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Shock Evaluation and Management

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0 International Trauma Life Support, 6e
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 cause. Discuss the 3 shock syndromes: Low volume (absolute hypovolemia) High space (relative hypovolemia) Mechanical (obstructive) Discuss the management of shock: Posttraumatic 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. Chapter 8 Shock Evaluation and Management

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 United States and United Kingdom in Iraq war has led to new thinking in management of exsanguinating hemorrhage. Shock Evaluation and Management

2 Overview Four vascular system components of perfusion
Progression of shock signs and symptoms Three common clinical shock syndromes Hemorrhagic and neurogenic shock pathophysiology Controllable and uncontrollable hemorrhage, nonhemorrhagic shock syndromes Hemostatic agents Current indications for fluid administration Shock -

3 Shock Perfusion of tissues with oxygen, electrolytes, glucose, and fluid becomes inadequate. Shock -

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. Shock -

5 Normal Perfusion Heart Rate x Stroke Volume = Cardiac Output Cardiac Output x PVR = Blood Pressure 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. Shock -

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 Shock -

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

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 Shock -

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. Shock -

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 Shock -

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 brain senses that perfusion to tissues is insufficient, it sends messages down 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 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 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 point at which patient in “compensated” shock suddenly “crashes.” Eventually, hypoxia and acidosis cause cardiac dysfunction, including cardiac arrest, and, ultimately, death. Shock -

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 Shock -

13 Classic Shock Pattern Early shock Late shock 15–25% blood volume
Tachycardia Pallor Narrowed pulse pressure Thirst Weakness Delayed capillary refill 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 following classic patterns of “early” and “late” shock. Early shock: In “early shock,” body is “compensating” for physical insult that is causing 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 body’s ability to compensate for physical insult has failed. The hypotensive patient, then, is near death, requiring aggressive assessment and management by 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 pulse. Weakened pulses taken with other signs of shock should quickly lead you to suspect decompensated shock. 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, but it is of little use for detecting early shock in adults. Shock -

15 Capillary Refill NOTE: Progression Shock -

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 patient with an elevated pulse rate, try to determine underlying cause. Shock -

17 Capnography Level of exhaled CO2 as waveform (EtCO2) Falling EtCO2
Typically ~35–40 mmHg Falling EtCO2 Hyperventilation or decreased oxygenation EtCO2 <20mmHg 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 40—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 (see Chapter 5, Figures 5-11 and 5-12). Shock -

18 International Trauma Life Support, 6e
Shock Syndromes Low-volume shock Mechanical shock Absolute hypovolemia Hemorrhagic or other fluid loss Obstructive Cardiac tamponade Tension pneumothorax Massive pulmonary embolism Cardiogenic Myocardial contusion Myocardial infarction High-space shock Relative hypovolemia Neurogenic shock Vasovagal syncope Sepsis Drug overdose 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. Shock -

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 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. 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 sympathetic nervous system and causes loss of this normal vasoconstriction allows vascular space to dilate, becoming much “too large” for amount of blood in 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”). Shock -

21 High-Space Shock Types
Neurogenic shock Most typically after injury to spinal cord Injury prevents additional catecholamine release Circulating catecholamines may briefly preserve Sepsis syndrome Drug overdoses and chemical exposures Such as nitroglycerin, calcium channel blockers, antihypertensive medications, cyanide Nerves of sympathetic nervous system come off of spinal cord in thoracic (chest) and lumbar area. This is why sympathetic nervous system is often called “thoracolumbar autonomic nervous system.” Conditions that cause high-space shock are listed on slide. Although several causes of high-space shock exist, neurogenic shock, commonly called spinal shock, is addressed here because it may be caused by trauma. Shock -

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 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 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. Shock -

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. Shock -

24 Current Shock Research
Prehospital management research Hemorrhagic shock due to trauma and traumatic brain injury in prehospital environment Intravenous solutions Hypertonic saline may support vascular status by pulling interstitial fluid into vascular space. 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. CURRENT PREHOSPITAL RESEARCH No question of need for control of hemorrhage, supplemental oxygen, and early transport, but indications for most other therapies are still being debated. National Institutes of Health (NIH) is sponsoring major international clinical trial at this time to determine optimal treatment for hemorrhagic shock due to trauma (and traumatic brain injury) in prehospital environment. Since early days of modern shock treatment (about middle of 20th century), intravenous crystalloid solutions (and sometimes colloid) have been tested and/or utilized to reverse effects of hypovolemia. In addition, it has been previously proposed that intra-abdominal and pelvic bleeding may possibly be diminished by use of pneumatic antishock garment (PASG, or military antishock trousers, MAST). Research showed that PASG seemed to cause a worsening death rate when garment was applied to patients with uncontrolled bleeding. Indeed, current research into management of hemorrhagic shock due to trauma suggests a modified approach. Shock -

25 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 setting of bleeding vessels within thorax, abdomen, and pelvis probably increases internal bleeding, raising chance of death due to exsanguination. Shock -

26 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. Shock -

27 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 Shock -

28 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 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). Shock -

29 Controllable Hemorrhage
Management Control bleeding Shock position High-flow oxygen Rapid safe transport Large-bore IV access 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. Shock -

30 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. Shock -

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 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. Shock -

32 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 Shock -

33 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. Shock -

34 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 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. Shock -

35 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 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. Shock -

36 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. Shock -

37 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. Shock -

38 Discussion Shock -

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