Unreliability of oxygen tension-based indices in reflecting intrapulmonary shunting in critically ill patients

Measurement of intrapulmonary shunting (Qsp/Qt), a widely used method for monitoring disturbances of pulmonary oxygen transfer in critically ill patients, involves calculation of arterial and mixed venous oxygen contents. In circumstances where mixed venous blood samples are not readily available, oxygen tension-based indices such as the alveolar to arterial oxygen tension differences (P[A-a]O2), arterial oxygen tension to alveolar oxygen tension ratio (PaO2/PAO2), PaO2 to FIO2 ratio (PaO2/FIO2) and respiratory index (RI) are widely utilized to reflect Qsp/Qt. Oxygen content-based indices such as the estimated shunt are not as widely utilized as the oxygen tension indices. In 75 critically ill patients in whom a pulmonary artery catheter was being utilized to augment clinical care, comparisons were made between Qsp/Qt and P(A-a)O2, PaO2/PAO2, PaO2/FIO2, RI, and estimated shunt to determine which index best reflected Qsp/Qt. Correlations between Qsp/Qt and estimated shunt were good (r = .94) and poor for the P(A-a)O2 (r = .62), PaO2/PAO2 (r = .72), PaO2/FIO2 (r = .71), and RI (r = .74). We conclude that there are no real substitutes for venous oxygen contents in critically ill patients. When pulmonary artery blood is not available for analysis, oxygen tension-based indices are unreliable reflectors of Qsp/Qt while the estimated shunt, an oxygen content-based index, provides a more reliable reflection of Qsp/Qt.     

Respiratory index/pulmonary shunt relationship: quantification of severity and prognosis in the post-traumatic adult respiratory distress syndrome

The relationship between the respiratory index (RI = alveolar-arterial oxygen gradient [P(A-a)O2] normalized by PaO2) and the pulmonary shunt (Qsp/Qt) has been examined in 929 studies from 240 critically ill post-traumatic patients. Of these, 88 patients (443 studies) were individuals who developed post-traumatic adult respiratory distress syndrome (ARDS) and 152 were patients (486 studies) who did not develop ARDS. This study demonstrates that the RI to Qsp/Qt [RI/(Qsp/Qt)] relationship was significantly (p less than .0001) increased in patients who developed fatal ARDS compared with those who did not develop ARDS, or with those whose ARDS resolved. Because of the increased oxygen consumption (VO2) in ARDS patients in association with their severe limitations in gas exchange (RI) and increased Qsp/Qt, surviving ARDS patients had a significant increase in the cardiac index which resulted in a higher oxygen delivery to VO2 ratio. ARDS patients showed significant (p less than .0001) evidence of increased pulmonary vascular tone, correlated with the increase in the RI/(Qsp/Qt) relationship. In addition, those patients with high RI/(Qsp/Qt) also had increased right ventricular (RVSW) to left ventricular work (LVSW) ratios which were shown to be a direct function of the rise in RI. This increase in both RVSW/LVSW and RI/(Qsp/Qt) ratios was significantly (p less than .0001) correlated with an increased mortality. Thus, the RI/(Qsp/Qt) relationship, which can be obtained from arterial and mixed venous blood gases and saturations only, can be used to predict the severity of the ARDS process as well as important pulmonary vascular and right ventricular overload consequences.     

Arterial blood gas derived variables as estimates of intrapulmonary shunt in critically ill children

Oxygen transport data, prospectively collected from 52 critically ill children, were analyzed to determine whether any derived variable accurately estimated intrapulmonary shunt (Qsp/Qt). Arterial hemoglobin saturation was more closely correlated with Qsp/Qt than was PaO2, alveolar-arterial oxygen gradient, arterial mixed venous oxygen difference (C[a-v]O2), arterial/alveolar oxygen ratio, and the ratio of PaO2 to inspired oxygen (FIO2) (r = 0.8, p less than .0001). When C(a-v)O2 was normal, hemoglobin saturation became a very accurate (r = 0.96) assessment of Qsp/Qt. We conclude that various arterial blood gas derived variables do not accurately reflect Qsp/Qt in critically ill children. In these patients, a pulmonary artery catheter is needed to accurately assess intrapulmonary shunt.     

