Blok 23

HYPOVOLEMIC SHOCK

Penyaji :
dr. Patiyus Agustiansyah, SpOG(K)

BAGIAN/DEPARTEMEN OBSTETRI DAN

GINEKOLOGI FK UNSRI / RSMH
PALEMBANG
 Introduction to
Hemorrhage and Shock
• Hemorrhage
– Abnormal internal or external loss of blood
• Homeostasis
– Tendency of the body to maintain a steady
and normal internal environment
• Shock
– INADEQUATE TISSUE PERFUSION
– Transition between homeostasis and death
Stages of Shock
Cellular Level
 Four Stages
• Stage 1: Vasoconstriction
• Stage 2: Capillary and venule opening
• Stage 3: Disseminated intravascular
coagulation
• Stage 4: Multiple organ failure
 Stage 1: Vasoconstriction (1 of 4)
• Vasoconstriction begins as minimal perfusion
to capillaries continues.
– Oxygen and substrate delivery to the cells
supplied by these capillaries decreases.
– Anaerobic metabolism replaces aerobic
metabolism.
 Stage 1: Vasoconstriction (2 of 4)
• Production of lactate and hydrogen ions
increases.
– The lining of the capillaries may begin to lose the
ability to retain large molecular structures within
its walls.
– Protein-containing fluid leaks into the interstitial
spaces (leaky capillary syndrome).
 Stage 1: Vasoconstriction (3 of 4)
• Sympathetic stimulation produces:
– Pale, sweaty skin
– Rapid, thready pulse
– Elevated blood glucose levels
• The release of epinephrine dilates coronary, cerebral,
and skeletal muscle arterioles and constricts other
arterioles.
– Blood is shunted to the heart, brain, skeletal muscle, and
capillary flow to the kidneys and abdominal viscera
decreases.
Stage 1: Vasoconstriction (4 of 4)

If this stage of shock is not treated by

prompt restoration of circulatory
volume, shock progresses to the next
stage.
Stage 2: Capillary and Venule Opening
(1 of 5)

• Stage 2 occurs with a 15% to 25% decrease in

intravascular blood volume. Heart rate,
respiratory rate, and capillary refill are
increased, and pulse pressure is decreased at
this stage. Blood pressure may still be normal.
Stage 2: Capillary and Venule Opening
(2 of 5)

• As the syndrome continues, the precapillary

sphincters relax with some expansion of the
vascular space.
• Postcapillary sphincters resist local effects and
remain closed, causing blood to pool or
stagnate in the capillary system, producing
capillary engorgement.
Stage 2: Capillary and Venule Opening
(3 of 5)

• As increasing hypoxemia and acidosis lead to

opening of additional venules and capillaries, the
vascular space expands greatly.
– Even normal blood volume may be inadequate to fill the
container.
• The capillary and venule capacity may become great
enough to reduce the volume of available blood for
the great veins and vena cava.
– Resulting in decreased venous return and a fall in cardiac
output.
Stage 2: Capillary and Venule Opening
(4 of 5)

• Low arterial blood pressure and many open

capillaries result in stagnant capillary flow.
• Sluggish blood flow and the reduced delivery of
oxygen result in increased anaerobic metabolism and
the production of lactic acid.
– The respiratory system attempts to compensate for the
acidosis by increasing ventilation to blow off carbon
dioxide.
Stage 2: Capillary and Venule Opening
(5 of 5)

