Non-steady state monitoring by respiratory gas exchange.

Traditionally, the study of CO2 and O2 kinetics in the body has been mostly confined to equilibrium conditions. However, the peri-anesthesia period and the critical care arena often involve conditions of non-steady state. The detection and explanation of CO2 kinetics during non-steady state pathophysiology have required the development of new methodologies, including the CO2 expirogram, average alveolar expired PCO2, and CO2 volume exhaled per breath. Several clinically relevant examples of non-steady state CO2 kinetics perturbations are examined, including abrupt decrease in cardiac output, application of positive end-expiratory pressure during mechanical ventilation, and occurrence of pulmonary embolism. The lesser known area of non-steady state O2 kinetics is introduced, including the measurement of pulmonary O2 uptake per breath. Future directions include the study of the respiratory quotient per breath, where the anaerobic threshold during anesthesia is identified by increasing respiratory quotient.

Protective effect of stroma-free methemoglobin during cyanide poisoning in dogs.

BACKGROUND: During fire exposure, cyanide toxicity can block aerobic metabolism. Oxygen and sodium thiosulfate are accepted therapy. However, nitrite-induced methemoglobinemia, which avidly binds cyanide, decreases oxygen-carrying capacity that is already reduced by the presence of carboxyhemoglobin (inhalation of carbon monoxide in smoke). This study tested whether exogenous stroma-free methemoglobin (SFmetHb) can prevent depression of hemodynamics and metabolism during canine cyanide poisoning. METHODS: In 10 dogs (weighing 18.8 +/- 3.5 kg) anesthetized with chloralose-urethane and mechanically ventilated with air, baseline hemodynamic and metabolic measurements were made. Then, 137 +/- 31 ml of 12 g% SFmetHb was infused into five dogs (SFmetHb group). Finally, the SFmetHb group and the control group (n = 5, no SFmetHb) received an intravenous potassium cyanide infusion (0.072 mg.kg-1.min-1) for 20 min. Oxygen consumption (VO2) was measured with a Datex Deltatrac (Datex Instruments, Helsinki, Finland) metabolic monitor and cardiac output (QT) was measured by pulmonary artery thermodilution. RESULTS: From baseline to cyanide infusion in the control group, QT decreased significantly (p < 0.05) from 2.9 +/- 0.8 to 1.5 +/- 0.4 l/min, mixed venous PCO2 (PvCO2) tended to decrease from 35 +/- 4 to 23 +/- 2 mmHg, PvO2 increased from 43 +/- 4 to 62 +/- 8 mmHg, VO2 decreased from 93 +/- 8 to 64 +/- 19 ml/min, and lactate increased from 2.3 +/- 0.5 to 7.1 +/- 0.7 mM. In the SFmetHb group, cyanide infusion did not significantly change these variables. From baseline to infused cyanide, the increases in blood cyanide (4.8 +/- 1.0 to 452 +/- 97 microM) and plasma thiocyanate cyanide (18 +/- 5 to 65 +/- 22 microM) in the SFmetHb group were significantly greater than those increases in the control group. SFmetHb itself caused no physiologic changes, except small decreases in heart rate and PvO2. Peak SFmetHb reached 7.7 +/- 1.0% of total hemoglobin. CONCLUSIONS: Prophylactic intravenous SFmetHb preserved cardiovascular and metabolic function in dogs exposed to significant intravenous cyanide. Blood concentrations of cyanide, and its metabolite, thiocyanate, revealed that SFmetHb trapped significant cyanide in blood before tissue penetration.

Measurement of blood CO2 concentration with a conventional PCO2 analyzer.

OBJECTIVES: CO2 content can be determined from the Pco2 in an acidified (forces all CO2 into solution) and diluted blood sample. However, Pco2 concentrations measured in conventional blood gas analyzers are only correct for samples with a significant buffer capacity (such as whole blood), so that mixing with the Pco2 in the rinse solution and tubing walls does not significantly change the sample Pco2. This study describes a calibration method and validation data for the Radiometer Medical ABL2 CO2 electrode system to accurately measure unbuffered blood samples used in the determination of blood CO2 content (or other aqueous fluids). DESIGN: Prospective, criterion standard. SETTING: Laboratory. MEASUREMENTS AND MAIN RESULTS: Blood samples (0.4 mL) were acidified and diluted with 0.2 M lactic acid. After measuring Pco2, CO2 content was calculated using the CO2 solubility coefficient and the dilution factor of 20. CO2 content was determined in a series of sodium carbonate (Na2CO3) solutions spanning the physiologic range of CO2 content. Regression of the measured vs. the actual CO2 content data generated a straight line with a slope of 0.796 and y-intercept of 12.5 (r2 = .99; n = 48). These coefficients were successfully used to correct CO2 content determined in blood samples into which graduated amounts of sodium carbonate were added. CONCLUSIONS: This calibration procedure allows accurate measurement of Pco2 in aqueous samples using the Radiometer ABL2 electrode system, and should be applicable to other blood gas analyzers. Necessary syringes and chemicals are readily available, the method is fast and simple, and the sample volume is small. In the practice of critical care medicine, accurate Pco2 measurement in aqueous acidified and diluted blood provides direct determination of blood CO2 content (useful in calculations of modified Fick cardiac output or tissue CO2 production). Determinations of absolute CO2 content in blood requiring complex methodology are not necessary. In addition, accurate measurement of aqueous gastric Pco2 can help determine gastric pH, which is an important marker of tissue perfusion.

