Erschienen in:
01.10.2008 | Editorial
Carbon dioxide and tissue oxygenation: is there sufficient evidence to support application of hypercapnia for hemodynamic stability and better tissue perfusion in sepsis?
verfasst von:
Ozan Akça
Erschienen in:
Intensive Care Medicine
|
Ausgabe 10/2008
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Excerpt
Hypercapnia increases cardiac output (CO), oxygen-carrying capacity of the blood, mixed venous oxygen, and peripheral tissue oxygenation [
1‐
4]. Recently, we have shown that even when CO is controlled, hypercapnia may alter vital organ perfusion (e.g. cerebral tissue) [
5]. This effect is likely due to changes in the balance of oxygen supply and demand. Increase in CO appears to be directly related to its inotropic effect through ß-adrenergic receptors or to hypercapnia-induced sympathetic activation [
6,
7] and release of catecholamines [
8]. In addition to increasing CO, hypercapnia decreases systemic vascular resistance [
9], which may further complement tissue perfusion under normal intravascular volume status. Unless moderate-to-high levels of carbon dioxide (ET PCO
2 > 70 mmHg) are reached, hypercapnia does not cause tachycardia in sedated or anesthetized humans. Most myocardial depression occurs at CO
2 concentrations greater than 10–15% (i.e., PaCO
2 > 75 mmHg) [
10,
11]. …
