WK 3 Shock

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation: Controlling active bleeding

(1) Step 1: Apply direct pressure (palm of hand) over the bleeding site using a single layer of sterile gauze unless contraindicated. (deep open skull wound). (2) Step 2: If bleeding persists and not contraindicated (open skull fx): hemostatic gauze. Multiple products are available with variations in how they work and time to clotting. (a) Indications for use: direct pressure ineffective or impractical; wound not amenable to tourniquet e.g. trunk, groin, neck, head or other location where a tourniquet cannot be used. (b) Process steps: Pack wound by covering all bleeding surfaces; including deep areas of wound, with hemostatic gauze so product mounds slightly out of wound. Press: Apply direct pressure over the gauze until the bleeding stops. If blood soaks through 1st layer, apply a 2nd. (c) Once bleeding stops, apply pressure bandage to hold dressing in place. Frequently check for bleeding. (3) Step 3: Tourniquets (a) "An acutely avascular extremity must be recognized promptly and treated emergently. The use of a tourniquet may be life and/or limb saving in the presence of ongoing hemorrhage uncontrolled by direct pressure or hemostatic gauze. A properly applied tourniquet, while endangering the limb, can save a life. A tourniquet must occlude all arterial flow, as occluding only the venous system can increase hemorrhage. The risks of tourniquet use increase with time. If a tourniquet must remain in place for a prolonged period to save a life, the physician must be clear that the choice of life over limb has been made". (b) If a tourniquet is needed, follow manufacturer recommendations for application. If bleeding continues, place 2nd proximal to 1st. Tourniquets should be visible/well marked at all times. Anticipate pain. Lactic acid, potassium and anaerobic metabolites can accumulate distal to the band. Once applied, do not release until distal bleeding has been controlled. (c) Document the following: (i) MOI: Blunt, penetrating (ii) Site of tourniquet application: arm, leg; R or L (iii) Measures used prior to tourniquet application (iv) Time tourniquet applied (v) Who applied and/or removed tourniquet (vi) Success of hemorrhage control (vii) Total tourniquet time in minutes (viii) Whether pt required pain meds d/t tourniquet pain (ix) Tourniquet-related complications if known: ischemia damage, compartment syndrome (4) iTClamp: Temporary closure device designed to be applied to areas that would otherwise be poorly controlled, such as inguinal areas, axillary areas, extremities and scalp. The device is clamped around the open wound to seal edges together causing blood to form a clot below the skin. It does not replace surgery, but slows bleeding significantly. (5) Abdominal Aortic and Junctional Tourniquet-StabilizedTM (AAJT-S): indicated to control difficult bleeding in the primary junctional areas (inguinal and axillary) as well as the pelvis. (6) T-PODTM external pelvic stabilization device provides circumferential compression to the pelvis in patients with suspected pelvic fracture for pelvic stabilization in an effort to reduce bleeding. (7) Endovascular control (REBOA) - Resuscitative endovascular balloon occlusion of the aorta

Phase II (Uncompensated - Progressive)

1. Anaerobic metabolism becomes widespread and leads to systemic acidosis and depletion of high energy reserves (ATP), producing only two moles of ATP (5-10% of normal). Hypoxia will decrease the rate of ATP synthesis in the cell but will not damage the mitochondria unless it is sustained, severe, and associated with ischemia. 2. Decompensated or progressive shock occurs when ATP is insufficient to maintain cellular function. The circulatory system starts to fail despite the body's maximum efforts to compensate and the SBP falls below 100 mmHg. This leads to global hypoperfusion and multiple organ dysfunction syndrome (MODS). 3. Arterioles are constricted and AV shunts are open further reducing O2 delivery to cells. There is slow flow in the upper capillary and other capillaries may open. When there is slow flow in all of them, the pH drop is marked. Blood vessels are unable to sustain vasoconstriction. Vasodilation results in decreased peripheral vascular resistance, hypotension, and capillary flooding. 4. Rouleaux formation: RBCs "pile up like coins" in the capillaries 5. Acidosis produces continued increases in extracellular potassium 6. Micro-circulatory failure and cellular membrane injury: Prolonged reduction in tissue perfusion and decreased ATP production cause the sodium-potassium-ATPase pump to become dysfunctional. 7. Influx of water into cells: Loss of Na+ pump allows water to flood into cell, depleting the interstitial compartment. All intracellular organelles swell and become dysfunctional. 8. Intracellular enzymes are bound in a relatively impermeable membrane. Hypoxia, acidosis, and cellular flooding cause lysosomal enzymes to be released which digest all intra and extracellular proteins. 9. Acids and waste products act as potent vasodilators of post-capillary sphincters, releasing hydrogen ion, lactic acid, carbon dioxide and columns of coagulated red blood cells (Rouleaux formations) into the venous circulation. This is known as capillary washout. Rouleaux formations microembolize in the lungs. 10. Leakage of intracellular contents into the extracellular space triggers the inflammatory cascade. 11. Arterial pressure falls to the point that even the "protected organs" (auto-regulated) such as brain, heart and kidneys are not perfused. 12. Decreased venous return causes sluggish blood flow and pooling in vessels; leading to platelet agglutination and formation of microthrombi. 13. Myocardial depressant factor (MDF) released from an ischemic pancreas decreases the pumping action of the heart and further depresses CO. 14. Ischemia and necrosis lead to widespread organ failure: Some tissues are more responsive to hypoxia than others. Skeletal and smooth muscles are highly resistant to hypoxia and irreversible damage does not occur in isolated hepatocytes until 2.5 hours of ischemia. Brain cells suffer permanent damage after only a few minutes of sustained hypoxia. a. Heart: Decreased preload = decreased CO = decreased MAP. If MAP < 60 mmHg, coronary perfusion is impaired resulting in dysrhythmias, muscle ischemia, infarction, and pump failure. Peripheral pulses are weak or absent. Extremities become cyanotic and cold. b. Lungs: Failure evidenced by ARDS or non-cardiogenic pulmonary edema. Hypoxic vasoconstriction of pulmonary beds increases pulmonary arterial pressures, creating pulmonary hypertension. Pulmonary capillary blood flow reduction results in increased physiologic dead space, impaired gas exchange, reduced pO2 and increased pCO2. Alveolar cells become ischemic and decrease production of surfactant resulting in massive atelectasis and decreased pulmonary compliance. Concurrently, pulmonary capillaries become permeable to water resulting in interstitial and intra- alveolar edema at low pulmonary artery occlusion pressures (<18 mmHg). Net result: respiratory failure, severe hypoxemia, and respiratory acidosis. c. CNS: Decreased cerebral perfusion pressure and cerebral blood flow results in confusion, reduced responses to stimuli (verbal and painful), and coma. d. Kidneys: Hypoperfusion or toxic damage to the kidneys results in acute kidney injury. Damaged tubules cannot regulate sodium, potassium or waste products. Urine output drops. Urea and creatinine levels rise and wastes remain in the circulatory system. Metabolic acidosis worsens as kidneys are unable to excrete acids or regulate bicarbonate levels. e. Liver: Hypoperfusion and altered metabolic functioning reduce liver function. Diffuse clotting causes clotting factor consumption and the patient develops disseminated intravascular clotting (DIC). Ability to mount a response to infection and metabolize toxins and waste is reduced. Ammonia and lactate levels rise, and hepatocellular death occurs. Elevations in LDH, AST and ALT result. Outcome: ischemic hepatitis, hypoxic hepatitis or shock liver results. f. GI tract: Ischemic gut syndrome. Translocation of bacteria into the blood stream. Release of vasodilating endotoxins contributes to shock progression.

Hypovolemic/ Hemorrhagic Shock: On-going monitoring: Imaging

10. Radiologic studies: Chest, pelvic, spine films; CT; arteriograms 11. Ultrasound (FAST or eFAST exam)

TO BE COMPLETED W/N 6 HOURS OF TIME OF PRESENTATION OF SHOCK

5. Apply vasopressors (for hypotension that does not respond to initial fluid resuscitation) to maintain a mean arterial pressure (MAP) ≥65mmHg 6. In the event of persistent hypotension after initial fluid administration (MAP < 65 mm Hg) or if initial lactate was ≥4 mmol/L, re-assess volume status and tissue perfusion and document findings. 7. Re-measure lactate if initial lactate elevated.

Post-trauma critical illness: ARDS Continued

5. Currently the definition being accepted, the Berlin Definition consists of the following: a. Respiratory failure meeting the below definitions that occur within 7 days of a specific triggering event (such as sepsis, pneumonia, trauma, or even worsening of respiratory symptoms). In the majority of cases, ARDS develops within 72 hours of a precipitating event. b. Bilateral pulmonary opacifications may be identified on CT or chest x-ray that are consistent with that of pulmonary edema. c. These opacifications are not fully explained by a presence of heart failure or fluid overload. (If unsure, echocardiogram is completed to determine cardiac function). d. Severity is determined by the ratio of PaO2 to FiO2 (ex. PaO2=50, FiO2=70%→ 50/.7=71) (1) Mild ARDS: PaO2/FiO2: 200-300 (2) Moderate ARDS: PaO2/FiO2: 100-200 (3) Severe ARDS: Pa02/Fi02: Less than 100 6. Symptoms: The patient presents in respiratory distress and/or respiratory failure: dyspnea, tachypnea, tachycardia, cyanosis and bilateral crackles. Chest pain and cough may also be present. The patient will have increased dead space (as evidenced by increasing CO2 and decreasing 02 levels), as well as decreased compliance (increased difficulty with breathing or increased resistance to bagging if intubated).

Irreversible/refractory shock

The total O2 debt and its rate of accumulation are critical determinants of survival. Inability to restore O2 to tissues invariably leads to death. Irreversible shock is diagnosed when the patient is refractory to therapeutic management. 1. Profound hypotension despite vasopressors 2. Severe hypoxemia despite oxygen therapy 3. Dilated, sluggish pupils 4. Severely decreased body temperature 5. Acute renal failure 6. Multiple emboli, diffuse intravascular clotting, severe coagulopathy 7. Infections 8. Decreased responsiveness 9. Decreased sympathetic response (bradycardia, hypotension, circulatory failure) 10. Tissue damage extensive and incompatible with life 11. Multi-system organ dysfunction syndrome (MODS) evident → patient dies

Hormonal compensation in Phase I of Shock: Renin - Angiotensin - Aldosterone cycle

This cycle causes the following compensations: (1) Hypoperfusion of the kidneys triggers the release of renin that reacts with alpha-2 globulin in the liver to release angiotensin I. Angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II in the lungs. (2) Angiotensin II is a potent vasoconstrictor. It also causes the adrenal gland to secrete the hormone aldosterone (mineralocorticoid). (3) Aldosterone causes sodium reabsorption and potassium excretion by the kidney to increase intravascular volume. (4) Net effects: Conservation of water (decreased urinary output), increased BP due to augmented blood volume and vasoconstriction, decreased urine sodium, increased urine potassium, and increased urine concentration or osmolality.

Classify patient as exsanguinating if:

a. Hemodynamic instability; b. Initial blood loss 40% or greater; and/or c. Massive ongoing blood loss

Post-trauma critical illness: Inflammatory and immune response syndromes: Sepsis and Septic Shock: Vasoactive agents

(1) "As a result of the effects of sepsis on the venous capacitance vessels and myocardial function, it is likely that less than 40% of hypotensive patients with septic shock are 'fluid responders'. In patients with sepsis and in experimental models, less than 5% of a crystalloid bolus remains intravascular an hour after the end of the infusion. It is therefore likely that the hemodynamic effects of a fluid bolus (in the fluid responders) are short-lived, with the net effect being the shift of fluid into the interstitial compartment with tissue edema". (2) An initial target MAP of 65 mmHg is recommended in patients with septic shock requiring vasopressors. (3) The Surviving Sepsis Campaign recommends norepinephrine as the first choice vasopressor. (Strong recommendation, moderate quality of evidence). Norepi increases preload, cardiac output, and MAP largely reversing the hemodynamic abnormalities of severe vasodilatory shock. It also increases cardiac index, systemic vascular resistance and central blood volumes. Norepinephrine may be safely given through a well-functioning peripheral venous catheter. (4) The Surviving Sepsis Campaign suggest adding either vasopressin (up to 0.03 U/min) or epinephrine to norepinephrine with the intent of raising MAP to target, or adding vasopressin (up to 0.03 U/min) to decrease norepi dosage. (Weak recommendation, low quality of evidence) i. If shock is not resolving quickly (1) Surviving Sepsis Campaign recommends further hemodynamic assessment (such as assessing cardiac function) to determine the type of shock if the clinical examination does not lead to a clear diagnosis. (2) Dynamic over static variables should be used to predict fluid responsiveness, where available. (Weak recommendation; low quality of evidence) (3) Guide resuscitation to normalize lactate in patients with elevated lactate levels as a marker of tissue hypoperfusion.(Weak recommendation; low quality of evidence)

Post-trauma critical illness: Inflammatory and immune response syndromes: Sepsis and Septic Shock: Antibiotics

(1) Administration of IV antimicrobials should be initiated as soon as possible after recognition and within 1 h for both sepsis and septic shock. (Strong recommendation, moderate quality of evidence). (2) They recommend empiric broad-spectrum therapy with one or more antimicrobials to cover all likely pathogens. (Strong recommendation, moderate quality of evidence). (3) If the severe inflammatory response is determined to be of non-infectious nature, antibiotics should not be used. k. Other recommendations: (1) Routine screening of potentially infected seriously ill patients for sepsis should occur with use of a standardized screening tool. (2) Serial re-evaluation, every 20-30 minutes should be completed to monitor response to resuscitative efforts. (3) Current science states that limiting fluids and beginning pressors early may be beneficial if increased CVP or filling pressures are noted without corresponding improvement in hemodynamic status. In addition the routine practice of fluid boluses for hypotension after the initial 6-hour fluid resuscitation phase can be damaging to patient outcomes l. Complications: MODS, DIC, ARDS, and death

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation: Massive Transfusion

(1) Defined as >10 units pRBC in 24 hours or more than 4 units in one hour (2) Foundations of replenishing with supplemental blood components is based on the idea that many patients in hemorrhagic shock have developed, due to their mechanism of hemorrhage, a complex coagulopathic disorder that is not resolved with the use of RBC units alone. (3) The need for massive transfusion can be identified by patients who have at least 2 of the following indicators: penetrating trauma, positive FAST for fluid, arrival systolic blood pressure of less than 90 mmHg, and /or pulse rate of over 120 bpm. (4) During initiating and continuation of massive transfusion protocols, it is vital that efforts are focused on stopping hemorrhage, including surgical control, damage control resuscitation, correction of shock, impaired tissue perfusion and hypoxia, and prevention or reversing coagulopathies.

