Shock, trauma, burns, hemodynamics,

Shock questions

1. Match each type of shock with the correct descriptive statement. Type of Shock Description a. Cardiogenic ___2___ b. Neurogenic ___4___ c. Anaphylactic ___5___ d. Septic ___1___ e. Hypovolemic ___3___ 1 Septic shock — Characterized by a profound inflammatory response, activation of the coagulation cascade, and increased capillary permeability. 2 cardiogenic shock — Primary pathophysiology is the inability of the left ventricle to pump blood to the rest of the body. 3. Hypovolemic- Burns and hemorrhage are common causes of this type of shock. 4. Neurogenic - Characterized by a loss of sympathetic tone, resulting in massive venous and arterial dilation. 5 anaphylactic - Caused by antigen-antibody response, as well as activation of mast cells and basophils. 2. Types of shock and their related clinical manifestations Hypovolemic Cardiogenic Neurogenic Anaphylactic Septic LOC Altered Altered Altered Altered Altered HR Increased Increased Decreased Increased Increased BP Hypotensive Hypotensive Hypotensive Hypotensive Hypotensive Pulse pressure Narrow Narrow Wide Wide Wide RR Increased Increased Increased Increased Increased Acid-base status Respiratory alkalosis, then acidosis Respiratory alkalosis, then acidosis Respiratory alkalosis, then acidosis Respiratory alkalosis, then acidosis Respiratory alkalosis, then acidosis Metabolic acidosis Skin Pale, cool Pale, cool Warm, pink Warm, pink Warm, pink Neck veins (JVD) Flat Distended Flat Flat Flat 3. Five (5) systems, with clinical indicators, included in the SOFA score Respiratory (PaO2/FiO2 ratio) Coagulation/Hematology (platelets) Liver/Hepatic (bilirubin) Cardiovascular (MAP, with/without vasopressors) CNS (GCS) Renal (creatinine, urine output) 4. Two key factors that distinguish SIRS from sepsis: life-threatening (urgency) and dysregulated host response 5. Septic shock is defined as sepsis-induced shock with hypotension (i.e., MAP ≤ 65 mm Hg) despite adequate fluid resuscitation and vasopressor therapy, along with the presence of perfusion abnormalities (i.e., lactate > 2 mmol/L). 6. Three main derangements that affect homeostasis during septic shock Inflammatory response Procoagulation responses Impaired fibrinolysis 7. Three main cardiovascular effects of sepsis Vasodilation: as a result of the activation of chemical mediators that cause a relative hypovolemia Maldistribution: as a result of selective vasoconstriction, vasodilation, and increased cell membrane permeability causing fluid to move from the intravascular space to the interstitium, and micro-emboli formation that decreases perfusion Myocardial depression: as a result of mediators releasing myocardial depressant factors 8. Ultimately, the pathophysiological response to shock will result in an imbalance between cellular oxygen demand and cellular oxygen supply and consumption, resulting in ineffective tissue perfusion and impaired metabolic metabolism. 9. Signs and symptoms of septic shock: "E" indicates an early sign and "L" indicates a late sign. Pink, warm skin E Hypotension L Narrow pulse pressure L Tachycardia; weak, thready pulse L Elevated temperature E Widened pulse pressure E Tachycardia; full, bounding pulse E Increased respiratory rate E Decreased urinary output (oliguria) E Decreased respiratory rate L Cool, pale, mottled skin L Decreased urinary output, leading to anuria L Irritability, confusion E Relatively normal blood pressure E Pulmonary edema, crackles L Extreme lethargy, coma L 10. ABG results in the early stages of septic shock Value Change PaO2, SaO2 Both are decreased. Supplemental O2 required to maintain PaO2 and SaO2. PaCO2 Respiratory rate increases to compensate for decreased PaO2 and SaO2, causing initial respiratory alkalosis. As the patient fatigues, respiratory acidosis will occur. pH, HCO3 Due to decreased tissue perfusion, anaerobic metabolism will take place, resulting in metabolic acidosis. pH and HCO3 will be decreased. 11. Laboratory results in septic shock Scvo2 Increased initially (due to inability of tissues to extract oxygen) PT/INR Increased WBC Increased initially, with elevated bands (immature neutrophils) in response to infection; decreased as illness progresses) PTT Increased Glucose Increased (due to hypermetabolism and insulin resistance) BUN Increased (due to decreased renal perfusion) Lactate Increased (due to shift to anaerobic metabolism) Cr Increased (due to decreased renal perfusion) Platelets Decreased Bili Increased (due to decreased hepatic perfusion) Alk Phos Increased (due to decreased hepatic perfusion) AST Increased (due to decreased hepatic perfusion) 12. Initial resuscitation interventions for patients with septic shock Crystalloid fluid bolus (30 ml/kg) IV within the first 3 hours (preferably within hour-1) Repeated bolus(es) guided by frequent assessment of hemodynamic status Reassessment should consist of thorough physical examination and analysis of dynamic variables (e.g., BP, HR, RR, SaO2, temperature, urine output, and others as available) Previous parameters (e.g.,CVP of 8-12 mmHg, Scvo2 of ≥ 70%) are no longer supported as lone indicators of resuscitation response (but may be considered in assessment of full clinical picture). MAP of ≥ 65 mm Hg if vasopressors required Normalize lactate levels in patients with elevated lactate (should also be used to guide resuscitation)

Bites and Stings

Bites Mammalian Bites In Canada, the most common mammalian bites seen in the ED are those caused by humans, dogs, and cats. The hand is the most common site involving bite injuries; however, the face is also a common site in children, particularly involving dog bites. Bites range in severity from minor cuts or punctures to traumatic crush wounds, soft tissue avulsion, and amputation of digits. Dogs can exert over 300 pounds of bite force, while cats have sharp, narrow teeth capable of piercing deep fascia and bone. Human bites can also cause significant trauma to soft tissues (Kennedy et al., 2015). The priorities of care for mammalian bites are always focused on the identification and management of life-threatening injuries (i.e., ABCDEs). An additional primary concern with mammalian bites is disease transmission and infection. Bites lead to direct inoculation with oral flora (bacterial and viral), some of which leading to severe infectious sequelae and invasive treatment. Human bites are known to cause severe infections; cat bites lead to infection in approximately 30-50% of cases, while less than 15-25% of dog bites result in infection. Bite wounds located over a joint or tendon, such as of the hand, are at higher risk for infection (Kennedy et al., 2015). Following stabilization of any life-threatening injuries (e.g., bleeding) and examination of the wound, the following medical and nursing interventions are recommended in the management of mammalian bites: Comprehensive history-taking (although this may be performed simultaneously with initial examination) Time of injury: signs/symptoms of infection may present within 12 hours, or as soon as 3 hours in cat bites Medical history: immunocompromised patients or those with prosthetic joints are at higher risk of infection Irrigation and debridement (with local anesthetic) Removal of foreign bodies (e.g., teeth, debris, pieces of clothing) Wound is left open (delay wound closure due to potential for infection and/or need for further debridement...facilitates bacterial egress); sterile dressing may be applied Elevate limb to heart level, if applicable Administer prophylaxis medications Antibiotics: dependent upon source of bite (e.g., dog, cat, human), location of bite (e.g., hand, face), medical history of patient Per os (PO, oral): e.g., amoxicillin-clavulanate (Augmentin) Intravenous (IV): e.g., piperacillin-tazobactam (Pip-Taz), ceftriaxone plus metronidazole (Rocephin plus Flagyl) Tetanus: recommended if the patient has not received a booster within the previous 5 years; immunoglobulin may be considered if two or fewer previous tetanus immunizations Antivirals: dependent upon source of bite (e.g., history of human immunodeficiency virus [HIV], hepatitis) Rabies: dependent upon signs/symptoms of dog/cat, level of patient exposure (e.g., veterinarian); strongly recommended if potential exposure to bats Obtain culture swab of wound (if infection suspected), as well as serology from source of bite (e.g., HIV, hepatitis, rabies) Tissue culture may also be considered Laboratory studies (if infection suspected [e.g., complete blood count, erythrocyte sedimentation rate, C-reactive protein]) Diagnostic imaging (if fracture(s), object impaction, and/or osteomyelitis suspected) Follow-up within 24-48 hours (e.g., ED, family physician, plastic surgery) Consult provincial regulations for reporting of disease guidelines (e.g., rabies) (Ellis & Ellis, 2014; Kennedy et al., 2015) Insect Bites Lyme disease is reportedly on the rise across the country (Government of Canada, 2018), thus tick bites are also worth discussion here. Lyme disease is caused by the transmission of the bacterium Borrelia burgdorferi (B. burgdorferi) by infected blacklegged (deer) and western blacklegged ticks, most commonly found in grassy or wooded areas. Once in contact with a host (e.g., humans, dogs), the tick must attach and feed for at least 24 hours in order for bacterial transfer to occur. Nymphs, or immature ticks, are most often responsible for infecting humans, but adult ticks may also transmit disease (Government of Canada, 2018). Current identified risk areas for Lyme disease in Canada, as well as illustrations of blacklegged ticks, can be found at the following link: https://www.canada.ca/en/public-health/services/diseases/lyme-disease/health-professionals-lyme-disease.html Clinical manifestations of Lyme disease can vary from person to person, often making diagnosis difficult. Symptoms may appear between 3 and 30 days after the infected bite, with general feelings of malaise or flu-like symptoms being most commonly reported; most patients present within 7 days of being bitten. It is important to note that many patients may not be aware they were bitten because ticks are very small in size. Signs and symptoms of Lyme disease often appear in overlapping stages, described as follows: Early localized (less than 30 days) Single, localized lesion (Erythema migrans [EM]), ranging in color from pinkish-red to dark bluish-purple Shape often resembles a "bull's eye" (see Figure 3.3 below) Unlike ecchymosis, EM has a uniform circular shape (may be mistaken for a "bruise") (see Figure 3.4 below) Slowly increases in size, non-pruritic Fatigue, malaise Fever Headache Myalgias Arthralgias Early disseminated (systemic manifestations; less than 3 months) Fatigue, general weakness Multiple EM lesions Cardiac disturbances (e.g., dysrhythmias, pericarditis, myocardial dysfunction) Neurological sequelae (e.g., aseptic meningitis, encephalopathy, cranial neuropathy) Ocular manifestations (e.g., uveitis, keratitis, conjunctivitis) Hepatitis (mild) Splenomegaly Late (more than 3 months; if left untreated, may last for months or years) Musculoskeletal manifestations (e.g., chronic arthritis, joint effusions) Neurological sequelae (e.g., subacute encephalopathy, axonal polyneuropathy) (Government of Canada, 2018, para. 3-6). Diagnosis of Lyme disease is largely based on clinical presentation and history of tick exposure (e.g., recent camping trip, outdoor activities). Serological testing for B. burgdorferi antibodies may also be performed (Government of Canada, 2018). Management of early Lyme disease involves antibiotics (e.g., doxycycline, amoxicillin) for 2 to 3 weeks. Persistent signs and symptoms seen in later in the disease course may be treated with anti-inflammatory drugs (Government of Canada, 2018). Stings In Canada, the most common sting injuries seen in the ED are those caused by insects, such as bees and wasps. The insect stings the individual by breaking the skin and leaving the stinger behind, which injects a venomous substance and causes rapid activation of inflammatory processes. Patients may present with minor localized inflammation at the site (e.g., erythema, tenderness) or more serious sequelae, such as urticaria, dyspnea, and laryngeal edema, leading to anaphylaxis (ENA, 2020). As describe above in the management of mammalian bites, the priorities of care are focused on the identification and management of life-threatening conditions (i.e., ABCDEs). In conjunction with stabilizing these components, patients experiencing an acute allergic reaction are also treated pharmacologically as follows, according to severity: Epinephrine (see Figure 3.5 below) Note: Pediatric dose is 0.01 mg/kg to maximum 0.5 mg Crystalloid infusions, with vasopressors (e.g., dopamine, norepinephrine) as needed Histamine blockers H1- blocker: Diphenhydramine 25-50 mg IV H2-blocker: Ranitidine 50 mg IV or 150 mg PO (if anaphylaxis is absent) H1- and H2-blockers given in combination are said to be more effective than H1-blockers alone; however, some research disputes their efficacy in anaphylaxis Beta2-agonists: Salbutamol 2.5-5mg via nebulizer, if bronchospasm present Corticosteroids Methylprednisolone 125 mg IV Onset of action is 1 to 2 hours, thus efficacy is disputed in anaphylaxis Prednisone 50 mg PO (if anaphylaxis is absent) (Tupper & Visser, 2010, pp. 1009-1010) ________________ Figure 3.5. Recommended doses of epinephrine in anaphylaxis. Reprinted from "Anaphylaxis: A Review and Update", by J. Tupper and S. Visser, 2010, Canadian Family Physician, 56, p. 1009 (http://www.cfp.ca/content/cfp/56/10/1009.full.pdf). Patient education is crucially important with regards to allergic reactions. Prior to discharge, patients should be informed about the risk of rebound anaphylaxis. This phenomenon occurs most often in the first 8 hours in patients who experienced a severe allergic reaction of rapid onset, but may occur as late as 72 hours. Depending on severity of signs and symptoms and response to treatment, patients should be monitored in the ED for at least 4 to 8 hours; admission should be considered for patients who experienced moderate to severe reactions. Patients must be informed of signs and symptoms to watch for and when to seek medical treatment, as well as the avoidance of triggers. They must also have access to an epinephrine injector (EpiPen) and receive instruction regarding its use (Tupper & Visser, 2010). Review Questions Which of the following is not an appropriate intervention in the acute management of a dog bite? Administration of antibiotic prophylaxis Irrigation of the wound with normal saline Closure of the wound Administration of tetanus vaccine Identify and describe the single, localized lesion seen in the early stage of Lyme disease. Which of the following is the primary drug used in the management of allergic reaction? Epinephrine 1:1,000 Epinephrine 1:10,000 Diphenhydramine Methylprednisolone Click here to view suggested ans Suggested Answers c. Closure of the wound is not an appropriate intervention in the acute management of a dog bite. The wound should be irrigated with copious amounts of normal saline and the patient's need for antibiotic and tetanus prophylaxis assessed. Wound closure would not occur until the extent of debridement required is determined. The single, localized lesion seen in the early stage of Lyme disease is referred to as Erythema migrans (EM). It can range in color from pinkish-red to dark bluish-purple and its shape often resembles a "bull's eye". Unlike ecchymosis, EM has a uniform circular shape, thus may be mistaken for a bruise. It slowly increases in size and is non-pruritic. a. Epinephrine 1:1,000 is the primary drug used in the management of allergic reaction. Epinephrine 1:10,000 is only used in refractory anaphylaxis (e.g., shock). Diphenhydramine and methylprednisolone are used as anti-inflammatory adjuncts in the management of allergic reaction.

Cardiogenic Shock

Cardiogenic shock results from failure of the heart to pump enough blood to meet the metabolic needs of the tissues, resulting in circulatory failure and inadequate tissue perfusion. The most common cause of cardiogenic shock is acute myocardial infarction (MI). Causes of cardiogenic shock include muscular (e.g., cardiomyopathy), mechanical (e.g., valvular disease), and rhythmic dysfunction (see Box 34.6 in Urden et al., 2022, p. 837). Cardiogenic shock is similar to hypovolemic shock in that both result from a decrease in stroke volume; however, cardiogenic shock occurs in the presence of adequate intravascular volume. In hypovolemic shock, the decrease in stroke volume is due to diminished preload, whereas in cardiogenic shock, the decrease in stroke volume is attributed to impaired contractility and/or valvular insufficiency. Regardless of the cause, the same compensatory mechanisms are initiated, leading to tachycardia, vasoconstriction, and reabsorption of Na+ and water. As left ventricular contractility falls, the volume of blood remaining in the ventricle increases; the back-up of blood into the pulmonary system and consequent pulmonary edema may actually worsen the cardiogenic shock state. Assessment findings of cardiogenic shock are similar to those of hypovolemic shock, including changes in LOC, BP, HR, RR, urine output, peripheral perfusion, JVD, and acid-base status. Identify the changes in clinical findings that would be expected in cardiogenic shock. Clinical Finding Change LOC ↓ Sensorium HR Tachycardia (with chest pain), weak/thready, ↓ heart sounds (S3, S4 may be present) Dysrhythmias BP SBP < 90 mmHg, or ≥ 30 mmHg drop in SBP/MAP Pulse pressure < 25% = left ventricular failure RR Tachypnea Crackles, rhonchi; pulmonary edema Peripheral perfusion Skin cool, pale, moist JVD Present with right-sided heart failure Urine output < 30 ml/hr ↓ Urine Na+ (kidneys retain Na+) ↑ Urine osmolality (concentrated) Acid-base status Respiratory alkalosis Hypoxemia Which assessment findings of cardiogenic shock differ from those of hypovolemic shock? Why? JVD is increased with cardiogenic shock (more so in right-sided heart failure), whereas jugular veins are flat with hypovolemic shock. The increase in JVD is due to an increased preload (secondary to impaired pump function of the left ventricle), which is reflected in the jugular veins. Medical and nursing management of cardiogenic shock includes addressing the underlying cause (e.g., impaired contractility), improving ventricular function, and optimizing cellular perfusion. Improving ventricular function may be achieved by the administration of combination therapy: vasopressor (e.g., Dopamine) and an inotrope (e.g., Dobutamine); evidence suggests that combination therapy is more effective than either drug alone. Dopamine binds to beta-1 receptors in the heart, resulting in increased inotropic and chronotropic effects. Dobutamine is a potent beta-adrenergic agent, with stronger inotropic than chronotropic effects. It increases contractility, but also may cause vasodilation and should be avoided if the systolic BP (SBP) is < 90 mmHg. Dobutamine is the mainstay of treatment for cardiogenic shock unless profound hypotension is present, in which case Dopamine is the preferred agent (Tintinalli et al., 2011). Milrinone is a phosphodiesterase inhibitor that increases the amount of intracellular calcium (Ca2+) and potassium (K+) in myocardial cells, thereby increasing contractility. Milrinone also increases Ca2+ uptake in smooth muscle cells, which enhances vasodilation and decreases resistance to ejection, thus must be used cautiously in hypotension. Excessive preload increases O2 consumption in the heart; therefore, nitrates and/or diuretics may be administered in order to decrease preload. Excessive afterload also increases myocardial O2 consumption, thus arterial vasodilators may be administered to minimize this effect. An intra-aortic balloon pump (IABP) may be utilized to optimize coronary artery perfusion and decrease afterload. An IABP is a temporary support to optimize myocardial O2 supply and demand. A balloon is placed in the descending aorta and inflation is timed to occur during ventricular diastole. This pushes blood retrogradely towards the ascending aorta, aortic arch, and coronary arteries, thereby increasing coronary artery blood flow. An intact aortic valve is essential to prevent regurgitation into the left ventricle. Blood is also pushed anterogradely to improve perfusion to the kidneys and lower extremities. Placement of the balloon above the renal arteries is imperative in order to prevent blockage of renal blood flow. Deflation of the IABP occurs immediately prior to ventricular systole, creating a vacuum effect in the descending aorta. This results in decreased resistance to left ventricular ejection (i.e., decreased afterload), thereby decreasing myocardial O2 consumption.