Continuous, in vivo pulmonary venous admixture from fiberoptically measured hemoglobin saturations

In six anesthetized swine, pulmonary venous admixture (Qsp/Qt) was calculated by four methods: a) Qsp/Qt 1, fiberoptically measured arterial and mixed venous Hgb saturation (SaO2 and SvO2), PaO2 and PvO2 derived from saturations; b) Qsp/Qt 2, fiberoptically measured SaO2 and SvO2, PaO2 and PvO2 measured by blood gas analysis; c) Qsp/Qt 3, PaO2 and PvO2 measured by blood gas analysis, SaO2 and SvO2 derived from tensions; d) Qsp/Qt 4, SaO2 and SvO2 measured by bench oximetry, PaO2 and PvO2 derived from saturations. Input from the fiberoptic catheters was fed into a computer programmed to calculate Qsp/Qt 1 every 20 sec. Fifty-eight of these values were compared with simultaneously calculated Qsp/Qt 2, 3, and 4. There was no difference between fiberoptic and derived SaO2 or fiberoptic and cooximetric SvO2. Correlations and slopes for Qsp/Qt 1 with Qsp/Qt 2, 3, and 4 were significant (p less than .05). Comparing mean differences, Qsp/Qt 1 was significantly different only from Qsp/Qt 3 (p less than .01). We conclude that dual oximetry reliably tracks Qsp/Qt.     

Continuous positive airway pressure is beneficial in treatment of smoke inhalation

This study demonstrates that continuous positive airway pressure (CPAP) improves pulmonary function after smoke inhalation by dogs. Sixteen dogs were anesthetized with iv sodium pentobarbital. Arterial and mixed venous blood gas tensions; carboxyhemoglobin concentration (COHgb); mean systemic arterial (MAP), mean pulmonary arterial (MPAP), and pulmonary arterial wedge (WP) pressures; heart (HR) and respiratory (f) rates; cardiac output (CO); and airway pressure (Paw) were measured. Intrapulmonary physiologic shunt (Qsp/Qt) and pulmonary (PVR) and systemic (SVR) vascular resistances were calculated. The animals then breathed an aerosol of smoke and were divided randomly into 2 groups. The treatment group breathed spontaneously on 8-torr CPAP whereas the control group continued to breathe spontaneously at ambient pressure. After inhalation of smoke, Qsp/Qt, MPAP, PVR, COHgb, HR, and f rose, whereas PaO2 and MAP fell in untreated animals. When CPAP was applied, PaO2 and Qsp/Qt returned nearly to baseline values. Mean f also was significantly lower in the treated animals. We found that the early institution of CPAP improves oxygen exchange in the lungs after the inhalation of smoke.     

Cardiovascular adjustments and gas exchange during extreme hemodilution in humans

