arterial and venous blood gas analysis edward omron md, mph

Arterial And Venous Blood Arterial And Venous Blood Gas AnalysisGas Analysis

ByBy

Edward Omron MD MPH FCCPEdward Omron MD MPH FCCP

Pulmonary Critical Care MedicinePulmonary Critical Care Medicine

Morgan Hill, CAMorgan Hill, CA

www.docomron.comwww.docomron.com

INDICATIONSINDICATIONS

• ABG– Oxygenation– Ventilation– Acid-Base Status

• VBG– Ventilation and Acid-Base Status

– Cardiac Output (venous arterial PCO2 difference)

– Endpoint of resuscitation (PvO2 and PCO2)

Blood Gas Report(Blood Gas Report(ArterialArterial))

• pH (No Units) 7.35-7.45

• PaCO2 (mm Hg) 35-45

• PaO2 (mm Hg) 110 - 0.5(age)

• HCO3- (mmol/L): calc. 22-26

• B.E. (mmol/L) -2 to 2

• O2 saturation: calc. >90%

Blood Gas ReportBlood Gas Report(mixed/central venous)(mixed/central venous)

• pH = 7.32-7.42

• PvCO2 = 40 - 50 (mm Hg)

• PvO2 = 36 - 42 (mm Hg)

• Oxygen Saturation > 70%

• Base Excess = -2 to +2

ANALYSIS OF OXYGENATIONANALYSIS OF OXYGENATION

• Alveolar Gas Equation– PAO2 = FIO2(PB - 47) - 1.2(PaCO2)

– PAO2 defines upper limit of PaO2

– FIO2 is 21% at all altitudes

– Factor 1.2 determined by RQ– Water vapor pressure = 47 mm Hg

– PAO2= 150 - 1.2(PaCO2) at room air

– PAO2 = 102

Alveolar-Arterial Oxygen DifferenceAlveolar-Arterial Oxygen Difference

• A-aDo2 = PAO2-PaO2(from ABG)

• Insight in the patients state of gas exchange– If elevated, defect in gas exchange

– Proper interpretation of the PaO2

Causes of a low PaOCauses of a low PaO22 and A-a Do and A-a Do22

• P(B): Altitude

• Alveolar Hypoventilation(Nl A-a Do2)

• V/Q mismatch

• Shunt

• Diffusion Impairment

• Decreased mixed / central venous O2 content

Alveolar HypoventilationAlveolar Hypoventilation

• No increase in P(A-a)O2 gradient

• Muscle weakness

• Neuromuscular Junction Disease

• Reduced Respiratory Drive (drugs)

• Chest wall elastic loads

• Brainstem injury

Approach To HypoxemiaApproach To Hypoxemia

PaO2 A-a Do2 pCO2N

FIO2N

Alv. Hypo.

100% O2 Corrects V/Q Mis.

No Correction Shunt

Diffusion

Changes in P(A-a)O2 with FIO2

Acute Lung Injury

• PaO2/FIO2 ratio

– Normal = 90 mm Hg/0.2 = 450– Acute lung injury < 300– Acute Respiratory Distress syndrome <200

OXIMETRYOXIMETRY

• Binding sites for O2 are heme groups• OXYGEN SATURATION

– % of all heme sites saturated with O2

• Measures the difference in the light absorbance characeteristics between Oxy Hb and Deoxy Hb

• SpO2 = Oxy Hb x 100 Oxy Hb + Deoxy Hb• ABG SaO2 is a calculated value from PaO2

Pulse OximetryPulse Oximetry

Whole Blood

PaO2

SaO2

SpO2:Pulse Oximetry

OximetryOximetry

• 54 yo WM with headaches, dyspnea and a Kerosene heater at home– ABG: PaO2 = 89, PaCO2 = 38, pH = 7.43– SaO2 = 98%– Whats the problem?

