iEqu.atio.n...(2.). shows that blood pressure is dependent on blood flow and vascular resistance. Systemically, blood flow is referenced to the cardiac output (which, in turn, is distributed into the blood flow delivered to individual organs). Therefore hypotension may complicate a fall in either resistance or cardiac output. A depression in cardiac output can be related to its determinants:
cardiac output - heart rate * stroke volume 0)
where stroke volume depends on ventricular preload, contractility, and afterload.
In this context, causes of hypotension can be classified. Briefly, some diseases cause hypotension primarily by affecting vascular resistance, while others predominantly depress cardiac output. Regardless of cause, a depression in blood pressure is accompanied by many autoregulatory responses, all of which attempt to maintain arterial perfusing pressures and local blood flows to prevent tissue ischemia ( eqnJl) and Fig 1(b)). Compensation involves all three major components of the circulation—the central circulation (the heart), the regional circulations (those supporting individual organs), and the microregional circulation (the capillary microcirculation)—and is dependent upon both neural and hormonal mechanisms.
The early response to hypotension is dominated by neural (sympathetic) activation which induces precapillary constriction, hence reducing capillary hydrostatic pressure. This mechanism acutely alters the balance of Starling forces and supports fluid redistribution from extravascular spaces into the capillary lumen, thereby augmenting intravascular fluid volume. This process, sometimes referred to as 'autotransfusion', helps to maintain (or even increase) cardiac output via the heart's Starling mechanism (the relationship between ventricular preload and cardiac output). Later responses to hypotension also attempt to maximize intravascular volume, including humoral mechanisms that increase sodium and water retention (i.e. stimulation of the renin-angiotension system, enhanced release of ADH, and activation of the ACTH-adrenocortical axis). In hypotension, sympathetic activation also augments myocardial contractility and heart rate, and promotes vasoconstriction of the arterial supply to non-vital organs. This latter response is the mechanism that facilitates redistribution of blood flow from non-vital organs to core vital organs. This autonomic response is mediated by decreased PaO2 or ischemia, although not by low blood pressure, and becomes extremely powerful at pressures below 60 mmHg
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