0. International Trauma Life Support, 7e
Shock Evaluation and Management 8
Key Lecture Points
Discuss the modern concept of “shock”: threat to normal cell function caused by diminished tissue perfusion and/or hypoxia.
Discuss the pathophysiology of hemorrhagic shock, including the classic signs and symptoms and their causes.
Discuss the 3 shock syndromes:
Low volume (absolute hypovolemia)
High space (relative hypovolemia)
Mechanical (obstructive)
Discuss the management of shock:
Post-traumatic hemorrhage
Exsanguinating external hemorrhage that can be controlled
Exsanguinating external hemorrhage that cannot be controlled
Exsanguinating internal hemorrhage
Nonhemorrhagic shock
Mechanical shock
High-space shock
Discuss the use of tourniquets and hemostatic agents in the situation of exsanguinating hemorrhage.
Stress that shock is, in general, recognized too late and treated insufficiently. Point out that delaying transport of a patient in shock is a critical mistake.

1. Shock Evaluation and Management
Management of shock has been subject of intensive research for decades and, as a result, changes have been made in recommendations for prehospital treatment of patient with hemorrhagic shock.
The experience of the United States military and its Coalition Partners in the Iraq and Afghanistan wars has led to new thinking in the management of life- threatening hemorrhage.
Courtesy of Eduardo Romero Hicks, MD, EMT

2. Overview Four vascular system components of perfusion
Progression of shock signs and symptoms
Three common clinical shock syndromes
Hemorrhagic, mechanical, and neurogenic shock pathophysiology

3. Overview
Controllable and uncontrollable hemorrhage, nonhemorrhagic shock syndromes
Hemostatic agents
Current indications for fluid administration

4. Normal Perfusion Perfusion “Steady state” activity
vascular system
air exchange
fluid volume
pump
Normal perfusion of body tissues requires 4 intact components:
An intact vascular system to deliver oxygenated blood throughout body: blood vessels
Adequate air exchange in lungs to allow oxygen to enter blood: oxygenation
An adequate volume of fluid in vascular system: blood cells and plasma
A functioning pump: heart
The heart must be pumping, blood volume must be adequate, blood vessels must be intact, and lungs must be oxygenating blood.

5. Normal Perfusion
Blood Pressure = Cardiac Output x PVR Cardiac Output = Heart Rate x Stroke Volume
NOTE: PVR is Peripheral Vascular Resistance.
Thus, if cardiac output falls (either due to falling heart rate or lowered stroke volume) or if peripheral vascular resistance falls (such as in dilated arteries that occur in neurogenic shock), blood pressure will fall.

6. Perfusion Preservation
Basic rules of shock management:
Maintain airway
Maintain oxygenation and ventilation
Control bleeding where possible
Maintain circulation
Adequate heart rate and intravascular volume

7. Shock Progression
Begins with injury, spreads throughout body, multisystem insult to major organs
NOTE: See progression cycle on next slide.

8. Shock Progression Red blood cells decreased Inadequate perfusion
Anaerobic processes
Hypoxia worsens
Catecholamine increases
Cell death
Shock progression details:
Decreased circulating blood volume
Red blood cell (RBC) loss means less oxygen transport
Inadequate perfusion of tissues
Anaerobic processes
Utilize energy sources less efficiently
Produce toxic by-products, such as lactic acid
Accumulating lactic acid creates systemic acidosis
Respiratory muscle weakens, failure develops
Hypoxia worsens
Increased catecholamine release
Increased heart rate and strength of contractions
Constricted peripheral arterial blood vessels
Increased respiratory rate
Cell death, if not corrected
Means less oxygen transport to tissues

9. Shock Shock is a continuum Compensated and decompensated:
Signs and symptoms are progressive
Many symptoms due to catecholamines
Cellular process has clinical manifestations
Compensated and decompensated:
Older, hypertensive, and/or head injury cannot tolerate hypotension for even short time
Shock state:
Low tissue perfusion in which body usually demonstrates similar signs of its response to this perfusion-deprived condition.
May not always demonstrate similar signs, however, as in high-space shock.
Shock state is a continuum:
Signs and symptoms are progressive.
Many symptoms due to catecholamine release.
Cellular process with clinical manifestations.
Compensated and decompensated:
Older, hypertensive, and/or head injury patient cannot tolerate hypotension for even short time.

