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Renal system > Arterial blood gas interpretation > Flashcards

Arterial blood gas interpretation Flashcards

1
Q

ABG

A

arterial blood gas

blood sample taken from the radial artery in the wrist

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2
Q

VBG

A

venous blood gas

blood sample taken from a vein in cubital fossa

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3
Q

when are ABGs used?

A

VGBs can tell almost as much as ABGs and is more comfortable for the patient.
used to check if a patient is a chronic CO2 retainer in COPD or initiating non-invasive ventilation

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4
Q

difference between VBGs and ABGs

A

interpretation technique is the same

pO2 cannot be interpreted on a VBG and the reference range values are slightly different

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5
Q

acidosis

A

pH <7.35
increased in CO2 - respiratory acidosis
decrease in HCO3- - metabolic acidosis

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6
Q

alkalosis

A

pH>7.45
increase in HCO3- - metabolic alkalosis
decrease in CO2 - respiratory alkalosis

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7
Q

pathophysiology of respiratory acidosis?

A

inadequate alveola ventilation

leading to CO2 retention

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8
Q

causes of respiratory acidosis

A 
respiratory depression - e.g. by opiates
guillain-Barre - paralysis 
asthma
COPD
iatrogenic - incorrect mechanical ventilation
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9
Q

pathophysiology of respiratory alkalosis

A

caused by excessive alveolar ventilation - hyperventilation

so more CO2 than normal is being exhaled

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10
Q

causes of respiratory alkalosis

A

anxiety - panic attack
pain - causing an increased respiratory rate
hypoxia - resulting in increased alveolar ventilation to compensate
pulmonary embolism
pneumothorax
iatrogenic - excessive mechanical ventilation

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11
Q

pathophysiology of metabolic acidosis

A
  1. increased acid production or ingestion

2. decreased acid excretion or rate of gastro and renal HCO3- loss

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12
Q

causes of metabolic acidosis mechanism 1

A

diabetic ketoacidosis - increased production
lactic acidosis - increased production
aspirin overdose - increased ingestion of acid

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13
Q

what does metabolic acidosis by mechanism 1 cause?

A

increased anion gap

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14
Q

causes of metabolic acidosis by mechanism 2

A

Gastrointestinal loss of HCO3- - diarrhoea, ileostomy, proximal colostomy
renal tubular acidosis - retention of H+
addison’s diseases - retention of H+

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15
Q

what does metabolic acidosis by mechanism 2 cause?

A

decreased anion gap/ normal anion gap

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16
Q

what is normal anion gap?

A

4-12mmol/L

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17
Q

how to calculate anion gap?

A

Na+ - (Cl- + HCO3-)

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18
Q

pathophysiology of metabolic alkalosis

A

occurs as a result of decreased hydrogen ion concentration causing an increased bicarbonate
or a direct result of increased bicarbonate concentrations

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19
Q

causes of metabolic alkalosis

A

gastrointestinal loss of H+ ions - vomiting/ diarrhoea
renal loss of H+ ions - loop and thiazide diuretics
heart failure
nephrotic syndrome
cirrhosis
conn’s syndrome
iatrogenic - addition of alkali

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20
Q

compensation

A

pH, CO2 and HCO3- will change on ABG

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21
Q

respiratory compensation

A

pH is not in range and so compensation is partial

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22
Q

metabolic compensation

A

more effective than respiratory and so may return pH to normal - full compensation, however, is usually only partial compensation

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23
Q

how quick is respiratory compensation?

A

reacts quickly by increasing or decreasing alveolar ventilation to blow off more or retain more CO2
fast but less effective

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24
Q

how quick is metabolic compensation?

