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Hypovolemic Shock

Definition
Hypovolemic shock refers to a medical or surgical condition in which rapid fluid loss results in multiple organ failure due to inadequate
perfusion. It is defined as approximately 1 Liter or 1/5 loss of circulating volume).
The following is the sequence of events that under perfused tissue goes through:

Profound ischemia for unperfused tissue causes a switch to anaerobic metabolism  leads to Lactic Acid waste  decreased ATP to
be available for cell work The cell membrane cannot function and it dies This causes release of intracellular enzymes and
inflammatory mediators  widespread destruction on the Lungs, Kidneys, Digestive Tract, Capillary Lining and Coagulation.

Risk Factors
1. Age
 Pediatric
 smaller total blood volumes
 The kidneys of children younger than 2 years are not mature
 the body surface area is increased relative to the weight, allowing for rapid heat loss and early hypothermia, possibly leading to
coagulopathy.
 Elderly
 altered physiology and preexisting medical conditions that may severely impair their ability to compensate for acute blood loss.
 less able to mount a tachycardia in response to decreased stoke volume because of decreased beta-adrenergic receptors in the
heart
 The kidneys also undergo age-related atrophy, and many older patients have significantly decreased creatinine clearance in the
presence of near-normal serum creatinine. Concentrating ability may be impaired by a relative insensitivity to antidiuretic
hormone.
2. Patient with Heart Disease
3. Patient with Kidney Disease

Epidemiology
Most often, hypovolemic shock is secondary to rapid blood loss (hemorrhagic shock).

Stages in Hypovolemic Shock:


1. Compensated: The body is still able to compensate for the decrease in perfusion.
a)Baroreceptor reflexes induce "sympathetic" vasoconstriction to increase blood vessel. Local hypoxic vasoconstriction also
assists, a little bit, in elevating b.p.
b)The renin-angiotensin system is activated (ANG-II causes peripheral vasoconstriction). Vasoconstriction increases the
resistance to bloodflow. In addition, ANG-II stimulates the release of antidiuretic hormone (ADH) from the posterior pituitary,
to increase reabsorption of water in the distal tubules and collecting ducts of the kidney. Thus, ADH will either increase b.p.
or help to slow the decline in b.p. Fluids will be absorbed from the gastrointestinal tract at a faster rate in an attempt to
increase b.p.
c)We may also see a CNS ischemic response from the vasomotor center (cardiovascular center) if mean arterial pressure
drops below 60 mmHg (mean arterial pressure in the systemic system: 90 to 95 mmHg. The CNS ischemic response
causes massive vasoconstriction via activation of the sympathetic nervous system in a last ditch effort to maintain b.p. and
kidney and brain function.

2. Uncompensated: The body’s compensation mechanisms are starting to fail.


a)Because of the lack of nutrients and oxygen arriving at the myocardium, cardiac activity is being depressed. The heart is
already hypoxic and sympathetic vasoconstriction of the coronary arteries makes the situation worse (even less oxygen to
the myocardium). The vasomotor center (cardiovascular center) eventually fails because it is not getting enough oxygen due
to restricted central blood flow resulting from sympathetic vasoconstriction in early shock (in the first 10-15 min).
b)With reduced tissue perfusion and exchange, we begin to see thrombosis in small vessels due to increased acid from the
tissues. This increase in acid (decrease in pH) causes circulating cells to agglutinate/clot.
c)Should prolonged hypoxia occur (hours), increased capillary fluid permeability ensues and fluid begins to transude from the
capillaries.
d)As the gut attempts to increase fluid reabsorption we see enhanced endotoxin absorption in the gut.
e)As blood flow continues to decline, we see generalized cellular deterioration and tissue necrosis.
f) Despite all this, it is still possible to retrieve this patient.

3. Irreversible: Cell and tissue ischemia leads to organ death due to lack of perfusion.
With lack of myocardial nutrition and severe depletion of ATP, the deterioration of the myocardium is extensive and
irreversible. Due to acidosis, we see extensive and irreversible clotting in the capillary beds and widespread tissue necrosis.
Under such circumstances, the patient should be re-evaluated to determine whether some reversible causes of the persistent
shock may have been overlooked.

