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Critical Care > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

Etiology of Peptic Ulcer Disease

A

NSAIDs

Helicobacter pylori

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2
Q

Etiology of Stress-Related Mucosal Disease

A

High physiologic stress (mechanical ventilation, burns, shock)

Increased acid production and decreased mucosal blood flow (ischemia)

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3
Q

Etiology of Esophagogastric Varices

A

Portal hypertension

Liver failure

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4
Q

Hematemesis

A

Bright red blood or coffee grounds (acid)

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5
Q

Hematochezia

A

Bright red blood in stool

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6
Q

Melena

A

UGI blood passed through bowels

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7
Q

Prophylaxis for GI Bleeding

A

Monitor gastric pH

Assess stools and gastric contents for blood

Histamine-2 Receptor Blocker (Cimetidine, Famotidine, Ranitidine)

PPI (Omeprazole, Pantoprazole)

Mucosal lining coating (Sucralfate)

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8
Q

Serum Bilirubin, direct

A

0 - 0.3 mg/dL

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9
Q

Serum Bilirubin, total

A

0 - 0.9 mg/dL

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10
Q

Serum Protein Total

A

7.0 - 7.5 g/dL

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11
Q

Serum Albumin

A

4.0 - 5.5 g/dL

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12
Q

Prothrombin Time

A

12 - 16 seconds

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13
Q

Ammonia

A

11 - 32 umol/L

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14
Q

Bleeding Etiology with Liver Involvement

A

Liver dysfunction (lack of clotting factors, hypoalbuminemia)

Decreased absorption (vitamin K, fat soluble vitamins)

Inadequate intake sufficient vitamins

Gastric erosion, ulceration

Portal hypertension

Esophageal varices

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15
Q

Stabilization of GI Bleeding

A

IV fluids

Blood transfusions

Blood products

Control bleeding

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16
Q

Control of GI Bleeding

A

Esophageal balloon tamponade

Vasopressin

Somatostatin and Octreotide

Beta blockers

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17
Q

Nursing Management of GI Bleeding

A

Fluid resuscitation

Blood and blood product transfusions

Gastric lavage

Maintaining surveillance for complications (neurological assessments hourly, assess renal perfusion with hourly outputs)

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18
Q

Medical Management of Esophageal Varices

A

Control bleeding (endoscopy)

Endoscopic injection therapy

Endoscopic variceal ligation

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19
Q

Hepatic Encephalopathy

A

Seen in chronic liver disease

Triggered by dehydration, electrolyte loss, increased protein intake, bleeding from GI tract, infections, alcohol ingestion

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20
Q

Signs and Symptoms of Hepatic Encephalopathy

A

Headache, hyperventilation, jaundice, mental status changes, palmar erythema, spider nevi, fetor hepaticus, bruises, hepatomegaly

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21
Q

Laboratory for Hepatic Encephalopathy

A

Serum bilirubin (unconjugated and tubal)

AST

Alkaline phosphatase

SERUM AMMONIA

Prothrombin time

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22
Q

Intellectual Function of Hepatic Encephalopathy

A

0: Normal
1: Personality changes, attention deficits, irritability, depressed state
2: Changes in sleep/wake cycle, lethargy, mood/behavioral changes, cognitive dysfunction
3: Altered LOC, somnolence, confusion, disorientation, amnesia
4: Stupor and coma

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23
Q

Neuromuscular Stages of Hepatic Encephalopathy

A

0: Normal
1: Tremor, incoordination
2: Asterixis, ataxic gait, speech abnormalities
3: Muscular rigidity, nystagmus, clonus, Babinski, hyporeflexia
4: Oculocephalic reflex, unresponsiveness to noxious stimuli

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24
Q

Acute Liver Failure

A

Severe acute liver injury with hepatic encephalopathy, elevated INR or Pro time

Seen in clients without cirrhosis or preexisting liver disease, illness less than 26 weeks duration

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25
Q

Etiology of Acute Liver Failure

A

Viral hepatitis

Medication-induced liver damage

Early recognition is key

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26
Q

Pathophysiology of Acute Liver Failure

A

ALF over 1 to 3 weeks

Hepatic encephalopathy within 8 weeks

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27
Q

Treatment of Acute Liver Failure

A

Control cerebral edema (Mannitol, positioning)

IV administration of glucose, electrolytes

LACTULOSE TO DECREASE AMMONIA/rectal tube

Bleeding monitoring and control

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28
Q

Etiologies of Chronic Liver Failure

A

Infections

Drugs or toxins (acetaminophen, alcohol)

Hypoperfusion

BILIARY (bile obstruction)

CARDIAC (right sided heart failure)

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29
Q

Treatment of Chronic Liver Failure

A

Safety –> FALL PREVENTION

Control ammonia levels (Neomycin, LACTULOSE)

Control bleeding (vitamin K, FFP, platelet transfusion)

Ascites (frequent paracenteses)

Spontaneous Bacterial Peritonitis–sudden pain, rigid abdomen, leads to sepsis

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30
Q

Nursing Care of Liver Failure

A

Provide comfort and emotional support

Family and patient education

Protect from injury (assess mental status)

Nutrition (protein intake 1 - 1.5 g/kg, assess fluid status)

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31
Q

Molecular Adsorbent Recirculating System (MARS)

A

Nonbiological artificial liver support system

Albumin used as dialysate to remove protein-bound toxins

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32
Q

MARS Effects

A

Stabilize condition

Bridge to transplant

Reduction of portal HTN

Improvement of ICP, encephalopathy

Increases MAP and SVR

Removes uremic toxins

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33
Q

Requirements for MARS

A

Central venous line for dialysis

FFP before line placement

Set up/prime takes 1-2 hours

MAP of 70-80

Intermittent treatment (lasts 8 hours for 3 days)

