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Pre-clinical review > ABGs > Flashcards

ABGs Flashcards

1
Q

Out of the following, which are measured values and which are calculated: pH, PCO2, PO2, HCO3, BE and SaO2?

A

Measured: pH, PCO2, PO2 and SaO2 (SaO2 via cooximeter)
Calculated: HCO3, BE and SaO2 (SaO2 via ABG machine).
*SaO2 is a measured parameter, but if it is reported directly from the ABG machine then it is calculated.

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2
Q 
What values do the following machine/test report and are they invasive or non-invasive:
Pulse Oximeter
Pulse co-oximeter
Blood gas machine
Co-oximeter
A

Pulse Ox: SpO2 (functional oxygen sat) –> non-invasive
Pulse Co-Ox: total Hb and oxyHb saturation –> non-invasive
Blood Gas machine: pH, CO2, PO2
Co-Ox: total Hb and various Hb species and SaO2 (fractional oxygen sat) –> invasive (uses a blood sample)

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3
Q

What are some things that can increase the risk of arterial blood flow obstruction during a blood gas?

A 
CVD (cardiovascular disease)
Larger catheter and needle gauges (larger gauge = smaller needle, smaller gauge = larger needle, therefore a small gauge needle increases the risk of obstruction)
Traumatic puncture
Multiple attempts/punctures
Long duration of cannulation
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4
Q

Describe the steps of the Modified Allen’s test (MAT), what is this test used for?

A

Used to assess for collateral circulation.
1. Place hand in neutral anatomical position
2. occlude both radial and ulnar arteries.
3. instruct patient to open and close hand rapidly
4. Once blanching of hand occurs, release ULNAR artery.
5. If colour returns in <10 seconds = collateral flow is adequate (+ve MAT)
If colour returns in >10 seconds = alternative site should be used (-ve MAT)
**ideally the want blood flow to return in 5-15 seconds.

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5
Q

What are the 3 sites of ABG collection and the appropriate angle the needle should enter at?

A

Radial: 30-45 degrees (**vessel of choice for it’s good access and it’s not close to many nerves)
Brachial: 45-60 degrees
Femoral: 90 degrees

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6
Q

How long should we tamponade for?

A

5 mins

*10 mins if they have any coagulopathies or are on anti-coagulants

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7
Q

What does it mean if the blood is dark and slow to fill?

A

It’s venous blood!

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8
Q

A pt will lose their radial pulse when systolic BP is:

A

< 80 mmHg

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9
Q

A pt will lose their femoral pulse when systolic BP is:

A

< 70 mmHg

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10
Q

A pt will lose their carotid pulse when systolic BP is:

A

<60 mmHg

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11
Q

What are the two collateral routes of circulation?

A

The deep palmar arch, which is a continuation of the radial artery, and attaches to the ulnar artery.
The superficial palmar arch, which is a continuation of the ulnar artery and attaches to the radial artery

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12
Q

When would we use the femoral artery as the sample site?

A

We avoid this area, unless the pt is hypotensive with a low perfusion state (ie. can’t palpate radial or brachial).
There is risk of inconspicuous hemorrhage or liberation of plaques and elevated infection risk.
Avoid if they had a Fem-Pop bypass.

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13
Q

What do you need to document/chart after taking an ABG sample?

A 
Puncture site location
# of attempts
Site appearance
MAT performed (+ve or -ve)
FiO2 
Amount of blood obtained (usually 3 ml)
Tamponade time
Complications (if any)
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14
Q

When is it appropriate to take an ABG sample?

A

Ask yourself: what is the pt’s status currently?
They should be 30 mins post exercise, 30 mins after a change to the their PPV, 30 mins after initiation in therapy for a spontaneous breathing pt (give them time to stabilize)

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15
Q

Why is leukocytosis a concern when taking an ABG sample?

A

Leukocytosis is an increased WBC count. Blood samples rich in leukocytosis have high metabolism –> transport on ICE.
Metabolism will consume O2 and produce CO2 –> decreasing pH.
O2 consumption increased by 10% with every degree temp increase

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16
Q

pH is buffered by what 3 things?

A

Lungs, Kidneys and blood buffers

*lungs being the most important organ for pH regulations

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17
Q

Are the kidneys responsible for acid or base regulation?

A

BOTH!
H+ regulation (so acid regulation) via excretion.
Base regulation via retaining or eliminating base.
Plasma HCO3- is the major blood base

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18
Q

T/F: The lungs and kidneys excrete the same chemical group of acids?

A

FALSE!
Lungs excrete volatile acids.
Kidneys excrete non-volatile acids.

