Shock: Mazen Kherallah, MD, FCCP
Shock: Mazen Kherallah, MD, FCCP
Shock: Mazen Kherallah, MD, FCCP
Mazen Kherallah, MD, FCCP Internal Medicine, Infectious Disease and Critical Care Medicine
First Step
Recognize its Presence
Shock Syndromes
Cardiogenic
Hypovolemic
Distributive
Obstructive
LVF
Hemorrhagic Nonhemorrhagic
Septic
P. Embolism
Arrhythmias
Neurogenic
Pneumothorax
Adrenal
Aortic Stenosis
Second Step
Identify the Probable Causes
Treatment should be initiated simultaneously with the identification of probable cause of the shock state
Tachycardia and cutaneous vasoconstriction are the usual and early physiologic response to volume loss Tachypnea Narrowed pulse pressure Hypotension when patients blood volume loss is more than 30% Hematocrit or hemoglobin concentration are not reliable
Nonhemorrhagic Shock
Cardiogenic Shock
Nonhemorrhagic Shock
Tension Pneumothorax Acute respiratory distress Subcutaneous emphysema Absent breath sounds Hyperresonance to percussion Tracheal shift
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
Nonhemorrhagic Shock
Septic Shock
Uncommon after injury May occur if patients 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
The patients 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
Blood pressure Normal Pulse pressure Respiratory rate Urine output (ml/h) CNS/mental status Fluid replacement Normal 14-20 >30 Slightly anxious Crystalloid
Obligatory edema
Airway and breathing Circulation: Hemorrhage control Disability: Neurologic examination Exposure: Complete examination Gastric dilatation: decompression Urinary catheter insertion
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 patients condition permits
Ringers 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
Blood pressure Normal Pulse pressure Respiratory rate Urine output (ml/h) CNS/mental status Fluid replacement Normal 14-20 >30 Slightly anxious Crystalloid
Blood pressure Pulse pressure Pulse rate Central nervous system status Skin circulation Changes in central venous pressure line Changes in PCWP and cardiac 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
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
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
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 typespecific is not available
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
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
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
Most patients receiving blood transfusion do not need calcium supplementation Excessive calcium supplementation may be harmful