OBJECTIVE: To examine the cardiovascular adjustments and pattern of gas exchange that occur during hemodilution. DESIGN: Nonrandomized prospective study. SETTING: Operating room in a university hospital. PATIENTS: Seven patients undergoing elective aortocoronary artery bypass surgery. INTERVENTIONS: Before initiating cardiopulmonary bypass, the patients' hematocrit levels were decreased to approximately 15%. This hemodilution was done by removing a sufficient amount of autologous blood from the aortic cannula and replacing it with a sufficient amount of crystalloid solution. After the discontinuation of cardiopulmonary bypass, measurements were made at a hematocrit of approximately 15%. Then, after autologous blood infusion, measurements were made at a hematocrit of 20%, followed by more blood infusion to approximately 25% with repeat measurements. MEASUREMENTS AND MAIN RESULTS: The following measurements were made before hemodilution and then at all three levels of hemodilution: heart rate, mean arterial pressure (MAP), right atrial pressure, mean pulmonary artery pressure, pulmonary artery occlusion pressure, and cardiac output. From these measurements, the following derived variables were calculated: cardiac index, systemic vascular resistance, and pulmonary vascular resistance. From measurements of arterial oxygen content, mixed venous oxygen content, and cardiac output, intrapulmonary shunt (Qsp/Qt), oxygen uptake (VO2), oxygen extraction ratio, and oxygen delivery (DO2) were derived. The MAP was lowest (57 +/- 3 [SD] vs. 92 +/- 3 mm Hg) at the lowest hematocrit. The cardiac index was highest (4.0 +/- 0.3 vs. 2.3 +/- 0.6 L/min.m2) at the lowest hematocrit. DO2 was lowest at the lowest hematocrit but VO2 remained constant at all levels of hematocrit. The oxygen extraction ratio increased as hematocrit decreased. With progressive increases in hematocrit, DO2 increased and Qsp/Qt decreased. CONCLUSIONS: The data suggest that, during hemodilution, tissue autoregulation of VO2 and utilization are not impaired, but gas exchange function (Qsp/Qt) is impaired.     

The impact of arterial oxygen tension on venous oxygen saturation in circulatory failure

Central and mixed venous oxygen saturations have been used to guide resuscitation in circulatory failure, but the impact of arterial oxygen tension on venous oxygen saturation has not been thoroughly evaluated. This observational study investigated the impact of arterial oxygen tension on venous oxygen saturation in circulatory failure. Twenty critically ill patients with circulatory failure requiring mechanical ventilation and a pulmonary artery catheter in an intensive care unit in a tertiary hospital in Western Australia were recruited. Samples of arterial blood, central venous blood, and mixed venous blood were simultaneously and slowly drawn from the arterial, central venous, and pulmonary artery catheter, respectively, at baseline and after the patient was ventilated with 100% inspired oxygen for 5 min. The blood samples were redrawn after a significant change in cardiac index (>or =10%) from the baseline, occurring within 24 h of study enrollment while the patient was ventilated with the same baseline inspired oxygen concentration, was detected. An increase in inspired oxygen concentration significantly increased the arterial oxygen tension from 12.5 to 38.4 kPa (93.8-288 mmHg) (mean difference, 25.9 kPa; 95% confidence interval [CI], 7.5-31.9 kPa; P < 0.001) and the venous oxygen saturation from 69.9% to 76.5% (mean difference, 6.6%; 95% CI, 5.3% - 7.9%; P < 0.001). The effect of arterial oxygen tension on venous oxygen saturation was more significant than the effect associated with changes in cardiac index (mean difference, 2.8%; 95% CI, -0.2% to 5.8%; P = 0.063). In conclusion, arterial oxygen tension has a significant effect on venous oxygen saturation, and this effect is more significant and consistent than the effect associated with changes in cardiac index.     

Extrapulmonary factors influencing the ratio of arterial oxygen tension to inspired oxygen concentration in burn patients.

The ratio of arterial oxygen tension to inspired oxygen concentration (PaO2/FIO2) as an index of respiratory function was evaluated in 22 patients with body surface area burns of 15--80%. These results indicate that this ratio is limited in its applicability because extrapulmonary factors, such as cardiac output, oxygen consumption, and arterial oxygen content, can affect this index by alterations in the amount of venous desaturation. Useful estimates of intrapulmonary right to left shunt (Qs/Qt) from PaO2/FIO2 were obtained only when arteriovenous oxygen content differences (avDO2) were between 3--5 ml/dl. There were avDO2 values above and below 3--5 ml/dl in at least 35% of the observations. Under these circumstances, PaO2/FIO2 did not correctly reflect changes in Qs/Qt. Blood gases from central venous catheters did not mirror changes in true mixed venous blood and, thus, can lead to erroneous estimations of Qs/Qt. Rational therapy of reduced arterial oxygen saturation requires measurement of both extra- and intrapulmonary factors contributing to arterial desaturation. Measurement of PaO2/FIO2 alone will not estimate these factors.     

