NOTES Mod #15 Trauma/Shock cmj
Module #15: Nursing Care of the Individual Requiring Critical Care: Trauma,
Shock, Emergenc...
2. Trauma: Sudden accidents or purposeful acts leading to injury, disability or
death
a. Impact: initial physical injuries...
c. Types of trauma
1) Blunt: no communication between damaged tissue and outside
environment; injuries internal...can be m...
Pre-hospital Care
a. Injury identification
1) Require rapid comprehensive trauma assessment (use different
systems) *Glasc...
2) B-breathing-? pneumothorax and tension pneumothorax (mediastinal
shift to unaffected side) and require chest tube; may ...
4) Physical Examination of Trauma requires:
a) Inspect, palpate each body area > identify obvious evidence
of injury (DCAP...
(Catheter placed in lower abdomen and aspiration for free blood;
infuse warm isotonic solution rapidly and drain by gravit...
Crystalloids (first line treatment) inexpensive; **initial
treatment-usually 1-2 L bolus of crystalloids (NS or RL); rapid...
3) Maintain chain of custody, i.e. preserve, label, document, and dispose
evidence (Important!)
3. Common Nursing Diagnose...
* Remember MAP of 60 or greater needed to maintain tissue
perfusion and oxygenation!
Regardless of cause- reaction and sym...
h) Fluid shifts into interstitial space; proteins shift into interstitial
space; fluid follows! * As cells die due to hypo...
acidosis; toxicity and bleeding (Liver- impaired circulation and may be
source of toxic materials; anoxic liver does not d...
b. Cardiogenic (See p. 155, Box 6-3 Assessment Findings in Clients in
Cardiogenic Shock) (review from heart failure)
1) Pu...
46-year-old man presented with nonnecrotizing cellulitis and
streptococcal toxic shock syndrome. The leg was incised to ex...
2) Neurogenic Shock See text. 156, Box 6-5 Assessment Findings in
clients in Neurogenic shock
a) Dec. sympathetic control ...
3) Anaphylactic Shock
(Click here for more)
See p. 157, Box 6-6 assessment Findings in Clients in Anaphylactic Shock
a) Re...
The most common etiologies of shock in children are
hypovolemia and sepsis.
The major type of shock in pregnancy is hemorr...
d. Dec. in B/P by 20 and Inc. HR by 20 = shock
e. Oliguria
f. Tachycardia
g. Decreased level of Consciousness
h. Rales and...
b. Early diet interventions dec. the risk of MODS
c. If cardiogenic- low Na and fluid restriction
d. High potassium if BUN...
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  1. 1. NOTES Mod #15 Trauma/Shock cmj Module #15: Nursing Care of the Individual Requiring Critical Care: Trauma, Shock, Emergency and Critical Care Nursing Trauma/Triage (click here-two separate sites) A. Etiology/Pathophysiology etc 1. Definition: *Regarding Emergency Care: there may appear to be “chaos” in the ED, however there is an inherent order in the timing and choice of interventions performed throughout (and prior to…pre-hospital) a client’s stay in the ED….organizational flow of events involves triage (prioritization), in- depth nursing assessment of the client, diagnostic testing, formulation of diagnoses, outcome management, evaluation, disposition, and documentation. RNSG 2432  87
  2. 2. 2. Trauma: Sudden accidents or purposeful acts leading to injury, disability or death a. Impact: initial physical injuries and long term effects; rehabilitation and psychosocial effects on clients and family members b. Components of Traumas 1) Host: person or group at risk of injury 2) Mechanism: source of energy that causes trauma *Most common: mechanical energy from motor vehicles in accidents 3) Intention: deliberate or unintentional 4) Environment: location and under what circumstances 88  RNSG 2432
