This patient was involved in a motorcycle collision and presented with signs of hemorrhagic shock. Key findings included shivering, pale skin, tachycardia and a weak radial pulse despite mild ambient temperatures, suggesting the patient was losing heat due to impaired energy production from hypoperfusion. Management of hemorrhagic shock focuses on restoring circulation through airway control, oxygenation, fluid resuscitation and hemorrhage control to improve tissue oxygen delivery until definitive care. While en route to the ED, the patient's blood pressure transiently responded to fluid but decreased, indicating ongoing hemorrhage as the likely shock etiology.
31. Signs of Shock 500 – 1000 Tibia or fibula 1000 – 2000 Femur Massive Pelvis 750 Humerus 250 – 500 Radius or ulna 125 Single rib Blood Loss (mL) Fracture
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Notas del editor
Instructor Notes: Solicit responses from participants rather than supply the information yourself. Ask follow-up questions as needed. For example, if participants respond with a list of potential injuries, follow up with a questions such as “What makes you say that?” This verifies understanding of the mechanism of injury. Key Points: Primary scene safety consideration is traffic. Leaking fuel and bystanders also may be considerations. The mechanism is suspicious for femur fractures, upper extremity fractures, head trauma, spinal trauma, and blunt/deceleration trauma. The patient is at risk of substantial hemorrhage associated with these injuries.
Key Points: Assessment is a process of seeking evidence of potential problems, including evidence of shock. Participants should note the following: The patient is awake and able to speak (LOC, airway, breathing) The patient has been described as shivering (general impression) The patient is pale (general impression) The patient is agitated and slightly confused (LOC) While these findings could have alternative explanations, based on the mechanism of injury, shock is extremely likely and will kill the patient more quickly than any other potential cause. The patient should be assumed to be in shock at this point.
Key Points: Additional information not obvious from the video clip: Breathing is slightly faster than normal Skin is cool Radial pulse is faster than 100
Instructor Notes: Solicit responses from participants rather than supply the information yourself. Ask follow-up questions as needed. For example, if participants respond with an answer of “Shock,” follow up with a question such as “What makes you say that?” This verifies understanding of how the patient’s signs and symptoms relate to shock. Key Points: The fact that the patient’s respiratory rate and heart rate are increased are additional evidence that the patient is in shock.
Key Points: Understanding what is happening to the patient is critical to understanding how shock kills and what EMS providers must do to intervene in the process. Signs and symptoms of shock are related to the pathophysiological process of shock and the body’s attempt to compensate for the pathophysiological changes. Transition: Discussion of pathophysiology follows.
Instructor Notes: It is critical that participants understand this basic definition of shock. Key Points: The patient is in shock. This means that his cells are not receiving enough oxygen to produce an adequate amount of energy for them to function.
Key Points: Loss of blood volume means oxygen cannot be delivered to the cells. Inadequate cellular oxygenation impairs metabolism.
Instructor Notes: For a combined or basic audience, explain that ATP is a molecule that produces energy when it is broken apart. It is the “energy molecule.” Key Points: ATP is required for cellular energy (metabolism). Cells cannot function without ATP. Oxygen is required for efficient production of ATP (adenosine triphosphate — a molecule used to produce energy). The production of ATP without oxygen is inefficient and results in the inability to convert lactic acid to carbon dioxide and water. Anaerobic metabolism is a short-term solution to inadequate oxygenation.
Key Points: Consequences of anaerobic metabolism include: Dysfunction of cell membranes such that potassium and lactic acid leave the cell and enter the interstitial fluid, resulting in hyperkalemia and acidosis. Sodium and water enter the cell resulting in cellular edema and further loss of intravascular fluid. The low pH (acidosis) causes the release of cellular enzymes that destroy cells, ultimately resulting in organ damage, organ death, and patient death. The process of anaerobic metabolism must be reversed by ensuring that oxygenated red blood cells reach the capillaries that supply the body’s cells.
Key Points: Blood loss is also heat loss. Without ATP the patient cannot produce heat to balance the heat loss associated with blood loss and the normal loss of heat to the environment. The body’s attempts to maintain its temperature is increasing the need for oxygen and resulting in increased anaerobic metabolism and worsening acidosis. Hypothermia impairs the ability of the blood to clot so that hemorrhage continues. The on-going hemorrhage worsens hypothermia and acidosis.