• As acidosis increases and pH falls, the RBCs may cluster

together (rouleaux formation).
– Halts perfusion
– Affects nutritional flow and prevents removal of cellular metabolites
• Clotting mechanisms are also affected, leading to
hypercoagulability.
• This stage of shock often progresses to the third stage if fluid
resuscitation is inadequate or delayed, or if the shock state is
complicated by trauma or sepsis.
Stage 3: Disseminated Intravascular
Coagulation (DIC) (1 of 4)
• Time of onset will depend on degree of shock,
patient age, and pre-existing medical conditions.
• Stage 3 occurs with 25% to 35% decrease in
intravascular blood volume. At this stage,
hypotension occurs. This stage of shock usually
requires blood replacement.
 Stage 3: Disseminated Intravascular
Coagulation (DIC) (2 of 4)
• Stage 3 is resistant to treatment (refractory
shock), but is still reversible.
• Blood begins to coagulate in the
microcirculation, clogging capillaries.
– Capillaries become occluded by clumps of RBCs.
• Decreases capillary perfusion and prevents removal of
metabolites
– Distal tissue cells use anaerobic metabolism, and
lactic acid production increases.
Stage 3: Disseminated Intravascular
Coagulation (DIC) (3 of 4)

• Lactic acid accumulates around the cell.

– Cell membranes no longer have the energy
needed to maintain homeostasis.
– Water and sodium leak in, potassium leaks
out, and the cells swell and die.
Stage 3: Disseminated Intravascular
Coagulation (DIC) (4 of 4)

• Pulmonary capillaries become permeable,

leading to pulmonary edema.
– Decreases the absorption of oxygen and results in
possible alterations in carbon dioxide elimination
– May lead to acute respiratory failure or adult
respiratory distress syndrome (ARDS)
• If shock and disseminated intravascular
coagulation (DIC) continue, the patient
progresses to multiple organ failure.
Stage 4: Multiple Organ Failure (1 of 2)
• The amount of cellular necrosis required to
produce organ failure varies with each organ and
the underlying condition of the organ.
– Usually hepatic failure occurs, followed by renal
failure, and then heart failure.
– If capillary occlusion persists for more than 1 to 2
hours, the cells nourished by that capillary undergo
changes that rapidly become irreversible.
• In this stage, blood pressure falls dramatically (to
levels of 60 mmHg or less).
– Cells can no longer use oxygen, and metabolism
stops.
Stage 4: Multiple Organ Failure (2 of 2)
• If a critical amount of the vital organ is damaged
by cellular necrosis, the organ soon fails.
– Failure of the liver is common and often presents
early.
– Capillary blockage may cause heart failure.
– GI bleeding and sepsis may result from GI mucosal
necrosis.
– Pancreatic necrosis may lead to further clotting
disorders and severe pancreatitis.
• Pulmonary thrombosis may produce
hemorrhage and fluid loss into the alveoli.
– Leading to death from respiratory failure.
Shock and Hemorrhage
 Defining Shock (1 of 2)
• Shock is best defined as inadequate tissue
perfusion.
– Can result from a variety of disease states
and injuries.
– Can affect the entire organism, or it can occur
at a tissue or cellular level.

“The rude unhinging of the machinery of Life”

Gross, 1877
 Defining Shock (2 of 2)
• Shock is not adequately defined by:
– Pulse rate
– Blood pressure
– Cardiac function
– Hypovolemia
– Loss of systemic vascular resistance
Physiological Response to Hemorrhage
• The body’s initial response to hemorrhage is
to stop bleeding by chemical means
(hemostasis).
– This vascular reaction involves:
• Local vasoconstriction
• Formation of a platelet plug
• Coagulation
• Growth of tissue into the blood clot that permanently
closes and seals the injured vessel
 Stages of Hemorrhage
• 60% of body weight is fluid.
– 7% circulating blood volume (CBV) in men
• 5 L (10 units)
– 6.5% CBV in women
• 4.6 L (9–10 units)
 Stages of Hemorrhage
Stage 1
• 15% loss of CBV
– 70 kg pt = 500–750 mL
• Compensation
– Vasoconstriction
– Normal BP, pulse pressure, respirations
– Slight elevation of pulse
– Release of catecholamines
• Epinephrine
• Norepinephrine
– Anxiety, slightly pale and clammy skin
 Stages of Hemorrhage
Stage 2 (1 of 2)
• 15–25% loss of CBV
– 750–1250 mL
• Early decompensation
– Unable to maintain BP
– Tachycardia and tachypnea
 Stages of Hemorrhage
Stage 2 (2 of 2)
• Decreased pulse strength
• Narrowing pulse pressure
• Significant catecholamine release
– Increase PVR
– Cool, clammy skin and thirst
– Increased anxiety and agitation
– Normal renal output
 Stages of Hemorrhage
Stage 3 (1 of 2)
• 25–35% loss of CBV
– 1250–1750 mL
• Late decompensation (early irreversible)
– Compensatory mechanisms unable to cope with
loss of blood volume
 Stages of Hemorrhage
Stage 3 (2 of 2)
• Classic Shock
– Weak, thready, rapid pulse
• Narrowing pulse pressure
– Tachypnea
– Anxiety, restlessness
– Decreased LOC and AMS
– Pale, cool, and clammy skin
 Stages of Hemorrhage
Stage 4
• >35% CBV loss
– >1750 mL
• Irreversible
– Pulse: Barely palpable
– Respiration: Rapid, shallow, and ineffective
– LOC: Lethargic, confused, unresponsive
– GU: Ceases
– Skin: Cool, clammy, and very pale
– Unlikely survival
 Postpartum Hemorrhage:
“Obstetrics is Bloody Business”*

