NURS MISC Study Guide: Shock/Burns/Emergency Summer 2019
1. Primary and Secondary Survey—assessments and interventions.
• Primary: ABCDE an
... [Show More] assessment of the pt triaged to the emergent or resuscitation category that focuses on stabilizing like threatening conditions.
• Secondary: an assessment of the pt triaged to the emergent or resuscitation category that commences after the primary survey is completed and life-threatening insults have been addressed. Includes obtaining v/s, completing head to toe assessment. Obtaining the pt.’s pertinent medical-surgical hx, including the history of the current event.
2. Priority assessments of the sexual assault victim
• The pt goes through several stages: the acute disorganized phase, a phase of denial (pt is unwilling to talk about the event), and phase of reorganization.
• The goals in management are to provide support, reduce the pt.’s emotional trauma, and gather evidence for possible legal proceedings.
3. Heat cramps, heat exhaustion, heat stroke. S/S?
• This is the inability to maintain cardiac output when faced with Moderately high body temps and in the presence of dehydration. The very old and very young are the ones affected the most.
• S/S: Heat Stroke Confusion, Delirium, bizarre behavior and coma. Temp above 40.6,
hot dry skin and no sweating (anhidrosis).
• Heat Exhaustion: High body temperature, HA, Anxiety, syncope, profuse diaphoresis, gooseflesh, orthostatic, cardinal sign is heat cramps- muscle spasms in the shoulders, abd and lower extremities.
• What type of treatment interventions will be done? For heat stroke: CAB’s are primary concern along with fluid resuscitation. The first thing to be done is to remove the pt.’s clothing. The core temp needs to be rapidly decreased to 39 or 102. This is facilitated by:
Cool sheets and towels or continuous sponging with cool water
• Ice applied to the neck, groin, chest, and axillae while spraying with tepid water
• Cooling blankets
• Immersion of the patient in a cold water bath is the optimal method for cooling
During the process a fan should blow on the pt as well. Throughout the cooling
process the pt v/s, ekg, LOC, s/s of mi, CVP. If pt has a sz due to rapid decline in temp, apply 02 and follow TX as needed, 100% 02.
• Main goal is bringing down the temp as quickly as possible!!! The long the
hyperthermic episode the higher the mortality rate.
• What is the priority of care? Bringing down the temp
4. You will be given several pts and will have to determine who needs to be seen first…. you must go by your ABCD’s and most critical/emergent!!!!!
5. In trauma pts, what s/s relate to the most life threatening conditions?
• Systolic B/P <90 mmHg
• MAP <65mmHg
• HR > 150bpm
• Rapid shallow breathing, crackles, Pa02< 80 mmHg, PC02> 45mmHG
• Skin Mottled or Petechiae
• Urine Output < 0.5ml/kg/hr.
• Mentation Lethargy or declining mental status
• Acid base: Metabolic Acidosis
6. Fluid resuscitation
• Two large-gauge IV lines are inserted (If an IV catheter cannot be quickly inserted, an intraosseous catheter may be used)
• Crystalloid solutions such as lactated Ringer’s solution or 0.9% sodium chloride solution are commonly used to treat hypovolemic shock
• 3:1 rule: If hypervolemia is primarily due to blood loss, the American College of Surgeons (2012) recommends administration of 3 mL of crystalloid solution for each milliliter of estimated blood loss. This is referred to as the 3:1 rule.
• Patients requiring massive transfusion respond better when blood products are given in a 1:1:1: ratio, meaning units of plasma, platelets, and packed red blood cells. This covers fluid replacement, 02 carrying and coagulopathy.
• 1 time bolus is 20ml/kg
7. Why is mechanism of injury significant? It reveals an injury pathway
Although blunt chest trauma is more common than penetrating trauma, it is often difficult to identify the extent of the damage because the symptoms may be generalized and vague. In addition, patients may not seek immediate medical attention, which may complicate the problem.
8. Blunt versus penetrating trauma
• Blunt trauma: blunt thoracic injuries are directly responsible for 20% to 25% of all trauma deaths.
