Venous hypercarbia associated with severe sepsis and systemic hypoperfusion

Mecher, Carter; Rackow, Eric C.; Astiz, Mark E.; Weil, Max Harry

doi:10.1097/00003246-199006000-00001

Cited by 119 publications

(73 citation statements)

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“…This mechanism has been elucidated by Mathias et al [3], who studied an acute cardiac tamponade model. In our study, the mechanism proposed by Mecher et al [ 1 ] and Grundler et al [2] would account for the increased P[v-a]C02 associated with elevated PvCCF and increased lactate. On the other hand, unlike increases in blood HCO3 and pH, increases in dissolved CO2 are accompanied by almost instanta neous decreases in intracellular pH [8][9][10].…”

Section: Discussionsupporting

confidence: 68%

“…venous hypercarbia. Mecher et al [1], who showed that P[v-a]C02 was increased in relation to the decrease in cardiac output in patients with severe sepsis, Grundler et al [2], who re ported the same finding after an experimental study with a cardiopulmonary resuscitation model, and many other experimental investi gators [4][5][6] have elucidated this mechanism. The venous hypercarbia also appears to result from another mechanism, impaired CO2 elimination secondary to reduced pulmonary blood flow.…”

Section: Discussionmentioning

confidence: 86%

“…Increased P[v-a]C02 is observed in various shock states, including septic, traumatic, hemorrhagic, hypovolemic and cardiogenic shock, associated with a decrease in cardiac output [1][2][3][4][5][6]. Of the several mechanisms which have been suggested, continued anaero bic CO2 production in the peripheral tissues secondary to buffering of acids, such as lactate and anaerobic decarboxylation associated with reduction in systemic blood flow [7], may cause an elevated PVCO2, i.e.…”

Section: Discussionmentioning

confidence: 99%

“…The venoarterial carbon dioxide tension gradient (P[v-a]C02) is increased in associa tion with various shock states [1][2][3][4][5][6], and it is suggested to be an indicator of intracellular acidosis [2]. However, there have been few clinical studies of P[v-a]CO?.…”

Section: Introductionmentioning

confidence: 99%

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Venoarterial Carbon Dioxide Tension Gradient in Acute Heart Failure

Inoue

Sakai²,

Morooka³

et al. 1993

Cardiology

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The venoarterial carbon dioxide tension gradient (P[v-a]CO₂) was studied in patients with acute myocardial infarction. Seven patients with congestive heart failure (CHF group) and 10 patients without heart failure (control) were enrolled in this study. In all patients, hemodynamics were continuously monitored. Simultaneously, arterial and mixed venous blood were sampled, and blood gases and lactate concentration were analyzed. At the initial measurement before therapy, arterial and mixed venous pH and bicarbonate values were within the normal range, and there was no significant difference between the CHF group and controls. There was also no difference in arterial oxygen tension under the differential conditions of oxygen inhalation. However, cardiac index and mixed venous oxygen saturation (SvO₂) were significantly lower, while the oxygen extraction ratio (OER) and arterial lactate were significantly higher in the CHF group than in the controls. On the other hand, P[v-a]CO₂ was significantly higher in the CHF group (7.8 ± 2.6 vs. 3.5 ± 2.2 mm Hg, p < 0.01). This finding was due to the elevated mixed venous carbon dioxide tension in the CHF group, since arterial carbon dioxide tension was the same in both groups. Analysis of a total of 42 measurements obtained during the therapeutic course in the CHF group revealed a correlation of P[v-a]CO₂ with cardiac index (r = -0.3, p < 0.05), OER (r = 0.57, p < 0.001), SvO₂ (r =-0.56, p < 0.001) and lactate (r = 0.62, p < 0.001). The increase in P[v-a]CO₂ observed in acute heart failure suggests the evidence of intracellular acidosis despite the absence of acidemia. Furthermore, P[v-a]CO₂ is related not only to the hemodynamics but also to the oxygen demand-supply relationships in peripheral tissues.

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Section: Discussionsupporting

confidence: 68%

Section: Discussionmentioning

confidence: 86%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Venoarterial Carbon Dioxide Tension Gradient in Acute Heart Failure

Inoue

Sakai²,

Morooka³

et al. 1993

Cardiology

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“…The Fick principle adapted to carbon dioxide demonstrates the inverse relationship between the CO and dCO 2 [45], in other words increased levels of dCO 2 reflect low flow states. It has been shown that in sepsis, heart failure and severe hypovolemia, its value can be elevated [46,47].…”

Section: Parameters Reflecting Vomentioning

confidence: 99%

Multimodal individualized concept of hemodynamic monitoring

Molnár

Szabó

Németh

2017

Current Opinion in Anaesthesiology

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Purpose of reviewTo discuss the pathophysiological rationale of advanced hemodynamic monitoring in the critically ill and also to highlight the importance of a multimodal, individualized approach. Recent findingsThere are several clinical studies and animal experiments evaluating, which hemodynamic endpoint should be the best target during fluid management. Recent systematic reviews and meta-analyses also investigated the effects of advanced hemodynamic endpoints targeted hemodynamic management on outcome mainly in high-risk surgical patients. Although most of these studies report positive results, this knowledge does not seem to affect our everyday practice. According to large international surveys, most physicians still rely on inappropriate indices. One of the reasons could be that target values applied in these studies can be misleading in the individual patient. Therefore, we describe the concept of an individualized approach, in which normalizing the components of oxygen delivery are put in the context of the patients' individual response by evaluating components of oxygen consumption, and organ perfusion. SummaryAdvanced hemodynamic monitoring-based management provides a number of benefits, which could be better tailored for the patients' actual needs by putting this into a multimodal, individualized approach.

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