2 Shock Recognition and Resuscitation

How shock develops

Shock is inadequate tissue perfusion and oxygen delivery, or impaired oxygen use, causing cellular dysfunction and, if uncorrected, organ failure. Oxygen delivery depends chiefly on cardiac output and the blood’s oxygen content. A fall in circulating volume, cardiac pumping, vascular tone, or unobstructed blood flow can therefore produce shock, and more than one mechanism may be present after trauma.

Blood pressure alone is not a reliable measure of perfusion. Compensation can preserve blood pressure early even while tissue hypoperfusion is developing, and hypotension can also have causes other than shock. Interpret the whole clinical picture and its trend.

Recognizing shock patterns

The main shock patterns reflect different problems, but categories can overlap. After spinal injury, for example, bleeding may also be present; assess for hemorrhage before attributing hypotension to neurogenic shock.

• Hypovolemic shock: Too little circulating volume reduces venous return, stroke volume, and cardiac output. Trauma-related causes include external or concealed bleeding. Common clues include tachycardia, narrow pulse pressure, cool or clammy skin, weak pulses, delayed capillary refill, and later hypotension.

• Obstructive shock: Mechanical impairment of cardiac filling or blood flow. Consider tension pneumothorax or cardiac tamponade when shock accompanies compatible chest findings or fails to improve as expected.

• Cardiogenic shock: The heart cannot pump effectively. Myocardial contusion, infarction, or arrhythmia may be responsible; suspect this pattern when poor perfusion occurs with evidence of cardiac dysfunction. Fluids may worsen some cases.

• Distributive shock: Abnormally low vascular tone causes blood maldistribution and relative hypovolemia. Neurogenic shock after spinal cord injury may cause hypotension with an inappropriately slow heart rate and warm skin. Sepsis and anaphylaxis can also cause distributive shock.

Assessing perfusion and trends

Assess repeatedly for changes in mental status; heart rate and pulse quality; skin temperature and color; capillary refill; respiratory pattern; blood pressure and pulse pressure; and urine output when available. Anxiety or confusion, cool mottled extremities, delayed refill, tachycardia, and decreasing urine output can signal impaired perfusion before marked hypotension appears. These signs are not specific: pain, cold exposure, medications, and brain injury can affect them.

The shock index is calculated as

A rising or elevated shock index can support concern for circulatory compromise, but cannot rule shock in or out by itself. Measure lactate and base deficit when available, and follow their trends alongside examination and vital signs. Lactate can reflect hypoperfusion but has other causes; an initially normal hemoglobin does not exclude acute blood loss.

For example, a patient with significant blunt trauma has a heart rate of $118$ beats/min and systolic pressure of $105$ mmHg, giving a shock index of about $1.1$. Even without hypotension, this finding—combined with cool skin or worsening mentation—should prompt urgent evaluation for bleeding and other causes of shock, rather than reassurance based on the blood-pressure number alone.

Resuscitating and treating the cause

Resuscitation should address immediate threats while treating the underlying cause. Use the trauma primary survey, control compressible external bleeding, and rapidly arrange definitive control of suspected internal bleeding. Do not delay hemorrhage control for tests that will not change immediate management.

Support circulation and activate local major-hemorrhage procedures when indicated. For suspected life-threatening blood loss, prioritize early blood-component resuscitation under the local protocol rather than repeated large crystalloid boluses. Warm the patient and blood products, and monitor and correct coagulopathy, acidosis, and hypocalcemia during major transfusion. As results and the clinical situation allow, transition from protocol-based transfusion to laboratory- or viscoelastic-guided treatment.

Use fluid and blood-pressure targets appropriate to the injury. In selected bleeding patients without brain injury, restricted-volume resuscitation may limit worsening hemorrhage until bleeding is controlled. It is not appropriate when it risks inadequate brain perfusion, including in significant traumatic brain injury; follow applicable trauma protocols and individualize targets.

Treat nonhemorrhagic causes directly: relieve obstructive causes urgently, address cardiac dysfunction and rhythm problems, and manage distributive causes. Fluids are not a universal treatment; additional volume may be harmful in cardiogenic shock or after adequate circulating volume has been restored.

Reassessing the response

Repeat the examination and vital signs frequently. Track mental status, pulse quality, skin perfusion, blood pressure and pulse pressure, urine output, ongoing bleeding, transfusion needs, and serial lactate or base deficit.

A brief improvement followed by renewed tachycardia or falling pressure suggests continued bleeding or another unresolved cause. Persistent abnormal perfusion despite initial treatment calls for renewed assessment, not automatic repeated fluid administration. Continue to consider ongoing or mixed shock.