Systemic Oxygen Extraction Ratio Research Articles

Abstract 9677: Therapeutic Improvements in Pulmonary Arterial Hypertension Are Related to Cardiopulmonary Function but Not Skeletal Muscle Oxygen Extraction

Introduction: World Symposium Group 1 pulmonary arterial hypertension (PAH) patients have impaired function from both central oxygen delivery and skeletal muscle oxygen extraction. The effect of PH-directed therapy on skeletal muscle oxygen extraction is unknown. The aim of this study is to determine if therapy associated changes in muscle extraction parallel changes in cardiopulmonary function. Methods: Retrospective analysis was performed on twenty-nine PAH patients (24 female, mean age 54±11.4 years) receiving prostacyclin therapy (18 on monotherapy). Subjects underwent invasive cardiopulmonary exercise testing (iCPET) for treatment response evaluation followed by repeat surveillance iCPET with mean follow-up of 10.4±5.2 months. Skeletal muscle oxygen extraction was quantified by arterio-venous difference indexed to hemoglobin (Ca-vO 2 /Hgb) and systemic oxygen extraction ratio (SER) (Ca-vO 2 /CaO 2 ). Central oxygen delivery (DO 2 ) was calculated as peak cardiac output X CaO2 at peak exercise. Functional capacity was semi-quantified by six-minute walk test (6MWT) distances between assessments (n=20). Subjects were stratified into two groups: those with improvement (n=10) vs unimproved (n=19) in currently accepted ERS/COMPERA score ( Figure ). Results: Improvements in ERS/COMPERA score were related to DO 2 (318.3±273.1 vs -38.3±684.9 mL/min, P=.016 ) and PVR (-4.8±3.0 vs -0.6±3.2 WU, P=.002 ) (Figure A & B). However, there was not a detectible difference between assessments in Ca-vO 2 /hgb (-0.01±0.14 vs 0.00±0.27 mL/g, P=.573 ), SER (-0.01±0.10 vs 0.00±0.20, P=.573 ), or 6MWT (7 improved, 13 unimproved) (77±115 vs 25±104 meters, P=.877 ) ( Figure C & D ). Conclusions: Although PH-directed therapy improves both PVR and oxygen delivery, its effects on skeletal muscle extraction are questionable. Clinicians should consider that oxygen extraction may influence functional capacity when evaluating therapeutic improvement.

Influence of variations in systemic blood flow and pressure on cerebral and systemic oxygen saturation in cardiopulmonary bypass patients

BackgroundAlthough both pressure and flow are considered important determinants of regional organ perfusion, the relative importance of each is less established. The aim of the present study was to evaluate the impact of variations in flow, pressure, or both on cerebral and whole-body oxygen saturation. MethodsThirty-four consenting patients undergoing elective cardiac surgery on cardiopulmonary bypass were included. Using a randomized cross-over design, four different haemodynamic states were simulated: (i) 20% flow decrease, (ii) 20% flow decrease with phenylephrine to restore baseline pressure, (iii) 20% pressure decrease with sodium nitroprusside (SNP) under baseline flow, and (iv) increased flow with baseline pressure. The effect of these changes was evaluated on cerebral ScO2 and systemic SvO2 oxygen saturation, and on systemic oxygen extraction ratio (OER). Data were assessed by within- and between-group comparisons. ResultsDecrease in flow was associated with a decrease in ScO2 [from 63.5 (7.4) to 62.0 (8.5) %, P<0.001]. When arterial pressure was restored with phenylephrine during low flow, ScO2 further decreased from 61.0 (9.7) to 59.2 (10.2) %, P<0.001. Increase in flow was associated with an increase in ScO2 from 62.6 (7.7) to 63.6 (8.9) %, P=0.03, while decreases in pressure with the use of SNP did not affect ScO2. SvO2 was significantly lower (P<0.001) and OER was significantly higher (P<0.001) in the low flow arms. ConclusionsIn the present elective cardiac surgery population, ScO2 and SvO2 were significantly lower with lower flow, regardless of systemic arterial pressure. Moreover, phenylephrine administration was associated with a reduced cerebral and systemic oxygen saturation.