A

takes a few days to occur as it requires the kidneys to either reduce HCO3- production or increase HCO3- production
slow but more effective

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25
Q

overcompensation

A

should never occur and so if results suggest this need to consider other pathologies

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26
Q

mixed respiratory and metabolic acidosis

A

decreased pH
increased CO2
decreased HCO3-
looks like both are the cause

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27
Q

causes of mixed respiratory and metabolic acidosis

A

cardiac arrest

multi-organ failure

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28
Q

mixed respiratory and metabolic alkalosis

A

increased pH
decreased CO2
increased HCO3-
looks like both are the cause

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29
Q

causes of mixed respiratory and metabolic alkalosis

A

liver cirrhosis in addition to diuretic use
hyperemesis gravidarum
excessive ventilation in COPD

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30
Q

how to treat mixed respiratory and metabolic acidosis/ alkalosis?

A

correct each primary acid-base disturbance

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31
Q

respiratory failure

A

paO2 <8

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32
Q

ABG

A

can measure partial pressure of oxygen

PaO2 - partial pressure of oxygen in arterial blood

33
Q

what are the types of respiratory failure?

A

type 1 and 2

34
Q

type 1 respiratory failure presentation

A

O2 low - <8kPa
CO2 normal - <6kPa
hypoxaemia and normocapnia

35
Q

type 2 respiratory failure presentation

A

O2 low - <8kPa
CO2 high - >6kPa
hypoxaemia and hypercapnia

36
Q

what causes type 1 respiratory failure?

A

occurs as a result of ventilation/ perfusion mismatch

volume of air flowing in and out of the lungs is not matched with the flow of blood to the lung tissue

37
Q

what happens in type 1 respiratory failure?

A 
due to V/Q mismatch 
PaO2 falls PaCO2 rises
rise in PaCO2 triggers an increase in patient's overall alveolar ventilation which corrects the PaCO2 by increasing CO2 elimination but not PaO2 due to the dissociation curve
normal CO2/ maybe low
low O2
38
Q

examples of VQ mismatching

A

reduced ventilation and normal perfusion = pulmonary oedema and bronchoconstriction
reduced perfusion with normal ventilation = pulmonary embolism

39
Q

what happens in type 2 respiratory failure?

A

occurs as a result of alveolar hypoventilation which prevents the patient from being able to oxygenate and eliminate CO2 from their blood

40
Q

how to treat respiratory failure?

A

non-invasive ventilation

determined by which type of respiratory failure

41
Q

treatment for type 1 resp failure

A

CPAP

42
Q

treatment for type 2 resp failure

A

IPAP

initial inspiratory positive airway pressure

43
Q

causes of hypoventilation

A

increased resistance of airways - COPD
reduced compliance of lungs/ chest wall - pneumonia/rib fractures/ obesity
reduced strength of respiratory muscles - Guillain-Barre/ motor neurone disease
drugs acting on the respiratory centre reducing ventilation - opiates

44
Q

steps to interpret ABG

A

look at pH - acidosis or alkalosis
Look at CO2 - low or high and cause or compensation
Look at HCO3- - low of high and cause or compensation
look at PaO2 - is it low? respiratory failure?

45
Q

how is a drug nebulised and what benefit does this provide?

A

nebulised drugs are given as a mist
with the drug dissolved in solution and then broken into tiny particles suspended in the air these reach further down the respiratory tree than normal aerosol inhalers which deliver the drug in powder form

46
Q

diabetic ketoacidosis

A

absence of enough insulin
causes excessive breakdown of glycogen, protein and fat
fat is converted by beta oxidation to acetyl coenzyme A which cannot all be utilised and the excess is converted into ketoacids

47
Q

another major problem associated with ketoacidosis

A

glycogen is converted to glucose which spills into urine causing osmotic diuresis and severe dehydration

48
Q

what would be the first treatment priority in diabetic ketoacidosis?

A

fluid depletion is the immediate life-threatening problem and so rehydration with 0.9% IV saline is needed first

49
Q

protracted vomiting

A

causes hug loss of gastric acid resulting in alkalosis
hypochloraemic
hypokalaemic - trying to retain H+ by kidneys

50
Q

what is hypochloraemia?

A

loss of HCl

51
Q

what causes mixed respiratory and metabolic acidosis during cardiac arrest?

