Shock and

hemorrhage
dr. Tri Hening Rahayatri Sp.B, Sp.BA
 Definition

• Shock defined as the

inadequate delivery of oxygen
to tissue leading to cellular
dysfunction and injury
• An abnormality of the circulatory
system that results in inadequate
organ perfusion and tissue
oxygenation
 Forms of Shock

• Blalock, 1943: • Hypovolemic

• Cardiogenic
– Hypovolemic • Neurogenic
– Vasogenic • Inflammatory (septic)
– Cardiogenic • Obstructive
– Neurogenic • Traumatic
• Hypovolemic shock: results from loss of circulating
blood or its component.
– May be due to decreased whole blood (hemorrhagic
shock), plasma, interstitial fluid or combination.
• Cardiogenic shock: results from failure of the pump
funcion as may occur with arrythmias or acute heart
failure.
• Neurogenic shock is a form of vasogenic shock in
which spinal cord injury (or spinal anesthesia) cause
vasodilatation.
• Inflammatory (septic) shock results from decreased
resistance to blood flow within capacitance vessels
of the circulatory systems causing an effective
decrease in circulationg volume.
• Obstructive shock occurs when circulatory flow is
mechanically impeded as with pulmonary embolism
or a tension pneumothorax.
• Traumatic shock: injury to soft tissue and fracture of
long bones that occur in association with
multysystem trauma can produce an upregulation of
proinflammatory regulation that can create a state
of shock that more complex than simple
hemorrhagic shock.

Hemorrhage is the most common cause of shock in the

injured patient.
Basic cardiac • Cardiac output: volume of
blood pumped by the blood
physiology per minute.
• Stroke volume: amount per
every contraction.
• Preload: the volume of
venous return to heart
determined by venous
capacitance, volume status,
and the difference between
mean venous systemic
pressure and right artrial
pressure
• Afterload is systemic
(peripheral) vascular
resistance or, simply stated,
resistance to the forward flow
of blood.
 Pathophysiology of blood loss
• Early responses to blood loss are
compensatory vasoconstriction of cutaneous,
muscle, and visceral circulation to preserve
blood flow to the kidneys, heart, and brain.
increase in heart rate/ tachycardia
• The release of endogenous catecholamines
increases peripheral vascular resistance
increase diastolic BP and reduce pulse
pressure.
 Pathophysiology of blood loss
• Other vasoactives hormones released:
histamine, bradykinin, ß-endorphins, and a
cascade of prostanoids and other cytokines.
• At the cellular level, inadequately perfused
and oxygenated cells are deprived of essential
substrates for normal aerobic metabolism and
energy production
formation of lactic acid and the
development of metabolic acidosis.
 Pathophysiology of blood loss
• Proinflammatory mediators, such as inducible
nitric oxide synthase (iNOS), tumor necrosis
factor (TNF), and other cytokines are released,
setting the stage for subsequent end-organ
damage and multiple organ dysfunction.
• If the process is not reversed, progressive
cellular damage, alterations in endothelial
permeability, additional tissue swelling, and
cellular death can occur.
 Recognition of shock
• pulse rate
• pulse character,
• respiratory rate
• skin circulation
• pulse pressure (the difference between systolic
and diastolic pressure).
• Tachycardia and cutaneous vasoconstriction are
the typical early physiologic responses to volume
loss in most adults.
 Definition of hemorrhage
• Hemorrhage is defined as an acute loss of
circulating blood volume.
• Normal adult blood volume is approximately
7% of body weight, and in childrean 8% to 9%
of body weight (80–90 mL/kg)
Hemorrhage classification
 Hemorrhage classification
• Class I hemorrhage is exemplified by the condition of
an individual who has donated a unit of blood.
• Class II hemorrhage is uncomplicated hemorrhage
for which crystalloid fluid resuscitation is required.
• Class III hemorrhage is a complicated hemorrhagic
state in which at least crystalloid infusion is required
and perhaps also blood replacement.
• Class IV hemorrhage is considered a preterminal
event; unless very aggressive measures are taken, the
patient will die within minutes.
 Initial management of hemorrhagic
shock
• The diagnosis and treatment of shock must occur
almost simultaneously

The basic management principle is to stop the

bleeding and replace the volume loss.

• Baseline recordings are important to monitor the

patient’s response to therapy, and measurements
of vital signs, urinary output, and level of
consciousness are essential
 Initial management of hemorrhagic
shock
• Priorities for managing circulation include
controlling obvious hemorrhage, obtaining
adequate intravenous access, and assessing
tissue perfusion.
• Bleeding from external wounds  direct
pressure to the bleeding site; pelvic binder for
pelvic fracture.
The priority is to stop bleeding
 Initial management of hemorrhagic
shock
• Access to the vascular system  inserting
two large-caliber (minimum of 16-gauge in an
adult) peripheral intravenous catheters.
• In children younger than 6 years, 
intraosseous needle.
• As intravenous lines are started, blood
samples are drawn for type and crossmatch,
appropriate laboratory analyses, BGA
 Fluid therapy
• Warmed isotonic electrolyte solutions, such as lactated Ringer’s and
normal saline.
• Warmed fluid bolus is given.
• The usual dose is 1 to 2 L for adults and 20 mL/kg for pediatric
patients.
• Absolute volumes of resuscitation fluids should be based on
patient response. It is important to remember that this initial fluid
amount includes any fluid given in the prehospital setting.
• The patient’s response is observed during this initial fluid
administration, and further therapeutic and diagnostic decisions are
based on this response.
• The amount of fluid and blood required for resuscitation is
difficult to predict on initial evaluation of the patient
 Initial management of hemorrhagic
shock
• If blood pressure is raised rapidly before the
hemorrhage has been definitively controlled,
increased bleeding can occur.

• Persistent infusion of large volumes of fluid

and blood in an attempt to achieve a normal
blood pressure is not a substitute for
definitive control of bleeding.
 Initial management of hemorrhagic
shock
• Excessive fluid administration can exacerbate the
lethal triad of coagulopathy, acidosis, and
hypothermia with activation of the inflammatory
cascade.
• Balancing the goal of organ perfusion with the
risks of rebleeding by accepting a lower-than-
normal blood pressure has been termed
“controlled resuscitation,” “balanced
resuscitation,” “hypotensive resuscitation,” and
“permissive hypotension.”
 Evaluation of resuscitation response
• The return of normal blood pressure, pulse
pressure, and pulse rate.
• Improvements in the CVP status and skin
circulation.
• The volume of urinary output is a reasonably
sensitive indicator of renal perfusion: 0.5
mL/kg/hr in adults 1 mL/kg/ hr for pediatric
patients for children under 1 year of age, 2
mL/kg/hour
 Initial management of hemorrhagic
shock
• It is most important to assess the patient’s
response to fluid resuscitation and identify
evidence of adequate end-organ perfusion
and oxygenation (urinary output, level of
consciousness, and peripheral perfusion).
Evaluation of resuscitation response
 Conclusion
• Inadequate volume replacement is the most
common complication of hemorrhagic shock.
• Immediate, appropriate, and aggressive therapy
that restores organ perfusion minimizes such
complications.
• An undiagnosed source of bleeding is the most
common cause of poor response to fluid therapy
• Immediate surgical intervention may be
necessary.