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    Guia Implementacion Iso45001

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    karelly molina
    Hypovolemic shock results from inadequate organ perfusion due to a reduction in circulating blood volume. It can be caused by hemorrhage, sepsis, trauma, or gastrointestinal accidents. Clinical signs may include depression, tachycardia, tachypnea, and reduced gastrointestinal sounds. Treatment focuses on rapid volume replacement with crystalloids or colloids to restore perfusion, as well as inotropes if needed. Goals are to maintain blood pressure and tissue oxygenation through normalization of physical parameters.

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    Guia Implementacion Iso45001

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    karelly molina
    10 views3 pages
    Hypovolemic shock results from inadequate organ perfusion due to a reduction in circulating blood volume. It can be caused by hemorrhage, sepsis, trauma, or gastrointestinal accidents. Clinical signs may include depression, tachycardia, tachypnea, and reduced gastrointestinal sounds. Treatment focuses on rapid volume replacement with crystalloids or colloids to restore perfusion, as well as inotropes if needed. Goals are to maintain blood pressure and tissue oxygenation through normalization of physical parameters.

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    Shock

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    Hypovolemic shock results from inadequate organ perfusion due to a reduction in circulating blood volume. It can be caused by hemorrhage, sepsis, trauma, or gastrointestinal accidents. Clinical signs may include depression, tachycardia, tachypnea, and reduced gastrointestinal sounds. Treatment focuses on rapid volume replacement with crystalloids or colloids to restore perfusion, as well as inotropes if needed. Goals are to maintain blood pressure and tissue oxygenation through normalization of physical parameters.

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    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    10 views3 pages

    Guia Implementacion Iso45001

    Uploaded by

    karelly molina
    Hypovolemic shock results from inadequate organ perfusion due to a reduction in circulating blood volume. It can be caused by hemorrhage, sepsis, trauma, or gastrointestinal accidents. Clinical signs may include depression, tachycardia, tachypnea, and reduced gastrointestinal sounds. Treatment focuses on rapid volume replacement with crystalloids or colloids to restore perfusion, as well as inotropes if needed. Goals are to maintain blood pressure and tissue oxygenation through normalization of physical parameters.

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    of 3

    Shock, Hypovolemic

    BASIC INFORMATION  ETIOLOGY AND PATHOPHYSIOLOGY  Gastrointestinal accidents (large


    • Etiology colon volvulus, gastric rupture)
    DEFINITION  Severe hemorrhage (guttural pouch (Figure 1)
    mycosis, uterine artery rupture,  Hyperthermia (endurance rides,
    A reduction in perfusion that results in
    inadequate organ perfusion and tissue trauma) long distance hauling)
    oxygenation
     Sepsis (neonatal septicemia, entero- • Pathophysiology
    colitis, metritis, pleuritis)  Reduced tissue perfusion caused by

    CLINICAL PRESENTATION a decrease in circulating volume


    DISEASE FORMS/SUBTYPES
    • Hemorrhagic
    • Maldistributive (sepsis, endotoxemia)
    • Traumatic
    HISTORY, CHIEF COMPLAINT
    • Ataxia, collapse
    • History of observed trauma
    • Weak, inappetent foals, often after
    dystocia
    • History of overt hemorrhage or recent
    foaling
    • Anorexia, colic, or signs of abdominal
    pain
    • Increased respiratory rate or labored
    breathing
    PHYSICAL EXAM FINDINGS  Physical
    examination findings may be normal in
    early, compensated shock.
    • Depression, stupor
    • Tachycardia, bright-red mucous mem-
    branes (progressing to purple), poor
    pulse quality, physiologic murmurs
    • Tachypnea, crackles, pleural friction
    rubs
    • Reduced gastrointestinal borborygmi FIGURE 1  Hyperemic mucous membranes in a horse with a gastric rupture demonstrating
    • Hyperthermia or hypothermia hypovolemic shock caused by dehydration, systemic inflammation, and endotoxemia.
    Shock, Hypovolemic 525

