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Chapter8 shock
- 1. International Trauma LifeSupport 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
- 2. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Shock Courtesy of Eduardo Romero Hicks, MD, EMT
- 3. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Objectives • List the four components of the vascular system necessary for normal tissue perfusion • Describe the symptoms and signs of shock in the order that they develop, from the very least to the very worst • Describe the four common clinical shock syndromes
- 4. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Objectives • Explain the pathophysiology of hemorrhagic shock, and compare it to the pathophysiology of mechanical and neurogenic shock • Describe the management of: – Hemorrhage that can be controlled – Hemorrhage that cannot be controlled – Nonhemorrhagic shock syndromes
- 5. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Objectives • Discuss the use of hemostatic agents for uncontrolled extremity hemorrhage • Discuss the current indications for the use of IV fluids in the treatment of hemorrhagic shock • Describe when it is appropriate to use tranexamic acid (TXA) in the management of hemorrhage
- 6. Copyright © 2016by Pearson Education, Inc. All Rights Reserved “Steady state” activity Normal Perfusion VASCULAR SYSTEM AIR EXCHANGE FLUID VOLUME PUMP Perfusion
- 7. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Normal Perfusion Blood Pressure = Cardiac Output × PVR Cardiac Output = Heart Rate × Stroke Volume
- 8. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Perfusion Preservation • Basic rules of shock management – Control bleeding where possible – Maintain airway – Maintain oxygenation and ventilation – Maintain circulation Adequate heart rate and intravascular volume
- 9. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Shock Progression Begins with injury, spreads throughout body, multisystem insult to major organs
- 10. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Shock Progression Red blood cells decreased Inadequate perfusion Anaerobic processes Hypoxia worsens Catecholamine increases Cell death
- 11. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Shock • Shock is a continuum – Signs and symptoms are progressive – Many symptoms due to catecholamines – Cellular process has clinical manifestations • Compensated and decompensated – How low can you go? – Healthy versus older or underlying problems
- 12. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Hypovolemic Shock • Compensated progression – Weakness and lightheadedness – Pallor – Tachycardia – Diaphoresis – Tachypnea – Urinary output decreased – Peripheral pulses weakened – Thirst
- 13. Copyright © 2016by Pearson Education, Inc. All Rights Reserved 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”
- 14. Copyright © 2016by Pearson Education, Inc. All Rights Reserved 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
- 15. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Classic Shock Pattern • Early shock – 15–25% blood volume – Weakness – Pallor – Tachycardia – Narrowed pulse pressure – Thirst – Delayed capillary refill • Late shock – 30–45% blood volume – Hypotension First sign of “late shock” – Weak or no peripheral pulse – Prolonged capillary refill
- 16. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Capillary Refill Courtesy of Louis B. Mallory, MBA, REMT-P
- 17. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Capillary Refill Courtesy of Louis B. Mallory, MBA, REMT-P
- 18. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Tachycardia • Most common early sign of illness – 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”
- 19. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Capnography Courtesy of Louis B. Mallory, MBA, REMT-P • Level of exhaled CO2 as waveform (ETCO2) – Typically ~35–40 mmHg • Falling ETCO2 – Hyperventilation or decreased oxygenation • ETCO2 <20 mmHg – May indicate circulatory collapse – Warning sign of worsening shock
- 20. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Shock Syndromes • Low-volume shock – Absolute hypovolemia Hemorrhagic or other fluid loss • Distributive 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
- 21. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Low-Volume Shock • Absolute hypovolemia – Loss of volume Blood vessels can 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
- 22. Copyright © 2016by Pearson Education, Inc. All Rights Reserved High-Space Shock • Relative hypovolemia – “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
- 23. Copyright © 2016by Pearson Education, Inc. All Rights Reserved 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
- 24. Copyright © 2016by Pearson Education, Inc. All Rights Reserved High-Space Shock • Neurogenic shock – 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
- 25. Copyright © 2016by Pearson Education, Inc. All Rights Reserved 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
- 26. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Treatment • General management of shock state – Control bleeding – Administer high-flow oxygen – Load and go
- 27. Copyright © 2016by Pearson Education, Inc. All Rights Reserved 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
- 28. Copyright © 2016by Pearson Education, Inc. All Rights Reserved PASG Research Courtesy of John Campbell • Pneumatic antishock garment – Uncontrollable internal hemorrhage due to penetrating injury May increase mortality, especially intrathoracic Probably increases bleeding, death due to exsanguination
- 29. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Controllable Hemorrhage • Management – Control bleeding – Shock position – High-flow oxygen – Rapid safe transport – Large-bore IV access
- 30. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Controllable Hemorrhage • Management – Fluid bolus (500–1,00 mL for adult and 20 ml/kg for pediatrics) rapidly, repeat if necessary – Cardiac monitor, SpO2, ETCO2 – Ongoing exam
- 31. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Uncontrollable Hemorrhage Courtesy of John Campbell • Management: External – Control bleeding – Shock position – High-flow oxygen – Rapid safe transport – Large-bore IV access – Fluid administration – Cardiac monitor, SpO2, ETCO2 – Ongoing exam