Post-trauma critical illness: Inflammatory and immune response syndromes: Sepsis and Septic Shock: Initial resuscitation

(1) Frequent assessment of the patients' volume status is crucial throughout the resuscitation period. (2) "Pathophysiologically, sepsis is characterized by vasoplegia with loss of arterial tone, venodilation with sequestration of blood in the unstressed blood compartment and changes in ventricular function with reduced compliance and reduced preload responsiveness. Data suggest that sepsis is primarily not a volume-depleted state and recent evidence demonstrates that most septic patients are poorly responsive to fluids. Furthermore, almost all of the administered fluid is sequestered in the tissues, resulting in severe edema in vital organs and, thereby, increasing the risk of organ dysfunction. A physiologic, hemodynamically guided conservative approach to fluid therapy in patients with sepsis would likely reduce the morbidity and improve the outcome of this disease" (3) Sepsis-induced hypoperfusion should be resuscitated with at least 30mL/kg of IV crystalloid fluid within the first 3 hours if hypotension persists. (Strong recommendation; low quality of evidence) (4) They recommend that following initial fluid resuscitation, additional fluids be guided by frequent reassessment of hemodynamic status. (5) "Diastolic dysfunction is becoming increasing recognized, particularly in patients with hypertension, diabetes, obesity and with advancing age. These conditions are associated with an increased risk of sepsis and may further increase the prevalence and severity of diastolic dysfunction in patients with sepsis. Patients' with diastolic dysfunction respond very poorly to fluid loading.

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation: Pharmaceutical plasma expanders

(1) Human plasma protein fraction (Plasmanate) (2) Hydroxyethelene starch - Hespan (a) Composition: A totally synthetic, nonbiologic colloid made from a heterogeneous group of starch molecules in NS that resembles glycogen. (b) The FDA has issued a box warning for Hespan because of the noted increases in mortality and/or severe renal injury when used on critically ill adult patients, including patients with sepsis and those admitted to the intensive care unit. Hespan should not be given to trauma patients in shock or with critical illness.

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation: Colloids

(1) Studies do not demonstrate a survival benefit over crystalloids. (2) Albumin (colloid): The use of albumin for resuscitation has also been studied. A summary published in 2011 by the Cochrane Collaboration demonstrates no evidence of reduced mortality with the use of albumin. (3) Most abundant protein in serum, accounting for 80% of the oncotic pressure in plasma. Albumin is produced in the liver at a rate of 150-200 mg/kg/day. Approximately 50-60% of endogenous albumin is found in the interstitial space. (4) The Cochrane Collaboration published summary data regarding the administration of albumin during resuscitation for critically ill patients. Thirty-eight trials were reviewed and it was determined that albumin carries no benefit for the patient when used during resuscitation or as a volume expander.

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation: Vascular access

(1) The number and size of vascular access catheters depend on the patient's age, size, nature of complaint, volume needs, and urgency of their condition. If large fluid volumes are needed, use the largest, shortest catheter that will easily fit into an accessible vessel. For most adult patients in shock, start two peripheral venous lines using 14-16 gauge catheters preferred (minimum 18 g for peripheral access); one above and one below diaphragm may be requested to limit vascular loss through the zone of injury. (2) Choice of site for alternate access based on clinician experience and skill. Consider IO infusion for those who are unresponsive and need urgent volume resuscitation when peripheral access is unobtainable. IO insertion into long bones, including proximal humerus, can provide rapid entry into the vascular space and high volume infusion. See IO procedure.

Hormonal compensation in Phase I of Shock: Adrenocorticotropic hormone (ACTH)

(1) The ventral hypothalamus is affected by sensory input from the ascending reticular activating system (ARAS), brain stem, subcortex, and limbic system. This leads to secretion of releasing factor for ACTH by the anterior hypothalamus, which acts on the anterior pituitary to secrete ACTH. (2) Normal release is triggered via circadian modulations and negative feedback via the adrenal glands. Stress and trauma override these. ACTH causes the adrenal cortex to ↑ production of glucocorticoids (cortisol), which ↑ metabolic processes in the liver and kidneys to ↑ blood glucose levels. (3) Quadriplegia inhibits ACTH release in response to surgery.

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation: Nursing considerations in fluid and blood administration

(1) Warm all crystalloids and blood products given to a patient in shock. The patient must mount sufficient kilocalories (energy) to warm room temperature fluids to body temperature (37° C) which rapidly depletes energy reserves. Large volumes of room temperature fluids will result in hypothermia and may result in clotting disorders (coagulopathies). Crystalloid solutions may be kept in a fluid warmer or given via rapid infusion warming devices. Research suggests that IVF may be warmed to 40° C. (2) Give blood using a high volume, rapid infusion warmer; Use standard blood administration filters and change tubing as needed. (3) Monitor lab values for calcium, potassium, acidosis and ECG for any changes. Notify physician so hypocalcemia, hyperkalemia, and acidosis is treated as changes develop. (4) Observe patient for signs of spontaneous bleeding. Platelets and fresh-frozen plasma may be needed when bleeding is apparent or the results of lab studies are abnormal. Adhere to local protocols. Some require FFP and/or platelets after units of packed cell or whole blood have been administered. (5) Eliminate extension sets and stopcocks from IV setups; may inhibit fluid flow. Pressure bags may be used on IV solutions and blood products to increase flow rates. o. Use of vasopressors in severe hemorrhagic shock may aid in resuscitation but must be used in such a way as to not increase severe vasoconstriction, and not used to take the place of adequate volume resuscitation and hemorrhage control.

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation: Packed red blood cells (PRBCs)

(250-300 mL/unit) (a) Composition: Remnants of whole blood after removal of 80%-90% of the plasma. Minimal clotting factors or platelets. Major limitation of PRBCs. (b) PRBC's are administered in boluses of 10 mL/kg. Each unit of PRBCs increases Hct by 3% if hemorrhage is controlled. (c) O2 carrying capacity of 1 unit PRBCs = 1 unit whole blood but Hct increases to 70%-75% of the infusion volume. (d) Indications for use: Packed red blood cells (PRBCs) should be administered if no response to crystalloid resuscitation. PRBC administration should coincide with administration of plasma and platelets. (e) Restore RBC deficiency, increase O2 carrying capacity while preventing fluid overload. (f) Advantages: Reduces the risk of transfusion reactions and disease transmission. Packed cells have less citrate, antigenic debris, phosphate, potassium, and negative thermal load than whole blood. (g) Precautions and nursing considerations: Increased viscosity can result in slow flow rates during administration. If used during transfusions, closely monitor the clotting factors, platelets and volume. Accentuates plasma protein dilution. Must infuse within four hours.

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation: Massive Transfusion: Resuscitation ratios

(a) A ratio of 1:1:1 platelet to plasma to RBC transfusion strategy was associated with decreased death by exsanguination in the first 24 hours and increased chance of hemostasis on post hoc analysis when compared to a ratio of 1:1:2, but the primary outcome of 24-hour and 30-day mortality did not differ. (b) Battlefield experience indicates reconstituting blood components to resemble whole blood improves the survival rate of patients. Optimal ratio of plasma to red blood cells appears to be in a range of 1:2.4 or higher. (6) Goals include fibrinogen levels of 1.5 g/L (150 mg/dL) which may be achieved through the use of cryoprecipitate 50 mg/kg or fibrinogen concentrate doses of 3-4 g. (7) Lactate levels and base deficits are monitored to assess responsiveness to therapy. (8) The following must be anticipated, monitored for, and corrected: (a) Hyperkalemia or hypokalemia: Banked blood has high K levels because of cell lysis that occurs during collection and storage. Hypokalemia is more common due to transient metabolic alkalosis (from citrate preservative in blood) that causes K to move into the cells. (b) Hypothermia if transfusion of large amounts of cold blood. Blood is stored at 4° C. All blood should be administered by a high volume warmer to prevent hypothermia (c) Hypocalcemia: Stored blood contains calcium citrate and EDTA that binds with ionized serum calcium and causes a Ca deficit. S&S: Prolonged QT segment, skeletal muscle tremors, perioral tingling. Monitor ionized Ca levels serially and/or administer 1 gram calcium gluconate for each 4 units of PRBCs transfused. (d) Early acidosis followed by alkalosis. Stored blood has a pH of 7.0; pH decreases over its storage life. The older the blood, the lower the pH. Citrate in stored blood is broken down by the liver to become bicarbonate, causing metabolic alkalosis. (e) Sodium and chloride abnormalities from crystalloid resuscitation. (9) PT, PTT, INR, fibrinogen and platelet levels should be monitored every 30-60 minutes. (10) Point of care coagulation testing (thromboelastography, thromboelastometry, Sonoclot®) is also being studied to determine their effectiveness in assessing response to massive transfusion therapy. (11) Once bleeding is stopped and the patient is stable, transfusion usually occurs if hemoglobin levels are less than 7 g/dL. Again assessment of the patient's clinical status may override this guideline.

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation: Whole blood

(a) Composition: Complete, undivided blood; contains 200 mL of RBCs and 250 mL of plasma that contains WBCs, platelets, and coagulation factors. (b) Indications for use: To replace lost whole blood and to increase hemoglobin and hematocrit values. (c) Advantages: Lower viscosity than packed cells and does not require saline. Lower risk of disease transmission because it is exposed to fewer donors. (d) Disadvantages: Stored whole blood has increased amounts of ammonia, potassium and cellular debris (decreased pH). (e) It is preferable to give type-specific and Rh compatible blood after obtaining a blood sample for T&CM. This requires 30 minutes preparation time. If time is of the essence, the universal donor type is O-neg. In men and women beyond childbearing age, type O Rh positive blood may be used until type-specific blood is available. If large amounts of type O blood are given and then type-specific blood is given later, a transfusion reaction may occur. Rh- negative blood will prevent Rh sensitization.

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation: Cryoprecipitate

(a) Composition: Concentrate removed from cold-thawed plasma which contains Factor I (fibrinogen), Factor VIII (antihemophilic factor), Factor XIII (fibrin stabilizing factor) and fibronectin in 10-15 mL of plasma. May freeze up to one year. (b) Usually dosed at 2-4 bags/10 kg body weight. The cryoprecipitate is usually diluted in the laboratory when the units are pooled together. They may be administered IV push with stopcock and syringe. (c) Indications for use: Restore fibrinogen when massive transfusion of stored blood has caused a dilutional coagulopathy. Indicated if fibrinogen is < 0.8.

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation: Platelets

(a) Composition: Obtained by centrifuging whole blood. Thrombocytes are extracted from plasma and resuspended in plasma. Available in single-dose or multiple-dose units in a 30-50 mL bag. Usually ordered 4- 10 units at a time. Blood bank may pool the entire order into one bag. (b) Indications for use: Promote clotting/control bleeding in patients with thrombocytopenia and when massive infusion of crystalloid and/or banked blood have caused a dilutional thrombocytopenia. Indicated if platelet count is < 50 to 100,000. (Blood stored > 72 hours has nonfunctional platelets). (c) Also consider the need for platelets in patients who are on antiplatelet therapy (aspirin (ASA), clopidogrel (Plavix), prasugrel (Effient), dipyridamole (Persantine) or ticlodipine (d) Precautions and nursing considerations: Must be infused rapidly or they lose their viability. May inject directly IV push via stopcock and syringe at 5-10 mL/min.

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation: Plasma (FFP)

(a) Composition: One unit of FFP contains 100 to 300 mL of plasma separated from a unit of uncoagulated whole blood; fresh or fresh frozen that contains clotting factors and plasma proteins, but no platelets. (b) Frozen within 6 hours of collection (c) Indications for use (i) Active uncontrolled bleeding; persistent base deficit due to hemodilution and/or hypovolemic shock. (ii) Correct coagulation defects if PT or PTT is > 1.5 times normal. (iii) Rapid reversal of Coumadin effects (iv) Thrombotic thrombocytopenia purpura (v) Selected clotting-factor deficiencies (d) Precautions: Not used as first choice volume expander. Use promptly after thawing to maximize quantity of clotting factors administered. (e) Hemoglobin-based carriers: Currently being studied due to blood shortage. Not available for use in the United States. This is acellular recombinant hemoglobin used as an oxygen carrier.

