Emergency Department (ED) Critical Care   Emergency medicine critical care podcast

 

Lab and Arterial Blood Gas Interpretation

Venous Blood Gas

pH .03 lower

PvCO2 5.8 higher

PvCO2 less than 45 on room air rules out hypercarbia (Journal of Emergency Medicine
Volume 28, Issue 4 , May 2005, Pages 377-379)

 

Venous is as good as arterial blood gases in DKA (Emerg Med Austr 2006;18:64)

pH was almost identical, bicarb was close enough

 

Central (SVC) pH, bicarb, BE, and lactate agrees with arterial (Emerg Med J 2006;23:622)

 

New method can calculate an ABG from a VBG (Emerg Med J 2009;26:268)

Lactate

A normal venous lactate rules out an elevated arterial, an elevated venous does not necessarily correlate with an elevated arterial.  Tourniquet time may contribute to this inaccuracy.  If you do venous lactate, draw as first tube and put on ice immediately.  (Annals EM 1997. Vol 29. Number 4)

 



Relative hyperlactatemia is still associated with mortality (>0.75 mmol/L) Crit Care 2010;14:R25

 

reanaylyzed in healthy subjects. no effect from tourniquet time or room temp holding if analyzed in 15 min or less (Acad Emerg Med 2007;14:587)

 

both arterial and venous lactates performed within 10 minutes.
Collected data included injury mechanism, demographics,
admission vital signs, disposition, length of stay, hospital
outcomes and injury severity score. The mean arterial lactate
concentration was 3.11 mmol/L (SD 3.45, 95% CI 2.67-3.55)
and the mean venous lactate concentration was 3.43 mmol/L
(SD 3.41, 95% CI 2.96-3.90) demonstrating no significant
differences between the two sources of blood lactate. The
correlation between venous and arterial lactate levels was 0.94 (Lavery RF, Livingston DH, Tortella BJ, Sambol JT, Slomovitz BM, Siegel JH. The utility
of venous lactate to triage injured patients in the trauma center. J Am Coll Surg.
2000;190(6):656-664.)

 

Adams et al. included all ED
patients over a seven month time period in whom a lactate
level was measured for any reason. They considered an AG
>12 abnormal and conducted sensitivity analyses of the AG
for detecting the presence of a lactate >2.5 mmol/L. The AG
was 52.8% sensitive, 81.0% specific with a negative predictive
value of 89.7% for the prediction of lactic acidosis.(

Adams BD, Bonzani TA, Hunter CJ. The anion gap does not accurately screen for lactic

acidosis in emergency department patients. Emerg Med J. 2006;23(3):179-182.)

 

Nguyen HB, Rivers EP, Knoblich BP, et al. Early lactate clearance is associated
with improved outcome in severe sepsis and septic shock. Crit Care Med.
2004;32(8):1637-1642.

 

 

In ARDS, the lung may be the major source of lactate Intens Care Med 2004;30:817

 

 

Whole blood venous point-of-care lactate concentrations in healthy subjects do not change significantly
over 15 minutes at either 18C or 238C, and the use of a tourniquet has no appreciable effect on
lactate concentrations. (Acad Emerg Med 2007; 14:587–591)

 

the utility of venous lactate to triage pts in trauma (J Am Coll Surg 2000;190(6):656)
VLAC equiv to ALAC; >=2 predicts need for ICU, etc.

another study correlating lactates with mortality (Inten Care Med 2007;33:1892)


 

---

if fiO2x5=PaO2 then lungs are fully recruited

 

Dead Space Ventilation V/Q>1

Venous Admixture V/Q<1

Shunt V/Q=0

 

Dead Space

Vd/Vt=(PaCO2-PECO2)/PaCO2

PECO2 is the CO2 in expired gas, but not same as ETCO2, it must be measured by resp therapy

 

Shunt Fraction

Qs/Qt=(CcO2-CaO2)/(CcO2-CvO2)

CcO2=pulmonary capillary blood

 

Aa Gradient=PA-Pa

PA=PIO2-(PaCO2/RQ)

PIO2=FiO2(760-47)
RQ=0.8

 

Normal Aa rises with Age

20 4-17

30 7-21

40 10-24

50 14-27

60 17-31

70 21-34

80 25-38

 

Normal Aa gradient increases 5-7 mmHG for every 10% increase in FiO2 due to the overcoming of hypoxic vasoconstriction opening blood flow to poorly ventilated lung areas.

 

Hypoxemia

Why: Hypoventilation, Pulmonary Disorder, DO2/VO2 Imbalance

 

In disorders with intrapulmonary shunt (pneumonia, ards), the mixed venous O2 will be a larger determinant of PaO2 and should be evaluated.

 

Evaluating Hypoxemia

Step I-Aa Gradient

Normal-generalized hypoventilation disorder. Drug induced or neuromuscular,

Increased-V/Q Abnormality and/or systemic supply/demand imbalance (DO2/VO2). Obtain a SvO2 or CvO2.