Mixed Venous Oxygen Saturation (Svo2) / Central Venous Oxygen Saturation (Scvo2)

Maintaining a balance between oxygen delivery and consumption is essential for critically ill patients. When supply is equal to demand, the tissues will be adequately oxygenated and cellular demands will be met. One way to measure how well the body is utilizing oxygen is to measure central venous oxygen saturation (Scvo2), which is the percentage of oxygen bound to hemoglobin (Hgb) returning to the right side of the heart from the body. This is indicative of the balance between oxygen supply and demand. Unlike the Scvo2, which uses a specialized CVC to monitor venous oxygen saturation, some critical care units may use a PA Svo2 catheter. If a CVC is used, a sample may be drawn from its distal port at the same time as an ABG sample is drawn from an arterial line. The percentage of oxygen available versus that actually used is then calculated to determine the Scvo2. General rule of thumb: Svo2 = SaO2 - 30% Conditions such as septic shock and multiple organ dysfunction syndrome (MODS) can more than double normal oxygen consumption; routine nursing care can also markedly increase consumption. In an effort to compensate for an oxygen imbalance, the body will increase either oxygen delivery or oxygen extraction. In the critically ill patient, cardiac output is frequently compromised, which usually affects oxygen delivery. If oxygen delivery to the tissues is insufficient, the body will attempt to extract more oxygen from the blood, decreasing both the amount of oxygen returned to the heart and the Scvo2. The body normally provides a balance between oxygen supply and demand. Factors that help maintain this balance are CO, Scvo2, Hgb, and tissue oxygen metabolism (vo2). CO contributes to oxygen supply to the tissues. The four hemodynamic factors that affect CO are preload, afterload, contractility, and heart rate; any change in these will affect CO and ultimately Scvo2. Any action or disease that decreases arterial oxygen saturation (SaO2) will decrease the Scvo2. Hgb also contributes to oxygen supply to the tissues. In healthy patients, the Hgb level would have to be extremely low to affect Scvo2; however, most critically ill patients are already anemic, so any decrease in Hgb will affect the Scvo2. VO2 describes oxygen consumption or the quantity of oxygen extracted at the tissue level in 1 minute. In critically ill patients, even normal activities can increase vo2, as well as conditions such as sepsis, MODS, and head injury. Note: The normal range for Scvo2 is 60-80%, with an absolute normal of 70%;however, the Scvo2 will always be a bit higher than Svo2 because the reading is taken before the blood enters the right side of the heart, where the cardiac sinus (vein) delivers venous blood into the right atrium. This blood, which is drained from the myocardium, is heavily desaturated, thus decreases the Svo2 slightly. Causes of high Scvo2 (i.e., 80-95%) are briefly outlined below: Anesthesia causes sedation and decreased muscle activity, thus lowering the metabolic demand for oxygen. Sepsis decreases the cells' ability to utilize oxygen. Even if supplemental oxygen is provided, the cells cannot extract it and the Scvo2 will be higher than normal. Hypothermia lowers metabolic demand, resulting in a higher Scvo2. Patients receiving more oxygen than required for their clinical condition. Causes of low Scvo2 (< 60%) include the following conditions: Hypoxemia Cardiogenic shock Severe anemia or blood loss with cardiovascular compromise Increased metabolic demand, which may occur due to prolonged shivering or seizures

Mechanism of Injury trauma

Trauma occurs when an external force of energy causes structural or physiologic alterations or injuries to the body. External forces include radiation and electrical, thermal, chemical, and mechanical forms of energy. Mechanical energy can produce either blunt or penetrating traumatic injuries. Knowledge of the mechanism of injury (MOI) is imperative for health care providers to anticipate and predict potential internal injuries. Describe blunt trauma and provide at least three (3) examples of blunt trauma injuries. Describe penetrating trauma and provide at least three (3) examples of penetrating trauma injuries. Match the following external forces of energy to the examples of each. Force of Energy Examples Mechanical _______ Electrical _______ Thermal _______ Radiation _______ Chemical _______ Rays of light, sound waves, explosions Plant and animal toxins Motor vehicle collisions, firearms, falls Heat, steam, fire Lightning; exposure to wires, sockets, plugs Click here to view suggested answers. Motor Vehicle Collisions One way to anticipate injuries in a patient involved in a motor vehicle collision (MVC) is to examine the vehicle. Emergency nurses should ask prehospital providers about the interior and exterior damage to the vehicle; emergency nurses should also provide this information to critical care nurses upon patient transfer to the intensive care unit (ICU). Head-on collisions (frontal impact) produce multiple injuries. With a down and under projectory, the occupant travels downward and into the steering column or dashboard, resulting in patella dislocation, femur fractures, and hip fractures. Alternatively, with an up and over projectory, the occupant's chest and/or abdomen hit the steering wheel. This can result in head injuries, skull fractures, facial fractures, cervical spine (C-spine) injuries, chest injuries and fractured ribs, myocardial contusion, pulmonary contusion, ruptured hollow organs, and lacerated solid organs. Rear-impact collisions occur when a stationary or slower-moving vehicle is struck from behind. Injuries to those in the vehicle that was struck may include hyperextension of the neck. With lateral (side-impact) collisions, occupants receive most of the injuries on the same side as the vehicle impact. Possible injuries include flail chest, pulmonary contusion, rib fractures, musculoskeletal (MSK) injuries, spinal fractures, and abdominal injuries. Mechanism of Injury Suggested answers Blunt trauma is an injury with no opening in the skin or communication with the outside environment. Common forces involved in blunt trauma are acceleration/deceleration, shearing, and compression. Blunt trauma is seen most often with MVCs, contact sports, blunt force injuries, and falls. Penetrating trauma is an injury that pierces the skin and damages internal structures along the path of penetration. Penetrating trauma is most often caused by gunshot or stab wounds and impalements. With regards to gunshot wounds, for example, the higher the velocity (e.g., rifles) the more tissue destruction. Projectile flight patterns must also be considered in penetrating trauma. Match the following external forces of energy to the examples of each. Force of Energy Examples Mechanical ___3____ Electrical ___5____ Thermal ___4____ Radiation ___1____ Chemical ___2____ Radiation — Rays of light, sound waves, explosions Chemical —- Plant and animal toxins Mechanical — Motor vehicle collisions, firearms, falls Thermal — Heat, steam, fire Electrical — Lightning; exposure to wires, sockets, plugs

serum lactate

this provides information regarding lactic acidosis the values will differ greatly with MODS

Preload, Afterload, and Contractility Notes

: HR x SV = CO preload - the volume in the left ventricle at the end of diastole. It is measured as pressure as it can not be measured with a transducer. Right sided preload is measured via CVP Right ventricle infarct - preload is lost due to damaged muscle The more you stretch, the more it will recoil unless it is overstretched preload is determined by - volume (not enough decreases preload), vascular tone (vasodilation decreases preload), and dysrhythmias (afib can reduce CO by as much as 30%) afterload - - pressure the ventricle has to overcome the resistance to ejection in the arteries/arterioles SVR systemic vascular resistance. an increase in afterload increases the workload of the heart and O2 demand. HTN and aortic stenosis are two conditions that will cause this to increase. Contractility - contractile force is known as inotropy. Dependant on preload and afterload. Influences include the SNS, medications, and is decreased by hypoxia, electrolyte imbalances, and medications

Arterial Pressure Monitoring

Arterial lines are used for the following reasons: To measure for hemodynamic instability To assess the efficacy of vasoactive medications To sample arterial blood for arterial blood gas (ABG) monitoring In an effort to decrease contamination, most EDs and critical care units use the arterial line to withdraw blood for all routine blood tests.

shock compensation text

Baroreceptors - respond to stretch and alert the autonomic nervous system in the medulla. If less than normal stretch, a reduction of receptors occurs and the sympathetic nervous system is activated. An increase activates the parasympathetic system Chemoreceptors - activate based on ph, oxygen, and CO2. With acidosis, the receptors increase the rate and depth of resps to blow off co2. Sns- a decrease in volume and CO will stimulate this causing a release in epi and norepi. This causes vasoconstriction. The adrenals are stimulated and fluid is retained. Shift of interstitial fluid - 25 % of fluid is extra cellular 2/3s of this is interstitial. This is maintained by colloids and hydrostatic pressure RRAS - renin is released from renal hypoperfusion. This causes vasoconstriction and the production of aldosterone. Promoting sodium and water retention. As shock progresses, this causes oliguria and renal fails Adrenal gland - stimulated by sns. Causes tachycardia which originally increases CO and organ perfusion.

Trauma and the Pediatric Patient

Children are prone to injury due to the following psychosocial and cognitive aspects of development: They are easily distracted and impulsive. They have difficulty localizing sound. Visually, they tend to focus on single objects at or near their own height. Blunt-force trauma is the most common mechanism of pediatric morbidity and mortality, with most injuries occurring in the home. Injuries outside the home may be caused by MVCs, falls, pedestrian incidents, and bicycle crashes. Most children who die in motor vehicles are not restrained in child safety seats or by seat belts. They are thrown about the vehicle, suffering injuries to the head, chest, abdomen, and extremities. They can be pinned beneath the dashboard, impaled on the gearshift, and bounced against doors, seats, and other passengers. Unrestrained children may be ejected through the front, side, or rear windows. List at least five (5) physiological differences between children and adults. Spinal precautions are initiated with pediatric trauma patients as well. Care must be taken to prevent C-spine flexion from the cervical collar or backboard, which may worsen the spinal cord injury or compromise the airway. 2. Suggest two modified C-spine immobilization techniques that can be implemented to ensure appropriate spinal precautions in pediatric patients. 3. What is the Broselow tape, and how is it used in the management of the critically ill pediatric patient? Further management of the pediatric patient is discussed in NURS 0473 Essentials of Pediatric Emergencies. Physiological differences in children Head is proportionally larger compared to body surface area and weight Cranium is thinner, more pliable; large occiput Anterior and posterior fontanels are open in infants (anterior closes by 18 mths on average, posterior closes by 2 mths) White matter is not well myelinated, more susceptible to shearing forces Tongue is large in proportion to oral cavity Obligatory nose-breathers ≤ 6 mths of age (any nasal blockage can cause significant respiratory distress) Larynx is higher, more anterior (cricoid cartilage narrowest portion of airway...no cuffed endotracheal tube if < 8 yrs of age, but practice is changing due to better manufacturing) Neck is short and wide, neck muscles/ligaments are weaker (airway cartilage also weaker) Chest wall is more pliable, does not provide as much protection to abdominal organs Less elastic tissue, lower tidal volumes Diaphragm more horizontal until 12 yrs of age Liver is more anterior, less protected by ribs Lower glycogen stores Kidneys are mobile, not protected by subcutaneous fat Injuries at or adjacent to growth plates can slow normal bone growth and development Spine is more flexible, less likely to be injured Bones of the extremities are more pliable and resilient to injury Blood volume depends on child's size (infant = 90 ml/kg; child = 80 ml/kg) For pediatric patients with possible spinal injuries, backboards can be modified by an occipital cut-out, or the child can be placed on a double mattress pad to raise the chest while the head and neck rest on one mattress pad. A small towel or padding can also be placed under the shoulders to ensure the external auditory meatus and shoulders are aligned. The Broselow tape is used as a rapid method for determining medication and fluid dosages for children, as well as equipment sizes (e.g., endotracheal tubes, suction catheters, nasogastric tubes, indwelling catheters). The patient is measured while lying on/beside the tape; the length of the child indicates precalculated drug dosages and equipment sizes. Many EDs and pediatric critical care areas also have color-coded equipment drawers on pediatric crash carts. Note: The Broselow tape may not be accurate across all populations. Given the increasing prevalence of childhood obesity among Canada's youth, the Broselow tape may significantly underestimate the weight of some children which must be considered during pediatric resuscitation (Bourdeau et al., 2011; Milne et al., 2012).

Heat- Related Emergencies

Heat Exhaustion Heat exhaustion is a clinical syndrome caused by prolonged heat exposure, leading to core temperature of 38.5°C to 40°C. Excessive perspiration and inadequate fluid and electrolyte replacement lead to fluid loss, electrolyte depletion, and dehydration. Rapid onset of extreme thirst, general malaise, muscle cramping, headache, nausea, vomiting, anxiety, and tachycardia can lead to hypotension, syncope, and collapse. Heat exhaustion can progress to heat stroke. The elderly and young are particularly at risk. Heat Stroke Heat stroke is characterized by thermoregulatory dysfunction, with a core body temperature exceeding 40º C. It presents in two forms: Classic heat stroke is due to prolonged exposure to sustained environmental high temperatures and humidity. Exertional heat stroke (EHS) occurs when heat production overcomes the internal heat dissipation mechanisms. Classic heat stroke affects mainly the elderly and very young, while EHS affects the young and healthy (e.g., athletes, military members, firefighters). What are the signs/symptoms of heat stroke? Describe the medical and nursing management of heat stroke. Suggested answers 1. Heat stroke is characterized by rapid onset of the following signs/symptoms: Hyperthermia > 40°C Decreased LOC (confusion, altered speech, anxiety, hallucinations, delirium, combativeness); ataxia; abnormal posturing, seizures; coma Dilated, fixed pupils Tachycardia, hypotension Tachypnea, hyperventilation Nausea, vomiting, diarrhea Decreased urinary output Coagulopathies Skin hot, dry but may be diaphoretic in early stages (i.e., in the young, healthy) 2. Medical and nursing management of heat stroke involves the following interventions: Maintenance of airway, breathing, and circulation (continuous cardiorespiratory monitoring) Initiate cooling measures (until mental status returns to baseline and core temperature < 38.8°C) Remove clothing Moist cloths, spray cool mist, use fan at bedside (promotes evaporative cooling, decreases shivering) Control any shivering (e.g., benzodiazepines) Ice packs in groin/axillae Cool/Cold water immersion, if EHS IV fluids (cool, 4ºC to room temperature)....fluid volume is usually not depleted in most cases of hyperthermia, thus NS 1-2 L over 4 hours is generally adequate (avoid LR due to lactate, potential hepatic impairment) Antipyretics should not be given (ineffective in heat stroke) Monitor electrolytes (e.g., sodium), coagulation Monitor urine output (> 1-2 ml/kg/hr); assess for myoglobinuria (rhabdomyolysis) (Worley, 2020) Corticosteroids (e.g., methylprednisolone) if cerebral edema Mannitol (> 12 yrs of age) to increase renal blood flow/urinary output (Sedlak, 2013). Thanks