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19
Q

What are volatile acids? Provide an example

A

Acids that can be converted from liquid to gas.

Eg. Carbonic acid

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20
Q

What are non-volatile acids? Provide an example.

A

These cannot be excreted as a gas (unlike volatile acids) and must be excreted as a liquid.
Eg. Lactic acid, ketones, uric acid.

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21
Q

What is anatomic deadspace? How much anatomic Deadspace is there in the body?

A

The gas that does not participate in gas exchange (i.e. the gas remaining in the lungs at the end of a breath).
Its about 2ml/kg (or 1 ml/lb)

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22
Q

What is the equation for deadspace ventilation?

A

alveolar DS = physiological DS - anatomic DS

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23
Q

What are some reasons for an increase in CO2 production?

A

Increased Temp
Diet (i.e. RQ - Fat = 0.7, CHO = 1 (produces most CO2), Protein = 0.8)
Exercise
Burns/Sepsis due to decrease V/Q
NaHCO3- administration - the pt enters hydrolysis and produces more CO2

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24
Q

Every year over ___, PaO2 decreases by ____ mmHG.

A

60, 1 mmHg

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25
Q

what is the PaO2 on a FiO2 of 1.0?

A

Use the “5x rule” - PaO2 is 5x FiO2.
FiO2 1.0 = PaO2 of 450-500 (“normal”)
FiO2 x 5 = ideal PaO2
*assuming pt has normal, healthy lungs

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26
Q

What are the PaO2/FiO2 range for mild, moderate and severe ARDS?

A 
Mild = 200-300
Moderate = 100-200
Severe = < 100
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27
Q

What is the normal range for SaO2?

A

aka Fractional Oxygen Saturation

97% (93-98%)

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28
Q

What is better: fractional (SaO2) or functional (SpO2) oxygen saturation?

A

Fractional, because it takes into account the total Hb (i.e. oxygenated, deoxygenated & dys Hb)
whereas functional only takes into account oxygenated and deoxygenated.

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29
Q

How is CNS depression an etiology for Respiratory acidosis?

A

CNS depression can decrease airway tone and frequency of ventilation, pt becomes apneic (thus alveolar ventilation decreases) and CO2 rises.
CNS depression may be due to administration of drugs that decrease LOC or potentially trauma

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30
Q

How is the NMJ an etiology for Respiratory acidosis?

A

with the use of neuromuscular blockades (NMB) that impede respiratory function OR neuromuscular disease that involves the NMJ like myasthenia graves.

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31
Q

How is metabolism an etiology for Respiratory acidosis?

A

CO2 is an end product of metabolic processes, so as metabolism proceeds, CO2 increases.

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32
Q

How is O2 excess an etiology for Respiratory acidosis?

A

Oxygen induced hypercarbia (or oxygen induced hypoventilation) –> interference with the hypoxic drive to breath when O2 is administer (rare occurrence, like the easter bunny haha).

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33
Q

How are the lungs an etiology for Respiratory acidosis?

A

damage or impairment of the lungs can affect V/Q matching, which contributes to respiratory acidosis.

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34
Q

How are drugs an etiology for Respiratory acidosis?

A

they can impair things like CNS function, LOC, normal ventilatory function my inhibiting respiratory muscles.

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35
Q

How can mechanical ventilation be an etiology for respiratory acidosis?

A

MV can hurt the lungs, but intended to maintain CO2 homeostasis however we do intentional respiratory acidosis sometimes (permissive hypercapnia)

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36
Q

How can muscle fatigue be an etiology for Respiratory acidosis?

A

Pronounced WOB that may not be able to maintain –> CO2 will rise since they can’t maintain the work to excrete CO2.

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37
Q

What is the most common source of chronic respiratory acidosis?

A

COPD!

38
Q

Why is hypercapnia dangerous for TBI?

A

Because hypercapnia increases cerebral perfusion.
Acute hypercapnia can increase cerebral blood low by 2x!.
Chronic hypercapnia may have NORMAL cerebral blood flow and reduced responsiveness to changes in PaCO2.

39
Q

what is permissive hypercapnia?

A

intentional withdrawal of ventilatory support; a protective lung strategy (avoids over distension due to trying to clear CO@2) where PaCo2 levels are allowed to rise.

40
Q

What are the physiological effects of permissive hypercapnia?