Causes of Hypovolemic Shock:


 Hemorrhage
 Laceration of a vein or artery  Fractured femur (may be associated with 500-1000cc blood
 Open wounds loss)
 Fractured pelvis (may be associated with 1500cc blood  Upper/Lower GI Bleed
loss)  Pnuemo/Hemothorax
 Saline or Combined Saline/Water Loss
 Gastrointestinal losses (vomiting, diarrhea)  Excessive sweating
 High Fever  Diuretics
 Third Spacing (Fluid shifts):
 Soft tissue trauma  Ascites (effusion & accumulation of serous fluid in
 Sepsis abdominal cavity)
 Peritonitis (intestinal obstruction)  Burn injuries
 Other causes of hypovolemic shock include:
 Inadequate fluid administration (even if the patient clinically  Adrenal insufficiency
appears to be overloaded with fluid)  Hypothermia
 Inadequate ventilation or oxygenation  Hypocalcemia

Symptoms
• Anxiety or agitation • Pale skin color (pallor)
• Cool, clammy skin • Rapid breathing
• Confusion • Sweating, moist skin
• Decreased or no urine output • Unconsciousness
• General weakness

Differential Diagnosis

Diagnostic Criteria
1. history taking
history of illness (cardiac, renal, GI problem, etc), history of trauma, some patients may report fatigue, generalized lethargy, or
lower back pain (ruptured abdominal aortic aneurysm), etc.
2. physical examination
 low blood pressure  weakness
 low body temperature  decreased urine output
 rapid pulse  check for any hemorrhage
 pale  etc
3. lab examination
CBC prothrombin time, activated partial thromboplastin time
electrolyte levels (eg, Na, K, Cl, HCO3, BUN, creatinine, urinalysis (in patients with trauma)
glucose levels), urine pregnancy test.
increased lactate
4. Imaging
 ultrasonographic examination in the ED if an abdominal aortic aneurysm is suspected.
 If GI bleeding is suspected, a nasogastric tube should be placed.
 An upright chest radiograph should be obtained if a perforated ulcer or Boerhaave syndrome is a possibility.
 Endoscopy can be performed (usually after the patient has been admitted) to further delineate the source of bleeding.
 A pregnancy test should be performed in all female patients of childbearing age
 If thoracic dissection is suspected because of the mechanism and initial chest radiographic findings, the workup may include
transesophageal echocardiography, aortography, or CT scanning of the chest.
 If a traumatic abdominal injury is suspected, a focused abdominal sonography for trauma (FAST) ultrasonography examination
may be performed in the stable or unstable patient. Computed tomography (CT) scanning typically is performed in the stable
patient.
 If long-bone fractures are suspected, radiographs should be obtained.

Possible Complication
 Kidney damage  Heart attack
 Brain damage  Severe shock can lead to death
 Gangrene of arms or legs, sometimes leading to amputation

Management
• Keep the person comfortable and warm (to avoid hypothermia).
• Have the person lie flat with the feet lifted about 12 inches to increase circulation (shock position). However, if the person has a head,
neck, back, or leg injury, do not change the person's position unless he or she is in immediate danger.
• Do not give fluids by mouth.
• If person is having an allergic reaction, treat the allergic reaction
• If the person must be carried, try to keep him or her flat, with the head down and feet lifted. Stabilize the head and neck before
moving a person with a suspected spinal injury.
• IV Therapy  fluid replacement
• Establish and maintain open airway
 Targeting O2 delivery to vital organs rather then a specific B/P or heart rate  supplemental oxygen, ventilation if needed
 Re-establishing circulation with Vasopressors & Inotropic agents  increasing blood pressure
 Blood component therapy
 Monitor mental status, skin color, blood gases, hemoglobin, urine output, electrolytes and Lactic Acid levels
 Heart monitoring, including Swan-Ganz catheterization
 Urinary catheter

Fluid Replacement Choices:


 Conventional “crystal”loids include both balanced salt solutions (BSS) and hypotonic salt solutions. Balanced salt solutions include
such fluids as 0.9% NaCl (normal saline), and Ringer's Lactate solutions. These solutions are characterized by having an electrolyte
composition or calculated osmolality approximating that of plasma (isotonic).
 Colloid solutions are solutions of proteins, starches, dextrans, and gelatins containing molecules sufficiently large enough so that
they do not normally cross capillary membranes. Under normal conditions most of the administered volume remains in the
intravascular space (unless tissue is damaged and then it can cross membranes). Once colloids have leaked into the interstitium,
they must be removed by the lymphatic system or they will exert a reverse pressure gradient, drawing water from the vascular space.
The removal of colloids from the interstitium is typically much slower than that of crystalloids.

