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Chapter8 shock
1. International Trauma Life Support
for Emergency Care Providers
CHAPTER
eighth edition
International Trauma Life Support for Emergency Care Providers, Eighth Edition
John Campbell • Alabama Chapter, American College of Emergency Physicians
Shock
8
Key Lecture Points
Review the four components of the vascular system necessary for normal perfusion
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.
Introduction to the use of tranexemic acid (TXA)
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.
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.
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.
NOTE: See progression cycle on next slide.
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
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
Healthy young patients can maintain perfusion despite hypotension.
Older, hypertensive, and/or head injury patient cannot tolerate hypotension for even a short time.
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
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
Thirst due to hypovolemia
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 in shock.
Decreased perfusion causes weakness and thirst initially, and 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.
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.
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.
NOTE: Progression
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.
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.
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). The tank is no longer full.
Distributive shock is caused by spinal injury, vasovagal syncope, sepsis, and certain drug overdoses. Also called high space shock.
Mechanical shock (also known as obstructive shock) is caused by pericardial tamponade, tension pneumothorax, massive pulmonary embolism.
Cardiogenic shock, 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.
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.
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”).
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).
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.
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.
Tension pneumothorax
Cardiac tamponade
Any traumatic or medical condition that obstructs flow of blood to or through heart can cause shock.
Tension pneumothorax
Cardiac tamponade
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.
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.
PASG
Worsening death rate when applied with uncontrolled bleeding
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.
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.
A tourniquet is rarely needed, but when it is needed, it should be applied quickly.
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.
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.
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.
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.
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).
Note: Head injury with hypovolemic shock BP is 100 mmHg systolic. Head injury with hypotension (hypovolemia not suspected)
Nonhemorrhagic hypovolemic shock
Example: fluid loss from burns, severe diarrhea
Fluid administration may be of value, but could worsen condition.
Should be used only with local EMS medical direction.
Fluid administration may be of value, but could worsen condition.
Should be used only with local EMS medical direction.
Pericardiocentesis must be performed immediately (if within care providers scope of practice).
Signs of acute heart failure: distended neck veins, tachycardia, cyanosis, arrhythmia
Not easily differentiated from cardiac tamponade
Remember: Survival after traumatic arrest is rare.
Signs of acute heart failure: distended neck veins, tachycardia, cyanosis, arrhythmia
Not easily differentiated from cardiac tamponade
Remember: Survival after traumatic arrest is rare.
Give 1 g over 10 minutes, then 1g over 8 hours.
All-cause mortality reduced with TXA 1463 [14·5%] vs 1613 [16·0%] placebo; RR 0·91, 95% CI 0·85–0·97; p=0·0035.
The risk of death due to bleeding was reduced 489 [4·9%] vs 574 [5·7%]; RR 0·85, 95% CI 0·76–0·96; p=0·0077.
Inclusion criteria set by clinical gestalt; no specific guidelines.
CRASH-2 led to ALL trauma patients in the UK (NHS) receiving TXA.
Several more studies have validated it.
Early tx (<1h) sig reduced the risk of death d/t bleeding (198/3747 [5·3%] deaths TXA vs 286/3704 [7·7%] deaths placebo; RR 0·68, 95% CI 0·57–0·82; p<0·0001).
Tx given b/w 1 & 3 h reduced risk of death d/t bleeding (147/3037 [4·8%] vs 184/2996 [6·1%]; RR 0·79, 0·64–0·97; p=0·03).
Tx >3h seemed to up risk of death d/t bleeding (144/3272 [4·4%] vs 103/3362 [3·1%]; RR 1·44, 1·12–1·84; p=0·004).
No evidence that the effect of TXA on death d/t bleeding varied by SBP, GCS, or type of injury
This puts TXA therapy squarely in the EMS/ED wheelhouse.
Early treatment with this drug seems to be much more effective than does late treatment.
Even after decades of research, it is not at all clear at this time what the best initial resuscitation fluid is.
Current research (Resuscitation Outcome Consortium – ROC’s study called “PROPPR”) 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.
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.
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.
The role of hypothermia in the care of critically ill patients is being evaluated.
