Chapter 5 Shock Starts on page 71 of the provider manual.

Chapter 5 Shock Starts on page 71 of the provider manual

Objectives Identify causes and characteristics of shock in the trauma patient Describe pathophysiologic changes as a basis for assessment of the trauma patient in shock Plan appropriate interventions for the trauma patient in shock Evaluate the effectiveness of interventions for the trauma patient in shock Image: iStock

Triggers compensatory mechanisms
Shock Insufficient oxygen supply Inadequate tissue perfusion Cellular hypoxia Increased metabolic demand Oxygen demand Oxygen supply Shock is a syndrome of inadequate tissue perfusion, which results from insufficient oxygen delivery, uptake, and utilization to meet the metabolic demands of cells and organs. The body will dynamically respond by preserving homeostasis, producing changes to all systems and organs in order to meet the needs of the oxygen deprived cells. However, if left untreated, the compensatory mechanisms will no longer correct the hypoxia effectively, and its efforts will lead to acidosis, tissue ischemia, and cellular death and destruction. The shock state is not always readily apparent. It may not be obvious until the patient is already in distress as the body’s compensatory mechanisms maintain some homeostasis. Often, it is only after these compensation mechanisms begin to fail that we see the signs and symptoms of shock. The trauma nurse must be alert to subtle assessment findings in order to prevent deterioration to end organ failure and death. Image: iStock Triggers compensatory mechanisms

Pathophysiology Aerobic metabolism Efficient production of ATP
ATP maintains cellular metabolic function Anaerobic metabolism Inefficient production of ATP Lactic acid is a byproduct of production Leads to metabolic acidosis Cellular dysfunction leads to cell death Normal cell Influx of fluid Cytosol and organelles swelling Shock begins at the cellular level. Cells require ATP, the principal molecule for storing and transferring energy in cells. In the presence of oxygen, aerobic metabolism efficiently produces ATP. Hypoperfusion deprives the cell of oxygen. In anaerobic metabolism, ATP production is much less efficient. The process results in lactic acid formation and metabolic acidosis. If shock is prolonged and ATP does not meet the cell’s metabolic demands, the cellular membrane loses the ability to carry out its cellular function and its ability to maintain its integrity, leading to cell death and destruction. Rupture of membrane, leakage of proteases and lysosomes

Pathophysiology x = PRELOAD AFTERLOAD CONTRACTILITY STROKE VOLUME
CARDIAC OUTPUT STROKE VOLUME HEART RATE x = PRELOAD AFTERLOAD All shock states are affected by the components of cardiac output. Cardiac output is the product of stroke volume (SV) multiplied by the heart rate (HR). Stroke volume is the volume of blood in the ventricles that is ejected with each contraction. The components of stroke volume include: PRELOAD: the volume of venous blood returning to the heart This represents circulatory volume. Dehydration, blood loss, and vasodilation result in loss of preload. Increased preload can also cause problems such as congestive failure or fluid overload. AFTERLOAD: the pressure the heart must overcome in order to pump blood This is represented by the diastolic blood pressure. Hypertension makes it harder to pump blood and is an example of increased afterload. Decreased afterload can be a result of hypovolemic or vasodilation. CONTRACTILITY: the strength of contraction of the cardiac muscle Stroke volume is important to understand because injury and illness can affect preload, afterload, and contractility We will discuss this in detail, but start thinking about how some traumatic injuries may impact all of these variables. Animated heart video: CONTRACTILITY

Stages of Shock: Overview
Stage III: Irreversible Shock Stage II: Decompensated (Progressive, Hypotensive) Shock Stage I: Compensated Shock In the early stages of shock, the body reacts by activating compensatory mechanisms to meet the increased metabolic needs. If the shock state goes unrecognized, widespread cellular damage will lead to multisystem organ failure and death. There are three recognized stages in the shock continuum, but movement from one to the next can be different for each individual and circumstance. Stage I: Compensated Shock Stage II: Decompensated (Progressive, Hypotensive) Shock Stage III: Irreversible Shock The STAGES of shock are not to be confused with the CLASSES of shock used by the American College of Surgeons to estimate the quantity of blood loss, although some parameters overlap. See page 78. Images: ENA Let’s review each phase …

