Hemorrhagic shock and resusitation

الرحيم الرحمن الله بسم

Hemorrhagic shock and resusitation

points1. Shock is hypoperfusion not

hypotension2. Rapid identification of HS and initiation

of ttt before hypotension occur is essential to minimize morbidity

Classification of HS

Class IA. 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 anxiety.

Class IIA. 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.

Class IIIA. Loss of 30% to 40% of total blood

volume (1,500 to 2,ooo) B. Characterized by hypotension,

tachycardia, tachypnea, decreased urine output , anxiety and confusion.

Class IVA. Loss of > 40% of total blood volume

(>2,ooo)B. Characterized by severe hypotension

and tachycardia, tachypnea, negligible urine output and lethargy

Notes that

BP is normal until significant blood loss occur.

( class III )

Tachycardia is the earliest reliable sign of shock.

ABG or VBG-PH 7.36

-pCO2 23

-PO2 75 or 32

-HCO3 17

-BE - 9

General rules of HS Resuscitation

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 experiments

B. Mortality for resuscitation with shed blood alone 80% shed blood plus

plasma was 70% lactated Ringer`s plus shed blood (in 3:1 ratio) 30%.

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 mortality.

2. Fluid resuscitation of the interstitial space is obligatory in HS.

Note The interstitial space volume in 70 –Kg

male is approximately 10 LThe resultant edema and fluid retention

is the expected result not a harmful side effect

Response to resuscitation

Rapid response I. Become hemodynamically stable after

initial fluid bolus II. Early surgical consultation is necessary

Transient responseI. 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 intervention

No response

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

Endpoints of resuscitation

The goal of HS resuscitation is restoration of end-organ perfusion

Traditional endpoints (normalization of BP- heart rate- urine output- capillary refill).

TricksBP does not equal cardiac output Increase systemic vascular resistance (SVR)

may raise BP Pt with shock but normal BP are referred to as

being “compansated shock” despite bleeding and hypoperfusion.

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.

Bitfalls in resuscitation

1-Albumin Albumin shown to decrease glomerular

filtration and urine output increase sodium retention worsen oxygenation 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 shock resuscitation.

VASOPRESSORS may have opposite effect of worsening perfusion through vasoconfusion

3. Diuretics 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 .

4. Bicarbonate HCO3 combined with hydrogen ion to

form water and carbon dioxide CO2 diffuses into cells and worsens

intracellular acidosis It is not indicated for lactic acidosis

from HS Best treatment of acidosis from HS is

restoring perfusion to ischemic tissue.

complications

MOF Multiple organ

failure

Coagulopathy

Multiple organ failure pt who survive HS but die in the hospital

later usually die of MOF or sepsis

MOF results from systemic inflammatory response

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

Coagulopathy1-Hypothermia

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

Note that Treate with warmed fluids and external

rewarming

2-Platelet dysfunction and deficiency

Second most common cause Hypothermia cause plt dysfunction Thrombocytopenia is common is

massive HS Degree of thrombocytopenia not

correlated directly with volume of blood loss

Platelets transfusion