    decreases the delivery of oxygen to TREATMENT   Oxyglobin (5–30 mL/kg, <10 


    tissues. mL/kg/h)
     Decreased circulating volume may  Side effects include increased
    THERAPEUTIC GOAL(S)
    result from loss of fluid (hemor- Restore tissue perfusion and oxygenation vascular resistance, formation
    rhage) or a relative decrease in of free radicals, methemoglo-
    volume (sepsis and endothelial dis- ACUTE GENERAL TREATMENT binemia, and fluid overload
    ruption, causing vascular leak • Cardiovascular support
    syndrome). DRUG INTERACTIONS
     Volume replacement
     Local hypoxia results in the conver- Calcium-containing crystalloid solutions
     Shock-dose crystalloid fluids
    sion to anaerobic metabolism for  Hypotensive resuscitation recom-
    may interfere with citrated blood
    energy production, with metabolic mended in uncontrolled hemor- transfusions.
    acids (lactate) as a byproduct. rhage
     Severe blood loss (>40% of circulat- POSSIBLE COMPLICATIONS
     Maintains hemostasis at the
    ing volume) or hypovolemia with site of hemorrhage; does not • Hypovolemia may lead to develop-
    severe hypotension (mean pres- dilute coagulation factors ment of the systemic inflammatory
    sures, 30–40 mm Hg) may lead to  Administer fluids at a 1 to 2 : 1
    response syndrome and multiorgan
    irreversible shock and death caused ratio to volume of blood lost. dysfunction (renal, pulmonary, cere-
    by:  Maintain a mean blood pres-
    bral, cardiac or hepatic dysfunction).
     Cellular dysfunction and death • Interstitial edema may result from
    sure of 60 mm Hg.
    from free radical production  May also delay fluid admi­ overaggressive fluid therapy or endo-
     Activation of the inflammatory thelial compromise, which may inhibit
    nistration until hemorrhage
    and coagulation cascades stopped if vasopressor support oxygen diffusion into tissues.
     Endothelial disruption permitting • Conservative fluid management is
    is provided
    endotoxemia and bacterial trans-  Colloids are recommended to required for congestive heart failure.
    location prolong fluid effects and as • May require earlier transfusions to
    therapy for vascular leakage. support oxygenation.
     Plasma (>1 L) may provide coag-
    • Maintain cerebral perfusion pressure
    DIAGNOSIS  ulation factors, fibronectin to with head trauma without fluid over-
    reduce endotoxemia, and antiin- load
    DIFFERENTIAL DIAGNOSIS flammatory protein C.
     Hypertonic saline

     Mannitol
    • Cardiogenic  Positive ionotropes are recom-
    • Hypoxic mended if volume resuscitation is
    • Anaphylactic RECOMMENDED MONITORING
    inadequate.
    • Neurogenic  Central venous pressure should
    Repeat physical examinations, arterial
    be 3 to 12 cm H2O in foals and blood pressure, central venous pressure,
    INITIAL DATABASE up to 24 cm H2O in adults lactate, arterial and venous blood gas,
    Hematocrit and hemoglobin may be  Dobutamine (2–15 µg/kg/min urine output, colloid oncotic pressure,
    normal in early hemorrhagic conditions. IV) cardiac output
    • Complete blood count  Dopamine (2–15 µg/kg/min IV)
    • Packed cell volume (PCV) and total  Vasopressors only if fluids and ion-
    protein otropes are unsuccessful or for
    PROGNOSIS AND
    • Serum chemistry delayed resuscitation OUTCOME 
    • Blood pressure  Norepinephrine (0.5 µg/kg/min
    • Colloid oncotic pressure IV) Depend on the success of treat-
    • Serum lactate  Vasopressin (0.3–1 µg/kg/min ment of the primary cause and
    • Coagulation profile IV): High doses of vasopressors rapid resolution of hypovolemic shock
    may reduce splanchnic perfusion through normalization of physical
    ADVANCED OR CONFIRMATORY • Oxygen supplementation (5–15 L/ parameters
    TESTING min)
    • Central venous pressure: Negative  Indicated with low PaO2 (<70 
    values may indicate hypovolemia (ref- mm Hg), PvO2 (<35 mm Hg), and PEARLS &
    erence range, 2–15 cm H2O) high lactate (>4 mmol/L) CONSIDERATIONS 
    • Ultrasonography of the abdomen or  Supplementation for low hemo­
    thorax (for specific infections, sus- globin concentrations may be Goal-directed early manage-
    pected rupture, or hemorrhage) detrimental; induces temporary ment is key to reducing mortal-
    • Abdominocentesis or thoracocentesis vasoconstriction ity from shock with goals of:
    to identify free fluid • Control of hemorrhage and PCV • Mean arterial pressure of 60 to
    • Coagulation profiles to monitor for  Surgical hemostasis 70 mm Hg
    disseminated intravascular coagulation  Therapy for DIC • Normal urine production
    (DIC)  Hemoglobin replacement: Recom- • Pink mucous membranes with a capil-
    • Endoscopy to identify guttural pouch mended for hemoglobin concentra- lary refill of less than 3 seconds
    mycosis tion below 7 g/dL, PCV below 15%, • Warm extremities
    • Cortisol levels and response to an and lactate above 4 mmol/L • Normal central venous pressures
    adrenocorticotropic hormone stimula-  Blood transfusion • Normalization of arterial and venous
    tion test to monitor appropriate endo-  Autotransfusion of blood in body oxygen
    crine response cavities • Blood lactate below 2 mmol/L
    • Cardiac output monitoring: Lithium  Hemoglobin-based fluids • Normalization of blood glucose
    dilution, echocardiography
    526 Shock, Hypovolemic Sinoatrial Block and Sinus Arrest

    SUGGESTED READING editors: Equine emergencies: treatment acute blood loss in horses. J Am Vet Med
    and procedures, St Louis, 2008, Saunders Assoc 229(9):1458–1462, 2006.
    Driessen B, Brainard B: Fluid therapy for the
    Elsevier, pp 544–552.
    traumatized patient. J Vet Emerg Crit Care AUTHOR: AMELIA MUNSTERMAN
    Magdesian KG, Fielding CL, Rhodes DM, et al:
    16(4):276–299, 2006.
    Changes in central venous pressure and EDITORS: R. REID HANSON and AMELIA
    Divers TJ: Shock and systemic inflammatory
    blood lactate concentration in response to MUNSTERMAN
    response syndrome. In Orsini JA, Divers TJ,

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