Stable and reproducible porcine model of acute lung injury induced by oleic acid

BACKGROUND AND METHODS: Previous studies on acute lung injury induced with oleic acid did not attempt to limit the influence of secondary changes on pulmonary circulation, and cardiopulmonary variable data were only collected and processed intermittently. Our study was designed to continuously monitor the following variables in five swine: systemic and pulmonary pressure; mixed venous oxygen saturation (SVO2) and arterial oxygen saturation (SaO2); minute oxygen consumption and CO2 production before, during, and for 4 hr after the infusion of oleic acid. A personal computer was programmed to produce 20-sec updates of deadspace ratio (VD/VT), venous admixture (Qsp/Qt), pulmonary (PVR) and systemic vascular resistance (SVR), and cardiac output (Qt) from these data. RESULTS: During the oleic acid infusion, there were increases in PVR, SVR, heart rate (HR), mean pulmonary arterial pressure (MPAP), Qsp/Qt, and VD/VT, and a decrease in Qt, SaO2, and SVO2. Thirty minutes after the oleic acid infusion, there was a further increase in HR, Qsp/Qt, and VD/VT, while MPAP, PVR, and SVR gradually decreased to pre-oleic acid infusion levels. No further decrease in SaO2, SVO2, and Qt was observed during that time. After the 30-min period, there was no further change in the cardiopulmonary variables. CONCLUSION: Our method of continuous monitoring was able to demonstrate in swine both the dynamic changes during, and stability after, the oleic acid infusion.     

Effect of hydralazine on intrapulmonary shunt

We compared the acute effects of bilateral arteriovenous may be related to levels of PvO2. The hydralazine-associated (p less than .05) decrease in resistance. Mixed venous oxygen fistulas to those of hydralazine infusion on hemodynamics and pulmonary gas exchange in dogs with pulmonary edema induced by administration of oleic acid. Oleic acid significantly (p less than .01) increased intrapulmonary shunt (Qsp/Qt) and pulmonary and systemic vascular resistance, and reduced cardiac output. Once the lesion stabilized, both opening the fistula and infusing hydralazine produced a similar and significant (p less than .01) increase in cardiac output, and a significant (p less than .05) decrease in resistance. Mixed venous oxygen tension (PvO2) closely followed the changes in cardiac output; however, PaO2 did not change. Qsp/Qt significantly (p less than .01) increased with the fistulas open and with hydralazine infusion. Closure of the fistulas or bleeding the animal at the end of the experiment reversed the changes in cardiac output and Qsp/Qt. The comparable increases in cardiac output and Qsp/Qt produced by opening the fistulas or infusing hydralazine may be related to levels of PvO2. The hydralazine-associated PvO2 increase indicates that this drug increased oxygen transport to the tissues even as Qsp/Qt became larger.     

Assessing pulmonary function in acute respiratory insufficiency: a clinical charting sheet

A sheet to chart the clinical respiratory variables relevant to acute respiratory insufficiency (ARI) therapy is presented. The chart permits plotting shunt fraction (Qsp/Qt) and efficiency (E or 1--Qsp/Qt) vs. load (L). L is the volume of oxygen (combined and dissolved) that would be exchanged in the lung per minute, if venous blood became fully equilibrated with alveolar gas. L relates cardiac output (Qt), hemoglobin concentration, alveolar oxygen tension, venous oxygen saturation and tension, and the oxygen-hemoglobin combining and oxygen solubility constants. Oxygen consumption (VO2) isopleths are added to the sheet (VO2 = L X E). Qt, VO2, and hence L are indexed per m2 (body surface area), and the approximate normal VO2 range is indicated. Using this sheet hopefully simplifies the correlation of complex pulmonary oxygen exchange data and enhances information recognition and analysis. It provides special help in determining the optimal PEEP in difficult ARI cases. To illustrate its use, a case is detailed.     