• Most common causes of blunt chest trauma are motor vehicle crashes (trauma from steering wheel, seat belt), falls, and bicycle crashes (trauma from handlebars). Types of blunt chest trauma include chest wall fractures,
dislocations, and barotraumas (including diaphragmatic injuries); injuries of the pleura, lungs, and aero digestive tracts; and blunt injuries of the heart, great arteries, veins, and lymphatic’s
o Hypoxemia from disruption of the airway; injury to the lung parenchyma, rib cage, and respiratory musculature; massive hemorrhage; collapsed lung; and pneumothorax
o Hypovolemic from massive fluid loss from the great vessels, cardiac rupture, or hemothorax
o Cardiac failure from cardiac tamponade, cardiac contusion, or increased intrathoracic pressure
o These pathologic states frequently result in impaired V./Q. leading to acute kidney injury, hypovolemic shock, and death.
• Penetrating trauma, any organ or structure within the chest is potentially
susceptible to traumatic penetration. These organs include the chest wall, lung and pleura, tracheobronchial system, esophagus, diaphragm, and major thoracic blood vessels, as well as heart and other mediastinal structures. The clinical consequence of penetrating trauma to the chest depends on the mechanism of injury, location, associated injuries, and underlying illnesses. Common injuries include pneumothorax and cardiac tamponade.
• Penetrating abd wounds have a high incidence of injury to hollow organs, especially the small bowel.
9. Be able to triage a pt as emergent, urgent, or non-urgent or Level I, II, or III.
• Immediate
intervention. Individuals in this group can progress rapidly to expectant if treatment is delayed. Prioirty: 1 Color: red. Things that would fall here: Sucking chest wound, airway obstruction secondary to mechanical cause, shock, hemothorax, tension pneumothorax, asphyxia, unstable chest and abdominal wounds, incomplete amputations, open fractures of long bones, and 2nd/3rd-degree burns of 15–40% total body surface area.
• Delayed: Injuries are significant and require medical care but can wait hours without threat to life or limb. Individuals in this group receive treatment only after immediate casualties are treated Priority: 2 Color: Yellow. Things that would fall here: Stable abdominal wounds without evidence of significant hemorrhage; soft tissue injuries; maxillofacial wounds without airway compromise; vascular injuries with adequate collateral circulation;
genitourinary tract disruption; fractures requiring open reduction, debridement, and external fixation; most eye and central nervous system injuries.
• Minimal: Injuries are minor, and treatment can be delayed hours to days. Individuals in this group should be moved away from the main triage area. Priority: 3 Color: Green. Thing that would fall here: Upper extremity fractures, minor burns, sprains, small lacerations without significant bleeding, behavioral disorders or psychological disturbances
• Expectant: Injuries are extensive, and chances of survival are unlikely even with definitive care. Persons in this group should be separated from other casualties, but not abandoned. Comfort measures should be provided when possible. Priority: 4 Color: Black. Things that would fall here: Patients who are unresponsive with penetrating head wounds, high spinal cord injuries, wounds involving multiple anatomic sites and organs, 2nd/3rd-degree
burns in excess of 60% of body surface area, seizures or vomiting within 24 hours after radiation exposure, profound shock with multiple injuries, agonal respirations; no pulse, no blood pressure, pupils fixed and dilated.
10. How should family presence during a resus or trauma be handled?
• The family is kept informed about where the patient is, how he or she is doing, and the care that is being given. Encouraging family members to stay with the patient.
• Family presence during resuscitation is permitted to assist the family to cope through this difficult time. Many family members respond very well to this approach.
11. Hypothermia—
• How are these types of injuries handled and treated?
• Nursing interventions?
• Priority intervention should be addressing the pt.’s hypothermia and attempting to correct it.
• When rewarming the pt be sure to maintain ekg monitoring
• Continuous assessment of core temp.
12. Alcohol intoxication and drug overdose—nursing interventions and priorities?
• ETOH: In the ED, the patient who is intoxicated with alcohol or who presents with alcohol poisoning is assessed for head injury, hypoglycemia (which mimics intoxication), and other health problems.
