Exam 3 Flashcards
stages of shock
1- compensatory “non-progressive”, reversible, switches from aerobic to anaerobic (lactate greater than 1); 2- decompensated “progressive”, compensation failing, extreme cardiovascular support takes place; 3- refractory, irreversible, severe tissue hypoxia, ischemia and necrosis occur
basic patho of shock
hypoxia -> reversible cell injury -> aerobic to anaerobic metabolism -> depletion of ATP -> lactic acidosis (metabolic) -> irreversible cell injury -> multiple organ dysfunction -> death
patho of stage 1 aka compensatory
no drop in BP; baroreceptors detect low perfusion and low O2; compensation mechanisms working; sympathetic response d/t release of epi and norepi causing increase HR and peripheral vasoconstriction (cool clammy pallor skin); endocrine system releases aldosterone, release renin, release ADH; hyperventilate; paralytic ileus
organs affected from stage 2 shock
brain- decreased CPP causing AMS and confusion; heart- cell death resulting in acute MI and dysrhythmia; kidney- acute tubular necrosis resulting in renal failure; lungs- increased capillary permeability causing pulmonary edema and ARDS; liver- acute failure; gut- decreased peristalsis in ileus and GI bleed; vessels use all clotting factors leading to DIC
patho of stage 2
drop in BP, persistent hypoperfusion; hypoxic injury d/t decreased perfusion and O2, increased capillary permeability (protein and fluids leaking); multiple organ failure
Patho stage 3
multiple organ dysfunction syndrome (MODS); end of septic continuum when tissue perfusion cannot be restored; fist occurs in lungs and heart then hepatic, GI, renal, Immune, CNS; patient cannot be saved
3 main types of shock
hypovolemic, cardiogenic, distributive
hypovolemic shock
decreased blood volume, decreased venous return (preload), decreased stroke volume; decreased cardiac output (CO = HR x SV); decreased tissue perfusion- tries to compensate with increasing HR and increasing vascular tone
signs and symptoms of hypovolemic shock
weak thready pulse, decreased cardiac output, tachycardia, hypotension, cyanosis, decreased capillary refill, cool pale skin, decreased central venous pressure, increased vasoconstriction, decreased O2 sat, tachypnea
labs associated with hypovolemic shock
lactic acid, CBC, ABGs, urine output (decreased)
treatment of hypovolemic shock
need two large bore IVs; stop bleeding or fluid loss; treat underlying cause; replace volume with crystalloids, blood products, or albumin; support BP with vasopressors; if >30% loss then need to replace blood volume
if administering vasopressors such as levophed…
need to give via central line; need A-line for monitoring
nursing management of hypovolemic shock
vitals q15; monitor cardiac and respiratory status; trendelenburg positioning; monitor temp for hypothermia; glucose <150; type and screen, get consent, and admin blood; meds like fluids and pressors
cardiogenic shock
pump failure; d/t problem with filling such as diastolic HF; contraction issues such as cardiomyopathy, HF, MI; d/t arrythmias causing conduction issues; structural issues like valvular diseases (regurgitation)
s/s of cardiogenic shock
weak peripheral pulse, decreased CO, increased HR, decreased BP, cool clammy skin, decreased capillary refill (>3sec), increased CVP, increased SVR from vasoconstriction, decreased O2 sat. JVD, chest pain, oliguria, confusion and agitation, dyspnea, pulmonary edema
labs associated with cardiogenic shock
lactate, troponin, ABG, CXR, EKG, echo, CRP, PCWP, CO, CI
management of cardiogenic
monitor O2 with ABGs and pulse ox; pain control via fentanyl and morphine; fluid control with diuretics; cardiovascular support with hemodynamic monitoring (increase SVR, increase contraction, fix arrhythmias, temporary assist device with intra-aortic balloon pump or ECMO; repair heart
how to increase SVR
vasopressors
how to increase contraction
inotropes
how to fix arrhythmias
Pacers, anti-arrhythmias, cardioversion
procedures to repair heart for cardiogenic shock
surgery, catheterization, LVAD, transplant