- 32. Copyright © 2016by Pearson Education, Inc. All Rights Reserved 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
- 33. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Uncontrollable Hemorrhage • Management: Internal – Rapid safe transport – Shock position – High-flow oxygen – Large-bore IV access – Fluid administration – Cardiac monitor, SpO2, ETCO2 – Ongoing Exam © Edward T. Dickinson, MD
- 34. Copyright © 2016by Pearson Education, Inc. All Rights Reserved 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
- 35. Copyright © 2016by Pearson Education, Inc. All Rights Reserved 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
- 36. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Special Situations • Severe head injury hypovolemic shock – Glasgow Coma Score of 8 or less – Fluid administration BP of 100 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
- 37. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Mechanical Shock • Tension pneumothorax – 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
- 38. Copyright © 2016by Pearson Education, Inc. All Rights Reserved 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
- 39. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Cardiac Tamponade • Management – Rapid safe transport to appropriate facility Cardiac arrest can occur in minutes – Fluid administration by local medical direction – Pericardiocentesis (if within scope of practice)
- 40. Copyright © 2016by Pearson Education, Inc. All Rights Reserved 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
- 41. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Myocardial Contusion • Management – Rapid safe transport Cardiac arrest may occur in 5–10 minutes – Cardiac monitoring and treat arrhythmias – Fluid administration may worsen condition
- 42. Copyright © 2016by Pearson Education, Inc. All Rights Reserved 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
- 43. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Tranexamic Acid (TXA) • Stabilizes fibrin clot after trauma • By mechanism it cannot be thrombogenic Dunn CJ, Goa KL: Tranexamic acid: A review of its use in surgery and other indications. Drugs 1999;57:1005-1032
- 44. Copyright © 2016by Pearson Education, Inc. All Rights Reserved CRASH-2 • Lancet 2010; 376: 23–32 Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant hemorrhage (CRASH-2): a randomized, placebo-controlled trial CRASH- 2 trial collaborators – Randomized, placebo controlled, double blind study – N>20,000
- 45. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Tranexamic Acid (TXA) • Tranexamic acid should be given as early as possible to bleeding trauma patients. For trauma patients seen late after injury (>3h), tranexamic acid is less effective and could be harmful. • TXA in EMS ─ Give in the field, early and when there is no other option ─ Give in the outlying hospital, prior to transport ─ Use 1:1:1 in the trauma center +/- TXA (if < 3h); the jury is still out.
- 46. Copyright © 2016by Pearson Education, Inc. All Rights Reserved Areas of Current Study • Finding the ideal resuscitation fluid • Blood administration to blood product ratio • Evaluating lactate levels to monitor shock • Hemostatic agents • Tourniquets • Monitoring lactate levels • Permissive hypothermia
- 47. Copyright © 2016by Pearson Education, Inc. All Rights Reserved 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
Editor's Notes
- #2 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)
- #3 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.
- #7 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.
- #8 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.
- #10 NOTE: See progression cycle on next slide.
- #11 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
- #12 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.
- #13 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
- #14 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.
- #16 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.
- #17 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.
- #18 NOTE: Progression
- #19 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.
- #20 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.
- #21 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.
- #22 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.
- #23 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”).
- #24 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).
- #25 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.
- #26 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
- #27 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.
- #28 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.
- #29 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.
- #30 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.
- #31 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.
- #32 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.
- #33 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.
- #34 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.
- #35 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).
- #37 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
- #38 NOTE: Decreased venous return = decreased cardiac output.
- #39 Fluid administration may be of value, but could worsen condition. Should be used only with local EMS medical direction.
- #40 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).
- #41 Signs of acute heart failure: distended neck veins, tachycardia, cyanosis, arrhythmia Not easily differentiated from cardiac tamponade Remember: Survival after traumatic arrest is rare.
- #42 Signs of acute heart failure: distended neck veins, tachycardia, cyanosis, arrhythmia Not easily differentiated from cardiac tamponade Remember: Survival after traumatic arrest is rare.
- #44 Give 1 g over 10 minutes, then 1g over 8 hours.
- #45 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.
- #46 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.
- #47 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.