Key Points: Keeping the patient warm is critical, but often overlooked. Transition: A discussion of classifications of shock follows.
Key Points: Trauma patients may suffer from any of three different types of shock: hypovolemic, distributive, or cardiogenic. Of these, hypovolemic is most common in the trauma patient. The most common cause of hypovolemia in trauma is hemorrhage. EMS providers should assume shock is hemorrhagic until proven otherwise. Patient assessment simultaneously provides information about whether the patient is in shock and about what the cause of shock may be in that patient.
Key Points: The ability of the body to compensate for volume loss is limited, therefore shock is progressive. It is important to understand the three levels of changes that occur due to on-going hemorrhage. Hemodynamic changes, or changes related to the heart and blood vessels Cellular changes related to anaerobic metabolism Microvascular changes, or changes that occur at the capillary level
Key Points: In order to maintain perfusion: The heart must act as an effective pump. There must be an adequate volume of blood in the body. The blood vessels must provide an adequate amount of resistance to flow.
Key Points: Cardiac output = stroke volume × heart rate To maintain cardiac output when the stroke volume drops, the heart rate must increase. Increased heart rate is one of the body’s compensatory mechanisms in hemorrhagic shock. Increased heart rate is stimulated by the sympathetic nervous system. An increase in heart rate can compensate for a decrease in stroke volume only to a point, then cardiac output begins to decrease. This is important because cardiac output is one of the factors that determines blood pressure.
Key Points: Blood pressure = cardiac output × systemic vascular resistance. Systemic vascular resistance is the amount of opposition supplied by the blood vessels to the force of blood flowing through them. SVR is increased by vasoconstriction, resulting in increased blood pressure. Vasoconstriction occurs through sympathetic nervous system stimulation. SVR can compensate for decreased cardiac output only to a point before blood pressure falls.
Key Points: There are three phases of shock at the capillary level: ischemic, stagnant, and washout. Blood flow to the tissues is controlled by sphincter muscles at both ends of the capillary beds that perfuse the tissues. The precapillary sphincter controls the flow of blood into the tissues. The postcapillary sphincter controls the flow of blood out of the tissues. Early in shock, both sphincters constrict to divert blood away from peripheral tissues into the core of the body in order to perfuse vital organs. This causes ischemia (lack of blood flow) in the tissues, which must then produce energy anaerobically. The acidosis produced by anaerobic metabolism causes the precapillary sphincters to fail so that blood flows into the capillary bed, but cannot flow out. The blood is then stagnant in the capillary bed. Finally, as acidosis increases, the post-capillary sphincter also fails and the accumulated acidotic blood and microemboli (small blood clots formed in the stagnant blood) are released into the circulation Systemically, this increases acidosis and causes infarction of organs by microemboli
Key Points: Organs and tissues have varying degrees of tolerance for ischemia, called ischemic sensitivity . Brain cells begin to die after 4 to 6 minutes of ischemic conditions. Organs such as the kidneys can tolerate ischemia for 45 to 90 minutes. After this time, cells of the renal tubules begin to die (acute tubular necrosis), which causes acute renal failure. Adequate prehospital resuscitation is important in reducing the patient’s likelihood of organ failure.
Key Points: Other types of shock in the trauma patient include distributive shock and cardiogenic shock. In trauma, distributive shock is typically due to neurogenic shock. Neurogenic shock results when damage to the spinal cord prevents the sympathetic nervous system from stimulating vasoconstriction. The amount of blood volume is constant, but unopposed parasympathetic nervous system stimulation results in vasodilation. Therefore the blood vessel “container” is larger than normal and cannot be adequately filled by the normal amount of blood present in the vascular system. The signs and pathophysiology of neurogenic shock are different than those of hemorrhagic shock. Warm, dry skin and normal skin color due to vasodilation — especially below the point of spinal cord injury Bradycardia Cardiogenic shock may occur in the trauma patient as a result of direct trauma or because of decreased stroke volume or preload as a result of pericardial tamponade or tension pneumothorax. Good patient assessment simultaneously determines that the patient is in shock and what the probable cause of shock is.