Stages of Shock: Compensated Shock
Assessment Findings OFTEN VERY SUBTLE Anxiety, confusion, restlessness Narrowing pulse pressure Rising diastolic BP Minimal change in systolic BP Tachycardia with bounding pulse Decreasing urinary output Assessment findings include: Mental status changes are noted, such as anxiety, confusion, and restlessness The blood pressure is usually within normal limits, with the diastolic beginning to rise with peripheral vasoconstriction and increased afterload The heart rate increases, and the pulse may be bounding due to catecholamine release As blood volume falls, the kidneys reabsorb sodium and water, decreasing output When low blood flow and poor tissue perfusion are detected, the body responds quickly with compensatory mechanisms. Slides review some compensatory mechanisms and corresponding physical findings. These compensatory mechanisms are meant to maintain homeostasis, so outward signs may be subtle. We rely on our knowledge of mechanism of injury to anticipate injuries that may cause shock and watch for these subtle cues. Images: ENA

Stages of Shock: Progressive or Decompensated Shock
Assessment Findings Decreased level of consciousness Hypotension Narrowed pulse pressure Tachycardia with weak pulses Tachypnea Cool, clammy, cyanotic skin In Stage II, decompensation begins as compensatory mechanisms begin to fail. Blood flow is reduced, leading to impaired oxygen and carbon dioxide transport. More cells are hypoperfused. Lactic acid levels rise as a byproduct of anaerobic metabolism. This lactic acid causes metabolic acidosis, which leads to further organ injury. Interventions can still turn the patient around, but it is more difficult to correct all of the problems and prevent deterioration to multiple organ dysfunction. Signs include: Mental status worsens - the patient may become obtunded The systolic blood pressure decreases; the pulse pressure narrows until vasoconstriction fails to provide cardiovascular support As the blood pressure drops, the pulses become weaker The heart rate is >100bpm The skin becomes cool and clammy, even cyanotic with peripheral vasoconstriction and loss of peripheral perfusion The serum lactate level rises as the cells are forced to resort to anaerobic metabolism due to hypoperfusion Images: ENA

Stages of Shock: Irreversible Shock
Assessment Findings Obtunded or comatose Profound hypotension Bradycardia Dysrhythmias Slow, shallow respirations Petechiae or purpura At Stage III, the shock state becomes irreversible. The body is unable to even TRY to compensate. Tissues and cells throughout the body become ischemic and necrotic, resulting in multiple organ dysfunction. Resuscitation interventions become increasingly difficult to restore tissue perfusion, with minimal ability to reverse morbidity and mortality. Assessment findings include: Mental status is obtunded, stuporous, or comatose Hypotension becomes profound Bradycardia with possible dysrhythmias Respirations become slow and shallow Skin is pale and cool Coagulopathies with petechiae, purpura, or bleeding Multiple organs begin to fail With worsening metabolic acidosis, lactate levels continue to rise and are an ominous sign of mortality Images: ENA

Compensatory Response to Shock
Baroreceptors sense decreased stretch Chemoreceptors detect increased CO2 and decreased pH Sympathetic nervous system is activated Adrenal glands release catecholamines Epinephrine Norepinephrine Picture shows the location and innervation of the arterial baroreceptors and chemoreceptors As blood flow decreases and arterial pressure falls below 80mmHg, oxygen delivery decreases as carbon dioxide levels increase. Baroreceptors, found in the carotid sinus and aortic arch sense the degree (or lack) of stretch, stimulating the “flight/fight” response, and the adrenal glands release epinephrine and norepinephrine to counter the loss of pressure by vasoconstriction and increasing the heart rate. Chemoreceptors in the carotid and aortic bodies and medulla detect an increase in CO2 and drop in pH, stimulating the CNS to increase respirations and increase blood pressure. High levels of epinephrine cause smooth muscle relaxation in the airways and increase arteriole smooth muscle contractility (potentiating the inotropic effect). Epinephrine also increases the heart rate (positive chronotropic effect), peripheral vasoconstriction, and glycogenolysis (breakdown of glycogen stores in the liver into glucose for cellular use). Peripheral vasoconstriction manifests as a narrowed pulse pressure. The rising diastolic pressure reflects an increase in systemic and peripheral vascular resistance (afterload). A narrowing pulse pressure may be one of the first concrete measurements signaling that the patient’s circulatory status is compromised and the body is trying to compensate. Norepinephrine increases heart rate and vascular tone through alpha-adrenergic receptor activation and triggers the release of glucose from energy stores. Image: ENA

