When Is Venous Blood Gas Analysis Enough?

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When Is Venous Blood Gas Analysis Enough?

Emerg Med 38(12):44-48, 2006

Since venipuncture is less painful, less costly, and safer for the practitioner, do you really need that arterial blood sample? The authors explain why, in many cases, the answer is no.

By Scott C. Sherman, MD, and Michael Schindlbeck, MD

Dr. Sherman is assistant professor of emergency medicine at Rush Medical College and assistant residency director in the department of emergency medicine at Cook County Hospital in Chicago, Illinois. Dr. Schindlbeck is a third-year resident in the department of emergency medicine at Cook County Hospital.

A 34-year-old man with a history significant for diabetes mellitus presents to the emergency department after experiencing progressive abdominal pain and vomiting for three days. His medications include insulin, but he states that he has missed several doses. A bedside glucose level taken in triage is 532 mg/dl. The patient appears to be in moderate discomfort with dry mucous membranes. His blood pressure is 118/80 mmHg; his heart rate, 124. He is in no apparent respiratory distress, but his respiratory rate is 22. Pulse oximetry reading on room air is 97%.

You order routine lab tests and a fluid bolus, then search for an arterial blood gas (ABG) kit. Just as you are about to draw blood from the patient’s radial artery, the nurse asks if you would like to order a venous blood gas (VBG) along with the cell count and chemistries.

CORNERSTONE OF MANAGEMENT

Arterial blood gas analysis has been a cornerstone in the management of acutely ill patients with presumed acid-base imbalances since automated blood gas analyzers first became available in the early 1960s. Decades of experience with ABG analysis have provided emergency physicians with an armamentarium of equations to diagnose multiple complicated and often concurrent metabolic derangements.

Recent studies have questioned this dogma, however. In specific scenarios, a VBG analysis may provide enough information to make the correct diagnosis and begin appropriate therapy.

In this article, we will review the practical advantages of VBG analysis and discuss its utility in the management of both metabolic and respiratory acid-base disorders.

advantages of vbg analysis

Blood gas analysis provides a great deal of data in a short period of time. When it has been set up in the emergency department as a point-of-care test, results can be obtained in about two minutes. In addition, most analyzers give more information than just the patient’s pH, PO₂, PCO₂, and HCO₃. Other data include hemoglobin, sodium, potassium, glucose, methemoglobin, carboxyhemoglobin, ionized calcium, and lactate levels.

The most obvious advantage to obtaining a VBG instead of an ABG is decreased pain for the patient. A 1996 double-blinded study by Giner found that pain scale ratings were reduced by almost half with VBG compared to ABG. (There was no significant difference in the ratings when a local anesthetic had been used prior to an arterial blood draw, but this is not always done.)

Also, a VBG sample can be drawn using the same intravenous (IV) line that is used to draw blood for other lab tests, thus necessitating only one puncture. This translates into decreased costs, labor, and risk of needlestick injury to the health care provider. Furthermore, complications such as arterial laceration, hematoma, and thrombosis are all but negated with venous blood sampling.

CRITICAL ILLNESS AND CARDIAC ARREST

So VBG analysis has several obvious advantages over ABG. But what about the data obtained with ABG analysis? Is it unique? Is it diagnostically superior to the data obtained with venous blood sampling?

Normal values for pH, PO₂, PCO₂, and HCO₃ in healthy individuals are listed in the table (below). However, because emergency department patients are generally not healthy, it is important to compare arterial and venous values in acutely ill individuals. A 1985 study by Gennis of critically ill emergency department patients revealed a breakdown in the linear relationship between arterial and venous values for pH, PCO₂, and HCO₃ seen in healthy individuals. However, the study did demonstrate that normal venous pH, PCO₂, and HCO₃ ruled out severe acid-base disturbances. For example, a venous pH of 7.25 or higher predicted an arterial pH of 7.2 or higher in 98% of all cases, which makes VBG testing valuable as a screening procedure. If the results are normal, ABG analysis should not be necessary. Conversely, abnormal venous levels predicted abnormal arterial values, but again in a nonlinear fashion. A venous pH of 7 or lower, for example, predicted an arterial pH of 7.2 or lower in 98% of cases.

