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Shock is defines defined as tissue hypoperfusion leading to inadequate delivery of
oxygen and nutrients to maintain normal tissue and cellular function and maintain
normal aerobic metabolism The resultant cellular injury is initially reversible; if the
hypoperfusion is severe enough and prolonged, the cellular injury becomes
irreversible, with end-organ dysfunction, cell death, and death of the patient .
The clinical manifestations of shock are the result of:
1. Stimulation of the sympathetic and neuroendocrine stress responses,
2. Inadequate oxygen delivery and end-organ dysfunction.
1. Blood pressure alone is an insensitive measure of shock; significant
hypoperfusion and cellular death may be ongoing, despite normal blood
pressure. Inadequate oxygen delivery is presumed to be the pathologic defect in
2. The clinical dilemma faced in a patient with trauma shock is that the etiology
may not be immediately apparent. Inadequate treatment results in ongoing
hypoperfusion and activation of inflammatory mediators. Thus, treatment of the
patient in shock is initially empiric, while the underlying etiology of the shock state
is investigated.

1. Hypovolemic shock, the most common type, results from loss of circulating blood
volume. This may result from loss of whole blood (hemorrhagic shock), third space
fluid loss or a combination of both.
2. Vasogenic shock ( vasidilatory) results from decreased resistance within capacitance
vessels. Resulting from spinal shock, anaphylactic shock and initial stage of septic shock
3. Neurogenic shock is a form of vasogenic shock in which spinal cord injury or spinal
anesthesia causes vasodilatation due to acute loss of sympathetic vascular tone.
4. Cardiogenic shock results from failure of the heart as a pump (the heart itself is
impaired as a pump) as in severe arrhythmias or acute myocardial infarction. In trauma it
results from rupture of one of the heart champers or valves, cardiac contusion, or
coronary artery injury

5. Obstructive shock, which results from mechanical impediment to heart and circulation
rather than a primary cardiac failure. It is caused by pulmonary embolism, cardiac
tamponade or tension pneumothorax, results in depressed cardiac output,
6. Traumatic shock, the soft tissue injury and long bone fractures that occur in
association with blood loss yield an upregulation of proinflammatory mediators that is
more complex than simple hemorrhagic shock resulting in third space loss.
(1) Definitive control of the airway must be secured,
(2) Control of active hemorrhage must occur promptly (generally in the operating room,
as delay in control of ongoing bleeding increases mortality),
(3) Adequate volume resuscitation with red blood cells and crystalloid solution
(4) Excessive fluid resuscitation may exacerbate bleeding.
Thus, both inadequate and uncontrolled volume resuscitation is harmful.

1. compensated phase of shock. With substantial physiologic compensatory

mechanisms for small volume blood loss, predominantly through the neuroendocrine
response, hemodynamics may be maintained.
2. Decompensated phase of shock : with continued hypoperfusion often not
apparent clinically, cell death and tissue injury are ongoing. At this point in
treatment, the cellular dysfunction can be reversed with appropriate volume

3. Irreversible phase of shock If volume loss continues or volume resuscitation is

insufficient; a vicious physiologic cycle will develop. With persistent hypoperfusion
with low cardiac output, regional tissue hypoperfusion and progressive tissue and
microcirculatory changes induce cardiovascular decompensation. Is often insidious
and recognized only in retrospect. Sufficient tissue injury and cell death have
occurred to this point that continued volume resuscitation fails to reverse the process.
Ultimately, even massive quantities of fluid resuscitation and vasopressors fail to
maintain adequate blood pressure. This vasodilatory response probably
represents the common late phase of all forms of shock, regardless of etiology.


Are directed at preservation of perfusion to the heart and brain even at the expense
of other organ systems by:
1. Selective vasoconstriction to non-vital organs (as skin and G.I.T.) to direct blood to
vital organs as heart and brain. Also constriction of the capacitant venous system leading
to increase venous return to the heart.
2. Fluid preservation by decreasing water loss and preserving water.
3. Fluid is shifted into the intravascular space fro interstitial space.
(1) Autonomic nervous system, prompt increase in cardiac contractility heart rate and
peripheral vascular tone.
(2) Hormonal response to preserve salt and intravascular volume.
(3) Changes in the local microcirculation to regulate regional blood flow.
Afferent impulses transmitted from the periphery are processed within the central nervous
system (CNS) and activate the reflexive effector responses or efferent impulses.
Afferent stimuli:
1. Loss of circulating blood volume, pain, hypoxemia, hypercarbia, acidosis,
infection, changes in temperature, emotional arousal, or hypoglycemia.
Activation of the hypothalamic-pituitary-adrenal axis and activation of the autonomic
nervous system (ANS) to induce direct sympathetic stimulation of the adrenal medulla to
release catecholamines.