Septic Shock

Septic shock is the most prevalent distributive shock seen in the critically ill patient population. Septic shock is part of a continuum of conditions that a patient with an infection may experience. This concept was originally developed in 1992 by the American College of Chest Physicians (ACCP) and the Society of Critical Care Medicine (SCCM). The definitions of sepsis and septic shock have subsequently been expanded in an effort to provide earlier recognition and treatment. Systemic Inflammatory Response Syndrome In normal circumstances, inflammation is a localized response to an invading microorganism or local tissue damage. This response is a protective mechanism and is self-limiting. Homeostasis is maintained by a balance between inflammatory and anti-inflammatory processes. The localized response activates endothelial cells near the initial insult, resulting in the release of mediators, such as histamine, bradykinin, and nitric oxide (NO), that cause vasodilation. Activation of the endothelial cells also influences coagulation and fibrinolysis (Cheek et al., 2009, p. 1189). Physiological manifestations of this response are capillary leakage, thrombi in the microvasculature, tissue hypoxia, abnormal vascular tone, and cell damage due to circulating O2 free radicals. Normally, these manifestations are contained at the local site. In SIRS, this localized response becomes systemic, affecting the whole body and causing inflammation in organs remote from the initial insult. The body is overwhelmed by uncontrolled inflammation, impairment of coagulation, fibrinolysis, endothelial dysfunction, immune cell disruption, hypermetabolism, and circulatory volume maldistribution. Patients present clinically with fever, peripheral edema, hypotension, tachycardia, increased or decreased white blood cell (WBC) count, and decreased tissue oxygenation (Cheek et al., 2009, p. 1189). Although SIRS is most frequently associated with sepsis, it can also occur as a result of conditions such as pancreatitis, ischemia, and other types of shock. Patients with SIRS may develop multiple organ dysfunction syndrome (MODS); however, it is important to remember that SIRS alone does not involve organ dysfunction (Singer et al., 2016). Sepsis and Septic Shock According to Singer et al., (2016), sepsis is defined as, "...life-threatening organ dysfunction caused by a dysregulated host response to infection" (p. 6). This definition highlights the dysregulation of host response and the urgency of care required in sepsis, as just a moderate degree of multiple organ dysfunction can lead to mortality rates of more than 10%. Septic shock can be defined as, "...a subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality" (Singer et al., 2016, p. 6). Clinically, patients with septic shock can be identified as requiring vasopressor therapy to "...maintain a mean arterial pressure of 65 mm Hg or greater and serum lactate level greater than 2 mmol/L (>18 mg/dL) in the absence of hypovolemia" (Singer et al., 2016, p. 2). Mortality rates are greater than 40% for patients who develop this combination of criteria (Singer et al., 2016). Etiology Sepsis and septic shock are progressive stages on the same illness continuum. They are initiated by infections caused by gram-negative or gram-positive organisms, viruses, or fungi. Gram-positive organisms are responsible for more than ½ of all cases of sepsis; a common gram-positive organism is Staphylococcus aureus. Gram-negative organisms include Escherichia coli (E. coli), Klebsiella, Serratia, Proteus, and Pseudomonas. In many patients, multiple causative organisms are identified. Both intrinsic and extrinsic precipitating factors contribute to the development of sepsis and septic shock. Extremes of age and co-morbidities, such as pneumonia and urinary tract infections (UTIs) in susceptible populations, are some intrinsic factors; extrinsic factors include invasive devices and procedures (see Box 34.15 in Urden et al., 2022, p. 846). Pathophysiology The pathophysiology of severe sepsis and septic shock involves a very complex interaction of many body systems, mainly a disturbance in the immune system's response to the original infection. Cellular mediators produced early in the onset of sepsis initiate a cascade of events, including activation of the coagulation and complement pathways, vasodilation leading to hypotension, endothelial dysfunction, fluid transudation, and generalized inflammation (Picard et al., 2006, p. 44). The derangements that affect homeostasis of the body during this insult are due to a variety of proinflammatory mediators, procoagulant factors, and inhibitors of fibrinolysis (Kleinpell, 2003, p. 18). Three main derangements related to sepsis and septic shock are: a profound inflammatory response, processes promoting the activation of coagulation, and impaired fibrinolysis (Tazbir, 2004, p. 41). These processes, along with disruption of the endothelial layer that results in increased capillary permeability and vasodilation, are the major foundations of the physiological response to sepsis. Ultimately, the imbalance of inflammation, procoagulation, and fibrinolysis as well as the resultant systemic inflammation, microvascular thrombosis, endothelial injury, and widespread coagulopathy, lead to impaired tissue perfusion and organ system dysfunction (Kleinpell, 2006, p. 22). In sepsis, another trigger of thrombus formation is the decrease in the circulating level of protein C, a natural component of the coagulation system that circulates in an inactive state. In order for it to be activated, it has to bind with two specific receptors found on the endothelial surface. As a result of the endothelial injury that occurs during sepsis, one of these receptors becomes down-regulated, leading to decreased levels of activated protein C (APC). APC has antithrombotic, anti-inflammatory, and profibrinolytic properties (Kleinpell, 2006, p. 22). Cardiovascular effects of sepsis include vasodilation, maldistribution of blood flow, and myocardial depression. Myocardial depression occurs in septic shock as a result of the release of myocardial depressant factors (Bridges & Dukes, 2005, p. 15). Vasodilation occurs as a result of the activation of chemical mediators, including NO, a major mediator that causes the vessels to dilate. Because intravascular volume is normal, the patient has a relative hypovolemia that will ultimately decrease venous return, preload, and cardiac output. Maldistribution of blood flow occurs as a result of selective vasoconstriction caused by various inflammatory mediators and a factor released from the endothelium, particularly at the level of the arterioles. Further maldistribution is caused by activation of the coagulation cascade that promotes thrombi development in the microvasculature, leading to decreased perfusion to tissue and organs. Cell membrane permeability is also affected, and transudation of fluid out of the cells and vascular space into the interstitium further contributes to the maldistribution of fluid. Effects of the activation of the central nervous system (CNS) and endocrine system further contribute to the abnormalities found in septic shock. The sympathetic nervous system (SNS) response results in the release of catecholamines. Other hormones are also stimulated to increase production, leading to hypermetabolism. This state contributes to selective vasoconstriction of the pulmonary, renal, and splanchnic (gut) vasculature. The last event contributes to hypoperfusion of the gastric mucosa, causing injury that further potentiates the inflammatory response. Hypermetabolism also results in severe metabolic derangements as the demand for cellular O2 and energy is increased without an adequate contributing O2 supply, further exacerbating cellular hypoxia. As a result, anaerobic metabolism leads to increased lactic acid production and subsequent lactic acidosis. Due to the metabolic derangements in sepsis and septic shock, cells are unable to utilize O2 even when perfusion and O2 supply are adequate, likely due to mitochondrial dysfunction. This dysfunction plays an integral role in the development of MODS. Figure 1.3 below illustrates the sepsis continuum, from local to systemic response, highlighting the key criteria of organ dysfunction and refractory hypotension despite fluid resuscitation. Clinical Signs and Symptoms of Sepsis and Septic Shock Clinical criteria for the diagnosis, or characterization, of sepsis have also been updated, as follows: Sepsis Sequential (Sepsis-related) Organ Failure Assessment (SOFA) score SOFA score serves as a means of quantifying abnormality(ies) by organ system while accounting for clinical interventions Five systems include: respiratory, coagulation, hepatic (liver), cardiovascular, central nervous (brain), and renal (see Figure 1.4 below) It is used to predict poorer outcomes and mortality for patients admitted to the intensive care unit (ICU) Higher SOFA score = higher probability of mortality (e.g., SOFA score ≥ 2 = in-hospital mortality rate of > 10%) (Singer et al., 2016, p. 2) Quick SOFA (qSOFA) qSOFA score was developed to rapidly identify patients with suspected infection at the bedside who may have poor outcomes outside the ICU (e. g., emergency department, inpatient ward) As outlined above (Figure 2), SOFA score requires laboratory investigations that may not be available in a timely manner Two (2) or more of the following (score out of 3): Respiratory rate ≥ 22 breaths/minute Altered mentation Systolic blood pressure (SBP) ≤ 100 mmHg Score of ≥ 2 = increased risk of mortality or prolonged ICU stay (three days or longer) (Seymour et al., 2016) In addition to the updated clinical definitions and criteria, nurses should be aware of other signs and symptoms as the patient's condition deteriorates. Sole et al. (2009, p. 301) outline the characteristics of early and late septic shock, as described below. Signs and symptoms of early septic shock: Altered LOC, usually presenting as irritability and confusion Pink, warm, dry skin as a result of vasodilation; slight hyperthermia Widened pulse pressure: increased SBP due to increased cardiac output, decreased diastolic BP (DBP) as a result of vasodilation BP that is relatively normal (low normal or slightly hypotensive) Tachycardia with a full, bounding pulse Increased RR due to hypoxemia Decreased urinary output (oliguria) Signs and symptoms of late septic shock: Further decrease in LOC leading to extreme lethargy or coma Cool, pale skin, may be grey/blue tinge or mottling; hypothermia Narrow pulse pressure; hypotension Tachycardia; weak, thready pulses Tachypnea that may progress to bradypnea Little or no urinary output (anuria) Pulmonary edema, with resultant crackles heard on auscultation Diagnosis The following are some diagnostic findings and trends in sepsis and septic shock: Arterial blood gases (ABGs): initially, respiratory alkalosis, metabolic acidosis, and hypoxemia occur; later, the respiratory alkalosis gives way to respiratory acidosis Central venous oxygen saturation (SCVO2): initally elevated, but decreases as the condition progresses WBC count: initially increases, but decreases as the condition progresses As sepsis worsens, a "shift to the left" occurs where mature neutrophils ("segs", "segmented neutrophils") become depleted and are replaced with immature neutrophils ("bands", > 10%) that are incapable of mounting an immune response. Thrombocytopenia (decreased platelets; component of SOFA score) Prothrombin time and international normalized ratio (PT/INR) and partial thromboplastin time (PTT) are increased Elevated C-reactive protein (CRP) Hyperglycemia occurs as a result of hypermetabolism and insulin resistance Lactate levels increase Blood urea nitrogen (BUN), creatinine (Cr; component of SOFA score) Alkaline phosphatase (Alk Phos) and aspartate transaminase (AST) increase, as well as bilirubin (Bili; component of SOFA score) Medical and Nursing Management Sepsis guidelines, known collectively as the Surviving Sepsis Campaign (SCC), continue to be updated and revised based on current evidence, research, and knowledge surrounding sepsis. The guidelines essentially grade recommendations according to the strength of evidence, specifically related to sepsis and the general care and management of the critically ill adult patient diagnosed with sepsis and septic shock (Rhodes et al., 2017). Originally, the guidelines included sets of interventions called "bundles," which outlined clinical measures to be taken within three and six hours of patient presentation or diagnosis. In the most recent update, the 3- and 6-hour bundles have been combined into a single "hour-1 bundle"; this change reflects the need to begin resuscitation and management immediately, particularly if the patient is hypotensive (Levy et al., 2018, p. 997). Resuscitation may not be completed within the first hour, but health care providers should strive to initiate the measures outlined in the hour-1 bundle immediately. Figure 1.5 below outlines the recommended priority interventions to be taken within the first hour of diagnosis or "time zero" ("hour-1 bundle"). Figure 1.5. "Hour-1 bundle" related to initial resuscitation for sepsis and septic shock. Reprinted from "The Surviving Sepsis Campaign Bundle: 2018 Update, by M. M. Levy, L. E. Evans, and A. Rhodes, 2018, Critical Care Medicine, 46(6), p. 998. Copyright 2018 by Society of Critical Care Medicine and European Society of Intensive Medicine. Initial resuscitation involves the immediate initiation of the following: Crystalloid fluid bolus (30 ml/kg) IV within the first 3 hours (preferably within hour-1) Need for repeated bolus(es) should be guided by frequent assessment of hemodynamic status Reassessment should consist of thorough physical examination and analysis of dynamic variables (e.g., blood pressure, heart rate, arterial oxygen saturation, respiratory rate, temperature, urine output, and others as available) Previous static quantitative parameters (e.g.,central venous pressure [CVP] of 8-12 mmHg, central venous oxygen saturation [Scvo2] of ≥ 70%) are no longer supported as lone indicators of resuscitation response (but may be considered in assessment of full clinical picture). Mean arterial pressure (MAP) of ≥ 65 mm Hg if vasopressors required Normalize lactate levels in patients with elevated lactate (marker of tissue hypoperfusion); lactate level should also be used to guide resuscitation (Rhodes et al., 2017) Further medical management of sepsis and septic shock includes the following measures: Infection is diagnosed by obtaining appropriate cultures (2 sets, aerobic/ anaerobic) prior to initiation of antimicrobial therapy, unless this results in significant delay of treatment (> 45 minutes). Imaging studies, such as ultrasound, may also be performed to aid in identifying the source of infection. Broad-spectrum antibiotics are administered within the first hour of diagnosis, followed by antibiotic therapy targeted at specific organisms as soon as they are identified. Control of the infection may include removing an infectious device, such as a central venous catheter or draining an abscess. As mentioned above, aggressive fluid therapy is targeted at improving hemodynamic status and increasing intravascular volume. Crystalloid solutions are recommended as the fluid of choice during initial sepsis resuscitation; however, albumin (colloid solution) may also be used when significant amounts of crystalloid solutions are required. Note: Sepsis is characterized by 'relative' hypovolemia; therefore, crystalloid volume must be closely monitored. Colloid solutions will draw fluid back into the intravascular space, thus less volume is often required. Vasopressor agents should be administered to help maintain the target MAP. The first-choice vasopressor agent is norepinephrine administered via a central venous line as soon as it is available. Epinephrine infusion is recommended as the first alternative to norepinephrine if response is poor. Any patient on vasopressor agents should have an arterial line inserted for BP monitoring. Vasopressin levels are decreased in septic shock; therefore, a very low dose of vasopressin may be added to norepinephrine, with the aim of increasing MAP or lowering norepinephrine dosage. Dopamine should only be used as an alternative to norepinephrine in select patients. Dobutamine may be considered in patients with refractory hypoperfusion despite adequate fluid resuscitation and vasopressors. Corticosteroids (i.e., hydrocortisone) may be considered in adult patients with septic shock if fluid resuscitation and vasopressor therapy have not restored hemodynamic stability. Red blood cell (RBC) transfusion should only be considered if hemoglobin (Hgb) levels less than 70 g/L, once resolution of tissue hypoperfusion (target Hgb level of 70-90 g/L). Prophylactic platelet administration is recommended is platelet count is < 10 x 109 with no apparent active bleeding or < 20 x 109 if patient is at high risk for bleeding. Glucose control is also a goal in sepsis treatment, as uncontrolled glucose levels have adversely affected outcomes. Rhodes et al. (2017) recommend instituting insulin infusion protocols when two consecutive blood glucose levels are > 10 mmol/L (10 mmol/L is also the recommended upper target blood glucose level for glucose control). Glucose levels should be monitored every 1-2 hours until stable, then every 4 hrs thereafter. The authors also caution against the use of capillary glucose readings, as they may not accurately reflect arterial/plasma glucose levels (Rhodes et al., 2017, pp. 540-544). Supportive medical therapy for patients with severe sepsis or septic shock includes the following measures: Mechanical ventilatory support with recommended parameters for sepsis-induced acute respiratory distress syndrome (ARDS), according to level of severity (mild, moderate, severe) Tidal volume of 6 ml/kg predicted body weight (12 ml/kg if ARDS) Plateau pressure ≤ 30 cmH20 Positive end-expiratory peep (PEEP): higher rather than lower in ARDS Recruitment measures (e.g., continuous positive airway pressure) if ARDS Prone position, if ARDS and PaO2/FiO2 ratio < 150 Neuromuscular blocking agents (NMBAs) should be used for ≤ 48 hours if ARDS and PaO2/FiO2 ratio < 150 Sedation protocols, with minimal use of intermittent or continuous sedation in mechanically ventilated patients Head-of-bed (HOB) should be elevated to 30-45º in all mechanically ventilated patients Nutritional support, initiated early preferably via enteral route, as tolerated (intravenous [IV] glucose and advancing of enteral feeds is preferred during first 7 days if enteral feeding alone is not tolerated) Continuous renal replacement therapy (CRRT) and intermittent hemodialysis may be considered for severe sepsis and acute kidney injury (AKI) Deep vein thrombosis (DVT) prophylaxis with daily low-molecular weight heparin (LMWH), if not contraindicated Stress ulcer prophylaxis (e.g., proton pump inhibitor, H2 blocker) only if bleeding risk factors (Rhodes, 2017, pp. 540-544) Note: Sodium bicarbonate (NaHCO3-) is not recommended in routine management of hypoperfusion-induced lactic acidosis if pH ≥ 7.15 (Rhodes et al., 2017, p. 516) For additional information about supportive medical therapy, refer to Urden et al. (2022, pp. 850-851). Nursing management of critically ill patients includes the following measures: Identifying patients at risk Reducing exposure Washing hands Adhering to strict aseptic technique practices Applying knowledge to prevent the entry of micro-organisms Monitoring closely for early signs of sepsis Monitoring ABCs and vital signs Maintaining accurate fluid balance Assessing response to interventions Nurse-directed weaning off mechanical ventilation Administering medications, fluids, and nutrition Providing comfort and emotional support Sepsis/septic shock is a multifaceted condition, and many interventions and supportive measures may be used in an effort to restore homeostasis. Mortality rates remain high; however, these rates may be contained somewhat through early recognition and intervention. While antibiotics are an essential part of the treatment for sepsis, they have a limited ability to cure severe sepsis. Surviving sepsis is dependent upon recovering function at the microcirculatory level and limiting the development of MODS.