OximetryOximetry

• Carboxyhemoglobin: Hb +CO– Does not affect PaO2 only SaO2– Pulse oximetry reads CO-HB as OxyHb

• Follow Up:– PaO2 = 79, PaCO2 = 31, SpO2 = 53%, pH =7.36 – CO-Hb46%

Correlation of symptoms and signs with carbon monoxide level Percent of CO in inspired

air Percent of HbCO in blood Signs and symptoms

0.007 10

Common in cigarette smokers; dyspnea during vigorousexertion; occasional tightness in forehead; dilation of cutaneous blood vessels

0.012 20 Dyspnea during moderate exertion; occasional throbbing headache in temples

0.022 30 Severe headache; irritability; easy fatigability; disturbed judgment; possible dizziness and possible dimness of vision

0.035 40+ Headache; confusion; fainting on exertion

0.080 60+ Unconsciousness; intermittent convulsions; respiratory failure; death if exposure prolonged

0.195 80 Fatal

Modified from Winter, P.M., and Miller, J.N.: JAMA 236:1503, 1976, Copyright 1976, American Medical Association.

ProblemProblem

• 42 yo HIV pt with fevers,chills, SOB,cough– Taking Dapsone for PCP prophylaxis– ABG: PaO2 82.5, PaCO2 35.2, pH 7.43, SaO2

89%– PCP Pneumonia, started onPrimaquine, Clinda,

and Prednisone– ABG: PaO2 378, PaCO2 of 35, pH 7.42, SaO2

80%– Whats Happening?

MethemoglobinMethemoglobin

• Oxidation of Fe++ to Fe+++ state

• Unlike CO-Hb, Met-Hb does depress the SpO2 reading

• Both Dapsone and Primaquine are oxidants

• Met-Hb depresses the SpO2 to 80’s– Further increaeses in Met-Hb do not depress

SpO2

• Methylene Blue administration is Rx

Some drugs implicated in causing methemoglobinemia Generic name Use

Dapsone Skin protectant

Benzocaine Local anesthetic

Metoclopramide Gastric stasis

Nitroglycerin Angina

Phenazopyridine Urinary tract analgesic

Prilocaine Local anesthetic

Primaquine Malaria prophylaxis and treatment

Trimethoprim Urinary antibacterial

Amyl nitrite Rarely used clinically; often used by drug abusers

ANALYSIS OF VENTILATONANALYSIS OF VENTILATON

• PaCO2 = VCO2 x K

VA

Hypercapnea > 45 mm Hg (Hypoventilation)

Respiratory Acidosis

Hypocapnea < 35 mm Hg (Hyperventilation)

Respiratory Alkalosis

Respiratory Acid-Base Status

• Respiratory Disturbances– CO2+H20 H2CO3 H+ + HCO3

– Acute changes:• Delta 10 mm Hg PaCO2, pH changes by 0.08• Chronic change: 40 + B.E

– Alveolar Ventilation• VA CO2 pH

• Respiratory Acidosis pCO2 > 45• Respiratory Alkalosis pCO2 < 35

BASE EXCESS (B.E.)BASE EXCESS (B.E.)

• Base Excess• Quantity of acid or base needed to restore plasma

pH to 7.4, at a PCO2 equillibrated to 40 mm Hg

• Positive value, excess base, metabolic alkalosis

• Negative value, excess acid, metabolic acidosis

• Metabolic component of acid-base status

• PCO2 independent

• Estimated by BE = (Total CO2 – 24)

Problem Solving

1. LOOK AT THE pH– Whatever side of pH 7.4 is the primary disorder

2. Look at pH, PCO2 direction

– Both decrease or increase, then metabolic– If move in opposite directions, respiratory

3. Respiration: acute or chronic?– Acute: 10 mm Hg / 0.08 change in pH– Chronic: 40+Base Excess

• Calculate the Adjusted Anion Gap– High vs normal ANG differential– 2.8 mmol of acid /gram serum albumin– Law of Electrical Neutrality

• Positive charges = negative charges or

• Positive charges - negative charges = 0

– [Na+] - [Cl-] -[HCO3-] - [Albumin-] = 0

– [Na+] - [Cl-] -[HCO3-] = [Albumin-]

– 140 - 104 -24 = 4.4 gm/dL* 2.8 12– Normal ANG = 12 = 2.8 * [Albumin-]– Adjusted ANG = ANG + 2.8(4.4 -Albumin)

Arterial Draw:• pH = 7.28, PaCO2 = 34, HCO3 = 16

• Na = 153 Cl = 106 Total CO2 = 17

• Alb = 3 g/dL

• Primary Acid-Base Disturbance?