A
  • Right shift on O2HB curve –> decreased affinity (increase P50) meaning might not pick up O2 with as great of an affinity.
  • decreased PAO2 –> as PCO2 levels increase, PAO2 decreases
  • CVS –> decreased contractility of the heart with decreased pH and increased CO2
  • CNS –> as CO2 levels exceed 70 mmHg, LOC may decrease.
  • Ventilatory drive is stimulated because CO2 levels are rising, which stimulates the central chemoreceptors –> **apply sedation
  • vasodilation –> low H+ or high CO2 causes vasodilation
  • Increased ICP via increase CBF
41
Q

What are common things that are presented with respiratory alkalosis?

A

Renal compensations (decrease HCO3-)
Decreased CBF (due to decreased CO2) **important for TBI.
PVR increases - so blood flow to areas decrease
Arrhythmias can develop due to decreased coronary blood flow from the increased PVR

42
Q

How can the CNS be an etiology for Respiratory alkalosis?

A

central chemoreceptors are sensitive to CO2 and CO2 changes the pH of the CSF and the CSF influences the medullary sensors promoting a pro-ventilatory response –> so the CNS increases alveolar ventilation (Va) to maintain CO2 at a homeostatic level.

43
Q

How can the CVS be an etiology for Respiratory alkalosis? (or how can hypoxemia be an etiology?)

A

peripheral chemoreceptors are located in the aortic arch and arteries, which are responsive to PO2. As the pt becomes hypoxemic, this will promote/increase Va.
*if the pt is in respiratory alkalosis, inspect their oxygenation!

44
Q

How can the lungs be an etiology for Respiratory alkalosis?

A

Via PULMONARY REFLEXES, which are stimulated as lung conditions change –> stimulates Va (alveolar ventilation) —> hyperventilation –> decreasing CO2 –> respiratory alkalosis

45
Q

How can drugs be an etiology for Respiratory alkalosis?

A

overdose of various drugs (such as aspirin for example) can promote resp alkalosis even though metabolic acidosis will commonly develop.

46
Q

How can mechanical ventilation be an etiology for Respiratory alkalosis?

A

May be targeting a higher minute ventilation, promoting respiratory alkalosis.

47
Q

If a pt is tachypneic does that mean they are hyperventilating?

A

NO.

Take an ABG to see PCO2 levels.

48
Q

What is metabolic acidosis?

A

Its the accumulation of fixed acid.
Loss of blood base (decreased HCO3-)
there is ALWAYS a decreased HCO3-
It is not a disease but a biochemical abnormality resulting from an imbalance between production and excretion of acids.

49
Q

what is the most commonly measured cation for metabolic acidosis?

A

Na+ (142 mEg/L)

50
Q

what is the most commonly measured anion for metabolic alkalosis?

A

Cl- (103 mEq/L) –> measured

HCO3- (27 mEq/L) –> calculated

51
Q

what is hyperchloremic metabolic acidosis?

A

when Cl- increased but there is not an increase in the unmeasured anion (A-). So it’s acidosis WITHOT an increase in the unmeasured anion (aka non-anion gap acidosis or anion gap -ve)
*HCO3- always decreased.

52
Q

what is anion gap positive metabolic acidosis?

A

When there IS an increase in the unmeasured anion (A-)

53
Q

What do BUN (urea) and creatine assess?

A

Renal function

54
Q

What is the range for Na+?

A

136-145 (142) mmol/L

55
Q

what is the range for Cl-?

A

95-105 (103) mmol/L

56
Q

what is the range for HCO3-?

A

22-26 mmol/l

57
Q

what is the range for BUN (urea)?

A

2.8-7.7 mmol/L

58
Q

what is the range for creatinine?

A

50-110 umol/L

59
Q

what is the range for glucose?

A

4-8 mmol/L

60
Q

How do you tell if there is an anion gap (AG) present? (HINT: what is the equation and the cut off for AG?)

A

[Na+] - ([Cl-] + [HCO3-])
If > 20 then AG present (AG +ve).
If < 20 then AG -ve

61
Q

How can toxins be an etiology for metabolic acidosis (+ AG)?

A

pharmaceuticals can take part in the metabolic breakdown which leads to AG +ve

62
Q

How can the kidneys be an etiology for metabolic acidosis (+ AG)?

A

If there is kidney failure, this can lead to + AG metabolic acidosis (look for problems with kidney perfusion, kidney function, decrease U/O, increased BUN or creatinine)

63
Q

What is the normal value for U/O

A

60 ml/hr for adults

1 ml/kg/hr for peds

64
Q

How can metabolism be an etiology for metabolic acidosis (+ AG)?

A

metabolism leads to tissue hypoxia and lactic acid production

65
Q

How can the liver be an etiology for metabolic acidosis (+ AG)?

A

certain metabolic processes and breakdown processes of toxic alcohols can lead to metabolites that can lead to metabolic acidosis

66
Q

What is the acronym for AG+ metabolic acidosis?