Respiratory Response ↑ Elimination of CO2 Smooth muscle relaxation
allows for increased air flow ↑ Oxygen exchange ↑ Respiratory rate ↑ Oxygen intake Epinephrine causes smooth muscle relaxation around the bronchioles, increasing air flow and oxygen exchange. The rate and depth of respirations increase to increase oxygen intake and blow off carbon dioxide as respiratory compensation for metabolic acidosis. If left untreated, the pulmonary response may fail and necessitate assisted ventilations. Image: ENA

Cerebral Autoregulation
Blood is preferentially shunted to the brain, which cannot store glucose Altered LOC noted when autoregulation fails (MAP less than 50 mm Hg) Cool, pale , diaphoretic skin Blood shunted away from the skin and splanchnic circulation (GI tract, spleen, liver) Capillary refill > 2 seconds Cerebral Response: Cerebral autoregulation maintains a constant cerebral vascular blood flow as long as the mean arterial pressure (MAP) is maintained in the range of 50–150 mm Hg. The autoregulation of the brain is especially important because the brain has no capacity to store oxygen or glucose for later use. When autoregulation fails, changes in the level of consciousness is appreciated. Image: ENA

Renal Response Angiotensin II Altered LOC  ADH Thirst, relentlessness
 H2O retention Altered LOC Thirst, relentlessness Dilated pupils Angiotensin II  aldosterone  Na and H2O reabsorption Vasoconstriction ↓ pulse pressure Angiotensin I converted to angiotensin II in the lungs Hypoperfusion of the kidneys triggers a complex compensatory mechanism in the adrenal glands in an attempt to improve tissue perfusion that triggers the renin-angiotensin-aldosterone response. Renal ischemia causes the kidneys to secrete renin Renin accelerates the production of angiotensin I Angiotensin I is converted to Angiotensin II in the lungs by angiotensin-converting enzyme Angiotensin II effects include: Potent vasoconstriction causing a rise in vascular resistance and arterial pressure The release of aldosterone, which increases reabsorption of sodium and water in the distal tubules to increase intravascular volume The stimulation of arginine vasopressin (AVP), also known as vasopressin or antidiuretic hormone (ADH), which further increases retention of water Decreased urinary output may be noted, which can be an indication of poor renal perfusion and progression of the shock state. If shock is left untreated, it will progress to oliguria and renal failure. Image: ENA Renal hypoperfusion  release of renin  angiotensin ↓urine output

Immune Response Systemic Inflammatory Response Syndrome (SIRS)
Designed to limit the initial tissue injury or blood loss Multiple organ systems are impacted Tissue damage Organ failure Altered LOC Thirst, relentlessness Dilated pupils ↑ Respiratory rate ↑ Heart rate Hypotension Release of aldosterone and cortisol Constriction of splanchnic vessels Severe injury is associated with the Systemic Inflammatory Response Syndrome (SIRS). This response is an inflammatory response to blood loss and tissue damage rather than infection. Tissue hypoxia activates this protective and necessary response. Neutrophils are sent to the injury sites, activating signaling pathways that mobilize inflammatory cells. Tissue hypoxia also stimulates the secretion of multiple inflammatory mediators or biomarkers. The immune system contains a series of feedback loops to restore homeostasis. An exaggerated immune inflammatory response can result from massive tissue injury and hemorrhage or a prolonged and untreated shock state. It can induce a generalized, acute inflammatory response that affects multiple organ systems and sets in motion a cycle of inflammation–tissue damage–inflammation that is driven by cytokines, chemokines, and products of damaged, dysfunctional, or stressed tissue. Activation of the immune system increases platelet activity as well, generating a self-perpetuating cycle. Platelets form leukocyte-platelet aggregates, which are potent activators of immune cells and cause endothelial cell damage. Image: ENA Cool, clammy, pale or cyanotic skin Capillary refill > 2 seconds ↓urine output ↑specific gravity

