Oxygenation and ventilation monitoring

54
OXYGENATION & VENTILATION MONITORING

description

Capnography, Pulse oximetry and blood gas monitoring

Transcript of Oxygenation and ventilation monitoring

Page 1: Oxygenation and ventilation monitoring

OXYGENATION & VENTILATION MONITORING

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Point of Discussion

1. Indices of oxygenation 2. Indices of ventilation3. Pulse oximetry4. Capnography5. Arterial and venous blood gases

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Indices of Oxygenation

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Alveolar Arterial O2 Gradient

Alveolar Gas Capillary Blood

initial Initial

Thickness

A-a Gradient

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Pulse Oximetry

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O2-Hg Dissociation Curve

PaO2 (mm Hg)

90

60

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Sources of error

Poor peripheral perfusion Dark skin False nails or nail varnish Lipaemia Bright ambient light Poorly adherent probe Excessive motion Carboxyhaemoglobin or methaemoglobin

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The Ventilation Vital Sign

Capnography

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Capnograhy vs Capnometry? Capnography- Continuous analysis and

recording of Carbon Dioxide concentrations in respiratory gases ( I.E. waveforms and numbers)

Capnometry- Analysis only of the gases no waveforms

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Semi-Quantitative Capnometry Relies on pH change Paper changes color

Purple to Brown to Yellow

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Quantitative Capnometry

Absorption of infra-red

light Gas source

Side Stream In-Line

Factors in choosing device:

Warm up time Cost Portability

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Waveform Capnometry

Adds continuous waveform display to the ETCO2 value. Additional information in waveform shape can provide clues about causes of poor oxygenation.

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Why ETCO2 I Have my Pulse Ox?

Oxygen SaturationReflects OxygenationSpO2 changes lag when patient is hypoventilating or apneicShould be used with Capnography

Carbon Dioxide

Reflects Ventilation

Hypoventilation/Apnea detected immediately

Should be used with pulse Oximetry

Pulse Oximetry Capnography

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What does it really do for me?

Bronchospasms: Asthma, COPD, AnaphlyaxisHypoventilation: Drugs, Stroke, CHF, Post-IctalShock & Circulatory compromiseHyperventilation Syndrome: Biofeedback

Verification of ETT placementETT surveillance during transportControl ventilations during CHI and increased ICPCPR: compression efficacy, early signs of ROSC, survival predictor

Non-Intubated Applications Intubated Applications

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NORMAL CAPNOGRAM

Phase I Phase IIIPhase II

Inspiratory PhaseExpiratory Phase

70

60

50

40

30

20

10

0

PetCO2

Time

mm Hg

Phase I: anatomical dead spacePhase II : alveolar gas begins to mix with the

dead space gas

Phase III: elimination of CO2

from the alveoli

Phase IV

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ABNORMALITIES

Abnormality Indication

Increased Phase III slope Obstructive lung disease

Phase III dip Spontaneous respiratio

Horizontal Phase III with large ET-art CO2 change

Pulmonary embolism cardiac outputHypovolemia

Sudden in ETCO2 to 0 Dislodged tubeVent malfunctionET obstruction

Sudden in ETCO2 Partial obstructionAir leak

Exponential Severe hyperventilationCardiopulmonary event

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ABNORMALITIES

Abnormality IndicationSudden increase in ETCO2 Sodium bicarb administration

Release of limb tourniquetGradual Hyperventilation

Decreasing tempGradual in volume

Increased baseline RebreathingExhausted CO2 absorber

Gradual increase FeverHypoventilation

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USES

Metabolic Assess energy expenditure

Cardiovascular Monitor trend in cardiac output Can use as an indirect Fick method, but

actual numbers are hard to quantify Measure of effectiveness in CPR Diagnosis of pulmonary embolism: measure

gradient

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PaCO2-PetCO2 gradient

Usually <6mm Hg PetCO2 is usually less Difference depends on the number of

underperfused alveoli Tend to mirror each other if the slope of

Phase III is horizontal or has a minimal slope Decreased cardiac output will increase the

gradient The gradient can be negative when healthy

lungs are ventilated with high TV and low rate Decreased FRC also gives a negative gradient

by increasing the number of slow alveoli

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LIMITATIONS

Critically ill patients often have rapidly changing dead space and V/Q mismatch

Higher rates and smaller TV can increase the amount of dead space ventilation

High mean airway pressures and PEEP restrict alveolar perfusion, leading to falsely decreased readings

Low cardiac output will decrease the reading

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PULMONARY USES

Effectiveness of therapy in bronchospasm Monitor PaCO2-PetCO2 gradient Worsening indicated by rising Phase III without

plateau Find optimal PEEP by following the gradient.

