Hypovolemic Shock

and
Disseminated Intravascular
Coagulopathy

Irma A. Lee, M.D.

Department of Obstetrics
and Gynecology
Hypovolemic Shock Dr. I. A. Lee
 Functions of Pregnancy-Induced
Hypervolemia
1. To meet the demands of the enlarged
uterus with its hypertrophied vascular
system
2. To protect the mother and fetus against
deleterious effects of impaired venous
return in the supine and erect position
3. To safeguard the mother against the
adverse effects of blood loss associated
with parturition

Hypovolemic Shock Dr. I. A. Lee

 Causes of Hemorrhage in
Pregnant Women
1. Bleeding from genital tract (antepartum
hemorrhage)
• Ruptured ectopic pregnancy, Molar pregnancy,
Abortion, Placenta previa, abruptio placenta,
Postpartum hemorrhage

2. Intra/Postpartum
• Retained placenta, uterine atony, uterine rupture,
post CS hemorrhage, lower genital tract injury

3. Others
• Subcapsular hematoma of the liver, coagulopathy
(AF embolism), trauma, GI bleeding, ruptured
aneurysm, burns
Hypovolemic Shock Dr. I. A. Lee
 Classification of Hemorrhage in
Pregnancy
Class Blood Loss % Loss Clinical Findings
(ml)
1 < 1,000 15 None

2 1,200-1,500 15-25 Orthostatic blood pressure changes,

positive tilt test, pulse pressure ≤ 30 mm
Hg, reduced peripheral perfusion with
prolonged capillary refill time
3 1,500-2,000 25-35 Cold, clammy skin, tachycardia,
tachypnea, hypotension

4 > 2,000 >35 Profound shock, nonpalpable blood

pressure

Hypovolemic Shock Dr. I. A. Lee

 Hypovolemic Shock

• Circulatory collapse due to inadequate

intravascular blood volume caused by
hemorrhage

Hypovolemic Shock Dr. I. A. Lee

 Clinical manifestations of
hypovolemic shock (symptoms)
Central nervous system Anxiety
Confusion
Respiratory system Shortness of breath
Air hunger
Cardiovascular system Palpitations
Skin Cold
Shivers
Gastrointestinal system Thirst
Apetite for salty food
Renal system Decreased urine
Hypovolemic Shock Dr. I. A. Lee
 Clinical manifestations of
hypovolemic shock (signs)
Central nervous system Delirium
Restlessness
Decreased level of consciousness
Respiratory system Hyperventilation
Cardiovascular system Tachycardia
Low blood pressure
Skin Cold
Pale
Clammy
Renal system Oliguria
Anuria
Pregnancy Fetal distress or death

Hypovolemic Shock Dr. I. A. Lee

 Stages of Shock
1. Non-Progressive- compensatory phase
caused by negative feedback control
mechanism of the circulation
• Baroreceptor reflexes eliciting sympathetic
stimulation within 30 seconds after hemorrhage
• CNS ischemic response eliciting sympathetic
stimulation occurring 10-60 minutes
• Absorption of large quantities of fluid from
intestinal tract and interstitial spaces
• Conservation of water and salt by the kidney

Hypovolemic Shock Dr. I. A. Lee

 Stages of Shock
2. Progressive – shock steadily worsens

3. Irreversible- shock has progressed to

state no known therapy can maintain life

Hypovolemic Shock Dr. I. A. Lee

 Maternal Compensatory Mechanism in response
to volume loss

Hypovolemic Shock Dr. I. A. Lee

Hypovolemic Shock Dr. I. A. Lee
 Complications of Hypovolemic
Shock
• Acute tubular necrosis
• ARDS
• DIC
• Hypothermia