Reduced venous admixture in hemorrhagic hypovolemia: maintenance of arterial oxygenation by selective pulmonary vascular collapse

In nine anesthetized and ventilated swine, a microcomputer calculated cardiac output, venous admixture (Qsp/Qt) and physiologic deadspace (VD/VT) every 20 sec, utilizing dual oximetry and a gas exchange analyzer. After lung injury with ethchlorvynol (ECV), animals were bled 40% blood volume over 40 min. Mean cardiac output decreased 7.0 to 2.2 L/min (p less than .05) accompanied by a decrease in mean Qsp/Qt from 0.28 to 0.14 (p less than .05) and an increase in mean VD/VT from 0.39 to 0.54 (p less than .05). Arterial Hgb saturation (Sao2) increased from 88 +/- 7% to 90 +/- 6%. On regression of all data points for each variable, Qsp/Qt had a positive correlation with cardiac output (r = .90), mean arterial pressure (MAP, r = .87), mean pulmonary artery pressure (MPAP, r = .86), and mixed venous Hgb saturation (Svo2, r = .89, p less than .001). VD/VT had an inverse correlation with cardiac output (r = -.90), MAP (r = -.82), Qsp/Qt (r = -.83), MPAP (r = -.77), and Svo2 (r = -.92, p less than .001). The decreasing Qsp/Qt and increasing VD/VT, with decreasing pulmonary perfusion pressures, were attributed to selective loss of perfusion to alveoli with low ventilation/perfusion ratios.     

Swine model of early adult respiratory distress syndrome induced by intravenous ethchlorvynol

Although ethchlorvynol (ECV) has been used to induce pulmonary damage in animals, changes after injection of this drug have not been studied, nor has the stability of the animal been assessed after injection. Continuously monitored hemodynamic and respiratory changes were followed during and after iv injection of 55 mg/kg ECV in ethanol into anesthetized, paralyzed, and ventilated swine (n = 5) and compared to changes in a control group given ethanol alone (n = 5). Arterial and mixed venous saturations were measured by fiberoptic vascular catheters and oxygen exchange by a gas monitor. Twelve direct and derived variables were monitored every 20 sec using a computer data acquisition system. Arterial oxygen saturation was kept at 90 +/- 2% by adjustment of FIO2. Ethanol produced only transitory changes during infusion. Significant elevations in pulmonary vascular resistance (PVR), shunt (Qsp/Qt) and deadspace (VD/VT) were observed during and after ECV. These were unaccompanied by changes in cardiac output or arterial pressure. PVR increased by 137%, Qsp/Qt by 67%, and VD/VT by 28% over 30 min. These changes were then sustained in the postinfusion period, producing a stable model of early adult respiratory distress syndrome for 3.5 h.     

原位肝移植非静-静脉转流围术期肺氧合及肺内分流的变化

目的观察非体外静静脉转流术下原位肝移植(OLT)围术期肺氧合功能及肺内分流的改变。方法对19例晚期肝病行OLT手术的患者采用静吸复合麻醉,无肝期均未使用体外静静脉转流术。常规经右颈内静脉放置SwanGanz导管持续监测心排血量(CO),测定肺氧合功能及肺内分流率。分别在麻醉诱导后、无肝前30min、无肝30min、新肝30min和术毕抽取桡动脉血和肺动脉血进行血气分析,记录不同时期的动脉血氧分压(PaO2)、动脉血二氧化碳分压(PaCO2)和心排血指数(CI),计算肺泡动脉氧分压差(PAaO2)。根据肺内分流标准模型公式计算肺内分流率(Qs/Qt)。结果麻醉诱导后吸入氧浓度(FiO2)1.00情况下,PaO2为(385.0±56.4)mmHg(1mmHg=0.133kPa),PAaO2和Qs/Qt均明显高于正常参考值。麻醉诱导后各项指标与无肝前30min相比差异均无显著性;无肝30minCO和CI明显下降(P均<0.01),Qs/Qt明显下降(P<0.05);新肝30minPaO2、PaCO2均明显升高(P均<0.05),PAaO2明显下降(P<0.05),CO和CI均明显升高(P均<0.01);术毕CO和CI也均明显升高(P均<0.05),并维持在较高的水平,Qs/Qt明显下降(P<0.05),但PaO2、PaCO2、PAaO2则均无明显变化。结论OLT患者非静静脉转流术前和术中均存在明显的肺氧合功能障碍。     

