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Shock

Def = an abnormality of the circulatory system that results in inadequate organ perfusion and
tissue oxygenation.
Hypovolemia is the cause of shock in most trauma patients

ATLS
Pathophysiology :
• Early circulatory responses to blood loss are com- pensatory and include progressive
vasoconstriction of cutaneous, muscle, and visceral circulation to preserve blood flow to
the kidneys, heart & brain.

• Response to acute circulating volume depletion associated with injury is an increase in


heart rate in an attempt to preserve cardiac output.

• Tachycardia is the earliest sign in most cases

• Release of endogenous catecholamines  increases peripheral vascular resistance 


increases diastolic blood pressure and reduces pulse pressure (but does little to increase
organ perfusion)

• In cellular level, compensation occurs by shifting to anaerobic metabolism, which results in


the formation of lactic acid and the development of metabolic acidosis.

• If shock is prolonged and substrate delivery for the gen- eration of adenosine triphosphate
(ATP) is inadequate, the cellular membrane loses the ability to maintain its integrity, and
the normal electrical gradient is lost
Hemorrhagic shock

• Hemorrhage is the most common cause of shock after injury, and virtually all
patients with multiple injuries have an element of hypovolemia.
• Hemorrhage is defined as an acute loss of circulating blood volume.
• Normal adult blood volume is approximately 7% of body weight.
Several confounding factors profoundly alter the classic hemodynamic response to an
acute loss of circulating blood volume :
• Patient’s age
• Severity of injury, with special attention to type and anatomic location of injury
• Time lapse between injury and initiation of treatment
• Prehospital fluid therapy
• Medications used for chronic conditions

Therapy :
• (A&B) Supplementary oxygen is provided to maintain oxygen saturation at greater than
95%.

• ( C ) Bleeding from external wounds usually can be controlled by direct pressure to the
bleeding site, although massive blood loss from an extremity may require a tourniquet.
Surgical or angiographic control may be required to control internal hemorrhage

• ( D ) Alterations in CNS function in patients who have hypotension as a result of


hypovolemic shock do not necessarily imply direct intracranial injury and may reflect
inadequate brain perfusion.

• ( E ) patient must be completely undressed and carefully exam- ined from head to toe to
search for associated injuries.
GASTRIC DILATION-DECOMPRESSION : In unconscious pa- tients, gastric distention
increases the risk of aspiration of gastric contents, which is a potentially fatal complication.
Gastric decompression is accomplished by intubating the stomach with a tube passed
nasally or orally and attaching it to suction to evacuate gastric contents.

UrinaryCatheterization :
Bladder catheterization allows for assessment of the urine for hematuria (indicating the
retroperitoneum may be a significant source of blood loss) and con- tinuous evaluation of
renal perfusion by monitoring urinary output.

INITIAL FLUID THERAPY :


Warmed isotonic electrolyte solutions, such as lactated Ringer’s and normal saline, are
used for initial resus- citation.

CROSSMATCHED, TYPE-SPECIFIC, AND TYPE O BLOOD

WARMING FLUIDS—PLASMA AND CRYSTALLOID

MASSIVE TRANSFUSION

COAGULOPATHY

CALCIUM
Nonhemorrhagic shock (cardiogenic)

• Myocardial dysfunction can be caused by blunt cardiac injury, cardiac


tamponade, an air embolus, or, rarely, a myocardial infarction associated with
the patient’s injury.
• All patients with blunt tho- racic trauma need constant electrocardiographic
(ECG) monitoring to detect injury patterns and dysrhythmias.
• FAST in the emergency department can identify pericardial fluid and the
likelihood of cardiac tamponade as the cause of shock.

Nonhemorrhagic shock (cardiac tamponade)

• Most commonly identified in penetrating thoracic trauma, but it can occur as


the result of blunt injury to the thorax.
• Tachycardia, muffled heart sounds, and dilated, engorged neck veins with
hypotension resistant to flu- id therapy suggest cardiac tamponade.
• Tension pneumothorax can mimic cardiac tamponade, but it is differentiated
from the latter condition by the findings of absent breath sounds, tracheal
deviation, and a hyperresonant percussion note over the affected hemithorax.
• Best managed by thoracotomy
Nonhemorrhagic shock (tension pneumothorax)

• Air enters the pleural space, but a flap-valve mechanism prevents its escape.
Acute respira- tory distress, subcutaneous emphysema, absent breath sounds,
hyperresonance to percussion, and tracheal shift supports the diagnosis
• Immediate thoracic decompression without waiting for x-ray confirmation of
the diagnosis.

Nonhemorrhagic shock (cardiac tamponade)

• Classic sign : hypotension without tachycardia or cutaneous vasoconstriction.


• Should be treated initially for hypovolemia.
• The failure of fluid resuscitation to restore organ perfusion suggests either
continuing hemorrhage or neurogenic shock.

Nonhemorrhagic shock (septic shock)

• Uncommon
• Difficult to distinguish from those in hypovolemic shock, as both groups can
manifest tachycardia, cutaneous vasoconstriction, impaired urinary output,
decreased systolic pressure, and narrow pulse pressure.