Hypovolemic Shock Dr. I. A. Lee

 Management of Hypovolemic
Shock
• Pre hospital care
– Prevent further injury
– Transport immediately to hospital
– Initiate appropriate treatment without delaying
transport (adequate airway, ventilation, and
circulation)
• Emergency department care
– Maximize O2 delivery
– Control further blood loss
– Fluid resuscitation
Hypovolemic Shock Dr. I. A. Lee
 Sequence of Therapeutic Diagnostic
Maneuvers
Priority Mnemonic Therapy Purpose

1 V Ventilate Adequate pulmona CO2

and O2 exchange
2 I Infusion Blood, fluid, electrolyte
balance
3 P Pump Restoration of cardiac
competence
4 P Pharmacologic Use of vasoactive
agents to improve
perfusion
5 S Specific, Medical and surgical
surgical management of primary
causes
Hypovolemic Shock Dr. I. A. Lee
 Ventilate
• Suspect ventilatory failure (thoracic
movement feeble, decreased breath
sounds)
• Respiratory acidosis pH <7.35, pCO2 >46
torr, pO2 <70 torr, 93 % saturation

• Mechanical assistance of ventilation

Hypovolemic Shock Dr. I. A. Lee

 Infuse
• To restore adequacy of intravascular blood
volume
• Hgb 7-10 g/dL
• CVP and PAWP- indicate relationship between
volume which enter the heart and effectivity of
volume ejected by heart
• Initial fluid resuscitation- isotonic crystalloid 1-2 L
lactated ringers or NSS
• Blood component therapy- (pRBC) to improve
O2 carrying capacity

Hypovolemic Shock Dr. I. A. Lee

 Pump

• Evaluate cardiac competence with ECG

and CVP

Hypovolemic Shock Dr. I. A. Lee

 Fluid Resuscitation
• Current recommendations are for
aggressive fluid resuscitation with
LACTATED RINGERS SOLUTION or
NORMAL SALINE SOLUTION in all
patients with signs and symptoms of
shock regardless of underlying cause

Hypovolemic Shock Dr. I. A. Lee

 Blood Component Therapy
Component Indication Notes

Packed red cells To improve O2 carrying capacity Raise Hb 1 g/dL

Fresh-frozen plasma Reduce clotting factors PT Start with 2 U FFP or 15-

and/or PTT >1.5 x upper normal 20 ml/kg ideal body
weight

Cryoprecipitate Fibrinogen <75-100 ug 1U/10-kg body weight

with fibrinogen<75

Platelets Platelets<50,000 Increase platelets 5000-

10,000/mm3 per unit
Albumin Volume replacement, bind Use 5% albumin
bilirubin in newborns albumin
<1.0 g/dl (total protein<4.0)

Hypovolemic Shock Dr. I. A. Lee

 Blood Component Therapy
1. pRBC
• Component of choice for anemic hypoxia
• For rapid transfusion, may dilute with 100 ml normal
saline
• 1 pRBC (300 ml) → 1 g/dL Hgb or Hct 3%
2. Fresh Frozen Plasma
• Component of whole blood once platelets and
cellular elements are removed
• Frozen at -18 to -30 °C
• 1u of whole blood → 200 ml ffp
• From plasma apheresis → 800 ml ffp
• Contains coagulation factors

Hypovolemic Shock Dr. I. A. Lee

 Blood Component Therapy
3. Cryoprecipitate
• Prepared by thawing a unit of ffp at 4°C and
collecting the formed precipitate in a
concentrated volume of 10-15 ml per bag
• A bag contains 200 to 300 mg of fibrinogen
and 100 units of Factor VIII, vWF, factor XIII
and 55 mg fibronectin
• 10 bags of cryoprecipitate from 10 units of
plasma → 2 g fibrinogen raising level to 65-
70 mg/dL

Hypovolemic Shock Dr. I. A. Lee

 Blood Component Therapy
4. Platelets
• Obtained from whole blood or by apheresis
• Indicated for thrombocytopenia or platelet
disorders prior to invasive procedures to
reach platelet level at 100,000/mm3
• Platelet count of 50,000/mm3 adequate if
platelets are normal
• Transfusion is initiated for non bleeding
patients with platelets 20,000/mm3 or less