10. Hypovolemic Shock Compensated progression Weakness and lightheadedness
Thirst
Pallor
Tachycardia
Diaphoresis
Tachypnea
Urinary output decreased
Peripheral pulses weakened
Clinical signs and symptoms of shock imply that critical processes are threatening every vulnerable cell in body, particularly those in vital organs. These signs and symptoms generally develop in this order:
Weakness and lightheadedness due to decreased blood volume
Thirst due to hypovolemia
Pallor due to catecholamine effect on skin and/or loss of red blood cells
Tachycardia due to increased activity of sympathetic nervous system
Diaphoresis due to catecholamine effect on sweat glands
Tachypnea due to stress, catecholamines, acidosis, hypoxia
Decreased urinary output due to hypovolemia, hypoxia, circulating catecholamines
Weakened peripheral pulses due to vasoconstriction, loss of blood volume

11. Shock Progression Compensated to decompensated
Initial rise in blood pressure due to shunting
Initial narrowing of pulse pressure
Diastolic raised more than systolic
Prolonged hypoxia leads to worsening acidosis
Ultimate loss of catecholamine response
Compensated shock suddenly “crashes”
Many of symptoms of shock of any etiology are caused by release of catecholamines.
When the brain senses that perfusion to tissues is insufficient, it sends messages down the spinal cord to sympathetic nervous system and adrenal glands, causing a release of catecholamines into circulation.
Circulating catecholamines cause tachycardia, anxiousness, diaphoresis, and vasoconstriction.
Vasoconstriction in arterioles shunts blood away from skin and intestines to heart, lungs, and brain.
Close monitoring early in the shock syndrome may allow you to detect an initial rise in blood pressure due to this shunting, though this does not always happen.
Vasoconstriction raises diastolic pressure more than systolic.
Shunting of blood from skin and loss of circulating red blood cells cause the sign of pallor of shock.
Decreased perfusion causes weakness and thirst initially, and then, later, an altered level of consciousness (confusion, restlessness, or combativeness) and worsening pallor.
As shock continues, prolonged tissue hypoxia leads to worsening acidosis.
This acidosis can ultimately cause a loss of response to catecholamines, worsening drop in blood pressure.
This is often the point at which a patient in “compensated” shock suddenly “crashes.”
Eventually, hypoxia and acidosis cause cardiac dysfunction, including cardiac arrest, and, ultimately, death.

12. Hypovolemic Shock Decompensated progression Hypotension
Hypovolemia and/or diminished cardiac output
Altered mental status
Decreased cerebral perfusion, acidosis, hypoxia, catecholamine stimulation
Cardiac arrest
Critical organ failure
Secondary to blood or fluid loss, hypoxia, arrhythmia

13. Classic Shock Pattern Early shock Late shock 15–25% blood volume
Tachycardia
Pallor
Narrowed pulse pressure
Thirst
Weakness
Delayed capillary refill
Late shock
30–45% blood volume
Hypotension
First sign of “late shock”
Weak or no peripheral pulse
Prolonged capillary refill
Although individual response to post-traumatic hemorrhage may vary, many patients will have the following classic patterns of “early” and “late” shock.
Early shock: In “early shock,” the body is “compensating” for physical insult that is causing a problem (hemorrhage, dehydration, tension pneumothorax, and so on).
NOTE: Emphasize tachycardia can be slight to moderate increase.
Late shock: When “late shock” has occurred, this means that the body's ability to compensate for physical insult has failed. The hypotensive patient, then, is near death, requiring aggressive assessment and management by the provider to prevent death.
Note that during Initial Assessment, early shock presents as a fast pulse with pallor and diaphoresis, while late shock may present as weak pulse or loss of peripheral pulses.
Weakened pulses taken with other signs of shock should quickly lead you to suspect decompensated shock.

14. Capillary Refill
NOTE: This slide is setup slide for next with progression. TALK ABOUT REFILL HERE—demo next slide.
Prolonged capillary refill time was previously thought to be very useful for detecting early shock. The test is suspicious for shock if blanched area remains pale for longer than 2 seconds.
Scientific evaluation of this test has shown it to have a high correlation with late shock but to be of little value for detecting early shock.
Test was associated with both frequent false-positive and false-negative results.
Low blood volume, cold temperatures, and catecholamine-induced vasoconstriction can all cause decreased perfusion of capillary bed in skin, and thus cause abnormal results.
Measurement of capillary refill is useful for small children in whom it is difficult to get an accurate blood pressure, and is tested centrally by placing pressure on the sternum, but it is of little use for detecting early shock in adults.
Courtesy of Louis B. Mallory, MBA, REMT-P