types of distributive shock
anaphylactic shock, neurogenic shock, septic shock; different reactions but all cause massive vasodilation
anaphylactic shock
massive release of histamine; allergen is entered into blood stream and interacts with B cells to produce antibodies (IgE); release H1 and H2 histamines
H1 histamine
bad one; increase capillary dilation (systemically) decreasing BP; increase capillary permeability systemically causing fluid shifts; bronchoconstriction of lungs; decrease conduction of AV node
H2 histamine
increase gastric acid production and can cause N/V and increase risk of aspiration; vascular smooth muscle relaxation causing decrease in BP
Type 1 vs Type 2 allergic reaction/anaphylaxis
type 1 needs sensitization and is IgE mediated; type 2 does not need sensitization and usually occurs with bee stings and IV contrast
signs of anaphylactic shock
rapid weak pulse, decreased CO, increased HR, decreased BP, generalized flushing of skin, decreased CVP, decreased SVP, decreased O2 sat, cardiac dysrhythmias/arrest, N/V, acute abdomen, wheezing/coughing, bronchoconstriction, itching, urticaria, flushing from massive vasodilation
nursing management of anaphylaxis
ABCs, Epinephrine to increase sympathetic response, intubate/ventilate, albuterol admin, IV fluids, H1 antihistamine (benadryl) and H2 antihistamine (zantac), corticosteroids to prevent rebound
Neurogenic shock
distributive shock caused from CNS injury; cervical or high thoracic injury (T6 and above); loss of sympathetic response and preserved parasympathetic activity, causes body to slow down (bradycardia)ca
causes of neurogenic shock
spinal cord injury, spinal anesthesia, nervous system damage, hypoglycemia, drug voerdose
patho of neurogenic shock
coronary vessels are impacted via decrease in afterload (SVR) and decrease in preload; loss of catecholamine response leading to decreased vascular tone and decreased BP; heart decreased in cardiac contraction and low heart rate; hypothermia from dysregulation in hypothalamus and no vasoconstriction
manifestations of neurogenic shock
decreased afterload (SVR), hypotension, bradycardia, decreased CO hypothermia (warm dry extrem.)
treatment of neurogenic shock
immobilize/protect spine; assess vitals and admin IV fluids, pressors, inotropes, increase HR (give epi); protect airway
septic shock stages
systemic inflammatory response (SIRS)- temp > 100.4F, respiration > 20, HR >90, WBC > 12000 or < 4000; sepsis- two or more of these conditions; severe sepsis- organ dysfunction hypotension, hypoperfusion; septic shock- symptoms despite adequate fluid resus, unable to fix
1 hour sepsis bundle
used to rapidly diagnose and provide immediate intervention; lactic acid draw > 2, cultures prior to antibx, broad spectrum antibiotics at first then narrow, Iv fluids like crystalloids, vasopressors to maintain map > 65 (levo), oxygenation, support failing organs
patho of septic shock
infection with bacteria, virus, or fungi in blood causing WBC to respond; result in pro-inflammatory mediators and nitric oxide that dilate blood vessels and decrease BP (drop SVR), leaky capillaries causing fluid shifts, less O2 and more fluid causes difficulty perfusing, lytic enzymes damage blood vessels and use up clotting factors (DIC), fluid accumulates in lungs (ARDS)
early clinical manifestations of septic shock
aka “warm”/compensated; fever, warm skin, increased RR, restless, anxious, glucose abnormalities (hyperglycemia d/t gluconeogenesis), elevated HR
late signs of septic shock
aka “cold”/uncompensated; cold clammy skin, respiratory distress/failure/ARDS, AMS/coma, glucose abnormalities (hypoglycemia), decrease in HR and BP
septic shock affects
heart, lungs, kidneys, GI, liver
septic shock affects on heart
stunned myocardium, HF; use IV fluids, vasopressors, blood products; DVT prohylaxis with lovenox
septic shock affects lunga
cyanosis, acidosis, ARDS; treat with BiPap and mechanical ventilation; sedate and neuromuscular blockade
septic shock affecting kidneys
oliguria, anuria, tubular necrosis, place on CRRT
septic shock affects liver