Hypovolemic Shock Dr. I. A. Lee

 Blood Component Therapy
5. Albumin
• Used for volume replacement, to bind
bilirubin in hemolytic disease of the newborn
• Albumin replacement cannot replace feeding
to improve patients’ nutritional status
• Low perioperative albumin levels correlate
with poor prognosis

Hypovolemic Shock Dr. I. A. Lee

 Transfusion Complications
• Infectious risks
– Viral and bacterial
• Immunologic risks
– Acute hemolytic reaction, delayed hemolytic reaction,
febrile reactions, allergic reactions, transfusion related
acute lung injury, post transfusion purpura
• Others
– Citrate toxicity, metabolic acidosis, hyperkalemia,
hypocalcemia, hypthermia, volume overload

* For every 5-7 units pRBC, give 10-20 ml of 10%

calcium gluconate or 2-5 ml of 10% calcium
chloride → ionized calcium level

Hypovolemic Shock Dr. I. A. Lee

 Definitive Treatment

As the patient is being

stabilized, steps should be
taken to arrest cause of
bleeding

Hypovolemic Shock Dr. I. A. Lee

Hypovolemic Shock Dr. I. A. Lee
 Summary

Reliance on blood pressure and initial

hematocrit level rather than signs of
decreased peripheral perfusion are errors
that lead to failure to recognize
hypovolemic shock

Hypovolemic Shock Dr. I. A. Lee

 Hemostasis
• Ingenious process that makes blood fluid
and free from clots and allows formation of
plugs to seal off vessel injury

Thrombosis
•A pathologic process whereby there is
blood clot formation within an injured vessel

Hypovolemic Shock Dr. I. A. Lee

 Maintaining Hemostatic Balance

Unobstructed blood flow -------- dilutes activated coagulation

factors

Humoral factors --------- inactivate stable coagulation factors

Reticuloendothelial system ------ removes products of

coagulation and clot disintegration

Prostacyclin endothelial cell -------- inhibits abnormal platelet

aggregation

Hypovolemic Shock Dr. I. A. Lee

 Tipping the Hemostatic Balance
Extensive activation of coagulation process (various diseases)

Endothelial damage
Pre-kallikrein Tissue injury
High molecular Platelet activation
weight kininogen Fibrin deposit in
Massive thrombosis micocirculation

Hypercoagulability
Activation of Infarction Hemolysis
fibrinolytic system
Consumption of coagulation
Factors and platelets

Secondary Hypocoagulability Massive bleeding

fibrinolysis

Death

Hypovolemic Shock Dr. I. A. Lee

 MAINTENANCE OF HEMOSTASIS
1. Vascular Wall
a. Endothelin – vasoconstriction
b. Collagen – needed for platelet
adherence
c. tPa – initiates fibrinolysis
d. PGI2 and NO – to limit size of thrombus

Hypovolemic Shock Dr. I. A. Lee

 2. Platelet reactions
a. Adhesion and shape changes
b. Secretion and release of ADP, calcium
ions, serotonin and thromboxane A2
c. Platelet aggregation – stimuli for
aggregation and recruitment are ADP,
thromboxane A2 and thrombin

Hypovolemic Shock Dr. I. A. Lee

Hypovolemic Shock Dr. I. A. Lee
 3. Coagulation Process – composed of
a. enzymes ( activated coagulation
factor)
b. substrate ( proenzyme form of
coagulation factor)
c. co-factor – reaction accelerator

Hypovolemic Shock Dr. I. A. Lee

Hypovolemic Shock Dr. I. A. Lee
Hypovolemic Shock Dr. I. A. Lee
 The Fibrinolytic System

Plasminogen

Tissue activator

Plasma activator

Urokinase

Plasmin

Fibrin-Fibrinogen

Fibrinolytic split products

Hypovolemic Shock Dr. I. A. Lee

Naturally Occurring Anticoagulants
1. Anti thrombin
• Inhibits activity of thrombin and serine
proteases factors IXa - XIIa
2. Protein C and S
• Inactivate cofactors Va and VIIIa
3. Plasminogen-plasmin system
• Breakdown fibrin

