Choque Hipovolemico

ANESTHESIOLOGY
CLINICS
ElSEVIER Anesthesiology Clin SAUNDERS
25 (2007) 23-34
Current Concepts in Hemorrhagic Shock
Richard P. Dutton, MD, MBAa,b,*
aUniversity of Maryland School of Medicine,
22 South Greene Street, Baltimore, MD 21201, USA
bDivision of Trauma Anesthesiology, R Adams Cowley Shock Trauma Center, University
of Maryland Medical System, 22 South Greene Street, Baltimore, MD21201, USA
Pathophysiology of hemorrhagic shock
Loss of intravascular volume triggers a predictable systemic response,
mediated by both local vascular signaling and the neuroendocrine system
[1]. Decreased filling pressures in the heart result in a decrease in cardiac
output, in accordance with Starling's Law. Vasoconstriction of ischemiatolerant
vascular beds (eg, skin, muscle, gut) allowspreservation of flow
to organs that depend on a continuous supply of oxygen, principally the
heart and the brain. Vasoconstriction is triggered by reduced blood pressure,
pain, and cortical perception of injury. In injured tissue, local mediators
act to constrict blood flow and reduce bleeding. Central sympathetic
outflow is increased and parasympathetic flow is decreased, leading to anincrease in heart rate and contractility. Adrenal stimulation results in the
"fight or flight" response, with increased levels of circulating epinephrine.
Persistent hypoperfusion leads to cellular death and organ system failure.
Cells that lose nutrient blood flow undergo necrotic cell death. Other cells
undergo apoptosis, or "programmed cell death," sacrificing themselves in
the face ofinsufficient resources. Cells in many organ systems have the ability
to hibernate. Cells in the renal cortex, for example, stop filtering fluid at
a level of ischemia less than that which causes necrosis.
Shock is more than a transient failure in oxygen supply, but also the systemic
disease that follows [2]. Cells in the liver and gut may remain ischemic
after flow is reestablished in themacrocirculation, because of the occlusion
of capillary networks caused by edema [3]. This "no-reflow" phenomenon
* Division of Trauma Anesthesiology, R Adams Cowley Shock Trauma Center,
University of Maryland Medical System, 22 South Greene Street, Baltimore, MD 21201.
E-mail address: rdutton@umaryland.edu
0889-8537/07/$ - see front matter © 2007 Elsevier Inc. All rights reserved.
doi: 10.1016/j.atc.2006.11.007 anesthesiology.theclinics.com
24 DUTTON
persists even after cardiac output is normalized. Reperfusion following hemorrhagic
shock releases toxic mediators into the circulation; these mediators
are potent immune modulators. Even short periods of relatively minor ischemia
can trigger a cascade of cellular signaling and response that results
in organ system failure (Fig. 1).
Theconsequences of ischemia first become apparent in the less critical
organs. Skin and muscle cells become anaerobic, producing lactic acid. Organs
of the splanchnic circulation hibernate (peristalsis and renal filtering
cease) and then suffer cellular damage, progressing to organ system failure.
Hypoperfusion of the liver results in decreased glucose availability, loss of
clotting factors, and,eventually, cell death [4]. Intestinal mucosal cells
lose the ability to transport nutrients; if ischemia persists, the barrier function
of the gut is lost, and translocation of bacteria occurs from the intestinal
lumen into the portal circulation.
The lungs are the downstream filter for toxic metabolites, inflammatory
mediators released by ischemic cells, and translocated bacteria from thegut. The lungs are also the sentinel organ for the development of multiple
organ system failure. The acute respiratory distress syndrome, occurring
after hemorrhagic shock, was first described in the 1960s as "Da Nang
lung" [5]. Pulmonary failure develops over 1 to 3 days following severe
trauma, is exacerbated by ventilator-associated pneumonia, and may require
weeks of supportive care to...