  3. 3. c. Types of trauma 1) Blunt: no communication between damaged tissue and outside environment; injuries internal...can be minor to lethal 2) Penetrating: actual tissue damage to body structures, obvious from outside; result of foreign objects set in motion; affect internal organs; ex gun shot wounds, stab wounds common 3) Often combination of blunt and penetrating 4) Pathophysiology/manifestations determined by location and extent of injury B. Common Manifestation/Complications * Determined by location/extent of injury; psychosocial impact also What potential “problems” do these photos suggest? C. Therapeutic Interventions/Collaborative Care 1. Goals of Collaborative Care: stabilization and appropriate intervention RNSG 2432  89
  4. 4. Pre-hospital Care a. Injury identification 1) Require rapid comprehensive trauma assessment (use different systems) *Glasco Coma scale is one aspect: See text p. 140 Table 6-2 Champion Revised Trauma Scoring Scale * modifications of this used in ER…estimates chance of survival...higher the score, the better the chance. (*know how to use this) 2) Determines need for trauma center and rapid transport 3) *Airway, Breathing, Circulation 4) Level of consciousness 5) Spinal cord injuries with deficit 6) Any obvious injuries (penetrating injuries to abdomen, chest, pelvis, neck head) 7) Evaluate crush injuries 8) Major burns b. Critical interventions 1) Life support 2) Immobilize cervical spine 3) Airway management (intubation); breathing 4) Treat hemorrhage and shock 5) Apply direct pressure over wounds c. Rapid Transport ASAP to regional trauma center! 2. Hospital Care: Emergency Department Care a. Support above critical interventions 1) In ER > triaged as to severity of problem 2) Triage categories include: Emergent (client must be treated immediately; otherwise life/limb /vision threaten); Urgent (client requires treatment, but life/limb/vision not threatened if care cannot be provided within 1-2 hours); Non-urgent (client requires evaluation and possible treatment, but time is not critical factor) b. Assessment to determine of injuries/plan of treatment 1) A- airway obstruction- blood, teeth tongue or vomiting (may required immediate intubation) 90  RNSG 2432
  5. 5. 2) B-breathing-? pneumothorax and tension pneumothorax (mediastinal shift to unaffected side) and require chest tube; may have cardiac contusion with cardiac tamponade; require open thoracotomy What is a pneumothorax, hemothorax?? 3) C- circulation-? signs of hemorrhage (external and internal) and hypovolemic shock Abd. Trauma-bleeding into abd. Cavity Pelvic fracture-bleed into retroperitoneal space; major blood loss! RNSG 2432  91 Blunt abdominal trauma; distended Why is abd distended?
  6. 6. 4) Physical Examination of Trauma requires: a) Inspect, palpate each body area > identify obvious evidence of injury (DCAP-BTLS) such as below: (mnemonic helps you remember!) Deformities Contusions (deep bruising) Abrasions (scrapes) Punctures or penetrations Burns Tenderness to palpation Lacerations (cuts) Swelling b) Primary Survey >determine immediate needs (several evaluative tools can be used); includes evaluation of LOC (A-alert, oriented X3; V-verbal, responds to verbal stimuli; P-pain, responds to painful stimuli; U- unresponsive) where does the client fall within this category? c) Secondary Assessment- Head to toe to determine extent of injuries and includes: (1) Integumentary- contusions, abrasions, punctures, lacerations (Consider risk for infection) (2) Abdominal-high risk for hemorrhage and peritonitis-(Bowel ischemia and infarction; Rupture of large bowel-peritonitis) (3) Musculoskeletal *High priority if threatens life or limb; dislocated hip/joint; pulseless extremity; significant blood loss from pelvic fracture (Note can look “bad”…priority is “ABC’s” (4) Neurological- head and spinal cord injuries **Must immobilize spinal cord… (5) Psychological- sudden death or serious injury c. Diagnostic Tests common to ER setting 1) Blood type and crossmatch: ? client’s blood type; ready donor blood for transfusion (Review blood administration; universal blood donor, etc, safety; autotransfusion) Hypovolemic-due to hemorrhage> adm blood, blood products> keep HCT 30-35% and HGB 12.5-14.5 g/100 ml. What blood products usually given? (p. 159) what crystalloid solution and why? (p. 159…understand rationale) See below also. 2) Blood Alcohol level: alters level of consciousness and pain response (20-50% of those injured are intoxicated!) 