15. Capillary Refill NOTE: Progression.
Courtesy of Louis B. Mallory, MBA, REMT-P

16. Tachycardia Early sign of illness—most common: Early sign of shock:
Transient rise with anxiety, quickly to normal
Determine underlying cause
Early sign of shock:
Suspect hemorrhage: sustained rate >100
Red flag for shock: pulse rate >120
No tachycardia does not rule out shock
“Relative bradycardia”
When confronted with a patient with an elevated pulse rate, try to determine an underlying cause.
Patients with traumatic hypotension may develop a “relative bradycardia.” As many as 20% of patients with bleeding into the abdomen may not show tachycardia.

17. Capnography Level of exhaled CO2 as waveform (ETCO2) Falling ETCO2
Typically ~35–40 mmHg
Falling ETCO2
Hyperventilation or decreased oxygenation
ETCO2 <20 mmHg
May indicate circulatory collapse
Warning sign of worsening shock
NOTE: “~” (tilde) means approximately.
Heart delivers oxygen and nutrients to cells of body by way of blood vessels.
Cells “burn” nutrients in presence of oxygen to produce energy, water, and carbon dioxide (CO2).
Water and CO2 move into bloodstream, CO2 being carried to lungs by red blood cells for excretion during exhalation.
CO2 then is exhaled by-product of metabolism.
When measured moment to moment at airway, level of CO2 being excreted may be graphed as a waveform.
Falling measured CO2 indicates either that patient is hyperventilating (from anxiety or acidosis) or that amount of oxygen being supplied to cells is falling.
Patients in shock have decreased oxygen being supplied to their cells.
Thus, if you are monitoring a patient who appears to be in shock or at risk of going into shock, monitor level of exhaled CO2.
A level of exhaled CO2 that falls much under 30—especially if it falls into 20s or below—may be an indication of circulatory collapse and thus can be an additional warning sign of worsening shock.
Courtesy of Louis B. Mallory, MBA, REMT-P

18. Shock Syndromes Low-volume shock High-space shock Mechanical shock
Absolute hypovolemia
Hemorrhagic or other fluid loss
High-space shock
Relative hypovolemia
Neurogenic shock
Vasovagal syncope
Sepsis
Drug overdose
Mechanical shock
Obstructive
Cardiac tamponade
Tension pneumothorax
Massive pulmonary embolism
Cardiogenic
Myocardial contusion
Myocardial infarction
NOTE: ANIMATED.
Although most common shock state seen in trauma patients is associated with hemorrhage and accompanying hypovolemia, there are actually 3 major classifications of shock. These “types of shock” relate directly to blood pressure equation discussed earlier in this chapter.
Low-volume shock is caused by hemorrhage or other major body fluid loss (diarrhea, vomiting, and “third spacing” due to burns, peritonitis, and other causes).
High-space shock is caused by spinal injury, vasovagal syncope, sepsis, and certain drug overdoses.
Mechanical shock (cardiogenic shock, also known as obstructive shock) is caused by pericardial tamponade, tension pneumothorax, massive pulmonary embolism, or conditions weakening heart muscle, such as myocardial contusion or infarction.
There are notable differences in appearance of patients with these conditions, and it is critical that you be aware of signs and symptoms that accompany each one.

19. Low-Volume Shock Absolute hypovolemia Clinical presentation
Large vascular space
Blood vessels hold more than actually flows
Catecholamines cause vasoconstriction
Minor blood loss: vasoconstriction sufficient
Severe blood loss: vasoconstriction insufficient
Clinical presentation
“Thready” pulse; tachycardia; pale, flat neck veins
Loss of blood from injury is called post-traumatic hemorrhage.
Hemorrhagic shock is the most preventable cause of death from injury.
When vasoconstriction is insufficient, hypotension occurs.
Normally, blood vessels are elastic and are distended by volume that is in them.
Produces a radial artery pulse that is full and wide.
Blood loss allows artery to shrink in width, becoming more threadlike in size; hence term “thready” pulse in shock.

20. High-Space Shock Relative hypovolemia Clinical presentation
“Vasodilatory shock”
Large intact vascular space
Interruption of sympathetic nervous system
Loss of normal vasoconstriction; vascular space becomes much “too large”
Clinical presentation
Varies dependent on type of high-space shock
Volume that blood vessels can hold is many liters more than blood volume in blood vessels.
Anything that interrupts outflow from the sympathetic nervous system and causes loss of this normal vasoconstriction allows vascular space to dilate, becoming much “too large” for amount of blood in the vascular system.
If blood vessels dilate, 5 liters or so of blood flowing through normal adult's vascular space may not be sufficient to maintain blood pressure and vital tissue perfusion.
Condition causing vascular space to be too large for a normal amount of blood has been called high-space shock or relative hypovolemia (also known as “vasodilatory shock”).

