VENOUS AND ARTERIAL BLOOD GAS ANALYSIS IN EMERGENCY DEPARTMENTS:

WHAT WE KNOW AND WHAT WE DON’T!

Anne-Maree KellyProfessor and DirectorJoseph Epstein Centre for Emergency Medicine Research @Western Health

Permissions

This presentation can be used in part or whole for educational purposes on the condition that the following appears on each slide used:

‘Re-produced with permission of Professor Anne-Maree Kelly, Joseph Epstein Centre for Emergency Medicine Research, Melbourne, Australia’

@kellyam_jec

Conflicts of interest

I received financial support for travel and accommodation from Radiometer Pty Ltd to present a similar presentation at 4th International Symposium on Blood Gas and Critical Care in France in 2008.

I am undertaking some research with A/Prof Rees into calculated values which may be commercialised. I have no pecuniary interest in this program.

I have not received industry funding for any of my blood gas research projects.

Objectives

After this presentation, participants will:

Understand the agreement performance of variables on arterial and venous blood gas analysis, in particular

pH pCO2

Bicarbonate Base excess

Be aware of the unanswered questions Be aware of new approaches being taken to improve accuracy of

prediction of arterial values from venous blood gas samples

Caveats

Discussion will be limited to comparisons between arterial and peripheral venous samples

Data is up-to-date as of publications to May 2012 Includes some of data only ‘published’ as abstract in

2012

Blood gases in emergency medicine

Establishing acid-base status Mainly pH; but also bicarbonate

Measuring respiratory function/ ventilation Mainly pCO2; but also pH

‘Quick check’ potassium, haematocrit, some electrolytes Not addressed in this presentation

Why venous rather than arterial?

Less pain for patients Fewer complications, especially vascular and

infection Fewer needle-stick injuries Easier blood draw Minimal training requirement

Setting the context

JANE

26 year old, insulin dependent diabetic

2 days of vomiting and diarrhoea.

Pulse 120 bpm, BP 100/-, BSL ‘Hi’

TRAN

74 year old COAD Acute respiratory distress.

Pulse 110, BP 140/-, SpO2

(air) 88%

The clinical questions

Can we Exclude / diagnose Monitor progress of Base therapeutic decisions for (eg use and settings of

NIV)

Metabolic acidosis or acute respiratory failure using venous blood gas analysis rather than arterial?

Statistical considerations

Outcome of interest is how closely venous and arterial values agree, not how well they correlate

Weighted mean difference gives an estimate of the accuracy between the methods

95% limits of agreement give information about precision

Arterial value

Venous value

95% LoA

Clinical considerations

There is limited data about the tolerance clinicians have with respect to agreement between arterial and venous values of blood gas parameters

Depending on this tolerance, the degree of agreement may be acceptable or unacceptable There is known variation between clinicians re this

Issues with the evidence

Patient cohorts highly varied

Patient groups of interest are those at high risk of acidosis or hypercarbia Reporting does not always report this detail Data may to be dominated by patients with normal pH,

pCO2 and blood pressure Need for research focussed on high risk patient groups

pH

13 studies Range from 44 to 346 patients

Various conditions DKA (3), COAD (4), trauma (1)

2009 patients

Weighted mean difference of 0.033 pH units

95% limits of agreement (7 studies) generally within +/- 0.1 pH units

pH in illness subgroups

DKA

3 studies (265 patients) Weighted mean

difference = 0.02 pH units

95% limits of agreement = -0.009 to 0.02 pH units (1 study)

COAD

5 studies (643 patients) Weighted mean

difference= 0.034 pH units

95% limits of agreement generally +/- 0.1 (3 studies)

pH- Other

One ICU-based study suggests that as hypotension increases, AV pH agreement deteriorates Very small patient numbers Finding not yet validated

What we know & evidence gaps

We know: Generally close AV agreement in both respiratory and

metabolic disease

Evidence gaps: AV agreement in various levels and types of shock AV difference in toxicology scenarios (1 small study in

TCA OD only) AV difference in mixed acid-base disease

Bicarbonate

8 studies

1211 patients

Various conditions (COAD 2)

Weighted mean difference = -1.3mmol/l

95% limits of agreement : up to +/- 5mmol/l (3 studies)

Bicarbonate in illness subgroups

DKA

1 study (21 patients) Weighted mean

difference = -1.88 mmol/l

95% limits of agreement = -2.8 to 0.9 mmol/l

COAD

2 studies (643 patients) Weighted mean

difference= -1.34 mmol/l 95% limits of agreement:

none reported

What we know and evidence gaps

We know: Limited data suggests good agreement

Very little data re limits of agreement ? +/- 5mmol/L

Evidence gaps: AV agreement in specific disease states AV agreement in various levels and types of shock AV difference in toxicology scenarios AV difference in mixed acid-base disease

pCO2

8 studies

965 patients

Various conditions (COAD 4)

Weighted mean difference = 6.2 mmHg

95% limits of agreement: up to -17.4 to +23.9 mmHg 5/7 studies reporting LoA report LoA band >20mmHg

pCO2 in COAD

4 studies

452 patients

Weighted man difference = 7.26 mmHg

95% limits of agreement: up to -14 to +26 All 3 studies that reported LoA report LoA band

>20mmHg

Venous pCO2: A screening test for hypercarbia?

