Oxygenation & Ventilation Monitoring

Oxygenation & Ventilation Monitoring

Point of Discussion Variable and fixed performance Oxygen devices
Pulse oximetry A-a gradient Ventilation equation Capnography Arterial and venous blood gases

The Oxygenation Vital Sign

O2-Hg Dissociation Curve
100% 90% Hb Saturation (%) The pulse oximeter is an extremely useful monitor which estimates arterial saturation the relationship between saturation and PaO2 is described by the oxyhaemoglobin dissociation curve a saturation ~90% is a critical threshold because below this level a small fall in PaO2 produces a sharp fall in SpO2 .Conversely a rise in arterial PO2 has little effect on saturation and therefore little effect on oxygen delivery to tissues 60 90 600 PaO2 (mm Hg)

Oxygen Saturation Monitoring by Pulse Oximetry

Patient Environments Ambient Light Excessive Motion
Any external light exposure to capillary bed where sampling is occurring may result in an erroneous reading Excessive Motion Always compare the palpable pulse rate with the pulse rate indicated on the pulse oximetry Fingernail polish and false nails Most commonly use nails and fingernail polish will not affect pulse oximetry accuracy Some shades of blue, black and green may affect accuracy (remove with acetone pad) Skin pigmentation Apply sensor to the fingertips of darkly pigmented patients

Conditions Affecting Accuracy
Patient conditions Carboxyhemoglobin Erroneously high reading may present Methaemoglobin Anemia Values as low as 5 g/dl may result in 100% SpO2 Hypovolemia/Hypotension: May not have adequate perfusion to be detected by oximetry Hypothermia: peripheral vasoconstriction may prevent oximetry detection

Nasal Cannula: Variable Flow

Simple Face Mask: Variable Flow

Venturi Mask: Fixed Flow
blue = 24%; yellow = 28%; white = 31%; green = 35%; pink = 40%; orange = 50%

Venturi Effect The pressure at "1" is higher than at "2" because the fluid speed at "1" is lower than at "2".

Venturi Effect 35-45 L/min 4-15 L/min
A flow of air through a venturi meter, showing the columns connected in a U-shape (a manometer) and partially filled with water. The meter is "read" as a differential pressure head in cm or inches of water.

Variable Performance Device: Nonrebreather Mask

Fractional inspired oxygen concentration %
100 90 5 L.min-1 80 10 L.min-1 70 20 L.min-1 60 30 L.min-1 Fractional inspired oxygen concentration % 50 40 30 20 10 5 15 25 35 45 55 65 75 85 Peak inspiratory flow (liters/minute)

Continuous Airway Pressure: CPAP

Alveolus Airways Interstitium Pleural cavity Pressure Inspiration Expiration Intrinsic PEEP Applied CPAP

Alveolar-arterial Oxygen Gradient
PAO2= (Patm-PH2O) FiO2- PACO2/0.8 760 47 0.21 40

Alveolar Arterial O2 Gradient
A-a Gradient Po2 Po2 initial Initial Epithelium Endothelium Alveolar Gas Capillary Blood Thickness

5 FIO2= 21% PAO2= 100 PaO2= 95 O2 Sat= 99% FIO2= 50% PAO2= 331 PaO2= 326 O2 Sat= 100% FIO2= 100% PAO2= 663 PaO2= 657 O2 Sat= 100% Epithelium Endothelium Alveolar Gas Capillary Blood Thickness

200 FIO2= 50% PAO2= 331 PaO2= 131 O2 Sat= 100% FIO2= 100% PAO2= 663 PaO2= 463 O2 Sat= 100% Epithelium Endothelium Alveolar Gas Capillary Blood Thickness

The Ventilation Vital Sign

PaCO3 Equation . VCO2 PaCO2= VE * (1- VD/VT) VDequip VDanat VDA
Low Production High Production Hypothermia Hyporthyroidism Underfeeding Neuromuscular blockade High fatty acid substrate Sepsis/inflammation Hyperthermia Hyperthyroidism High carbohydrates Seizure and agitation Cell Metabolism . VCO2 PaCO2= VE * (1- VD/VT) VDequip HME Respiratory Rate Tidal Volume VDanat VDA PEEP Low BP

Dead Space VDA VDequip VDanat ETT Alveoli High PEEP Alveolus Airways

Semi-Quantitative Capnometry
Relies on pH change Paper changes color Purple to Brown to Yellow

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Hypercapnia ↑VCO2 ↑PaCO2 = ↔VA = VE – VD Increased CO2 production but not able to hyperventilate: Fever Sepsis Hyperthyroidism Overfeeding with carbohydrates Agitation

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Hypercapnia ↔VCO2 ↑PaCO2 = ↓VA = ↓VE – VD Decreased Alveolar Ventilation due to Decreased Minute Ventilation (VE= ↓VT X ↓RR) Sedative drug overdose Respiratory muscle paralysis Central hypoventilation