 

Mixed Venous PO2

breakpoint is 40 mmHg

Normal-Problem is solely V/Q abnormality.

Low-Systemic DO2/VO2 imbalance. Either decreased oxygen delivery (anemia, Low CO) or increased consumption (hypermetabolic state)

 

Hypercapnia

PaCO2=k x (VCO2/VA)

k is a constant

VA=VE(1-Vd/Vt)

VE is expired volume

VA is non-deadspace ventilation

Overfeeding can cause hypercarbia

 

Alveolar Hypoventilation

Resp Muscle Weakness (Get PImax)

Central Hypoventilation Syndromes

 

 

Dual Oximetry

SaO2-SvO2=VO2/(Q x Hb)

Normal is 20-30%

30-50 low cardiac output, anemia, hypermetabolism

50-60 High Risk of dysoxia, transfusion trigger.

 

 

Hypocapnia

(N Engl J Med, Vol. 347, No. 1 July 4, 2002)

.
In such cases, there is a dissociation between
the condition of central venous blood, with a
high partial pressure of arterial carbon dioxide and a
low pH, and that of the systemic arterial blood, with
a low carbon dioxide tension and an alkalemic pH;
this dissociation is due to the combination of low pulmonary
perfusion and normal ventilation, and this
condition is called pseudorespiratory alkalosis.
16

Hypocapnia may cause
or aggravate cellular or tissue ischemia by both decreasing
the cellular oxygen supply and increasing the
cellular oxygen demand (Fig. 3). Although hypocapnia
induced by hyperventilation may increase alveolar
oxygen tension, multiple important pulmonary effects
of hypocapnic alkalosis (e.g., bronchoconstriction,
48
attenuation of hypoxic pulmonary vasoconstriction,
49
and increased intrapulmonary shunting
49
) result in a
net decrease in the partial pressure of arterial oxygen.

Because both hypocapnia and alkalosis cause a leftward
shift of the oxyhemoglobin dissociation curve,
off-loading of oxygen at the tissue level is restricted.
50
In addition, hypocapnia causes systemic arterial
vasoconstriction, decreasing the global and regional
oxygen supply and compounding the reduction in
the delivery of oxygen to tissue

 

the time required for equillibration of PaO2 after PEEP adjustment is 20 minutes (Crit Care Med 2005;33(5):995)

 

if fiO2x5=PaO2 then lungs are fully recruited

 

Dead Space Ventilation V/Q>1

Venous Admixture V/Q<1

Shunt V/Q=0

 

Dead Space

Vd/Vt=(PaCO2-PECO2)/PaCO2

PECO2 is the CO2 in expired gas, but not same as ETCO2, it must be measured by resp therapy

 

Shunt Fraction

Qs/Qt=(CcO2-CaO2)/(CcO2-CvO2)

CcO2=pulmonary capillary blood

Place pt on 100% O2 for 5-15 minutes. The Aa Gradient is entirely from shunt. Dive Aa by 20 to get the shunt fraction

 

 

Aa Gradient=PA-Pa

PA=PIO2-(PaCO2/RQ)

PIO2=FiO2(760-47)
RQ=0.8

 

Normal Aa rises with Age

20 4-17

30 7-21

40 10-24

50 14-27

60 17-31

70 21-34

80 25-38

 

Normal Aa gradient increases 5-7 mmHG for every 10% increase in FiO2 due to the overcoming of hypoxic vasoconstriction opening blood flow to poorly ventilated lung areas.

 

Hypoxemia

Why: Hypoventilation, Pulmonary Disorder, DO2/VO2 Imbalance

 

In disorders with intrapulmonary shunt (pneumonia, ards), the mixed venous O2 will be a larger determinant of PaO2 and should be evaluated.

 

Evaluating Hypoxemia

Step I-Aa Gradient

Normal-generalized hypoventilation disorder. Drug induced or neuromuscular,

Increased-V/Q Abnormality and/or systemic supply/demand imbalance (DO2/VO2). Obtain a SvO2 or CvO2.

 

Mixed Venous PO2

breakpoint is 40 mmHg

Normal-Problem is solely V/Q abnormality.

Low-Systemic DO2/VO2 imbalance. Either decreased oxygen delivery (anemia, Low CO) or increased consumption (hypermetabolic state)

 

Hypercapnia

PaCO2=k x (VCO2/VA)

k is a constant

VA=VE(1-Vd/Vt)

VE is expired volume

VA is non-deadspace ventilation

Overfeeding can cause hypercarbia

 

Alveolar Hypoventilation

Resp Muscle Weakness (Get PImax)

Central Hypoventilation Syndromes

 

 

Dual Oximetry

SaO2-SvO2=VO2/(Q x Hb)

Normal is 20-30%

30-50 low cardiac output, anemia, hypermetabolism

50-60 High Risk of dysoxia, transfusion trigger.