• Nursing interventions?
• Treatment goals for a patient with a drug overdose are to support the respiratory and cardiovascular functions, to enhance clearance of the agent, and to provide for safety of the patient and staff. People who abuse
IV/injection drugs are at increased risk for HIV infection, acquired immune deficiency syndrome, hepatitis B and C, and tetanus.
• Supportive TX for drug overdose this depends on the drug used.
• Treatment involves detoxification of the acute poisoning, recovery, and
rehabilitation.
• A blood specimen is obtained for analysis of the blood alcohol level.
• Maintenance of a patent airway and observation for symptoms of CNS depression are essential.
13. S/S related to food poisoning?
• Nursing priorities?
• The key to treatment is determining the source and type of food poisoning.
• V/S: RR. PR, B/P, LOC, Muscular activity is monitored
• Antiemetic medication
• Clear liquids are usually prescribed for 12 to 24 hours, and the diet is gradually progressed to a low-residue, bland diet.
14. Can shock occur in a burn pt?
• Yes because when a burn injury occurs, there is an immediate decrease in cardiac output that precedes the loss of plasma volume. Why or why not?
• Hypovolemia is the immediate consequence of ensuing plasma volume loss and results in decreased perfusion and oxygen delivery. As fluid loss
continues due to capillary leakage, and vascular volume decreases, cardiac output continues to decrease and the blood pressure drops. This is the onset of burn shock. Burn shock is initially a type of hypovolemic shock.
• The greatest volume of fluid leak occurs in the first 24 to 36 hours after the burn, peaking by 6 to 8 hours. As the capillaries begin to regain their integrity, burn shock resolves and fluid returns to the vascular compartment.
Intrinsic diuresis will begin and continue for several days to 2 weeks in the previously healthy adult.
15. Why do electrical burn pts often experience acute renal failure?
• Myoglobinuria, common with muscle damage, may cause kidney failure if not treated. IV fluid administration titrated to a higher target of urine output per hour
than usual may be indicated until the urine is no longer red. It is common practice to add 50 mEq of sodium bicarbonate per liter of IV fluid in an effort to assist in alkalinizing the urine. Serum myoglobin and urine myoglobin levels may be monitored as indicators of the need for continued resuscitation.
16. Know the different burn depths based on s/s.
• 1st degree: Sunburn, Low-intensity flash, superficial scald. Layer: Epidermis Clinical manesfesataion: Tingling, Hyperesthesia (hypersensitivity), Pain that is soothed by cooling, Peeling, Itching.
• 2nd Degree (Partial thickness): Scalds Flash flame Contact Layer: Epidermis, portion
of dermis. Clinical manifestation: Pain Hyperesthesia Sensitive to air currents.
• 3rd degree (Full Thickness): Flame Prolonged exposure to hot liquids Electric current Chemical Contact Layer: Epidermis, dermis, and sometimes subcutaneous tissue; may involve connective tissue, and muscle. Clinical manifestation: Insensate Shock Myoglobinuria (red pigment in urine) and possible hemolysis (blood cell destruction) Possible contact points (entrance or exit wounds in electrical burns).
• 4th Degree (Full Thickness That Includes Fat, Fascia, Muscle, and/or Bone): Prolonged exposure or high voltage electrical injury. Layer: Deep tissue, muscle and bone. Clinical manifestation: Shock Myoglobinuria (red pigment in urine) and possible hemolysis (blood cell destruction)
• Nursing interventions for burn pts.
Emergent/resuscita tive
From onset of injury to completion of fluid resuscitation
• Primary survey: A, B, C, D, E
• Prevention of shock
• Prevention of respiratory
distress
• Detection and treatment of concomitant injuries
• Wound assessment and initial care
Expected blood work results in the emergent/resuscitative phase of burn injury include:
• Hyperkalemia, hyponatremia, elevated hematocrit and metabolic acidosis.
17. Burns--rule of 9’s.
• This system is based on anatomic regions, each representing approximately 9% of the TBSA, allowing clinicians to quickly obtain an estimate of burn size. If a portion of an anatomic area is burned, the TBSA is calculated accordingly
—for example, if approximately half of one arm were burned, the TBSA burned would be 4.5%.