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Hypercapnia ↔VCO2 ↑PaCO2 = ↓VA = VE – ↑VD Decreased Alveolar Ventilation due to Increased Dead Space Ventilation (VD= Dead Space Volume X RR) Pulmonary embolism High PEEP Pulmonary hypertension Chronic obstructive pulmonary disease

Dangers of Hypercapnia
An elevated PaCO2 will lower the PAO2 (Alveolar gas equation), and as a result will lower the PaO2. An elevated PaCO2 will lower the pH ( Henderson-Hasselbalch equation). The higher the baseline PaCO2, the greater it will rise for a given fall in alveolar ventilation, e.g., a 1 L/min decrease in VA will raise PaCO2 a greater amount when the baseline PaCO2 is 50 mm Hg than when it is 40 mm Hg.

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Hypocapnia ↓VCO2 ↓PaCO2 = ↔VA = VE – VD Decreased CO2 production but same minute ventilation: Hypothermia Paralysis Hypothyroidism Underfeeding with carbohydrates Sedation

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Hypocapnia ↔VCO2 ↓PaCO2 = ↑VA = ↑VE – VD Increased Alveolar Ventilation due to Increased Minute Ventilation (VE= ↑ VT X ↑ RR) CNS stimulants Agitation Central hyperventilation

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Eucapnia ↑VCO2 ↔PaCO2 = ↑VA = ↑VE – VD Increased CO2 production and Increased Alveolar Ventilation: Fever and sepsis Hyperthyroidism Agitation

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Eucapnia ↓VCO2 ↔PaCO2 = ↓VA = ↓VE – VD Decreased CO2 production and decreased Alveolar Ventilation Hypothermia Hypothyroidism

PCO2 vs. Alveolar Ventilation
The relationship is shown for metabolic carbon dioxide production rates of 200 ml/min and 300 ml/min (curved lines). A fixed decrease in alveolar ventilation (x-axis) in the hypercapnic patient will result in a greater rise in PaCO2 (y-axis) than the same VA change when PaCO2 is low or normal. This graph also shows that if alveolar ventilation is fixed, an increase in carbon dioxide production will result in an increase in PaCO2.

PaCO2 and Alveolar Ventilation: Test Your Understanding
What is the PaCO2 of a patient with respiratory rate 24/min, tidal volume 300 ml, dead space volume 150 ml, CO2 production 300 ml/min? The patient shows some evidence of respiratory distress. VCO2 X 0.863 VCO2=300 X .863 VCO2=259 PaCO2=71.9 PaCO2 = VA = VE – VD VA = 3.6 VA = VE (300X24) – VD (150 X 24) VA = VE (7.2) – VD (3.6)

What is the PaCO2 of a patient with respiratory rate 10/min, tidal volume 600 ml, dead space volume 150 ml, CO2 production 200 ml/min? The patient shows some evidence of respiratory distress VCO2 X 0.863 VCO2=200 X .863 VCO2=173 PaCO2=38.4 PaCO2 = VA = VE – VD VA = 4.5 VA = VE (600X10) – VD (150 X 10) VA = VE (6) – VD (1.5)

A man with severe chronic obstructive pulmonary disease exercises on a treadmill at 3 miles/hr. His rate of CO2 production increases by 50% but he is unable to augment alveolar ventilation. If his resting PaCO2 is 40 mm Hg and resting VCO2 is 200 ml/min, what will be his exercise PaCO2? VCO2 X 0.863 ↑300 X 0.863 200 X 0.863 PaCO2=59.9 PaCO2=40 PaCO2 = VA = 4.32 L/min VA = VE – VD

Effective Ventilation
Alveolus VDA Alveolus Airways Alveoli ETT VDequip VDanat VT= 500 RR= 10 VDequip= 50 VDanat= 125 VDA= 25 VTe= 300 VT= 250 RR= 20 VDequip= 50 VDanat= 125 VDA= 25 VTe= 50 VE= 5 L/min

NORMAL CAPNOGRAM Phase I: anatomical dead space mm Hg
Phase II : alveolar gas begins to mix with the dead space gas 70 60 50 40 30 20 10 Phase I Phase II Phase III Phase IV Phase III: elimination of CO2 from the alveoli PetCO2 Time Expiratory Phase Inspiratory Phase

NORMAL Waveform Square box waveform ETCO2 35-45 mm Hg
Management: Monitor Patient mm Hg 70 60 50 40 30 20 10 Time

Sudden  in ETCO2 to 0 Loss of waveform Loss of ETCO2 reading
Dislodged tube ET obstruction Management: Replace ETT mm Hg 70 60 50 40 30 20 10 Time

Esophageal Intubation
Absence of waveform Absence of ETCO2 Management: Re-Intubate mm Hg 70 60 50 40 30 20 10 Time

CPR Square box waveform ETCO2 15-20 mm Hg with adequate CPR
ETCO2 falls bellow 10 mm Hg Management: Change Rescuers mm Hg 70 60 50 40 30 20 10 Time