Trauma Triad of Death Coagulopathy Trauma-induced
Resuscitation-related Acidosis Reduced pH Elevated lactate level Excessive fluids Hypothermia Exposure Excessive bleeding Worsens acidosis Acute endogenous coagulopathy often occurs within minutes following injury. Other causes such as hypothermia and metabolic acidosis induce coagulopathy after injury. The Trauma Triad of Death highlights 3 factors that can be lethal for the trauma patient. Coagulopathy: Whole blood loss results in depletion of clotting factors and the impaired ability to produce clotting factors Hypothermia: Inhibits the function of platelets and production of thrombin Acidosis: pH < 7.4 prolongs clotting times and reduces clot strength The result is disseminated intravascular coagulopathy (DIC), multiple organ dysfunction syndrome (MODS), and death. The trauma nurse can influence each of these factors by avoiding excessive fluids, initiating early hemostatic resuscitation, and keeping the patient warm. Picture Source based on:

Shock: Types and Causes
OBSTRUCTIVE SHOCK Compression/obstruction Cardiac tamponade Tension pneumothorax CARDIOGENIC SHOCK Pump failure Blunt cardiac injury Dysrhythmia Myocardial infarction DISTRIBUTIVE SHOCK Vasodilation Anaphylaxis Sepsis Spinal cord injury (neurogenic shock) HYPOVOLEMIC SHOCK Reservoir depletion Hemorrhage Hypovolemia There are 4 etiologies of shock Hypovolemic Shock – Volume problem Obstructive Shock – Mechanical problem Distributive Shock – “Pipe” problem Cardiogenic Shock – “Pump” problem The common denominator of them all is inadequate tissue perfusion and cellular oxygenation. Images: ENA

Hypovolemic Shock Hypovolemic shock is caused by a decrease in circulating volume. Hemorrhagic shock, as in trauma, is the loss of circulating whole blood. Other causes of hypovolemia can be from vomiting, diarrhea, and burns. Hemorrhage is the most common type of shock and the leading preventable cause of death. When volume is lost from the central circulation, preload is decreased, resulting in a decrease in cardiac output. The purpose of goal-directed therapy in hypovolemic shock is to stop the loss of volume and replace the lost volume. With hemorrhagic shock, replacement of volume includes blood and blood products. Images: ENA

Obstructive Shock Conditions that may cause obstructive shock include tension pneumothorax and cardiac tamponade. When pressure increases within the thorax, such as occurs with tension pneumothorax, or when the pericardial sac fills with blood, such as in cardiac tamponade, it prevents proper blood flow through the heart and great vessels. Goal directed therapy is aimed at relieving the obstruction and improving perfusion For tension pneumothorax, a needle decompression and chest thoracostomy is performed For cardiac tamponade, a pericardiocentesis or pericardial window is performed Refer to the Thoracic and Neck Trauma chapter and discussion for more information Images: ENA – tension pneumothorax

Cardiogenic Shock Cardiogenic shock is primarily a pump problem. There is no substantial blood loss and no obstruction. This is a problem in which the heart does not generate adequate cardiac output to move blood throughout the circulation. It is usually a deficit in cardiac contractility. “Pump” Problem: Common causes may be direct, such as blunt cardiac injury, or indirect, such as myocardial infarction or dysrhythmia. Goal directed therapy includes administration of inotropic or antidysrhythmic medications. If fluids are given before the cardiac function is supported, overload may occur. Images: ENA

