This chapter focuses on the effects of hypo- and hypercapnia at the organ and tissue level. Carbon dioxide's role in determining acid-base status and tissue oxygenation is described, followed by its effects on major organ systems. The higher lipid solubility of CO2 compared to hydrogen ions allows acid-base changes caused by respiratory acidosis and alkalosis to equilibrate between extra- and intracellular fluids much faster than changes caused by metabolic acidosis or alkalosis. The primary determinants of tissue oxygen availability are arterial O2 tension, cardiac output, and local perfusion. Hypocapnia induced by hyperventilation is clinically used for treatment of increased intracranial pressure (ICP), but the compromise in tissue perfusion, and thus the resulting secondary ischemia, should be factored into the risk-benefit equation. The active management of CO2 is a promising strategy to consider for improving tissue perfusion, providing anti-inflammatory effects, and preventing apoptotic injury.

Common clinical situations that lead to shock include hemorrhage, myocardial infarction, heart failure, trauma, sepsis, and cardiac arrest. Regardless of the cause, clinicians are better able to treat shock if they understand the underlying mechanisms, shared mechanisms, and physiologic events. It is the relationship between VO2 and carbon dioxide (CO2) production (VOCO2) that forms the general foundation for the utility of VOCO2 and end-tidal PCO2 (PETCO2) monitoring in shock states. The ability of the measurement of the partial pressure of expired carbon dioxide (PETCO2) monitoring to reflect tissue perfusion lies in its ability to closely reflect alveolar CO2. Several options to monitor tissue CO2 in various shock states have been studied, and include transcutaneous CO2(PtcCO2) skin monitoring, interstitial fiberoptic PCO2, gastric mucosal CO2 via gastric tonometry (PgCO2), and sublingual tonometry (PslCO2). These measurements detect changes in tissue CO2 as a reflection of changes in DO2.

The failure of cardiovascular system to maintain adequate organ perfusion pressure causes inadequate oxygen delivery resulting in tissue hypoxia, lactic acidosis and end organ damage. Inotropes affect the force of myocardial contraction. A positive inotrope will increase myocardial contractility. Vasopressors cause vasoconstriction of blood vessels (most act by α1 receptor activation) and therefore increase mean arterial blood pressure (MAP) and systemic vascular resistance (SVR). Vasoactive drugs are used to support tissue perfusion and hence oxygenation. Vasoactive drugs act on various receptors in the body to produce their effects. Treatment with vasoactive drugs should be considered, if optimization of oxygenation, ventilation and adequate fluid resuscitation fail to restore cardiac output. Therapy may need to be started with minute-by-minute assessment of the patient's response. The response to vasoactive drugs is often unpredictable and dependent on the cause of shock and baseline circulation.