Oxygen in CHF ============= Several months ago someone raised the issue of why supplemntal oxygen was needed in patients with good O2 sats in the setting of acute MI. At that time I related the rationale that I had been taught, namely that oxygen increased systemic vacular resistance and thus diatolic pressure and coronary blood flow. Although stopping short of wholeheartedly endorsing this theory, I did believe that it was an interesting proposition. Now comes a study on the use of 100% oxygen in patients with CHF (1). The authors suggest that in that setting high concentrations of oxygen are detremental precisely because they do indeed cause an increase of SVR and wedge pressure and consequent decrease in stroke volume and CO. This is not to suggest that a patient with CHF who is blue does not need O2 but, rather, that perhaps, a more reasonable goal in treating these patients is to use the lowest concentration of O2 that will result in 90% saturation of Hb. Interesting proposition. H. Louzon MD (1) Haque WA, Boehmer J, Clemson BS, Leuenberger UA, Silber DH, Sinoway LI Hemodynamic effects of supplemental oxygen administration in congestive heart failure. J Am Coll Cardiol 1996 Feb;27(2):353-7 OBJECTIVES. This study sought to determine the hemodynamic effects of oxygen therapy in heart failure. BACKGROUND. High dose **oxygen** has detrimental hemodynamic effects in normal subjects, yet oxygen is a common therapy for heart failure. Whether oxygen alters hemodynamic variables in heart failure is unknown. METHODS. We studied 10 patients with New York Heart Association functional class III and IV congestive heart failure who inhaled room air and 100% oxygen for 20 min. Variables measured included cardiac output, stroke volume, pulmonary capillary wedge pressure, systemic and pulmonary vascular resistance, mean arterial pressure and heart rate. Graded oxygen concentrations were also studied (room air, 24%, 40% and 100% oxygen, respectively; n = 7). In five separate patients, muscle sympathetic nerve activity and ventilation were measured during 100% oxygen. RESULTS. The 100% oxygen reduced cardiac output (from 3.7 +/- 0.3 to 3.1 +/- 0.4 liters/min [mean +/- SE], p < 0.01) and stroke volume (from 46 +/- 4 to 38 +/- 5 ml/beat per min, p < 0.01) and increased pulmonary capillary wedge pressure (from 25 +/- 2 to 29 +/- 3 mm Hg, p < 0.05) and systemic vascular resistance (from 1,628 +/- 154 to 2,203 +/- 199 dynes.s/cm5, p < 0.01). Graded oxygen led to a progressive decline in cardiac output (one-way analysis of variance, p < 0.0001) and stroke volume (p < 0.017) and an increase in systemic vascular resistance (p < 0.005). The 100% oxygen did not alter sympathetic activity or ventilation. CONCLUSIONS. In heart failure, oxygen has a detrimental effect on cardiac output, stroke volume, pulmonary capillary wedge pressure and systemic vascular resistance. These changes are independent of sympathetic activity and ventilation. -------------------- All of the subjects had been admited to the hospital with severe heart failure. Many were under consideration for heart transplantation. All were NYHA Class III-IV (symptomatic with less than usual exertion and symptomatic at rest respectively). In the first experiment hemodynamic variables were measured at rest and then after 20 minutes of O2 per nonrebreather mask ("100%"). Average CO dropped from 3.7 to 3.1 L/min. This was due entirely to a fall in stroke volume (SV) from 46 to 38 ml/beat inasmuch as heart rate did not change. MVO2 rose from 8.8 to 10.4 vol%. Oxygen saturation increased from 92.6% to 99.8% (pO2 was not reported). By my calculation (the authors did not actually persue this line of reasoning), oxygen delivery to tissues actually fell from CDO2 = 37.0*0.926*1.34*Hb = 45.9*Hb on RA to CDO2 = 31.0*0.998*1.34*Hb = 41.5*Hb on 100% O2 because the fall in CO was disproportional to the rise in arterial oxygen content. In the second phase of the study the subjects were exposed to progressively increasing concentrations of O2 from 24% to 100%. Oxygen was found to cause a consistent DOSE-DEPENDENT decrease in cardiac output. Again, at baseline (RA) CDO2 = 38.0*0.936*1.34*Hb = 47.7*Hb whereas CDO2 = 35.0*.961*1.34*Hb = 45.0*Hb at 24% O2 and CDO2 = 32.0*0.981*1.34*Hb = 42.0*Hb at 40% O2 etc. Where CO has fallen from 3.8 to 3.5 to 3.2 L/min (or 38 dl/min etc). In a third phase of the study muscle nerve sympathetic activity was measured and was unchanged by the administration of oxygen implying that these effects on the vasculature were not mediated centrally but were, rather, a direct effect of O2 in causing vasoconstriction. If I read Don's question about pO2 correctly he seems to be implying that, perhaps, oxygen was being administered in supraphysiologic quantities (beyond the need to nearly fully saturate Hb) and that this may explain the deleterious effects. I would note that the reduction in CO was observed even in patients with moderate FIO2 (0.24). The authors point to studies done in healthy volunteers and in patients with acute MI that came to similar conclusions (increased SVR and decreased CO). They note that previous studies have found decreased coronary blood flow (so much for my CCU attending's theories), cardiac contractility and systemic oxygen consumption with O2 administration. They conclude that "...in the absence of substantial arterial desaturation, supplmental oxygen should be used cautiously during the hospital period in subjects with severe heart failure." Setting aside the issue of O2 in CHF, what effect does the production of hyperoxia have in critically ill patients in general? The answer is that it appears to be detrimental in that it tends to cause a paradoxical DECREASE in oxygen consumption (1). Perhaps we should not be so complacent when the ABGs on our intubated patients come back 300 - 400. Unlike the common wisdom about never being too rich or too thin it does appear to be possible, in some cases, to have too much oxygen. H. Louzon MD (1) Reinhart K, Bloos F, Konig F, Bredle D, Hannemann L Reversible decrease of oxygen consumption by hyperoxia. Chest 1991 Mar;99(3):690-4 The hemodynamic and metabolic effects of 90 minutes normobaric hyperoxia were studied in 20 critically ill patients (11 septic, 9 nonseptic) requiring mechanical ventilation with inspired O2 fraction (FIO2) less than 0.40. Thirty minutes after increasing the FIO2 to 1.0, arterial PO2 had increased from about 100 to about 400 mm Hg, and whole body oxygen uptake (VO2) was decreased 10 percent (p less than 0.05) due to an 18 percent decrease in O2 extraction ratio. During the subsequent 60 minutes of hyperoxia, there was no further significant change in VO2. Cardiac index did not change in hyperoxia, but it increased 10 percent (p less than 0.05) in recovery as systemic vascular resistance decreased. VO2 returned to baseline after 30 minutes recovery at original FIO2 due to increased O2 extraction as well as the increased cardiac output. The decrease in VO2 without a decrease in O2 delivery may reflect maldistribution of blood flow and functional O2 shunting to protect tissue from unphysiologically high PO2. While brief oxygenation is advisable before periods of hypoventilation, the present data suggest that hyperoxic ventilation in these patients with already adequate O2 delivery was counterproductive.