Distributive Shock Distributive shock is primarily a problem with the vasculature or the pipes. There is no loss of circulating volume, and the pump is adequate. “Pipe” Problem: The vasculature, or pipes, becomes larger due to vasodilation. There are three general causes of distributive shock: With anaphylactic shock, histamine and other inflammatory mediators are released causing vasodilation and an increase in vascular permeability, which causes fluid to shift from the intravascular space to the interstitial space. This increases the size of the vasculature while decreasing the volume within, making the shock state more severe. In septic shock, vasodilation is related to release of endotoxins and cellular residue from bacterial cells. The effect is similar to the histamine response in anaphylaxis. In neurogenic shock, the form most commonly seen in trauma, the response is related to spinal cord injury. Injury causes a loss of sympathetic control over vascular tone and heart rate, resulting in vasodilation and bradycardia. While volume might not be directly lost, the vasculature is dilated. which decreases preload. Cardiac output does benefit from volume administration. The goal-directed therapy in neurogenic shock is judicious volume replacement along with the use of medications to promote vasoconstriction. Images: ENA

Current Management Strategies
Tourniquets Damage control resuscitation Hypotensive resuscitation Hemostatic resuscitation Tourniquets: early application of the tourniquet on an actively bleeding limb will minimize the likelihood of mortality from hemorrhagic shock Damage control resuscitation has two important components: Hypotensive resuscitation: Plasma and blood products are the primary fluids to correct blood loss and inadequate coagulation. Initial fluid management for the adult trauma patient in hemorrhagic shock consist of 500 mL boluses of isotonic crystalloid solution until blood products are available or a systolic blood pressure (SBP) of 90 mm Hg is achieved with a maximum of 1 liter (permissive hypotension). The goal is not hypotension, but adequate resuscitation without producing hypertension so as to not “pop the clot” and cause further bleeding or re-bleeding. Don’t pop the clot Hemostatic resuscitation: Balanced fluid resuscitation is an approach to resuscitation that addresses all components that are lost with hemorrhage, including fluid, packed red blood cells, plasma, and platelets while surgically controlling the source of bleeding. Traditional methods of large volumes of isotonic crystalloid produce hemodilution and loss of oxygen-carrying red blood cells and clotting factors. Administering packed red blood cells (PRBCs), platelets, and plasma replaces needed losses without hemodilution. Replace what they have lost Image: INDNAM [CC BY-SA 3.0 ( or GFDL ( from Wikimedia Commons Image: page 76 of provider manual INDNAM [CC BY-SA 3.0 ( or GFDL ( from Wikimedia Commons

Current Management Strategies
Massive Transfusion Protocol (MTP) Tranexamic acid (TXA) Damage control surgery Massive transfusion protocol (MTP) is dependent on early recognition and implementation, using a defined ratio of one part red blood cells to one part thawed plasma to one part platelets (1:1:1 ratio) and providing a detailed process for implementation. Hypocalcemia is a concern with massive transfusion because citrate is added as a preservative to banked blood to prevent coagulation. Citrate chelates, or binds with, calcium rendering it inactive. Because calcium is a vital part of the clotting cascade, hypocalcemia, as a result of massive transfusion, can actually worsen hypovolemic shock by permitting continued bleeding. Replacement of calcium chloride may be needed. Tranexamic acid (TXA) is a synthetic version of the amino acid lysine. It is an antifibrinolytic that inhibits activation of plasminogen, a substance that is responsible for dissolving clots. The first dose is typically given over 10 minutes with a follow-up dose of 1 gram given over 8 hours – research on TXA continues. Damage control surgery is a shift from rapid definitive surgery and complete repair to surgery that is intended to stop the bleeding, restore normothermia, and treat coagulopathy and acidosis This limits the strain on the patient in the early period of trauma This abbreviated surgery typically lasts no longer than 90 minutes in order to prevent hypothermia, acidosis, and coagulopathy (Trauma Triad of Death) Goal is to treat the physiology, NOT the anatomy Image: Mark Oniffrey [CC BY-SA 4.0 ( from Wikimedia Commons Image: iStock Mark Oniffrey [CC BY-SA 4.0 ( from Wikimedia Commons