REDUCED SYSTEMIC OXYGEN EXTRACTION DOES NOT PROVE MUSCLE DYSFUNCTION IN PAH

Dear Editor-in-Chief: With interest, we have read the article of Tolle et al. (7)reporting on the systemic oxygen extraction using the Fick principle in patients with either pulmonary arterial hypertension (PAH) or left ventricular systolic (LVSD) and diastolic dysfunction (LVDD). The authors found in PAH patients an impaired systemic oxygen extraction ratio (SER) and concluded that it was pathologic, and they sought explanation in dysfunctioning skeletal muscles in these patients because cardiac output (Q˙t) was found to be normal; this is in contrast to the LVSD patients who are known to have a reduced V˙O2peak but have an increased SER in response to an abnormal Q˙t. We disagree with the authors' conclusion for the following reason: In their Figure 2, Tolle et al. (7) used a Q˙t percentage, normalized to the maximal predicted cardiac output that is calculated from a predicted V˙O2peak, which was derived from a population of healthy men (3). The figure showed that Q˙t in the PAH patients was higher than in theLVSD patients and eventually exceeds 100% of predicted values. Ahyperdynamic circulation is an abnormal phenomenon in PAH patients only encountered in portopulmonary hypertension or PAH secondary to a right-to-left shunt phenomenon. By inserting the PAH patients with a hyperdynamic circulation (Q˙t more than 100% predicted), Tolle et al. (7) concluded that the PAH population has a different linear correlation compared with the LVSD group, and thus another pathophysiological cause, in the skeletal muscles, resulting in a reduced SER. However, many studies performed in different patient groups-including those of Jain et al. (4) in chronic heart failure patients, Ruokonen et al. (6) in ICU patients, and Buheitel et al. (1) in children with congenital heart disease-have shown that the relation between cardiac output and SER is nonlinear (2). Moreover, it is a physiological response of the body that SER is reduced at increased Q˙t because muscle mitochondria operate close to the maximum rate at the predicted V˙O2peak (5). Fitting linear lines for different patient groups with different ranges of cardiac output will automatically lead to different slopes. It is additionally clear from their Figure 2 that if the PAH patients with the hyperdynamic flow are excluded, slopes between the different patient groups will not differ. We conclude that the difference in slopes between the PAH patients and LVSD patients cannot be interpreted as the consequence of dysfunctioning skeletal muscles in the PAH patients, rather it reflects the curvilinear relation between SER and Q˙t. Yeun Ying Wong, MD Willem J. van der Laarse, PhD Anton Vonk-Noordegraaf, MD, PhD Departments of Pulmonology and Physiology Institute of Cardiovascular Disease VU University Medical Center Amsterdam, The Netherlands

Cardio-renal recovery of hypoxic newborn pigs after 18%, 21% and 100% reoxygenation

We examined the effects of 18%, 21% or 100% oxygen on the recovery of the heart and kidneys in a short-term survival model of neonatal hypoxia-reoxygenation (HR). Controlled, block-randomized animal study. University animal research laboratory. Large White piglets (1-3 days, 1.7-2.5 kg). Piglets received normocapnic hypoxia (15% oxygen) (2 h) and were reoxygenated with 18%, 21% or 100% oxygen (1 h) (n=7 per group) then 21% oxygen (2 h). Sham-operated pigs (n=7) had no HR. Seventeen of 21 HR piglets recovered from moderate hypoxemia (mean PaO(2) 27-33 mmHg and pH 7.20-7.22, associated with tachycardia and hypotension). Systemic arterial pressure, heart rate, left renal arterial flow, oxygen transport, plasma troponin-I and creatinine levels were monitored and recovered with no differences among HR groups over 4 days after resuscitation. The 100% group had increased myocardial oxidative stress (oxidized glutathione levels) and the most cardiac HR-induced injury. There were no differences in renal oxidative stress and HR-induced injury among groups. Early oxygenation at 1 h after resuscitation correlated with the plasma troponin-I level at 6 h (r = -0.51 and 0.64 for SaO(2) and systemic oxygen extraction ratio, p<0.05, respectively) and renal HR-induced injury at 4 days (r =0.61 for renal oxygen delivery, p<0.05). In hypoxic piglets, 18%, 21% and 100% reoxygenation caused similar systemic and renal hemodynamic and functional recovery. The indicators of oxidative stress and HR injury in myocardial and renal tissues suggest that the reoxygenation with 100% oxygen appears sub-optimal and the use of 18% oxygen offers no further benefit, when compared with 21% oxygen.