Should be lowest at optimal PEEP. Can predict successful extubation.

Dead space ratio to tidal volume ratio of >0.6 predicts failure. Normal is 0.33-0.45

Limited usefulness in weaning the vent when patient is unstable from cardiovascular or pulmonary standpoint

Confirm ET tube placement

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NORMAL Waveform

70

60

50

40

30

20

10

0 Time

mm Hg

• Square box waveform• ETCO2 35-45 mm Hg• Management: Monitor Patient

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Sudden in ETCO2 to 0

70

60

50

40

30

20

10

0 Time

mm Hg

• Loss of waveform• Loss of ETCO2 reading• Dislodged tube• ET obstruction• Management: Replace ETT

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Esophageal Intubation

70

60

50

40

30

20

10

0 Time

mm Hg

• Absence of waveform• Absence of ETCO2• Management: Re-Intubate

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CPR

70

60

50

40

30

20

10

0 Time

mm Hg

• Square box waveform• ETCO2 15-20 mm Hg with adequate CPR• ETCO2 falls bellow 10 mm Hg • Management: Change Rescuers

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Return of Spontaneous Circulation

70

60

50

40

30

20

10

0 Time

mm Hg

• During CPR sudden increase of ETCO2 above 10-15 mm Hg• Management: Check for pulse

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Gradual Decrease in ETCO2

70

60

50

40

30

20

10

0 Time

mm Hg

• Hyperventilation• Decreasing temp• Gradual in volume

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Hyperventilation

70

60

50

40

30

20

10

0 Time

mm Hg

• Shortened waveform• ETCO2 < 35 mm Hg• Management: If conscious gives biofeedback. If ventilating slow ventilations

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Gradual Increase in ETCO2

70

60

50

40

30

20

10

0 Time

mm Hg

• Fever• Hypoventilation

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Hypoventilation

70

60

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30

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0 Time

mm Hg

• Prolonged waveform• ETCO2 >45 mm Hg• Management: Assist ventilations

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Rising Baseline

70

60

50

40

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10

0 Time

mm Hg

• Patient is re-breathing CO2• Management: Check equipment for adequate oxygen flow• If patient is intubated allow more time to exhale

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Curare Cleft

70

60

50

40

30

20

10

0 Time

mm Hg

• Curare Cleft is when a neuromuscular blockade wears off

• The patient takes small breaths that causes the cleft

• Management: Consider neuromuscular blockade re-administration

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Breathing around ETT

70

60

50

40

30

20

10

0 Time

mm Hg

• Angled, sloping down stroke on the waveform• In adults may mean ruptured cuff or tube too small• Management: Assess patient, Oxygenate, ventilate and possible re-intubation

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Obstructive Airway

70

60

50

40

30

20

10

0 Time

mm Hg

• Shark fin waveform• With or without prolonged expiratory phase• Can be seen before actual attack• Indicative of Bronchospasm( asthma, COPD, allergic reaction)

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Oscillation in Inspiratory Phase

70

60

50

40

30

20

10

0 Time

mm Hg

J Int Care Med, 12(1): 18-32, 1997J Int Care Med, 12(1): 18-32, 1997

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Oscillation in Inspiratory Phase

70

60

50

40

30

20

10

0 Time

mm Hg J Int Care Med, 12(1): 18-32, 1997J Int Care Med, 12(1): 18-32, 1997

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Oscillation and slow Inspiration

70

60

50

40

30

20

10

0 Time

mm Hg

J Int Care Med, 12(1): 18-32, 1997J Int Care Med, 12(1): 18-32, 1997

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6 Step ABG’s Analysis

Blood Gases

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1. Acidemic/Alkalemic?

This refers to the pH Normal pH= 7.40 ± 0.05 Acidemia pH < 7.40 Alkalemia pH > 7.40 Normal PaCO2 = 40 ± 5 (35-45) Normal HCO3 = 24 ± 2 (22-26)

