Quick-and-dirty ABG calculations for arrest: 1. Calculate predicted pH just due to hyper- or hypo- carbia: pCO2 10 =  pH 0.08 2. for each  pH beyond predicted give i amp bicarb (for 70 kg pt.) > The arterio-venous differential in blood gas readings was described several > years by Weil and colleagues. Due to poor pulmonary perfusion, the venous > pCO2 rises considerably (along with a decrease in the pH) while the arterial > pH remained the same or went up a little bit -- at least in the first 10 > minutes of the resuscitation. This is why venous gasses during codes are an > unreliable indicator of the need for bicarbonate. I don't have all the > references at hand, but you can find them by doing a medline search (go back > at least 10 years) -- look for Max Weil and/or Erik Rackow as authors. Correct. The acidosis early (in the first 8 minutes or so) of cardiac arrest is predominantly due to CO2 retention and not lactic acidosis. However the venous blood gas (VBG) is a more reliable indicator of tissue perfusion than is the arterial blood gas (ABG). Even in non-arrest situations this is a strong inverse correlation between cardiac index and the difference between arterial and venous CO2 (1). Thus in these circumstances ABGs underestimate the degree of tissue hypoperfusion (2,3,4) and (central) venous samples are a better indicator in the arrest situation. In at least one (animal) model (5) there was good correlation between central venous and femoral blood samples. One final interesting observation: Pulsations felt in the groin during cardiac arrest are probably of femoral venous and not of arterial origin (6). People who are unaware of this may be inadvertantly drawing venous specimens. Thus their dual errors (believing the pulsations overlie the femoral artery AND their belief that ABGs are a better indicator of tissue perfusion than are venous specimens) *precisely* cancel one another out! Of course they are actually obtaining venous specimens and using that to guide therapy which is precisely what they should be doing. But no bicarb please. H. Louzon MD ------------------------------------------ > So what therapy are we guiding with the venous/arterial blood gas > samples taken during cardiac arrests. I no longer routinely do them > as they provided no added information. > I'd be interested in hearing those who do take them. Outside of a research setting I agree. Don't think I've done one in 5 - 6 years. The practice of obtaining blood gases is a leftover from the days when bicarb was given freely. In those circumstances ACLS protocol recommended that alkali therapy be guided by results of ABG. Now that bicarb is rarely used that rationale is gone. Nevertheless I mentioned it in response to the suggestion that a difference exists between arterial and venous CO2 levels as an interesting observation. Furthermore current guidelines suggest that HCO3, although not recommended 'can be considered' in cases or pre-existing acidosis with/without hyperkalemia. Perhaps there are a few souls out there still using it. In the future the value of ABG (or VBG) may be in predicting futile resusitation attempts. It's correlation with poor tissue perfusion and bad outcome (1) (if persisting in the face of a reassessment of CPR) may identify those cases where early termination of a code is indicated. ------------------------------------------ (1) Durkin R, Gergits MA, Reed JF 3rd, Fitzgibbons J The relationship between the arteriovenous carbon dioxide gradient and cardiac index. J Crit Care 1993 Dec;8(4):217-21 It has been reported that under normal conditions, mixed venous blood gases have approximated arterial samples; however, during cardiac arrest or severe cardiogenic shock, marked differences between arterial and venous blood gases have been noted. To further assess the relationships between arterial and mixed venous blood gases and cardiac index, a study population was chosen consisting of patients with less severe states of cardiac impairment. The differences between arterial and mixed venous PCO2s and pHs were compared with cardiac indexes (CI) of 44 patients in an intensive care unit with arterial lines and Swan-Ganz catheters in place. Twenty-six patients with normal CIs (2.6 to 4.1 L/min/m2) had a mean difference in mixed venous-arterial PCO2 (delta PCO2) of 4.88 +/- 0.40 mm Hg. In patients with low CIs (< 2.6), the delta PCO2 was 7.44 +/- 0.63 mm Hg (P = .001). The difference of mixed venous and arterial pH (delta pH) was 0.027 +/- 0.004 pH units for patients with normal CIs and 0.04 +/- 0.003 pH units for those with low CIs (P < .002). When the CIs of all patients were plotted against the delta PCO2s, there was an inverse linear relationship wherein delta PCO2 increased as CI decreased (r = -.47, P = .0011). There is an inverse relationship between delta PCO2 and CI that has not been previously