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Hypovolemic Shock
Hypovolemic Shock
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).
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.
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
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.