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation: Thresholds to treat with blood or blood products

(a) Good Clinical Practice Statement: "When deciding to transfuse an individual patient, it is good practice to consider not only the hemoglobin level, but the overall clinical context and alternative therapies to transfusion. Variables to take into consideration include the rate of decline in hemoglobin level, intravascular volume status, shortness of breath, exercise tolerance, lightheadedness, chest pain thought to be cardiac in origin, hypotension or tachycardia unresponsive to fluid challenge, and patient preferences." (b) Definitions: Restrictive (threshold of 7 g/dL) and liberal (10 g/dL). (c) Patients with acute hemorrhage can still have normal or high hemoglobin concentrates. Hgb levels in active hemorrhage fail to accurately predict the actual RBC mass present and anemia is often only discovered when non- RBC fluid replacement is provided. Thus, the decision to transfuse in the face of acute hemorrhage is based on assessment of ongoing blood loss, patient hemodynamic status, comorbidities, risks and benefits of transfusion, concentration of hemoglobin, and clinical setting. (d) At this time, in acute trauma, a specific transfusion threshold is not warranted as a trigger for transfusion. Resuscitation of the trauma patient with hemorrhage should be performed based on clinical status and not laboratory values. If the patient is in hemorrhagic shock, with acute hemorrhage and hemodynamic instability, transfusion is warranted. Once the patient is hemodynamically stable, transfusion should be considered in the setting of anemic symptoms (e.g., chest pain, shortness of breath, or poor distal perfusion), with 1 unit of RBCs given at 1 time. (e) Note: A restrictive hemoglobin threshold of 7 g/dL is now generally recommended in the new American Association of Blood Banks guidelines and multiple meta-analyses and is supported in GI bleeding, sepsis, critical illness, and trauma. Patients with active ischemia in acute coronary syndrome and neurologic injury require additional study. However, most physicians agree that transfusion is required in the setting of acute, life-threatening trauma with massive hemorrhage. (f) Studies in patients with traumatic brain injuries and subarachnoid hemorrhages have suggested using a transfusion threshold of Hgb 8 to 9 g/dL, but more information is needed to develop true recommendations for transfusion. A 2016 meta-analysis evaluated RBC transfusion in patients with TBI and found no difference in mortality, with the transfusion threshold varying from Hgb 6 g/dL to 10 g/dL.

Hypovolemic/ Hemorrhagic Shock: On-going monitoring: Intra-abdominal hypertension

(abdominal compartment syndrome [ACS]) a. If intra-abdominal pressure becomes higher than pressure in inferior vena cava, CO decreases. If intra-abdominal pressure is higher than pressure in the renal veins, renal blood flow decreases, resulting in decreased urinary output and increased chance of renal failure. Pressure increase mechanically impairs diaphragmatic movement leading to ARDS and death in the early post-op period. b. Intra-abdominal hypertension is an on-going sign of hemorrhage, third space losses into intestine and abdominal cavity, and must be detected and corrected as soon as possible. c. Intra-abdominal pressures should be measured for any patient with a known risk factor for the development of abdominal compartment syndrome. "Intra- abdominal pressures should be measured every 4-6 hours or continuously". If elevated intra-abdominal pressures (>20 mmHg) are noted, notify the physician immediately and follow hospital protocol for control of abdominal compartment syndrome. Anticipate orders for analgesia, sedation and possibly paralysis in an attempt to control pressure. If pressure is uncontrollable with the use of medications and other medical therapy, the patient may need to go to surgery and have the abdomen surgically decompressed. d. Although intra-abdominal hypertension is more common, the rate of ACS has been reduced. Resuscitation and surgical strategies such as leaving the abdomen open on at risk patients have reduced the morbidity of patients due to ACS.

Class IV hemorrhage

(exsanguination per ATLS) a. Acute loss of >40% total blood volume; >2,000 mL in an adult. b. Compensatory mechanisms ineffective and may shut down; classic shock symptoms c. Signs & symptoms (1) Mental status: Confusion, lethargy, coma (2) HR: Tachycardia > 140; barely palpable in central arteries if they can be found at all (3) Cardiac dysrhythmias (4) SBP < 60 mmHg (5) Pulse pressure very narrow: 10 mmHg (6) RR: Tachypnea > 35/minute; shallow and ineffective (7) Cyanotic lips, nailbeds; cyanotic, ashen gray skin; diaphoretic (8) Negligible urinary output (9) Base deficit: -10 or greater (10) Need for blood products: Massive transfusion protocols 6. These stages assume a previously healthy person. Any pre-existing condition may affect volume loss or patient response in terms of the speed at which they move from one stage to the next. The rate of blood loss affects the effectiveness of compensatory mechanisms; the slower the loss, the better compensatory mechanisms will work.

Hypovolemic shock: Effects on Hct (% of RBCs in blood)

1. Adult male 7.2% of ideal weight or 40%-54% 2. Adult female = 7.0% of idea weight or 37%-47% 3. Acute loss of circulating volume so that Hct drops below 30 4. Decrease in Hct is influenced by transcapillary refill that takes some time to occur. As hydrostatic pressure decreases in the capillary bed due to reduced blood flow and vasoconstriction, fluid is drawn in from the interstitial space. This accounts for the decrease in hematocrit several hours after admission. 5. Takes 6-24 hours to see maximal effects so need serial Hct determinations to assess actual volume loss. 6. One unit of whole blood or packed red cells will increase Hb concentration 1 g/dL or 3 to 4% hematocrit units if the person is not actively bleeding. 7. The kidneys release erythropoietin, a protein that stimulates RBC production in red bone marrow, to help restore RBCs lost through hemorrhage.

Hypovolemic shock: Precipitating factors

1. Hemorrhage a. Most prevalent in the trauma patients due to (1) blunt or penetrating injury to vessels and/or organs; (2) long bone or pelvic fractures; (3) major vascular injuries including traumatic amputation; and (4) multi-system injury. b. Organs/organ systems with high incidence of exsanguination from penetrating injuries (1) Heart (2) Thoracic vascular system (3) Abdominal vascular system (a) Abdominal aorta (b) Superior mesenteric artery (4) Venous system (a) Inferior vena cava (b) Portal vein (5) Liver c. Severe hemorrhage = blood loss >150 mL/min. A rate of 250 mL/min leads to exsanguination that causes the patient to lose 1⁄2 of their entire blood volume in about 10 minutes. 2. Fluid (plasma) shifts: Plasma shifts from intravascular to interstitial space as a result of increased capillary permeability, i.e., crush, burn injuries. 3. Body fluid may also be lost due to a. dehydration; b. excess GI drainage; diarrhea; c. ascites; d. diabetes insipidus; e. excess wound drainage; f. acute renal failure - high output phase; g. insensible losses through skin and lungs; and/or h. osmotic diuresis secondary to hyperosmolar states.

Post-trauma critical illness: Summary

1. Inflammatory and immune system responses that become wide spread, produce havoc on the body, playing a major role in all syndromes discussed here: DIC, ARDS, SIRS/sepsis, MODS and PICS. 2. Many times, infection is the culprit initiating the processes from which these syndromes arise. However, trauma can cause these syndromes as well. 3. In order to positively impact patient outcomes, the trauma nurse must work in conjunction with resuscitative personnel, identifying potential risks, and treating patients aggressively. 4. Goals of shock resuscitation should include: restoration of adequate oxygenation and perfusion, rapid hemorrhage control and normalization of base deficit and serum lactate levels; adequate volume repletion without causing fluid overload or positive fluid balance; conservation of energy stores by administration of appropriate amounts of warmed fluids (to prevent hypothermia, DIC, ALI, SIRS/Sepsis); identification and treatment of those patients needing protective lung strategies; and optimizing hemodynamic status to repay oxygen debt and prevent stagnation of circulation. 5. Review of literature suggests that treatment of our most critical patients is a delicate balance of aggressive resuscitation with avoidance of over-resuscitation. Vigilant assessment and monitoring of these patients can help identify strategies for resuscitation. 6. More research is needed regarding prophylactic strategies in the emergency department and their impact on the long term functioning of the surviving trauma patient.

TO BE COMPLETED W/N 3 HOURS OF TIME OF PRESENTATION OF SEPSIS

1. Measure lactate level 2. Obtain blood cultures prior to administration of antibiotics 3. Administer broad spectrum antibiotics 4. Administer 30mL/kg crystalloid for hypotension or lactate ≥4mmol/L * "Time of presentation" is defined as the time of triage in the emergency department or, if presenting from another care venue, from the earliest chart annotation consistent with all elements of severe sepsis or septic shock ascertained through chart review.

Post-trauma critical illness: ARDS

1. Overview: ARDS is the most common complication affecting the morbidity and mortality of critically ill or injured patients in the ICU. Transfusion-related acute lung injury (TRALI) and ventilator-associated lung injury (VALI) are discussed in the literature, and according to the new classification system, are considered etiologies of ARDS. 2. Physiology: ARDS is an inflammatory pulmonary process that results in increased leakage of the pulmonary vascular bed, increased lung weight, and loss of functioning lung (increased dead space) associated with hypoxemia, pulmonary opacification, pulmonary shunting and decreased lung compliance. Injury or trauma occurs directly to the tissues (such as with pulmonary contusions, aspiration pneumonia, near drowning, pulmonary barotrauma or inhalation injury) or indirectly from inflammatory or autoimmune responses (such as with pancreatitis, certain blood transfusions, sepsis, drug reactions or fat emboli). 3. Risk Factors: Risk factors may include shock, trauma, sepsis, pneumonia, aspiration, pancreatitis, drug overdose, blood transfusion (TRALI), burns, and smoke or toxic gas inhalation. The highest risk of ARDS is severe sepsis and multiple blood transfusions; however the ratio of blood to fresh frozen plasma is irrelevant. Patients who are elderly, have pre-existing problems, such as chronic alcohol abuse, chronic lung disease, or widespread, direct injury to pulmonary tissues are more likely to develop ARDS. For trauma patients ONLY, studies suggest incidence is higher among females. 4. Outcomes: Mortality rates are generally lower in trauma, but are up to 40% in those patients with pneumonia, sepsis or aspiration. ARDS patients are more at risk for developing nosocomial infections and ventilator associated pneumonia. The syndrome causes a hypermetabolic state which manifests itself in severe weight loss, muscle wasting, immune system compromise and functional impairment. For those that survive, long- term quality of life is affected.

Post-trauma critical illness: Disseminated Intravascular Clotting/Coagulation (DIC)

1. Overview: DIC is a pathologic condition in which widespread activation of the coagulation cascade causes microvascular thrombus formation and depletion of platelets and other coagulation factors. DIC causes thrombosis of both small and medium sized vessels and diminished thrombolysis. Therefore, a consumptive state occurs, reducing the body stores of coagulation factors. Widespread coagulation can lead to global cellular hypoxia and multiple organ dysfunction syndrome (MODS). 2. Physiology: Tissue damage, vascular disruption, inflammatory pathway activation or immune system activation triggers initiation of the coagulation cascade. A vicious cycle of inflammation and immune system over response occurs, causing release of pro-inflammatory mediators, cytokines and other chemical mediators that increase tissue damage and further coagulation activation. The body is no longer able to localize its response to damage. Fibrin is no longer removed normally due to impairment of the fibrinolytic pathway. Coagulation components are consumed, and the body is unable to keep up with the demand. Additional hemodynamic instability increases clotting within the tissues due to stagnation of circulation. Clotting occurs in the small and medium vascular bed and coagulation components are depleted, leaving the body unprotected from actual or potential bleeding events. 3. Risk factors associated with DIC: a. Systemic inflammatory response due to infection or trauma causes release of tissue material, tissue factor or fat into the circulation and activation of cytokines or other mediators. Cytokines patterns appear very similar for both trauma and sepsis. b. Malignancies (acute myelocytic leukemia or other cancers) c. Eclampsia, amniotic fluid embolism, hemorrhagic obstetric emergencies such as abruptio placenta d. Severe trauma e. Toxins (such as envenomation, drug overdose) f. Hemolytic reactions, blood transfusion g. Liver disease or dysfunction

Post-trauma critical illness: Multiple Organ Dysfunction Syndrome (MODS)

1. Overview: First identified in the 1960's, multiple organ dysfunction syndrome is a clinical syndrome characterized by the development of progressive and potentially reversible physiologic dysfunction in 2 or more organs or organ systems that is induced by a variety of acute insults, including sepsis. Past studies have dealt with the 'two hit' theory of late onset organ failure. Currently the thoughts regarding organ failure evolve around primary MODS and a secondary, less defined failure of organs. This ill-defined failure is fueled by persistent inflammation and immunosuppression resulting in catabolism and development of secondary infections, causing permanent dysfunction and disability. 2. Types a. Primary MODS is a direct response to a well-defined insult or injury. It occurs early in the injury and illness. b. Secondary MODS occurs from malignant stimulation of the inflammatory response from toxins other mediators or substances, and many times occurs as a response to SIRS or sepsis. This type of MODS has been virtually eliminated due to treatment strategies aimed at aggressive identification and resuscitation , and has been replaced by insidious persistent inflammation - immunosuppression and catabolism syndrome (PICS). Patients with this syndrome linger in the ICU, continuing to need life support and have frequent or recurrent infections, poor nutritional intake, poor wound healing, immunosuppression and ongoing protein breakdown causing loss of muscle mass, progressive weakness and failure to regain strength. These patients may be discharged to long term care facilities, but will continue to do poorly and will rarely return to the functional level they had prior to that hospitalization.