*Cunningham, et. al: Williams Obstetrics, 21st ed., 2001

Postpartum Hemorrhage

Etiology is linked to Risk Factors

Bleeding from Hypotonic myometrium—uterine atony
Placental Some general anesthetics
Implantation Site Poorly perfused myometrium
Over distended uterus
Prolonged labor
Very rapid labor
Oxytocin-induced or augmented labor
High parity
Uterine atony in previous pregnancy
Chorioamnionitis
Retained placental tissue
Avulsed cotyledon, succenturiate lobe
Abnormally adherent—accreta, increta,
percreta
Postpartum Hemorrhage

Etiology is linked to Risk Factors

Large episiotomy, including extensions

Trauma to the
Genital Tract Lacerations of perineum, vagina or
cervix
Ruptured uterus

Coagulation Defects Intensify all of the above

Postpartum Hemorrhage
DO NOT UNDERESTIMATE BLOOD LOSS
Clinical Features of Shock
System Early Shock Late Shock
CNS Altered mental states Obtunded

Cardiac Tachycardia Cardiac failure

Orthostatic hypotension Arrhythmias
Hypotension

Renal Oliguria Anuria

Respiratory Tachypnea Tachypnea
Respiratory failure

Hepatic No change Liver failure

Gastrointestinal No change Mucosal bleeding
Hematological Anemia Coagulopathy

Metabolic None Acidosis

Hypocalcemia
Hypomagnesemia
Postpartum Hemorrhage

Categorization of Acute Hemorrhage

Class 1 Class 2 Class 3 Class 4

Blood loss 15% 15%-30% 30%-40% >40%
(% blood volume)

Pulse rate <100 >100 >120 >140

Pulse pressure Normal Decreased Decreased Decreased

Blood pressure Normal or Decreased Decreased Decreased

increased
Postpartum Hemorrhage

Goals of Therapy

• Maintain the following:

Systolic pressure >90mm Hg
Urine output >0.5 mL/kg/hr
Normal mental status
• Eliminate the source of hemorrhage
• Avoid overzealous volume replacement that may
contribute to pulmonary edema
Postpartum Hemorrhage

Management Protocol
To be undertaken simultaneously with
management of hypovolemic shock

• Examine the uterus to rule out atony

• Examine the vagina and cervix to rule out
lacerations; repair if present
• Explore the uterus and perform curettage to rule
out retained placenta
Postpartum Hemorrhage

Management Protocol (cont’d.)

• For uterine atony:

• Firm bimanual compression
• Oxytocin infusion, 40 units in 1 liter of D5RL
• 15-methyl prostglandin F2a, 0.25 to 0.50 mg
intramuscularly; may be repeated
• Methergine 0.2 mg IM, PGE1 200 mg, or PGE2 20 mg are
second line drugs in appropriate patients
• Bilateral uterine artery ligation
• Bilateral hypogastric artery ligation (if patient is clinically
stable and future childbearing is of great importance)
• Hysterectomy
Postpartum Hemorrhage

Management of Hypovolemic Shock

• Insert at least two large catheters. Start saline infusion.