3) Urine Drug screen: alters level of consciousness and pain response 4) Pregnancy test for women of child-bearing age: treatment concerns 5) Diagnostic Peritoneal Lavage (click here for more): test presence of free blood (or bile, or food, feces…) in peritoneal cavity; determines if hemorrhaging, injury internally and need for exploratory laparotomy 92  RNSG 2432
  7. 7. (Catheter placed in lower abdomen and aspiration for free blood; infuse warm isotonic solution rapidly and drain by gravity; check for presence of blood) (if blood, bile, feces, send to OR) 6) Computerized Tomography (CT Scan) special x-ray of body area in layers with computerized views; brain, chest, abdomen and MRI; critical to early identification of injury. d. Medications/Treatment/Surgical Intervention 1) Most likely initiated at scene; oxygenation! Why important? 2) Intravenous access (2 large bore large bore IVs; NS (give with blood); or Ringers Lactate) blood components (See text p. 143 & 159; Table 6-3 Types of Blood components Used in Transfusion Therapy RNSG 2432  93
  8. 8. Crystalloids (first line treatment) inexpensive; **initial treatment-usually 1-2 L bolus of crystalloids (NS or RL); rapid based upon client’s needs; (more than 4-5 L causes internal and external edema, does not provide RBC’s) (FYI…recall colloids- albumin for volume expansion) What are nursing implications re use of plasma expanders such as albumin & dextran? (p. 157) *Hypovolemic shock with massive bleeding; rule –“3-1” - replace blood loss with crystalloids; for every 1 ml of blood loss, 3 ml crystalloids given; once blood loss = 1500cc; blood transfusion with packed red blood given along with other blood products as FFP and platelets to restore clotting factors. Transfusion recommended when hemoglobulin = 7-8 g/dl and hematocrit - 21% to 24%.) 3) Cardiovascular support may require inotropic agents (vasopressors) *If volume replacement does not adequately support CO and MAP to ensure and maintain tissue perfusion; may need vasopressors as dopamine (Inotropin) and norepinephrine (Levophed) to support BP and increase cardiac contractility. How does dopamine work? (p. 142, 880) 4) Hypovolemic shock-volume loading (blood & fluid) > major intervention; drug therapy- last choice! 5) Pain control; opiates, however, cautiously as will altered LOC 6) Tetanus immunization, if indicated & potential for gas gangrene later and tetanus! What organism causes this? 7) Blood Transfusions (Blood type O-Universal donor) (Use NS only when adm blood-review “transfusions”) 8) Emergency surgery (determined by injury) e. Organ Donation *not tested with this unit…read, cover in Mod 13 1) What are brain death criteria? (p. 145-box 6-1) & below 2) Uniform Anatomical Gift Act (1968, 1987) 3) Care given to maintain circulation and perfuse organs if organs to be donated *Note; hepatitis, even HIV not absolute contraindications for organ donation any longer; nurses and physicians MUST call the Donor Referral Line (1-800-275-1744) in event of potential donor; nurses and physicians are NOT to communicate information about donor request etc (contrary to text) 4) Supportive care to family member; assist with grief 5) Brain Death Criteria: a) Irreversible condition b) Apnea with PACO2 >60 c) No response to deep stimuli d) No spontaneous movement e) No gag or corneal reflex f) No oculocephalic or oculovestibular reflex g) Absence of toxic or metabolic disorders. f. Forensic Considerations 1) Trauma due to illegal activity 2) Determine if client under influence of alcohol, illegal drugs 94  RNSG 2432