Return of Spontaneous Circulation
During CPR sudden increase of ETCO2 above mm Hg Management: Check for pulse mm Hg 70 60 50 40 30 20 10 Time

Gradual Decrease in ETCO2
Hyperventilation Decreasing temp Gradual  in volume mm Hg 70 60 50 40 30 20 10 Time

Hyperventilation Shortened waveform ETCO2 < 35 mm Hg
Management: If conscious gives biofeedback. If ventilating slow ventilations mm Hg 70 60 50 40 30 20 10 Time

Gradual Increase in ETCO2
Fever Hypoventilation mm Hg 70 60 50 40 30 20 10 Time

Hypoventilation Prolonged waveform ETCO2 >45 mm Hg
Management: Assist ventilations mm Hg 70 60 50 40 30 20 10 Time

Rising Baseline Patient is re-breathing CO2
Management: Check equipment for adequate oxygen flow If patient is intubated allow more time to exhale mm Hg 70 60 50 40 30 20 10 Time

Curare Cleft Curare Cleft is when a neuromuscular blockade wears off
The patient takes small breaths that causes the cleft Management: Consider neuromuscular blockade re-administration mm Hg 70 60 50 40 30 20 10 Time

Breathing around ETT 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 mm Hg 70 60 50 40 30 20 10 Time

Obstructive Airway Shark fin waveform
With or without prolonged expiratory phase Can be seen before actual attack Indicative of Bronchospasm( asthma, COPD, allergic reaction) mm Hg 70 60 50 40 30 20 10 Time

Oscillation in Inspiratory Phase
mm Hg 70 60 50 40 30 20 10 Time J Int Care Med, 12(1): 18-32, 1997

Oscillation and slow Inspiration
mm Hg 70 60 50 40 30 20 10 Time J Int Care Med, 12(1): 18-32, 1997

Blood Gases

Acidemia or Alkalemia Is there Is the PaCO2 Is the HCO3- It is
Acidaemia High Normal/high Respiratory acidosis Low Metabolic acidosis Alkalaemia Normal/low Respiratory alkalosis Metabolic alkalosis We are going to use this table to define the causes of pH abnormalities. We assess the change in ph and then by looking at the changes in CO2 and bicarbonate we can work out the primary problem and the type and amount of compensation.

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

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

Adequate degree of compensation?
Primary problem Compensation For every  in Expected  Metabolic Acidosis Respiratory alkalosis 1 ↓ HCO3 PaCO2 ↓ 1.2 Metabolic Alkalosis Respiratory acidosis 1 ↑ HCO3 PaCO2 ↑ 0.6 Respiratory Acidosis Acute 1 ↑ PaCO2 HCO3 ↑ 0.1 Respiratory Acidosis Chronic HCO3 ↑ 0.4 Respiratory Alkalosis Acute 1 ↓ PaCO2 HCO3 ↓ 0.2 Respiratory Alkalosis Chronic HCO3 ↓ 0.4

Adequate degree of compensation for Metabolic Acidosis ?
Calculated PaCO2=(1.5 x HCO3) +8±2 Measured PaCO2>Calculated PaCO2 then concomitant respiratory acidosis Measured PaCO2<Calculated PaCO2 then concomitant respiratory alkalosis

 HCO3 = Normal HCO3- Measured HCO3
Delta Delta    HCO3 = Normal HCO3- Measured HCO3  AG= Measured AG-Normal AG  HCO3 >  AG: associated metabolic alkalosis  HCO3 <  AG: associated nongap metabolic acidosis

ABG Problems: 7.2/26/85/95% on RA Metabolic acidosis
145 100 16 4.0 12 1.0 Metabolic acidosis 145-(100-12)=AG =33 Expected PaCO2 1.5x12 +8 ±2=26±2 appropriate  AG= 21 >  HCO3= 12 Concomitant metabolic alkalosis

ABG Problems 7.1/35/60/90% on RA Metabolic acidosis 135-106-10 = AG 19
16 4.2 10 1.0 Metabolic acidosis = AG 19 Expected PaCO2 1.5 x ±2=23±2 Measured >calculated Concomitant respiratory acidosis  AG= 7 <  HCO3= 14 Concomitant nongap metabolic acidosis Next calculate UAG

[HCO3-] mmol/l 100 20 10 30 40 50 60 80 90 70 13.3 2.7 1.3 4.0 5.3 6.7 8.0 10.6 12.0 9.3 PCO2 (kPa) 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 7.8 8.5 H+ (nmol/l) pH 6 9 12 15 18 21 24 27 33 36 39 42 45 48 51 57 63 69 74 Acute respiratory alkalosis Chronic respiratory alkalosis Metabolic acidosis Acute respiratory acidosis Metabolic alkalosis HCO3-(mmol/l) N Chronic respiratory acidosis Acid-base nomogram

Thank You

Ventilator Course in Sudan: December 15-16, 2011

Oxygenation & Ventilation Monitoring

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