呼吸指数在低氧血症时的临床意义

呼吸指数（ＲＩ）是肺泡－动脉氧压差与动脉氧分压之比。其值受心输出量、混合静脉血氧分压、肺内分流、通气／血流比、通气状况及弥散功能的影响，是反映呼吸功能的重要指标。通过对８０例低氧血症危重病患者的ＲＩ分析显示，ＲＩ的改变可确定低氧血症的存在与程度的变化，动态观察ＲＩ可评价低氧血症的疗效和预后。建议在ＩＣＵ病房将ＲＩ与血气指标配合应用，以便更好地反映病人体内病理生理变化。     

Validation of oxygen saturation monitoring in neonates.

BACKGROUND: Pulse oximetry is commonly used to monitor oxygenation in neonates, but cannot detect variations in hemoglobin. Venous and arterial oxygen saturations are rarely monitored. Few data are available to validate measurements of oxygen saturation in neonates (venous, arterial, or pulse oximetric). Purpose To validate oxygen saturation displayed on clinical monitors against analyses (with correction for fetal hemoglobin) of blood samples from neonates and to present the oxyhemoglobin dissociation curve for neonates. METHOD: Seventy-eight neonates, 25 to 38 weeks' gestational age, had 660 arterial and 111 venous blood samples collected for analysis. RESULTS: The mean difference between oxygen saturation and oxyhemoglobin level was 3% (SD 1.0) in arterial blood and 3% (SD 1.1) in venous blood. The mean difference between arterial oxygen saturation displayed on the monitor and oxyhemoglobin in arterial blood samples was 2% (SD 2.0); between venous oxygen saturation displayed on the monitor and oxyhemoglobin in venous blood samples it was 3% (SD 2.1) and between oxygen saturation as determined by pulse oximetry and oxyhemoglobin in arterial blood samples it was 2.5% (SD 3.1). At a Pao(2) of 50 to 75 mm Hg on the oxyhemoglobin dissociation curve, oxyhemoglobin in arterial blood samples was from 92% to 95%; oxygen saturation was from 95% to 98% in arterial blood samples, from 94% to 97% on the monitor, and from 95% to 97% according to pulse oximetry. CONCLUSIONS: The safety limits for pulse oximeters are higher and narrower in neonates (95%-97%) than in adults, and clinical guidelines for neonates may require modification.     

Respiratory function and carbonic anhydrase inhibition

Acetazolamide (Diamox) induced carbonic anhydrase inhibition is an efficient means of eliminating surplus water and bicarbonate in the overhydrated and alkalotic patient. Previous studies have demonstrated an unexpected and unexplained increase in arterial and venous oxygenation during acute carbonic anhydrase inhibition. In the present investigation we assessed the effect of acetazolamide 15 mg kg^-1 on pulmonary gas exchange in 10 critically ill, mechanically ventilated patients. Median arterial oxygen tension increased by 0.9 kPa and central venous oxygen tension and content by 16–18% and 6–8% respectively. The improved oxygenation could, however, not be attributed to an improved pulmonary oxygen exchange as both pulmonary venous admixture (Q_sQ_t ^–1) and physiological dead space ventilation (V_DV_T ^-1) increased. The increase in arterial oxygen tension can be explained by a rightward shift of the oxyhemoglobin dissociation curve due to the increased acidity of the blood during carbonic anhydrase inhibition (Bohr effect). Acetazolamide does not depress oxygen consumption, so the increase in central venous oxygen content probably reflects an improved cardiac performance. This could conceivably be mediated via sympathetic activation in response to acetazolamide induced carbon dioxide retention.     