described. An elevated delta PCO2 may be a marker of a low cardiac index. (2) Selective venous hypercarbia during human CPR: implications regarding blood flow. Ann Emerg Med 1987 May;16(5):527-30 Thirty-five patients presenting to the emergency department in cardiopulmonary arrest had simultaneous measurement of central venous (cv) and arterial (a) blood gases during CPR with a pneumatic chest compressor and ventilator. The mean cv, arterial pH, and PCO2 values were markedly different (P less than .001). The mean pH gradient (pHa - pHcv) was .31 +/- .10 units and the mean PCO2 gradient (PcvCO2 - PaCO2) was 60.5 +/- 23.6 torr. This selective venous hypercarbia is probably due to a cardiac output that is inadequate to eliminate the CO2 produced from both residual aerobic metabolism and the buffering of anaerobically produced lactic acid. Central venous blood gases are probably a better reflection of actual tissue environment during prolonged cardiac arrest than are arterial blood gases. (3) Grundler W, Weil MH, Rackow EC Arteriovenous carbon dioxide and pH gradients during cardiac arrest. Circulation 1986 Nov;74(5):1071-4 In a porcine preparation of cardiac arrest, we demonstrated that there is a marked paradox of venous acidemia and arterial alkalemia. This paradox is related to decreased clearance of CO2 from the lungs when pulmonary blood flow is critically reduced. Accordingly, increased venous PCO2 rather than metabolic acidosis due to lactic acidosis predominates during the initial 8 min of cardiopulmonary resuscitation. Arterial blood gases fail as indicators of systemic acid-base status and therefore as indicators of tissue acidosis. (4) Weil MH, Rackow EC, Trevino R, Grundler W, Falk JL, Griffel MI Difference in acid-base state between venous and arterial blood during cardiopulmonary resuscitation. N Engl J Med 1986 Jul 17;315(3):153-6 We investigated the acid-base condition of arterial and mixed venous blood during cardiopulmonary resuscitation in 16 critically ill patients who had arterial and pulmonary arterial catheters in place at the time of cardiac arrest. During cardiopulmonary resuscitation, the arterial blood pH averaged 7.41, whereas the average mixed venous blood pH was 7.15 (P less than 0.001). The mean arterial partial pressure of carbon dioxide (PCO2) was 32 mm Hg, whereas the mixed venous PCO2 was 74 mm Hg (P less than 0.001). In a subgroup of 13 patients in whom blood gases were measured before, as well as during, cardiac arrest, arterial pH, PCO2, and bicarbonate were not significantly changed during arrest. However, mixed venous blood demonstrated striking decreases in pH (P less than 0.001) and increases in PCO2 (P less than 0.004). We conclude that mixed venous blood most accurately reflects the acid-base state during cardiopulmonary resuscitation, especially the rapid increase in PCO2. Arterial blood does not reflect the marked reduction in mixed venous (and therefore tissue) pH, and thus arterial blood gases may fail as appropriate guides for acid-base management in this emergency. (5) Emerman CL, Pinchak AC, Hagen JF, Hancock D A comparison of venous blood gases during cardiac arrest. Am J Emerg Med 1988 Nov;6(6):580-3 Previous reports have advocated the use of mixed venous blood gases to estimate arterial pH and as a reflection of tissue acid-based balance. However, true mixed venous samples are difficult to obtain during cardiac arrest as they require a pulmonary artery catheter. The purpose of this study was to determine whether central or femoral venous samples could be used in place of pulmonary artery samples. Blood gases from these sites were drawn at intervals during experimental cardiac arrest in dogs. The PO2, PCO2, and pH from the pulmonary artery samples were strongly correlated with those from the central venous (r = .93, .99, and .99, respectively) and from the femoral venous samples (r = .73, .93, and .97, respectively). There were no significant differences in the pulmonary artery, central, or femoral venous gases. This animal model suggests that femoral and central venous samples mirror true mixed venous blood gases from the pulmonary artery and could be used in their place. (6) Connick M, Berg RA Femoral venous pulsations during open-chest cardiac massage. Ann Emerg Med 1994 Dec;24(6):1176-9 We describe the cases of two children with easily palpated femoral pulses during open-chest cardiac massage after aortic occlusion. These pulsations must have arisen from the femoral veins, implying that during CPR in children the usual anatomic landmarks for femoral venous access may be unreliable, and femoral pulsations do not necessarily reflect arterial flow. Femoral pulses may signify to-and-fro inferior vena caval flow that compromises venous return, adversely affecting cardiac output and the effectiveness of medication administration to the lower extremity.