In cardiac arrest victims, the disparity between arterial and venous values is even greater. During cardiac arrest, tissue hypoxia is all but a certainty and is reflected by the lower pH and higher PCO₂ on the venous side. A 1986 study by Weil demonstrated a significantly lower pH in venous samples (mean, 7.15 vs 7.41 in arterial samples) and a significantly elevated PCO₂ (mean, 74 mm Hg vs 32 mm Hg) in these patients. In clinical practice, however, knowledge of either the arterial or venous pH or PCO₂ during cardiac arrest does not alter management, making the debate less relevant.

A similar 1989 study by Androque confirmed the above findings in cardiac arrest, but it also included patients in severe hemodynamic failure not related to cardiac arrest. The study found that as cardiac output declines, the differences between arterial and venous measurements increase. These authors concluded that VBG analysis in cardiac arrest provides values more indicative of the true cellular environment.

lactate levels

Elevated arterial lactate levels are an early sensitive marker of tissue hypoperfusion, predicting both the severity of hemodynamic compromise and overall patient prognosis. Unlike the pH during cardiac arrest, interpreting a venous lactate level in relation to an arterial value could be useful in the workup and management of critically ill patients. Based on the available evidence, the correlation between arterial and venous lactate values appears to be quite close. A 1996 study by Younger of 48 emergency department patients in whom concurrent arterial and venous blood gas analyses were performed demonstrated that an abnormally elevated venous lactate level (1.6 mmol/L or greater) was 100% sensitive and 89% specific in predicting elevated arterial lactate levels. A 2000 study by Lavery bolstered these results, demonstrating a close correlation between arterial and venous lactate levels in a population of 375 hypovolemic trauma patients. A venous lactate level above 2 mmol/L predicted an elevated injury severity score, ICU admission, and length of stay.

The bottom line: Venous lactate levels are similar to those found in arterial samples. A normal venous lactate measurement predicts a normal arterial lactate reading, precluding the need to perform an arterial puncture.

METABOLIC CONDITIONS

Using ABG measurements and serum electrolyte levels, the emergency physician can perform the six steps involved in calculating mixed acid-base disturbances (see box below). Venous pH values can aid in the first step because they closely mirror arterial values for several metabolic conditions, including diabetic ketoacidosis (DKA) and uremia.

A 1998 study by Brandenburg of emergency department patients with DKA found remarkably similar values for arterial and venous pH (mean arterial, 7.20; mean venous, 7.17). HCO₃ levels are also very similar (mean arterial, 11.0 +/- 6.0 mmol/L; mean venous, 12.8 +/- 5.5 mmol/L). A 2003 study by Ma of DKA patients presenting to the emergency department corroborated these findings. More importantly, it examined the effect that knowing a patient’s ABG values had on the clinician’s diagnosis, treatment plan, and patient disposition. Rarely did it alter care in the emergency department.

Other forms of metabolic acidosis have been studied. A similar relationship has been found, for example, between arterial and venous measurements in patients with metabolic acidosis due to uremia. A 2000 study by Gokel of 100 uremic patients found a mean arterial pH of 7.17 +/- 0.14 compared to a mean venous pH of 7.13 +/- 0.14, and a mean arterial HCO₃ of 10.13 +/- 4.26 mmol/L compared to a mean venous HCO₃ of 11.86 +/- 4.23 mmol/L. Some caution is warranted in interpreting a high potassium level in a uremic patient obtained on an arterial or venous blood gas sample because the analyzer will not distinguish true hyperkalemia from pseudohyperkalemia due to a hemolyzed sample.

The six steps in calculating mixed acid-base abnormalities cannot be completed without knowing the patient’s arterial PCO₂ level. Specifically, concomitant respiratory conditions cannot be excluded. Other metabolic disorders can still be detected, however, by using information obtained from the serum electrolytes—namely, the anion and delta gaps.

The anion gap is determined by subtracting the sum of the patient’s serum bicarbonate and chloride levels from the sodium level, or AG = Na – (HCO₃ + Cl). It is not a true gap, but an indirect estimate of the amount of unmeasured serum anions, from which one can infer the presence of an acid causing the patient’s acid-base derangement. Anion gap values above 12 are generally considered positive and should prompt a specific workup to identify the etiology and direct appropriate treatment.