Post-trauma critical illness: Inflammatory and immune response syndromes

1. Overview: SIRS and sepsis are often discussed as a single syndrome. Their definitions are similar and the processes by which each syndrome affects the body are similar. For purposes of this presentation, they will be discussed in this manner. 2. Systemic Inflammatory Response Syndrome (SIRS): An inflammatory and autoimmune response due to a specific insult to the body. That insult may be infectious or non-infectious. SIRS is defined as having 2 or more of the following conditions: a. Temperature over 38 C (100.4 F) or less than 36 C (96.8 F) b. HR greater than 90 c. Respiratory rate over 20 or PaC02 less than 32 mmHg d. WBC greater than 12,000/mm3 or less than 4,000/mm3 or over 10% immature (band) cells e. SIRS does NOT need to have infection as a causative agent. Other mechanisms include but are not limited to ischemia, inflammation, and trauma. f. SIRS is usually followed by compensatory anti-inflammatory response syndrome (CARS).

Special patient populations react differently to blood loss

1. Pregnant women: Patient has extra blood and may appear to compensate longer; fetus will be in distress. 2. Athletes: Greater fluid and cardiac reserves; moves more slowly through the early phases with greater percentages lost before moving to the next phase 3. Obese patients: Blood volume as an actual percentage of real body weight is lower than 7%. Small losses may have a more serious effect. 4. Children: Blood volume is 8% to 9% of body weight; may not show early S&S of compensation as clearly as adults; crash quickly 5. Elderly: Compensatory mechanisms are less responsive to fluid losses; medications may block typical signs and symptoms of tachycardia or affect clotting cascade. BPs will drop faster than a healthy adult. They have reduced perception of pain and may already have AMS due to disease. Cannot tolerate hypoperfusion as they have reduced reserves in all organ systems.

STAGES OR CLASSES of hemorrhage

1. Progressive stages based on percentage of approximate blood lost. The classic stages of hemorrhagic shock are of limited clinical relevance in real world, because of: a. Differences in compensation (blunt vs. penetrating) b. Age: large or small reserve capacity c. Elderly: If HTN, may present "normotensive" d. Comorbidities e. Medications may conceal shock by preventing tachycardia

Phase I (compensated/reversible) of Shock

1. Something occurs to cause a perfusion deficit with an early drop in cardiac output that alters cellular function. The body attempts to maintain hemodynamic stability through compensatory mechanisms and by neutralizing elevated lactate levels. Interrelated neural, hormonal, and chemical mechanisms restore cardiac output and perfusion to keep the circulatory system functioning at normal or near normal levels so there are no early clinical S&S.

Hypovolemic/ Hemorrhagic Shock: Summary on evolving science regarding end points of shock resuscitation

1. Standard hemodynamic parameters do not adequately quantify the degree of physiologic derangement in trauma patients. The initial base deficit, lactate level, or gastric pHi can be used to stratify patients with regard to the need for ongoing fluid resuscitation, including blood products, and the risk of MODS and death. 2. The time to normalize base deficit (BD), lactate, and pHi is predictive of survival. 3. Persistently high BD or low pH (or worsening of these parameters) may be an early indicator of complications, e.g., ongoing hemorrhage, under-resuscitation, or abdominal compartment syndrome. 4. The predictive value of the BD may be limited by ethanol intoxication or a hyperchloremic metabolic acidosis, as well as administration of NaHCO3. 5. The ability of a patient to attain supranormal O2 delivery parameters correlates with an improved chance for survival. 6. Right ventricular end diastolic volume index (RVEDVI) measurement may be a better indicator of adequate volume resuscitation (preload) than CVP or pulmonary capillary wedge pressure (PCWP). 7. Patients that don't reach established end point goals by 12 hours post-trauma are at risk for developing MODS.

Hypovolemic shock: Clotting/process of hemostasis

1. Vascular phase: Smooth muscle contraction of the torn vessel reduces the size of the lumen and the volume and strength of blood flow. 2. Platelet phase: When the inner vessel lining is damaged it causes turbulent blood flow. This causes frictional damage to platelets, making them more adherent. Platelets (thrombocytes) stick to collagen, a protein fiber found in connective tissue on the vessel's inner surface, and to other injured tissue in the area. Small vessels may stick together. As platelets adhere to vessel walls, they aggregate (clump) to form a platelet plug. Resulting white clot is unstable. 3. Coagulation: Enzymes are released initiating a complex series of events called the clotting cascade. a. Enzymes released from the damaged blood vessels and surrounding tissues initiate the extrinsic pathway. b. Enzymes released from the damaged platelets initiate the intrinsic pathway. c. The end point of this process is a stable clot made of protein fibers called fibrin that normally takes 7 to 10 minutes to form. d. Over time, the clot contracts, drawing the wound margins together. e. Amount of bleeding may depend on the nature of the vessel injury (1) A transverse transection permits the vessel to retract, thickening the vessel wall (media). This further reduces the lumen size, reduces blood flow, and assists the clotting process. (2) A longitudinal wound pulls the vessel open when smooth muscle contracts. The lumen does not constrict; bleeding is heavy and continues for a longer period of time. Crushing mechanisms often produce this type of damage. f. Factors affecting the clotting process (1) Movement at or around the wound site can loosen clots and disrupt fibrin formation. Benefit of immediate splinting. (2) Fluids infused during resuscitation can dilute the clotting factors, platelets and RBCs further inhibiting the clotting process. (3) Body temp <98.6° F: Hypothermia may worsen bleeding by delaying thrombin formation, reducing the speed of clot formation and clot growth. This is made markedly worse by acidosis. Treatments focused on correcting coagulopathy are more successful if acidosis is corrected first. (4) Medications may interrupt or interfere with clotting mechanisms. Example: aspirin, anti-platelet agents, Heparin and warfarin (Coumadin) interfere with the normal generation of a stable clot. These drugs may prolong or worsen hemorrhage in trauma patients. Try to determine if patients are taking any of these medications when obtaining a history.

Post-trauma critical illness: Disseminated Intravascular Clotting/Coagulation (DIC) Continued

4. Outcomes: Morbidity and mortality rates vary depending on severity. Generally, patients with sepsis have higher mortality rates. In the most severe cases, mortality rates are approximately 50-75%. Development of hypotension and/or high injury severity score which is associated with coagulopathy due to trauma increases mortality. However, it increases fourfold in the presence of concurrent brain injury. 5. Clinical Presentation a. General presentation includes bleeding/thrombosis, fever, hypotension, acidosis, proteinuria, and hypoxia. b. Thrombi formation causes: (1) impairment of blood flow; (2) ischemia; and (3) associated end-organ failure or damage to the following systems: cardiac, pulmonary, renal, hepatic and CNS. c. Hemorrhagic: Usually bleeds from three or more unrelated sites (1) Petechiae and purpura (2) Hemorrhagic bullae (3) Bleeding from surgical wounds, venipuncture sites (4) Subcutaneous hematomas or deep tissue bleeding d. Laboratory Indications (1) Low platelet count (2) Elevated prothrombin time (3) Low fibrinogen levels (4) Elevated D-dimer (5) Elevated fibrin degradation products (6) Additional lab studies are being researched to determine their effectiveness in identifying DIC. These include coagulation inhibitors, fibrinopeptide A levels and prothrombin fragment levels. (7) Additional radiographic studies may be ordered to determine the etiology of DIC.

Phase 1 of Shock summation

6. Catecholamines: Catecholamine and glucocorticoid release creates a catabolic state that prompts glycogenolysis and lipolysis. Patients may have hyperglycemia as well as elevated lactate and fatty acid levels as shock progresses. 7. Net result: Compensatory mechanisms successfully restore cardiac output and tissue perfusion to vital organs at the expense of the non-vital organs. 8. Note: Compensated hypotension can be caused by a fall in cardiac output or by vasodilation.

Post-trauma critical illness: Disseminated Intravascular Clotting/Coagulation (DIC): Emergency Department Management

6. Emergency Department Management a. Identify and treat the cause of DIC. Sepsis, trauma, obstetric emergencies and malignancies are common causes. b. Transfuse platelets or plasma if bleeding or there is a high risk of bleeding (platelet count below 50 x 103 /L; anticipated invasive procedure or recently post-op). c. If administration of plasma is not possible, consider administration of factor concentrates. d. For thrombotic presentation such as thromboembolism or severe purpura fulminans, heparin may be administered. e. For patients presenting with hyperfibrinolysis and severe bleeding, TXA may be administered. 7. Prevent worsening of DIC by: a. Providing or maintaining appropriate vascular volume and supporting hemodynamic status, thus preventing further circulatory stagnation. b. Preventing or reducing blood loss c. Promote comfort.

Factors necessary to maintain perfusion

A. Adequate pump: The heart must generate the power necessary to keep the vascular container filled and to move blood forward to meet body demands. It does this by generating a cardiac output to maintain circulation. B. Circulating fluid: There must be sufficient blood volume to fill the vascular container plus the ability to carry oxygen to the tissues and remove waste products. 1. The average adult's estimated blood volume (EBV) is about 70 mL/kg of body weight or 5 liters, but this varies with age and physiologic state. Infants have approximately 90 mL/kg of body weight, and children 80 mL/kg. It is important to remember relatively small amounts of blood loss can lead to shock in pediatric patients. 2. Red cell oxygenation depends on an adequate oxygen delivery to the alveoli and adequate oxygen exchange with the blood: a. Adequate oxygen diffusion into blood. b. Adequate RBC flow past alveoli c. Adequate RBC mass/hemoglobin (Hb) levels d. Adequate RBC capacity to bind O2: pH, temp, acid/base status C. Intact vascular container: Resistance vessels (arterioles) and capacitance vessels (veins) control the blood flow through the capillary bed for gas exchange. This system must be intact and able to respond to local tissue and oxygen demands. The container cannot be too large for the volume of blood. Dilation of vessels without volume compensation can result in shock.

Factors affecting fluid volume

A. Fluid volume deficits can be absolute or relative, causing decreased venous return, decreased preload and therefore decreased cardiac output. B. Examples of absolute volume deficits include: 1. Loss of blood plasma or fluids outside of the body. 2. Loss of blood plasma or fluids outside of the vascular tree into body cavities (such as the pelvis) or into interstitial spaces (third spacing). C. Relative volume loss can occur if the vascular compartment enlarges without additional blood volume or fluid to fill it.

Shock syndrome defined

A. Nothing brings the body's machinery to a grinding halt quite like the process that occurs when essential nutrients and metabolic fuel like oxygen fail to be delivered to cells to meet their demands at the moment. "A rude unhinging of the machinery of life" B. While the word, shock, may conjure up mental images of patients that are cool, sweaty, hypotensive, and tachycardic, clinical signs can vary remarkably based on the cause or etiology of the problem. To understand the essence of shock, one needs to consider what is happening at the cellular level. C. All body cells require a constant supply of oxygen and other nutrients like glucose. They cannot storehouse O2 for even a minute when breathing room air. This just in time supply is provided by the constant passage of blood through the body's tissues in a process called perfusion. D. The simplest definition of shock begins with two words, cellular hypoxia. This hypoxia usually stems from a sustained perfusion deficit producing a cellular insult where blood flow is restricted despite compensatory adjustments. Shock occurs when oxygen and nutrient delivery to cellular mitochondria throughout the body occurs at a rate below that of total oxygen consumption (oxygen debt) and waste products (CO2 and acids) are not effectively removed. If unchecked, the perfusion failure will end in eventual organ failure. E. In a more complete definition, shock is a metabolic condition resulting from a sustained perfusion deficit leading to oxygen debt (cellular hypoxia), anaerobic metabolism, cellular membrane dysfunction, fluid influx, and cellular death.v

Post-trauma critical illness: Inflammatory, Immune and Organ Failure Syndromes

A. Overview: Many of the syndromes described below are interrelated and it is nearly impossible to talk about one syndrome without referring to another. The scope of this section will be to describe the syndromes and comment BRIEFLY on their pathogenesis, signs & symptoms, lab work and current treatments. B. Generalizations 1. These syndromes occur as an inappropriate response to an event triggering inflammation or immune responses. This can be from the initial insult or injury, under-resuscitation, or can be from specific methods of resuscitation such as massive transfusions, or use of large volumes of isotonic crystalloids for resuscitation. Infection usually is a key risk factor in the development of these organ failure syndromes. 2. When severe, trauma can cause significant complications, prolonging hospital stay and increasing morbidity and mortality rates. Such complications include SIRS/sepsis, acute respiratory distress syndrome (ARDS), multiple organ dysfunction syndrome (MODS) and disseminated intravascular coagulation (DIC). The stimulation of the inflammatory and immune system mechanisms occurs and becomes dysfunctional, causing the inability to localize response to injury, insult or infection. This causes dramatic rises in both metabolic drive and metabolic needs, rapid losses of fat and muscle mass and produces immunosuppression. 3. The key to prevention and/or reduction in severity of syndrome response is early detection and treatment. In the emergency department the objectives are multifold. Early identification of potential risks and conditions associated with development of these syndromes can reduce morbidity and mortality. Treatment of these syndromes according to evidence based standards and utilizing preventative measures (such as early administration of antibiotics, volume limited ventilation to patients at risk for ARDS, control of hemorrhage, tight glucose control and rapid treatment and reversal of shock) may reduce frequency and severity of complications.

