Shock consists of inadequate tissue perfusion marked by decreased delivery of required
metabolic substrates and inadequate removal of cellular waste products. This involves
failure of oxidative metabolism that can involves defects of oxygen delivery, transport or
Classification of Shock
▫ Septic (vasogenic)
3. Pathophysiology of Shock
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.
Ischemia/reperfusion injury will often exacerbate the initial insult, thus leading to the “vicious
cycle” of shock.
5. Neuroendocrine and Organ-Specific Responses
The goal of the neuroendocrine response to hemorrhage is to maintain perfusion to the
heart and the brain.
The mechanisms include autonomic control of peripheral vascular tone and cardiac
contractility, hormonal response to stress and volume depletion, and local microcirculatory
The magnitude of the neuroendocrine response is based on both the volume of blood lost
and the rate at which it is lost.
6. Afferent Signals
Afferent impulses transmitted from the periphery are processed within the central nervous
system (CNS) and activate the reflexive effector responses or efferent impulses.
The afferent impulses originate from a variety of sources. The initial inciting event usually is loss
of circulating blood volume. Other stimuli that can produce the neuroendocrine response
include pain, hypoxemia, hypercarbia, acidosis.
Baroreceptors also are an important afferent pathway. Are present within the atria of the heart.
They become activated with low volume hemorrhage or mild reductions in right atrial pressure.
When activated, these baroreceptors diminish their output, thus disinhibiting the effect of the
7. Efferent Signals
Hemorrhage results in diminished venous return to the heart and decreased cardiac output.
Stimulation of sympathetic fibers innervating the heart. Increase heart rate and contractility.
Increased myocardial O2 consumption.
Direct sympathetic stimulation of the peripheral circulation via the activation of α1-adrenergic
receptors induces vasoconstriction and increase in systemic vascular resistance and blood
The arterial vasoconstriction is not uniform; marked redistribution of blood flow results.
Increased sympathetic output induces catecholamine release from the adrenal medulla.
8. Hormonal Response
Shock stimulates the hypothalamus, anterior pituitary leading to stimulation of the adrenal
cortex to release cortisol. Cortisol causes retention of sodium and water.
The renin-angiotensin system is activated in shock.
The pituitary also releases vasopressin or ADH in response to hypovolemia.
ADH acts as a potent mesenteric vasoconstrictor, shunting circulating blood away from the
splanchnic organs during hypovolemia. This may contribute to intestinal ischemia.
Following hemorrhage, larger arterioles vasoconstrict; however, in the setting of sepsis or
neurogenic shock, these vessels vasodilate.
Pathophysiologic response of the microcirculation to shock is failure of the integrity of the
endothelium and development of capillary leak, and the development of an extracellular fluid
Capillary dysfunction also occurs secondary to activation of endothelial cells by circulating
inflammatory mediators generated in septic or traumatic shock.
10. Metabolic Effects
Cellular metabolism is based primarily on the hydrolysis of adenosine triphosphate (ATP).
When oxidative phosphorylation is insufficient, the cells shift to anaerobic metabolism and
glycolysis to generate ATP.
Under hypoxic conditions in anaerobic metabolism, pyruvate is converted into lactate, leading
to an intracellular metabolic acidosis.
11. Immune and Inflammatory
The inflammatory and immune responses are a complex set of interactions between circulating
soluble factors and cells that can arise in response to trauma, infection, ischemia, toxic, or
Following direct tissue injury or infection, there are several mechanisms that lead to the activation
of the active inflammatory and immune responses.
The immune response to shock encompasses the
elaboration of mediators with both
proinflammatory and anti-inflammatory
Furthermore, new mediators, new relationships
between mediators, and new functions of known
mediators are continually being identified.
14. TNF-a can produce peripheral vasodilation, activate the release of other cytokines.
Interleukin-1 (IL-1) has actions similar to those of TNF-a.
Some investigators have postulated that increased IL-2 secretion promotes shock-induced
tissue injury and the development of shock.
Elevated IL-6 levels correlate with mortality in shock states.IL-6 may play a role in the
development of diffuse alveolar damage and ARDS.
IL-10 is considered an anti-inflammatory cytokine that may have immunosuppressive
properties. Administration of IL-10 depresses cytokine production.
15. Hypovolemic/Hemorrhagic Shock
The most common cause of shock in the surgical or trauma patient.
Treatment of shock is initially empiric. Shock in a trauma patient or postoperative patient
should be presumed to be due to hemorrhage until proven otherwise.
The clinical signs of shock may be evidenced by agitation, cool clammy extremities,
tachycardia, weak or absent peripheral pulses, and hypotension.
The clinical and physiologic response to hemorrhage has been classified according to the
magnitude of volume loss.
16. Young healthy patients with vigorous compensatory mechanisms may tolerate larger volumes
of blood loss.
Elderly patients with diminished cardiac compliance, atherosclerotic vascular disease, are less
able to tolerate hemorrhage.
17. Serum lactate and base deficit are measurements that are helpful to both estimate and monitor
the extent of bleeding and shock.
Identifying the sources of blood loss in patients with penetrating wounds is relatively simple.