21. High-Space Shock Types
Several causes
Sepsis syndrome
Drug overdose
Trauma
Neurogenic shock
Most typically after injury to spinal cord
Injury prevents additional catecholamine release
Circulating catecholamines may briefly preserve
Although several causes of high-space shock exist (such as sepsis syndrome and drug overdose), neurogenic shock, commonly called spinal shock, is addressed here because it may be caused by trauma.
The nerves of the sympathetic nervous system come off of the spinal cord in the thoracic (chest) and lumbar area.
This is why the sympathetic nervous system is often called the “thoracolumbar autonomic nervous system.”
Neurogenic shock occurs most typically after an injury to the spinal cord. An injury to the spinal cord in the neck can prevent the brain from being able to send out the sympathetic nervous system signals.
Thus, a cervical spinal-cord injury can prevent the brain from raising the pulse rate from raising the strength of the heart's contraction, or from constricting the peripheral arterioles (the vessels that maintain blood pressure).

22. High-Space Shock Neurogenic shock Drug overdose, sepsis Hypotension
Heart rate normal or slow
Skin warm, dry, pink
Paralysis or deficit
No chest movement, simple diaphragmatic
Drug overdose, sepsis
Tachycardia
Skin pale or flushed
Flat neck veins
Clinical presentation of neurogenic shock differs from hemorrhagic shock in that there is no catecholamine release, thus no pallor, tachycardia, or sweating.
Patient will have a decreased blood pressure, but heart rate will be normal or slow, and skin is usually warm, dry, and pink.
May also have accompanying paralysis and/or sensory deficit corresponding to spinal-cord injury.
May see lack of chest wall movement and only simple diaphragmatic movement when patient is asked to take a deep breath, seen as protruding of abdomen during inspiration.
Important point: Neurogenic shock does NOT have typical picture of hemorrhagic shock, even when associated with severe bleeding.
Neurologic assessment is therefore very important:
Do not rely on typical shock symptoms and signs to suspect internal bleeding or accompanying hemorrhage-associated shock.
Neurogenic shock patients may “look better” than their actual condition really is.
Whereas neurogenic shock (due to spinal-cord injury) is bradycardic, pink, and has flat neck veins, other forms of high-space shock (drug overdoses, cyanide, sepsis) typically are tachycardic, pale or flushed, and have flat neck veins.

23. Mechanical Shock Obstructs blood flow to or through heart
Slows venous return
Decreases cardiac output
Clinical presentation
Distended neck veins
Cyanosis
Catecholamine effects
Pallor, tachycardia, diaphoresis
Heart is a pump; it has a “power” stroke and a “filling” stroke.
Normal adult resting state, heart pumps out about 5 liters of blood per minute and must take in about 5 liters of blood per minute.
Any traumatic or medical condition that slows or prevents venous return of blood can cause shock by lowering cardiac output and thus oxygen delivery to tissues.
Any traumatic or medical condition that obstructs flow of blood to or through heart can cause shock.

24. Treatment General management of shock state Control bleeding
Administer high-flow oxygen
Load and go
Control bleeding. Red blood cells are necessary to carry oxygen. Control of bleeding must be obtained either by direct pressure, tourniquet, hemostatic agent, or rapid transport to surgery.
Administer high-flow oxygen. Patients in shock need oxygen supplementation.
Evaluation of skin color in shock patients may not tell you what the patient's oxygen requirement is. Generally, patients in hemorrhagic shock are pale.
Someone bleeding to death, literally, may not have enough hemoglobin around to manifest cyanosis.
Try to maintain a pulse oximeter reading greater than 95 percent.
Load and go. Trauma patients in shock from any cause are considered to be in the load-and-go category. Transport as soon as you finish the ITLS Primary Survey (initial assessment and rapid trauma survey). Almost all critical interventions should be done in the ambulance.

