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Med Surg 3 (theory class) > NURS 444 week 12 > Flashcards

NURS 444 week 12 Flashcards

1
Q

shock

A

A SYNDROME of whole body

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2
Q

Classification of shock: functional impairment

A
  • hypovolemic shock
  • cardiogenic shock
  • distributive shock
  • obstructive shock
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3
Q

Classification of shock based on eitology

A
  • hypovolemic
  • cardiogenic
  • vasogenic ?
  • septic
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4
Q

What do oxygenation and perfusion depend on?

A

total blood volume

cardiac output

size of vascular bed

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5
Q

Hypovolemic shock

A

15- 30% fluid volume loss

commonly caused by hemorrhage and dehydration

Absolute or Relative

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6
Q

Cardiogenic shock

A

actual heart muscle is not doing it’s job

**most common is MI

cardiomyopathy, dysrhythmias, blunt injury, severe systemic pulm. htn

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7
Q

Obstructive shock

A

something that impairs heart muscle to pump.

  • pericarditis
  • cardiac tamponade
  • tension pneumo.
  • PE?
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8
Q

Distributive shock

A

Blood vol. is not lost, widespread vasodilation and re-distribution

3 types:
1. neuro-genic shock
2. anaphylactic shock
3. septic shock

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9
Q

Neuro-genic shock

A

loss of sympathetic tone

hypotension and bradycardia

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10
Q

Anaphylactic shock

A

massive dilation

increased permeability (leak)

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11
Q

Sepsis and Septic shock

A

complex type of distributive shock
- usually bacterial or fungal

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12
Q

Sepsis

A

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

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13
Q

Severe Sepsis

A

progression of sepsis with amplified inflammatory response

dysfunction of at least one organ

shock: sepsis with hypotension despite fluids

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14
Q

Septic shock

A

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

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15
Q

QSOFA

A

score for sepsis

  • GCS < 15
  • resp. >/equal 22
  • systolic </equal 100
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16
Q

Lactate levels

A
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17
Q

CVP

A

we ideally want above 6 to give vasopressor (book says > 2-8) we’ll give if fluid expanders don’t work

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18
Q

MODS: multiorgan dysfunction syndrome

A

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

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19
Q

shock: stages

A

initial: early shock

nonprogressive: compensatory stage

progressive: intermediate

refractory: irreversible

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20
Q

shock
Initial stage (early)

A
  • 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)

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21
Q

shock:
Nonprogressive (compensatory)

A

> 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

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22
Q

shock:
Progressive (intermediate)

A

< 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

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23
Q

shock:
refractory (irreversible)

A

too much cell death and tissue damage result from hypoxia

body can no longer respond effectively to interventions, and shock continues

IRREVERSIBLE

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24
Q

shock management:
Goals

A

+ 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

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25
Q

Assessment/ Clinical manifestations (shock)

A
  • 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

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26
Q

Nursing management (shock)

A

> 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

27
Q

Drugs and hemodynamics

A

+ 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

28
Q

extra shock notes or values

A

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

29
Q

Types of Burns

A

> Thermal (hot)
chemical
electrical
cold thermal injuries (frostbite)
smoke and inhalation injuries

30
Q

Classification of Burn Injury

A

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

31
Q

depth of burn

A
  • Superficial partial-thickness burn:
    involves epidermis
  • deep partial-thickness
    involves dermis
  • deep full-thickness
    involves fat, muscle, bone
32
Q

Superficial

A
  • painful
  • no edema
  • redness
  • blanches with pressure
33
Q

partial thickness

A
  • blistered
  • moist
  • painful
34
Q

Classification of burn
Full thickness burns

A
  • dry
  • discolored
  • no pain
35
Q

Classification of burn
Extent of burn

A
  • Lund-Browder’s chart
    more accurate
  • Rules of Nines
    adequate for initial assessment of adult patients
36
Q

Classification of burn
Location of burn

A

location r/t severity
- face, neck, chest» resp. obstruction

  • hands, feet, joints, eyes&raquo_space; self care
  • ears, nose&raquo_space; infection