•
18. Pain management in the burn pt?
• Burn injury is considered one of the most painful types of trauma that a patient can experience. The nature of the injury may expose nerve endings; and the patient may require multiple debridement, surgeries, and treatments. Moving,
changing position, and receiving occupational and physical therapy cause additional discomfort. Adequate pain management must address background, procedural, and breakthrough pain.
• Patient-controlled analgesia gives control to the patient and achieves this goal.
• Break though pain Short-acting agents are used for breakthrough pain
• Pharmacologic treatment for the management of burn pain includes the use of opioids, nonsteroidal anti-inflammatory drugs, anxiolytics, and anesthetic
agents.
• No pharmacologic therapies include relaxation techniques, distraction, guided imagery, hypnosis, therapeutic touch, humor, music therapy, and more recently virtual reality techniques.
19. Know the different stages of shock and what signs and symptoms you would expect a pt to exhibit in the different stages.
• Compensatory Stage: BP remains within normal limits. Vasoconstriction, increased heart rate, and increased contractility of the heart contribute to maintaining adequate cardiac output. This results from stimulation of the sympathetic nervous system and subsequent release of catecholamines. Skin may be cool and pale, bowel sounds are hypoactive, and urine output decreases in response to the release of aldosterone and ADH. V/s B/P- Normal, HR >100 bpm, Skin is Cold and clammy, Urine output is Decreased, Mentation- Confusion and/or agitation. RR- >20/min and PC02 <32mmHg, Acid base- Resp. alkalosis.
• Progressive Stage: second stage of shock, the mechanisms that regulate BP can no longer compensate, and the MAP falls below normal limits. Patients are clinically hypotensive; this is defined as a systolic BP of less than 90 mm Hg or a decrease in systolic BP of 40 mm Hg from baseline. The patient shows signs of declining mental status. V/S: Systolic B/P <90 mmHg, MAP <65 mmHg (Fluid resuscitation is required to maintain B/P). HR->150bpm, Resp- Rapid, shallow respirations; crackles PaO2 <80 mm Hg PaCO2 >45 mm Hg. Skin: Mottled and petechaie. Urine 0.5ml/kg/hr. mental status- lethargic. Acid-Base: Metabolic acidosis.
• Irreversible Stage: Despite TX, BP remains low. Renal and liver dysfunction occurs, compounded by the release of biochemical mediators create acute metabolic acidosis. B/P: requires mechanical support or pharmacologic support. HR- Erratic. Resp: Requires intubation and mechanical ventilation and oxygenation. Skin- Jaundice. Mentation- Unconscious. Acid/Base: profound cyanosis.
20. Be sure to include the different types of shock. What is happening with the compensatory mechanisms in the different stages of shock?
• Hypovolemic: The fluid is attempting to shift from the intravascular space to the interstitial space to try in compensate for the fluid loss. This in turn Causes a drop in cardiac output, leading to shunting of the blood and lack of circulating blood. Which eventually causes a lack in tissue perfusion.
• Cardiogenic: occurs when the heart’s ability to contract and to pump blood is impaired and the supply of oxygen is inadequate for the heart and the tissues. S/S can be angina and dysrhythmias. Stroke volume and heart rate decrease or become erratic, BP falls and tissue perfusion is reduced. Blood supply for tissues and organs and for the heart muscle itself is inadequate, resulting in impaired tissue perfusion. Because impaired tissue perfusion weakens the heart and impairs its ability to pump, the ventricle does not fully eject its volume of blood during systole. As a result, fluid accumulates in the lungs. This sequence of events can occur rapidly or over a period of days
• Obstructive: Cardiogenic, PE, Cardiac tamonade, pneumothorax, Obstruction of the great vessels of some sort. Vessel is obstructive
• Distributive: The vessel widens and blood pools. Examples: Neurogenic, Anaphylactic and septic.