CRRT between MARS sessions

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34
Q

Etiology of Acute Pancreatitis

A

Gallstone migration

Alcoholism

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35
Q

RANSON’S Criteria for Acute Pancreatitis

A

Age > 55 years

Hypotension

Abnormal pulmonary findings

Abdominal mass

Hemorrhagic/discolored peritoneal fluid

Neurological deficits (confusion, localizing)

LDH > 350, AST > 250

Leukocytosis > 16,000

Hyperglycemia > 200

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36
Q

RANSON’S Criteria for First 48 Hours

A

Decrease in Hct > 10% with hydration

Fall in Hct < 30%

Need for massive fluid/colloid replacement

Hypocalcemia < 8

PaO2 < 60 without ALI

Hypoalbuminemia < 3.2

Azotemia

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37
Q

Pathophysiology of Acute Pancreatitis

A

Edematous pancreatitis

Acute necrotizing pancreatitis

Local tissue injury

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38
Q

Assessment and Diagnosis of Acute Pancreatitis

A

Physical examination (hypoactive bowel sounds, abdominal tenderness, Cullen sign, Grey-Turner sign)

LOW CALCIUM

Laboratory studies (elevated serum amylase and lipase)

Diagnostic procedures (abdominal ultrasound, CT)

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39
Q

Medical Management of Acute Pancreatitis

A

FLUID RESUSCITATION (IV crystalloid, isotonic) for distributive shock

Pain management

Nutritional support (enteral feedings, TPN may be very helpful)

Systemic complications (hypovolemic shock, ARDS, AKI, GI hemorrhage)

Local complications (infected pancreatic necrosis and pseudocyst)

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40
Q

Nursing Management of Acute Pancreatitis

A

Providing comfort and emotional support

Maintaining surveillance for complications

Educating patient and family

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41
Q

Functions of the Skin

A

Protection

Sensation

Water balance

Temperature regulation

Vitamin production

Immune response function

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42
Q

Burn

A

Injury to the skin or other organic tissue primarily caused by heat or due to radiation, radioactivity, electricity, friction, or contact with chemicals

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43
Q

ABLS

A

Initial assessment/management

Airway, smoke injury

Shock and fluid resuscitation

Burn wound management

Electrical injury

Chemical burns

Pediatric burns

Stabilization, transfer, transport

Burn disaster management

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44
Q

Significant Factors Related to Burn Injury

A

Type of injury

Location of injury (of incident, on client)

Age

Previous health history

Size-Area

Depth

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45
Q

Assessment: Sources of Burn Injuries

A

Thermal (heat, flame, scalds)

Electrical

Chemical

Radiation

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46
Q

Care of Thermal Burn Injuries

A

Stop, Drop, Roll

Remove clothing

Flush with water or saline

Saline compresses if TBSA < 10%; do not chill patient

Dry, sterile dressing/”burn sheet” otherwise

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47
Q

Care of Electrical Burn Injuries

A

TURN OFF SOURCE OF ELECTRICITY FIRST

CPR priorities of Airway, Breathing, Circulation

Treat dysrhythmias

Entry and exit wounds

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48
Q

Pathophysiology of Burns

A

DYSFUNCTION OF ALMOST EVERY CELL AND CELLULAR SIGNALING PATHWAYS

Hypermetabolic state = CELL DEATH

Chronic inflammation

FLUID SHIFTING (3RD SPACING)

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49
Q

Care of Chemical Burn Injuries

A

Protect self (clothing)

Remove from source

Remove client’s clothing

Continuous flushing with water or saline for 20-30 minutes (except lime powder or carbolic acid)

Eye care

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50
Q

Care of Radiation Burn Injuries

A

Protect self (shielding)

Remove from source

Isolate client

Decontamination

Severity: type of radiation, duration of exposure, distance from source, absorbed dose, depth of body penetration

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51
Q

Children and Burns

A

Greater risk for injury

Head greater ratio of TBSA

Legs smaller ratio of TBSA

Skin thinner

Fluid loss more critical

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52
Q

Elderly and Burns

A

Thinner, tougher skin

Slower regeneration time

More sensitive to fluid volume loss

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53
Q

Assessment: Area of Burn

A

TBSA

Rule of 9s

Rule of 9s for child: Head (18%), Leg (14%)

Berkow Formula (detailed assessment based on age and TBSA, Rule of 9s)

TBSA not final until debridement is complete

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54
Q

Rule of Palms

A

Measure the palmar surface of the victim’s hand (fingertip to wrist)

Represents 1% of the TBSA

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55
Q

Assessment: Depth of Burns

A

Amount of injured epidermis or dermis

Depth of destruction of epidermis and/or dermis

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56
Q

Superficial/First Degree Burns

A

Only first 2-3/5 layers of epidermis

Erythema–heals within 2-7 days

Mild discomfort (resolves 48-72 hours)

Cause: sunburns, steam burns

Treatment: pain relief, pruritus relief, oral fluids

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57
Q

Partial-Thickness/Second Degree Burns

A

Superficial, mid-dermal, deep dermal

Involved upper 1/3 of dermis

Cause: brief contact with flames, hot liquid, exposure to chemicals

Light/bright red, or mottled appearance

May appear wet, weeping, bull

Painful, sensitive to air currents

Heals 7-21 days with minimal scarring

Deep-dermal involves entire epidermis and part of dermis (red with patchy white, blanches with pressure, prolonged healing time, scarring contractures if untreated)