Instructor Notes: Solicit responses from participants rather than supply the information yourself. Ask follow-up questions as needed to verify understanding of how the pathophysiology of shock explains the patient’s signs and symptoms. Key Points: The patient is compensating hemodynamically. His heart rate is increased to maintain cardiac output. His cool skin indicates vasoconstriction to increase systemic vascular resistance. The patient’s respiratory rate is increased in an attempt to deliver more oxygen to his ischemic tissues. The patient’s attempts to compensate are indications that he is hypoperfusing his tissues and becoming acidotic due to anaerobic metabolism. Without intervention, shock will progress.
Instructor Notes: Ask participants how the pathophysiology of shock contributes to each of these findings. Key Points: Increased respirations are an early sign of shock. Increased hydrogen ion (acidosis) and hypoxia increase the respiratory drive. A rate of 20 to 30 breaths per minute is moderately increased, indicating the need for supplemental oxygen. A rate greater than 30 breaths per minute is accompanied by a decrease in tidal volume and generally requires ventilatory assistance. The sensation of “air hunger” and the feeling that something over the face interferes with getting air can lead hypoxic patients to be intolerant of oxygen face masks. This is a clue to hypoxia.
Instructor Notes: Ask participants how the pathophysiology of shock contributes to each of these findings. Key Points: Significant external hemorrhage is an indication of shock. Other efforts to treat the patient will be futile if hemorrhage is allowed to continue. Altered level of consciousness is an indication of cerebral ischemia. There may be other causes of altered LOC, but ischemia should be suspected and treated. Heart rate A heart rate between 100 and 120 indicates early shock. A heart rate above 120 indicates shock, but fear and pain may be contributory. A heart rate of 140 or above is critical, and the patient should be assumed to be near death. Pulse Loss of peripheral pulses indicates severe hypovolemia and/or vascular damage to the extremity. A weak, thready pulse indicates shock. Skin color and temperature The skin may be cool and pale due to vasoconstriction (compensatory), loss of RBCs, or localized vascular causes. Mottling or cyanosis indicates desaturated hemoglobin. Capillary refill is an important indication of peripheral perfusion. Other environmental and physiological conditions may contribute to delayed capillary refill and must be taken into consideration. Blood pressure Generally, blood loss must reach 30% of the patient’s volume (Class III hemorrhage) before blood pressure drops. While the patient is compensating, the pulse pressure narrows. Adequate blood pressure does not equate to adequate tissue perfusion.
Key Points: A single rib fracture may result in blood loss of 125 mL. Fractures of the radius or ulna may result in blood loss of 250 to 500 mL. Humerus fractures can result in up to 750 mL of blood loss. Tibia or fibula fractures can result in 500 to 100 mL of blood loss. Femur fractures can result in 1000 to 2000 mL of blood loss. Blood loss from pelvic fractures can be massive.
Key Points: A single rib fracture may result in 125 mL of blood loss. Fractures of the radius or ulna may result in blood loss of 250 to 500 mL. Humerus fractures can result in up to 750 mL of blood loss. Tibia or fibula fractures can result in 500 to 1000 mL of blood loss. Femur fractures can result in 1000 to 2000 mL of blood loss. Blood loss from pelvic fractures can be massive.
Key Points: Abdominal tenderness, rigidity, and distention are all very late signs of abdominal hemorrhage. These signs are not always present in the case of significant abdominal injury.
Additional information: The patient’s breath sounds are equal bilaterally and his abdomen is soft and nontender. His pelvis is stable. The patient is experiencing significant pain in the areas of deformity. This information is important in determining the cause of shock in this patient. Key Points: The patient’s vital signs provide important information about the amount of blood loss and where the patient is in the shock continuum. The presence of multiple major fractures is significant for hemorrhage. Absence of significant findings in the chest and abdomen and the fact that the patient has intact sensation make distributive and cardiogenic causes of shock unlikely.
Key Points: There is no indication that the patient has cardiogenic or distributive shock, so the signs of shock are attributed to hemorrhage. The severity of hemorrhage is classified according to the amount of blood loss.