• ANG and Adjusted ANG

• Metabolic Acid-Base Status

74 yo male found unresponsive and pulseless

• Primary Disorder– Acidosis and acidemia (pH < 7.4)

• pH and PCO2 direction– Both down: Metabolic Acidosis

• Base Excess– 16 – 24 = -8 mmols/L

• Adjusted Anion Gap– ANG + 2.8*(4.4 - 3) or 30 + 4 = 34 – Anion Gap Acidosis

• Compensation? – 40 + BE or 32 mm Hg

Venous Draw

• pH = 7.08, pCO2 = 75, HCO3 = 21

• Na = 145, Cl = 103, Total CO2 =22

• Alb = 3 g/dL

• Primary Acid-Base Disorder?

• ANG and expected ANG?

• Metabolic Acid-Base Status?

• Primary Disorder– pH < 7.4, acidosis and acidemia

• pH and PCO2 direction– Opposite therefore RESPIRATORY acidosis

• Base Excess

– 22 – 24 = -2 mmol/L

• Adjusted Anion Gap– ANG + 2.8(4.4 -3) = 20+4 =24– Anion Gap Acidosis

• 40 + BE rule Comp in VBG

74 yo male found unresponsive and pulseless

• Why a metabolic acidosis in arterial bed and respiratory acidosis in venous bed?– Venous arterial PCO2 difference?– PaCO2 = 34 and PvCO2 = 75– PvCO2 – PaCO2 1 / cardiac index

• Venous vs Arterial saturation difference?– PaO2 = 50 mm Hg, saturation = 84%– PvO2 =18, Venous Saturation = 20%– Increased oxygen extraction from circulatory

failure

Central Venous Oxygen Saturation ScvO2

• Easily measured with venous blood gas• Surrogate measurement of mixed venous oxygen sat.

– 5-18% higher

– A low ScvO2 always means a low SvO2!

• Normal ScvO2 68-76%– 25% extraction coefficient of normal physiology

– Peripheral venous gas as a screen for further investigation

PaO2 vs PvO2 in Cardiogenic Shock

Paradoxical Respiratory Acidosis of Cardiopulmonary Arrest

Four Determinants of Central Venous Oximetry

ScvOScvO22 SvO SvO22 = SaO = SaO2 2 - VO - VO22 / C.O. x Hgb x 1.36 / C.O. x Hgb x 1.36

ScvO2 = Central venous saturation (%)

SvO2 = Mixed venous saturation (%)

SaO2 = Arterial oxygen saturation (%)

VO2 = Oxygen consumption mL (O2/min)

Hgb = Hemoglobin concentration (g/dL)Cardiac Output (C.O.) = dL/min

Effect of changes in PaO2 on SvO2

600200

10080

60

40

0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

0.9

1

0 100 200 300 400 500 600 700

PaO2 (mm Hg)

SvO

2

SvO2

Effect of changes in Hgn on SvO2

13

10

7.5

5

0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

0.9

0 2 4 6 8 10 12 14

Hemoglobin (g/dL)

Sv

O2

SvO2

The Effects of Cardiac Output on SvO2

0.870.83

0.73

0.66

0.55

0.31

0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

0.9

1

0 2 4 6 8 10 12

Cardiac Output (L/min)

Sv

O2

SvO2

Effect of Oxygen Consumption (VO2) on SvO2

0.850.79

0.74

0.68

0.57

0.46

0

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

0.9

0 100 200 300 400 500 600

Oxygen Consumption (VO2)

Sv

O2

SvO2

Venous Arterial CO2 Difference

• Circulatory Failure– Associated with Tissue Hypercarbic Acidosis– Hypovolemia, sepsis, shock …

• Cardiac Index = e (1.787 – 0.151(v-a CO2))

– Endpoint of Resuscitation

• PvO2– Enpoint of Resuscitation

SvO2 vs SaO2 response in Septic Shock "Golden Hour"

27

51

6873

100 100 9891

0

10

20

30

40

50

60

70

80

90

100

1 2 3 4

Days

Per

cen

tag

e

SvO2

SaO2

REFERENCES

• Current Opinion Critical Care 2001; 7: 204-211• NEJM 2001; 345: 1368-1377• Critical Care Medicine 2002; 30: 1686-1692• Circulation 1969; 40: 165• Thorax 2002; 57: 170-177• Academic Emer Med 1999; 6: 421