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58
Q

Full Thickness/Third Degree Burn

A

Destruction of all layers of skin, may include subcutaneous tissue

Pale white or charred, red, brown, leathery

Surface dry

Painless, insensitive to palpation

Requires skin grafting

Susceptible to infection, fluid/electrolyte imbalances, alterations in thermoregulation, metabolic disturbances

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59
Q

Zone of Coagulation

A

Irreversible damage

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60
Q

Zone of Stasis

A

Impaired circulation

Inflammatory response

Can be converted to full thickness

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61
Q

Zone of Hyperemia

A

Vasodilation, increased blood flow

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62
Q

Minor Burn Severity Criteria

A

PT < 15% TBSA

FT < 2% TBSA

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63
Q

Moderate Burn Severity Criteria

A

PT: 15-25% TBSA

FT: 10% TBSA

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64
Q

Critical Burn Severity Criteria

A

Breathing problems

PT > 25% TBSA

FT > 10% TBSA

Face, hands, feet, genitalia

Deep chemical burns

Complicated by fracture or concurrent disease (e.g. diabetes)

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65
Q

Emergent or Resuscitative Phase of Burn

A

First 24-48 hours

Until 3rd spacing has stopped

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66
Q

Acute Phase of Burn

A

3-6 months

Until wound closure

Shock and hyper metabolic phase

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67
Q

Rehabilitative Phase of Burn

A

Several years

Scar and graft management

PT/OT, contractures

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68
Q

Phases of Burn Care

A

First TWO minutes: Prehospital

First TWO hours: ED care

First TWO days: Resuscitation

First TWO weeks: Surgical excision/graft

First TWO months: Rehab, psychology

First TWO years: Reconstruction

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69
Q

Nursing Management of Burns

A

Inflammatory Phase (immediately after injury)

Proliferative Phase (4-20 days after injury)

Maturation Phase (20 days after injury)

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70
Q

Airway Management with Burns

A

ASSESSMENT OF RISK (facial burns, singed facial hair, stridor)

Visualize larynx for redness

Endotracheal intubation

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71
Q

Respiratory Problems with Burns

A

Carbon monoxide poisoning (carboxyhemoglobin serum level)

Smoke poisoning

ALI

Pulmonary fluid overload

Thoracic eschar impairment

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72
Q

Interventions for Respiratory Problems with Burns

A

100% O2 therapy

Monitor fluid balance

ET intubation

Mechanical ventilation

Humidification

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73
Q

Renal and GI Complications with Burns

A

Renal: myoglobinuria, hypovolemic AKI

Paralytic ileus: NG tube insertion and low intermittent suctioning, monitor bowel sounds

Curlings ulcers: H2 Histamine Blockers, gastric pH checks, antacids PRN

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74
Q

Integumentary Complications with Burns

A

HYPOTHERMIA (monitor client’s core temperature, keep client warm with heated blankets and warm irrigation solutions)

NUTRITION DEFICIT (high calorie, high protein needs for restoration)

SEQUESTRATION OF MEDICATIONS (only IM injection is tetanus toxoid)

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75
Q

Fluid Replacement Therapy for Burns

A

Baxter Equation

Monitor fluid replacement with CVP, BP, and hourly urine output

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76
Q

Baxter Equation

A

24 hour IV = 4 mL x Wt (kg) x %TBSA

(Child) = 1 mL x Wt (kg) x %TBSA

FIRST HALF 24 hour intake within 8 HOURS OF TIME OF BURN INJURY

Second half 24 hour intake during next 16 hours

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77
Q

Alteration in Comfort: Pain for Burns

A

Narcotic therapy IV

Administer medications by routine schedule

Medicate prior to procedures

Promote adequate sleep cycle

Adjunctive therapies: therapeutic touch, music therapy, distraction

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78
Q

Impaired Skin Integrity with Burns

A

Preserve integrity of non-burned skin

Restoration of viable tissue (debridement) to remove tissue contaminated by foreign bodies and bacteria and remove devitalized tissue

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79
Q

Alteration in Nutrition with Burns

A

TOTAL PARENTERAL NUTRITION

Diet: high calorie, high protein

Caloric needs: 2-3x normal

Protein needs: 1.5 - 3 grams/kg body weight

BURNS REQUIRE SUBSTANTIAL NUTRITION FOR RESTORATION

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80
Q

Debridement

A

Mechanical: hydrotherapy, whirlpool baths, surgical excision

Enzymatic (eschar): autolysis, proteolytic

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81
Q

Autolytic Debridement

A

Natural process, occurs in all wounds

Phagocytic cells

Proteolytic enzymes in wound bed

Results in significant wound fluid, not damaging surrounding tissue, minimal pain

Dressing must contain moist wound bed

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82
Q

Impaired Skin Integrity Interventions for Burns

A

Antimicrobial agents

Dressings (open vs. closed)

Grafts (heterograft/pigskin, homograft/cadaver, autograft/own skin)

Synthetic dressings

Hyperbaric therapy

ESCAROTOMY to restore circulation

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83
Q

Stem Cell Research

A

Use of patient’s own cells

Need biopsy of all layers of skin

EPICEL (keratinocytes–expanded into confluent epidermal autograft, takes 2-3 weeks)

Bone marrow, hair follicle, adipose can be used

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84
Q

Infection with Burns

A

Tetanus toxoid and immunoglobulin

Topical drugs: silver sulfadiazine, silver nitrate, nitrofurazone, mafenide acetate

Antibiotic IV therapy: Aminoglycosides (check renal function)

Protective isolation

Good handwashing

No plants (risk of pseudomonas)