Author, year No. Screening cut-off

Sens. Spec. NPV %ABG avoided

Kelly, 2002 196 45 100 57 100 43

Kelly, 2005 107 45 100 47 100 29

Ak, 2006 132 45 100 * 100 33

McCanny, 2011

94 45 100 34 100 23

POOLED DATA

529

45 100 (95% CI 97-100)

53(95% CI 57-58)

100(95% CI 97-100)

35%(95% CI 32-41)

Data limited to studies in cohorts with respiratory disease

Using venous pH and CO2 to track progress?

Preliminary data presented at this meeting as a poster

41 comparisons in 29 patients Arteriovenous difference for change in pH =0.004 (95%

LoA -0.09 to 0.1) Arteriovenous difference for change in pCO2 = 0.55mmHg

(95% LoA -16.6 to 17.6mmHg)

What we know & evidence gaps

We know: AV agreement is NOT good enough for clinical inter-

changeability Wide limits of agreement

Venous pCO2 has potential as a screening test for hypercarbia Excellent NPV AV agreement in change in pCO2 is NOT good enough for clinical

inter-changeability (pilot data only) Wide limits of agreement

Evidence gaps: Whether trend in venous pCO2 and pH can safely drive a care pathway

for COAD Subject of current international research project

Base excess

Two studies only In a sample of 103 patients (various conditions), they

report: mean difference of 0.089mmol/L 95% limits of agreement -0.974 to +0.552 mmol/L

In 326 trauma patients mean difference -0.3 BE units 95% limits of agreement -4.4 to +3.9 BE units 20% did not fall within pre-defined clinical equivalence threshold

Current view: LOA too wide. If accuracy needed in critically ill, need ABG

Clinical application

JANE

DKA AV agreement is

acceptable; at least in non-shocked patients

Can use venous pH to diagnose/ monitor

TRAN

Acute respiratory distress

pH agreement good but pCO2 has considerable imprecision

Can use venous pCO2 as a screening test for hypercarbia

Another approach

Team from Center for Model Based Medical Decision Support Systems, Dept of Health Science and Technology, Aalborg University, Denmark (A/Prof Steven Rees)

Developed venous to arterial conversion method using venous blood gas variables and pulse oximetry

Designed to be incorporated into blood gas analysers

The model

The method calculates arterial values using mathematical models

Assumes: Constant value of the

respiratory quotient of 0.82 Change in base excess from

arterial to venous blood is 0 mmol/l

Rees SE, Toftegaard M, Andreassen S. A method for calculation of arterial acid–base and blood gas status from measurements in the peripheral venous blood. Comp Methods Programs Biomed. 2006, Vol 81, 18-25.

Validations

Respiratory patients N=40 (55% acute

admissions) Arterial-calculated pH

difference = -0.001pH units (95% LoA -0.026 to +0.026)

Arterial-calculated pCO2 difference = -0.68mmHg (95% LoA -4.81 to +3.45 mmHg)

Respiratory/ ICU N=103 Arterial-calculated pH

difference = -0.002pH units (95% LoA -0.029 to +0.025)

Arterial-calculated pCO2 difference = 0.3mmHg (95% LoA -3.58 to +4.18 mmHg)

Toftegaard et al. Emergency Medicine Journal. 2009;26:268-72

Rees et al. Eur Respir J. 2009;33:1141-7.

Validations

Emergency dept patients

N=148 patients (47 clinical need for ABG, 101 without)

pH can be calculated to within 0.02 pH units (95% LoA)

pCO2 can be calculated to within 4mmHg (0.5kPa)

Tygesen et al. Eur J Emerg Med. 2011 Nov 11. [Epub ahead of print]

Monitoring over time: Example

Red=measured arterialBlack dots =calculated arterialBlue dashes=measured venous

pH pCO2

Courtesy of SE Rees (unpublished)

Comments

Hard to know how many patients were acidotic or hypercarbic

No validation in patients undergoing respiratory support e.g. NIV

Model undergoing commercialisation Add on licence to blood gas machine No app planned at this stage (personal communication)

Take home messages

pH and bicarbonate probably close enough agreement for clinical

purposes in DKA, acute respiratory failure, isolated metabolic acidosis

More work needed in toxicology, shock, mixed disease

Take home messages

pCO2 NOT enough agreement for clinical purposes, either as

one-off or to monitor change Data suggests venous pCO2 is useful as a screening test

Base excess Probably not enough agreement for clinical purposes

Take home messages

Mathematical modelling approaches might be more accurate especially for pCO2

For broad applicability an app/ similar would be more feasible than integration into blood gas machines

More work needed to prove accuracy and precision in high risk groups

Questions?

Questions?

Questions?

@kellyam_jec