Cardiovascular Response
1. Hemorrhage results in diminished venous return to the heart and decreased
cardiac output.
2. This is compensated by increased cardiac heart rate and contractility in an
attempt to increase cardiac output.
3. Venous and arterial vasoconstriction is not uniform. Blood is shunted away from
less essential organ such as the intestine, kidney, and skin. In contrast, the brain and
heart preserve their blood flow despite decrease in cardiac output.

4. The majority of the blood volume is within the venous system. In shock there is
contraction of the capacitant veins increasing venous return to the heart and
maintaining ventricular filling.
1. Increased sympathetic output induces catecholamine release from the
adrenal medulla. Catecholamine effects on peripheral tissues include stimulation
of hepatic glycogenolysis and gluconeogenesis to increase circulating glucose
availability to peripheral tissues, an increase in skeletal muscle glycogenolysis,
suppression of insulin release, and increased glucagon release.
2. Activation of the hypothalamic-pituitary-adrenal axis Shock stimulates the
hypothalamus to release corticotropin-releasing hormone that results in the release
of adrenocorticotropic hormone (ACTH) by the pituitary. ACTH subsequently
stimulates the adrenal cortex to release cortisol. Cortisol acts synergistically
with epinephrine and glucagon to induce a catabolic state. Cortisol stimulates
gluconeogenesis and insulin resistance, resulting in hyperglycemia as well as
muscle cell protein breakdown and lipolysis to provide substrates for hepatic
gluconeogenesis. Cortisol causes retention of sodium and water by the nephrons
of the kidney.
3. The renin-angiotensin system is activated in shock. This result in release of
aldosterone, ACTH, and antidiuretic hormone (ADH). Aldosterone, a mineralocorticoid,
acts on the nephron to promote reabsorption of sodium. ADH acts on the distal tubule and
collecting duct of the nephron to decrease water and sodium losses, and preserve
intravascular volume.


1. Recognition of shock.
The clinical manifestations of shock are related to tissue hypoperfusion and the
body response to shock by neuroendocrine response.
a. Due to compensatory mechanisms, (including preservation of venous return)
hypotension is noted only in stage III (loss of >30% of blood volume).
b. Tachycardia is an early sign of shock; it is an attempt to increase cardiac output.
Elderly patients however may not exhibit tachycardia because: (1) Limited
cardiac response to catecholamines stimulation. (2)Use of drugs as beta blockers
and (3) Presence of cardiac bacemaker.
c. Release of endogenous catecholamines increase peripheral vascular resistance
increasing diastolic pressure (decrease pulse pressure which is the difference

between systolic and diastolic blood pressure). So decrease pulse pressure is seen
in stage II and before decrease systolic blood pressure which is seen in stageIII.
d. Vasoconstriction of cutaneous circulation leads to pallor and cold skin.
e. Renal hypoperfusion and kidney attempts to preserve fluids would lead to
decreased urine output.
f. Due to cerebral hypoperfusion patient is irritable initially and later has altered
level of consciousness and coma.
g. Hemoglobin level or hematocrit concentration is not reliable to estimate
blood loss and diagnose shock.

2. Identify the etiology of shock;

1. Hemorrhagic shock
1. Hemorrhage is the most common etiology of shock in injured patients. Start treating
shock as hypovolemic shock. If no response, think of inadequate resuscitation,
continuing blood loss or other causes of shock.
2. Non-hemorrhagic shock.
a.Carcinogenic shock: blunt cardiac injury, valvular rupture, cardiac tamponade,
tension pneunothorax, air embolus, or rarely acute myocardial infarction. All cases of
cardiogenic shock are characterized by congested neck veins or increased CVP or
b. Spinal shock: vasodilatory shock due to loss of sympathetic tone. The classical
clinical picture is hypotension without tachycardia or cutaneous
c. Septic shock: Uncommon, may be due to penetrating abdominal injuries
leading to peritonitis. Early septic shock has warm pink skin and wide pulse

Hemorrhagic shock
In adults, blood= 7% of ideal body weight= 5 liters

In children, 8-9% of body weight= 80-90 ml/ kg.