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85
Q

Impaired Physical Mobility with Burns

A

Contractures and deformities resulting from burns

Position client in anatomical position

ROM Immediately

Ambulation as soon as fluid shift is resolved

STATIC SPLINTS immobilize joints

DYNAMIC SPLINTS exercise joints

PRESSURE GARMENTS AND DRESSINGS

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86
Q

Stressors of Burn Units

A

Fast-paced, high-technology

Complex management

Multidisciplinary

Equipment

Limited workspace

Warm temperatures

Unpleasant odors

High noise levels

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87
Q

Trauma

A

Accidental or unintentional injury sustained through an external mechanism of injury

Falls, shootings, burns, auto accidents, farm accidents, altercations, natural disasters

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88
Q

Blunt Trauma

A

Motor vehicle collisions

Contact sports

Blunt force injuries

Falls

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89
Q

Penetrating Trauma

A

Stabbings

Firearm injuries

Impalement

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90
Q

First Peak of Injury

A

50% of deaths occur

Minutes from injury

Location: at scene, en route to medical facility

Cause of death: laceration of brain or brainstem, high spinal cord injury, injury to heart or other large vessels

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91
Q

Second Peak of Injury

A

30% of deaths occur

Minutes to few hours after injury

Location: emergency room, operating room

Cause of death: subdural or epidural hematoma, hemo-pneumothorax, ruptured spleen, liver laceration, pelvic fracture, injuries associated with extensive blood loss

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92
Q

Third Peak of Injury

A

20% of deaths occur

Days to weeks after injury

Location: critical care unit

Cause of death: sepsis, multiple organ dysfunction syndrome

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93
Q

Victim of a Trauma

A

Real fear of dying/disfigurement

Anger or guilt toward causing agent

Anxiety over alien environment

Intrusion by impersonal strangers

High level of stress (sympathetic NS stimulation, inability to relax or concentrate)

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94
Q

Six Phases of Trauma Care

A

Prehospital resuscitation

Hospital resuscitation

Definitive care and operative phase

Critical care

Intermediate care

Rehabilitation

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95
Q

Primary Survey of Advanced Trauma Life Support

A

Airway with C-spine protection

Breathing and ventilation

Circulation with hemorrhage control

Disability/Neuro assessment

Exposure and environmental control

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96
Q

Personal Safety of Nurse in Trauma

A

Unknown risk of infections –> universal precautions

Displacement of anger by client or family

Physical threat to safety

Toxic agents

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97
Q

Prehospital Care of Trauma

A

Security and safety of scene

Initial assessment (ABCDE)

Triage and prioritize all victims

Focused history and physical exam

Stabilization of victims

Transportation

98
Q

Primary Evaluation in ED

A

ABCs

Mechanism of injury

Scene

99
Q

Resuscitation in ED

A

Intubation

O2

IV fluids

Stop bleeding

100
Q

Secondary Assessment in ED

A

Pertinent health history

Physical exam

101
Q

Definitive Care in ED

A

CCU, OR

Decisions to direct client’s care

102
Q

Primary Trauma Assessment

A 
Airway
Breathing
Circulation
Disability
Exposure/Environmental Control
103
Q

Secondary Trauma Assessment

A

Full set of vitals
Get resuscitation adjuncts (LMNOP)
History (MIST)
Inspect posterior surfaces

104
Q

Resuscitation Adjuncts

A 
Laboratory studies
Monitoring, cardiac
NG/OG tube
Oxygenation/ventilation
Pain assessment/management
105
Q

MIST for Head to Toe

A

Mechanism of injury
Injuries sustained
Signs/symptoms before arrival
Treatment before arrival

106
Q

Secondary Assessment History (SAMPLE)

A 
Symptoms associated with injury
Allergies, tetanus status
Medications currently used
Past medical history
Last meal/oral intake
Events/environmental factors related to injury/illness
107
Q

Definitive Care of Trauma

A

Dressing of wounds

Suturing as needed

Stabilization of fractures or dislocations

Surgery if indicated

CCU admission

Medications as needed

Pain control

108
Q

Lethal Triad

A

Coagulopathy

Hypothermia

Acidosis

109
Q

Critical Wounds

A

Sucking chest wound

Gunshot wound

Impaled object

110
Q

Sucking Chest Wound

A

Seal with occlusive dressing

One way valve dressing or dart

111
Q

Gunshot Wound

A

Look for exit wound

Extensive internal injuries

112
Q

Impaled Object

A

Do not remove the object!

Bulk dress the object in place

113
Q

Chest Wall Injuries

A

Rib fractures

Flail chest (two or more ribs fractured in two or more places, free floating, pulmonary contusion under fracture)

Blunt chest trauma (cardiac trauma, contact with steering wheel, cardiac perfusion problems)

114
Q

Trauma to Extremities

A

Immobilization of fractures

Assessment of distal circulation and nerve function

Assess extremities bilaterally

Lower priority injuries

Dress traumatic amputations and bring extremity with client

115
Q

Spinal Cord Injury

A

Cord vs. Vertebral injury and level

Neck immobilization with cervical collar

Spinal cord immobilization with long spine board

Paralysis may be present without loss of sensation

Hypoventilation if cord injury is above C7

116
Q

Complications of Trauma

A

Hypermetabolism (initiate enteral feedings within 72 hours for patients with blunt and penetrating abdominal injuries and those with head injuries)

Infection

Sepsis

Pulmonary (respiratory failure, ALI, fat embolism)

Pain

Renal complications (renal failure, AKI, myoglobinuria)

Vascular complications (compartment syndrome, venous thromboembolism, missed injury, MODS)