A

MULEPAK

67
Q

What’s the M in MULEPAK?

A

Methanol - indicates a toxic alcohol that has been ingested that can be broken down into toxic metabolites (antifreeze, solvent, wood alcohol, ethylene glycol (ingredient of antifreeze), cleaning materials).
Alcoholics are the usual suspects

68
Q

What’s the U in MULEPAK?

A

Uremia - renal failure –> high levels of BUN (urea) and/or creatinine

69
Q

What’s the L in MULEPAK?

A

Lactic acidosis –> lactic acid > 4-5 mmol/L indicates anaerobic metabolic.
Anything that can lead to tissue hypoxia (eg. anemia, sepsis, hypotension, MI)

70
Q

What’s the E in MULEPAK?

A

ETOH (AKA) - alcoholic ketoacidosis (alcoholic on a binge and ceases drinking).
The pt enters ketosis from fatty acid breakdown.

71
Q

What’s the P in MULEPAK?

A

Paraldehyde - anticonvulsant/hypnotic –> rare pharmaceutical, overdose can lead to acidosis

72
Q

What’s the A in MULEPAK?

A

ASA (salicylate) - aspirin overdose

resp acidosis is usually the more pronounced acid-base disorder

73
Q

What’s the K in MULEPAK?

A

ketoacidosis - metabolic pathway of lipid metabolism seen in diabetic patients; insulin deficiency.
**look at glucose #

74
Q

what breathing pattern will you see when the patient becomes acidotic?

A

Kussmal’s breathing pattern - pt is trying to normalize pH by expelling CO2.

75
Q

Whats the normal range for lactate?

A

0.6-2.4 mmol/L

76
Q

whats the normal AG range?

A

8-12 +/- 4 mmol/L

77
Q

Without calculating the AG, how could you tell it’s AG -ve?

A

If Cl- has increased

78
Q

How can the intestine be an etiology for metabolic acidosis (-ve AG)?

A

Diarrhea can result in BASE LOSS, resulting in metabolic acidosis (AG -ve)

79
Q

How can surgery be an etiology for metabolic acidosis (-ve AG)?

A

the use of surgical drains to remove alkaline secretions (i.e. base loss).

80
Q

How can the kidneys be an etiology for metabolic acidosis (-ve AG)?

A

renal tubular acidosis can manifest and create a situation where the renal tubules fail to absorb bicarb –> base loss

81
Q

How can drugs be an etiology for metabolic acidosis (-ve AG)?

A

A variety of drugs can lead to metabolic acidosis.
Infusion of certain acidic substances like HCl or NaCl (chloride containing acids) dilutes the blood making is more acidosis

82
Q

How can the stomach be an etiology for metabolic alkalosis?

A

If gastric secretions that have a lower pH are removed, the pH will become more alkalotic

83
Q

How can mechanical ventilation be an etiology for metabolic alkalosis?

A

If the patient has been managing hypercarbia for a couple days, this is when you want to apply protective ventilation strategies.
Compensation occurs by the kidneys and then we return to homeostatic PCO2 levels – the ABG would look like metabolic alkalosis

84
Q

How can NaHCO3 be an etiology for metabolic alkalosis?

A

this is administered to correct the acid/base disturbance, increasing bicarb –> metabolic alkalosis

85
Q

How can the adrenal cortex be an etiology for metabolic alkalosis?

A

Adrenal hypersecretion?

86
Q

How can hypokalemia be an etiology for metabolic alkalosis?

A

Low K+ = Kidneys excrete H+ and Na+ retention –> so H+ is lost, thus more alkalotic

87
Q

How can drugs be an etiology for metabolic alkalosis?

A

Loop diuretics can cause volume loss which leads to hypokalemia –> metabolic alkalosis

88
Q

How can oral bases be an etiology for metabolic alkalosis?

A

Overconsumption of sodium or potassium hydroxide tablets may adversely affect its acid/base status.

89
Q

What are the effects of metabolic alkalosis?

A

Mild to moderate metabolic alkalosis: lethargy & confusion.
Severe: seizures.
Depressed myocardial contractility and arrhythmias

90
Q

What is creatinine?

A

it’s a waste-end product of metabolism in skeletal muscle.
A high creatinine level may mean kidney function is reduced.
Normal: 5-110 mmol/l

91
Q

What is urea nitrogen?

A

Referred to a BUN (blood urea nitrogen)
It is nitrogen containing waste formed from PROTEIN catabolism.
Formed in the liver and excreted by kidneys.
Normal: 2.8-7.7 mmol/l

Pre-clinical review (19 decks)

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