Physiopathology Of Shock

| |
Principio del formulario

Final del formulario
|
J Emerg Trauma Shock. 2011 Apr-Jun; 4(2): 222–232. | PMCID: PMC3132363 |
Physiopathology of shockFabrizio Giuseppe BonannoChris Hani Baragwanath Hospital, Johannesburg, South AfricaAbstractShock syndromes are of three types: cardiogenic, hemorrhagic and inflammatory. Hemorrhagic shock has its initial deranged macro-hemodynamicvariables in the blood volume and venous return. In cardiogenic shock there is a primary pump failure that has cardiac output/mean arterial pressure as initial deranged variables. In Inflammatory Shock it is the microcirculation that is mainly affected, while the initial deranged macrocirculation variable is the total peripheral resistance hit by systemic inflammatory response.Keywords: Physiology,physiopathology, shockINTRODUCTIONThe three main shocks (cardiogenic, hemorrhagic and inflammatory) differ in the primum movens i.e., the initial circulation variable that becomes deranged: HS is a failure of the peripheral circulation that has its initial deranged variables in the blood volume and venous return, and to follow, cardiac output/mean arterial pressure; in CS is the pump that fails andhas its initial deranged variables in cardiac output/mean arterial pressure; in IS the microcirculation is affected while the initial deranged macrocirculation variable is the total peripheral resistance hit by systemic inflammatory response (SIR) or by I-R phenomenon [Figure 1] [Schemes ​[Schemes11–3]. All shocks in full-blownout phase are effectively vasoconstrictors, including the IS [Schemes​[Schemes11–3]. What makes SS different from the other variants of IS is the initial hyperdynamic response of SS, lipopolysaccharide (LPS) and other bacterial toxins mediated, that is responsible of the hyperdynamic, physiologically compensatory, vasodilatory phase.OXYGEN DELIVERYThe delivery of oxygen to cells (DO2) depends on the content of oxygen in the blood mainly combined to hemoglobin (Hb),which is regulated by the respiratory system, and from its transport in the blood, which is function of the cardiac output/mean arterial pressure/peripheral vascular resistance inter-relationships and of the oxygen extraction/consumption rate at cellular/tissues level, the latter being the main driver, controller and modulator of the oxygen delivery system. [Appendix A] Because oxygen has a lowsolubility in plasma, it is oxygen carried by red blood cells (RBC) specifically, and not ‘blood’ (plasma and RBCs) in general, which determines arterial oxygen content (CaO2) in the oxygen delivery equation. O2 loose in the blood which is not combined to Hb accounts instead for the component of partial pressure of oxygen (PaO2) that can be increased. Once Hb is completely saturated with oxygen (HbO2)oxygenation is increased either by increasing its concentration on air (fraction inspired oxygen-FiO2) or by increasing the pressure into the alveoli with which is administered in the air-oxygen mixture (intra-alveolar pressure). Hypoxia, which is low oxygen to tissues, is classified into three main categories: scarce oxygen offer from macrocirculation, maldistribution of offer and incapacity ofconsumption. Hypoxemia or respiratory failure, is a frequent cause of hypoxia pertaining to the ingress/egress of gases in and out the body; shock, a cause of hypoxemia or dysoxia, pertains instead to their exchange in the target organs and tissues. There is an indissoluble inter-relation and overlapping between shock and hypoxia in biological and conceptual terms: etiology and treatment oftenoverlap.Chronic anemia is practically irrelevant as cause of hypoxia. In the absence of pathological Hb or acute RBCs loss (acute hemorrhage), hypoxia is never observed to be symptomatic or clinically significant until Hb goes at around 3 g/dL.[1] The author has seen few patients with chronic anemia of 3 g/dL of Hb living normal life, maybe not classifiable as such for an athlete, but enough to...