117
Q

Compartment Syndrome

A

Increased pressure within limited space

Compromises circulation, results in ischemia and necrosis of tissues

High risk patients (LE trauma, fractures, penetrating injuries)

Signs/Symptoms: swelling, paresis, PAIN, decreased pulses, decreased capillary refill

DECREASED PULSES ARE VERY LATE SIGN OF COMPARTMENT SYNDROME

118
Q

Disseminated Intravascular Coagulation

A

A systemic clotting cycle that begins with the systemic circulation of thrombin

Thrombin promotes clotting in the microvasculature of the organs

As the coagulation process continues to deplete the circulatory system of clotting factors/platelets, signs of bleeding begin to occur

PROFUSE BLEEDING AND A LOW PLATELET COUNT

119
Q

Nontraumatic Causes of DIC

A

Obstetric conditions (50% of DIC cases)

Cancer (35% of DIC cases)

Sepsis

Autoimmune reactions

Pulmonary embolism

120
Q

Thrombotic Signs of DIC

A 
Angina
Acrocyanosis
Dyspnea
Headache
Confusion
Severe pain
Visual changes
121
Q

Hemorrhagic Signs of DIC

A 
Bleeding from puncture sites
Renewed bleeding from dressings or drains
Epistaxis
Hematemesis, melena stools
Petechiae
Ecchymosis
122
Q

Diagnostic Tests of DIC

A

PT and PTT prolonged

Low platelet count (<50,000)

Low fibrinogen level

Elevated fibrin degradation products

D-dimer serum screen > 50

123
Q

Interventions for DIC

A

Treat underlying cause

Whole blood if needed for bleeding replacement

Replace clotting factors (platelets, cryoprecipitate, fresh frozen plasma)

Antithrombin III

124
Q

Trauma-Induced Coagulopathy

A

Different from DIC (can happen immediately after trauma)

Initiated by tissue injury and hemorrhagic shock

Caused by platelet dysfunction, clotting factor inhibition due to hypo perfusion, dilution by fluid administration

125
Q

Treatment of Trauma-Induced Coagulopathy

A

Administration of specific ratios of blood products (PRBCs, FFP, platelets)

Administration of clotting factors and antifibrinolytic agents

126
Q

Disaster

A

Large group of people ( > 100)

Man-made and natural causes

May be predictable or foreseeable

Involves more voluntary care

First aid, field station, evacuation, designated hospital, temporary morgue

Triage field casualties with tags

Improvise from limited supplies

127
Q

Multiple Casualty

A

One to a few victims

Accidental causes

Unpredictable

Involves highly professional care

First aid, transport, emergency department, surgery, CCCU

ABCs of primary survey

Sophisticated equipment

128
Q

Agent

A

Physical item causes injury or destruction

129
Q

Primary Agent

A

Heat, wind, water

130
Q

Secondary Agent

A

Bacteria or viruses thriving as a result of the disaster

131
Q

Pre-Impact of Disaster

A

Prior to the actual occurrence

Period of earliest warning

Planning: Assess probability and risk

Mitigation: Prevent and reduce damages

132
Q

Impact of Disaster

A

From the time of onset until the threat of further destruction has passed

Enduring hardship and surviving

133
Q

Postimpact of Disaster

A

Beginning during the impact phase

Ends with the return of normal community order

Emergency (rescue and first aid)

Recovery (from emergency to recovery)

134
Q

Phases of a Community’s Reaction to a Disaster

A

Heroic –> Honeymoon –> Disillusionment –> Reconstruction

135
Q

Heroic Phase

A

Strong emotions focusing on helping people to survive

136
Q

Honeymoon Phase

A

Drawing people together in common experience

137
Q

Disillusionment Phase

A

Feelings of disappointment due to unfulfilled promises, individualization of consequences

138
Q

Reconstruction Phase

A

A reaffirmation of faith in the community during recovery

139
Q

Dimensions of a Disaster

A

Predictability (natural/manmade)

Frequency (in certain locations)

Controllability (prevent/reduce damage)

Time (speed of onset)

Scope (geographical area)

Intensity (ability to inflict damage and injury)

140
Q

Effects of Disaster on Community

A

Public service personnel are overworked

Lifelines are disrupted

Resources depleted

Public/private buildings are damaged

141
Q

Primary Prevention of Disasters

A

Safety Measures (levies, construction, storm cellars, engineering controls of high risk areas)

Drills

Evacuation plans

Emergency communication plan

Disaster supplies (CASH)

142
Q

Secondary Prevention of Disasters

A

Monitoring systems

Warning system

Elements of a disaster plan

Rescue operations

Psychological impact and response

Critical incident stress debriefing

143
Q

Elements of a Disaster Plan

A

Notification of residents

Warning

Control measures of the disaster

Logistical coordination

Evacuation

Rescue

Immediate care

Supportive care

144
Q

Levels of Response

A

Agency (NRMC)

Local (fire + police departments)

State (MO government, National Guard)

Regional (Midwest, state support)

International (Red Cross)

145
Q

Labeling System for Casualties

A

Red: Life threatening, STAT TREATMENT (chest trauma, head injury, hypoxia, shock, chest pain, big burns)

Yellow: Systemic injuries (need treatment within 45-60 minutes)

Green: Localized injuries (may wait several hours)