Normal cellular metabolism

A. Oxygen delivery to tissues depends on an adequate RBC mass, adequate Hb levels, the distance between capillaries and cells, and the RBC capacity to unbind O2. B. Normal flow in the microcirculation 1. The microcirculation is composed of arterioles, capillaries and venules. 2. Each arteriole feeds a specific area of the capillary bed. 3. Sphincters before and after the capillary bed (called pre- and post-capillary sphincters) maintain peripheral vascular resistance and determine blood flow through the capillaries. The SNS controls this mechanism. 4. Capillary sphincters open and close depending on the local metabolic needs of the cells. Acidosis and hypoxia influence the opening of the capillary sphincters which regulates local tissue oxygenation and perfusion. 5. When an arteriole is widely opened, flow is rapid, pH drop is minimal and the arterio-venous (AV) shunt is closed. Oxygen and waste products are exchanged across the membrane based on hydrostatic and osmotic pressure gradients. The post-capillary sphincter opens to empty blood into the venue. 6. In cases of shock, these normal mechanisms are not enough to sustain tissue oxygenation and perfusion, and anaerobic metabolism and cellular hypoxia occur. C. Tissues are dependent on aerobic metabolism The primary energy source for cells is glucose. Glucose must be broken down through a process called glycolysis. This step does not require oxygen. Glycolysis produces pyruvate but very little energy. The second stage of metabolism is aerobic. In the presence of O2, calcium (Ca++), and ADP, the cell mitochondria (through the Krebs cycle) metabolizes pyruvate to produce CO2, water, and 36 moles of ATP (adenosine triphosphate) per mole of glucose. The cell uses ATP to maintain the Na+/K+ pump and to regulate its intracellular water component. Oxygen consumption is not dependent on oxygen delivery under aerobic metabolism. When needed, cells can extract extra oxygen necessary for energy production.

Pathophysiology of shock

A. Shock occurs when oxygen and nutrient delivery is insufficient to meet the mitochondrial needs of the cells. Decreased perfusion and oxygen debt occurs. Metabolic wastes are not effectively removed, and in an effort to produce energy, the cells start to change from aerobic to anaerobic metabolism. B. The progress of shock is described in stages that reflect the severity of the decline in tissue perfusion and the intensity of cellular membrane damage. C. If precipitating factors are promptly reversed, compensatory mechanisms usually restore perfusion. The longer a patient remains in shock, the longer vital organs are deprived of O2. After cellular destruction begins, shock cannot be reversed and organs will fail. D. A patient can be in shock with high or low systemic vascular resistance, high or low cardiac output, and high, low, or normal BP. Hypoxia acts at the cellular level. Signs and symptoms are manifestations of the cellular response.

Assessment/resuscitation of the hypovolemic/hemorrhagic shock patient

A. Shock resuscitation begins in the prehospital environment and continues through the ED, OR, and ICU. Everyone knows when it begins, but very few know where it ends. The end points of effective resuscitation are in the process of being redefined. Classic end points were considered to be a normalizing heart rate and BP and good urine output. B. Traditional markers are global measures that reflect the general circulation to large tissue beds and may be slow to exhibit signs of severe perfusion deficits to cells. C. Another limitation is that preexisting diseases or the aging process may alter a patient's response to volume losses and blunt changes in vital signs or renal function. D. Priorities: Stop the source of hemorrhage/volume shifts, restore tissue perfusion and oxygenation; detect and correct the cause(s); and maintain the blood's ability to clot. Without intervening for the hemorrhaging/hypovolemic patient, death will result. There are three peaks of mortality for the hemorrhagic shock patient. The first occurs within minutes due to immediate exsanguination, the second peak occurs up to several hours later due to decompensation, and the last peak occurs days to weeks after the trauma due to sepsis or organ failure syndrome.

Factors affecting vessels

A. Total peripheral resistance (TPR) or systemic vascular resistance (SVR) 1. Within limits, a. Increasing either SVR or cardiac output increases blood pressure. b. Decreasing either SVR or cardiac output decreases blood pressure. 2. Compensatory mechanisms in shock include rapid changes in the diameter of the arterioles. As arterioles constrict, SVR increases. As arterioles dilate, SVR decreases. 3. SVR in itself is a function of blood viscosity, vessel diameter and length. Manipulating vessel diameter and blood viscosity will allow for changes in SVR, allowing for compensation of reduced cardiac output. B. Local auto-regulatory vascular control 1. Blood vessels autoregulate vascular tone to maintain flow over a wide range of perfusion pressures, independent of neurogenic or humoral influence. Vascular beds vary in their ability to autoregulate flow. The cerebral, coronary and ?vascular beds are the most sensitive. 2. Triggers for autoregulation may be influenced by osmolality, accumulation of metabolic waste, and hypoxia from hypoperfusion. 3. Sympathetic nervous system (SNS) autoregulatory mechanisms are effective but are lost in severe hypoxic or hypercarbic states. C. Hemodynamics 1. Blood pressure may appear stable in shock, but it is important to understand that blood pressure does not equate to tissue perfusion 2. Blood pressure can be maintained through increased resistance. The higher the resistance, the less flow through the tissues, and the less perfusion is present.

Acid-base disturbances in Phase I of Shock

Aerobic metabolism begins to change to anaerobic. Pyruvic acid cannot be converted to Acetyl Coenzyme A without oxygen. With cellular hypoxia, pyruvate is alternatively transformed in greater amounts to lactate and other non-volatile acid by-products. a. Acidosis develops because ATP is hydrolyzed to ADP and phosphate with the release of a proton. Hydrogen ion accumulates, decreasing the pool of bicarbonate buffer. Lactate also buffers protons and lactic acid accumulates. b. Increased CO2 in tissues is a universal phenomenon during ischemia. CO2 levels rise in stomach, under the tongue, in esophagus, duodenum, jejunum, brain, liver, and kidneys. The higher the organ's metabolic rate, the higher the CO2 level in states of hypoperfusion.

Types of shock

All forms of shock are due to failure of one or more of these three separate, but related, functions: pump, circulating fluid, and/or vessels (resistance and capacitance). A. Cardiogenic: Caused by intrinsic pump failure as seen in AMI/heart failure. B. Obstructive or compressive cardiac shock is an inadequate venous return to the heart caused by extrinsic compression, i.e., tension pneumothorax, pericardial tamponade. C. Hypovolemic/hemorrhagic: The most common type of shock seen in trauma patients is due to loss of circulating volume, initially producing hypovolemic or hemorrhagic shock. D. Distributive, vasogenic, low resistance: Loss of peripheral vascular resistance (vasodilation) causes maldistribution of blood flow to cells. 1. Septic: Sepsis comes from the Greek word meaning "to putrefy" and can occur after even a minor infection. It is currently defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection. Septic shock is a subset of sepsis defined as persisting hypotension requiring vasopressors to maintain MAP ≥65 and having a serum lactate level >2 despite adequate volume resuscitation. This produces circulatory and metabolic failure associated with high mortality. Hemodynamic parameters include systolic BP less than 90 mmHg, mean arterial pressure (MAP) less than 65 mm Hg or a systolic BP decrease of greater than 40 mmHg or 2 standard deviations below the norm for age in absence of other causes for hypotension. It may be caused by bacteria, virus, fungi, protozoa, parasites, and prions. The leading causes of sepsis are UTI, pneumonia, GI infections, wounds and post-op. 2. Neurogenic: Loss of sympathetic tone below the level of a high spinal cord injury or a brainstem lesion. 3. Anaphylactic: Vasodilation due to antigen/antibody (immune system) reaction with release of vasoactive mediators such as histamine.

Factors affecting pump performance

Cardiac output (CO) = stroke volume (SV) X heart rate (HR) also myocardial contractility

Class II hemorrhage

Compensated a. Acute loss of 15-30% total blood volume or ~750-1,500 mL in an adult b. Most patients with major acute blood loss arrive at the hospital in the supine position. Most have a decreased cardiac output, but will have retained an essentially normal MAP due to compensatory mechanisms (peripheral vasoconstriction). Organ perfusion, however, may be markedly reduced. This state is termed normotensive hypoperfusion. Peripheral metabolism is impaired and metabolic acidosis develops. c. Signs & symptoms of Class II hemorrhage (1) Anxious restless, weakness (2) HR normal to increased (> 100); pulse strength begins to diminish (3) RR normal to mild tachypnea (4) BP: Increased diastolic pressure; systolic pressure maintained > 100 mmHg = narrowed pulse pressure (5) Cool, pale, moist skin; feels cold (6) Thirst (7) Urinary output maintained or slightly diminished (20-30 mL/hr) (8) Base deficit: -2 to -6 mEq/L (9) Need for blood products: Possible

Class I hemorrhage

Compensated a. Acute loss of <15% total blood volume or about <750 mL in an adult b. Signs & symptoms if compensatory mechanisms intact (1) Normal CNS to mild anxiety (2) Normal or minimal increase in pulse to < 100 (3) Venoconstriction; marginally cool skin w/ slight pallor possible (4) Normal BP and pulse pressure (5) Normal RR (12-20), ventilatory volume (6) Normal urinary output (> 30 mL/h) (7) Base deficit 0 to -2 mEq/L (8) Need for blood products: Monitor

Hypovolemic/ Hemorrhagic Shock Secondary survey

Complete this after initial resuscitation 1. Patient history 2. Full set of vital signs; assess for orthostatic changes in early shock. Positive if HR increases 15-30 BPM or if SBP drops 20 mmHg or DBP drops 10 mmHg after changing position from supine to sitting or sitting to standing. Ask about dizziness or lightheadedness. Change in HR is more sensitive. May indicate a 15% volume deficit or blunting of homeostatic mechanisms (especially in elderly). Any injured patient who is cool and tachycardic is considered to be in shock until proven otherwise. 3. Review of systems a. HEENT: sclera, mucous membranes, pupils; S&S of injury? b. Neck: JVD, hematomas c. Lungs: S&S trauma, accessory muscle use, retractions, splinting, normal or abnormal breath sounds d. CVS: Dysrhythmias, murmurs, muffled heart sounds, strength/equality of pulses e. Abdomen: Scars, contour, bowel sounds, guarding, rebound, peritoneal signs, ascites f. Rectal: Tone, blood, prostate g. Extremities: motor, sensory, circulatory status, S&S injury/fracture h. Back/spine i. Neuro: Focal deficits, seizure activity j. Skin: temperature, petechiae

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation: D5W

Contraindicated in trauma patients due to H2O intoxication (1) Will not act as a volume expander. Once infused, glucose is taken up by cells leaving free water in the vascular tree that rapidly diffuses out to cells. (2) Body already liberates sugar (gluconeogenesis) from liver and adult patients may be hyperglycemic. (3) May have sugar in urine (glycosuria) which results in an osmotic diuresis which gives a false sense of well-being. Insufficient osmotic pressure.

Hypovolemic/ Hemorrhagic Shock: On-going monitoring

End points of resuscitation 1. We need accurate end points of resuscitation. a. Shock index (HR/Systolic BP) is a marker of acute critical illness. It is not accurate in discriminating between major and minor traumatic injury. However, when prehospital shock index scores and hospital arrival shock index scores are compared for correlation, they are able to more accurately identify which patients will have a more complicated hospital course (such as longer stay in the ICU, longer ventilator dependency, higher use of blood products). b. Modified shock index (MSI) (HR ÷ MAP) has been shown to be a more superior indicator of mortality in emergency department patients. c. ATLS strongly cautions not to correlate a rise in blood pressure with a reduction in shock state. Patient response must be continually assessed. Return of normal BP, pulse pressure and HR are indications that perfusion may be normalizing. However, it is also recognized that these measurements do not equate to end organ perfusion. Urinary output is correlated with renal perfusion, and therefore is considered a more sensitive indicator (as long as diuretics are not given). d. Resuscitation is complete when the oxygen debt has been repaid, tissue acidosis eliminated and normal aerobic metabolism restored in all tissue beds. 2. End points of resuscitation fall into two categories: global and regional a. Global indicators include traditional assessments that reflect general circulation to large tissue beds and may be slow to exhibit signs of ongoing perfusion deficits including vital signs, urine output, hemodynamic monitoring parameters and global acid-base status using base deficit and lactate levels. Another limitation is that preexisting disease may alter a patient's response to volume losses and blunt changes in vital signs or renal function. b. Regional indicators are more sensitive to identifying compensated shock as it continues to decrease blood flow to the splanchnic bed to maintain cerebral and coronary blood flow. Gut-related markers (such as gastric pHi) are useful markers to determine the severity of shock and the pathophys connection between gut ischemia and later MODS. 3. Direct arterial monitoring a. A drop in SV diminishes Korotkoff sounds and markedly limits the usefulness of the auscultatory technique at pressures < 60 mmHg. b. 5-10% of patients who have an unobtainable cuff pressure have abnormal or high intra-arterial pressure. c. Affords continued access to arterial blood gases.