Circumferential burns
compartment syndrome

37
Q

Thermal Burns

A

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)
38
Q

Chemical burns

A
  • 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

39
Q

Alkali burns

A

neutralized with mild acid
- 5% acetic acid
- household vinegar
- water dilution

40
Q

Smoke inhalation injuries

A
  • inhalation of hot air or noxious chemicals
  • damage to resp. tract
  • need to be treated fast

** Major predictor of mortality in burn victims

41
Q

three types of smoke inhalation injuries

A

1) Carbon monoxide poisoning
2) Inhalation injury above the glottis
3) inhalation injury below the glottis

42
Q

What does inhaling carbon monoxide do?

A
  • displaces oxygen
  • hypoxia
  • carboxyhemoglobinemia
  • death
43
Q

Carbon monoxide treatment

A

+ treat with 100% humidified oxygen

+ CO poisoning may occur in absence of burn

+ skin color described as “Cherry Red”

44
Q

Inhalation injury above the glottis

A
  • 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

45
Q

inhalation below the glottis

A
  • 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
46
Q

Electrical burns

A

result from coagulation necrosis caused by intense heat from an electrical current

  • tissue anoxia and death
  • injury depends on;
    amount of voltage tissue resistance
    current pathways surface area
    `duration of the flow
47
Q

Criteria for referral of burn

A
  • electrical
  • chemical
  • trauma
  • circumferential
  • > 5% third degree
  • > 10% second or third degree
  • children
  • face, hands, or genitals (2nd or 3rd)
48
Q

Phases of burn management

A
  • prehospital care (EMS)
  • Emergent (resucitative)
  • Acute (wound healing)
  • Rehabilitative (restorative)
49
Q

Prehospital and emergency Tx of burns

A
  • 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
50
Q

burns: EMERGENCY tx

A
  • Airway: check for inhalation, soot, stridor, wheezing
  • Breathing
  • circulation: keep burned limb above heart to reduce swelling

-emergent burn phase: first 24-48 hours

51
Q

biggest. risk of burns

A

hypovolemic shock from fluid shifts

  • electrolyte shifts
  • K
    -Na
52
Q

Burns: inflammation, healing and immunity

A

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

53
Q

Burns: clinical manifestations

A
  • shock from pain and hypovolemia
  • blisters
  • Adynamic ileus
  • altered mental status
54
Q

Burns: abnormal lab findings

A

> During initial fluid shift (first 24 hr)
H&H elevated (fluid loss) Na+ decreased
`K+^ from cell destruction

> after 24 hr
H&H decreased Na+ decreased
`K+ decrease from loss and movement back into cells

55
Q

What to do in Emergent phase

A

+ airway management
+ fluid therapy!!!
+ wound care
+ pain & anxiety
+ pain meds are always IV due to edema and impaired circulation
+ psychosocial
+ PT/OT
+ nutrition

56
Q

Burns: Complications

A

!! electrolyte imbalance (need to know difference from emergent phase and later phases)
!! hypothermia
!! infection
!! scarring/ contractures (rehab phase)
!! Curling’s ulcers (stress ulcers)
!! hyperglycemia

57
Q

Burns: acute phase

A

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

58
Q

Burns: rehab phase collaborative care

A

beginning: when burn wounds are covered with skin or healed.

the patient is able to resume a level of self-care

59
Q

Burns: acute phase care

A

+ 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

60
Q

Burns: rehab phase carre

A

+ self care
+ continue nutritional therapy
+ wound care
+ adjustment and coping
+ occupational therapy

61
Q

Carbon monoxide poisoning intevention

A

(will look cherry red; CO will attack to hemoglobin)

100% humidified oxygen ASAP

62
Q

biggest risk in emergent phase

A
  • edema
  • hypovolemia
  • glottis edema

prevent infection (cover wound) and consider nutrition

*AIRWAY
*CIRCULATION
*WOUND CARE
*PAIN

63
Q

underlying pain that is present all the time in burns

A

hypnosis

biofeedback

alternative management

Med Surg 3 (theory class) (13 decks)

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