Black: Dead or fatally wounded

146
Q

Nursing Responsibilities in Disaster Management

A

Adapting nursing skills to recognize and meet needs resulting from a disaster

Includes C/PHN from state/local health department

Volunteers from disaster teams

American Red Cross

US Public Health Service

147
Q

Responsibilities of Agencies in Disaster Management

A

Comprehensive plan: mitigation, preparedness, response, recovery

Federal Government: supports state and local governments

FEMA: coordinating federal assistance

148
Q

Principles of Disaster Management

A
  1. Prevent disaster
  2. Minimize casualties
  3. Prevent further casualties
  4. Rescue victims
  5. Provide first aid
  6. Evacuate injured
  7. Provide medical care
  8. Promote reconstruction of lives
149
Q

Responsiveness

A

State of general awareness of oneself and the environment

Reflects functional integrity of the brain as a whole

150
Q

Specialized Neurological Assessment for Unresponsive Patient

A

Assess arousal first (stimulus, response, abnormal posturing such as decorticate/decerebrate)

Glasgow Coma Scale (eyes open, verbal response, motor response)

151
Q

Nursing Care of Unresponsive Patient

A

Maintaining ventilation and airway

Optimizing cerebral perfusion pressure (BP control, temperature control, promoting venous return)

Safe and protective environment (temperature control, side rails, pressure ulcers, VAP)

152
Q

Poisoning

A

More than 2.4 million cases reported in the US annually

Most poisoning deaths caused by drugs

75% of suicides caused by drugs

153
Q

Management of Poisoning

A

Sources: medications, plants, environmental sources, pollutants, and drugs of abuse

Entry: oral, inhalation, injection, absorption through skin

Intentional or accidental

Symptoms often mimic a disease

154
Q

Fundamentals of Poisoning Treatment

A

Emergency that requires rapid treatment

Supportive care, identification of poison, prevention of further absorption, poison removal, antidotes

155
Q

Drug Overdose Phase I

A

Assessment (history, identification of toxidromes)

156
Q

Anticholinergic Toxidromes

A

Atropine, Antihistamines, Tricyclics

Delirium

Flushed, dry skin

Dilated pupils, elevated temperature

Decreased bowel sounds, urinary retention

Tachycardia

157
Q

Cholinergic Toxidromes

A

Pesticides, Organophosphates

Excessive salivation, lacrimation, urination, diarrhea, and emesis

Diaphoresis, bronchorrhea, bradycardia

Fasciculations, CNS depression

Constricted pupils

158
Q

Opioid Toxidromes

A

Narcotics, Fentanyl

CNS depression, respiratory depression

Constricted pupils

Hypotension

Hypothermia

159
Q

Sympathomimetic Toxidromes

A

PCP, Angel Dust

Agitation

Tachycardia, hypertension

Seizures

Metabolic acidosis

160
Q

Acetaminophen Toxidromes

A

Nausea/Vomiting

Appear okay, then sudden altered mental status

161
Q

Aspirin Toxidromes

A

Nausea, vomiting

TINNITUS

Metabolic acidosis arrhythmias

Appear okay, then rapid decline

162
Q

Anticholinergic Mnemonic

A

MAD as a hatter

RED as a beet

BLIND as a bat

HOT as a hare

DRY as a bone

163
Q

Drug Overdose Phase II

A

Stabilization

ABCs

ACID-BASE AND ELECTROLYTE

Injuries and disease processes

164
Q

Drug Overdose Phase III

A

Initial decontamination

Prevent absorption

Ocular (eye irrigation)

Dermal (flushing/showering)

Inhalation

Ingestion

165
Q

Drug Overdose Phase IV

A

Advanced management

GI decontamination (lavage, absorbents, cathartics)

Enhancement of elimination (activated charcoal, whole bowel irrigation, urine alkalization, hemodialysis hyperbaric oxygenation, exchange transfusion

Antagonists

NO UNIVERSAL ANTIDOTE

Antivenin/Antitoxin

166
Q

Gastric Lavage

A

Ewald tube

Contraindications: caustic, alkali, petroleum distillates

167
Q

Absorbents

A

Activated charcoal

168
Q

Cathartics

A

Magnesium citrate

Sorbitol

169
Q

Antidote for Acetaminophen

A

Acetylcysteine (Mucomyst)

170
Q

Antidote for Anticholinergics

A

Physostigmine (Antilirium)

171
Q

Antidote for Benzodiazepines

A

Flumazenil (Romazicon)

172
Q

Antidote for Cyanide

A

Amyl nitrite

173
Q

Antidote for Ethlyne Glycol/Methanol

A

Ethanol, Fomepizole

174
Q

Antidote for Opiates

A

Naloxone (Narcan)

175
Q

Antidote for Organophosphatase Insecticides

A

Atropine

176
Q

Drug Overdose Phase V

A

Continuous monitoring

Respiratory and airway

Cardiac (BP, Pulse, and Rhythm)

Chemistry (Electrolytes, Serum Levels)

LOC

177
Q

Drug Overdose Phase VI

A

Prevention (patient/family teaching)

Rehabilitation

178
Q

Managing Blood Sugar in the Surgical CCU

A

Strict glycemic control (80-110)

Insulin drips

Reduced mortality in surgical CCU patients

High incidence of hypoglycemia

Enhanced wound healing

179
Q

Managing Blood Sugar in the Medical CCU

A

Target: 140-180

Insulin drip if BS > 180

Hourly blood sugar assessments

Titration of insulin (immediate BS and rate of change in BS)

