1. Shock is hypoperfusion not hypotension
2. Rapid identification of HS and initiation of
ttt before hypotension occur is essential to
A. Loss of up to 15% of total blood volume (0 to
750 ml in 70 kg person).
B. Characterized by normal blood pressure, urine
output, slight tachycardia, tachypnea, slight
A. Loss of 15 % to 30% of total blood volume
(750 to 1,500 ml )
B. Characterized by normal blood pressure,
tachycardia, mild tachypnea, decrease urine
output and mild anxiety.
A. Loss of 30% to 40% of total blood volume
(1,500 to 2,ooo)
B. Characterized by hypotension, tachycardia,
tachypnea, decreased urine output , anxiety
A. Loss of > 40% of total blood volume
B. Characterized by severe hypotension and
tachycardia, tachypnea, negligible urine
output and lethargy
BP is normal until significant blood loss occur.
( class III )
Tachycardia is the earliest reliable sign of
1. Replace three times the volume of blood lost
with warm crystalloids. (1L of blood lost
should be replaced with 3L of crystalloids)
A. The 3-to-1 rule comes from classic
B. Mortality for resuscitation with shed blood
alone 80% shed blood plus plasma was 70%
lactated Ringer`s plus shed blood (in 3:1
1. Replacement of hemorrhage with blood
only or less than the required ratio of
crystalloid to blood loss results in persistent
hypoperfusion and acidosis and increase
2. Fluid resuscitation of the interstitial space is
obligatory in HS.
The interstitial space volume in 70 –Kg male is
approximately 10 L
The resultant edema and fluid retention is the
expected result not a harmful side effect
I. Become hemodynamically stable after initial
II. Early surgical consultation is necessary
I. Pts respond to initial fluid bolus but again
become hemodynamically unstable or
shown signs of hypoperfusion.
II. Cont` with fluid & blood transfusion
maintain normal hemodynamics
III. These Pts most often require rapid surgical
I. Pt who show no response to fluid boluses
and blood transfusion have continued
hemorrhage and require Immediate
surgical intervention to stop bleeding.
II. Must keep in mind non hemorrhagic
causes of shock .
A. Tension pneumothorax.
B. Cardiac tamponade.
C. Spinal cord injury.
D. Cardiogenic shock..
E. Septic shock
The goal of HS resuscitation is restoration of end-
Traditional endpoints (normalization of BP- heart
rate- urine output- capillary refill).
BP does not equal cardiac output
Increase systemic vascular resistance (SVR) may raise
Pt with shock but normal BP are referred to as being
“compansated shock” despite bleeding and
Even experienced practitioners can be
fooled by patient in compensated shock.
Normalization of acidosis and oxygen
consumption are the best current indicators
of adequate resuscitation
Base deficit and lactate level are good
indications of tissue perfusion.
Albumin shown to decrease glomerular
filtration and urine output
increase sodium retention
Increase coagulopathy when used in HS
2. Inotropes and vasopressors
Increase SVR and rise BP according to
formula BP = CO X SVR
Increase BP not mean PERFUSION
NORMAL tissue perfusion is the GOAL of
VASOPRESSORS may have opposite effect
of worsening perfusion through
Well resuscitated Pts mobilize 3th space
fluid naturally 3 to 5 days after resuscitation
Induced diuresis (eg. Furosemide ) is
unnecessary and may be harmful if it
reduces intravascular volume and perfusion
Since normal edema resulting from proper
shock resuscitation is the result of an
inflammatory response (not cardiogenic
failure) and is obligatory it is not reversible
in the early stages of shock.
Intravascular volume status should be
estimated by measurements of
central venous pressure .
HCO3 combined with hydrogen ion to form
water and carbon dioxide
CO2 diffuses into cells and worsens
It is not indicated for lactic acidosis from HS
Best treatment of acidosis from HS is
restoring perfusion to ischemic tissue.
Multiple organ failure
pt who survive HS but die in the hospital later
usually die of MOF or sepsis
MOF results from systemic inflammatory
Duration and severity of HS correlate with
incidence of MOF
Patients who get > 6 units of packed RBCs in
the first 12 hours of HS resusitation have higher
risk of MOF
Most common cause of coagulopathy in HS
Significant coagulopathy begins at 34o c
Undetectable on lab tests of coagulation
,blood warmed to 37 c before testing
Treate with warmed fluids and external
2-Platelet dysfunction and deficiency
Second most common cause
Hypothermia cause plt dysfunction
Thrombocytopenia is common is massive
Degree of thrombocytopenia not correlated
directly with volume of blood loss