Peter H. Breen

Can Changes in End-tidal Pco2 Measure Changes in Cardiac Output?

In recent studies of cardiopulmonary resuscitation, an increase in end-tidal carbon dioxide tension (Petco2) signifies an increase in cardiac output (&OV0422;T) as spontaneous circulation resumes. We hypothesized that changes in &OV0422;T might generally be measured by changes in Petco2. In five pentobarbital-anesthetized dogs, we inflated percutaneously inserted vena cava balloons to impede venous return and to decrease &OV0422;T (measured by pulmonary thermodilution). The Petco2 was measured at the airway opening by sidestream infrared capnometry. In 32 vena cava balloon inflation sequences during constant ventilation in five dogs, the percent decrease in Petco2 directly correlated with the percent decrease in QT (slope = 0.73, R2 = 0.89, P < 0.001). During decreased &OV0422;T, reduced CO2 delivery to the lungs decreased alveolar Pco2 to cause part of the decrease in Petco2. The remaining reduction in Petco2 resulted from the increase in alveolar dead space (in turn due to lower pulmonary perfusion pressures during reduced &OV0422;T), which diluted the CO2 from perfused alveolar spaces to further reduce Petco2. During a sustained reduction in &OV0422;T, increasing CO2 accumulation in the peripheral tissues and in venous blood began to restore CO2 delivery to the lung and Petco2 toward baseline levels. Reciprocal changes occurred during increases in QT when the vena cava balloons were deflated. The linear relationship between changes in Petco2 and &OV0422;T in animals supports a decision to perform clinical studies necessary to determine whether a change in Petco2 will be useful as a noninvasive, continuous monitor of a change in &OV0422;T during anesthesia or intensive care.

Carbon dioxide kinetics and capnography during critical care

Greater understanding of the pathophysiology of carbon dioxide kinetics during steady and nonsteady state should improve, we believe, clinical care during intensive care treatment. Capnography and the measurement of end-tidal partial pressure of carbon dioxide (PETCO2) will gradually be augmented by relatively new measurement methodology, including the volume of carbon dioxide exhaled per breath (VCO2,br) and average alveolar expired PCO2 (PǢCO2). Future directions include the study of oxygen kinetics.

Comparison of end-tidal PCO2 and average alveolar expired PCO2 during positive end-expiratory pressure

The measurement of average alveolar expired PCO2 (PAECO2) weights each PCO2 value on the alveolar plateau of the CO2 expirogram by the simultaneous change in exhaled volume.PAECO2 can be determined from a modified analysis of the Fowler anatomic dead space (VDANAT). In contrast, end-tidal PCO2 (PETCO2) only measures PCO2 in the last small volume of exhalate. In conditions such as mechanical ventilation with positive end-expiratory pressure (PEEP), where the alveolar plateau can have a significant positive slope, we questioned how much PETCO2 could overestimate PAECO2. Accordingly, in six anesthetized ventilated dogs, we digitally measured and processed tidal PCO2 and flow to determine VD (ANAT). We determined PETCO2 and PAECO before and after the application of 7.6 cm H2 O PEEP. Alveolar dead space to tidal volume fraction (VD/VT) was determined by [arterial PCO2-alveolar PCO2]/arterial PCO2, where alveolar PCO (2) was determined by either PETCO2 or PAECO2. During baseline ventilation, PETCO2 was 3.4 mm Hg (approximately 11%) greater than PAECO2. Because PEEP significantly increased the slope of the alveolar plateau from 28 to 74 mm Hg/L, the difference between PETCO2 and PAECO2 significantly increased to 6.6 mm Hg (approximately 20% difference. The concurrent increase in VDANAT during PEEP decreased alveolar tidal volume and tended to limit the overestimation of PETCO (2) compared to PAECO2. When alveolar PCO2 was estimated by PETCO2, alveolar VD/VT was 18%, compared to an alveolar VD/VT of 26% when alveolar PCO (2) was estimated by PAECO2. This difference was significantly magnified during PEEP ventilation. The overestimation of PAECO2 by PETCO2 can result in a falsely high assessment of overall alveolar PCO2. Moreover, the use of PETCO (2) to estimate alveolar PCO2 in the determination of the alveolar dead space fraction can result in falsely low and even negative values of alveolar dead space. (Anesth Analg 1996;82:368-73)

How does positive end-expiratory pressure decrease CO2 elimination from the lung?

Six chloralose-urethane anesthetized dogs (23 +/- 2 kg) underwent median thoracotomy (open pleural spaces) and constant mechanical ventilation with O2. We conducted measurements at baseline and during 25 min of ventilation with 3.3 cmH2O positive end-expiratory pressure (PEEP3) or 10.7 cmH2O PEEP (PEEP 11), including breath-by-breath values in the first 2 min after PEEP began. PEEP 11 immediately decreased pulmonary CO2 elimination per breath (VCO2,br, digital integration and multiplication of exhaled flow and FCO2) from 8.4 +/- 2.0 to 4.5 +/- 1.6 ml (P < 0.05) by significantly decreasing alveolar ventilation (VA) (29% increase in anatomical dead space (VDana) and generation of high VA/Q regions) and by decreasing alveolar PCO2 (PACO2) from 42.5 +/- 3.5 to 35.9 +/- 3.5 Torr (decreased CO2 transfer to the lung as electromagnetic aortic cardiac output (QT) decreased by 51%). The immediate dilution of alveolar gas and PACO2 by fresh gas as PEEP increased functional residual capacity by 1152 +/- 216 ml was offset by simultaneous decreased expiratory volume and, hence, CO2 accumulation. Compared to baseline, the 17% reduction in VCO2,br was sustained at 25 min after addition of PEEP 11 because VA remained depressed. Then, VCO2,br could only be restored to baseline if PACO2 sufficiently increased. However, CO2 transport was still in unsteady state at 25 min of PEEP. Peripheral tissue retention of CO2 and the significant increase in mixed venous PCO2 (PVCO2, 62.4 +/- 6.2 Torr) were not enough to normalize CO2 transfer to the lung and to sufficiently increase PACO2, especially during the continued depression in QT that occurred at higher PEEP. The sustained decrease in VCO2,br during PEEP was not mirrored by changes in end-tidal PCO2 (PETCO2).

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 (IV) infused (0.072 mg centered dot kg-1 centered dot 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. The elimination half-life of CN in the blood was 129 min and significant blood [CN] persisted at least 25 min after the CN infusion. We suggest that, after extraction of a victim from a fire, mechanical ventilation alone should facilitate the return of critical body functions, and that the presence of persistent blood [CN] and lactic acidosis indicate the need for specific therapy for CN toxicity. (Anesth Analg 1995;80:671-7)

Bymixer provides on-line calibration of measurement of CO2 volume exhaled per breath

AbstractThe measurement of CO2 volume exhaled per breath

Arterial blood gas and pH analysis: Clinical approach and interpretation

(V_{CO_2 ,br} )

CARBON DIOXIDE KINETICS DURING ANESTHESIA: Pathophysiology and Monitoring

can be determined during anesthesia by the multiplication and integration of tidal flow