A

respiratory acidosis caused by respiratory arrest
metabolic acidosis caused by lactic acid production in the tissues as they switch to anaerobic metabolism with no oxygen being supplied during cardiac standstill

52
Q

a normal PaO2 in patient on high flow oxygen

A

you would expect the patient to have a PaO2 well above the normal range with this level of oxygen therapy
should be >18 if on 28% oxygen supply

53
Q

normal PaCO2 in hypoxic asthmatic patient

A

SOB
high ventilation rate
blowing off lots of CO2 as they hyperventilate
should have low PaCO2 and low PaO2
if PaCO2 becomes normal they may be tiring and no longer able to hyperventilated and will need ITU intervention

54
Q

very low PaO2 in patient who seems completely well, has normal O2 sats and is not short of breath

A

likely accidentally hit a vein not artery and taken a venous sample

55
Q

what is a common cause of respiratory alkalosis with no compensation?

A

anxiety/ panic attack

56
Q

what causes symptoms of paraesthesia during a panic attack induced respiratory alkalosis?

A

alkalosis increases neural excitability due to lowered free ionised calcium (alkalosis promotes its binding to albumin)
fall in K+ may be invovled

57
Q

how to treat respiratory alkalosis caused by panic attack?

A

rebreathe into a bag - increasing PCO2 and restoring pH

58
Q

aspirin overdose

A

can produce direct stimulation of the respiratory centre and change blood pH

59
Q

what specific methods can be used to limit/ reduce aspirin concentration in blood?

A

further absorption from GI tract can be lessened by activated charcoal
renal excretion of aspirin can be increased by giving IV bicarbonate and increasing the ionised drug fraction which then not reabsorbed by the nephron

60
Q

long-standing respiratory acidosis

A

elevated HCO3-
chronically elevated PCO2 can blunt the responsiveness of central chemoreceptors so ventilation becomes driven by hypoxia via peripheral chemoreceptors - which normally become active at PO2 of 6Kpa

61
Q

chronic retainer

A

requires controlled O2 to titrate oxygen sats to 88-92%
can have normal pH if fully compensated by metabolic compensation
COPD

62
Q

what precautions should be taken with a chronic retainer?

A

giving oxygen at a concentration that raises PO2 substantially risks switching off the respiratory drive which will cause a hugely dangerous rise in PCO2
oxygen should be administered in low concentrations - monitoring the response and aiming for an adequate PO2

63
Q

umbilical cord values for ABG

A

different to normal adult values

64
Q

what would be the best indicator of prolonged fetal hypoxia in utero?

A

low pH of metabolic origin - indicates sustained hypoxia with a switch to anaerobic metabolism in tissues - producing lactic acid
fetal scalp capillary pH can be measured during labour to guide management

65
Q

how is oxygen content in the fetus maximised at a low PO2?

A

fetal haemoglobin

concentration of haemoglobin is higher - polycythaemia

66
Q

fetal haemoglobin

A

has a higher affinity for O2

left shift of the dissociation curve so saturation is higher at a low PO2

67
Q

polycythaemia in fetus

A

180-200g/L of haemoglobin

68
Q

umbilical artery normal pH

A

7.27

69
Q

umbilical artery normal PCO2

A

5.8kPa

70
Q

umbilical artery normal PO2

A

2.9kPa

71
Q

umbilical artery normal HCO3-

A

24mmol/L

72
Q

umbilical vein normal pH

A

7.31

73
Q

umbilical vein normal PCO2

A

5.6kPa

74
Q

umbilical vein normal PO2

A

4.1kPa

75
Q

umbilical vein normal HCO3-

A

25mmol/L

76
Q

what else can be shown by a VBG or ABG?

A 
electrolytes - sodium/ potassium
haemoglobin
lactate
glucose
should be interpreted with caution and repeated on a lab blood test
77
Q

lactate >2

A

dehydration and end organ damage

78
Q

repeated VBGs

A

useful for monitoring metabolic acidosis and glucose in diabetic ketoacidosis treatment

Renal system (17 decks)

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