Effect of oxygen and sodium thiosulfate during combined carbon monoxide and cyanide poisoning.

In a canine model of combined carbon monoxide (CO) and cyanide (CN) poisoning, cardiac output (QT) and oxygen consumption (Vo2) decreased but recovered to baseline values by 15 min after toxic exposure; elevated blood CN and lactic acidosis persisted for at least another 10 min. Given the rapid spontaneous recovery after cessation of toxic exposure, we questioned the efficacy of usual treatment with oxygen (O2) and sodium thiosulfate (Na2S2O3) for CN poisoning. Accordingly, in seven dogs (26 +/- 3 kg, chloralose and urethane anesthesia), we sequentially administered CO by closed circuit inhalation (231 +/- 42 ml) and potassium CN by intravenous infusion (0.072 mg.kg-1.min-1 for 17 +/- 3 min). Fifteen minutes after toxic exposure, O2 breathing began and Na2S2O3 (150 mg/kg) was infused. Measurements were repeated 10 and 45 min after treatment. At the end of the CN infusion, QT decreased by 43% and Vo2 decreased by 51%, compared to baseline values. Both variables recovered to baseline by 15 min after stopping toxic exposure. Significant lactic (4.8 +/- 2.9 mM) acidosis (7.14 +/- 0.10) persisted for at least another 10 min. Treatment with oxygen and Na2S2O3 did not hasten the recovery of this lactic acidosis or decrease blood cyanide levels compared to nontreated dogs. However, after treatment, plasma thiocyanate significantly increased from 16.3 +/- 12.5 to 94.4 +/- 72.2 microM, as Na2S2O3 participated in the increased metabolism of cyanide to thiocyanate. We conclude that O2 and Na2S2O3 therapy should be continued during combined CO and HCN poisoning. Oxygen increases CO elimination and can enhance anti-CN treatment. After infusion or inhalation of CN, when most CN has already penetrated the intracellular compartment, postexposure sodium thiosulfate increased the metabolism of CN.

Combined carbon monoxide and cyanide poisoning: a place for treatment.

During fires, victims can inhale significant carbon monoxide (CO) and cyanide (CN) gases, which may cause synergistic toxicity in humans. Oxygen therapy is the specific treatment for CO poisoning, but the treatment of CN toxicity is controversial. To examine the indication for treatment of CN toxicity, we have established a canine model to delineate the natural history of combined CO and CN poisoning. In seven dogs (24 +/- 3 kg), CO gas (201 +/- 43 mL) was administered by closed-circuit inhalation. Then, potassium CN was intravenously (i.v.) infused (0.072 mg.kg-1.min-1) for 17.5 +/- 3.0 min. Cardiorespiratory measurements were conducted before and after these toxic challenges. Despite significant CO poisoning (peak carboxyhemoglobin fractions [COHb] = 46% of total hemoglobin [Hb]; elimination t1/2 = 114 +/- 42 min) with attendant decrease in blood O2 content, CO had essentially little effect on any hemodynamic or metabolic variable. On the other hand, CN severely depressed most hemodynamic and metabolic functions. Compared to baseline values, CN caused significant (P < 0.01) decreases in cardiac output (6.4 +/- 2.0 to 3.1 +/- 0.5 L/min) and heart rate (169 +/- 44 to 115 +/- 29 bpm) and decreases in oxygen consumption (VO2) (133 +/- 19 to 69 +/- 21 mL/min) and carbon dioxide production (VCO2) (128 +/- 27 to 103 +/- 22 mL/min). However, these critical hemodynamic and metabolic variables recovered to baseline values by 15 min after stopping the CN infusion, except lactic acidosis which persisted for at least 25 min after the CN infusion.(ABSTRACT TRUNCATED AT 250 WORDS)