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2. Primary -osis

pH emia PaCO2 HCO3 1 ° osis

<7.40 acidemia <40 <24 1°Metabolic acidosis

<7.40 acidemia >40 >24 Respiratory acidosis

>7.40 alkalemia

>40 >24 Metabolic alkalosis

>7.40 alkalemia

<40 <24 Respiratory alkalosis

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2. Respiratory process acute or chronic ? Respiratory Acidosis Acute :

pH= 0.08x(PaCO2-40)/10 Respiratory Acidosis Chronic :

pH= 0.03x(PaCO2-40)/10 Respiratory Alkalosis Acute :

pH= 0.08 x (40-PaCO2)/10 Respiratory Alkalosis Chronic :

pH= 0.03 x (40-PaCO2)/10

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4. Metabolic acidosis

Anion gap vs. Nongap acidosis Anion gap (AG) = Na-Cl-HCO3

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3. Adequate degree of compensation for Metabolic Acidosis ? Calculated (expected) PaCO2 for Gap

acidosis (Winter’s formula) Calculated PaCO2=(1.5 x HCO3) +8±2 Measured PaCO2>Calculated PaCO2

then concomitant respiratory acidosis Measured PaCO2<Calculated PaCO2

then concomitant respiratory alkalosis

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4. Calculated (expected) HCO3 Calculated (expected) HCO3 =

(Pt.’s AG-nl gap) + measured HCO3 Calculated HCO3>30 associated metabolic

alkalosis Calculated HCO3<23 associated nongap

metabolic acidosis AKA Delta Delta

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4. Metabolic acidosis

Check for Osmolar gap (OG)OG:Measured osmol – Calculated > 10Calculated Osmol=(2xNa) + glucose/18 + BUN/2.8 +ethanol/4.6

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5. Calculate Urinary AG

Determines renal vs. extrarenal causes UAG=UNa+UK-UCl (nl -10 to 10). UAG <-10 = extrarenal b/c kidneys

making a lot of NH3Cl to buffer acidosis UCl nl/high (>40) AKA saline unresponsive

UAG> 10 = renal b/c kidneys unable to make NH3Cl to excrete acid. UCl low (<25) saline responsive

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6. Adequate degree of compensation for

Metabolic Alkalosis ?

For every 1 in HCO3 the paCO2 0.6

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Adequate degree of compensation ?

Primary Primary problemproblem

CompensatioCompensationn

For For every every inin

ExpecteExpected d

Metabolic Metabolic AcidosisAcidosis

Respiratory alkalosisRespiratory alkalosis1 1 ↓↓ HCO3 HCO3 PaCO2 PaCO2 ↓↓ 1.2 1.2

Metabolic Metabolic AlkalosisAlkalosis

Respiratory acidosisRespiratory acidosis1 1 ↑↑ HCO3 HCO3 PaCO2 PaCO2 ↑↑ 0.6 0.6

Respiratory Respiratory Acidosis AcuteAcidosis Acute

Metabolic AlkalosisMetabolic Alkalosis1 1 ↑↑ PaCO2 PaCO2 HCO3 HCO3 ↑↑ 0.1 0.1

Respiratory Respiratory Acidosis ChronicAcidosis Chronic

Metabolic AlkalosisMetabolic Alkalosis1 1 ↑↑ PaCO2 PaCO2 HCO3 HCO3 ↑↑ 0.4 0.4

Respiratory Respiratory Alkalosis AcuteAlkalosis Acute

Metabolic AcidosisMetabolic Acidosis1 1 ↓↓ PaCO2 PaCO2 HCO3 HCO3 ↓↓ 0.2 0.2

Respiratory Respiratory Alkalosis ChronicAlkalosis Chronic

Metabolic AcidosisMetabolic Acidosis1 1 ↓↓ PaCO2 PaCO2 HCO3 HCO3 ↓↓ 0.4 0.4

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ABG Problems:

145145 100100 1616

4.04.0 1212 1.01.0

7.2/26/85/95% on RA

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Answer

Metabolic acidosis 145-100-12=AG 33 Expected PaCO2 1.5x12 +8 ±2=26±2

appropriate Expected HCO3= (33-12) + 12 =33 Concomitant metabolic alkalosis

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ABG Problems

7.1/35/60/90% on RA

135135 106106 1616

4.24.2 1010 1.01.0

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Answer

Metabolic acidosis 135-106-10 = AG 19 Expected PaCO2 1.5 x 10 +8 ±2=23±2

Measured >calculated Concomitant respiratory acidosis Expected HCO3 = 19-12 +10 = 17 Concomitant nongap metabolic acidosis Next calculate UAG

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ABG Problems

HIV, HBV associated ESLD, ARF with pleural effusions, tachypneic RR 34

7.48/28/55/90% on 4L NC 155|97|41/117

4.7| 18|1.7\

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Answer

Respiratory alkalosis H:748-740=8 paCO2: 40-28=128/12=0.67 Acute on chronic respiratory

alkalosis. Acute from tachypnea chronic from ESLD

7.47/18/98 on 50% face mask