• Neurogenic: vasodilation occurs as a result of a loss of balance between parasympathetic and sympathetic stimulation. Sympathetic stimulation causes vascular smooth muscle to constrict, and parasympathetic stimulation causes vascular smooth muscle to relax or dilate. Neurogenic shock can be caused by spinal cord injury, spinal anesthesia, or other nervous system damage. It is said to be Prolonged (spinal cord injury) or Short (syncope/ fainting). Defining charteristic is Bradycardia unlike the other forms of shock.
• Anaphylactic: is caused by a severe allergic reaction when patients who have already produced antibodies to a foreign substance (antigen) develop a systemic antigen–antibody reaction; specifically, an immunoglobulin E (IgE)-mediated response. This antigen– antibody reaction provokes mast cells to release potent vasoactive substances, such as histamine or bradykinin, and activates inflammatory cytokines, causing widespread vasodilation and capillary permeability. The most common triggers are foods (especially peanuts), medications, and insects. There are 3 defining things: Acute onset of symptoms, Presence of two or more symptoms that include respiratory compromise, reduced BP, GI distress, and skin or mucosal tissue irritation, Cardiovascular compromise from minutes to hours after exposure to the antigen.
• Septic: the most common type of distributive shock is caused by widespread infection or sepsis. Finding and aggressively treating the source of infection and quickly restoring tissue perfusion are important interventions that may positively influence the clinical outcome. Gram-negative bacteria traditionally have been the most commonly implicated microorganisms in sepsis
21. How do you treat the different types of shock?
• Hypovolemic: Restore fluid Volume and stopping the bleeding. 3:1 vlm replacement
• Cardiogenic: correcting the underlying cause. Returning O2 supply back to the myocardium and improve cardiac function by increasing cardiac contractility, decreasing ventricular afterload, or both. Dopamine is used to restore complete HF. MS04 can be given for pain as it also dilates the blood vessels. Remember to watch out for dysrhythmias.
• Neurogenic: Treatment of neurogenic shock involves restoring sympathetic tone. Elevate and maintain the head of the bed at least 30 degrees to prevent neurogenic shock. Using interventions are directed toward supporting cardiovascular and neurologic function until the usually transient episode of neurogenic shock resolves. Patients with neurogenic shock have a higher risk for venous thromboembolism (VTE) formation.
• Anaphylactic: Treatment of anaphylactic shock requires removing the causative antigen. Intramuscular epinephrine is given for its vasoconstrictive action. Diphenhydramine (Benadryl) is given intravenously to reverse the effects of histamine, thereby reducing capillary permeability. Nebulized medications, such as albuterol (Proventil), may be given to reverse histamine-induced bronchospasm. If cardiac arrest and respiratory arrest are imminent or have occurred, cardiopulmonary resuscitation (CPR) is performed. Endotracheal intubation may be necessary to establish an airway. IV lines are inserted to provide access for administering fluids and medications.
• Septic: Current treatment of sepsis and septic shock involves rapid identification and elimination of the cause of infection. Current goals are to identify and treat patients in early sepsis within 3 hours to optimize patient outcome. Initial fluid challenge, which includes an IV infusion of at least 30 mL/kg of crystalloids over 30 minutes. If infecting organism is unknown, broad-spectrum antibiotic agents are started until culture and sensitivity reports are received. If fluid therapy alone does not effectively improve tissue perfusion, vasopressor agents, specifically norepinephrine or dopamine, may be initiated to achieve a MAP of 65 mm Hg or higher. Inotropic agents may also be given to provide pharmacologic support to the myocardium. Packed red blood cells may be ordered to support oxygen delivery and transport to the tissues. Neuromuscular blockade agents and sedation agents may be required to reduce metabolic demands and provide comfort to the patient. Deep vein thrombosis (DVT) prophylaxis with low- dose unfractionated heparin or low–molecular-weight heparin, in combination with mechanical prophylaxis (e.g., sequential compression devices) should be initiated, as well as medications for stress ulcer prophylaxis (e.g., H2 blocking agents, proton pump inhibitors).