  9. 9. 3) Maintain chain of custody, i.e. preserve, label, document, and dispose evidence (Important!) 3. Common Nursing Diagnoses for Trauma Clients (p. 146-148) a. Ineffective Airway Clearance (assess airway, check O2 sats, LOC) b. Risk for Infection c. Impaired Physical Mobility d. Spiritual Distress: Client and Family e. Risk for Post-Trauma Syndrome 1) Intense emotional response to disastrous event 2) Impaired coping mechanisms 3) Nurses assist client and family to express feelings 4) Referrals for counseling, support groups f. Teaching Need: Prevention of Trauma: educate the public about trauma prevention and safety e.g. seatbelts, bicycle helmets *Read carefully-recognize priority nsg problem/dx and intervention Shock (Click here-article- hypovolemic shock) A. Etiology/Pathophysiology etc 1. Definition: Clinical syndrome, systemic imbalance between oxygen supply and demand; Inadequate blood flow to body organs and tissue >life- threatening cellular dysfunction resulting in: *inadequate tissue perfusion and *decreased O2 at cellular level 2. Pathophysiology: Shock triggered by a stimulus (**drop in the MAP) > leads to alteration in hemodynamics within body a. Body responds by maintaining perfusion to vital organs, heart and brain b. Results in inadequate tissue and cellular perfusion; if not reversed, body develops acidosis; if untreated, progresses to organ hypoxia, ischemia and death c. Alteration in hemodynamics results in drop in arterial blood pressure by one of these mechanisms 1) Decrease in cardiac output (ability of heart to supply adequate circulation) 2) Decrease in circulating blood volume 3) Increase in size of vascular bed d. Terms: pathophysiology of shock (review only): Stroke Volume (SV): amount of blood pumped into aorta by contraction of left ventricle; Cardiac Output (CO): amount of blood pumped into aorta by contraction of left ventricle in one minute; Systemic Vascular Resistance (SVR): amount of resistance provided by vascular bed against flow of blood being ejected from left ventricle (vasoconstriction increases SVR); and Mean arterial pressure (MAP): product of cardiac output and systemic vascular resistance * Review Class Lab#4 Hemodynamic Monitoring and Mod #4 Heart Failure MAP = systolic BP + 2 (Diastolic BP) 3 RNSG 2432  95
  10. 10. * Remember MAP of 60 or greater needed to maintain tissue perfusion and oxygenation! Regardless of cause- reaction and symptoms typically follow same course-differentiate stages/type of shock/ underlying cause * Important to understand this concept e. Stages of Shock/type of shock! 1) Stage 1-Early reversible and Compensatory Shock (p. 150) *Initial stage: MAP dec. to less than 10 mmHg; circulating blood volume usually less than 500 mL; SNS inc. HR and force contraction > CO; peripheral vasoconstriction, inc. SVR and yields inc. arterial pressure; individual does not note symptoms unless progressive insult a) MAP 10 -15 mm Hg below normal levels b) Decrease in circulating blood volume (25-35% less) loss of 1000 mL or more c) Sympathetic nervous system stimulated; release catecholamines (epinephrines and norepinephrines); bronchodilation and increased cardiac output occurs due to beta receptor stimulation d) To maintain blood pressure: inc. heart rate and contractility; inc. in peripheral vasoconstriction due to stimulation of beta adrenergic fibers (cause vasoconstriction of blood vessels of skin and abdominal viscera) and inc. in heart rate and contractility e) Renin-angiotensin-release of aldosterone to reabsorb H2O and sodium; loose potassium (increase fluid volume to compensate for decreased renal perfusion) f) Posterior pituitary releases ADH (antidiuretic hormone, also called vasopressin) to increase intravascular fluid volume) g) Get fluid shift from interstitial to capillaries due to decrease in hydrostatic pressure in capillaries h) Circulation maintained, but only sustained short time without harm to tissues; must treat underlying cause of shock; will progress to next stage ***Preserve perfusion of heart and brain! 