jaundice, glucose problems, liver failure; treat with IV insulin d/t TPN increasing BGL
septic shock affects GI
N/V, diarrhea, ileus; treat with parenteral or enteral nutrition; prophylaxis to prevent stress ulcer
Summary of hypovolemic shock symptoms
elevated HR, elevated SVR, decreased CO, decreased CVP, decreased O2, cold clammy skin
summary of cardiogenic shock symptoms
elevated HR, increased SVR, decreased CO, increased CVP, decreased O2 sat, cold clammy skin
summary of neurogenic shock symptoms
decreased HR, decreased SVR, decreased CO, decreased CVP, decreased O2, warm dry skin
summary of septic shock symptoms
increased then decreased HR, decreased SVR, increased Co then decreased, decreased CVP, decreased O2 sat the increased, warm hot dry skin then cold clammy skin
green triage tag; “minor”
able to walk; victim with relatively minor injuries; status unlikely to deteriorate over days; may be able to assist in own care; “walking wounded”
yellow triage tag “delayed”
unable to walk, spontaneous breathing, RR <30, radial pulse present or capillary refill <2, mental status able to obey commands; transport can be delayed; serious and potentially life-threatening injuries but status not expected to deteriorate significantly over several hours
red triage tag; “immediate”
unable to walk, spontaneous airway absent but recurs with airway repositioning, respiratory rate >30, radial pulse absent or capillary refill >2 sec, mental status does not obey commands; victim can be helped by immediate intervention and transport; requires medical attention within 60 minutes for survival; compromise to ABCs
black triage tag; “expectant”
unable to walk, no spontaneous breathing even with airway adjustment; victim unlikely to survive given severity of injuries or level of available care, palliative care and pain relief should be provided
tick bite diseases
rocky moutain spotted fever, tularemia, lyme disease
tularemia
tick transmitted disease; tick and deer fly bites; skin contact with infected animals; contaminated water; inhalation of infected dust; lab exposure; treat with antibiotics like streptomycin or gentamycin; caused by bacterium francisella tularensis
rocky mountain spotted fever
caused by bacterium rickettsiia rickettsii; dx with signs and symptoms and hx; confirmed dx with antibody testing like enzyme immunoassay (ELISA); treat with doxycycline before day 5
signs and symptoms of rocky mountain spotted fever
fever, headache, abdominal pain, vomiting, myalgia, rash may be apparent, can be fatal within days
lyme disease
caused by bacterium borrelia burgdoferi; may see headache, fatigue, flu-like symptoms, skin rash erythema migrans; treat with doxycycline or penicillin
stages of lye disease
stage 1- within 4 weeks, bulls eye rash, flu-like symptoms; stage 2- 4 to 10 weeks, joint pain, memory loss, poor motor coordination, meningitis; stage 3- arthritis, neuropathy, myalgias, myocarditis
bites to be aware of
animal + human, snakes such as copper head and timber rattlesnake, spiders such as brown recluse and black widow
bites to report
report human and animal bites to public health authorities in order to proved follow up screening of animals for rabies
nursing interventions for animal and human bites
assess the bite, control bleeding, clean wound with soap and water, pain management, tetanus booster of needed (within last 5 years), rabis risk if animal unknown wild or rabid (prophylactic vaccine)
snake bites
medical emergency; most common in children 1-9 during daylight during summer; pit vipers most common; 20-25% envenomation
s/s of snake bites
edema, ecchymosis, hemorrhagic bullae (necrosis at site), lymph node enlargement, N/V or metallic taste in mouth, numbness
s/s of snake bite without treatment
fasciculation, hypotension, parasthesia, seizures, coma
snake bites nursing interventions
assessment of bite, maintain ABCs, immobilize and light sterile dressing, remove constrictive clothing/jewelry, do not apply tourniquet or ice, first aid care to cleanse with soap and water, VS, pain management, antivenom admin., fluid resus.
