helping to increase conc in the final urine therefore lowering the blood conc and pH
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14
Q

Metabiolic factors can affect acid/base balance and therefore blood gases (4)

A

Alkaline tide

kidney failure

ketone bodies

vomiting

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15
Q

Alkaline tide

A

when bicarbonate is produced in the intestine is not absorbed by the gut. bicarb bypassses the reabsorption mechanisms

e.g., bowel obstruction

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16
Q

kidney failure

A

reduced excretion of uric acid leading to metabolic acidosis

17
Q

ketone bodies

A

in starvation, diabetic ketoacidosis, sepsis or severe exercise can result in greater lactic acid production

18
Q

vomiting

A

loss of H+ from vomiting

19
Q

Kussmaul’s breathing

A

Breathing patterns can affect acid/base balance

When we have metabolic acidosis due to:

K= Ketones (diabetic ketoacidosis)

U= Uremia

S= Sepsis

S= salicylates (aspirin)

M= menthanol

A= Aldehydes

U

L= lactic acid

breathing pattern changes to kussmaul’s breathing, deep sighing respiration pattern where we increase tidal volume, allowing us to breathe out more CO2

20
Q

Lungs excrete excess non volatile gases in the form of

A

CO2

21
Q

Reflex increase in ventilation rate

A
  1. Increase firing of chemoreceptors
  2. detected peripherally and centrally
  3. transmitted to the Central Pattern Generator in the brainstem
  4. Increased and more frequent phrenic and intercostal nerve activity
  5. more forceful and drequent contraction of diaphragm and intercostals
  6. increase rate and depth of breathing (increase V rate)
22
Q

Respiratory compensation for chronic metabolic acidosis

A

decrease pH

Increased firing of peripheral chemoreceptors

transmitted APs via the glossopharyngeal and vagus nerves to

Central Pattern Generator in Brainstem

Increased more frequent phrenic and intercostal nerve activity

Increased ventilation rate

increased exhalation of CO2

decreased PCO2 and increased pH

23
Q

Arterial blood gas

A

take arterial blood sample (usually from radial artery)

send to specific analyser

electrodes for arterial pH, O2 and CO2

gives info on pH, pCO2, Bicarbonate, pO2 and (base excess?)

Go though steps O, A, B, C

24
Q

Step O

A

Normal pO2= 13.3 kPa

  • <10 suggests respiratory problem
  • >10 but pH is normal suggets a metabolic problem

If the patient is breathing artificial oxygen concentrations then it should

Where pO2 is less than 10 we should look at:

  • Normal/ low (type 1 RF) caused by V/Q mismatch
  • High, then (type II RF) due to conditions that reduce our tidal volume
25
Q

Normal ranges for ABG

A

O2- 13.3 kPa (<10 resp problem // >10 but pH normal is metabolic problem)

pH- 7.35-7.45

CO2- <4.7 is alkalitic >6.00 is acidic

HCO3- <20mM is acidotic >28 is alkolitic

26
Q

Step A

A

Acidosis or alkalosis? (look at pH)

normally under a very tight control of 7.35-7.45

  • <7.35 = too acidic = acidosis
  • >7.45 = to
  • o basic = alkalosis

NB- type 1 RF or mixed/ base disorder may be balancing each other out for a patient to have a normal pH. e.g., patient with ketoacidosis who is vomiting.

27
Q

Step B

A

Buffers (CO2/HCO3-)

Acidotic blood- look at CO2

  • CO2 high - resp failure - resp failure
  • CO2 normal/ low - bicarb low - metabolic acidosis

Alkalotic blood

  • CO2 too low- resp. alkalosis - breathing too much- blow off too much CO2
  • Bicarb levels too high - metabolic alkalosis

28
Q

Step C- Chronic/ compensated

A

Identify how acute the acid/base disturbance is by whether the body has started its compensatory mechanisms yet

Resp. acidosis- Bicarb level – body tries to produce more bicarb

Met. acidosis- PCO2 level –Falls as we start to breathe more

Resp. alkalosis- Bicarb level –Falls to balance poeple breathing too much

Met. Alkalosis- PCO2 –risen to compensate for too much bicarb

29
Q

Base excess

A

useful in conjunction with [HC03-] to confirm any component of an acid-base disorder

“the amount of strong acid that has to be added to fully oxygenate blood held at body temperature and normal PCO2 to return ut to a pH of 7.40”

negative value indicates a base deficit

-2 t0 +2 is normal range

+2 is metabolic alkalosis

-2 is metabolic acidosis

30
Q

Example 1

Patient is brought into casualty department semi-conscious. Patient was found at home with an empty bottle of sleeping pills nearby.

pH 7.16 (low 7.16< 7.35)

PCO2 10.7 (high 10>6)

Bic 28 (normal)

pO2 5.3 (low 5.3< 10)

Base excess -0.4 (normal)

A

Step O- O2 low

Step A- acidosis

Step B- high CO2 + low O2 (resp. acidosis)

Step C- bicarb is normal (acute resp.acidosis)

Presentation fits with clinical history – reduced consciousness causes a reduction in tidal volume

Alternatively:

31
Q

Example 2

Patient suffers catastrophic stroke and following the event was seen to be irregular and inadequate. Patient was intubated and ventilated with an inspired oxygen concentration of 40%.

pH 7.63 High

pCO2 low

Bic 20 mmol.L-1 normal

pO2 35.3 high

base excess normal

A

O- high

A- alkalosis

B- CO2 low Bic low? (respiratory alkalosis)

C- Bicarb starting to get low- beginings of compensation?

Patient is being overventilated. Setting on ventilator needs to be changed.

Alternatively it is someone who is hyperventilating.

32
Q

Example 3

Patient with abdominal pain due to a duodenal ulcer has been admitted to the medical ward with persistent vomiting. He was also taking large quantities of sodium bicarbonate to ease the pain.

pH- 7.54 High

pCO2- 6.7 High

Bic- 33 mmol high

pO2- 11.1 High

Base excess- 17.6 (large amounts of acid had to be added - excess bicarb)

A

O- high

A- high- alkalosis

B- CO2 high Bic high (metabolic alkalosis)

C- starting to see a degree of compensation as CO2 Is starting to rise

Patient has been vomiting too much acid out- not enough left to balance base

33
Q

Example 4-

A 52-year-old man was admitted unconscious to casualty. He was a known diabetic on daily insulin. One week ago he had developed a chest infection. He stayed at home and because he stopped eating he stopped his insulin. Over the preceding days he had become increasingly drowsy and in the morning of admission he was unrousable.

pH 7.19

PCO2: 4.0

bic: 11.1

pO2; 13.3

Base excess; 15.3

A

O; normal

A; acidic

B; low + base excess suggesting too much acid most likley metabolic

C; CO2 is starting to fall - most likley respiratory response to acidosis- KUSSMAUL breathing

Started to have ketoacidosis. Could be a septic patient with lactic acidosis.