25. Current Shock Research
Prehospital management research
Hemorrhagic shock due to trauma and traumatic brain injury in prehospital environment
Intravenous solutions
Hypertonic saline may not have benefit over conventional IV fluids
Artificial blood products carry oxygen
Shock management has been subject of intensive research for decades and changes have been made in recommendations for prehospital treatment of patient with hemorrhagic shock. Specific prehospital management of patient in shock remains both controversial and subject of ongoing research.
The results of the National Institutes of Health Resuscitation Outcomes Consortium trial on the treatment of hemorrhagic shock due to trauma–reported in 2010–indicated that low volume resuscitation with hypertonic saline in patients in severe hemorrhagic shock showed no benefit over conventional IV fluids. Further studies to find the “best” resuscitation fluid, including how much fluid should be administered, are ongoing at this time.

26. PASG Research Pneumatic antishock garment
Uncontrollable internal hemorrhage due to penetrating injury
May increase mortality, especially intrathoracic
Probably increases bleeding, death due to exsanguination
PASG:
Worsening death rate when applied with uncontrolled bleeding, and
May increase death with penetrating injury, especially intrathoracic bleed.
PASG raises blood pressure, and raising blood pressure in the setting of bleeding vessels within thorax, abdomen, and pelvis probably increases internal bleeding, raising chance of death due to exsanguination.
Courtesy of John Campbell

27. Controllable Hemorrhage
Management
Control bleeding
Shock position
High-flow oxygen
Rapid safe transport
Large-bore IV access
A patient with controllable bleeding is fairly easy to manage.
Most bleeding can be stopped with direct pressure.
In some situations (usually blast or tactical injuries), there may be exsanguinating hemorrhage that you cannot control with direct pressure.
In these most extreme circumstances, you should not hesitate to apply a tourniquet.
Tourniquet is rarely needed, but when it is needed, it should be applied quickly.

28. Controllable Hemorrhage
Management
Fluid bolus 20 ml/kg rapidly, repeat if necessary
Cardiac monitor, SpO2, ETCO2
Ongoing Exam
A patient with controllable bleeding is fairly easy to manage.
Most bleeding can be stopped with direct pressure.
In some situations (usually blast or tactical injuries), there may be exsanguinating hemorrhage that you cannot control with direct pressure.
In these most extreme circumstances, you should not hesitate to apply a tourniquet.
Tourniquet is rarely needed, but when it is needed, it should be applied quickly.

29. Uncontrollable Hemorrhage
Management: External
Control bleeding
Shock position
High-flow oxygen
Rapid safe transport
Large-bore IV access
Fluid administration
Cardiac monitor, SpO2, ETCO2
Ongoing Exam
Most bleeding can be stopped with direct pressure.
In some situations (usually blast or tactical injuries), there may be exsanguinating hemorrhage that you cannot control with direct pressure.
In these most extreme circumstances, you should not hesitate to apply a tourniquet.
A tourniquet is rarely needed, but when it is needed, it should be applied quickly.
If need be, consider hemostatic agent.
Courtesy of John Campbell

30. Fluid Administration Uncontrollable hemorrhage
May increase bleeding and death
Dilutes clotting factors
Early blood transfusion in severe cases
IV fluids carry almost no oxygen
Moribund trauma patients
Fluid may be indicated to maintain some circulation
Local medical direction
Moribund trauma patients (ones in very deep shock with blood pressures under 50 mmHg systolic, i.e., nonpalpable pulses) usually die, but fluid administration may be indicated to maintain some degree of circulation.
Treatment of this extreme amount of hemorrhage may override concerns for increased hemorrhage secondary to use of these interventions. However, this approach is still controversial.
Local medical direction should guide such therapy pending further research.

31. Uncontrollable Hemorrhage
Management: Internal
Rapid safe transport
Shock position
High-flow oxygen
Large-bore IV access
Fluid administration
Cardiac monitor, SpO2, ETCO2
Ongoing Exam
Uncontrolled internal hemorrhage is the classic critical trauma victim who will almost certainly die unless you promptly transport to an appropriate facility where rapid operative hemostasis can be obtained.
Results of most current medical research on management of patients with exsanguinating internal hemorrhage is that there exists no substitute for gaining surgical control of bleeding.
© Edward T. Dickinson, MD

32. Fluid Administration Internal hemorrhage from blunt trauma
Large-bone fractures
Usually self-limiting bleed, except pelvis
Fluid administration for volume expansion
Large internal blood vessel tear, or laceration or avulsion of internal organ
Fluid may increase bleeding and death
Fluid administration to maintain peripheral perfusion
Local medical direction
Current published research has not yet adequately addressed treatment of patient with presumed internal hemorrhage in setting of blunt injuries (MVCs, falls, and so on).
Creates a dilemma since many patients with blunt injuries can lose a significant amount of blood and fluid from intravascular space into sites of large-bone fractures (hematoma and edema).
This loss can be enough to cause shock, and yet blood loss from these fractures is usually self-limited, with exception of pelvic fractures.
Pelvic fractures can result in exsanguination and death. In theory, this situation should be treated with oxygen and intravascular volume expansion (IV fluids).