Impaired Systemic Oxygen Extraction at Maximum Exercise in Pulmonary Hypertension

To determine the relative contributions of the Fick principle variables to impaired exercise tolerance in pulmonary arterial hypertension compared with pulmonary venous hypertension. One hundred forty-seven consecutive, complete, clinically indicated cardiopulmonary exercise tests done with radial and pulmonary arterial catheters and radionuclide ventriculographic scanning were screened for an exercise limit attributable to 1) pulmonary arterial hypertension (N = 34), 2) left ventricular systolic (N = 23), or 3) diastolic dysfunction (N = 36), defined by mean pulmonary artery pressure, pulmonary capillary wedge pressure, and left ventricular ejection fraction. Systolic and diastolic dysfunction are together referred to as pulmonary venous hypertension. Patients with other limits were excluded, including those with a pulmonary mechanical limit. For the resulting 93 exercise tests, the Fick principle variables' contributions to a depressed maximum oxygen consumption were compared by ANOVA and ANCOVA. Maximum oxygen consumption (54.5 +/- 15.5 vs 73.2 +/- 20.1 vs 66.0 +/- 15.7% predicted) and oxygen delivery (1457 +/- 456 vs 2161 +/- 824 vs 2007 +/- 665 mL x min(-1)) were reduced in systolic dysfunction versus both diastolic dysfunction and pulmonary arterial hypertension, respectively (P < 0.05 by ANOVA). Maximum systemic oxygen extraction ratio was highest in systolic dysfunction, intermediate in diastolic dysfunction, and lowest in pulmonary arterial hypertension (0.744 +/- 0.091 vs 0.680 +/- 0.091 vs 0.619 +/- 0.113, respectively, P < 0.05 among all groups). Systemic oxygen extraction at peak exercise was inversely related to maximum cardiac output in pulmonary arterial hypertension, but it was blunted versus systolic dysfunction throughout the range of peak cardiac outputs (P < 0.05 by ANCOVA). Maximum systemic oxygen extraction is impaired in pulmonary arterial versus pulmonary venous hypertension and contributes to the exercise limit.

What is the meaning of standard venous admixture formula results in septic patients?

The standard venous admixture formula is widely used in the bedside assessment of intrapulmonary shunt in intensive care units. The intrapulmonary shunt fraction calculated by the standard venous admixture formula is affected by the systemic oxygen extraction ratio and thus reflects both systemic and intrapulmonary shunts, especially in septic patients with decreased oxygen extraction ratios. The standard venous admixture formula may cause misestimation of the intrapulmonary shunt fraction, especially in septic patients. Inert gas rebreathing techniques and simultaneous measurement of cardiac output by thermodilution and oxygen consumption by indirect calorimetry may be useful in septic patients.

The aetiology of hypoxaemia in chickens selected for rapid growth

In comparison to other classes of chickens, broilers selected for rapid growth tend to be hypoxaemic, and many develop congestive heart failure (CHF). In order to explain the physiological mechanisms associated with hypoxaemia in fast-growing broiler chickens ( Gallus gallus), this study examined several basic physiological parameters including the blood gas profile in arterial [left atrial (LA)] and mixed venous [right atrial (RA)] blood, systemic oxygen extraction ratio, and intrapulmonary shunt fraction. These parameters were further studied in the context of blood flow in the pulmonary circulation, structural characteristics of the lungs, and cardiac function [measured as cardiac index (CI)]. Overall, broilers had lower arterial and mixed venous blood pO 2 levels and higher pCO 2 levels compared to leghorns. The cardiac index was lower in fast-growing and CHF broilers compared to leghorn chickens or feed-restricted broilers. Systemic oxygen extraction ratio (ER) and intrapulmonary shunt fraction were significantly higher in fast-growing broilers and birds with CHF (all P < 0.01). Lungs of all broilers, but not leghorns, contained ectopic, irregular nodular formations located within air spaces. Broilers with clinical signs of hypoxaemia revealed the highest number of these formations in their lung. Taken together, the present findings indicate that key factors associated with the development of hypoxaemia in fast-growing broilers include: (1) high demand for oxygen as evidenced by high oxygen ER; (2) inadequate cardiac output (CO) to fulfill the higher oxygen demands, leading to severe depletion of O 2 in mixed venous blood; and (3) elevated intrapulmonary shunt fraction and possibly dead space associated with specific pathological and anatomical characteristics within the lung.