2) Stage II- Intermediate or progressive shock (severe or decompensated) a) Further drop in MAP (20 mm below normal values) * As shock continues to progress, compensatory mechanisms from the previous phase continue unchecked, worsening the status! b) Increase in fluid loss of 35-50% (1800 – 2500 ml) due to hemorrhage or fluid leakage c) Vasoconstriction continues; cells become more O2 deficient>start anaerobic metabolism ) d) **Body switches to anaerobic metabolism > lactic acid as a waste product. e) Body inc. heart rate and vasoconstriction. f) Heart and brain cells become hypoxic g) More severe effects on other tissues > become ischemic and anoxic 96  RNSG 2432
  11. 11. h) Fluid shifts into interstitial space; proteins shift into interstitial space; fluid follows! * As cells die due to hypoxic state, > release destructive enzymes and proteins into surrounding tissues >inc. oncotic pressure into interstitial space (third-spacing) >,circulating volume is further decreased i) Metabolic acidosis with hyperkalemia develops j) Needs rapid treatment; poor survival rate! 3) Stage III-Refractory or irreversible shock (also called MODS… multiple organ dysfunction> death) a) Tissues anoxic, cellular death widespread b) Even with restoration of blood pressure and fluid volume > too much damage to restore homeostasis of tissues c) Cellular death leads > tissue death > vital organs fail and death occurs *Know understand these stages B. Common Manifestation/Complications 1. Effects of Shock on Body Systems (See text p. 152 Multsystem effects of Shock) a. Cardiovascular/hematologic 1) Initially: slight tachycardia, normal blood pressure 2) Progresses to weak, rapid pulse with dysrhythmias 3) Progressive dec. in systolic and diastolic blood pressures with narrowing of pulse pressure; blood pressure > inaudible 4) DIC [disseminated intravascular coagulation); late effect of hypoxia; slow-moving acid blood - hypercoagulable, does not coagulate unless clot-initiating factor present a) Factors= bacterial endotoxins and thromboplastin of RBCs; hemolysis (destruction of RBC’s b) Massive crush injury occurs c) Stagnant acidic blood b. Respiratory 1) Initially: inc. respiratory rate (chemoreceptors sense dec. pH, depth of respiration inc. to “blow-off” CO2 to compensate for metabolic acidosis; cellular hypoxia not caused by inadequate ventilation but by inadequate tissue perfusion > inc. respiratory effort does not correct the problem > lactic acid accumulates> becomes more acidic > blood pH and bicarbonate levels dec. a) Gas exchange impaired >leads to anaerobic metabolism b) Leads to acidosis (metabolic and respiratory) 2) Acute Respiratory Distress Syndrome (ARDS): complication of decreased lung perfusion (Review Mod 1 ARDS) c. Gastrointestinal and Hepatic 1) GI organs > ischemic, with blood circulation shunted to heart and brain > Stress Ulcers (GI mucosa > ischemic, prone to rapid ulceration) and Paralytic Ileus (dec. gastrointestinal motility with decreased blood flow) 2) Altered liver metabolism: initially glucose made available, then hypoglycemia, fat breakdown leads to ketones and metabolic RNSG 2432  97
  12. 12. acidosis; toxicity and bleeding (Liver- impaired circulation and may be source of toxic materials; anoxic liver does not detoxify; may release vasoactive substances; bacterial invasion from intestines. d. Neurologic 1) Develops cerebral hypoxia (cerebral edema due to hypoxia) 2) Restlessness initially > altered level of consciousness, lethargy, coma; have emboli 3) Circulatory collapse- sympathetic stimulation lost > bradycardia > death e. Renal: Dec. kidney perfusion > to oliguria (urine output < 20 ml/o ) ; develop ATN (can recover function if basement membrane intact; epithelial cells regenerate) f. Skin, temperature, thirst; Skin: cool, pale, hypothermic due to vasoconstriction g. Immune System: All forms of shock severely deplete macrophages (found in blood cells and tissues) > cannot remove bacteria and endotoxins from the blood stream > increased chance for sepsis! h. MODS (multiple organ dysfunction)- Ultimately all body systems fail and death. 