33. Fluid Administration Uncontrollable hemorrhage
Maintain peripheral perfusion
Peripheral pulse
Higher systolic may be required with increased ICP or with history of hypertension
Maintaining consciousness
In absence of traumatic brain injury
“Adequate blood pressure”
Controversial with ongoing research
Local medical direction

34. High-Space Shock Management High-flow oxygen Shock position
Rapid safe transport
Large-bore IV access
Fluid bolus 20 ml/kg rapidly
Consider vasopressors for vasodilatory shock
Calcium channel blocker overdose or sepsis
Ongoing Exam
Courtesy of John Campbell

35. Special Situations Severe head injury hypovolemic shock
Glasgow Coma Score of 8 or less
Fluid administration
BP of 120 mmHg systolic to maintain cerebral perfusion pressure of at least 60 mmHg
Nonhemorrhagic hypovolemic shock
General management same as controllable
Fluid administration for volume replacement
Nonhemorrhagic hypovolemic shock:
Example: fluid loss from burns, severe diarrhea.

36. Mechanical Shock Tension pneumothorax Management
Vena cava collapses, prevents venous return
Mediastinal shift lowers venous return
Tracheal deviation away from affected side
Decreased cardiac output
Management
Chest decompression
Prompt decompression of pleural pressure
NOTE: Decreased venous return = decreased cardiac output.

37. Mechanical Shock Causes
Cardiac tamponade
Blood fills “potential” space; prevents heart filling
May occur >75% with penetrating cardiac injury
“Beck's triad”
Shock, muffled heart tones, distended neck veins
Fluid administration may be of value, but could worsen condition.
Should be used only with local EMS medical direction.

38. Mechanical Shock Causes
Management
Rapid safe transport to appropriate facility
Cardiac arrest can occur in minutes
Fluid administration by local medical direction
Fluid administration may be of value, but could worsen condition.
Should be used only with local EMS medical direction.

39. Mechanical Shock Causes
Myocardial contusion
Heart muscle injury and/or cardiac dysrhythmias
Rarely causes shock; mostly little or no signs
Severe may cause acute heart failure
Signs of acute heart failure: distended neck veins, tachycardia, cyanosis, arrhythmia.
Not easily differentiated from cardiac tamponade.
Remember: Survival after traumatic arrest is rare.

40. Mechanical Shock Causes
Management
Rapid safe transport
Cardiac arrest may occur in 5–10 minutes
Cardiac monitoring and treat arrhythmias
Fluid administration may worsen condition
Signs of acute heart failure: distended neck veins, tachycardia, cyanosis, arrhythmia.
Not easily differentiated from cardiac tamponade.
Remember: Survival after traumatic arrest is rare.

41. Areas of Current Study Finding the ideal resuscitation fluid
Blood administration to blood product ratio
Evaluating lactate levels to monitor shock
Hemostatic agents
Tourniquets
Permissive hypothermia
Even after decades of research, it is not at all clear at this time what the best initial resuscitation fluid is.
Current research is examining what the ratio of “blood administration” to “blood product” administration should be. While beyond the scope of this chapter, this is an important area that will continue to guide emergency medicine and surgery in the resuscitation of these patients.
One important method that is being evaluated is in the use of “lactate levels” in the prehospital arena to monitor patients in shock. Early work at this time suggests that increasing lactate levels may be predictive of worsening outcome for the patient.
It should be stressed that hemostatic agents should only be used in the setting of an overall hemorrhage control protocol and not as agents that control bleeding by themselves. This is an area in which the recommended agent to use seems to change frequently, so consult your medical director or state protocols for current recommendations.
Tourniquets are lifesaving devices and should be part of all EMS education. The rapid control of massive external bleeding–by tourniquets if necessary–is a critical part of patient care.
The role of hypothermia in the care of critically ill patients is being evaluated.

42. Summary
Knowledge about pathophysiology and treatment of shock is essential
Critical condition that leads to death
Assessment and intervention must be rapid
Monitor closely for early signs
Be aware of management controversies
Rely on local medical direction