Arginine vasopressin reduces intestinal oxygen supply and mucosal tissue oxygen tension

We investigated intestinal oxygen supply and mucosal tissue PO2 during administration of increasing dosages of continuously infused arginine vasopressin (AVP) in an autoperfused, innervated jejunal segments in anesthetized pigs. Mucosal tissue PO2 was measured by employing two Clark-type surface oxygen electrodes. Oxygen saturation of jejunal microvascular hemoglobin was determined by tissue reflectance spectrophotometry. Microvascular blood flow was assessed by laser-Doppler velocimetry. Systemic hemodynamic variables, mesenteric venous and systemic acid-base and blood gas variables, and lactate measurements were recorded. Measurements were performed at baseline and at 20-min intervals during incremental AVP infusion (n = 8; 0.007, 0.014, 0.029, 0.057, 0.114, and 0.229 IU.kg(-1).h(-1), respectively) or infusion of saline (n=8). AVP infusion led to a significant (P < .05), dose-dependent decrease in cardiac index (from 121 +/- 31 to 77 +/- 27 ml.kg(-1).min(-1) at 0.229 IU.kg(-1).h(-1)) and systemic oxygen delivery (from 14 +/- 3 to 9 +/- 3 ml.kg(-1).min(-1) at 0.229 IU.kg(-1).h(-1)) concomitant with an increase in systemic oxygen extraction ratio (from 31 +/- 4 to 48 +/- 10%). AVP decreased microvascular blood flow (from 133 +/- 47 to 82 +/- 35 perfusion units at 0.114 IU.kg(-1).h(-1)), mucosal tissue PO2 (from 26 +/- 7 to 7 +/- 2 mmHg at 0.229 IU.kg(-1).h(-1)), and microvascular hemoglobin oxygen saturation (from 51 +/- 9 to 26 +/- 12% at 0.229 IU.kg(-1).h(-1)) without a significant increase in mesenteric venous lactate concentration (2.3 +/- 0.8 vs. 3.4 +/- 0.7 mmol/l). We conclude that continuously infused AVP decreases intestinal oxygen supply and mucosal tissue PO2 due to a reduction in microvascular blood flow and due to the special vascular supply in the jejunal mucosa in a dose-dependent manner in pigs.

Circulatory effects of hypoxia, acute normovolemic hemodilution, and their combination in anesthetized pigs.

Because hemodilution decreases the oxygen-carrying capacity of blood, it was hypothesized that severe hemodilution would decrease the tolerance to alveolar hypoxia. Hemodynamics, oxygen transport, and blood lactate concentrations were compared in ten pigs with normal hematocrit (33 +/- 4%), and ten hemodiluted pigs (hematocrit 11 +/- 1%; mean +/- SD) anesthetized with ketamine-fentanyl-pancuronium during stepwise decreases in inspired oxygen fraction (FIO2; 1.0, 0.35, 0.21, 0.15, 0.10, 0.05). Median systemic oxygen delivery (DO2SY) became critical (the DO2SY value when arterial lactate exceeded 2.0 mmol.l-1) at 10.4 ml.kg-1.min-1 (range 6.9-16.1) in hemodiluted animals and at 11.8 ml.kg-1.min-1 (5.9-32.2) in animals with normal hematocrits (NS). The relationship between mixed venous oxygen saturation and arterial lactate values was less consistent and median critical mixed venous oxygen saturation was higher (P < 0.05) in the hemodiluted group (35%, range 21-64), than in animals with normal hematocrits (21%, 7-68%). In animals with normal hematocrit, decreasing FIO2 from 1.0 to 0.10 resulted in a decrease in DO2SY from 26.3 +/- 9.1 to 9.3 +/- 3.9 ml.kg-1.min-1 (P < 0.01). Cardiac output did not change, systemic oxygen extraction ratio increased from 0.23 +/- 0.08 to 0.68 +/- 0.13 (P < 0.01), and arterial lactate from 0.9 +/- 0.2 to 3.4 +/- 3.0 mmol.l-1 (P < 0.05). Cardiac venous blood flow, as measured by retrograde thermodilution, increased from 5.7 +/- 2.9 to 12.6 +/- 5.7 ml.kg-1.min-1 (P < 0.01). When FIO2 was reduced to 0.05, three animals became hypotensive and died. In the second group, hemodilution increased cardiac output and systemic oxygen extraction ratio (P < 0.01). Cardiac venous blood flow increased from 4.1 +/- 1.7 to 9.8 +/- 5.1 ml.kg-1.min-1 (P < 0.01), and cardiac venous oxygen saturation from 22 +/- 5 to 41 +/- 10% (P < 0.01). During the subsequent hypoxia, cardiac output and DO2SY were maintained until FIO2 = 0.15 (DO2SY = 10.1 +/- 3.3 ml.kg-1.min-1). Cardiac venous blood flow was then 18.5 +/- 10.7 ml.kg-1.min-1 (P < 0.01), but in spite of this, myocardial lactate production occurred. At FIO2 = 0.10 (DO2SY = 7.7 +/- 3.0 ml.kg-1.min-1), arterial lactate concentration increased to 8.5 +/- 2.3 mmol.l-1 (P < 0.01), and most animals became hypotensive. All hemodiluted animals died when FIO2 was decreased to 0.05 (P < 0.01 when compared to animals with normal hematocrit). Systemic and myocardial lactate production occurred at similar systemic oxygen delivery rates in hemodiluted and nonhemodiluted animals. Mixed venous oxygen saturation may be a less reliable indicator of inadequate oxygen delivery during hemodilution.

