NURS 444 week 12 Flashcards
shock
A SYNDROME of whole body
Classification of shock: functional impairment
- hypovolemic shock
- cardiogenic shock
- distributive shock
- obstructive shock
Classification of shock based on eitology
- hypovolemic
- cardiogenic
- vasogenic ?
- septic
What do oxygenation and perfusion depend on?
total blood volume
cardiac output
size of vascular bed
Hypovolemic shock
15- 30% fluid volume loss
commonly caused by hemorrhage and dehydration
Absolute or Relative
Cardiogenic shock
actual heart muscle is not doing it’s job
**most common is MI
cardiomyopathy, dysrhythmias, blunt injury, severe systemic pulm. htn
Obstructive shock
something that impairs heart muscle to pump.
- pericarditis
- cardiac tamponade
- tension pneumo.
- PE?
Distributive shock
Blood vol. is not lost, widespread vasodilation and re-distribution
3 types:
1. neuro-genic shock
2. anaphylactic shock
3. septic shock
Neuro-genic shock
loss of sympathetic tone
hypotension and bradycardia
Anaphylactic shock
massive dilation
increased permeability (leak)
Sepsis and Septic shock
complex type of distributive shock
- usually bacterial or fungal
Sepsis
widespread infection
- coupled with more general inflammatory response, known as systemic inflammatory response syndrome (SIRS), that is triggered when infection escapes local control
SIRS can also occur with other shock BUT most common with septic
Severe Sepsis
progression of sepsis with amplified inflammatory response
dysfunction of at least one organ
shock: sepsis with hypotension despite fluids
Septic shock
when multi-organ failure is evident and bleeding occurs (micro-clots, DIC)
death rate in this stage exceeds 60%
unable to correct with fluids
begins with hyperventilation: alkalosis results but goes back to acidodic
probably on vent.
disorientation, resp., kidneys affected
QSOFA
score for sepsis
- GCS < 15
- resp. >/equal 22
- systolic </equal 100
Lactate levels
CVP
we ideally want above 6 to give vasopressor (book says > 2-8) we’ll give if fluid expanders don’t work
MODS: multiorgan dysfunction syndrome
massive release of toxic metabolites and enzymes cause cell damage
- metabolites released from dead cells
- microthrombi
- MODS occurs first in the liver, heart, brain, and kidney
- myocardial depressant factor from the ischemic pancreas
MODS can occur with other shocks but mainly with sepsis and septic shock
shock: stages
initial: early shock
nonprogressive: compensatory stage
progressive: intermediate
refractory: irreversible
shock
Initial stage (early)
- baseline MAP decreased by < 10
- heart and RR ^ from the baseline or a slight ^ in diastolic pressure
- adaptive responses of vascular constriction and ^ HR
(liver is affected because it cannot clear lactic acid)
shock:
Nonprogressive (compensatory)
> MAP decreases by 10-15
kidney and hormonal adaptive mechanisms activated
tissue hypoxia in non-vital organs
acidosis and hyperkalemia
> stopping conditions that started shock and supportive interventions can prevent shock from progressing
more clinically noticeable in this stage
noticeable; neuro, BP, vitals
MAY HAVE OXYGEN NOW
shock:
Progressive (intermediate)
< sustained decrease in MAP of > 20 from baseline
< vital organs develop hypoxia
< life-threatening emergency
< immediate interventions!!!
< conditions causing shock need to be corrected within 1 hr of the onset of the progressive stage
CALL A RAPID
GET TPN STARTED
shock:
refractory (irreversible)
too much cell death and tissue damage result from hypoxia
body can no longer respond effectively to interventions, and shock continues
IRREVERSIBLE
shock management:
Goals
+ maintain tissue oxygenation
+ ^ vascular volume to normal range
+ support compensatory mechanisms
` oxygen therapy
` IV therapy
` drug therapy
` hemodynamic monitoring
` nutrition (protein)
DEXTRAN- fluid volume expanders
Assessment/ Clinical manifestations (shock)
- cardiovascular changes
- pulse
- BP
- oxygen saturation
- skin changed
- resp. changes
- renal and urinary changes
- CNS changes
- musculoskeletal changes
- cap. refills
think of original reason they came in
Nursing management (shock)
> frequent assessment: physical, psychosocial
> Identify trends: labs, vitals, LOC
> Plan and implement interventions
> evaluate responses
> provide support
> collaborate w/ team
manage DM if they have it
Drugs and hemodynamics
+ vasoconstrictors
+ agents that enhance contractility (dobutamine)
+ agents that enhance myocardial perfusion
+ hemodynamics:
` CVP: right atrium pressur
` pulm. artery pressure PCWP
` mixed venous set (Svo2): venous 60-80. tells us about oxygen consumption
` cardiac index
extra shock notes or values
CVP- 2-8 tells us pre-load
pulmonary artery pressure PCWP: left artery pressure
SV02: only monitored with PA line
Cardiac index: 2.2-4 normal for septic patient. This is a more specific measure of cardiac output based on body mass
START FLUID BOLUS if lactate >4 OR hypotensive
Types of Burns
> Thermal (hot)
chemical
electrical
cold thermal injuries (frostbite)
smoke and inhalation injuries
Classification of Burn Injury
Severity determined by;
- depth of burn
- extent of burn
- location of burn
- patient risk factors
ABA» depth of skin destruction
- partial-thickness burn
- full-thickness burn
depth of burn
- Superficial partial-thickness burn:
involves epidermis - deep partial-thickness
involves dermis - deep full-thickness
involves fat, muscle, bone
Superficial
- painful
- no edema
- redness
- blanches with pressure
partial thickness
- blistered
- moist
- painful
Classification of burn
Full thickness burns
- dry
- discolored
- no pain
Classification of burn
Extent of burn
- Lund-Browder’s chart
more accurate - Rules of Nines
adequate for initial assessment of adult patients
Classification of burn
Location of burn
location r/t severity
- face, neck, chest» resp. obstruction
- hands, feet, joints, eyes»_space; self care
- ears, nose»_space; infection
Circumferential burns
compartment syndrome
Thermal Burns
caused by;
flame, flash, scald, or contact with hot objects
**most common type of burn
- full-thickness burn (A)
- partial thickness (B)
- partial thickness d/t hot water immersion (C)
Chemical burns
- burn from acid, alkalis, organic compounds
- alkali burns hard to manage because they cause protein hydrolysis and liquefaction. *damage continues after alkali is neutralized
** chemical should be quickly removed from the skin: includes clothing
** tissue destruction may continue up to 72 hr after chem. injury
Alkali burns
neutralized with mild acid
- 5% acetic acid
- household vinegar
- water dilution
Smoke inhalation injuries
- inhalation of hot air or noxious chemicals
- damage to resp. tract
- need to be treated fast
** Major predictor of mortality in burn victims
three types of smoke inhalation injuries
1) Carbon monoxide poisoning
2) Inhalation injury above the glottis
3) inhalation injury below the glottis
What does inhaling carbon monoxide do?