2. Types of Shock (categorized according to underlying causes) a. Hypovolemic; loss of intravascular volume > 15-25% (See p. 154, Box 6-2, Assessment Findings in Clients in Hypovolemic Shock) 1) Most common: occurs with other types of shock 2) Common stimuli/causes hemorrhage, burns, severe dehydration, third spacing such as bowel obstruction, burns, liver 3) Progresses through stages of shock unless restoration of fluid volume 98  RNSG 2432
  13. 13. b. Cardiogenic (See p. 155, Box 6-3 Assessment Findings in Clients in Cardiogenic Shock) (review from heart failure) 1) Pumping ability of heart compromised to degree that cannot maintain cardiac output (CO) and adequate tissue perfusion (pump failure); 2) Common causes: MI, cardiomyopathy, arrhythmia, cardiac tamponade; cardiac arrest 3) Leads to left and right sided heart failure; decreased CO and MAP; increased LVEDP (*decreased MAP stimulates sympathetic system; beta receptors stimulated; increases O2 needs; cardiac stress!) 4) Cyanosis common c. Obstructive (hard to diagnose)*** 1) Heart or great vessels obstructed; venous return or cardiac pumping action impeded; cardiac preload dec./severely compromised; inc. pressure on right side of heart and an inadequate blood return (different from cardiogenic shock- heart itself has adequate pumping abilities and is not necessarily diseased) 2) Common cause: *pulmonary embolism, pneumothorax d. Distributive (Vasogenic); includes several types of shock-result in widespread vasodilatation and dec. peripheral resistance; *blood volume does not change, have relative hypvolemia! (need to understand this concept!) 1) Septic Shock (Toxic shock (click here to learn more) found in menstruating women who use tampons) (See text p. 156, Box 6-4 Assessment Findings in Clients with Septic Shock) a) Leading cause of death in intensive care units b) Common stimuli: Gram negative bacterial most often causative agent; others (pseudomonas, E coli); Gram positive bacterial infections (staphylococcus and streptococcus) 60% mortality rate despite treatment RNSG 2432  99 May lead to cadiogenic shock
  14. 14. 46-year-old man presented with nonnecrotizing cellulitis and streptococcal toxic shock syndrome. The leg was incised to exclude underlying necrotizing infection. Courtesy of Rob Green, MD. c) Increased risk: clients with chronic illness, poor nutritional status, invasive procedure or tubes, as central lines, foley catheters d) Course: Septicemia (bacteremia initially) develops> pathogens and their toxins in blood > endotoxins disrupt circulation > cause massive vasodilation in response to pathogen’s release of toxins into bloodstream> normal coagulation mechanisms altered> inflammatory response triggered > DIC (*understand this concept) e) Phases Septic Shock (SIRS) systemic inflammatory response syndrome: (1) Warm Phase (early); skin flushed, warm due to vasodilatation; (2) Cold Phase (late): skin cool due to fluid deficit with shock. Have deep respirations, lethargic, coma f) CO high and SVR low (warm phase) g) DIC high risk with septic shock h) Priority: early recognition; tachycardia, hyperthermia (or hypothermia) and hypotension due to decreased SVR; blood volume adequate, but misplaced i) Interventions: Some controversy over management and treatment (not in text) (1) Maintain airway -adequate cardiac output; oxygen, IV access, hemodynamic monitoring, BP support with fluids and medications, cultures and appropriate antibiotics; treat elevated temperature (some controversy) but inc. temperature inc. metabolic demands. (High mortality rate) 100  RNSG 2432 Patient in septic shock can exhibit can exhibit skin lesions; most often on lower extremities; associated with development of DIC;