Primary assessment of hypovolemic/hemorrhagic shock: Exposure

Expose to examine; keep warm! Monitor core temperatures. The risk of bleeding increases dramatically in hypothermic patients with moderate-to-severe acidosis. It occurs in trauma patients with minimal cold stress secondary to inadequate tissue oxygenation and perfusion preventing the body from generating enough heat to maintain normothermia. Predisposing factors are age, injury severity, impaired thermogenesis, elevated serum alcohol levels, fluid resuscitation, blood product transfusions, and exposure of body cavities during surgery. Hypothermia shifts the oxyhemoglobin dissociation curve to the left, impairing oxygen delivery to cells and worsening the shock state.

Hypovolemic shock: Sources of blood loss

Hemorrhage is classified based on the injured vessel from which it flows: capillary, venous or arterial. 1. Arterial: Flows very rapidly and often spurts with the heartbeat. Appears bright red as it is fully oxygenated. Blood losses can be enormous due to intravascular pressures. 2. Venous blood flows quickly, but can be stopped in a few minutes with direct pressure. It is generally dark red as blood has already given up some oxygen flowing through the capillary beds. Ex: Superficial cut. 3. Capillaries ooze and clot quickly on their own. Blood is generally bright red as it is well oxygenated. Ex: abrasion.

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation: Impact on hemoglobin levels

In a healthy adult, the normal daily production of RBCs is 0.25/kg, with an average RBC lifespan of 120 days. Transfused blood cells have a lifespan of 60 days. One unit of RBCs increases Hgb by 1 g/dL and Hct by 3% in adults, but these levels may not be reached in the setting of occult bleeding, repeated laboratory draws, fever, hypersplenism, immunologic disease, or hemolysis. (6) Hospital policies should be followed regarding obtaining, storing and infusing all blood components. (a) Regulations allow the storage of products ≤ 42 days, though the majority of transfusions include products stored 16 to 21 days. The process of storing RBCs changes cell wall deformability, increases proinflammatory cytokines, and decreases 2,3-diphosphoglycerate (2,3-DPG), which shifts the oxyhemoglobin dissociation curve to the left. In fact, levels of 2,3-DPG are depleted within 2 weeks of storage, decreasing the ability of RBCs to release oxygen to peripheral tissues. (b) Currently, insufficient evidence exists that true harm is present with older products. Studies are retrospective in design, observational, and have small sample sizes. Several randomized trials are currently underway evaluating the effect of transfusion age. However, if possible, products < 21 days should be given, with studies suggesting harm with older products (i.e., those stored for > 21 days).

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation: Indications for blood or blood products:

In the face of acute hemorrhage, RBC transfusion can increase O2 delivery, increase cell mass, and potentially resolve anemic symptoms and shock. (a) Symptoms of volume depletion do not usually occur until 15% or more of blood volume is lost. When loss is between 15-30%, tachycardia may be present, but transfusion is only indicated for those patients with pre-existing anemia, cardiac, or pulmonary disease. (b) Blood loss of 31-40% produces signs of progressive or refractory shock and increases the need for volume replacement with RBCs. Transfusion is considered life- saving when blood loss is over 40%.

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation: Volume replacement

Maintain adequate fluid, oxygen and hemodynamic support: Volume replacement: The most expeditious way to increase cardiac output and improve the distribution and delivery of oxygen in hypovolemic shock is by restoring plasma volume. Fluid therapy must support the patient in three phases: emergency, replacement, and maintenance. (1) The ideal fluid or combination of fluids for definitive shock resuscitation has not been established. "Warmed isotonic electrolyte solutions (crystalloids, e.g. lactated Ringers or normal saline) are used for initial resuscitation to provide transient intravascular expansion to increase BP to a level that maintains organ perfusion and further stabilize the vascular volume by replacing accompanying fluid losses into the interstitial and intracellular spaces, replace interstitial fluid losses, and replace electrolyte deficits. (a) Lactated Ringers (i) Hypovolemic shock is caused by a functional volume loss in the ECF compartment. LR is the closest mimic to ECF: containing 130 mEq/L Na, 4 mEq/L K, 3 mEq/L Ca, 109 mEq/L Cl, and 28 mEq/L sodium lactate. Preferred by burn physicians. (ii) Cannot be mixed with blood or blood products. (b) Normal saline (0.9% NaCl) (i) 154 mEq. Na + 154 mEq. Cl. NS has excessive Cl ion and an acidic pH: May produce hyperchloremic metabolic acidosis when given in large quantities, especially in patients w/ renal impairment (such as in shock). (ii) Can be mixed with blood and blood products. (c) Hypertonic saline (3-7.5% NaCl) (i) Alternative initial fluid option although current literature does not demonstrate any survival advantage". It is estimated that 250 mL hypertonic saline increases vascular volume as effectively as 2,500 mL NS and could be used for hemodilution without massive volume infusions. (ii) Possible benefits: reduction in polymorphonuclear neutrophil activation, prevention of liver and kidney damage, prevention of increased ICP in head injury, substitution of hypertonic saline and hemoglobin-based carriers until blood and blood products are administered for hemorrhagic shock, and possible use as low-volume resuscitation fluid for patients undergoing damage control surgery as well as burn resuscitation.

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation: Patient response

Patient response can be divided into three categories: (1) Rapid response; Patients who demonstrate rapid improvement in clinical status after initial fluid bolus is given, without apparent need for additional fluids. However, surgical consultation and evaluation are still needed to determine the need for operative intervention. (2) Transient response: Patients who respond to the initial fluid bolus but do not remain stable once fluids are slowed to maintenance rates. These patients need additional fluids (blood/ blood products). Patients who transiently respond require either operative or angiographic control of hemorrhage. If the patient has transient response to blood products, the patient will require rapid surgical intervention due to continued bleeding. (3) Minimal or no response: These patients do not stabilize or respond to either crystalloid or blood administration and should undergo immediate control of exsanguinating hemorrhage.

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation: Amount to infuse

The goal of fluid resuscitation is to restore perfusion and to provide efficient oxygen transport without creating a coagulopathic state. A hematocrit of 30%-35% is optimal for maintaining the oxygen-carrying capacity of the blood and for slightly decreasing blood viscosity, which improves circulation to tissues. (1) ATLS guidelines: Initial crystalloid fluid bolus of 1 liter may be required. Fluids are administered judiciously because aggressive resuscitation before control of bleeding has been shown to increase mortality (prehospital fluid resuscitation volumes must be included in this amount). (2) Excess crystalloid infusion during the first 24 hours of resuscitation is associated with uncontrolled hemorrhage, hypothermia, hypocoagulable state, development of acute respiratory distress syndrome (ARDS), multiple organ dysfunction syndrome (MODS), surgical site infections as well as abdominal compartment syndrome and extremity compartment syndrome. (3) Increased intravascular volume affects active bleeding by hindering clotting. Administration of IV fluids can lead to hemodilution, because they do not contain clotting factors or erythrocytes, and to hypothermia, if unwarmed, because of the increased infusion rate (>4 mL/kg per minute). (4) Fluid resuscitation that results in a MAP greater than 80 to 90 mm Hg before surgical hemostasis is associated with increased bleeding as an increased MAP may "pop a clot" by increasing the vascular hydrostatic pressure and dislodging a soft, unstable, white clot that has begun to seal over the opening in a vessel, adversely affecting the patient's condition. (5) Although complications associated with resuscitation are undesirable, the alternative of exsanguination is even less so. A careful, balanced approach with frequent reevaluation is required. (6) Balancing the goal of organ perfusion with the risks of rebleeding by accepting a lower than normal BP has been called "Controlled resuscitation", "Balanced resuscitation", "Hypotensive resuscitation", and "Permissive hypotension". (7) Contraindications to permissive hypotension (a) Can be fatal in some patients: Traumatic brain injuries because adequate cerebral perfusion pressure (CPP) is crucial to ensure tissue oxygenation of the CNS. (b) Patients who are near circulatory collapse (i.e., Classes III and IV of hypovolemic shock). (c) In preexisting conditions such as hypertension, angina pectoris, coronary disease, and carotid stenosis: permissive hypotension following trauma may lead to severe cardiovascular dysfunction. These conditions are common mainly in the elderly (>65 years old), but also occur in other age groups because of occult disease. (d) Pregnant trauma patients (8) Guideline: Resuscitate with crystalloids just to a minimum SBP that maintains a MAP that perfuses protected organs until blood products can be added and definitive hemorrhage control is accomplished in the OR. (a) Penetrating trauma to torso: SBP of 80. In penetrating trauma with hemorrhage, delaying aggressive fluid resuscitation until definitive control may prevent additional bleeding. (b) Blunt trauma: SBP of 90 (MAP of ≥65) (c) TBI: The CNS is dependent on a consistent metabolic supply of nutrients, including oxygen, because the brain and spinal cord have little anaerobic reserve and are not able to compensate for decreased oxygen delivery. Higher systolic pressures (110-120) are needed for patients who have impaired cerebral perfusion or traumatic brain injury. (d) Crystalloid fluid resuscitation for pediatric patients occurs in boluses, 20 mL/kg up to a total of 60 mL/kg. (9) Assessment of end-organ perfusion and oxygenation (level of consciousness, urine output, lactate, and/or base deficit measurements, and trending of serial vital sign measurements) should guide resuscitation. (10) Sufficient volume expansion usually brings cardiac preload pressures and cardiac output to acceptable levels at least temporarily. Continue to carefully monitor perfusion. (11) Be alert to signs of over resuscitation that can result in pulmonary congestion/edema, especially in those with cardiovascular disease.

Hormonal compensation in Phase I of Shock: Antidiuretic hormone (ADH or Vasopressin)

This hormone causes the following compensations: (1) Synthesized in ventral hypothalamus, stored in posterior pituitary. (2) Released in response to hypovolemia or hyperosmolality via receptors in the carotid bodies and atria and by osmoreceptors in the hypothalamus. (3) Effects (a) Decreases urine output by stimulating water reabsorption. (b) Causes peripheral vasoconstriction

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation: RBC transfusion risks

Transfusion can contribute to transfusion-associated circulatory overload (TACO), febrile nonhemolytic transfusion reaction, acute hemolytic transfusion reaction, immunomodulation, multiple organ dysfunction (>9.5 units), transfusion- associated acute lung injury (TRALI), iron overload, delayed hemolytic reaction, hypothermia, coagulopathy, infection (absolute pooled risk of serious infection of 11.8% with a restrictive strategy vs. 16.9% with a liberal strategy), and potentially increased mortality. (1) Product transfusion can increase intrinsic blood viscosity and decrease cardiac output, and these effects actually diminish the ability of RBCs to improve oxygenation in critically ill patients. (2) Transfusing RBCs introduces foreign antigens into the patient, and the host response varies with modifications to intrinsic T cells, lymphocyte response, natural killer cell function, cytokine production, and phagocyte function. This effect is known as transfusion-related immunomodulation (TRIM), which may be associated with increased adverse effects of transfusion. (3) Incompatibility/Transfusion reactions (a) Hemolytic: Occur as a result of the interaction of antibodies in the plasma of the recipient with antigens present in donor RBCs. Acute intravascular hemolysis: ABO incompatibility may be fatal. Often caused by human error in identifying blood samples or in giving properly cross-matched blood to the wrong patient. Acute extravascular hemolysis due to antibodies other than ABO; usually benign. (b) Non-hemolytic: More common; related to reactions to WBCs or proteins in the donor blood. S&S: rash, mild bronchoconstriction, fever - 5% of all transfusions. Mitigate by premedication with antipyretics and antihistamines.

Post-trauma critical illness: Acute Lung Injury (ALI)

Transfusion-related acute lung injury (TRALI): Acute lung injury findings that occur within 6 hours of a patient receiving a transfusion with a clear temporal relationship to the transfusion. It is underdiagnosed due to lack of awareness of the syndrome. Clinicians believe that a large number of critically ill patients receiving blood or blood by-products develop this syndrome, but that it is not recognized. It is important to understand that infusion of red blood cells alone may not just trigger TRALI, but can trigger Acute Respiratory Distress Syndrome (ARDS). 1. Presentation: hypoxia, acute shortness of breath, respiratory distress, cyanosis and non-cardiogenic pulmonary edema. These symptoms may develop acutely but are present within 6 hours of the infusion. Symptoms and presentation are difficult to differentiate from ARDS. 2. Risk factors: most commonly occurs in patients receiving fresh frozen plasma, whole blood or packed red blood cells, but can be caused (rarely) by administration of cryoprecipitate or other blood components. Albumin is not implicated in this syndrome. 3. Etiology: White blood cells and inflammatory responses to antibodies in the blood products cause permeability of the alveolar- capillary interface and leakage of fluid from vessels into the alveoli and interstitium. Most patients who develop this have concomitant infection, recent surgery, cytokine administration or massive transfusions. 4. Treatment: Is supportive in nature, including supplemental oxygen and supporting hemodynamic status. General guidelines are to prevent hypovolemia. Diuretics are not indicated in this syndrome, but actually are being looked at as a part of a combination treatment in ARDS. 5. Prognosis: Generally better than ARDS, usually resolves on its own. Mortalities have been reported however.