Instructor Notes: Solicit responses from participants rather than supply the information yourself. Ask follow-up questions as needed. This verifies understanding of the cause of shock and where the patient is in the shock continuum. Key Points: This patient’s presentation is most consistent with a Class II hemorrhage. Increased respiratory rate Increased heart rate Narrowed pulse pressure Normotensive Although it is possible that the patient has hemorrhage due to abdominal trauma, he unquestionably has hemorrhage due to multiple major fractures. Each femur fracture may result in 1000 to 2000 mL of blood loss. The humerus fracture may result in 500 to 750 mL of blood loss. Assuming the patient is an average-sized male (150 lb or 70 kg), his normal blood volume is 6 L; he may have lost up to 2 L at this point. Because of the potential for hemorrhage associated with his injuries, significant on-going hemorrhage should be anticipated.
Key Points: A number of factors may cause patients in shock to present atypically. Pregnancy Later in pregnancy a woman may lose 30% to 35% of blood volume before signs are apparent. The weight of the uterus compresses the vena cava, impeding blood return to the heart if the patient is supine. Placental blood vessels are sensitive to catecholamines (epinephrine) resulting in vasoconstriction and decreased blood flow to the placenta. This results in fetal hypoxia. Medications may interfere with compensatory mechanisms. Beta blockers and calcium channel blockers may prevent tachycardia and vasoconstriction . Aspirin and NSAIDS may interfere with blood clotting. Age Neonates and the elderly do not compensate well. Children compensate well — decompensation represents a dire emergency. Well-conditioned athletes may not show the same increase in heart rate, despite being in shock. Preexisting medical conditions Patients with cardiovascular and pulmonary disease cannot compensate well. Patients with pacemakers cannot show an increase in heart rate.
Key Points: Four critical questions guide shock resuscitation. Assessment should simultaneously provide evidence that the patient is in shock and clues about what type of shock the patient is suffering from. Hemorrhagic shock is most common in trauma.
Key Points: Anaerobic metabolism is occurring before signs and symptoms of shock are evident. Managing shock requires definitive treatment of the cause, as well as restoration of tissue perfusion.
Instructor Notes: Solicit responses from participants rather than supply the information yourself. Ask follow-up questions as needed. For example, ask how a suggested intervention will address the patient’s needs and/or why that intervention is a better choice than other interventions. This verifies understanding of the need to address the underlying pathophysiology of shock with interventions. Key Points: The patient is awake and able to speak. He does not need an airway intervention at this point. Because shock is progressive and we cannot definitively treat this patient, on-going assessment of the airway is warranted.
Instructor Notes: Solicit responses from participants rather than supply the information yourself. Ask follow-up questions as needed. For example, ask how a suggested intervention will address the patient’s needs and/or why that intervention is a better choice than other interventions. This verifies understanding of the need to address the underlying pathophysiology of shock with interventions. Key Points: Ischemia and anaerobic metabolism occur prior to outward signs of shock. This patient is exhibiting signs of compensation, including an increased respiratory rate. The increased respiratory rate is an indication of inadequate cellular oxygenation. This patient needs oxygen. The goal is to maintain an oxygen saturation level of at least 95%. The best way to accomplish this is to provide the patient with 12 to 15 liters per minute of oxygen via a non-rebreathing mask.
Instructor Notes: Solicit responses from participants rather than supply the information yourself. Ask follow-up questions as needed. For example, ask how a suggested intervention will address the patient’s needs and/or why that intervention is a better choice than other interventions. This verifies understanding of the need to address the underlying pathophysiology of shock with interventions. Key Points: The patient’s respiratory rate is 28. Also consider the depth of ventilation to determine adequacy of ventilation. In this case, because the patient does not have clear indications of chest, abdominal, or cervical spine trauma, it is likely that his tidal volume is adequate. Once the ventilatory rate exceeds 30, the tidal volume may be inadequate. He does not yet need assistance, but is approaching the point where ventilatory assistance should be considered. Shock is progressive and we cannot definitively treat this patient; therefore the need for ventilatory assistance must be continually assessed.