连续性血液净化对感染性多脏器功能障碍综合征患者血流动力学及氧代谢的影响

目的 探讨连续性血液净化(CBP)对感染所致多脏器功能障碍综合征(MODS)患者血流动力学及氧代谢的影响。方法 选择感染所致MODS患者17例,应用连续静脉-静脉血液滤过(CVVH)联合血浆置换(PE)进行治疗,治疗期间用Swant-Ganz漂浮导管监测血流动力学变化并检测氧代谢指标。结果 与CBP前比较,CBP治疗后,体血管阻力指数(SWRI)明显改善,平均动脉压(MAP)回升,心率(HR)下降,肺动脉压及肺动脉楔压(PAP、PCWP)也明显降低,动脉血氧分压明显上升(P<0.01),氧供及氧耗均有所增加(P<0.05),动脉血乳酸含量明显降低(P<0.01),混合静脉血氧分压、静脉血氧饱和度及氧摄取率无明显变化(P>0.05)。结论 CBP可改善MODS患者的全身血流动力学状况,提高患者的氧供,但对氧摄取率无明显影响。     

Sequential cardiorespiratory patterns in septic shock

Sequential hemodynamic and oxygen transport monitoring was performed in 33 patients with septic shock to define the temporal pattern of physiologic events. Measurements taken over a 24-h period before the hypotensive crisis, defined as the lowest initial mean arterial pressure (MAP), were compared to those taken during the 48 h thereafter. In the 24-h period before the hypotensive crisis, there were increases in cardiac index (CI), central venous pressure (CVP), pulmonary capillary wedge pressure (WP), pulmonary vascular resistance index (PVRI), and pulmonary shunt (Qsp/Qt), but decreases in MAP, systemic vascular resistance index (SVRI) and oxygen delivery (Do2). When sequential cardiorespiratory patterns were examined, oxygen consumption (VO2) fell transiently to significantly low values 12 h before as well as at the time of the hypotensive crisis. SVRI fell and CI rose to values significantly different from normal in the 4 h before the low MAP. During the subsequent 48 h after the hypotensive crisis, CI, CVP, WP, PVRI and Qsp/Qt remained elevated. Values for MAP, SVRI, DO2, and VO2 were significantly reduced. These results demonstrate the existence of antecedent cardiorespiratory alterations that precede the hypotensive episode in septic shock and suggest that flow maldistribution in the systemic circulation is an early event with possible pathogenic significance.     

Reliability of in vivo mixed venous oximetry during experimental hypertriglyceridemia.

BACKGROUND AND METHODS: The spectral absorbance of iv lipid emulsion produces interference in the in vitro spectrophotometric measurement of hemoglobin saturation. Therefore, we investigated in vivo mixed venous oximetry during lipid emulsion infusions. Boluses of lipid emulsion, increasing by 0.1-g/kg increments, were infused every 30 mins into nine anesthetized dogs. After each lipid bolus, laboratory and hemodynamic data measurements were repeated, and arterial and mixed venous blood gases were analyzed on a laboratory cooximeter that was equipped for canine blood. The in vivo mixed venous oxygen saturation was continuously monitored via an indwelling, optically equipped pulmonary artery catheter. RESULTS: As expected, increasing concentrations of lipid emulsion increased (r2 = .92) serum triglyceride concentration. As a result, the in vitro measurements of percentage methemoglobin increased artifactually, reducing in vitro measurements of arterial (r2 = .74) and mixed venous (r2 = .44) oxygen saturations. The in vivo mixed venous oxygen saturation, however, remained constant during hypertriglyceridemia (r2 less than .01). CONCLUSIONS: In vivo mixed venous oximetry remained constant during hypertriglyceridemia, while in vitro measurements of arterial and mixed venous saturations were artifactually reduced.