Abdominal Injuries

Abdominal injuries are the third leading cause of death among trauma patients. They may be caused by penetrating injuries, such as gunshot or stab wounds, or blunt injuries resulting from MVCs, assaults, or falls. The liver and spleen are the most commonly injured organs by blunt trauma; the liver, small intestine, and stomach are the organs most commonly injured by penetrating trauma. Discuss the clinical significance of Kehr's sign, including its pathophysiological basis. List at least four (4) signs/symptoms of hepatic injury. List at least five (5) signs/symptoms of a hollow organ injury (e.g., small intestine). Kehr's sign is associated with splenic rupture and is characterized by pain radiating to the left shoulder (referred pain). The left phrenic nerve originates from C3-C5 spinal nerves and travels down through the chest, passes over the pericardium, and penetrates the diaphragm. Blood accumulating below the diaphragm may irritate the phrenic nerve, thus sending the sensory information up the nerve to the shoulder area. Signs/Symptoms of hepatic injury Right upper quadrant pain Abdominal wall muscle rigidity and/or spasm Involuntary guarding Rebound tenderness Hypoactive or absent bowel sounds Signs of hemorrhage and/or hypovolemic shock Signs/Symptoms of hollow organ injury (e.g., small intestine) Peritoneal irritation Abdominal wall muscle rigidity and/or spasm Involuntary guarding Rebound tenderness Abdominal distension Hypoactive or absent bowel sounds Fever, elevated WBC count Evisceration (e.g., small intestine, stomach)

Anaphylactic Shock

Anaphylactic shock is caused by an immediate hypersensitivity reaction, often mediated by immunoglobulin E (IgE), that affects multiple organ systems. IgE-mediated responses involve activation of the antigen-antibody response, while non-IgE-mediated responses involve direct activation of mast cells during first-time exposure. Regardless of the mechanism, anaphylactic shock is caused by the release of many biochemical mediators, including histamine, serotonin, heparin, and prostaglandins. The pathophysiology of anaphylactic shock is outlined in the diagram below. Identify the physiological effects of inflammatory mediators on the following: Component Effect(s) Airway/Respiratory Laryngeal edema, bronchoconstriction, wheezing, ↑ mucous Cardiac Hypovolemia, ↓ venous return Tachycardia Coronary vasoconstriction, myocardial depression Vascular Vasodilation, ↑ capillary permeability (massive fluid shifts from intravascular to interstitial space) Angioedema Inflammation Integument Urticaria, erythema, pruritis, pain Warm periphery Gastrointestinal Smooth muscle constriction Nausea, vomiting, abdominal pain Genitourinary Smooth muscle constriction Goals in the management of anaphylactic shock include immediate removal of the offending substance, reversing the effects of inflammatory mediators, and ensuring adequate tissue perfusion. Aggressive fluid resuscitation and medications (e.g., Epinephrine, Diphenhydramine, Ranitidine, vasopressors [refractory hypotension]) are the standard of care, as well as patient education specifically related to the trigger(s) involved (e.g., prevention, self-administration of Epinephrine). Indicate whether the following statements are True or False? Correct the statements that are False. The most effective treatment for mild to moderate anaphylaxis is Epinephrine 0.3-0.5 mg IV (1:1000 concentration). Patients on beta-blockers may experience a heightened response to Epinephrine. Corticosteroids are administered during the acute phase of anaphylactic shock. False The most effective treatment for mild to moderate anaphylaxis is Epinephrine 0.3-0.5 mg intramuscularly (IM) (1:1000 concentration). False Patients on beta-blockers may experience a limited response to Epinephrine. False Corticosteroids are administered during the recovery phase of anaphylactic shock (prevent prolonged or delayed reaction). Describe the role of Glucagon in the management of anaphylactic shock, including its mechanism of action. Glucagon is used (off-labeled) in the treatment of cardiovascular emergencies, namely shock states (e.g., anaphylactic shock). Although not a primary reason for its use, glucagon is known to have positive inotropic and chronotropic effects via its stimulation of cyclic adenosine monophosphate (cAMP) synthesis. cAMP is a second messenger that facilitates the cellular effects of glucagon via intracellular conduction. Glucagon is also used in the management of beta-blocker toxicity.

Trauma and the Pregnant Patient

Anatomic and physiologic changes during pregnancy can obscure the mother's response to trauma. Maternal compensatory mechanisms preserve vital functions at the expense of the fetus. Fetal survival depends on adequate gas exchange and uterine perfusion. Blunt trauma is the most frequent cause of maternal and fetal injury, and head injury is the major cause of maternal death. Major causes of fetal death are as follows: Maternal cardiopulmonary arrest Maternal shock Preterm labor Disruption of the placenta Direct fetal injury Resuscitation priorities for the pregnant patient are identical to those for the non-pregnant patient. 1. What interventions can the nurse initiate if a pregnant trauma patient presents with a BP of 80/40 mmHg? Emergency delivery of the fetus is performed due to maternal stress, fetal stress, or both. Indications include the following: Placental abruption Uterine rupture Unstable pelvis or lumbosacral fracture Impending maternal death The following conditions are associated with successful delivery of a fetus during a maternal trauma code: Stat caesarean section (C-section) performed within 5 minutes of maternal cardiac arrest Continuation of cardiopulmonary resuscitation (CPR) throughout C-section Viable fetal gestational age (>26-28 weeks) Availability of a neonatal resuscitation team Once the fetus is delivered, the health care team should perform assessment and resuscitation of the neonate simultaneously. Drying, warming, suctioning, and tactile stimulation are the first interventions. Administer bag-valve-mask (BVM) ventilation with 100% O2 for a compromised neonate when minimal respiratory effort is made with an adequate HR. Start chest compressions when the HR is absent or < 60 beats/minute. Intubation and medications are the final steps. Further management of the obstetric patient is discussed in NURS 0472 Essentials of Obstetric and Gynecological Emergencies. Nursing interventions for a pregnant trauma patient with BP 80/40 mmHg Place patient in left lateral position at approximately 15-20° (while maintaining C-spine immobilization, if appropriate). This moves the uterus away from the vena cava, allowing venous return to the heart, which increases cardiac output and, therefore, BP. Initiate 2 x large-bore IVs, administer isotonic fluid bolus as ordered if repositioning has little or no effect on BP. Administer blood products, as ordered Continuous monitoring of hemodynamic status (e.g., vital signs, LOC, urinary output) Control external hemorrhage

Central Venous Pressure (CVP)

CVP is a measurement of right heart filling pressures. The CVP accurately reflects right ventricular end diastolic pressure (RVEDP). The normal CVP is generally considered to be 2-5 mmHg, although many critical care literature resources suggest 2-6 mmHg as the range. The same pressurized tubing used for all hemodynamic monitoring is used for CVP monitoring, and the phlebostatic axis is used as the reference point. A low CVP may reflect hypovolemia, as stroke volume is decreased when volume in the right ventricle at the end of diastole is inadequate. In the hypovolemic patient, CVP falls before any significant change in MAP because peripheral vasoconstriction will maintain a normal MAP; peripheral vasodilation also reflects a low CVP. The CVP therefore is an excellent indicator of decreased fluid status in conditions such as severe hemorrhage and severe vasodilation that may occur due to distributive shock or the use of vasodilating drugs. In contrast, a high CVP may reflect volume overload. In some circumstances, treatment goals are directed at maintaining the CVP above normal. For example, the goal in sepsis resuscitation is to maintain the CVP at 8-12 mmHg, due in part to massive vasodilation that occurs but also due to cardiac stiffening that tends to reflect euvolemia in critical illness at higher than normal ranges. With mechanical ventilation, right ventricular compliance is further diminished, requiring a CVP of 12-15 mmHg for optimal outcomes in the septic patient (Tuggle, 2009, p. 1104). The CVP reads pressure, not volume, so it is important for nurses to be aware of clinical situations that may increase pressure and in turn elevate CVP without a commensurate increase in volume. For example, cardiac tamponade and positive-end expiratory pressure (PEEP) can elevate pressures without volume. It is important that the CVP be read consistently; in many critical care units, it is read at end expiration. Three positive components of the CVP waveforms are the "a" wave, which denotes atrial contraction; the "c" wave, denoting the closed tricuspid valve bulging into the right atria during ventricular systole; and the "v" wave, representing atrial filling. There are also two descent waves, the "x" and "y." Because these waveforms are considerably smaller than arterial waveforms, they are difficult to identify without a commensurate electrocardiogram (ECG) tracing on the monitor. The "a" wave is usually just below the PR interval, the "c" wave is found midway to near the end of the QRS, and the "v" wave is found after the T wave. The figure below depicts CVP waveforms with corresponding cardiac events and ECG. ______________ Figure 2. CVP waveforms with corresponding cardiac events and ECG. Reprinted from " 'X' " descent of CVP: An indirect measure of RV dysfunction?, by M. S. Raut and A. Maheshwari, 2014, Journal of Anaesthesiology Clinical Pharmacology, 30(3), p. 430. Elevated "a" waves are usually a result of increased resistance to right ventricular filling and may be seen in patients with tricuspid stenosis and pulmonary hypertension. Elevated "v" waves result from blood reflux into the right atria during ventricular systole and may be seen in patients with tricuspid regurgitation and right ventricular failure. Certain dysrhythmias can also change the shape of CVP waveforms.

Stages of shock

Carlson and Fitzsimmons (2022) identify four stages of shock based on estimated blood loss; however, the Emergency Nurses Association (ENA, 2020, pp. 74-75) combines the Initial and Compensatory stages, categorizing them as Stage 1: Compensated Shock, based on subtle compensatory changes. For the purpose of this module, shock will be divided into the four stages identified by Carlson and Fitzsimmons (2018); however, it is paramount that the emergency nurse recognizes the "...narrow window of opportunity to rapidly intervene and restore perfusion" (ENA, 2020, p. 74) before the patient progresses to irreversible shock. Shock is believed to progress through the following four (4) stages: 1. Initial (Class I, Mild) During this stage, hypoxia causes damage at the cellular level which results in mitochondria being unable to produce energy, damaged cell membranes, and cellular anaerobic metabolism. Volume loss during this stage is approximately 15% (or up to 750 ml), thus clinical signs and symptoms are most often not noticeable due to compensatory mechanisms. If present, subtle signs/symptoms may include slight anxiety and increased pulse pressure due to decreased cardiac output. 2. Compensatory (Class II, Moderate) Compensatory mechanisms (sympathetic nervous system [SNS], hormonal) are able to maintain tissue perfusion, allowing shock to proceed potentially unrecognized. Volume loss ranges from 15-30% (750-1500 ml), resulting in decreased cardiac output and profound compensatory mechanisms. The neural response consists of activation of the SNS, which results in venous and arterial vasoconstriction and an increase in heart rate (HR) and contractility to shunt blood to vital organs. Hormonal responses include activation of the renin-angiotensin-aldosterone system (RAAS), secretion of antidiuretic hormone (ADH), and stimulation of the adrenal medulla. RAAS causes vasoconstriction of the arterioles, along with reabsorption of sodium (Na+) and water (ADH also causes reabsorption of water). The RAAS and ADH work together to restore circulating blood volume. Stimulation of the adrenal medulla causes the release of catecholamines (epinephrine, norepinephrine), which enhances the effects of the SNS. The adrenal response also includes the release of cortisol, which increases serum glucose levels and aids in renal absorption of Na+ and water. 3. Progressive (Class III, Moderate-Severe) Compensatory mechanisms are no longer able to maintain adequate perfusion; however, shock may still be reversible in this stage. Activation of the inflammatory and immune responses is initiated, and one or more organ systems may begin to fail. 4. Refractory (Class IV, Severe) Cellular function can no longer be maintained. Shock becomes irreversible and unresponsive to therapy, resulting in multiple organ dysfunction.

Central Venous Lines

Central lines are used for the following reasons: To measure right heart pressures (they do not tell us anything about the left side of the heart) To estimate the patient's fluid status To guide volume resuscitation and allow larger volumes to be administered To assess central venous oxygen saturation (Scvo2) To administer irritant drugs, inotropes, vasopressors, and hyperosmolar solutions such as total parenteral nutrition (TPN)

Catheters

Central venous catheters (CVCs) are made of many different materials and may be single or multiple lumen. A triple-lumen catheter is usually selected to allow for the administration of other therapies while monitoring CVP. The lumens are usually labeled as distal, proximal, and medial. The CVP is monitored via the distal port, and therefore this is where the specialized monitoring tubing is attached. The distal lumen is usually the largest and may also be used for blood, large volumes, and viscous solutions. Any catheter inserted into a great vessel is considered a central line; however, to enable CVP monitoring, the tip of the catheter has to be in the superior vena cava (SVC), or the inferior vena cava (IVC). The subclavian (SC), internal jugular (IJ), and femoral veins are the three major sites of cannulation, each with its own advantages and disadvantages. The SC vein site has lower infection rates and is more comfortable for the patient, thus is preferred for dwelling times longer than 5 days. However, the SC vein is more difficult to cannulate and has higher risk of pneumothorax or hemothorax on insertion (dependent upon provider experience). The IJ vein is most easily accessible and has highest blood flow, but it tends to be more uncomfortable for the patient when moving the head or neck; the external jugular vein is also an option if the IJ vein is not accessible. The femoral vein is the easiest to cannulate and also has higher blood flow; however, it has higher rates of nosocomial infections, such as when an indwelling urinary catheter is insitu. The femoral site is typically reserved for circumstances in which thoracic sites are not accessible. Of note, if the femoral vein is cannulated and used for CVP monitoring, an extra-long catheter will be necessary. Open-ended peripherally inserted central catheters (PICC) are increasingly being utilized. These very long catheters are usually inserted via the cephalic or basilic veins, with the tip terminating in the SVC. A chest x-ray (CXR) is obtained following insertion if the CVC is placed in the upper thorax. In addition, ultrasound guidance is increasingly being used when central lines are inserted.

Complications and Nursing Management

Central venous catheters are not without complications. Pneumothorax, hemothorax, dysrhythmias (especially on insertion), air emboli, thrombosis, and infection may occur throughout the course of therapy. As mentioned above, a CXR should always be done following the insertion of central lines to ensure the placement is correct and also to check for possible complications such as pneumothorax. Measures to decrease the risk of air embolus include using Luer-Lock connections, ensuring they are secure, and placing the patient in supine or Trendelenberg position during catheter removal. The use of any invasive line carries a risk for the development of a fully formed thrombus or a fibrin sheath. Either of these not only interferes with pressure monitoring readings, but also provides a nidus for infection. The longer an invasive line is used, the greater the risk of thrombus. Any lumen that does not have a continuous infusion running should be regularly flushed. Because of the concern for development of heparin-induced thrombocytopenia (HIT), alternatives such as NS or sodium citrate should be considered. The nurse's role in helping to prevent infection is paramount. Well-documented interventions for nurses and other members of the health care team include a group of evidence-based interventions known as "bundles" that have been endorsed by infection control experts, the Institute for Health Improvement (IHI) in the United States, and Safer Healthcare Now! in Canada, a program within the Canadian Patient Safety Institute (www.saferhealthcarenow.ca). These measures include: Use effective hand-washing techniques, both on insertion and during maintenance. Follow infection control guidelines. Nurses should be empowered to stop the procedure if these guidelines are not being followed. Use maximal barrier precautions during insertion. Use chlorhexidine 2% as antisepsis for insertion and for continued maintenance, such as site cleansing and lumen access. Use a transparent semipermeable membrane dressing (impregnated with chlorexidine 2%) to allow continuous visualization of the site, thus decreasing the risk of contamination. If infection is suspected, obtain blood and catheter cultures. If CVC infection is suspected, the catheter should be removed and the patient should be treated with IV antibiotics. Daily review of need for central (and arterial) line, with prompt removal when warranted (Safer Healthcare Now!, 2012). The nurse caring for a patient with a CVC is also responsible for monitoring the waveform and numerical values of pressures and intervening as necessary. As previously indicated, the CVC does not provide information related to the left side of the heart.