Instructor Notes: Solicit responses from participants rather than supply the information yourself. Ask follow-up questions as needed. For example, ask how a suggested intervention will address the patient’s needs and/or why that intervention is a better choice than other interventions. This verifies understanding of the need to address the underlying pathophysiology of shock with interventions. Key Points: The best way to improve the patient’s circulation is to transport him to definitive care. He most likely needs surgery and blood products. Interventions aimed at improving circulation prior to definitive care are among the most controversial issues in trauma care. Evidence for the best way of accomplishing this goal in the prehospital setting is being aggressively sought. Splinting fractures decreases hemorrhage. Transition: Discussion of potential treatments aimed at improving circulatory status follows.
Key Points: Most external hemorrhage can be controlled with direct pressure. Tourniquet use is being reconsidered. Immobilizing fractures is important in controlling hemorrhage due to fractures. Depending on the patient’s condition, immobilization to a long backboard may be the best way of accomplishing this. Consider elevating extremities that continue to bleed after direct pressure is applied if fracture is not suspected. Bleeding from extremities that continues after direct pressure and elevation may be controlled with pressure to proximal arterial pressure points. Evidence is lacking for the efficacy of elevation and use of arterial pressure points. Topical hemostatic agents are being used in military applications but have risks that may not be acceptable in nonlethal situations.
Key Points: Prehospital fluid resuscitation seems to “make sense.” Increased circulatory volume should improve circulation. But there is no evidence that fluid therapy in the prehospital setting improves survival. Moderate hypotension may be beneficial in reducing bleeding. Hemodilution and increased blood pressure may impair clotting. Transport is not delayed to gain vascular access and administer fluids. Blood is the fluid of choice, but impractical in prehospital care. Alternatives Isotonic crystalloids Short-term volume expanders Lactated Ringers preferred Traditionally, a 3:1 ratio of crystalloid solution to the amount of blood loss has guided resuscitation, but the end-points of prehospital resuscitation are not known. Hypertonic crystalloids No improvement in survival rate over isotonic crystalloids Advantageous in military settings where large volumes of fluid cannot be carried Synthetic colloids Large protein molecules help maintain vascular volume Drawbacks: cost, allergic reactions, interference with blood typing, transmission of infectious diseases Blood substitutes Clinical trials show promise, but there are drawbacks
Key Points: Recommendations Adult patients in Classes II, III, or IV shock should receive an initial rapid bolus of 1000 to 2000 mL of warmed lactated Ringer’s solution. Ideal fluid temperature is 102 ° F (39 ° C) Pediatric patients should receive 20 mL/kg Maintain systolic blood pressure at 85 to 90 mm Hg or MAP of 60 to 65 mm Hg
Key Points: The best position for the patient in shock is the supine position. Trendelenburg position allows the abdominal organs to impede movement of the diaphragm, further compromising ventilation and oxygenation. Patients in hemorrhagic shock are maximally vasoconstricted; no blood is available in the lower extremity vasculature to provide an autotransfusion.
Key Points: Studies of PASG showed no benefit in urban areas. PASG has not been adequately studied in suburban and rural areas and may have been prematurely removed from suburban and rural ambulances. Indications Suspected pelvic fracture with hypotension Profound hypotension (systolic blood pressure below 50 to 60 mm Hg) Suspected intraperitoneal or retroperitoneal hemorrhage with hypotension Contraindications Penetrating thoracic trauma Splinting of lower extremity fractures Evisceration of abdominal organs Impaled object in the abdomen Pregnancy Traumatic cardiopulmonary arrest Not effective for control of external hemorrhage
Key Points: Patients must receive appropriate management without delay in transporting. The temperature of the patient compartment must meet the needs of the patient, not necessarily the needs of the crew.
Instructor Notes: Solicit responses from participants.
Key Points: A rapid return to normal vital signs and stabilization of the patient’s condition usually indicates that the patient has lost up to 20% of his blood volume but that hemorrhage has stopped. Surgery may still be necessary. An initial improvement followed by deterioration indicates 20% to 40% volume loss and on-going hemorrhage. The patient requires rapid surgical intervention. No change in condition after a rapid infusion of 1000 to 2000 mL of fluid indicates massive exsanguinating hemorrhage and the need for immediate surgical intervention to prevent death.
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