Inhibitory effect of Escherichia coli endotoxin on skeletal muscle contractility

Endotoxemia in rabbits is associated with decreases in oxygen transport, tissue hypoxia, metabolic acidosis, and impaired oxygen extraction. In this study, we tested the hypothesis that endotoxin also inhibits skeletal muscle contractility directly. Randomized animal study. Accredited animal research facility. New Zealand white rabbits of either sex, weighing 2.55 +/- 0.20 kg. We compared two groups of rabbits (n = 10 each) undergoing continuous electrical stimulation of the left hindlimb (maximal isometric twitch contraction at 0.25 Hz). One group (septic) was given an intravenous infusion of Escherichia coli endotoxin. The control group was subjected to decreases in cardiac output by inflating a balloon placed in the right ventricle. Endotoxin or balloon inflation resulted in comparable decreases in cardiac output (49% and 53%, respectively). Hindlimb oxygen transport decreased to similar values for both groups (4.9 +/- 0.3 and 4.2 +/- 0.5 mL/min/kg, respectively). Systemic oxygen extraction ratio was greater in the control group (0.72 +/- 0.03) than in the septic group (0.55 +/- 0.04; p < .05). There were no differences in hindlimb oxygen extraction ratio. Decreases in hindlimb forces were greater in the septic group (42 +/- 4%) than in the control group (18 +/- 3%, p < .01). Force frequency curves obtained at the beginning and the end of the experiment showed greater fatigue in the septic group. The intravenous infusion of Escherichia coli endotoxin produces a direct inhibitory effect on skeletal muscle contractility in rabbits. This phenomenon is independent of decreases in oxygen transport and blood pH. Our data support the notion of a direct cellular effect of endotoxin, or of an associated cytokine, on skeletal muscle contractility. The mechanism responsible for this phenomenon is unknown.

The Effect of the Total Cumulative Epinephrine Dose Administered During Human CPR on Hemodynamic, Oxygen Transport, and Utilization Variables in the Postresuscitation Period