*Based on percentage of acute volume loss

*Volume replacement should depend on response to initial therapy rather than on
initial assessment.


2. Nasogasrtic decompression
3. Urinary catherization
4. Vascular access

a. 2 large caliber (minimum of no 16- gauge) peripheral catheters forearm or

antecubital veins.
b. Central venous access (femoral, jugular or subclavian), consider
c. Saphenous cutdown.
d. In children less than 6 years of age: insert intraosseous needle before
central line insertion.
e. Draw blood for: Type and crossmatch, appropriate lab tests, toxicology,
and pregnancy tests.

Initial fluid therapy

a. Initially, warmed isotonic electrolyte solutions are rapidly infused.
b. In adults 1-2 liters, in children 20ml/kg
c. Ringers lactate or Normal saline are the initial fluid of choice.
d. Amount of resuscitation fluid depends on evaluation of body response rather
than initial estimation.
1. Clinical: BP, Pulse pressure, Heart rate, Respiratory rate, skin color and
temperature, CVP readings.
2. Urine output: Sensitive indicator of renal perfusion, in adults 0.51ml/kg/hour, in children 1-2 ml/kg/hour.
3. Acid/base balance: Metabolic acidosis due to anaerobic metabolism indicates
inadequate resuscitation or continuing blood loss, so it should be treated by
fluid resuscitation not by bicarbonates.

Therapeutic decisions based on response to initial fluid resuscitation.

1. Identify patients whose blood loss was greater than initially estimated.
This avoids unnecessary fluid and blood transfusion
2. Identify patients with ongoing bleeding who need operative control of
3. Operating room resuscitation go hand in hand with operative control of
1. Rapid response: Patients respond rapidly to the initial fluid bolus
and remain hemodynamically stable. These patients have lost less
than 20% of their blood. No further boluses or blood transfusion is
needed. These patients should be maintained on fluid maintenance
rate. Typed and cross-matched blood should be prepared, operative
intervention is still a possibility.
2. Transient response: These patients have lost 20%-40% of their
blood. They respond initially to initial fluid therapy, but deteriorate
when I.V. fluids is lowered to the maintenance rate. This indicates
inadequate resuscitation or continued blood loss. They need
further Fluids and initiation of blood transfusion. In this group of

patients you should identify those patients who have continued

blood loss and manage them by surgical intervention.
3. Minimal or no response. Failure to respond to initial fluid bolus and
blood transfusion dictates the need for immediate operative
intervention to control bleeding. Rarely this may indicate nonhemorrhagic cause of shock as blunt cardiac injury, cardiac
tamponede or tension pneumothorax.
Blood transfusion: restore the oxygen carrying capacity of intravascular volume.
Intrvascular volume can be maintained with crystalloids which also replace the
lost interstitial and intracellular losses.
1. Fully crossmatched blood: the safest, but needs 1 hour to be ready. It should
be prepared for rapid responders, as we have time and the patient is stable.
2. Type-specific blood: ready within 10 minutes, compatible with ABO and Rh
blood types. Incompatibility to other antibodies may exist. It is suitable for
transient responders.
Type-specific blood is better than Type O blood, unless multiple causalities
are present that may increase the chance of lab errors.
3. Type O packed RBCs. Needed in severe hemorrhage. It should be Rhnegative in females.
The administered fluids should be warm to avoid hypothermia.
Crystalloids are warmed to 39 degree centigrade by a fluid-warmer or
microwave oven.
Blood and blood products should not be warmed by microwave oven but by
blood warmers.
AUTOTRNSFUSION: shed blood from thoracic or abdominal cavities may be
collected under srerile conditions anticoagulated (sodium citrate) and then auto

1. Patients with shock and hypothermia dont respond normally to
fluid resuscitation.
2. They may develop coagulopathy.

3. Monitoring of body temperature is important in initial

management; bladder or esophageal temperature is accurate
measure of body core temperature.
4. Patients under the influence of alcohol intake, or who were
exposed to low temperature, or those with spinal shock are liable
for hypothermia. Also seen in children and elderly
5. Treatment is by rapid re-warming, warmed inspired gases, warmed
intra-venous fluids and blood.
6. They may need core re-warming by irrigation of peritoneal cavity
by saline heated to 39 degrees.