Class III hemorrhage

Uncompensated a. Acute loss of 31-40% total blood volume, about 1,500-2,000 mL in an adult: major hemorrhage. b. Compensatory mechanisms ineffective in maintaining SBP over 100 (MAP ≥65); physical responses dramatic. Classic S & S of shock appear. c. Signs & symptoms (1) Mental status: restlessness, confused, agitation (2) HR: Tachycardia > 120; thready (3) SBP < 100; pulse pressure narrow (4) RR: Tachypnea; 30-40 with air hunger (5) Skin: cold, pale, diaphoretic (6) Thirst more severe (7) Decreased urinary output (5-15 mL/hr) (8) Base deficit: -6 to -10 mEq/L (9) Need for blood products: Yes

Hypovolemic/ Hemorrhagic Shock: On-going monitoring: Urine output

Very important to measure! a. Need a minimum of 0.5 -1 mL/kg/hour in adults, 1mL/kg/hour for pediatric patients, and for infants 2 mL/kg/hour. b. Oliguria may not be a sign of renal failure but of good renal conservation of fluid. Monitor over time with osmolality. Attempt to elicit past medical history for preexisting renal dysfunction. c. Specific gravity > 1.020 indicates fluid deprivation d. Fixed specific gravity of less than 1.010 indicates renal insufficiency e. Specific gravity depends on the weight, not the concentration of solutes in the urine f. Kidney responds to changes in concentration of particles, not weight g. High molecular weight substances (glucose, albumen, urea) contribute much less to osmolarity than to specific gravity. 6. Urine osmolarity a. Is a more accurate and physiological reflection of renal concentrating ability than is specific gravity b. Increased osmolarity = hypovolemia c. Decreased osmolarity = renal failure

Heart Rate

Within limits, an increased HR will increase CO. At very fast rates (>150), filling time is compromised and stroke volume is decreased, thus CO falls. a. Intrinsic HR is a function of the excitability and rhythmicity of pacemaker cells. b. Extensive neural regulation (1) Sympathetic nervous system (SNS): B1 receptors (2) Parasympathetic nervous system (PNS): Vagus nerve

Primary assessment of hypovolemic/hemorrhagic shock: Adjuncts to primary survey as indicated

a. ABGs b. Labs: Trauma profile: Complete blood count (H&H), clotting profile, type and screen for six units; basic metabolic panel, liver function tests and disseminated intravascular coagulation panel (1) Coagulation testing (a) Activated Partial Thromboplastin Time (aPTT) is a measure of the intrinsic pathway); (b) Prothrombin time (PT)/international normalized ration (INR) is a measure of the extrinsic and common pathway (c) Thrombin Time (TT - also Known as Thrombin Clotting Time) directly assesses the activity of thrombin and is useful in patients receiving dabigatran (Pradaxa) (d) Chromogenic AntiFactor Xa measures the concentration of anticoagulants that inhibit factor Xa. This test is useful in patients receiving LMWHs, fondaparinux (Arixtra) and direct oral factor "Xabans" (2) Serum bicarbonate; serum lactate levels: may be substituted for base deficit levels (3) BUN: increased; serum creatinine: increased (4) Serum osmolality (5) Mixed venous gases from fiberoptic pulmonary artery (Swan Ganz) catheter in right atrium correlate in linear fashion to cardiac index c. Indwelling urinary catheter (UA), naso/orogastric tube d. Anticoagulation reversal and treatment options in major bleeding: Protamine, phytonadione (Vitamin K), hemodialysis, oral activated charcoal, antifibrinolytic agents including tranexamic acid, desmopressin, blood products including packed red blood cells (PRBCs) and platelets, prothrombin complex concentrates (PCCs), and specific reversal agents.

Hypovolemic/ Hemorrhagic Shock: On-going monitoring: Global markers of tissue perfusion

a. Base deficit: Base deficit and/or lactate can be useful in determining the presence and severity of shock. Serial measurement of these parameters can be used to monitor the response to therapy. (1) Base deficit is the amount of base in millimoles (mmol) required to titrate 1 L of whole arterial blood to a normal pH (7.4) when the sample is fully saturated, warm, and has a normal CO2. Base deficit has a strong correlation to lactate levels and is a good predictor of ischemic insult, O2 debt, on-going volume loss, blood product requirement, and mortality. (2) High base deficits are associated with lower BPs on admission and greater fluid requirements. Levels of severity: (a) Mild: -5 mmol/L or greater (b) Moderate: 6-14 mmol/L (c) Severe: BD > 15 mmol/L (3) Alcohol intoxication can worsen BD for similar injury severity and hemodynamics after trauma. A BD of 4.1 mmol/L is concerning in intoxicated patients. b. Serum lactate levels: A normal blood lactate level is 0.5-1 mmol/L. Hyperlactatemia is defined as a persistent, mild to moderately elevated (2-4 mmol/L) lactate level without metabolic acidosis. This can occur with adequate tissue perfusion and tissue oxygenation. A level > 4 mmol/L reflects lactic acidosis, and a level high enough create an acid-base imbalance which may result in a serum pH < 7.35 in association with metabolic acidosis. Lactate can be measured from both venous and arterial blood. Serum samples should be processed within 15 minutes to avoid falsely elevated results. If processing cannot occur within this time frame, the sample should be kept on ice. Lactate increases as the pyruvate that is normally metabolized via the Krebs cycle is shunted to lactate during anaerobic metabolism. If # > 4, the patient is in shock. An ETCO2 reading of 31 correlates to a lactate level of 2 and an ETCO2 of 25 correlates to a lactate level of 4.

Primary assessment of hypovolemic/hemorrhagic shock: Circulatory/perfusion/cardiac assessment

a. Compare carotid and radial pulse rate (fast, normal, or slow, don't count yet), amplitude, and regularity. If hypovolemic shock, anticipate tachycardia except in the elderly, those with pacemakers or patients on medications that would artificially suppress the HR. If neurogenic shock, anticipate bradycardia. Absent central pulses at more than one location without local injury signifies the need for immediate resuscitative measures to restore depleted blood volume, cardiac output or both, including CPR. b. Assess mental status as one measure of central perfusion. Anticipate anxiety and restlessness that may progress to altered mental status (AMS) due to decreased perfusion. c. Re-inspect for external bleeding (internal or external) from wounds, mouth, rectum or other orifices. Assess type (arterial, venous, capillary), amount, source, and rate of bleeding. d. Inspect for concealed internal bleeding if shock is present without external bleeding. Bleeding into the thoracic, abdominal, pelvic or retroperitoneal cavities or into the muscle body surrounding a long bone fracture (femur) can cause major blood loss. e. Assess skin color, temperature, and moisture: The skin is one of the first organs to lose blood flow due to vasoconstriction in the presence of hypovolemia, hypothermia, fear, or a stress response. A patient with normal skin color, temperature, and moisture is rarely in shock. Conversely, cyanosis of the lips or face with diaphoresis or the mottled skin of vasoconstricted extremities (particularly in children) are ominous signs. If skin is moist, the SNS has been activated. Anticipate pale, cool, moist skin in all but neurogenic shock. f. Patients in shock will c/o being cold and may have shaking chills. g. Apply cardiac monitor: anticipate ST changes or dysrhythmias.

Post-trauma critical illness: Inflammatory and immune response syndromes: Sepsis and Septic Shock

a. Definitions: (1) Sepsis: Life-threatening organ dysfunction caused by dysregulated host response to infection. (2) Sepsis-induced hypotension: Systolic blood pressure (SBP) <90 mmHg or (MAP)<70 mmHg or a SBP decrease > 40 mmHg or less than two standard deviations below normal for age in the absence of other causes of hypotension (3) Septic shock: New definition: Subset of sepsis with circulatory and cellular/metabolic dysfunction associated with higher risk of mortality. (4) Sepsis-induced tissue hypoperfusion: "infection-induced hypotension, elevated lactate or oliguria" b. Overview: Sepsis is a significant issue worldwide. Mortality rates vary, and can be as high as 50%. Early recognition and treatment of sepsis significantly reduces morbidity and mortality rates. The identification and treatment of sepsis is so important, international guidelines are updated regularly, identifying processes, pathways and treatments that prove to be more effective than others. c. "Sepsis and septic shock are medical emergencies and treatment and resuscitation should begin immediately" d. Applied to trauma: Trauma patients, due to the nature of injury itself, ramp a complex immune response to tissue damage. This includes the activation of inflammatory mediators throughout the body. e. Start resuscitation early with source control, intravenous fluids and antibiotics f. Source Control: "We recommend that a specific anatomic diagnosis of infection requiring emergent source control be identified or excluded as rapidly as possible in patients with sepsis or septic shock, and that any required source control intervention be implemented as soon as medically and logistically practical after the diagnosis is made." (1) If at all possible, source control should be completed using the least invasive method possible. (2) If vascular access devices are a possible source, they should be removed once alternative vascular access is established.

Primary assessment of hypovolemic/hemorrhagic shock: D = Disability/drugs

a. Mental status; GCS; pupils b. Inotropic agents (SNS stimulants) are sometimes prescribed for patients who fail to respond to volume replacement (1) Dopamine (a) Low dose potentially causes increased renal and mesenteric flow, although this finding is now questionable. (b) Moderate dose (2-10 mcg/kg/min) causes increased force of myocardial contraction (inotrope - beta effects) (c) High dose (10-20 mcg/kg/min) causes a predominately alpha adrenergic response (vasoconstriction) (2) Norepinephrine (Levophed) (3) Neo-Synephrine (4) Dobutamine

Post-trauma critical illness: Multiple Organ Dysfunction Syndrome (MODS): Patterns and predictability

a. Organ failures present on day of admission to ICU are commonly cardiovascular and respiratory. Organ failure patterns that commonly develop in the ICU are respiratory and renal. Mortality rates vary according to the degree and number of failed organs. The highest mortality rates occurred in patients having failure of liver or coagulation systems, and in patients with failure of central nervous system and either liver or coagulation systems. In these cases, mortality reached 80%. b. Treatment: Current treatment of MODS supports failing organ systems involved, attempts to identify the cause of persistent inflammation if possible (such as untreated infection), administers antibiotics as prescribed, and continues to correct base deficits through adequate resuscitation, oxygenation and identifies and controls hemorrhage and other life threats. c. Treatment of PICS involves the management of continuous inflammation, immunosuppression and protection against subsequent infection. In addition, supporting the patient's hypermetabolic state by providing adequate nutrition can help prevent severe muscle wasting and protein catabolism. This is a new concept on the forefront of critical care medicine, and will require more research to determine best approaches and treatments.

Post-trauma critical illness: ARDS Emergency Department Management

a. Provide appropriate airway, support ventilation and oxygenation. Endotracheal intubation with positive pressure ventilation is needed for the severely hypoxic, those in acute severe respiratory failure or who do not respond to supplemental oxygen or (CPAP). b. Reduce risk of secondary injury through appropriate ventilator management: Appropriate ventilator management has made the biggest impact on the treatment of ARDS patients. High volumes and high plateau pressures increase damage to fragile lung tissue (ventilator-associated lung injury). A recent study examined ventilator strategies used in the emergency department (ED). It was identified that use of protective lung ventilation was uncommon in the ED regardless of clinical presentation. Newer strategies balance adequate gas exchange by taking into consideration potential worsening of lung injury. c. Protective lung ventilation: Limit tidal volumes to 6 mL/kg of ideal body weight. (1) Initial management technique for ARDS. (2) Limit plateau pressures to less than or equal to 30 cm H20. (3) Blood gas goals: pH of 7.30-7.45, p02 55-80 mmHg; Sp02 88-95% (4) High frequency oscillatory ventilation (HFOV): Used when lung protective ventilation is ineffective. Studies are inconclusive about its effectiveness. (5) Venovenous extracorporeal membranous oxygenation (VV -ECMO): usually reserved for younger patients who fail protective lung ventilator strategies but possibly have reversible disease. d. Adjunctive treatment (1) Use of prone positioning (2) Recruitment techniques (such as permissive hypocapnia) (3) Inhaled nitric oxide (4) Inhaled prostacyclin (5) Administration of steroids (6) Administration of surfactant (7) Neuromuscular blockade/analgesia/sedation (8) Frequent assessment and re-assessment to determine effectiveness of therapy e. Prevention: Aimed at preventing infection and treating underlying cause (1) Early aggressive treatment when respiratory deterioration is identified (2) Aggressive adequate volume restoration for patients in shock

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation

a. Treatment of hemorrhagic shock - Priorities: Immediate hemorrhage control and balanced fluid resuscitation. Volume restoration with appropriate solutions should be initiated as soon as early signs and symptoms of shock are identified or suspected. Fluid resuscitation is not a substitute for definitive surgical intervention. The best way to manage life-threatening hemorrhage is surgical control in the operating room. Any resuscitation strategy is only a temporary measure. Whatever strategy is followed, it should not lead to additional delay in the transfer of a patient to the operating room if indicated. b. Control active bleeding: Resuscitation is impossible without hemostasis. Options: direct pressure, hemostatic dressings, sutures, staples, pelvic binder or tourniquet. The Federal Government has a massive campaign to teach first responders to stop bleeding even before EMS can arrive.