Current and Emerging Management Strategies for shock management

Damage Control Resuscitation (DCR): emphasis on early recognition and prevention of shock, rather than intervention Hypotensive resuscitation Traditionally, practice has been rapid infusion of large volumes of crystalloid solution; however, research demonstrates that this results in increased bleeding (hemodilutional coagulopathy) and mortality. Goal of therapy is to replace the type of volume the patient has lost (i.e., nonhemorrhagic = electrolytes, crystalloids; hemorrhagic = blood products). Plasma and blood products are primary corrective measures for blood loss and coagulopathy. 'Hypotension' also needs to be redefined. Research suggests a SBP threshold of 110 mmHg, particularly in the elderly population. Hemostatic resuscitation Early prevention of hemodilutional coagulopathy (loss of clotting factors and platelets in hemorrhagic blood loss, compounded by excessive crystalloid infusion) Ratio of PRBCs : plasma administration should be 1 :1 (if platelets are added for actual or anticipated thrombocytopenia, ratio is 1:1:1) Fluid Resuscitation: As mentioned above, traditional practice resulted in hemodilution, lower O2-carrying capacity (less Hgb), worsening acidosis, abdominal compartment syndrome, ARDS, and mortality. 'Permissive hypotension' is the current philosophy (trauma patients are now managed 'drier' than previously....bleeding and/or volume loss is controlled before fluid resuscitation is initiated leading to a more balanced resuscitation). 500 ml of warmed IV fluid boluses (including that given by prehospital providers) should be administered until blood products are available or SBP of 90 mmHg is achieved (maximum of 1 L crystalloid solution) (ENA, 2020, p. 80) Fluid warmer/rapid infuser is recommended for crystalloid and/or blood product administration. Massive Transfusion: Similar to the above, historical massive transfusion practices have been replaced with judicious administration of IV fluids and blood products. Research indicates that balanced resuscitation and use of predefined massive transfusion protocol (MTP), such as blood-to-plasma ratio, results in hemostasis and decreased mortality in hemorrhaging patients (ENA, 2020, p. 81) Preferred PRBCs : thawed plasma : platelets ratio is 1:1:1. Calcium Chloride Replacement: Citrate, which is added to blood products to prevent clotting, binds with calcium (Ca2+) resulting in its inactivation and subsequent hypocalcemia (worsens bleeding). Each unit of PRBCs (≈ 300 ml) contains citrate 3 g. Healthy, adult liver can metabolize citrate 3 g every 5 minutes (Murgo & Leslie, as cited in ENA, 2014, p. 81), thus patient's risk of hypocalcemia can be predicted according to volume of blood administered. Ca2+ gluconate or Ca2+ chloride should be administered in hypocalcemia. Autotransfusion: transfusion of patient's own blood from chest tube collection chamber Advantages: no risk of transfusion reaction; blood already at room temperature; RBCs likely not degraded, thus increased O2-carrying capacity; less communicable disease; less costly; lower K+ level than banked blood; anticoagulation not required. Disadvantages: use limited to patients with hemothorax; chest drainage may be contaminated; hemorrhage may involve hemolysis of RBCs and destruction of clotting factors; enhanced inflammatory response may occur, resulting in MODS. Damage Control Surgery: resuscitative surgery (no more than 90 mins) aimed at correcting the 'trauma triad' of bleeding, hypothermia, and coagulopathy. Tranexamic Acid (TXA): synthetic antifibrinolytic agent (synthetic version of lysine) that inhibits plasminogen activation, thus stopping fibrin breakdown; prevents the dissolving of clots to reduce bleeding Its use in trauma-related hemorrhage is becoming more common in Canadian trauma centers. Research suggests decreased mortality if administered within 3 hours of injury (ENA 2020, p. 82). Dose: 1g IV over 10 minutes, followed by 1 g IV over 8 hours (Ackery & Rizoli, 2014, p. E587) Tourniquet Use: early use of tourniquet, if applied properly, saves lives and stops major limb hemorrhage (ENA, 2020, pp. 80-82).

Distributive Shock

Distributive shock is caused by the maldistribution of blood volume. Regardless of etiology, decreased venous return occurs as a result of systemic vasodilation and subsequent enlargement of the vascular compartment. Vasodilation is due to the loss of sympathetic tone (neurogenic shock) or presence of inflammatory mediators in the blood (anaphylactic and septic shock). Neurogenic shock is discussed extensively in NURS 0456 Essentials and Management of Neurological Disorders (Spinal Cord Injuries), thus will only be briefly mentioned here. Neurogenic Shock Neurogenic shock is a hemodynamic phenomenon that occurs when the transmission or outflow of sympathetic impulses from the brain to the spinal cord is interrupted, resulting in loss of sympathetic tone. The most common cause of neurogenic shock is spinal cord injury (SCI), typically at the cervical or thoracic level. The loss of sympathetic tone causes extensive peripheral vasodilation, ineffective baroreceptor response, and impaired regulation of body temperature (unopposed vagal activity). Goals in the management of neurogenic shock include treating the cause (e.g., SCI) and restoration of cardiovascular function. Fluid resuscitation, vasopressors, Atropine or transcutaneous pacing (if profound bradycardia), and warming measures are priority interventions for neurogenic shock. Which assessment findings for neurogenic shock differ from those of all other types of shock? Why? Bradycardia is present in neurogenic shock due to the loss of sympathetic innervation and tone (unopposed vagal stimulation), whereas tachycardia occurs in other forms of shock.

Zeroing and Leveling Hemodynamic Systems

Ensuring the accuracy of hemodynamic parameters is essential for decision-making relative to critically ill patients. Two necessary measurements are zeroing and leveling the transducer. Most cardiovascular pressures, such as arterial and CVP, are referenced to the heart to eliminate hydrostatic pressure, which is proportional to the height of the column of blood between the heart and the peripheral vasculature. All cardiovascular pressure devices are zeroed to ambient atmospheric pressure so that the actual pressure measured reflects the pressure above atmospheric pressure (McGhee & Bridges, 2002, p. 62). Zeroing the system involves using the top port of the stopcock closest to the transducer. Maintaining sterility of the system, the cap of this port is removed and the stopcock is opened to air and closed to the patient. The monitor is adjusted so the zero ("0") is displayed, which is equal to atmospheric pressure; this takes only seconds. Once the zeroing is complete, the air port is closed, a closed sterile cap is added, and the system is again opened to the patient. A waveform and pressures will now be displayed on the monitor. Leveling the transducer involves aligning the air fluid interface (zero stopcock) with the level of the left atrium, using an external reference point known as the phlebostatic axis, which is approximately at the level of the atria. This axis is determined by identifying the 4th intercostal space and following this with your finger to a point midway between the anterior and posterior chest wall. When more than one clinician is monitoring the patient, it is appropriate to mark the spot with a permanent marker to ensure continued accuracy. Once the phlebostatic axis is identified, it can be leveled with a carpenter's level or a laser level (refer to Urden et al., 2022, p. 207).

Cold-Related Emergencies

Frostbite Frostbite occurs when ice crystals form in intracellular spaces as tissue freezes, causing vasoconstriction and thrombus formation. These crystals enlarge and compress cells, causing membrane rupture, interruption of enzyme activity, and altered metabolic processes. The patient with frostbite may also have hypothermia, the treatment of which takes precedence over the management of frostbite. The degree of frostbite depends on ambient temperature, wind-chill factor, duration of exposure, and type of clothing worn. The signs/symptoms of each classification below are similar to its heat-related counterpart (Tintinalli et al., 2011, p. 1333). First-degree frostbite ('frostnip') is similar to a superficial burn. The skin may be hyperemic with edema and tingling sensation/numbness. Second-degree frostbite involves the formation of blisters, which may contain blood indicating full-thickness damage. Third-degree frostbite involves complete skin and subcutaneous necrosis and tissue loss. Fourth-degree frostbite extends the entire thickness, including deep structures (e.g., muscle, tendon, bone). The skin is black, with eschar formation resulting in eventual loss of the part. Thawing and rewarming frozen tissue is extremely painful, thus liberal administration of parenteral opioids is needed in severe cases. If severe vasoconstriction is present, an escharotomy may be required. Amputation is never considered in the ED, as the depth of the injury may not be known for several weeks. ______________ Figure 3.2. Third-degree frostbite to fingers. Reprinted from Friday philosophy - Shivering, by C. Grothaus, 2008, Retrieved March 10, 2021, from https://dailytri.wordpress.com/2008/01/18/friday-philosophy-shivering/ Hypothermia Mild hypothermia is defined as a core temperature of at least 32ºC-35°C, moderate hypothermia ranges from 28°C-32ºC, and severe hypothermia occurs at less than 28ºC (Worley, 2020, p. 325). A core temperature of less than 25.6ºC is usually fatal (Sedlak, 2013). Cellular activity and organ function progressively decline as the core body temperature decreases. A 10°C drop in temperature results in a significant decrease in basal metabolic rate. CNS effects are most evident and widespread, with other clinical manifestations including the following: Apathy, weakness, and fatigue, with impaired reasoning, coordination, and gait Loss of consciousness likely if core temperature reaches 30°C-32ºC Cold heart muscle is irritable and prone to dysrhythmias (e.g., atrial and ventricular fibrillation) Ventricular fibrillation does not respond to conventional treatment without prior rewarming (> 28°C) Decreased respiratory rate and effort lead to CO2 retention, hypoxia, and acidosis Decreased drug metabolism below 30°C, potentially leading to toxic levels once rewarmed Hold resuscitation medications if below 30°C Double interval between doses if above 30°C Resume normal advanced cardiovascular dosing and intervals once above 35°C (Worley, 2020, p. 325) Decreased renal blood flow leads to decline in glomerular filtration rate (GFR) Impaired water reabsorption leads to dehydration Shivering consumes glucose stores, thus hypoglycemia ensues Loss of shivering below 30°C List at least four (4) passive external and internal rewarming techniques. In severe hypothermia, active internal and external rewarming procedures are necessary to prevent rewarming shock. If the periphery is rewarmed faster than the core, the lactic acid that has accumulated in the periphery is shunted to the core, resulting in ventricular irritability and fibrillation (rewarming shock). Once rewarming is initiated, providers must also be on the alert for afterdrop. As heat from the core moves into colder tissues, and blood from the periphery travels to the core, the patient's core temperature may decrease by 5ºC-6ºC before it rises again (Worley, 2020). Rewarming also causes vasodilation and hypotension, thus intravascular volume must be replaced, albeit judiciously (relative hypovolemia). The philosophy of 'not dead until warm and dead' remains the standard of practice today...current guidelines recommend rewarming (targeted temperature management) until a core temperature of 32-36°C is reached. If there is no return of spontaneous circulation (ROSC) at that temperature, termination of resuscitation efforts may be considered (AHA, 2016; Hazinski et al., 2015). List at least eight (8) active external and internal rewarming techniques. Passive rewarming (External/Internal) External Warm room temperature Remove wet clothing Cover patient with warm blankets Avoid bathing until normothermic Internal Warmed, humidified O2 Warmed IV fluids Active rewarming (External/Internal) External Radiant heat lamps Heating blankets/pads Bair hugger warming blanket Hot-water bottles Internal Warmed gastrointestinal (GI) irrigation/lavage Esophageal rewarming tubes Extracorporeal warming if severely hypothermic (e.g., hemodialysis, bypass) (see Table 33.4 in Urden et al., 2022, p. 796)

Genitourinary Injuries

Genitourinary (GU) injuries should always be suspected in any trauma patient with one or more of the following: Penetrating injury to the torso Pelvic fracture Blunt trauma to the lower chest or flank Contusions, hematomas, or tenderness over the flank(s), lower abdomen, or perineum Blood at the urethral meatus Hematuria is the most common assessment finding with GU trauma. Urethral trauma is more common in males than females, as the male urethra is longer and less protected. When is the insertion of an indwelling urinary catheter contraindicated in a trauma patient? List at least five (5) signs/symptoms of GU trauma. Suggested answers The insertion of an indwelling urinary catheter is contraindicated in a trauma patient when blood is present at the urethral meatus. This may indicate bladder or urethral injury. Signs/Symptoms of GU trauma Sense of urgency, but inability to urinate Hematuria Suprapubic pain Rebound tenderness Abdominal wall muscle rigidity and/or spasm Involuntary abdominal guarding Blood at the urethral meatus Blood/Edema in the scrotum Displacement of the prostate gland Signs/Symptoms of hemorrhage or hypovolemic shock (e.g., renal arteries)

Nonhemorrhagic causes of hypovolemic shock

Heatstroke, burns, diarrhea, vomiting, hypoaldosteronism, diuresis, and third spacing

septic shock

Higher SOFA score = higher probability of mortality (e.g., SOFA score ≥ 2 = in-hospital mortality rate of > 10%) Tachycardia RR increases due to hypoxemia Interventions: measure lactate level administer antibiotics ONLY after blood cultures begin 30 ml/kg crystalloid infusion for hypotension or lactate >4 Administer vasopressors after fluid resusicatation to maintain MAP greater than >65

Hypovolemic Shock

Hypovolemic shock is the most common form of widespread impaired perfusion. It is caused by a loss of circulating blood volume related to an absolute loss, such as with hemorrhage, or a shift in fluid from the intravascular to interstitial space, such as with a burn injury (absolute hypovolemia). Relative hypovolemia mainly occurs due to vasodilation, resulting in increased venous capacity (see Box 34.4 in Urden et al., 2022, p. 834 for the etiology of hypovolemic shock). Decreased cardiac output and venous return (preload), and ultimately inadequate oxygenation, are responsible for the clinical manifestations associated with hypovolemic shock. In addition, assessment findings are related to the onset and severity of volume loss. They generally include changes in level of consciousness (LOC), HR, blood pressure (BP), respiratory rate (RR), urine output, peripheral perfusion, jugular vein distension (JVD), and acid-base balance. Applying the Frank-Starling law of the heart, what would happen to cardiac output with a decrease in circulating blood volume (preload)? In which direction along the curve below would the star move? Based on Starling's law of the heart, decreased preload will result in a decrease in cardiac output; the star will move down and to the left on the curve Identify the changes in clinical findings that would be expected in the four (4) stages/classifications of hypovolemic shock. Clinical Finding Initial (Class I, Mild) ≤ 15% volume loss, 750 ml Compensatory (Class II, Moderate) 15-30% volume loss, 750-1500 ml Progressive (Class III, Moderate-Severe) 30-40% volume loss, 1500-2000 ml Refractory (Class IV, Severe) > 40% volume loss, > 2000ml ORGAN FAILURE LOC Slight anxiety ↑ Anxiety ↑↑ Anxiety Confusion ↑ Confusion, agitation Lethargic Unresponsive HR Asymptomatic (< 100 beats/min) Tachycardia (100-120 beats/min) Tachycardia (120-140 beats/min) Dysrhythmias (myocardial ischemia) ↑ Tachycardia (> 140 beats/min) BP Normal or slightly ↑ pulse pressure ↑ DBP (narrowing of pulse pressure) Postural hypotension Hypotension Profound hypotension RR Asymptomatic (< 20 breaths/min) Tachypnea (20-30 breaths/min) ↑ Tachypnea (30-40 breaths/min) ↑ Tachypnea (> 35 breaths/min) Peripheral perfusion Asymptomatic Pale, cool skin Delayed capillary refill Significant hypoperfusion (skin ashen, cold, clammy; very sluggish capillary refill) Absent peripheral pulses, capillary refill Skin cyanotic, mottled, diaphoretic JVD Asymptomatic Flat (↓ venous return) Flat Flat Urinary output Asymptomatic (> 30 ml/hr) ↓ to 20-30 ml/hr Oliguria (5-15 ml/hr) Anuria Acid-base status Asymptomatic Respiratory alkalosis Metabolic acidosis (↑ Lactate, ↓ bicarbonate [HCO3]) Severe lactic acidosis Medical and nursing management of hypovolemic shock focuses on identifying and treating the cause of volume loss, and replacing this loss by administering crystalloid or colloid solutions, as well as blood products. Vasopressors may also be administered to restore BP; however, the 'tank must be topped up' first. Crystalloid solutions (e.g., 0.9% sodium chloride [0.9% NaCl, normal saline [NS], Ringer's lactate [RL, LR]). The main benefit of crystalloids is their Na+ content, which is comparable to the serum Na+ concentration. Na+ pulls water with it, thus aiding in increasing intravascular volume; however, approximately only 25-30% of crystalloid solutions remain in the intravascular space, with the remainder diffusing to other fluid compartments (Muzzy & Snyder, 2013). This can be an advantage for some patients, such as in chronic dehydration, whereas it may be a disadvantage for others (e.g., patients requiring rapid vascular expansion). Of note, NS may cause neutrophil activation and adhesion; however, this response is dose-dependent. Lastly, crystalloids have no O2-carrying capacity. Colloids rely on oncotic pressure to rapidly expand intravascular volume, with most of the solution remaining within the vessels. Whether they are more effective than crystalloids in the treatment of hypovolemic shock remains unclear. In shock states that affect capillary permeability (e.g., sepsis), colloids may leak into the extravascular space, drawing water out of the intravascular compartment and exacerbate volume loss. Blood products (e.g., packed red blood cells [PRBCs]) may also be administered for hypovolemic shock; however, their purpose is not to expand intravascular volume per se. PRBCs, for example, are given to increase the patient's O2-carrying capacity, typically when the hemoglobin (Hgb) level reaches < 70-80 g/L. The recommended ratio of PRBCs : plasma : platelets is 1:1:1 in order to prevent coagulopathies (Emergency Nurses Association [ENA], 2020, p. 80). Discuss factors that may determine the type of solution administered. Generally, the type of solution administered will reflect the type of fluid lost. Crystalloids may be administered to quickly replace intravascular volume; however, they do not have any O2-carrying capacity and only 25-30% stays in the intravascular compartment (blood products may be an adjunct, depending on the situation). NS may also cause neutrophil activation and adhesion, but this effect is dose-dependent. On the other hand, colloids will also rapidly increase intravascular volume and smaller volumes are required, most of which stays within the vessels. However, colloids may cross capillary membranes, pulling fluid with them and exacerbating hypovolemia. Additional factors, such as Hgb/electrolyte levels and acid-base status, will also influence the selection of fluids.

Obtaining Arterial Pressures

Intra-arterial pressure monitoring allows for continuous evaluation of systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP). While trending of systole and diastole are important in assessing how well a patient is perfusing, the MAP is a more stable hemodynamic parameter and provides a more accurate interpretation of a patient's hemodynamic status (McGhee & Bridges, 2002, p.78). A MAP of at least 60 mm Hg is required for coronary artery perfusion, and greater MAPs may be required for other organs. The normal MAP is 70-90 mm Hg. The formula for assessing MAP in the non-monitored patient is: SBP + (DBP x 2 ) = MAP 3 Pulse pressure, the difference between the systolic and diastolic pressures, is also a valuable parameter that nurses can assess, as it is an indirect reflection of stroke volume (SV). Normal pulse pressure is 40 mm Hg; however, this parameter is not measured or displayed on the monitor, so trending does not occur as it does with MAP. A narrow pulse pressure often occurs in conditions associated with hypovolemia which results in a rise in diastolic pressure, whereas a wide pulse pressure is typically due to a rise in systolic pressure (e.g., aortic regurgitation, vascular conditions).

