Choque Flashcards
Livro
The failure to meet the metabolic needs of the cell and the consequences that ensue.
shock
reversible
the initial injury
if tissue perfusion is prolonged or severe enough such that, at the cellular level, compensation in no longer possible
the injury will become irreversible
hemodynamic parameters such as ____ and___ are relatively insensitive measures of stock.
blood pressure; heart rate
Shock is defined as a failure to meet the metabolic demands of
cells and tissues and the consequences that ensue.
A central component of shock is decreased tissue perfusion.
This may be a direct consequence of the etiology of shock,
such as in hypovolemic/hemorrhagic, cardiogenic, or neurogenic
etiologies, or may be secondary to elaborated or released
molecules or cellular products that result in endothelial/cellular
activation, such as in septic shock or traumatic shock.
Physiologic responses to shock are based on a series of afferent
(sensing) signals and efferent responses that include neuroendocrine,
metabolic, and immune/inflammatory signaling.
The mainstay of treatment of hemorrhagic/hypovolemic shock
includes volume resuscitation with blood products. In the case
of hemorrhagic shock, timely control of bleeding is essential
and influences outcome.
Prevention of hypothermia, acidemia, and coagulopathy is
essential in the management of patients in hemorrhagic
shock.
The mainstay of treatment of septic shock is fluid resuscitation,
initiation of appropriate antibiotic therapy, and control
of the source of infection. This includes drainage of
infected fluid collections, removal of infected foreign bodies,
and débridement of devitalized tissues.
A combination of physiologic parameters and markers of
organ perfusion/tissue oxygenation are used to determine if
patients are in shock and to follow the efficacy of resuscitation
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Many of the organ-specific responses are aimed at maintaining
perfusion in the cerebral and coronary circulation
These are
regulated at multiple levels including (a) stretch receptors
and baroreceptors in the heart and vasculature (carotid sinus
and aortic arch), (b) chemoreceptors, (c) cerebral ischemia
responses, (d) release of endogenous vasoconstrictors, (e) shifting
of fluid into the intravascular space, and (f) renal reabsorption
and conservation of salt and water
Neuroendocrine and Organ-Specific Responses
to Hemorrhage
The goal of the neuroendocrine response to hemorrhage is to
maintain perfusion to the heart and the brain, even at the expense
of other organ systems. Peripheral vasoconstriction occurs, and
fluid excretion is inhibited. The mechanisms include autonomic
control of peripheral vascular tone and cardiac contractility,
hormonal response to stress and volume depletion, and local
microcirculatory mechanisms that are organ specific and regulate
regional blood flow. The initial stimulus is loss of circulating
blood volume in hemorrhagic shock. The magnitude of the
neuroendocrine response is based on both the volume of blood
lost and the rate at which it is lost.
FORMS OF SHOCK
Hypovolemic/Hemorrhagic
The most common cause of shock in the surgical or trauma
patient is loss of circulating volume from hemorrhage. Acute
blood loss results in reflexive decreased baroreceptor stimulation
from stretch receptors in the large arteries, resulting in decreased
inhibition of vasoconstrictor centers in the brain stem, increased
chemoreceptor stimulation of vasomotor centers, and diminished
output from atrial stretch receptors. These changes increase vasoconstriction
and peripheral arterial resistance. Hypovolemia also
induces sympathetic stimulation, leading to epinephrine and norepinephrine
release, activation of the renin-angiotensin cascade,
and increased vasopressin release. Peripheral vasoconstriction
is prominent, while lack of sympathetic effects on cerebral and
coronary vessels and local autoregulation promote maintenance
of cardiac and CNS blood flow.
The appropriate priorities in these patients are (a) secure
the airway, (b) control the source of blood loss, and (c) intravenous
(IV) volume resuscitation. In trauma, identifying the body
cavity harboring active hemorrhage will help focus operative
efforts; however, because time is of the essence, rapid treatment
is essential and diagnostic laparotomy or thoracotomy
may be indicated. The actively bleeding patient cannot be
resuscitated until control of ongoing hemorrhage is achieved.
Our current understanding has led to the management strategy
known as damage control resuscitation.62 This strategy begins
in the emergency department and continues into the operating
room and into the intensive care unit (ICU). Initial resuscitation
is limited to keep SBP around 80 to 90 mmHg. This prevents
renewed bleeding from recently clotted vessels. Resuscitation
and intravascular volume resuscitation are accomplished with
blood products and limited crystalloids,
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Traumatic Shock
The systemic response after trauma, combining the effects
of soft tissue injury, long bone fractures, and blood loss, is
clearly a different physiologic insult than simple hemorrhagic
shock. Multiple organ failure, including ARDS, develops relatively
often in the blunt trauma patient, but rarely after pure
hemorrhagic shock (such as a GI bleed). The hypoperfusion
deficit in traumatic shock is magnified by the proinflammatory
activation that occurs following the induction of shock.
Examples of
traumatic shock include small-volume hemorrhage accompanied
by soft tissue injury (femur fracture, crush injury) or any
combination of hypovolemic, neurogenic, cardiogenic, and
obstructive shock that precipitates rapidly progressive proinflammatory
activation.
traumatic shock is focused on correction of the individual elements
to diminish the cascade of proinflammatory activation
and includes prompt control of hemorrhage, adequate volume
resuscitation to correct O2 debt, débridement of nonviable tissue,
stabilization of bony injuries, and appropriate treatment
of soft tissue injuries.
Septic Shock (Vasodilatory Shock)
In the peripheral circulation, profound vasoconstriction is the
typical physiologic response to the decreased arterial pressure
and tissue perfusion with hemorrhage, hypovolemia, or acute
heart failure. This is not the characteristic response in vasodilatory
shock. Vasodilatory shock is the result of dysfunction of the
endothelium and vasculature secondary to circulating inflammatory
mediators and cells or as a response to prolonged and
severe hypoperfusion. Thus, in vasodilatory shock, hypotension
results from failure of the vascular smooth muscle to constrict
appropriately. Vasodilatory shock is characterized by peripheral
vasodilation with resultant hypotension and resistance to treatment
with vasopressors. Despite the hypotension, plasma catecholamine
levels are elevated, and the renin-angiotensin system
is activated in vasodilatory shock. The most frequently encountered
form of vasodilatory shock is septic shock. Other causes
of vasodilatory shock include hypoxic lactic acidosis, carbon
monoxide poisoning, decompensated and irreversible hemorrhagic
shock, terminal cardiogenic shock, and postcardiotomy
shock (Table 5-6). Thus, vasodilatory shock seems to represent
the final common pathway for profound and prolonged shock
of any etiology.