Chemical (respiratory) compensation in Phase I of Shock

a. Vasoconstriction of pulmonary beds results in alveoli that are ventilated but not perfused, increasing alveolar and physiological dead space. These result in ventilation/perfusion (VA/Q) mismatches, impaired gas exchange, and decreased PaO2 (hypoxemia). b. Hypoxic or hypotensive stimulation of the aortic and carotid chemoreceptors, the presence of metabolic acidosis and painful stimuli all activate the ventilatory center, causing hyperventilation. Ventilatory rate and depth increase in an effort to reduce levels of CO2. On room air, there is a 1:1 inverse correlation between pCO2 and pO2 levels. For each 1 torr decrease in pCO2, there is a corresponding rise of 1 torr in pO2. In mild to moderate shock, the most commonly seen acid-base disturbance is respiratory alkalosis. c. Hypoxemia + respiratory alkalosis affects mental status resulting in restlessness, agitation, excitability, confusion, and lethargy.

Hormonal compensation in Phase I of Shock: Cortisol, Gonadotrophins, Kinins, Serotonin and histamine, and Prostaglandins

e. Cortisol (1) Base level changes in trauma, and although it may rise, adrenal insufficiency may also occur (corticosteroid insufficiency brought about by critical illness, traumatic brain injury or etomidate). (2) Elevated levels stimulate glucose production via gluconeogenesis. (3) Cortisol release is an adaptation response in trauma patients. (4) Dying patients have high levels of cortisol. (5) Effects (a) Decreased fever and edema (b) Decreased vascular extravasation (c) Decreased fibroblastic proliferation (d) Young lymphoid B and T cells appear cortisol-sensitive and may be destroyed by the absence of energy generating pathways using glucose (e) Increases the pressor effects of catecholamines (f) Enhances the hepatic synthesis of angiotensinogen (g) Increased secretion of H+ by the gastric mucosa f. Gonadotrophins are inhibited (amenorrhea) g. Kinins (bradykinin): Potent vasodilator polypeptides formed by the action of proteolytic enzymes on precursors in the plasma. They are thought to be responsible for the dramatic hypotension and hyperemia associated with anaphylactic shock. h. Serotonin and histamine: Vasoactive substances released from platelets and mast cells respectively and regulate local vascular tone and capillary permeability. Anaphylaxis and complement activation trigger their release. i. Prostaglandins: Endogenous acidic lipid soluble materials distributed widely in the body. They are generally released in response to ischemia or hypoxia from the endothelial tissue or platelets and may cause intravascular platelet aggregation, clumping and vasoconstriction.

Neural compensation of Phase I of Shock

homeostatic neuroreflexes a. The vasomotor center in the medulla receives input from various receptors in the body which either suppress or stimulate the sympathetic NS (SNS) and adrenal axis to stabilize BP. b. Peripheral receptors all feed information to the vasomotor center (1) Baroreceptors (pressure receptors in the aortic arch and carotid sinuses) are triggered by a decrease in cardiac output. The vasomotor center increases SNS outflow causing release of epinephrine and norepinephrine. This increases heart rate and contractility and causes venous then arterial vasoconstriction. (2) Chemoreceptors detect hypoxia (pO2 < 80), high pCO2 levels or a low pH (< 7.4). Increased CO2 levels usually trigger ventilations. If increased ventilations do not normalize the pH, chemoreceptors activate the Vagus nerve resulting in bradycardia and coronary vasodilation. (3) Osmoreceptors (hypothalamus) sense concentration of body fluids. (4) Stretch receptors (ventricles) sense the volume of blood return to the heart. c. Recap: In shock, the combination of hypoxia, acidosis, hypotension and volume abnormalities cause simultaneous and synergistic stimulation of the above receptors to increase SNS and adrenal output. The SNS releases norepinephrine from nerve endings and the adrenal gland releases catecholamines (epinephrine & norepinephrine).

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation: Tranexamic acid (TXA)

may be administered in some jurisdictions to severely injured patients in the field within 3 hours of injury. If the bolus is given in the field (1 Gm over 10 minutes), start the follow up dose (1 Gm over 8 hours) in the trauma bay. It was approved by the FDA as adjuvant therapy for patients expected to require massive transfusion and has been used in the US military as a strategy to limit the amount of blood needed during resuscitation. Risk of death is significantly lower when TXA is administered within 1-3 hours of injury. In addition, studies demonstrated the need for blood transfusion was reduced about 33%. The CRASH-2 studies have indicated reduced morbidity and mortality for patients with hemorrhagic traumatic brain injury when TXA is administered.

Hypovolemic/ Hemorrhagic Shock: On-going monitoring: Hemodynamic monitoring

not often done in ED - nice to know only a. Current indications for use (1) Shock (2) Hypotension requiring vasopressors (3) Significant pulmonary congestion (4) Persistent or refractory chest pain (5) Unexplained hypoxemia, cyanosis, or acidosis b. CVP (1) Determined by four components (a) Blood volume (b) Intrathoracic pressure (c) Right ventricular function (d) Venomotor tone (2) Normal values: 6 to 12 cmH2O. (3) Because it reflects right atrial filling pressure (preload) it is an indirect measure of volume status. A reading < 6 cmH2O generally suggests hypovolemia. (4) An elevated reading does NOT rule out hypovolemia. Cardiac tamponade and tension pneumothorax will falsely elevate the CVP in the presence of a low ventricular filling pressure. (5) Dynamic process; response to fluid loading over time is important. (6) Proper positioning can only be verified by chest x-ray. (7) Does not reflect left heart function. (8) May not reflect hemodynamic status due to changes in ventricular compliance (edema, ischemia or blunt cardiac injury) and intrathoracic pressure (mechanical ventilation).

Primary assessment of hypovolemic/hemorrhagic shock

resuscitate immediate life-threats as found. Varies with cause of shock. This begins with an across the room assessment. If life threatening hemorrhage or cardiac arrest is occurring, resuscitation should begin with hemorrhage control and/or circulatory support, revising the typical Airway, Breathing, Circulation assessments and interventions to Circulation, Airway, Breathing, and Circulation (C-A-B-C). 1. Circulatory/perfusion/cardiac status assessment: This step comes first if uncontrolled, life-threatening hemorrhage or if in cardiac arrest. Control life-threatening hemorrhage prior to beginning airway interventions/control. If in cardiac arrest, initiate cardiopulmonary resuscitation beginning with chest compressions. 2. Airway; access/maintain using appropriate positioning, suction, adjuncts prn 3. B: Ventilatory/oxygen status; Assess general respiratory rate, depth, effort, (capnography) and adequacy of gas exchange (SpO2); mental status, and skin signs. Pulse ox implications a. Ideal: 94%-100% (Non-pregnant adults w/o COPD) b. Mild-mod hypoxemia: 90%-93% c. Severely low SpO2 (< 90%) predictor of poor outcomes. Assess for and immediately resuscitate clinically evident immediate life-threats: Tension pneumothorax, open pneumothorax; flail chest Provide O2 per appropriate device and FiO2; assist/ventilate as needed. Ensure that blood has adequate O2 carrying capacity and that tissue can extract and use O2. Acidosis will shift oxyhemoglobin dissociation curve to the right, thus loosening the bonds of oxygen on hemoglobin.

Primary assessment of hypovolemic/hemorrhagic shock: Cardiovascular (cardiocerebral) resuscitation: Coagulopathy

this is associated with severe trauma can be fueled by resuscitative measures. Early resuscitation with blood and blood products must be considered in patients with evidence of Class III and IV hemorrhage. Early administration of blood products at a low and/or predefined ratio of packed red blood cells to plasma and platelets can prevent development of coagulopathy and thrombocytopenia. Initiate massive transfusion protocols, if necessary. "A vital component of patient blood management (PBM) is to minimize procedural and surgical blood loss. Meticulous hemostasis and prevention of bleeding is of paramount importance and results in significant reduction in blood transfusions. Additional PBM efforts include managing anticoagulants, clotting factors, fibrinogen, platelets, and fibrinolysis. PBM may include prompt reversal of anticoagulants for treatment of bleeding and hemorrhage and concurrent treatment of coagulopathy and thrombocytopenia with hemostatic resuscitation and factor replacements as required. Treatment of hyperfibrinolysis may require Tranexamic acid or aminocaproic acid. Most recent advances evaluate the coagulation defect by viscoelastic testing (thromboelastography and rotational thromboelastometry). In select situations, this may direct more specific treatment strategies focused on specific coagulation defects that are identified". (1) Oxygenation is dependent on Hgb concentration, Hgb saturation, O2 supply, cardiac output, and pulmonary extraction and perfusion. Oxygen delivery to tissues occurs predominantly through attachment to Hgb. A large reservoir of oxygen delivery exists, as the rate of delivery in the normal individual exceeds the consumption of oxygen by a factor of 4; however, if Hgb decreases, O2 delivery may be affected. (2) Patients with critical illness have multiple causes of anemia, including active hemorrhage, blunted erythropoietin production, inflammatory cytokine production, increased hepcidin, iron deficiency, and underlying organ dysfunction (e.g., renal failure).

Hormonal compensation in Phase I of Shock: Adrenal medulla

this nerologic structure helps compensate by: (1) Release of epinephrine and norepinephrine from the adrenal glands cause tachycardia, narrowed pulse pressure, sweating, peripheral vasoconstriction and dilated pupils, commonly seen in any marked stress response ('fight, flight or freeze'). These hormones help to sustain the stress response for hours to days. (2) Vasoconstriction redistributes blood to the vital (protected) organs (heart and brain) and shunts blood away from non-priority organs (skin, gut, kidneys, and lungs). (3) Venoconstriction precedes arterial constriction during the initial stage of shock which adequately restores MAP, producing no discernible clinical signs. If O2 debt and acidosis persist or worsen, more catecholamines are released, causing increases in HR, myocardial contractility, cardiac output, MAP and tissue perfusion. Coronary arteries dilate to supply O2 to the myocardium. (4) Over a period of hours, constricted arterioles reduce capillary hydrostatic pressure, causing translocation of fluid from the interstitial space into the intravascular space (transcapillary refill) thus increasing circulating fluid volume. This causes a drop in hemoglobin as fluid dilutes vascular volume to increase perfusion. (5) Constriction of dermal capillary beds causes the skin to be pale and cool. (6) The intense SNS/catecholamine metabolic response generates heat and activates sweat glands producing moist skin. (7) Decreased GI perfusion slows peristalsis.

Stroke volume

volume (avg. 70 mL), is a function of several factors. a. End diastolic filling pressure (Preload) (1) Depends on the rate and duration of filling, ventricular compliance, venous tone, the total blood volume, and the amount of venous return. Normal preload pressures are 4-12 mmHg. End diastolic pressure is influenced by intrathoracic and intrapericardial pressures. (2) These pressures determine the amount of blood the ventricle ejects during systole, thus also affecting the myocardial fiber length or stretch (review Starling's Law). Ventricular volume will also influence myocardial fiber length or stretch. (3) Starling's Law: optimal stretch = optimal contractility b. Afterload: Resistance the chamber must pump against to empty. (1) Ventricles must be able to generate more tension than that in the vessels into which they empty in order to eject any blood. Afterload pressures are determined by systemic and pulmonary vascular resistance and the degree of vasoconstriction. Constricted or diseased arteries have smaller internal diameters and provide high resistance (afterload pressures). Dilated arteries provide little resistance (afterload) and allow for increased stroke volumes. (a) Right ventricle afterload: pulmonary arteries (b) Left ventricle afterload: aorta and arterioles (2) Afterload pressures are increased in hypovolemic or cardiogenic shock or following administration of alpha stimulants such as epinephrine, norepinephrine. NeoSynephrine, or dopamine in high doses (greater than 10 mcg/kg/min). (3) Afterload is decreased in the presence of severe hypoxemia and low resistance or distributive forms of shock, e.g., neurogenic, anaphylactic, and septic. Vasodilating drugs such as nitroprusside, nitrates in high doses, alpha or calcium blockers, ACE inhibitors and angiotensin II blockers reduce afterload pressures. c. Myocardial contractility - Independent of preload and/or afterload. Decreased contractility is the primary cause of cardiogenic shock and contributes to the late phase of any shock. This is due to the effects of acidosis. A patient with an arterial pH of less than 7.2 may exhibit impaired myocardial functioning and reduced responsiveness to vasoactive drugs. (1) Hypoxia, resulting from ventilation/perfusion abnormalities, occurs in early shock and "stuns" the cardiac cells, decreasing contractility. In late shock it worsens, and becomes "malignant" or irreversible because of the low perfusion state. (2) Myocardial ischemia develops when the mean arterial pressure (MAP) falls below 60 mmHg impairing perfusion into the coronary arteries, further decreasing contractility. This situation is compounded in the patient with pre-existing CAD. (3) Drugs: Negative inotropes like barbiturates, beta blockers, calcium blockers, ganglionic blockers, and lidocaine decrease contractility. (4) Myocardial remodeling as seen with chronic volume overload or acute myocardial infarction decreases contractility. (5) MDF - Myocardial depressant factor is thought to be a low molecular weight peptide released from damaged pancreatic cells which markedly decreases contractility and compounds shock. d. Mechanical obstruction to flow: Stroke volume is diminished during pericardial tamponade, tension pneumothorax, or with extensive pulmonary embolization as venous blood cannot return to the heart.