Studies evaluating the dose of epinephrine required to optimize return of spontaneous circulation and survival after CPR have shown that doses greater than recommended by advanced cardiac life support (ACLS) improve coronary perfusion pressure and short-term resuscitation rates. Since survival has not improved, it is possible that higher doses of epinephrine may be physiologically detrimental in the postresuscitation period. The object of this study is to measure the effect of the total cumulative dose of epinephrine given during ACLS on the hemodynamic, oxygen transport, and utilization variables in the postresuscitation period. A prospective nonrandomized control trial of inception cohorts. A large urban emergency department and intensive care unit. Forty-nine successfully resuscitated witnessed, normothermic, nontraumatic, out-of-hospital patients, who had suffered cardiac arrests. All patients were treated according to ACLS guidelines; however, the epinephrine dose (0.01 to 0.2 mg/kg or 1 to 14 mg) was selected at the clinician's discretion and given through central venous access every 3 to 5 min. Hemodynamic, oxygen transport, and utilization variables were measured on a return of spontaneous circulation, and at least every 30 min thereafter under a standardized postresuscitation protocol. Hemodynamic, oxygen transport/utilization variables, and mortality in patients resuscitated from cardiac arrest. The total cumulative dose of epinephrine given during ACLS until a return of spontaneous circulation was recorded. A total cumulative epinephrine dose of 15 mg was found to best predict 24-h mortality. Of the 49 patients, 20 received less than 15 mg (group 1) and 29 received greater than 15 mg (group 2). Age, premorbid health status, sex, presenting rhythm, and duration of cardiac arrest were similar in both groups. The 24-h survival was 17 of 20 (85%) and 12 of 29 (41%) in group 1 and 2, respectively (p < 0.002). Over the first 6 h of the postresuscitation period, both groups had similar mean arterial pressure (MAP), mixed venous oxygen saturation, and systemic oxygen extraction ratio (all p > 0.1). Group 2, however, had a significantly lower cardiac index (CI), systemic oxygen consumption (VO2), and systemic oxygen delivery (DO2) (all p < 0.01). Systemic vascular resistance index (SVRI), initial and 6-h lactic acid levels were significantly higher in group 2 (all p < 0.03). The administration of all doses of epinephrine during the resuscitation of out-of-hospital cardiac arrest is associated with impairment of DO2 and VO2 in the postresuscitation period. Both duration and severity of these impairments correlate with the total cumulative epinephrine dose given during the resuscitation. Thus, inadvertent catecholamine toxicity represents a further complicating factor in the production of postresuscitation disease. Diagnostic and therapeutic interventions addressed toward mitigating these potentially reversible adverse effects may impact morbidity and mortality in out-of-hospital cardiac arrests.

Characterization of systemic oxygen transport in end-stage chronic congestive heart failure

Chronic congestive heart failure (CHF) is characterized by low cardiac index (CI) and low systemic oxygen delivery (Ḋ o 2), which frequently are associated with lethal cardiogenic shock after acute myocardial infarction. Nevertheless, patients with severe CHF are able to survive with these low levels of systemic Ḋ o 2 and Cl. It was hypothesized that patients with CHF survive low Cl and Ḋ o 2 by downregulation of global metabolism and resting oxygen consumption (V̇ o 2) and a concomitant increase in systemic oxygen extraction ratio ( o 2ER). Therefore the objective of this study was to characterize the resting pattern of systemic oxygen transport ( o 2T) and utilization in patients with stable CHF. Seventeen patients with CHF (New York Heart Association functional class III or IV) for ≥ 3 months and with left ventricular ejection fraction (EF) <25% and whose condition was stable with conventional oral therapy were studied. The control group comprised 10 subjects (NYHA class I) who had coronary angiography and who were found to have normal left ventricular function and EF >60%. Subjects underwent right-heart catheterization for measurement and calculation of hemodynamic and o 2T variables (V̇ o 2, Ḋ o 2, and o 2ER). There were no significant differences in mean age (67 ± 6 vs 64 ± 17 years) or gender ratio (male:female 14:3 vs 7:3) between CHF and control groups, respectively. The cause of CHF was ischemic in 13 and idiopathic in 4 patients. There were 9 patients in NYHA class III and 8 in class IV. Although heart rate (84 ± 15 vs 80 ± 15 beats/min) and mean arterial pressure (89 ± 19 vs 99 ± 10 mm Hg) were similar, pulmonary capillary wedge pressure was significantly raised (26 ± 9 mm Hg, vs 10 ± 3 mm Hg, p < 0.001) in CHF vs control, respectively. Cl (1.7 ± 0.4 L/min/m 2 vs 2.9 ± 0.3 L/min/m 2, p < 0.001), left ventricular EF (17% ± 6% vs 70% ± 10%, p < 0.001), systemic Ḋ o 2 (279 ± 52 ml/min/m 2 vs 531 ± 86 ml/min/m 2, p < 0.001), V̇ o 2 (160 ± 14 vs 150 ± 28, p < 0.001), and mixed venous oxygen saturation (60 ± 6 vs 67 ± 4, p < 0.02) were significantly reduced in CHF group vs control, respectively. In conclusion, end-stage CHF is characterized by decreases in Cl and Ḋ o 2 that are associated with a significant reduction in systemic V̇ o 2 and an increase in o 2ER. This level of V̇ o 2 would be lethal in other clinical shock states; however, downregulation of metabolic and oxygen demands (or hibernation) may be an adaptive response in end-stage CHF to enhance survival.