Monitoring Procedures and Equipment

Invasive methods of hemodynamic monitoring are used to obtain detailed physiological information to guide therapy for critically ill patients. Invasive monitoring techniques require the insertion of a catheter into an artery to directly measure blood pressure (BP), into a central vein to measure central venous pressure (CVP), or into a pulmonary artery (PA) for continuous cardiac output monitoring. This module concentrates on the first two monitoring processes, as PA monitoring is generally not practiced in the emergency department (ED). (Refer to Urden et al., 2022, pp. 237-242 for information about newer non-invasive methods of hemodynamic monitoring).

Shock Introduction

Shock is, quite simply, a state of inadequate tissue perfusion resulting in insufficient oxygen (O2) delivery and/or inadequate O2 utilization at the cellular level. Without adequate O2 delivery and utilization, cells are no longer able to produce energy via aerobic metabolism and must use anaerobic metabolism instead, which results in the accumulation of lactic acid and cellular acidosis. Eventually, progressive tissue acidosis and organ dysfunction occur. This study guide will enable you to review the pathophysiology and management of shock syndromes. It is not all-inclusive, but focuses on essential introductory information. Shock can be classified as hypovolemic, cardiogenic, or distributive. Distributive shock can be further classified as neurogenic, anaphylactic, or septic.

Site Selection

Site selection for arterial line insertion involves consideration of the following factors: Size of the artery: the artery must be large enough to accommodate the catheter without occluding or impeding blood flow. Accessibility: site must be readily accessible and free from contamination (i.e. away from bodily secretions) Distal blood flow: adequate collateral circulation must be present distal to the site should the cannulated artery become occluded The most common site for insertion of an arterial line in the adult patient is the radial artery. The femoral artery is an alternative site; brachial, axillary, and dorsalis pedis arteries are less preferable. The Allen test should be performed prior to radial site insertion to assess collateral circulation (Morton et al., 2018).

Positioning the Patient and Transducer

Studies have shown that CVP can be reliably measured between 0-60° head-of-bed (HOB) supine position, as well as 30°-90° lateral position with the HOB flat (see Urden et al., 2022, p. 207 for lateral position landmarking). When the transducer is placed above the phlebostatic axis, gravity and lack of fluid pressure will cause an erroneously low reading. It can read 1.87 mm Hg less than the true value for every inch above the level of the catheter tip. When the transducer is placed below the catheter tip, the fluid pressure will cause an erroneously high reading, increasing by 1.87 mm Hg for every inch below the phlebostatic axis. Although leveling must be done every time the patient or transducer is moved, due to the accuracy of disposable transducers it is not necessary to re-zero; however, most ED and critical care unit protocols require zeroing to be completed at the beginning of each shift.

Hemodynamics review question answers

Suggested answers List three criteria for hemodynamic monitoring tubing. It must be stiff and non-compliant. It should be no longer than 92 cm (36 in.). It must have a minimum amount of stopcocks (two to three). The phlebostatic axis is located at the 4th intercostal space (ICS) and a midway point between the anterior and posterior chest wall. When the transducer is placed above the phlebostatic axis, pressures will be erroneously low. image01 The illustration is of an arterial pressure waveform. Systolic blood pressure (SBP) - Systole Dicrotic notch (DCN), denoting aortic valve closure and beginning of diastole Diastolic blood pressure (DBP) - Diastole image02 a. This is an overdamped waveform. b. Nursing interventions Check the integrity of the system for leaks. Ensure all connections are tight. Check for kinks in the line or catheter. Ensure a continuous pressurized solution is infusing to help prevent clot formation. Make sure transducer is clear of air. c. Overdamped waveforms may result in underestimated systolic pressure and overestimated diastolic pressures. image03 a. This is an optimally damped waveform, which is normal. There are 1.5-2 oscillations following the square wave. b. No nursing interventions are necessary. c. The nurse can be reassured the pressures and waveform are accurate. image04 a. This is an underdamped waveform. It has more than 2-3 oscillations following the square wave. b. Nursing interventions include ensuring the tubing is stiff and non-compliant, the tubing is not too long, and a minimum amount of stopcocks are present. c. Underdamping may result in overestimating the systolic blood pressure and underestimating the diastolic pressure. Complications of central venous lines Air embolus Thrombosis formation Infection Pneumothorax Hemothorax Dysrhythmias Interventions to prevent and manage infection in central lines Use effective hand washing on insertion and during maintenance Follow infection control guidelines Use maximal barrier precautions during insertion (sterile technique) Use chlorhexidine 2% as antisepsis Use blood and catheter cultures to confirm suspected infection Treat infection with IV antibiotics and remove the catheter Use a transparent semipermeable membrane dressing Sudden hypotension may be the first indicator of an air embolus; other signs include confusion, lightheadedness, anxiety, and unresponsiveness. Roughly 10-20 ml of air must enter the venous system in order for the patient to become symptomatic. The air creates 'foam' in the right ventricle with each contraction, and subsequent drop in SV due to air rather than blood being ejected (loss of CO). If you suspect an air embolus, your immediate action is to turn the patient onto his/her left side in Trendelenburg position, which facilitates the air rising to the wall of the right ventricle and increases blood flow. Oxygen should also be administered immediately, unless contraindicated. Causes of low CVP Hemorrhage Vasodilation from any cause, including drugs such as nitroglycerine Distributive shock Use of diuretics Re-warming following cardiac surgery Causes of high CVP Fluid overload (the major cause of increased CVP) Conditions causing vasoconstriction or decreased myocardial contractility Mechanical ventilation Right ventricular failure image05 a. The illustrations are of an ECG waveform and central venous pressure waveform. b. Events shown in the lower waveform a wave atrial contraction x descent atrial relaxation, downward movement of contracting right ventricle c wave closed tricuspid valve bulging into atrium during ventricular systole v wave atrial filling y wave valve opens, beginning of ventricular filling c. There is no recognizable CVP pattern in atrial fibrillation due to atrial disorganization. Term Definition a. __2__ Preload b. __3__ Afterload c. __1__ Contractility This can be positive or negative and is influenced by Starling's mechanism and the sympathetic nervous system. The volume in the left ventricle at the end of diastole. It is measured as pressure because volume cannot be measured by a transducer. The pressure or resistance that the ventricle has to overcome to eject blood. It may be increased due to aortic impedance. Determinants of Scvo2 Cardiac output (CO) Arterial oxygen saturation (SaO2) Hemoglobin (Hgb) Tissue oxygen metabolism (vo2). Causes of high Scvo2 Anesthesia Sepsis Hypothermia Excessive supplemental oxygen

septic shock clinical manifestations

Tachypnea / hyperventilation as a compensatory mechanism, temperature dysregulation, urine output down, altered neurological status, GI dysfunction and respiratory failure increased CO and cardiac index, decreased SVR, decreased right arterial pressure, decreased pulmonary occlusion pressure

Burn Injuries

The end result of burn injury is tissue loss or damage, which involves multisystem alterations if the burn is severe. Enzyme malfunction, protein denaturation (loss of structure), and cellular necrosis are responsible for the massive tissue damage. In order to provide appropriate care, nurses must be aware of local and systemic changes associated with burns. Mechanism of Burn Injury Injury to tissue results from exposure to heat, electricity, chemicals, or radiation. Thermal burns account for 60% of all burns, and are the result of exposure to flame, flash, steam, or scalding liquid. Burns involving direct contact or flame are most often deep partial-thickness or full-thickness injuries. Electrical burns occur when electricity passes through the body, via the path of least resistance towards the ground, and is converted to heat. Nerves, blood vessels, and muscles are less resistant and more easily damaged than bone or fat. Alternating current (AC) is more dangerous than direct current (DC), but both may produce entry and exit wounds. Little surface damage may be visible; however, underlying tissue and muscle burns can be extensive. Chemical burns vary in severity; their extent is determined by the concentration of the substance and length of exposure. All chemical burns should be considered deep partial-thickness or full-thickness until proven otherwise. Alkalis cause more damage than acids as they penetrate deeper into tissue. Radiation burns due to radiation beams are uncommon, and injuries may not be apparent for days or even weeks. They are usually localized, resulting from high doses of radiation to the affected area. Sunburn is also an example of a radiation burn. Zones of Injury Three specific zones are present in burn injury: Zone of coagulation - centre portion of injury, site of greatest heat transfer. Irreversible necrosis occurs in this area. Zone of stasis - area surrounding the zone of coagulation, where impaired circulation can lead to cessation of blood flow due to inflammation. The skin in this area is potentially salvageable. Zone of hyperemia - area of minimal cell involvement where vasodilation and increased blood flow are present. Recovery can occur in this area. Classification of Burn Injuries Burns are classified by size and depth. Size of Injury The size (total body surface area [TBSA]) of thermal and chemical injuries is assessed using formulas, such as the following: Rule of Nines (adults, children > 10 years of age) Lund and Browder table (more accurate during childhood growth; see Urden et al., 2022, p. 868) Rule of Palms (small or scattered burns; 1% = size of patient's hand, including fingers; calculate TBSA burned) For electrical burns, surface damage is minimal when compared with underlying damage (e.g., muscle). Describing the injury anatomically is more important than calculating the percentage of TBSA burned. Depth of Injury Burns are classified as superficial, partial-thickness, or full-thickness. These descriptions are based on the surface appearance of the wound. A superficial (first-degree) burn involves the first two layers of the epidermis; it appears dry and red, blanches with pressure, and is quite painful. Examples include sunburns and minor burns caused by steam. The wound heals in 2-7 days. A superficial partial-thickness (second-degree) burn is usually caused by brief contact with flames or hot liquid, or exposure to dilute chemicals. The wound is light to bright red or mottled, blanches with pressure, may appear wet and weeping, and may contain bullae; blister formation is also very common. These burns are very painful and sensitive to temperature and air currents. Healing typically occurs within 7-21 days. A deep partial-thickness (second-degree) burn is often the result of contact with hot liquids or solids, or intense radiant energy. It may or may not be characterized by blister formation, and may be wet or waxy dry. The surface of the wound is usually red with patchy white areas that have slow to no blanching with pressure. Dermal necrosis and coagulated protein change the color of the wound from white to yellow. The burned area is sensitive to pressure only. Healing may require up to 6 weeks and often requires grafting. A full-thickness (third-degree) burn destroys all layers of the skin. The area appears pale white, charred, red, or brown and leathery, and does not blanch. The surface may be dry, or subcutaneous fat may be exposed. The burned area is usually painless and sensitive to deep palpation only. Surgical skin grafting is required for closure. Patients with full-thickness burns are extremely susceptible to infection, fluid and electrolyte imbalances, alterations in thermoregulation, and metabolic disturbances. A full-thickness (fourth-degree) burn extends into the fascia and muscle. It is sensitive to deep pressure only and requires extensive surgical grafting. Emergency Burn Management The goals are to save life, minimize disability, and prepare the patient for definitive care. Priorities in the assessment and management of burn patients are listed in order below: Airway management Inhalation injuries can occur in either the presence or absence of cutaneous injury, and are strongly associated with burns sustained in a closed space. Observe for facial burns, singed eyebrow(s) and nasal hair, carbon deposits (soot) in the oropharynx and/or spututm Respiratory management If inhalation injury is suspected, immediate intubation and ventilatory support must be considered (high peak airway pressures most often needed). Carbon monoxide (CO) toxicity leads to hypoxia (further discussed in NURS 0464 Endocrine and Toxicological Emergencies). Circulatory management Burn shock: may result when ≥ 20% TBSA involved (see fluid resuscitation guidelines below) Hypovolemic shock due to capillary dilation and increased capillary permeability...plasma leaks from intravascular to interstitial space leading to significant edema...capillary leak syndrome Release of local and systemic inflammatory mediators increases arteriolar dilation Decreased myocardial contractility and cardiac output Increased systemic and pulmonary vascular resistance Renal management Hourly assessment of urine output (best indicator of the effectiveness of fluid resuscitation), particularly if ≥ 15-20% TBSA burned Adequate urine output: adults (0.5 ml/kg/hr, or 30-50 ml/hr); children (0.5-1 ml/kg/hr) If electrical injury with myoglobinuria in adult patient, maintain urine output at 1.0-1.5 ml/kg/hr (or 75-100 ml/hr) until urine is clear Gastrointestinal management Prone to paralytic ileus, Curling stress ulcers (sloughing of duodenal mucosa due to hypovolemia) Pain management Acute phase: analgesics (i.e., opioids) IV, titrated to effect Subcutaneous (SC) and intramuscular (IM) routes must be avoided due to altered absorption Maintenance: patient-controlled analgesia; oral opioids/narcotics Extremity pulse assessment Neurovascular compromise due to edema, particularly if circumferential burns...assess peripheral pulses with Doppler; escharotomy may be required Wound care A comprehensive review of burn care is beyond the scope of this Module, and is most often institution and/or unit specific (e.g., burn unit); however, general principles of wound care (e.g., partial-thickness) include the following: Remove clothing, jewelry, etc. (if able) in order to assess the wound (soak the wound with sterile water/0.9% sodium chloride (0.9% NaCl, normal saline [NS]) during removal to limit further tissue damage; provide analgesia) Cover wounds with clean, dry dressings or sheets (prevents infection, but also provides pain relief from being exposed to oxygen [O2]-rich room air, as well as hypothermia) Infection is of significant concern in the burn patient (direct contact - cross-contamination most common cause of sepsis), thus strict infection control precautions must be adhered to by all (i.e., physicians, nurses, family, visitors) Fluid Resuscitation There are several formulas that can be utilized to guide the fluid resuscitation of a burn patient. Regardless of which formula is used, "... the volume of fluid actually infused in practice is adjusted according to the individual patient's urinary output and clinical response" (American Burn Association [ABA], 2018, p. 33). When estimating TBSA for fluid resuscitation, only second-degree and third-degree total burn surface are calculated (e.g., Rule of Nines). "First-degree burns should not be included in the fluid resuscitation calculations as it is unnecessary and increases the likelihood of over-resuscitation" (ABA, 2018, p. 32). The recommended formula for fluid resuscitation (modified Parkland formula) has recently been updated, as follows: Fluid requirements = TBSA burned (%) x patient's weight (kg) x 2 ml = TBSA (%) x 2 ml/kg Note: Half of the calculated volume is delivered in the first 8 hours after injury, with the second half administered in the remaining 16 hours. However, if resuscitation is delayed for 2 hours, for example, half of the calculated volume would be delivered in the first 6 hours post-burn (time adjusted) (ABA, 2018). Traditionally, the Parkland formula (4 ml/kg rather than 2 ml/kg) has been used to replace lost fluid volume and resuscitate the burn patient in the first 24 hours. However, evidence now suggests that 4 ml/kg results in over-resuscitation, particularly given that burn-related edema reaches its maximum in the second 24 hours post-burn. Although patient response to fluid resuscitation is variable, higher volumes (i.e., 4 ml/kg) should be reserved for patients with significant myoglobinuria due to second-degree and third-degree high-voltage electrical burns (ABA, 2018). Lactated Ringer's (LR) is the isotonic fluid of choice in burn patients due to its similarity to intravascular solute content (ABA, 2018, p. 32) (infants and young children ≤ 30 kg should also receive Dextrose 5% in LR as maintenance fluid). Hyperchloremic solutions, such as 0.9% normal saline, should be avoided in fluid resuscitation of the burn patient.

Complications of Arterial Lines

The following complications may be related to arterial lines: Air embolus Infection Thrombosis Hemorrhage Arterial spasm Hematoma Neurovascular compromise Nursing actions related to these complications include prevention, troubleshooting, and interventions (review Table 13.2 in Urden et al., 2022, pp. 211-212).

Equipment for Hemodynamic Monitoring

The following equipment is common to all invasive hemodynamic monitoring systems: Catheter Non-compliant (stiff) pressure tubing Transducer, plus stopcocks Pressurized flush system Bedside monitoring system Catheters used for arterial monitoring are usually relatively short single-lumen catheters. Catheters for central venous monitoring are longer and are usually multi-lumen. The catheters and tubing are often referred to as "lines". The tubing used for hemodynamic monitoring is stiff and non-compliant, with a transducer and stopcocks attached. This specialized tubing is made to minimize artifact and increase data accuracy. In order to provide accurate data, the tubing should be no longer than 92 cm (36 in) and have a minimum amount of stopcocks (most standard sets come with two to three). Using ordinary tubing would result in inaccurate readings. Tubing should be changed every 72-96 hours; however, individual ED and critical care unit policies vary. Closed system tubing such as the American Edwards VAMP® system may be used for arterial line set-up, as most of the blood sampling in critical care patients is via the arterial line. From an infection control standpoint, this type of tubing is less likely to result in contamination and also allows "discard" blood to be returned to the patient, thus decreasing the risk of further anemia in a critically ill individual. The transducer is a device that allows the physiological (mechanical) signal transmitted from the patient via the catheter and tubing to be converted into an electrical signal so that waveforms and numerical values can be displayed on the bedside monitor. A stopcock attached at the transducer level is the reference point for leveling and zeroing, which must be done to obtain accurate readings. An in-line flow device is also attached at this level to allow manual flushing of the system, particularly following blood withdrawals. The transducer is usually attached to an intravenous (IV) pole in a holder. A pressurized flush system maintains the patency of the arterial line. Some facilities still use low-dose heparin in the flush solution; however, due to increasing concerns about heparin-induced thrombocytopenia (HIT), plain normal saline (NS) is now the preferred solution. This is placed in a pressure infuser bag inflated to 300 mm Hg, maintaining an administration rate of approximately 3 ml/hr. Transducers are usually disposable and are attached to the monitor by cables. The bedside monitoring system amplifies the electrical signal, enabling easier visualization and also allowing trending and storage of data.

