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Shock Mazen Kherallah, MD, FCCP Internal Medicine, Infectious Disease and Critical Care Medicine
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First Step Recognize its Presence
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No Laboratory Test Diagnoses Shock
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Shock Syndromes CardiogenicHypovolemicDistributiveObstructive LVF Arrhythmias Hemorrhagic Non- hemorrhagic Septic Neurogenic Adrenal P. Embolism Pneumothorax Aortic Stenosis
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Clinical Appreciation of the Presence of Inadequate Organ Perfusion and Tissue Oxygenation
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Second Step Identify the Probable Causes
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Traumatized and Shocked Patients Hypovolemic shock Cardiogenic shock Neurogenic shock Septic shock
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Treatment should be initiated simultaneously with the identification of probable cause of the shock state
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Hemorrhage is the most common cause of shock in the injured patient
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I. Initial Patient Assessment Recognition of Shock Tachycardia and cutaneous vasoconstriction are the usual and early physiologic response to volume loss Tachypnea Narrowed pulse pressure Hypotension when patient’s blood volume loss is more than 30% Hematocrit or hemoglobin concentration are not reliable
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I. Initial Patient Assessment Recognition of Shock Tachycardia Greater than 160 in infant Greater than 140 in preschool age child Greater than 120 in school age child Greater than 100 in an adult
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I. Initial Patient Assessment Recognition of Shock Unable to produce Tachycardia Limited cardiac response to catecholamine stimulation: elderly Concurrent use of beta-adrenergic blocking agents The presence of a pacemaker
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I. Initial Patient Assessment Clinical Differentiation of Etiology of Shock Hemorrhagic Shock The most common cause of shock after injury All patients with multiple injuries have an element of hypovolemia Most patients with nonhemorrhagic shock state respond partially or briefly to volume resuscitation All patients with shock should initially be treated with volume replacement
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I. Initial Patient Assessment Clinical Differentiation of Etiology of Shock Nonhemorrhagic Shock Cardiogenic shock Tension pneumothorax Neurogenic shock Septic shock
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Nonhemorrhagic Shock Cardiogenic Shock Blunt cardiac injury Cardiac tamponade Air embolus Myocardial infarction
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Nonhemorrhagic Shock Tension Pneumothorax Acute respiratory distress Subcutaneous emphysema Absent breath sounds Hyperresonance to percussion Tracheal shift
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Nonhemorrhagic Shock Neurogenic Shock Isolated intracranial injuries do not cause shock Spinal cord injury may produce hypotension due to loss of sympathetic tone Hypotension without tachycardia or cutaneous vasoconstriction
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Nonhemorrhagic Shock Septic Shock Uncommon after injury May occur if patient’s arrival to ER is delayed several hours Penetrating abdominal injuries and contamination of the peritoneal cavity with intestinal contents Normal circulating volume, modest tachycardia, warm and pink skin, and a wide pulse pressure
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II. Hemorrhagic Shock in the Injured Patient Definition of Hemorrhage Acute loss of circulating blood volume Normal adult blood volume is 7% of body weight Normal pediatric blood volume is 8-9% of the body weight Calculation is based on ideal body weight
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II. Hemorrhagic Shock in the Injured Patient Direct Effect of Hemorrhage The distinction between classes may not be apparent in an individual patient Volume replacement should be directed by the response to initial therapy rather than by relying solely on the initial classification Several confounding factors profoundly alter the classic hemodynamic response
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Confounding Factors that alter the Classic Hemodynamic Response The patient’s age Severity of the injury Type and anatomical location of the injury Time lapse between injury and initiation of treatment Prehospital therapy Medication used for chronic conditions
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Classification of Hemorrhagic Shock
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II. Hemorrhagic Shock in the Injured Patient Fluid Changes Secondary to Soft Tissue Injury Blood loss at the site of injury: –Fractured tibia: 750 ml of blood loss –Fractured femur: 1500 ml of blood loss –Retroperitneal hematoma: several liters Obligatory edema
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III. Initial Management of Hemorrhagic Shock Physical Examination Airway and breathing Circulation: Hemorrhage control Disability: Neurologic examination Exposure: Complete examination Gastric dilatation: decompression Urinary catheter insertion
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Contraindication to Insertion of Transurethral catheter prior to Radiological confirmation of an intact Urethra Blood at the urethral meatus High-riding, mobile, or nonpalpable prostate
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III. Initial Management of Hemorrhagic Shock Vascular Access Lines Must be obtained promptly Two large-caliber (minimum of 16 gauge) peripheral intravenous catheters Large-caliber, central venous access Central lines should be changed in more controlled environment as soon as patient’s condition permits
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III. Initial Management of Hemorrhagic Shock Initial Fluid Therapy Ringer’s lactate solution is the initial fluid of choice Normal saline is the second choice Normal saline has the potential of causing hyperchloremic acidosis Initial fluid bolus is given as rapidly as possible, 1-2 liters for an adult and 20 mg/kg for pediatric patient “3 for 1 rule”: each mL of blood loss is replaced with 3 mL of crystalloid fluid
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Estimated Fluid and Blood Losses
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IV. Evaluation of Fluid Resuscitation and Organ Perfusion General Blood pressure Pulse pressure Pulse rate Central nervous system status Skin circulation Changes in central venous pressure line Changes in PCWP and cardiac output
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IV. Evaluation of Fluid Resuscitation and Organ Perfusion Urinary Output Adequate volume replacement should produce a urinary output of approximately 0.5 mL/kg/hour in the adult One mL/kg/hour is an adequate urinary output for the pediatric patients 2 mL/kg/hour for children under 1 year of age
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IV. Evaluation of Fluid Resuscitation and Organ Perfusion Acid/Base Balance Respiratory alkalosis followed by metabolic acidosis is seen in patients with early hypovolemic shock Severe metabolic acidosis may develop from long-standing shock Persistent acidosis is due to inadequate resuscitation or ongoing blood loss
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V. Response to Initial Fluid Resuscitation 2000 mL Ringer’s lactate in adults or 20 mL/kg bolus in children
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VI. Blood Replacement Packed Red Blood Cells Versus Whole Blood Therapy Restore the oxygen-carrying capacity of the intravascular volume Either whole blood or packed red cells can be used. Component therapy is used to maximize blood product availability
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VI. Blood Replacement Crossmatched, Type-specific, and Type O Blood Crossmatched blood is preferable but it requires approximately 1 hour to be completed: should be used for patients who stabilize rapidly Type-specific blood can be provided in 10 minutes: this blood is compatible with ABO an Rh blood types Type O blood can be used in patients with exanguinating hemorrhage when type- specific is not available
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VI. Blood Replacement Warming Fluids-Plasma and Crystalloid In patients receiving massive volume of crystalloid, heat the fluid to 39 C before using it to prevent hypothermia Storage of crystalloids in a warmer with the use of microwave oven Blood products cannot be warmed in the microwave ovenbut can be heated with the passage through intravenous fluid warmer
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VI. Blood Replacement Autotransfusion Patients with a major hemothoarax Sterile collection of blood through standard tube thoracotomy collection devices Anticoagulation with sodium-citrate solution, not heparin Retransfusion of shed blood
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VI. Blood Replacement Coagulopathy Dilution of platelets and clotting factors Averse effect of hypothermia on platelets aggregation Release of tissue thromboplastin by the damaged neural tissue in patients with closed head injury
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VI. Blood Replacement Calcium Administration Most patients receiving blood transfusion do not need calcium supplementation Excessive calcium supplementation may be harmful
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