 

 

Hypocapnia

(N Engl J Med, Vol. 347, No. 1 July 4, 2002)

.
In such cases, there is a dissociation between
the condition of central venous blood, with a
high partial pressure of arterial carbon dioxide and a
low pH, and that of the systemic arterial blood, with
a low carbon dioxide tension and an alkalemic pH;
this dissociation is due to the combination of low pulmonary
perfusion and normal ventilation, and this
condition is called pseudorespiratory alkalosis.
16

Hypocapnia may cause
or aggravate cellular or tissue ischemia by both decreasing
the cellular oxygen supply and increasing the
cellular oxygen demand (Fig. 3). Although hypocapnia
induced by hyperventilation may increase alveolar
oxygen tension, multiple important pulmonary effects
of hypocapnic alkalosis (e.g., bronchoconstriction,
48
attenuation of hypoxic pulmonary vasoconstriction,
49
and increased intrapulmonary shunting
49
) result in a
net decrease in the partial pressure of arterial oxygen.

Because both hypocapnia and alkalosis cause a leftward
shift of the oxyhemoglobin dissociation curve,
off-loading of oxygen at the tissue level is restricted.
50
In addition, hypocapnia causes systemic arterial
vasoconstriction, decreasing the global and regional
oxygen supply and compounding the reduction in
the delivery of oxygen to tissue

 

the time required for equilibration of PaO2 after PEEP adjustment is 20 minutes (Crit Care Med 2005;33(5):995)

 

 

 

Lab Tubes

What's in those vacuum-filled blood sample tubes?

Worth knowing:

 

 

"Routine Screening"
 
 
 

Contents of tubes

A large SST vacutainer.
A large SST vacutainer.

The tubes may contain additional substances that preserve the blood for processing in the medical laboratory. Using the wrong tube may therefore make the blood sample unuseable.

The substances may include anticoagulants (EDTA, lithium citrate , heparin) or a gel with intermediate density between blood cells and blood plasma. When the tube is centrifuged, the blood cells sink to the bottom of the tube, are covered by a layer of the gel, and the plasma (or serum) is left on top. The gel enables the tube to be tipped upside-down, and transported without the blood cells remixing with the plasma.

The meaning of the different colors are standardized across manufacturers. For more details on the meaning of these different colors, see [1], [2], or the bottom of [3].

The Order of Draw refers to the sequence in which these tubes should be filled. The needle which pierces the tubes can carry additives from one tube into the next, and so the sequence is standardized so that any cross-contamination of additives will not affect laboratory results [3].

[edit ]

Containers containing coagulants

Containers containing anticoagulants

[edit]

Other

[edit]

Miscellaneous

The purple top tube became an issue in the O. J. Simpson murder trial when the defense alleged that small droplets of blood found at the crime scene contained the preservative EDTA; had this been true, it would have meant that the droplet might have been taken from the purple top tube used to collect Simpson's blood and planted at the crime scene. [4]

 

 

 

 


MGH Lab Callback (Am J Clin Pathol 125(5) 2006)

Table 1. Massachusetts General Hospital Critical Value List

 


 
Test Critical Values
Chemistry (blood gas)
   Bilirubin, total, 0-3 mo old, mg/dL (µmol/L) >20 (>342)
   Calcium, ionized, mg/dL (mmol/L) <3.20 or >6.16 (<0.8 or >1.54)
   Hemoglobin, g/dL (g/L) <6.5 (<65)
   pco2, mm Hg <20 or >75
   pH <7.10 or >7.59
   po2, mm Hg <40
Chemistry (main laboratory)
   Calcium, mg/dL (mmol/L) <6.5 or >14.0 (<1.63 or >3.53)
   Carbon dioxide, total, mEq/L (mmol/L) <11 (<11)
   Glucose, CSF, mg/dL (mmol/L) <40 (<2.2)
   Glucose, plasma, mg/dL (mmol/L) <45 or >500 (<2.5 or >27.8)
   Magnesium, mEq/L (mmol/L) <1.0 or >4.9 (<0.50 or >2.45)
   Osmolality, plasma or serum, mOsm/kg H2O (mmol/kg H2O) <250 or >335 (<250 or >335)
   Phosphorus, mg/dL (mmol/L) <1.1 (<0.36)
   Potassium, mEq/L (mmol/L) <2.8 or >6.0 (<2.8 or >6.0)
   Sodium, mEq/L (mmol/L) <120 or >160 (<120 or >160)
Hematology
   All hematocrit values, % >56% (>0.56)
   δ values Various δ checks for platelet and hematocrit values
   Differential Presence of blasts on initial smear
   Initial hematocrit, % <20 (<0.20)
   Initial platelet count, × 103/µL (× 109/L) <50 or >999 (<50 or >999)
   Initial WBC count, /µL (× 109/L) <2,000 or >50,000 (<2.0 or >50.0)
   Partial thromboplastin time, s >100
   Prothrombin time, s >30

CSF, cerebrospinal fluid.

 

 

 

 

 

 

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