Delta gap refers to the principle that in an uncomplicated anion gap metabolic acidosis (AGMA), for every 1 mmol/L elevation in the anion gap, there should be a reflexive 1 mmol/L drop in the serum HCO₃ level. Any deviation from this suggests a mixed acid-base disorder—either a combined metabolic acidosis/alkalosis or mixed anion gap and non-anion gap metabolic acidosis (NAGMA). There are several ways to calculate the delta gap. One commonly used method is: delta gap equals the change in the anion gap (from the normal of 12) minus the change in the serum bicarbonate (from the normal of 24), or DG = (AG – 12) – (24 – HCO₃). When the delta gap is greater than 6, there is a combination of AGMA and metabolic alkalosis. When it is less than -6, there is a combination of AGMA and NAGMA.

RESPIRATORY ILLNESS

In physiologic terms, ABG composition reflects the relationship between ventilation and perfusion and thus is an important reflection of overall pulmonary function. In clinical practice, respiratory insufficiency can be broken down into two categories—namely, ventilatory failure (inadequate clearance of CO₂, or hypercarbia) and oxygenation failure (inadequate plasma oxygenation, or hypoxemia). Arterial blood gas analysis has long been used to diagnose and quantify the severity of either or both of the above conditions in patients with apparent respiratory distress.

A close correlation between arterial and venous PCO₂ that would decrease dependency on an ABG does not exist. However, a venous PCO₂ value that predicts significant arterial hypercarbia might be useful. In a study published in 2002 by Kelly, a venous PCO₂ level above 45 mm Hg predicted an arterial PCO₂ above 50 mm Hg (the designated value for significant hypercarbia) with a sensitivity of 100% and specificity of 57%. In this study, a venous PCO₂ value above 45 mm Hg detected all cases of significant arterial hypercarbia (negative predictive value, 100%) and reduced the requirement for arterial blood sampling in 41% of cases.

Venous PO₂ values do not provide any significant reflection of arterial PO₂ levels and are therefore a poor surrogate to quantify oxygen delivery to target tissues. However, the widespread availability of pulse oximetry makes it an attractive alternative. A 2001 study by Witting of more than 700 emergency department patients showed that an oxygen saturation level of 96% or less on room air predicted a PO₂ below 70 mm Hg with a sensitivity of 100% and a specificity of 54%.

CASE RESOLUTION

With the conclusions from the various studies cited above in mind, you tell the nurse to add a VBG to the rest of the labs and you hold off on an ABG analysis. Within two minutes, the results of the VBG return: pH, 7.12; PCO₂, 27; PO₂, 27; HCO₃, 9, and lactate, 1.2. The nurse notifies you that the urine dipstick test is positive for ketones.

You begin treating the patient with fluids and insulin for presumed DKA based on the elevated serum glucose level, urine dipstick test, and VBG results showing a low pH and a low HCO₃ consistent with a metabolic acidosis. Forty minutes later, the chemistries come back and confirm an AGMA (sodium, 129; chloride, 101; potassium, 7.3; HCO₃, 9; blood urea nitrogen, 55; creatinine, 3.0; glucose, 686; anion gap, 19). The decision is made to admit the patient to the hospital, but the floor resident accepting the patient calls down and requests that you perform an ABG. You know you have not ruled out a mixed acid-base disorder, but you can’t remember the last time you calculated it or changed your management based on it. Nonetheless, you decide to calculate a delta gap based on the chemistry results as follows: DG = [(AG-12) – (24 – HCO₃)] = [(19 – 12) – (24 – 9)] = (7 – 15) = -8. Given a delta gap of less than -6, you diagnose an additional metabolic derangement—an NAGMA.

Your thoughts next turn to the possibility that a significant respiratory disorder may be present. The patient is tachypneic, but this may be due to his acidosis. Knowing that a venous PCO₂ below 45 mm Hg indicates an arterial PCO₂ below 50 mm Hg, you feel confident that significant hypercarbia in this patient is unlikely given his venous PCO₂ of 27 mm Hg. Additionally, the patient’s pulse oximeter shows an oxygen saturation of 97%, and you conclude that there is no significant hypoxia (PO₂ above 70 mm Hg).

The patient is admitted to the hospital, where the insulin drip is continued. His symptoms improve and his anion gap closes. He is discharged two days later without an ABG analysis having been performed.

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