180
Q

Hypoglycemia Assessment

A

Early: irritability, dizziness, shakiness, slurred speech

Late: vertigo, unresponsive, seizures, tachycardia, pallor, diaphoresis

Finger Stick BS

181
Q

Causes of Hypoglycemia

A

Response to insulin

Stress

Weight loss, malnutrition

Prolonged exercise

Alcohol ingestion

Fasting

Salicylates

Severe sepsis

182
Q

Treatment of Hypoglycemia

A

GLUCOSE

Oral agents if conscious

BS: 40-70 –> 25 gm Dextrose 50% slow IVP

BS: < 40 –> 50 gm Dextrose 50% slow IVP

Monitor blood sugars q15 min

Neuro and VS assessment q15 min

183
Q

Diabetic Ketoacidosis Etiologies

A

Type I DM

Acute pancreatitis

184
Q

Pathophysiology of DKA

A

Hyperglycemia

Hyperosmolality

Metabolic ketoacidosis

Dehydration–volume depletion

185
Q

Early DKA Assessment

A

Polyuria, thirst, N/V, loss of appetite, abdominal cramps, fatigue, progressive hyperventilation, tachycardia

BS > 250

Decreased pH, decreased bicarbonate

Glycosuria (BS > 180)

Anion gap > 10

186
Q

DKA Late Assessment

A

Kussmaul respirations, fruity breath odor, hypotension, dry mucous membranes, lethargy, coma, poor skin turgor

BS: 300-800

pH: < 7

Decreased bicarbonate

Anion gap > 12

INCREASED POTASSIUM, SODIUM, BUN, MAGNESIUM, PHOSPHATE

187
Q

Pathophysiology of Hyperosmolar Hyperglycemic State

A

Type II DM

Hyperglycemia

Hyperosmolality

Osmotic diuresis

Dehydration –> Hypovolemic shock

188
Q

Assessment of HHS

A

Gradual onset over 5 or more days

Increased fatigue, drowsiness

Loss of appetite

Polyuria, polydipsia

BS > 600

Increased sodium

189
Q

Comparison of DKA to HHS

A

Mean Glucose: DKA 600, HHS 1100

Serum Osmolarity: DKA 320, HHS 400

Arterial pH: DKA 7.07, HHS 7.26

Anion Gap: DKA > 12, HHS < 12

Mortality: DKA 1-15%, HHS 20-40%

190
Q

Volume Replacement Protocol for DKA and HHS

A

REHYDRATION IS VERY IMPORTANT

0.9% NS 1 L/hour

If Na > 140, 0.45% saline and 20-30 mEq KCl

If Na < 140, 0.9% NS and 20-30 mEq KCl

When BS < 200, D5/0.45% saline and 20-30 mEq KCl

191
Q

Insulin Protocol for DKA

A
  1. 1 U/kg IV bolus
  2. 1 U/kg/hour IV drip

Target of 50-70 mg/dL to decrease BS per hour

Hourly blood glucose monitoring

When BS < 200, decrease insulin to 0.02 U/kg/hour

192
Q

Insulin Protocol for HHS

A
  1. 1 U/kg IV bolus
  2. 1 U/kg/hour IV drip

Hourly blood glucose monitoring

If BS does not fall 10% in first hour, 0.14 U/kg IV bolus

When BS < 300, decrease insulin to 0.02 U/kg/hour

Maintain BS 200-300

193
Q

Reversing DKA

A

pH > 7.0: No intervention

pH < 7.0: 100 mol Bicarbonate, 400 mL water, 20 mEq KCl infused over 2 hours

Monitor pH, bicarbonate, potassium, and phosphate hourly until stable

194
Q

Reversing HHS

A

Not a likely goal

Otherwise, follow DKA protocol

195
Q

Restoring Potassium with DKA and HHS

A

Establish adequate urine function (UO > 50 mL/hour)

K < 3.8: 20-30 mEq K+/hour IV drip until K+ > 4.0

K > 5.2: Hold potassium, monitor q2h

196
Q

Restoring Phosphate with DKA and HHS

A

Establish adequate urine renal function (UO > 50 mL/hour)

Phosphate < 1.0 mg/L: add phosphate to IV

Monitor phosphate q2h

197
Q

Monitor Response to Therapies for DKA and HHS

A

Fluid volume overload (hourly CVP, UO, BP, pulse, jugular veins)

Hypoglycemia (hourly or more frequent BS)

Hypo/Hyperkalemia (hourly lab assessment)

Hyponatremia (hourly lab assessment)

Cerebral edema (hourly neuro assessment)

Risk for infection

198
Q

pH and Potassium

A

INVERSE RELATIONSHIP

199
Q

CABG

A

Artery or vein from another area used to create a detour around the blockage

Saphenous vein or mammary artery most common

200
Q

Cardiopulmonary Bypass

A

Extracorporal circuit

Carries blood to perfusion machine from vena cava and back to aorta

Requires extra fluid volume

201
Q

Cardiopulmonary Bypass Nursing Concerns

A

Intravascular fluid deficit –> hypotension

Third spacing –> edema, weight gain

Myocardial depression –> decreased CO

Coagulopathy –> bleeding

Pulmonary dysfunction, neurological dysfunction

AKI –> clamp time

202
Q

How to Care for Post-Op Open Heart Patient

A

Pre-Op education is key

Benchmark is 6 hours to extubation

Important to prepare patient and keep calm during weaning

Chest tube drainage monitoring

203
Q

Beck’s Triad for Cardiac Tamponade

A

JVD

Hypotension

Distant heart sounds

204
Q

Monitoring for Cardiac Tamponade with Chest Tube

A

Chest tube drainage monitoring is key; not too much, not too little

Hourly milking–no longer strip tubes

No more than 200 mL/hour, but ensure tubes are patent

205
Q

Caring for Patient after Extubation

A

IS is key

Sternal precautions

Ambulation

Pain control

Wound care

206
Q

Care for Organ Transplant Recipients

A

Immunosuppression

Rejection

Organ-specific complications

207
Q

Caring for Heart Patients

A

Extracorporal circuit complications

Contractility issues

Denervation problems

Bleeding/tamponade

208
Q

Caring for Lung Patients

A

Double will require bypass-pump complications

Especially susceptible to fluid overload and ALI

Bleeding, cancer, infection

Requires more immunosuppression than other organs

209
Q

Caring for Liver Patients

A

At risk for bleeding, but do not want to overcorrect

T-tube for bile drainage

Frequent monitoring of liver enzymes

Fluid shifts may occur

May have swings in blood sugar due to steroid immunosuppression and graft function