- displaces oxygen
- hypoxia
- carboxyhemoglobinemia
- death
Carbon monoxide treatment
+ treat with 100% humidified oxygen
+ CO poisoning may occur in absence of burn
+ skin color described as “Cherry Red”
Inhalation injury above the glottis
- thermally produced
- hot air, steam, or smoke
- mucosal burns of oropharynx and larynx
- mechanical obstruction can occur quickly
** true medical emergency
** presence of facial burns
singed nasal hair
hoarseness, painful swallowing
darkened oral and nasal mucosa
inhalation below the glottis
- r/t length of time of exposure to smoke or toxic fumes
- pulm. edema may not appear until 12 to 24 hr after burn.
- then may manifest as acute resp. distress syndrome
Electrical burns
result from coagulation necrosis caused by intense heat from an electrical current
- tissue anoxia and death
- injury depends on;
amount of voltagetissue resistancecurrent pathwayssurface area
`duration of the flow
Criteria for referral of burn
- electrical
- chemical
- trauma
- circumferential
- > 5% third degree
- > 10% second or third degree
- children
- face, hands, or genitals (2nd or 3rd)
Phases of burn management
- prehospital care (EMS)
- Emergent (resucitative)
- Acute (wound healing)
- Rehabilitative (restorative)
Prehospital and emergency Tx of burns
- remove source
- chemical, remove dry particles and irrigate continuously
- small thermal (<10%) may be covered with cool tap-water, dampened towel
-** no ice - LARGE BURNS SHOULD NOT BE EMERSED IN WATER DUE TO RISKS OF HYPOTHERMIA
burns: EMERGENCY tx
- Airway: check for inhalation, soot, stridor, wheezing
- Breathing
- circulation: keep burned limb above heart to reduce swelling
-emergent burn phase: first 24-48 hours
biggest. risk of burns
hypovolemic shock from fluid shifts
- electrolyte shifts
- K
-Na
Burns: inflammation, healing and immunity
inflammation/ healing
< neutrophils and monocytes accumulate at site of injury
< fibroblasts, collagen fibers begin repair within first 6-12 hr
< burns injuries cause widespread impairment of immune system
` decreased T cells
` ^ suppressor cells
` decreased interlukins
Burns: clinical manifestations
- shock from pain and hypovolemia
- blisters
- Adynamic ileus
- altered mental status
Burns: abnormal lab findings
> During initial fluid shift (first 24 hr)H&H elevated (fluid loss)
Na+ decreased
`K+^ from cell destruction
> after 24 hrH&H decreased
Na+ decreased
`K+ decrease from loss and movement back into cells
What to do in Emergent phase
+ airway management
+ fluid therapy!!!
+ wound care
+ pain & anxiety
+ pain meds are always IV due to edema and impaired circulation
+ psychosocial
+ PT/OT
+ nutrition
Burns: Complications
!! electrolyte imbalance (need to know difference from emergent phase and later phases)
!! hypothermia
!! infection
!! scarring/ contractures (rehab phase)
!! Curling’s ulcers (stress ulcers)
!! hyperglycemia
Burns: acute phase
begins with the metabolization of extracellular fluid and subsequent diuresis.
Acute phase is concluded when burned area is completely covered by skin grafts or wounds are healed
*greatest risk: infection
Burns: rehab phase collaborative care
beginning: when burn wounds are covered with skin or healed.
the patient is able to resume a level of self-care
Burns: acute phase care
+ continue fluid therapy
+ labs: sodium, potassium
+ cont. nutritional therapy
+ wound care
+ assess for complications
+ debridement and grafting
+ pain and anxiety
depends on the patient
-can develop paralytic ileus
-can be combative r/t anxiety
Burns: rehab phase carre
+ self care
+ continue nutritional therapy
+ wound care
+ adjustment and coping
+ occupational therapy
Carbon monoxide poisoning intevention
(will look cherry red; CO will attack to hemoglobin)
100% humidified oxygen ASAP
biggest risk in emergent phase
- edema
- hypovolemia
- glottis edema
prevent infection (cover wound) and consider nutrition
*AIRWAY
*CIRCULATION
*WOUND CARE
*PAIN
underlying pain that is present all the time in burns
hypnosis
biofeedback
alternative management