Hypovolemic Shock Dr. I. A. Lee

 Disseminated Intravascular
Coagulopathy
Acute, subacute or chronic thrombo-
hemorrhagic disorder characterized by
activation of coagulation sequence leading
to formation of microthrombi throughout
the microcirculation as a consequence
there is consumption of platelets, fibrin
and coagulation factors and activation of
fibrinolytic system

Hypovolemic Shock Dr. I. A. Lee

 Mechanisms that Trigger DIC
1. Release of tissue factor or
thrombocytoplastic materials into the
circulation
2. Widespread injury to the endothelial cells

Hypovolemic Shock Dr. I. A. Lee

 Extrinsic Pathway

Tissue Injury Abruptio placenta

Amniotic Fluid Embolism
Thromboplastin Retained Dead Fetus
Saline induced abortion
VII

X V PF 3
Ca++

II Thrombin

Fibrinogen Fibrin (clot)

Hypovolemic Shock Dr. I. A. Lee

 Intrinsic Pathway
Endothelial damage Septic abortion

Chorioamnionitis
Contact activation

XII

XI

IX

VIII Platelet
factor 3 Ca++

II Thrombin

Fibrinogen Fibrin (clot)

Hypovolemic Shock Dr. I. A. Lee
 Initiation of DIC by platelet activation

PLATELET ACTIVATION
(Platelet activation factor, diminished prostacyclin)

Severe Pre-eclampsia

Increased aggregation and adhesion

X V PF3
Ca++

II Thrombin

Fibrinogen Fibrin (clot)

Hypovolemic Shock Dr. I. A. Lee
Hypovolemic Shock Dr. I. A. Lee
 Major Disorders Associated with DIC

Hypovolemic Shock Dr. I. A. Lee

Hypovolemic Shock Dr. I. A. Lee
 Consequences of DIC

1. Widespread fibrin deposition → ischemia

and hemolytic anemia
2. Hemorrhagic diathesis secondary to
consumption of platelets and clotting
factors and activation of plasminogen
and fibrinolysis

Hypovolemic Shock Dr. I. A. Lee

 CLINICAL MANIFESTATIONS
1. Microangiopathic hemolytic anemia
2. Respiratory – dyspnea, cyanosis
3. Neurologic – convulsions, coma
4. Renal – oliguria, acute renal failure
5. Circulatory failure and SHOCK

Hypovolemic Shock Dr. I. A. Lee

 Laboratory Diagnosis
1. Fibrinogen level ------ Clot observation test
5ml of blood in a 15ml test tube inverted 4-5
times
* clot within 6-12 minutes or stable clot that
does not lyse

If clot <6mins = fibrinogen level (150mg/100ml)

If clot >12mins = fibinogen level (100-
150mg/100ml)
If no clot in 30 mins = fibinogen level
(<100mg/100ml)
Hypovolemic Shock Dr. I. A. Lee
 Laboratory Diagnosis

2. Platelets
<4 platelets / hpf = suggest thrombocytopenia
3. Partial thromboplastin time
4, Prothrombin time
5. Fibrin degradation products- D-dimer

Hypovolemic Shock Dr. I. A. Lee

 Goals in Management
2. Good clinical judgement
3. Recognition and treatment of underlying
disorder (abruptio placenta, IUFD, Amniotic
fluid embolism, septic abortion, and sepsis,
eclampsia)
4. Supportive measures
(replacement therapy –FFP, cryoprecipitate)
4. Epsilon-Aminocaproic Acid – control
fibrinolysis by inhibiting conversion of
plasminogen to plasmin

Hypovolemic Shock Dr. I. A. Lee

 Thank you !

Hypovolemic Shock Dr. I. A. Lee