Emerging Trends TEG or ROTEM REBOA Whole Blood Freeze Dried Plasma
Thromboelastometry (TEG/ROTEM): Unlike the standard coagulation assays, such as prothrombin time (PT INR) or partial thromboplastin time (PTT), which only measure clotting factor function, TEG® can also evaluate platelet function, clot strength and fibrinolysis. Rotational Thromboelastometry (ROTEM®) is similar to TEG® but uses a rotational technology. Both tests are used to guide transfusion strategies (including MTP) in the actively bleeding patient as well as reduce the need for unnecessary transfusions. Resuscitative endovascular balloon occlusion of the aorta (REBOA) is an emerging technique used in trauma patients to stop life threatening hemorrhage within the chest, abdomen, and pelvis. A balloon is inserted in the aorta, occluding blood flow below it and stopping the bleeding. It can temporarily restore blood pressure to within normal physiological values by increasing cardiac afterload, thereby increasing cerebral and myocardial perfusion until the patient can be taken to the operating room for definitive hemorrhage control. The use of whole blood, compared to individual blood components, may result in faster resolution of shock and coagulopathy, reduced transfusion requirements, and decreased donor exposure to the recipient. Freeze dried plasma can remain effective in its freeze dried form for up to two years, until it is reconstituted with sterile water and used. Images: ENA, iStock Image based on:

Emerging Trends Hemostatic dressings
Bleeding control education for the community Hemostatic dressings contain a hemostatic agent that hastens clotting until definitive hemorrhage control can be initiated. The “STOP The Bleed®” campaign is a public education initiative aimed at the layperson to use bleeding control kits placed in public spaces to provide hemorrhage control prior to the arrival of prehospital providers. This program continues to be offered to communities nationwide and trauma nurses are uniquely positioned to actively participate. Picture Source: Pfc. David Devich [Public domain], via Wikimedia Commons Picture Source: ReAl [CC BY-SA 4.0 ( from Wikimedia Commons ReAl [CC BY-SA 4.0 ( from Wikimedia Commons Pfc. David Devich [Public domain], via Wikimedia Commons

Correlate each type of shock with its identifying characteristics
Shock Activity Match each piece provided to the 5 spaces on your card Causative factors are placed over the shock image Think about what this looks like clinically Instructions Correlate each type of shock with its identifying characteristics Use printable activity cards and cut-outs of answers. Allow approximately 5-10 minutes for this activity. When the groups have completed their cards, BRIEFLY review the correct answers on slides 25–28. Give each group: 4 blank activity cards, one for each type of shock 1 set of 5 activity pieces for each card (20 pieces total, shuffled) Mechanism of injury Other clues Goal-directed therapy Values (HIGH, LOW, NO CHANGE, VARIES) Causative factors Match each piece provided to the 5 spaces on the card. The causative factors piece is placed over the Shock image.

Obstructive Shock BRIEFLY review the correct answers on slides 25-28.

BRIEFLY review the correct answers on slides 25-28.
Cardiogenic shock Variable for both preload and afterload

BRIEFLY review the correct answers on slides 25–28.
Distributive shock Respiratory rate MIGHT be low in neurogenic shock IF the cord injury affects the patient’s ability to breathe

BRIEFLY review the correct answers on slides 25-28.
Hypovolemic shock

Summary Shock is the mismatch between supply and demand of oxygen and nutrients Hemorrhagic shock is the most common preventable cause of death in a trauma patient Early recognition and goal-directed therapy leads to optimal outcomes It is important to remember the primary pathology of shock and its most common causes. It provides a framework in which to anticipate the appropriate goal-directed therapy for an optimal outcome. ADVANCE to next slide for 15-minute break timer, if desired. To use these slides, the sleep timer and screen saver must be modified to last longer than 15 minutes. If your version of PPT/Windows supports it, you may also turn on Presentation Mode by going to the Windows Mobility Center. Image: iStock

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Chapter 5 Shock Starts on page 71 of the provider manual.

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Chapter 5 Shock Starts on page 71 of the provider manual.

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