  15. 15. 2) Neurogenic Shock See text. 156, Box 6-5 Assessment Findings in clients in Neurogenic shock a) Dec. sympathetic control of vasomotor responses; parasympathetic stimulation unchecked > **sustained peripheral vasodilation > dec. MAP b) Common stimuli: head injury, spinal cord trauma, insulin reactions, anesthesia (somewhat rare associated with significant spinal trauma) R/O hypvolemic shock initially, NCS depressant drugs c) Bradycardia due to parasympathetic influence early then tachycardia d) Decreased CO due to bradycardia; dec. PAP, pulmonary capillary wedge pressure; dec. SVR due to vasodilation; hypotension and hypothermia e) Early neurogenic shock: blood pools in venous & capillary beds; skin warm and pink; pulse slow and bounding; dec. BP; dec. temperature; have vasodilation and cec. MAP; Late skin pale and cool and heart rate inc. f) Priority problem: maintain tissue perfusion (1) Interventions- assessment and pulse oximetry; identify cause and attempt to correct; maintain ABC; may involve infusing IV fluids for volume replacement and initiating vasopressors to control BP levels. If symptomatic bradycardia, use atropine, maybe a transvenous pacemaker. RNSG 2432  101
  16. 16. 3) Anaphylactic Shock (Click here for more) See p. 157, Box 6-6 assessment Findings in Clients in Anaphylactic Shock a) Result of widespread hypersensitivity (anaphylaxis); first symptoms-dermatologic : pruritus, generalized erythemia, urticaria usually on chest, then on face and angioedema b) Vasodilation > hypovolemia and altered cellular metabolism c) Sensitized in past, re-contact with the allergen (medication, bee sting, food allergen) d) Allergic reaction with large amounts of histamine released e) Histamine > vasoconstriction of smooth muscles in bronchioles (causes bronchospasm, laryngospasm), bladder, intestines > leads to inc. permeability and massive vasodilatation (pooling of blood in periphery)= hypovolemia f) Serotonin- increases capillary permeability (can cause pulmonary) g) Key manifestations: dyspnea, stridor, wheeze dec. BP, inc. heart rate, dysrhythmias, laryngospasm/bronchospasm, warm, edematous skin, restless to coma; oliguria to anuria h) Priorities: Maintain airway (1) Interventions: Find cause and remove!; administer epinephrine (Adrenaline); provide oxygen, give antihistamine; give corticosteroids i) Need Medic Alert bracelet (teaching!) 3. Life Span and Effects of Shock 102  RNSG 2432 Urticaria wheal
  17. 17. The most common etiologies of shock in children are hypovolemia and sepsis. The major type of shock in pregnancy is hemorrhagic (hypovolemic) and is the leading cause of maternal death. Postpartum hemorrhage occurs most often in the first hour following delivery (fundus and lochia should be assessed every 15 minutes for the first hour postpartum) but can occur up to a week following childbirth. Because the uterus is a nonessential body organ, danger to the fetal blood supply occurs when the woman's body begins to decrease blood flow to the peripheral organs. (Pillitteri, 2003, p. 380) Sepsis is a major cause of death in the elderly; shock of any type is a strong predictor of mortality. Due to the decrease in chronotropic response with aging, tachycardia may not be present in the elderly hypovolemic patient despite very low cardiac output. Fluid resuscitation is best achieved with colloids such as blood products as the elderly require higher hemoglobin levels to facilitate oxygen delivery. Large amounts of normal saline should be avoided; with decreased renal function, metabolic acidosis may result. Treatment is aimed not at normalizing hemodynamic parameters, but at correcting any oxygen deficit. (Fulmer, et al., 2001) C. Therapeutic Interventions/Collaborative Care (summary all types) 1. Collaborative Care: focus on treating underlying cause to stop progress through stages of shock; rapid shock identification; rapid diagnosis of cause; rapid aggressive treatment: better outcome for client 2. Goal: improve arterial oxygenation and tissue perfusion; determine type of shock 3. Assessment: **Keys: a. Cool, clammy skin b. Hypotension-widened pulse pressure c. MAP<60 (need more than 60 for organs to be perfused)*Takes 40 minutes of MAP<60 to develop acute renal failure. *May see slighly different values.. RNSG 2432  103