Submersion Injury

The highest incidence of water-related deaths in Canada involves the 18-24 years age group, mainly due to their high risk-taking behaviors. Interestingly, drowning victims in Canada are getting older: the 50-64 years age group and elderly (65+ years) are the fastest growing groups of drowning victims. Despite the decrease in number of drownings in children < 5 years of age, they remain a high-risk age group for drowning accidents (Drowning Prevention Research Centre Canada, 2013). Submersion injury involves surviving suffocation while submerged in liquid (i.e., water). Reflex laryngospasm occurs in 15% of submersion victims, preventing significant aspiration of water/liquid; however, 1-3 ml/kg is enough aspirate to interfere with surfactant function (washout) and gas exchange. Hypoxemia and contaminants (e.g., algae, soil, chlorine) cause pulmonary damage and dysfunction, specifically the inflammation, obstruction, and collapse of bronchioles and smaller airways. Capillary permeability is altered, leading to leakage and pulmonary edema (ARDS). Most submersion victims experience an influx of fluid. Regardless of the mechanism, the common denominators in submersions are hypoxia and acidosis. Note: Currently, the preferred terminology is drowning death (fatal), drowning with morbidity (non-fatal), and drowning without morbidity (non-fatal). Clinical manifestations of submersion injury are directly proportional to the severity of hypoxia, and may include the following: Pulmonary: tachypnea/apnea, pulmonary edema, pneumonitis; ARDS Cerebral: hypothermia; dilated pupils ('fish eyes'); anoxic encephalopathy, cerebral edema Cardiovascular: cold skin with ashen, blue-grey coloring; hypotension, bradycardia (severe); cardiac arrest Hematological: DIC Gastrointestinal: vomiting Renal: acute kidney injury (AKI; acute tubular necrosis [ATN]) It is important to note that complications from a non-fatal drowning may be delayed, up to 2-3 days after the submersion event. Delayed inflammatory responses damage the alveolar-capillary membrane (site of gas exchange) and impair surfactant function. Regardless of the duration of submersion or seemingly asymptomatic presentation, all submersion victims should be observed in the ED for a minimum of 24 hours to monitor for complications (e.g., ARDS). Worley (2020) suggests that only those who present asymptomatic, have a normal chest x-ray, and have normal vital signs including oxygen saturation for 6 to 8 hours should be discharged home (with explicit instructions regarding signs/symptoms that warrant return to the ED). All others, with abnormal laboratory findings and/or chest x-ray, should be admitted (p. 327). Prehospital management of submersion injury is crucial in decreasing anoxic brain injury and improving overall survival. The duration of submersion, water (liquid) quality and temperature, and time elapsed before effective basic life support (BLS) could be initiated are the most important factors in predicting the severity of neurological outcomes. Saltwater or freshwater aspirate is usually insignificant in the management of submersion victims. Submersion in cold water (< 5°C) may have a cerebral protective effect if resuscitation is initiated early; however, cold submersion predisposes the patient to hypothermia and cardiac arrest due to immersion syndrome (vagal stimulation resulting in cardiac arrest). Hypothermia following warm water submersion is associated with a poorer prognosis; it is indicative of prolonged submersion time and poor/absent perfusion. Discuss the medical and nursing management of submersion injury. Medical and nursing management of submersion injury Immediate BLS/advanced life support (ALS) measures Assess for neck/spinal injuries Assess core body temperature frequently (continuous rectal temperature if on cardiorespiratory monitoring); initiate rewarming measures as needed Assess ABGs, SaO2; correct acid-base imbalances Insert 2 x large bore IVs Insert NG tube for gastric decompression (reduce vomiting) Consider positive airway pressure (e.g., bi-level [BIPAP]), which will help to force open the collapsed alveoli Consider prophylactic antibiotics (this is controversial: uncommon organisms may not be sensitive to commonly prescribed regimen; depends on type of submersion and comorbidities)

Normal and Abnormal Waveforms

The normal arterial wave form consists of a sharp upstroke, the top of which is systole and the SBP. The downstroke after the peak contains the dicrotic notch reflecting aortic valve closure and the beginning of diastole. The lowest point of the waveform represents the DBP (diastole). A normal arterial waveform is shown below. Figure 1. Normal arterial waveform. Copyright 2011 by MacEwan University. Changes in the arterial waveform can occur as a result of certain conditions. For example, if cardiac output is low as a result of non-perfusing or poorly perfusing premature ventricular contractions (PVCs), the arterial waveform will be decreased or non-existent. During pulsus paradoxus (such as that which may occur with cardiac tamponade), arterial waveforms will be markedly diminished on inhalation. Changes to the arterial waveform may be due to other conditions such as pulsus alternans or pulse deficit situations. Note that changes to arterial waveforms may also occur as a result of problems with the monitoring system (refer to Table 13.2 in Urden et al., 2022, pp. 211-212). When low pressures are seen on the monitor, it is the nurse's responsibility to determine whether the problem is related to the patient or the equipment. One way of determining this involves performing a bedside dynamic frequency response or fast-flush square waveform test (square wave test). When performing the square wave test, the nurse is attempting to establish that the waveform is being accurately transmitted back to the transducer, in effect, that the transducer is performing accurately. This is known as optimal damping (or normal damping). The test is done by activating the fast-flush device on the tubing system for about one second. The expected response is a rapid upstroke with a plateau before a return to baseline (the square wave), followed by 1.5 to 2 oscillations close together. An optimally damped waveform should reassure the nurse that the pressures and waveform are accurate (see Figure 13.11 in Urden et al., 2022, p. 212). An overdamped waveform will display a less crisp, more slurred-looking square wave with fewer than 1.5 oscillations below or above baseline. This can be due to leaks in the system, blood clots, kinks in the line or catheter, or air. Systolic pressures may be underestimated (lower than they actually are) and diastolic pressures may be erroneously elevated. An underdamped waveform will display a narrow upward systolic peak, and the square wave will look fairly normal but taller. It will be followed by more than 2 or 3 oscillations below and above baseline. This can be due to excessively long tubing, use of ordinary IV tubing, or too many stopcocks. Underdamped systems can show erroneously high systolic pressures and erroneously low diastolic pressures. It is important to do the square wave test whenever the waveform appears overdamped or underdamped. An arterial waveform with a narrow systolic peak may be present in a patient with hypertension; it appears underdamped but is not caused by equipment problems. The square wave test should also be considered whenever the accuracy of the arterial blood pressure is in doubt, or when physiological changes, such as higher heart rate or vasoconstriction, increase the demands on the patient's circulatory system. Many critical care units (and EDs) have policies indicating the test should be performed at least once a shift (McGhee & Bridges, 2002, p. 76). If the arterial line waveform becomes unreliable, a cuff pressure may be used; however, the square wave test is probably more accurate than a cuff blood pressure reading alone.

Maxillofacial Injuries

These injuries can result from either blunt or penetrating trauma. The nasal bones, zygoma, and mandible are most susceptible to fractures. Fractures of the maxilla are diagnosed according to LeFort's classification. LeFort I fractures are horizontal fractures in which the teeth are separated from the rest of the maxilla (above the palate, below the zygomatic process). The fractured portion of the maxilla is free-floating from the rest of the face. Malocclusion may be evident, as well as slight maxillary edema; however, the nasal bones remain intact. They may be unilateral or bilateral in presentation. Figure 2.1. LeFort I fracture. LeFort II fractures involve the orbit, ethnoid, and nasal bones, resulting in a tripod or pyramidal shape. Again, the fractured portion is free-floating from the remaining face/skull. LeFort II fracture is characterized by massive facial edema, obvious nasal deformity, malocclusion, and cerebrospinal fluid (CSF) rhinorrhea. Figure 2.2. LeFort II fracture. LeFort III fractures involve complete craniofacial separation; the orbits, maxilla, zygoma, mandible, and nasal and ethmoid bones are free-floating. When in the upright position, the patient's face appears elongated, whereas it appears sunken in the supine position. LeFort 2.3. LeFort III fracture. List at least four (4) major complications that may be associated with maxillofacial trauma. Possible complications related to maxillofacial trauma Maxillary fractures require a tremendous amount of force, thus concomitant fractures and injuries are also likely present (e.g., head/spinal injuries) Airway compromise involving difficulty swallowing, edema, and traumatic debris (e.g., teeth, blood) is a common concern with these injuries Difficult endotracheal intubation due to edema and loss of normal anatomic contour LeFort II and III often involve cerebrospinal fluid (CSF) leakage, thus infection is a significant concern Fluid volume deficit due to hemorrhage

Thoracic Injuries

These injuries may be caused by blunt or penetrating forces and involve trauma to the chest wall, lungs, heart, great vessels, and esophagus. Rib Fractures Fractures of the 1st and 2nd ribs are often associated with what underlying injuries? Right-sided fractures at the 8th rib and below are associated with injury to the _____________. Left-sided fractures at the same level are associated with injury to the ______________. Identify at least four (4) signs/symptoms of rib fractures. See bottom of page to view suggested answers. Flail Chest A flail chest occurs when two or more ribs are fractured in two or more places and are no longer attached to the thoracic cage. This results in a free-floating segment that moves independently from the chest wall. A flail chest may also result from bilateral detachment of the sternum from the costal cartilage. The chest wall moves paradoxically: with inspiration the flail segment moves in, and with expiration the flail segment moves out. Muscle spasms occur immediately following chest injury, thus paradoxical movement may not present for several hours (more visible following analgesia). ____________ Figure 2.4. Left-sided flail chest. Reprinted from Flail Chest [PowerPoint slides], by S. N. Bhagirath, 2014 (http://www.slideshare.net/bhagirathsn/flail-chest-34161720). The following are additional signs/symptoms of flail chest: Hypoventilation, atelectasis Decreased tidal volume and vital capacity Dyspnea Impaired cough Chest wall pain and/or contusions Crepitus Emergency management of a flail chest includes oxygen (O2), analgesia, IV fluids, stabilization of the flail segment, and chest tube insertion (pneumo/hemothorax often present). Assisted ventilation and endotracheal intubation may also be required. Pulmonary Contusion Pulmonary contusion is the most common traumatic chest injury, and also the most potentially-fatal. Essentially a 'bruised lung', a pulmonary contusion is typically caused by blunt-force trauma and often presents with the rib injuries noted above. Like any other 'bruise', pulmonary contusion begins with localized hemorrhage, in addition to alveolar and interstitial edema. As this process spreads to other areas of the lung(s), the alveoli become susceptible to inflammation and the lung becomes less compliant. Hemorrhage and inflammatory processes result in increased pulmonary vascular resistance and limited pulmonary blood flow, leading to ventilation-perfusion (V/Q) mismatch. Clinical manifestations often occur gradually over a 24-48 hour period, thus may not be evident until the patient arrives in the critical care environment (although pulmonary infiltrates can be seen on chest x-ray [CXR] within 12-24 hours). Inspection of the chest reveals ecchymosis and edema, alerting the medical and nursing team that a pulmonary contusion is likely. Signs/Symptoms of a pulmonary contusion include crackles on auscultation, productive cough with hemoptysis, dyspnea, and chest pain. Aggressive management of pulmonary contusion is essential in preventing complications (e.g., infection, ARDS). Early ambulation, deep breathing/spirometry exercises, judicious use of IV fluids, and pain control are required. Describe the position in which a patient with unilateral pulmonary contusion should be placed, including rationale. Pneumothorax A pneumothorax occurs when air accumulates in the pleural space, resulting in partial or complete collapse of the affected lung. Figure 2.5. Left-sided pneumothorax. Identify at least four (4) signs/symptoms of a pneumothorax. Discuss the medical and nursing management of a pneumothorax. Hemothorax A hemothorax (bleeding into the pleural space) may be caused by lung parenchymal damage, blunt injuries or bruising affecting the heart or major vessels, or injury to internal mammary arteries. Mechanisms of injury include steering wheel impact, falls, assaults, and direct blows to the chest. Figure 2.6. Left-sided hemothorax. A hemothorax is characterized by the following: Absent or diminished breath sounds over the affected lung Dyspnea, tachypnea Chest pain Cardiac dysrhythmias Signs/Symptoms of hypovolemic shock Medical and nursing management is similar to that of a pneumothorax, with the exception of the potential for hypovolemic shock (see the module above). Chest tube insertion and care of patients with chest tube drainage systems are described in the following videos: https://www.youtube.com/watch?v=IdmMR8JxmFo https://www.youtube.com/watch?v=j8xNaN7TRC0 Tension pneumothorax is a life-threatening condition that occurs due to increased air pressure in the pleural space (may also occur due to hemorrhage in the pleural space = tension hemothorax). As the pressure increases, the lung on the injured side collapses and causes the mediastinum to shift to the opposite side. This shift exerts pressure on the heart and great vessels, which results in decreased cardiac output and venous return. Discuss the treatment for tension pneumothorax. Define cardiac (pericardial) tamponade. What are the three (3) classic signs/symptoms of Beck's triad? Aortic Injuries Aortic injuries are caused by penetrating or blunt trauma, most often via rapid deceleration/acceleration forces. In most cases, injuries to the ascending aorta are immediately fatal; mortality rates for injuries to the descending aorta are roughly 85%. List at least four (4) signs/symptoms of an aortic injury. Emergency management of aortic injury is aimed at maintaining hemodynamic stability, specifically BP. Depending on the site of rupture or laceration, the patient may present as hypo- or hypertensive. Early surgical repair is required. Fractures of the 1st and 2nd ribs are often associated with injuries to the brachial plexus and great vessels (intrathoracic vasculature). Right-sided fractures at the 8th rib and below are associated with injury to the liver. Left-sided fractures at the same level are associated with injury to the spleen. Signs/Symptoms of rib fractures Pain Shallow respirations Guarding or splinting of chest wall Ecchymosis or sternal contusions Bony crepitus Deformity Ventilation and perfusion depend on body position, meaning the areas of the lungs that are most dependent in the supine/side-lying positions will be the most perfused and ventilated (preferential blood flow to dependent areas). Thus, a patient with a (unilateral) pulmonary contusion should be placed with the uninjured side down ("down with the good lung") (Urden et al., 2022, p. 812) to allow for maximal ventilation and perfusion. Signs/Symptoms of a pneumothorax Decreased breath sounds upon auscultation of affected side Hyperresonance upon percussion of affected side Dyspnea, tachypnea Pain Tachycardia Open, sucking wound on affected side (open pneumothorax) Subcutaneous emphysema (open pneumothorax) Medical and nursing management of pneumothorax Vigilant assessment of cardiorespiratory status High-flow O2 Chest tube insertion Analgesia Ensure patient is positioned upright Provision of support and comfort measures Treatment of tension pneumothorax Emergent needle thoracentesis (decompression) 14 g needle inserted at 2nd intercostal space, midclavicular line (high failure rates at this position) Alternative site: 5th intercostal space, anterior axillary line (higher success rates due to thinner chest wall in this area) Generally speaking, needle decompression is reserved for those patients who are hemodynamically unstable and for whom definitive treatment is not readily available (i.e., pre-hospital, rural setting). Needle decompression involves significant failure rates (> in women) due to inadequate length of angiocath (must be > 4.5 cm long) and needle malposition (creation of new hemo/pneumothorax). Chest tube insertion involves significant risk as well; however, it is the preferred and definitive treatment for unstable patients with a tension pneumothorax (Mattu et al., 2010; Yarmus & Feller-Kopman, 2012). Cardiac tamponade occurs when accumulation of blood in the pericardial sac decreases ventricular filling. As little as 50 ml of blood in the pericardial sac can adversely affect stroke volume and cardiac output. An accumulation of approximately 120-150 ml of blood compresses the atria and ventricles, resulting in myocardial hypoxia and cardiogenic shock. Three classic signs/symptoms of Beck's triad Hypotension (decreased cardiac output) Muffled heart sounds (impaired pumping ability) JVD (elevated central venous pressure [CVP]) Signs/Symptoms of aortic injury Dyspnea Hemoptysis Chest/Sternal pain, pain between scapulae Discrepancy between right- and left-sided BPs Hypertension in upper extremities Hypotension in lower extremities Decreased femoral pulses Decreased sensation to lower extremities Widened mediastinum on CXR

Trauma Emergencies

Trauma is recognized as a national and global public health concern. Trauma is the leading cause of death in Canada among those less than 45 years of age; injuries can also have substantial social and economic consequences for the individual, family, and community. This module discusses trauma from the perspective of emergency care; assessment, management, and evaluation of the trauma patient are included. Specific conditions that will be discussed include facial, thoracic, and abdominal injuries. Traumatic brain injuries and spinal cord injuries are extensively covered in NURS 0456 Essentials and Management of Neurological Disorders, thus will not be addressed here.