210
Q

Caring for Kidney Patients

A

Monitor fluid-volume status every hour; replace 1:1

Output monitoring is essential

Irrigate catheter to get rid of clots

211
Q

Caring for Pancreas Patients

A

Monitor glucose and urine amylase

212
Q

Hematopoietic Stem Cell Transplant

A

Used to treat myeloma, lymphoma, AML, ALL, aplastic anemia

Autogenic vs. Allogenic

213
Q

Graft vs. Host Disease

A

Seen in stem cell transplants

New immune system attacks body as foreign

Attacks liver, skin, gut

Use prophylactic immunosuppression

Will need TPN and IV medications

214
Q

Hyperacute Rejection

A

Occurs within minutes to hours

Result of presensitized antibodies

Graft failure/removal common

Life-threatening, high mortality, hemodynamic shock, collapse

215
Q

Acute Rejection

A

Occurs between week 1 to 3 months

SIRS

Responds to steroids and higher immunosuppression

Cell-mediated; most patients experience at least once

216
Q

Chronic Rejection

A

Gradual deterioration

B and T cell mediation

Not responsive to steroids

May need another transplant

217
Q

Signs of Heart Rejection

A

Asymptomatic

Need a biopsy

218
Q

Signs of Lung Rejection

A

Distinguish from pulmonary infection or reperfusion injury

219
Q

Signs of Pancreas Rejection

A

Hyperglycemia

Urine amylase

220
Q

Signs of Liver Rejection

A

Elevated liver enzymes and total bilirubin

221
Q

Signs of Kidney Rejection

A

Increased serum BUN, creatinine

Decreased urine output

Weight gain, edema, hypertension

222
Q

Immunosuppression

A

Must be started right after surgery, then lifelong commitment

Multidrug regimen

Need to prevent rejection and treat autoimmune diseases

Toxicity, neoplasms

Side effects include hirsutism, moon face

223
Q

Calcineuron Inhibitors

A

Tacrolimus, Cyclosporin

Nephrotoxicity common

Sharp increase in BUN and creatinine

Avoid NSAIDs

224
Q

Glucocorticoids

A

In combination: thin skin, GI tract, glucose issues

225
Q

Cytotoxic Agents

A

Methotrexate, Remicaid, Mycophenalate

226
Q

Antibodies

A

Rabbit antithymocyte given once in OR, once post-op in kidneys

Blocks activation of T-Cells

227
Q

Prevention of Post-Op Infection

A

Meticulous wound care

CLABSI and CAUTI bundles

IS

Mobility

Nutrition

Hand hygiene, oral care

Pharmacological prophylaxis

228
Q

Brain Surgeries

A

Craniotomy, Brain Hemorrhage Evacuation, Tumor/Abscess Removal

Relieve pressure to maintain brain perfusion

229
Q

Traumatic Brain Injury

A

Battles Sign (bruising behind ears)

Raccoon Eyes

Coup/Contra-Coup

230
Q

Epidural Hematoma

A

Skull fracture with ARTERIAL rupture

Lucid interval followed by a rapid increase in ICP

231
Q

Subdural Space Hematoma

A

Rupture of VENOUS sinuses or small bridging veins due to torsion forces

Acute presentation with a rapid increase in ICP

Chronic presentation with personality change, memory loss/confusion, particularly in the elderly

232
Q

Subarachnoid Space Hematoma

A

ARTERIAL RUPTURE

Meningeal irritation with a rapid increase in ICP

233
Q

Cerebral Hemisphere Hematoma

A

CORTICAL CONTUSIONS

Rupture of small intrinsic vessels with intracerebral hematoma

Increased ICP with focal deficits; usually fatal

Profound coma

234
Q

Post-Op Craniotomy

A

Frequent neuro checks (q15, then q30, then q1h)

Frequent vitals

Urine output, drain output

235
Q

Decorticate Posturing

A

Flexion

“Toward the core”

236
Q

Decerebrate Posturing

A

Away from the core

WORSE

237
Q

ICP Monitoring

A

Catheter inserted into brain to monitor pressure

Monroe-Kellie Hypothesis: 80% brain, 10% blood, 10% CSF

Cerebral Perfusion Pressure = MAP - ICP

238
Q

Intercranial Hypertension Prevention/Treatment

A

HOB > 30

Decreased stimulation

Mannitol or 3% NS

Hyperventilation, Hyperthermia

239
Q

Cushing’s Triad

A

Bradycardia

Extreme HTN

Respiratory issues (apnea)

240
Q

Brain Death

A

Notify donor as GCS falls

Oculocephalic reflex test (doll’s eyes)

Oculovestibular reflex test (cold calorics)

Apnea test

Do not withdraw any care until donor has been notified

241
Q

Diabetes Insipidus

A

Central or neurogenic causes

Brain damage to hypothalamus or pituitary gland

Absence of ADH production

Urine output > 250

Spec Grav 1.000-1.005

Polyuria, polydipsia

Hyperosmolar serum

Hypernatremia

Critical Care (3 decks)

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