Venous Hyperoxia after Cardiac Arrest: Characterization of a Defect in Systemic Oxygen Utilization

Supranormal mixed venous oxygen saturation (mixed venous hyperoxia), although reported, has never been characterized in humans resuscitated from cardiac arrest (postarrest cardiogenic shock). By contrast, cardiogenic shock without cardiopulmonary arrest (primary cardiogenic shock) is accompanied by mixed venous hypoxia under similar conditions of low oxygen delivery (DO2). The appearance of mixed venous hyperoxia indicates an excessive supply relative to demand in perfused tissue or cellular impairment of oxygen utilization, ie, low systemic oxygen consumption (VO2). Failure to improve VO2 has been associated with a poor outcome in other shock states. This study evaluates the clinical significance of mixed venous hyperoxia and its implications for impaired systemic oxygen utilization. The oxygen transport patterns in surviving and nonsurviving cardiac arrest patients are compared for their prognostic and therapeutic implications. Consecutive, nonrandomized series. Large urban emergency department (ED). Adult normothermic, nontraumatic out-of-hospital cardiac arrest patients presenting to the ED who develop a return of spontaneous circulation (ROSC). On arrival to the ED, a fiberoptic catheter was placed in the central venous position for continuous central venous oxygen saturation monitoring (ScvO2). A proximal aortic catheter was placed via the femoral artery for blood pressure monitoring. Upon ROSC, the fiberoptic catheter was advanced to the pulmonary artery. Mean arterial pressure (MAP), cardiac index (CI), VO2, DO2, systemic oxygen extraction ratio (OER), and systemic vascular resistance index (SVRI-dynes.s/cm5.m2) were measured immediately and every 30 min. The duration of cardiac arrest (DCA) in minutes and amount of epinephrine (milligrams) administered during ACLS was recorded. Twenty-three patients were entered into the study. Survivors (living more than 24 h) and nonsurvivors (living less than 24 h) were compared. These findings indicate an impairment of systemic oxygen utilization in postarrest cardiogenic shock patients. In spite of a lower DO2 than survivors, the OER in nonsurvivors remained lower than expected. Venous hyperoxia is a clinical manifestation of this derangement. Epinephrine dose may have a causal relationship. The inability to attain a VO2 of greater than 90 ml/min.m2 after the first 6 h of aggressive therapy was associated with a 100 percent mortality in 24 h.

Myocardial metabolism and adaptation during extreme hemodilution in humans after coronary revascularization.

This study was designed to evaluate the oxygen transport adjustments and myocardial metabolic adaptation that occurs with different levels of hemodilution during normothermia after cardiopulmonary bypass. Prospective, nonrandomized study. Operating room in a university hospital. Eight patients with ejection fractions (> 40%) undergoing elective coronary artery bypass grafting. Before the institution of cardiopulmonary bypass, blood was withdrawn from patients to a target hematocrit of 15%. After coronary artery bypass grafting, a catheter was inserted directly into the coronary sinus. After the patients were rewarmed to 37 degrees C, they were weaned from cardiopulmonary bypass. Hemodynamic indices were measured, as well as measurements of myocardial oxygen consumption (VO2) and myocardial metabolism (lactate extraction and coronary sinus hypoxanthine). Measurements were made at three different hematocrit values: 15%, 20%, and 25%. Hematocrit was increased by autologous blood transfusion. The three levels of hemodilution (hematocrit: 17.4 +/- 3.4%; 23.0 +/- 3.7%; 27.8 +/- 4.8%) were significantly different from baseline (hematocrit 37 +/- 2.6%; p < .05). Oxygen delivery, which increased with autologous transfusion, exceeded 350 mL/min/m2 at each level of dilution. The myocardial VO2 increased significantly after autologous transfusion compared with the most dilute condition (7.0 +/- 3.7 mL/min at hematocrit 17.4% vs. 11.2 +/- 4.8 mL/min at hematocrit 23.0% and 12.4 +/- 4.0 mL/min at hematocrit 27.8%). This transfusion-induced increase was also true of myocardial oxygen extraction. Lactate extraction and hypoxanthine release were normal and unchanged at each level of hemodilution. Systemic oxygen extraction ratio increased with hemodilution and decreased with autologous transfusion. Hemodilution to a hematocrit of approximately 15% is tolerated in anesthetized humans after coronary artery bypass surgery. There was no evidence of myocardial ischemia, as demonstrated by absence of S-T depression on the electrocardiogram, lactate extraction, or hypoxanthine release. In selected patients, postoperative transfusion may be based on systemic physiologic end-points, such as oxygen extraction ratio, rather than set hematocrit values.