Preload, Afterload, and Contractility

We cannot discuss arterial and central venous pressure monitoring without a short discussion of preload, afterload, and contractility. First, we must review the relationship of cardiac output (CO) to these parameters. CO reflects the efficiency of the cardiac pump (heart), and is the amount of blood ejected from the heart over one minute (cardiac index [CI] reflects CO standardized to body size). The two parameters responsible for CO are the SV, the amount of blood ejected from the heart with every heartbeat, and the minute heart rate (HR). The formula used for this is: HR x SV = CO The SV is determined by preload, afterload, and contractility. Preload Preload is the volume in the left ventricle at the end of diastole. The pressure created by this volume is known as left ventricular end-diastolic pressure (LVEDP). Preload is measured as pressure because we cannot measure volume with a transducer. Right-sided preload is measured via CVP. In order to understand the basis of preload, it is important to understand Starling's law, which, simply stated, says as diastolic volume increases, it stretches the cardiac muscles in their resting state. When contraction occurs, contractility is increased as a result of this increased stretch; however, if the muscle is overstretched, contractility will decrease. If the stretch is not optimized or not manipulated enough, contractility is decreased and the heart will begin to fail. In clinical situations such as right ventricular infarct, in which preload is lost due to damaged muscle and/or decreased vascular tone, if the stretch is not manipulated or optimized by fluid replacement, the right side of the heart will start to fail and subsequently the left side will also fail. As an analogy, think of an elastic band. The more you stretch it, the more it will recoil; however, if you stretch it too much, the band loses its elasticity (stretch) and will not function adequately. Preload is determined by the following: Circulating blood volume: when there is not enough blood, the preload decreases. Vascular tone: if the patient has massive vasodilation, such as that which occurs in septic shock, preload will be decreased. Conversely, fluid overload and conditions that cause vasoconstriction may increase preload. Compliance (the ability of muscle to stretch) or stiffness or thickness of the muscle wall also affects preload by increasing pressures even though the volume has not changed. Dysrhythmias. Atrial fibrillation reduces CO by approximately 30% as a result of loss of atrial kick, and tachycardias can decrease diastolic filling time, resulting in decreased preload. It is important to be aware that a critically ill patient may have a volume problem despite having an adequate CVP. If a patient is ventilated, PEEP will increase, but the patient may still be hypovolemic or have a volume distribution problem. Afterload Afterload is the pressure the ventricle has to exert to overcome the resistance to ejection created by arteries/arterioles (the force the ventricle must pump against), otherwise known as systemic vascular resistance (SVR). An increase in afterload increases the work of the heart and myocardial oxygen demand. Hypertension and aortic stenosis are two conditions that will increase afterload. Medications that cause arterial vasodilation and conditions such as septic shock and anaphylaxis will decrease afterload. Contractility The contractile force of the heart is also referred to as inotropy. It is dependent on preload and afterload and can be increased by the Starling mechanism. Influences on contractility include the sympathetic nervous system (SNS) and sympathomimetic drugs, such as dopamine, that increase contractility. Contractility is decreased by hypoxia, electrolyte imbalances, and drugs, such as beta blockers and calcium channel blockers.

Initial Assessment trauma

When caring for a trauma patient, time is critical. Thus, the "...approach to trauma patient care requires a process to identify and treat or stabilize life-threatening injuries in an efficient and timely manner (Emergency Nurses Association [ENA], 2020, p. 25). The systematic approach to trauma care involves components of the initial assessment, specifically the A -J mnemonic, which allows the nurse to "...rapidly assess for and intervene in life-threatening injuries and identify all injuries in a systematic manner" (ENA, 2020, p. 25). This approach also serves as the basis for the trauma nursing process (TNP). Although the TNP focuses on assessment and care of the trauma patient, the principles and approach can be applied to any patient in any clinical setting. Components of the initial assessment (i.e., A-J mnemonic) are outlined below, as per current guidelines (ENA, 2020). Primary Survey (Assessment) The primary survey begins as soon as the trauma patient arrives in the emergency department (ED), or other clinical setting (e.g., intensive care unit [ICU]. The purpose of the primary survey is to identify life-threatening injuries, and treat them accordingly, before moving on to the secondary survey. The primary survey consists of five steps (ABCDE), plus corresponding interventions or adjuncts (FG) as required, in the following order: A: Across-the-room assessment for uncontrolled hemorrhage; Airway and Alertness with simultaneous C-spine immobilization B: Breathing and ventilation C: Circulation and Control of hemorrhage D: Disability (neurological status) E: Exposure and Environmental control F: Full set of vital signs and Family presence G: Get monitoring devices and Give comfort (LMNOP) ***Reevaluation: assess need for portable x-rays, patient transfer*** Across-the-room observation involves rapid assessment of patient's overall physiological stability and any uncontrolled external hemorrhage as soon as the patient arrives in the room (ENA, 2020, p. 28). Providers must assess for the need to reprioritize (i.e., C-ABC), such as in uncontrolled external hemorrhage, before moving on in the primary survey. It should be noted that, while the mnemonic steps are presented in sequential linear order, in reality, providers work together to assess components (and intervene as needed) simultaneously. Airway, with simultaneous C-spine immobilization, is assessed for ineffective airway clearance and airway obstruction. 1. a. What may cause an airway to be ineffective or obstructed? b. Identify nursing interventions related to ensuring a patent and effective airway. 2. AVPU is an acronym used to rapidly assess and describe a patient's LOC. What does it stand for? Why might it be introduced so early in the primary survey? Breathing and ventilation are assessed for ineffective ventilatory patterns and impaired gas exchange. 3. a. Describe how the nurse should assess the breathing status of a trauma patient. b. List some nursing interventions that may be required to assist with breathing. Circulation is assessed to determine the presence of decreased cardiac output, impaired tissue perfusion, and fluid volume deficit (Control of hemorrhage). 4. a. List signs/symptoms of poor circulatory status. b. Identify immediate nursing interventions that can be implemented to treat ineffective circulatory status. Disability is determined by a neurologic assessment, specifically the patient's LOC and pupil size/reaction. The Glasgow Coma Scale (GCS) is the universal clinical standard for assessing a patient's LOC. Capillary blood glucose and ABG may be considered at this stage, as derangements related to these investigations may adversely affect LOC (e.g., hypoglycemia, hypoxemia). Exposure involves removing the patient's clothing to facilitate the identification and assessment of other injuries. Environmental control involves protecting the patient from hypothermia by applying warm blankets and administering warmed IV solutions, for example. Full set of vital signs must be obtained and monitored frequently in order to evaluate resuscitation efforts. Family presence must also be considered; however, a member of the trauma team should remain with the family member to offer support and act as a liaison. Get monitoring devices and Give comfort: L = Laboratory studies (e.g., ABGs, venous blood gases [VBGs], lactate, type and cross-match) M = Monitor cardiac rate/rhythm (e.g., dysrhythmias, pulseless electrical activity [PEA]) N = Nasogastric or orogastric tube O = Oxygenation (e.g., SpO2) and ventilation (capnography: end-tidal CO2 [ETCO2]) assessment P = Pain assessment/management (pharmacologic, nonpharmacologic) Suggested Answers Secondary Survey (Assessment) The secondary survey begins when the primary survey is completed, and potentially life-threatening problems have been identified, treated, and reevaluated. As the primary survey consisted of ABCDE (FG), the secondary survey continues the alphabet mnemonic with HIJ. H History / Head-to-toe assessment History can be obtained using the mnemonics MIST and SAMPLE. MIST M - MOI I - Injuries sustained S - Signs/Symptoms (on scene, on route, on arrival in ED/ICU) T - Treatment received prior to arrival at hospital and patient's response SAMPLE S - Symptoms A - Allergies, Tetanus status M - Medications (prescription, non-prescription) P - Past medical, surgical, social, environmental, and family history L - Last meal / Last menstrual period (LMP) / Last output (void, bowel movement) E - Events/Environmental factors related to illness or injury Head-to-toe assessment evaluates the overall general appearance of the patient. Head and face Inspect for wounds, ecchymosis, deformities, drainage from nose and ears, and pupils. LACE (lacerations, abrasions, avulsions, contusions, edema, or ecchymosis) when inspecting for any soft-tissue injuries Palpate for tenderness; note bony crepitus and deformities. Neck Inspect then palpate the anterior portion of the neck. Inspect for LACE, deformities, and distended neck veins. Palpate for tenderness, bony crepitus, deformity, subcutaneous emphysema, and tracheal position. Chest Inspect for breathing rate and depth, wounds, deformities to chest wall, LACE , use of accessory muscles, and paradoxical chest movement. Auscultate lung and heart sounds Palpate for tenderness, bony crepitus, subcutaneous emphysema, and deformity. Abdomen and flanks Inspect for distension, LACE, and scars Auscultate bowel sounds Palpate four quadrants for tenderness, rigidity, guarding, masses, and femoral pulses Pelvis and perineum Inspect for wounds, deformities, LACE, priapism, and blood at the urinary meatus or perineal area Palpate the pelvis and anal sphincter for tone Extremities Inspect for LACE, movement, wounds, and deformities Palpate for pulses, pallor, paresthesia, paralysis, and pain (the five Ps), and bony crepitus I - Inspect posterior surfaces. Maintain C-spine immobilization while the patient is log-rolled If spinal or pelvic trauma suspected, imaging is recommended prior to log-rolling due to increased risk of secondary injury(ies) Inspect posterior surfaces for wounds, deformities, and LACE Palpate posterior surfaces for tenderness and deformities Palpate anal sphincter for tone (digital rectal exam [DRE]) Sensitivity is questionable....alternative is to ask alert patient to squeeze buttocks, thereby assessing spinal cord function (ENA, 2020, p. 41) J - Just keep reevaluating VIPP Vital signs (F) Injuries identified in H and I (and interventions) Primary survey (ABCDE) Pain level (P, of G [LMNOP]) (ENA, 2020, pp. 25-42) Primary and Secondary Surveys Suggested answers a. A trauma patient's airway may be compromised by the following: Tongue obstruction due to decreased LOC Loose teeth Foreign objects Bleeding Vomitus or other secretions Edema b. Nursing interventions to ensure a patent airway Positioning the patient with head tilt/chin lift or jaw thrust (C-spine injury) Suctioning secretions Removing any foreign object(s) Inserting an oral or nasal airway Preparing for endotracheal intubation or emergency cricothyrotomy 2. AVPU stands for Alert, Verbal (responds to verbal stimuli), Pain (responds to painful stimuli), or Unresponsive (patient does not respond to any of the above). The AVPU mneumonic is introduced early in the primary survey because it provides valuable information in the selection of an appropriate airway. If the patient is Alert, he/she will likely be able to protect his/her own airway; however, all other responses are indicative of potential airway compromise. 3. a. Assessment of breathing status of trauma patient involves the following: Presence of spontaneous breathing, chest rise and fall Bilateral breath sounds Rate and depth of respirations Use of accessory or abdominal muscles Skin colour Tissue and bony chest wall integrity Position of trachea Presence of JVD b. Nursing interventions to assist with breathing Supplemental O2 Administration of medications (e.g., bronchodilators) Positive airway pressure ventilation (e.g., continuous, bi-level) BVM ventilation Three-sided chest wall dressing (for an open, sucking chest wound) Prepare for needle decompression/thoracentesis, chest tube insertion Prepare for endotracheal intubation, mechanical ventilation a. Signs/Symptoms of poor circulatory status Altered LOC Tachycardia; weak, thready pulses Hypotension Tachypnea Cool, pale, ashen skin Delayed capillary refill Nausea, vomiting Decreased urinary output Obvious bleeding, exsanguination b. Immediate nursing interventions to treat ineffective circulatory status High-flow O2 Direct pressure on bleeding wound (Control hemorrhage - primary survey) Elevation of affected extremity Two large-bore IVs with isotonic fluid bolus(es), blood products Administration of vasopressors (once volume restored)

decrease O2 consumption with MODS

antipyretics and sedative agents O2 demand can be decreased by --sedation, paralytics, antipyretics, external cooling, administering pain meds

shock review questions notes

cardiogenic shock - inability of the heart to pump blood to the rest of the body *distended JVD, pale and cool skin septic - profound inflammation response, coagulation cascade, increased cap permeability hypovolemic - typically caused by burns and hemmorhage *narrow pulse pressure, pale cool skin neurogenic - caused by a loss of sympathetic tone resulting in massive vasodilation *decreased HR, skin warm and pink anaphylatic - caused by a antigen-antibody response activating mast cells and basophils *increased HR SOFA: respiratory, coagulation, liver, cardio (MAP), CNS (LOC), renal (output) cardio effects of sepsis: vasodilation, maldistribution of perfusion, myocardial depression

Mixed Venous Oxygen Saturation (Svo2) / Central Venous Oxygen Saturation (Scvo2) NOTES

central venous oxygen saturation (Scvo2), which is the percentage of oxygen bound to hemoglobin (Hgb) returning to the right side of the heart from the body. This is indicative of the balance between oxygen supply and demand. Uses a special CVC to monitor. Svo2 = SaO2 - 30% The normal range for Scvo2 is 60-80%, with an absolute normal of 70%;however, the Scvo2 will always be a bit higher than Svo2 because the reading is taken before the blood enters the right side of the heart, where the cardiac sinus (vein) delivers venous blood into the right atrium. This blood, which is drained from the myocardium, is heavily desaturated, thus decreases the Svo2 slightly. Causes of high Scvo2 (i.e., 80-95%) are briefly outlined below: Anesthesia causes sedation and decreased muscle activity, thus lowering the metabolic demand for oxygen. Sepsis decreases the cells' ability to utilize oxygen. Even if supplemental oxygen is provided, the cells cannot extract it and the Scvo2 will be higher than normal. Hypothermia lowers metabolic demand, resulting in a higher Scvo2. Patients receiving more oxygen than required for their clinical condition. Causes of low Scvo2 (< 60%) include the following conditions: Hypoxemia Cardiogenic shock Severe anemia or blood loss with cardiovascular compromise Increased metabolic demand, which may occur due to prolonged shivering or seizures

manifestation of cardiogenic shock

decreased cardiac index to less than 2.2 L/min initially there will be a decline in cardiac output , increased pulmonary occlusion pressure, increased right atrial pressure, increased SVR

septic shock

includes hypotension dispite fluid resusitation along with perfusion abnormalities other things that occur: lactic acidosis, oliguria, alertation in mental status

cardiogenic shock

occurs in the prescence of *adequate* intravascular volume (main difference from hypovolemic) both cardiogenic and hypovolemic cause a decrease in stroke volume cardiogenic is caused by imparied contractility or valve dysfunction (not from a decrease in volume) Dobutamine is the mainstay of treatment for cardiogenic shock unless profound hypotension is present, in which case Dopamine is the preferred agent

hemodynamics review questions

tubing must be stiff and noncompliant no longer than 36 in it must have a minimum of 2-3 stopcocks The phlebostatic axis is located at the 4th intercostal space (ICS) and a midway point between the anterior and posterior chest wall. When the transducer is placed above the phlebostatic axis, pressures will be erroneously low. overdamped waveform: Check the integrity of the system for leaks. Ensure all connections are tight. Check for kinks in the line or catheter. Ensure a continuous pressurized solution is infusing to help prevent clot formation. Make sure transducer is clear of air. This is an underdamped waveform. It has more than 2-3 oscillations following the square wave.b. Nursing interventions include ensuring the tubing is stiff and non-compliant, the tubing is not too long, and a minimum amount of stopcocks are present.c. Underdamping may result in overestimating the systolic blood pressure and underestimating the diastolic pressure. Complications of central venous lines Air embolus Thrombosis formation Infection Pneumothorax Hemothorax Dysrhythmias Sudden hypotension may be the first indicator of an air embolus; other signs include confusion, lightheadedness, anxiety, and unresponsiveness. Roughly 10-20 ml of air must enter the venous system in order for the patient to become symptomatic. The air creates 'foam' in the right ventricle with each contraction, and subsequent drop in SV due to air rather than blood being ejected (loss of CO).If you suspect an air embolus, your immediate action is to turn the patient onto his/her left side in Trendelenburg position, which facilitates the air rising to the wall of the right ventricle and increases blood flow. Oxygen should also be administered immediately, unless contraindicated. Causes of low CVP Hemorrhage Vasodilation from any cause, including drugs such as nitroglycerine Distributive shockUse of diuretics Re-warming following cardiac surgery Causes of high CVP Fluid overload (the major cause of increased CVP) Conditions causing vasoconstriction or decreased myocardial contractility Mechanical ventilation Right ventricular failure The illustrations are of an ECG waveform and central venous pressure waveform .b. Events shown in the lower waveform a wave atrial contraction x descent atrial relaxation, downward movement of contracting right ventricle c wave closed tricuspid valve bulging into atrium during ventricular systole v wave atrial fillingy wave valve opens, beginning of ventricular filling c. There is no recognizable CVP pattern in atrial fibrillation due to atrial disorganization.

Medical and nursing management of hypovolemic shock

vasopressors to restore BP but tank must be topped up first Crystalloids - NS or LR High Na+ content - 25-30% remains intravascular Colloids - rely on oncotic pressure and may exacerbate volume loss if they leak out into the intravascular space Blood - to increase O2 carrying capacity