Apply compression cuff to infusion pack. Monitor central
venous pressure (CVP) and arterial pressure.
• Alert blood bank. Take samples for transfusion and
coagulation screen. Order at least 6 units of red cells. Do
not insist on cross matched blood if transfusion is urgently
needed
• Place patient in the Trendelenburg position
• Warm the resuscitation fluids
• Call extra staff, including consultant anesthesiologist and
obstetrician.
• Rapidly infuse 5% dextrose in lactated Ringer’s solution
while blood products are obtained.
Postpartum Hemorrhage

Management of Hypovolemic Shock (cont’d)

• Transfuse red cells as soon as possible. Until then:
•crystalloid, maximum of 2 liters
•colloid, maximum of 1.5 liters
• Restore normovolaemia as priority, monitor red cell
replacement with Hematocrit or Hemoglobin
• Use coagulation screens to guide and monitor use of blood
components
• If massive bleeding continues, give FFP 1 unit,
cryoprecipitate 10 units while awaiting coagulation results
• Monitor pulse rate, blood pressure, CVP, blood gases, acid-
base status and urinary output (catheterization)
Consider adding oxygen by mask.
Emergency Obstetrics Hemorrhage Orders

• Transfuse two units of packed red blood cells

immediately. Use cross matched blood if available;
otherwise use type specific or O negative packed red
blood cells. Call the blood bank with the patient’s
name, medical record number and DOB to request
the two units.
• Bring a “request for release of blood” form for cross
matched blood [or a “Blood Bank Emergency Blood
Release” {Downtime} Form signed by the physician
for 0 negative blood (uncross matched)].
Hemorrhage causes 30% of All
Maternal Mortality
Causes of 763 Deaths due to hemorrhage
- Abruptio Placentae 19%
- Laceration or rupture 19%
- Atonic uterus 15%
- Coagulopathy 14%
- Placenta Previa 7%
- Placental accreta 6%
- Uterine Bleeding 6%
- Retained placenta 4%
Chichaki, et al, 1999
Intravenous Fluid Therapy
and Blood Component
 Fluid Compartments
• Total body consists of 60% water by
weight in adults
• Body fluids divided into:
– Intracellular compartment
– Extracellular compartment, further
divided into:
• Interstitial compartment
• Intravascular compartment
 Fluid Compartments
Extracellular Fluid
Intracellular Fluid 2/3 1/3

Interstitial
Fluid=75%

IntracellularFluid

Intravascular
Fluid=25%
Intravascular compartement
• Consists of:
– Cellular components of blood
– Proteins
– Ions – mainly sodium, chloride and

bicarbonates
– Potassium – only a small portion in plasma

• Normal blood volume is about 72 mL/kg of body

weight
 Interstitial compartement
• Larger than intravascular compartment
• Water and electrolytes pass freely between blood
and interstitial spaces, which have similar ionic
composition
• Plasma proteins are not free to pass out of the
intravascular space unless there is damage to
capillaries, e.g., septic shock or burns
• With fluid loss or fall in blood pressure, water and
electrolytes pass from interstitial compartment
into blood (intravascular) to maintain volume
(physiologic priority)
 Intracellular Compartement
• Water within cells: Largest reservoir of body water
• Ionic composition different from extracellular fluid
• Contains high concentration of potassium ions and
low sodium and chloride ions
• Normal saline given IV: Tends to remain in
extracellular compartment
• Glucose solution gets distributed throughout all
body compartments
• Pure water given IV: Causes massive hemolysis
(dangerous)
 Principles of Fluid Therapy
• Fluid replacement should be as close as possible
in volume and composition to those fluids lost
• Acute losses should be replaced quickly
• Chronic losses—replace with caution; rapid
infusion may cause fluid overload and heart
failure
– Better replaced by oral or rectal rehydration