Blood Component Therapy:


 Packed Red Blood Cells
 Platelets - Platelet transfusion therapy after massive transfusion is an accepted intervention in the presence of micro-vascular
bleeding prior to documentation of thrombocytopenia. The platelet transfusion dose recommended is 1 unit per 10 kg body weight for
platelet counts <50,000 or when platelet dysfunction is suspected.
 Plasma – Plasma (FFP) transfusion therapy should be instituted after laboratory confirmation of coagulation factor
deficiencies. The recommended dose is 10-15 mL/kg body weight for PT/PTT>1.5 normal range.
 Cryoprecipitate - Cryoprecipitate therapy should be instituted for the correction of laboratory evidence of hypo-fibrinogenemia
(fibrinogen <100 mg/dl). Dosing will depend on the degree of hypo-fibrinogenemia and the patient’s weight. For an average size
adult, 6-unit pool for fibrinogen levels between 50-100 mg/dl and 12-unit pool for fibrinogen levels <50 mg/dl.

Re-establishing Circulation:
 Norepinephrine:
Secreted by nerve cells,
potent alpha adrenoceptor agonist and is therefore a strong vasoconstrictor, increasing systolic and diastolic blood pressures.
In addition, Norepinephrine stimulates beta 1 cells so it increases both heart rate and contractility.

 Epinephrine:
A hormone secreted by the adrenal medulla.
Epinephrine is used intravenously during advanced cardiac life support and may also be used to treat other conditions, including
anaphylactic shock and acute, severe asthma unresponsive to normal treatment.
potent alpha and beta adrenoceptor agonist, it is also a powerful vasoconstrictor with both positive inotropic, and chronotropic effects.
Epinephrine causes increased heart rate, increased force of contraction, an increase in cardiac output, and increased systolic blood
pressure.

 Dopamine:
 A neurotransmitter, precursor of norepinephrine and epinephrine.
 indicated in the treatment of shock due to myocardial infarction, trauma, septicemia, open-heart surgery, renal failure, and chronic
cardiac decompensation.
 directly stimulates dopaminergic receptors, alpha and beta adrenoceptors, and it indirectly causes the release of endogenous
norepinephrine.
 At low doses (l to 5mcg/kg/minute), dopamine directly stimulates dopaminergic receptors on arteries in the kidneys, abdomen, heart,
and brain and causes vasodilatation. At these doses, urine output may increase, but blood pressure and heart rate are usually not
affected.
 As the dose is increased (5 to 10 mcg/kg/min), dopamine stimulates beta 1 adrenoceptors, resulting in positive inotropic and
chronotropic effects, which increases myocardial contractility, and heart rate, which results in, enhanced cardiac output.
 At higher doses (greater than 10 mcg/kg/min), dopamine exerts effects primarily alpha-receptors, and extensive vasoconstriction
causes blood pressure to increase.

 Vasopressin
an antidiuretic hormone indicated to inhibit diuresis in patients with diabetes insipidus.
at higher doses, vasopressin causes vasoconstriction.
Because there is a fair amount of evidence to support its effectiveness as a vasopressor, vasopressin is now considered as an
alternative to epinephrine for the treatment of adult shock-refractory ventricular fibrillation during advanced cardiac life support.
vasoconstriction arises from vasopressin's actions on vasopressin receptors. Vasopressin receptors are classified as V-1 and V-2
receptors. V-1 receptors are located on arterial smooth muscle, and V-2 receptors are found in renal tubules. It is Vasopressin's
interaction with V-1 receptors that is responsible for its potent vasopressor effects.

Prevention
 Quickly treating the cause will reduce the risk of developing severe shock.
 Early first aid can help control shock.