Blood loss sufficient to cause shock is generally of a large volume, and there are a limited
number of sites (e.g., external, intrathoracic, intra-abdominal, retroperitoneal, and long bone
Control of ongoing hemorrhage is an essential component of the resuscitation of the patient in
Patients who fail to respond to initial resuscitative efforts should be assumed to have ongoing
active hemorrhage from large vessels and require prompt operative intervention.
The appropriate priorities in these patients are as follows: (a) control the source of blood loss,
(b) perform IV volume resuscitation with blood products in the hypotensive patient, and (c)
secure the airway.
19. The management strategy known as damage control resuscitation. This strategy begins in the
emergency department, continues into the operating room, and into the intensive care unit
Initial resuscitation is limited to keep SBP around 80 to 90 mmHg. This prevents renewed
bleeding from recently clotted vessels.
Control of hemorrhage is achieved in the operating room .
Patients who respond to initial resuscitative effort but then deteriorate hemodynamically
frequently have injuries that require operative intervention.
20. Failure to respond to resuscitative efforts despite adequate control of ongoing hemorrhage.
These patients have ongoing fluid requirements despite adequate control of hemorrhage,
necessitating vasopressor support.
Fluid resuscitation is a major adjunct in patients with shock. The ideal type of fluid to be used
continues to be debated; however, crystalloids continue to be the mainstay fluid of choice.
Ongoing studies continue to evaluate the use of hypertonic saline as a resuscitative adjunct in
bleeding patients. The benefit of hypertonic saline solutions may be immunomodulatory.
21. Transfusion of packed red blood cells and other blood products is essential in the treatment of
patients in hemorrhagic shock. Current recommendations in stable ICU patients aim for a
target hemoglobin of 7 to 9 g/dl.
There is a potential role for other coagulation factor based products.
Data also support the use of antifibrinolytic agents in bleeding trauma patients, specifically
tranexamic acid limits rebleeding and reduces mortality.
Additional resuscitative adjuncts in patients with hemorrhagic shock include minimization of
heat loss and maintaining normothermia.
22. Septic Shock (Vasodilatory
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
Despite the hypotension, plasma catecholamine levels are elevated, and the renin-angiotensin
system is activated in vasodilatory shock.
Causes of septic and vasodilatory shock:
Systemic response to infection
Noninfectious systemic inflammation
Acute adrenal insufficiency
23. Despite advances in intensive care, the mortality rate for severe sepsis remains at 30% to 50%.
In septic shock, the vasodilatory effects are due, in part, to the upregulation of the inducible
isoform of nitric oxide synthase (iNOS or NOS 2) in the vessel wall. Additionally, endothelial
activation or injury likely contributes to some degree of vascular dysfunction.
Recognizing septic shock begins with defining the patient at risk.
The clinical manifestations of septic shock will usually become evident and prompt the
initiation of treatment before bacteriologic confirmation of an organism or the source of an
organism is identified.
Fever, tachycardia, and tachypnea, signs of hypoperfusion such as confusion, malaise,
oliguria, or hypotension may be present. These should prompt an aggressive search for
The Surviving Sepsis Campaign has updated
treatment recommendations and care bundles
with a most recent goal for care within the
Serum lactate should be measured as a marker
of shock. Fluid resuscitation should begin
within the first hour and should be at least 30
mL/kg for hypotensive patients.
Blood cultures should be obtained. Empiric
antibiotics must be chosen carefully based on
the most likely pathogens.
26. After first-line therapy of the septic patient with antibiotics, IV fluids, and intubation if
necessary, vasopressors may be necessary to treat patients with septic shock.
Catecholamines are the vasopressors used most often, with norepinephrine being the first-line
agent followed by epinephrine.
Dobutamine therapy is recommended for patients with cardiac dysfunction. Mortality in this
group is high.
Goal-directed therapy of septic shock and severe sepsis initiated in the emergency department
and continued for 6 hours significantly improved outcome.
27. The use of corticosteroids in the treatment of sepsis and septic shock has been controversial
for decades. The observation that severe sepsis often is associated with adrenal insufficiency
has generated renewed interest in therapy for septic shock with corticosteroids.
A single IV dose of 50 mg of hydrocortisone improved mean arterial blood pressure response
relationships to norepinephrine and phenylephrine in patients with septic shock
Additional adjunctive immune modulation strategies have been developed for the treatment of
septic shock. These include the use of antiendotoxin antibodies, anticytokine antibodies.
28. Obstructive Shock
Caused by mechanical obstruction of venous return such as:
• Tension pneumothorax
• Cardiac tamponade
• Pulmonary embolism
• IVC obstruction
Diagnosis and Treatment
The diagnosis of tension pneumothorax should be made on clinical exam, pleural decompression
is indicated rather than delaying wait for confirmation, definitive treatment is immediate tube
The goal in the treatment of shock is restoration of adequate organ perfusion and tissue
Resuscitation is complete when O2 debt is repaid, tissue acidosis is corrected, and aerobic
Hemorrhagic shock, septic shock, and traumatic shock are the most common types of shock
encountered on surgical services.
Any intervention that delays the arrival of a bleeding patient to the operating room for control
of hemorrhage increases mortality.