– Mostly deficient in water: Do not overload with

sodium
 Fluid Therapy During
Operation
• Use salt solution – Normal saline or Ringer s
lactate
• Preload 1 L before spinal anesthesia
• Ketamine anesthesia does not need preloading
• Maintenance fluid 4mL/kg/hour
 Fluid Therapy During
Operation

• Replacement for the loss of fluid

• Blood loss replace with crystalloid 3 times the
volume of blood loss
• Blood loss more than 1 L consider giving
blood
– Desirable to have a hemoglobin minimum

8–9 mg after surgery

Intravenous Fluid
Therapy
 Estimation of Blood Loss
• Subjective
• Fully soaked and dripping mop – approximately
100 mL
• Monitor heart rate, blood pressure throughout the
operation
• Urine output – 0.5 mL/kg/hr considered adequate
fluid replacement
 Types of IV Fluids
• Crystolloids
– 5% dextrose in aqua
– 5% dextrose in NaCl
– Normal saline (NaCl)

– Hartman s solution

– Ringer s lactate solution

– Cholera saline

• Colloids
– Dextran 40, 70

– Gelatin preparations e.g., Haemacel

– Hetastarch, Pentastarch

Intravenous Fluid
Therapy
TRANSFUSI DARAH
 Pemberian Transfusi Darah
Pada Pasien
• Nilai ulang:
- check list pelaksanaan transfusi darah
- golongan darah pasien = donor ?
(tanyakan/peneng)
- identitas pasien tepat ?
- identitas donor dan golongan darah donor
- awasi selama dan setelah transfusi
(tanggung jawab dokter)
- awasi reaksi transfusi darah
Component/Product Composition Volume Indications

Whole Blood RBCs (approx. Hct 40%); plasma; 500 ml Increase both cell mass & plasma
WBCs; platelets volume (WBCs & platelets not
functional; plasma deficient in labile
clotting Factors V and VIII)

Red Blood Cells RBC (approx. Hct 75%); reduced 250 ml Increase red cell mass in symptom
plasma, WBCs, and platelets atic anemia (WBCs & platelets not
functional)

RBCs Leukocytes > 85% original volume of RBC; 225 ml Increased red cell mass; < 5 x 106WBCs
Reduced (prepa- < 5 x 106WBC; few platelets; to decrease the likelihood of febrile reac-
red by filtration) minimal plasma tions, immunization to leukocytes (HLA)
antigens) of CMV transmission

RBCs Washed RBCs (approx, Hct 75%); 180 ml Increase red cell mass; reduced risk of
< 5 x 108 WBCs; no plasma allergic reactions to plasma proteins

(Continued)
Component/Product Composition Volume Indications

Platelets Platelets (> 5.5 x 1010/unit); 300 ml Bleeding due to thrombocytopenia or

RBC; WBCs; plasma thrombocytopathy

Platelets Pheresis Platelets (> 3 x 1011); 300 ml Same as platelets;l sometimes HLA
RBCs; WBCs; plasma matched

FFP; FFP Donor Plasma; anticoagulation factors; 220 ml Treatment of some coagulation
Retested plasma; complement (no platelets)
Solvent/detergent-
Treated plasma

Cryoprecipitated Fibrinogen; Factors VIII and XIII;15 ml Deficiency of fibrinogen; Factor XIII;
AHF von Willebrand factor second choice in treatment of
hemophilia A, von Willebrand s disease