brown recluse spider bite
systemic effects like fever, N/V, chills, malaise; initially no pain at site; red purple to necrotic; cleanse and hyperbaric O2
black widow spider bite
systemic effects like N/V, abdominal rigidity, HTN, tachycardia, paresthesia’s, painful, admin antivenom
chemical burn of eye
irrigate eye immediately with NS or water
ABCDE
a- airway with cervical spine; b- breathing, c- circulation, d- disability (neuro) with AVPU, E- exposure
management of overdose pt
support respiratory and cardiovascular function; enhance clearance of agent causing OD; provide safety of patient and staff; IV drug users at high risk of HIV, HEP B, hep C, and tetanus
management of sexual assault pt
provide support, reduce emotional trauma, gather evidence for possible legal proceedings; may be SANE certified nurse; physical exam; specimen collection; treatment of consequences like STI or pregnancy; encourage follow up care
nursing role/intervention for human trafficking
offer for pt to speak alone without companion; ask if control of own money?, able to come and go as they please?, who is the person accompanying you?; pt may decline assistance; resource available is The national human trafficking hotline
when collecting evidence for forensics
meticulous documentation including wound descriptions, mechanism of injury, time of events, and collection of evidence
implications of forensics
trauma pt (dead/alive) that has potential legal and forensic implications if criminal activity is suspected; carefully remove clothing and place in individual BROWN BAGS; inventory valuables and place in hospital safe; if police present have them label items as evidence; take photographs (possibility)
CO poisoning
inhaled Co binds to hemoglobin and does not transport O2; manifestations include CNS symptoms, skin color and pulse ox are not reliable; treat with fresh air immediately, CPR as necessary, 100% O2 or hyperbaric O2 pressure; monitor continuously with CO monitor and serial labs to look at carboxyhemoglobin
types of burns
thermal- most common, exposure to heat dry or moist; chemical- tissue injury and destruction from necrotizing substances; electrical- electrical current or lightning, injury to muscle and bone; radiation- caused by sun, tanning booth, xrays; cold- frost bite; friction- abrasion to skin
thermal burn interventions
remove charred clothing, saline or water to cool tissues, fluffed gauze for fingers and toes (wrap individually)
chemical burn interventions
remove by brushing off or with water, remove and clothing, neutralizing agent are not recommended, tissue destruction occurs for up to 72 hours, is it acidic or alkaline
acidic vs alkaline bruns
acid- damage resulting in protein denaturation and necrosis, usually short-lived and localized; alkaline- far worse, cause progressive liquefaction necrosis, deeper tissue penetration, prolonged effect
electrical brun intervention
remove electrical current before touching pt, causes cell rupture (release of potassium can cause arrhythmias), iceberg effect (worse below the surface), can fracture bones, identify entrance and exit, can cause compartment syndrome (may need fasciotomy)
assessing extent of burns
depth, age of pt, location, medical Hx, total percentage of body surface area (TBSA) where 1st degree or superficial are not included (use rule of 9s and parkland formula)
rule of 9s
entire head and neck = 9%
entire right arm = 9% (posterior is 4.5 and anterior is 4.5)
entire left arm = 9%
entire trunk = 36% (18 posterior and 18 anterior)
groin = 1%
entire right leg is 18% (anterior 9 and posterior 9)
entire left leg = 18%
greater than 20% TBSA is considered
systemic; superficial burns do not count
less than 20% TBSA burn
considered local burn
different layers of skin
epidermis, dermis, hypodermis, muscle and bone
epidermis contains
protection from infection
dermis contains
blood vessels, nerve endings (feel pain after epidermis is burned), sweat and oil glands, cells to create new skin (need skin graft if damaged)
hypodermis contains
subcutaneous tissue, veins, arteries, nerves, insulation that regulates temp (cannot regulate if burned); if burned to hypodermis keep room at 85-100 degrees
muscle and bone exposure after burn
if burned this far then everything is destroyed; release of myoglobin that travels to kidney and results in AKI
superficial burn aka epidermal
1st degree burn, does not count towards rule of 9s, appears dry and red, blanches with pressure, painful sensation, heals in 3-6 days
superficial partial thickness
2nd degree burn; appears blistering, moist, red, weeping, blanches with pressure; painful sensation to temperature, air and touch; heals in 7-21 days
deep partial thickness burn
2nd degree burn; appears blisters (easily unroofed), wet or waxy, variable color from patchy to cheesy white to red, blanching with pressure may be sluggish; painful to pressure only; heals >21 days and usually requires surgical intervention
full thickness burn
3rd degree burn, travels into hypodermis; appears waxy white to leathery gray to charred and black; painful to pressure only; rare to heal unless surgically treated