  18. 18. d. Dec. in B/P by 20 and Inc. HR by 20 = shock e. Oliguria f. Tachycardia g. Decreased level of Consciousness h. Rales and edema-only in cardiogenic 4. Diagnostic tests for clients in shock a. Blood hemoglobin and hematocrit: hypovolemic shock b. Arterial Blood Gases: identify body compensatory mechanisms, such as acidosis c. Electrolytes (Na level decreases, K dec, later inc. K with cellular breakdown d. BUN and creatinine (renal failure), osmolality: renal function e. Blood cultures: identify causative organism in septic shock; treat f. White blood count and differential: septic shock g. Cardiac enzymes: diagnosis of cardiogenic shock (Cardiac enzymes are: lactate dehydrogenase (LDH); Creatine phosphokinase (CPK); serum glutamic-oxaloacetic transaminase (SGOT): h. CVP- Measures right heart pressure (Normal 4-10 cm H20 or 2-5 mmHg); 1) High reading means fluid overload 2) Low reading means fluid deficit i. Swan Ganz or PA catheter for hemodynamic monitoring of left heart pressures (Review values) What do altered hemodynamic reading readings indicate related to shock? Low CVP? High CO? 5. Medications/Treatment (depend upon cause of shock/trauma) a. Oxygen Therapy: Patent airway and adequate oxygenation-critical! Interventions; Monitor ABGs, pulse oximetry (more accurate in early stage); Mechanical ventilation b. Inotropic agents: improve cardiac contractility (dopamine, dobutamine) c. Vasoactive agents according to symptoms: vasoconstrictors for distributive shock (Levophed and epinephrine); vasodilator (Nipride and Nitroglycerine) for cardiogenic shock d. Other meds according to cause as antibiotics, steroids; diuretics, digoxin, etc e. Fluid Replacement: appropriate solutions-Types of Intravenous Fluids 1) Crystalloid solutions: Dextrose or electrolyte solutions; inc. intravascular and interstitial fluid volume; ex Isotonic (0.9% NaCl, lactated Ringers) and hypotonic (5% dextrose in water, .45% NaCl) 2) Colloids: Do not diffuse easily through capillary walls; stay in vascular compartment; increase osmotic pressure; ex: albumin, hetastarch, plasma protein fraction, dextran. 3) Blood and Blood Products: treatment of hemorrhage; restore coagulation properties 6. Nutrition : hypermetabolic state a. Enteral feeding first choice (food in GI tract, dec risk GI bleed) 104  RNSG 2432
  19. 19. b. Early diet interventions dec. the risk of MODS c. If cardiogenic- low Na and fluid restriction d. High potassium if BUN and Creat OK 7. Surgery/Invasive a. IABP for cardiogenic shock *review how they work! b. VAD :BRIDGE TO HEART TRANSPLANT:USED IN PATIENTS WITH CARDIOMYOPATHY 8. Other: Treat underlying cause a. Positioning-flat with legs elevated b. Assess for MODS 9. Nursing Process/Nursing Diagnosis a. Nurse assess/analyze client situation and change in condition b. Notify physician >early treatment before shock advanced and less responsive to treatment c. Care of client in shock: constant assessment /modify treatment d. Transfer to intensive care unit for hemodynamic monitoring and respiratory support e. Complexities of changing status of fluid, acid-base, cardiovascular function f. Support of client and family 10.Common Nursing Diagnoses a. Decreased Cardiac Output b. Altered Tissue Perfusion c. Fluid volume deficit d. Anxiety RNSG 2432  105

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