(Continued)
 Transfusi Trombosit

• Trombosit disimpan dalam kondisi digoyang terus

(Reciprocal agitator), pada suhu kamar (20˚C)
• Harus segera diberikan (tidak boleh disimpan di
kulkas/ di ruangan)
• Kecepatan cepat
• Gunakan infus set khusus (jangan menggunakan
set transfusi darah merah)
 Kebutuhan Trombosit
• Trombosit:
- dosis umumnya: 1 unit per 10 kg BB
(5-7 unit untuk orang dewasa)
- 1 unit meningkatkan 5000/mm3
(dewasa 70 kg)
- ABO-Rh typing saja, tak perlu cross
match, kecuali pada keadaan tertentu
 KEBUTUHAN PLASMA/FFP
• Dosis bergantung kondisi klinis dan penyakit
dasarnya
• Coagulation factor replacement:
10 – 20 ml/kg BB (= 4-6 unit pd dewasa)
• Dosis ini diharapkan dapat meningkatkan faktor
koagulasi 20 % segera setelah transfusi
• Plasma yang dicairkan (suhu 30 - 37º C) harus
segera ditransfusikan
• ABO-Rh typing saja (tak perlu cross match)

Transfusi Plasma
KEBUTUHAN KRIOPRESIPITAT

• Diencerkan pada suhu 30 – 37 C

• 1 unit akan meningkatkan fibrinogen 5
mg/dl pada dewasa
• Target hemostasis level: fibrinogen
> 100 mg %
• Segera transfusikan dalam 4 jam

Transfusi Kriopresipitat
 REAKSI REAKSI
TRANSFUSI DARAH
• Bila dilaksanakan pemeriksaan laboratorium
sebelum pemberian transfusi darah, mayoritas
transfusi darah tidak memberikan efek samping
kepada pasien

• Namun, kadang-kadang timbul reaksi pada

pasien, walaupun pemeriksaan laboratorium pra-
transfusi darah telah dilaksanakan dan hasilnya
COMPATIBLE
(= cocok antara darah resipien dan donor)

• Reaksi: reaksi RINGAN (suhu meningkat, sakit

kepala) s/d BERAT (reaksi hemolisis), bahkan
dapat meninggal
Reaksi Transfusi Darah
 KOMPLIKASI TRANSFUSI
DARAH
• Komplikasi LOKAL:
- kegagalan memperoleh akses vena
- fiksasi vena tidak baik
- masalah ditempat tusukan
- vena pecah saat ditusuk, dll

• Komplikasi UMUM:
- reaksi reaksi transfusi
- penularan/transmisi penyakit infeksi
- sensitisasi imunologis
- kemokromatosis

Komplikasi Transfusi Darah

 REAKSI TRANSFUSI DARAH

• Reaksi Tranfusi Darah AKUT:

hemolitik, panas, alergi, hipervolume,
sepsis bakteria, lung injury, dll

• Reaksi Transfusi Darah LAMBAT

 REAKSI REAKSI
REAKSI TRANSFUSI
TRANSFUSI DARAH
DARAH

• Yang paling sering timbul:

- reaksi febris
- reaksi alergi
- reaksi hemolitik
 REAKSI FEBRIS

• Nyeri kepala  menggigil dan gemetar

tiba tiba  suhu meningkat
• Reaksi jarang berat
• Berespon terhadap pengobatan
 REAKSI ALERGI

• Reaksi alergi berat (anafilaksis): jarang

• Urtikaria kulit, bronkospasme moderat,

edema larings: respon cepat terhadap
pengobatan
 REAKSI HEMOLITIK

• REAKSI YANG PALING BERAT

• Diawali oleh reaksi:
- antibodi dalam serum pasien >< antigen
corresponding pada eritrosit donor
- antibodi dalam plasma donor >< antigen
corresponding pada eritrosit pasien
• Reaksi hemolitik: - intravaskular
- ekstravaskular
 REAKSI HEMOLITIK
• REAKSI INTRAVASKULAR:
- hemolisis dalam sirkulasi darah
- jaundice dan hemogolobinemia
- antibodi IgM
- paling bahaya anti-A dan anti-B spesifik
dari sistem ABO
- fatal  akibat perdarahan tidak terkontrol
dan gagal ginjal
 REAKSI HEMOLITIK
• REAKSI EKSTRAVASKULAR:
- jarang sehebat reaksi intravaskular
- reaksi fatal jarang
- disebabkan antibodi IgG  destruksi
eritrosit via makrofag
- menimbulkan penurunan tiba triba
kadar
Hb s/d 10 hari pasca transfusi