deeper injury
4th degree; appears to extend into fascia and muscle; pain with deep pressure; never heals unless surgically treated
1st degree burn
superficial, only the epidermis, very red pink and warm, no blisters, brisk capillary refill, minimal to no edema, painful, sunburn
2nd degree burn
superficial partial burn, affects epidermis and dermis (varies), shiny moist red/pink, blisters, can still blanch, very painful; deep partial- damage deeper into the dermis, hair follicles and glands, painful to pressure only, blisters, does not blanch
3rd degree burn
full thickness, consists of epidermis dermis and hypodermis, not painful/deccreased pain, skin will not heal without grafting, color is black yellow red, matte/dry, hard areas are eschar
eschar
burned dead tissue that has to be removed; hard
4th degree burn
extends through all layers, muscle and bone, appears black and charred, eschar present, all sensation is gone, grafting is necessary, shock can occur, myoglobinuria to kidneys, hemolysis, AKI, risk for contractures due to tight skin
inhalatio n injury
damage to respiratory system due to breathing in smoke, thermal, or chemical; if suspected do not hesitate to intubate
inhalation injury s/s
charred burned or bright red lips, head neck or face burn, wheezing, change in voice, difficulty breathing, singed nose hairs or eye brows, dark mucus from soot; can affect upper and lower respiratory system
when to refer to burn unit
deep partial thickness burns > 10% TBSA; burns involving face, hands, feet, genitalia, perineum, or major joints or throat; full thickness of any age group; electrical burns including lightning; inhalation burns requiring intubation; chemical burns that involve deep and extensive TBSA; circumferential burns; complicated medical or social HX
phases of burn care
emergent, acute, rehabilitation
emergent phase of burn care
firs 48hrs (resuscitative); onset of injury to completion of fluid resus; priorities - ABCDE, prevent shock, prevent compartment syndrome, prevent resp. distress, assess wound and initial care; fluid accumulation phase
acute phase of burn care
intermediate, 48-72 hours after injury; from beginning of diuresis to near completion of wound closure; priorities- wound care like hydrotherapy, warm room; infection prevention via PPE, handwashing, sterility; pain management with narcotics; nutritional support; ends TBSA <20% or skin graft
rehabilitation phase of burn care
wound closure to return to optimal level; priorities- prevention and treatment of scars and contractures; PT, OT, and vocational rehab; functional and cosmetic reconstruction; psychosocial counseling
fluid resuscitation parkland formula
first half over 8 hours; 2nd half over 16 hours; fluid requirements = Weight (Kg) x TBSA burned (%) x 4 mL
systems that can become dysfunctional from burns
respiratory, cardiovascular, immune, GI, renal/endocrine, skin
respiratory dysfunction from burna
occurs after face, mouth, neck, or torso burns; inhalation injury; monitor ABG, potential intubationcard
cardiovascular system dysfunction
hypovolemia due to increased fluid shifts (3rd spacing)
immune dysfunction from burns
infection possible; perineum burns susceptible; depends on %TBSA
GI dysfunction from burns
paralytic ileus, less blood flow, ulcers, risk for bleeding; bowel sounds, NPO, NG tube, parenteral nutrition
renal/endocrine dysfunction from burns
hyperglycemia occurs from gluconeogenesis
skin dysfunction from burns
poor blood supply; nose and ears require cosmetic surgery; skin tightening acts as tourniquet and requires escharotomy; eyes and contractures attribute to disability; compartment syndrome can occur
treatment of circumferential burn
elevate above the hear; escharatomy to cut bands of dead tissue in order to restore normal perfusion
open woundd care of burn
antimicrtobial cream applied as prescribed and left open to air without dressing/; use silvidine; allows for visualizing wound, easier mobility, easier ROM, simple wound care; increased chance of hypothermia d/t exposure
closed wound care for burn
gauze dressing carefully wrapped to ensure circulation is not compromised, changed q8-12h; decreased evaporative fluid and heat loss, aids in debridement; limited mobility and ROM, unable to assess wound as easily
silver impregnated dressings
antimicrobial properties; disrupts cell wall and membrane, denatures proteins, interrupts ATP production, disrupts DNA replication; silvadene or silver nitrate
wound debridement
removal of eschar or necrotic tissue to prevent bacterial proliferation under eschar an to promote wound healing; can be mechanical, chemical, autolytic, or surgical excisionco
complications with wound debridement
pain (need to premedicate with narcotics), bleeding, infection, delayed healing, removal of healthy tissue
skin grafting
surgical procedure where skin or skin substitute is placed over burn or non-healing wound; reduces course of treatment needed and improves function/appearance