22. Be able to prioritize treatment. Sepsis, septic shock—what is the difference?
• Sepsis is “life-threatening organ dysfunction caused by a dysregulated host response to infection
• Septic shock is “a subset of sepsis in which underlying circulatory and cellular metabolism abnormalities are profound enough to substantially increase mortality
Treatment: Correction of underlying cause,
Surviving Sepsis Campaign Bundle
Complete within 3 hours of patient presentation/symptoms
• Obtain serum lactate level
• Obtain blood culture prior to administration of antibiotics
• Administer prescribed broad-spectrum antibiotics
• Initiate aggressive fluid resuscitation in patients with hypotension or elevated serum lactate (>4 mmol/L):
• Minimum initial fluid bolus of 30 mL/kg using crystalloid solutions
Complete as soon as possible or within the first 6 hours of patient presentation/symptoms
• Begin vasopressor agents if hypotension is not improved (MAP < 65 mm Hg) after initial fluid resuscitation
• If hypotension persists after initial fluid administration (MAP <65 mm Hg) or initial lactate was ≥4 mmol/L, reassess intravascular volume status and tissue perfusion using two of the following assessment parameters:
• Measure CVP (goal 8–12 mm Hg)
• Measure Scv¯O2 (goal > 70%)
• Bedside cardiovascular ultrasound
• Dynamic assessment of fluid responsiveness with passive leg raise or fluid challenge
Additional interventions and targets for therapy in the early management of sepsis
• Support blood pressure to achieve a urine output >0.5 mL/kg/h
• Administer vasopressor agents if fluid resuscitation does not restore an effective BP and cardiac output:
• Norepinephrine centrally given is the initial vasopressor of choice.
• Epinephrine, phenylephrine, or vasopressin should not be given as the initial vasopressor in septic shock.
• Obtain blood, sputum, urine, and wound cultures and administer broad-spectrum antibiotics:
• Cultures should be obtained prior to antibiotic administration.
• Antibiotic administration should occur within 3 hours of admission to the emergency department or within 1 hour of inpatient admission.
• Support the respiratory system with supplemental oxygen and mechanical ventilation.
• Transfuse with packed red blood cells when hemoglobin is <7 g/dL to achieve target hemoglobin of 7–9 g/dL in adults.
• Provide adequate IV sedation and analgesia; avoid the use of neuromuscular blockade agents when possible.
• Control serum glucose <180 mg/dL with IV insulin therapy.
• Implement interventions and medications to prevent deep vein thrombosis and stress ulcer prophylaxis.
• Discuss advance care planning with patients and families
23. Lactic acid level. The lactic acid level increases when the organs are not getting enough 02. This is considered an early warning sign.
• What is normal? 0.5-1 mmol/l Pt.’s w/ critical illness can be considered to be wnl until 2mmol/l.
• What do abnormal values indicate? 2-4 mmol/l. This means that a lactic acid is higher due to not enough circulating blood or 02. Secondary to a lower circulation vlm of blood and 02. This is very true since the very pathophysiology is cells lacking an adequate blood supply and is being deprived of 02 and nutrients.
24. IVF in shock—nursing interventions and priorities?
• Initial fluid challenge, which includes an IV infusion of at least 30 mL/kg of crystalloids over 30 minutes, may be required to aggressively treat sepsis- induced tissue hypo perfusion. In addition to monitoring BP, CVP, fluid
responsiveness with passive leg raise, urine output, and serum lactate levels are monitored to assess effectiveness of fluid resuscitation.
•
25. How would you know a pt is adequately perfused?
• Cardiac output and MAP
• Skin s/s like mottling and petechaie
MODS? Multiple Organ Dysfunction Syndrome This is a big problem and End Of Life care is most likely the next step. Presence of altered function of two or more organs in an acutely ill patient such that interventions are necessary to support continued organ function. How would you know a pt is experiencing MODS?
• Drop in systolic blood pressure of 40 mmHg from baselines or <90 mmHg
• MAP <65 mmHg
• Serum Lactate > 4mmol/L
26. Don’t forget about studying your drug list! This is also a crucial step! ACTIVELY STUDY!!!! [Show Less]